What Doctors Don't Tell YouNew evidence links this misunderstood disease with chemical or drug damage, even those used for fertility.
Endometriosis is the second most common gynaecological disorder requiring hospital treatment, and an increasing number of women are being diagnosed as having the condition. This may, however, be due to technical advancement in diagnostic techniques, particularly laparoscopy, rather than an increasing incidence of the disease itself.
No one knows what causes endometriosis, or how to cure it, and yet medical science continues to throw powerful hormonal drugs with physically and psychologically damaging side effects at it, or perform varying degrees of surgery despite the fact that the problem usually returns when treatment is discontinued. “A single form of therapy with consistent results for all patients is lacking,” said the Department of Obstetrics and Gynaecology, University of Tennessee, Memphis (Obstetrics & Gynaecology Clinics of North America, December 1993).
Endometriosis occurs when tissue similar to that of the endometrium (lining of the womb) is found in other parts of the body, usually on the ovaries, tubes and peritoneum. However, deposits have been found all over the body even, in rare instances, on the eye. Adenomyosis is another form of endometriosis found in the muscle of the uterus.
The tissue behaves in the same way as the womb lining, bleeding every time menstruation occurs, causing inflammation and often forming fibrous adhesions which may make organs stick to one another. Infertility may result if the reproductive organs, particularly the fallopian tubes, become inflamed and scarred. However, according to one report, “controlled studies offer strong evidence that endometriosis per se is not a direct cause of infertility” (Annals of Medicine, April 1990).
The most common symptoms are painful ovulation, painful periods and painful intercourse, although there are many others including bloating, heavy or irregular bleeding, constipation and/or diarrhea, constant tiredness, insomnia and depression.
Various theories exist as to what causes endometriosis. The most popular is that, during monthly menstruation, the endometrium not only flows from the womb down the vagina but also back along the fallopian tubes and out over the ovaries, tubes, womb and peritoneum. Sometimes some of this endometrium sticks to the structures in the pelvis and grows as new tissue. This may be normal, to a certain degree, in most women.
An increasing number of women who have not experienced any of the previously mentioned symptoms only discover they have endometrial deposits when undergoing exploratory operations for infertility or other gynecological and abdominal operations. Also the extent of visually diagnosed disease does not necessarily equate with severity of symptoms ie, a woman diagnosed as having mild endometriosis may complain of extreme symptoms, while another with many more endometrial “patches” and adhesions may not experience any symptoms.
This has led Eric J Thomas, Professor of Obstetrics and Gynaecology at the University of Southampton, Princess Anne Hospital, to argue that the presence of ectopic endometrium may, therefore, be normal and should be considered a disease state only if associated with symptoms or signs of progression and tissue damage (British Medical Journal, 16 January 1993).
In three studies following the natural course of the disease without medical treatment, he notes the disease progressed in about half the patients and in the other half either remained the same, improved or disappeared. Increased disease was not necessarily symptomatic. Professor Thomas concluded that “endometriosis should not, therefore, be treated just because it is there”.
Why then are some women more susceptible to endometriosis?
One of the most recent theories is that it may be due to individual immune deficiency caused by, among other things, immuno suppressive drugs, toxic overload from other drugs or environmental pollutants.
There is strong evidence linking endometriosis with immune system damage caused by the environmental pollutant dioxin. Research done by the US Endometriosis Protection Agency indicates a close association between dioxin levels in the body and the severity and incidence of endometriosis.
Dioxins are unintentional by products of chemical manufacturing processes involving chlorine, such as plastic, PVC, many solvents such as drycleaning fluid, pesticides and wood preservatives, disinfectants and drugs. They are produced when the waste containing these chlorine chemicals is burnt or incinerated. They then become airborne, fall on grass and plants and are eaten by animals such as cows, which become dioxin concentrators. Animal fat, such as meat and dairy produce, is the major source of dioxins for humans, and surveys of breastmilk suggest that UK dioxin levels are among the highest in the world.
It is well known that dioxins attack the immune system, and the US Environmental Protection Agency (EPA) has stated that immune system effects are likely at the levels of dioxins some of us already have in our bodies: “Some more highly exposed members of the population may be at risk. . . of decreased sperm counts, higher probability of experiencing endometriosis in women, reduced ability to withstand immunological challenge and others.”
An experiment carried out on rhesus monkeys exposed to the most toxic dioxin, TCDD, concluded that “the incidence of endometriosis was directly correlated with dioxin exposure and the severity of disease was dependent upon the dose administered” (Fundamental & Applied Toxicology, November 1993).
Until the use of chlorine is reduced, the only way in which we can cut dioxins intake is by eating fewer foods containing animal fat.
Drugs administered to women for conditions other than endometriosis may also lead to an immune deficiency.
A 76 year old woman who had, for several years, been taking tamoxifen (see WDDTY vol 3, no 11) an increasingly questionable drug used in the prevention and treatment of breast cancer, died from neutropenia, a blood disease linked to immune deficiency (The Lancet, 20 August 1994).
