📱

Get Our Mobile App

Take your business learning on the go!

Download on the App StoreGet it on Google Play

How to Recover Hypothalamus-Pituitary Function after PED's

Leo and Longevity11:56

Transcription

although I don't think it is clear that aromatisse inhibitors cause atherosclerosis, which was thought for a very long time, it is in fact, it seems to be the case that tamoxifen prevents some of those cardiovascular problems, not that AIs cause them.

[Music]

hello friends, welcome to the third episode in my four-episode series on how to recover natural testosterone production and fertility after the use of anabolic androgenic steroids. of course, this series is only for educational purposes. I'd like to make you aware of the fact that in the description to this video below, you'll find a link to a blog post that I made on the subject. each of the videos has a respective blog post. I highly recommend you read them. they are more straightforward and, to be honest, easier to understand than my video descriptions. and also, they're not too detailed. they're not like the cholinergic system one that got very detailed or the upcoming certain urging system one that will be very detailed and more interesting for people that are academically inclined or or even inquisitive or curious nature. this one is meant mainly to be useful to people that are thinking about how they may or how people may go about fixing this problem.

so, in the last episode, we talked about the use of HCG and HMG to simulate the production of LH and FSH from the brain. that results in increases in intratesticular testosterone and the maturation and differentiation of sperm, respectively. however, in this episode, we're going to talk about SERMs, which are selective estrogen receptor modulators, and AIs, which are aromatase inhibitors. now, I want you guys to notice something. the HCGs and the HCG and HMG, what they're really doing there is bypassing the brain to try to make sure that the rest of the body responds as if the brain is producing signals that include the gonadotropins, luteinizing hormone, and follicle-stimulating hormone. in this episode, we're going to talk about things that actually try to get to the root of the problem, which is to get the brain to start actually producing those gonadotropins again. so, this is actually more of a solution to the real problem than a quick fix on fertility or testosterone production, as well as, yeah, you know, it's HCG and HMG aren't just a quick fix because, again, I mentioned in the last episode, they use a "use it or lose it" theory in biology that we need things to be working. so, if we can just get the testes, the gonads, to be working, that's still something good, and it may be useful if you're trying to get pregnant or trying to have your own endogenous testosterone production. but we also want to address the root cause or the root of the matter, which is the brain. so, and that's what SERMs do.

so, selective estrogen receptor modulators are less harsh than AIs. what they do is modulate the estrogen receptors to a lesser extent than completely blocking their activity. and they are similar to SARMs, which are selective androgen receptor modulators. now, in this class, the most famous chemical or pharmaceutical is called tamoxifen, which is also called Nolvadex as a brand name of it. tamoxifen is very well-known in breast cancer communities because it is a mainlined treatment for breast cancer. and tamoxifen is an interesting drug because it also has some protective qualities. it may protect against the development of fatty liver. it may, it definitely is chemoprotective in some ways, which means it may protect you from the development of cancers. it's a very interesting drug. however, I won't discuss tamoxifen too much here because it's not usually the preferred drug when it comes to fertility. when it comes to fertility, we're mainly talking about a drug called clomiphene citrate. one of the two brand names for this drug is Clomid, which is how it the name is usually gone by in the AAS circles. now, clomiphene citrate is composed of two chemicals, actually. one is called enclomiphene citrate, and one is called zuclomiphene citrate. and enclomiphene, I'm gonna call them EC and ZC. EC is enclomiphene citrate, or Clomid. ZC is zuclomiphene citrate. now, the interesting thing about Clomid, or clomiphene citrate, is that it is not completely antagonistic to the estrogen receptor because enclomiphene citrate, EC, is completely antagonistic to the receptor. but ZC, zuclomiphene citrate, is both antagonistic and agonistic. so, zuclomiphene citrate is not really desirable because we're only trying to antagonize the receptor. so, for this reason, recently, there are several trials testing a specific preparation of EC alone and clomiphene citrate at doses of 25 milligrams for the purposes of fertility, and they are very promising. but as of yet, the FDA has not approved it for this use.

