DHT may increase abdominal fat (beware of DHT and DHT prohormones during recomp)

[DR_P]

From anecdotal experience, DHT and/or DHT related precursors may vastly improve mood and overall well-being, but some anecdotal feedback also pointed to unexpectedly slow loss of abdominal fat during a strong cut (with significant caloric deficit, high levels of cardio etc.).

So, despite DHT precurosors are being touted to yield "dry" effects and to support body recomposition during a cut or lean bulk, I wondered what the scientific rationale for the industry claims of increased fat loss and improved body recomposition due to DHT and DHT prohormones, respectively.

To my big surprise, the literature offered some results (in vitro experiments as well as human clinical trials) which actually suggest the opposite of what the industry claims: The results from these studies actually show that DHT may lead to a complex modulation of gene expression patterns, a part of which indicate upregulation of adipogenic signaling pathways in visceral adipose tisse, and - to add worse to the bad - even controlled human trials found that DHT administration led to an INCREASE of visceral fat in humans. The interesting point was, however, that humans treated with testosterone showed reduction in abdominal fat mass - in strong contrast to the DHT treated study participants.

In essence: These study results support the anecdotal observation of unusally hampered loss of abdominal fat during the intake of DHT-related prohormones and suggest to rather take a good test booster that will primarily boost testosterone and not DHT.

Shame on the industry for claims being exactely the opposite to what science says (and anecdotal feedback). Boooh!


Here are the cited articles:

Obes Res. 1995 Nov;3 Suppl 4:609S-612S.
Testosterone and regional fat distribution.
Marin P.


The effects of testosterone treatment of abdominally obese men have been assessed by evaluating the following parameters: The metabolic activity of different adipose tissue regions in vivo (using lipid label as a tracer) and in vitro (measuring lipoprotein lipase (LPL) activity), the total and visceral adipose tissue mass, insulin sensitivity, fasting blood glucose, blood lipids, and blood pressure as well as prostate volume. Middle-aged men with abdominal obesity were treated with transdermal administration of testosterone (T), dihydrotestosterone (DHT) or placebo (P) during 9 months. The study was double-blind. Treatment with T was followed by an inhibited uptake of lipid label in adipose tissue triglycerides, a decreased LPL-activity and an increased turn-over rate of lipid label in the abdominal adipose tissue region in comparisons with the DHT and P groups. These effects on adipose tissue metabolism were not detected in the femoral adipose tissue region in any of the groups. T treatment was also followed by a specific decrease of visceral fat mass (measured by CT-scan), by increased insulin sensitivity (measured with the euglycemic glucose clamp), by a decrease in fasting blood glucose, plasma cholesterol and triglycerides as well as a decrease in diastolic blood pressure. In the DHT group an increased visceral mass was detected. No other changes in these variables were found in the DHT and P groups. There were no detectable changes in prostate volume (measured by ultra-sound), prostate specific antigen concentration, genito-urinary history or urinary flow measurements in any of the groups. It is suggested that T substitution to a selected group of men results in general metabolic and circulatory improvements. The prostate area needs further careful attention.

J Mol Endocrinol. 2004 Oct;33(2):429-44.
Effects of dihydrotestosterone on adipose tissue measured by serial analysis of gene expression.
Bolduc C, Larose M, Yoshioka M, Ye P, Belleau P, Labrie C, Morissette J, Raymond V, Labrie F, St-Amand J.
Source

Molecular Endocrinology and Oncology Research Center, Laval University Medical Center, Department of Anatomy and Physiology, Université Laval, Québec, Canada.
Abstract

