Cause of Endometriosis

Introduction
Definition
Incidence
Cause
Symptoms
Intestinal Endometriosis
Infertility
Diagnosis
Treatment
Adenomyosis
Are you too young to have
a laparoscopy?
Endometriosis and cancer
Treatment summary
Endometriosis and heredity

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When something is poorly understood, in medicine as in other pursuits, numerous theories arise to explain the unexplainable. As a result, over the years, many different mechanisms have been proposed to try to explain how endometriosis develops. These have included retrograde menstruation, embryonic rest cells (cells leftover from the time that you were an embryo - such cells have the ability to develop into almost anything), and what is termed "coelomic metaplasia" - the transformation of cells that line the abdominal and pelvic cavity into endometriosis cells. All of these theories had their proponents and their detractors. None of them really seemed to explain exactly how endometriosis develops.

With advances in medicine and a better understanding of what is occurring, we now have a mechanism that seems to fit the known and observed facts. If it is not the correct theory, it will probably be the best we have until something substantially better comes along.

It has been known for many many years that virtually all women have retrograde menstruation. During the menstrual period, almost all of the blood flows out through the cervix and into the vagina. However, a tiny portion does flow back through the fallopian tubes into the pelvic cavity. It is this backward flow that we term "retrograde menstruation".

Studies have been done looking at the fallopian tubes in women who were actively menstruating at the time of hysterectomy. Virtually all women have menstrual blood in their fallopian tubes at that time.

It has also been known for many many years that women who have any congenital anomaly or any acquired abnormality of the uterus, cervix or vagina, that either partially or completely obstructs the normal flow of menstrual blood into the vagina, are at greater risk to develop endometriosis. The theory holds that these women are more likely to have retrograde menstruation or that the retrograde menstruation which they are experiencing would be significantly greater than that which occurs in women who are not obstructed in some fashion.

The retrograde menstruation theory is the one that has been most popular and is believed by most physicians to be the precipitating cause of endometriosis. However, this does not fully resolve the matter. Since all women experience retrograde menstruation, why do only a certain percentage ever goes on to develop endometriosis?

Personally, I am not convinced that it is retrograde menstruation that causes endometriosis or at least sets the stage for its development. My belief is based upon the fact that the cells that are being shed during your menstrual flow are cells that are dying and are not very capable of implanting and growing in your pelvic cavity. However, women are constantly shedding cells from their endometrium throughout the menstrual cycle. It has been shown that you can recover these cells from the early stages of the menstrual cycle from the pelvic fluid. These are normal, healthy cells and they can even be grown in tissue culture. If indeed it is the retrograde migration of these abnormal cells (which is in a sense a variant of retrograde menstruation), the question still remains - why only some women when the phenomenon itself is virtually universal?

The answer is most likely to be found in your immune system. The primary purpose of your immune system is to get rid of anything that shouldn't be there. This applies to infectious agents such as viruses and bacteria. It also applies to cells that are dead or dying. When a cell is in the process of dying, it has a mechanism by which it alerts the immune system that it is no longer a normal, healthy cell. The immune system attacks it and gets rid of it. Your body also gets rid of cancer cells the same way. It is believed that we are all constantly forming cells that could become cancer. Again, the immune system has the ability to recognize these cells as being abnormal and it destroys them.

Using this same line of reasoning, endometrial cells in the pelvic cavity may be normal but they are found in an abnormal location. Again, the immune system recognizes this and destroys them.

There are cells throughout your body that we call macrophages. These are your immune system's scavengers. They are the cells that literally gobble up abnormal cells, viruses, bacteria, etc. There is increasing evidence that the macrophages in the pelvic cavity of women with endometriosis do not function properly and, therefore, they have an impaired ability to destroy the endometrial cells that are deposited there in the early stages of the menstrual cycle.

There is also evidence that these macrophages function abnormally insofar as they produce excess amounts of various hormones and other tissue factors that promote the growth of the endometrial cells and allow them to survive and proliferate. Many of these tissue factors also play a major role in inflammation and pain, which may also contribute to the symptoms the Endometriosis is causing.

This theory also explains why it is believed that virtually all women will develop "temporary endometriosis". By this it is meant that endometrial cells will begin to grow in the pelvis but, within three to six months, the body will destroy them. Studies have been done looking at women who appear to have this condition. In such women, if the endometriosis is left untreated for six months and they undergo a repeat laparoscopy, a substantial percentage of these women will no longer have detectable endometriosis. These women cannot, therefore, really be classified as having the "disease" endometriosis. This condition suggests that their immune system is not working completely normally but it is not as defective as it would be in those women who actually go on to develop the clinical disease that we term endometriosis.

