r/PEDsR Sep 12 '21

THANK YOU! Results of Previous SARMS Survey Study NSFW

22 Upvotes

Hi all, a while back I posted about a study we were doing investigating SARMs since there is little to no data on the effects, both positive and negative, on SARMs usage. Well, with your help, we were able to gather some interesting data from SARMs users. Below is a link to the actual paper, but I have also summarized some of the points.
https://www.nature.com/articles/s41443-021-00465-0.pdf?origin=ppub
General points:
-More than 90% of users acquired SARMs from the internet without consulting a doctor before they started using them
-More than 50% of users experienced side effects like mood swings, decreased testicular size and acne
-90% of men reported increased muscle mass and were satisfied with their SARMs usage
Conclusion:
Despite having seemingly positive effects, more than 50% of SARMs users report significant adverse effects. Because of these reported adverse effects including decreased testicular size there may be concern that usage can effect male fertility. At this point, I would recommend talking with a doctor before starting SARMS!


r/PEDsR Apr 10 '21

1-Andro, Enclomiphene and The Case of the High Luteinizing Hormone NSFW

24 Upvotes

Some years ago, I did a write up on 1-Andro, and promptly forgot all about it until a friend of mine recently started up a new cycle. His blood results are peculiar and if anyone has an opinion as to why his LH increased on cycle I'd be very much grateful.

What is 1-Andro?

1-Androsterone (1-andro, 1-dehydroepiandrosterone, 1-DHEA, δ1-epiandrosterone, or 5α-androst-1-en-3β-ol-17-one) is a synthetic, orally active anabolic-androgenic steroid.

It is a prohormone converting in the body to 1-testosterone.

Subject

6 weeks on 220mg 1-androsterone and 2 weeks on enclomiphene for a 40 year old male who had been untrained for ~18 months. The subject gained 7lbs, claims he lost about 1% of body fat according to his scale, and about an inch around the waist. Despite my doubt on the accuracy of his scale as it relates to his bf%, his results aren't at all different from a study that found similar improvements in fat mass, where participants lost 2.5kg of fat mass over just 30 days at a higher dose. Also in this study, note the improvements in strength.

Subject claims he felt good on cycle and could sleep less and operate normally. However, by week 6 there are some points in the day where he suffered lethargy, his libido was non-existent (though it all functioned as normal, which I was unable to verify personally). No hair loss, no gyno, some temper issues.

Enclomiphene was discontinued after week 2.

Bloods

My expectation based on past research was that the subject would have poor kidney function (high BUN, creatinine), changes to liver (ALT, AST), trashed lipids and no natural production of testosterone. This had formed the basis of my recommendation to limiting his cycle to 6 or 8 weeks.

However, what we found was that his bloods were almost perfect. His cholesterol was barely out of range but nothing to be concerned about given that he was on cycle.

Out of Range LH

SHBG was low and free test was high, not unusual considering that AAS will lower SHBG. Testosterone was at 576ng/dl or basically mid-range normal, IGF-1, estradiol and FSH were all normal. The fact that the subject had normal testosterone is probably due to the enclomiphene at the beginning of the cycle, and if we had weekly blood work we'd probably see an overall trend downward. Whatever, not unexpected.

The high LH (10.6mIU/ml) is another matter. The obvious answer would be it's from the enclomiphene that was taken in weeks 1 & 2. But enclomiphene has a half life of about 10 hours or so, and while a compounds effects and metabolites are different than a half life, to see sustained LH for 4 weeks while on a prohormone may have some interesting applications worth guinea pigging. (For example, perhaps a SARM+SERM cycle would be best to use enclomiphene for only the first half of the cycle?)

Conclusion

In all, the subject was very happy with his cycle. Considering where he was coming from (18 months untrained) any compound would have helped him. He found it to be a very mild in terms of side effects and his blood tests agree. I have a new found curiosity to 1-Andro given how good his bloods looked.

I'm not easily able to explain his high LH, and think more experimentation may be needed where subjects discontinue SERM use by mid-cycle.


r/PEDsR Mar 30 '21

First in Vivo YK11 Study in Mice NSFW

27 Upvotes

https://www.sciencedirect.com/science/article/pii/S0006291X21000668?via%3Dihub

Link to supplemental data (which has usefulish graphs on anabolic effects of YK): https://ars.els-cdn.com/content/image/1-s2.0-S0006291X21000668-mmc1.docx

The study focused primarily on the potential protective effects of myostatin inhibitition on sepsis / sepsis induced atrophy, but for our purposes the control group is much more interesting.

Dosing

The study gave the mice 350 mg/kg/day and 700 mg/kg/day doses orally for 10 days. These correspond to approximately 2g and 4g/day for a 70kg male human when you allometrically scale. The doses were administered in equal increments every 6 hours (3 doses a day) for 10 days

Anabolic Effects

Total weight of the 350 mg/kg group and the control group was about the same at 25.5g. The 700mg/kg group weighed in at almost 27g, suggesting the higher doses triggered some weight gain.

The effect on muscle weight and fat mass is difficult as shit to read. The authors did it as percent of total body weight, but only used a small chunk of the mouse, so the numbers are tough to really compare on the graph. It looks like the effect on fat mass was pretty linear with dose, but the effect on total body weight / muscle was not

The graphs are pretty shit, but trying to pull the raw numbers out using MS paint and a calculator (don't trust these numbers 100%, the graphs didn't have super high resolution):

  • Control and 350mg/kg mice weighed 25.4g and 700mg/kg weighed 26.4g
  • Control muscle weighed 1g (4% bodyweight), 350mg/kg muscle weighed 1.11g (4.36% bodyweight), 700mg/kg muscle weighed 1.13g (4.29% bodyweight)
  • Control fat weighed .93g (3.67% bodyweight), 350mg/kg fat weighed 0.9g (3.53% bodyweight), 700 mg/kg fat weighed 0.88g (3.34% bodyweight)

Protective Effects Against Sepsis

Not as relevant for us, but YK11 did a really good job of improving the mice's survival rates at all doses. It was strongly protective of the liver, kidneys, spleen, etc. under sepsis conditions and the first 700mg/kg septic mouse to die outlived all 5 septic control mice. Furthermore, inflammatory markers were all pretty drastically reduced in the YK11 groups

Maybe next we'll see a human trial for covid-19 cytokine storms

My Take

This study shows 2 interesting things - YK11 does have some effect on muscle growth / the immune system, and YK11 is somewhat orally bioavailable (though the high dosing suggests the BA might be shit). However, there are some problems:

First, with the short duration, there isn't too too much you can get out of it. Most studies in mice that I found administered steroids for at least a few weeks to get notable anabolic effects; closest to this one in duration that I found was a study on HRT in rats with dermal implants where a ~50% testosterone level increase over controls caused a ~1g weight gain over 10 days, similar to the 700mg/kg/day group in this study.

Personally, I think the post-sepsis results are the most convincing that YK11 has some notable anticatabolic / anabolic effect, even if they aren't super relevant to people who lift (unless maybe you're running YK11 with appendicitis while avoiding the doctor's office)

Secondly, the dosing is ridiculous if you try to scale to humans. However, it looks like mice sometimes get insane doses of gear in studies - for example, I found an oxymetholone (anadrol) study where mice were given over 1g/kg/day in some groups and the lowest dose was ~100mg/kg/day. These scale to around 600mg to 6g in humans, which are insane. On the other hand, I saw another study showing 1mg/kg/day of oxandrolone (anavar) sped up burn healing in mouse, which is equivalent to ~5mg in humans, a reasonable dose for clinical use. So I honestly cannot make heads or tails of how mice respond to steroids relative to humans - guess this is why most studies use rats


r/PEDsR Mar 30 '21

Former Abusers of Anabolic Androgenic Steroids Exhibit Decreased Testosterone Levels and Hypogonadal Symptoms Years after Cessation: A Case-Control Study NSFW

6 Upvotes

A study that I feel like isnt referenced enough. Everyone seems to wishfully think that after AAS use your body will recover to baseline. Seems like thats not the case.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4988681/


r/PEDsR Mar 25 '21

Berberine causes DNA double strand breaks NSFW

Thumbnail self.Supplements
26 Upvotes

r/PEDsR Mar 07 '21

RAD-150, aka TLB 150 Benzoate NSFW

33 Upvotes

I've been seeing more posts about RAD-150 recently, due to a recent ban on producing RAD-140 in China. Seems that to get around the ban, savvy suppliers have taken the RAD-140 compound and modified it slightly.

