Endometriosis: Theory and Understanding

Part one of a two part series.

Endometriosis is a misunderstood, chronic disease that affects an estimated 6 million women in the US and 89 million worldwide. There is a higher incidence in women with early menarche, short cycles or menorrhagia, outflow obstruction, and is 6 to 7 times more prevalent in first degree relatives of affected women. Endometriosis is the most common cause of secondary dysmenorrhea, and has been found in 30-70% of women investigated for infertility. ⁽⁷⁾

The endometrium is tissue that covers the whole cavity inside the uterus. Endometriosis is defined by the presence of endometrial cells outside of the uterus. It is most commonly found on the ovaries but may be found in nearly any part of the body in the abdomen: pelvic cavity, fallopian tubes, between the uterus and rectum, uterosacral ligament, as well as the bladder, bowel, vagina, even in the lung, or extremities. These ectopic cells respond to hormones of the menstrual cycle, especially estrogens and are characterized by abnormal growth of endometrial tissues. All monthly changes that occur in the normal endometrium, also occur in the abnormal endometrium, but the blood shed from this tissue has no way of leaving the body. Abnormal endometrial tissue tends to continue to increase in size and invade deeper lying tissues, causing bleeding, lesions, inflammation, adhesions, infertility, pain and bowel problems.

Symptoms
Endometriosis is multi-symptomatic and symptoms such as chronic pelvic pain, dysmenorrhea, pre-menstrual spotting, bowel problems, and lumbago are worse during menses. Additional symptoms include:  dyspareunia (pain during intercourse), gastrointestinal and bladder problems, infertility, high rates of atopic diseases are common, allergies, food intolerances, asthma, eczema; sometimes debilitating sensitivities to environmental chemicals such as perfumes, cigarette smoke, cleaning agents, PCB’s, and others; a tendency towards infections and mononucleosis, problems with candida albicans, mitral valve prolapse, Fibromyalgia and chronic fatigue immune dysfunctions syndrome, and greater risk for autoimmune disorders including lupus and Hashimoto’s thyroiditis. ⁽¹⁾

Due to endometriosis’ misunderstood nature, causation is more commonly overlooked in favor of theory. The following are nine theories, which may occur simultaneously with some overlap or individuality.

1. Sampson’s retrograde theory
2. Coelomic metaplasia
3. Inflammation
4. Iatrogenic origin
5. Environmental toxins
6. Lymphatics
7. Immune function
8. Genetic Factors
9. Abdominal wall/pelvic floor dysfunction

In 1921, John Sampson described a series of hemorrhagic cysts, which clump or row together forming blue or dark brown cysts as “chocolate cysts.” Sampson’s theory said that, “it was due to dissemination of endometrial tissue into the peritoneal cavity.” This endometrial tissue contains pieces of glands, blood vessels and connective tissue required to start a new endometrium. This is now referred to as retrograde menstruation (backward menstruation into the peritoneal cavity). 75 to 95% of all women have retrograde menstruation, but it does not cause endometriosis in all women.

Coelemic metaplasia occurs when some of the cells of the peritoneum develop into endometrial cells instead of normal peritoneal cells. Peritoneal epithelium can be “transformed” into endometrial tissue, perhaps because of chronic inflammation or chemical irritation from refluxed menstrual blood.  Peritoneal inflammation from bacteria, parasites or viruses may also result in coelemic metaplasia. This theory based on the observation that coelomic epithelium is the common ancestor of endometrial and peritoneal cells, which allow transformation of one type of cell into another

Pain and inflammation are multifactorial and multisymptomatic. Pelvic pain most often starts 1-2 days before the period and lasts throughout it; however, there is no direct correlation between the extent of endometriosis and the severity of pain. Dyspareunia is a common occurence in which pain related to penetration, such as during intercourse. Inflammatory cytokines that enter the uterus create an environment that is hostile to the fetus. Low back pain during menses may be due to endometriosis in the cul-de-sac between the uterus and rectum. Endometrium tends to respond to progesterone and estrogens, and which causes pain. Endometriosis forms on the peritoneum in the pelvic bowel, due to blood dropping from fimbriae at the opening of the fallopian tubes. Endometrial tissue here bleeds during menses affecting nerves and causing pain. Moderate pain occurs during defecation due to adhesions distorting the bowel or without gastrointestinal problems, even when not menstruating.

Iatrogenic origin is not uncommon in surgeries where uterine wall cells are accidentally transferred to the abdominal cavity. Inadvertent direct transplantation of endometrial cells can occur with c-sections, or other pelvic surgeries.