This, however, also does not fully answer the question as to why these women were having a laparoscopy in the first place since that is the only way you can diagnose this condition. The only women who would be undergoing a laparoscopy completely electively are those women who are having a tubal sterilization. Otherwise, women who are having laparoscopies are doing so because they are either infertile or having pain. Nonetheless, the evidence does indicate that an abnormality in the immune system is the most likely and most logical explanation to explain the development of endometriosis. It also goes a long way in explaining why women with endometriosis and their close relatives have an increased incidence of other diseases that we either know or suspect involve abnormalities in the immune system.

OTHER FACTORS IN ASSOCIATION WITH ENDOMETRIOSIS

Over the years, many theories have been advanced to explain Endometriosis. They are discussed in this section for your information in case you should come across them in your reading. A great deal of information has also been accumulated. Some of this is also included to help you better understand the problems often associated with Endometriosis.

In order to understand how Endometriosis gets started, it is necessary to understand what happens during a normal menstrual cycle. In a normally ovulating woman, each month an egg begins to grow and develop within a structure called the follicle. The follicle is comprised of the egg and the surrounding ovarian cells that are necessary for the growth and development of the egg. The cells of the follicle also serve as the source of estrogen which is produced during the menstrual cycle.

As the follicle develops, fluid begins to collect inside it and at the time of ovulation when the follicle is fully developed, the follicle is approximately 1 inch in diameter and contains about 1/2 teaspoon of fluid. The follicle is, by strict definition, a small cyst. Because of the fluid which the follicle contains, it is possible to visualize it on ultrasound and this, of course, is very important in tracking an infertile woman during her menstrual cycle.

Once the follicle has reached full maturity, the follicle wall ruptures and the egg is expelled. This is the process of ovulation. After the egg is released from the follicle, it is picked up by the fallopian tube. Following ovulation, fluid begins to accumulate in the deep pelvis where it can be seen on ultrasound. This is one of the indicators that ovulation has occurred.

After ovulation takes place, the follicular cells undergo a transformation and the structure that was once the follicle now becomes the corpus luteum. Prior to ovulation, the follicle produces estrogen; after ovulation, the corpus luteum produces estrogen and progesterone.

Our bodies are composed of cells and we are always creating new cells as older ones die. Some cells are shed. You are always losing cells from your skin, your intestinal tract, etc. Similarly, women constantly shed cells from the endometrium and some of these cells work their way back through the fallopian tube out into the abdomen, then down into the deep pelvis. If a laparoscopy is carried out on a woman, it is almost always possible to find endometrial cells in the deep pelvis in the small amount of fluid that naturally collects there. These endometrial cells that have been sloughed off throughout the menstrual cycle are living cells that can be made to grow under appropriate laboratory conditions.

You may have heard that Endometriosis is caused by retrograde menstruation. By this, it is meant that menstrual blood and cells flow back through the fallopian tube out into the abdomen at the time of the menstrual period. While retrograde menstruation certainly does take place, the cells that are being shed at the time of the menstrual period are in the process of dying and, therefore, are probably not the cause of Endometriosis. I believe it is the healthy, actively growing cells which are shed early in the menstrual cycle that give rise to Endometriosis.

Other theories, such as the transformation of the lining cells of the abdomen (the peritoneum) into Endometriosis have been recently shown not to be the cause of Endometriosis.

Since it is evident that nearly all women have endometrial cells in their deep pelvis, the natural question would be - why don't all women develop Endometriosis? What is it that allows those cells to implant and grow in some women but not in others? In those women who develop early stage Endometriosis, what allows the endometrial tissue to persist (and perhaps progress) in some and causes it to be eliminated in others?

For many years, those of us in the field of Reproductive Endocrinology have recognized that women with Endometriosis are less fertile than women who do not have Endometriosis. It was believed that in these women, the Endometriosis caused the infertility. Certainly when a woman has severe Endometriosis with considerable scar tissue around the tubes and ovaries, there is no question that the Endometriosis is causing the infertility.

