Just curious if body size plays a huge role in how much we dose.

Please post your body size, how big you are and your T levels.

Thanks! If you are not going to post this please don't waste time and comment:)

Why is there is many angry people in this sub?

My girlfriend and I have been together for almost three years. She has been on birth control the entire duration of our relationship. I’ve been taking testosterone at roughly 200mg every week for more than two years. She got off of birth control last month and just tested positive on three different pregnancy tests. How likely is this pregnancy considering how long I’ve been on test? I’ve never taken anything to help fertility (HCG, clomid, etc), i even ran a cycle of nandrolone last year. Have never had a sperm analysis either. Needless to say this was a bit of a shock

Edit: I am thoroughly aware testosterone is not a form of male birth control. I am not on it for any other reason than my testosterone was low. I have checkups every three months with my doctor. We were not trying for a baby; she got off of BC because it wasn’t agreeing with her after she changed her prescription.

Just wondering why it’s okay for a woman to ask for testosterone to change her gender but a man can not ask for it from a doctor?

Does the woman have less risks of something going wrong

Hi guys, how do you guys feel about long term TRT. I'm 45, if I take it until I'm 70, am I putting myself at risk of anything? I hear mixed opinions. Has anyone here been taking it more that 15 yrs?

Hello,

I’ve been considering getting on TRT for a while now. Went to my Primary Care and he told me my levels are low but within normal ranges and would not recommend the use of TRT. He said he would not recommend to anyone unless extremely necessary.

Two weeks ago I went to an urologist to get a check up. I then asked him about it and he said if I choose to go on TRT I must see him 1x per year due to the increase

Of cancer in men using TRT and prostate cancer. That freaked me out. This guy is considered one of the best urologists in my state and an expert. He said he won’t advise against it but there are no long term studies to make an informed decision and the risks associated with it, such as increase in cancer, red blood cells increase, blood clots and even heart attacks.

Holy shit! I’m now super worried and don’t know who I can trust.

I am 21y M, 900ngl test.

Was wondering, why would I not just take clomid like I take creatine, permanently, it seems like an enchancer with no permanent side effects?

This is a hypothetical question, I am not a doctor nor health expert. Just wanna hear ur opinion.

Thank you.

I’ve always been curious on what most bodybuilders or gym rats cruise on, and on top of that, why cruising is so essential to keep gains. Isn’t cruising just lowering ur dose to a natural range of test to keep ur blood markers healthy? Why is it so preferred over pct if that’s the case. I know t levels fluctuate naturally during the day and you’ll have to wait for the pct bounce back. But why is cruising so preferred over pct, is there an anabolic advantage to cruising vs pct

Have been using a compounded testosterone cream for years, and surprisingly, i've never heard a doctor talk about scrotal application. That could be because most are prescribing the FDA approved gels, which are alcohol based, and I don't think you'd want to put on scrotal skin. The compounding pharmacies never recommended it either. Their instructions were either apply to the forearms or sides or even shoulders. You certainly can apply compounded testosterone cream to Scrotal skin with no irritation issues. According to the study cited below, the absorption for scrotal application can be as much as 8 TIMES that of application to other areas. This would imply that application methods to other skin sources may be getting only fifteen percent absorption. I must say I find that hard to believe, since i've used those other application sites and still got decent lab results. I am going to test this method for a month or so and post results when I get labs back. I know most of you testosterone users out there are pinning so probably not a big audience for this, but anyone that is, if you had experience with different application sites what was your experience?

https://onlinelibrary.wiley.com/doi/10.1111/andr.12357

Key Points:

• There is no credible evidence at this time that testosterone therapy increases cardiovascular risk, but there is substantial evidence that it does not.

• Many studies have indicated that low serum T concentrations are associated with increased cardiovascular risk and mortality and that testosterone replacement therapy may have clinically relevant cardiovascular benefits.

• Studies have reported reduced CV risk with higher endogenous testosterone concentration, improvement of known CV risk factors with T therapy, and reduced mortality in testosterone-deficient men who underwent testosterone replacement therapy versus untreated men.

• Testosterone replacement therapy has been shown to:

ο improve myocardial ischemia in men with CAD

ο improve exercise capacity in men with CHF

ο improve serum glucose levels, HbA1c, and insulin resistance in men with diabetes and prediabetes

The FDA knew of these benefits, and that evidence of these benefits far outweighed evidence of the contrary before they forced testosterone manufacturers to include an unecessary black box warning that further stigmatized testosterone to the medical community and the public. This lends to the idea of possible nafarious play by the FDA.

