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Endometriosis - The Common, Yet Under-Diagnosed Condition

Endometriosis - The Common, Yet Under-Diagnosed Condition
By Raihane Palagi 3 months ago 9144 Views

The average woman can spend 10 years, or 3650 days, having a period. For many, these are years of life-affecting symptoms, such as debilitating pain and fatigue. This is especially the case for women with endometriosis. One in ten women in the UK have endometriosis, but diagnosis is tricky and can take up to a staggering 7.5 years.1

Endometriosis is the growth of cells from the uterine lining, the endometrium, in other areas such as the ovaries or colon. These cells respond to hormone fluctuations in the same way as in the uterus, thickening under the influence of oestrogen and then shedding after the sudden drop of progesterone, in absence of fertilisation. However, unlike the cells in the uterus, these cells have nowhere to escape, making menstruations extremely painful and causing a whole lot of symptoms.

Key Symptoms:

Hormonal fluctuations are part of a normal female monthly cycle, so experiencing mild abdominal cramps and breast tenderness, can be normal for some individuals. For endometriosis, other symptoms can include:

  • Painful and heavy periods
  • Infertility
  • Back, pelvic, and ovulation pain
  • Painful bowel movements, urination, and intercourse
  • Bleeding between periods
  • Nausea
  • Extreme tiredness

What Are The Main Drivers?

Retrograde menstruation, when menstrual blood containing endometrial cells flows back through the fallopian tubes, has long been deemed as the main cause of endometriosis.2,3 However, more recent research highlights many other compounding factors.

Oestrogen dominance, is often debated when discussing endometriosis.4 Oestrogen is one of the main hormones that regulates the menstrual cycle. It drives the development of the reproductive tract and thickens the endometrium to prepare the uterus for the ovulation and egg implantation. This stems from the ability of oestrogen to promote cell proliferation. However, if oestrogenic activity becomes enhanced, it can drive excessive cell proliferation, possibly contributing to endometriosis.

This can happen when oestrogen synthesis is stimulated by factors such as excessive carbohydrate intake,5 being overweight,6 stress,7 and working night-shifts.8 Shift work has been associated with a 50% increased risk of endometriosis.9 Oestrogenic activity can also be heightened by exposure to environmental chemicals which mimic its activity, for example xenoestrogens from plastics.10,11

Oestrogen is kept within balance thanks to complex detoxification processes performed by your body, mainly methylation, glucuronidation, and sulphation. Unfortunately, many women have a reduced ability to perform these processes and effectively metabolise and eliminate oestrogen. This is exacerbated by high intake of paracetamol12 and smoking,13 coupled with low intake of cruciferous vegetables,14 folate, B12,15 and magnesium.16,17 Disrupted methylation, in particular, has been directly linked with endometriosis.18

Gut health can also play a role. Under normal circumstances, oestrogen metabolites are shunted from the liver into the gut in bile, and eliminated through daily bowel movements. Dysbiosis, constipation, and intestinal permeability (‘Leaky Gut’), can increase the risk of oestrogen metabolites being re-absorbed, rather than eliminated, and so, oestrogen dominance. Women with endometriosis can also be prone to irritable bowel syndrome (IBS),19 highlighting the gut-hormone connection.

Elevated inflammation has been identified during, and as a driver of, endometriosis.20 Excess weight,21 disrupted sleep,22 processed food,23 low omega-3 intake,24 and stress,25 can further increase inflammation and may worsen symptoms. Wider immune dysfunction also seems to be involved. Antibodies targeting our own cells have been identified in extra-uterine endometrial tissue,26 indicating an autoimmune component to this condition.27 Low vitamin D is a risk factor for autoimmunity,28 and interestingly, increases endometriosis risk.29

What You Can Do?

  • If overweight, implement sustainable weight loss. Consider daily exercise, reduced carbohydrate intake, and increased intake of nutrients to support blood glucose regulation, such as chromium.30
  • Enjoy daily relaxation and increase intake of calming nutrients, such as magnesium.31
  • Reduce xenoestrogen exposure by minimising plastic use and switching to natural cosmetics.
  • Increase phytoestrogen intake from red clover and flaxseeds, which weakly bind to oestrogen receptors, blocking more stimulating oestrogens.32,33
  • Support oestrogen detoxification by increasing intake of sulphoraphane,34 N-acetyl cysteine,35 and glucobrassicin through dietary sources, such as cruciferous vegetables, or supplementation.
  • Quit smoking and reduce intake of smoked/charred and non-organic food, caffeine, and alcohol to further take pressure off the liver.
  • Test for nutrient deficiencies such as folate, B12, B6, iron, and vitamin D via the GP or privately.
  • Increase omega-3 intake though oily fish, hemp and flaxseeds to reduce inflammation and endometriosis risk.36

If you are concerned about your monthly cycle and any symptoms you may be experiencing, or if you have a family history of endometriosis, seek the advice of a Registered Nutritional Therapist for targeted, personalised advice.