However, there are many women in whom laparoscopy demonstrates only the presence of minimal or mild Endometriosis. By this it is meant that there is surface disease or some scar tissue but the Endometriosis has not progressed to the point where there is significant scar tissue or large ovarian Endometriosis cysts. I have long held the belief that at least for some of these women, they were infertile for some other reason and that other reason permitted the Endometriosis to develop. The problem is that we never had a good explanation for "that other reason". Now we may.

I and other Reproductive Endocrinologists have long recognized that women with Endometriosis very often have evidence of other hormonal disorders. It is very common for me to see women with Endometriosis who have evidence of increased male hormone production such as facial hirsutism and/or acne. I see many women with Endometriosis who also have Poly-Cystic Ovary Syndrome. We also have recognized for many years that other types of abnormalities in the endocrine system, particularly as it affects ovulation, occur more frequently in women with Endometriosis. It was once believed that these abnormalities in ovulation were the result of the Endometriosis. It is now becoming apparent that these ovulatory abnormalities may play a major role in the development of Endometriosis.

Three principal types of ovulatory abnormalities are commonly seen in women with Endometriosis. One problem - easy to diagnose - is the failure of ovulation to occur at all. The second ovulatory abnormality is also fairly common and also fairly easy to diagnose. This is a "luteal phase defect" in which there is inadequate or insufficient amounts of progesterone produced by the corpus luteum after ovulation has occurred.

There probably truly is an entity we call the luteal phase defect. It would take a pamphlet as long as this one to explain everything about it. It is a highly controversial situation in Reproductive Endocrinology. Most women who are told they have it are not diagnosed properly. The true significance of this condition is debatable. Further confusing the whole matter is newer evidence that the real problem for most women is not inadequate progesterone production but the inability of the endometrium to respond to the progesterone. None-the-less, there are well documented cases of women who have it and it probably does play a role in Endometriosis but I am not fully certain what that role is.

The third principal ovulatory abnormality is a problem that has been recognized for many years but was thought to be a medical curiosity. It is now becoming increasingly apparent that this abnormality is quite common in women with Endometriosis. This third abnormality to which I refer is the so-called "Luteinized Unruptured Follicle Syndrome."

In the Luteinized Unruptured Follicle (LUF) Syndrome, the egg develops within the follicle quite normally and then, after mid cycle, the follicle turns into the corpus luteum. All the hormones are made in reasonably normal amounts. It is important to remember that when a woman is being assessed for ovulation, we are not determining whether ovulation, the actual release of the egg from the ovary, has taken place. Rather, we are measuring the biological effects of the hormones that are being produced during the menstrual cycle. We make the assumption that if the hormones are being produced in proper amounts, then ovulation is presumed to be normal.

New evidence suggests that, particularly in women with Endometriosis, this is no longer a valid assumption. What happens in the Unruptured Follicle Syndrome is that even though all hormonal changes take place reasonably normally, the follicle never ruptures and the egg is never expelled from the ovary. However, since the hormones are being produced, the basal body temperature chart will show a rise; measurement of blood hormone levels will be "normal"; and if an endometrial biopsy is done, it will show that "ovulation" has taken place. However, the follicle will not collapse and there will not be any significant increase in fluid in the pelvis when an ultrasound is done.

The next question is then - how do these various abnormalities in ovulation lead to Endometriosis. The answer is found when one looks at the fluid that normally accumulates in the pelvis throughout the menstrual cycle and analyzes this fluid for its hormone content. In normally ovulating women, after ovulation has taken place, the concentration of estrogen and progesterone in the pelvic fluid rises dramatically and achieves a level much higher than the hormone concentration found in the blood. Keep in mind that estrogen is produced throughout the menstrual cycle whereas progesterone is produced only after ovulation. Keep in mind also, as was pointed out earlier, the endometrial cells are also found in this pelvic fluid. It now appears that the progesterone that accumulates in this pelvic fluid after ovulation kills the endometrial cells that have accumulated there. If there is a defect in ovulation, the progesterone accumulation either does not occur or is below normal. This then permits those endometrial cells to live and eventually implant and grow. Thus, Endometriosis is allowed to develop.