now, clomiphene citrate, which is approved and is easier to get, its half-life is, I think, around five days. it stays in the system quite long, and it's usually used in clinical studies at between 25 milligrams to 100 milligrams a day. of course, this is a pill, for those of you that don't know, that can be taken once a day. now, what I'd like to say is what's going on here with it with the clomiphene citrate or Clomid or CC, or whatever we call it, is that it is preventing your body from recognizing the feedback system which comes from estrogen, which causes the hypothalamus to stop producing gonadotropin-releasing hormone, which in turn causes the pituitary to stop releasing luteinizing hormone and follicle-stimulating hormone, LH and FSH. so, what we're doing is sort of dampening that estrogenic response, which in turn should lead, we hope, to the pituitary releasing hormones of its own. now, in studies, this actually does seem to happen. there is clinical evidence of hypogonadism, which means smaller testes, being alleviated by the singular monotherapy use of clomiphene citrate. as well, there is evidence that the serum testosterone levels rise from the monotherapy clomiphene citrate.

now, aside from SERMs, aromatase inhibitors are also quite interesting. they're usually called AIs. what they do is inhibit the activity of the enzyme aromatase, which synthesizes estrogen from testosterone in the male and female body. although it does it, it accounts for much less of the estrogen production in the female body. most is produced by the ovaries, but they also get some from the aromatase enzyme. now, what AIs do, and by the way, AIs are continuously being made more so. even anastrozole, we're only going to talk about anastrozole in this video, but even anastrozole is considered a much more specific AI than its predecessors. now, what these things do is they prevent, basically, your body from converting testosterone into estrogen in the body. so, they reduce the amount of actual estrogen that you have in the body. now, they're mainly used clinically on obese men because obese men convert much more testosterone into estrogen than men that have a ratio of testosterone to estrogen that's higher than about 10, or lower than about 10. so, if you have a ratio of testosterone to estrogen that's lower than 10, sometimes the clinician will prescribe an aromatase inhibitor.

now, I just want to make a side note here while we're talking about this, that as you, if you're a long-term viewer of mine, you may know that I am not very fond of aromatase inhibitors because, as I will discuss in, I think soon, and maybe I'll do a series on estrogen at some point, estrogen has numerous benefits in the body, I mean, very great benefits. although I don't think it is clear that aromatase inhibitors cause atherosclerosis, which was thought for a very long time, it is in fact, it seems to be the case that tamoxifen prevents some of those cardiovascular problems, not that AIs cause them. but as I discussed before, AIs definitely lower estrogen in the body, and estrogen has so many great neuroprotective and cardioprotective and mood-enhancing and cognitive-enhancing benefits that I generally, I'm not want to encourage the use of AIs. with that said, when working on a fertility program or or endogenous testosterone production program, we would want to be careful of the fact that it seems to be that the more out of whack the testosterone to estrogen ratio, the harder it is to recover natural function. so, what I would want to see as well is that on their own, aromatase inhibitors, including anastrozole at one milligram a day, whereas letrozole is usually used at 2.5 milligrams a day, by the way, one milligram a day, and anastrozole has been shown to increase sperm count, although it's not clear if it works for low sperm motility.

now, keep in mind, sperm is judged according to three parameters. one is count, one is motility, which means how much it moves, and one is morphology, which means whether it is not DNA. morphology doesn't have to do with DNA damage in the sperm, it has to do with the shape of the sperm, whether the sperm are visually shaped correctly, and it's originally told by a microscope, just looking at the sperm in a microscope. but anyway, so, it's not so clear that using an AI on its own may help with motility, but it is clearer that in a minority of patients, it does help with sperm count. and in fact, you know, letrozole, for example, has worked to raise sperm count in about 20% of patients studied. so, it isn't a minority. and I do believe on its own is less effective than Clomid. however, there are clinicians who have speculated that a combination of Clomid, or clomiphene citrate, or ideally enclomiphene citrate, but also clomiphene citrate in combination with an AI may be the ideal package to take. and remember, this is all to stimulate the hormones being produced directly in the pituitary, as opposed to bypassing the pituitary like HCG and HMG are doing and going to the testes.

so, I hope you guys enjoyed this shorter episode. tomorrow, I will describe to you guys my, and it may be a bit more along with that, I don't know, maybe I'll talk a bit about my experience, but I'll describe to you guys my views also from the clinical literature, but my views on what may be the ideal program and how to how to develop it, because it's not, these kind of programs cannot be, they're not supposed to be simple like the programs currently out there. they're a little bit simple, and there's reason to have a little bit more complexity in it. thank you guys so much for watching, and stay tuned for tomorrow, which I think will be a good episode. thank you so much for listening. we'll see you next time.

[Music]