The Effect of Testosterone With / Without Training on Size, Morphology, Neuronal Wiring of Elderly Muscle (Rat Model)

How do youthful+ (probably slightly above range) levels of testosterone affect muscle size, strength, and morphology as we age? That's more or less what the authors of a recent study wanted to know when they injected aging rats with testosterone propionate and observed if/how this would affect aging in the presence or absence of resistance training.

Yes, I know, this is only a rodent study, and no one can tell for sure if similar effects will be observed in human beings... I know. What you can be sure about, however, is that an identical study is not going to be conducted with human subjects. So, all smartasses who don't give a damn about rodent studies and are unwilling to or unable to take them for what they are - basic physiological studies for hypothesis formation - please stop reading here.

Since you have not stopped reading, yet, I guess you will be interested in what the researchers from the São Judas Tadeu University and the São Paulo State University did to analyze the effects of resistance training associated with and without the concomitant the administration of exogenous significant amounts of testosterone.

Read more about studies involving TRT/HRT & co on suppversity.com:

What to expect from normalizing Testosterone

Testosterone Gel Augmens 'ur Gainz

PWO T-Increases Don't Determine Your Gainz

The Hormonal + Other Underpin-nings of Gainz

Impressive 12% T-Boost (+20% IGF1) W/ Tribulus

Low Testosterone = Low Life Expectancy?

For their study, the scientists used 30 Wistar male rats (Rattus norvegicus). With an initial age of 20 months and a study duration of 4 months, the scientists observed their hairy subjects over a period that's roughly equivalent 11.5 years in human terms (Sengupta 2013). If the results of the study are representative of what we would see in human beings, it would thus be representative of roughly 57-60-year-old human beings. The rats were divided into five groups  ...

• SEI - 20 months-old that were used as initial control (n = 6);
• SEF - 24 months-old which remained as final control of the procedures (n = 6);
• T - 20 months-old which received injections of testosterone propionate (n = 6);
• S – 20 months-old which underwent resistance training (n = 6) and
• ST - 20 months-old which were trained and received testosterone injections (n = 6).

The resistance training that was done thrice a week consisted, as it is common practice in rodent studies, of 6-8 'sets' of climbing a ladder with an inter-set rest of 2 minutes, a progressively increased weight on their backs (initial load 50% body weight).

The study used a dosages that are probably slightly higher than the equivalent of what you'd see in the average human TRT -- With respect to the previously voiced concerns about how representative the data from this rodent study would be for humans, it's important to note that the scientists chose a dosage that has previously been shown to (a) increase bone mineral density and growth hormone and (b) trigger significant increases in muscular hypertrophy in aged rats. This means that (a) it is certainly not representative of a classic testosterone cycle in bodybuilders, where the dosing will probably be significantly higher. On the other hand, the levels may be slightly higher than in conservative TRT, where T is often boosted only to "age-appropriate" (whatever that may be), not high(er) youthful levels.

The testosterone was administered in form of 200 mg/20 ml of testosterone propionate (TP), which was administered by intraperitoneal injection, twice a week (Tuesdays and Fridays), starting from the first day of the experiment in the T and ST groups. All rats were euthanized at the end of the study period, soleus and plantaris muscles were removed and prepared for histochemistry and cytofluorescence.

Figure 1: Final body weight (g) and relative muscle mass (as % of total mass) after 4 months (Krause Neto 2017).

As you can see in Figure 1 all three treatments, i.e. testosterone alone (T), training alone (S) and testosterone + training (ST), led to significant increases in the relative soleus and plantaris mass of the rodents - statistically significant were these benefits yet only for the plantaris muscle (note: unfortunately, the total lean and fat mass/body composition of the rodents was not assessed / the relative muscle mass, i.e. indiv. muscle/total mass in Figure 1, right is thus the best proxy we have).

Figure 2: Cross sectional area of type I, II-a & IIx fibers (µm²) of the soleus muscles (Kause Neto 2017); a indicates a significant difference in relation to SEI, b indicates a significant difference in relation to SEF.