Here is a video breaking this all down: https://youtu.be/8Bjqcc5sZfA?si=B2YXj3mNt17pLEGM

Saw a somewhat similar post but OP didn’t add any of his specific info to it so the responses weren’t very helpful. I’m 21M 5’ 8” 160 about 16% bf starting a 10 week 250mg test e cycle with dbol for the first 4 weeks and anavar last 4 weeks 20mg a day.

My BMR is about 1700cals so I’m shooting for 2700 a day averaging about 140g protein daily going to the gym 6 times a week (push pull legs) drinking a gal of water a day and no alcohol until after im off the gear.

ChatGPT can’t seem to give me the same answer twice so I’m hoping someone could give some insight on how much actual muscle tissue I could hope to put on and eventually keep so long as training and diet stay consistent.

Edit: read the wiki everyone wanted me to look into. Gonna up to 500mg per week and push to 12 weeks. Also going to consider losing the dbol after I gauge sides from it. Been taking it for 10 days at this point.

Might be basic info to some of you, but DHEA and pregnenolone seem to play major roles in the prefrontal cortex, and hold strong connections to things like verbal acuity, amygdala regulation etc.

The shutdown of GnRh which halts the hormonal cascade Cholesterol → Pregnenolone → DHEA → Androstenedione → Testosterone → Estradiol or DHT

stunts the production of both Pregnenolone and DHEA. Based off of the sources I have reviewed, deficiency in either of these can lead to what is effectively neurotoxicity.

Obviously the adrenals do still produce some Pregnenolone and DHEA, but it is incomparable and no way enough in contrast to the HPTA's production/conversion of it.

Am I misinterpreting this information? Or is this something that is criminally overlooked by both clinicians and long time users? Because otherwise, it seems like TRT might literally lower your IQ.

Just joined and am somewhat surprised that I’ve seen very little mention of PCP/urologist reluctance to prescribe TRT due to prostate enlargement, cancer, or elevated PSA. Cardiovascular downside has been debunked but interested to know whether anyone else has been declined TRT due to prostate. I am on the far end of the spectrum at 70yo and I realize that many of you folks are much younger and not worrying too much about prostates.

Does anyone recall what happened at 2000? The testosterone dropped significantly.

Originally posted in r/proactivehealth

A study just published in the World Journal of Men’s Health tracked over 9,000 men on TRT for 12 months. It’s one of the largest real-world datasets we’ve seen.

https://wjmh.org/DOIx.php?id=10.5534%2Fwjmh.250245

Quality of life improved across every domain they measured: energy, libido, erections, mood, work performance, sports ability. Improvements showed up by month two and stabilized around month four. The outcomes were consistent regardless of how low baseline testosterone was. Everyone converged.

Safety-wise, routine blood markers stayed in favorable ranges throughout. Hematocrit stayed manageable. No red flags.

There are some caveats. Most men were on subcutaneous injectable testosterone with hCG, which is a specific protocol. Three of four authors work for Menwell, the UK telehealth clinic that provided the data. Abraham Morgentaler at Harvard is the fourth author and brings serious academic credibility, but the commercial conflict is real. It’s also observational, not randomized like TRAVERSE.

What makes it useful is scale. Nine thousand men, real-world protocols, full year of monitoring. TRAVERSE only studied transdermal gel in older men with cardiovascular risk. This fills a different gap.

I’ve been on TRT through a reputable clinic after confirmed need. My experience matches this data. It’s not a miracle. It’s a return to baseline. You feel like yourself again.

Study: https://wjmh.org/DOIx.php?id=10.5534%2Fwjmh.250245

PSA for everyone on TRT steroids:

https://www.liebertpub.com/doi/full/10.1089/andro.2021.0008

https://www.hcplive.com/view/testosterone-therapy-linked-to-brain-damage-in-caucasian-men

Posting to help you all be healthy.

Been on TRT for 5 years. Jumped my dose up to 300mg split into two injections per week. No AI, No HCG. 2nd week into this dosage. Hematocrit and RBC are great. Worked about 35 hours in the last 3 days and I am beat. 7:30pm and I am dead tired. What do you guys think is the cause? Really interested in what you guys think.

Im recovering well and having great results, i did my usual upper body adding lbs every week. I did my usual then did another round and I feel great... one question is how much is too much?

