VATTACHARYYA

WARNING

2007-06-29T23:38:00.000-07:00

WARNING

THIS SITE IS MEANT FOR EDUCATIONAL PURPOSES ONLY. THIS IS MEANT TO BE FRANK DISCUSSION OF HUMAN REPRODUCTIVE HEALTH WITH SPECIAL PAPERS ON ADOLESCENT REPRODUCTIVE HEALTH AND WALEFARE.

THE PAGES CONTAINS PHOTOS, DIAGRAMS AND SKETCHES OF HUMAN SEXUAL ORGANS, AND ANATOMY AND PHYSIOLOGY INCLUDING CHEMISTRY OF IT. SO SOME ARTICLES ARE NOT SUITABLE FOR BOYS / GIRLS UNDER 12 YRS OF AGE.

SOME MAY FIND IT OFFENSIVE.
SO I SUGGEST THE PARENTS TO GO THROUGH THE LABELES FIRST AND DECIDE ON ITS DEGREE AND GUIDE THEIR WARDS ACORDINGLY.

AND IF YOU ARE NOT 18

PARENTAL SUPERVISION IS ADVISED.

IF YOU DO NOT WISH TO CONTINUE PLEASE QUIT THE SITE AND GO BACK NOW.

SEXUAL HEALTH.......PART 3

2007-06-27T22:23:00.000-07:00

SEXUAL HEALTH………PART 3

Menstruation (a period) is a major stage of puberty in girls; it's one of the many physical signs that a girl is turning into a woman. And like a lot of the other changes associated with puberty, menstruation can be confusing. Some girls can't wait to start their periods, whereas others may feel afraid or anxious. Many girls (and guys!) don't have a complete understanding of a woman's reproductive system or what actually happens during the menstrual cycle, making the process seem even more mysterious.

Puberty and Periods

When girls begin to go through puberty (usually starting between the ages of 8 and 13), their bodies and minds change in many ways. The hormones in their bodies stimulate new physical development, such as growth and breast development. About 2 to 2½ years after a girl's breasts begin to develop, she usually gets her first menstrual period.
About 6 months or so before getting her first period, a girl might notice an increased amount of clear vaginal discharge. This discharge is common. There's no need for a girl to worry about discharge unless it has a strong odor or causes itchiness.
The start of periods is known as menarche. Menarche doesn't happen until all the parts of a girl's reproductive system have matured and are working together.
Baby girls are born with ovaries, fallopian tubes, and a uterus. The two ovaries are oval-shaped and sit on either side of the uterus (womb) in the lowest part of the abdomen called the pelvis. They contain thousands of eggs, or ova. The two fallopian tubes are long and thin. Each fallopian tube stretches from an ovary to the uterus, a pear-shaped organ that sits in the middle of the pelvis. The muscles in a female's uterus are powerful and are able to expand to allow the uterus to accommodate a growing fetus and then help push the baby out during labor.
As a girl matures and enters puberty, the pituitary gland releases hormones that stimulate the ovaries to produce other hormones called estrogen and progesterone. These hormones have many effects on a girl's body, including physical maturation, growth, and emotions.
About once a month, a tiny egg leaves one of the ovaries — a process called ovulation — and travels down one of the fallopian tubes toward the uterus. In the days before ovulation, the hormone estrogen stimulates the uterus to build up its lining with extra blood and tissue, making the walls of the uterus thick and cushioned. This happens to prepare the uterus for pregnancy: If the egg is fertilized by a sperm cell, it travels to the uterus and attaches to the cushiony wall of the uterus, where it slowly develops into a baby.

If the egg isn't fertilized, though — which is the case during most of a woman's monthly cycles — it doesn't attach to the wall of the uterus. When this happens, the uterus sheds the extra tissue lining. The blood, tissue, and unfertilized egg leave the uterus, going through the vagina on the way out of the body. This is a menstrual period. This cycle happens almost every month for several more decades (except, of course, when a female is pregnant) until a woman reaches menopause and no longer releases eggs from her ovaries.

Just as some girls begin puberty earlier or later than others, the same applies to periods. Some girls may start menstruating as early as age 10, but others may not get their first period until they are 15 years old.
The amount of time between a girl's periods is called her menstrual cycle (the cycle is counted from the start of one period to the start of the next). Some girls will find that their menstrual cycle lasts 28 days, whereas others might have a 24-day cycle, a 30-day cycle, or even longer. Following menarche, menstrual cycles last 21–45 days. After a couple of years, cycles shorten to an adult length of 21–34 days.
Irregular periods are common in girls who are just beginning to menstruate. It may take the body a while to sort out all the changes going on, so a girl may have a 28-day cycle for 2 months, then miss a month, for example. Usually, after a year or two, the menstrual cycle will become more regular. Some women continue to have irregular periods into adulthood, though.
As a girl gets older and her periods settle down — or she gets more used to her own unique cycle — she will probably find that she can predict when her period will come. In the meantime, it's a good idea to keep track of your menstrual cycle with a calendar.
The amount of time that a girl has her period also can vary. Some girls have periods that last just 2 or 3 days. Other girls may have periods that last 7 days or longer. The menstrual flow — meaning how much blood comes out of the vagina — can vary widely from girl to girl, too.
Some girls may be concerned that they're losing too much blood. It can be a shock to see all that blood, but it's unlikely that a girl will lose too much, unless she has a medical condition like von Willebrand disease. Though it may look like a lot, the average amount of blood is only about 2 tablespoons (30 milliliters) for an entire period. Most teens will change pads 3 to 6 times a day, with more frequent changes when their period is heaviest, usually at the start of the period.

Especially when menstrual periods are new, you may be worried about your blood flow or whether your period is normal in other ways. Talk to a doctor or nurse if:
your period lasts longer than a week
you have to change your pad very often (soaking more than one pad every 1–2 hours)
you go longer than 3 months between periods
you have bleeding in between periods
you have an unusual amount of pain before or during your period
your periods were regular then became irregular
Cramps, PMS, and Pimples

Some girls may notice physical or emotional changes around the time of their periods. Menstrual cramps are pretty common — in fact, more than half of all women who menstruate say they have cramps during the first few days of their periods. Doctors think that cramps are caused by prostaglandin, a chemical that causes the muscles of the uterus to contract.
Depending on the girl, menstrual cramps can be dull and achy or sharp and intense, and they can sometimes be felt in the back as well as the abdomen. These cramps often become less uncomfortable and sometimes even disappear completely as a girl gets older.
Many girls and women find that over-the-counter pain medications (like acetaminophen or ibuprofen) can relieve cramps, as can taking a warm bath or applying a warm heating pad to the lower abdomen. Exercising regularly throughout the monthly cycle may help lessen cramps, too. If these things don't help, ask your doctor for advice.
Some girls and women find that they feel sad or easily irritated during the few days or week before their periods. Others may get angry more quickly than normal or cry more than usual. Some girls crave certain foods. These types of emotional changes may be the result of premenstrual syndrome (PMS).

PMS is related to changes in the body's hormones. As hormone levels rise and fall during a woman's menstrual cycle, they can affect the way she feels, both emotionally and physically. Some girls, in addition to feeling more intense emotions than they usually do, notice physical changes along with their periods — some feel bloated or puffy because of water retention, others notice swollen and sore breasts, and some get headaches.
PMS usually goes away soon after a period begins, but it can come back month after month. Eating right, getting enough sleep, and exercising may help relieve some of the symptoms of PMS. Talk to your doctor if you are concerned about your premenstrual symptoms.
It's also not uncommon for girls to have an acne flare-up during certain times of their cycle; again, this is due to hormones. Fortunately, the pimples associated with periods tend to become less of a problem as girls get older.
Pads, Tampons, and Liners
Once you begin menstruating, you'll need to use something to absorb the blood. Most girls use a pad or a tampon. But some use menstrual cups, which a girl inserts into her vagina to catch and hold the blood (instead of absorbing it, like a tampon).
There are so many products out there that it may take some experimenting before you find the one that works best for you. Some girls use only pads (particularly when they first start menstruating), some use only tampons, and some switch around — tampons during the day and pads at night, for example.
Girls who worry about leakage from a tampon often use a pantiliner, too, and some girls use liners alone on very light days of their periods.
Periods shouldn't get in the way of exercising, having fun, and enjoying life. Girls who are very active, particularly those who enjoy swimming, often find that tampons are the best option during sports.

If you have questions about pads, tampons, or coping with periods, ask a parent, health teacher, school nurse, or older sister.

Some girls worry that if they use tampons, they will no longer be virgins. The truth is, a virgin is someone who has never had sexual intercourse. Inserting a tampon is definitely not the same as having sex!
So why do girls ask this question so often? Girls who are virgins usually have a hymen, a very thin piece of skin-like tissue that stretches partly across the opening of the vagina. A lot of people mistakenly think that a girl is still a virgin if her hymen has not been broken. Most of the time a girl's hymen breaks after having sex for the first time.
But a girl's hymen can tear in ways that have nothing to do with having sex. For example, it is possible that inserting a tampon might tear the hymen (although that usually doesn't happen). So even if a tampon does break a girl's hymen, she is still a virgin until she has had sexual intercourse.

Normal vaginal discharge has several purposes: cleaning and moistening the vagina and helping to prevent and fight infections. Although it's normal for the color, texture, and amount of vaginal fluids to vary throughout a girl's menstrual cycle, some changes in discharge may indicate a problem.
If you think you may have a problem, you should see a doctor as soon as possible. First, though, it helps to learn some of the differences between normal and abnormal vaginal discharge. This will help you to recognize changes that may occur.
Normal vaginal fluids can vary somewhat in texture and color. They can be somewhat thin, sticky, and elastic or thick and gooey. Vaginal fluids should be clear, white, or off-white in color.
It's important to keep an eye out for changes in vaginal fluids. The following changes may indicate a problem:
change in odor (especially an unpleasant odor)
change in color or texture (especially greenish, grayish, or anything looking like pus)
vaginal itching, burning, swelling, or redness
change in color that is caused by vaginal bleeding or spotting that is not a menstrual period
Vaginal infections, such as bacterial vaginosis, candidiasis (yeast infection), and trichomoniasis are common causes of abnormal vaginal discharge. Some infections are transmitted by having sex, such as gonorrhea. Other infections can occur with or without having sex, such as bacterial vaginosis or yeast infection.

Although the symptoms of these infections can be very similar, there are some differences to look for:
Yeast infections may cause your discharge to become very white and thick, resembling cottage cheese. A yeast infection usually does not cause a strong odor, but it may cause severe itching and burning.
Bacterial vaginosis (BV) may cause your discharge to be heavier than usual. The fluids may become foamy or frothy and grayish in color. BV often causes vaginal fluids to have an unpleasant, fishy odor.
Trichomoniasis, a common sexually transmitted disease (STD), may cause a musty, stale odor. Discharge may become grayish or yellow-green and may become thicker. Trichomoniasis also often causes vaginal itching and pain during urination.
It's very important to see a doctor or go to a teen clinic if you have any of the symptoms of abnormal vaginal discharge. This is really important for girls who have had sex, especially those who have had sex without using a condom. Many STDs cause changes in vaginal discharge or cause other infections that affect discharge as well.

The examination girls need:

Your mom just made an appointment for your first gynecologic exam and you're feeling:
Totally panicked. You start praying for an avalanche, four flat tires on the car, anything to avoid that appointment.
Pretty calm. You don't really mind going to the doctor that much, and if your friends can handle it, so can you.
Confused. You don't feel sick at all, and you just had some vaccinations for school and a physical for sports. Why waste time going to a doctor when you're OK?
These are just some of the feelings that girls may have before their first gynecologic (or "gyn") exam, and it's not surprising. You might be asking yourself "Why me? Why now?" The answer is that you're older and have gone through puberty, so you need to have a physical exam appropriate for a young woman. That's where breast and pelvic exams come in.

Why You Need These Exams
The American College of Obstetricians and Gynecologists recommends that a girl make her first visit to a gynecologist when she is between the ages of 13 and 15. Not all girls will need a pelvic exam during this initial visit, though. Many gynecologists will just do a regular health exam and talk to the girl about her development.
Yearly gyn visits are important for a number of reasons, including:
as a routine check. You'll want to be sure you're developing normally.
to prevent pregnancy or infection. If you have ever had sex, you are probably going to need a pelvic exam. Girls should have a pelvic exam before having sex to discuss methods of birth control and preventing sexually transmitted diseases (STDs).
to deal with a problem. There may be a number of concerns that lead to a pelvic exam. For example, if you have problems with your periods, missed periods, pain, signs of infection, and worries about development, it's a good idea to see a doctor.
If you're going to be involved in deciding who you'll see for your pelvic exam, you have a few choices. Many family doctors and pediatricians perform pelvic and breast exams and advise teens on birth control and STD prevention. So you may be able to see a doctor you already know and feel comfortable with for your first pelvic exam.

Also, a number of different kinds of doctors and nurses have special training in women's reproductive health:
Gynecologists are doctors who have been specially trained in women's health issues. Gynecologists are one of the doctors who can prescribe birth control and teach patients how to use it.
Adolescent medicine doctors have been trained in the health and management of teen issues. They are familiar with the concerns most young women have about their reproductive systems and can advise them on birth control and STD prevention.
Nurse practitioners have had advanced training that allows them to give gynecological exams and pay special attention to women's reproductive health.

Whether you want to see a male or female health care professional is up to you. Some women say that they prefer being examined by a female doctor or nurse because it puts them more at ease and they feel like they can talk more openly about women's health problems and sexuality issues. Other women feel comfortable being examined by a male doctor or nurse. If the doctor or nurse is male, he will usually have a female assistant in the room with him during all parts of the exam.
It's best to involve your parents in your health care. If you want to go to a doctor's office for your exam, you may need to involve an adult for insurance purposes (it may be expensive otherwise).
If for some reason you can't involve your parents, you can take advantage of health clinics like Planned Parenthood or your local teen clinic. These clinics have fully trained staff who often can care for you at a lower cost and respect your need for confidentiality. Each state has different guidelines on which medical issues teens can get confidential care for. Your doctor should be able to explain these issues to you.
The most important thing is that you feel comfortable with the person who is examining you. You want to be able to talk with him or her about important personal health and relationship issues, including birth control.

What Happens When You Go for Your Pelvic Exam

You don't need to do anything special before going for your exam. When you make the appointment, try to schedule the exam for a time when you won't have your period. For many young women, that can be hard to predict, though — lots of girls have irregular periods at first. Ask the doctor's office or clinic when you make the appointment what you should do if you get your period. Some doctors say it's OK to come for an exam if your period is just beginning or just ending and it's very light, but everyone has a different policy.
When you arrive for your appointment, you may be asked to fill out some forms while you wait. These forms ask questions about any illnesses or conditions you have, your health habits (like whether you drink or smoke), any family illnesses that you know of, and your history regarding sexual activity, pregnancy, and birth control. You might also be asked for the date of your last period (or a doctor or nurse will ask during your exam).

When you first go into the exam room, a nurse or medical assistant will do a few things that your doctor has probably done a million times before, such as recording your weight and taking your blood pressure. You'll then be left alone to change out of your clothes. It may feel weird taking off even your underwear because you may not have had to undress completely for a medical exam before. The nurse or medical assistant will leave you a paper sheet or gown — or maybe both — to cover you. If you're cold, most doctors and nurses won't mind if you keep your socks on.
After a few minutes, the doctor (or nurse practitioner, if that is who you choose to see) will knock on the door to make sure you're in your gown. If you're ready, he or she will come in and start the exam. The doctor may start by going over anything you wrote down on your forms, or you may talk about these things later.
If this is your first gynecologic exam, let the doctor know. That way, he or she will know to go slowly and explain everything that's going on. Now is also the time to ask about birth control or sexuality if you need to. Some doctors like to discuss these things before the exam, and some like to do it after. Your aim is to make sure you get your questions answered.

The Breast Exam
During the physical part of the gynecologic exam, you'll be asked to lie on your back on the table. You'll have the paper sheet or gown covering you, and the doctor will only uncover the parts of your body being examined.
The doctor will give you a breast exam by lightly pressing on different parts of your breasts. After finishing, he or she may show you how to examine your own breasts. This helps you become familiar with how your breasts feel so you know which lumps are normal and which may be the result of a change.

The Pelvic Exam

During the pelvic part of the exam, the doctor or nurse practitioner will ask you to move down so your behind is at the end of the table. You'll bend your knees and rest your feet in two stirrups, which are metal triangular loops that stick out from the end of the table. These might look a little scary, but they're just there to rest your feet in and keep you more comfortable. The doctor will ask you to relax your knees out to the sides as far as they will go. It might feel a little funny to be lying with your legs opened like this, but everyone feels that way at first.
The doctor will put on gloves and examine the outside of your vagina to make sure that there are no sores or swelling and that everything looks OK on the outside.
Next, the doctor will want to look at the inside of your vagina and will do so with the help of a speculum (pronounced: speh-kyuh-lum). A speculum is a thin piece of plastic or metal with a hinged piece on one end that allows it to open and close. The doctor or nurse will warm the speculum with water (some offices keep the speculum warmed in a drawer with a heating pad). The doctor or nurse will then slide the speculum into your vagina. Usually the doctor will tell you when he or she is about to place the speculum inside you so it doesn't come as a surprise.
Once the speculum is in the vagina, it can be opened to allow the doctor to see inside. Putting in and opening the speculum should not be painful, although some women say that it can cause a bit of pressure and discomfort. Naturally, if this is your first exam, you might feel a little tense. Because the vagina is surrounded by muscles that can contract or relax, the exam can be more comfortable if you try to stay calm and relax the muscles in that area.
If you feel like you're tensing up the muscles in your vagina, try breathing deeply or doing some breathing exercises to help you stay relaxed. Sometimes humming your favorite song or making small talk can distract you and allow you to feel more relaxed.
After the speculum is in place, the doctor will shine a light inside the vagina to look for anything unusual, like redness, swelling, discharge, or sores. He or she may then do a Pap smear, which involves touching the cervix to pick up cells from that area.
The cervix is the opening to the uterus, and it's located at the very top of the vagina. The Pap smear should not hurt, but it might be uncomfortable, especially if this is your first pelvic exam. The good news is this part of the exam is over quickly.
The cells that have been collected are sent to a laboratory where they are studied for any abnormal cells, which might indicate infection or warning signs of cervical cancer. (Like breast cancer, cervical cancer is very unusual in teen girls.)
If you have had sex, the doctor or nurse practitioner may test for STDs. He or she will swab the inside of the cervix with what looks like a cotton swab. The speculum is then slid out of the vagina. As with the Pap smear, the sample is sent out to a laboratory where it is tested for various STDs.
Talk to your doctor or a nurse about how you want to be contacted with results, and what they should do if they are unable to reach you. Again, doctors and nurses will do their best to maintain confidentiality, but they need to be able to reach you.

Because the ovaries and uterus are so far inside a girl's body that they can't be seen at all, even with the speculum, the doctor will need to feel them to be sure they're healthy. While your feet are still in the stirrups, and after the speculum is removed from the vagina, the doctor will put lubricant on two fingers (while still wearing the gloves) and slide them inside your vagina. Using the other hand, he or she will press on the outside of your lower abdomen (the area between your vagina and your stomach). With two hands, one on the outside and one on the inside, the doctor can make sure that the ovaries and uterus are the right size and free of cysts or other growths.
During this part of the exam, you may feel a little pressure or discomfort. Again, it's important to relax your muscles and take slow, deep breaths if you feel nervous.

At this point, the physical part of the exam is usually over. Your own doctor may do the exam in a different order, but it will probably include all these steps.

After the Exam:

Although reading this article may make it seem long, the entire pelvic exam (the parts involving your vagina, cervix, uterus, and ovaries) really only takes about 3 to 5 minutes.
Afterward, you'll be left alone to get dressed. Some women say that they bleed a tiny bit from the Pap smear after the exam, so they like to put a pantiliner in their underwear as they get dressed. If you bleed a tiny bit, it's no big deal — it's nothing like a period and it won't last.
If you haven't discussed your questions before the exam, now's the time. Don't be afraid of questions that sound stupid or silly — no question about your body is stupid, and this is the best time to get answers.
The Pap smear is almost always normal in teen girls. But if for any reason the doctor or nurse practitioner needs to see you again, the office or clinic will let you know. Unless you notice any health problems, you won't need to go for an exam for another 6 months to a year.
It's very important to go for pelvic exams on a yearly basis — even when you're feeling good — because they help detect any problems early on. If you don't want to return for another exam because you didn't like the doctor or nurse practitioner, look into finding a new doctor or clinic.
And if the physical discomfort of the exam left you not wanting another, remember that each time it gets easier and easier to relax. Naturally, no one loves getting an exam, but having a doctor or nurse practitioner you trust can really help.

Making breasts bigger:
Although many products (from special creams to exercise techniques) claim to boost breast size, you should save your money: They don't work. The truth is that the only way to permanently change breast size is cosmetic surgery.
Most doctors won't perform breast enlargement surgery until a girl reaches 18 because the body takes time to develop and some girls develop (and have changes in the size of their breasts) later than others. Even after 18 there are certain physical and psychological risks involved with breast implants.
Everyone goes through times when they don't like parts of their bodies. These feelings are part of normal development and the process of adjusting to our changing bodies. Even girls with large breasts can be unhappy about them. Some find that their backs or shoulders hurt or that the large breasts attract unwanted attention and they may wish their breasts were smaller.
If you're unhappy with the size or development of your breasts, talk to your doctor or gynecologist, who can probably reassure you that you're developing normally.

Can a girl get pregnant if she has sex during her period?
A lot of people think that if a girl has sex during her period, she can't get pregnant. But it is possible for a girl to get pregnant while she is bleeding. This can happen for a couple of reasons:
Not all vaginal bleeding is the result of a menstrual period. Sometimes a girl will have a small amount of vaginal bleeding at the time of ovulation — the time when she is most fertile. During ovulation, an egg is released from one of the ovaries and travels down a fallopian tube to the uterus. It's common for girls who are ovulating to have some vaginal bleeding that can be mistaken for a period.
Sometimes ovulation can occur before the bleeding from a girl's period has stopped, or it may occur within a few days after her period is over. Sperm can fertilize an egg for several days after ejaculation. So in both cases, having sex before the period is finished can result in pregnancy.
Having unprotected sex at any time is very risky. Along with the chance of becoming pregnant, there is also the risk of getting a sexually transmitted disease (STD), such as chlamydia, genital warts, or HIV. The only surefire way to prevent pregnancy and STDs is abstinence. If you do have sex, use a condom every time to protect against STDs. And talk to your doctor about additional forms of contraception.

SEXUAL HEALTH FOR ADOLESCENT.....PART 2

2007-06-25T22:56:00.000-07:00

SEXUAL HEALTH…….PART 2

OK, so it's a funny word . . . but what is puberty, anyway?
Puberty is the name for when your body begins to develop and change. During puberty, your body will grow faster than any other time in your life, except for when you were an infant. Back then, your body was growing rapidly and you were learning new things — you'll be doing these things and much more during puberty. Except this time, you won't have diapers or a rattle and you'll have to dress yourself!
It's good to know about the changes that come along with puberty before they happen, and it's really important to remember that everybody goes through it. No matter where you live, whether you're a guy or a girl, or whether you like hip-hop or country music, you will experience the changes that occur during puberty. No two people are exactly alike. But one thing all adults have in common is they made it through puberty.

When your body reaches a certain age, your brain releases a special hormone that starts the changes of puberty. It's called gonadotropin-releasing hormone, or GnRH for short. When GnRH reaches the pituitary gland (a pea-shaped gland that sits just under the brain), this gland releases into the bloodstream two more puberty hormones: luteinizing hormone (LH for short) and follicle-stimulating hormone (FSH for short). Guys and girls have both of these hormones in their bodies. And depending on whether you're a guy or a girl, these hormones go to work on different parts of the body.

For guys, these hormones travel through the blood and give the testes the signal to begin the production of testosterone and sperm. Testosterone is the hormone that causes most of the changes in a guy's body during puberty. Sperm cells must be produced for men to reproduce.

In girls, FSH and LH target the ovaries, which contain eggs that have been there since birth. The hormones stimulate the ovaries to begin producing another hormone called estrogen. Estrogen, along with FSH and LH, causes a girl's body to mature and prepares her for pregnancy.

So that's what's really happening during puberty — it's all these new chemicals moving around inside your body, turning you from a teen into an adult with adult levels of hormones.

Puberty usually starts some time between age 8 and 13 in girls and 10 and 15 in guys. Some people start puberty a bit earlier or later, though. Each person is a little different, so everyone starts and goes through puberty on his or her body's own schedule. This is one of the reasons why some of your friends might still look like kids, whereas others look more like adults.

"Spurt" is the word used to describe a short burst of activity, something that happens in a hurry. And a growth spurt is just that: Your body is growing, and it's happening really fast! When you enter puberty, it might seem like your sleeves are always getting shorter and your pants always look like you're ready for a flood — that's because you're experiencing a major growth spurt. It lasts for about 2 to 3 years. When that growth spurt is at its peak, some people grow 4 or more inches in a year.
This growth during puberty will be the last time your body grows taller. After that, you will be at your adult height. But your height isn't the only thing that will be changing.

As your body grows taller, it will change in other ways, too. You will gain weight, and as your body becomes heavier, you'll start to notice changes in its overall shape. Guys' shoulders will grow wider, and their bodies will become more muscular. Their voices will become deeper. For some guys, the breasts may grow a bit, but for most of them this growth goes away by the end of puberty.

Guys will notice other changes, too, like the lengthening and widening of the penis and the enlargement of the testes. All of these changes mean that their bodies are developing as expected during puberty.

Girls' bodies usually become curvier. They gain weight on their hips, and their breasts develop, starting with just a little swelling under the nipple. Sometimes one breast might develop more quickly than the other, but most of the time they soon even out. With all this growing and developing going on, girls will notice an increase in body fat and occasional soreness under the nipples as the breasts start to enlarge — and that's normal.

Gaining some weight is part of developing into a woman, and it's unhealthy for girls to go on a diet to try to stop this normal weight gain. If you ever have questions or concerns about your weight, talk it over with your doctor.
Usually about 2 to 2 1/2 years after girls' breasts start to develop, they get their first menstrual period. This is one more thing that lets a girl know puberty is progressing and the puberty hormones have been doing their job. Girls have two ovaries, and each ovary holds thousands of eggs. During the menstrual cycle, one of the eggs comes out of an ovary and begins a trip through the fallopian tube, ending up in the uterus (the uterus is also called the womb).
Before the egg is released from the ovary, the uterus has been building up its lining with extra blood and tissue. If the egg is fertilized by a sperm cell, it stays in the uterus and grows into a baby, using that extra blood and tissue to keep it healthy and protected as it's developing.
Most of the time, though, the egg is only passing through. When the egg doesn't get fertilized, the uterus no longer needs the extra blood and tissue, so it leaves the body through the vagina as a menstrual period. A period usually lasts from 5 to 7 days, and about 2 weeks after the start of the period a new egg is released, which marks the middle of each cycle.

Hair, Hair, Everywhere:

Well, maybe not everywhere. But one of the first signs of puberty is hair growing where it didn't grow before. Guys and girls both begin to grow hair under their arms and in their pubic areas (on and around the genitals). It starts out looking light and sparse. Then as you go through puberty, it becomes longer, thicker, heavier, and darker. Eventually, guys also start to grow hair on their faces.

Another thing that comes with puberty is acne, or pimples. Acne is triggered by puberty hormones. Pimples usually start around the beginning of puberty and can stick around during adolescence (the teen years). You may notice pimples on your face, your upper back, or your upper chest. It helps to keep your skin clean, and your doctor will be able to offer some suggestions for clearing up acne. The good news about acne is that it usually gets better or disappears by the end of adolescence.
A lot of teens notice that they have a new smell under their arms and elsewhere on their bodies when they enter puberty, and it's not a pretty one. That smell is body odor, and everyone gets it. As you enter puberty, the puberty hormones affect glands in your skin, and the glands make chemicals that smell bad. These chemicals put the scent in adolescent!
So what can you do to feel less stinky? Well, keeping clean is a good way to lessen the smell. You might want to take a shower every day, either in the morning before school, or the night before. Using deodorant (or deodorant with antiperspirant) every day can help keep body odor in check, too.

Guys and girls will also notice other body changes as they enter puberty, and they're all normal changes. Girls might see and feel a white, mucous-like discharge from the vagina. This doesn't mean anything is wrong — it is just another sign of your changing body and hormones.
Guys will begin to get erections (this is when the penis fills with blood and becomes hard) sometimes. Erections happen when guys fantasize and think about sexual things or sometimes for no reason at all. They may experience something called nocturnal emissions (or wet dreams). This is when the penis becomes erect while a guy is sleeping, and he ejaculates. When a guy ejaculates, semen comes out of the penis — semen is a fluid that contains sperm. That's why they're called wet dreams — they happen when you're sleeping and your underwear or the bed might be a little wet when you wake up. Wet dreams become less frequent as guys progress through puberty, and they eventually stop. Guys will also notice that their voices may "crack" and eventually get deeper.
Change Can Feel Kind of Strange
Just as those hormones create changes in the way your body looks on the outside, they also create changes on the inside. While your body is adjusting to all the new hormones, so is your mind. During puberty, you might feel confused or have strong emotions that you've never experienced before. You may feel anxious about how your changing body looks.
You might feel overly sensitive or become easily upset. Some teens lose their tempers more than usual and get angry at their friends or families.
Sometimes it can be difficult to deal with all of these new emotions. Usually people aren't trying to hurt your feelings or upset you on purpose. It might not be your family or friends making you angry — it might be your new "puberty brain" trying to adjust. And while the adjustment can feel difficult in the beginning, it will gradually become easier. It can help to talk to someone and share the burden of how you're feeling — a friend or, even better, a parent, older sibling, or adult who's gone through it all before.
You might have new, confusing feelings about sex — and lot of questions. The adult hormones estrogen and testosterone are signals that your body is giving you new responsibilities, like the ability to create a child. That's why it's important to get all your questions answered.
It's easy to feel embarrassed or anxious when talking about sex, but you need to be sure you have all the right information. Some teens can talk to their parents about sex and get all their questions answered. But if you feel funny talking to your parents about sex, there are many other people to talk to, like your doctor, a school nurse, a teacher, a school counselor, or another adult you feel comfortable talking with.

Developing Differently:

People are all a little different from one another, so it makes sense that they don't all develop in the same way. No two people are at exactly the same stage as they go through puberty, and everyone changes at his or her own pace. Some of your friends may be getting curves, whereas you don't have any yet. Maybe your best friend's voice has changed, and you think you still sound like a kid with a high, squeaky voice. Or maybe you're sick of being the tallest girl in your class or the only boy who has to shave.

But eventually everyone catches up, and the differences between you and your friends will even out. It's also good to keep in mind that there is no right or wrong way to look. That's what makes us human — we all have qualities that make us unique, on the inside and the outside.

What Is the Male Reproductive System?

Most species have two sexes: male and female. Each sex has its own unique reproductive system. They are different in shape and structure, but both are specifically designed to produce, nourish, and transport either the egg or sperm.

Unlike the female, whose sex organs are located entirely within the pelvis, the male has reproductive organs, or genitals (pronounced: jeh-nuh-tulz), that are both inside and outside the pelvis. The male genitals include:
the testicles
the duct system, which is made up of the epididymis and the vas deferens
the accessory glands, which include the seminal vesicles and prostate gland
the penis

In a guy who's reached sexual maturity, the two testicles (pronounced: tes-tih-kulz), or testes (pronounced: tes-teez), produce and store millions of tiny sperm cells. The testicles are oval-shaped and grow to be about 2 inches (5 centimeters) in length and 1 inch (3 centimeters) in diameter. The testicles are also part of the endocrine system because they produce hormones, including testosterone (pronounced: teh-stass-tuh-rone). Testosterone is a major part of puberty in guys, and as a guy makes his way through puberty, his testicles produce more and more of it. Testosterone is the hormone that causes guys to develop deeper voices, bigger muscles, and body and facial hair, and it also stimulates the production of sperm.
Alongside the testicles are the epididymis (pronounced: eh-puh-dih-duh-mus) and the vas deferens (pronounced: vass de-fuh-runz), which make up the duct system of the male reproductive organs. The vas deferens is a muscular tube that passes upward alongside the testicles and transports the sperm-containing fluid called semen (pronounced: see-mun). The epididymis is a set of coiled tubes (one for each testicle) that connects to the vas deferens.
The epididymis and the testicles hang in a pouch-like structure outside the pelvis called the scrotum. This bag of skin helps to regulate the temperature of testicles, which need to be kept cooler than body temperature to produce sperm. The scrotum changes size to maintain the right temperature. When the body is cold, the scrotum shrinks and becomes tighter to hold in body heat. When it's warm, the scrotum becomes larger and more floppy to get rid of extra heat. This happens without a guy ever having to think about it. The brain and the nervous system give the scrotum the cue to change size.
The accessory glands, including the seminal vesicles and the prostate gland, provide fluids that lubricate the duct system and nourish the sperm. The seminal vesicles (pronounced: seh-muh-nul veh-sih-kulz) are sac-like structures attached to the vas deferens to the side of the bladder. The prostate gland, which produces some of the parts of semen, surrounds the ejaculatory ducts at the base of the urethra (pronounced: yoo-ree-thruh), just below the bladder. The urethra is the channel that carries the semen to the outside of the body through the penis. The urethra is also part of the urinary system because it is also the channel through which urine passes as it leaves the bladder and exits the body.
The penis is actually made up of two parts: the shaft and the glans (pronounced: glanz). The shaft is the main part of the penis and the glans is the tip (sometimes called the head). At the end of the glans is a small slit or opening, which is where semen and urine exit the body through the urethra. The inside of the penis is made of a spongy tissue that can expand and contract.
All boys are born with a foreskin, a fold of skin at the end of the penis covering the glans. Some boys have a circumcision (pronounced: sur-kum-sih-zhun), which means that a doctor or clergy member cuts away the foreskin. Circumcision is usually performed during a baby boy's first few days of life. Although circumcision is not medically necessary, parents who choose to have their children circumcised often do so based on religious beliefs, concerns about hygiene, or cultural or social reasons. Boys who have circumcised penises and those who don't are no different: All penises work and feel the same, regardless of whether the foreskin has been removed.

What Does the Male Reproductive System Do?

The male sex organs work together to produce and release semen into the reproductive system of the female during sexual intercourse. The male reproductive system also produces sex hormones, which help a boy develop into a sexually mature man during puberty (pronounced: pyoo-bur-tee).
When a baby boy is born, he has all the parts of his reproductive system in place, but it isn't until puberty that he is able to reproduce. When puberty begins, usually between the ages of 10 and 14, the pituitary (pronounced: puh-too-uh-ter-ee) gland - which is located in the brain - secretes hormones that stimulate the testicles to produce testosterone. The production of testosterone brings about many physical changes. Although the timing of these changes is different for every guy, the stages of puberty generally follow a set sequence.
During the first stage of male puberty, the scrotum and testes grow larger.
Next, the penis becomes longer, and the seminal vesicles and prostate gland grow.
Hair begins to appear in the pubic area and later it grows on the face and underarms. During this time, a male's voice also deepens.

Boys also undergo a growth spurt during puberty as they reach their adult height and weight.

Once a guy has reached puberty, he will produce millions of sperm cells every day. Each sperm is extremely small: only 1/600 of an inch (0.05 millimeters long). Sperm develop in the testicles within a system of tiny tubes called the seminiferous tubules (pronounced: seh-muh-nih-fuh-rus too-byoolz). At birth, these tubules contain simple round cells, but during puberty, testosterone and other hormones cause these cells to transform into sperm cells. The cells divide and change until they have a head and short tail, like tadpoles. The head contains genetic material (genes). The sperm use their tails to push themselves into the epididymis, where they complete their development. It takes sperm about 4 to 6 weeks to travel through the epididymis.
The sperm then move to the vas deferens, or sperm duct. The seminal vesicles and prostate gland produce a whitish fluid called seminal fluid, which mixes with sperm to form semen when a male is sexually stimulated. The penis, which usually hangs limp, becomes hard when a male is sexually excited. Tissues in the penis fill with blood and it becomes stiff and erect (an erection). The rigidity of the erect penis makes it easier to insert into the female's vagina during sexual intercourse. When the erect penis is stimulated, muscles around the reproductive organs contract and force the semen through the duct system and urethra. Semen is pushed out of the male's body through his urethra - this process is called ejaculation (pronounced: ih-jah-kyuh-lay-shun). Each time a guy ejaculates, it can contain up to 500 million sperm.
When the male ejaculates during intercourse, semen is deposited into the female's vagina. From the vagina the sperm make their way up through the cervix and move through the uterus with help from uterine contractions. If a mature egg is in one of the female's fallopian tubes, a single sperm may penetrate it, and fertilization, or conception, occurs.

This fertilized egg is now called a zygote (pronounced: zy-goat) and contains 46 chromosomes - half from the egg and half from the sperm. The genetic material from the male and female has combined so that a new individual can be created. The zygote divides again and again as it grows in the female's uterus, maturing over the course of the pregnancy into an embryo, a fetus, and finally a newborn baby.
Things

That Can Go Wrong With the Male Reproductive System

Guys may sometimes experience reproductive system problems. Below are some examples of disorders that affect the male reproductive system:
Disorders of the Scrotum, Testicles, or Epididymis

Conditions affecting the scrotal contents may involve the testicles, epididymis, or the scrotum itself.
Testicular injury. Even a mild injury to the testicles can cause severe pain, bruising, or swelling. Most testicular injuries occur when the testicles are struck, hit, kicked, or crushed, usually during sports or due to other trauma. Testicular torsion (pronounced: tor-zhun), when one of the testicles twists around, cutting off the blood supply, is also a problem that some teen guys experience - although it's not common.
Varicocele (pronounced: var-uh-koh-seal). This is a varicose vein (an abnormally swollen vein) in the network of veins that run from the testicles. Varicoceles commonly develop while a guy is going through puberty. A varicocele is usually not harmful, although in some people it may damage the testicle or decrease sperm production, so it helps for a guy to see his doctor if he's concerned about changes in his testicles.
Testicular cancer. This is one of the most common cancers in men younger than 40. It occurs when cells in the testicle divide abnormally and form a tumor. Testicular cancer can spread to other parts of the body, but if it's detected early, the cure rate is excellent. All guys should perform testicular self-examinations regularly to help with early detection.
Epididymitis (pronounced: eh-puh-dih-duh-my-tus) is inflammation of the epididymis, the coiled tubes that connect the testes with the vas deferens. It is usually caused by an infection, such as the sexually transmitted disease chlamydia, and results in pain and swelling next to one of the testicles.
Hydrocele. A hydrocele (pronounced: high-druh-seel) occurs when fluid collects in the membranes surrounding the testes. Hydroceles may cause swelling of the testicle but are generally painless. In some cases, surgery may be needed to correct the condition.
Inguinal hernia. When a portion of the intestines pushes through an abnormal opening or weakening of the abdominal wall and into the groin or scrotum, it is known as an inguinal hernia (pronounced: in-gwuh-nul her-nee-uh). The hernia may look like a bulge or swelling in the groin area. It can be corrected with surgery.