In women who do not ovulate at all, it is obvious that no progesterone is produced. In women with a luteal phase defect, inadequate progesterone is produced. The puzzle was what was going on in women with the Unruptured follicle syndrome. For reasons that are not yet apparent, in order for the progesterone level to rise in the pelvic fluid, actual ovulation must have taken place. If the follicle does not rupture and the egg is not expelled, the progesterone level in the pelvic fluid does not rise. This then serves to explain why women with the Unruptured follicle syndrome develop Endometriosis and indeed, recent evidence suggests that whereas in the general population, the Unruptured follicle syndrome is fairly rare, it occurs with significant frequency in women with Endometriosis and probably serves as one of the main causative factors. The definitive diagnosis of the Unruptured follicle syndrome is made by laparoscopy but it can be strongly suspected and sometimes even diagnosed by the use of ultrasound examinations.

Abnormalities of ovulation such as the ones that I have just described are usually fairly easy to diagnose. They are simple straightforward concepts and the diagnostic criteria for each of them is now fairly well established. However, there are a substantial number of women who do not appear to have any obvious defect in ovulation. How then can these women be explained and still preserve the integrity of the theory?

Several studies from England revealed some very interesting data concerning not only the cause of Endometriosis but also its effects on a woman's fertility. What these studies looked at was couples who were presented in the infertility clinic and put them through a standard fertility workup. When they reached the point in the evaluation that laparoscopy was indicated, they combined the laparoscopy with an attempt at in-vitro fertilization. They then analyzed their data in the following way. They did not consider the overall pregnancy rate from the attempt at IVF because that was too low(at that time) to draw any meaningful conclusions. Instead, they looked at the percentage of eggs that were fertilized in relationship to the cause of that couple's infertility after they had examined all of the data.

What they found was very interesting and very enlightening. The results showed that if the couple's main reason for infertility was tubal damage, the fertilization rate for the eggs obtained from these women was 90%. A similar figure was obtained for those couples with "unexplained infertility". However, for those women who had early untreated Endometriosis, the fertilization rate was only 60%. This study has been expanded and the additional data confirms the original findings that the eggs from infertile women with early stage Endometriosis do not fertilize as often as those from women with other causes of infertility.

This data indicates that there may be an inherent defect in the egg of those women who develop Endometriosis. This further supports the theory that a defect in ovulation is probably a major cause of Endometriosis. This is true because the egg, in ways we do not fully understand, plays a major role in controlling its destiny during a given menstrual cycle. If there is a problem with the egg itself, then it would follow that normal ovulation could not occur.

More recently, by carefully monitoring the menstrual cycle using frequent vaginal ultrasound examinations combined with the measurement of serum hormone levels, we have been able to discover that most women with Endometriosis have subtle but definite abnormalities of ovulation that can not be detected by other means. These abnormalities do not fall into any one given pattern so they are lumped under the overall heading of "ovulatory dysfunction". I have found that many women with Endometriosis have one or more abnormalities of ovulation when the time is spent to search for them.

The other question that must be answered is whether the ovulatory abnormalities are a cause of Endometriosis or simply an associated phenomenon.

Endometriosis is often called the "career woman's disease". It is a common belief that the longer a woman goes without having had a baby, the more likely she is to develop Endometriosis. In point of fact, while this is true, it is not true in the way most people think of it. The age at which a woman has her first baby may alter the time course of the Endometriosis in terms of when the symptoms may initially appear but does not affect her chances of ultimately developing the disease. In other words, if a woman has her children at a younger age, she will develop her symptoms later, but she will still develop them. Nonetheless, I assume that a woman over the age of 30 who has never had a baby has Endometriosis until proven otherwise. Perhaps we simply look for Endometriosis more diligently in an older women who is infertile because her age becomes a factor.

The question is, does simply delaying childbearing predispose a woman to Endometriosis? Maybe! Probably. In a very real sense, Endometriosis is a "career woman's disease". Calculations have been made looking at women who were in their reproductive years 50 to 100 years ago and compared them to women today. Once upon a time, women graduated from high school and their formal education ceased. They got married and had children. In the absence of good contraception, women would have a large number of children and breast feeding was more common than it is today. Life expectancies were much shorter.

It has been calculated that women from our grandmother's generation and before would ovulate perhaps 50 times in their entire lives. The rest of the time they would be pregnant or breast feeding.

Today women are marrying later and having fewer children. Breast feeding, although making a come-back, is still not as common as it once was. It is estimated that currently, women will ovulate 450 times in their life.