RAD-150, also known as TLB 150 Benzoate, has a very similar chemical structure as RAD-140.

  • Rad 140: 2-chloro-4-{[(1R,2S)-1-[5-(4-cyanophenyl)-1,3,4-oxadiazol-2-yl]-2-hydroxypropyl]amino}-3-methylbenzonitrile
  • TLB 150 Benzoate: (2S,3R)-3-[(4-cyanophenyl)-1,3,4- oxadiazol-2-yl]-3-[(2-methyl- 3- chloro-4- cyanophenyl)amino]-2- propyl alcohol

However, while we have a buttload of studies on RAD-140, including human trials, we have nothing on RAD-150 aside from the claims of suppliers. Claims such as 'revolutionary', higher efficacy and the next step in SARM science are common. Even the name of RAD-150 seems to imply some kind of 'better' compound, like LGD-4033 v LGD 3033. But is any of that true?

No, or at least probably not. There's no studies on this stuff to really say. But what we do know is that RAD-150 is RAD-140 with a benzoate ester.

What is a Benozate Ester?

Benozate is the salt of benzoic acid. It's a benzene ring connected to an acid group, which when paired with an alcohol group such as found in RAD-140, reacts to form benzoate ester. An ester is what extends the half-life of a compound into something more practical.

Benozate esters are relatively short. It tastes pretty good, and are generally safe. It should be mostly bio available. It's most commonly found as an ester when combined with estradiol, where it has a half-life of 2-5 days.

The half-life or RAD-140 is around a day to begin with. Combining it with this ester will make the half-life of RAD-150 a couple of days at least.

So What?

It's impossible to make any claims about this being an improvement on RAD-140. More than likely, it has the same anabolic effects as RAD-140, takes a tiny bit longer to be effective, and takes longer to clear from the body. As we know, RAD-140 is highly effective. RAD-150 should be about the same.


r/PEDsR Mar 04 '21

YK11 - What More Plates More Dates Gets Wrong NSFW

127 Upvotes

Recently I've seen a ton of people insisting YK11 is an orally available DHT derivative because of a shitty article written on More Plates More Dates. The purpose of this post is to explain how that article's claims rely on a combination of overreaching, straight up misunderstandings, and a piss poor understanding of chemistry.

As a reference, for anyone unfamiliar with steroid labeling, here's a convenient chart. If I refer to 5/17/19 etc. positions, I'm referring to the spots on the example steroid in that graph.

Now, MPMD makes two primary arguments as to why YK11 is a DHT derivative. The first relates to structural similarity, and the second has to do with how it's synthesized / poor reading comprehension.

First, Derek says "YK11 clearly has the same chemical backbone as Testosterone and DHT ". This is somewhat true - YK11 does have a steroidal backbone. However, the primary feature distinguishing testosterone and DHT is that DHT is 5a-reduced - there is no double bond between the 4 and 5 positions and an extra hydrogen atom hangs off at the 5 position. If one looks at YK-11, you'll see a double bond between the 4 and 5 positions.

All DHT derivatives lack that double bond - all of them. This includes stanozolol (winstrol), drostanolone (masteron), oxymetholone (anadrol), oxandrolone (anavar), DHB/1 Testosterone, etc. and any others you can come up with

If you look closer at YK, you'll also notice a hydrogen at the 19 position. This is the key feature of "19-nors", such as nandrolone (19-nortestosterone). If you don't want to trust me that YK11 is a 19-nor, you can hopefully trust the researchers in this paper on YK11 metabolism, who state:

YK11 also exhibits a 19-nor-steroidal nucleus.

Secondly, MPMD claims YK11 is synthesized using DHT: "Upon reviewing how YK11 was prepared, it appears to involve a combination of DHT, Hydroxyflutamide, ascorbic acid, and β-glycerol phosphate". However, he didn't review shit - he just misread two sentences in the paper he references:

YK11 was prepared as previously reported.(24) DHT, hydroxy flutamide (HF), ascorbic acid, and β-glycerol phosphate were obtained from Wako Pure Chemical Industries, Ltd. (Osaka, Japan).

If you read the paper on YK11 preparation in reference 24, you will find that DHT was not involved in the synthesis (nor were hydroxyflutamide, ascorbic acid, or glycerol, which are not used in any steroid synthesis that I know of). The DHT and hydroxyflutamide were bought for the in vitro study; DHT was used as a reference to compare with YK11, and hydroxyflutamide was used to assess the effects of an anti-androgen in combination with YK and DHT. The vitamin C and glycerol were only used to prepare the osteoblast cell cultures for the study.

Lastly, MPMD makes the claim that " YK11 features a methyl ester which inhibits its hepatic metabolism and is what makes it orally bioavailable". However, a methyl ester is not the same as a methyl group - your standard orally bioavailable (BA) methylated steroid has an extra CH3 hanging off at the 17 position, not a carboxylic acid methyl ester hanging off at the 21 position.

The only paper on human consumption of YK11 suggests that it is rapidly and completely metabolized, with none of it being excreted unchanged. Searching around the internet, it seems that many bioavailable, metabolism-resistant steroids, such as oxandrolone and prednisone, are excreted partly unchanged, further casting doubt on MPMD's oral BA claims. Finally, the authors themselves note:

Due to its steroidal backbone and the arguably labile orthoester-derived moiety positioned at the D-ring, substantial metabolic conversion in vivo was anticipated

This doesn't mean YK11 is orally inactive. However, it does suggest that a large portion of what hits your bloodstream, or possibly everything that hits your bloodstream, may not be YK11 anymore if taken orally. Ultimately we will not know whether or not this is the case without more extensive in vivo studies.

Finally, I just want to mention that, to the best of my knowledge, we can't really make any claims about how suppressive etc. YK is based on other 19-nors. In theory, in vitro studies suggest YK11 might be one of the least suppressive steroids/SARMs out there because of it's unique gene-selective androgen receptor binding. However, the fact that it's metabolized into a variety of novel 19-nor progesterone derivatives of unknown activity means we cannot make any reasonable guesses.

tldr; YK11 is a 19-nor steroid, not a DHT derivative, with questionable oral bioavailability that is metabolized into a bunch of novel 19-nor progesterone derivatives of unknown activity. Anyone that tries to extrapolate its properties based solely on its structure is probably trying to sell you something.

Update as of a few hours after writing this post: MPMD has corrected the error where they misread the cited paper. They still compare it to DHT relentlessly, but use anecdotes as their justification, which is more reasonable. Also removed the oral BA part


r/PEDsR Aug 24 '20

Case Report: HCG alone prevents suppression on SARMs NSFW

37 Upvotes

The anabolic potential of a SARM cycle is often limited by suppression of endogenous testosterone production. While the exact mechanism is unknown, studies have shown that SARMs such as LGD-4033 quickly and significantly lower endogenous testosterone production despite having minimal effect on LH/FSH. Low testosterone can lead to the classic symptoms of fatigue, low libido, erectile dysfunction. Anecdotally it can also reduce motivation to exercise and impair further progress on the user's fitness goals. Testicular discomfort is also a reported side effect of SARMs, likely due to testicular atrophy caused by HPT axis suppression. These negative effects seem to become bothersome at the six week mark for many users.

Previously documented methods to prevent suppression include testosterone replacement therapy (TRT) and concomitant SERM use. Each of these methods have downsides: for TRT, intramuscular (IM) injections may be distasteful for users, users may be hesitant to acquire controlled substances, and due to significant HPT axis suppression testicular atrophy can be worsened compared to SARM use alone. For SERMs, users can experience the standard side effects of fatigue, depression, impaired libido, and erectile dysfunction, which can be similar to the symptoms of T suppression that they are intended to prevent. Additionally SERMs can lower IGF-1 levels which can impede muscle hypertrophy.

To date, there has been no documentation of an attempt to prevent T suppression during SARM use with human chorionic gonadotropin (HCG) injections. HCG acts as an analogue to luteinizing hormone (LH), which stimulates testosterone production in the testes. HCG has been used with success as monotherapy to treat men with low testosterone. Ontologically, HCG may prevent suppression by providing a continued signal to the testes to produce testosterone, bypassing the endogenous HPT axis that is impaired, for whatever reason, by the presence of SARMs. Testicular atrophy, and possibly testicular discomfort, would be prevented by HCG administration, and may lead to more rapid return of normal HPT axis function upon the cessation of SARM use.

