Endometriosis is a painful disorder characterized by endometrial cells that grow in another area in the reproductive organs, such as ovaries, fallopian tubes,..... and the tissue lining your pelvis, outside of the uterus.
The causes of endometriosis are debatable. Some researchers suggested that normally a layer of endometrial lining in the inside of the uterus is expelled through menstruation, during the last stage of menstrual cycle, instead, some of the endometrial tissues grow somewhere else in the body, causing endometriosis.
There are numbers of the theory proposed that endometrial tissues grow somewhere else in the body are results of
* Uterine structure abnormalities
The theory suggested women with uterine structure abnormalities are associated to increase the risk of dysfunctional uterine peristalsis. As the condition progress, dysperistalsis of uterus constructions might underlie disorders of endometriosis(6).
* Retrograde menstruation
Sampson’s theory of retrograde menstruation is the oldest principle explaining the etiology of endometriosis. The theory suggested. that endometriosis is the result of the retrograde flow of endometrial cells that are transported through the fallopian tubes into the peritoneal cavity during menstruation.
* Genetic alternation
There are numbers of gene that cause uterine structural abnormalities and abnormal endometrial development, including HOX gene.
However, the joint study of "Genetics and Genomics of Endometriosis" lead by the Sanford School of Medicine of the University of South Dakota, " the etiology of endometriosis remains enigmatic but it does appear to cluster in families. Genetic studies have demonstrated an increased frequency of the disease in close relatives with the type of inheritance most likely polygenic/multifactorial. Genomic studies continue to explore differences in gene expression and understanding the basic biology of the disease"(9).
Endometriosis also reacts to hormone signals of the monthly menstrual cycle by building up tissues, breaking them and eliminating them through the menstrual period.
Types of food to prevent and treat endometriosis
1. Flaxseed and fish oil (EPA/DHA)
In the study of the effect of oral administration of pure EPA on endometriosis surgically induced in the experimental rabbits in compared to control, researchers found that pure EPA treatment group s exerts significant decrease of peritoneal fluid PGE2 and IL-1-beta concentrations in compared to control that shows increased significantly after induction of endometriosis(1).
Prostaglandin E(2), PGF2-alpha and proinflammatory IL-1-beta concentrations are up-regulated in patients with endometriosis in compared to healthy women.
Furthermore, in endometriosis surgically induced animal study, researchers indicated that at day 10, injection of EPA/DHA in endometrial infected group shows a decrease of concentrations of both peritoneal fluid PGE2 and PGF2-alpha(2).
Moreover, total endometrial implant diameter 8 weeks after induction of endometriosis was significantly smaller in the experimental group compared to the controls(2).
Dr. Covens AL, the lead scientist at the final report of the experiment said, "dietary supplementation with fish oil, containing the n-3 polyunsaturated fatty acids EPA and DHA, can decrease intraperitoneal PGE2 and PGF2-alpha production and retard endometriotic implant growth in this animal model of endometriosis"(2).
2. Organic Soy(Isoflavone)
In the study to examine the associations among soy isoflavone intake, estrogen receptor 2 (ESR2) gene polymorphisms and risk of endometriosis, researchers showed that higher levels of urinary genistein and daidzein were associated with decreased risk of advanced endometriosis but not early endometriosis(3).
In advanced endometriosis, the adjusted odds ratio for the highest quartile group was 0.21 for genistein and 0.29 for daidzein in compared with the lowest group(30.
Inverse associations were also noted between urinary isoflavones and the severity of endometriosis. For advanced endometriosis(3).
However, the study is based on a total of 138 Japanese women age 20-45 years old who had consulted a university hospital for infertility in Tokyo, Japan in 1999 or 2000. due to endometriosis.
Therefore, a large example size and multi-centers study different ethnic groups involved are necessary to reconfirm the isoflavone anti endometriosis possibility.
3. Green tea (epigallocatechin-3-gallate (EGCG))
In the study to evaluate the antiangiogenesis mechanism of epigallocatechin-3-gallate (EGCG) in an endometriosis model in vivo, researchers at The Chinese University of Hong Kong, showed that EGCG inhibits microvessels in endometriotic implants.
EGCG selectively also suppressed vascular endothelial
* Growth factor C (VEGFC), the expression is increased eutopic and ectopic endometrium of endometriosis patients(10)
* Tyrosine kinase receptor which is targeted by a number of pharmaceutical compounds for the treatment of endometriosis successfully in vitro and animal models(11).
* VEGF receptor 2 (VEGFR2) or Flk-1 expression which is significantly higher in endometriotic lesions and confirmed the angiogenic potential of these lesions(12)..
4. Skin and seed of grape (Resveratrol)
In the study to investigate the effects of resveratrol on human endometriotic implants in a nude mouse model and to examine its impact on human endometrial stromal (HES) cell invasiveness in vitro, scientists found that(5)
* Resveratrol treatment group demonstrated a decreased number of endometrial implants by 60% and the total volume of lesions per mouse by 80%.
* Resveratrol injection at a concentration of 10-30 μM also induced a reduction of invasiveness of HES by up to 78%.
These results suggested that resveratrol may be considered as a functional supplement for reduced risk of endometriosis in the nude mouse and invasiveness of HES cells(5).
5. Olive oil (Melatonin)
The study of Melatonin protects against endometriosis via regulation of matrix metalloproteinase-3 and an apoptotic pathway by Dr. Paul S, and scientist at the Indian Institute of Chemical Biology, showed that during the early phase of endometriosis, MMP-3, a protein was found to promote endometriosis(13) is increased and associated with the expression of transcription factor, c-Fos gene which may play a role in the molecular mechanisms of estrogen action on the induction, promotion or progression of endometriosis(14).
These increased levels of MMP-3 activity that parallel to c-Fos gene expression in endometriosis were inhibited by melatonin, a major bioactive ingredient found in olive oil pre-treatment, researchers after taking into account other co and confounders.
Melatonin-treated group also demonstrated a significant effect on regression of glandular epithelium when compared to untreated mice through apoptotic pathway involving increased cells death in endometrial zones(6).
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Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blogs, self-growth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bioscience, ISSN 0975-6299.
Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/1607749
(2) http://www.ncbi.nlm.nih.gov/pubmed/2832216
(3) http://www.ncbi.nlm.nih.gov/pubmed/17474167
(4) http://www.ncbi.nlm.nih.gov/pubmed/21821246
(5) http://www.ncbi.nlm.nih.gov/pubmed/20844278
(6) http://www.ncbi.nlm.nih.gov/pubmed/20609072
(7) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5209923/
(8) https://www.hindawi.com/journals/ijrmed/2014/179515/
(9) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4346178/
(10) https://www.ncbi.nlm.nih.gov/pubmed/23334337
(11) https://watermark.silverchair.com/dmv060.pdf
(12) https://www.ncbi.nlm.nih.gov/pubmed/20085636
(13) https://www.ncbi.nlm.nih.gov/pubmed/15879464
(14) https://www.ncbi.nlm.nih.gov/pubmed/19199093
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