For the soleus muscle, significant changes in the cross-sectional area were observed only for the type I fibers in the T, S, and ST group and the type I + type IIA fibers in the ST group.

Training alone makes rodents strong(est)

While the rodents in all three intervention groups got stronger over the 4-months study, it was not the training + testosterone (ST) group that got the strongest. Rather than that, the training only (S) group saw the greatest increases in muscle strength (+81% vs. 43% in T and 66% in ST groups).
In contrast to the maximal strength, though, the absolute training weights showed no significant inter-group difference for the T (training only) and ST (steroids + training) group, yet. With 154.3 g and 147.1 g in the S and ST group respectively, there is, however, a visible "training only" advantage.

Neither resistance training nor testosterone alone or in combination prevented the deterioration of the wiring between brain and muscle: The neuromuscular junction (NMJ) is the link between the brain and your muscles. It's deterioration and the subsequent denervation of muscle fibers often precedes (if not triggers) the onset of muscle loss. Accordingly, the absence of changes in the corresponding parameters assessed in the study at hand is a problem, because a severe degeneration of the NMJ may trigger problems you'd otherwise associate with sarcopenia, i.e. the loss of skeletal muscle mass and strength as a result of aging. This result is in line with previous resistance training studies (Deschenes 2015), but in contrast to studies which used an endurance training protocol that kept the NMJs functional (Deschenes 2016).

Hormone/Testosterone replacement therapy is one of the top-sellers in so-called/self-proclaimed anti-aging clinics. Now, the study at hand has been conducted in rodents, not men, but with its design, it is still representative of the average healthy, non-hypogonadal, but aging man who's fed up of progressive muscle and strength loss. The same guy who would pay the aforementioned clinics a visit to get testosterone shots that will up his levels to the upper end of the normal range of men in their twenties.

Steroids alone will reverse the age-related decline in muscle strength and size

If we assume for the time being, that the results Krause Neto et al. observed in this model of aging translate (not necessarily 1:1, but at least as far as the general results are concerned) to human beings, our guy from the previously described example will see results - after all, significant increases in muscle strength and size (esp. in fast-twitch muscles you'd use to lift or sprint, those muscles that deteriorate most as you age and thus affect the jacked look you may have had in your 20-40s) were observed in all three treatment groups.

Before you run to the next best HRT clinic, though, I suggest you take a look at the effects of training alone. With strength and size increases that were similar to the ones the scientists observed in the steroid (T) and steroid + training (ST) groups, the study at hand clearly confirms the potent anti-(muscle-)aging effects of a simplistic strength training (weight carrying) protocol.

Body composition probably benefits most from adding testosterone to training

A non-deniable downside to training with suboptimal testosterone levels, however, is the reduced effect on body composition. Even though the scientists didn't measure the body fat of their hairy subjects directly, the reduced reduction in body weight (-14-15% w/ testosterone vs. -10% w/ training only) clearly suggests that the rodents on "T" lost more body fat than their peers in the training-only group.

Figure 2: Relative change in lean and fat mass in response to changes in serum testosterone (calculated based on Bhasin. 2001) - you can read up on the different effect size of T on fat and muscle in my previous article "Quantifying the Big T".

And that's a result that should not surprise you if you've read my detailed elaborations on the effects of testosterone on muscle size in the "Intermittent Thoughts on Building Muscle" (go to the article overview and conclusion or read up on the different effect size of low/high testosterone on body fat and skeletal muscle in the corresponding part of the article series: "Quantifying the Big T"), in which I showcase that the effect of low testosterone on body fat is much more pronounced than its effects on skeletal muscle size.