Disorders of the Penis

Disorders affecting the penis include the following:
Inflammation of the penis. Symptoms of penile inflammation include redness, itching, swelling, and pain. Balanitis occurs when the glans (the head of the penis) becomes inflamed. Posthitis is foreskin inflammation, which is usually due to a yeast or bacterial infection.
Hypospadius is a disorder in which the urethra opens on the underside of the penis, not at the tip.
Sexually transmitted diseases. Sexually transmitted diseases (STDs) that can affect guys include human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS), human papilloma virus (HPV, or genital warts), syphilis, chlamydia, gonorrhea, herpes genitalis, and hepatitis B. They are spread from one person to another mainly through sexual intercourse.

If you think you have symptoms of a problem with your reproductive system or if you have questions about your growth and development, talk to your parent or doctor - many problems with the male reproductive system can be treated.

A minute ago your voice sounded normal. You could talk and laugh with no worries. But now when you open your mouth, it's a completely different story. The noise coming from your throat kind of sounds like you, but it's croaking, squeaking, honking, and peeping. You can barely get through a sentence without your voice sounding like it's out of control: high one minute, low the next, then high again. You don't have a cold or a sore throat. In fact, everything feels normal — but nothing sounds right.
Your voice is changing! It's one of the many developments that happen to both girls and guys when they reach puberty. A guy's voice gets way deeper than a girl's, though.

At puberty, guys' bodies begin producing a lot of the hormone testosterone (pronounced: tes-tass-tuh-rone), which causes changes in several parts of the body, including the voice. For starters, a guy's larynx (pronounced: lar-inks), also known as the voice box, grows bigger.
The larynx, which is located in the throat at the top of the trachea (pronounced: tray-kee-ah) or windpipe, is like a hollow tube about 2 inches (5 centimeters) high. The larynx is responsible for creating the sound of your voice.
Stretched across your larynx are two muscles, your vocal cords, which are kind of like rubber bands. When you breathe, your vocal cords relax against the walls of the larynx and completely open to allow air to get in and out of your lungs. When you speak, though, your vocal cords close together by stretching across the larynx. Air from your lungs is then forced out between your vocal cords, causing them to vibrate and produce the tone of your voice. When you lower your voice, your vocal cords are lengthened and relaxed. When you make your voice higher, your vocal cords become shortened and tightened. (You can notice this difference in how they feel as you adjust your speech.)
As your larynx grows, your vocal cords grow longer and thicker. Also, your facial bones begin to grow. Cavities in the sinuses, the nose, and the back of the throat grow bigger, creating more space in the face that gives your voice more room to echo. All of these factors cause your voice to get deeper.
Think of a guitar. When a thin string is plucked, it vibrates and produces a high-sounding tone. When a thicker string is plucked, it sounds much deeper when it vibrates. That's kind of what happens to your voice. Before your growth spurt, your larynx is relatively small and your vocal cords are relatively thin. So your voice is high and kid-like. But as bones, cartilage, and vocal cords grow, your voice starts to sound like an adult's.
Along with all the other changes in your body, you might notice that your throat area looks a little different. For guys, when the larynx grows bigger, it tilts to a different angle inside the neck. Part of it sticks out in the part of the neck at the front of the throat and forms the Adam's apple. For girls, the larynx also grows bigger but not as much as a guy's. That's why girls don't have Adam's apples.

While your body is getting used to these changes, your voice can be difficult to control. A guy's voice "cracks" or "breaks" because his body is getting used to the changing size of his larynx. Fortunately, the cracking and breaking is only temporary. It usually lasts no longer than a few months. And even during that time, your voice won't crack every time you speak.
Some guys' voices might drop gradually, whereas others' might drop quickly. You may feel concerned, stressed, or embarrassed about the sound of your voice, but people usually understand — especially friends or brothers who've gone through it, too. Everyone goes through it, and once it happens, it takes a while to adjust to your larger larynx and the new sound of your voice.

You may have noticed that some of your friends have cracking and breaking voices, some might already have deep voices, and some still have the same voice they've always had. Everyone's timetable is different, so some voices might start to change earlier and some might start a little later. Generally, a guy's voice will start to change somewhere between the ages of 11 and 15 — although it can be earlier or later for some people. It all depends on when a guy goes through puberty, and some normal guys enter puberty earlier or later than others.
How deep a guy's voice gets depends on his genes: The larger a guy's larynx, the thicker the vocal cords, and the bigger the resonating area, the deeper his voice will be.
Once your larynx has grown, your voice will be more stable and easier to control. But even then your voice hasn't finished developing! Even after the quick change that happens in your teens, your voice continues to develop. Although the squeaking and cracking stage doesn't last long, most guys' voices don't fully mature until they're in their twenties.

SEXUAL HEALTH FOR ADOLESCENT......PART1

2007-06-24T22:39:00.000-07:00

SEXUAL HEALTH………part..1

Al's friend Rachel invited him to go to the lake for the day with her family. Rachel thought Al was fun to be around — plus he was cute. Rachel really hoped he'd say yes.

Al turned Rachel down. He liked Rachel, too, but was self-conscious about taking off his T-shirt. He worried that her family and others at the lake would see what he saw when he looked in the mirror — a scrawny excuse for a man. Al hadn't gone to the pool in more than a year because he was so self-conscious about his appearance.

The Truth About Guys:

Many people think of guys as being carefree when it comes to their appearance. But the reality is that a lot of guys spend plenty of time in front of the mirror. It's a fact — some guys care just as much as girls do about their appearance.
You may hear a lot about being a tough guy, but how often do you hear that being a guy is tough? Guys might think that they shouldn't worry about how they look, but body image can be a real problem for them. Unlike girls, guys are less likely to talk to friends and relatives about their bodies and how they're developing. Without support from friends and family, they may develop a negative self-image. The good news is that self-image and body image can be changed.
Body image is a person's opinions, thoughts, and feelings about his or her own body and physical appearance. Having a positive body image means feeling pretty satisfied with the way you look, appreciating your body for its capabilities and accepting its imperfections. Body image is part of someone's total self-image. So how a guy feels about his body can affect how he feels about himself. If he gets too focused on not liking the way he looks, a guy's self-esteem can take a hit and his confidence can slide. (The same thing can happen to girls, too.)
Although body image is just one part of our self-image, during the teen years, and especially during puberty, it can be easy for a guy's whole self-image to be based on how his body looks. That's because our bodies are changing so much during this time that they can become the main focus of our attention.
A change in your body can be tough to deal with emotionally — mainly because, well, your body is yours and you have become used to it.
Some guys don't feel comfortable in their changing bodies and can feel as if they don't know who they are anymore. Being the only guy whose voice is changing or who's growing body hair (or the only guy who isn't) can also make some guys feel self-conscious for a while.
Some guys go into puberty not feeling too satisfied with their body or appearance to begin with. They may have wrestled with body image even before puberty started (for example, battles with weight or dissatisfaction with height). For them, puberty may add to their insecurities.

The gene factor:

It can be tough to balance what you expect to happen to your body with what actually does happen. Lots of guys can have high expectations for puberty, thinking they'll develop quickly or in a certain way.
The best way to approach your own growth and development is to not assume you'll be a certain way. Look at everyone in your family — uncles, grandfathers, and even female relatives — to get an idea of the kinds of options your genes may have in store for you.

Not everyone's body changes at the same time or even at the same pace. It can be tough if all of your friends have already matured physically and are taller and more muscular. Most guys eventually catch up in terms of growth, although some will always be taller or more muscular than others — it's in their genes.
It's natural to observe friends and classmates and notice the different ways they're growing and developing. Guys often compare themselves with other guys in certain settings, and one of the most common is the locker room. Whether at a local gym or getting ready for a game at school, time in the locker room can be daunting for any guy.
Try to keep in mind in these situations that you aren't alone if you feel you don't "measure up." Many guys feel exactly the same way about their own bodies — even those whose physiques you envy. Just knowing that almost everyone else will go through the same thing can make all the difference.
You could try talking to a trusted male adult — maybe a coach, a doctor, a teacher, or your dad. Chances are they went through similar experiences and had some of the same feelings and apprehensions when their bodies were changing.
Guys put enough pressure on themselves, but what about the pressure society puts on them to be perfect?
It used to be that only girls felt the pressure of picture-perfect images, but these days the media emphasis on men's looks creates a sense of pressure for guys, too. And sometimes (actually many times) that "as advertised" body is just not attainable. The men you see in those pictures may not even be real. Magazines and ad agencies often alter photographs of models, either by airbrushing the facial and muscular features, or by putting a good-looking face on someone else's buff body.
So in the face of all the pressure society places on guys — and guys place on themselves — what can you do to fuel a positive body image? Here are some ideas:
Recognize your strengths. Different physical attributes and body types are good for different things — and sometimes the things you did well as a kid can change during puberty. What does your body do well? Maybe your speed, flexibility, strength, or coordination leads you to excel at a certain sport. Or perhaps you have non-sports skills, like drawing, painting, singing, playing a musical instrument, writing, or acting. Just exploring talents that you feel good about can help your self-esteem and how you think of yourself.
A good body doesn't always translate into athletic success. Too often, the way guys see their body image is closely associated with their performance on a sports field or in the gym. The upside to this is that if you're good at a team sport, you might have a pretty good view of your body. But what if you don't like team sports or you got cut from a team you really wanted to make? In these cases, it helps to look at individual accomplishments.
If you don't like team sports, that's OK. Try finding another form of physical activity that really gets you going. Depending on your interests and where you live, that may be mountain biking, rock climbing, dancing, yoga, or even jogging. This will help you stay in shape and help you to appreciate skills may not have realized you had in a team environment.
If you like team sports but didn't make a particular team, don't let it get you down. Use this as an opportunity to discover what you're good at, not to lament what you aren't best at. Maybe try out for another team — so soccer wasn't for you, but maybe cross-country running will be.
If none of these appeal to you, continue to practice the sport you were cut from and try again next year. The people around you probably won't remember that you didn't make the team — not being picked was a much bigger deal to you than it was to them.
Look into starting a strength training program. Exercise can help you look good and feel good about yourself. Good physiques don't just happen — they take hard work, regular workouts, and a healthy diet. There's no need to work out obsessively. A healthy routine can be as simple as exercising 20 minutes to 1 hour three days a week. Another benefit to working out properly is that it can boost your mood — lifting weights can lift your spirits.
Don't trash your body, respect it! To help improve your view of your body, take care of it. Smoking and other things you know to be harmful will take a toll after a while. Treating yourself well over time results in a healthier, stronger body — and that contributes to a better body image. Practicing good grooming habits — regular showering; taking care of your teeth, hair, and skin; wearing clean clothes, etc. — also can help you build a positive body image.

Be yourself. Your body is just one part of who you are — along with your talent for comedy, a quick wit, or all the other things that make you unique. Your talents, skills, and beliefs are just as much a part of you as the casing they come in. So try not to let minor imperfections take over.
While it's important to have a positive body image, getting too focused on body image and appearance can cause a guy to overlook the other positive parts of himself. If you're like most guys who take care of their bodies and wear clothes that look good, you probably look great to others. You just might not be aware of that if you're too busy being self-critical.

Tom’s story:

Tom hates gym class. It's not that he minds playing soccer or basketball or any of the other activities. But he does dread going into the locker room at the end of class and showering in front of his friends. Although the other guys' bodies are growing and changing, his body seems to be stuck at a younger age. He's shorter than most of the other guys in his grade, and his voice hasn't deepened at all. It's embarrassing to still look like a little kid.

Abby’s story:

Abby knows what it's like to feel different, too. The bikini tops that her friends fill out lie flat on her. Most of them have their periods, too, and she hasn't had even a sign of one. Abby doesn't even really have to shave her legs or underarms, although she does it just to be like everyone else.

Both Tom and Abby wonder and worry, "What's wrong with me?"

What Is Delayed Puberty?

Puberty is the time when your body grows from a child's to an adult's. You'll know that you are going through puberty by the way that your body changes. If you're a girl, you'll notice that your breasts develop and your pubic hair grows, that you have a growth spurt, and that you get your period (menstruation). The overall shape of your body will probably change, too — your hips will widen and your body will become curvier.
If you're a guy, you'll start growing pubic and facial hair, have a growth spurt, and your testicles and penis will get larger. Your body shape will also begin to change — your shoulders will widen and your body will become more muscular.
These changes are caused by the sex hormones (testosterone in guys and estrogen in girls) that your body begins producing in much larger amounts than before.

Puberty takes place over a number of years, and the age at which it starts and ends varies widely. It generally begins somewhere between the ages of 7 and 13 for girls, and somewhere between the ages of 9 and 15 for guys, although it can be earlier or later for some people. This wide range in age is normal, and it's why you may develop several years earlier (or later) than most of your friends.

Sometimes, though, people pass this normal age range for puberty without showing any signs of body changes. This is called delayed puberty.

Causes Delayed Puberty?

There are several reasons why puberty may be delayed. Most often, it's simply a pattern of growth and development in a family. A guy or girl may find that his or her parent, uncle, aunt, brothers, sisters, or cousins developed later than usual, too. This is called constitutional delay (or being a late bloomer), and it usually doesn't require any kind of treatment. These teens will eventually develop normally, just later than most of their peers.
Medical problems also can cause delays in puberty. Some people with chronic illnesses like diabetes, cystic fibrosis, kidney disease, or even asthma may go through puberty at an older age because their illnesses can make it harder for their bodies to grow and develop. Proper treatment and better control of many of these conditions can help make delayed puberty less likely to occur.
A person who's malnourished — without enough food to eat or without the proper nutrients — may also develop later than peers who eat a healthy, balanced diet. For example, teens with the eating disorder anorexia nervosa often lose so much weight that their bodies can't develop properly. Girls who are extremely active in sports may be late developers because their level of exercise keeps them so lean. Girls' bodies require a certain amount of fat before they can go through puberty or get their periods.
Delayed puberty can also happen because of problems in the pituitary or thyroid glands. These glands produce hormones important for body growth and development.
Some people who don't go through puberty at the normal time have problems with their chromosomes (pronounced: kro-muh-soamz), which are made up of DNA that contain our body's construction plans. Problems with the chromosomes can interfere with normal growth processes.
Turner syndrome is an example of a chromosome disorder. It happens when one of a female's two X chromosomes is abnormal or missing. This causes problems with how a girl grows and with the development of her ovaries and production of sex hormones. Women who have untreated Turner syndrome are shorter than normal, are infertile, and may have other medical problems.

Males with Klinefelter syndrome are born with an extra X chromosome (XXY instead of XY). This condition can slow sexual development.

TREATMENT:

1PHYSICAL EXAMINATION
2FAMILY HISTORY
3BONEAGE DIAGONASIS

The good news is that if there is a problem, doctors usually can help teens with delayed puberty to develop more normally. So if you are worried that you're not developing as you should, you should ask your parents to make an appointment with your doctor.
In addition to doing a physical examination, the doctor will take your medical history by asking you about any concerns and symptoms you have, your past health, your family's health, any medications you're taking, any allergies you may have, and other issues like growth patterns of your family members. He or she will chart your growth to see if your growth pattern points to a problem and also may order blood tests to check for thyroid, pituitary, chromosomal, or other problems. You may also have a "bone age" X-ray, which allows the doctor to see whether your bones are maturing normally.
In many cases, the doctor will be able to reassure you that there's no underlying physical problem; you're just a bit later than average in developing. If the doctor does find a problem, though, he or she might refer you to a pediatric endocrinologist (pronounced: en-doh-krih-nah-leh-jist), a doctor who specializes in treating kids and teens who have growth problems, or to another specialist for further tests or treatment.
Some teens who are late developers may have a difficult time waiting for the changes of puberty to finally get going - even after a doctor has reassured them that they are normal. In some cases, doctors may offer teens a short course (usually a few months) of treatment with hormone medications to get the changes of puberty started. Usually, when the treatment is stopped a few months later, the teen's own hormones will take over from there to complete the process of puberty.

It can be really hard to watch your friends grow and develop when the same thing's not happening to you. You may feel like you're never going to catch up. People at school may joke about your small size or your flat chest. Even when the doctor or your parents reassure you that things will be OK eventually - and even when you believe they're right — it's difficult to wait for something that can affect how you feel about yourself.
If you're feeling depressed or having school or other problems related to delays in your growth and development, talk to your mom or dad, your doctor, or another trusted adult about finding a counselor or therapist you can talk to. This person can help you sort out your feelings and suggest ways to cope with them.
Delayed puberty can be difficult for anyone to accept and deal with — but it's a problem that usually gets solved.

PEYRONIE'S DISEASE

2007-06-11T23:03:00.000-07:00

PENILE PROBLEM:…………….1

PEYRONIE’S DISEASE:

Peyronie's disease, a condition of uncertain cause, is characterized by a plaque, or hard lump, that forms on the penis. The plaque develops on the upper or lower side of the penis in layers containing erectile tissue. It begins as a localized inflammation and can develop into a hardened scar.

Cases of Peyronie's disease range from mild to severe. Symptoms may develop slowly or appear overnight. In severe cases, the hardened plaque reduces flexibility, causing pain and forcing the penis to bend or arc during erection. In many cases, the pain decreases over time, but the bend in the penis may remain a problem, making sexual intercourse difficult. The sexual problems that result can disrupt a couple's physical and emotional relationship and lead to lowered self-esteem in the man. In a small percentage of patients with the milder form of the disease, inflammation may resolve without causing significant pain or permanent bending.

The plaque itself is benign, or noncancerous. A plaque on the top of the shaft (most common) causes the penis to bend upward; a plaque on the underside causes it to bend downward. In some cases, the plaque develops on both top and bottom, leading to indentation and shortening of the penis. At times, pain, bending, and emotional distress prohibit sexual intercourse.

One study found Peyronie's disease in 1 percent of men. Although the disease occurs mostly in middle age, younger and older men can develop it. About 30 percent of men with Peyronie's disease develop fibrosis (hardened cells) in other elastic tissues of the body, such as on the hand or foot. A common example is a condition known as Dupuytren's contracture of the hand. In some cases, men who are related by blood tend to develop Peyronie's disease, which suggests that genetic factors might make a man vulnerable to the disease.
Men with Peyronie's disease usually seek medical attention because of painful erections and difficulty with intercourse. Since the cause of the disease and its development are not well understood, doctors treat the disease empirically; that is, they prescribe and continue methods that seem to help. The goal of therapy is to keep the Peyronie's patient sexually active. Providing education about the disease and its course often is all that is required. No strong evidence shows that any treatment other than surgery is effective. Experts usually recommend surgery only in long-term cases in which the disease is stabilized and the deformity prevents intercourse.
A French surgeon, François de la Peyronie, first described Peyronie's disease in 1743. The problem was noted in print as early as 1687. Early writers classified it as a form of impotence, now called erectile dysfunction (ED). Peyronie's disease can be associated with ED; however, experts now recognize ED as only one factor associated with the disease—a factor that is not always present.

Course of the Disease:
Many researchers believe the plaque of Peyronie's disease develops following trauma (hitting or bending) that causes localized bleeding inside the penis. Two chambers known as the corpora cavernosa run the length of the penis. The inner-surface membrane of the chambers is a sheath of elastic fibers. A connecting tissue, called a septum, runs between the two chambers and attaches at the top and bottom.

If the penis is abnormally bumped or bent, an area where the septum attaches to the elastic fibers may stretch beyond a limit, injuring the lining of the erectile chamber and, for example, rupturing small blood vessels. As a result of aging, diminished elasticity near the point of attachment of the septum might increase the chances of injury.

The damaged area might heal slowly or abnormally for two reasons: repeated trauma and a minimal amount of blood flow in the sheath-like fibers. In cases that heal within about a year, the plaque does not advance beyond an initial inflammatory phase. In cases that persist for years, the plaque undergoes fibrosis, or formation of tough fibrous tissue, and even calcification, or formation of calcium deposits.

While trauma might explain acute cases of Peyronie's disease, it does not explain why most cases develop slowly and with no apparent traumatic event. It also does not explain why some cases disappear quickly or why similar conditions such as Dupuytren's contracture do not seem to result from severe trauma.
Some researchers theorize that Peyronie's disease may be an autoimmune disorder.

Diagnosis and Evaluation:
Doctors can usually diagnose Peyronie’s disease based on a physical examination. The plaque is visible and palpable whether the penis is flaccid or erect. Full evaluation, however, may require examination during erection to determine the severity of the curvature. The erection may be induced by injecting medicine into the penis or through self-stimulation. Some patients may eliminate the need to induce an erection in the doctor’s office by taking a digital or Polaroid picture in the home. The examination may include an ultrasound scan of the penis to pinpoint the location and extent of the plaque and evaluate blood flow throughout the penis.

Treatment:
Because the course of Peyronie's disease is different in each patient and because some patients experience improvement without treatment, medical experts suggest waiting 1 to 2 years or longer before attempting to correct it surgically. During that wait, patients often are willing to undergo treatments whose effectiveness has not been proven.

Experimental Treatments:
Some researchers have given vitamin E orally to men with Peyronie's disease in small-scale studies and have reported improvements. Yet, no controlled studies have established the effectiveness of vitamin E therapy. Similar inconclusive success has been attributed to oral application of para-aminobenzoate, a substance belonging to the family of B-complex molecules.

Researchers have injected chemical agents such as verapamil, collagenase, steroids, calcium channel blockers, and interferon alpha-2b directly into the plaques. These interventions are still considered unproven because studies included small numbers of patients and lacked adequate control groups. Steroids, such as cortisone, have produced unwanted side effects, such as the atrophy or death of healthy tissues. Another intervention involves iontophoresis, the use of a painless current of electricity to deliver verapamil or some other agent under the skin into the plaque.

Radiation therapy, in which high-energy rays are aimed at the plaque, has also been used. Like some of the chemical treatments, radiation appears to reduce pain, but it has no effect at all on the plaque itself and can cause unwelcome side effects. Although the variety of agents and methods used points to the lack of a proven treatment, new insights into the wound healing process may one day yield more effective therapies.

Surgery:
Peyronie's disease has been treated surgically with some success. The two most common surgical procedures are removal or expansion of the plaque followed by placement of a patch of skin or artificial material, and removal or pinching of tissue from the side of the penis opposite the plaque, which cancels out the bending effect. The first method can involve partial loss of erectile function, especially rigidity. The second method, known as the Nesbit procedure, causes a shortening of the erect penis.
Some men choose to receive an implanted device that increases rigidity of the penis. In some cases, an implant alone will straighten the penis adequately. In other cases, implantation is combined with a technique of incisions and grafting or plication (pinching or folding the skin) if the implant alone does not straighten the penis.
Most types of surgery produce positive results. But because complications can occur, and because many of the phenomena associated with Peyronie's disease (for example, shortening of the penis) are not corrected by surgery, most doctors prefer to perform surgery only on the small number of men with curvature so severe that it prevents sexual intercourse.

Signs and Symptoms:
Peyronie's disease may be mild or severe, and may develop rapidly or over time. Symptoms include the following:
Hardened tissue (plaque) in the penis
Pain during erection
Curve in the penis during erection
Distortion of the penis (e.g., indentation, shortening)
Plaque usually develops on the top of the shaft, causing the penis to bend upward during erection, but it may occur on the bottom, causing a downward bend. If plaque develops on the top and the bottom, indentations and shortening may occur. In about 13% of cases, plaque does not cause severe pain or curvature, and the condition resolves on its own.

In severe cases, pain and curvature result in erectile dysfunction (impotence). If there are several areas of plaque, incomplete erection may occur.

Overview:
Peyronie's disease is characterized by the formation of hardened tissue (fibrosis) in the penis that causes pain, curvature, and distortion, usually during erection. The penis is the male organ for reproduction and urination. It is composed of two columns of erectile tissue (the corpora cavernosa); the corpus spongiosum, which contains the tube that carries urine and semen from the body (urethra); and the sheath that surrounds the erectile tissue (tunica albuginea). In Peyronie's disease, dense, fibrous scar tissue (plaque) forms in the tunica albuginea.

Incidence and Prevalence:
According to a report published in 1995 by the National Institutes of Health, Peyronie's disease occurs in about 1% of men. It is most common between the ages of 45 and 60, but it also occurs in young and elderly men. Prevalence may be higher because of reluctance to seek medical attention for the condition and failure to report in cases with mild symptoms.

Treatment:
Treatment options for patients with Peyronie's disease are limited. The goal of treatment is to reduce pain and maintain sexual function. Surgery is the only effective treatment, and because Peyronie's may resolve on its own, physicians often advise waiting 1 or 2 years before choosing this option.

Nonsurgical treatment should be implemented within 6 months of the onset of symptoms and before the plaque has calcified. Vitamin E supplementation and para-aminobenzoate tablets (B- complex substance) may be taken for several months. Chemical agents such as a calcium channel-blocker (e.g., verapamil), an enzyme that breaks down connective tissue (collagenase), and steroids (e.g., cortisone) may be injected into plaque or delivered by iontophoresis.

Iontophoresis is a painless method of delivering medication to localized tissue using electrical current. Like electrical charges repel, therefore a positive charge applied to a positively charged solution repels the medication into the tissue. Low-dose radiation (high-energy rays) therapy may reduce pain, but it does not effectively diminish plaque.

Complications:

Tissue atrophy may occur with these treatments, and successful results are not well documented.

Surgery:
Surgical treatment may be used in severe, persistent cases of Peyronie's that have not responded to nonsurgical treatment. Procedures involve the removal (excision) of hardened tissue and skin graft, the removal or pinching (plication) of tissue opposite the plaque to reduce curvature (called the Nesbit procedure), a penile implant, or a combination of these.

The removal of plaque requires a skin graft from another area of the patient's body and may result in a partial loss of erectile function (e.g., less rigidity). The Nesbit procedure reduces the length of the erect penis.

Penile implant involves implanting a device in the corpora cavernosa that increases rigidity. This procedure may be combined with incisions and skin grafts, or plication to effectively reduce curvature.
During the recovery period, patients are prescribed medication that prevents them from having an erection and are advised to avoid sexual activity. Antibiotics are also prescribed to reduce the risk for infection.

Complications:

Complications that may develop as a result of surgery include the following:
Adverse reaction to anesthesia
Damage to the tube that carries urine and semen from the body (urethra)
Excessive bleeding
Infection
Neurovascular damage resulting in a lack of sensation
Prosthesis malfunction
Scar tissue resulting in impotence
Prognosis

The prognosis for maintaining sexual function is good when treatment is started within 6 months of the onset of symptoms.

MORE ON PENILE PROBLEM TO FOLLOW

TESTOSTERONE

2007-06-02T23:27:00.000-07:00

TESTOSTERONE THERAPY:

The possibilities are enticing — increase your muscle mass, sharpen your memory and mental focus, boost your libido, and improve your energy level. If you're an aging man, this may sound like the ultimate anti-aging formula. But such health benefits from testosterone therapy aren't quite so clear-cut.

Testosterone therapy has been used successfully for years to treat men with abnormally low testosterone levels — a medical condition called male hypogonadism. More recently, healthy, aging men have taken the hormone to boost waning testosterone levels. But not enough is known about the effects of testosterone therapy for this purpose. No long-term studies have weighed the potential benefits against the possible risks, including infertility and prostate problems.

Despite the lack of scientific evidence, testosterone therapy is growing in popularity. Pharmacies filled 2.4 million testosterone prescriptions in 2004 — more than twice the number filled in 2000, according to IMS Health, a company that tracks pharmaceutical sales. Though the number appears to be growing, there are no data that track who's filling these prescriptions — men or women — and for what purpose.

At the core of the controversy is whether gradually declining testosterone levels are a natural phenomenon or a health problem. And the practical question for men and their doctors is whether to treat it, particularly in the absence of scientific evidence. Before you buy into the tempting claims, find out what's known — and not known — about testosterone therapy so that you can make the best decision for you and your long-term health.

The natural decline of testosterone
Starting around age 40, a man's body produces less testosterone. Testosterone is the main male hormone that maintains muscle mass and strength, fat distribution, bone mass, sperm production, sex drive, and potency.

Many call this progressive decline of hormones "male menopause" or "andropause" and equate it to women's menopause. But this isn't a valid comparison, says Todd Nippoldt, M.D., an endocrinologist at Mayo Clinic, Rochester, Minn. "In women, ovulation ceases and female hormone production plummets over a relatively short time frame," says Dr. Nippoldt. "In men, there's a gradual decline in the production of male hormones."

For most men, testosterone levels naturally decline but still remain within the normal range throughout their lifetimes, causing no significant problems. But about two in 10 men age 60 and older have testosterone levels below the normal range (testosterone deficiency).

Testosterone deficiency can have several effects on the body, including:
Decreased energy
Reduced muscle mass and strength
Decreased cognitive function
Less sexual interest or potency
Depressed mood

If you experience these signs or symptoms, you may have testosterone deficiency. Other medical conditions — such as liver disease, hypothyroidism and depression — can cause these effects as can certain medications, including beta blockers, painkillers and certain drugs for depression or anxiety. In addition, some healthy men encounter these changes as a part of the aging process, possibly because of declining hormones other than testosterone.

Talk to your doctor if you're experiencing these signs and symptoms. He or she can help determine the likely cause and suggest the best treatment plan, if any.

The male hormone testosterone plays an important role in the development and maintenance of typical masculine physical characteristics.
Potential benefits and risks

In men with testosterone deficiency, testosterone therapy can restore sexual function and muscle strength, prevent bone loss and protect against heart disease (atherosclerosis). Also, some men taking testosterone therapy report an increase in energy, sex drive and well-being.

Some anti-aging enthusiasts claim that increasing the level of testosterone in older and healthy men provides these same benefits. Though potentially beneficial for some of these men, testosterone therapy isn't risk-free. High doses of testosterone may result in sleep apnea, infertility and excess blood production, which could increase the risk of stroke.

Increasing testosterone levels may also pose problems for the prostate, a small male gland that produces most of the fluids in semen. Testosterone naturally stimulates the growth of the prostate. Long-term testosterone treatment could cause prostate gland enlargement. Also, doctors are concerned that testosterone therapy might fuel the growth of prostate cancer that is already present. This is especially worrisome since prostate cancer is common in older men, and many men may have prostate cancer that is undiagnosed.

In addition, scientists have linked testosterone therapy to breast cancer in men. Breast cancer, like prostate cancer, is a hormone-dependent cancer. Because long-term testosterone treatment could cause breast enlargement in men (gynecomastia), doctors are concerned that testosterone therapy might also fuel the growth of breast cancer that is already present.

All men, especially those with a family history of prostate or breast cancer, should discuss the potential benefits and risks of testosterone therapy with their doctors before beginning treatment.

To carefully weigh the potential pros and cons for you, consider the following:Potential benefits Potential risks
Improve muscle mass and strength
Increase bone mineral density
Thicken body hair and skin
Improve sexual desire
Boost energy
Decrease irritability and depression
Improve cognitive function Cause skin reactions
Cause fluid retention
Cause baldness
Cause or aggravate sleep apnea (brief, repeated cessation of breathing during sleep)
Stimulate noncancerous (benign) growth of the prostate and cause or worsen urinary symptoms
Stimulate growth of prostate cancer that's already present
Enlarge breasts (gynecomastia)
Stimulate growth of breast cancer that's already present
Cause testicle shrinkage (testicular atrophy)
Limit sperm production (infertility)
Stimulate excess blood production (polycythemia)
Cause acne

Learning from experience
Men aren't the only ones evaluating the benefits and risks of hormone therapy. For years, women have wrestled with the decision whether to take hormone therapy for the treatment of menopausal symptoms. They've had to assess the pros and cons based on the available scientific evidence. Dr. Nippoldt says that men should learn from women's experience.

"Early studies suggested that taking hormone therapy might protect postmenopausal women from heart disease. But a large, long-term study found just the opposite results," he says. "We learned from these studies that we just can't predict all the potential harmful effects of taking hormones even though on the surface they may seem beneficial."
Who should take testosterone therapy?

Testosterone therapy is clearly beneficial for men whose testicles fail to produce sufficient levels of testosterone (male hypogonadism). For this group of men, it can restore sexual function and muscle strength and prevent bone loss.

Few studies have evaluated possible benefits and risks of testosterone therapy for healthy aging men. And those that have been done provide conflicting results. Many questions remain unanswered, particularly the extent and the duration of the beneficial effects, which men might benefit, and the possible long-term risks.

In November 2003, the Institute of Medicine (IOM) reviewed the current evidence surrounding testosterone therapy and reported that this treatment is appropriate only for men who produce little or no testosterone. The IOM concluded that the long-term effects of supplemental testosterone on otherwise healthy men aren't known. And until more studies have been done, the institute recommends that testosterone therapy not be used to prevent or relieve the physical or psychological effects of aging.

TYPES OF TESTOSTERONE THERAPY:
Several types of testosterone therapy exist. Choosing a specific therapy depends on your preference of a particular delivery system, the side effects and the cost. Types include:
Injection. Intramuscular testosterone injections (Delatestryl, Depo-Testosterone) are safe and effective. Injections are given approximately every two weeks. You may experience fluctuations in symptom relief between doses. You or a family member can learn to administer this method of testosterone replacement therapy at home. If you're uncomfortable administering injections, a nurse or doctor can give the injection.
Patch. A patch containing testosterone (Androderm) is applied each night to your back, abdomen, upper arm or thigh. The site of the application is rotated to maintain seven-day intervals between applications to the same site to lessen skin reactions.
Gel. You rub testosterone gel (AndroGel, Testim) into your skin on your lower abdomen, upper arm or shoulder. As the gel dries, your body absorbs testosterone through your skin. Gel application of testosterone replacement therapy appears to cause fewer skin reactions than patches cause. Avoid showering or bathing for several hours after an application to ensure adequate absorption. A potential side effect of the gel is the possibility of transferring the medication to your partner. You can avoid this by avoiding skin-to-skin contact until the gel is completely dry or by covering the area after an application.

Gum and cheek (buccal cavity). Striant, a small putty-like substance, delivers testosterone through the natural depression above your top teeth where your gum meets your upper lip (buccal cavity). This product rapidly adheres to your gumline and, as exposed to saliva, softens into a gel-like form, allowing testosterone to be absorbed directly into your bloodstream. Side effects may include gum irritation or pain, bitter taste or headache. A recent study found this form of testosterone therapy may deliver a steadier dose of testosterone throughout the day.

Oral. Taking testosterone orally (Android, Testred, Virilon) is not recommended for long-term replacement. Testosterone taken by this method may cause an unfavorable cholesterol profile and increase your risk of blood clots and heart and liver problems.
The debate continues

There's no question a man faces emotional and physical challenges as he gets older. Changes at home, at work and within his body all can affect a man's general health. If you're concerned that you might have a hormone deficiency, talk to your doctor. A decline in testosterone that falls below normal values may be a reason to take supplemental testosterone. But it remains unclear whether restoring the testosterone levels to those of youth benefits older men.

PRECOCIOUS PUBERTY:

Important
It is possible that the main title of the report Precocious Puberty is not the name you expected. Please check the synonyms listing to find the alternate name(s) and disorder subdivision(s) covered by this report.

General Discussion

Precocious Puberty means an abnormally early onset of puberty. A sequence of events occurs during which a child develops into a young adult beginning at an unexpectedly early age. Glands that secrete growth and sex hormones begin to function abnormally early in life resulting in this condition. The exact cause of Precocious Puberty is not known.

For a Complete Report

This is an abstract of a report from the National Organization for Rare Disorders, Inc. ® (NORD). A copy of the complete report can be obtained for a small fee by visiting the NORD website. The complete report contains additional information including symptoms, causes, affected population, related disorders, standard and investigational treatments (if available), and references from medical literature. For a full-text version of this topic, see http://www.rarediseases.org/search/rdblist.html

The information provided in this report is not intended for diagnostic purposes. It is provided for informational purposes only. NORD recommends that affected individuals seek the advice or counsel of their own personal physicians.

It is possible that the title of this topic is not the name you selected. Please check the Synonyms listing to find the alternate name(s) and Disorder Subdivision(s) covered by this report.

This disease entry is based upon medical information available through the date at the end of the topic. Since NORD's resources are limited, it is not possible to keep every entry in the Rare Disease Database completely current and accurate. Please check with the agencies listed in the Resources section for the most current information about this disorder.

This information is not intended to replace the advice of a doctor. Healthwise disclaims any liability for the decisions you make based on this information. For more information, click here. Privacy Policy. How this information was developed.

In case of further enquiry contact

bhattacharyyad@scientist.com

EJACULATION

2007-06-01T22:59:00.001-07:00

EJACULATION:

EJACULATION:
This article is about male ejaculation. For female ejaculation, see Female ejaculation. For the grammatical term, see Ejaculation (grammar).

Ejaculation is the ejecting of semen from the penis, and is usually accompanied by orgasm. It is usually the result of sexual stimulation, which may include prostate stimulation. Rarely, it is due to prostatic disease. Ejaculation may occur spontaneously during sleep (a nocturnal emission). Anejaculation is the condition of being unable to ejaculate.

The process of ejaculation is an intense sensation, part of orgasm (French "la petite mort" - the little death), which can be immensely pleasureable and satisfying. Each spurt is associated with a wave of sexual pleasure, especially in the penis and loins. The first and second convulsions are usually the most intense in sensation, and produce the greatest quantity of semen. Thereafter, each contraction is associated with a diminishing volume of semen and a milder wave of pleasure. During sexual intercourse or masturbation, most males will find it difficult to resist the psychological temptation to continue the stimulation of the penis to the point of ejaculation once the feeling of orgasm becomes imminent.

