News on USP Labs' "Pink Magic": High Dose Massularia Acuminata Increases Testosterone and Makes Bucks Horny as Hell

Faithful readers of the SuppVersity will probably remember my short write-up on USP Labs Test Booster "Pink Magic". Now that the initial fuss about how "brilliant" and "unique" the product is, is over there is finally another study on the efficiency of its main ingredient, a shrub called massularia acuminata.

Two scientists from Nigeria (Yakubo. 2011) published an article on the "Effect of Aqueous Extract of Massularia acuminata Stem on Sexual Behaviour of Male Wistar Rats" in the January issue of Evidence Based Complementary Alternative Medicine. The scientists found that supplementation with 500 and 1000mg/kg body weight (equivalent to 6.8g and 13.6g) of an aqueous extract of the stem of the botanical...

... increased the frequencies of mount and intromission. In addition, the ejaculation latency was significantly prolonged (P < .05). The latencies of mount and intromission were reduced significantly whereas ejaculation frequency increased. The extract also reduced the postejaculatory interval of the animals. Computed percentages of index of libido, mounted, intromitted, ejaculated and copulatory efficiency were higher in the extract treated animals compared to the distilled water-administered control whereas the intercopulatory interval decreased significantly.

In short: the rats were horny as hell ;-) But there was more to it:

The extract also significantly (P < .05) increased the serum testosterone content of the animals except in those administered with 250mg/kg body weight on days 1 and 3.

In view of these results it is interesting to have a look at the amount of massularia in Pink Magic. Unfortunately, USP provides no data on the amount of the individual ingredients - so, we only know that there is 1.6g of a mixture of massularia and two other botanicals in one serving. Massularia is mentioned first which tells us that it should be the main ingredient. So, let's be generous and assume that there is 1.0g of massularia per serving. USP recommends 3 servings per day. This would amount to 3.0g of massularia, which has now been clinically proven to be insufficient; and what's more even with 6.8g/day (equivalent to 500mg/kg in rats) the increase in testosterone (cf. Table 1) is still almost negligible.

Table 1: Effect of aqueous extract of Massularia acuminata stem on serum testosterone concentrations of male rats. (Yakubo. 2011)

What about all the positive feedback on various message boards, then? Well, we do not know how the dosing protocol used in rats eventually translates to human beings. The above calculation is based on a standard human equivalence dose formula, the accuracy of which is certainly questionable. Thus, the results of the study are actually good news for USP Labs, as they prove that massularia which, by the way is not a USP Labs exclusive anymore, actually works.

Resveratrol Increases Lipolysis and Reduces Lipogenesis in Mature Adipocytes

If you are (as I hope) an avid reader and daily visitor of the SuppVersity, you probably remember Friday's news on the "Side Effects of Polyphenol Supplementation". I just hope you did not throw away all your supplements immediately, because eventually the question of side effects is always relative. If, for example, you are a sumo competitor and in dire need of gaining mass, no matter what. It would be an unwelcome side-effect of resveratrol supplementation not to gain or even to lose body fat...

A report (Baile. 2011), recently published in the Annals of the New York Academy of Sciences does now confirm, what supplement companies have been promising all along: the right dose of supplemental resveratrol will limit fat gain and improve lipolysis in a mouse model:

Treatment of mice with resveratrol alone was shown to improve resistance to weight gain caused by a high-fat diet. Moreover, dietary supplementation of aged ovariectomized rats with a combination of resveratrol and vitamin D, quercetin, and genistein not only decreased weight gain but also inhibited bone loss.

The human equivalent dose to that used in the cited study would be about 35mg/kg (= 2.800mg for a 80kg human being), which, unfortunately, is much more than your average resveratrol product contains. So, what does this tell you? Either you spend a fortune for minor improvements in your resistance to an unhealthy diet OR you just consume a healthy diet in the first place - I bet you will end up leaner and healthier using the second option.

