Thursday, 21 November 2013

Phytochemicals and Endometriosis

During the last stage of menstrual cycle, normally a layer of endometrial lining in the inside of uterus is expelled which is known as menstruation blood, but instead some of the endometrial tissues grow somewhere in the body causing endometriosis. Endometriosis also react to hormone signals of the monthly menstrual cycle by building up tissues, breaking it and eliminating it through the menstrual period.

Types of food to prevent and treat endometriosis
1. Flax seed and fish oil
In the study of  the effect of oral administration of pure EPA on endometriosis, indicated that Endometriosis was surgically induced by a previously described experimental technique. Peritoneal fluid PGE2, PGF2-alpha and IL-1-beta concentrations in the experimental rabbits and controls were measured before and after induction of endometriosis by laparotomy. Following the treatment, EPA levels in plasma and peritoneal fluid increased significantly. However, no differences were seen in AA levels. Peritoneal fluid PGE2 and IL-1-beta concentrations increased significantly after induction of endometriosis in the control group. In contrast, they were not significantly changed after endometrial implantation in the experimental group. Peritoneal fluid PGF2-alpha concentrations were lower in the EPA group than in the controls, but there were no significant differences(1). Others found that Endometriosis was surgically induced 10 days later using a previously described experimental technique. Peritoneal fluid PGE2 and PGF2-alpha concentrations were significantly lower in the EPA/DHA group versus controls (P less than 0.05, P = 0.05, respectively). Total endometrial implant diameter 8 weeks after induction of endometriosis was significantly smaller in the experimental group (3.1 +/- 0.2 cm) compared with the controls (4.0 +/- 0.3 cm) (P less than 0.03). The authors conclude that 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
In the study to examine the associations among soy isoflavone intake, estrogen receptor 2 (ESR2) gene polymorphisms and risk of endometriosis, showed that Higher levels of urinary genistein and daidzein were associated with decreased risk of advanced endometriosis (P for trend = 0.01 and 0.06, respectively) but not early endometriosis. For advanced endometriosis, the adjusted odds ratio for the highest quartile group was 0.21 (95% confidence interval = 0.06-0.76) for genistein and 0.29 (0.08-1.03) for daidzein, when compared with the lowest group. Inverse associations were also noted between urinary isoflavones and the severity of endometriosis (P for trend = 0.01 for genistein and 0.07 for daidzein). For advanced endometriosis, ESR2 gene RsaI polymorphism appeared to modify the effects of genistein (P for interaction = 0.03)(3).

3. Green tea
In the study to evaluate  the antiangiogenesis mechanism of epigallocatechin-3-gallate (EGCG) in an endometriosis model in vivo. Dr. Xu H, and the research team atThe Chinese University of Hong Kong, showed that GCG, but not vitamin E, inhibited microvessels in endometriotic implants. EGCG selectively suppressed vascular endothelial growth factor C (VEGFC) and tyrosine kinase receptor VEGF receptor 2 (VEGFR2) expression. EGCG down-regulated VEGFC/VEGFR2 signaling through c-JUN, interferon-γ, matrix metalloproteinase 9, and chemokine (C-X-C motif) ligand 3 pathways for endothelial proliferation, inflammatory response, and mobility. EGCG also suppressed VEGFC expression and reduced VEGFR2 and ERK activation in endothelial cells. VEGFC supplementation attenuated the inhibitory effects by EGCG(4).

4. Skin and seed of grape
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, found that resveratrol decreased the number of endometrial implants per mouse by 60% (P < 0.001) and the total volume of lesions per mouse by 80% (P < 0.001). Resveratrol (10-30 μM) also induced a concentration-dependent reduction of invasiveness of HES by up to 78% (P < 0.0001). Resveratrol inhibits development of endometriosis in the nude mouse and reduces invasiveness of HES cells. These observations may aid in the development of novel treatments of endometriosis(5).

5. Olive oil
In 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 but not MMP-9 was increased and associated with the expression of transcription factor, c-Fos. Moreover, urokinase plasminogen activator and tissue inhibitor of metalloproteinase (TIMP)-3 were involved in MMP-3 regulation during endometriosis. Furthermore, MMP-3 activity that was parallel to c-Fos expression in endometriosis was reduced by melatonin pretreatment as characterized by diminished activator protein (AP)-1 DNA-binding activity. Because decreased apoptosis is an explanation for the perpetuation of endometriosis, we tested the role of melatonin on apoptotic pathway in preventing endometriosis. Significant regression of glandular epithelium was observed in melatonin-treated when compared to untreated mice. Melatonin treatment increased apoptotic cells in endometriotic zones. This was related to reduced Bcl-2 expression along with increased Bax expression and caspase-9 activation(6).

6. Etc.

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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

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