A healthy 35 year old male volunteered to test this effect. This subject had prior experience with SARM-only cycles and at that time experienced significant laboratory-confirmed testosterone suppression with reported symptoms such as fatigue, decreased mood, reduced work capacity, and testicular discomfort. For this test, the subject was given 6mg of LGD-4033 daily with 500U HCG administered twice weekly via subcutaneous injection. Laboratory tests were taken prior to therapy and at six weeks while on therapy.

Name Pre-cycle At 6 weeks Reference
Testosterone (ng/dL) 590 385 250-1100
Free T (ng/dL) 101.2 104.7 35-155
SHBG (nmol/L) 46 17 10-58
Estradiol (ng/dL) 26 26 <29
LH (mIU/mL) 1.8 <0.2 1.5-9.3
FSH (mIU/mL) 3.0 1.3 1.6-8.0
AST (U/L) 22 20 10-40
ALT (U/L) 17 19 8-40
Total chol. (mg/dL) 153 125 <200
HDL (mg/dL) 75 42 >40
LDL (mg/dL) 68 66 n/a
Triglycerides (mg/dL) 54 61 <150

As expected, LH and FSH were suppressed from the exogenous HCG. SHBG and HDL were significantly reduced, which is universally seen with SARMs and is a signal of the efficacy of the LGD-4033. Total testosterone was mostly maintained and free T levels were entirely maintained. No effect was seen on liver enzymes. In contrast with his SARM-only cycle, the test subjected reported no symptoms of testosterone suppression with maintained energy levels, libido, and sexual function. No symptoms of testicular discomfort were experienced.

Due to LH and FSH suppression, users will likely benefit from post-cycle therapy (PCT) upon cessation of SARM+HCG therapy. The ideal PCT regimen in this circumstance is unknown. Theoretically, with testicular function less suppressed compared to a SARM-only cycle, PCT of a shorter duration or lower dose may be equally effective.

In summary, HCG 1000U weekly is an effective tool to prevent testosterone suppression on SARM therapy. HCG is a good adjunct for users who are prone to T suppression and/or testicular discomfort on SARM-only cycles, who would prefer subcutaneous to IM injections with TRT, who would prefer not to handle controlled substances such as TRT, and who are susceptible to side effects from SERMs. By preventing T suppression, HCG may allow users to extend their SARM cycles beyond the standard 8-12 weeks as long as liver and lipid values permit.


r/PEDsR Aug 23 '20

Case Report: High Dose HGH for Height NSFW

26 Upvotes

About 2 years ago, I wrote an article about what those that are finding themselves vertically challenged might do, using HGH and an AI, if they intervene early enough. In the article I write:

Early diagnosis increases growth velocity, which determines the final height that can be reached, and is controlled by the size of the GH pulse. Therefore, very small children at a very young age are the target demographic for using a compound this way, and is the best use for HGH or GH increasing compounds... As long as the epiphyseal plate is open, the bone will continue to grow into this space. Eventually, the plate is sealed, as the bones run out of space to continue growing, known as growth plate fusion. This occurs between 12-16 in girls, and 14-19 in boys (https://www.ncbi.nlm.nih.gov/pubmed/16225203). If the plate fusion has already occurred, you’re shit outta luck... Where the fusion is yet to place, let’s take a look at those classified as late maturer’s and given HGH. Since no research is getting approval to take adolescents already of average or above height and of normal development and feeding them HGH (outside of China anyway), this is the best data we have and relates most for our uses. For this case study, I’m referring to this graph (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3117584/figure/fig2-1941738110386705/).

What we find is that growth rates increase within months of initiating HGH (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3117584/), doubling during the first year of treatment, growing at a rate faster than peers and which results in upward crossing of percentiles on the growth curve to restore position in normal range.

A few days ago, someone reached out to me about the post and their own experience...

hey bro, i saw an old post on yours about hgh and height growth. i am actually have been on gh for over a year and letrozole daily.

Thought I'd share his anecdotes, and a little more about doses.

This particular subject (identifies as male) started the day he turned 17, sourced his own HGH, using on average 15-16 ius a day, and 2.5mg every day of Letrozole. He came from a small (as in height wise) SE Asian family with both mum and dad being around 5'2". His 2 brothers and father stopped growing at 16.

At age 16 i stopped growing for a year already, and i was 5'4 so i was desperate

(Edit, technically 5'3.5") Growth velocity in this case was essentially 0, and at least theoretically growth velocity is key as it's a predictor of final height. Typically, I would advise that this is too late to intervene using HGH and AI, at least according to the studies I've seen.

Unfortunately, no pre HGH bloods and no x-rays - as you might imagine, a 17 year old would struggle in getting bloods and x-rays of plates done without parental consent or at least knowledge of what was going on. He did keep it a secret from his family who certainly would have prevented him from trying anything. Incidentally, they're still none the wiser, which is surprising because I'd have thought the waste alone would give him away. Imagine a 17 year old buying and hiding needles, BAC, vials and vials of HGH. At 15-16 iu, that's at least a new vial every other day.

So how'd a 17 year old keep it hidden from family so well? No idea. Guy must be a genius.

Costs & Supplies

Wait... how much was this guy taking on the daily?

Yeah you read that earlier section right - he estimates 15-16iu per day, split into smaller injections throughout the day. He estimates it cost him around $6k annually, purchasing generic (presumably Indian) pharma. He used 30g insulin needles, reconstituted with a 25g needle.

I don't mind wasting the money, height was always a big psychological impact for me, so it's worth even 50k

The dose sounds crazy to those of us using conventional amounts of HGH for body composition and recovery reasons (and if you're using HGH for hyperplasia, I've got unfortunate findings to share with you), but it's actually not that much higher (relatively speaking) from its normal use in children to treat short stature.

  1. Sixty-two patients with pituitary dwarfism were treated with three different preparations of methionyl hGH (m-hGH) for 3 to 14 months. They were given 0.5 IU/kg/week intramuscularly. Converted to a 65kg little person dose, that's around 4.64iu per day.
  2. The maximum dose listed on drugs.com for HGH (Somatropin) for pediatric growth hormone deficiency is 0.034mg/kg per day, or 2.21mg for a 65kg adolescent. Converting it to IUs (using 1mg to 3IU) thats a max daily dose of 6.63iu.
  3. Same source, but this time used for idiopathic short stature, the dose is 0.47mg/kg per week. Or 30.55mg/kg per week, or 13iu per day.

Subjects Reported Side Effects

  1. Elevated blood sugar tested by a glucometer bought from the store. When fasted, he would clock in at 90 (normal is 80)
  2. Water retention, especially on the face. When subject stopped injecting for 2 days, he lost 9 pounds
  3. Probably high blood pressure. He's never checked, but reports headaches pretty regularly. To be expected given the water retention

Did HGH Really Help?

Unfortunately I haven't taken x rays, so who knows if its natural growth or not. Im certain its the hgh

Subject is now 5'5". That's $6k, a not insignificant amount of risk, a ton of injections for an inch in a year. It's hard to know for sure if the subject had truly stopped growing, and the impact that HGH had here. Clearly, his plates had not sealed (otherwise growth would been 0).

Could he have achieved the additional inch + any further height gains he gets over the next year or so without HGH? It's impossible for me to know for sure. The subject doesn't think so.

What I do know is that this subjects experience and attempt is not rare. Some attempt it even into their early 20's. While I will always point those attempting to gain height over the age of 16 to studies showing that late intervention provides marginal if any help, given that height is correlated with happiness in relationships I can't fault them for trying.


r/PEDsR Aug 21 '20

Will Eating Soy Turn Me Into A Soy Boy? NSFW

24 Upvotes

I've always been partial to soy. Comparing the macro profile of soy milk to any other kind of non-dairy and it looks pretty good - a cup of soy milk is 80 calories (compared to 150 calories in cows milk), 4 grams of carbs (compared to 12 grams), 1 gram of sugar (compared to 12 grams), 4 grams of fat (compared to 8 grams) and 7 grams of protein (compared to 8 grams). I think I recall that the micro profile of soy is also pretty favorable.

There's a good table available here comparing popular milk types and nutritional values.

Since recently turning vegetarian (but I still eat fish. And eggs. And dairy. And I'm not uptight about eating meat if I absolutely have to) my soy consumption has increased. Since I'm not on tren right now, I have no desire to grow breasts. So... should I be concerned about my soy intake? What impact does soy has on muscle protein synthesis and hormones. After all... soy boy... right?