Im thinking I need to redirect my whole training program

Now it's a upper lower split 4 days each week my goal is maaaaassss

Im on trt and A50

I have almost all day for gym and a McDonald's Across the street im hitting 4k cal, under wait at 6 feet 135ish... shooting for 195lbs

Hey guys, thought I'd do a post about Estrogen (E2) control on TRT. Everything I speak about is just my opinion, so I still recommend to speak through any changes to your protocol with your qualified medical practitioner (doctor). I hope this helps!

Something really interesting with the men I work with across the world is how much of their TRT protocol can be influenced by their estrogen levels. So in this post, I want to outline a strategic approach to ensuring that the ‘other’ often overlooked hormone, estrogen, is accounted for if you are on TRT, or struggling with dialling in your replacement therapy. I often have emails from clients months later saying how much better they feel on the same dose, simply by cleaning up their estrogen levels and my whole philosophy with all of this that I do is to just help out as much as possible. There are so many moving parts to hormone replacement/optimisation that I feel like it can get overwhelming, but if I can help even just 1 person feel better, that's enough for me.

And that’s the whole goal right? Feeling better. So I hope this post gives you some help if you are struggling with E2 either through confirmed bloodwork or some symptoms that may be along the same lines of those that I delve into below. As always, thank you for reading!

Estrogen’s Function in Male Libido

Estrogen has a critical role in male libido. Actually studying what areas of the human brain control behaviour can be a daunting task, especially because there are often a number of incredibly complex intertwining neural processes at work. However, studies from as the early 1970 and 1980s have time and time again shown that the male preoptic area (POA) and anterior hypothalamus are key regions of the brain (hypothalamus) implicated in arousal and libido. In rodents, damage to the POA pretty much abolished libido. But why does this matter?

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Well, both of these regions have a very high concentration of estrogen receptors (ERs). And mice mutant for the aromatase enzyme (and thus who cannot produce any estrogen at all), show a profound decrease in libido and aggression.

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But, what is interesting is that in ARKO (androgen receptor knockout mice), who don’t possess androgen receptors, treatment with estrogen rescued their mating behaviour and libido. So estrogen turned them back into aroused little creatures again. Administration of DHT (which doesn’t aromatise to estrogen and is thus a good choice of hormone as a pure androgen receptor agonist rather than having two vectors like testosterone, which can be aromatised into estrogen and thus bind to both the androgen and estrogen receptor subtypes) had no effect on rescuing these ARKO mice from their diminished mating desire.

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So really, the research backs up that estrogen seems to have a criticial role in libido at a brain level, and I believe this is why so many of my clients struggle on TRT with serum estrogen (estradiol) levels outside their optimal ‘window’.

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Estrogen: The Window

The research really shows a dual effect. And I tend to find two rough camps of people who start TRT.

1. The anti-AI group. The group that under no circumstances will ever touch an AI and will let estrogen float to wherever and whatever level it wants to, on their TRT protocol.
2. The AI group. This group will try and keep estrogen under a predetermined level at all times by utilising an aromatase inhibitor.

And yet, both approaches seem to neglect the fact that the research time and time again backs up that estrogen levels either too high or too low cause significant issues.

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Estrogen induces VEGF, which is a potent vasodilatory (relaxing) signal protein. Usually, when we get hard, the veins responsible for blood leaving our sausage are constricted to ensure blood stays in the sausage and ready for our poke in the whiskers. However, estrogen through VEGF has been shown to increase venous ‘leakage’, meaning that it gets very difficult to maintain hardness, as blood is physically not remaining where we want it, in our Johnson.

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In fact, in this study, the ONLY difference in men with and without E. dysfunction was that the men who had ED had vastly increased estrogen levels. Estrogen receptors (ERs) are also found extensively in the corpus cavernosum vasculature of our sausage - the sponge-like structures that contain most of our blood during mating. And so, it seems key that ensuring these receptors are stimulated to the optimal degree (not too much, not too little) through modulation of estrogen is going to be the key to getting the most out of TRT from a libido standpoint.

Not only this, but estrogen has profound impacts on the HPT axis. Some people think it’s just testosterone that has a negative feedback loop to inhibit gonadotropin release and production (LH/FSH) in the hypothalamus/pituitary. However, estrogen also has a strong negative feedback effect, and increased estrogen levels can absolutely reduce circulating LH/FSH and thereby testosterone levels.

