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Pro-inflammatory Roles of Estrogens

Majid Ali, M.D.

Synthetic estrogens and xenoestrogens are potent pro-inflammatory agents. A clear understanding of the pro-inflammatory roles of synthetic estrogens, progestins, and androgens is key to understanding the Unifying Dysox Model of Hormone Dysfunctions. Oxygen governs the inflammatory response and adjudicates man-microbe conflicts. That was the title of my column in Townsend Letter of May 2005. The following are major mechanisms by which synthetic estrogens, xenoestrogens, and synthetic androgens evoke and perpetuate pathologic inflammatory responses, and thereby set the stage for dysoxic hormonal disorders:

* Postmenopausal hormone therapy (PHT) is associated with raised blood levels of a protein called CRP, a well established marker of inflammation.

* PHT is also associated with raised blood levels of another well established marker of inflammation called IL-6.

* PHT is associated with raised blood levels of a class of proteins found in the matrix—materials that hold cells together in tissues—called MMP-9. The increased levels of these proteins indicate an accelerated breakdown of the matrix substances.

*PHT is associated with raised blood levels of a substance that anchors cells together called sICAM. Again, the raised levels of this substance indicate the presence of molecular inflammation and increased stress on normal cohesion among cells .

* The case for pathologic proinflammatory effects of synthetic hormones becomes even stronger when the effects of controlled ovarian hyperstimulation (COH) caused by potent synthetic hormones used for in vitro fertilization (IVF) are carefully examined

Estrogen receptors, of course, are proteine embedded in cell membranes. Below is some general information to show hormone functions are integrated with oxygen homeostasis.

Related Tutorials

The above inflammatory roles of estrogen are further discussed in the following tutorials:

The Unifying Oxygen Model of Gonadal Health

* Amenorrhea, Oligomenorrhea, and Polymenorrhea in CFS and Fibromyalgia Are Caused by Oxidative Menstrual Dysfunction

* Hormone Replacement Therapy (HRT) or Receptor Restoration Therapy (RRT)?

* Pro-inflammatory Roles of Estrogens

 

Oxygen, Hypoxia Inducible Factors, and Hormone Receptors

Protein systems in living tissues are dynamic. Proteins fold and unfold in response to cues in their molecular environment to assume various functions.19-21 Though well-protected by chaperons (which are proteins and so require their own chaperons), proteins misfold with excessive stress and become dysfunctional. The protein biosynthesis is closely matched with proteolysis to replace the disfigured or broken down units. The proteins that make up hormone receptors are not an exception to this protein order of human biology. It is well established that for a large number of proteins, proteolysis occurs in response to changes in the prevailing conditions of oxygen. In the following paragraph, I present some information about one family of proteins that display a high degree of responsiveness to oxygen signalling, which is of evident relevance to the Unifying Dysox Model of Hormone Dysfunctions.

Hypoxia-inducible factors (HIF) are a large family of proteins that display a high degree of responsiveness to oxygen signalling. I include here brief comments about one member of this family, hypoxia-inducible factor 1a (HIF-1a1) to shed light on one important aspect of the Unifying Dysox Model of Hormone Dysfunction. (HIF-1a is a basic helix-loop-helix transcription factor of the PAS superfamily. It plays a central role in cellular adaptation to diminished reduced oxygen availability.22,23 It senses and responds to oxygen deficit (becomes activated) and strives to restore oxygen homeostasis by: (1) inducing glycolysis, and angiogenesis to maintain cellular energetics; (2) inhibits cell proliferation and DNA repair to limit energy consumption; (3) activating a sleuth of its target genes, including those that encode erythropoietin, vascular endothelial growth factor, PGK1, and ARNT (also known as HIF-1ß)24); (4) recruiting the transcription co-activator p300/CBP; (5) binding to the hypoxia-responsive element in the promoter27; (6) functionally antagonizing the oncogene Myc via protein-protein interactions; (7) up-regulating the CDKN1A/p21cip system; and (8) down-regulating MSH2 and MSH6 down-regulation. For all those, and probably others as yet unrecognized roles, HIF-1a has been designated as a master regulator of oxygen homeostasis for cell survival. Disruptions of all the above genetic and signaling pathways create the dysoxic conditions that set the stage—directly or indirectly—for the development of menstrual and menopausal disorders.

 

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