NSARMs and other non-steroidal PEDs as a low risk training shortcut

[Vastness]

I am interested in using NSARMS and similar chemicals as a shortcut to increased muscle mass and stamina, ideally with a low to zero risk profile, and was wondering if anyone has any experience doing the same. I did use the search function but did not really find much.

I will be honest, I am basically looking for a shortcut to increased size and strength. I am 28, male, and in generally good health, I eat clean, and already do a lot of high intensity exercise, although mostly cardio with some bodyweight/calisthenics type things thrown in. Every few months I will try to focus on weightlifting a little more for perhaps the same duration (a few months). I know that I am gradually, gradually improving in all areas but I feel like the pace of my improvement has pretty much plateaud. I'm not a professional athlete and I don't know if realistically I will ever compete in any sport I do. I also feel like I am kind of at the limit of how much time I can devote to training. For these reasons, as well as pure vanity and impatience, I have recently been considering chemical aids.

However I am not really interested in using anything steroidal, and the idea that I could permanently fuck up my HPTA by doing such scares me. I also do not see myself injecting anything in the near future. So that rules out the obvious candidates.


From my research so far, Ostarine, LGD-4033, MK-677 and SR9009 seem the most interesting. I think the first 2 however are a little too close to true steroids in their effects, and I have read some reports of people experiencing long term negative effects from them for quite temporary gains. However the latter 2, MK-677 and SR9009, seem to be very benign and with almost no downsides... SR9009 especially - I know this one is not active orally but I have read a few anecdotal reports of sublingual being effective. There seems to also be some debate over whether MK-677, a "growth hormone secretagogue" causes an increased risk of cancer which obviously is potentially worrying.

Anyway, does anyone have experience using any of the mentioned substances, or similar, in pursuit of similar goals?

Does anyone with more knowledge on the topic know if it would be possible for me to do a short "cycle", with perhaps the 2 seemingly safest substances I mentioned (or similar) with, again, almost no risk of fucking up my hormones?

 

[CFC]

As a person looking for a low side-effect profile, your biggest concern here will be the fact that none of these newer research chemicals has had anything like sufficient testing or analysis in humans (and barely on any other lifeform either). If you choose to use them, you're potentially going to expose yourself to various risks that haven't yet been documented. People often turn to these chemicals as 'safer' alternatives to AAS, yet many of the known risks of AAS use are only now coming to light some 70 years after they were first introduced.

As for SR specifically, its use is focused more on those seeking to lose bodyfat rather than gain LBM (rather like cardarine (GW), another of the newer compounds). It appears to enhance mitochondrial density and function, among other effects, which likely improves insulin sensitivity and increases the efficienty of beta-oxidation of fatty acids (one reason they're often combined with injectable carnitine). I've never used it, though I did try GW and didn't find it effective enough to risk using repeatedly.

Ibutamoren (MK-677) does have more research behind it, especially in elderly patients and those with sarcopenia (aged-related muscle loss). As an oral secretagogue of GH (ghrelin-mimetic) it does seem to be a viable alternative to regular injectable GHRPs. From actual blood testing I personally found it to be about as potent at releasing GH as CJC, which is a similar injectable 'bleed-like' releaser of GH, unlike the more pulsatile Mod-GRF/GHRP combos, which stimulate far greater amplitude GH releases.

As for SARMs, you'll want to steer clear of them completely, since their capacity to shutdown the HPTA seems to be more potent than most real AAS, and some are being investigated as the first reliable male contraceptives.

 

[Vastness]

Thanks for your response! Yeah, I guess it is something to consider that a lot of these chemicals have barely any research behind them. I guess I was drawn to them as I also experiment with various novel nootropics of the mental performance variety, as well as various psychoactive RCs, so I figure if I am going to be taking untested substances anyway I may as well take one that can help me to get bigger.

I didn't know that about SARMs being more HPTA-destabilising than AAS, if that's the case I will likely just abandon that avenue entirely.

I guess my next question would be, what other substances are there that have minimal to no side effects, and can be taken orally (or sublingually, or some other kind of mucus-membrane absorption)? I guess I wouldn't completely rule out AAS type substances if there are any that are safe enough. Would taking Ibutamoren on it's own be worth doing?

