According to Galbraith & Michnovicz's 1989 study:

Radiometric analysis of urine and serum samples from nine normal male volunteers showed that the extent of 2-hydroxylation of estradiol was significantly reduced from a mean (±SEM) of 31.7±2.3 percent to 19.7±2.3 percent (P<0.0001) after two weeks of oral treatment with cimetidine (800 mg twice a day); the 16α-hydroxylation of estradiol was unaffected. At the same time, the urinary excretion of 2-hydroxyestrone decreased by approximately 25 percent (P<0.0002), and the serum concentration of estradiol increased by approximately 20 percent (P<0.04). The mean percentage of estradiol 2-hydroxylation was also rapidly reduced, from 36.8±4.4 percent to 24.5±3.4 percent in six men after one week of oral cimetidine at a lower dosage (400 mg twice a day; P<0.0006).

Perhaps this would be enough to avoid 'crashed estrogen' symptoms, particularly where this is associated with SARMs (which may suppress testosterone production less than AAS) and/or combination with DHEA/pregnenolone?

Cimetadine also seems to promote weight loss in obese individuals, possibly sparing lean body mass (pdf, 150kb), so might make more sense during cutting cycles.

It does also interfere with the CYP enzymes though, so there's a lot of potential for unwanted drug interactions.

YMMV...

It's often observed that, since it binds a proportion of total testosterone (tT), lowering SHBG will tend to raise free testosterone (fT); this is a common rationale for lowering (or 'crushing') SHBG.

However, as it stands, this 'raise free/total theory' suffers from two problems:

1. lowering SHBG will also release estrogen, raising free estrogen (fE). Meanwhile, increasing fT will tend to increase aromatization of T into estrogen, raising total estrogen (tE). fE has a strongly suppressive action on production of T via the HTPA, so other things being equal, wouldn't the boost to fT from lower SHBG would be cancelled by the suppressive effects of higher fE on T production?
2. SHBG plays a (poorly elucidated) role in protecting &/ transporting T & E. Lowering it may interfere with this.

SHBG's role is not yet well understood by medical science, so there's not much to be said about (2). However, there is some research out there that seems broadly consistent with (1), the 'raise free/total theory', albeit involving rather more complex mechanisms.

Why lowering SHBG may sustainably raise both free and total T, and the free androgen/free estrogen ratio

First of all, it turns out that while SHBG binds DHT, T & E, these have very different binding affinities:

The active androgen, 5α-dihydrotestosterone (DHT), has the highest affinity ∼1 nm Kd for SHBG followed by testosterone and estradiol, which bind with ∼5 and ∼20 times lower affinities, respectively, when compared with DHT

So, when SHBG is lowered, the initial hormonal responses will be ordered DHT>T>E (as a proportion of their total levels). This happens to be the reverse of the ordering of the negative feedback 'coefficients' of these hormones upon testoterone production via the HTPA (ie E>T>DHT; E is by far the most suppressive of T production, DHT is the least suppressive).

Second, DHT functions as an aromatase antagonist (reducing conversion of E) and doesn't itself aromatize.

After the initial changes (DHT>T>E) in hormone levels, the larger increase in DHT may therefore reduce production of E, & the effect of the newly increased (due to the reduction of SHBG) fE/tE ratio on fE may be offset by this effect (eg because of the impact of DHT reducing tE). The initial changes will have increased the free androgen/free estrogen (fA/fE) ratio; this second round effect will certainly tend to increase it further, and may even reduce the level of fE itself (or at least its biological activity).

Longer term, the increased fA/fE ratio will tend favor accumulation/ preservation of lean body mass over fat mass. Since fat mass has aromatase activity, this may permanently lower a man's E production, 'resetting' his fA/fE & body composition.

In short: yes, 'crushing' SHBG may 'raise T', with potential for a lasting impact on body composition and hormonal baseline (&/ side effects related to (2), above) . But the explanation is a bit complicated.