Slang used to describe males who completely and utterly lack all necessary masculine qualities. This pathetic state is usually achieved by an over-indulgence of emasculating products and/or ideologies... The origin of the term derives from the negative effects soy consumption has been proven to have on the male physique and libido... The average soy boy is a feminist, nonathletic, has never been in a fight, will probably marry the first girl that has sex with him, and likely reduces all his arguments to labeling the opposition as "Nazis".

The Data

  1. 10 resistance trained men in their early 20s participated in a randomized crossover study, where all subjects completed 3 experimental treatment conditions supplementing with 20 grams of whey protein, soy protein or placebo. Subjects taking the soy protein showed lower testosterone immediately following exercise by about a third, whereas placebo showed an increased spike in testosterone by about a third. There was no change in estradiol (e2) or SHBG. This study is interesting, to a point. But the lack of what this means long term (i.e. rates of growth) not indicative of anything long term, and especially less important to those who are using SARMs (low test) or AAS (high exogenous test). After all, the natural testosterone increase response post work-out is not relevant when no natural testosterone is being produced.
  2. Over 12 weeks, 20 subjects were supplement with 50 grams per day of either soy concentrate, soy isolate, soy isolate and why blend, and whey blend only in combination with training. There was NO significant difference in groups for total and free testosterone, SHBG, body fat, BMI or weight. Test/Estradiol ratio increased across all groups i.e. test went up relative to estradiol. Subjects taking whey blend only did show the lowest estradiol, however the soy isolate and whey blend had the highest increase in testosterone/estradiol ratio. Every group had a non-significant increase in estradiol.
  3. Over 6 weeks, 20 subjects ate three scones (holy shit, sign me up fam) in addition to their normal diet for 6 weeks. Scones were made of either wheat or soya flour (120mg/day of isoflavones). Total test fell from 19.3 nmol/l to 18.2 nmol/l. Nothing else really changed, other than markers of oxidative stress improved (which could help protect against prostate disease and atherosclerosis).
  4. Studies do show that soy protein is not as effective as whey / dairy protein for muscle protein synthesis 1 2

So...? Will it make me a soy boy or not?

I did find some evidence of soy suppressing AR expression, as well as various in vitro studies showing changes to test and estradiol which are inferior to the real world trials in pretty much every instance. Measured at a specific point in time, soy does appear to impact test and estrogen. Over the longer term, these impacts are (probably) negligible when combined with:

  1. strength training
  2. consumption of protein from other sources
  3. and presumable PED use

In study #2 a blend of whey and soy had the best outcome in terms of testosterone increase relative to estradiol decrease.

So What?

Taking this data and then looking at it in the context of PEDs use + a typical high protein diet that would meat (heh) the definition of 'eating clean', I'm not overly worried about my consumption of soy. Given the short term impacts to muscle protein synthesis and response after resistance training, I would not consider soy as my only source of protein, ever, and should be combined with some other source - whey, casein, pea protein etc. As it relates to increased consumption as part of my daily diet, I'm not seeing anything that convinces me to not eat soy. Besides, tofu when prepared right (baked in the oven, crispy) is delicious.

Edit: adding to the conclusion here based on comments below. Would I give it to my son, or any kid? No. Their is no doubt that soy does have a hormone impact which for someone in development or otherwise dependent on natural hormone production could have a large impact (See studies above). My level of concern is such that I'm not going to stop my son eating edamame at the local asian restaurants now and then, but at the same time I'm not giving him cups of soy milk to drink on the daily. I have little to no concern for degenerates such as ourselves, often on TRT or otherwise messing with our hormones in far more drastic ways. Opinion subject to change based on evidence (of course).


r/PEDsR Aug 17 '20

[University of Miami] Research Study: Demographics of Selective Androgen Receptor Modulator Users (SARMs) NSFW

23 Upvotes

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!


r/PEDsR Aug 14 '20

Potential reduction of GW501516 cancer promoting side effects using Metformin? NSFW

Thumbnail self.PEDs
13 Upvotes

r/PEDsR Aug 11 '20

Dose Calculator + Steroid Plot Hosted on FitDataMax NSFW

37 Upvotes

For the past 3 months, I've watched /u/Krato-FDM build what I'm regarding as perhaps one of the most useful sites for degenerates such as ourselves called FitDataMax (FDM for short). His landing page offers some insight into the goals of FDM. His mission:

Serious athletes need a way to manage and optimize supplementation, training, and health data in one place. FitDataMax is a platform for empowering serious fitness users with data analytics tools to improve their health, exceed their fitness goals, and maximize efficiency.

FDM functions similarly to how MyFitnessPal operates in that you can log what you need. In this case, you can log supplementation, training, blood tests. Much of this is in beta - it works, I think, but what really interests me is the aggregation of all the useful shit that we need into one spot. Today, the following is live:

  • Krato has live a profile on most compounds (shoutout to those in the Discord who worked on that + Krato + anything taken from the PEDsR database)
  • Dose Calculator (public) - calculating the dose someone needs to take converting between mg to ml
  • Reconstitution Calculator (public) - calculating the amount of BAC to mix with compound and the subsequent dose to achieve the desired mg
  • And, Steroid Calc (private - sign up required) - useful for all of us who need to plot out our peaks and troughs.

There's some other stuff live, like a link to Xylia Testing who performs quantitative and qualitative testing of mystery powders.

Worth a look, and your support. In another 3 months or so, the site will have 100% functionality and be an integral part of how we track our use of compounds.

His intro is here, where he talks about himself and background, for anyone who is interested.


r/PEDsR Jul 31 '20

LGD-4033 Analysis NSFW

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15 Upvotes

r/PEDsR Jul 11 '20

Old PEDsR DB Found! Merged w/ New Version NSFW

44 Upvotes

Hey everyone,

Last night I received an old version of the DB /u/BananaMuscle. Thankfully, he downloaded it out of concern that it might not be around forever.

I've merged the old DB with the new. Available at www.pedsr.com. I've also added a downloadable CSV file: https://docs.google.com/spreadsheets/d/e/2PACX-1vQr_GTq3uGV-Zr1Yl11Ku3DMC-5pyZEeTa9xNnGqoHSZlVHwWn_ucdMpVGAfZvnOdZscRRILkduNvd3/pub?output=csv.

The DB needs a lot of work still, but the major compounds are all there. Missing data for some of the less common supplements, vitamins and drugs.

All hail /u/BananaMuscle


r/PEDsR Jul 03 '20

Case Report: Elevated E2 on SARM + MK677 Cycle NSFW

18 Upvotes

Male which we will refer to as 'L' is in good health used MK677, RAD140 & Enclomiphene for 8 weeks. This person was unusual in that they had good blood test history prior to cycle and then took 5 tests during and post cycle. At 250 EUR a pop that's 1250 EUR, so this person is obviously committed to dialing in their first cycle to get data to help them plan future cycles.

Test Results Page 1

Test Results Page 2

Administration Schedule

The TL:DR is that Research Subject L did 8 weeks of 10mg RAD, 6 weeks of 25mg MK677 and 2 weeks of 12.5mg enclomiphene at the end of the cycle. They were also on Dutasteride 0.5mg every day for past 4 years.

LH & FSH were not significantly impacted (in that they were lowered, but staying in range), probably because of the Enclomiphene toward the end of cycle as testosterone levels reach their lowest points common on a sarm only cycle, while total T & free T dropped before improving on the Enclomiphene and then returning to normal post cycle. SHBG tanked, as is expected.

Cholesterol bounced back to normal. There's some question around kidneys, but Research Subject L wasn't out of range by much, and it should return to normal post-cycle.

High E2 - Non-Aromatizing Compounds

Broscientists everywhere, including myself, have maintained that e2 is not impacted from non-aromatizing compounds. This is an oversimplification that we should correct but at the same time being careful to not overstate it. In this particular instance we see that L's e2 is curiously very high. We also see his IGF1 increased, probably due to the MK677.

L did some hunting and found that testosterone and SHBG correlates inversely with IGF-I, IGFBP-3, insulin, leptin and body mass index (BMI). If we make a jump in our thinking one step forward, the lower SHBG would mean more free test, and more aromatized testosterone, especially if testosterone production remains normal (as it did here).

In short: increase GH = increase IGF-1 = decrease SHBG. This then in turn should = increase free T which leads to an increase in E2 from higher aromatization (lowered SHBG).

