Vegancrossfit
Member
- Joined
- Jul 24, 2020
- Messages
- 170
High T is oftentimes high shbg anyway
what I’ve never seen is high free T in naturals
what I’ve never seen is high free T in naturals
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High T is oftentimes high shbg anyway
what I’ve never seen is high free T in naturals
What does that synergy entail?Sure. Just search for "estradiol" and filter by user to get only Georgi's (haidut) posts. You'll find hundreds of posts highlighting studies on estradiol going back 5+ years.
Just want to say that I appreciate that you're questioning things, but Ray has referenced a gazillion studies on estrogen and estradiol specifically in his articles and newsletters over the years, and as you'll find, Georgi has posted a great deal on the topic in this forum.
There is overwhelming evidence that estradiol can and is often associated with deleterious effects. It's not just us Peat-heads parroting a theory. I think it plays an important physiological role (of cellular division and growth for instance), but there is a synergy between E2 and P4 which is often overlooked by most of the researchers.
Because popping an ai does nothing to fix the actual problem -- of course it'll make you feel worse.
Beyond increasing concentrations of serotonin, E2 also modulates the actions of serotonin because the activation of E2 receptors affects the distribution and state of serotonin receptors. Higher levels of E2 in the presence of progesterone upregulate E2 β receptors (ERβ) and down regulate E2 α receptors (ERα) [24]. ERβ activation results in upregulation of the 5HT2A receptor,[25] while ERα activation results in an increase in 5HT1A receptors via nuclear factor kappa B (NFkB) [26]. Therefore, increasing E2 causes an increase in the density and binding of the 5HT2A receptor,[27,28] which could explain the observed increases in 5HT2A density for post-menstrual teenage girls [29]. 5HT2A activity stimulates an increase in intracellular Ca++,[30] which causes changes in cellular function [17,31]. 5HT2A activation subsequently causes Protein Kinase C (PKC) activation. The effects of increased Ca++ and PKC in cells are system-specific and explain many of the physiological consequences of serotonin activation. One effect of PKC activation is the uncoupling of 5HT1A auto-receptors[32] and decreasing serotonin's effect at these receptors [33,34]. Following 5HT2A activation of PKC, 5HT1A receptors become unable to reduce serotonin production through negative feedback, and serotonin concentrations increase [32-34] E2 compounds this effect by directly inhibiting 5HT1A function [35,36].
edit source: An overlooked connection: serotonergic mediation of estrogen-related physiology and pathologyWith reduced levels of E2, 5HT1A receptors are disinhibited and counter the effects of 5HT2A receptor activation. Increased activation of 5HT1A in the immune system results in greater mitotic potential via cyclic adenosine monophosphate (cAMP) and extra cellular response kinase (ERK) [37-40]. Additionally, the reinstatement of 5HT1A auto-regulation decreases serotonin concentrations by allowing negative feedback inhibition of serotonin production and release. Normal physiology depends on maintaining a balance between 5HT2A receptor produced Ca++ inflow and 5HT1A receptor suppression of cAMP production. Pathologies result when this balance is perturbed, and the specific manifestation of these pathologies depend on which system is affected.
Both naturally-occurring and pharmacologically-induced changes in E2 alter the concentration of serotonin through two mechanisms. First, E2 increases production of tryptophan hydroxylase[18,19] (TPH, the rate-limiting step in synthesis of serotonin from tryptophan), increasing the concentrations of serotonin in the body [20,21]. Second, E2 inhibits the expression of the gene for the serotonin reuptake transporter (SERT) and acts as an antagonist at the SERT, thus promoting the actions of serotonin by increasing the time that it remains available in synapses and interstitial spaces [22,23].