Endometriosis: a disease of oxidative stress?

by endosolu

Unless you have been hiding under a rock… I assume you realize that lower antioxidant levels in women with endometriosis is par for the course.

I thought this study below measuring the low levels of Vitamin E was worth the post.

Vitamin E is known to ensure that animals have healthy uterine linings, and it has been used by farmers since the 1930’s.

WARNING: don’t go just buying any Vitamin E on the market… it needs to be sourced from whole foods, have all 8 tocopherols in it and be in the same ratio as found in nature otherwise you are wasting your money.

The product we use in our endometriosis program is…

  • Whole food sourced natural vitamin E is full spectrum.
  • Breakthrough water-miscible technology improves absorption

ABSTRACT

Our central hypothesis proposes that oxidatively damaged red blood cells (RBCs), apoptotic endometrial cells or undigested endometrial tissue may signal the recruitment and activation of mononuclear phagocytes. Women with endometriosis are prone to respond to this stimulus with an inadequate macrophage scavenger receptor response although the secretory response is not impaired. Activated macrophages in the peritoneal cavity generate an oxidative stress, which consists of lipidperoxides, their degradation products, and products formed from their interaction with low-density lipoprotein (LDL) apoprotein and other proteins. The lipoproteins of the peritoneal fluid (interstitial fluid) have been shown to have lower vitamin E levels and to be more readily oxidized than plasma, so peritoneal fluid may actually contribute to the disease process actively rather than as a passive carrier of mediators of inflammation and growth. As a result of such a stress, a sterile, inflammatory reaction with secretion of growth factors, cytokines, and chemokines is generated, which is deleterious especially to successful reproduction. We propose that such a pro-oxidant environment (peritoneal fluid as well as activated macrophages) promotes growth of ectopic endometrium. The data presented in this review are just the beginning of exploring the role of oxidative stress in mediating the pathophysiology of endometriosis. Only by understanding the mechanisms involved in theĀ pathogenesis of endometriosis can we develop the basis for new diagnostic and therapeutic approaches.

Jackson, L. W., et al. “Oxidative stress and endometriosis.” Human reproduction 20.7 (2005): 2014-2020.

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