You don't need TRT to counter the age-related loss of muscle strength and size: Yes, the effect on the rodents body composition seems to be more pronounced with youthful (or even higher) testosterone levels. Before jumping to the conclusion that you cannot get along without HRT/TRT as you age, though, there are yet three things you shouldn't forget:

• 

  Learn more about the effects of TRT on body comp (if T is low), here

  First, the strength-decline that's probably the greatest obstacle to normal physiological function in the elderly was countered at least as, if not more effectively, by training alone.  
• Second, even if the body fat loss was probably lower for the T than for the S and ST group, the muscle-to-total-body-weight ratio leaves little doubt that the training only (T) group saw improvements in body composition, too. 
• Third, a more elaborate workout that isn't limited to carrying weight upstairs for 6-8 sets may have significantly more pronounced effects on older men's body composition, would thus reduce the testosterone advantage in terms of body composition, and could, on top of that, augment the training-induced changes in muscle size and strength even further - regardless of whether you are or aren't on TRT.

So, overall, there's little doubt: the study clearly confirms the potential benefits of HRT/TRT as an anti-aging program for aging muscles, guys. It does, however, and I believe that's at least as important, also demonstrate that a little training will also go a long way - at least, if your testosterone levels suffered only the natural decline and are not rock bottom, to begin with. | Comment!

References:

• Bhasin, Shalender, et al. "Testosterone dose-response relationships in healthy young men." American Journal of Physiology-Endocrinology And Metabolism 281.6 (2001): E1172-E1181.
• Deschenes, Michael R., et al. "Effects of resistance training on neuromuscular junction morphology." Muscle & nerve 23.10 (2000): 1576-1581.
• Deschenes, Michael R., et al. "Effect of resistance training on neuromuscular junctions of young and aged muscles featuring different recruitment patterns." Journal of neuroscience research 93.3 (2015): 504-513.
• Deschenes, Michael R., et al. "Effects of exercise training on neuromuscular junction morphology and pre-to post-synaptic coupling in young and aged rats." Neuroscience 316 (2016): 167-177.
• Krause Neto, Walter et al. "Divergent effects of resistance training and anabolic steroid on the postsynaptic region of different skeletal muscles of aged rats." Experimental Gerontology 98 (2017): 80-90.
• Sengupta, Pallav. "The laboratory rat: relating its age with human's." International journal of preventive medicine 4.6 (2013): 624.

Mercury, From Fish to Toenail; Less Testosterone Needed W/ TRT + Tongkat Ali; R,R-Monatin the Next Stevia From South Africa! Plus: Magnesium Protects Mitochondria from LPS & Caffeine Arteries from HIIT Induced Platelet Activity!

Image 1: Looks like the Terminator was concerned about "bone" health, maybe he should consider Tonkgat ali as an addition to his TRT... or whatever regimen;-)

If you want to, you can call today's news a special installment of "On Short Notice", I have already had a couple of interesting news and before I am piling up another truckload, I thought I could make at least some of you happy and put a handful of them out before the Super Human Radio & SuppVersity Science Round-Up on Thursday (you better make time to listen live, Thursday, 12PM/EST and download the first installment if you haven't done so, already ;-) and the "official" Saturdaily installment of "On Short Notice", here at the SuppVersity.

So let's see what we have here: Contrary to the order in the headline we will check out your toenails later, after all, I don't know what they look like and don't want to kill your appetite so that you cannot fully appreciate the findings of Fry et al. who discuss the potential application of an extract from the bark of Sclerochiton ilicifolius A.Meeuse as an all natural sweetener that's probably at least as, if not sweeter than stevia and - you guessed it - 100% calorie free! The same, i.e. being calorie free is obviously true for magnesium aspartate... whatever, in view of its potent protective effects against lipopolysaccharide induced mitochondrial damage and decay, you should not care about that, anyways.  And despite the fact that I would hope that the same goes for the minor pro-thrombotic effects of interval training, there may be one or another of the SuppVersity readers who's having issues with platelet activity already and will therefore be relieved to hear that a cup of coffee before your workout will not increase, but rather decrease the risk of thrombosis in response to the post-exercise increase in platelet activity.

You don't want to miss this week's installment of the joint Super Human Radio + SuppVersity
Science News Roundup - the show airs each Thursday, 12PM/EST (tune in live!)