1.200 IU Vitamin D Won't Raise 25OH-D Levels Enough to See Beneficial Effects on Markers of Cardiovascular Health

In the course of the last weeks, I have refrained from posting each of the 1001 studies on vitamin D that appear in the myriad of medical magazines each month. It is simply too much, mostly very irrelevant information. A recent study by Maki et al. (Maki. 2011) is yet interesting insofar, as it provides some insight into the amounts of supplemental vitamin D one would probably need to see some cardiovascular benefits.

After supplementing the diets of their subjects with either a standard multi-vitamin or the multi-vitamin + 1,200IU of vitamin D for 8 weeks, the researcers measured serum 25-hydroxyvitamin D [25(OH)D] and high-density lipoprotein cholesterol (HDL-C) in subjects with high waist circumference and found:

There was a significant difference in mean change for 25(OH)D between the MVM and MVM+D treatment groups ( − 1.2 ± 2.5 nmol/l vs. 11.7 ± 3.0 nmol/l, respectively; P = 0.003). Vitamin D 1,200 IU/day did not increase 25(OH)D to a desirable level ( ≥ 75 nmol/l) in 61% of participants. There were no significant changes in cardiovascular disease risk markers. 

This is quite interesting, because even after all the fuss about vitamin D defiency that has even reached the mass media in the course of the last months, the general recommendation is not to take more than 1.000IU of vitamin D (sometimes even less) per day. For most people, this study seems to indicate, this is far too little to even get their vitamin D levels into the desirable ranges. Whether or not this would provide them with the beneficial results many scientists hope for, remains to be elucidated, though.

Another Good Reason to Take Creatine: Creatine Helps with Exercise Induced Arterial Stiffness

If there is one supplement out there on the fitness market that is really worth each cent you spend on it, it is probably creatine monohydrate.

In a recent study, scientists from the Florida State University (Sanchez-Gonzalez. 2011) report on the positive effects, of creatine supplementation (creatine monohydrate @ 2x5g /day for 3 weeks) on arterial stiffness and hemodynamics in 16 healthy male subjects:

Compared with the Pl group, the Cr group had attenuated (P\0.05) increases in SBP [systolic blood pressure] at PE5 [5 minutes post exercise] (Pl 14.0 ± 2.5, Cr 5.6 ± 2.3 mmHg), HR [heart rate] at both P5 (Pl 28 ± 4 vs. Cr 16 ± 2 beats/min) and PE15 (Pl 21 ± 3, Cr 11 ± 2 beats/min) and rate pressure product at P5 (Pl 45.8 ± 6.4, Cr 24.8 ± 2.2) and P15 (Pl 34.2 ± 5.0, Cr 15.9 ± 6.0). Compared with the Pl group, the Cr group had suppressed
increases in baPWV [brachial-ankle pulse wave velocity] at PE5 (Pl 1.5 ± 0.4, Cr-0.1 ± 0.4 m/s) and PE15 (Pl 1.1 ± 0.2, Cr -0.3 ± 0.3 m/s) and returned SBP to pre-exercise values at PE15 (Pl 10.6 ± 2.8, Cr 2.1 ± 2.6 mmHg). PWV in the exercised leg decreased at PE5 in both groups.

Overall, this indicates that creatine supplementation reduces cardiac stress from strength training. It would have been interesting, though, to see a more realistic setting for the study - with the single-leg extension exercise in an isokinetic dynamometer used in this you probably don't induce much cardiac stress, anyway. Sometimes, I am asking myself if any of those researchers have ever been to the gym to take a look at the intensity levels at which many ambitious gymrats work out...

Unexpected Side Effects of Flavonoid Supplementation: Do You have to Re-Evaluate the Use of EGCG, Grape Seed Extract & Co?

It is pretty exciting to see how scientists find new beneficial constituents in common foods on a daily basis. A group of these phytoprotectants is called "flavonoids". Respective extracts from grapes, green tea, etc. have been shown to exhibit various health benefits and supplement companies make a fortune selling them to health-conscious costumers. The question however remains: Did nature really intend us to consume these trace nutrients in such significant amounts?

