Endometriosis is a puzzling and sometimes debilitating disease that affects millions of women around the world. Women suffering from endometriosis experience a variety of symptoms, with lower abdominal pain being most common. Pain can be especially intense before and during menstrual periods. Some women experience pain throughout the menstrual cycle; some during sex. The disease forces more than 100,000 hysterectomies each year in the United States alone, and the costs of the disease exceed $1 billion annually.

Particularly troubling is the fact that it is showing up more than ever before in very young women. Given the poor quality of data, however, it is difficult to document long term trends or determine the precise number of women afflicted with the disease. Many cases go unreported and accurate, confirmed diagnosis requires an invasive surgical procedure.

Nonetheless, specialists in the field believe that the prevalence of the disease has increased greatly since World War II. The National Institute of Child Health and Human Development estimates that endometriosis afflicts 10 to 20 percent of women of childbearing age in the U.S. Prior to 1921, there were only twenty reports of the disease in the worldwide medical literature.

Endometriosis develops when endometrial-like tissue starts growing in places where it shouldn’t be, away from the lining of the uterus, often in the abdominal cavity or pelvic region, but sometimes in lungs or arms, and elsewhere. These tissue growths respond to hormonal signals in the menstrual cycle in the same way that uterine lining does, building up and breaking down each month. But while the uterine lining can be flushed out of the body during menstruation, the tissue remains of endometrial growths have no place to go. Internal bleeding, inflammation and other problems result.

While these facts about endometriosis are clear, the causes of the disease are much more obscure and debated. There are four key parts to the puzzle.

First, how does endometrial tissue wind up in inappropriate locations? One suggestion is that endometrial cells are transported by reverse flow off blood during menstruation into the abdominal cavity, or through the blood stream and lymphatic system to more remote sites. Another is that cells in the remote locations are transformed from their original condition into endometrial cells. These explanations are not mutually exclusive.
Second, why doesn’t the immune system prevent endometrial tissue from becoming established and growing? Recent research has revealed that women with endometriosis are also likely to experience an array of immune system problems, suggesting that immune system dysfunction may be the proximal cause of endometriosis. The challenge then is to understand what has happened to the endometriosis victim's immune system.
Third, what would lead some women to develop severe endometriosis, while others none at all? There appears to be some heriditary component to the risk of endometriosis, possibly involving multiple genes, but environmental factors are also implicated. The most telling evidence on environment comes from animal studies in which dioxin increases the risk of endometriosis in Rhesus monkeys, and also increases the likelihood that endometrial implants will thrive in rodents. Monkeys exposed to radiation also are more likely to develop endometriosis.
And fourth, what are the patterns of the disease over time? As indicated above, it is widely believed that endometriosis is more common now than mid-20th century, and data also suggest that more cases are now developing earlier in life than before and becoming more severe.
As we describe in Chapter 10 of Our Stolen Future, the medical causes of endometriosis are shrouded in uncertainty. A few studies completed by the time we published OSF pointed toward contamination. Since then a small number of studies have been reported consistent with this trend. None contradict it.


In 1992, German scientists reported an association between heavy PCB contamination and endometriosis that hinted at a new chapter in the search for causes of endometriosis. Then in 1993 researchers from the Harlow Primate Center at the University of Wisconsin published dramatic and unexpected findings . Their study was of monkeys used in research on the long-term reproductive effects of dioxin. When three of the dioxin treated animals died of severe endometriosis, a new study was initiated to compare the presence and severity of endometriosis with the animals exposure to dioxin. The study found a dose-dependent relationship between dioxin and endometriosis. Animals with more exposure were more likely to develop the disease, and the greater a female monkey's exposure to dioxin, the greater the severity of the disease. Only one of 7 animals exposed to 25 parts per trillion dioxin was free of endometriosis. This was much higher than the rate of endometriosis experienced in the general population of monkeys at the research center, about 30%.

Experimental work has now afforded additional clues. In mice and rats, exposure to dioxin increases the size of endometriotic sites that are experimentally induced. A furan also promotes endometrial growth.

More about dioxin and endometriosis...

While we still lack scientific certainty about the causes of endometriosis, exposures to environmental factors that undermine the immune system are emerging as one of the most likely causative agents. Both dioxin (and other dioxin-like compounds) and radiation harm immune system action, in monkeys as well as in people. Widespread exposures to dioxins increased during the 20th century, as most likely did endometriosis. Other contaminants also are toxic to the immune system including a variety of pesticides and industrial compounds.

This combination of experimental data from animals and circumstantial evidence from people suggests that preventative steps to reduce exposures could assist in the fight against endometriosis.