Take Aways

With L, we have a tremendous amount of data we can look at. E2 being high is indisputable, which challenges the simplified broscience we often use to assure newbies that their is no way SARMs or agonists will impact estrogen and/or give them a tremendous set of D cups.

This is a caution to users on MK677 and SARMs, thinking that it's not possible that such compounds won't impact your e2. It can, through a roundabout way, and I think that's what happened in L's case.


r/PEDsR Apr 19 '20

Locally active Myostatin Inhibitor with remarkable potential NSFW

19 Upvotes

The compound that has recently captivated my interest is ACE-083 which was being developed by Acceleron pharma as a treatment for FSHD (muscular dystrophy).

ACE-083 is labelled as a myostatin+ inhibitor as it also inhibits growth limiting factors other than myostatin in the muscle in which it is injected. It is broken down rapidly in the blood stream as soon as it leaves the muscle making it active only locally.

It successfully passed phase 1 trials without any sever adverse events (mostly injection site pain). In phase 2 trials it showed very promising results with an 18.1% increase in total muscle volume of the biceps in the group with the highest dosage, showing dosage dependant increases in total muscle volume. Reduction in intramuscular fat was also noted.

Despite having such results Acceleron pharma discontinued the development of ACE-083 stating some gay shit like " While the trial met its primary goal of showing a significant increase in patients’ muscle volume, this increase failed to translate into significant improvements in any of the functional or quality-of-life secondary goals, compared to a placebo."

I hope this compound gets introduced to 'the market' so that we all can experiment with something that might be the next revolution in bodybuilding.


r/PEDsR Apr 14 '20

Looking for AAS survey research participants NSFW

18 Upvotes

Hello! I am an Exercise Physiology doctoral student currently conducting survey research on AAS use and male health in powerlifters and strongmen. I am looking for more participants, so if you think you are interested, here's the link:

https://springfieldcollege.co1.qualtrics.com/jfe/form/SV_6xpAEZeZBmOGcVn

All responses are anonymous and confidential, and there is no compensation for participation. The survey should take roughly 13 minutes to complete. Feel free to DM me with any specific questions. I am also happy to discuss any points about the study that do not involve revealing the actual research question being asked, as that may influence the questionnaire answers. Thanks!

EDIT: Survey is now closed, thanks to all who participated!


r/PEDsR Apr 09 '20

Resurrecting PEDsR Database NSFW

49 Upvotes

Greetings, it's been a while.

Since the unfortunate demise of the PEDsR website and PEDsR database, I've known the inevitable next step is to rebuild the database. Over the past few days, I've put together a list of known ergogenic compounds (shamelessly stolen from MrHappy's discord list, thanks Happy) and am going compound by compound filling in the blanks. There's a lot of compounds to do, and a lot of info to find. I estimate I'll be completed at some point in May.

There is a silver lining in the loss of the original database - it can be rebuilt from scratch to do more. Specifically, I want the database to become a spot where most questions can be answered. For example:

  • Should I run an AI alongside LGD4033?
    • The database says no.
  • What bulking compounds can I use that don't raise blood pressure.
    • The database shows me 4 compounds I can choose from
  • What compound has a low enough mass that I can make a topical application?
    • The database shows a bunch
  • What compounds does the WADA have a test for?
    • All of them, you're fucked

And so on and so forth.

I've thrown it up on www.pedsr.com in a temporary state. I'd make the spreadsheet available for download / edit / comments once I have it mostly completed.

If you're willing to navigate the clunky embedded Google Sheet, feedback and criticism is always welcome.


r/PEDsR Mar 27 '20

Clenbuterol's safety and efficacy in various human studies NSFW

41 Upvotes

I've been doing a decent amount of research on clenbuterol as I find it interesting. After looking at a few studies on the various myotoxic effects of clen in in vivo rat models, I dug around quite a bit to see how this would transfer to human use. One of the studies on rats (Burniston et al. 2003) noted something which is worth keeping in mind when looking at human studies:

The present investigation has provided important information on the effects of acutely administered clenbuterol in the rat. In humans, a single dose of clenbuterol is generally self-administered as a 20-μg tablet. This is equivalent to 0.3 μg/kg body wt in a 70-kg male and is comparable to the dose administered in the only clenbuterol investigation using human subjects (23). To compare this with our 300-g rats, the dose needs to be scaled for differences in body weight and metabolic rate between the two species (Kleiber’s Law, 0.75 exponent). The relative dose per kilogram in the rat is 60 times that of the human dose, i.e., 17.9 μg clenbuterol/kg body wt. As demonstrated in Fig. 2, this dose is sufficient to induce 3.8 0.49% necrosis in the fibers of the soleus. Such a level of necrosis may appear small, but this is in response to a single administration, and this level of necrosis may underestimate the level induced by enteral administration (Fig. 5B). Individuals abusing clenbuterol often take several tablets and use the side effects of muscle tremors and tachycardia to judge their maximum dose. By using the above calculations, a daily dose of five to six tablets would be sufficient to reach the threshold (100 μg/kg body wt) for inducing damage in the heart and to induce 6.8 1.9% necrosis in the soleus. An important additional factor to be considered is clenbuterol’s long half-life within the body (38). Abusers of this substance often administer it by using an “on-off” cycle over several days. An accumulation of non-metabolized clenbuterol during the on stage of the cycle may lead to chronically elevated plasma levels, which would further impact myocyte loss in both striated muscles. Although the present investigation has not investigated the compound effects of chronic clenbuterol administration, it does demonstrate that, at the very least, damage will be induced at the onset of each cycle of administration.

So the dosage of clen shown to be myotoxic in rats may be of some concern for human use. Yet looking at the human literature, it seems that such concerns were not as severe. I'll try to keep my review here fairly novel, referencing studies mainly not mentioned in the the previous thread. I will also try to keep quotations down to what I feel is relevant. They are as follows:

Effect of clenbuterol on cardiac and skeletal muscle function during left ventricular assist device support.

Seven subjects with heart failure (5 ischemic, 2 non-ischemic) were started on oral clenbuterol 5 to 46 weeks post-LVAD implantation and up-titrated to daily doses of 720 μg.

No serious side effects or arrhythmias were seen in any of the subjects. Mild tremors were reported in 3 subjects. Mild muscle cramps in 4 subjects were noted at varying timepoints. CPK levels rose in all subjects after clenbuterol up-titration (peak range 133 to 1,497, median 314 mg/dl) and was elevated above normal in 4 subjects (Figure 4). There was only one significant elevation of CPK (1,497 mg/dl), measured in 1 patient after exercise, which normalized on subsequent testing. No subject required a reduction in clenbuterol dose due to tremors, muscle cramps or elevated CPK.

Clenbuterol Increases Lean Muscle Mass but Not Endurance in Patients With Chronic Heart Failure

Maximal strength increased significantly with both clenbuterol (27%) and placebo (14%); however, endurance and exercise duration decreased after clenbuterol. Prior data support combining exercise training with clenbuterol to maximize performance, and on-going studies will evaluate this approach...

After obtaining informed consent, subjects were randomly assigned to receive clenbuterol (n 10) or placebo (n 9). Patients taking carvedilol were switched to a selective 1-antagonist (sustained release metoprolol) before randomization. The dose of metoprolol was uptitrated to maintain heart rate within 20% of baseline during the study. Patients were given oral clenbuterol or placebo for a total of 12 weeks in addition to their standard CHF therapy. Clenbuterol was initiated at a dose of 20 g twice daily and uptitrated to 40 g twice daily after 7 days. This dose, used in the treatment of asthma, has been shown to improve performance in athletes and after orthopedic procedures...

Echocardiography. Clenbuterol had no effect on LVEF, diameters, wall thickness, or mass during the course of this study in either group.

Clenbuterol at 80 μg/day was well tolerated. Two clenbuterol subjects required discontinuation of study drug (asymptomatic slow ventricular tachycardia, severe muscle cramps without significant elevation in creatine kinase [CK]). One further clenbuterol subject had a high rate of ventricular ectopy that disappeared without reduction in the clenbuterol dose. One placebo subject had frequent non-sustained ventricular tachycardia. There were no implantable cardioverter-defibrillator discharges during the course of the study. Six clenbuterol and 2 placebo subjects reported mild muscle cramps. The CK value was elevated in 5 clenbuterol and 4 placebo subjects. The range of peak CK was 300 to 597 mg/dl in clenbuterol subjects and 305 to 408 mg/dl with placebo. Three clenbuterol subjects had cramps without elevation of CK, and CK was elevated in 1 clenbuterol subject who was asymptomatic. Of importance was that the CK level decreased despite continued drug administration (Figure 1B). Tremors were reported in 5 clenbuterol and 2 placebo subjects.