Intra-abdominal fat accumulation is related to several diseases, especially diabetes and heart disease. Molecular mechanisms associated with this independent risk factor are not well established. Through the serial analysis of gene expression (SAGE) strategy, we have studied the transcriptomic effects of castration and dihydrotestosterone (DHT) in retroperitoneal adipose tissue of C57BL6 male mice. Approximately 50,000 SAGE tags were isolated in intact and gonadectomized mice, as well as 3 and 24 h after DHT administration. Transcripts involved in energy metabolism, such as glyceraldehyde-3-phosphate dehydrogenase, malic enzyme supernatant, fatty acid synthase, lipoprotein lipase, hormone-sensitive lipase and monoglyceride lipase, were upregulated by DHT. Transcripts involved in adipogenesis, and cell cycle and cell shape organization, such as DDX5, C/EBPalpha, cyclin I, procollagen types I, III, IV, V and VI, SPARC and matrix metalloproteinase 2, were upregulated by DHT. Cell defense, division and signaling, protein expression and many novel transcripts were regulated by castration and DHT. The present results provide global genomic evidence for a stimulation of glycolysis, fatty acids and triacylglycerol production, lipolysis and cell shape reorganization, as well as cell proliferation and differentiation, by DHT. The novel transcripts regulated by DHT may contribute to identify new mechanisms involved in the action of sex hormones and their potential role in obesity.

The last article points to very complex effects of DHT, however, the fact that it upregulates adipogenetic pathways as well may provide the molecular basis for the observed clinical effect of increased visceral adipose tissue in DHT treated men.

[Mr.Cooper69]

Very interesting, good read!

[powercage]

So in theory Finasteride will become a weightloss stack supp

[DR_P]

So in theory Finasteride will become a weightloss stack supp

interesting idea. However, you would have to stack this potent 5-Alpha-Reductase inhibitor at least with an effective aromatase inhibitor, because Finasteride solo might shuttle a dysproportionate amount of testosterone into the aromatization pathway, which in turn would cause an unfavorably low testosterone:estradiol ratio, which ultimately may hamper fat loss as well.

I hate to say it (haha), but I think that the test booster by muscletech (I think it's called cryotest if I am not mistaken) is designed around a parallel inhibition of aromatase and inhibiton of 5-AR, which may be the ideal scenario for fat loss.

[THEHUGE]

Interestingly, many people taking finasteride report fat gain.

[DR_P]

Interestingly, many people taking finasteride report fat gain.

exactely, this observation would support my theoretical insertions right above in the previous post. Too much estrogenic impact (which is inevitable after strong 5AR inhibition) is definitely bad for fat loss.

[THEHUGE]

exactely, this observation would support my theoretical insertions right above in the previous post. Too much estrogenic impact (which is inevitable after strong 5AR inhibition) is definitely bad for fat loss.

This seems to apply (anecdotically) to any unbalanced hormonal scenario actually.

[SwolenONE]

people used to swear by M5AA and Methyl DHT (scivation methyl rage) years back for cutting, this news is pretty shocking!

[TheGoodBro]

Strong cherry-picking "Doc".

First of all, a big fat LOL at this statement:

but some anecdotal feedback also pointed to unexpectedly slow loss of abdominal fat during a strong cut (with significant caloric deficit, high levels of cardio etc.).

You must be new to hormonal compounds. I've NEVER heard DHT related compounds slow fat loss. In contrary, they're being used IN A CUT to retain mass while accelerate fat loss. I don't know which of the voices in your head told you these anectdotes but they aren't real. Forget about them.

After you can't keep your diet and training on track you are now blaiming a DHT related compound for your laziness. And worse, you're cherry-picking the literature to substantiate your lack of dedication. This thread doesn't even belong in the science section. Well, upon closer consideration maybe it does, but the title should be 'Voices in the head of a psychiatric patient claiming to be a doctor on the internet'.

I'm only responding to keep the discussion balanced and take the momentum out of your alarmist hands:

Long-term effects of dihydrotestosterone treatment on prostate growth in healthy, middle-aged men without prostate disease: a randomized, placebo-controlled trial.
Idan A, Griffiths KA, Harwood DT, Seibel MJ, Turner L, Conway AJ, Handelsman DJ.
Source
Concord Hospital, ANZAC Research Institute, University of Sydney, Sydney, Australia.
Abstract
BACKGROUND:
Benign prostatic hypertrophy increases with age and can result in substantially decreased quality of life for older men. Surgery is often required to control symptoms. It has been hypothesized that long-term administration of a nonamplifiable pure androgen might decrease prostate growth, thereby decreasing or delaying the need for surgical intervention.

OBJECTIVE:
To test the hypothesis that dihydrotestosterone (DHT), a nonamplifiable and nonaromatizable pure androgen, reduces late-life prostate growth in middle-aged men.