The latter, i.e. the risk of thrombosis would by the way be even higher, if you were one of Xun et al.'s study participants who consumes one or more servings of fish per day. This would place you at greater risk of having high toenail mercury levels and with those being representative of whole body and tissue mercury levels you would already have higher baseline platelet activity than Mr. or Mrs. Healthy Average Joe, which would probably be a reason for your doctor to tell you that he cannot, by any means, put you on TRT (testosterone replacement therapy) - and that even if you were about as hypogonadal as the castrated rats in the Saadiah Abdul Razak study from the latest issue of Evidence Based Complementary Medicine. A study by the way you could print, show it to your doctor and say: "Look, I don't want to lose my muscle and break my bone, so let's do this you give me a script for low dose TRT and I get myself some quality Eurycoma longifolia extract and we will see how my values look like in 6 weeks from now." 

You see, as usual, even doctors can learn something, here at the SuppVersity so let's not put them on the rack for another paragraph or two and start right with our first item for today:

• 

  Image 2: Could the bark of these twigs from a spiny-leafed, hardwood shrub from South Africa hold a likewise natural stevia alternative?

  Is R,R-Monatin the new stevia? I know you all love your stevia, but there are people who simply hate the taste and still don't want to resort to any of the dubious sugar alcohols let alone the 100% artificial sweeteners, who may be interested that John C. Fry and a couple of other researchers published ad paper on a novel all natural sweetener from the bark of a South African spiny-leafed, hardwood shrub that goes by the name of  Sclerochiton ilicifolius A.Meeuse (Fry. 2012).
  According to the Fry et al., the compound has a potency above 3000 at 5% sucrose equivalent, which would make it (theoretically) even sweeter than stevia. Since the latter hit the market, we do yet all know how unrealiable these theoretical values are so that we will probably have to wait until the first monatin-based sweeteners become available - and you as a SuppVersity would be the first to know what's in there ;-)
  If we assume that there are no hitherto undisclosed health issues with monatin and it does in fact taste sweet and not disgusting, metallic or whatever, it is also likely that we are going to see new "proprietary" blends of stevia + monatin, similar to their artificial counterparts you still see in Coke Zero & Co - the quasi "natural" way to get as close as possible to the "true sugar taste", people are still craving, these days... if they don't hurry, I do yet doubt that there will be a market for products like that very long, as we are more or less trained to crave the "real sugar" taste, but this would be the topic for another blogpost ;-)

• 

  Figure 1: Effect of different doses of pre-supplementation with magnesium aspartate on markers of LPS induced mitochondrial decay, antioxidant activity and oxidative damage (data calculated based on Ahmed. 2012)

  250mg/day magnesium counter the metabolic derangements from lipopolysaccharide (LPS) intoxication When Lamiaa A. Ahmed added 20mg/kg or 40mg/kg (~125mg or 250mg in human equivalents) of magnesium aspartate to the chow mice that were pretreated with LPS injections, the researcher from the Faculty of Pharmacy at the University of Cairo found that this regimen restored body temperature (low dose) and heart rate (high dose) of the profoundly inflamed to normal, restored the lowered glutathione levels (both doses) and reduced (low dose) and normalized (high dose) the elevated creatine kinase (marker of cell damage) and thiobarbituric acid reactive substances (TBARS; marker of oxidative damage) levels that had been elevated by the lipopolysaccharide treatment (Ahmed. 2012).
  The ATP:ADP ratio, the activity of the sodium potassium pumps and the creatine phosphate levels (CrPh protects the cell wall from damage as you remember from a previous installment, right?) were not completely restored to, but the pathological changes were minimized dose-dependently. In conjunction with the normalization of the lactate to pyruvate ratio, a sign of either exertional exercise or - if it occurs at rest, as it does here - mitochondrial failure, these observations indicate that Mg therapy could be a reliable protective agent in LPS-induced cardio- and general myotoxicity. In that it should be noted that higher, but not exorbitantly high (250mg is roughly 2/3 of what you should aim to get from our diet everyday, anyway) doses were more effective in reducing cell membrane damage as well as in improving the intracellular acidosis, energy production, oxidative stress and Na+,K+-ATPase activity and corresponded with a better perseverance of the mitochondrial ultrastructure.
  And while Ahmed sees the main application of Mg aspartate therapy in "critically ill" patients, I would say that the large group of patients (and non-patients) with other pathologies such as a leaky gut would benefit as well, since the defective gut barrier opens the door for the "excrements" of your gut bacteria, to induce all sorts of pathologies including mitochondrial damage and decay, but also depression, obesity, diabetes, etc. (Maes. 2008; Musso. 2010)... and before I forget to mention it is not unlikely that cheap magnesium citrate (if tolerated) would do the job just as well - maybe in a slightly higher dosage of say 300mg per day (best taken in divided doses with food).