A study from Italy showed a correlation between the chances of a woman developing Endometriosis and the total number of ovulations she experienced. One part of this theory holds that it is the repeated insult to the peritoneal cavity during retrograde menstruation that may disrupt the normal protective mechanisms in the abdominal cavity and allow the Endometriosis to occur.
The time interval since a woman's last baby also plays a major role in whether or not she develops Endometriosis. The longer the time from a woman's last pregnancy, the more likely Endometriosis will be identified if that woman undergoes a laparoscopy. This is true even if the woman has had several children. This was shown in a study which looked at the incidence of Endometriosis diagnosed in women undergoing laparoscopy for the purpose of having a tubal sterilization. The longer the time since the woman's last baby, the more likely Endometriosis would be found. This most likely explains why women who have their children early show up with Endometriosis in their 30's and 40's.

A newborn baby girl has approximately one million eggs in her ovaries and at the time she becomes a teenager and goes through puberty, the number of eggs has dwindled to approximately 400,000. Menopause occurs when the ovary literally runs out of eggs. It is important to understand that even though, under normal circumstances, only one mature egg is produced during each menstrual cycle, many eggs begin to develop each day but never go on to maturity. It is also known that pregnancy, at least temporarily, suppresses Endometriosis. It was this observation that formed the basis for much of our hormonal therapy of Endometriosis.

In order for an egg to develop, it must be stimulated by two pituitary hormones - FSH and LH. It is known that as a woman reaches her late thirties or early forties, the level of FSH begins to rise. Although the increase is not dramatic, it is definitely detectable. From what we do know about the physiology of the ovary and ovulation, this rise in FSH is the result of the aging process in the ovary and reflects a decreased sensitivity of the eggs to respond to the pituitary hormones. The body must therefore produce more of the stimulating hormones. Putting all these facts together, it becomes apparent that the ovary uses up its "better" eggs earlier in life and the eggs that remain in the woman's ovaries in her late thirties and early forties are not her best eggs. Therefore, as a woman ages, she begins to ovulate eggs that are not as good as the eggs she produced in her teens and her twenties.

This is all consistent with the known facts that a woman does not conceive as readily over the age of 30 as she did in her twenties and that a woman who does become pregnant over the age of 35 has a greater chance of having a baby with a genetic abnormality. Therefore, if a woman does not have a baby at all, she has never had the protective effect of a pregnancy against her developing Endometriosis. As she begins to ovulate from her poorer eggs, she is therefore more prone to have a defect in ovulation. This entire combination of factors probably accounts for the (possible) increase in Endometriosis just on the basis of age alone.

It seems that every month, a new article appears in the infertility literature describing a new abnormality of ovulation in association with Endometriosis. For instance, under normal circumstances, the corpus luteum "dies" just prior to menstruation and the serum levels of estrogen and progesterone decline rather quickly. It has recently been discovered in women with early Endometriosis, the corpus luteum continues to produce progesterone into the early days of the next menstrual cycle. In fact, the authors of this article coined a new term and talk about what they call the "Minimal Endometriosis Infertility Syndrome", referring to all the women with a multitude of ovulatory defects in association with early Endometriosis.

Another article recently published from England tracked women through their menstrual cycles with frequent ultrasound examinations and hormone levels. They found that up to 60% of women who were infertile had ovulatory defects, even when at first glance, they appeared to ovulate normally.

For years, it was traditionally taught that Endometriosis causes infertility. In fact, it makes much more sense and provides much better answers to turn that phrase around. Infertility should be thought of as a cause of Endometriosis - not its result. In other words, women who develop Endometriosis do so because they have a basic underlying infertility ( i.e. reproductive) problem. This also applies to women who are not actively trying to conceive. It means that women who develop Endometriosis do so because they have a basic defect in their reproductive physiology irrespective of whether or not they are trying to conceive at that time.

There is now strong evidence that Endometriosis is, at least in part, an "auto-immune" disease. In such a situation, the body forms antibodies against its own tissues. There are many common illnesses that are auto-immune including Type I Diabetes, Psoriasis, Rheumatic Fever, Lupus, Hyperthyroidism, Hashimoto's Thyroiditis (a very common cause of enlarged thyroid glands and hypothyroidism), and Rheumatoid Arthritis. It has been shown that women with Endometriosis have a much higher incidence of auto-immune diseases than the general population. Women generally tend to have a higher incidence of auto-immune diseases than do men, particularly the "collagen-vascular" diseases such as Lupus. Preliminary studies that have been done indicate that women with Endometriosis have abnormalities in the functioning of the cells within the abdominal cavity that are the initiators of the immune response. Women with Endometriosis often have detectable antibodies against their own endometrial tissue. Abnormalities in the immune system would go a long way in helping to explain the significant discrepancy between the severity of the Endometriosis and the severity of the symptoms that exists in many women with this disease. It would also explain why, at least in my experience, severe Endometriosis seems to behave in a different biological fashion than does the earlier stages of the disease. Some of the worst cases of Endometriosis I have seen have occurred in young women - often teenagers.