Table 1: Potential beneficial and adverse effect of flavonoid supplements. (Egert. 2011)

Scientists from the Department of Nutrition and Food Science of the University in Bonn, Germany (Egert. 2011), have now taken a closer look at possible side-effects of a selection of these phytoprotectants. Among the possible interaction and health concerns the scientists have found were

• Flavonoid - trace element interactions - reduced the uptake of iron (and possible other trace elements)
• Flavonoid - vitamin interactions - folate, vitamin E and vitamin C absorption may be inhibited
• Flavonoid - thyroid interactions - increased risk of goiter and higher incidence of various forms of thyroid related illnesses

Last but not least, there are the effects on the cytochrome P450 pathway (hormonal interactions), possible interferences with specific medications and interactions with liver detoxification pathways (phase II enzymes in particular).

All this does not mean, that you should generally shy away from these nutrients. It shall only remind you of the fact that isolated in-vitro studies on certain beneficial effects of certain plant / fruit / legume extracts may not be enough to decide whether its worth risking unwanted side effects of inadequately researched "wonder supplements". Maybe, trying to get a diversified menu of flavonoids from a healthy and varied diet (yes, I am thinking of those of you who live on chicken breasts and broccoli), would be a viable alternative!?

Melatonin, Magnesium and Zinc for a Healthy Night of High Quality Sleep

Sleeping disorders are very common in our hectic society and sleeping pills are among the no.1 drugs (ab-)used by the general public. At least in a very restricted group of subjects, the combination of melatonin, magnesium and zinc has now proven a very viable and certainly more natural alternative to the highly advertised "chemical maces" of the big pharma companies.

Figure 1: Effects of treatment of the primary end point. Mean Pittsburgh Sleep Quality Index (PSQI) (marker) are reported at baseline and at 8 weeks for the melatonin, magnesium, and zinc (left) and placebo (right) participants, together with their standard deviations (whiskers). (Figure 2 from Rondanelli. 2011)

In a double-blind, placebo-controlled clinical trial set in along-term care facility in Pavia, Italy, researchers from the University of Pavia (Rondanelli. 2011) found a combination of 5 mg melatonin, 225 mg magnesium, and 11.25 mg zinc, mixed with 100 g of pear pulp taken 1 hour before bedtime to be an effective treatment for primary insomnia in elderly subjects:

The food supplement resulted in considerably better overall PSQI [Pittsburgh Sleep Quality Index] scores than placebo (difference between groups in change from baseline PSQI score=6.8; 95% confidence interval=5.4-8.3, P<.001). Moreover, the significant improvements in all four domains of the LSEQ [Leeds Sleep Evaluation Questionnaire] (ease of getting to sleep, P<.001; quality of sleep, P<.001; hangover on awakening from sleep, P=.005; alertness and behavioral integrity the following morning, P=.001), in SDQ [Short Insomnia Questionnaire] score (P<.001), in total sleep time (P<.001), and in SF-36 physical score (P=.006) suggest that treatment had a beneficial effect on the restorative value of sleep.

To summarize the results, the patients receiving the treatment for 8 weeks, slept longer, slept deeper, found it easier to get up in the morning and were overall more alert than those receiving placebo treatment. While it would certainly be necessary to verify these beneficial effects in younger subjects, it appears that the days of ZMA could well be over, with MMZ, i.e. Melatonin-Magnesium-Zinc being the new buzz-word of the industry.

Ginkgo, Ginseng, Green Tea: Only one of the G's may be worth Supplementing

In the most recent episode of their supplement review (which is usually very critical) the British Journal of Sports Medicine (BJSM Review. Part 17) has a look at studies on the ergogenic potential of ginkgo, ginseng and green tea, all of which are heavily advertised for their beneficial effects on health, long jeopardy and mental, as well as physical performance.