• 

  Image 3: Coffee is full of wonders ;-)

  Antithrombotic effects of caffeine blunt platelet activity in response to interval training The use of 3mg/kg (equiv. to ~1 large cup of strong coffee or 2 smaller cups of regular coffee) of caffeine as an ergogenic aid during aerobic interval training cannot just improve your performance, it will also prevent the pro-thrombotic platelet function activation that occurs during exercise. That's the somewhat surprising finding of the one of the latest studies from the Health Innovations Research Institute at the School of Medical Sciences on the campus of the RMIT University in Melbourne, Australia (Whittaker. 2012).
  Whether this effect is of any importance to you certainly depends on your personal health. Personally, I would say that it is negligible for the vast majority of people who engage in strenuous athletic activities, if you belong to a risk group where platelet function is either high (risk of developing thromboses) or low (risk of bleeding) you may want to keep these results in mind.
  And if you don't care about platelet function, you may be considering to have another cup of coffee, when I tell you that ~3 cups per day appear to offer some protection against skin cancer, parkinson's and non-alcoholic-fatty-liver disease (click on the links to read the full stories on the SuppVersity Facebook Wall).

• 

  Image 4: Remember last week's post on the mercury in fish and how it's not simply excreted with the selenium, let alone the cysteine it's bound to? It looks like the toenails of young Americans would confirm those lab results.

  Something fishy about toenail mercury levels I guess all of you will remember my "shocking" post about the mercury toxicity from fish (cf. "Mercury in Fish NOT Harmless, Regardless of Cysteine, Selenium, EPA or DHA!"), this one could actually go as sort of a follow up post, as it deals with the real-world consequences of mercury exposure and the subsequent deposition of the heavy metal in the toe nails of the 4,344 American male and female participants (age 20–32y) in the CARDIA Trace Element Study researchers from the Gillings School of Global Public Health and School of Medicine at the University of North Carolina have recently examined (Xun. 2012).
  I know, it may sound gross, but toenails have, among the various biological specimens you could theoretically analyze, the advantage of providing a relatively reliable long-term measure of Hg exposure (from a few months to a year), are easily collected, transported,stored, and cleaned and are relatively sheltered from environmental contaminants and less likely to be contaminated by shampoo, hair treatments, and medication (Morris. 1983, He 2011).

  

  Image 5: Who would have thought that your toenails provide a way better measure of the toxic load you have accumulated than your hair, for example? Just looking at them is yet not enough for a thorough analysis