Ejaculation has two phases: emission and ejaculation proper. The emission phase of the ejaculatory reflex is under control of the sympathetic nervous system, while the ejaculatory phase is under control of a spinal reflex at the level of the spinal nerves S2-4 via the pudendal nerve. During emission, the two ducts known as vas deferens contract to propel sperm from the epididymis where it was stored up to the ampullae at the top end of the vas deferens. The beginning of emission is typically experienced as a "point of no return," also known as point of ejaculatory inevitability. The sperm then passes through the ejaculatory ducts and is mixed with fluids from the seminal vesicles, the prostate, and the bulbourethral glands to form the semen, or ejaculate. During ejaculation proper, the semen is ejected through the urethra with rhythmic contractions.[1]

DEMONSTRATION OF EJACULATION PROPER:
These rhythmic contractions are part of the male orgasm. The typical male orgasm lasts about 17 seconds but can vary from a few seconds up to about a minute. After the start of orgasm, pulses of semen begin to flow from the urethra, reach a peak discharge and then diminish in flow. The typical orgasm consists of 10 to 15 contractions. The rate of contractions gradually slows during the orgasm. Initial contractions occur at an average interval of 0.6 seconds with an increasing increment of 0.1 second per contraction. Contractions of most men procede at regular rhythmic intervals for the duration of the orgasm. Many men also experience additional irregular contractions at the conclusion of the orgasm.[2]

Semen begins to spurt from the penis during the first or second contraction of orgasm. For most men the first spurt occurs during the second contraction. A small study of seven men found the initial spurt occurring on the first contraction for 2 men and occurring on the second contraction for 5 men. This same study showed between 26 and 60 percent of the contractions during orgasm were accompanied by a spurt of semen.[3]

The force and amount of ejaculate vary widely from male to male. A normal ejaculation may contain anywhere from 1.5 to 5 milliliters.[4]Boys that are going through puberty might produce a very small amount of semen, clear semen, or none at all. Adult ejaculate volume is affected by the amount of time that has passed since the previous ejaculation. Larger ejaculate volumes are seen with greater durations of abstinence. However, a recent Australian study has suggested a positive correlation between prostate cancer and infrequent ejaculation and/or prostate milking, which performs essentially the same function. That is, frequent masturbation appears to reduce the risk of prostate cancer. Frequent ejaculation is more easily obtained and sustained over time with the aid of masturbation and it is these ejaculations which are important, not the mechanism. [5] Also, the duration of the stimulation leading up to the ejaculation can affect the volume. Abnormally low volume is known as hypospermia, though it is normal for the amount of ejaculate to diminish with age.

The number of sperm in an ejaculation also varies widely, depending on many factors, including the recentness of last ejaculation, the average warmth of the testicles, the degree and length of time of sexual excitement prior to ejaculation, the age, testosterone level, the nutrition and especially hydration and the total volume of seminal fluid. An unusually low sperm count, not the same as low semen volume, is known as oligospermia, and the absence of any sperm from the ejaculate is termed azoospermia.

Most men experience a lag time between the ability to ejaculate consecutively, and this lag time varies among men. Age also affects the recovery time; younger men typically recover faster than older men. During this refractory period it is difficult or impossible to attain an erection, because the sympathetic nervous system counteracts the effects of the parasympathetic nervous system.

There are wide variations in how long sexual stimulation can last before ejaculation occurs.

When a man ejaculates before he wants to it is called premature ejaculation. If a man is unable to ejaculate in a timely manner after prolonged sexual stimulation, in spite of his desire to do so, it is called delayed ejaculation or anorgasmia. An orgasm that is not accompanied by ejaculation is known as a dry orgasm.

CENTRAL NERVOUS SYSTEM CONTROL:
To map the neuronal activation of the brain during the ejaculatory response, researchers have studied the expression of c-fos, a proto-oncogene expressed in neurons in response to stimulation by hormones and neurotransmitters [6] Expression of c-fos in the following areas have been observed: [7],[8]

medial preoptic area (MPOA) // lateral septum, bed nucleus of the stria terminalis // paraventricular nucleus of the hypothalamus (PVN) // ventromedial hypothalamus, medial amygdala // ventral premammillary nuclei // ventral tegmentum // central tegmental field // mesencephalic central gray // peripeduncular nuclei // parvocellular subparafascicular nucleus (SPF) within the posterior thalamus

FERTILIZATION:
Normally, ejaculation is required for emission of sperm, which can fertilize a woman's egg and impregnate her. However, almost all men produce a small amount of pre-ejaculate fluid when their penis is erect and they are sexually stimulated, and this pre-ejaculate may contain some sperm which can also lead to pregnancy. For this reason, coitus interruptus may still lead to unwanted pregnancies for couples engaging in vaginal intercourse if other forms of birth control are not used as well.

EUPHEMISMS:
Because sexual topics are often an uncomfortable topic among peers, a huge variety of euphemisms and dysphemisms have been invented to describe ejaculation and semen. For a complete list of terms, see: "Sexual slang".

EJACULATION FACTS:
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Please help improve this article by adding citations to reliable sources. (help, get involved!)
Any material not supported by sources may be challenged and removed at any time. This article has been tagged since June 2006.
Average energy in a tablespoon of semen: 2-7 kilocalories, 8-29 kilojoules
Average number of sperm cells in the ejaculate of a healthy man: 40 million to 600 million (avg. 250 million)
Distance sperm travels to fertilize an egg: 7.5-10 centimeters or 3-4 inches
Sperm lifespan: 2.5 months from development to ejaculation
Sperm lifespan after ejaculation: 30 seconds to 6 days depending on conditions

SEMEN:
Semen is an organic fluid (also known as seminal fluid) that usually contains spermatozoa. It is secreted by the gonads (sexual glands) and other sexual organs of male or hermaphroditic animals for fertilization of female ova. The process of discharge is called ejaculation.

COMPOSITION OF HUMAN SEMEN:
The components of semen come from two sources: sperm, and "seminal plasma". Seminal plasma, in turn, is produced by contributions from the seminal vesicle, prostate, and bulbourethral glands.

Seminal plasma of humans contains a complex range of organic and inorganic constituents.

The seminal plasma provides a nutritive and protective medium for the spermatozoa during their journey through the female reproductive tract. The normal environment of the vagina is a hostile one for sperm cells, as it is very acidic (from the native microflora producing lactic acid), viscous, and patrolled by immune cells. The components in the seminal plasma attempt to compensate for this hostile environment. Basic amines such as putrescine, spermine, spermidine and cadaverine are responsible for the smell and flavor of semen. These alkaline bases counteract the acidic environment of the vaginal canal, and protect DNA inside the sperm from acidic denaturation.

THE COMPONENTS AND CONTRIBUTIONOF SEMEN ARE AS FOLLOWS:

Gland Approximate % Description

testes 2-5%[1] Approximately 200- to 500-million spermatozoa
. produced in the testes, are released per ejaculation

seminal vesicle 65-75% amino acids, citrate, enzymes, flavins, fructose (the main energy source of sperm cells, which rely entirely on sugars from the seminal plasma for energy), phosphorylcholine, prostaglandins (involved in suppressing an immune response by the female against the foreign semen), proteins, vitamin C

prostate 25-30% acid phosphatase, citric acid, fibrinolysin, prostate specific antigen, proteolytic enzymes, zinc (serves to help to stabilize the DNA-containing chromatin in the sperm cells. A zinc deficiency may result in lowered fertility because of increased sperm fragility. Zinc deficiency can also adversely affect spermatogenesis.)

bulbourethral glands < 1% galactose, mucus (serve to increase the mobility of sperm cells in the vagina and cervix by creating a less viscous channel for the sperm cells to swim through, and preventing their diffusion out of the semen. Contributes to the cohesive jelly-like texture of semen.), pre-ejaculate, sialic acid

1992 World Health Organization report described normal human semen as having a volume of 2 ml or greater, pH of 7.2 to 8.0, sperm concentration of 20x106 spermatozoa/ml or more, sperm count of 40x106 spermatozoa per ejaculate or more and motility of 50% or more with forward progression (categories a and b) of 25% or more with rapid progression (category a) within 60 minutes of ejaculation.[2

SEMEN AND TRANSMISSION OF DISEASE:
The semen of a disease-free individual is harmless on the skin. However, semen can be the vehicle for many sexually transmitted diseases, including HIV, the virus that causes AIDS.

It is also hypothesized that components of semen, such as the spermatozoa as well as the seminal plasma, can cause immunosuppression in the body when introduced to the bloodstream or lymph. Evidence for this dates back to 1898, when Elie Metchnikoff injected a guinea pig with its own and foreign guinea pig sperm, finding that an antibody was produced in response; however the antibody was inactive, pointing to a suppression response by the immune system.

Further research, such as that by S. Mathur and J.M. Goust, demonstrated that non-preexisting antibodies were produced in humans in response to the sperm. These antibodies mistakenly recognized native T lymphocytes as foreign antigens, and consequently the T lymphocytes would fall under attack by the body's B lymphocytes. []

Other semen components shown to spur an immunosuppressive effect are seminal plasma and seminal lymphocytes.

BLOOD IN THE SEMEN (hematospermia)
The presence of blood in the semen may be undetectable (it only can be seen microscopically) or visible in the fluid. Its cause could be the result of inflammation, infection, blockage, or injury of the male reproductive tract or a problem within the urethra, testicles, epididymis and prostate.

Further semen analysis and other Urogenital system tests might be needed to find out the cause of blood in the semen.
Sexual stimulation is any stimulus that leads to sexual arousal or orgasm. The term often implies stimulation of the genitals but may also include stimulation of other areas of the body, stimulation of the senses (such as sight or hearing), and mental stimulation (such as that gotten from reading or fantasizing).

PHYSICAL SEXUAL STIMULATION:
Physical sexual stimulation usually consists of the touching of parts of the human body, especially erogenous zones. Masturbation is considered a type of sexual stimulation. Physiological reactions are usually triggered through sensitive nerves in these body parts which cause the release of pleasure-causing chemicals that act as mental rewards to pursue such stimulation. Arousal is usually the term used to describe such a physiological reaction. Physical sexual stimulation may also involve the touching of other people's body parts and may trigger similar physiological reactions.

MENTAL SEXUAL STIMOLATION
Mental sexual stimulation consists of any visual images, imagination, reading material, auditory stimulation that causes sexual stimulation and leads to arousal. The degree of sexual stimulation derived from any such activity depends upon the person and the circumstance. Pornography is considered to be the most prominent example of mental stimulation and the watching of pornographic material can lead to arousal in many people, especially for young men and boys in their teenage years

AROUSAL
The capability for arousal from sleep provides an organism with the energy, strength, and opportunity to become mobile and to direct its sensory organs to locate and ingest food, to procreate, and avoid predation or other potentially dangerous situations. The energy and strength of a mobile organism, and its sensory organs serve to protect an animal in its search for nutrition and in its ability to ingest it, thus ensuring its survival. These same factors also make possible its attempts to procreate, thus ensuring its success as an organism. The balance of sleep and wakefulness is essential to the survival and the success of every animal that sleeps.

NOCTURNAL EMISSION
"Wet Dream" and "Wet Dreams" redirect here. For other uses, see Wet Dream (disambiguation).
A nocturnal emission is an ejaculation of semen experienced during sleep. It is also called a "wet dream", an involuntary orgasm, or simply an orgasm during sleep.
Nocturnal emissions are most common during teenage and early adult years. However, nocturnal emissions may happen any time after puberty. They may or may not be accompanied by erotic dreams. It is possible to wake up during, or to simply sleep through, the ejaculation in what is sometimes called a "sex dream".

FREQUENCY
The frequency of nocturnal emissions is highly variable. Some men have experienced large numbers of nocturnal emissions as teenagers, while some men have never experienced one. 83 percent of men in the United States will eventually experience nocturnal emissions at some time in their lives.[1] Surveys in non-western countries where masturbation is culturally suppressed show 98 percent or more of the men eventually experience nocturnal emissions. [2] For males that have experienced nocturnal emissions the mean frequency ranges from 0.36 times per week for single 15 year old males to 0.18 times per week for 40 year old single males. For married males the mean ranges from 0.23 times per week for 19 year old married males to 0.15 times per week for 50 year old married males.[3]

Men who experience wet dreams more (or less) frequently than others usually do not have any sort of disease or problem. Some have the dreams only at a certain age, while others have them throughout their lives following puberty. The frequency that one has nocturnal emissions has not been conclusively linked to one's frequency of masturbation. Widely-known sex researcher Alfred Kinsey found "There may be some correlation between the frequencies of masturbation and the frequencies of nocturnal dreams. In general the males who have the highest frequencies of nocturnal emissions may have somewhat lower rates of masturbation. Some of these males credit the frequent emissions to the fact that they do not masturbate; but it is just as likely that the reverse relationship is true, namely, that they do not masturbate because they have frequent emissions."[4] For women the correlation is also short of conclusive "According to Kinsey's findings, women who suddenly lost the opportunity for several coital orgasms per week had only a few more orgasms in their sleep per year."[5]

One factor that can affect the number of nocturnal emissions a person has is whether they take testosterone-based drugs. In a 1998 study, the number of boys reporting nocturnal emissions drastically increased as their testosterone doses were increased, from 17% of subjects with no treatment to 90% of subjects at a high dose.[6]

During puberty, 13 percent of males experience their first ejaculation as a result of a nocturnal emission.[7] Kinsey found that males experiencing their first ejaculation through a nocturnal emission were older than those experiencing their first ejaculation by means of masturbation. The study indicates that such a first ejaculation resulting from a nocturnal emission was delayed a year or more from what would have been developmentally possible for such males through physical stimulation.[8]

Whereas an ejaculation normally terminates an erection, in the case of nocturnal emission, the subject often still has a functional erection afterward.[citation needed]

Although purported treatments to help prevent or diminish nocturnal emissions are available in abundance, none are known to have undergone any kind of rigorous experimentation or approval process such as that required by the Food and Drug Administration. Like the hiccups, there are a huge variety of "home remedies" with no scientific basis. Moreover, because no physical harm (beyond the inconvenience of the semen ejaculate) is caused by the event and it is not symptomatic of any underlying problem, it is generally considered inadvisable to undergo any sort of treatment except in cases of severe psychological trauma.

Involuntary orgasms can occur during waking hours in both sexes, but these are rare. The German word Pollution which does not have the same meaning as the English word "pollution", describes all these involuntary orgasms collectively.[9]

Regarding women, Kinsey found in 1953 that nearly 40 percent of the 5,628 women he interviewed experienced at least one nocturnal orgasm (orgasm during sleep), or "wet dream," by the time they were forty-five years old. A smaller study published in the Journal of Sex Research in 1986 found that 85 percent of the women who had experienced nocturnal orgasms had done so by the age of twenty-one, some even before they turned thirteen. In addition, women who have orgasms during sleep usually have them several times a year. Dr. Kinsey and his colleagues defined female nocturnal orgasm as sexual arousal during sleep that awakens one to perceive the experience of orgasm. Girls and women who don't have orgasms in their sleep, or who don't know whether or not they've had them, are perfectly normal. It may be easier for men to identify their wet dreams because of the "ejaculatory evidence." Vaginal secretions could be a sign of sexual arousal without orgasm.

ORGASM:
Orgasm is the conclusion of the plateau phase of the sexual response cycle, and is experienced by both males and females. Orgasm is controlled by our involuntary, or autonomic, nervous system [1]. It is accompanied by quick cycles of muscle contraction in the lower pelvic muscles, which surround the primary sexual organs and the anus. Orgasms are often associated with other involuntary actions, including vocalizations and muscular spasms in other areas of the body, and a generally euphoric sensation.

After orgasm, humans often feel tired and a need to rest. This was recently attributed to the release of prolactin.[2] Prolactin is a typical neuroendocrine response in depressed mood and irritation.[3] Ongoing research at the University Medical Center of Groningen, the Netherlands, studies brain events that accompany orgasm in men and women. Techniques used involve Positron Emission Tomography (PET) and fMRI. Male and female brains act almost the same during orgasm. Brain scans showed that large parts of the cerebral cortex temporarily reduced their activity.

FROM THE ERECTILE ORGAN:
Orgasm is achieved after direct stimulation of the penis or clitoris for a period of time. This stimulation can be caused by sexual intercourse, manual masturbation, oral sex, or a sensual vibrator. Any sexual stimulation of the penis or clitoris may eventually result in orgasm.

MULTIPLE ORGASM:
In some cases, women either do not have a refractory period or have a very short one and thus can experience a second orgasm soon after the first; some women can even follow this with additional consecutive orgasms. This is known as having multiple orgasms. After the initial orgasm, subsequent climaxes may be stronger or more pleasurable as the stimulation accumulates. Research shows that about 13% of women experience multiple orgasms[citation needed]; a larger number may be able to experience this with the proper stimulation (such as a vibrator) and frame of mind. However, for some women, their clitoris and nipples are very sensitive after climax, making additional stimulation initially painful. Taking deep, rapid breaths while continuing stimulation can assist in releasing this tension. [5]There are sensational reports of women having too many orgasms, including an unauthenticated claim that a young British woman has them constantly throughout the day, whenever she experiences the slightest vibration.

It is possible to have an orgasm without ejaculation (dry orgasm) or to ejaculate without reaching orgasm. Some men have reported having multiple consecutive orgasms, particularly without ejaculation. Males who experience dry orgasms can often produce multiple orgasms, as the need for a rest period, the refractory period, is reduced.[7] Some males are able to masturbate for hours at a time, achieving orgasm many times.[7] In recent years, a number of books have described various techniques to achieve multiple orgasms. Most multi-orgasmic men (and their partners) report that refraining from ejaculation results in a far more energetic post-orgasm state[citation needed]. Additionally, some men have also reported that this can produce more powerful ejaculatory orgasms when they choose to have them.

One technique is to put pressure on the perineum, about halfway between the scrotum and the anus, just before ejaculating to prevent ejaculation. This can, however, lead to retrograde ejaculation, i.e. redirecting semen into the urinary bladder rather than through the urethra to the outside. It may also cause long term damage due to the pressure put on the nerves and blood vessels in the perineum. Men who have had prostate or bladder surgery, for whatever reason, may also experience dry orgasms because of retrograde ejaculation.

Other techniques are analogous to reports by multi-orgasmic women indicating that they must relax and "let go" to experience multiple orgasms. These techniques involve mental and physical controls over pre-ejaculatory vasocongestion and emissions, rather than ejaculatory contractions or forced retention as above. Sexual energy, though focused in the groin, can be channeled throughout the body. Anecdotally, successful implementation of these techniques can result in continuous or multiple "full-body" orgasms.[8]. Gentle digital stimulation of the prostate, seminal vesicles, and vas deferens provides erogenous pleasure that sustains intense emissions orgasms for some men. A dildo device (the Aneros) claims to stimulate the prostate and help men reach these kinds of orgasms.

Many men who began masturbation or other sexual activity prior to puberty report having been able to achieve multiple non-ejaculatory orgasms. Young male children are capable of having multiple orgasms due to the lack of refractory period until they reach their first ejaculation. In female children it is always possible, even after the onset of puberty. This capacity generally disappears in males with the subject's first ejaculation. Some evidence indicates that orgasms of men before puberty are qualitatively similar to the "normal" female experience of orgasm, suggesting that hormonal changes during puberty have a strong influence on the character of male orgasm.[9]

Internet rumors and a few scientific studies have pointed to the hormone prolactin as the likely cause of male refractory period. Because of this, there is currently an experimental interest in drugs which inhibit prolactin, such as Dostinex (also known as Cabeser, or Cabergoline). Anecdotal reports on Dostinex suggest it may be able to eliminate the refractory period altogether, allowing men to experience multiple ejaculatory orgasms in rapid succession. At least one scientific study supports these claims.[10] Dostinex is a hormone-altering drug and has many potential side effects. It has not been approved for treating sexual dysfunction. Another possible reason may be an increased infusion of the hormone oxytocin. Furthermore, it is believed that the amount by which oxytocin is increased may affect the length of each refractory period.

A scientific study to successfully document natural, fully ejaculatory, multiple orgasms in an adult man was conducted at Rutgers University in 1995. During the study, six fully ejaculatory orgasms were experienced in 36 minutes, with no apparent refractory period.[11] It can also be said that in some cases, the refractory period can be reduced or even eliminated through the course of puberty and on into adulthood. Later, P. Haake et al. observed a single male individual producing multiple orgasms without elevated prolactin response.[12]

SPONTENEOUS ORGASM:
Orgasm can be spontaneous, seeming to occur with no direct stimulation. Many people find this to be quite embarrassing but enjoyable. Occasionally, orgasm can occur during sexual dreams.

The first orgasm of this type was reported among people who had spinal cord injury (SCI). Although SCI very often leads to loss of certain sensations and altered self-perception, a person with this disturbance is not deprived of sexual feelings such as sexual arousal and erotic desires. Thus some individuals are able to initiate orgasm by mere mental stimulation. Some non-sexual activity may result in a spontaneous orgasm. The best example of such activity is a release of tension that unintentionally involves slight genital stimulation, like rubbing of the seat of the bicycle against genitals during riding, exercising, when pelvic muscles are tightened or when yawning.

It was also discovered that some anti-depressant drugs may provoke spontaneous climax as a side effect. There is no accurate data for how many patients who were on treatment with antidepressant drugs experienced spontaneous orgasm, as most were unwilling to accept the fact.

THE PROSTATIC STRUCTURE:
Some people are able to achieve orgasm through stimulation of the prostatic structure, which in men is the prostate and in women is the Skene's glands; in women the location of the Skenes's glands is often known as the g-spot, or Grafenberg Spot. Grafenberg being the physician who first identified the spot as having orgasmic potential. The stimulation can come from receptive intercourse, being fingered, fisted, or penetrated with a dildo. Orgasms of this kind can cause both male and female ejaculation. With sufficient stimulation, the prostatic structure can also be "milked." Providing that there is no simultaneous stimulation of the penis or clitoris, prostate milking can cause ejaculation without orgasm. When combined with penile stimulation, some men report that prostate stimulation increases the volume of their ejaculation. The prostatic structure produces a secretion that forms one of the components of ejaculate; in males sperm are transmitted from the ductus deferens into the male urethra via the ejaculatory ducts, which lie within the prostate gland, during orgasm.

Other categorizations of orgasm

Certain types and categorization of orgasm have become widely enough acknowledged to be discussed as distinctive forms of orgasm.

VAGINAL ORGASM
The concept of purely vaginal orgasm was first postulated by Sigmund Freud. In 1905, Freud argued that clitoral orgasm was an adolescent phenomenon, and upon reaching puberty the proper response of mature women changes to vaginal orgasms. While Freud provided no evidence for this basic assumption, the consequences of the theory were greatly elaborated, partly because many women felt inadequate when they could not achieve orgasm via vaginal intercourse that involved little or no clitoral stimulation. Freud's claims about this and many other biological subjects, were later largely proven false or based on supposition.

In 1966, Masters and Johnson published pivotal research about the phases of sexual stimulation. Their work included women and men, and unlike Alfred Kinsey earlier (in 1948 and 1953), tried to determine the physiological stages before and after orgasm.[14] One of the results was the promotion of the idea that vaginal and clitoral orgasms follow the same stages of physical response. Masters and Johnson also argued that clitoral stimulation is the primary source of orgasms.

Recent discoveries about the size of the clitoris - it extends inside the body, around the vagina[15] - complicate or may invalidate attempts to distinguish clitoral vs. vaginal orgasms. Recent anatomical research shows that there are nerves connecting intravaginal tissues and the clitoris[citation needed]. This, with the anatomical evidence that the internal part of the clitoris is a much larger organ than previously thought, could explain credible reports of orgasms in women who have undergone clitorectomy as part of so-called female circumcision (also called female genital mutilation). The link between the clitoris and the vagina is evidence that the clitoris is the 'seat' of the female orgasm and is far wider-spread than the visible part most people associate with it. But it is possible that some women have more extensive clitoral tissues and nerves than others, and so that some women can achieve orgasm only by direct stimulation of the external part of the clitoris

MASTURBATION:
Masturbation refers to sexual stimulation, especially of one's own genitals and often to the point of orgasm, which is performed manually, by other types of bodily contact (except for sexual intercourse), by use of objects or tools, or by some combination of these methods.[1] Masturbation is the most common form of autoeroticism, and the two words are often used as synonyms, although masturbation with a partner (mutual masturbation) is also common. Animal masturbation has been observed in many species, both in the wild and in captivity.

Origins
Masturbation exercises sexual functions to increase fertility during intercourse.

FEMALE:
Masturbation in females is a tool to regulate the conditions in the vagina, cervix and uterus, which is used to either increase or decrease the chances of conception from intercourse, depending on the timing of the masturbation. This timing is a subconscious decision. If she has intercourse with more than one male, it favors the chances of one or the other male's sperm reaching her egg.
During orgasm, the woman's cervix extends and retracts at each contraction (cervical tenting), and the opening to the cervix gapes open. If a seminal pool is still present in the vagina when she masturbates, a significant number of sperm will be sucked up into her cervix
She can also increase the acidity of the cervical mucus to provide protection against infections.

MALE:
The function of masturbation is to flush out old sperm with low motility from the male's genital tract. The next ejaculate contains more fresh sperm, which has higher chances of achieving conception during intercourse. If more than one male is having intercourse with a female, the sperm with the highest motility will compete more effectively.[4]

MASTURBATION TECHNIQUES:

Ways of masturbating common to members of both sexes include pressing or rubbing the genital area, either with the fingers or against an object such as a pillow; inserting fingers or an object into the anus (see anal masturbation); and stimulating the penis or vulva/clitoris with electric vibrators, which may also be inserted into the vagina or anus. Members of both sexes may also enjoy touching, rubbing, or pinching the nipples or other erogenous zones while masturbating. Both sexes sometimes use lubricating substances to intensify sensation.

Reading or viewing pornography, or sexual fantasy, are often common adjuncts to masturbation. Masturbation activities are often ritualised. Various fetishes and paraphilias can also play a part in the masturbation ritual. Some potentially harmful or fatal activities include autoerotic asphyxiation and self-bondage

Some people get sexual pleasure by inserting objects into the urethra [5] (The urethra is the tube through which urine and, in men, semen, flows.) If these objects are urethral sounds, the practice is known as "sounding."[6] Other objects such as ball point pens and thermometers may be used. This practice can cause injury and infection.[7]

Some people masturbate by using machines that simulate intercourse.

Some people may masturbate until they are close to orgasm, stop for a while to reduce excitement, and then resume masturbating. They may repeat this cycle multiple times. This "stop and go" method is practiced in order to achieve even stronger orgasms.

Rarely, people quit stimulation just before orgasm to retain a heightened energy that normally comes down after orgasm [8] due to the release of prolactin hormone. A hazard of this technique is pelvic congestion.

FEMALE:
Female masturbation techniques are quite numerous and much more varied than those of males. Techniques include stroking or rubbing of the vulva, especially the clitoris, with the index and/or middle fingers. Sometimes one or more fingers may be inserted into the vagina to repeatedly stroke the frontal wall of the vagina where the g-spot is located. This gives a sensation close to that of orgasm.[9] Masturbation aids such as a vibrator, dildo or Ben Wa balls can also be used to stimulate the vagina and clitoris. Many women caress their breasts or stimulate a nipple with the free hand, if these are receptive areas for sexual stimulation. Anal stimulation is also enjoyed by some.

Lubrication is sometimes used during masturbation, especially when penetration is involved, but this is by no means universal and many women find their natural lubrication sufficient — some even produce more lubricant alone than with a partner[citation needed], though the reasons for this seem to be primarily psychological.

A vibrating duck. By de-dramatising the vibrator, these toys have gained a wider acceptance.

Common positions include lying on back or face down, sitting, squatting, or even standing. While sitting in a bath a female may use a tap which thrusts water out at a high pressure aimed at the clitoris to provide an extremely pleasureable experience. Lying face down, one may straddle a pillow, the corner or edge of the bed, a partner's leg or some scrunched-up clothing and "hump" the vulva and clitoris against it. Standing up, the corner of an item of furniture, or even a washing machine, can be used to stimulate the clitoris through the labia and clothing. Havelock Ellis reported that turn-of-the-century seamstresses using treadle-operated sewing machines could achieve orgasm by sitting near the edge of their chairs.[10]

Some can reach orgasm merely by crossing their legs tightly and clenching the muscles in their legs, which creates pressure on the genitals. This can potentially be done in public without observers noticing. Some prefer to use only pressure, applied to the clitoris without direct contact, for example by pressing the palm or ball of the hand against underwear or other clothing.

A few women can orgasm spontaneously, after experiencing prior sexual arousal, due to intellectual stimulation alone, for instance listening to certain pieces of music. Often, these mental triggers have associations with previous instances of arousal and orgasm. Some women even claim to be able to orgasm spontaneously by force of will alone, but that ability, if it exists at all, may not strictly qualify as masturbation as no physical stimulus is involved.[11] Sex therapists will sometimes recommend that female patients take time to masturbate to orgasm, especially if they have not done so before.[12][13]

MALE
Male masturbation techniques are also influenced by a number of factors and personal preferences. Techniques may also differ between circumcised and uncircumcised males, as some techniques which may work for one can often be quite painful for the other.
The most common male masturbation technique is simply to hold the penis with a loose fist and then to move the hand up and down the shaft until orgasm and ejaculation take place. The speed of the hand motion will vary from male to male, although it is not uncommon for the speed to increase as ejaculation nears and for it to decrease during the ejaculation itself. When uncircumcised, stimulation of the penis in this way comes from the "pumping" of the foreskin. This gliding motion of the foreskin reduces friction. When circumcised, there is more direct contact between the hand and the glans, thus a personal lubricant is sometimes used to reduce friction.

Circumcised or not, men may rub or massage the glans, the rim of the glans, and the frenular delta.

Another technique is to place just the index finger and thumb around the penis about halfway along the shaft and move the skin up and down. A variation on this is to place the fingers and thumb on the penis as if playing a flute, and then shuttle them back and forth. A less common technique is to lie face down on a comfortable surface such as a mattress or pillow and rub the penis against it until orgasm is achieved. This technique may include the use of a simulacrum, or artificial vagina.

There are many other variations on male masturbation techniques. Some men place both hands directly on their penis during masturbation, while others use their free hand to fondle their testicles, nipples, or other parts of their body. Some may keep their hand stationary while pumping into it with pelvic thrusts in order to simulate the motions of sexual intercourse. Others may also use vibrators and other sexual devices more commonly associated with female masturbation. A few extremely flexible males can reach and stimulate their penis with their tongue or lips, and so perform autofellatio.

The prostate gland is one of the organs that contributes fluid to semen. As the prostate is touch-sensitive, some directly stimulate it using a well-lubricated finger or dildo inserted through the anus into the rectum. Stimulating the prostate from outside, via pressure on the perineum, can be pleasurable as well.

Ejaculation of semen is sometimes controlled by wearing a condom or by ejaculating onto a tissue or some other item. The individual male's ability to project his semen over a distance during ejaculation may also influence a male's behaviour at ejaculation, as some males on rare occasions have been known to ejaculate up to three meters (about ten feet). Most males rarely ejaculate much farther than a fraction of that distance however.

A somewhat controversial ejaculation control technique is to put pressure on the perineum, about halfway between the scrotum and the anus, just before ejaculating. This can, however, redirect semen into the bladder (referred to as retrograde ejaculation). If repeated on a regular basis, this technique could cause long term damage due to the pressure put on the nerves and blood vessels in the perineum. A dry orgasm is one that is reached while withholding ejaculation (or where retrograde ejaculation has taken place). Proponents of dry orgasm say that this is a learnable skill that can shorten the refractory period.

FREQUENCY:
Frequency of masturbation is determined by many factors, e.g., one's resistance to transient sexual tension, hormone levels influencing sexual arousal, sexual habits established during youth, peer influences, health, intensity of the ejaculatory urge,[14] and one's attitude to masturbation formed by culture.[15] Medical causes have also been associated with masturbation.[16][17][18]

"Forty-eight female college students were asked to complete a sexual attitudes questionnaire in which a frequency of masturbation scale was embedded. Twenty-four of the women (the experimental group) then individually viewed an explicit modeling film involving female masturbation. One month later, all subjects again completed the same questionnaire. Subjects in the experimental group also completed a questionnaire evaluating aspects of the film. Results indicated that the experimental group reported a significant increase in the average monthly frequency of masturbation, as compared to the control group. This same group, however, reported that the film had no effect on sexual attitudes or behavior."

It is thought that most people begin masturbating when reaching adolescence ,however many scholarly and clinical studies have been done on the matter, and many informal surveys have asked the question. A 2004 survey by Toronto magazine NOW was answered by an unspecified number of thousands.[19] The results show that an overwhelming majority of the males — 81% — began masturbating between the ages of 10 and 15. Among females, the same figure was a more modest majority of 55%. (Note that surveys on sexual practices are prone to self-selection bias.) It is not uncommon however to begin much earlier, and this is more frequent among females: 18% had begun by the time they turned 10, and 6% already by the time they turned 6. Being the main outlet of child sexuality, masturbation has been observed in very young children. In the book Human Sexuality: Diversity in Contemporary America, by Strong, Devault and Sayad, the authors point out, "A baby boy may laugh in his crib while playing with his erect penis (although he does not ejaculate). Baby girls sometimes move their bodies rhythmically, almost violently, appearing to experience orgasm."

According to a Canadian survey of Now magazine readers cited above, the frequency of masturbation declines after the age of 17. However, most males masturbate daily or even more frequently well into their 20s and sometimes far beyond. This decline is more drastic among females, and more gradual among males. While females aged 13–17 masturbated almost once a day on average (and almost as often as their male peers), adult women only masturbated 8–9 times a month, compared to the 18–22 among men. It is also apparent that masturbation frequency declines with age. Adolescent youths report being able to masturbate to ejaculation six or more times per day, while men in middle age report being hard pressed to ejaculate even once per day. The survey does not give a full demographic breakdown of respondents, however, and the sexual history of respondents to this poll, who are readers of an urban Toronto lifestyle magazine, may not extend to the general population.

This may be because females are less likely to masturbate while in a heterosexual relationship than men. Both sexes occasionally engage in this activity, however, even when in sexually active relationships. Popular belief asserts that individuals of either sex who are not in sexually active relationships tend to masturbate more frequently than those who are; however, much of the time this is not true as masturbation alone or with a partner is often a feature of a relationship. Contrary to conventional wisdom, several studies actually reveal a positive correlation between the frequency of masturbation and the frequency of intercourse as well as the number multiple sex partners. One study reported a significantly higher rate of masturbation in gay men and women who were in a relationship. [20] [21] [22] [23]
For both males and females, masturbation is a way to relieve stress, anxiety and even boredom. For many with compressed schedules or frequent travel, regular masturbation enables them to maintain sexual output and performance for when opportunity eventually knocks.

Other cultures have rites of passage into manhood that culminate in the first ejaculation of a male, usually by the hands of a tribal elder. In some tribes such as the Agta, Philippines, stimulation of the genitals is encouraged from an early age.[25] Upon puberty, the young male is then paired off with a "wise elder" or "witch doctor" who uses masturbation to build his ability to ejaculate in preparation for a ceremony. The ceremony culminates in a public ejaculation before a celebration. The ejaculate is saved in a wad of animal skin and worn later to help conceive children. In this and other tribes, the measure of manhood is actually associated more with the amount of ejaculate and his need than penis size. Frequent ejaculation through masturbation from an early age fosters frequent ejaculation well into adulthood. [26]

Masturbation is becoming accepted as a healthy practice and safe method for sharing pleasure without the strings. It is socially accepted and even celebrated in certain circles. Group masturbation events can be found online in just about any state. Masturbation marathons are yearly events and are occurring across the globe from the U.S. to the UK. These events provide a supportive environment where masturbation can be performed openly among young and old without embarrassment. Participants talk openly with onlookers while masturbating to share techniques and describe their pleasure.[27] [28]

HEALTH AND PSYCOLOGICAL EFFECT

BENEFITS

It is held in many mental health circles that masturbation can relieve depression, stress and lead to a higher sense of self-worth (Hurlbert & Whittaker, 1991). Masturbation can also be particularly useful in relationships where one partner wants more sex than the other — in which case masturbation provides a balancing effect and thus a more harmonious relationship.[citation needed]

In 2003, an Australian research team led by Graham Giles of The Cancer Council Australia [2] concluded that frequent masturbation by males appears to help prevent the development of prostate cancer. The study also indicated that this would be more helpful than ejaculation through sexual intercourse because intercourse can transmit diseases that may increase the risk of cancer instead. Also, frequent ejaculation is more easily obtained and sustained over time with the aid of masturbation.

Masturbation is also seen as a sexual technique that protects individuals from the risk of contracting sexually transmitted diseases. Support for such a view, and for making it part of the American sex education curriculum, led to the dismissal of US Surgeon General Joycelyn Elders during the Clinton administration.

Many people see masturbation as an effective, natural cure for insomnia. Sexual climax, from masturbation or otherwise, leaves one in a relaxed and contented state. This is frequently followed closely by drowsiness and sleep - particularly when one masturbates in bed.[citation needed]

Some people actually consider masturbation as a cardiovascular workout.[29] And while doctors have no proof of this actually being true, those suffering from cardiovascular disorders (particularly those recovering from myocardial infarction, or heart attacks) should resume physical activity (including sexual intercourse and masturbation) gradually and with the frequency and rigor which their physical status will allow. Some doctors will advise those recovering from heart attacks to resume sexual activity (solitary or with a partner) when one is able to climb two flights of stairs without experiencing shortness of breath or chest pain.[citation needed]

Blood pressure
A small study has shown that a test group which only had intercourse experienced, as a whole, lower blood pressure in stressful situations than those who had intercourse but also had masturbated for one or more days.

PENIS ANATOMY.............1

2007-05-28T22:56:00.000-07:00

PENIS ANATOMY AND PHYSIOLOGY

AVERAGE PENIS SIZE

Difficulty in researching average penis size:

Determining what the average penis size is seems like it shouldn’t be that complicated. It’s a physical body part, you measure it, and repeat hundreds of thousands of times around the world, then take an average. Unfortunately, arriving at an accurate idea of what is an average penis size, is more complicated. Some of the problems with figuring out average penis size include:
Is penis size considered to be the length, the girth, or both?
When measuring penis length, where do you start?
Is penis girth measured at the base of the penis, at the glans (head), or around the shaft?
Are the people measured in these studies representative of the general population?
Do all studies include measurements taken by others, or self-reported measurements (which are historically bigger than measurements reported by others)?

