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Chapter 162 Endometriosis

image General Considerations

Endometriosis affects 10% to 15% of menstruating women between 24 and 40 years of age. The main risk factor for endometriosis is heredity. Women with a mother or a sister who has endometriosis have an increased risk. Also, women with shorter menstrual cycles and a longer duration of flow have been found to be at higher risk for endometriosis. Lack of exercise from an early age, a high-fat diet, use of intrauterine devices, increased or unbalanced estrogen levels, and even natural red hair color have been suggested as factors in the development of endometriosis. A greater number of women with adhesions, endometriosis, or both have reported abuse in their histories. Increased immune action within the pelvic cavity and the possibility of antibody reactions to sperm has prompted recognition of an immunologic basis for endometriosis.

Additional possible risk factors are immune dysfunction; prenatal exposure to high levels of estrogens; exposure to environmental estrogens or endocrine disruptors (polychlorinated biphenyls [PCBs], weed killers, plastics, detergents, household cleaners, tin can liners); long-term dioxin exposure; and inappropriate liver metabolism and excretion of estrogens.

Etiologic Theories

Retrograde flow, the predominant theory first proposed in 1927, suggests that during menses blood flows backward and provides seeds of implants in the pelvic cavity. The problem with this theory is that more than 90% of menstruating women without endometriosis have retrograde flow; thus, this theory was challenged and questions were raised as to the biochemical and immunologic factors causing the implantation of endometrial tissue within the pelvic environment.1 Some theories are based on findings that endometrial implants from women with endometriosis are biochemically different from those from normal women.2

Other findings suggest that cells may implant only in women with altered cell immunity.1 Implants found in odd locations, such as the nose and lungs, suggest the transportation of endometrial tissue through lymphatic channels and blood vessels. Some researchers believe the implants to be of embryologic origin, when pieces of the uterus were left behind during development, and that these implants, when activated, secrete a chemical causing the nearby capillaries to bleed.3

Other research on endometriosis in baboons suggests activation by environmental toxins that mimic estrogens.4 Exposure to radiation and dioxin has been associated with a higher frequency of endometriosis.5,6 The highest incidence of endometriosis appears to be in Belgium, which is also the home to the highest level of dioxin pollution in the world.7

Two studies, however, one in Belgium, found no significantly increased risk with dioxins or polychlorinated biphenyls.8 The other study, in Italy, found no significantly increased risk of endometriosis in women who had high levels of dioxin in their blood.9 Although there is currently no definitive epidemiologic evidence linking any one class of chemicals to the risk of endometriosis, there does appear to be some suggestion of a link with estrogen-like compounds in the environment,10 called xenoestrogens, which can disrupt estrogen and estrogen metabolism. Substances that have been shown to have estrogenic effects in the body include PCBs, weed killers, liners in tin cans, plastics, detergents, and household cleaners.11

Immunologic alterations may exist in women with endometriosis. Increasingly, we are finding evidence that a lack of proper immune surveillance in the pelvic area is the cause of endometriosis and that impairment in other aspects of the immune system function are involved in the progression of the disease.12

Women with endometriosis have been found to have suppressed natural killer cell activity in their peritoneal fluid,13,14 high levels of immunoglobulins IgG and IgM,15 and high levels of autoantibodies against ovary and endometrial cells.16,17

Both types of immunity, cell-mediated and humoral, have been implicated in endometriosis, with immunologic defects present even in the mildest forms of the disease.18 Macrophages are found in greater numbers in the early stages of endometriosis.19

Cytokines, macrophages, T lymphocytes, and tumor necrosis factors have all been found to be increased in the peritoneal fluid in women with endometriosis,2022 and their increase correlates with the severity of the disease. Growth factors, angiogenic factors, and lipid peroxidation in the peritoneal fluid may stimulate endometrial cell growth. Targeting of these proinflammatory compounds and blocking their action with antioxidants and other compounds provide a good rationale for new treatment strategies, both conventional and with natural compounds.