Symptoms of endometriosis usually disappear after the menopause (either naturally or medically induced), but hormone replacement therapy, in which there is little control over the amount of estrogen released into the bloodstream, has been shown to reactivate symptoms in post menopausal women (Australian & New Zealand Journal of Obstetrics & Gynaecology, November 1992).
The anti estrogen drug clomiphene citrate (Clomid), which is used to treat infertility, may also cause endometriosis, which is somewhat ironic considering that endometriosis is also being touted as a cause of infertility. In a letter to the BMJ (24 February, 1990) John M Svigos reported that in a study group of infertile women with no previous evidence of endometriosis, 57 per cent were found to have the disease following treatment with clomiphene citrate, compared to 7 per cent in the control group.
Psychotherapeutic and gastroenteric drugs have also been shown to cause adenomyosis in mice (Life Sciences 49 (3) 201-6, 1991).
The link between endometriosis and infertility is a moot one. Professor Thomas states that “none of the published randomized trials have shown that medical treatment improves fertility”, and suggests that “endometriosis should be considered to be coincidental unless it has caused tubal and ovarian damage that requires repair”.
Most current drug therapy for endometriosis suppresses ovulation, inducing either pseudo pregnancy (through the contraceptive pill or other progestogens) or, more commonly, pseudo menopause. It is therefore not a suitable treatment if a woman is infertile and wishes to conceive. If she does conceive while on hormone therapy, there is a chance of infant abnormality. Progestogens are also not a good idea as suppression of ovulation can continue for a long time after treatment has ended.
A quantitative overview of commonly used treatments for endometriosis associated infertility concluded that “ovulation suppression is an ineffective treatment” (Fertility & Sterility, May 1993).
Hormone treatment has proved quite effective in temporarily suppressing some of the worse symptoms of endometriosis, but the symptoms usually return once treatment stops (The Lancet, 31 October, 1992).
Even relief from symptoms has to be weighed up against the side effects associated with these drugs. These include hot flushes, depression, changes in breast size, dry vagina, sweating, mood changes, loss of libido, headaches, nausea, muscle pains and a reduction in bone density (which increases the risk of osteoporosis).
Danazol one of the most commonly used drugs and gestrinone, both induce a post menopausal state with the possibility of these sorts of side effects. But they are also both androgens which are similar to male reproductive hormones. Male hormonal side effects such as greasy skin, acne, hirsutism and voice changes (the latter non reversible) can cause additional distress.
Surgery may be offered to women with advanced endometriosis whose symptoms are extreme or who are infertile. The British Journal of Clinical Practice (Symposium Supplement, Autumn 1991) took the view that the only lasting cure for endometriosis was radical surgery with removal of both ovaries.
As for infertility, Prof Thomas points out that there have been no scientific studies of the experiences of surgical treatment of endometriosis on future fertility. Surgery itself can cause adhesions, which could further contribute to the problem.
Conservative surgery involves trying to conserve or improve reproductive capacity while removing endometrial patches and adhesions and repairing any damaged organs.
Radical surgery means a hysterectomy and removal of ovaries. This usually brings on the menopause, which is often more severe than natural menopause because its onset is sudden rather than gradual. Women who go through the menopause much earlier than normal also have an increased risk of osteoporosis and possibly even heart disease and hardening of the arteries. If the ovaries are removed, HRT may be recommended, which could of course reactivate the endometriosis.
A recently developed alternative to conventional hysterectomy is endometrial ablation (removal of the lining of the womb to stop heavy bleeding, using laser, radiofrequency electromagnetic energy or electrocoagulation). This technique is popular in the US and UK. However, a report in JAMA (8 September 1993) highlights four cases of hyponatremia (potentialy life threatening lack of sodium in the blood, possibly leading to convulsions and coma) following endometrial ablation, in which one woman died. The report concluded: “Menstruant women are at high risk for death or permanent brain damage from even modest postoperative hyponatremia. . ..
Endometrial ablation is becoming a more popular procedure, and unless appropriate safeguards are taken, more such cases will likely follow.”
Surgery is usually performed using either laparotomy the traditional method of performing abdominal or pelvic surgery through an abdominal incision or laparoscopy, which is minimally invasive endoscopic surgery mainly used for the diagnosis of endometriosis.
Few gynecologists are well trained in laparoscopic surgery, The Royal College of Obstetricians and Gynecologists admits in its Information Pamphlet on Endometriosis, which was published in 1994. “Some surgeons have become skilled in destroying the endometriosis with either the laser or cautery during a laparoscopy. A few surgeons are also able to remove endometriotic cysts and divide fibrous adhesions at laparoscopy. There is no doubt that the number of surgeons with these skills will increase over the next few years”.
Microsurgery and laser surgery are also being used by some surgeons. As the British Journal of Clinical Practice concluded: “Although their effectiveness remains to be confirmed in controlled clinical trials, they appear to produce good results and are safe in experienced hands”.
Maryon Stewart
Daniel Redwood DC
Tom Ferguson MD