DESIGN:
Randomized, placebo-controlled, parallel-group trial. (Australian New Zealand Clinical Trials Registry number: ACTRN12605000358640)

SETTING:
Ambulatory care research center.

PARTICIPANTS:
Healthy men (n = 114) older than 50 years without known prostate disease. Intervention: Transdermal DHT (70 mg) or placebo gel daily for 2 years.

MEASUREMENTS:
Prostate volume was measured by ultrasonography; bone mineral density (BMD) and body composition were measured by dual-energy x-ray absorptiometry; and blood samples and questionnaires were collected every 6 months, with data analyzed by mixed-model analysis for repeated measures.

RESULTS:
Over 24 months, there was an increase in total (29% [95% CI, 23% to 34%]) and central (75% [CI, 64% to 86%]; P < 0.01) prostate volume and serum prostate-specific antigen level (15% [CI, 6% to 24%]) with time on study, but DHT had no effect (P > 0.2). Dihydrotestosterone treatment decreased spinal BMD (1.4% [CI, 0.6% to 2.3%]; P < 0.001) at 24 months but not hip BMD (P > 0.2) and increased serum aminoterminal propeptide of type I procollagen in the second year of the study compared with placebo. Dihydrotestosterone increased serum DHT levels and its metabolites (5α-androstane-3α,17β-diol and 5α-androstane-3β,17β-diol) and suppressed serum testosterone, estradiol, luteinizing hormone, and follicle-stimulating hormone levels. Dihydrotestosterone increased hemoglobin levels (7% [CI, 5% to 9%]), serum creatinine levels (9% [CI, 5% to 11%]), and lean mass (2.4% [CI, 1.6% to 3.1%) but decreased fat mass (5.2% [CI, 2.6% to 7.7%]) (P <0.001 for all). Protocol-specific discontinuations due to DHT were asymptomatic increased hematocrit (n = 8), which resolved after stopping treatment, and increased prostate-specific antigen levels (n = 3; none with prostate cancer) in the DHT group. No serious adverse effects due to DHT occurred.

LIMITATION:
Negative findings on prostate growth cannot exclude adverse effects on the natural history of prostate cancer.

CONCLUSION:
Dihydrotestosterone treatment for 24 months has no beneficial or adverse effect on prostate growth but causes a decrease in spinal but not hip BMD. These findings have important implications for the wider use of nonsteroidal pure androgens in older men.

The FT of the second study you quoted states DHT does hundreds of things (including stimulating lypolysis). The net effect on adipose tissue is unknown. The paper also states the observed increased visceral fat mass in Marin's paper is in contradiction with various other observations. Why didn't you include this valuable information in your OP?

WHY WHY WHY?? Cause you're biased.

[TheGoodBro]

And since you're blaiming other in the industry?

Where are your 3 promised nitrate studies? Don't you think your customers deserve to know about that....?

Tell us 'dr' P DID YOU DO THEM OR NOT????!!!

[TheGoodBro]

And since you're blaiming other in the industry?

Where are your 3 promised nitrate studies? Don't you think your customers deserve to know about that....?

Tell us 'dr' P DID YOU DO THEM OR NOT????!!!

I just got this CP comment

Better yet, ask if the scientist performing those studies was recently fired...

Maybe the person can jump in or you can start answering some questions 'doc'?

[DR_P]

SNIP.

Sir, this thread is about "abdominal fat" - please re-read the thread title. So is the cited literature specifically related to visceral abdominal adipose tissue.
If you don't have anything worthwile to contribute to this topic, it would be kind to leave this civilized and science-related thread. The literature you have provided does not relate to abdominal fat, let alone visceral fat, so it doesn't really help to evaluate the hypothesis of the thread.

Thank you.

[TheGoodBro]

Sir, this thread is about "abdominal fat" - please re-read the thread title. So is the cited literature specifically related to visceral abdominal adipose tissue.
If you don't have anything worthwile to contribute to this topic, it would be kind to leave this civilized and science-related thread. The literature you have provided does not relate to abdominal fat, let alone visceral fat, so it doesn't really help to evaluate the hypothesis of the thread.

Thank you.

