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--- home:othertreatments:hormone_therapy [08.01.2019] – [Hormone replacement therapy upsets cellular homeostasis] sallieq
+++ home:othertreatments:hormone_therapy [09.14.2022] (current) – external edit 127.0.0.1
@@ Line 36: / Line 36: @@
-When the Vitamin D Receptor (VDR) becomes blocked by 25-D, bacterial ligands, or other compounds, the Receptor can no longer transcribe an important enzyme that keeps the active D metabolite, 1,25-D, in the correct range. As 1,25-D rises without a feedback system to keep it in check, the hormone dysregulates the nuclear receptors including PPAR-gamma which control the body's hormones and affects the levels of hormones including the male, female, and thyroid hormones.(({{pubmed>long:19758159}}))
+When the Vitamin D Receptor (VDR) becomes blocked by 25-D, bacterial ligands, or other compounds, the Receptor can no longer transcribe an important enzyme that keeps the active D metabolite, 1,25-D, in the correct range. As 1,25-D rises without a feedback system to keep it in check, the hormone dysregulates the nuclear receptors including PPAR-gamma which control the body's hormones and affects the levels of hormones including the male, female, and thyroid hormones.(({{pmid>long:19758159}}))
 ===== Hormone replacement therapy upsets cellular homeostasis =====
 When a patient takes exogenous (supplemental) hormones including the male, female, and thyroid hormones, those hormones enter the blood stream with some leaching into the cell. It is not known how exactly hormones affect activity of the body's nuclear receptors. However, it may be the case that just as with elevated levels of 1,25-D, the presence of supplemental hormones triggers a feedback pathway which leads to reduced production of that hormone.
-For example, if a patient is given testosterone, some of that testosterone enters the cell. Increased levels of testosterone may reduce the transcriptional activity of the Androgen Receptor, the nuclear receptor which produces it. One possibility is that with reduced production of testosterone, the Androgen Receptor also reduces transcription in other ways, leading to a reduction in the production of certain families of antimicrobial peptides, which many active Type I nuclear receptors also produce.(({{pubmed>long:17254313}})) Therefore, hormone replacement therapy //may// compromise innate immune function in dose-dependent fashion. Research is needed to validate this theory.
+For example, if a patient is given testosterone, some of that testosterone enters the cell. Increased levels of testosterone may reduce the transcriptional activity of the Androgen Receptor, the nuclear receptor which produces it. One possibility is that with reduced production of testosterone, the Androgen Receptor also reduces transcription in other ways, leading to a reduction in the production of certain families of antimicrobial peptides, which many active Type I nuclear receptors also produce.(({{pmid>long:17254313}})) Therefore, hormone replacement therapy //may// compromise innate immune function in dose-dependent fashion. Research is needed to validate this theory.
-Research into estrogen plus progestin therapy showed increased risks, 7 more CHD events, 8 more strokes, 8 more PEs, and 8 more invasive breast cancers. (16608 healthy postmenopausal women studied over 5 years) (({{pubmed>long:12117397}}))
+Research into estrogen plus progestin therapy showed increased risks, 7 more CHD events, 8 more strokes, 8 more PEs, and 8 more invasive breast cancers. (16608 healthy postmenopausal women studied over 5 years) (({{pmid>long:12117397}}))
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+<nodisp>
 ===== Notes and comments =====
   * Legacy content
     *
-===== References =====
+===== References =====</nodisp>

home/othertreatments/hormone_therapy.txt · Last modified: 09.14.2022 by 127.0.0.1