Different studies answer these questions differently, which makes arriving at a single average penis size almost impossible. Also, many researchers believe that those who are willing to participate in a study about penis size may have larger than average penises, which would also skew the results.

With all that in mind, here are some figures from different studies published in academic journals.

MEASURMENT OF AVERAGE PENIS SIZE IN RESEARCH:

The results from three studies of penis size where the measurements were taken in a laboratory setting give the following ranges:

Average penis length (flaccid/not erect): from 3.4 inches to 3.7 inches (8.6 cm to 9.3 cm)

Average penis length (erect): from 5.1 inches to 5.7 inches (12.9 cm to 14.5 cm)

Average penis girth (circumference when erect): from 3.5 inches to 3.9 inches (8.8 cm to 10 cm)

These numbers are obviously very different from the sizes we hear (and see) in adult movies, and even the kinds of numbers you read on line. Why such a difference?

Many, possibly most, statistics you read are not from legitimate research, but from marketing companies who want you to feel bad about your penis size (so you’ll buy their product).

Other important things to know about average penis size

There is much greater variation in size of flaccid (non-erect) penises than of penises when they are erect. A soft penis that looks large may be roughly the same size when erect as a soft penis that looks smaller.
Because most men see other penises when they are not erect it can appear as if there is a big difference, and men may be likely to assume their erect penis is much smaller when compared to others.
Male porn stars are often chosen specifically because they have larger than average penises. Also, there are a variety of techniques used to make penises look bigger on camera. Lighting, camera angle, and even shaving of pubic hair can all make things look bigger on camera.

PENIS ANATOMY:

MALE SEXUAL ANATOMY - Parts of the Penis

The penis is made up of spongy erectile tissue, which fills with blood when a man is turned on or aroused and usually becomes erect. Penises come in all sizes, and penis size in almost all cases has nothing to do with how a penis works or how well a penis works. There are several different parts to the penis, each of which has some impact on feeling sexual arousal and pleasure.

PENIS SHAFT:
The shaft of the penis is the part that extends out of the body to the tip of the penis. When flaccid (no erect) the skin on the shaft of the penis will be loose and stretchy. While many people think that the shaft of the penis is not as sensitive as the head, some men have areas on the shaft that are highly sensitive.

GLANS PENIS:
The head of the penis is called the glans, and at the tip is the urethral opening (where both urine and semen come out).
The glans is a highly sensitive area, with many nerve endings. The glans is often considered to be similar in function to the clitoris in the woman, and the tissue that the glans develops out of is the same tissue that the clitoris develops from.

FRENULUM:
The frenulum is the indentation on the underside of the penis where the glans meets the shaft. For most men the frenulum is an area of great sensitivity. In some cases the frenulum can be short on a man, a condition called frenulum breve, which can cause sex play and intercourse to be painful.

FORESKIN:
Almost all men are born with a foreskin, which is the skin that covers the glans when the penis is flaccid. When the penis is erect, the foreskin retracts to just below the head. Men who are circumcised have had their foreskins removed, so the glans is exposed at all times. There is tremendous debate about the practice of circumcision for religious, cultural, and medical purposes. There is also debate about the connection between circumcision and sexuality.

INSIDE THE PENIS:
Despite the countless slang terms for the penis (boner, rod, etc…) and men’s bravado about their sexual strength, the penis has no bones and no muscle in it. An erection happens as a result of stimulation and blood flow (and sometimes as a reflex). Inside the penis are three spongy tubes, two on top and one on the bottom. The bottom one also has the urethra running through it.

An erection happens when blood flows into the penis and fills the tissue making it firm. Erectile dysfunctions usually occur as a result of some problem with getting the blood to the penis, having enough of it flow in, or keeping the blood there.
Urethra
The urethra is the tube through which urine and semen pass to get out of the body. The urethra runs from the bladder to the tip of the penis. In the process of normal functioning there are certain passages that are blocked and others that open up to insure that semen flows out of the urethra and not into the bladder, however problems can happen which cause semen to not be expelled.

The urethra is also a source of sexual pleasure for some men. Some men like the feeling of stimulation right at the urethral opening (which is called meatus) and others will stimulate the urethra itself. Internal urethral stimulation can cause serious harm, and it should only be engaged in with a great deal of education and care.

FRENULUM BREVE

Definition:

This is a condition where the frenulum is short and it makes movement of the foreskin, and erection, difficult and sometimes painful. It can make sexual activity painful leading to a diagnosis of dyspareunia. It is also possible that the frenulum can tear during sexual activity as a result of frenulum breve.

Frenulum breve can be caused by small “malformations” from birth or chronic infections.

Typically treatment has been surgical, including circumcision. A 1996 Polish study reported favorably on the use of laser surgery for frenulum breve.

SEX AND CIRCUMCISSION:

The imapact of circumcision on sexual behavior, pleasure, and research::

Most men don’t talk much about the sexual impact of circumcision. Because the majority of men who are circumcised had the procedure done prior to having sexual experiences, they don’t have a point of comparison when the question of how circumcision impacts sex is raised. Women who have sex with men probably talk about it a bit more, often comparing their experiences between circumcised and uncircumcised men, and talking about aesthetic preferences. But there is still a great deal of controversy, and not nearly enough research, on the actual impact of circumcision on both sexual behavior and more broadly on sexuality. In fact the question “does circumcision impact sexuality” can really be broken down into several more specific questions.
Does circumcision impact physical sexual sensitivity?

There is general agreement that physical sexual sensitivity is altered as a result of circumcision.

By definition, circumcision is the cutting away of the foreskin, a part of the body that is rich with nerve endings. Circumcision has an impact on the physical structure of the penis, and a corresponding impact on penile sensation.

Does circumcision impact the experience of sexual pleasure and/or sexual satisfaction?

These are, of course, two different questions. And both are different from the question of sensitivity. Sexual satisfaction and pleasure are related to sexual sensitivity, but they are much more complicated than the number of intact nerve endings we have.
Read more about the impact of circumcision on the experience of sexual pleasure and/or sexual satisfaction.

Does circumcision impact sexual behavior?

Because sexual behaviors naturally change over time it is near impossible to say for sure that circumcision is the reason for someone engaging in a specific kind of sexual behavior. In fact there has only been one study that has examined the self-reported sexual behaviors of circumcised and uncircumcised men.

It’s important to remember that from a sexual quality of life perspective one penis is not better than the other. The human body is capable of unimaginable pleasure, and when we think so narrowly as to say, if you’re missing this piece of skin your sex life isn’t as good, we’re doing ourselves (and our bodies) a great disservice.

Whats wrong with research on circumcision and sexuality?

It’s hard to know what research to trust when it comes to circumcision and sexuality. Most studies begin with a premise that is clearly pro or anti-circumcision, and the results tend to do little more than confirm the original hypotheses. If you’re interested in learning more about the sexual impact of circumcision, consider some of these problems that can be found in much of the research in this area:
Most of the anti-circumcision research suffers from a bias both in the interpretation of data and in data collection. For example, in one survey, participants who were meant to be representative were recruited from an anti-circumcision organization.

Studies of men who are circumcised as adults are complicated by the fact that these men are usually being circumcised for a medical reason, and therefore the circumcision may be alleviating a form of sexual pain.

As such we would expect that sexual pleasure be increased after circumcision, despite the possible reduction in sexual sensitivity.

Researchers often use words like “sexual sensitivity” and “sexual pleasure” interchangeably, and don’t provide their definitions for these terms, raising questions such as:

Does sensitivity mean the number of nerve endings in a penis?

Does it mean how the penis responds to being pinched or poked with a needle?

Does it mean how much the man says he feels during sex?

From one study to the next these terms are used and not defined, making it difficult to piece studies together

Almost all of this research is correlational, and isn’t able to imply causality. Researchers may find that circumcised men experience sexuality differently than uncircumcised men, but they have no way of knowing whether it is the circumcision that is the cause of this difference.

Because the research is correlational, it is left to the authors to “explain” their findings. These explanations usually fit their original positions. A great example of how personal bias can impact the explanation of research findings can be found in a large study of the sexual behavior of circumcised versus uncircumcised men.

The study, which analyzed data from a huge national probability sample in the U.S., found that men who were circumcised reported engaging more frequently in oral sex and anal sex than men who were not circumcised. These findings were more significant for white men than African American or Latino men.

The authors of the study proposed that because the findings were tied to ethnicity and race, it was unlikely that the finding is only related to the physical difference of circumcision, rather it is probably related to social and psychological forces as well.

Yet in a different study, these same results were interpreted as proof that circumcised men require more stimulation (which they say is what both oral and anal sex provided).

Both theories need to be seriously questioned.

One review study correlated circumcision with everything from reduced sexual satisfaction, to increased violent feelings towards women, to addiction to low self-esteem. Another study claimed that feelings of inferiority are almost “universal” in the “self-selected” circumcised participants.

In another study, of 150 men between the ages of 15 and 40 who were circumcised as adults 74% of the men had no change in their libidos, and only 18% of men reported a reduction in penile sensation.

With such conflicting results, one has to wonder about how careful these researchers are being in both their data collection and analysis, and simply wonder if they are measuring what they think they’re measuring. It also raises the possibility that there are no meaningful generalizations to be made about the impact of circumcision on sexuality.

Whatever the case, such confusing data should make anyone think twice before taking “expert advice” as the final word on this subject.

SYMOND'S SYNDROME............I

2007-05-24T23:25:00.000-07:00

SIMMONDS DISEASE:

Simmonds' disease (also Simmonds' syndrome) refers to panhypopituitarism caused by the destruction of the pituitary gland due to infiltrative processes (e.g. lymphocytic), tumours (pituitary adenomas or craniopharyngiomas) or trauma (cranial injury or following surgery).

Sheehan's syndrome is a sub-classification of Simmond's disease occurring specifically in the peripartum period.

EPONYM

It was first described by Morris Simmonds when a patient presented with 'fatal cachexia', although his patient went on to live for 11 more years. [1][2]

SYMPTOMS

Although cachexia may be present, the disease is characterised by symptoms due to decreased gonadal, thyroidal and adrenal function. These include:
amenorrhoea or oligomenorrhoea, impotence, loss of libido
tiredness, hypotension
waxy skin, loss of body hair

HYPOPITUTARISM

Hypopituitarism is a medical term describing the deficiency (hypo) of one or more hormones of the pituitary gland. The hypothalamus regulates pituitary secretion by the production of releasing hormones and posterior pituitary hormones and hence its dysfunction can also lead to hypopituitarism.

In endocrinology, deficiency of one or multiple hormones of the anterior pituitary is generally referred to as hypopituitarism, while deficiency of the posterior lobe generally only leads to central diabetes insipidus. The deficiency of all anterior pituitary hormones is termed panhypopituitarism.

PHYSIOLOGY

The hormones of the anterior pituitary include 2 proteins, 3 glycoproteins and a polypeptide:
prolactin (PRL) - stimulates milk production in the breast
growth hormone (GH) - growth and glucose homeostasis
luteinizing hormone (LH) - menstrual cycle and reproduction
follicle stimulating hormone (FSH) - same
thyroid stimulating hormone (TSH) - stimulates thyroxine production in the thyroid
adrenocorticotropic hormone (ACTH) - stimulates glucocorticoid production in the adrenal gland

These hormones are secreted in individually characteristic pulsatile patterns, often with distinct circadian rhythm, rather than at steady rates throughout 24 hours.

The posterior pituitary is the site of release of the nonapeptide hormones antidiuretic hormone (ADH) and oxytocin, the former regulating plasma osmolarity and the latter regulating uterine contractions during childbirth as well milk ejection from the breasts.

Multiple hormone deficiencies:

Deficiency of a single pituitary hormone occurs less commonly than deficiency of more than one hormone. Sometimes referred to as progressive pituitary hormone deficiency or partial hypopituitarism, there is usually a predictable order of hormone loss.

Generally, growth hormone is lost first, then luteinizing hormone deficiency follows. The loss of follicle-stimulating hormone, thyroid stimulating hormone and adrenocorticotopic hormones follow much later. The progressive loss of pituitary hormone secretion is usually a slow process, which can occur over a period of months or years. Hypopituitarism does occasionally start suddenly with rapid onset of symptoms

Most people with hypopituitarism lack growth hormone as well as one or more others. As for the posterior pituitary, antidiuretic hormone deficiency is the main problem, while oxytocin deficiency rarely causes clinically significant problems.

CASUSES

Hypopituitarism and panhypopituitarism can be congenital or acquired. A partial list of causes and forms:
Congenital hypopituitarism
Hypoplasia of the pituitary
Isolated idiopathic congenital hypopituitarism
Associated with other congenital syndromes and birth defects
Septo-optic dysplasia
Holoprosencephaly
Chromosome 22 deletion syndrome
Rapaport syndrome
Single gene defect forms of anterior pituitary hormone deficiency
Acquired hypopituitarism (Simmonds' disease)
trauma (e.g., skull base fracture)
surgery (e.g., removal of pituitary neoplasm)
tumor - secretory and non-secretory (20%) pituitary or hypothalamic neoplasms, cause hypopituitarism by compressing the remaining tissue
inflammation (e.g. sarcoidosis or autoimmune hypophysitis)
radiation (e.g., after cranial irradiation for childhood leukemia)
shock
(Sheehan's syndrome is hypopituitarism after heavy bleeding in childbirth)
hemochromatosis
other diseases.

DIAGNOSIS

Hypopituitarism may come to medical attention by symptoms or features of pituitary hormone deficiency (e.g., poor growth, hypoglycemia, micropenis, delayed puberty, polyuria, impaired libido, fatigue, and many others), or because the physician has diagnosed one of the many disorders and conditions associated with hypopituitarism listed above and tests for it. A provocative test (triple bolus test) measures the secretory response of the pituitary to a stimulus (other hormones, drugs, exercise, etc.) by measuring serum levels of the hormone involved.

REPLACEMENT THERAPY

Hypopituitarism and panhypopituitarism are treated by replacement of appropriate hormones. Since most of the anterior pituitary hormones are proteins or glycoproteins released in pulsatile patterns, whose functions are to induce secretion of smaller molecule hormones (thyroid hormones and steroids), it is simpler and less expensive for most purposes to simply replace the target gland hormones. There are a few exceptions, such as fertility induction.
GH is replaced with growth hormone.
TSH is replaced with thyroxine.
ACTH is usually replaced with hydrocortisone but any glucocorticoid may be used.
LH and FSH are most often replaced by supplying the appropriate sex steroids (e.g., testosterone or estrogen and progestin). Virtually all people who need T or E2 replacement for hypopituitarism rarely have spontaneous, effective spermatogenesis or follicular maturation. Both GnRH by subcutaneous pump and gonadotropins (Pergonal) by daily subcutaneous injections have been used effectively to induce fertility.
Prolactin is not usually replaced, as infant formula is readily available, simpler, and much cheaper.
ADH is replaced most commonly with oral, nasal, and sometimes intravenous or subcutaneous desmopressin.
Oxytocin is most important during labor and delivery at the end of pregnancy, and can be replaced in that circumstance by pitressin.

THE PITUTARY:

The pituitary gland, or hypophysis, is an endocrine gland about the size of a pea that sits in a small, boney cavity (pituitary fossa) covered by a dural fold (sellar diaphragm) at the base of the brain. The pituitary fossa, in which the pituitary gland sits, is situated in the sphenoid bone in the middle cranial fossa at the base of the brain.

The pituitary gland secretes hormones regulating homeostasis, including trophic hormones that stimulate other endocrine glands. It is functionally connected to the hypothalamus by the median eminence. It also secretes hormones for sexual eminence and desires.

SECTIONS:

Located at the base of the brain, the pituitary is functionally linked to the hypothalamus. It is divided into two lobes: the anterior or front lobe (adenohypophysis) and the posterior or rear lobe (neurohypophysis).

Anterior pituitary (Adenohypophysis)
Main article: Anterior pituitary

The anterior lobe is derived from the oral ectoderm and is composed of glandular epithelium. The anterior pituitary is functionally linked to the hypothalamus via the hypophysial-portal vascular connection in the pituitary stalk. Through this vascular connection the hypothalamus integrates stimulatory and inhibitory central and peripheral signals to the five phenotypically distinct pituitary cell types.

The anterior pituitary synthesizes and secrets important endocrine hormones, such as ACTH, TSH, prolactin, growth hormone, endorphins, FSH, and LH. Most of these hormones are released from the anterior petuitary under the influence of hypothalamic hormones. The hypothalamic hormones travel to the anterior lobe by way of a special capillary system, called the hypothalamic-hypophyseal portal system.

The control of hormones from the anterior pituitary exerts a negative feedback loop. Their release is inhibited by increasing levels of hormones from the target gland on which they act.

Posterior pituitary (neurohypophysis)
Main article: Posterior pituitary

The posterior lobe is connected to a part of the brain called the hypothalamus via the infundibulum (or stalk), giving rise to the tuberoinfundibular pathway. Hormones are made in nerve cell bodies positioned in the hypothalamus, and these hormones are then transported down the nerve cell's axons to the posterior pituitary. Hypothalamic neurons fire such hormones, releasing them into the capillaries of the pituitary gland.

The hormones secreted by the posterior pituitary are
Oxytocin comes from the paraventricular nucleus in the Hypothalamus
Antidiuretic hormone (ADH, also known as vasopressin and AVP, arginine vasopressin), comes from the supraoptic nucleus in the Hypothalamus

Intermediate lobe

There is also an intermediate lobe in many animals. For instance in fish it is believed to control physiological colour change. In adult humans it is just a thin layer of cells between the anterior and posterior pituitary, nearly indistinguishable from the anterior lobe. The intermediate lobe produces melanocyte-stimulating hormone (MSH), although this function is often (imprecisely) attributed to the anterior pituitary.

Functions

The pituitary gland helps control the following body processes:
Growth
Blood pressure
Some aspects of pregnancy and childbirth
Breast milk production
Sex organ functions in both women and men
Thyroid gland function
The conversion of food into energy (metabolism)
Water and osmolarity regulation in the body.

Pathology

Disorders involving the pituitary gland include:Condition Direction Hormone
Acromegaly overproduction growth hormone
Growth hormone deficiency underproduction growth hormone
Syndrome of inappropriate antidiuretic hormone overproduction vasopressin
Diabetes insipidus underproduction vasopressin
Sheehan syndrome underproduction prolactin
Pituitary adenoma overproduction any pituitary hormone
Hypopituitarism underproduction any pituitary hormone

FUNCTIONS OF PITUTARY

Human development is the process of growing to maturity. In biological terms, this entails growth from a one-celled zygote to an adult human being.

Biological development

Development begins with fertilization, the process by which the male gamete, the sperm cell, and the female gamete, the oocyte, fuse to give rise to a diploid cell, the zygote.

In medicine, pregnancy is defined as beginning when a fertilized zygote becomes implanted in a woman's uterus. This occurs when the zygote then becomes embedded into the endometrium (lining of the uterus) where it forms a placenta, for the purpose of receiving essential nutrients through the uterus wall. The umbilical cord in a newborn child signifies the remnants of implantation.

The zygote undergoes rapid mitotic divisions with no significant growth (a process known as cleavage) and cellular differentiation, leading to development of an embryo.

Childbirth is the process in which the baby is born. It is considered by many to be the beginning of a person's life, where age is defined relative to this event in most cultures.

Growth is normally controlled and moderated by the Pituitary Gland, located at the base of the skull in humans.

Physical stages

Terms for stages of age-related physical development include, with their approximate age ranges:
Zygote, the point of conception, fertilization
Blastocyst the period between conception and embryonic stages
Embryo; the embryonic period starts at three weeks and continues until the end of the 8th week of pregnancy
Fetus; the fetal stage begins at the end of the 8th week and continues until childbirth
Birth
Child
Neonate (newborn) (0-30 days)
Infant (baby) (1 month-1 year)
Toddler (1-4)
Primary school age (also called prepubescence) (4-12)
Elementary school age (also called middle childhood) (4-8)
Preadolescence (preteen, or late childhood. The child in this and the previous phase are called schoolchild (schoolboy or schoolgirl), when still of primary school age.) (9-12)
Adolescence and puberty (teenage) (13-19)
Young adult (19-25)
Adult (exact minimum age may vary)
Early adulthood (20-39)
Middle age (40-59)
Advanced adult/Senior citizen/Old age (60+)
Death (occurs at various ages, depending on person)
Decomposition (breakdown of the physical body after death)

Also sometimes used are terms that specify one's age in decades, such as:
Twenty something (20-29)
Thirty something (30-39)
Forty something (40-49) (Formerly also Quadragenarian, rarely used since 1980)
Quinquagenarian (50-59)
Sexagenarian (60-69)
Septuagenarian (70-79)
Octogenarian (80-89)
Nonagenarian (90-99)
Centenarian (100-109)
Supercentenarian (110+)

Physical development milestones
Ability to lift and control the orientation of the head
Crawling begins
Walking begins
Speech begins
Voice lowers in pitch (especially noticeable in boys)
Pubic hair appears
Genitals and reproductive organs mature
Menses begin (females)
Body hair and facial hair appears

Note: the Tanner stages can be used to approximately judge a child's age based on physical development.

A fetus (or foetus, or fœtus) is a developing mammal or other viviparous vertebrate, after the embryonic stage and before birth. The plural is fetuses (foetuses, fœtuses) or, very rarely, foeti.

In humans, the fetal stage of development begins at the end of the eighth week after fertilisation, when the major structures and organ systems have formed, until birth.

Etymology and spelling variations

The word "fetus" is from the Latin fetus, meaning "offspring", "bringing forth", or "hatching of young".[1] It has Indo-European roots related to sucking or suckling.[2]

Foetus is an English variation on this, rather than a Latin or Greek word, but has been in use since at least 1594 according to the Oxford English Dictionary, which describes "fetus" as the etymologically preferable spelling. "Fetus" is derived from the Latin verb fere, to conceive, not from the Latin verb foetare, to give birth. The superior etymological spelling is therefore "fetus",[3] and the variant foetus or fœtus may have originated with an error by Saint Isidore of Seville, in AD 620.[4] The preferred spelling in the United States is fetus, but the variant foetus or fœtus persists in other English-speaking countries, and in some medical contexts, as well as in some other languages (e.g. French).

Human fetus

he fetal stage begins eight weeks after fertilization. The fetus is not as sensitive to damage from environmental exposures as the embryo was, though toxic exposures can often cause physiological abnormalities or minor congenital malformation. Fetal growth can be terminated by various factors, including miscarriage, feticide committed by a third party, or induced abortion.

DEVELOPMENT

The following timeline describes some of the specific changes in fetal anatomy and physiology by fertilization age (i.e. the time elapsed since fertilization). However, it should be noted that obstetricians often use "gestational age" which, by convention, is measured from 2 weeks earlier than fertilization. For purposes of this article, age is measured from fertilization, except as noted.
8 weeks (condition at start of fetal stage). The risk of miscarriage decreases sharply at the beginning of the fetal stage.[5] At this point, all major structures, including hands, feet, head, brain, and other organs are present, but they continue to grow, develop, and become more functional.[6] When the fetal stage commences, a fetus is typically about 30 mm (1.2 inches) in length, and the heart is beating.[7] The fetus bends the head, and also makes general movements and startles that involve the whole body.[8] Brain stem activity has been detected as early as 54 days after conception.[9] Some fingerprint formation can be seen from the beginning of the fetal stage.[10]
8 to 15 weeks. The fetus continues to move in distinct motor patterns, picking up new patterns such as localized movement of the arms and legs, hiccups, breathing-like movements, and stretches and yawns .[8] [11] The breathing-like movement of the fetus is necessary for stimulation of lung development, rather than for obtaining oxygen.[12] At nine weeks, the fetus is able to bend fingers around an object; in response to a touch on the foot, the fetus will bend the legs or curl the toes to move away from the object.[13] The face is well-formed and develops a more human appearance. Eyelids close and remain closed for several months. The different appearance of the genitals in males and females becomes pronounced. Tooth buds appear, the limbs are long and thin, and red blood cells are produced in the liver. A fine hair called lanugo develops on the head. The gastrointestinal tract, still forming, starts to collect sloughed skin and lanugo, as well as hepatic products, forming meconium (stool). Fetal skin is almost transparent. More muscle tissue and bones have developed, and the bones become harder. The first measurable signs of EEG activity occur

n the 12th week.[9][14] By the end of this stage, the fetus has reached about 15 cm (6 inches).
16 to 25 weeks. The lanugo covers the entire body. Eyebrows, eyelashes, fingernails, and toenails appear. The fetus has increased muscle development. Alveoli (air sacs) are forming in lungs. The nervous system develops enough to control some body functions. The cochlea are now developed, though the myelin sheaths in the neural portion of the auditory system will continue to develop until 18 months after birth. The respiratory system has developed to the point where gas exchange is possible. The quickening, the first maternally discernable fetal movements, are often felt during this period. A woman pregnant for the first time (i.e. a primiparous woman) typically feels fetal movements at about 18-19 weeks, whereas a woman who has already given birth at least two times (i.e. a multiparous woman) will typically feel movements around 16 weeks.[15] By the end of the fifth month, the fetus is about 20 cm (8 inches).
26 to 38 weeks. The amount of body fat rapidly increases. Lungs are not fully mature. Thalamic brain connections, which mediate sensory input, form. Bones are fully developed, but are still soft and pliable. Iron, calcium, and phosphorus become more abundant. Continuous EEG readings have been observed by the 30th week.[9] Fingernails reach the end of the fingertips. The lanugo begins to disappear, until it is gone except on the upper arms and shoulders. Small breast buds are present on both sexes. Head hair becomes coarse and thicker. Birth is imminent and occurs around the 40th gestational week. The fetus is considered full-term by week 35, which means that the baby is considered sufficiently developed for life outside the womb.[16] It may be 48 to 53 cm (19 to 21 inches) in length, when born.

VARIATION IN GROWTH

There is much variation in the growth of the fetus. When fetal size is less than expected, that condition is known as intrauterine growth restriction (IUGR) also called fetal growth restriction (FGR); factors affecting fetal growth can be maternal, placental, or fetal.[17]

Maternal factors include maternal weight, body mass index, nutritional state, emotional stress, toxin exposure (including tobacco, alcohol, heroin, and other drugs which can also harm the fetus in other ways), and uterine blood flow. A woman's primiparity also may affect fetal weight (firstborns tend to weigh less).

Placental factors include size, microstructure (densities and architecture), umbilical blood flow, transporters and binding proteins, nutrient utilization and nutrient production.

Fetal factors include the fetus genome, nutrient production, and hormone output. Also, female fetuses tend to weigh less than males, at full term.[17]

Fetal growth is often classified as follows: small for gestational age (SGA), appropriate for gestational age (AGA), and large for gestational age (LGA).[18] SGA can result in low birth weight, although premature birth can also result in low birth weight. Low birth weight increases risk for perinatal mortality (death shortly after birth), asphyxia, hypothermia, polycythemia, hypocalcemia, immune dysfunction, neurologic abnormalities, and other long-term health problems. SGA may be associated with growth delay, or it may instead be associated with absolute stunting of growth.

VIABILITY

Five months is currently the lower limit of viability, and viability usually occurs later.[19] According to The Developing Human:

Viability is defined as the ability of fetuses to survive in the extrauterine environment... There is no sharp limit of development, age, or weight at which a fetus automatically becomes viable or beyond which survival is assured, but experience has shown that it is rare for a baby to survive whose weight is less than 500 gm or whose fertilization age is less than 22 weeks. Even fetuses born between 26 and 28 weeks have difficulty surviving, mainly because the respiratory system and the central nervous system are not completely differentiated... If given expert postnatal care, some fetuses weighing less than 500 gm may survive; they are referred to as extremely low birth weight or immature infants.... Prematurity is one of the most common causes of morbidity and prenatal death.[20]

During the past several decades, expert postnatal care has improved with advances in medical science, and therefore the point of viability has moved earlier.[21] As of 2006, the youngest child to survive a premature birth was Amillia Taylor, born at the Baptist Hospital of Miami at 21 weeks and 6 days' gestational age.[22]

FETAL PAIN

The subject of fetal pain and suffering is controversial. The ability of a fetus to feel pain is often part of the abortion debate. However, according to Arthur Caplan, "there is no consensus among the medical and scientific experts about precisely when a fetus becomes pain-capable."[23] Different sources have estimated that the earliest point for pain sensation may be during the first 12 weeks or after 20, 24, or 26 weeks gestation, or months after birth.

THE CIRCULATORY SYSTEM OF FETUS

The circulatory system of a human fetus works differently from that of born humans, mainly because the lungs are not in use: the fetus obtains oxygen and nutrients from the woman through the placenta and the umbilical cord.[24]

Blood from the placenta is carried to the fetus by the umbilical vein. About half of this enters the fetal ductus venosus and is carried to the inferior vena cava, while the other half enters the liver proper from the inferior border of the liver. The branch of the umbilical vein that supplies the right lobe of the liver first joins with the portal vein. The blood then moves to the right atrium of the heart. In the fetus, there is an opening between the right and left atrium (the foramen ovale), and most of the blood flows from the right into the left atrium, thus bypassing pulmonary circulation. The majority of blood flow is into the left ventricle from where it is pumped through the aorta into the body. Some of the blood moves from the aorta through the internal iliac arteries to the umbilical arteries, and re-enters the placenta, where carbon dioxide and other waste products from the fetus are taken up and enter the woman's circulation.[24]

Some of the blood from the right atrium does not enter the left atrium, but enters the right ventricle and is pumped into the pulmonary artery. In the fetus, there is a special connection between the pulmonary artery and the aorta, called the ductus arteriosus, which directs most of this blood away from the lungs (which aren't being used for respiration at this point as the fetus is suspended in amniotic fluid).[24]

POSTNATAL DEVELOPMENT

With the first breath after birth, the system changes suddenly. The pulmonary resistance is dramatically reduced ("pulmo" is from the Latin for "lung"). More blood moves from the right atrium to the right ventricle and into the pulmonary arteries, and less flows through the foramen ovale to the left atrium. The blood from the lungs travels through the pulmonary veins to the left atrium, increasing the pressure there. The decreased right atrial pressure and the increased left atrial pressure pushes the septum primum against the septum secundum, closing the foramen ovale, which now becomes the fossa ovalis. This completes the separation of the circulatory system into two halves, the left and the right.

The ductus arteriosus normally closes off within one or two days of birth, leaving behind the ligamentum arteriosum. The umbilical vein and the ductus venosus closes off within two to five days after birth, leaving behind the ligamentum teres and the ligamentum venosus of the liver respectively.

Differences from the adult circulatory system

Remnants of the fetal circulation can be found in adults:[25][26]

In addition to differences in circulation, the developing fetus also employs a different type of oxygen transport molecule than adults (adults use adult hemoglobin). Fetal hemoglobin enhances the fetus' ability to draw oxygen from the placenta. Its association curve to oxygen is shifted to the left, meaning that it will take up oxygen at a lower concentration than adult hemoglobin will. This enables fetal hemoglobin to absorb oxygen from adult hemoglobin in the placenta, which has a lower pressure of oxygen than at the lungs.

Developmental problems

Congenital anomalies are anomalies that are acquired before birth. Infants with certain congenital anomalies of the heart can survive only as long as the ductus remains open: in such cases the closure of the ductus can be delayed by the administration of prostaglandins to permit sufficient time for the surgical correction of the anomalies. Conversely, in cases of patent ductus arteriosus, where the ductus does not properly close, drugs that inhibit prostaglandin synthesis can be used to encourage its closure, so that surgery can be avoided.

A developing fetus is highly susceptible to anomalies in its growth and metabolism, increasing the risk of birth defects. One area of concern is the mother's lifestyle choices made during pregnancy. Diet is especially important in the early stages of development. Studies show that supplementation of the mother's diet with folic acid reduces the risk of spina bifida and other neural tube defects. Another dietary concern is the consumption of breakfast by the mother. This one factor could lead to extended periods of lower than normal nutrients in the mother's blood, leading to a higher risk of prematurity, or other birth defects in the fetus. During this time alcohol consumption may increase the risk of the development of Fetal alcohol syndrome, a condition leading to mental retardation in some infants.[27] Smoking during pregnancy may also lead to reduced birth weight. Low birth weight is defined as 2500 grams (5.5 lb). Low birth weight is a concern for medical providers due to the tendency of these infants, described as premature by weight, to have a higher risk of secondary medical problems.

Umbilical vein

Circulation

Attached to the uterine lining, the placenta is the site of gas exchange between mother and fetus. The singular umbilical vein carries oxygenated blood from the placenta to the fetus, while two umbilical arteries return deoxygenated blood to the placenta. The three vessels coil around one another within the Wharton's jelly of the umbilical cord and enter the abdomen at the umbilicus.

Inside the fetus, the vein courses alongside the falciform ligament and then to the liver's underside. At the transverse fissure, the vein divides into two vessels, one larger than the other. The larger of the two is joined by the portal vein, and together they enter the right lobe of the liver. The smaller vessel, now called the ductus venosus, diverges away from the liver and joins with the inferior vena cava.

Closure

Within a week of birth, the infant's umbilical vein is completely obliterated and is replaced by a fibrous cord called the round ligament of the liver (also called the ligamentum teres hepatis, from the Latin meaning the same). It extends from the umbilicus to the transverse fissure, where it joins with the ligamentum venosum to separate the left and right lobes of the liver.

Closure of the umbilical vein usually occurs after the umbilical arteries have closed. This prolongs the communication between the placenta and fetal heart, allowing for a sort of autotransfusion of remaining blood from the placenta to the fetus.

Recanalization

Under extreme pressure, the round ligament may reopen to allow the passage of blood. Such recanalization is common in patients with cirrhosis and portal hypertension. Patients with cirrhosis experience rapid growth of scar tissue in and around the liver, often functionally obstructing nearby vessels. Vessel occlusion increases vascular resistance and therefore leads to hypertension. In portal hypertension, the vessels surrounding the liver are subjected to abnormally high blood pressure—so high, in fact, that the force of the blood pressing against the round ligament is sufficient to recanalize the structure.

Catheterization

A newborn baby has a patent umbilical vein for at least a few months. This umbilical vein may be catheterised for ready intravenous access. It may be used as a site for regular transfusion in cases of erythroblastosis or hemolytic disease.

Childbirth

Childbirth (also called labour, birth, partus or parturition) is the culmination of a human pregnancy with the emergence of a newborn infant/s from the mother's uterus.

The process of human childbirth is categorized in 3 stages of labour. In the first stage, the uterus begins rhythmic contractions which steadily increase in strength and frequency, gradually widening and thinning the cervix. During the second stage, the infant passes from the uterus, through the cervix and birth canal. In the third stage, the placenta pulls from the uterine wall and is expelled through the birth canal.[1]

The natural birth

Mother and newborn with umbilical cord still attached after a water birth

First stage: contractions

A typical childbirth will begin with the onset of contractions of the uterus. The frequency and duration of these contractions varies with the individual. The onset of labour may be sudden or gradual, and is defined as regular uterine activity in the presence of cervical dilatation.

During a contraction the long muscles of the uterus contract, starting at the top of the uterus and working their way down to the bottom. At the end of the contraction, the muscles relax to a state shorter than at the beginning of the contraction. This draws the cervix up over the baby's head. Each contraction dilates the cervix until it becomes completely dilated, often referred to as 10+ cm (4") in diameter.

A gradual onset with slow cervical change towards 3 cm (just over 1 inch) dilation is referred to as the "latent phase". A woman is said to be in "active labour" when contractions have become regular in frequency (3-4 in 10 minutes) and about 60 seconds in duration. The cervix must shorten (efface) before it can dilate; for first time mothers this can take a substantial period of time and can often be a very tiring and disheartening time. However, it is also a very positive time, as once the cervix is effaced dilatation can occur and the downward journey of the fetus can commence. The now powerful contractions are accompanied by cervical effacement and dilation greater than 3 cm. The labour may begin with a rupture of the amniotic sac, the paired amnion and chorion ("breaking of the water"). The contractions will accelerate in frequency and strengthen. In the "transition phase" from 8 cm–10 cm (3 or 4 inches) of dilation, the contractions often come every two minutes and are typically lasting 70–90 seconds. Transition is often regarded as the most challenging and intense for the mother. It is also the shortest phase.

During this stage, the expectant mother typically goes through several emotional phases. At first, the mother may be excited and nervous. Then, as the contractions become stronger, demanding more energy from the mother, mothers generally become more serious and focused. However, as the cervix finishes its dilation, some mothers experience confusion or bouts of self-doubt or giving up. It is important during this time for the birth partners to stay positive and supportive of the mother; to actively encourage if this is what she wishes and to provide nutrition and hydration in order to keep her energy reserves up.

The duration of labour varies widely, but averages some 13 hours for women giving birth to their first child ("primiparae") and 8 hours for women who have already given birth.

If there is a significant medical risk to continuing the pregnancy, induction may be necessary. As this carries some risk, it is only done if the child or the mother are in danger from prolonged pregnancy. Forty-two weeks' gestation without spontaneous labour is often said to be an indication for induction although evidence does not show improved outcomes when labour is induced for post-term pregnancies. Inducing labour increases the risk of cesarean section uterine rupture in mothers that have had a previous cesarean section.

Second stage: delivery

In the second stage of labour, the baby is expelled from the womb through the vagina by both the uterine contractions and by the additional maternal efforts of "bearing down," which many women describe as similar in sensation to straining to expel a large bowel movement. The imminence of this stage can be evaluated by the Malinas score.

The baby is most commonly born head-first. In some cases the baby is "breech" meaning either the feet or buttocks are descending first. Babies in the breech position can be helped to be born vaginally by a midwife, although caesarean births are becoming more common for breech presentation.

There are several types of breech presentations, but the most common is where the baby's buttocks are born first and the legs are folded onto the baby's body with the knees bent and feet near the buttocks (full or breech). Others include frank breech, much like full breech but the baby's legs are extended toward his ears, and footling or incomplete breech, in which one or both legs are extended and the foot or feet are the presenting part. Another rare presentation is a transverse lie. This is where the baby is sideways in the womb and a hand or elbow has entered the birth canal first. While babies who present transverse will often move to a different position, this is not always the case and a cesarean birth then becomes necessary.