Abstract*:

Resistance exercise training is well documented as having cardiovascular benefits, but paradoxically, it seems to increase arterial stiffness, favoring the development of high blood pressure. The present study investigates the potential effects of oral supplementation with arginine in healthy individuals performing exercise resistance training. We studied 70 non-smoking male subjects between the ages of 30 and 45 with normal or mildly increased blood pressure on ambulatory monitoring (for 24 h) and normal blood samples and echocardiography, who performed regular resistance exercise training for at least five years with a minimum of three workouts per week. They were divided into two groups in a random manner: 35 males were placed in the arginine group (AG) that followed a 6-month supplementation of their regular diets with 5 g of oral arginine powder taken before their exercise workout, and the control (non-arginine) group (NAG) consisted of 35 males. All subjects underwent body composition analysis, 24 h blood pressure monitoring and pulse wave analysis at enrollment and at six months. After six months of supplementation, blood pressure values did not change in the NAG, while in the AG, we found a decrease of 5.6 mmHg (p < 0.05) in mean systolic blood pressure and a decrease of 4.5 mmHg (p < 0.05) in diastolic values. There was also a 0.62% increase in muscle mass in the AG vs. the NAG (p < 0.05), while the body fat decreased by 1% (p < 0.05 in AG vs. NAG). Overall, the AG gained twice the amount of muscle mass and lost twice as much body fat as the NAG. No effects on the mean weighted average heart rate were recorded in the subjects. The results suggest that oral supplementation with arginine can improve blood pressure and body composition, potentially counteracting the stress induced by resistance exercise training. Supplementation with arginine can be a suitable adjuvant for these health benefits in individuals undertaking regular resistance training.

Not a significant effect according to the p<0.05 convention, but the study may simply have been underpowered for the body composition effect size.

This earlier study also found non-significant effects in the same directions (see Table 3), despite being shorter and using a lower arginine dose, and cites several other suppoortive studies (of mixed comparability in terms of subjects and treatment).

More research (&/ a meta-analysis) necessary!

*From article full text.

Two 2015 meta analyses in J Am Coll Nutr and J Acad Nutr Diet point to modest 'repartioning' effects related to MCT ingestion. (0.9kg fat loss & 0.7kg bodyweight loss, implying 0.2kg lean mass gain in the first one; fat loss with stable lean mass in the second*.)

Unlike MCT (medium chain triglycerides), coconut oil is on the supermarket shelves in many countries. Does it have a similar effect? A priori, it's unclear, because coconut oil is mostly MCTs, but also contains long chain triglycerides, which are metabolized differently.

This Malaysian study obtained a 0.6kg increase in lean mass combined with a 0.5kg decrease in fat mass, via feeding obese subjects 30ml virgin coconut oil daily (before meals). These changes weren't statistically significant, but there was a significant reduction in waist circumference that suggests there were 'real' changes in body composition terms.

But this was virgin coconut oil... apparently this has more MCT and less LCT. What about plain ol' coconut oil?

At least one study suggests this also works - in women with abdominal obesity who are dieting, at least. This used 30ml/day of 'filtered pressed coconut oil' with soya oil as a control. Both groups lost similar amounts of weight (0.4-0.5 BMI units), but only the coconut oil group reduced waist circumference, which points to an increased proportion of the weight loss being fat (esp as they had abdominal obesity).

It's not definitive, but this suggests ordinary coconut oil may have a modest body composition repartitioning effect. If anyone's aware of further research bearing on that specific point, please link in the comments!

*Taking the -0.39 kg change in total body fat at face value; it's unclear how this squares with the changes in subcutaneous (-0.46) and (-0.55) visceral fat though, eg ~1kg total fat loss, which would imply a 0.5kg gain in lean mass... (???)

Paper here

Abstract:

Purpose: To investigate the impact of supplementation with a targeted micronutrient formulation on the visual discomfort associated with vitreous degeneration.

Methods: In this clinical trial, 61 patients with symptomatic vitreous floaters were randomized to consume daily, the active supplement consisting of 125 mg L-lysine, 40 mg vitamin C, 26. 3 mg Vitis vinifera [grape seed?] extract, 5 mg zinc, and 100 mg Citrus aurantium or placebo for 6 months. Change in visual discomfort from floaters, assessed with the Floater Disturbance Questionnaire, was the primary outcome measure. Secondary outcome measures included best-corrected visual acuity, letter contrast sensitivity, photopic functional contrast sensitivity with positive and negative contrast polarity, and quantitative vitreous opacity areas.