Again, recognizing that all women "spill" endometrial cells into the pelvic cavity, a defect in the immune system would allow these cells to persist and survive. In woman with an normally functioning immune system, these cells would be destroyed.
Please understand that having an auto-immune disease or a problem with your immune system does not mean that you have AIDS. One has absolutely nothing to do with the other.

Alterations in immune function would also explain why, for many women, Endometriosis is not a rapidly progressive disease. If it were, minimal disease would be seen primarily in teenagers, mild disease in women in their 20's, moderate disease in the 30's, and severe disease would only be seen in women in their 40's. In fact, such is not the case. For many women, their disease tends to remain relatively stable over long periods of time.

On the other hand, abnormalities in the immune system would also explain why, at least in my experience, the worst cases of Endometriosis often occur in young women in their late teens or early twenties. It would also explain why for some women, Endometriosis is a progressive disease that keeps coming back as bad as ever, despite whatever therapy is given.
Endometriosis affects much more than a woman's ability to become pregnant - it affects her overall ability to have a baby. Statistically, women with Endometriosis have fewer children than women who do not have Endometriosis. Women with Endometriosis take longer to become pregnant and they have a lesser chance of conceiving in any one given month than do women who do not have Endometriosis.

Although there have been no major breakthroughs recently, our understanding of Endometriosis does go forward, sometimes in fits and starts. Every new bit of information does bring about a better understanding as to what is going on.

Our bodies are collections of cells. These cells are held together by special "sticky" molecules calls Integrins. In studying infertile women for whom no obvious reason could be found, it was discovered that many of them do not produce Integrins in the endometrium. This lack of endometrial Integrins prevents the embryo from literally sticking to the lining of the uterus and subsequently implanting.

Additional research has shown that many women with early Endometriosis lack endometrial Integrins. Whether this is a cause and effect or simply a coincidence is not yet known. However, there is some preliminary data to suggest that if a woman has early Endometriosis, destroying that Endometriosis at laparoscopy somehow restores normal endometrial Integrins and therefore might allow that woman to become pregnant. To be sure, this is contrary to most data that suggests treating early Endometriosis does not improve a woman's chances of getting pregnant. However, the group of women with deficient Integrins may represent a different category that might indeed benefit from an operative laparoscopy.

Endometriosis is also an environmental disease. In fact, environmental factors may be one of the more important causes of endometriosis. The incidence of Endometriosis is increasing throughout the world. Is it because we are more aware of it? Is it because it is far easier to recommend a laparoscopy than open surgery, thereby facilitating the diagnosis. Both of these are no doubt true. But what is also true is that we live in an environmental cesspool and I do not believe we fully understand the degree to which our environment has been polluted by the "advances" in our modern civilization over the past 50-75 years.

The Endometriosis Association recently took over a monkey research colony in Oregon that the original "owners" could no longer support. Except for baboons, Endometriosis does not occur naturally in any other animal species but the human female. Now, for the first time, Endometriosis could be created experimentally in animals.

To be sure, you can also create Endometriosis by sewing up the cervix of an animal and forcing retrograde menstruation in such a large amount that Endometriosis will occur. However, this is probably not true Endometriosis since the "disease" regresses if the animal's cervix is opened. A similar situation occurs in women. Women with congenital anomalies of the reproductive system which create any outflow obstruction will create "Endometriosis" although again, this may be a different disease than the Endometriosis which arises in women without obstruction.

Getting back to the monkey colony, researchers were studying the effect of dioxin, PCB's, and related chemicals on these animals. It was soon recognized that these monkeys developed Endometriosis! Similar "experiments" are occurring in nature. Underdeveloped countries such as Indonesia which previously had very low rates of Endometriosis are now experiencing an epidemic. Because many Western manufacturing companies are building plants in Indonesia, it has become a very polluted country. The rising rate of Endometriosis is probably not coincidental.

Evidence is rapidly accumulating that many diseases are the result of environmental pollution - breast cancer and male infertility are two of the most important.