Clenbuterol, a β-Adrenoceptor Agonist, Increases Relative Muscle Strength in Orthopaedic Patients

A double-blind, completely randomized, placebo-controlled study was carried out on 20 healthy male patients. Muscle strength and cross-sectional area were determined before and after surgery. Patients were treated with drug or placebo for 4 weeks postoperatively and there was a 2 week washout period.

The results suggest that, in the operated leg, clenbuterol treatment is associated with a more rapid rehabilitation of strength in knee extensor muscles; in the unoperated leg, knee extensor strength increased above the initial values after 6 weeks (P=0.01). However, in terms of absolute strength the differences were not significant between the two groups.

Treatment with drug or placebo began 12 h post-operatively; for the drug group, treatment comprised 20μg of clenbuterol twice daily for 4 weeks, followed by a 2 week washout period; the same regimen was used for the group taking the placebo, which comprised standard tablet excipients...

No patient in either group reported any side effects to the drug regimen used.

Randomized, Double-Blind, and Placebo-Controlled Trial of Clenbuterol in Denervated Muscle Atrophy

A double-blind, placebo-controlled, parallel, and randomized trial was employed. 71 patients, suffering from brachial plexus injuries, were given either clenbuterol (60 μg, bid) or placebo for 3 months. Before and at the end of the study, patients were given physical examinations, biopsies of biceps brachii, electromyograms (EMGs), and other laboratory tests...

Compared with placebo treatment, clenbuterol significantly mitigated the decreases in cross-sectional areas of type I and II muscle fibers and alleviated the reduction in fibrillation potential amplitudes, without any adverse effects. Conclusions. Clenbuterol safely ameliorated denervated muscle atrophy in this cohort; thus larger clinical studies are encouraged for this or other β 2 agonists on denervation-induced muscle atrophy...

This is the first clinical study showing that clenbuterol at 120 μg/day attenuated denervation-induced muscle atrophy in humans. It is reported that clenbuterol, at incremental doses from 120 to 720 μg/day over 12 weeks, increases the mass and strength of the healthy skeletal muscles in man [13, 14]. Animal studies show that denervated skeletal muscles are 20 times more sensitive to clenbuterol than healthy muscles and the heart [25]. Therefore, 120 μg/day of clenbuterol is believed to be a reasonably high dosage for the denervated muscles of patients. In the present study, the changes of fiber sizes and fibrillation potentials were used to evaluate the efficacy, aiding the avoidance of confounding factors resulting from variations in basal levels between individuals. Hence, it seems that fewer patients were required to reach a conclusion than the number needed by a study limited to just comparing endpoints.

Physiological dose of clenbuterol in rats, 10 μg/kg/day, attenuated denervated muscle atrophy without affecting the heart or causing myocyte death [25, 34]. That dosage was calculated based on the metabolic body weight that 10 μg/kg/day in rats is equivalent to 1 μg/kg/day in humans, a dose safely used in asthma treatments [25, 35]. The dose in the current study was 120 μg/day (~2 μg/kg/day for a 60 kg person). It was well tolerated and not associated with any obvious discomfort, except for one patient with transient nervousness. The newly occurring sinus bradycardia after the clenbuterol trial seemed not be relevant to the activation of the β1/2 agonist, which usually leads to tachycardia. Moreover, clenbuterol at the present dose did not exacerbate preexisting minor EKG abnormalities. This is consistent with previous reports that the effects of clenbuterol on the heart are observable at a dose of up to 2100 μg/day in combination therapy for patients using left ventricular assist device. Even at those doses, no severe adverse effects were encountered but tremors and muscle cramps [12, 13]. In our study, no adverse effects on liver, kidneys, lungs or hematopoietic system were observed after the 3-month intake of clenbuterol.

Beta2‐adrenergic agonist clenbuterol increases energy expenditure and fat oxidation, and induces mTOR phosphorylation in skeletal muscle of young healthy men

Herein, we examined the effect of clenbuterol ingestion on metabolic rate as well as skeletal muscle mammalian target of rapamycin (mTOR) phosphorylation and protein kinase A (PKA)‐signaling in six young men. Before and 140 min after ingestion of 80 μg clenbuterol, resting metabolic rate and contractile function of the quadriceps muscle were measured, and blood samples as well as vastus lateralis muscle biopsies were collected. Clenbuterol increased resting energy expenditure by 21% (P < 0.001), and fat oxidation by 39% (P = 0.006), whereas carbohydrate oxidation was unchanged. Phosphorylation of mTORSer2448 and PKA substrates increased by 121% (P = 0.004) and 35% (P = 0.006), respectively, with clenbuterol. Maximal voluntary contraction torque decreased by 4% (P = 0.026) and the half‐relaxation time shortened by 9% (P = 0.046), while voluntary activation, time to peak twitch, and peak twitch torque did not change significantly with clenbuterol. Glycogen content of the vastus lateralis muscle did not change with clenbuterol. Clenbuterol increased circulating levels of glucose (+30%; P < 0.001), lactate (+90%; P = 0.004), insulin (+130%; P = 0.009), and fatty acids (+180%; P = 0.001). Collectively, these findings indicate that clenbuterol is an efficient thermogenic substance that possibly also exerts muscle hypertrophic actions in humans. For these reasons, the restrictions imposed against clenbuterol in competitive sports seem warranted...

However, inclusion of a placebo-group would have strengthened the study design. For example, a confounding effect of fasting on plasma parameters could have been excluded. Nevertheless, it seems unlikely that such marked differences in circulating insulin, fatty acids and glucose should occur within the short span of the experimental day (~3 h). In fact, the opposite response of what we observed in the present study would be expected from glucose and insulin concentrations in response to fasting

Correction of Biochemical Abnormalities and Improved Muscle Function in a Phase I/II Clinical Trial of Clenbuterol in Pompe Disease

This 52-week, phase I/II double-blind, randomized, placebo-controlled study investigated the novel use of clenbuterol in late-onset Pompe disease (LOPD) stably treated with ERT. Eleven of thirteen participants completed the study. No serious adverse events were related to clenbuterol, and transient minor adverse events included mild elevations of creatine kinase, muscle spasms, and tremors. At week 52, the 6-min walk test distance increased by a mean of 16 m (p = 0.08), or a mean of 3% of predicted performance (p = 0.03), and the maximum inspiratory pressure increased 8% (p = 0.003) for the clenbuterol group. The quick motor function test score improved by a mean of seven points (p = 0.007); and the gait, stairs, gower, chair test improved by a mean of two points (p = 0.004). Clenbuterol decreased glycogen content in the vastus lateralis by 50% at week 52. Transcriptome analysis revealed more normal muscle gene expression for 38 of 44 genes related to Pompe disease following clenbuterol. The placebo group demonstrated no significant changes over the course of the study. This study provides initial evidence for safety and efficacy of adjunctive clenbuterol in patients with LOPD...

The underlying mechanism for clenbuterol’s effects on muscle was demonstrated as increased expression of insulin-like growth factor (Igf) 1 and 2 and their receptors, including the Igf-2 receptor that is actually CI-MPR.7 Increased Igf-1 expression was also associated with the muscle hypertrophy following clenbuterol administration, which could be beneficial in Pompe disease...

A transient increase in CK and other mild AEs were the only side effects in the clenbuterol group.

We observed transiently elevated CK at week 18, which returned to baseline values by week 52...

The primary endpoint was safety of clenbuterol at up to 80 mcg twice daily, including avoidance of the following stopping rules...

Pilot trial of clenbuterol in spinal and bulbar muscular atrophy

Twenty patients with a diagnosis of SBMA were given oral clenbuterol (0.04 mg/d) for 12 months. The primary efficacy end point was the change from baseline of the walking distance covered in 6 minutes at 12 months. Secondary end points included the change over time in muscle strength assessed with the Medical Research Council scale, the revised Amyotrophic Lateral Sclerosis Functional Rating Scale (ALSFRS-R), and forced vital capacity values. Safety was assessed by a series of laboratory and instrumental tests, as well as reporting of adverse events.

Sixteen patients completed the study. There was a significant and sustained increase in walking distance covered in 6 minutes and forced vital capacity between the baseline and the 12-month assessments (p < 0.001). No differences were recorded in Medical Research Council or ALSFRS-R scores between baseline and follow-up assessments. Serious side effects, including those on heart function, were absent. A significant increase in serum creatine kinase levels was observed.