Results: After supplementation, the active group reported a significant decrease in their visual discomfort from floaters (P < 0.001), whereas the placebo group had no significant change in their visual discomfort (P = 0.416). At 6 months, there was a significant decrease in vitreous opacity areas in the active group (P < 0.001) and an insignificant increase in vitreous opacity areas in the placebo group (P = 0.081). Also, there was a significant improvement in photopic functional contrast sensitivity with positive contrast polarity in the active group after supplementation (P = 0.047).

Conclusions: The findings of this study indicate improvements in vision-related quality of life and visual function of patients suffering from vitreous floaters after supplementation with a formulation of antioxidative and antiglycation micronutrients. Notably, these improvements were confirmed by the decrease in vitreous opacity areas in the active group.

Translational Relevance: This targeted dietary intervention should be considered to support patients with symptomatic vitreous degeneration.

It's a small study, & IDK if the problems from SERMs &/ SARMs (only S4 AFAIK) relate to the same mechanisms, but these supplements might be worth a try for anyone experiencing problems, or as a form of 'vision support' for someone using compounds prone to cause them.

Although the evidence isn't incredibly solid, there are some studies pointing to TA improving body composition, particularly in conjunction with exercise &/ in older people

Generally speaking, this is attributed to TA increasing testosterone in older people &/ reducing the cortisol response exercise or dieting.

Recently, an anti-hyperglycemic effect of TA mediated by PDX1-associated pancreatic beta-cells [has also been identified] (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7400842/) (in mice):

Powdered EL root showed significant antihyperglycemic activity along with the control of body weight. After eight weeks of treatment, both the blood cholesterol level and the glycogen deposit in hepatocytes were remarkably lower, whereas the secreting insulin level was elevated. ... This study confirms the antihyperglycemic activity of EL through PDX1-associated beta-cell expansion resulting in an enhancement of islet performance.

Prior to this though, there had also been some in vitro research on Fetuin-A (alpha-2-HS-glycoprotein, AHSG),

a liver borne plasma protein, [which] contributes to the prevention of soft tissue calcification, modulates inflammation ['good'], reduces insulin sensitivity and fosters weight gain following high fat diet or ageing ['bad'].

This suggests Fetuin-A may play a role in the 'metabolic syndrome' associated with aging, and its level turns out to be partly androgen mediated:

Testosterone participates in the [up]regulation of hepatic fetuin-A expression, an effect mediated, at least partially, by androgen receptor activation.

But isn't this effect in the 'wrong' direction? Both metabolic syndrome and hypogonadism are associated with aging, so one might expect androgens to downregulate fetuin-A (increasing insulin sensitivity and reducing fat gain).

In short, it doesn't look like fetuin-A is very well-understood; the best way to think of it perhaps is as an "androgen-responsive double-edged metabolic sword".

Nonetheless, in rats at least, Tongkat Ali (TA) reduces fetuin-A:

In the present study, we have investigated the effect of standardized E. longifolia extract on serum protein expression up to 28 days following oral administration in rats. ... AHS [fetuin-A] expression is known to be associated with insulin resistance and diabetes. Our data indicated that serum AHS was reduced in rats treated with standardized E. longifolia extract

So modulation of fetuin-A might just be another way in which TA may be helpful for metabolic syndrome, and worth being aware of. Unlike SHBG and DHEA, it looks like rodent fetuin-A metabolism is somewhat similar to humans'; useful animal research may eventually be forthcoming.

A 2004 paper, Dihydrotestosterone may inhibit hypothalamo-pituitary-adrenal activity by acting through estrogen receptor in the male mouse found that "In agreement with previous studies, the CORT [cortisol] response to immobilization [eg stress] was enhanced by EB [estradiol benzoate] and inhibited by DHT."

This inhibition was pretty significant, ~40% for DHT and a DHT metabolite 3β-Androstanediol*. So the anabolic effect from SARMs (& AAS, esp DHT derivatives) may stem partly from a dampened cortisol response.

However, to check whether the estrogen receptor was mediating this effect, the researchers also added a SERM (tamoxifen). This undid about 1/3 of the reduction in cortisol from DHT, and completely undid the effect of 3β-Androstanediol.

How significant is this 'unblunted cortisol stress response' effect? IDK - not least because I'm not sure how important the blunted cortisol stress response in the first place... But we've known for a while that SERMs' impact on IGF-1 may blunt the anabolism of the SARM in a SERM-SARM cycle, and this is another pathway through which that might also occur.

