Please discuss, and you can vote in the /r/truscum poll that I made here.
I myself plan on initially just using the usual antiandrogen plus normal dose (not microdose) estradiol when I am able to restart HRT, and switching to that strategy if I were to become dysphoric over breast development.
https://en.wikipedia.org/wiki/Zuranolone
Won't that result in benzodiazepine esque dependence and withdrawals considering its same receptor?
Selective Androgen Receptor Modulators (aka SARMs) are synthetic drugs being tested for, but are not yet approved for, use in various medical conditions, and often marketed as "legal steroids" or "steroid alternatives". They are NOT recognized by FDA as dietary supplements, and are prohibited for use by DoD, NCAA, and WADA. In addition, these drugs have been known to adversely effect the liver and cholesterol levels.
For more information SARMs you can check out the article here from Operation Supplement Safety. Additionally, there are links to a list of product with SARMs in them to be wary of, and an infographic you can find here.
I just found out about SERMs, they're nicknamed "designer estrogen" because of their estrogen-like effects on bone density, and their anti-estrogen effects on chest tissue. However, similar to how hormone suppressants were designed as uterine and prostate chemo, SERMs are for breast cancer. I don't make enough hormones (afab he/him), just found out, but my endocrinologist doesn't want to give me SERMs because it's used to prevent osteoporosis in people with breast cancer who are over age 65. He said it's mostly concerning due to my age, mid 20s.
I'm prescribed half of an estrogen patch, but I don't realistically see myself being able to take estrogen or testosterone, regardless of consequences. The hope is having such a low dose of estrogen I don't really notice, we'll see. Any effects would be too distressing. Same goes for testosterone, so I'm out of options. Testosterone with finasteride to block some of it might be less terrible, but again not ideal or likely tolerable.
I know this may be seen as basic stuff that might be pathetic that I donβt know. But please explain to me
https://www.frontiersin.org/articles/10.3389/fendo.2021.701364/full
> Here, we discuss the theoretical use of Selective Estrogen Receptor Modulators (SERMs) for non-binary people assigned male at birth (AMAB) who are seeking an androgynous appearance through partial feminization without breast growth. Given their unique range of pharmacodynamic effects, SERMs may represent a potential gender-affirming treatment for this population, but there is a lack of knowledge regarding their use and potentially adverse effects in this context.
Using a Positive allosteric modulator increases the response to agonists.
Has anyone tried this? I'll be running some tests with it.
Inspired by this study which used "Combination of Nicotine with Galantamine may have enhanced therapeutic effect in patients with Alzheimer's disease."
https://staticweb.bmj.com/clinmed/original/2002080001v1/Comb__nic_plus_galant_in_AD-YES.htm
Positive allosteric modulator:
Galantamine.
Agonist:
Nicotine.
Phenylpiracetam.
GTS-21.
I propose Phenylpiracetam and Galantamine as the best stack to utilize this mechanism. See studies below.
This should be a potent pre-workout aswell, as both activate muscle type nicotinic acetylcholine receptors.
What Galantamine was missing all along may have been an agonist.
Studies:
https://www.nature.com/articles/1301256
"Galantamine (3βmg/kg p.o.) significantly increased the extracellular dopamine release in the hippocampus of saline- and AΞ²25β35-injected mice. The effects of nicotine on the extracellular dopamine release were potentiated by galantamine, but antagonized by mecamylamine, a nAChR antagonist."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC29386/
"Nicotinic receptor binding was significantly increased in rabbits treated for 15 days with Galantamine."
http://europepmc.org/article/PMC/1576175
"Galantamine, described as a molecule with anticholinesterasic properties, is also an allosteric enhancer of human alpha4beta2 neuronal nicotinic receptor activity. "
"Phenylpiracetam binds to Ξ±4Ξ²2 nicotinic acetylcholine receptors in the mouse brain cortex with IC50 = 5.86 ΞΌM.[6]."
https://link.springer.com/article/10.1007/s00213-019-05363-4
This may reflect specific nAChR subtype involvement, or additional pharmacological actions of galantamine may have overshadowed similar interactions on other measures. The finding suggests that allosteric potentiation of nAChR agonist-induced cognitive benefits is possible in principle."
https://www.jneurosci.org/content/25/8/1992.short
"Galantamine Activates Muscle-Type Nicotinic Acetylcholine Receptors."
https://fscimage.fishersci.com/images/D00599~.pdf
"Galantamine is a potent allosteric potentiating ligand (APL) of human τ°alpha3beta4, alpha4beta2, and alpha6beta4 nicotinic receptors (nAChRs). Galantamine potentiates agonist responses of the four nAChR subtypes studied.