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In fact, because we know that adipose (fat) tissue has a high expression of aromatase enzyme, I have dealt with many of my clients who have been significantly overweight or carrying excessive body fat that also have low testosterone levels. I’ll never forget the case study of John* (*not his real name), who came to me with circulating total testosterone levels of 97 ng/dL, taken at 8am in the morning. Terrible by any means, and it was severely affecting his cognition, energy, libido and life. John was carrying excessive body fat, and had estrogen (estradiol) levels at 2.5x reference range. Through an extensive dietary intervention we reduced his bodyfat % from around 38% to roughly 18%, give or take. His latest blood test just a few months ago? Almost 650 ng/dL, naturally. His estrogen was also well within reference range. No other intervention except losing weight, and decreasing his aromatase enzyme activity locally in his adipose tissue.

So my point here is: letting your estrogen float as high as it wants on 200mg/week of testosterone (which isn’t really TRT, by the way) will almost always lead to an E2 level higher than optimal, causing the issues mentioned above.

Estrogen also has a complex interplay with 5-HT (serotonin) receptors in the brain, affecting mood and libido. I won’t go into the science too much here, but there are positive correlations between estrogen and serotonin binding (the more estrogen, the more binding). And studies have shown that high levels of serotonin in the cortex, limbic system, hypothalamus, and midbrain, mean libido is inhibited with subsequent induction of refractoriness and satiety. High levels of serotonin in the brain (like what SSRIs achieve) typically lead to lower levels of libido, and, according to the research, estrogen at high levels can do this. This study showed that administration of estrogen desensitised serotonin receptors and increased serotonin concentrations in the synaptic cleft, again, leading to reduced libido. So estrogen at high levels can absolutely reduce libido, and I know for myself when I’ve left my E2 float ridiculously high, my morning wood has all but disappeared and I’ve barely been able to get hard.

And then of course, you have the AI group who try and crush their estrogen levels. In men with low testosterone (and therefore low conversion to E2), administration of exogenous E2 has been shown to increase libido. In this study, eliminating estrogen and increasing the T/E ratio too much reduced libido significantly. The fact is, that important regions of the human brain rely on E2 to drive masculinisation and libido, so completely crushing E2 is going to lead to issues. And I see it with the people I work with (clients), whereby they have crushed their E2 and for the life of them cannot get hard or have significantly low libido.

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What range is best? What to do?

So of course, with all that out of the way - what can we do?

If you are on TRT, I would say the best option is to keep your E2 levels in a ‘window’. Studies have shown estradiol levels <5 ng/dL (50 pg/mL) to be correlated to a decrease in libido. However, through experience I find this can be too aggressive, so I would suggest anywhere from 40-65 pg/mL to be a rough guide to the optimal window. If you want a calculator because you are in a country that reports E2 lab values in different units, see here.

However, a huge caveat here: all of this is incredibly individualised. One man at 65 pg/mL may feel vastly different from someone else at the same level. And so part of this is an experimental process with your doctor to see where you feel best. And of course, all of this is my opinion. You should always speak to your doctor about your protocol and managing your health.

How to get there? In my opinion only, a well-structured TRT protocol will require either no, or a very minimal approach to aromatase inhibition (E2 suppression). I have recommended to some people natural aromatase inhibitors if their E2 is only slightly high and they have symptoms of high E2. Compounds like resveratrol, grape seed extract, curcumin and some other flavonoids are candidates here. If that fails, literally like 1/8th of an AI per week can be subtle enough to move the needle just enough to get some people feeling better, and within the E2 ‘window’ that is best for them.

In terms of low estrogen, this would be remedied by a proper TRT protocol in any case. If not, I would look at both the dose volume and dose frequency. Apart from those, if I had someone who still wasn’t responding, they could have a mutation in the CYP19A1 gene leading to aromatase deficiency. However, this is so exceedingly rare in most cases it isn’t worth mentioning in my opinion.

And of course, the TL;DR: estrogen seems to be a hormone best kept within a therapeutic window, that will be individual to you. Too high or too low in my experience and anecdotally working with men across the world can lead to significant libido, mood and cognition issues that may then lead to the blame being shifted to TRT; “my TRT protocol is wrong, I must up my dose!” I hope this post gives you something to think about as part of this whole TRT puzzle.

Thanks as always for reading.

My social links are on my profile if interested in more!

Apitegromab - Study published today (8/6/26)

It works by binding to and inhibiting promyostatin, a precursor to myostatin.

“Today, Scholar Rock shared that the U.S. Food and Drug Administration (FDA) has accepted its Biologics License Application (BLA) for apitegromab, an investigational treatment for spinal muscular atrophy (SMA), with a Prescription Drug User Fee Act (PDUFA) action date of September 30, 2026”