 

[Vastness]

Would you be able to provide some source for this?

As for SARMs, you'll want to steer clear of them completely, since their capacity to shutdown the HPTA seems to be more potent than most real AAS

...Because this seems counter to a lot of what I've read, which indicates that a lot of SARMS are less suppressing than traditional steroids, although, granted, I am a layperson as far as this stuff goes and I may be looking in the wrong places.

 

[CFC]

...Because this seems counter to a lot of what I've read

Well of course, because the theory promoted by companies working on the largely untested compounds was that SARMs would give all the 'good' effects of AAS with none of the 'bad'. And so online bros took this to mean it wouldn't significantly affect gonadotrophin levels either - until repeated blood work analyses demonstrated the suppressive impact on LH and FSH.

Quite why it was assumed compounds that - by their nature - are designed to activate androgen receptors would not cause hypogonadism isn't obvious - particularly as the original researchers never made that claim (admittedly newer ones have, but they're not 'researchers' in the traditional sense, rather mostly Chinese companies simply trying to cash in on the SARM bandwagon). Hypogonadism isn't really an issue when your target population is already largely hypogonadic and SARMs are intentionally designed as a less androgenic and more convenient oral replacement therapy for testosterone.

If you've done some researching, you might also note that many of the early papers on SARMs were full of promise and requesting follow-ups with human trials and longer-term studies. Many of those latter-stage trials for the early batch would have completed between 2007-2013. The complete absence of their publication implicitly suggests that those trials didn't work out very well. Either the SARMs were causing too many side-effects, or were not significantly superior (or just inferior all-round) to regular AAS treatments to warrant further development.

Given that, there's not enough solid research out there. You can find some info reading through the full results of some of the earlier papers where they did bother to examine the effect on the HPTA. Aside from that, these following papers should give you a pretty decent idea:

https://www.ncbi.nlm.nih.gov/pubmed/18772237

In intact male rats treated for 14 d, S-23 alone suppressed LH levels by greater than 50% at doses greater than 0.1 mg/d, with corresponding decreases in the size of the prostate but increases in the size of levator ani muscle. In intact male rats treated for up to 10 wk with S-23 and estradiol benzoate (necessary to maintain sexual behavior in rats), S-23 showed biphasic effects on androgenic tissues and spermatogenesis by suppressing serum concentrations of LH and FSH

https://www.ncbi.nlm.nih.gov/pubmed/16099859

S-4 (3 and 10 mg/kg) also demonstrated agonist activity in the pituitary and significantly decreased plasma LH and FSH levels in castrated animals in a dose-dependent manner.

https://www.ncbi.nlm.nih.gov/pubmed/15347734

Gonadotropin levels in C-6-treated groups were significantly lower than control values. C-6 also significantly decreased serum testosterone concentration in intact rats after 2 weeks of treatment. Marked suppression of spermatogenesis was observed after 10 weeks of treatment with C-6 in intact male rats.

https://www.ncbi.nlm.nih.gov/pubmed/22459616

LGD-4033 administration was associated with dose-dependent suppression of total testosterone, sex hormone-binding globulin, high density lipoprotein cholesterol, and triglyceride levels. Follicle-stimulating hormone and free testosterone showed significant suppression at 1.0-mg dose

https://www.ncbi.nlm.nih.gov/pubmed/19017848

LGD-3303 suppresses serum LH to eugonadal levels. In no case did LGD-3303 restore LH, prostate, or preputial gland weights.

If you're really keen to use a PED with a lesser side-effect profile, you may want to start researching the oral AAS Anavar (oxandrolone), which has very few androgenic side-effects and is probably easier to recover from than most SARMs.

 

[Vastness]

Thanks for such an informative answer! I think I will definitely be staying away from SARMs then. I did look into Oxandrolone, and it sounds interesting with minimal sides, BUT I did read a few places that some people consider it to be not too useful for bulking, only for cutting, as the effects are fairly "mild"... would you agree? Additionally I see some people recommending to take it with testosterone which I would prefer not to do, partly because of an aversion to injections and partly because of a desire to take as few substances as possible initially.