A newborn baby with umbilical cord ready to be clamped

The length of the second stage varies and may be affected by whether a woman has given birth before, the position she is in and mobility. The length of the second stage should be guided by the condition of the fetus and health of the mother. Problems may be encountered at this stage due to reasons such as maternal exhaustion, the front of the baby's head facing forwards instead of backwards (posterior baby), or extremely rarely, because the baby's head does not fit properly into the mother's pelvis (Cephalo-Pelvic Disproportion (CPD)). True CPD is typically seen in women with rickets and bone deforming illnesses or injuries, as well as arbitrary time limits placed on second stage by caregivers or medical facilities.

Immediately after birth, the child undergoes extensive physiological modifications as it acclimatizes to independent breathing. Several cardiovascular structures start regressing soon after birth, such as the ductus arteriosus and the foramen ovale. In some cultures, the father cuts the umbilical cord and the infant is given a lukewarm bath to remove blood and some of the vernix on its skin before being handed back to its parents.

The practice of leaving the umbilical cord to detach naturally is known as a Lotus Birth.

The medical condition of the child is assessed with the Apgar score, based on five parameters: heart rate, respiration, muscle tone, skin color, and response to stimuli. Apgar scores are typically assessed at both 1 and 5 minutes after birth.

Third stage: placenta

Breastfeeding during and after the third stage

In this stage, the uterus expels the placenta (afterbirth). Breastfeeding the baby will help to cause this. The mother normally loses less than 500 mL (2 cups) of blood. It is important to note that the placenta is to never be pulled from the mother by an untrained person; this could cause it to tear and not be expelled in whole. It is essential that the placenta be examined to ensure that it was expelled whole. Remaining parts can cause postpartum bleeding or infection.

The alternative to natural delivery of the placenta is what is called Active Management - this involves administration of a prophylactic oxytocic before delivery of the placenta, and usually early cord clamping and cutting, and controlled cord traction of the umbilical cord.

A Cochrane database study[2] suggests strongly that blood loss and the risk of postpartum bleeding will be reduced in women offered active management of the third stage of labour. However, the group treated with active third phase management, there was an increased risk of unpleasant side effects (eg nausea and vomiting), and hypertension. The authors suggest that this is due to the use of ergometrine as a component of the oxytocic. No advantages or disadvantages were apparent for the baby.

Details of CCT may be found at: http://library.med.utah.edu/nmw/mod2/Tutorial2/menu_norm.html It is important to emphasise that this procedure must not be attempted unless you have been appropriately trained.

After the birth

Medical professionals typically recommend breastfeeding of the first milk, colostrum, to reduce postpartum bleeding/hemorrhage in the mother, and to pass immunities and other benefits to the baby.

Parents usually bestow the infant its given names soon after birth.

Often people visit and bring a gift for the baby.

Many cultures feature initiation rites for newborns, such as naming ceremonies, baptism, and others.

Mothers are often allowed a period where they are relieved of their normal duties to recover from childbirth. The length of this period varies. In China it is 30 days and is referred to as "doing the month" (see Postpartum period). In other countries taking time off from work to care for a newborn is called "maternity leave" and varies from a few days to several months.

Variations

When the amniotic sac has not ruptured during labour or pushing, the infant can be born with the membranes intact. This is referred to as "being born in the caul." The caul is harmless and its membranes are easily broken and wiped away by the doctor or midwife assisting with the childbirth. In medieval times, and in some cultures still today, a caul was seen as a sign of good fortune for the baby, even giving the child psychic gifts such as clairvoyance, and in some cultures was seen as protection against drowning. The caul was often impressed onto paper and stored away as an heirloom for the child. With the advent of modern interventive obstetrics, premature artificial rupture of the membranes has become common, so babies are rarely born in the caul.

Pain

The amounts of pain experienced by women during childbirth varies. For some women, the pain is intense and agonizing; for other women there is little to no pain. Many factors affect pain perception; fear, number of previous births, fetal presentation, cultural ideas of childbirth, birthing position, support given during labor, beta-endorphin levels, and a woman's natural pain threshold. Uterine contractions are always intense during childbirth. Some women report these sensations as painful, though the degree of pain varies from individual to individual. Some women even find the sensations pleasurable.

Non-medical pain control

Some women believe that reliance on analgesic medication is unnatural, or believe that it may harm the child. They still can alleviate labour pain using psychological preparation, education, massage, hypnosis, water therapy in a tub or shower. Some women like to have someone to support them during labour and birth; often female family members such as her mother, a sister, the father of the baby, a close friend, a partner or a trained professional doula. Some women deliver in a squatting or crawling position in order to more effectively push during the second stage and so that gravity can aid the descent of the baby through the birth canal.

The human body also has its own method of pain control for labour and childbirth in the form of beta-endorphins. As a naturally occurring opiate, beta-endorphin has properties similar to pethidine, morphine, and heroin, and has been shown to work on the same receptors of the brain.[3] Like oxytocin, beta-endorphin is secreted from the pituitary gland, and high levels are present during sex, pregnancy, birth, and breastfeeding. This hormone can induce feelings of pleasure and euphoria during childbirth.[4]

Water births are being increasingly chosen by many women as an option for pain relief during labour and childbirth, and waterbirth has been proven in many trials to be not only a safe option for mother and baby, but in many cases show a reduction in the need for further analgesia, and a higher rate of birth 'without injuries'.[5][6][7][8] Many hospitals and birthing centres now offer women the option of waterbirth, either via custom-made 'birthing pools' or large bath tubs, and have policies to safeguard their use.

Meditation and mind medicine techniques for the use of pain control during labor and delivery. These techniques are used in conjunction with progressive muscle relaxation and many other forms of relaxation for the mind and body to aid in pain control for mothers during childbirth. These techniques are a form of natural pain control. One such technique is Calm Birth. This technique is a form of meditation that empowers and liberates the mother by uplifting her body and its natural process to welcoming her new child into the world.[citation needed]

Medical pain control

In Europe, doctors commonly prescribe inhaled nitrous oxide gas for pain control; in the UK, midwives may use this gas without a doctor's prescription. Pethidine (with or without promethazine) may be used early in labour, as well as other opioids, but if given too close to birth there is a risk of respiratory depression in the infant.

Popular medical pain control in hospitals include the regional anesthetics epidural blocks, and spinal anaesthesia. Doctors and many parents favor the epidural block because medication does not enter the mother's circulatory system, thus it does not cross the placenta and enter the bloodstream of the fetus. Some studies find that although epidural use can lengthen the labour and increase the need for operative intervention, it has no adverse effect on perinatal outcome, and is a safe and effective method of pain control.[9][10]

Different measures for pain control have varying degrees of success and side effects to mother and baby. The risks of medical pain control should be balanced against the fact that childbirth can be extremely painful, and anesthetics are an effective and generally safe way to control pain.

Complications and risks of birth

Problems that occur during childbirth are called complications. They can affect the mother or the baby. Sometimes they cause injury or even death. Doctors and midwives are trained to deal with these problems if they should occur.

Infant deaths (neonatal deaths from birth to 28 days, or perinatal deaths if including fetal deaths at 28 weeks gestation and later) are around 1% in modernized countries. The risk of maternal death during childbirth in developed nations is comparatively low; only about 1 in 1800 mothers die in childbirth (only 1 in 3700 in North America). In the Third World, it is a much riskier proposition: neonatal deaths rates in Sub-Saharan Africa and South Asia are more than 3.7%,[11] and on average 1 in 48 women die during childbirth.[12] The "natural" mortality rate of childbirth—where nothing is done to avert maternal death—has been estimated as being between 1,000 and 1,500 deaths per 100,000 births.[13] (See main article: neonatal death, maternal death)

Emergency airlift of woman in labor by the US Coast Guard

The most important factors affecting mortality in childbirth are adequate nutrition and access to quality medical care ("access" is affected both by the cost of available care, and distance from health services). "Medical care" in this context does not refer specifically to treatment in hospitals, but simply routine prenatal care and the presence, at the birth, of an attendant with midwifery skills. A 1983-1989 study by the Texas Department of Health revealed that the infant death rate was 0.57% for doctor-attended births, and 0.19% for births attended by non-nurse midwives. (The comparison may be misleading because higher-risk births are less likely to be attended solely by a midwife.) Conversely, some studies demonstrate a higher perinatal mortality rate with assisted home births.[14] Around 80% of pregnancies are low-risk. Factors that may make a birth high risk include prematurity, high blood pressure, diabetes and a previous cesarean section.

One of the most dangerous risks to the fetus is that of premature birth, and its associated low neonatal weight. The more premature (or underweight) a baby is, the greater the risks for neonatal death and for pulmonary, respiratory, neurological or other sequelae. About 12% of all infants born in the United States are born prematurely. In the past 25 years, medical technology has greatly improved the chances of survival of premature infants in industrialized nations. In the 1950s and 1960s, approximately half of all low birth weight babies in the US died. Today, more than 90% survive. The first hours of life for "premies" are critical, especially the very first hour of life. Rapid access to a Neonatal Intensive Care Unit is of paramount importance.

Some of the possible complications are:

Heavy bleeding during or after childbirth, which is the most common cause of mortality in new mothers, in both developed and undeveloped nations.[11] Heavy blood loss leads to hypovolemic shock, insufficient perfusion of vital organs and death if not rapidly treated by stemming the blood loss (medically with ergometrine and pitocin or surgically) and blood transfusion. Hypopituitarism after obstetric hypovolemic shock is termed Sheehan's syndrome.
Non-progression of labour (longterm contractions without adequate cervical dilation) is generally treated with intravenous synthetic oxytocin preparations. If this is ineffective, Caesarean section may be necessary. Changes in maternal position is effective in many cases.
Fetal distress is the development of signs of distress by the child. These may include rising or decreasing heartbeat (monitored on cardiotocography/CTG), shedding of meconium in the amniotic fluid, and other signs.
Non-progression of expulsion (the head or presenting parts are not delivered despite adequate contractions): this can require interventions such as vacuum extraction, forceps extraction or Caesarean section.
In the past, a large proportion of women died from infection puerperal fever, but since the introduction of basic hygiene during parturition by Ignaz Semmelweis, this number has fallen precipitously.
Lacerations can be painful. An episiotomy was once thought necessary to avoid tears involving the anal sphincter, but its routine use—once normal—has now been shown to increase the risk of deep lacerations especially involving and extending through the anal sphincter.

Instrumental delivery (Forceps and Ventouse)
The mother will have her legs apart supported in stirrups.
If an anaesthetic is not already in place it will be given.
For a forceps delivery an episiotomy will be done (a cut in the perineum or the region between the vagina and anus), for ventouse extraction an episiotomy is not always done.
After the head is delivered the rest of the delivery is done in the manual method.
After episiotomy or tears the mother is stitched up.
In some cases a 'Trial of Forceps' will be tried out, this will be done in the operating theatre, meaning they will try a forceps delivery and will switch to a caesarean section if it fails.

WARNING

2007-05-23T23:19:00.000-07:00

WARNING : FOR 18 YRS AND ABOVE ONLY

THIS SITE IS MEANT FOR EDUCATIONAL PURPOSES ONLY. THIS IS MEANT TO BE FRANK DISCUSSION OF HUMAN REPRODUCTIVE HEALTH WITH SPECIAL PAPERS ON ADOLESCENT REPRODUCTIVE HEALTH AND WALEFARE.
THE PAGES CONTAINS PHOTOS, DIAGRAMS AND SKETCHES OF HUMAN SEXUAL ORGANS, AND ANATOMY AND PHYSIOLOGY INCLUDING CHEMISTRY OF IT. SO SOME ARTICLES ARE NOT SUITABLE FOR BOYS / GIRLS UNDER 12 YRS OF AGE, AND SOME MAY FIND IT OFFENSIVE.
SO I SUGGEST THE PARENTS TO GO THROUGH THE ARTICLE AND DECIDE ON ITS DEGREE AND GUIDE THEIR WARDS ACORDINGLY. AND IF YOU ARE NOT 18
PARENTAL SUPERVISION IS ADVISED.
IF YOU DO NOT WISH TO CONTINUE PLEASE QUIT THE SITE AND GO BACK NOW.

ADOLESCENCE

2007-05-22T23:32:00.000-07:00

ADOLESCENCE:

Adolescence is recognized as both a cultural/social phenomenon and as a standardized human development phase.

In sociology, adolescence is seen as a cultural phenomenon for the working world and therefore its end points are not easily tied to physical milestones. The time is identified with dramatic changes in the body, along with developments in a person's psychology and academic career. In the onset of adolescence, children usually complete elementary school and enter secondary education, such as middle school or high school. A person between early childhood and the teenage years is sometimes referred to as a pre-teen or tween.

As a transitional stage of human development, adolescence is the period in which a child matures into an adult. This transition involves biological (i.e. pubertal), social, and psychological changes, though the biological ones are the easiest to measure objectively.

The ages of adolescence vary by culture. The World Health Organization (WHO) defines adolescence as the period of life between 10 and 19 years of age.[1] In contrast, in the United States, adolescence is generally considered to begin somewhere between ages 12 and 14, and end at 19 or 20. As distinct from the varied interpretations of who is considered an "adolescent", the word "teenager" is more easily defined: it describes a person who is thirteen to nineteen years of age.

During this period of life, most children go through the physical stages of puberty which often begins between the ages of nine and thirteen.

Most cultures regard people as becoming adults at various ages of the teenage years.

PUBERTY:

MAIN ARTICLE: PUBERTY

Puberty is the stage of the lifespan in which a child develops secondary sex characteristics (for example deeper voice in boys, and development of breasts in girls) as his or her hormonal balance shifts strongly towards an adult state. This is triggered by the pituitary gland, which secretes a surge of hormones into the blood stream and begins the rapid maturation of the gonads: the girl's ovaries and the boy's testicles.

The onset of puberty in girls appears to be related to body fat percentage. In most Western countries, the average age of menarche fell, in a secular trend, over the last century, possibly because of improved nutrition and increased caloric intake. Some theorists believe that analysis of data shows the age of onset of menarche to correlate to whether a girl lives with her natural father, a stepfather, or no father at all. Yet others propose a climatological connection and attribute the decreased average age of menarche in part to climate change or global warming. The debates regarding both of these theories are politically charged.

PRETEENS

MAIN ARTICLE: PRETEEN

The word preteen describes a child approaching the teenage years. The neologism tween has the same meaning, and isn't in general use as either a colloquial or scientific term. This word comes from the age being between that of a child and a teenager, and perhaps it has also been inspired by the first sounds of numeral twelve and the similarity to teen.

There is no universally agreed definition of "preteen", but the term may roughly be considered as covering the ages from 10 to 13 inclusive.

TEENAGERS

MAIN ARTICLE: YOUTH

The term teenager, or teen, is the usual Western designation for an Adolescent and derives from the western view that adolescence starts at 13 and ends at 20, the seven numbers, 13,14,15,16,17,18 and 19 all end in Teen if expressed in the decimal numerical representation.

Equivalent words in other languages may apply to a larger age bracket, including (at least some) preteens; e.g. tiener in Dutch officially from 12, colloquially from 10.

There are numerous activities in which teenagers engage, namely family, education, work and recreation; these occur in school, home, youth organizations and other settings throughout the community. Many argue that in Western cultures, a distinct youth culture has developed. This culture is often distinctly different from the mainstream culture, sometimes in rebellion against it, and thus is often referred to as a subculture or counterculture, although subcultures or countercultures themselves are not always necessarily youth-oriented. This rebellion is also referred to as youth voice, and is used in positively ways, including youth leadership and youth participation activities.

EMERGING ADULTHOOD

Some scholars have theorized a new stage of development, post-adolescence and pre-adulthood. Arnett (2000) calls this stage "emerging adulthood," and argues that it is characterized by "relative independence from social roles and from normative expectations...Emerging adulthood is a time of life when many different directions remain possible, when the scope of independent exploration of life's possibilities is greater for most people than it will be at any other period of the life course." Arnett notes, however, that this stage is situationally and culturally constructed (i.e., people in other countries may not experience this as a unique life stage).

PSYCHOLOGY OF ADOLESCENTS

MAIN ARTICLE: ADOLESCENT PSYCOLOGY

Adolescent psychology is associated with the notable changes in the behavior and characteristics of adolescents, cognitive, emotional and attitudal changes take place during this period, which can be a cause of conflict on one hand and positive personality development on the other.

Due to the adolescents' experiencing various cognitive and physical changes, it is frequently notable that they start giving more importance to their peer group and less to their parents, due to the aggregated influence of whom they might go on to indulge in activities not deemed as socially acceptable, although this may be more of a social phenomenon than a psychological one.

In the search for a unique social identity for themselves, adolescents are frequently found confused between the right and wrong. G. Stanley Hall denoted this period as one of "Storm and Stress" and, according to him, conflict at this developmental stage is normal and not unusual. Margaret Mead, on the other hand, attributed the behavior of adolescents to their culture and upbringing.[3] However, Piaget, attributed this stage in development with greatly increased cognitive abilities; at this stage of life the individual's thoughts start taking more of an abstract form and the egocentric thoughts decrease, hence the individual is able to think and reason in a wider perspective.[4]

Positive Psychology is sometimes brought up when addressing adolescent psychology as well. This approach towards adolescents refers to providing them with motivation to become socially acceptable and notable individuals, since many adolescents find themselves bored and unmotivated.[5]

It should also be noted that adolescence is the stage of a psychological breakthrough in a person's life when the cognitive development is rapid[6] and the thoughts, ideas and concepts developed at this period of life greatly influence the individual's life in future and play a major role in character and personality formation.[7]

ADOLSCENT SEXUALITY

Adolescent sexuality refers to sexual feelings, behavior and development in adolescents and is a stage of human sexuality. Sexuality and sexual desire usually begins to appear along with the onset of puberty. The expression of sexual desire among adolescents (or anyone, for that matter), might be influenced by social engineering, social control, taboos, and other kinds of social mores.

In the United States, sexual activity among adolescents is sometimes associated with a number of risks as well as stigmas and taboos. The risks of adolescent sexual activity is sometimes associated with include emotional distress, sexually transmitted diseases (including HIV/AIDS) and pregnancy through failure or non-use of birth control. In terms of sexual identity, sexual preferences among adolescents may vary greatly across the spectrum from heterosexuality and LGBT orientations to pansexuality and sexual fetishism.

SOCIAL CULTURAL

Entering post-secondary education is often considered a rite of passage in Western cultures.

In commerce, this generation is seen as an important target. Mobile phones, contemporary popular music, movies, television programs, sports, video games and clothes are heavily marketed and often popular amongst adolescents.

In the past (and still in some cultures) there were ceremonies that celebrated adulthood, typically occurring during adolescence. Seijin shiki (literally "adult ceremony") is a Japanese example of this. Upanayanam is a coming of age ceremony for males in the Hindu world. In Judaism, 12-year-old females and 13-year-old males become b'nai mitzvah and often have a celebration to mark this coming of age. Among some denominations of Christianity, the rite or sacrament of Confirmation is received by adolescents and may be considered the time at which adolescents becomes members of the church in their own right. African boys also have a coming of age ceremony in which, upon reaching adolescence, the males state a promise to never do anything to shame their families or their village. This was also continued among African-American slaves in the early days of slavery before the practice was outlawed. In United States, girls will often have a "sweet sixteen" party to celebrate turning the aforementioned age, a tradition similar to the quinceañera in Latino culture.

Adolescents have also been an important factor in many movements for positive social change around the world. The popular history of adolescents participating in these movements may perhaps start with Joan of Arc, and extend to present times with popular youth activism, student activism, and other efforts to make youth voice heard.

PRE EJACULATE:

Pre-ejaculate (also known as pre-ejaculatory fluid or Cowper's fluid, and colloquially as precum) is the clear, colorless, viscous fluid that is issued from the urethra of a man's penis when he is sexually aroused. The fluid is usually secreted by Cowper's glands during arousal, masturbation, foreplay or at an early stage during sex, some time before the man fully reaches orgasm and semen is ejaculated.

FUNCTION

Pre-ejaculatory fluid prepares the urethra for the passage of semen by neutralizing acidity due to any residual urine. It also lubricates the movement of the penis and the foreskin over the glans. The amount of fluid that the human male can issue varies widely among individuals, from imperceptible amounts to a copious flow.

COMPONENTS

There have been no large-scale studies of sperm in pre-ejaculate, but some smaller-scale studies suggest that any sperm present may be ineffectual at causing pregnancy.[1][2] This may account for the surprisingly low pregnancy rate (approximately 4% per year) among couples that practice perfect use of coitus interruptus.

The same studies have shown the presence of HIV, the virus responsible for the disease AIDS, in pre-ejaculate.

SEXUAL INTERCOURSE:

Vaginal sexual intercourse, also called coitus, is the human form of copulation. While its primary purpose is the reproduction and continued survival of the human species, it is often performed exclusively for pleasure and/or as an expression of love and emotional intimacy. Sexual intercourse typically plays a powerful bonding role; in many societies it is normal for couples to have frequent intercourse while using birth control, sharing pleasure and strengthening their emotional bond through sex even though they are deliberately avoiding pregnancy.

Sexual intercourse is also defined as referring to any form of insertive sexual behavior, including oral sex, as well as anal intercourse. The phrase to have sex can mean any or all of these behaviors, as well as other non-penetrative acts not considered here.

Coitus may be preceded by foreplay, which leads to sexual arousal of the partners, resulting in the erection of the penis and natural lubrication of the vagina.

To engage in coitus, the erect penis is inserted into the vagina and one or both of the partners move their hips to move the penis backward and forward inside the vagina to cause friction, typically without fully removing the penis. In this way, they stimulate themselves and each other, often continuing until highly pleasurable orgasm and ejaculation are achieved. Penetration by the hardened erect penis is also known as intromission, or by the Latin name immissio penis.

SEXUAL REPRODUCTION

Coitus is the basic reproductive method of humans. During ejaculation, which usually accompanies male orgasm, a series of muscular contractions delivers semen containing male gametes known as sperm cells or spermatozoa from the penis into the vagina. (While this is the norm, if one is wearing a condom, the sperm will almost never reach the egg.) The subsequent route of the sperm from the vault of the vagina is through the cervix and into the uterus, and then into the fallopian tubes. Millions of sperm are present in each ejaculation, to increase the chances of one fertilizing an egg or ovum. If female orgasm occurs during or after male ejaculation, the corresponding temporary reduction in the size of the vagina and the contractions of the uterus that occur can help the sperm to reach the fallopian tubes, though female orgasm is not necessary to achieve pregnancy. When a fertile ovum from the female is present in the fallopian tubes, the male gamete joins with the ovum resulting in fertilization and the formation of a new embryo. When a fertilized ovum reaches the uterus, it becomes implanted in the lining of the uterus, known as endometrium and a pregnancy begins.

OTHER FORMS OF SEXUAL INTERCOURSE

ORAL SEX
Oral sex consists of all the sexual activities that involve the use of the mouth, tongue, and possibly throat to stimulate genitalia. It is sometimes performed to the exclusion of all other forms of sexual activity. Oral sex may include the ingestion or absorption of semen or vaginal fluids.

ANAL SEX

Representation of Hadrian having anal sex with Antinous in Egypt

While there are many sexual acts involving the anus, anal cavity, sphincter valve and/or rectum, the specific meaning describes the insertion of a man's penis into another person's rectum.

Functions of sex beyond reproduction
The reverse missionary position is frequently combined with kissing, caressing and embracing.

Humans, bonobos[1] and dolphins[2] are all species that engage in heterosexual behaviors even when the female is not in estrus, that is, at a point in her reproductive cycle suitable for successful impregnation. (These three species, and others besides, are also known to engage in homosexual behaviors.[3])

In both humans and bonobos the female undergoes relatively concealed ovulation, so that both male and female partners commonly do not know whether she is fertile at any given moment. One possible reason for this distinct biological feature may be formation of strong emotional bonds between sexual partners important for social interactions and, in the case of humans, long-term partnership rather than immediate sexual reproduction.[4]

Humans, bonobos and dolphins are all intelligent social animals, whose cooperative behavior proves far more successful than that of any individual alone. In these animals, the use of sex has evolved beyond reproduction apparently to serve additional social functions. Sex reinforces intimate social bonds between individuals to form larger social structures. The resulting cooperation encourages collective tasks that promote the survival of each member of the group.

Alex Comfort[citation needed] and others [4] posit three potential advantages of intercourse in humans, which are not mutually exclusive: reproductive, relational, and recreational. While the development of the Pill and other highly-effective forms of contraception in the mid- and late 20th century increased peoples' ability to segregate these three functions, they still overlap a great deal and in complex patterns. For example: A fertile couple may have intercourse while contracepting not only to experience sexual pleasure (recreational), but also as a means of emotional intimacy (relational), thus making their relationship more stable and more capable of sustaining children in the future (deferred reproductive). This same couple may emphasize different aspects of intercourse on different occasions, being playful during one episode of intercourse (recreational), experiencing deep emotional connection on another occasion (relational), and later, after discontinuing contraception, seeking to achieve pregnancy (reproductive, or more likely reproductive and relational).

COITUS DIFFICULTIES:

While well-suited for effective stimulation of the penis, certain forms of coitus are much less effective at stimulating the clitoris, the seat of the female orgasm, because it is small and outside the vagina. Up to 70 percent of women[5] rarely or never achieve orgasm during coitus without simultaneous direct stimulation of the clitoris with the fingers or other implement. Most women do require such direct stimulation, and ignorance or disregard of this fact is seen as a common cause of female anorgasmia.

Anorgasmia is the lack of orgasm during otherwise pleasurable stimulation. It is much more common in women than men. The condition may be related to a psychological discomfort with or aversion to sexual pleasure, or to a basic lack of knowledge of what the woman finds physically pleasing and is likely to result in orgasm.[citation needed] A sense of shame, or the feeling that she "should" be able to climax can compound the problem, along with feelings of shame on the part of her partner, who may believe that he does not excite her sufficiently.[citation needed] Masturbation is a well supported method for a woman to explore her body and discover what feels good for her. The absence of a partner can remove the sense of performance anxiety and allow the woman to relax and enjoy. Good communication and patience are essential in helping an anorgasmic woman achieve orgasm. Whether a woman considers anorgasmia a problem or not is highly individual, though many women find it very frustrating.

Some males suffer from erectile dysfunction (ED), or impotence, at least occasionally. For those whose impotence is caused by medical conditions, prescription drugs such as Viagra, Cialis, and Levitra are available. However, doctors caution against the unnecessary use of these drugs because they are accompanied by serious risks such as increased chance of heart attack. Moreover, using a drug to counteract the symptom — impotence — can mask the underlying problem causing the impotence and does not resolve it. A serious medical condition might be aggravated if left untreated.

A more common sexual disorder in males is premature ejaculation (PE). The U.S. Food and Drug Administration is examining the drug dapoxetine to treat premature ejaculation. In clinical trials, those with PE who took dapoxetine experienced intercourse three to four times longer before orgasm than without the drug.

Vaginismus is involuntary tensing of the pelvic floor musculature, making coitus distressing, painful, and sometimes impossible.

Dyspareunia is a medical term signifying painful or uncomfortable intercourse, but does not specify the cause.

SEXUAL ETHICS AND LEGALITY:

Unlike some other sexual activities, vaginal intercourse has rarely been made taboo on religious grounds or by government authorities, as procreation is inherently essential to the continuation to the species or of any particular genetic line, which is considered to be a positive factor, and indeed, enables most societies to continue in the first place. Many of the cultures that had prohibited sexual intercourse entirely no longer exist; an exception is the Shakers, a sect of Christianity that has four adherents at current. There are, however, many communities within cultures that prohibit their members to engage in any form of sex, especially members of religious orders and the priesthood in the Roman Catholic Church and priests in Buddhist monasteries. Within some ideologies, coitus has been considered the only "acceptable" sexual activity. Relatively strict designations of "appropriate" and "inappropriate" sexual intercourse have been in human culture for hundreds of years. These have included prohibitions against specific positions, but even more often against:
Coitus among partners who are not married (this is sometimes referred to as fornication)

Coitus where a married person has sex with someone to whom they are not married. (called adultery or extramarital sex)

Coitus mongst partners who are not married for consideration (called prostitution).

Coitus amongst partners of the same sex (called sodomy).

Coitus with a close relative (called incest). This may also be called inbreeding in slang terms.

Coitus with children (called pedophilia).

Coitus amongst partners of different species (called bestiality).

More controversially in some societies there are (or have been in the past) taboos (social, religious and sometimes legal) against sexual relations with persons of differing ethnic, tribal or social (e.g caste) backgrounds.

Some cultures and religions, such as Islam and Judaism, prohibit coitus during a woman's menstrual period. This is because sacred texts specifically forbids it. There is no medical reason for abstaining during this time.

Often a community adapts its legal definitions during case laws for settling disputes. For example, in 2003 the New Hampshire Supreme Court ruled that same-sex relations do not constitute sexual intercourse, based on a 1961 definition from Webster's Third New International Dictionary, in Blanchflower v. Blanchflower, and thereby an accused spouse in a divorce case was found not guilty of adultery based on this technicality.

Most countries have age of consent laws specifying the minimum legal age for engaging in sexual intercourse. Sexual intercourse with a person against their will, or without their informed legal consent, is referred to as rape, and is considered a serious crime in many cultures around the world, including those found in Europe, northern and eastern Asia, and the Americas. Sex, regardless of consent, with a person under the age of consent is often considered to be sexual assault or statutory rape. The age of consent varies from country to country and often by state or region; commonly, the age of consent is set anywhere between twelve and eighteen years of age, with sixteen years being the most common age the law sets. Sometimes, the age of consent is lowered for people near the same age wishing to participate in intercourse. For example, in Canada, the minimum age of consent for all couples is 14. However, the age of consent can go below 14 on the condition that the couple still aren't 2 years of age apart. Religions may also set differing ages for consent, with Islam setting the age at puberty, which can vary from around 10 to 14. There are exceptions in the case of anal sex or people in a position of trust/authority

DURATION OF SEXUAL INTERCOURSE:

Many men suffer from premature ejaculation. Since most men, unlike women, cannot have multiple orgasms, intercourse normally ends when the man has ejaculated. Thus the woman might not have time to have an orgasm.

Vaginal sexual intercourse typically consists of a period of foreplay, followed by intromission and ejaculation. According to a Kinsey study, just under half of men reported a time to ejaculation from intromission of five minutes or less during their first marriage. Slowly the time increases but on an average duration of sexual intercourse from the time of insertion of the penis into the vagina and ejaculation is 4min to 6 min. Some form of local anesthesia can expand the time but not good for the health of penis and in future it may lead to severe sexual dysfunction.

SEXUAL AROUSAL

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SEXUAL AROUSAL

HUMAN SEXUAL AROUSAL

Unlike most animals, human beings of both sexes are potentially capable of sexual arousal throughout the year, therefore, there is no human mating season. Things that precipitate human sexual arousal are colloquially known as turn-ons. Turn-ons may be physical or mental in nature. Given the right stimulation, sexual arousal in humans will typically end in an orgasm, but may be pursued for its own sake, even in the absence of an orgasm.

MALE SEXUAL AROUSAL

Penile tumescence and erection (usually the most prominent and reliable sign of sexual arousal in males; however, adolescent males experience frequent 'non-sexual' erections stemming from their high level of testosterone.)
Retraction and tightening of the foreskin if present, often exposing the glans penis if not normally exposed (though this is not always the case)
Emission of pre-ejaculatory fluid
Swelling of the testes
Ascension of the testes
Tensing and thickening of the scrotum

HUMAN SEXUAL RESPONSE CYCLE:

During the 1950s and 1960s, William H. Masters and Virginia E. Johnson conducted many important studies within the field of human sexuality. In 1966, the two released a book, Human Sexual Response, detailing four stages of physiological changes in humans during sexual stimulation. These phases, in order of their occurrence, are excitement, plateau, orgasmic, and resolution.[1]

ERECTILE DYSFUNCTION

Erectile dysfunction (ED) or impotence is a sexual dysfunction characterized by the inability to develop or maintain an erection of the penis. There are various underlying causes, such as damage to the sigmoid mesocolon nerves which prevents or delays erection, or diabetes, which simply decreases blood flow to the tissue in the penis, many of which are medically reversible.

The causes of erectile dysfunction may be psychological or physical. Psychological impotence can often be helped by almost anything that the patient believes in; there is a very strong placebo effect. Physical damage is much more severe. One leading physical cause of ED is continual or severe damage taken to the sigmoid mesocolon nerves. These nerves are located directly behind the upper portion of the kidneys. Continual pressure or painful strikes to the area can affect the ability to achieve erection.

In the 1920's, Dr. Howard Flitz, a famous surgeon, conducted a series of experiments in which he applied pressure and series of electric shocks to the sigmoid mesocolon nerve of his patients. After a few weeks many of his patients reported back that they were having trouble obtaining an erection. It has been said that damage to this nerve can cause permanent ED. This experiment would not be able to be conducted today as it is ruled unethical.

Due to its embarrassing nature and the shame felt by sufferers, the subject was taboo for a long time, and is the subject of many urban legends. Folk remedies have long been advocated, with some being advertised widely since the 1930s. The introduction of perhaps the first pharmacologically effective remedy for impotence, sildenafil (trade name Viagra), in the 1990s caused a wave of public attention, propelled in part by the news-worthiness of stories about it and heavy advertising.

The Latin term impotentia coeundiae describes simple inability to insert the penis into the vagina. It is now mostly replaced by more precise terms.

NEURAL BIAS OF PUBERTY

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THE NEURAL BASIS OF PUBERTY AND ADOLESCENCE:

The pubertal transition to adulthood involves both gonadal and behavioral maturation. A developmental clock, along with permissive signals that provide information on somatic growth, energy balance and season, time the awakening of gonadotropin releasing hormone (GnRH) neurons at the onset of puberty. High-frequency GnRH release results from disinhibition and activation of GnRH neurons at puberty onset, leading to gametogenesis and an increase in gonadal steroid hormone secretion. Steroid hormones, in turn, both remodel and activate neural circuits during adolescent brain development, leading to the development of sexual salience of sensory stimuli, sexual motivation, and expression of copulatory behaviors in specific social contexts. These influences of hormones on reproductive behavior depend in part on changes in the adolescent brain that occur independently of gonadal maturation. Reproductive maturity is therefore the product of developmentally timed, brain-driven and recurrent interactions between steroid hormones and the adolescent nervous system.

Puberty and adolescence mark the metamorphosis of the child into the adult. Biologists have typically viewed puberty from an endocrine perspective because the overt signs of reproductive maturation are driven by hormonal changes occurring during this period of development. Over the past four decades, an appreciation for the neural control of hormone secretion and a gradual awareness of extensive brain remodeling during adolescence have shifted the emphasis to a neural basis for reproductive maturation. Neuroscientists wish to answer two main questions about puberty: how is it timed and what are the underlying neural mechanisms? This review summarizes the neurobiology of puberty and describes the complexity of the maturational processes that underlie the transition into adulthood.

The terms puberty and adolescence are often used interchangeably. To specialists, however, puberty refers to the activation of the hypothalamic-pituitary-gonadal axis that culminates in gonadal maturation. Adolescence refers to the maturation of adult social and cognitive behaviors. These nuances of terminology capture the two essential elements of adulthood: production of gametes and a behavioral means for bringing male and female gametes together. The central position of this review is that gonadal maturation and behavioral maturation are two distinct brain-driven processes with separate timing and neurobiological mechanisms, but they are intimately coupled through iterative interactions between the nervous system and gonadal steroid hormones. The collective endpoint of these two processes is the reproductively mature adult.

GnRH neurons are central to gonadal and behavioral maturation
The control of GnRH secretion is fundamental to reproductive maturation. GnRH is a decapeptide produced by specialized neurons that intermittently secrete pulses of hormone from nerve terminals positioned in the median eminence of the basal hypothalamus. GnRH enters the pituitary portal vasculature and travels to the pituitary to signal the synthesis and secretion of the pituitary gonadotropins: luteinizing hormone (LH) and follicle stimulating hormone (FSH). Blood-borne LH and FSH act on target cells in the testes and ovaries to direct the production of sperm and eggs, as well as the secretion of steroid hormones. Gonadal steroids are vital to both gonadal function and reproductive behavior. Within the gonads, steroid hormones participate in spermatogenesis and follicle maturation. Within the brain, steroids influence GnRH secretion via neuroendocrine feedback loops and facilitate sexual behavior. Modulation of GnRH pulse frequency is the primary mechanism by which the body alters its reproductive status during development, and a relatively short interpulse interval is required to produce a pattern of gonadotropin and steroid hormone secretion that supports gonadal function and reproductive behavior.

Sex steroids promote secondary sex characteristics in peripheral tissues, regulate GnRH neurons via a neuroendocrine feedback loop and facilitate social behaviors by acting on central neural circuits. The pubertal increase in GnRH neuronal activity and episodic gonadotropin secretion is grossly timed by a developmental clock and fine-tuned by the neural integration of multiple permissive internal and external signals. At the onset of puberty, steroid feedback and steroid-independent neural mechanisms are engaged to disinhibit and excite GnRH neurons.

Determining the neural mechanisms that underlie episodic GnRH secretion has proved to be a major conceptual and technical challenge due to the neuroanatomy of the GnRH system . First, despite their enormous responsibility, GnRH neurons are surprisingly few in number, with only 1,000−3,000 cells consistently found across mammalian species. Second, GnRH neurons arise from the nasal placode region during early embryologic development, migrate into the brain and spread diffusely throughout the diagonal band of Broca, septum, organum vasculosum of the lamina terminalis, preoptic area and hypothalamus. The widespread distribution of GnRH cell bodies has hampered efforts to describe the sources and phenotypes of direct afferent inputs to these neurons. Finally, most GnRH neurons have a simple bipolar or unipolar morphology, and innervation of GnRH cell bodies is sparse compared to neighboring neurons. Yet GnRH neurons somehow fire synchronously to produce the intermittent episodes of hormone release in the median eminence. Recent successes with in vivo electrophysiological monitoring of GnRH activity are beginning to shed light on how amino acid neurotransmitters and steroid hormones alter GnRH excitability and synchrony 3, 4, 5, 6, 7, 8, but the neurobiological basis of the GnRH pulse generator remains elusive.