Oh, you mean the literature mentioned by Bolduc et al. (your second reference) who state Marin's paper (your first reference) is in contradiction with other research IS NOT A WORTHWILE CONTRIBUTION?

Besides that the doses used in the Marin paper are not as high as in other studies. (let alone the amounts used in a typical cycle) Indeed studies using a higher dose of DHT (Simon et al., 2001) show different effects. Also Marin didn't even monitor of sex hormones levels, so he couldn't adapt the dose when necessary.

And just for the record; in the case of anabolic steroids I do think anecdotal information is generally highly valuable. Especially in this case were millions of bbers use DHT related compounds on a cut. Your study is not only in direct contrast with this anecdotal information, but also with most of the (scarce) literature. You're just an alarmist.

[TheGoodBro]

And FFS when are you going to answer the CN questions? Don't you think you guys are obligated that to your customers?

[DR_P]

Indeed studies using a higher dose of DHT (Simon et al., 2001) show different effects.

Can you provide the full citation of Simon et al., 2001?

[TheGoodBro]

Can you provide the full citation of Simon et al., 2001?

I'll answer that question when you answer mine. I know, very childish, but unfortunately that are all 'discussions' with you.

[DR_P]

Can you provide the full citation of Simon et al., 2001?

Assuming that it is this one:

Diabetes Care. 2001 Dec;24(12):2149-51.
Androgen therapy improves insulin sensitivity and decreases leptin level in healthy adult men with low plasma total testosterone: a 3-month randomized placebo-controlled trial.
Simon D, Charles MA, Lahlou N, Nahoul K, Oppert JM, Gouault-Heilmann M, Lemort N, Thibult N, Joubert E, Balkau B, Eschwege E.

This study has not assessed abdominal / visceral fat mass, so it is quite irrelevant to the discussion of this thread.

[TheGoodBro]

Assuming that it is this one:

Diabetes Care. 2001 Dec;24(12):2149-51.
Androgen therapy improves insulin sensitivity and decreases leptin level in healthy adult men with low plasma total testosterone: a 3-month randomized placebo-controlled trial.
Simon D, Charles MA, Lahlou N, Nahoul K, Oppert JM, Gouault-Heilmann M, Lemort N, Thibult N, Joubert E, Balkau B, Eschwege E.

This study has not assessed abdominal / visceral fat mass, so it is quite irrelevant to the discussion of this thread.

I didn't claim that, either. However it does show (with a huge leap of fait, and in this case there are very few relevant studies) that different doses of DHT have different effects on insulin sensitivity. And as the authors speculate:

From the literature, we can speculate that the effect of androgens on insulin sensitivity could be caused by changes in body composition and fat mass distribution. Indeed, androgens are known to increase fat-free mass and muscle size and to decrease visceral fat mass (8) by inhibiting lipoprotein lipase activity, therefore inhibiting triglyceride uptake and accelerating triglyceride release from abdominal adipose tissue (9). In turn, a decrease in abdominal fat mass may induce an improvement in insulin sensitivity via a reduction in circulating free fatty acids (10)

I'd be much happier if they indeed measured abdominal adipose tissue, but I wouldn't just dismiss this as irrelevant.

Now you answer my questions.

[TheGoodBro]

For some reason I can't edit my post. Just dismiss this sentence, as it was refering to abdominal adipose tissue:

(with a huge leap of fait, and in this case there are very few relevant studies)

[DR_P]

I didn't claim that, either. However it does show (with a huge leap of fait, and in this case there are very few relevant studies) that different doses of DHT have different effects on insulin sensitivity.

This study has investigated a variable dosing regimen of DHT that was aimed to reach normal plasma DHT levels in hypogonadal men. THis study has no relevance to the question of differential dosing effects on insulin sensitivity because it did only have one DHT arm and has not compared different DHT doses. Let alone that it allows any inferences on visceral fat mass.

[TheGoodBro]

This study has investigated a variable dosing regimen of DHT that was aimed to reach normal plasma DHT levels in hypogonadal men. THis study has no relevance to the question of differential dosing effects on insulin sensitivity because it did only have one DHT arm and has not compared different DHT doses. Let alone that it allows any inferences on visceral fat mass.

Yep and the authors totally disagree with you.