  Since the Hg levels in toenails also have relatively high correlation with both mercury intake (r = 0.54; Ohno. 2007) and the mercury deposition in critical organs (spec. in the brain - r = 0.65 ; Bjorkman. 2007), it should be obvious that the association between toe nail mercury levels and fish intake in all, but those participants who lived in Oakland and had the lowest (0.45 servings per day) fish intake per day could have a significant impact on the health of the subjects that consume more than one serving of fish per day and have a 76% higher beta coefficient of the natural logarithm of toenail Hg level than those who consume fish / seafood less than once per day (this mean that the mercury in the toenails of daily fish eaters increases 75% more rapidly towards that level than in those who eat 0.35 to 1.03 servings). Interestingly this was particularly true for the Caucasian men in the study, where the beta coefficient was another 45% higher (beta = 0.64 vs. beta = 0.44).
  Despite the fact that these results seem to confirm that eating one dose of untested canned tuna (which would probably go as way more than one serving in the eyes of the scientists) is not necessarily the best idea. It does however not mean that you cannot have you once or even twice a weak salmon steak or sushi - just keep your diet more versatile and don't make fish (or any other single foodstuff your only "allowed" source of protein or fat.

• 

  Figure 2: Weight of castrated rats on TRT, TRT (50% dose) + Eurycoma longifolia  (EL) or Eurycoma longifolia, alone, at the end of the 6-week supplementation phase, ratio of bone building osteocalcin to CRX a marker of bone resorption and actual bone strength, as measure by maximal tolerable load and Young's Modulus; all data expressed relative to sham operated (=intact) rats (data calculated based on Saadiah Abdul Razak. 2012)

  Low dose testosterone + long jack better than TRT alone? The results Saadiah Abdul Razak et al. present in the latest issue of Evidence Based Complementary Medicine don't actually look like they were interesting for muscle heads, I mean "androgen dependent osteoporosis", where are the word hypertrophy, skeletal muscle, or at least ripped & jacked? And I have to admit that of these only "skeletal muscle" makes its appearance somewhere in the introductory remarks of the discussion and only in the context of the "auxiliary functions" of testosterone as a growth hormone and IGF-1 booster and muscle builder. I do still believe that the data in the figure 2 on the right is going to get your attention - after all, the combination treatment of testosterone + Eurycoma longifolia did not "just" restore the balance of the "bone builder" osteocalcin to the "bone eater" ORX (actually it's just a marker of bone resorption) to normal (=sham levels), it did also effectively build the strongest bones, with the highest maximal load in Newton and the greatest elastic stability, as measured by the Young's Modulus.
  What's interesting, as well, is that all treatments were equally effective in restoring normal body weight - who knows maybe 15mg/kg/day (HED: 2.4mg/kg; ~170-250mg/day) of Eurycoma longifolia (EL) extract would even make a valuable stand alone (no pun intended ;-) testosterone booster for mild cases of real hypogonadism (not the one where your diet is shitty, your training sucks and it's your "low T" that you believe is to to blame that you make no gains), or an adjunct to HRT that would allow you to use only half the regular dose (this was done in the study at hand) and see similar results!? That it's good for sperm quality and testosterone, when it's administered in ~13x higher dosages in rodents (Chan. 2009) and for sperm health in men (at about the dosage used here; cf. Tambi. 2010) has already been established.
  And still, the "major gap" of which Bhat et al. postulated that it existed "in [sic!] providing scientific base for commercial utilization and clearance of the Tongkat Ali products with regard to consumer's safety" is still in existence. Moreover, the same could be said about our knowledge with respect to the individual effects of the potentially biologically active component(s) in the plant and respective extracts. Before those issues are not solved, the "extract" you may buy could be anything from uberpotent to simply toxic... although I suspect that it is still most likely that it will simply be ineffective.

What? That went too fast? Don't worry, it's just two days to the Thursdaily Science News Roundup on SHR, four days to the next official installment of "On Short Notice" and just one click away from a handful of additional up-to-the-minute news on the SuppVersity Facebook Wall such as

• the correlation of low growth hormone levels with NAFLD (= non-alcoholic fatty liver disease), 
• a study on how digestion potentates the antimicrobial activity of coconut oil,
• a potential successor to metformin that triples muscular glucose uptake in the absence of insulin 

and all the other interesting tidbits I have already and am still going to post there even before the next SuppVersity news is going to be published right here, tomorrow! Ah,... and by the way it's not prohibited to share articles you like on Facebook and other social media outlets ;-)