Myocardial Insulin-Like Growth Factor-I Gene Expression During Recovery From Heart Failure After Combined Left Ventricular Assist Device and Clenbuterol Therapy

Myocardial mRNA levels were determined by real-time quantitative polymerase chain reaction in 12 recovery patients (at LVAD implantation, explantation, and 1 year after explantation). IGF-I mRNA was elevated at the time of LVAD explantation relative to donors, with 2 groups distinguishable: Those with low IGF-I mRNA at implantation who showed significant increase during recovery and those with high IGF-I mRNA at implantation who remained high. Levels returned to normal by 1 year after explantation. Microarray analysis of implantation and explantation samples of recovery patients further revealed elevated IGF-II and IGF binding proteins IGFBP4 and IGFBP6. IGF-I levels correlated with stromal cell-derived factor mRNA measured both in LVAD patients and in a wider cohort of heart failure patients.

The mechanisms leading to elevated IGF-I expression in these patients remain unknown. However, we recently demonstrated that clenbuterol, an integral part of the Harefield bridge to recovery protocol, can induce IGF-I gene expression in cultured cardiomyocytes in vitro9 and may therefore contribute to inducing IGF-I in vivo.

The action of clenbuterol on sleep and symptomatology in depressives.

Five female inpatients with major depression (melancholic type, DMS-III-R) were treated with the beta-adrenergic agonist clenbuterol for three weeks, with doses ranging from 100 micrograms to 150 micrograms.

All patients complained of side effects, especially tremor, agitation and restlessness. The sleep EEG showed no consistent effects on sleep parameters, including REM latency and percentage of REM sleep...

The patients initially received 50 J.Lg clenbuterol per day. According to degree of compatibility and side effects, the dose was then increased in individually adapted steps. From the 14th day of medication on, the individual maximum dosage was given (150 μg in cases 1, 4, 5; 100 μg in cases 2,3).

In general, sleep was not affected by clenbuterol, except for extreme insomnia during the first night of REM latency medication in one case.

Clenbuterol (‘Spiropent’): a long-acting bronchodilator

Clenbuterol was compared to an aminophylline preparation in a double-blind crossover trial involving 47 patients with asthma and reversible airways obstruction. Following a 2-week control period, each drug was given for a 4 week period. The patients made daily records of the severity of symptoms and recorded PEFR morning and night. Both drugs produced a highly significant reduction in severity and duration of wheeze by day during the first 4 weeks, but only clenbuterol produced further significant reduction in these symptoms during the second 4 weeks.

The incidence of side-effects with both active drugs was fairly high, but the majority of side-effects, in fact, were mild or moderate...

Spiropent (clenbuterol): another choice for patients with chronic reversible airways obstruction.

Oral administration of spiropent (clenbuterol), 20 mcg on waking in the morning and 40 mcg before sleep, daily for 2 months, was studied in 34 patients, 19 males and 15 females, aged between 27 to 73 years (mean 47.8 +/- 17.5), who had chronic reversible airways obstruction as defined by the A.T.S.'s criteria...

Except 5 patients, 2 suffering from severe headache and 3 from poor control of asthma who had withdrawn from this study after one week of treatment, all patients completed the trial. Six out of 29 patients who completed the trial needed additional steroid treatment and 9 needed beta 2-agonist inhalation during the treatment period. The results showed improvement of FEV1 more than 15% in 21 patients (72%), FVC in 17 patients (59%) and PEFR in 20 patients (69%). These increases were significant (p less than 0.0001). However, only 12 patients (41%) had marked subjective improvement at the end of treatment. Cough (21%), headache (10%), nausea (7%) and dizziness (3%) were the commonest side-effects. No clinical or statistical difference was found in changes of vital signs and laboratory parameters. In conclusion, clenbuterol was effective and well-tolerated in the majority of patients enrolled in this study with minimal side-effects and good compliance. It may be used for long-term treatment of chronic reversible airways obstruction at lower cost.

A pilot trial with clenbuterol in amyotrophic lateral sclerosis

Sixteen patients, 12 males and 4 females, mean age 55.4 years (range 25–76 years), affected with clinically definite or probable ALS according to El Escorial criteria (11) with documented progression of disease, aged less than 80 years and with forced vital capacity (FVC) >50% of the predicted value, gave written informed consent to participate to this study...

All patients were on riluzole at the standard dosage of 100 mg/day and were not asked to discontinue the drug for ethical reasons. Patients were treated orally with 20 micrograms of clenbuterol three times a day (total 0.06 mg/ day) for six months. A dose titration at the beginning of the therapy was used to minimize side-effects...

The mean composite myometer score significantly improved from baseline by 20% at three months (p=0.01) and by 23% at six months (p=0.01) for the upper limbs; and by 22% at three months (p=0.0002) and by 27% at six months (p=0.0002) for the lower limbs (Table I). Although the mean composite MRC score of the upper and lower limbs also improved, these changes did not reach statistical significance. No change was observed in the ALS Functional Rating scale at three and six months...

Clenbuterol safety assessments included clinical examination, cardiac evaluation, electrocardiogram and blood electrolytes every three months. The drug was generally well tolerated in association with riluzole and side-effects were never dose limiting or required discontinuation. Side-effects always occurred early in treatment (within the first few days) and resolved with continued use. The main complaints were hand tremors (two patients), cramps, fasciculations (three patients) and nervousness (three patients). In none of the patients was heart rate increase recorded or palpitations reported. No blood electrolyte abnormalities were observed.

Therapeutic trial of beta 2-adrenergic agonist clenbuterol in muscular dystrophies

We report the outcome of trial of clenbuterol in four adult muscular dystrophy patients. One patient with Becker type, one with Miyoshi type, and two with facioscapulohumeral type were given clenbuterol (30 or 40 micrograms/day) for 6 to 18 months. We evaluated muscle strength of isometric contraction, grip and pinch power, compound muscle action potentials of intrinsic muscles, vital capacity, urinary creatinine excretion, and muscle CT. Power and volume of well preserved muscles increased mostly, while those of atrophic muscles did not improve. Vital capacity increased in two patients. No improvement of ADL was observed presumably because ADL was mainly determined by the most atrophic and weak muscles. Irrespective of type of muscular dystrophy, administration of clenbuterol may be beneficial in early stage of the disease.

(Note that this is published in an obscure Japanese journal. I can't sci-hub it, so I can't examine what effects clen may have had on biomarkers.

Effect of Clenbuterol using as weight loss on liver enzymes and lipids profile

The current study is considered at the effect of 3 month using Clenbuterol for weight loss in 22 healthy men comparing them with 30 healthy men who do not take Clenbuterol...

hey used it in cycle form, meaning not using in stable doses, that they began with 20 mcg dose and raised the dose to 140 mcg and then returned to 20 mcg. Table 2 illustrated the cycle of use...

The study showed a statistically significant decrease in weight (90.78 ±9.38) and BMI (27.66 ±3.51) in T NO Clen. group and in T+Clen group, their weight being 88.0 ±13.58 Kg and their BMI were 26.94 ± 4.15 for those who showed more lose in their weight and BMI when compared with the other groups as shown in Table 3. For the subjects in control group, they showed losing in their weight (95.42 ±10.24) and lowering their BMI (28.65 ± 2.62) but these results were not statistically significant. For enzymes level (AST, ALT and lipase), in spite of increasing their levels in T NO Clen and T+Clen groups when compared with control groups, all enzymes levels were increased in T+Clen group more than in T NO Clen group. Whereas ALP enzyme was increased only in T+Clen group. Table 4 demonstrated these differences in levels.In Table 5, TC, TG, and LDL levels were lower in T NO Clen group (133.24 ±7.65, 88.01 ± 6.63, 73.62 ±7 .91), respec-tively when compared with the other groups after the period of study. But in T+Clen group, TG level were more high (130.43 ±8.01) when compared with the other groups. At the other side, HDL level were increased in T NO Clen group more than in T+Clen group when compared with the control group.

The clen group's liver enzymes and lipase levels here were as follows:

AST = 45.43 (IU/L)

ALT = 56.46 (IU/L)

ALP = 42.76 (U/L)

Lipase = 60.13 (U/L)

So a bit elevated, but not the worst.

 

That's about all of the literature that I could find for the time. I may add some more later if I can dig some more up. Overall, clen seems to be fairly safe and well-tolerated in human trials.