In most mammals, transient activation of the hypothalamic-pituitary-gonadal axis during late prenatal or early postnatal life results in an increase in circulating gonadal steroids, which participate in sexual differentiation and other programming of the nervous system. GnRH secretion declines soon thereafter, and hormone pulse frequency slows to about one discharge every few hours throughout the prepubertal period, which may last several years in long-lived species. After this period of quiescence, puberty begins when GnRH secretion once again gradually increases and remains high to stimulate gonadotropin and steroid hormone secretion, this time resulting in complete gonadal maturation and the capacity to express reproductive behavior. But what times the resumption of frequent GnRH secretion to drive the pubertal transition?

Multiple permissive signals time onset of puberty:

A perpetual goal for researchers is to find the 'trigger' that induces the re-emergence of GnRH secretion at puberty. Findings reported in the scientific and popular press have implicated various candidates, including melatonin, body fat, leptin and most recently a single gene! Hope is now fading for finding a single trigger for puberty because of the number and complexity of the variables that determine reproductive success9, 10, 11. Rather, we are finding that multiple signals are involved. Thus far, scientists have identified signals that permit puberty to occur or progress, but do not cause puberty. We call these 'permissive' signals.

Researchers have made much progress toward identifying the permissive signals and locating their respective sensors. Not surprisingly, the permissive signals vary with species and sex, and most relate to energy balance. The consequences of puberty, such as the defense of territory or mate, pregnancy and care of young, are energetically expensive. For this reason, the timing of puberty is critical: the individual must perceive whether it has grown sufficiently (through metabolic cues), what its relationship is to other individuals (through social cues) and whether conditions are optimal to begin the reproductive process (through environmental cues). For example, metabolic fuel availability, insulin, glucose and leptin in females serve as important signals for the attainment of somatic growth sufficient to support pregnancy. Sensors in the hypothalamus and hindbrain monitor these signals and permit high-frequency GnRH release when the signals reach appropriate levels12, 13, 14, 15, 16, 17, 18. Except in the extreme, energy imbalance affects reproductive maturation and fertility relatively less in males, perhaps because males do not face the risk of pregnancy and lactation. For many seasonal breeders, the photoperiod signals the optimal time of year for puberty onset19, 20. The circadian clock in the suprachiasmatic nucleus measures day length by controlling melatonin production in the pineal gland. The duration of the nocturnal elevation in melatonin encodes day length, and melatonin receptors in the thalamus and hypothalamus transduce this signal to GnRH neurons . In other species, sensory cues from conspecifics permit the onset of GnRH secretion at puberty 22, 23.

Multiple permissive signals determine the precise timing of puberty onset and are integrated in a species-specific manner to allow or not allow the pubertal increase in GnRH to proceed, depending on the interplay, balance and hierarchy among the signals . The integrating mechanism is still unknown. A matter of debate is whether integration is intrinsic to the GnRH neuronal system, with subpopulations of GnRH neurons receiving different types of synaptic input corresponding to the various signals, or whether there is an independent master integrator providing a 'go/no-go' signal to GnRH neurons.

A developmental clock ultimately times puberty onset:

Combinations of permissive signals cannot fully explain the timing of puberty, as the use of such signals is not unique to this period of life. Many are used later on to time other transitions from low- to high-frequency GnRH secretion, such as the resumption of fertility after birth and lactation, seasonal anestrus, restricted diet or high energy expenditure. One could argue that puberty is unique because it represents the first alignment of several permissive signals that result in a maturation that is never again replicated. However, this line of reasoning is unsatisfying because the starting point for an infertile juvenile is not the same as for an infertile adult. We are left with the simple recognition that there is a maturational component in the juvenile that makes puberty unique. Such a view leads to the concept of an innate developmental clock that times the unfolding of primary genetic programs and produces the internally derived signals that in turn determine the responses to both internal and external permissive signals. According to this broad reasoning, permissive signals would not influence the ticks of the developmental clock, but their combination would determine precisely when the puberty alarm would sound.

If the maturational component of puberty is a clock mechanism, then there must be key regulatory genes that are an integral part of the developmental process. Among the candidates, genes encoding members of the POU homeodomain family of transcription factors were first proposed as master regulators for the onset of puberty because of their temporal and spatial expression patterns in the hypothalamus and their ability to transactivate genes encoding GnRHor proximal regulators of GnRH synthesis and secretion 24, 25, 26, 27. More recent reports have nominated GPR54 as the 'puberty gene.' GPR54 encodes a G protein−coupled receptor, and mutations in the gene lead to the absence of increased GnRH secretion at puberty 28, 29. Despite these identified genetic mechanisms, we are extremely cautious about designating any of these genes to be a master regulator of puberty. Rather than being part of a developmental clock, they may simply act as downstream mechanisms governing GnRH synthesis and release. Identification of master regulatory genes directing the unique maturational component of the first and most important transition to fertility remains an unsolved part of the puberty mystery.

Sex differences in the timing of puberty:

Males and females often initiate and end puberty at different times, and the magnitude and tempo of these differences are species dependent. The order is as well. For example, girls show outward signs of puberty before boys, but male lambs begin puberty before female lambs. We know little about the mechanisms for these timing differences, but whatever they are, they must originate within the brain, given its essential role in regulating GnRH secretion. Most likely, these mechanisms are both genetic and programmed, but a pure genetic basis is difficult to evaluate because neurons are bathed in a variety of substances during development. We are beginning to appreciate how the timing of puberty can be prenatally programmed by sex steroids. For example, studies in sheep reveal that prenatal administration of testosterone to the developing female will advance the time of the pubertal GnRH rise by several months such that it resembles the earlier timing seen in males. Moreover, the timing of the pubertal GnRH rise depends on when the female is first exposed to the sex steroid, as well as the amount and duration of exposure. Although it is attractive to suppose that the timing of puberty and certain dysfunctions in adult reproduction may have fetal origins, the neuroanatomical basis of such effects is not clear. Prenatal steroid organization of postnatal GnRH secretion does not involve changes in the number, distribution or morphology of GnRH neurons in the rat, monkey or sheep as they are the same in both sexes. This reinforces the notion that whereas the basal activity of these 'pacemaker' neurons could be endogenous, the GnRH neurosecretory system requires external input to modulate physiologically meaningful changes in activity. Thus, sexual differentiation of presynaptic input to the GnRH system is important for its differential function in the developing male and female. Indeed, this hypothesis is supported by electron microscopy in the sheep, where there are more synaptic contacts on GnRH neurons of adult females than males, and prenatal exposure of females to testosterone decreases the number of synapses in females.

Steroid-independent vs. steroid-dependent mechanisms:

The developmental clock and permissive signals that time the onset of puberty engage two broad types of neural mechanisms that impose prepubertal quiescence of GnRH neurons and their subsequent activation at the onset of puberty. As a theoretical framework, these mechanisms can be categorized as those that act without hormonal information from the gonads (steroid independent) and those that act in the presence of gonadal steroids (steroid dependent).

In some altricial species, those that are not well developed at birth, steroid-independent mechanisms are primarily responsible for the postnatal changes in the pattern of GnRH secretion. Researchers have studied this most in the rhesus monkey and rat For example, after elimination of gonadal steroids by neonatal castration of male monkeys, gonadotropin levels remain very low during the two-to-three-year prepubertal period, but then gradually rise to high levels at the expected age of puberty, a pattern of hormone secretion that is the same as that observed in gonad-intact males. Similarly, peripubertal LH secretion increases in both gonad-intact and ovariectomized female rats and in humans with no circulating gonadal steroids due to gonadal dysgenesis. These same steroid-independent mechanisms also operate prenatally in precocious species such as the guinea pig and sheep, which are well developed at birth.

Steroid-dependent mechanisms that regulate GnRH release involve changes in sensitivity to gonadal steroid negative-feedback regulation of GnRH neurons. During the prepubertal period, GnRH neurons are highly sensitive to negative feedback, which permits only a slow frequency of GnRH release so that the gonads remain immature. At the onset of puberty, sensitivity to negative feedback decreases, which permits expression of high-frequency GnRH pulses that subsequently drives the pubertal increase in gonadotropin secretion and leads to gonadal maturation. This remarkable change in the 'gonadostat' clearly underlies the pubertal increase in GnRH secretion in some species, most notably in sheep, hamsters and ferrets. In these species, early postnatal gonadectomy results in an immediate increase in gonadotropin secretion, and levels remain elevated during the prepubertal period in the absence of steroid hormones. Replacing steroid hormones causes gonadotropins to return to the typically low levels during the prepubertal period of high sensitivity to negative feedback. During the pubertal transition, the 'escape' from negative feedback is manifest by an increase in gonadotropin levels at the time of puberty in face of constant levels of steroid hormone.

As a theoretical construct, the dichotomy of steroid-independent and steroid-dependent mechanisms has increased our appreciation of the different ways that the body controls GnRH secretion. However, in most species, both types of mechanisms come into play at different points during puberty to boost GnRH secretion. For example, after a steroid-independent increase in GnRH secretion at the onset of puberty in female monkeys, a decrease in sensitivity to steroid negative feedback drives a late puberty increase in GnRH pulse frequency. Perhaps the steroid-independent system provides coarse control and the steroid-dependent system provides fine control. In this sense, in nonhuman primates and children, the steroid-independent control of GnRH secretion would determine the year when first ovulation is possible, whereas the steroid-dependent control mechanism would determine the week when first ovulation occurs. This may not be the case in all species, for a decrease in sensitivity to negative feedback in male hamsters leads to the initial pubertal increase in gonadotropin secretion, which is enhanced during late puberty by steroid-independent mechanisms.

GnRH neurons are excited at puberty:

Both steroid-independent and -dependent mechanisms, driven by the brain, suppress GnRH secretion during the prepubertal period and enhance GnRH secretion during puberty, but what are the downstream mechanisms that regulate GnRH neurons? Although these mechanisms do not control the timing of puberty, they form a critical part of the terminal pathway that conveys temporal information from the upstream steroid-independent and -dependent integrator systems and regulates the GnRH neurosecretory network. In the search for neural mechanisms that directly modulate GnRH secretion, most research has focused on whether pubertal activation of GnRH neurons results from a decrease in inhibitory input or an increase in excitatory input to the GnRH system, as well as which neurochemicals provide the inhibitory and excitatory tone . The answers are species- and sex-dependent. In female monkeys, the pubertal rise in GnRH secretion seems to result from a decrease in GABAergic inhibition and a concomitant increase in glutamatergic excitation of GnRH neurons, along with potentiation of glutamate excitation by norepinephrine and neuropeptide Y38. In male monkeys, a similar disinhibition/excitation of GnRH neurons operates at the onset of puberty, except that neuropeptide Y is the prime candidate for prepubertal inhibition of GnRH release. In rats, the evidence for strong tonic prepubertal inhibition of GnRH is not clear; however, glutamatergic NMDA receptor activation accelerates, and NMDA receptor blockade delays, the onset of puberty, indicating an increased excitatory drive of GnRH neurons at puberty. Researchers have also proposed that glial-neuronal interactions at the level of GnRH terminals are involved in the onset of puberty through facilitation of GnRH release by glial-derived growth factors in the epidermal and transforming growth factor families.

In no species do we definitively know whether pubertal disinhibition and excitation of GnRH secretion involves changes in direct or indirect synaptic input to GnRH neurons. Some GnRH neurons express receptors for GABA and glutamate and the proportion of GnRH neurons that express the NMDA-R1 subunit increases with pubertal development in female rats. In addition, the number of synaptic contacts onto GnRH perikarya increases with pubertal development in rats and monkeys. The unraveling of how GnRH neurons are inhibited before puberty and activated at the onset of puberty will no doubt keep neuroscientists occupied for some time to come, and the final picture will surely be complicated. As a case in point, recent reports of a switch from GABA depolarization of GnRH neurons before puberty to GABA hyperpolarization of GnRH neurons at the time of puberty must be reconciled with the finding that blockade of GABA action increases GnRH secretion.

A pubertal decrease in sensitivity to steroid negative feedback does not seem to be related to changes in nuclear steroid hormone receptor expression within GnRH or other types of neurons, although this conclusion remains tentative because the direct sites and mechanisms of action for steroid regulation of GnRH secretion are unknown. In addition to nuclear receptor-mediated alterations in gene transcription within neurons, steroid hormones influence GnRH cell excitability by modulating ion conductance across potassium, chloride and calcium channels. One interesting but unexplored possibility is that pubertal changes in the gonadostat are mediated by developmental changes in ion channel subunit expression in GnRH neurons or their upstream neuronal regulators, which could also be involved in the dynamic interplay between GABAergic and glutamatergic control of GnRH secretion described above. Finally, it must be noted that these immediate controls of GnRH secretion, including those described for neurotransmitters and even steroid-dependent and -independent regulation, may not be unique to the pubertal transition because numerous reversals to infertility may occur during the lifespan. The re-emergence of high-level GnRH secretion after these periods of adult infertility may use these same immediate, general mechanisms.

Behavioral maturation during adolescence:

Up to this point, we have considered that the timing of gonadal activation lies in an elusive developmental clock whose signals integrate with permissive cues to modulate a passive GnRH neurosecretory system and drive the maturational changes in sex steroids. How does this scheme relate to the parallel changes occurring in behavior during maturation? In one sense, the timing of adolescent behavioral maturation depends on the timing of gonadal maturation because steroid hormones are required for the overt expression of reproductive behavior. However, it is clear that some important aspects of behavioral maturation are not driven solely by the appearance of steroid hormones at the time of puberty, because hormone treatment fails to fully activate copulatory behavior in prepubertal animals, indicating a need for further maturation of central and peripheral tissues before behavior can be expressed. Thus, as with puberty, there appears to be a developmental clock that times behavioral maturation during adolescence and that limits the age at which fully mature adult reproductive behavior can be expressed. A critical question is whether the developmental clock timing behavioral maturation is the same as that timing gonadal maturation.

Gonadal steroids are well-known regulators of reproductive behavior, influencing the structure and function of behavioral circuits during both early development and in adulthood. In males, testosterone and its metabolites facilitate sexual motivation and copulatory behaviors. In females, estradiol and progesterone facilitate proceptive and receptive behaviors that signal a readiness to mate. Traditional thinking holds that gonadal steroids, acting during a sensitive period spanning late embryonic and early neonatal development, sexually differentiate neural circuits that are destined to mediate adult male and female reproductive behavior (see accompanying review in this issue). In adulthood, steroid hormones facilitate reproductive behavior in specific social contexts by eliciting cellular responses within the previously sexually differentiated neural circuits. The irreversible changes in nervous system structure and the programming of adult behavioral responses to hormones caused by exposure to steroids during early neural development are called 'organizational effects'; the facilitation of reproductive behavior by steroids in adulthood, which is reversible if hormone is removed, is called an 'activational effect'.

As originally conceived, the organizational-activational framework for steroid control of reproductive behavior presumed a strictly activational role for gonadal steroids during adolescence. A recent modernization of this thinking incorporates dual roles for steroid hormones, which not only activate, but also organize neural circuits during adolescence68. For example, castration of male hamsters after the neonatal period of sexual differentiation, but before puberty, reduces testosterone-induced activation of behavior in adulthood compared to castration of males after puberty. Furthermore, neither prolonged hormone replacement nor sexual experience in adulthood reverses these behavioral deficits, demonstrating irreversible and adverse consequences for behavior if gonadal hormones are absent during adolescence. Two other examples of behaviors that are organized during adolescence are territorial scent marking in tree shrews and social interactions in a novel environment in rats. In both cases, the absence of gonadal hormones or pharmacological blockade of their action during adolescence prohibits adult-typical expression of the behavior, even if hormones are replaced in adulthood. Moreover, the inability of hormone treatment in adulthood to reverse the consequences of hormone absence during adolescence in all of these cases suggests that adolescence may be a sensitive period for further steroid-dependent organization of neural circuits mediating reproductively relevant social behaviors.

The sequence of events during steroid-dependent adolescent maturation of reproductive behavior may be an initial reorganization of circuits that further sensitizes them to hormone activation, followed by activation of behavior in an appropriate social context. This could explain why exogenous steroid treatments that reliably activate reproductive behavior in adults are less effective at doing so in prepubertal animals. Steroid treatments may be more efficacious in adults either because adult brains have already been organized and primed for more rapid activational responses, or because the prepubertal brain is less sensitive to organization and activation by steroid hormones.

The neural circuits mediating reproductive behavior include areas involved in sensory associations and motivation (amygdala), male mounting and female receptive behaviors (preoptic area, ventromedial nucleus of the hypothalamus) and motor control of behavior (central gray, ventral tegmentum, spinal nucleus of the bulbocavernosus, dorsal horn). Cells in many of these regions express nuclear receptors specific for androgens, estrogens and progestins. Receptor activation by hormone elicits a variety of cellular responses through receptor-mediated transcriptional activity and alterations in cell excitability. Reproductive behavior is complex and its manifestation relies on receipt of sensory stimuli from a partner, motivation to mate and motor output . Not surprisingly, virtually all of the classical amino acid and gaseous neurotransmitter systems are involved, as well as numerous neuropeptides and scores of receptor subtypes. A summary is beyond the scope of this review, but neural mechanisms of male and female reproductive behavior have been extensively reviewed by others

Adolescent maturation of reproductive behavior requires remodeling and activation of neural circuits involved in salience of sexual stimuli and sensory associations, sexual motivation and sexual performance.

Structural remodeling of the brain during adolescence occurs through both steroid-dependent and steroid-independent mechanisms.

Compared with activation of neural circuits by steroid hormones, we know relatively little about steroid-dependent organization during adolescence. Presumably, there are many similarities to the processes involved in steroid-dependent sexual differentiation during early neural development, such as regulation of cell death and survival, and synaptic density and connectivity (see accompanying review67 in this issue). Some structural sexual dimorphisms are established during puberty and adolescence, such as size of the rat hypothalamic anteroventral periventricular nucleus, cell number in the rat visual cortex, size of the rat locus coeruleus, dendritic arborizations of spinal motor neurons and size of the human bed nucleus of the stria terminalis. The enduring structural and functional changes resulting from adolescent reorganization of the brain impart uniqueness to behavioral maturation that is never exactly repeated, even, for example, during annual reactivation of reproductive behavior in seasonally breeding species. A challenge for future research will be to clarify which changes in behavioral circuits during adolescence result from activational effects and which result from organizational effects of steroid hormones.

Steroid-independent behavioral maturation

Although we have recognized for decades the contribution of both steroid-dependent and steroid-independent mechanisms to the pubertal rise in GnRH secretion, the idea that both types of mechanisms contribute to behavioral maturation is even newer than the understanding that steroid hormones both organize and activate reproductive behavior during adolescence. An experimental protocol similar to that used to show steroid-independent influences on pubertal activation of GnRH secretion reveals that the propensity for male reproductive behavior increases during adolescence, even if the organizational and activational effects of steroids during adolescent development are eliminated by prepubertal castration. Specifically, copulatory behaviors in adult male hamsters can still be activated by an activational dose of testosterone, even though the hamsters were castrated before puberty. However, the levels of behavior are not as high as those seen in males in which gonadal hormones were present during adolescence. In contrast, copulatory behavior cannot be activated in prepubertal males. That behavior cannot be activated before puberty, but can be activated in adulthood even when gonadal hormones are absent during adolescence, demonstrates that steroid-independent maturational changes occurring during adolescence contribute to the ability to express adult reproductive behavior, and underscores the separation of gonadal maturation and behavioral maturation.

The neurobiological underpinnings of steroid-independent maturational changes in circuits mediating reproductive behavior are unknown. However, steroid-independent structural changes during adolescence have been described for other neural systems. For example, high expression of dopamine receptors in the striatum characterizes early adolescence in the rat and is followed by a pruning of these receptors in later adolescence. This pattern is more pronounced in males than in females, but in both sexes it proceeds even when gonadal hormones are removed before puberty. Disturbances in this developmental programming have been linked to schizophrenia and attention-deficit hyperactivity disorder. Identifying the structural correlates of behavioral maturation, and distinguishing between those that are driven by steroid hormones and those that are not, is an area ripe for discovery.

Sexual salience of sensory stimuli and sexual motivation
Steroid activation of reproductive behavior does not occur in a vacuum. It also requires perception of sexually salient sensory stimuli, which are encountered in social interactions and modulate activity within steroid-sensitive behavioral circuits. Maturation of adult reproductive behavior also requires the acquisition of sexual salience of sensory stimuli . For example, the odor of an adult female is likely to mean one thing to a weanling male (mom) and yet another thing to an adult male (potential mate).

Odor preferences, neural and behavioral responses to sensory stimuli, and social affiliations all change with adolescent development. For example, in species in which chemosensory stimuli are important, preference for opposite-sex odors emerges with adolescent development and neuroendocrine and neurochemical responses to odors that are typical in adults do not occur in juveniles. In rhesus monkeys, juvenile males indiscriminately mount males and females, whereas adult males almost exclusively mount females in sexual contexts, indicative of maturation of sensory and behavioral cues that motivate the behavior.

In adulthood, steroid hormones alter both the quality of sensory stimuli produced by a potential mate and the responses elicited by those stimuli. In addition to these activational effects, steroids may organize circuits during adolescence in a way that programs sensory responses and associations. Gonadal steroids organize both primary sensory cortex and sensory association areas such as the amygdala and hippocampus during perinatal and/or adolescent development. For example, ovarian hormones during adolescence promote programmed cell death in rat visual cortex, leading to an adult sex difference in cell number and cortical volume. Via an androgen receptor−mediated process, testicular hormones during adolescence program a shift from long-term potentiation to long-term depression in hippocampal CA1 synaptic plasticity. These organizing effects are likely to influence responses to sensory stimuli in adulthood.

Closely linked to acquisition of sensory associations and sexual salience is the development of sexual motivation . Behavioral indicators of sexual motivation are generally not present in juvenile animals, and it has been argued for both males and females that acquisition of sexual motivation is a key component of reproductive maturation. Researchers further postulate that steroid hormones stimulate sexual motivation, and that some process occurring during adolescence links sexual behavior to a hormonally modulated motivational system. Research has also proposed that pubertal activation of the adrenal gland (adrenarche) is related to adolescent development of sexual attraction.

A better understanding of the neural mechanisms that underlie adolescent development of sexual motivation is likely to come from our increasing awareness of adolescent remodeling of cortical, limbic and reward areas of the brain. This remodeling includes processes such as increased myelination and decreased gray matter volume in cortical areas synaptic elaboration and subsequent pruning in striatum and prefrontal cortex, cell death in primary visual cortex and changes in connectivity in the amygdala and prefrontal cortex. There are also sex differences in the timing and magnitude of these structural changes. Brain areas involved in sensory associations and motivation mature much later than primary sensory and motor areas, and adolescent brain maturation in humans continues through the early twenties. Collectively, these brain rearrangements are postulated to be linked to adolescent changes in decision making, risk taking, planning, drug sensitivity and reward incentive

Summary:

We have attempted to make the case that attainment of adult reproductive status involves both gonadal and behavioral maturation, and that both processes come about through a series of brain-driven, developmentally timed events that are modulated by internal and external sensory cues. Gonadal and behavioral maturation are intimately linked through multiple and complex interactions between the nervous system and gonadal steroid hormones. The brain initiates activation of the GnRH system at puberty onset, leading to an increase in steroid hormone production. Steroid hormones in turn modulate GnRH secretion in the brain, and organize and activate neural circuits mediating reproductive behavior during adolescence. These effects of hormones on behavior depend in part on pubertal changes in the nervous system that occur independently of gonadal maturation. Thus, while gonadal maturation and behavioral maturation are separate and interacting processes, the two are normally temporally coordinated, presumably maximizing reproductive success. Research in animal models unambiguously shows that disruptions in this temporal coordination influence neural responses and behavior in adulthood. This, together with evidence that adolescent development is a time of experience-dependent brain reorganization suggests that individual differences in adult behavior could arise in part from normal variation in temporal coordination between gonadal and behavioral maturational processes .

Neuroscientists have made enormous strides in calling attention to the role of the brain in reproductive maturation, in identifying the proximal signals and neural mechanisms that drive the activation of GnRH neurons at the onset of puberty, in characterizing the neural circuits that mediate reproductive behavior and in recognizing adolescence as a time of profound remodeling of the brain. Three fundamental questions remain. What are the workings of the developmental clock(s) that provides gross timing of reproductive maturation? What is the neural basis for the integration of permissive signals that fine-tune the timing of reproductive maturation? What are the consequences of adolescent remodeling of the brain for adult behavior? Future work on these questions will deepen our understanding of the process of puberty and adolescence.

PENIS ANATOMY:

Penis size is of great concern to many people. Some consider having a large penis a mark of masculinity; others are concerned that their penis is too small to satisfy their sexual partners. These insecurities have led to many myths about penis size, and the creation of a whole industry devoted to penis enlargemen

MEASURING THE PENIS:

There are a variety of different ways to measure a penis, and there are a number of difficulties in doing so. First of all, a penis must be maximally erect to do so, and in a clinical setting this is difficult to achieve. At least one Brazilian doctor resorted to injecting penises with drugs to induce an erection, giving much more consistent results[citation needed]. Relying on self-reporting of penis size is problematic, since some patients exaggerate or are unable or unwilling to measure the penis correctly.

Length of a penis is typically measured with the subject standing and the penis held parallel to the floor. Measurement of length goes horizontally along the top of the penis from the patient's body to the tip. The length is usually quoted as either "bone-pressed" or "non-bone-pressed". "Bone-pressed" means that the ruler is pressed to the pubic bone; this largely removes the problem of body fat interfering with the measuring process, as the penis will appear shorter for subjects with a high level of body fat.

Girth is measured by using a tape measure. It is variously quoted as an average, or at 3 places along the penis, or just the penile head, or in the middle of the shaft, at the base, or from the thickest part.
Data

There have been several studies regarding the average size of the human penis. The majority of such studies could be flawed due to Self-selection bias: Men with a below-average sized penis might be less likely to allow themselves to be measured (making the figures noted below above the true average), or men with a larger-than average sized penis might be more likely to allow themselves to be measured (making the figures noted below also above the true average).

There is an ongoing penis size government study in India, commissioned with the goal of helping reduce the high condom failure rate there. [citation needed]

SIZE AT BIRTH:

Average stretched penile length at birth is about 4 cm, and 90% of newborn boys will be between 2.4 and 5.5 cm (0.94 and 2.17 inches). Limited growth of the penis occurs between birth and 5 years of age, but very little occurs between 5 years and the onset of puberty. The average size at the beginning of puberty is 6 cm with adult size reached about 5 years later.

ERECT LENGTH:

Frequency graph of LifeStyles data

Percentile plot of LifeStyles data

Regarding the length of the adult fully erect penis (measured along the top of the penis from the groin to the tip), several studies have been performed. Studies that have relied on self-measurement consistently reported a higher average than those that had staff take the measurements.
A study published in the September 1996 Journal of Urology concluded that average erect length was 12.9 cm (5 inches. (Measured by staff).

A UCSF study by Wessells et.al. published in 1996 found an average of 5.1 inches (13.0 cm). (Measured by staff)

A study by a Brazilian urologist found an average of 5.7 inches (14.5 cm). (Measured by staff)

A German study in 1996 also reported an average of 5.7 inches (14.5 cm). (Measured by staff)

A study conducted by LifeStyles Condoms during 2001 Spring Break in Cancún found an average of 5.9 inches (15.0 cm). (Measured by staff)
A study conducted by the Korean Consumer Protection Board (KCPB) at a college campus found an average of 6.1 inches (15.5 cm).[citation needed]

A study conducted by the Journal of Sexology in Japan found an average of 5.1 inches (12.9 cm). (Measured by staff)

ERECT CIRCUMFERENCE:

Similarly, regarding the circumference of the adult fully erect penis (with the measurement taken from the midshaft of the penis), several studies have been performed. Just as with length, those studies that relied on self-measurement consistently reported a higher average than those that had staff take the measurements.

An UCSF study by Wessells et.al. published in 1996 found an average of 4.9 inches (12.5 cm). (Measured by staff).

A study by a Brazilian urologist found an average of 4.7 inches (12.0 cm). (Measured by staff)

A study conducted by LifeStyles Condoms during 2001 Spring Break in Cancún found an average of 5.0 inches (12.7 cm). (Measured by staff)

A study conducted by the Korean Consumer Protection Board (KCPB) at a college campus found an average of 5.0 inches. 14.cm

A study conducted by the Journal of Sexology in Japan found an average of 5.1 inches (12.9 cm). (Measured by staff)

FLACCID LENGTH:

The flaccid penis is measured when fully stretched, from the belly to the tip, excluding the foreskin. The length of a stretched flaccid penis closely conforms to erect length. [citation needed]

The length of the unstretched flaccid penis is no guide to the size of the erect penis [citation needed]; indeed, some men with small flaccid penes may have larger erections than men with larger flaccid penes. When a man with a relatively large flaccid penis has a normal or below average length penis when he is fully aroused, or when a man with a relatively small flaccid penis has a normal or above average length penis when he is fully aroused.

Although there are differences in flaccid penis sizes, it is generally accepted that every man's flaccid penis is approximately the same size. At most, there is usually only 0.5cm of a difference between all men over 18[citation needed], however irregularities do exist.

Present environmental conditions play a role in the size of a relaxed flaccid penis, in particular cool temperatures. One general physiological response to cold is decreased circulation of blood to the appendages. As the size of the penis very much relies on blood supply, this results in a decreased flaccid size. The slang term "shrinkage" is sometimes used to describe this phenomenon; this was featured in a famous episode of Seinfeld. As humorist Garrison Keillor once said, "At forty degrees below zero, all men are indeed equal."

Perceptions

In a 2005 study by the University of California Los Angeles, 45% of men responded they would prefer their penis size increased.[1] 84% of respondents rated their penis size as average to above average. (There is a similar perception gap in women's perceptions of their breasts.)

Men may tend to misjudge the size of their penis relative to that of other men they have seen naked, simply because of the foreshortening effect obtained from always looking down at the penis from above. In addition, as Paul Fussell noted in his memoirs, men who are overweight or have large stomachs may fail to allow for the partial concealment of the penis by their abdomen. The accumulation of fat on the pubic bone above the penis may give a shorter appearance even though the length of the penis from the base is normal.

A survey by sexologists showed that many men who believed that their penis was of inadequate size actually had a normal-sized penis. Most sexologists believe that worries about penis size come from some other source of anxiety or perceived inadequacy.

Past perceptions

In ancient Greek and Roman art, it is common to see the male genitalia to be smaller than one would expect for the size of the man. [2] Renaissance art also followed this aesthetic; note Michelangelo's David. This was due to the belief that the genitalia should not distract from the male form in sculpture.
Myths

In some cultures, mass hysteria involving the believed removal or shrinking of the penis has been observed. See penis panic for a detailed discussion.

Many theories are held in popular culture, that it is possible to predict the size of someone's penis by observing other features. The features usually selected are
Size of hands
Size of feet, or shoe size
Size of nose
Height of a person

One of these theories says that the size of a fully erect penis is the length from the tip of a man's thumb to the tip of his index finger, when a 90° angle is made with those two fingers.

The suggested link between penis size, foot size and height has been investigated by a relatively small number of groups. Two of these studies have suggested a link between penis size and foot size, while the most recent report dismissed these findings. One of the studies suggesting a link relied on the subjects measuring the size of their own penis, which may well be inaccurate. The second study found statistically significant although "weak correlation" with the size of the stretched penis with foot size and height. A potential explanation for these observations is that the development of the penis in an embryo is controlled by some of the same Hox genes (in particular HOXA13) as the limbs. Mutations of some Hox genes that control the growth of limbs cause malformed genitalia (hand–foot–genital syndrome). However the most recent investigation failed to find any evidence for a link between shoe size and stretched penis size. Given the large number of genes which control the development of the human body shape and effects of hormones during childhood and adolescence it would seem unlikely that an accurate prediction of penis size could be made by measuring a different part of the human body.

Other studies correlating the size of the human penis with other factors have given intriguing results. Notably one study analysing the Kinsey data set found that homosexual men had statistically larger penises than their heterosexual counterparts. One potential explanation given is a difference in the exposure to androgen hormones in the developing embryo.
Penis size and vaginal stimulation

According to Dr. Louanne Cole Weston, in a May 2002 report by WedMD, several misconceptions have developed surrounding penile-vaginal intercourse. Cultural preferences may have enlarged the importance of deep vaginal penetration in obtaining female orgasm.

The vagina itself is a very elastic environment through which an infant can pass, yet it also easily retains a tampon. It will accommodate and adjust to the entity it surrounds.

The perception of the vaginal canal as being the primary source of orgasmic stimulation may be exaggerated in many cultural circles. The most sensitive area of the vagina is the section closest to the outside of a woman's body, which is roughly 4 inches in length. Given that the average penis size is above this length, most men should be able to easily reach and stimulate these erotic nerve endings. [3]

In stark contrast, minor surgery without anesthetic can be conducted on the inner portion of a woman's vagina without discomfort. Most woman attest to a feeling of being "filled up" by larger than average penises, yet few can claim to feel erotic sensations in the deeper regions of the vagina. In fact, stimulation of the G-Spot is often more effective if the man's penis is slightly shorter than average, as this highly sensitive area of the vagina is located closer to the opening of vagina than to the recesses of its canal.[4]

Stimulation of the G-Spot may be more effective if the man's penis is thicker than average, since the pleasure sensations from this area are activated by pressure more than anything else. A thicker penis supposedly provides more friction against the clitoral bulbs, which are located internally under the clitoris, itself. Additionally, some claim that if a penis is thick enough compared with the vaginal opening, i.e. vulva, stretching will occur. This stretching can supposedly cause the clitoral hood to pass back and forth across the clitoris, effecting extra stimulation of that massive cluster of nerve endings. This stretching is claimed to pull the clitoris down into the path of the thrusting penis, causing it to make contact with, and rub across, the top or dorsal section of the penis. This may facilitate even greater clitoral stimulation.

Women have confirmed in surveys the primary focus of the clitoris in sexual stimulation. Roughly three-quarters of women surveyed have reported difficulty reaching orgasm by vaginal intercourse alone. Many report requiring simultaneous clitoral stimulation -- regardless of the size of the inserted object. [5]

Micropenis
Main article: Micropenis

A penis whose stretched flaccid length is more than approximately 2.5 standard deviations below average size for the age group but otherwise formed normally is referred to in a medical context as a micropenis. Some of the identifiable causes are deficiency of pituitary growth hormone and/or gonadotropins, mild degrees of androgen insensitivity, a variety of genetic syndromes, and variations in certain Homeobox genes. Some types of micropenis can be improved with growth hormone or testosterone treatment in early childhood. Penis-enlargement self-treatments are not effective for this condition.

A news post on New Scientist dated Dec 6, 2004 reads "A new surgical procedure has allowed men with abnormally short penises to enjoy a full sex life and urinate standing up, some for the first time. Tiny "micro-penises" have been enlarged to normal size without losing any erogenous sensation, say UK doctors."

Female preference

One source of continued debate is the extent to which women actually prefer certain penis sizes. In the 2005 UCLA study, 85% of women said they were "very satisfied" with their partner's size.

Recently, there has been greater media attention to the issue of penis size and women being more vocal about their preferences. Television shows such as Sex and the City and Ally McBeal popularized the penis size issue when characters in these TV shows stated their preference for well-endowed men and rejected men who had only average endowment. In HBO's Sex and the City, a female character is portrayed crying in bed when she experiences her boyfriend's penis for the first time and discovers that it is below average length, as opposed to the large length she had expected and anticipated. In the same episode the characters debate whether it's proper to dump a man because of displeasure over the size of his penis; they conclude that it's OK and at the end of the episode that one of the women does indeed dump her boyfriend because she doesn't like the size of his penis, even though earlier in the episode she reveals that she thinks she loves him.

The media image of women's preference may have had an impact on some average sized men, and caused even more damage to below-average sized men who are likely already self conscious. In recent years, penis pumps, pills, and other dubious means of penis enlargement have had increased sales.

Surveys of women's actual preference have consistently shown that penis size is only a priority for a minority of women, and some women dislike large penises. The media have been criticized for making "penis envy" into a male body issue equivalent to Cosmopolitan Magazine being criticized for their coverage of women's weight. Indeed, one episode of Sex and the City also shows a character expressing displeasure over her partner having too large a penis, though the penis is described in hyperbolic terms and implied to be something of impossibly gargantuan proportions. It has also been recorded in many cases that some women have a hard time with men with above average sized penis, with the sexual experience being uncomfortable or painful for the woman. Some women request that the man does not fully penetrate her, making sex somewhat more awkward and controlled.
Race and penis size

While physical differences between each race do exist, the stereotypes of penis size variation between different races has been a taboo, while not untrue, since it could imply one race is "superior" or "inferior" to another.

In one study, J. Philippe Rushton, a highly controversial Canadian psychologist, pointed out that: "Penis size also varies moderately across populations, being largest among African populations, smaller among European populations, and smallest among East Asian populations,..." However, this is a common misconception. A man's penis size is not dependent on race, but on what he inherited genetically.

Frantz Fanon covers this subject in some detail in Black Skin, White Masks (1952), where he tends towards the view that the supposed positive correlation between large penises and African ancestry is a myth, a conclusion that he backs up with statistics. On the other hand, J. Philippe Rushton has published statistics claiming otherwise (Race, Evolution, and Behavior: A Life History Perspective, 1995). He points out that the World Health Organization specifies 53 mm wide condoms for Africa, 52 mm wide condoms for Europe, and 39 mm condoms for Asia. [10] This fact itself is not stable nor it is substantially suitable because the statistical results are found to be scientificly inconclusive.

According to Family Health International, "The World Health Organization bases its specifications for condom width on consumer preference and penis size, citing three studies. Taken together, the studies show significant variations in penis size within all population groups, but also indicate that men of African descent on average have a slightly wider and longer penis size, Caucasian men have a medium size, and Asian men a slightly narrower and shorter size." [11]

The cultural issues involved with the question of race and penis size are complex. For example, in American history, African-American slaves were often perceived as hyper-sexual animals, as illustrated by the main character in Ralph Ellison's novel Invisible Man.
Penis size and condom use

In a British study examining condom use and reproductive health, the author pointed out that "penis size could affect condom failure." The cross-sectional study looked at race factors on condom use. In this comprehensive study, 18% of Africans descent, 7% of Caucasians and no Asians reported frequent breakage. In contrast, 21% of Asians, 8% of blacks and 2% of whites reported frequent complete slippage.

