This for real? Maybe this the reason why you feel more aggressive when on peps?
@Whisky
@ValiantThor08
EXOGENOUSLY ADMINISTERED GROWTH HORMONE LEADS TO FEMINIZED SECRETORY PATTERN AND ALTERED STEROID METABOLISM
Men and women release growth hormone (GH) in patterns unique to their sex. Adult men secrete growth hormone in a pulsatile pattern with well pronounced peaks of plasma growth hormone occurring approximately every 3.5 hours followed by periods without measurable growth hormone (GH off-time) lasting about two hours.
In contrast, adult females have a more frequent growth hormone release which results in near-continuous presence of GH in plasma.
These adult patterns of GH release are set during the first month of life by exposure to gonadal steroids, which program the hypothalamus and its regulation of pituitary GH secretion to behave in sexually distinct ways at the onset of puberty and during adulthood 1.
This difference in pattern has significant consequence primarily determined by the “off time” or period when no detectable GH is present in males or is elevated in females. This “off time”, a period when there is no (or very low) growth hormone present is required for the expression of male-specific liver enzymes, such as cytochrome P450 (CYP) 2C11 2. Without this off time those liver enzymes needed to metabolize male hormones do not get expressed to a significant degree. The reason for this failure appears to primarily result from the fact that the intracellular pathway STAT5b responsible for the synthesis of these enzymes needs time off. If it doesn’t get time off it fails to reset.
The following image will serve to give a quick understanding. Growth Hormone is a molecule that may be visualized as a peg which lands on a receptor where it flips a switch and sets things in motion. One of the things it sets in motion is an intracellular pathway known as signal transducer and activator of transcription 5b (STAT5b). This protein once activated moves to the cell nucleus and initiates the transcription of end product proteins such as liver enzymes. It then is deactivated returns to the receptor and is reactivated to again mediate transcription.
When a pulse of growth hormone activates growth hormone receptors it does so with a strong enough punch that STAT5b undergoes multiple rounds of activity during this single pulse. When a non-pulsatile more feminine continuous growth hormone “bleed” activates growth hormone receptors STAT5b activity is not as vigorous and this activity or mediating cycle is terminated more quickly.
When exogenous growth hormone is administered in a way that causes prolonged elevation of plasma growth hormone the GH pulse induced expression of male specific liver genes is reduced and if long enough completely abolished while the expression of female specific genes is significantly induced 3. This can primarily be attributed to the failure to give STAT5b an “off time” which reduces its activation and partially desensitizes it to growth hormone 4.
The time period required to reset the STAT5b pathway after a GH pulse is two to three hours 5,6.
Specific Examples
The female P450 isoform CYP3A4 can be thought of as having a role in estradiol homeostasis. Specifically it hydroxylates estradiol at the 2, 4 and 16 alpha positions. It also catablyzes 6 beta-hydroxylation of testosterone which it converts to estradiol by the action of aromatase. This activity is welcome for mammary gland development and lactation if you are a female. But if you are a male with a lot of substrate in the form of testosterone you don’t want this enzyme to be active 15.
Yet patients suffering from acromegaly and men who are given continuous forms of GH treatment end up with greatly upregulated expression of this female liver enzyme 16,17. This female liver enzyme is suppressed by intermittent pulsatile GH 18.
The female P450 isoform CYP3A4 also metabolizes other steroids such as cortisol as well which is converted more rapidly in women then men 19.
Many of the male P450 isoforms have roles in testosterone metabolism such as CYP2C11 which hydroxylases testosterone and converts testosterone to androstenedione for use in resynthesis. This activity is lost when a female pattern of GH release is instituted.
The female GH release profile stimulates the full expression of testosterone 5 alpha reductase activity 20,21. In men with the substrate testosterone this female GH release profile can lead to a substantial conversion of testosterone to Dihydrotestosterone (DHT).
It is also thought that certain environmental triggers and food additives can trigger autoimmune diseases for those genetically predisposed. Alterations in GH release profile brought about by environmental factors make middle aged women more susceptible then men to such triggers as MSG and Aspartame in invoking auto-immune hepatitis 22.
The full treatment of this topic is beyond the scope of this review. This section was meant to underscore the fact that imbalances are created in ways not often considered. Health and a reduction in toxicity require countermeasures which could include the use of compounds such as the Arginine/Lysine combination to reduce cortisol or Sodium Glucuronate to bind and eliminate the byproducts of P450 enzymal activity. Of course another beneficial method would be to optimize sex specific GH release patterns rather then eliminate them.
Copied and pasted from:
https://synthetek.com/en/the-science-behind-synthergine-liver-protectant/
The references are found on said page, I could not include them as the post was too long.