In the case of Ginkgo an Ginseng, the studies that have been considered in this review provide very inconclusive evidence for and against their use as ergogenics or medical plants. With regards to the underlying reasons for the discrepancies which have been reported, the reviewers argument that both, the origin, as well as the processing techniques may have influenced the efficiency of ginkgo and ginseng products. green tea, on the other hand, "shows some promise" - regular readers of this review series will know that this is already a great praise!

Although evidence is limited, green tea extract, and particularly the active component EGCG, has shown some consistency from animal to human models regarding a delay in fatigue during prolonged exercise. In humans this appears to be due to the effect of an increase in fat oxidation.

Against this background and in view of the declining prices of quality green tea products (especially if bought in bulk) green tea should obviously be the "G" of choice in your supplement regimen. Ah, and before I forget: green tea is actually something you drink, basically the counterpart to real food, which is what you probably have forgotten to eat facing the stash of capsuled supplements you're popping everyday ;-)

Resveratrol Fails to Ameliorate inflammatory response and Delayed Onset Muscle Soreness After a Marathon

Resveratrol, an antioxidant polyphenol from the skin of red grapes, has now been around for quite a while and as it was in the case of almost every other antioxidant which was hailed as a powerful panaceum (e.g. vitamin E) it slowly transpires that the real life value of resveratrol may well fall short of the expectations its potency in (mostly) in vitro studies rose among scientists and laymen alike.

For some of you it may yet still come as a surprise that the results of a double placebo-controlled randomised trial conducted at the London Marathon 2010 (Laupheimer. 2011) fall short of the expectations the colorful advertisements and cited abstracts from in vitro studies may raise in many half-informed customers:

There was no significant difference between the two groups in terms of changes occurring between pre and post-tests for WBC [white blood cell count], CRP [C reactive protein] or VAS [a measure of muscle soreness] (p=0.857, 0.629 and 0.70 respectively).

And, although the author remarks that the dose and loading protocol (600mg of resveratrol /day for 7 days before the event) may have been insufficient to produce favorable results, I would like to remind everyone that these 600mg is three times the dose one would get from the suggested usage of NOW's high quality Resveratrol 200. So, even if 1.200mg would work, this would be quite an expensive supplementation protocol.

And again: Vitamin E Supplementation has no Effect on All Cause Mortality

I suppose, only few of you will be surprised to read this: A very recent review by scientists from the University of Kentucky (Abner. 2011) confirmed the results of previous reviews of the available literature:

Based on the present meta-analysis, supplementation with vitamin E appears to have no effect on allcause mortality at doses up to  5,500 IU/d.

The scientists had compiled a selection of randomized, controlled trials published between 1988 and 2009 that investigated the treatment effect of vitamin E supplementation in adults for at least one year. What they got was a data pool comprising 246,371 subjects and 29,295 all-cause deaths with an overall risk ratio of 1.00 that was independent of whether or not the subjects received supplementary vitamin E.

On a side note: Instead of another review of the literature, I would have liked to see a study investigating the differential effects of the various forms of tocopherols and tocotrienols, of which I assume that the interaction / ratio between those is where the magic happens. So, if you happen to own a big laboratory and do not know what to do with it, I would certainly post the results of such a study ;-)

High Protein Diet Safe for Bones! Acid Load due to Meat Protein does not Compromise Calcium Metabolism.

Reading the caption of this post, some of you may rightly ask themselves: "Why does he even mention this? Of course, meat is safe - meat is natural and eating meat is what man is made for!" So, if you already knew all that, you can stop reading now. If, however, you still belong to the misguided brotherhood of the followers of the holy food pyramid with your "healthy" grains, pasta and cereals at the bottom, you may be interested in the results from an older scientific paper I just came across while posting an answer to a forum post of someone who was concerned that his bones will become brittle if he increases his protein intake beyond the 0.8g/kg body weight barrier.