They also point at the flaws of the Marin study and considering you also ignored the 'evidence' provided by Bolduc et al. I strongly believe discussing with you is hopeless as you only seem to want to confirm your own personal experience.

[DR_P]

Yep and the authors totally disagree with you.

They also point at the flaws of the Marin study and considering you also ignored the 'evidence' provided by Bolduc et al. I strongly believe discussing with you is hopeless as you only seem to want to confirm your own personal experience.

Sorry, but this post does not make any sense. What 'evidence' from the Balduc study are you speaking about? The Balduc study investigated gene expression patterns in abdominal visceral adipose tissue in DHT treated mice. As I have stated in the first post of this thread, DHT induces a plethora of signaling pathways including - but not limited to - adipogenic pathways. It is absolutely impossible to deduce any net effects on visceral adipose tissue from these complex gene expression effects. However, the effects on the adipogenic pathways could provide an explanation for the observed results from the human clinical trial that found increased visceral adipose mass in DHT treated humans.
FYI, the Balduc study is not a meta-analysis nor is it a systematic review; it is an experimental study and evidence from this study refers to its experimental results.

[TheGoodBro]

Sorry, but this post does not make any sense. What 'evidence' from the Balduc study are you speaking about? The Balduc study investigated gene expression patterns in abdominal visceral adipose tissue in DHT treated mice. As I have stated in the first post of this thread, DHT induces a plethora of signaling pathways including - but not limited to - adipogenic pathways. It is absolutely impossible to deduce any net effects on visceral adipose tissue from these complex gene expression effects. However, the effects on the adipogenic pathways could provide an explanation for the observed results from the human clinical trial that found increased visceral adipose mass in DHT treated humans.
FYI, the Balduc study is not a meta-analysis nor is it a systematic review; it is an experimental study and evidence from this study refers to its experimental results.

Well, if you actually read the Bolduc et al. paper you would have noticed that they discussed the Marin paper where they said that paper seemed to contradict others.

Your only evidence is the Marin paper. Considering the many critics and contradictory results in other papers I believe your claims are based on quicksand, and do definitely not warrant a thread with an alarmistic approach like this one. Don't you agree?

[DR_P]

Considering the many critics and contradictory results in other papers ...

where are these contradictory results from other papers? So far, you have presented none.

[TheGoodBro]

where are these contradictory results from other papers? So far, you have presented none.

Lol you're again being misleading. Read the thread, 'doc'.

Is it direct evidence DHT decreases visceral fat. No of course not, but your data is far from convincing either. If we correctly weight the (lack of) literature, the only conclusion we can make is that there needs to be more research.

You're just an alarmist trying to prove your point with one study (in the OP you even say there are more human trials) and ignoring the evidence pointing to the contrary.

Inb4 you delete this thread also.

[TheGoodBro]

And now we're looking at actual DHT derivative (oxandrolone/anavar), how the hell do you explain this?

Oral anabolic steroid treatment, but not parenteral androgen treatment, decreases abdominal fat in obese, older men.
Lovejoy JC, Bray GA, Greeson CS, Klemperer M, Morris J, Partington C, Tulley R.
Source
Pennington Biomedical Research Center, Baton Rouge, Louisiana 70808-4124, USA.
Abstract
OBJECTIVE:
To compare the effects of testosterone enanthate (TE), anabolic steroid (AS) or placebo (PL) on regional fat distribution and health risk factors in obese middle-aged men undergoing weight loss by dietary means.

DESIGN:
Randomized, double-blind, placebo-controlled clinical trial, carried out for 9 months with primary assessments at 3 month intervals. Due to adverse blood lipid changes, the AS group was switched from oral oxandrolone (ASOX) to parenteral nandrolone decaoate (ASND) after the 3 month assessment point.

SUBJECTS:
Thirty healthy, obese men, aged 40-60 years, with serum testosterone (T) levels in the low-normal range (2-5 ng/mL).

MAIN OUTCOME MEASURES:
Abdominal fat distribution and thigh muscle volume by CT scan, body composition by dual energy X-ray absorptiometry (DEXA), insulin sensitivity by the Minimal Model method, blood lipids, blood chemistry, blood pressure, thyroid hormones and urological parameters.