TNSTAAFL & YMMV!

*AKA 5alpha-androstan-3beta, 17beta-diol. The paper refers to this as a DHT metabolite, but I think it can also be formed by the action of 5-alpha reductase on Androstenediol.

Several anecdotal accounts suggest that DHEA can reduce of prevent (some of?) the subjective symptoms of suppressed testosterone production during SARM or possibly AAS cycles.

Looking at the steroidogenesis diagram it's hard to understand how this could be the case, because suppression "works" by reducing the activity of the enzymes required to convert DHEA into testosterone (ie the ones in green rectangles). If the pathway for producing androgens, which provide the substrates for onward conversion to estrogens, is blocked, then how can estrogen production be increased? (The point of a test base, since maintaining an adequate level of estrogens is likely more important than maintaining endogenous androgen production after all there are plenty of exogenous androgens present.)

Just now I stumbled across a possible resolution to this puzzle in Dehydroepiandrosterone Sulfate (DHEAS) Stimulates the First Step in the Biosynthesis of Steroid Hormones:

These [in vitro] findings indicate that DHEAS affects steroid hormone biosynthesis on a molecular level [by modulating the catalytic efficiency of CYP11A1] resulting in an increased formation of pregnenolone.

Reviewing the steroidogenesis chart, this alone doesn't solve the puzzle: CYP11A1 is too high up in the chain of reactions, and additional pregnenolone and DHEA should still be bottlenecked by the enzymes involved in getting 'sht down', preventing their conversion to testosterone and estrogen.

However: EDIT: 0) DHEA interacts directly with estrogen receptors, particularly estrogen receptor beta

1. perhaps increased availability of DHEA can overpower reduced enzyme activity? [Not related to the finding in the paper.]
2. increasing conversion of cholesterol to pregnenolone could magnify increases in DHEA levels resulting from DHEA supplementation, reinforcing this &
3. if the level of DHEAS modulates the catalytic efficiency of one enzyme, it may also modulate the efficiency of other steroidogenesis enzymes.
4. the levels of other steroid hormones may also modulate the efficiency of other relevant enzymes.

So there does seem to be some (currently rather vague) theory behind the idea of DHEA as a test base.

While (0), direct estrogenic activity, is the simplest mechanism via which DHEA could be acting as a test base, DHEAS levels are also known to decline with age; (1)-(4) could tie that in with the declines also typical in androgen and estrogen levels. (Supplementing DHEA alone only seems capable of raising estrogen levels in males, however.)

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!

A (deserved) reputation for visual side effects has led to andarine falling out of favour. However, the drug seems to have some advantages relative to ostarine, and there may a way to get the best of both worlds.

Andarine pros vs ostarine: greater acute strength benefit, better cosmetic effects, possibly less suppressive. Cons: visual side effects, (more frequent dosing).

Andarine's visual side effects include tinting (generally yellow) of vision, deterioration of night vision and ability to adapt to changes in brightness, and blurry vision.

Andarine's benefits: Strength "According to anecdotal information, Andarine’s strength increase is slightly greater than that of Ostarine." {TSH} "I like to refer to this SARM as 'weak Winny'" {GD} "if I tense my arm I could feel that my arm tenses differently, I just can't explain it to people, it's the same feeling I would get when I took winny or anavar, like a more powerful feeling" {GD}

Cosmetics "This compound is known for providing a very dry, vascular and tight look." {TSH} "it's awesome if you're trying to dry out and look good and if you're on a cycle and it's summer and you're always with your shirt off and you want to look good every day" {GD}

Suppression "Andarine is one of the least suppressive SARMs out there... [suppression] comparable to that of Ostarine." {TSH} Several redditors have commented that they found Andarine noticeably less suppressive than ostarine. (Possible explanation below.)

Otherwise the two SARMs are similar, with one further important difference: ostarine's half life is about 24 hours, while andarine's seems to be 3-6 hours {TSH}.