Based on the consideration that anatomical differences exist among regions, a series of FHI studies were conducted in three Asian countries to compare small and standard width condoms (39 mm and 49 mm), and in three African countries to compare larger and standard width condoms (55 mm and 52 mm). Among the African sites, breakage rates were slightly higher and slippage was slightly lower for the smaller of the two condoms being compared. (Joanis) However, results from the Asian sites were inconsistent. (Neupane; Andrada) Moreover, almost none of the differences in breakage and slippage rates from either the Asian or African sites were statistically significant. Thus, results from these studies pertaining to penis size and condom failure were conclusive.[12]

Overall, condom failures are rare so there are little "legitimate" facts that can actually support or validate the correlation between penis size and condom breakage/slippage.

HYPOSPADIAS

2007-05-22T23:25:00.000-07:00

HYPOSPADIAS:

Hypospadias is a birth defect of the urethra in the male that involves an abnormally placed urethral meatus (opening). Instead of opening at the tip of the glans of the penis, a hypospadic urethra opens anywhere along a line (the urethral groove) running from the tip along the underside (ventral aspect) of the shaft to the junction of the penis and scrotum or perineum. A distal hypospadias may be suspected even in an uncircumcised boy from an abnormally formed foreskin and downward tilt of the glans.

The urethral meatus opens on the glans penis in about 50-75% of cases; these are categorized as first degree hypospadias. Second degree (when the urethra opens on the shaft), and third degree (when the urethra opens on the perineum) occur in up to 20 and 30% of cases respectively. The more severe degrees are more likely to be associated with chordee, in which the phallus is incompletely separated from the perineum or is still tethered downwards by connective tissue, or with undescended testes (cryptorchidism).

INCIDENCE:

Hypospadias are among the most common birth defects of the male genitalia (second to cryptorchidism), but widely varying incidences have been reported from different countries, from as low as 1 in 4000 to as high as 1 in 125 boys.

There has been some evidence that the incidence of hypospadias around the world has been increasing in recent decades. In the United States, two surveillance studies reported that the incidence had increased from about 1 in 500 total births (1 in 250 boys) in the 1970s to 1 in 250 total births (1 in 125 boys) in the 1990s. Although a slight worldwide increase in hypospadias was reported in the 1980s, studies in different countries and regions have yielded conflicting results and some registries have reported decreases.

CAUSES

Most hypospadias are sporadic, without inheritance or family recurrence. For most cases, no cause can be identified though a number of hypotheses related to inadequate androgen effect, or environmental agents interfering with androgen effect, have been offered. Among the suspected environmental agents have been various chemicals, sometimes termed endocrine disruptors, that interact with steroid receptors. Putative endocrine disruptors include phthalates, DDT, and PCB. A recent questionnaire study of mothers who bore infants with hypospadias reported fivefold higher risk association with vegetarian diet (with plant phytoestrogens the hypothetical link) during pregnancy, and weaker associations with iron supplementation or influenza during early pregnancy [1]. The associations are as yet uncorroborated by additional surveys or other methods.

Prenatal testosterone, converted in the genital skin to dihydrotestosterone, causes migration of skin fibroblasts to fully enclose the urethral groove in fetal males, normally resulting in an enclosed penile urethra by the second trimester of pregnancy. Failure of adequate prenatal androgen effect is therefore thought to be involved in many cases, making hypospadias a very mild form of intersex (undervirilization of a genetic male). Since postnatal androgen deficiency can only be demonstrated in a minority of cases, it has been proposed that transient deficiency of testosterone can occur during critical periods of fetal genital development, due to elevation of anti-müllerian hormone or more subtle degrees of pituitary-gonadal dysfunction. More recently, abnormalities of transcription factors have been proposed.

In a minority of cases a postnatal deficiency of, or reduced sensitivity to, androgens (testosterone and dihydrotestosterone) can be demonstrated. These are often associated with a chordee, and in severe cases a residual perineal urogenital opening and small phallus. This combination of birth defects is referred to as pseudovaginal perineoscrotal hypospadias and is part of the spectrum of ambiguous genitalia. Treatment with testosterone postnatally does not close the urethra.

Genetic factors are likely involved in at least some cases, as there is about a 7% familial recurrence risk.

Rare iatrogenic urethral injuries similar to hypospadias after procedures such as surgery, catheterization, or circumcision have been reported.

TREATMENT

First degree hypospadias are primarily a cosmetic defect and have little effect on function except for direction of the urinary stream. If uncorrected, a second or third degree hypospadias can make male urination messy, necessitate that it be performed sitting, impair delivery of semen into the vagina (possibly creating problems with fertility), or interfere with erections. In developed countries, most hypospadias are surgically repaired in infancy. Surgical repair of first and second degree hypospadias is nearly always successful in one procedure, usually performed in the first year of life by a pediatric urologist or a plastic surgeon.

When the hypospadias is third degree, or there are associated birth defects such as chordee or cryptorchidism, the best management can be a more complicated decision. A karyotype and endocrine evaluation should be performed to detect intersex conditions or hormone deficiencies. If the penis is small, testosterone or human chorionic gonadotropin (hCG) injections may be given to enlarge it prior to surgery.

Surgical repair of severe hypospadias may require multiple procedures and mucosal grafting. Preputial skin is often used for grafting and circumcision should be avoided prior to repair. In a minority of patients with severe hypospadias surgery produces unsatisfactory results, such as scarring, curvature, or formation of urethral fistulas, diverticula, or strictures. A fistula is an unwanted opening through the skin along the course of the urethra, and can result in urinary leakage or an abnormal stream. A diverticulum is an "outpocketing" of the lining of the urethra which interferes with urinary flow and may result in post-urination leakage. A stricture is a narrowing of the urethra severe enough to obstruct flow. Reduced complication rates even for third degree repair (e.g., fistula rates below 5%) have been reported in recent years from centers with the most experience, and surgical repair is now performed for the vast majority of infants with hypospadias.

Because of the difficulties and lower success rates of surgical repair of the most severe degrees of undervirilization, some of these genetically male but severely undervirilized infants have been assigned and raised as girls, with feminizing surgical reconstruction. Opinion has shifted against this approach in the last decade because adult sexual function as a female has often been poor, and development of a male gender identity despite female sex assignment and rearing, has occurred in some XY children after reassignment for a more severe type of genital birth defect, cloacal exstrophy.

ASSOCIATED BIRTH DEFECTS:

Mild hypospadias most often occurs as an isolated birth defect without detectable abnormality of the remainder of the reproductive or endocrine system. However, a minority of infants, especially those with more severe degrees of hypospadias will have additional structural anomalies of the genitourinary tract. Up to 10% of boys with hypospadias have at least one undescended testis, and a similar number have an inguinal hernia. An enlarged prostatic utricle is common when the hypospadias is severe (scrotal or perineal), and can predispose to urinary tract infections, pseudo-incontinence, or even stone formation.

EPISPADIAS:

A much rarer and unrelated type of urethral malformation is an epispadias. This is not a problem of the urethral groove or meatus, but a failure of midline penile fusion much earlier in embryogenesis. An isolated opening of the dorsal ("top") side of the penis is rare, and most of these children have much more severe defects, involving a small and bifid phallus with bladder exstrophy or more severely, cloacal exstrophy involving the entire perineum. The cause of this defect of early embryogenesis is unknown but does not involve androgens.

In human anatomy, the perineum is generally defined as the surface region in both males and females between the pubic symphysis and the coccyx.

It is a diamond-shaped area on the inferior surface of the trunk which includes the anus and, in females, the vagina[1]. Its definition varies: it can refer to only the superficial structures in this region, or it can be used to include both superficial and deep structures.

The perineum corresponds to the outlet of the pelvis.

BOUNDARIES:

Its deep boundaries are as follows:[2]
In front: the pubic arch and the arcuate ligament of the pubis
Behind: the tip of the coccyx
On either side: the inferior rami of the pubis and ischium, and the sacrotuberous ligament

TRIANGLES:

A line drawn transversely across in front of the ischial tuberosities divides the space into two triangles:Name Location Contents
Urogenital triangle the anterior triangle in females, contains the vagina
Anal triangle the posterior triangle contains the anus

PERINEAL FASCIA:

The terminology of the perineal fascia can be confusing, and there is some controversy over the nomenclature. This stems from the fact that there are two parts to the fascia, the superficial and deep parts, and each of these can be subdivided into superficial and deep parts.

The layers and contents are as follows, from superficial to deep:
1) Skin
2) superficial perineal fascia: Subcutaneous tissue divided into two layers: (a) A superficial fatty layer, and (b) Colles' fascia, a deeper, membranous layer.
3) deep perineal fascia and muscles:

uperficial perineal pouch Contains superficial perineal muscles: transversus perinei superficialis, bulbospongiosus, ischiocavernosus
inferior fascia of urogenital diaphragm, or perineal membrane A membranous layer of the deep fascia.
deep perineal pouch Contains the deep perineal muscles: transversus perinei profundus, sphincter urethrae membranaceae
superior fascia of the urogenital diaphragm Considered hypothetical by some modern anatomists, but still commonly used to logically divide the contents of the region.

4) facia and muscles of pelvic floor (levator ani, coccygeus)

AREAS OF THE PERINEUM:

The region of the perineum can be considered a distinct area from pelvic cavity, with the two regions separated by the pelvic diaphragm. The following areas are thus classified as parts of the perineal region:
perineal pouches: superficial and deep (see above for details)
Ischioanal fossa - a fat filled space
Anal canal
Pudendal canal - contains internal pudendal artery and the pudendal nerve.

RIDING:

This area can become extremely sore among inexperienced bicyclists, horseback riders, motocross riders, and even ATV'ers

GLANS

The glans (Latin for "acorn", because the glans of an uncircumcised penis often looks like an acorn popping out of its cap) is a structure internally composed of corpus spongiosum in males or of corpus cavernosa and vestibular tissue in females that is located at the tip of homologous genital structures involved in sexual arousal.

STRUCTURE

The exterior structure of the glans consists of mucous membrane, which is usually covered by foreskin or clitoral hood in naturally developed genitalia. This covering, called the prepuce, is normally retractable in adulthood.

The glans naturally joins with the inner labia, and the frenulum of the penis or clitoris. In non-technical or sexual discussions, often the word "clitoris" refers to the external glans alone, excluding the clitoral hood, frenulum, and internal body of the clitoris.

GENDER DIFFERENCES

In males the glans is known as the glans penis, while in females the glans is known as the glans clitoris.

In females, the clitoris is above the urethra. This organ was once thought to serve no function other than sexual arousal, but research is beginning to prove otherwise. The glans of the clitoris is the most highly innervated part.

ABNORMAL DEVELOPMENT OF PENIS AND URETHRA:

If the fusion of the urethral folds fail to progress distally on the ventral penis, the urethra will be shortened. Hypospadias occurs when the fusion of the urethral folds stops proximal to the tip of the glans penis. The term, hypospadias, means under [hypo] the rent [spadon]. The rent refers to the appearance of the ventral glans penis. It appears to have been ripped (rent) apart. Hypospadias can occur anywhere along the urethral groove. In mild forms, the urethra opens just under the corona glandis. This is called coronal hypospadias.
When the internal urethral folds fail to fuse, causing hypospadias, the external urethral folds usually fail to fuse, causing a dorsal hood foreskin. Notice that the median raphé lies at an angle on the penile shaft.
Occasionally, the urethra develops only to the junction of the penis and scrotum. This boy has peno-scrotal hypospadias. As in this case, severe forms of hypospadias are accompanied by shortening of the urethral groove that causes ventral tethering of the penis. This condition, called chordee, can be severe enough to make sexual function impossible.

Whenever the foreskin appears shortened or abnormal on the ventral surface of the penis, one should suspect hypospadias. Occasionally, the external urethral folds develop and fuse despite failure of fusion of the internal urethral folds. In these boys, distal hypospadias occurs despite the presence of a complete prepuce. The urethral meatus must be examined before any circumcision is performed to make sure the boy does not have hypospadias.

Hypospadias occurs in about 1/125 infant males. In most cases, the cause of the hypospadias is not known. Certain conditions, however, are known to result in hypospadias. If the testes fail to produce adequate amounts of testosterone, virilization (enlargement and development of the genital tubercle and scrotal swellings) will not be complete and hypospadias will result. Similarly, if the cells of the genital structures lack adequate androgen receptors, hypospadias will occur. If those cells lack the androgen converting enzyme, 5 alpha reductase, inadequate androgen stimulation will follow and hypospadias will occur.

When severe forms of virilization failure occur (perineal hypospadias, or penoscrotal hypospadias with at least one undescended testicle) the infant must be evaluated for intersex (ambiguous genitalia). Intersex can be caused by hormonal abnormalities (congenital adrenal hyperplasia, ect.) and also by abnormal chromosomes (hermaphroditism, etc.).

TANNER STAGE

2007-05-19T23:43:00.000-07:00

The major abnormalities of menstruation during the reproductive years number two: amenorrhea and abnormal uterine bleeding. Because any abnormality of menstruation may be associated with pregnancy, pregnancy always must be ruled out as a cause for the abnormality.

Amenorrhea

The prevalence of amenorrhea that is not due to pregnancy, lactation, or menopause is 3 to 4%.1,2 Amenorrhea indicates failure of the hypothalamic-pituitary-gonadal axis to induce cyclic changes in the endometrium that normally result in menses and also may result from the absence of end organs or from obstruction of the outflow tract. It is important to remember that amenorrhea may result from an abnormality at any level of the reproductive tract. How long a woman must be amenorrheic before it is considered pathologic is arbitrary; however, any woman who presents with concerns about the absence of menses should be evaluated.

Amenorrhea may be defined as 1) the absence of menstruation for 3 or more months in women with past menses (i.e., secondary amenorrhea) or 2) the absence of menarche by the age of 16 years in girls who have never menstruated (i.e., primary amenorrhea). Recent data suggest that pubertal development, and hence menarche, continues to begin earlier in American girls.3 Consequently, some clinicians would consider initiating evaluation of a girl with primary amenorrhea by age 14, particularly if 5 or more years had passed since the first evidence of pubertal development. Women who menstruate fewer than 9 times in any 12-month period should be evaluated identically to women with secondary amenorrhea. These women are typically oligo- or anovulatory. The separation of amenorrhea into the categories primary and secondary is artificial and should not be considered in the evaluation of the amenorrheic woman. Likewise, the term “postpill amenorrhea”, sometimes used to refer to women who do not menstruate within 3 months of discontinuing oral contraceptives, conveys nothing about the cause of the amenorrhea and should not alter the evaluation.

Amenorrhea is not a diagnosis in itself but rather a sign of a disorder. In general, menses general occur at intervals of 28 ± 3 days in two-thirds of women, with a normal range of 18-40 days.

It is useful to think about 3 broad categories of amenorrhea (Table 1)

Table 1. Causes of Amenorrhea

Anatomic Causes

Pregnancy

Müllerian agenesis or dysgenesis (uterine, cervical, or vaginal)

Imperforate hymen

Cervical stenosis

Various disorders of sexual differentiation

Intrauterine adhesions (Asherman syndrome)

Tentative Classification of Premature Ovarian Failure

Cytogenetic Alterations of the X Chromosome

Absence of an X chromosome

Trisomy X with or without mosaicism

Structural abnormalities of the X chromosome

Mutations of Specific Genes

Premutation of FMRl gene (Fragile X; 6% of cases)

INHA (inhibin alpha)

FOXL2 (a forkhead transcription factor associated with the blepharophimosis/ptosis/epicanthus inverse syndrome)

ELF2B (a family of genes associated with CNS leukodystrophy and ovarian failure)

BMP15 (bone morphogenetic factor 15, involved with folliculogenesis)

PMM2 (phosphomannomutase)

AIRE (autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy syndrome)

Enzymatic Defects

Steroidogenic enzyme defects

17α-Hydroxylase or 17,20-lyase deficiency

20,22-Desmolase deficiency

c. Aromatase deficiency

2. Galactosemia

Defects in Gonadotropin Secretion or Action

Receptor and post-receptor defects

FSH receptor (FSHR) mutations

LH receptor (LHR) mutations

G-protein alterations

Secretion of biologically inactive gonadotropin

α- or β-Subunit defects

Immune Dysfunction

Association with other autoimmune disorders (15-20% of cases, 4% with steroidogenic cell autoimmunity)

Isolated

In association with congenital thymic aplasia

Physical Insults

Chemotherapeutic (especially alkylating) agents

Ionizing radiation

Viral agents

Surgical extirpation

Gonadotropin-Secreting Pituitary Tumors (Extremely Rare)

Idiopathic

Chronic anovulation

Hypothalamic

Psychogenic, including pseudocyesis

Exercise-associated

Eating disorders, nutritional

2° to systemic illness

Hypothalamic neoplasms

Pituitary

Isolated gonadotropin deficiency (including Kallmann syndrome)

Hypopituitarism

Pituitary neoplasms, including mucroadenomas

With inappropriate steroid feedback

Functional androgen excess (PCOS)

Adrenal Hypoplasia

Neoplasms producing androgens or estrogens

Neoplasms producing hCG (including trophoblastic disease)

Liver and renal disease

Obesity

Other endocrine disorders

Thyroid dysfunction

Adrenal hyperfunction

Anatomic causes, including pregnancy, that almost always can be identified by physical examination alone.

Ovarian failure.

Chronic anovulation resulting from any of a number of endocrine disturbances.

It is generally impossible to distinguish between ovarian failure and chronic anovulation without laboratory testing.

The most important aspect of the clinical evaluation is the history and physical examination. During the physical examination, special attention should be directed toward evaluating:

Body dimensions and habitus.

Distribution and extent of terminal androgen-stimulated body hair.

Extent of breast development by Tanner staging and the presence or absence of any breast secretions.

External and internal genitalia, with emphasis on evidence of exposure to androgens and estrogens.

History, physical examination and determination of basal concentrations of follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), and prolactin will identify the most common causes of amenorrhea. Administration of exogenous progestin has been recommended in the past, both as a clinical aid to diagnosis and to evaluate the biological levels of estrogen. Either progesterone in oil (100 – 200 mg im) or medroxyprogesterone acetate (5 – 10 mg orally daily for 5 – 10 days) can be given. Any genital bleeding within 10 days of the completion of these regimens is regarded as a positive test. If the test is negative (suggesting low levels of endogenous estrogen), then an estrogen and a progestin together (e.g., oral conjugated estrogen, 2.5 mg daily for 25 days, together with oral medroxyprogesterone acetate, 5-10 mg for the last 10 days of estrogen therapy) should induce bleeding if the endometrium is normal. This test will determine with certainty if the outflow tract is intact. However, the results are not always definitive. In fact, in one survey almost half the women with so-called premature ovarian “failure” bled in response to progestin.4 Thus, progestin challenge should never be used as the sole diagnostic test by which amenorrheic women should be evaluated. In women with evidence of hirsutism, at least total testosterone and dehydroepiandrosterone sulfate levels should be determined to rule out any serious cause (Figure 1).

Figure 1. Flow diagram for the laboratory evaluation of amenorrhea. Such a scheme must be considered as an adjunct to the clinical evaluation of the patient. CAH -= congenital adrenal hyperplasia; DHEAS = dehydroepiandrosterone sulfate; FSH = follicle-stimulating hormone; HCA = hypothalamic chronic anovulation; PCO = polycystic ovary syndrome; PRL = prolactin; T = testosterone; TSH = thyroid-stimulating hormone. Originally from Rebar RW, The ovaries. In: Smith LH Jr, ed. Cecil textbook of medicine, ed. 18. Philadelphia. WB Saunders, 1992:1367)

In 1976 the WHO Scientific Group divided women with amenorrhea into two groups based upon a suggestion of Insler5:

Group I, termed Hypothalamic-Pituitary Failure, consists of women with no evidence of endogenous estrogen production (based on urinary measurements), nonelevated prolactin levels, normal or low FSH levels, and no detectable space-occupying lesion in the hypothalamic-pituitary region.

Group II, termed Hypothalamic-Pituitary Dysfunction, consists of women with a variety of menstrual cycle disturbances, including amenorrhea with evidence of endogenous estrogen production (on urinary measurement) and normal levels of prolactin and FSH. Thus, this group includes women with polycystic ovarian syndrome, who in reality may or may not have hypothalamic-pituitary dysfunction.
HYPERGONADOTROPIC AMENORRHEA (Primary Hypogonadism; Gonadal Failure)

It is frequently impossible to diagnose hypergonadotropic amenorrhea, also called presumptive ovarian failure, without the measurement of basal serum FSH levels. This is especially true because ovarian failure may occur at any time from embryonic development onward. The ovaries normally fail at the time of menopause, when virtually no viable oocytes remain. Premature ovarian failure (POF) or premature menopause generally is defined as consisting of the triad of amenorrhea, hypergonadotropinism, and hypoestrogenism in women under the age of 40 years. From what is known about follicular development and atresia, it appears that premature ovarian failure can arise from abnormalities in the recruitment and selection of oocytes. The follicles may undergo atresia at an accelerated rate or a smaller than normal pool may undergo atresia at the normal rate to yield early oocyte depletion. FSH must be involved, because it is the principal hormonal regulator of folliculogenesis. Circulating gonadotropin levels rise whenever ovarian failure occurs because of decreased negative estrogen feedback to the hypothalamic-pituitary unit. Gonadotropin levels sometimes increase even in the presence of viable oocytes, but the explanation for such increases is unclear. Thus, use of the term POF is inappropriate. In 5-10% of patients, spontaneous pregnancy has occurred many years after the initial diagnosis.4,6 Thus, it is more appropriate to refer to this disorder as hypergonadotropic amenorrhea, primary hypogonadism, or hypergonadotropic hypogonadism, but the term premature ovarian failure is well established in the literature.
TYPES OF PREMATURE OVARIAN FAILURE

It is now clear that POF is a heterogeneous disorder. Premature loss of oocytes could result from a reduced germ cell endowment in utero, accelerated atresia, or failure of all germ cells to migrate to the genital ridges in early development. There may be marked differences in oocyte endowment and rates of follicular atresia among women.7,8 Only now are investigators learning about the molecular factors that regulate oocyte number and development. Because information in this field is changing rapidly, it is probably impossible to provide a definitive classification of the disorder, but it is possible to enumerate many of the apparent causes (Table 1).

It is becoming clear that genetic abnormalities are perhaps the most important cause of premature ovarian failure (Table 1). Individuals with the various forms of gonadal dysgenesis typically present with hypergonadotropic amenorrhea regardless of the extent of pubertal development and the presence or absence of associated anomalies or stigmata. It is well known that cytogenetic abnormalities of the X chromosome can impair ovarian development and function. Studies of 46,XX individuals and those with various X chromosomal depletions have confirmed that two intact X chromosomes are necessary for maintenance of oocytes.9 The gonads of 45,X fetuses contain the normal complement of oocytes at 20 to 24 weeks of fetal age, but these rapidly undergo atresia so that none are typically present by the time of birth.10 Primary or secondary amenorrhea is typically occurs in women with deletions in either the short or the long arm of one X chromosome.9 Mutations at independent loci on the X chromosome at Xq26-28 (POF1) and Xq13.3-22 (POF2) have been identified that also are linked to POF. One gene in the POF2 region has homology to the DIA allele in Drosophila, mutants of which result in male and female infertility. A breakpoint in the last intron of the DIAPH2 gene (the homologue of the Drosophila diaphanous gene) has been associated with familial POF in women.11

Although individuals with Turner syndrome usually are apparent on physical examination, patients with pure and mixed gonadal dysgenesis typically have no obvious identifying features. Women with pure gonadal dysgenesis, who generally present with sexual infantilism and primary amenorrhea, are of normal height and have none of the somatic abnormalities associated with Turner syndrome.12,9 Affected individuals have either a 46,XX or 46,XY karyotype. In mixed gonadal dysgenesis, a germ cell tumor or testis accounts for one gonad, with a streak, rudimentary gonad, or no gonad accounting for the other.9,13 The 45,X/46,XY karyotype is most frequent, but affected individuals may have any of several other reported karyotypes. The vast majority of affected individuals are raised as females, with mild to moderate virilization occurring at puberty. Abnormal genitalia may be noted at birth. Because of the malignant potential of intraabdominal gonads in individuals with a Y chromosomal component14-16 the gonads should be removed.

Additional X chromosomes also are present in some women with POF.17 These women typically develop normally and may bear children early in adulthood and commonly develop POF after age 30.

Mutations in the Familial Mental Retardation-1 (FMR1) gene, located at Xq27 and which can lead to fragile X syndrome, can also lead to POF.18 Although the genetics involved in the abnormalities associated with this gene is quite complex, the basic principles can be summarized. Normal individuals have 5-50 repeats of the cytosine-guanine-guanine (CGG) trinucleotide in the gene. Expansion of this trinucleotide to greater than 200 repeats inactivates the gene and leads to the fragile X syndrome. In addition to mild to severe mental retardation, affected males typically present with long narrow faces, increased head circumference, dysmorphic ears, prominent jaws and foreheads, and large testes. Females are less severely affected, presumably because one of the two X chromosomes is inactivated independently in every cell in the body, and only one of the chromosomes carries the mutations. Some individuals have 50-200 repeats of the CGG sequences, and these individuals are considered premutations carriers. The women who are carriers of this unstable premutation can have further expansion of the trinucleotide in their germ cells and transmit the full syndrome to their offspring; in some families, the carrier state can be transmitted for several generations before expansion occurs. Men who are premutation carriers virtually never have further expansion in germ cells but can transmit the premutation to their female offspring. It is now recognized that POF develops in about 20% of female premutation carriers.19,20 In addition, about 2% of women with sporadic POF and 14% of women with familial POF have this unstable mutation.21,22 These observations make a convincing argument for testing women with POF for mutations of FMR1.

Several other specific gene mutations (not necessarily located on the X chromosome) also can result in POF. These include mutations involving the inhibin alpha gene (INHA), a gene at chromosome 3q23 involving a forkhead transcription factor associated with blepharophimosis-ptosis-epicanthus inversus (BPES) type I syndrome,23,24 a family of genes associated with central nervous system leukodystrophy and ovarian failure (EIF2B),25 the gene involving bone morphogenetic factor 15 (BMP15) which is known to play a role in folliculogenesis26, the phosphomannomutase (PMM) gene, and the gene associated with the autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy syndrome (AIRE).27 No doubt other mutations will be identified as causes of POF in some affected women. Several rare inherited enzymatic defects also may be associated with premature ovarian failure. These include partial deficiencies in four enzymes in the steroidogenic pathway, 17a-hydroxylase, 17,20-desmolase, 20,22-desmolase, and aromatase, as well as galactosemia.

Girls with 17a-hydroxylase deficiency who survive to their teens present with sexual infantilism; primary amenorrhea; increased circulating levels of LH, FSH, deoxycorticosterone, and progesterone; and hypertension with hypokalemic alkalosis.28-30 Ovarian biopsy has revealed no evidence of orderly follicular maturation but instead has demonstrated numerous, large cysts and primordial follicles. Presumably, the enzyme deficiency does not permit normal follicular development. The startling observation that normal follicular growth and development with successful fertilization in vitro can be achieved with exogenous gonadotropins in individuals with 17a-hydroxylase deficiency raises significant questions about why there is no follicular development in affected girls.31

Several case reports have described individuals with mutations in the CYP19 (aromatase P450) gene.32-34 Aromatase deficiency appears to be inherited in an autosomal recessive manner and is manifested in 46,XX individuals by female pseudohermaphroditism with clitoromegaly and posterior labioscrotal fusion at birth; enlarged cystic ovaries associated with elevated FSH levels during childhood; lack of pubertal development in association with further enlargement of the clitoris, normal development of pubic and axillary hair, and continued existence of enlarged multicystic ovaries during the teenage years; and severe estrogen deficiency, virilization, and enlarged multicystic ovaries in association with markedly elevated gonadotropin levels in adulthood. Administration of exogenous estrogen results in prompt lowering of circulating gonadotropin levels. Ovarian biopsy showed many closely packed primordial follicles in an affected 17-month old,33 but biopsy in a 13-year old showed excessive atresia.34

Girls with galactosemia, a disorder in which galactose-1-phosphate uridyltransferase activity is decreased and that is characterized by mental retardation, cataracts, hepatosplenomegaly, and renal tubular dysfunction, also may develop premature ovarian failure with hypergonadotropinism even when a galactose-restricted diet is introduced early in infancy.35

Data from a variety of sources indicate that abnormalities in the structure, secretion, metabolism, or action of gonadotropins can cause POF. It is now known that at least one form of premature ovarian failure is caused by mutations in the FSH receptor (FSHR). Affected individuals present with primary or secondary amenorrhea and elevated levels of FSH and may have ovarian follicles present on transvaginal ultrasound. One specific mutation on chromosome 2p –(C566T:alanine to valine)- in exon 7 of the FSHR was identified in several Finnish families36,37 but the mutation must be very rare outside of Finland because it has not been detected in some other populations.38,39

The “resistant ovary” syndrome may be the result of a gonadotropin postreceptor defect. As originally described, the Savage syndrome (named after the first patient described) consisted of young amenorrheic women with elevated peripheral gonadotropin concentrations, normal but immature follicles in the ovaries on biopsy, 46,XX karyotype with no evidence of mosaicism, and complete sexual development, and hyposensitivity (i.e., “resistance”) to exogenous gonadotropin stimulation.40

Altered forms of immunoreactive LH and FSH in urinary extracts from women with POF compared to those from oophorectomized and postmenopausal women have been reported, suggesting that metabolism and/or excretion of gonadotropin is altered in some cases.41 Some individuals with POF and evidence of intermittent follicular activity may have low molecular weight receptor-binding activity that antagonizes normal FSH binding.42

Destruction of oocytes by any of several environmental insults, including ionizing radiation, various chemotherapeutic (especially alkylating) agents, and certain viral infections may accelerate follicular atresia.43 Although there is no evidence that cigarette smoking will result in POF, cigarette smokers experience menopause several months before nonsmokers.

More and more girls and young women who are treated for a variety of malignancies are surviving free of disease and subsequently presenting with transient or permanent ovarian failure. Strategies for reducing the likelihood of ovarian failure in women cured of their malignancies are being investigated by several groups. Cryopreservation of oocytes and ovarian tissue before therapy remains experimental at this point in time.

Approximately half of all individuals receiving 400-500 rads to the ovaries over four to six weeks will develop permanent ovarian failure.44 For any given dose of radiation, the older the woman, the greater the likelihood of her developing ovarian failure. It appears that about 800 rads is sufficient to result in permanent ovarian failure in all women. The transient nature of the hypergonadotropic amenorrhea in some women suggests that some follicles may be damaged but not destroyed by lower doses of radiation. To minimize the dose of radiation received by the ovaries, transposition to the pelvic sidewalls, often by laparoscopy, is recommended. One series noted preservation of ovarian function in about 90% of women undergoing transposition.45 Similarly, the older the woman at the of chemotherapy, the more likely is the ovarian failure.46 In general, it appears that the greater the number of oocytes present in the ovaries at the time of therapy with radiation or chemotherapy, the more likely it is that normal ovarian function will continue. Although the data are limited, the frequency of congenital anomalies does not appear to be increased in the children of women previously treated with chemotherapeutic agents.47

Premature ovarian failure may be associated with a number of autoimmune disorders.4 The most common association may be with thyroiditis. Ovarian failure occurs commonly in women with polyglandular failure, including hypoparathyroidism, hypoadrenalism, and mucocutaneous candidiasis4. The heterogeneous nature of this disorder is suggested by the many different endocrinopathies that may be associated with premature ovarian failure. Autoimmune ovarian failure may occur independently of any other autoimmune disorder.

Autoimmune lymphocytic oophoritis was originally reported in association with adrenal insufficiency (Addison disease). Women with steroidogenic cell autoimmunity have lymphocytic oophoritis resulting in the ovarian failure. When POF occurs in association with adrenal insufficiency, the ovarian failure presents first about 90% of the time. The presence of antibodies to the 21-hydroxylase enzyme measured by a commercially available immunoprecipitation assay will identify who who may have occult adrenal insufficiency at the time of initial presentation as well as those who should be followed closely for the subsequent development of adrenal insufficiency.48,49 At the present time there is no good test to document the presence of antibodies to any specific ovarian antigens. The best evidence of antibodies to ovarian tissue comes from a study documenting FSH receptor antibodies in two women with myasthenia gravis and hypergonadotropic amenorrhea.50 Immunoglobulins that block the trophic actions of FSH but not LH also have been reported.51

The thymus gland influences reproductive function52. Congenitally athymic girls have ovaries devoid of oocytes.53 Irradiation and chemotherapeutic (especially alkylating) agents used to treat various malignancies are increasingly causes of premature ovarian failure.54-56 Inexplicably, both of these modalities have been associated with “reversible” ovarian failure. Ovulation and cyclic menses return in some individuals after prolonged intervals of hypergonadotropic amenorrhea associated with signs and symptoms of profound hypoestrogenism. Preliminary studies suggest that gonadotropin-releasing hormone analogues (but not oral contraceptive agents) may provide some protection from ovarian damage.57 Rarely, the mumps virus can affect the ovaries and cause ovarian failure.58
DIAGNOSIS AND THERAPY OF PREMATURE OVARIAN FAILURE

Individuals with premature ovarian failure warrant thorough evaluation to eliminate potentially treatable causes and to identify associated disorders that may require therapy. In general, young women who experience loss of regular menses for three or more consecutive months should be evaluated. Failure to initiate pubertal development by age 13 or begin menstruating by age 15 also warrants evaluation.

Several laboratory tests are indicated in women with POF, beginning with measurement of basal levels of prolactin, FSH, and TSH (after pregnancy is ruled out). FSH levels are typically greater than 30 mIU/ml in women with ovarian failure. If the FSH level is greater than 15 mIU/ml on initial screening, then the measurement should be repeated and serum estradiol should be measured as well to document hypogonadism. In addition, the simultaneous measurement of basal LH levels may be helpful in discerning if any oocytes remain. In general, if the estradiol concentration is greater than 50 pg/mL or if the LH level is significantly greater than the FSH level (in terms of mIU/mL) in any sample, the probability of viable oocytes is considerable. Irregular uterine bleeding, as an indication of estrogen stimulation, also provides good evidence of remaining functional ovarian follicles. It is not uncommon to identify women with intermittent menstruation, hypoestrogenism, and hypergonadotropinism. Visualization of follicles on transvaginal ultrasound also provides evidence of functional oocytes. Because a number of pregnancies have occurred after biopsy of ovaries devoid of oocytes, ovarian biopsy cannot be recommended for affected women.

Other indicated laboratory tests include measurement of thyroid-stimulating immunoglobulins (because of the frequency of thyroiditis), adrenal antibodies, fasting glucose, electrolytes, and bone density by dual-energy X-ray absorptiometry. Also indicated are an analysis of karyotype and fragile X premutation screening, particularly in the presence of a family history of mental retardation. If adrenal antibodies are detected, then a corticotropin stimulation test is indicated to identify women with adrenal insufficiency. One series evaluated 119 women with karyotypically normal spontaneous POF and found that 32 patients had hypothyroidism (27%) and 3 had adrenal insufficiency (2.5%).59

Even women with X-chromosomal abnormalities have delivered normal children and subsequently developed POF prior to age 40. Thus, neither parity nor age rules out the possibility of a chromosomal abnormality. Unexpected karyotypic findings that may be inherited have important implications for other family members. Also, by finding an explanation for the POF, patients with normal karyotypes may be reassured, and the patients with abnormal karyotypes can be counselled. Surgical removal of the gonads is indicated in any individual in whom a Y chromosome is identified.

Women who experience spontaneous POF are unprepared for the diagnosis. Taking the time to present the findings with sensitivity and to counsel appropriately is most important. Patients may benefit from referral to a psychologist and/or to an organization such as the POF Support Group ( www.pofsupport.org). Patients should be reassessed at intervals of one to two years for the presence of other disorders associated with POF.

Even in women with intermittent ovarian failure, estrogen replacement is appropriate to prevent the accelerated bone loss that occurs in affected women.4 Although exogenous estrogen may be given either as part of combined estrogen-progestin therapy or in the form of combined oral contraceptives, sequential therapy with exogenous estrogen and progestin is most physiologic. The estrogen should always be given with a progestin to prevent endometrial hyperplasia. Because women with ovarian failure may conceive while on estrogen therapy (including combined oral contraceptive agents), affected women should be counseled appropriately and cautioned to have a pregnancy test if withdrawal bleeding does not occur or if signs and symptoms suggestive of pregnancy develop. Despite these considerations, probably no other contraceptive agent is required for those women who do not wish pregnancy but who are sexually active, because pregnancy occurs in less than 10%.4 Although rare pregnancies in women with premature ovarian failure have occurred after ovulation induction with human menopausal and chorionic gonadotropins, the low likelihood should lead the physician to discourage patients from selecting such therapy. There is no evidence that ovulation and pregnancy occur more commonly in response to ovulation induction than spontaneously in these patients. Hormone replacement treatment to mimic the normal menstrual cycle, with oocyte donation for embryo transfer, provides the greatest possibility for pregnancy in women desiring pregnancy.60,61

There are no data documenting safety of estrogen-progestin in young women with POF, but there are no reports of excessive risks either. Findings documenting risks in postmenopausal women do not apply to women with POF for whom estrogen therapy really represents replacement. Similarly, there are no data documenting the optimal form of estrogen and progestin to use in women with POF. It is important to remember that these young patients typically require twice as much estrogen as postmenopausal women to relieve any signs and symptoms of estrogen deficiency. Thus, one reasonable regimen would be 100 mm of estradiol per day by a skin patch, combined with 5-10 mg of medroyprogesterone acetate for 12 calendar days each month. The skin patch deliver a constant infusion of estradiol, avoids the “first pass” effect on the liver, and will maintain regular menses and be well tolerated by most patients.
CHRONIC ANOVULATION

Chronic anovulation may be viewed as a steady state in which the monthly rhythms associated with ovulation are not functional. Although amenorrhea is common, irregular menses and oligomenorrhea may occur as well. Chronic anovulation further implies that viable oocytes remain in the ovary and that ovulation can be induced with appropriate therapy.