RESULTS:
After 3 months, there was a significantly greater decrease in subcutaneous (SQ) abdominal fat in the ASOX group compared to the TE and PL groups although body weight changes did not differ by treatment group. There was also a tendency for the ASOX group to exhibit greater losses in visceral fat, and the absolute level of visceral fat in this group was significantly lower at 3 months than in the TE and PL groups. There were significant main effects of treatment at 3 months on serum T and free T (increased in the TE group and decreased in the ASOX group) and on thyroid hormone parameters (T4 and T3 resin uptake significantly decreased in the ASOX group compared with the other two groups). There was a significant decrease in HDL-C, and increase in LDL-C in the ASOX group, which led to their being switched to the parenteral nandrolone decanoate (ASND) after 3 months. ASND had opposite effects on visceral fat from ASOX, producing a significant increase from 3 to 9 months while continuing to decrease SQ abdominal fat. ASND treatment also decreased thigh muscle area, while ASOX treatment increased high muscle. ASND reversed the effects of ASOX on lipoproteins and thyroid hormones. The previously reported effect of T to decrease visceral fat was not observed, in fact, visceral fat in the TE group increased slightly from 3 to 9 months, although SQ fat continued to decrease. Neither TE nor AS treatment resulted in any change in urologic parameters.

CONCLUSIONS:
Oral oxandrolone decreased SQ abdominal fat more than TE or weight loss alone and also tended to produce favorable changes in visceral fat. TE and ASND injections given every 2 weeks had similar effects to weight loss alone on regional body fat. Most of the beneficial effects observed on metabolic and cardiovascular risk factors were due to weight loss per se. These results suggest that SQ and visceral abdominal fat can be independently modulated by androgens and that at least some anabolic steroids are capable of influencing abdominal fat.

Effects of androgen therapy on adipose tissue and metabolism in older men.
Schroeder ET, Zheng L, Ong MD, Martinez C, Flores C, Stewart Y, Azen C, Sattler FR.
Source
Department of Medicine and Division of Infectious Diseases, University of Southern California, Los Angeles, California 90033, USA.
Abstract
We investigated the effects of oxandrolone on regional fat compartments and markers of metabolism. Thirty-two 60- to 87-yr-old men (body mass index, 28.1 +/- 3.4 kg/m(2)) were randomized to oxandrolone (20 mg/d; n = 20) or matching placebo (n = 12) treatment for 12 wk. Oxandrolone reduced total (-1.8 +/- 1.0 kg; P < 0.001), trunk (-1.2 +/- 0.6 kg; P < 0.001), and appendicular (-0.6 +/- 0.6 kg; P < 0.001) fat, as determined by dual energy x-ray absorptiometry. The changes in total and trunk fat were greater (P < 0.001) than the changes with placebo. By magnetic resonance imaging, visceral adipose tissue decreased (-20.9 +/- 12 cm(2); P < 0.001), abdominal sc adipose tissue (SAT) declined (-10.7 +/- 12.1 cm(2); P = 0.043), the ratio VAT/SAT declined from 0.57 +/- 0.23 to 0.49 +/- 0.19 (P = 0.002), and proximal and distal thigh SC fat declined [-8.3 +/- 6.7 cm(2) (P < 0.001) and -2.2 +/- 3.0 kg (P = 0.004), respectively]. Changes in proximal and distal thigh SC fat with oxandrolone were different than with placebo (P = 0.018 and P = 0.059). A marker of insulin sensitivity (quantitative insulin sensitivity check index) improved with oxandrolone by 0.0041 +/- 0.0071 (P = 0.018) at study wk 12. Changes in total fat, abdominal SAT, and proximal extremity SC fat were correlated with changes in fasting insulin from baseline to study wk 12 (r >or= 0.45; P < 0.05). Losses of total fat and SAT were greater in men with baseline testosterone of 10.4 nmol/liter or less (<or= 300 ng/dl) than in those with higher levels [-2.5 +/- 1.1 vs. -1.5 +/- 0.8 kg (P = 0.036) and -24.1 +/- 14.3 vs. -2.9 +/- 21.3 cm(2) (P = 0.03), respectively]. Twelve weeks after discontinuing oxandrolone, 83% of the reductions in total, trunk, and extremity fat by dual energy x-ray absorptiometry scanning were sustained (P < 0.02). Androgen therapy, therefore, produced significant and durable reductions in regional abdominal and peripheral adipose tissue that were associated with improvements in estimates of insulin sensitivity. However, high-density lipoprotein cholesterol decreased by -0.49 +/- 0.21 mmol/liter and directly measured low-density lipoprotein cholesterol increased by 0.57 +/- 0.67 mmol/liter and non-high-density lipoprotein cholesterol increased by 0.54 +/- 0.97 mmol/liter (P < 0.03 for each) during treatment with oxandrolone; these changes were largely reversible. Thus, therapy with an androgen that does not adversely affect lipids may be beneficial for some components of the metabolic syndrome in overweight older men with low testosterone levels.