I am still quite interested in MK-677 also, I read a few studies and it seems to be well tolerated with minimal sides. BUT I did also read a report of someone developing early stage gynomasteia (sp?) with MK-677 alone, which apparently is highly unusual but maybe 1% of the population are prone to this from a short term rise in prolactin levels. Any way to avoid this?

Anyway, I formulated a preliminary cycle idea for myself which I hope is a reasonably sensible one, if a little cautious (too cautious?), and is based on a conglomeration of doses used in the studies I read and other sources. For reference, I currently weight 76kg, I haven't measured my body fat percentage although I guesstimate it to be around 15%, maybe just under.


For 6 weeks on cycle:
25mg MK-677
25mg Oxandrolone (increasing 5mg/week thereafter)

4 weeks PCT: (Is a PCT even necessary here?)
20mg Tamoxifen (is this the best choice? My research so far on PCT is minimal at best but this seems to be widely recommended)

 

[Genetic Freak]

Thanks for such an informative answer! I think I will definitely be staying away from SARMs then. I did look into Oxandrolone, and it sounds interesting with minimal sides, BUT I did read a few places that some people consider it to be not too useful for bulking, only for cutting, as the effects are fairly "mild"... would you agree? Additionally I see some people recommending to take it with testosterone which I would prefer not to do, partly because of an aversion to injections and partly because of a desire to take as few substances as possible initially.

I am still quite interested in MK-677 also, I read a few studies and it seems to be well tolerated with minimal sides. BUT I did also read a report of someone developing early stage gynomasteia (sp?) with MK-677 alone, which apparently is highly unusual but maybe 1% of the population are prone to this from a short term rise in prolactin levels. Any way to avoid this?

Anyway, I formulated a preliminary cycle idea for myself which I hope is a reasonably sensible one, if a little cautious (too cautious?), and is based on a conglomeration of doses used in the studies I read and other sources. For reference, I currently weight 76kg, I haven't measured my body fat percentage although I guesstimate it to be around 15%, maybe just under.


For 6 weeks on cycle:
25mg MK-677
25mg Oxandrolone (increasing 5mg/week thereafter)

4 weeks PCT: (Is a PCT even necessary here?)
20mg Tamoxifen (is this the best choice? My research so far on PCT is minimal at best but this seems to be widely recommended)

Anavar is like any hormone, it can be used to hold on to muscle mass as part of a cut, or as part of a bulk, the only thing that changes is calorific intake.. (don't believe everything you read on popular steroid boards)..
We first used anavar back in 1983 at a max of 25mg/day for 6 weeks, tapering up and tapering down.. (very conservative by today's standards)..

You won't need PCT, we didn't need it 34 years ago, neither should you now....

 

[Serotonin101]

^^would you recommend taurine ran with it to hopefully prevent or minimize shutdown? I believe you posted studies of it showing it helped with deca shutdown which is far more than what anavar would yield.

 

[Vastness]

We first used anavar back in 1983 at a max of 25mg/day for 6 weeks, tapering up and tapering down.. (very conservative by today's standards)..

You won't need PCT, we didn't need it 34 years ago, neither should you now....

That's interesting, and I thought I was being conservative! Would you mind going into a little more detail about what the taper would look like? What dose would you start and finish on, and how quickly would you go up and down?

I assume with tapering, this is what removes the need for a PCT? But still, wouldn't it be advisable to have something on hand in case, during the cycle, I turn out to be prone to gyno? Would Tamoxifen be suitable for this?

I have more questions but am on my phone and already lost my first attempt at this post, so I will leave it there for now, but thank you in advance for any help you can provide!

 

[Genetic Freak]

That's interesting, and I thought I was being conservative! Would you mind going into a little more detail about what the taper would look like? What dose would you start and finish on, and how quickly would you go up and down?

I assume with tapering, this is what removes the need for a PCT? But still, wouldn't it be advisable to have something on hand in case, during the cycle, I turn out to be prone to gyno? Would Tamoxifen be suitable for this?

I have more questions but am on my phone and already lost my first attempt at this post, so I will leave it there for now, but thank you in advance for any help you can provide!

The taper we used was 15mg - 20mg - 25mg - 25mg - 20mg - 15mg Off..