References:

• Ahmed, L.A., Protective effects of magnesium supplementation on metabolic energy derangements in
  lipopolysaccharide-induced cardiotoxicity in mice. Eur J Pharmacol. 2012.
• Bhat R, Karim AA. Tongkat Ali (Eurycoma longifolia Jack): a review on its ethnobotany and pharmacological importance. Fitoterapia. 2010 Oct;81(7):669-79. Epub 2010 Apr 29. 
• Bjorkman L, Lundekvam BF, Laegreid T, Bertelsen BI, Morild I, Lilleng P, Lind B, Palm B, Vahter M. Mercury in human brain, blood, muscle and toenails in relation to exposure: an
  autopsy study. Environ Health. 2007; 6:30 
• Chan KL, Low BS, Teh CH, Das PK. The effect of Eurycoma longifolia on sperm quality of male rats. Nat Prod Commun. 2009 Oct;4(10):1331-6. 
• Fry JC, Yurttas N, Biermann KL, Lindley MG, Goulson MJ. The Sweetness Concentration-Response of R,R-Monatin, a Naturally Occurring High-Potency Sweetener. J Food Sci. 2012 Aug 27.  
• He K. Trace elements in nails as biomarkers in clinical research. Eur J Clin Invest. 2011;  41(1):98–102.
• Maes M, Kubera M, Leunis JC. The gut-brain barrier in major depression: intestinal mucosal dysfunction with an increased translocation of LPS from gram negative enterobacteria (leaky gut) plays a role in the inflammatory pathophysiology of depression. Neuro Endocrinol Lett. 2008 Feb;29(1):117-24.
• Morris JS, Stampfer MJ, Willett WC Dietary selenium in humans: toenails as an indicator. Biol Trace Elem Res. 1983; 5:529–537.
• Ohno T, Sakamoto M, Kurosawa T, Dakeishi M, Iwata T, Murata K. Total mercury levels in hair, toenail, and urine among women free from occupational exposure and their relations to renal tubular function. Environ Res. 2007;103(2):191–1.
• Saadiah Abdul Razak H, Shuid AN, Naina Mohamed I. Combined Effects of Eurycoma
  longifolia and Testosterone on Androgen-Deficient Osteoporosis in a Male Rat Model. Evid Based Complement Alternat Med. 2012;2012:872406. Epub 2012 Aug 9.
• Whittaker JP, Linden MD, Coffey VG. Effect of Aerobic Interval Training and Caffeine on Blood Platelet Function. Med Sci Sports Exerc. 2012 Aug 29.
• Xun P, Liu K, Morris JS, Jordan JM, He K. Distributions and determinants of mercury concentrations in toenails among American young adults: the CARDIA Trace Element Study. Environ Sci Pollut Res Int. 2012 Aug 25.

Positive/Negative Effects of Normal/High DHT on Metabolic Pathways

Regular visitors of the SuppVersity will certainly remember some of my previous posts about the false demonization of DHT. A new study coming from the Institute of Endocrinology in Prague (Duskova. 2010) supports the view that "optimal" and not low DHT levels are what men should be striving for.

Theorizing that DHT as a non-aromatizable androgen could be responsible for a male type fat distribution, the scientists reviewed the results of both animal and human studies and found that "physiological levels of DHT [do not only] inhibit growth of mature adipocytes", but also have positive levels on body composition in patients on hormone replacement therapy (HRT). On the other hand, there is also evidence that high (super-physiological) DHT levels are associated with obesity:

In obese people, DHT metabolism in adipose tissue is altered. Local abundance of non-aromatizable androgen has a negative effect on adipose tissue and it could be involved in pathogenesis of metabolic and cardiovascular diseases.

So, in view of getting/staying lean and healthy, you want your DHT levels within normal ranges and you certainly don't want to block it by taking Saw Palmetto or (God forbid) Finasteride or other drugs out of fear of developing prostate cancer, even if you do not even know if your DHT levels are pathologically elevated.