Alarmist status confirmed.

Like I said, in the case of AAS/PH/DS anecdotes are IMO highly relevant.

[DR_P]

You're just an alarmist trying to prove your point with one study

where again were the "many contradictory findings" that you have announced? Of course is more research needed, but you have been attacking the hypothesis of that thread without ANY evidence whatsoever.

[TheGoodBro]

Treatment with Oxandrolone and the Durability of Effects in Older Men.

Schroeder ET, Zheng L, Yarasheski KE, Qian D, Stewart Y, Flores C, Martinez C, Terk M, Sattler FR.

Division of Infectious Diseases, University of Southern California, Keck School of Medicine, Los Angeles, CA, USA; Biokinesiology and Physical Therapy, University of Southern California, Los Angeles, CA, USA.

We investigated the effects of the anabolic androgen, oxandrolone, on lean body mass (LBM), muscle size, fat, and maximum voluntary muscle strength, and determined the durability of effects after stopping treatment. Thirty-two healthy 60-87 year old men were randomized to receive 20 mg oxandrolone/day (n = 20) or placebo (n = 12) for 12 weeks. Body composition (DEXA, MRI and D2O dilution) and muscle strength (1-repetition maximum; 1-RM) were evaluated at baseline and after 12 weeks of treatment; body composition (DEXA) and 1-RM strength were then assessed 12 week after discontinuing treatment (week 24). At week 12, oxandrolone increased LBM 3.0+/-1.5kg (P<0.001), total body water 2.9+/-3.7kg (P=0.002), proximal thigh muscle area 12.4+/-8.4cm(2) (P<0.001); these increases were greater (P<0.003) than in the placebo group. Oxandrolone increased 1-RM strength for leg press 6.7+/-6.4% (P<0.001), leg flexion 7.0+/-7.8% (P<0.001), chest press 9.3+/-6.7% (P<0.001), and latissimus pull-down 5.1+/-9.1% (P=0.02) exercises; these increases were greater than placebo. Oxandrolone reduced total (-1.9+/-1.0kg) and trunk fat (-1.3 +/-0.6kg; P<0.001) and these decreases were greater (P<0.001) than placebo. Twelve weeks after discontinuing oxandrolone (week 24), the increments in LBM and muscle strength were no longer different from baseline (P>0.15). However, the decreases in total and trunk fat were sustained (-1.5+/-1.8, P=0.001 and -1.0+/-1.1kg, P<0.001, respectively). Thus, oxandrolone induced short-term improvements in lean body mass, muscle area, and strength, while reducing whole-body and trunk adiposity. Anabolic improvements were lost 12 weeks after discontinuing oxandrolone, while improvements in fat mass were largely sustained.

...

[DR_P]

And now we're looking at actual DHT derivative (oxandrolone/anavar), how the hell do you explain this?

oxandrolone is NOT DHT.

As I have already stated in the introduction to this thread, different androgens may have differential effects on visceral adipose tissue. For example, testosterone has been found to decrease visceral abdominal fat while DHT was found to increase it.
This thread is solely about DHT and DHT prohormones, not about any other androgens.

[TheGoodBro]

where again were the "many contradictory findings" that you have announced? Of course is more research needed, but you have been attacking the hypothesis of that thread without ANY evidence whatsoever.

Damn, you're harsh. Post #9, #13, #18 #21.