Anavar isn't known for its aromatisation properties, therefore negates the need for SERM's or AI's..

Putting things in perspective, you are looking at doses from 105mg - 175mg/week... Compared to popular steroid boards recommending 500mg+/week as a starting dose..
You don't need PCT on 6 weeks anavar...

As previously stated, include 3-5g taurine a day for healthy testicular function...

 

[CFC]

I think I will definitely be staying away from SARMs then

Just to clarify, I'm not saying SARMs don't have their place. The point I was making is simply that (a) there's lack of research and (b) what research we have proves they cause HPTA shutdown, just like regular AAS. So from the perspective of low risk, we can't say they're a safer alternative, either on this issue or others. Meanwhile, we do know more about oxandrolone, and it has been proven to be relatively benign in women and children.

 

[RedLeader]

CFC, GF, etc...If you guys are arguing against popular opinion and saying no PCT and just a two week taper of test e/c following a mild first AAS cycle, I'm guessing you'll say no SERMs at all, nor an AI, at the end of a SARMs cycle? Assuming the answer is no, would the SARM(s) be tapered at the end? In the spirit of HR, I know your risk/reward argument against SARMs.

 

[Genetic Freak]

CFC, GF, etc...If you guys are arguing against popular opinion and saying no PCT and just a two week taper of test e/c following a mild first AAS cycle, I'm guessing you'll say no SERMs at all, nor an AI, at the end of a SARMs cycle? Assuming the answer is no, would the SARM(s) be tapered at the end? In the spirit of HR, I know your risk/reward argument against SARMs.

I would say our argument is promoting current research to opposed popular bro'science..

With test-e/c, in conjunction with a taper minimal use of an AI has been advised (dose dependent obviously) to lower estrogen end of cycle as exogenous testosterone levels decline also..
We know estrogen metabolizes at a slower rate than testosterone therefore it seems prudent to add an AI to avoid A:E ratio to elevate in favor of estrogens..

Regarding SARM's they are a bit new-school for me, so can't comment Sorry...

 

[CFC]

To add to what GF has already said, the point I've made repeatedly is that PCTs don't appear to improve long-term recovery, particularly in cases of primary hypogonadism, and this is not just an anecdotal observation, we have some decent studies of large numbers of men pointing to this poor recovery now.

And most guys following a sensible low-dosed AAS cycle don't appear to suffer from secondary hypogonadism anyway (in other words less harm is caused to the hypothalamus and pituitary on low doses). LH and FSH levels typically return to baseline quite rapidly for most guys who haven't harmed that part of the axis.

Meanwhile you can use potent antioxidants and/or AIs to either (a) neuter free radicals or (b) inhibit the build up of oestrogens that lead to the oxidative cascade that's implicated in the causation of primary hypogonadism during a cycle. Whether this is an issue on SARMs is an issue for debate, partly because we have so little research on them, and because they don't directly cause E2 build-up (directly being the key word, because like with winstrol or other supposedly non-aromatisable AAS, they may indirectly do so).

Therefore it's hard to see what utility most PCT drugs have on your average androgen cycle - be it SARMs or 'normal' AAS (and frankly since SARMs are AAS in all but name and structure, the distinction is ridiculous and mostly a marketing scam).

Many will say "ah, but I had my test levels taken after my PCT and it showed I'd recovered," and I will say (a) you have no idea whether you would simply have recovered anyway, with or without PCT (because if you want to trade anecdotes, this is what I've found repeatedly over the years with hundreds of guys), and (b) have a blood test in a few weeks, and watch your levels crash again.

And if you thus need to use SERMs or AIs continuously post-cycle in order to maintain normal levels of LH/FSH or test after a cycle (because otherwise levels drop again), then clearly that is not recovery and the term PCT is meaningless.

As for tapering down/off, I say it not particularly because of recovery of the HPTA. Even with abysmally low levels of androgens, you can hold on to plenty of muscle. The point about tapering is to enable the body to adjust to a less anabolic environment without the shock of going cold-turkey. Homeostatic physiological systems take a while to kick into a new equilibrium, so tapering buffers the shock a little. Because it is the change that leads to muscle loss, in exactly the same way as it can cause our desired muscle gains.

