- Joined
- Feb 20, 2021
GnRH agonist drugs are no joke and I cannot believe that doctors are willing to fuck around with them.
Regarding the possible link to T2D and obesity, per this source, it's a known issue with this drug class. "Effects on glucose and lipid metabolism have been noted, with data suggesting that low testosterone levels lead to insulin resistance, central obesity, hypercholesterolemia and hypertriglyceridemia, and other precursors of metabolic syndrome."
It's not fully understood why the use of androgen deprivation therapy (ADT) increases risk of obesity. The therapy was originally intended for the treatment of prostate cancer, as has been discussed at various points in this thread. In pharmacology, an "agonist" is a type of molecule (a "ligand") that binds to a receptor on the surface of a cell and activates it, causing a physiological effect. A receptor can be activated by an "endogenous agonist", which is naturally produced by the body, or by an "exogenous agonist", which must be introduced to the body by outside means. The exogenous agonist must be similar enough in structure to bind to the correct receptor, thus "tricking" it into doing something. The drugs we're talking about here are gonadotropin releasing hormone agonists, which means they are modeled after endogenous GnRH, a neuropeptide that is produced and released by specialized neurons (brain cells) in the hypothalamus, a structure deep within the brain. The endogenous GnRH is carried to the anterior pituitary gland, another deep brain structure, by the blood vessels within the brain. In the pituitary gland, it binds to the GnRH receptors and activates them. A bunch of complicated and unfathomably elegant shit happens once the ligand binds to the correct receptor site, and the ultimate result is the production and release of two gonadotropins, called follicle stimulating hormone and luteinizing hormone. The pituitary gland's release of gonadotropins is what "tells" the testis or ovary to produce testosterone or estrogen, respectively.
These drugs bind (act as ligands) at the GnRH receptor site as if they were endogenous GnRH, causing those receptors to "activate".
So, taking a "puberty blocker" drug like a GnRH agonist is really inhibiting the process way, way upstream from the gonads. Specifically, it's inhibiting the GnRH neurons from starting the cascade of events that causes the testis or ovary to release sex hormone. This means you cannot prevent the other effects of the reduced testosterone within the body, because the action is happening well before the testes ever produce or secrete anything. This is also why these drugs have such gnarly consequences. I don't think many of these trans-friendly doctors are going out of their way to make clear that the "puberty blocker" medication they offer acts within the brain, preventing a whole sequence of events from occurring. Referring to them as "puberty blocker" drugs and saying that they simply stop the development of secondary sex characteristics is disingenuous, at best. There are GnRH receptors in other cell types, not just in the pituitary gland. They exist in lymphocytes (white blood cells), as well as breast, ovary, and prostate tissue.
These drugs bind (act as ligands) at the GnRH receptor site as if they were endogenous GnRH, causing those receptors to "activate".
So, taking a "puberty blocker" drug like a GnRH agonist is really inhibiting the process way, way upstream from the gonads. Specifically, it's inhibiting the GnRH neurons from starting the cascade of events that causes the testis or ovary to release sex hormone. This means you cannot prevent the other effects of the reduced testosterone within the body, because the action is happening well before the testes ever produce or secrete anything. This is also why these drugs have such gnarly consequences. I don't think many of these trans-friendly doctors are going out of their way to make clear that the "puberty blocker" medication they offer acts within the brain, preventing a whole sequence of events from occurring. Referring to them as "puberty blocker" drugs and saying that they simply stop the development of secondary sex characteristics is disingenuous, at best. There are GnRH receptors in other cell types, not just in the pituitary gland. They exist in lymphocytes (white blood cells), as well as breast, ovary, and prostate tissue.
"Blocking" the effects of testosterone in the body can help shrink the prostate gland, reducing the bothersome symptoms of prostate cancer, like urinary incontinence and compression of the spinal cord. However, there's no way to prevent the effects of decreased testosterone on other tissues in the body. The same source I linked to above explains, "Stimulation of FSH receptors on the endothelial surface of proliferating tissues could lead to decreased lipid metabolism and increased fat accumulation, leading to increased cardiovascular risk with GNRH agonists. Additionally, GNRH agonists, but not antagonists, bind to and stimulate GNRH receptors on T cells that could result in a hyperinflammatory state causing plaque destabilization."
So, in short, not only does GnRH agonist therapy make you fat and diabetic, it also contributes to development of an inflammatory state within the entire body, which is what will really fuck a person up.
#transgender #allytotall #straighttiktok