Genetic influences the area also likely involved in endometriosis. Grouping of endometriosis within families has been found in clinical studies,23,24 populations-based studies,25 and even studies of twins.2628 Several abnormalities in detoxification enzymes, tumor suppressor genes, and other genetic factors occurring in multistep fashion may be involved both in the development and the progression of the disease.29

image Diagnosis

In some cases symptoms begin with the onset of menstruation, but in most symptoms begin later and worsen progressively over time. The triad of symptoms is dysmenorrhea (pain with menses), dyspareunia (pain with vaginal intercourse), and infertility. Acute pain occurs before the onset of menses; it can last for a day or two during the menses or throughout the month. In some women, vomiting, diarrhea, and fainting can occur concurrently with the intense pelvic/abdominal cramping and even labor-like pains. Other pains can involve a chronic bearing-down pain and pressure in the lower back, with pain sometimes radiating down the legs. There is not necessarily any correlation between pain and the extent of disease. Women with fixed ovaries and large endometriomas may report only mild discomfort, whereas those with visibly smaller lesions may report severe chronic pain. Upon surgery, these lesions are found to extend more deeply; they are possibly more influenced by circulating estrogens.30 Research has found that the severity of symptoms is correlated with the depth of the lesions rather than the number of lesions.31

Other symptoms may include pain with urination or bowel movements, bleeding from the nose/bladder or bowels, and fatigue.

Endometriomas, enlarged areas of ectopic endometrial involvement on the ovaries, are found in two of three patients with endometriosis. Infertility may be a cause of endometriosis rather than a result. There may be immune action within the pelvic cavity and the possibility of antibody reactions to sperm, which would suggest an immunologic basis for endometriosis.

Endometriosis can result in infertility and miscarriage. Data suggest that excessive amounts of free radicals are produced in endometriosis. Other findings suggest that infertility is a cause of endometriosis, due to the unruptured follicle, rather than a result. Whether infertility is a cause or result of endometriosis, tubal scarring, adhesions, and unruptured follicles are common findings in women having endometriosis and infertility problems.

Physical examination reveals one or more of the following: tenderness of the pelvic area, cul-de-sac, or both; enlarged or tender ovaries; a uterus that tips backward and lacks mobility; fixed pelvic structure; and adhesions. Endometrial tissue can be found on surgical scar tissue, in the vagina, and on the cervix. Physical examination during the first or second day of menses highlights tender areas in the septum between the rectum and vagina, most likely correlated with endometriosis.

An ultrasound examination of the pelvis can be useful in assessing pelvic pain and tumors but is not a definitive tool in diagnosing endometriosis. It can detect a mass on the ovary and determine size, characteristics, and consistency of the endometriomas. A blood test, CA-125, can have positive results in endometriosis but cannot differentiate among that and uterine fibroids, malignancies, and even normal tissue.

Definitive diagnosis of endometriosis can only be accomplished with a biopsy via either laparoscopy or laparotomy. Endometrial implants, endometriomas, or both are then visualized.

image Therapeutic Considerations

No single theory explains the development of endometriosis in all cases. More than likely, it stems from a combination of these postulated mechanisms with variable influences from case to case. The therapeutic plan may vary while targeting one or more of these possible mechanisms.


Several dietary principles are key in a natural medicine approach to endometriosis:

The consumption of trans fats appears to increase the risk of endometriosis, whereas long-chain omega-3 fats appear to be protective. Twelve years of prospective data from the Nurses’ Health Study II, which began in 1989, weres analyzed for dietary fat and its association with many health problems, including endometriosis.32 Although there was no association with total fat consumption and endometriosis risk, those women with the highest consumption of long-chain omega-3 fatty acids were 22% less likely to be diagnosed with endometriosis compared with women who had the lowest intake of these fats. Those women who had the highest intake of trans unsaturated fats were 48% more likely to be diagnosed with endometriosis.

Foods high in fiber are associated with optimal transit time in the intestines and an optimal balance of friendly microorganisms within the large intestines (see Chapter 52). These microorganisms, better known as gut flora, crowd out the other types of flora that deconjugate estrogens and allow estrogens to recycle back through the body. Studies suggest that a predominantly vegetarian diet emphasizing less protein and more fiber can lead to a decrease of biologically active unconjugated estrogens in the blood plasma.33 Although higher-protein diets are found to provide enzymes for the detoxification pathways of estradiol,34 vegetarian diets are of greater value owing to their lower fat content. Diets containing large amounts of animal protein, especially in the form of red meat, contain large amounts of arachidonic acid, which promotes inflammatory prostaglandins and thus inflammation and pain. By adding vegetable protein, soy, nut butters such as almond, and salmon to our diets, we tip the inflammatory pathway toward antiinflammatory prostaglandins that inhibit tumor growth—and possibly endometrial growth.

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