 

[Genetic Freak]

To add to what GF has already said, the point I've made repeatedly is that PCTs don't appear to improve long-term recovery, particularly in cases of primary hypogonadism, and this is not just an anecdotal observation, we have some decent studies of large numbers of men pointing to this poor recovery now.

And most guys following a sensible low-dosed AAS cycle don't appear to suffer from secondary hypogonadism anyway (in other words less harm is caused to the hypothalamus and pituitary on low doses). LH and FSH levels typically return to baseline quite rapidly for most guys who haven't harmed that part of the axis.

Meanwhile you can use potent antioxidants and/or AIs to either (a) neuter free radicals or (b) inhibit the build up of oestrogens that lead to the oxidative cascade that's implicated in the causation of primary hypogonadism during a cycle. Whether this is an issue on SARMs is an issue for debate, partly because we have so little research on them, and because they don't directly cause E2 build-up (directly being the key word, because like with winstrol or other supposedly non-aromatisable AAS, they may indirectly do so).

Therefore it's hard to see what utility most PCT drugs have on your average androgen cycle - be it SARMs or 'normal' AAS (and frankly since SARMs are AAS the distinction is ridiculous and mostly a marketing scam).

Many will say "ah, but I had my test levels taken after my PCT and it showed I'd recovered," and I will say (a) you have no idea whether you would simply have recovered anyway, with or without PCT (because if you want to trade anecdotes, this is what I've found repeatedly over the years with hundreds of guys), and (b) have a blood test in a few weeks, and watch your levels crash again.

And if you thus need to use SERMs or AIs continuously post-cycle in order to maintain normal levels of LH/FSH or test after a cycle (because otherwise levels drop again), then clearly that is not recovery and the term PCT is meaningless.

As for tapering, I say it not particularly because of recovery of the HPTA. Even with abysmally low levels of androgens, you can hold on to plenty of muscle. The point about tapering is to enable the body to adjust to a less anabolic environment without the shock of going cold-turkey. Homeostatic physiological systems take a while to kick into a new equilibrium, so tapering buffers the shock a little. Because it is the change that leads to muscle loss, in exactly the same way as it can cause our desired muscle gains.

Wonderful post again CFC.. It's an awful shame you don't see informative information like this regarding PCT/recovery on other forums..

 

[CFC]

Thanks mate. I think for many guys who aren't convinced of the need for PCT, there's still a sense of "well I might as well anyway, just to be sure" and I can appreciate that. But I'm not going to recommend something - particularly something that unsurprisingly makes some people extra money - if all the arguments in favour are mostly hollow or based on a flawed understanding of the problem. Sometimes the PCT costs as much as the cycle itself these days lol.

 

[Genetic Freak]

Thanks mate. I think for many guys who aren't convinced of the need for PCT, there's still a sense of "well I might as well anyway, just to be sure" and I can appreciate that. But I'm not going to recommend something - particularly something that unsurprisingly makes some people extra money - if all the arguments in favour are mostly hollow or based on a flawed understanding of the problem. Sometimes the PCT costs as much as the cycle itself these days lol.

Therein lies the answer...

 

[RedLeader]

I think that a lot of people fear losing their gains (clean gains, not water weight from something like dbol) if they don't run PCT. Now under the assumption that muscle can be preserved on a tiny amount of androgens, can we say that the discussion of how to preserve muscle post-cycle is independent of the PCT debate?

 

[CFC]

Someone said to me that PCT could still act as a buffer to falling test levels once exogenous AAS levels are fully depleted. True (partially and potentially). Unfortunately that's like closing the gate after the horse has bolted. You're going to lose most muscle during the immediate post-cycle phase when levels are plummeting fastest. And as already stated, that assumes the PCT is doing something that wouldn't just happen naturally anyway (*LH/FSH rebound).

It's thus more sensible to buffer by slowly tapering exogenous AAS levels down to physiological levels/TRT and then coming off. At which point, your own natural production (whether forced with PCT or natural) won't be so different from the end of your taper and will soon match or exceed what you came off at.

 

[Gratefulchicken]

Late to the party but do either of you two have bloods from pre/during/post cycle with and without pot??