Why 'seems to be'? MPMD's Derek claims it's a lot longer: "I speculate that the half-life in humans is probably closer to 36 to 48 hours if not more and I have no idea where this four hour statistic came from ... based on my own eyeballs I can tell you that's certainly not the case" {MPMD}

However, this claim is based on the visual side effects, and the "Eye is a distinctive organ with protective anatomy and physiology. Several pharmacokinetics compartment model[s] of ocular drug delivery has [sic] been developed for describing the absorption, distribution and elimination of ocular drugs in the eye." {AEL} A 4 hour plasma half life could be consistent with Derek's experience, if the relevant ocular compartment half life is much longer.

And that short half life would likely govern the acute strength effects, which are noticeable with dosing: "it's got a short half-life ... I notice then when I take my next dose and like later in the afternoon I can again feel that same [stronger contraction] feeling" {GD}

So how can we get (some of) the benefits of andarine without the vision side effect? One recommendation I've seen is to dose andarine 5 days on, 2 days off. However, I think there's a better way: use andarine preworkout, 3-4 days per week stacked over ostarine dosed daily.

Using the minimum bro doses (ostarine 10mg, andarine 25mg/day) as an example, working out on T, TH, S, something like this: M: O 10mg (morning) T: O 10mg, A 25mg (~1h preworkout) W: O 10mg " Th: O 10mg, A 25mg " F: O 10mg " S: O 10mg, A 25mg " Su: O 10mg "

Total O: 70mg, A 75mg

The short exposure of the ocular compartment to andarine, and ~40 hour periods with minimal exposure, should make visual side effects very rare; many people could likely titrate to higher anderine doses.

Increased anabolic activity during the post-workout anabolic window might also deliver improved gains, and, given the pulsatile nature of gonadotropin release, the short daytime spikes of andarine could be minimally suppressive of the HTPA (possibly the reason some redditors found this).

But won't andarine compete with ostarine for ARs, and simply replace it, giving little added benefit? Sure, ligands all compete, but the binding affinities of ostarine and andarine are very similar (Ki = 3.8 and 4.0, respectively*). If andarine is dosed several hours away from ostarine, much of the ostarine will have bound; given their similar affinities, andarine shouldn't be able to displace much of it, and should bind to other ARs. (If my bropharmacodynamics are off here, please let me know...)

Then won't andarine displace testosterone/DHT bound to ARs or SHBG? Yes. But so will andarine alone dosed several times a day. With a relatively stable level of ostarine also present, I can't see why this should create more problems than the standard andarine-only scenario (in which, AFAIK, related problems aren't specially common).

A small dose of a SERM alongside this dosing schedule should also be enough to mitigate suppression.

{S} = The SARM Handbook (Sarminfo, 4th Ed) {GD} = Greg Doucette: https://www.youtube.com/watch?v=s5r7dns8oNo {MPMD} = More Plates More Dates: https://www.youtube.com/watch?v=aS1Fwpn6N0Y {AEL} = Agrahari et al: https://dx.doi.org/10.1007%2Fs13346-016-0339-2

*ostarine 3.8 nM Ki https://www.caymanchem.com/pdfs/11603.pdf andarine 4.0 nM Ki https://dx.doi.org/10.1124/jpet.102.040840

I just stumbled across this: https://www.reddit.com/r/PEDsR/comments/aip16s/prevalence_of_serm_side_effects_results/

There was very little info on some SERMs (notably enclomiphene and toremifene) when this was done. I think there'd be more now, so together with the increased popularity of SERM + SARM cycles, it might be a good time for a revisit...

Icariins are major active components of epimedium grandiflorum aka Horny Goat Weed, (淫羊藿叶) which has long been used as a "yang tonic" in Chinese medicine. Epimedium leaf extracts are widely available, and, in contrast to many herbs, it seems to be quite easy to find extracts specifying icariin concentration (rather than the far less helpful X:1 concentration metric). Epimedium also seems to be safe to use singly (a lot of Chinese herbs really need to be used in multi-herb formulas).

Icariin as a SERM in female animals

Prenylflavonoid Icariin Induces Estrogen Response Element–Independent Estrogenic Responses in a Tissue-Selective Manner. 2019 seems to be the first study identifying icariin's SERM-like properties:

Long-term treatment with icariin effectively prevented [sic] bone of ovariectomized (OVX) rats from estrogen deficiency–induced osteoporotic changes in bone structure, bone mineral density, and trabecular properties. Moreover, icariin ... prevented [sic] dopaminergic neurons against OVX-induced changes by rescuing expression of estrogen-regulated tyrosine hydroxylase and dopamine transporter in the striatum. Unlike estrogen, icariin did not induce estrogenic effects in the uterus and breast in mature OVX rats or immature CD-1 mice. ... Our results support the hypothesis that icariin, through its distinct mechanism of actions in activating ER, selectively exerts estrogenic activities in different tissues and cell types.