Chronic anovulation is the most common pathological cause of oligomenorrhea or amenorrhea in women of reproductive age (Table 2). Appropriate management requires determination of the cause of the anovulation. However, anovulation can be interrupted transiently by nonspecific induction of ovulation in most affected women.
CHRONIC ANOVULATION OF CENTRAL ORIGIN
Hypothalamic Chronic Anovulation

Hypothalamic chronic anovulation may be defined as anovulation in which dysfunction of hypothalamic signals to the pituitary gland causes failure to ovulate. It remains unclear whether the primary abnormality is always present within the hypothalamus or sometimes occurs as a result of altered inputs to the hypothalamus. The term is used to refer to women who may be affected with suprahypothalamic or hypothalamic chronic anovulation. Although isolated gonadotropin deficiency frequently is caused by hypothalamic dysfunction, it is preferable to consider such individuals separately. However, partial forms of isolated gonadotropin deficiency may be virtually impossible to differentiate from hypothalamic chronic anovulation.

Numerous studies have documented an increased incidence of amenorrhea in women who exercise strenuously, diet excessively, or are exposed to severe emotional or physical stresses of any kind.1,62.63 Such amenorrheic persons fall into this group of women considered as having hypothalamic chronic anovulation, which is sometimes called functional amenorrhea. The diagnosis of hypothalamic chronic anovulation is suggested by the abrupt cessation of menses in women younger than 30 years of age who have no clinically evident anatomic abnormalities of the hypothalamic-pituitary-ovarian axis or any other endocrine abnormalities. The term hypothalamic amenorrhea was first proposed by Klinefelter and colleagues in 1943 for anovulation in which hypothalamic dysfunction is thought to interfere with the pituitary secretion of gonadotropin.64

Although hypothalamic chronic anovulation is a common cause of oligomenorrhea and amenorrhea, relatively little is known about its pathophysiologic basis. The diversity of women presenting with hypothalamic chronic anovulation indicates that this is a heterogeneous group of disorders with similar manifestations. Compared with a matched control population, young women with secondary amenorrhea are more likely to be unmarried, to engage in intellectual occupations, to have had stressful life events, to use sedative and hypnotic drugs, to be underweight, and to have a history of previous menstrual irregularities.1 Although it has been suggested that the percentage of body fat controls the maintenance of normal menstrual cycles, it is more likely that diet, exercise, stress, body composition, and other unrecognized nutritional and environmental factors contribute in various proportions to amenorrhea.

Hormonally, basal circulating concentrations of pituitary (i.e., LH, FSH, TSH, prolactin, growth hormone), ovarian (i.e., estrogens, androgens), and adrenal hormones (i.e., dehydroepiandrosterone, DHEAS, cortisol) typically are within the normal range for women of reproductive age.65 However, mean serum gonadotropin, gonadal steroid, and DHEAS levels often are slightly decreased, and circulating and urinary cortisol levels are generally increased compared with those in normal women in the early follicular phase of the menstrual cycle.63,66 Despite low levels of circulating estrogen, affected women rarely have symptoms related to estrogen deficiency. Typically, the pulsatile secretion of gonadotropin is diminished, but these individuals respond normally to exogenous gonadotropin-releasing hormone.
ANOREXIA NERVOSA, BULIMIA NERVOSA AND ATYPICAL EATING DISORDERS.

Eating disorders are common in adolescents and young women and may represent the most severe forms of functional hypothalamic chronic anovulation.67,68 Eating disorders are generally divided into three diagnostic categories: 1) anorexia nervosa, 2) bulimia nervosa, and 3) atypical eating disorders. Binge eating disorder has been proposed as a possible fourth group.

All eating disorders are characterized by altered eating habits or weight-control behavior. Poor nutrition can impact physical health. In addition, disturbed behavior in bulimia and anorexia is not due to any general medical disorder or any other psychiatric condition.

The constellation of amenorrhea often preceding weight loss, a distorted and bizarre attitude toward eating, food, or weight, extreme inanition, and a disordered body image makes the diagnosis of anorexia nervosa obvious in almost all cases.69-71 Demographically, 90% to 95% of anorectic women are white and come from middle- and upper-income families.

What distinguishes bulimia nervosa from anorexia nervosa is repeated binges during which there is loss of self control with unusually large amounts of food eaten. In most cases, binge eating is followed by compensatory self-induced vomiting or laxative abuse. Individuals with bulimia seldom have body weights that are significantly altered from ideal. Thus, body weight is the most obvious difference that distinguishes bulimia from anorexia nervosa. Many women with bulimia are ashamed or distress by their actions and are often more willing to accept treatment than individuals with anorexia. Symptoms of depression and anxiety disorders are common.

Anorexia nervosa most commonly arises in the mid-adolescent years. Self-induced dietary restrictions quickly gets out of control. In some cases, the disorder is of short-standing and self-limited, whereas in others the disorder becomes well entrenched and long-standing.

Bulimia nervosa usually begins later in adolescence. Often bulimia begins similarly to anorexia. However, episodes of binge eating eventually interrupt the dietary restriction, and body weight increases to near normal levels. Women with bulimia commonly seek treatment more than five years after disease onset.

Peripheral gonadotropin and gonadal steroid levels generally are lower than in the early follicular phase of the menstrual cycle.72 As patients with anorexia undergo therapy, gain weight, and improve psychologically, sequential studies of the ultradian gonadotropin rhythms show progressive gonadotropin changes paralleling those normally seen during puberty. Initially, there is a nocturnal rise in gonadotropins, followed by an increase in mean basal gonadotropin levels throughout the 24-hour period.73-75 The responses of severely ill anorectics to GnRH are also similar to those observed in prepubertal children and become adult-like with recovery or with treatment with pulsatile GnRH.76 Because the metabolism of estradiol and testosterone is also abnormal, normalizing with weight gain, some of the gonadotropin changes may be secondary to peripheral alterations in steroids.77

Several abnormalities indicate hypothalamic dysfunction, including mild diabetes insipidus and abnormal thermoregulatory responses to heat and cold.71 Affected individuals have altered body images as well.78

Still other central and peripheral abnormalities exist. There is evidence of chemical hypothyroidism, with affected patients having decreased body temperature, bradycardia, low serum triiodothyronine (T3) levels, and increased reverse T3 concentrations.79,80 Circulating cortisol levels also are elevated, but the circadian cortisol rhythm is normal.81 The increased cortisol seems to be caused by the reduced metabolic clearance of cortisol as a result of the reduced affinity constant for corticosteroid binding globulin (CBG) present in such patients.82 Moreover, like women with endogenous depression, anorectics suppress significantly less after dexamethasone administration than do normal subjects.83 Anorectics also have reduced ACTH responses to exogenous corticotropin-releasing hormone (CRH), suggesting normal negative pituitary feedback by the increased circulating cortisol.84

Although rigorous studies have not been performed in women with bulimia, presumably such individuals have endocrine disturbances similar to those of women with anorexia nervosa.
SIMPLE WEIGHT LOSS AND AMENORRHEA

Societal attitudes encourage dieting and pursuit of thinness, particularly in young women. Several reproductive problems, including hypothalamic chronic anovulation, have been associated with simple weight loss. Affected women are distinctly different from anorectics in that they do not fulfill the psychiatric criteria for anorexia. The cessation of menses does not occur before significant weight loss in such women, although this sequence is common in anorectics. The few studies that have been conducted in amenorrheic women with simple weight loss suggest that the abnormalities are similar to those observed in anorectics, but are more minor and more easily reversed with weight gain.85 Although it has been suggested that the amenorrhea in these women is secondary to metabolic defects resulting from undernutrition, the possibility of separate central defects has not been excluded.86 The importance of normal body weight to normal reproductive function is evident in studies of a tribe of desert-dwelling hunter-gatherers in Botswana.87 The weights of the women vary markedly with the season, being greatest in the summer, and the peak incidence of parturition follows exactly 9 months after the attainment of maximal weight.
EXERCISE-ASSOCIATED AMENORRHEA

Regular endurance training in women is associated with at least three distinct disorders of reproductive function: delayed menarche, luteal dysfunction, and amenorrhea.88,89 In 1992 the American College of Sports Medicine coined the term the “female athletic triad” to describe the three disorders recognized as sometimes occurring together in female athletes: disordered eating, amenorrhea, and osteoporosis.90 Activities associated with an increased frequency of reproductive dysfunction include those favoring a slimmer, lower-body-weight physique such as middle and long distance running, ballet dancing, and gymnastics. Swimmers and bicyclists appear to have lower rates of amenorrhea despite comparable training intensities. The cause of these disorders remains to be established and may involve many factors. Dietary changes, the hormonal effects of acute and chronic exercise, alterations in hormone metabolism because of the increased lean to fat ratio, and the psychological and physical “stress” of exercise itself may all contribute and may vary in importance in different individuals. Women engaged in endurance training frequently also have disordered attitudes toward eating, and a number of studies have documented low leptin levels and the absence of normal circadian leptin variation.91-94

In untrained women who underwent a program of strenuous aerobic exercise (running 4—10 miles/day) combined with caloric restriction, menstrual dysfunction was induced.95 The spectrum of abnormalities in these women included luteal phase dysfunction, loss of the midcycle LH surge, prolonged menstrual cycles, altered patterns of gonadotropin secretion, and amenorrhea. Subsequent studies have indicated that luteal phase defects can occur soon after beginning endurance training in the majority of untrained women.96 However, in contrast to these findings, others observed that a progressive exercise program of moderate intensity did not affect the reproductive system of gynecologically mature (mean age, 31.4 years), untrained, eumenorrheic women.97 It was suggested that relatively young gynecologic age or an earlier age of training onset in particular adversely affects menstrual cyclicity.

Many amenorrheic athletes welcome the onset of amenorrhea. However, significant osteopenia, usually affecting trabecular bone, has been reported in these women.98-100 It appears that the loss in bone density secondary to hypoestrogenism nullifies the beneficial effects of weight-bearing exercise in strengthening and remodeling bone.99,101 Such women are at risk for stress fractures, particularly in the weight-bearing lower extremities, and bone density may remain below those of eumenorrheic athletes even after resumption of menses.102

Stress is generally acknowledged to play a role in the cause of this form of amenorrhea, even though the term stress itself remains difficult to define. Amenorrheic runners subjectively associate greater stress with running than do runners with regular menses.103 (Fig.2)

Figure 2. Subjective stress associated with running. Subjects were asked to evaluate the stress associated with running on a scale from 0 to 10, with 10 being maximal. The means + standard errors are shown. The number of subjects in each group is shown in the bar. MDR - middle distance runners (15-30 miles per week) with regular menses; LDR - long distance runners (>30 miles per week) with regular menses; AR = amenorrheic runners. Stress was significantly greater (p<0.001) in both long distance and amenorrheic runners compared to middle distance runners. (Data from Schwartz et al., reference 103).

However, no increase in amenorrhea was observed in a competitive group of young classical musicians, who presumably were experiencing similar stress, compared with a group of young ballet dancers, in whom the incidence of amenorrhea was quite high.104 Basal levels of circulating cortisol and urinary free cortisol excretion, indicative of increased stress, are increased in eumenorrheic and amenorrheic runners.105 (Fig.3)

Figure 3. 24 Hour-urinary free cortisol excretion in normal control subjects (NC) eumenorrheic runners (R) and amenorrheic runners (AR). The number of subjects is shown in each bar. (Data from Villaneuva et al, reference 105).

Because levels of CBG, the disappearance rate of cortisol from the circulation, and the response of cortisol to adrenocorticotropin (ACTH) were not altered in the women runners compared with sedentary control subjects, secretion of ACTH and possibly of CRH must be increased in women who run. Abnormalities of the hypothalamic-pituitary-adrenal axis also are indicated by the observations that serum ACTH and cortisol responses to exogenous CRH are blunted as are the responses to meals.105,106

The observation that amenorrheic runners also have subtle abnormalities in hypothalamic-pituitary-thyroidal function provides support for the concept that exercise-associated amenorrhea is similar to other forms of hypothalamic amenorrhea.107
PSYCHOGENIC HYPOTHALAMIC AMENORRHEA

Amenorrhea may occur in women with a definite history of psychological and socioenvironmental trauma.86,108 The incidence of amenorrhea is quite high among depressed women, and the effects of lifestyle and nutritional status are difficult to differentiate from variables such as stress. Studies of individuals in whom a definite psychological traumatic event preceded the onset of amenorrhea have revealed low to normal basal levels of serum gonadotropins with normal responses to GnRH, prolonged suppression of gonadotropins in response to estradiol, and failure of a positive feedback response to estradiol.86,108-110 Increased basal levels of cortisol and decreased levels of DHEAS also have been noticed in women with psychogenic amenorrhea compared with eumenorrheic women.62 The mean levels of circulating cortisol are increased in such women largely because of an increase in the amplitude of the pulses of cortisol.111 Moreover, studies of depressed women have revealed abnormal circadian rhythms of cortisol and early “escape” from dexamethasone suppression.112,113

The mechanism by which emotional states or stressful experiences cause psychogenic amenorrhea is not yet established. Evidence suggests, however, that a cascade of neuroendocrine events that may begin with limbic system responses to psychic stimuli impairs hypothalamic-pituitary activity.114 It has been suggested that increased hypothalamic b-endorphin is important in inhibiting gonadotropin secretion.114

Psychological studies have found several social and psychological correlates of psychogenic amenorrhea: a history of previous pregnancy losses, including spontaneous abortion;115,116 stressful life events within the 6-month period preceding the amenorrhea;117,118 and poor social support or separation from significant family members during childhood and adolescence.113,118 Many women with psychogenic amenorrhea report stressful events associated with psychosexual problems and socioenvironmental stresses during the teenage years.108 Women with psychogenic amenorrhea also tend to have negative attitudes toward sexually related body parts, more partner-related sexual problems, and greater fear of or aversion to menstruation than do eumenorrheic women.117 Distortions of body image and confusion about basic bodily functions, especially sexuality and reproduction, are common.116
DIMINISHED GONADOTROPIN-RELEASING HORMONE AND LUTEINIZING HORMONE SECRETION IN ALL FORMS

The various forms of hypothalamic chronic anovulation associated with altered lifestyles have several features in common. Altered GnRH and LH secretion seems to be the common result from altered hypothalamic input. It remains unclear if these disorders form a single disorder or several closely related disorders. Moreover, similar forms of amenorrhea are sometimes seen in women with severe systemic illnesses or with hypothalamic damage from tumors, infection, irradiation, trauma, or other causes.
TREATMENT

The treatment of patients with hypothalamic chronic anovulation is controversial. Psychological therapy and support or a change in lifestyle may cause cyclic ovulation and menses to resume. However, ovulation does not always resume, even after the lifestyle is altered. The treatment of affected women in whom menses do not resume and who do not desire pregnancy is difficult. Most physicians now advocate the use of exogenous sex steroids to prevent osteoporosis. Therapy consisting of oral conjugated estrogens (0.625—1.25 mg), ethinyl estradiol (20 mg), micronized estradiol-17b (1—2 mg), or estrone sulfate (0.625—2.5 mg) or of transdermal estradiol-17b (0.05—0.1 mg) continuously with oral medroxyprogesterone acetate (5 to 10 mg) or oral micronized progesterone (200 mg) added for 12-14 days each month is appropriate. Sexually active women can be treated with oral contraceptive agents. These women appear to be particularly sensitive to the undesired side effects of sex steroid therapy, and close contact with the physician may be required until the appropriate dosage is established. If sex steroid therapy is provided, patients must be informed that the amenorrhea may still be present after therapy is discontinued.

Some physicians believe that only periodic observation of affected women is indicated, with barrier methods of contraception recommended for fertility control. Contraception is necessary for sexually active women with hypothalamic chronic anovulation because spontaneous ovulation may resume at any time (before menstrual bleeding) in these mildly affected individuals. Women who refuse sex steroid therapy should be encouraged to have spinal bone density evaluated at intervals to document that bone loss is not accelerated. Adequate calcium ingestion should be encouraged in all affected women.

For women desiring pregnancy who do not ovulate spontaneously, clomiphene citrate (50—100 mg/d for 5 days beginning on the third to fifth day of withdrawal bleeding) can be used. However, clomiphene is frequently ineffective in these hypoestrogenic women. Treatment with human menopausal and chorionic gonadotropins (hMG-hCG) or with pulsatile GnRH may be effective in women who do not ovulate in response to clomiphene. Because the underlying defect in hypothalamic amenorrhea is decreased endogenous GnRH secretion, administration of pulsatile GnRH to induce ovulation can be viewed as physiologic; it offers the additional advantages of decreased need for ultrasonographic and serum estradiol monitoring, a decreased risk of multiple pregnancies, and a virtual absence of ovarian hyperstimulation. A starting intravenous dose of GnRH of 5 mg every 90 minutes is effective.119 After ovulation is detected by urinary LH testing or ultrasound, the corpus luteum can be supported by continuation of pulsatile GnRH or by hCG (1500 IU every 3 days for four doses). Ovulation rates of 90% and conception rates of 30% per ovulatory cycle can be expected.120

One recent report noted improvements in reproductive function in a group of eight women with hypothalamic amenorrhea due to strenuous exercise or low weight who received recombinant human leptin for up to three months.121 As might be expected for a heterogeneous disorder, however, only three of the women ovulated in response to this therapy.

In general, women with anorexia and bulimia nervosa should not have ovulation induced until their disease is in remission. It is clear that cognitve-behavioral therapy that focuses on modification of the specific behaviors and ways of thinking that support the patient’s eating disorder should be a part of any treatment plan.122 Addition of antidepressant drugs, especially selective serotonin reuptake inhibitors, may be of additional benefit in treating women with bulimia nervosa.
Isolated Gonadotropin Deficiency

As originally described in 1944, Kallmann syndrome consisted of the triad of anosmia, hypogonadism, and color blindness in men.123 Women may be affected as well, and other midline defects may be associated.124-126 Because autopsy studies have shown partial or complete agenesis of the olfactory bulb, the term olfactogenital dysplasia also has been used to describe the syndrome.127 Because isolated gonadotropin deficiency may also occur in the absence of anosmia, the syndrome is considered to be quite heterogeneous.

Data indicate that in many patients the defect is a failure of GnRH neurons to form completely in the medial olfactory placode of the developing nose or the failure of GnRH neurons to migrate from the olfactory bulb to the medial basal hypothalamus during embryogenesis.128 In some patients, structural defects of the olfactory bulbs can be seen on magnetic resonance imaging.129 It appears likely that this disorder forms a structural continuum with other midline defects, with septo-optic dysplasia representing the most severe disorder.

Clinically, affected individuals typically present with sexual infantilism and a eunuchoidal habitus, but moderate breast development may also occur. Primary amenorrhea is the rule. The ovaries usually are small and appear immature, with follicles rarely developed beyond the primordial stage.130 These immature follicles respond readily to exogenous gonadotropin with ovulation and pregnancy, and exogenous pulsatile GnRH can also be used to induce ovulation.131 Replacement therapy with estrogen and progestin should be given to affected women not desiring pregnancy.

Circulating LH and FSH levels generally are quite low. The response to exogenous GnRH is variable, sometimes being diminished and sometimes normal in magnitude, but rarely may be absent.132,133 Although the primary defect in most individuals appears to be hypothalamic, with reduced GnRH synthesis or secretion, a primary pituitary defect may occasionally be present. In addition, partial gonadotropin deficiency may be more frequent than has been appreciated.
Hyperprolactinemic Chronic Anovulation

About 15% of amenorrheic women have increased circulating concentrations of prolactin, but prolactin levels are increased in more than 75% of patients with galactorrhea and amenorrhea.134 Radiologic evidence of a pituitary tumor is present in about 50% of hyperprolactinemic women, and primary hypothyroidism always must be considered. Individuals with galactorrhea-amenorrhea (i.e., hyperprolactinemic chronic anovulation) frequently complain of symptoms of estrogen deficiency, including hot flushes and dyspareunia. However, estrogen secretion may be essentially normal.135 It is not clear if the hyperprolactinemia or the “hypoestrogenism” causes the accelerated bone loss seen in such individuals.136 Signs of androgen excess are observed in some women with hyperprolactinemia; androgen excess may rarely result in PCO. In hyperprolactinemic women, serum gonadotropin and estradiol levels are low or normal.

Most hyperprolactinemic women have disordered reproductive function, and it appears that the effects on gonadotropin secretion are primarily hypothalamic. The mechanism by which hypothalamic GnRH secretion is disrupted is unknown but may involve an inhibitory effect of tuberoinfundibular dopaminergic neurons.135, 137 It has been proposed that increased hypothalamic dopamine is present in hyperprolactinemic women with pituitary tumors but is ineffective in reducing prolactin secretion by adenomatous lactotropes. The dopamine can, however, reduce pulsatile LH secretion and produce acyclic gonadotropin secretion through a direct effect on hypothalamic GnRH secretion.

It has been suggested that mild nocturnal hyperprolactinemia may be present in some women with regular menses and unexplained infertility.138 Galactorrhea in women with unexplained infertility may reflect increased bioavailable prolactin and may be treated appropriately with bromocriptine.139 Bromocriptine or cabergoline therapy may also be indicated in normoprolactinemic women with amenorrhea and increased prolactin responses to provocative stimuli.140
Hypopituitarism

Hypopituitarism may be obvious on cursory inspection or it may be quite subtle. The clinical presentation depends on the age at onset, the cause, and the woman's nutritional status. Loss of axillary and pubic hair and atrophy of the external genitalia should lead the physician to suspect hypopituitarism in a previously menstruating young woman who develops amenorrhea. In such cases, a history of past obstetric hemorrhage suggesting postpartum pituitary necrosis (i.e., Sheehan syndrome) should be sought.141 Failure to develop secondary sexual characteristics or to progress in development once puberty begins must always prompt a workup for hypopituitarism.

Individuals with pituitary insufficiency often complain of weakness, easy fatigability, lack of libido, and cold intolerance. Short stature may occur in individuals developing hypopituitarism during childhood. Symptoms of diabetes insipidus may be observed if the posterior pituitary gland is involved. On physical examination, the skin is generally thin, smooth, cool, and pale (i.e., “alabaster skin”) with fine wrinkling about the eyes; the pulse is slow and thready; and the blood pressure is low.

An evaluation of thyroid and adrenal function is of paramount importance in these individuals. Thyroid replacement therapy must be instituted and the patient must be euthyroid before adrenal testing is initiated. Serum gonadotropin and gonadal steroid levels typically are low in hypopituitarism. Responses to exogenously administered hypothalamic hormones have failed to localize the cause to the hypothalamus or the pituitary gland in affected patients.

Radiographic evaluation of the sella turcica is indicated in any individual with suspected hypopituitarism. The ovaries appear immature and unstimulated, but because oocytes still are present, ovulation can be induced with exogenous gonadotropins when pregnancy is desired. Exogenous pulsatile GnRH may also be used to induce ovulation if the disorder is hypothalamic. Moreover, oocytes may undergo some development, and even ovarian cysts may appear in the absence of significant gonadotropic stimulation. When pregnancy is not desired, maintenance therapy with cyclic estrogen and progestin is indicated to prevent signs and symptoms of estrogen deficiency.
CHRONIC ANOVULATION DUE TO INAPPROPRIATE FEEDBACK IN POLYCYSTIC OVARY SYNDROME (PCOS)

A Heterogeneous Disorder. In 1935, Stein and Leventhal focused attention on a common disorder in which amenorrhea, hirsutism, and obesity were frequently associated.142 (Fig.4)

Figure 4. Facial hirsutism in a 17-year-old woman with polycystic ovary syndrome (PCOS).

With the development of radioimmunoassays for measuring reproductive hormones, it became clear that women with what is called PCOS shared several distinctive biochemical features. Compared with eumenorrheic women in the early follicular phase of the menstrual cycle, affected women typically have elevated serum LH levels and low to normal FSH levels143. Virtually all serum androgens are moderately increased, and estrone levels are generally greater than estradiol levels105. Ovarian inhibin physiology is normal.145

Many women with the biochemical features of PCOS have small or even morphologically normal ovaries and are not overweight or hirsute. Not all women with PCOS present with the characteristic features. Moreover, excess androgen from any source or increased conversion of androgens to estrogens can lead to the constellation of findings observed in PCOS.146 Included are such disorders as Cushing syndrome, congenital adrenal hyperplasia, virilizing tumors of ovarian or adrenal origin, hyperthyroidism and hypothyroidism, and obesity. In all of these disorders, the ovaries may be morphologically polycystic. Although no clinical and biochemical criteria describe the syndrome strictly, a conference convened by the National Institutes of Health147 developed diagnostic criteria for PCOS:

1. Clinical evidence of hyperandrogenism (e.g., hirsutism, acne, androgenetic alopecia) and/or hyperandrogemia (e.g., elevated total or free testosterone).

2. Oligoovulation (i.e., cycle duration >35 days or <8 cycles per year).

3. Exclusion of related disorders (e.g., hyperprolactinemia, thyroid dysfunction, androgen-secreting tumors, 21-hydroxylase-deficient nonclassical congenital adrenal hyperplasia.)

A subsequent expert conference convened in Rotterdam, The Netherlands, in 2003 and sponsored in part by the American Society for Reproductive Medicine (ASRM) and the European Society for Human Reproduction and Embryology (ESHRE) recommended that PCOS be defined when at least two of the following three features are present: 1) oligo- and/or anovulation, 2) clinical and/or biochemical signs of hyperandrogenism, and 3) polycystic ovaries. This definition also states that other androgen excess or related disorders should be excluded prior to assigning the diagnosis of PCOS.148,149 By these criteria neither hyperandrogenism nor ovulatory dysfunction is required to make the definition of PCOS. This definition has been widely accepted in Europe but has been greeted with skepticism in the United States.

PCOS may be viewed as a state of chronic anovulation associated with LH-dependent ovarian overproduction of androgens. Clinically, the perimenarcheal onset of symptoms is a common feature. It has been estimated that PCOS affects approximately 5% of women of reproductive age.150, 151 Although the cause of this disorder remains unknown, there is some evidence of autosomal dominant transmission in some affected individuals.152, 153 Disorders presenting similarly but with different underlying causes can be considered as having chronic anovulation with inappropriate feedback.
Polycystic Ovaries

Grossly, the ovaries of most women with PCOS are bilaterally enlarged and globular. (Fig.5)

Figure 5. Gross and cut appearance of typical polycystic ovaries. Multiple small follicular cysts are apparent in the cut section.

They are often described as having an “oyster shell” appearance because they have smooth, glistening capsules and are the appropriate color. The tunica albuginea is often thickened diffusely, and many cysts 3 to 7 mm in diameter are present on cut section. Because ovulation rarely occurs, corpora lutea are rarely present. Histologically, the follicular cysts are usually lined by granulosa cells and surrounded by a thickened and luteinized theca interna and are in various stages of maturation and atresia. When islands of luteinized thecal cells are found scattered throughout the ovarian stroma, not just around the follicles, the term hyperthecosis is sometimes used. The clinical syndrome accompanying this pathologic finding is typically characterized by massive obesity, severe hirsutism reflecting particularly excessive ovarian overproduction of androgens, acanthosis nigricans, glucose intolerance with insulin resistance, and hyperuricemia. (Fig.6)

Figure 6. Appearance of a woman with hyperthecosis, sometimes referred to as the HAIR-AN syndrome (hyperandrogenism, insulin resistance, acanthosis nigricans). The obesity, hirsutism, acne, and acanthosis nigricans are obvious.

Insulin action at the target cell appears defective in these patients, with some individuals having antibodies to insulin receptors and others apparently having a postreceptor defect.154, 155 PCOS and hyperthecosis appear to represent facets of the same disease process rather than two distinct entities. Some authorities, however, maintain that the two represent different disorders.

The follicles in the ovaries of women with PCOS do not mature completely. However, in vitro studies have failed to detect any primary defect in the steroidogenic capacity of polycystic ovaries.156 Although there seems to be a relative deficiency in aromatase activity in the granulosa cells of polycystic ovaries, this deficiency can be corrected by FSH in vitro and in vivo.

Other Clinical and Biochemical Features. Although all women with PCOS produce androgens at increased rates compared with eumenorrheic women, only some present with hirsutism, largely because of varying sensitivity at the level of the hair follicle. The hyperandrogenism is rarely sufficient to produce overt virilization. Signs of markedly elevated androgen levels, including clitoromegaly, temporal balding, and deepening of the voice, may suggest an androgen-producing tumor, especially if these features developed rapidly. Women with PCOS invariably are well estrogenized, with normal breast development and abundant cervical mucus on examination. Because obesity is found in only about 50% of women with PCOS, it is doubtful that obesity is central to its cause.

About 50% of women with PCOS have amenorrhea, about 30% have irregular bleeding, and about 12% have “cyclic menses.”146 No particular pattern of menstrual bleeding is characteristic of women with PCO, although a history of oligomenorrhea is probably most common. Because only about 75% of women with PCOS are infertile, women with PCOS do ovulate occasionally.

Two other biochemical features warrant discussion. First, obese and normal-weight women with PCOS generally release increased quantities of insulin in response to a standard glucose challenge compared with weight-matched eumenorrheic individuals.157, 158 Many investigators now regard the insulin resistance as the central abnormality in the disorder, but this has not been established with certainty. Thus, regardless of body weight, 30 to 80 percent of women with PCOS experience insulin resistance and compensatory hyperinsulinemia.159 Based on studies in a very well characterized subset of obese women with the disorder, the insulin resistance present in PCOS appears to represent a postreceptor signalling aberration and differs from the insulin resistance observed in non-insulin dependent diabetes mellitus and simple obesity.118 The compensatory hyperinsulinemia that results causes exaggerated effects in other tissues as well. These effects include increased ovarian androgen secretion; excessive growth of the basal cells of the skin leading to acanthosis nigricans in some women; increased vascular and endothelial reactivity, which may lead to hypertension and vascular disease; and abnormal hepatic and peripheral lipid metabolism, which may cause dyslipidemia. Thus, it is now recognized that women with PCOS are at increased risk of cardiovascular disease and non-insulin-dependent diabetes mellitus in addition to endometrial carcinoma because of anovulation. Because treatment with a GnRH analogue reduces ovarian androgen secretion but does not correct the insulin resistance in women with PCOS, the defect in insulin action presumably is not due to abnormal sex steroid levels.160 The possibility that a defect in the secretion or action of insulin or some related growth factor is central to the cause of PCOS cannot be entirely excluded and is gaining increasing support as the cause of hyperandrogenemia in women with PCOS.161 The pivotal role of insulin resistance in PCOS is strongly suggested by the beneficial effects of insulin-sensitizing agents such as metformin, troglitazone, and D-chiro-inositol on metabolic and reproductive function, regardless of the patient’s weight.162-165

In addition, perhaps 10% to 15% of women with PCOS have mild hyperprolactinemia in the absence of radiographic evidence of a pituitary tumor, possibly because of chronic acyclic estrogen secretion.166 Although hyperprolactinemia is associated with increased adrenal production of DHEAS, the increased adrenal androgen production seen in women with PCOS usually does not correlate with the hyperprolactinemia.
Pathophysiology of the Chronic Anovulation

A growing body of evidence indicates that disordered insulin action precedes the increase in androgens in PCOS. The administration of insulin to women with PCOS increases circulating androgen levels.161, 167 The administration of glucose to hyperandrogenic women increases circulating levels of insulin and androgen.168 Weight loss decreases levels of insulin and androgens.128 The suppression of circulating insulin levels experimentally by diazoxide reduces androgen levels.170 The suppression of androgen secretion to normal levels with GnRH agonists does not lead to normal insulin responses to glucose tolerance testing in obese women with PCOS.160, 171, 172

The hyperinsulinemia may cause hyperandrogenemia by binding to IGF-I receptors in the ovary.173 Activation of ovarian IGF-I receptors by insulin can lead to increased androgen production by thecal cells.174 Moreover, independent of any effect on ovarian steroid production, increased insulin inhibits the hepatic synthesis of SHBG.175 Insulin directly inhibits insulin-like growth factor binding protein-1 in the liver, permitting greater local activity of IGF-I in the ovary.176

Regardless of the cause of PCOS, it is possible to construct a rational pathophysiologic mechanism to explain the disorder. (Fig.7)

Figure 7. Pathophysiologic mechanisms associated with PCOS that may help explain the chronic anovulation.

Regardless of the source or cause of androgen excess, a vicious cycle of events causing persistent anovulation commences. The androgen is converted to estrogen, primarily estrone, in the periphery. The estrogen feeds back on the central nervous system-hypothalamic-pituitary unit to induce inappropriate gonadotropin secretion with an increased LH to FSH ratio. The estrogen stimulates GnRH synthesis and secretion in the hypothalamus, causing preferential LH release by the pituitary gland. The estrogen may also increase GnRH by decreasing hypothalamic dopamine. Selective inhibition of FSH secretion by increased ovarian inhibin may also occur in PCOS. Possible inhibition of FSH secretion by increased androgen secretion has not been considered. The increased LH secretion stimulates thecal cells in the ovary to produce excess androgen. The androgen also inhibits production of SHBG, resulting in increased free androgen and predisposing affected women to hirsutism. The morphologic ovarian changes undoubtedly are secondary to hormonal changes. The absence of follicular maturation and the reduced estradiol production by the ovaries apparently result from a combination of inadequate FSH stimulation and inhibition by the increased concentrations of intraovarian androgen. The low levels of SHBG probably facilitate tissue uptake of free androgen, leading to increased peripheral formation of estrogen and perpetuating the acyclic chronic anovulation. The androgenic basis for the inappropriate estrogen feedback is partly shifted from the site of origin to the ovaries. The increased estrogens (and perhaps androgens) may also stimulate fat cell proliferation, leading to obesity. The current data suggest that there is no defect in the hypothalamic-pituitary axis in PCOS but rather that peripheral alterations result in abnormal gonadotropin secretion.
Therapy

Appropriate therapy demands that potential causes such as neoplasms be eliminated. Besides facilitating fertility, the aims of treatment in women with PCOS are three-fold: to control hirsutism, to prevent endometrial hyperplasia from unopposed acyclic estrogen secretion, and to prevent the long-term consequences of insulin resistance. The treatment must be individualized according to the needs and desires of each patient.

For the anovulatory woman with PCOS who is not hirsute and who does not desire pregnancy, therapy with an intermittent progestin (e.g., medroxyprogesterone acetate, 5 to 10 mg orally, or micronized progesterone, 200 mg orally, for 10 to 14 days each month) or oral contraceptives if she is younger than 35 years of age, does not smoke, and has no other significant risk factor should be provided to reduce the increased risk of endometrial hyperplasia and carcinoma present in such a woman because of the unopposed estrogen secretion. The woman taking progestins intermittently should be informed of the need for effective barrier contraception if she is sexually active, because these agents as administered do not inhibit ovulation, and ovulation occasionally occurs in PCOS. There is no evidence that the use of low-dose combined oral contraceptive agents increases the risks associated with insulin resistance in women with PCOS, and the benefits in preventing endometrial hyperplasia are clearly established.

Therapy for the woman with PCOS who is hirsute is somewhat different in some circumstances. In general, oral contraceptives provide initial therapy for affected women with mild hirsutism and provide protection from endometrial hyperplasia.

For women with PCOS who are overweight, it is reasonable to encourage lifestyle changes. Weight loss alone (of even less than 10%) may result in decreased insulin resistance and resumption of ovulation.177-179 However, lifestyle changes are difficult for patients to adopt. The use of insulin-sensitizing agents such as metformin is increasing but is not approved by the FDA. Whether the use of such agents will decrease the likelihood of the consequences of the metabolic alterations associated with insulin resistance is unclear. At present no data regarding the long-term safety and efficacy of these agents exist. What is clear is that only short-term trials of perhaps 3 months duration are needed to determine if insulin-sensitizing agents will be useful: responsive individuals will resume cyclic menstruation and ovulation in this short time frame and insulin levels will fall substantially.162, 163 180 181

Predicting which individuals with PCOS will respond is not possible at the present time. However, many clinicians believe that the therapy is low in risk, and the agents are relatively inexpensive. The use of these agents should probably be contemplated only in women with well documented insulin resistance and PCOS. Metformin should be administered only if the patient’s creatinine is normal and should be discontinued during illnesses to prevent the occurrence of lactic acidosis. Individuals should be cautioned that they may anticipate nausea or diarrhea on beginning metformin. Consequently the drug should be increased slowly to the maximal dose of 2.5 g per day orally.

For the woman with PCOS who wants to conceive, clomiphene citrate is used initially because of its high success rate and relative simplicity and inexpensiveness. Other possible therapeutic approaches to ovulation induction include the use of gonadotropins (perhaps preceded by a GnRH analogue), FSH alone, pulsatile GnRH, and wedge resection of the ovaries at laparotomy. Wedge resection or any other surgical manipulation of the ovaries should be performed only after all other methods of ovulation induction fail, an ovarian tumor is possible because of ovarian size or circulating androgen levels, or fertility is unimportant, because pelvic adhesions frequently result from surgery and may contribute to infertility. Laparoscopic ovarian follicular cautery or laser vaporization can also be used successfully to induce ovulation.182,183 However, these procedures also cause adhesion formation in a significant percentage of women. In addition, the success of medical therapy does not justify routine use of these procedures.

Data indicate that insulin-sensitizing agents, alone or in combination with clomiphene citrate, may improve both ovulatory function and fertility in some women with PCOS.162, 163,180 A trial may be warranted in women who do not respond to clomiphene before considering the use of more expensive agents to induce ovulation.
CHRONIC ANOVULATION DUE TO OTHER ENDOCRINE AND METABOLIC DISORDERS
Cushing Syndrome

Along with the well-known physical manifestations in Cushing syndrome—central obesity, moon facies, and pigmented striae—are the less visible endocrinologic changes of amenorrhea, hirsutism, and infertility. The mechanisms responsible for the chronic anovulation are unclear, but several possibilities exist. The various degrees of adrenal androgen excess in Cushing syndrome of all causes together with obesity may cause excessive extraglandular conversion of androgens to estrogens in fat cells and inappropriate acyclic feedback to the hypothalamic-pituitary unit.184 The increased levels of CRH and ACTH in Cushing disease may affect the hypothalamic-pituitary secretion of GnRH and LH, as suggested for hypothalamic chronic anovulation.
Thyroid Dysfunction

As a result of significant changes in the metabolism and interconversion of androgens and estrogens, hyperthyroidism and hypothyroidism are associated with menstrual disorders ranging from excessive and prolonged uterine bleeding to amenorrhea. The altered sex steroid metabolism leads to inappropriate feedback and chronic anovulation. The changes are corrected by appropriate treatment of the underlying thyroid disease. Next
Abnormal Uterine Bleeding in Women of Reproductive Age