Exposure to environmental toxins such as dioxin, a chemical byproduct of pesticides and certain types of waste incineration increase the risk of endometriosis. Cigarette smoke, cleaning agents, PCB’s (Poly Chlorinated Biphenyls), remain in the body for 14 to 15 years and can be passed on to developing fetuses, and all contribute to the formation of endometriosis.

Lymphatic system or cardiovascular system transport of endometrial tissues is a possibility and explains why it may be found in the brain, lungs, or parts of the body not near the uterus.

Endometriosis starts off with a reduction in immune cells, which allows endometrial tissues to form. At the onset of disease the immune system becomes hyperactive. Endometriosis itself has a barrier around it, which the immune system is inadequate to deal with. Alterations in cellular immunity result in inadequate removal of ectopic endometrial cells from the peritoneal cavity. Increased levels of growth factors and cytokines, secreted by the endometrial and immune cells seem to promote implantation and growth of ectopic endometrium by producing new cells and new blood vessels. Endometriosis is considered an autoimmune disease because of its association with the presence of auto-antibodies, other autoimmune diseases, and possible immune related abortion. Instead of acting as scavengers to eliminate ectopic endometrial cells, macrophages seem to promote the disease by secreting growth factors that stimulate the growth of ectopic endometrium. Endometrial cells in women with endometriosis are resistant to apoptosis that contributes to menses and ectopic endometrium is even more resistant to apoptosis and macrophage mediated clearance.

Genetics play a role in families that have predisposing factors, particularly genes that control the survival of detached endometrial cells, abnormal proliferation, angiogenesis and the inflammatory response.

The abdominal wall stops functioning as a result of or in conjunction with pelvic floor dysfunction, this may be due to poor posture, faulty biomechanics, inadequate breathing patterns, long term emotional stress or injury. In this situation the transverse colon and the small intestine drop down, collapse the uterus and the bladder and starve the uterus for oxygen and blood. Anything that interrupts the blood supply through the abdominal cavity decreases the tissue’s capacity to heal and causes chronic problems. In women that may lead to uterine prolapse, irritation or direct infiltration of nerves in the pelvic floor. Structural integrity has been linked, back to the early 1900’s, to uterine fibroids and what today is called endometriosis.⁽²⁾

Diagnosis
Endometriosis is usually diagnosed 8 to 11 years after it first develops. Diagnosis is prone to subjective misinterpretation and difficult differentiation due to the fact that many pathologies in women present with similar symptoms and can range from irritable bowel, primary dysmenorrhea, pelvic inflammatory disease, ovarian tumors to uterine myomas. Diagnosis of endometriosis is accomplished via a personal health history and family history. Today laparoscopy is the gold standard in diagnosis. Further testing includes FSH and estradiol, hysteroscopy orMRI.

Treatment
Treatment is usually administered with surgery or drugs that alter the estrogen-based hormonal stimulus that affect endometrial tissue, but are highly ineffective. It may go away with pregnancy or on its own, only to return later. In women under the age of 40 drugs are usually prescribed to inhibit LH and FSH, or decrease estrogens, while other hormones are created. Most drugs are discontinued if a woman is trying to become pregnant. Surgeons may opt for bilateral salpingo-oophorectomy (ovary and fallopian tube removal), use polyester ligaments to tie the uterus up to the spine or remove it all together via hysterectomies. For many women, they are told to become pregnant to hold off symptoms and complications, and to have children while they still can. In general healthcare providers do not emphasize prevention, diet, abdominal wall function, stress management, nor exercise.

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2. Chek, P. (2005) Abdominal Wall Function and Organ Health. Video series. SD, CA.
3. Chen, J. and Chen, T. (2009) Chinese Herbal Formulas and Applications. City of Industry, CA: Art of Medicine Press, Inc.
4. Endo-Online The Voice of the Endometriosis Association http://www.endometriosisassn.org/endo.html
5. Flaws, B. (1989) Endometriosis, Infertility and Traditional Chinese Medicine A Laywoman’s Guide. 1^st Ed. Boulder, CO: Blue Poppy Press.
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7. Maciocia. G. (1998) Obstetrics & Gynecology in Chinese Medicine. Churchill Livingston. 258-259.
8. Porth, C. (2005) Pathophysiology 7^th Ed. PA: Lippincott Williams & Wilkins.
9. Werner, Ruth. (2005) A Massage Therapist’s guide to Pathology 3^rd Ed. Lippincott Williams & Wilkins.

Part two : Endometriosis in Traditional Chinese Medicine .