If it quacks like a SERM, it is a SERM... and the nature of this selectivity - avoiding uterus and breast tissue - seems useful.

A 2021 paper followed up, also examining the interactions of icariin with Tamoxifen and Raloxifene in bone cells and tissues:

HEP [Herba Epimedii Extract] exerted bone protective activity and the use of HEP did not alter the bone protective activities of SERMs when they were used simultaneously in an estrogen-deficient rat model.

So it appears icariin does selectively interact with estrogen receptors in females, and doesn't interfere with pharmacological SERMs. But what does it do in males?

Icariin in male animals

Quite a lot - as we might expect from it's history of use as an aphrodisiac/ED herb in men. From (Effects of Icariin on Reproductive Functions in Male Rats, 2014):

Adult rats were treated orally with icariin at doses of 0 (control), 50, 100, or 200 mg/kg body weight for 35 consecutive days. ... 100 mg/kg icariin significantly increased epididymal sperm counts. In addition, 50 and 100 mg/kg icariin significantly increased [serum] testosterone levels. These increases were about 75% and 200%; this is evidence of the effect needed for icariin to work as a SERM in a SERM+SARM cycle. In addition:, there were modest (non-significant) increases in LH & LHrH - possibly suited to SARMs' weaker inhibition of LH - and: Superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels were measured in the testes; 50 and 100 mg/kg icariin treatment improved antioxidative capacity... These results collectively suggest that icariin within a certain dose range is beneficial to male reproductive functions, ; meanwhile, higher doses of icariin may damage reproductive functions by increasing oxidative stress in the testes.

Similar positive results, also identifying the NO pathway, from a 2017 study:

All icariin groups exhibited... higher testicular and prostate [probably not good] indexes compared with controls (p < .001). These groups had higher serum testosterone and NO concentrations (p < .001), hypothalamic DA [dopamine] and 5-HT levels, and eNOS, PI3K and phosphorylated AKT expressions in penile tissue (p < .05). The effect of icariin was dose-dependently increased. Our study suggests that icariin improves the sexual function of male mice, which might be associated with the hypothalamic–pituitary–gonadal axis and the PI3K/AKT/eNOS/NO signalling pathway

And also from a 2020 study on aging mice, which noted:

Icariin, a flavonoid from Epimedium, has been reported to exhibit anti-aging effects and improve testicular dysfunction in the clinical setting. ... Dietary administration of icariin for 4 months significantly ameliorated the age-related decline in testicular function by increasing testicular and epididymal weights and indices, sperm count and sperm viability, testicular testosterone and estradiol concentrations, and seminiferous tubule diameters and heights. In addition, icariin protected age-related Sertoli cells from injury [sic] as evidenced by an analysis of Sertoli cell number, ultrastructure, and function. ... Our data suggest that icariin effectively ameliorates age-related degeneration of testicular function by alleviating Sertoli cell injury via the ERα/Nrf2 signal-transduction pathway.

Icariin also prevented testicular damage due to nicotine:

The nicotine-treated group showed significantly decreased epididymal sperm density and serum testosterone concentration relative to the control group. Nicotine also caused oxidative damage shown by significant reduction in the activities of antioxidant enzymes and elevation in Malondialdehyde (MDA) levels. ICA [icariin group] on the other hand, improved the reduction in sperm density, hormone levels, and activities of antioxidant enzymes altered in the nicotine treated mice.

So icariin has demonstrated clinical efficacy, and may not only be able maintain testicular production of testosterone during use of SARMs or AAS, but also to protect testicular tissue from injury directly due to that usage (assuming that supraphysiological androgens cause damage via mechanisms similar to aging &/ nicotine).

There's more evidence for all this out there in published studies, including direct research on icariin as a PDE5 inhibitor. But I'm already a bit out of my depth :)

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.

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/

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

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.

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

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.

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.

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.

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).

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!

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.