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References

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2 Sampson JA. Metastatic or embolic endometriosis, due to the menstrual dissemination of endometrial tissue into the venous circulation. Am J Pathol.1927;93:110–43.

3 D’Hooghe, T, Debrock, S. Endometriosis, retrograde menstruation and peritoneal inflammation in women and in baboons. Human Reproduction Update. 2002; 8 (1): 84-88.

4 Vercellini P et al. Endometriosis: pathogenesis and treatment. Nat Rev Endocrinol. 2014; 10(5): 261-75

5 Fulghesu AM et al. The impact of insulin secretion on the ovarian response to exogenous gonadotropins in polycystic ovary syndrome. J Clin Endocrinol Metab. 1997; 82 (2): 644-8.

6 Williams G. Aromatase up-regulation, insulin and raised intracellular oestrogens in men, induce adiposity, metabolic syndrome and prostate disease, via aberrant ER-? and GPER signalling. Mol Cell Endocrinol. 2012;351(2):269-78

7 McTernan PG et al. Gender differences in the regulation of P450 aromatase expression and activity in human adipose tissue. International Journal of Obesity. 2000; 24:875-881

8 Nagata C et al. Light exposure at night, urinary 6-sulfatoxymelatonin and serum estrogens and androgens in postmenopausal Japanese women. Cancer Epidemiol Bio Prev. 2008; 17 (6).

9 Marino JL et al. Shift work, hCLOCK T3111C polymorphism and endometriosis risk. Epidemiology.2008;19(3):477-84.

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11 Krishnan AV et al. Bisphenol-A: an estrogenic substance is released from polycarbonate flasks during autoclaving. Endocrinology. 1993;132:2279–86.

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15 Herrmann W et al. Vitamin B-12 status, particularly holotranscobalamin II and methylmalonic acid concentrations, and hyperhomocysteinemia in vegetarians. Am J Clin Nutr. 2003;78(1):131-6.

16 Tsao D et al. Structural mechanisms of S-adenosyl methionine binding to catechol O-methyltransferase. PLoS One. 2011; 6 (8): e24287

17 Dawling S et al. Catechol-O-methyltransferase (COMT)-mediated metabolism of catechol estrogens: comparison of wild-type and variant COMT isoforms. Cancer Res. 2001;15;61(18):6716-22.

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20 Meng-Hsing W et al. Endometriosis and possible inflammation markers. Gynecology and Minimally Invasive Therapy. 2015; 4 (3): 61-67.

21 Coppack SW. Pro-inflammatory cytokines and adipose tissue. Proc Nutr Soc. 2001;60(3):349-56. Review.

22 Morris et al. Sleep Quality and Duration are Associated with Higher Levels of In ammatory Biomarkers: the META-Health Study. Circulation. 2010; 122: A17806.

23 Erridge C. The capacity of foodstuffs to induce innate immune activation of human monocytes in vitro is dependent on food content of stimulants of Toll-like receptors 2 and 4. Br J Nutr. 2011;105 (1): 15-23.

24 Bokor S et al. Single nucleotide polymorphisms in the FADS gene cluster are associated with delta-5 and delta-6 desaturase activities estimated by serum fatty acid ratios. J Lipid Res. 2010; 51 (8): 2325-2333.

25 Gouin. Chronic Stress, Immune Dysregulation, and Health. Am J Life Med. 2011; 5: 476-85.

26 Zhang et al. The link between immunity, autoimmunity and endometriosis: a literature update. Autoimmunity Reviews 17 (2018) 945–955

27 Olof et al. Risk of endometriosis in 11 000 women with celiac disease. Human Reproduction, Vol.26, No.10 pp. 2896–2901, 2011

28 Simpson et al. Latitude is significantly associated with the prevalence of multiple sclerosis: a meta-analysis. J Neurol Neurosurg Psychiatry. 2011; 82 (10): 1132-41.

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33 Brzezinski et al. Phytooestrogens: the "natural" selective oestrogen receptor modulators? Eur J Obstet Gynecol 1999;85:47-51.

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35 Porpora et al. A promise in the treatment of endometriosis: an observational cohort study on ovarian endometrioma reduction by N-acetylcysteine Evidence-based complementary and alternative medicine : eCAM vol. 2013: 240702.

36 Stacey et al. A prospective study of dietary fat consumption and endometriosis risk. Hum Reprod. 2010 Jun; 25(6): 1528–1535.

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