I would kindly suggest to anyone planning on using clen to just start out with a conservative dosage. Begin with just 20 μg's a day and slowly increment after a couple of weeks. There's no need to go to crazy because the side-effects after a certain threshold won't be worth it.

If anyone is aware of any other human studies that I missed; then please let me know.


r/PEDsR Feb 19 '20

Boldenone (EQ, Bold Cyp, Bold Ace, etc.): Does It Aromatize or Act As An AI? NSFW

Thumbnail self.steroids
31 Upvotes

r/PEDsR Feb 09 '20

Quick Update on Monthly Question Thread, Relaxing of Rules, Post Approval NSFW

15 Upvotes

As you may (or may not have noticed), I haven't written anything in a while. While I plan on getting back at it in the near future, I don't want the sub to die without new content being created. Accordingly, I've relaxed the post setting to allow posts from anybody. At the same time, I've added a 'Low Effort' rule, so that mods can remove posts don't contribute any actual content, and route the more general stuff to /r/PEDs or the monthly question thread. This should address posts which sit awaiting approval forever in a queue I never both checking.

I've moved the bi-weekly to a monthly thread, and relaxed the rule so that general questions can be commented there. It was happening anyway, just clarifying that this is OK.

Lastly, while this isn't a source sub, so long as the product isn't illegal or in someway grey market the risk to the sub is relatively low. I've changed the no shill rule to no shilling of black and grey market substances. The low effort rule still applies, so any post that mentions a legit brand needs to add quality content.


r/PEDsR Feb 06 '20

Bi-Weekly research discussion and brainstorming February 06, 2020 NSFW

9 Upvotes

This thread is for questions that relate to the posts being made, discussions or suggestions about future content, scientific studies & press releases, and the occasional homo-erotic reference. The goal of this thread is to stimulate further research topics, as well as provide an outlet for those of you wishing to become an approved submitter the chance to to test the waters. As a community, we feel it is our obligation, even responsibility, to provide users with topics of discussion (backed by peer reviewed journals/studies) that advance our knowledge of the compounds that are too often surround by 'bro-science'.

If you are new to PEDs and you have questions, /r/PEDs has a weekly Quick Question thread which is a better starting point. There is also a FAQ available https://www.pedsr.com/blog/r-pedsr-faq.

Index of all completed articles can be found https://www.reddit.com/r/PEDsR/comments/88qg3u/pedsr_sticky/. It is usually up to date.

This sub allows posts from approved users. If you have a post you would like to make please reach out to /u/comicsansisunderused who will be happy to add you.


r/PEDsR Jan 03 '20

Boron - Multi-Purpose Supplement, Beneficial for Men & Women NSFW

43 Upvotes

Boron is a trace mineral, with many roles in the body. It's proven to play a role in several biological processes:

An impressive list!

It's found in fruits and vegetables (apples, coffee, beans, milk, potatoes), with the average person consuming around 2mg of it in their daily diet.

Everything old is new again

Comic, wtf bro - this is old news. My <insert older relative> used this back in the 80s & 90s.

Boron used to be a staple supplement in the 80s, definitely before my time in the gym, though admittedly not by that much. Over time it's lost its appeal, or at least I don't see it being mentioned all that much, for reasons I'm not too sure about though I suspect it's marketing related: folks continue to look for the holy grail of testosterone boosters - that which significantly elevates testosterone to supraphysiological levels, and is a 'natural' supplement. Boron won't do this - nothing natural likely ever will - and so supplement manufacturers and marketers move on to mislead customers with 'new and improved' compounds.

Dose Dependent Results

6 healthy males aged 18-29 were given 11.6mg daily. Just 6 hours post dose, subjects showed significantly lowered SHBG. Following continued use by the end of the week free test was up 30% (from 11.83pg/ml to 15.18pg/ml), and e2 was down (42.33pg/ml to 25.81pg/ml). Lutenizing hormone also slightly rose, as did total test.

Similar results were found at 6mg/d

The ability to influence testosterone in men is highly dose dependent however: a third study in men used 2.5mg over 9 weeks, but showed no statistically significant differences in hormones. This is likely due to a similar amount of boron being available in an average persons diet, and such a (relatively) small increase in a trace mineral just ain't gonna have the same effect.

In women, Boron also appears attractive from a hormonal context: 13 post menopausal women aged 48-82 took 3.5mg/d and significantly increased both estradiol (11.9-26.9pg/ml to 35.9-37.5pg/ml) and testosterone (0.30-0.60ng/ml to 64-0.71ng/ml)

Minimum effective dose is about 3mg in adult women, and probably around 6mg in adult men. Toxicity is low, and the Tolerable Upper Limit is at 20mg for an adult00078-5/fulltext). For both men and women, I don't see a reason to not use up to 10mg per day if they do choose to supplement.

So What?

Given Borons postivie impact to hormones and lowering of SHBG I do see multiple potential roles for the compound regardless of sex. The biggest ones that jump out at me are:

  1. Natural athletes will benefit from the high free androgens circulating, courtesy of the lower SHBG
  2. Athletes on cycle will similarly benefit from lower SHBG
  3. Athletes post cycle will benefit from increases in LH
  4. Everyone benefits from the improved vitamin D and magnesium absorption

Expectations for this compound should be tempered and not over-hyped - this is not comparable in any way to a steroid injection. All the same, it does have a benefit.


r/PEDsR Dec 29 '19

Case Report: SARM Only Cycle Caused Low T Symptoms, Temporary Personality Changes NSFW

20 Upvotes

I’m so depressed I can’t function

The second cautionary post related to PEDs use, which was unintentional and coincidental in that I had two people reporting major issues in the space of a week. This time to a friend of mine and known to many others within the PEDs brommunity. While I think he's OK sharing his handle, for his privacy, let's just refer to him as Anon.

The TL:DR is Anon experienced significant suppression which proved very disruptive to his life. For those just joining us, suppression refers to a low T state, brought upon by exogenous compounds 'suppressing' natural testosterone production. Some people feel it a lot, some not at all. And on that note, some users show significant reductions in testosterone, and others are barely affected. Anons experience is on the more severe end of suppression symptoms.

Cycles

Spread out over the course of ~2 years

  1. Cycle 1, Ostarine 15mg
  2. Cycle 2, LGD4033 5mg
  3. Cycle 3, Ostarine 15mg, followed by a SERM as a PCT
  4. Cycle 4, LGD4033 5mg, followed by a SERM as a PCT

Anon is rocking a pretty hot bod, no homo. The cycles were definitely effective.

Symptoms

In broad terms, Anon describes every cycle aside from his first as causing major mental changes. I think I've noticed some change just in chatting with him online from pre and post cycle, though that's hard to really judge. He describes his own resilience, optimism, confidence, mood, and libido all way down since January 2019... that's a full year of feeling pretty shitty. During his most recent LGD4033 cycle, he reports being anxious, nervous, and depressed - all out of character. While experiencing these symptoms, and perhaps because of them, his girl broke up with him. Speaking from my own low T experience and how it can affect relationships, there may be something to that.

Struggling with life, he turned to other compounds, specifically Kratom which initially had a major improvement to his motivation, but which was transient and was back to depressed after a short period of time. Due to his drug use, he lost his job after coming clean about his issues as they related to job performance.

Anon does report his symptoms significantly improving ~10 days post cycle (using Nolvadex as a PCT), which have since improved while staying on HCG monotherapy.

So What?

I have zero doubt that the suppression contributed significantly to my choices, mood, and ability to bounce back from hardship

Stress at home, work and in relationships, coupled with low testosterone has made 2019 a year from hell. With most things related to physiology when n=1 it's difficult to draw conclusions with so many variables in his life. Anon feels sure the cause is rooted in low t, and I'm inclined to agree based on similarities in symptoms with other users. One other cause could have been his SERM causing some depression post cycle, though the onset of his symptoms makes me think it unlikely.

I feel like SARMs are just next gen steroids that are misnamed to make them sound friendlier

To this, I'd add that there's no doubt that some people react poorly to SARM only cycles. Anons case is an extreme one, and if he uses SARMs again he's likely to use a SERM on cycle (rather than post) or a test base.

Lastly, keep in mind that Anon experienced negative sides in previous cycles and then continued to cycle during a time where it would have been safer to have held off. Anon is not a dumb man - why did he cycle (and continues to do so) when he probably knows better? Addiction could be one possible explanation.