These studies support our previous proposal that the therapeutic action of galantamine is mainly produced by its sensiti
... keep reading on reddit β‘Hi all,
As far as I'm aware, the most potent anxiolytic drugs available are gaba a agonists that increase inhibitory transmission (alcohol, benzodiazepines...).
Conversely, gaba antagonists such as flumazenil have an opposite effect, with the potential to cause seizures at higher doses.
I was looking into Quercetin, described by multiple sources as a negative allosteric modulator at the gaba a receptor
"Quercetin markedly reduced the GABA-activated currents in a noncompetitive manner in cultured cortical neurons, and moderately inhibited spontaneous and electrically-evoked GABAergic inhibitory postsynaptic current in mouse prefrontal cortical slices. "
Quercetin as negative allosteric modulator.
However, other papers conclude that quercetin likely exerts an anxiolytic effect through the gabaergic system, and that that effect is BLOCKED by co administration of a gaba a agonist; *"As shown inΒ Fig. 3Β , the anxiolytic-like effects of quercetin were not antagonized either by WAY-100635 (0.3 mg/kg) or flumazenil (10 mg/kg). However, interestingly, the anxiolytic-like effects of quercetin (5 mg/kg) were * *blocked by TACA (20 mg/kg), a GABAΒ A-ΟΒ receptor potent agonist."
How does this work? How can the administration of a gaba agonist block an anxiolytic effect? How can the inhibition of gabaergic transmission have an anxiolytic effect, rather than the opposite such as is the case with flumazenil?
Thank you.
Hi everyone! My name is Dr. Justin Dubin and I am a Urologist at the University of Miami. I am asking members of this subreddit to take part in a research study evaluating the demographics of selective androgen receptor modulator users (Commonly known as SARMs). SARMs are very commonly used throughout communities like this but little is known about their side effects and impact on fertility. We feel it is an important topic that has not been discussed and we would like to shed some light on it through our research.
Below is the link to an anonymous survey that asks questions on the topic. We are asking all adults 18 and older to participate. The survey can range from approximately 10-30 questions (depending on your answers) and should take no longer than 6 minutes to complete.
Demographics of Selective Androgen Receptor Modulators (SARMs) Users
This survey has been approved by the moderators (/u/Troythetoyboy) and the study is IRB approved at UMiami. This is a one time survey and no follow up will be required. If you have any further questions feel free to message me or reach out via my contact information on the survey.
Thanks for your participation!
https://en.wikipedia.org/wiki/Zuranolone
Zuranolone (INN;[1] developmental code names SAGE-217, S-812217) is an investigational medication which is under development by SAGE Therapeutics for the treatment of depressive disorders and a variety of other indications.[2][3] It is a synthetic, orally active, inhibitory pregnane neurosteroid, and acts as a positive allosteric modulator of the GABAA receptor.[2][3][4] The drug was developed as an improvement of allopregnanolone (brexanolone) with high oral bioavailability and a biological half-life suitable for once-daily administration.[3] As of October 2019, zuranolone is in phase III clinical trials for major depressive disorder, postpartum depression, and insomnia and is in phase II clinical studies for bipolar depression, essential tremor, and [Parkinson's disease](https://en.wikipedia.org/wiki/Parkinson
... keep reading on reddit β‘Hi everyone! My name is Dr. Justin Dubin and I am a Urologist at the University of Miami. I am asking members of this subreddit to take part in a research study evaluating the demographics of selective androgen receptor modulator users (Commonly known as SARMs). SARMs are very commonly used throughout communities like this but little is known about their side effects and impact on fertility. We feel it is an important topic that has not been discussed and we would like to shed some light on it through our research.
Below is the link to an anonymous survey that asks questions on the topic. We are asking all adults 18 and older to participate. The survey can range from approximately 10-30 questions (depending on your answers) and should take no longer than 6 minutes to complete.
Demographics of Selective Androgen Receptor Modulators (SARMs) Users
This survey has been approved by the moderators and the study is IRB approved at UMiami. This is a one time survey and no follow up will be required. If you have any further questions feel free to message me or reach out via my contact information on the survey.
Thanks for your participation!