In November 2010, Cao & Nilsen (Cao. 2010) published a review which analyzed the outcome of studies that investigated the effect of the purported renal acid load resulting from a high protein intake (above the current Recommended Dietary Allowance of 0.8 g protein/kg body weight) on increased urinary calcium excretion. With reference to more recent findings they write:

Neither whole body calcium balance is, nor are bone status indicators, negatively affected by the increased acid load. Contrary to the supposed detrimental effect of protein, the majority of epidemiological studies have shown that long-term high-protein intake increases bone mineral density and reduces bone fracture incidence. The beneficial effects of protein such as increasing intestinal calcium absorption and circulating IGF-I whereas lowering serum parathyroid hormone sufficiently offset any negative effects of the acid load of protein on bone health.

By the way, I am already looking forward to the huge steaks I am going to have for lunch, today ;-)

Beta-Hydroxy-Beta Methylbutyrate Strikes Back: HMB Increases GH and IGF-1 at the Expense of Insulin Resistance

"HMB" - do you remember these three letters? If you have been around the supplement world in the early 2000s, you probably will. Beta-hydroxy-beta methylbutyrate (HMβ) is a metabolite of leucine which has been advertised to enhance exercise performance, reduce fatigue and promote muscle gains. Nothing of that has been substantiated within larger human studies, though; and thus HMB a former star among the amino acid supplements has almost been forgotten.

Now, a recent study from Brazil (Gerlinger-Romero. 2011) provides data suggesting that HMB may in effect raise the content of pituitary GH mRNA and growth hormone [GH], as well as hepatic IGF-I mRNA and serum IGF-I concentrations.

It was observed that the HMβ treatment induced an increase in GH mRNA by 65% (P < 0.001) and in GH content by 20% (P < 0.05) compared to control group. The IGF-I mRNA expression in liver, as well as the serum IGF-I concentration was also significantly increased in the HMβ-treated animals.

There are some downsides to these results, however. Firstly, this is another rodent study, so we do not know how the results of this 4 week intervention would translate to human beings. At least, other than in previous investigations, the amount of HMB, 320mg/kg body weight, which is equivalent to roughly 52mg/kg body weight in a human being, would be affordable, but ...

Figure 1: Effect of the HMβ-treatment on Insulin concentrations.
Data are expressed as mean ± SEM. *P < 0.05; n = 9–16 animals per group
(Gerlinger-Romero. 2011)

... and here comes secondly, the rats became hyperinsulinemic (cf. figure 1), or in other words HMB supplementation induced insulin resistance. With the latter being at the heart of the metabolic syndrome I would think twice before attempting to boost my growth hormone level with an amino acid metabolite that will compromise my body's insulin management.

Drink Your Milk! Scientists Unlock the Health Secrets of the White Elixir of Life

Arnold said "Milk is for babies", yet recent studies showed that chocolate milk is among the most effective post-workout drinks you can consume and whey proteins are a stable not only of almost every bodybuilder's diet regimens.

In a recent review, a group of Irish scientists (Mills. 2011) attempt to summarize all the available information on the "ever-accumulating range of bioactivities associated with milk substituents"; and the sheer size of the paper underlines that there probably is much more to milk than Arnold would have imagined.

Table 1: Milk-derived bioactive peptides in commercially available functional foods and ingredients (Mills. 2011)

Table 1 (truncated from Mills. 2011) shows a summary of the most important components of milk and their proclaimed beneficial health effects. So, don't let anyone tell you milk was for babies, only ;-)

Edit: I think it is noteworthy to say that (of course) this review was supported by the milk industry. While this does not change the reliability of the scientific evidence cited, one should keep that in mind when looking at which studies the authors selected.

Role of Magnesium in Blood Sugar Management

In a recent study (Guerrero-Romero. 2011) a group of scientists from the Research Group on Diabetes and Chronic Illnesses from Durango, Mexico, investigated the effect of oral supplementation with magnesium chloride (MgCl(2) ) on "the ability of beta-cells to compensate for variations in insulin sensitivity in [52; placebo + treatment] non-diabetic individual". Obviously, we hear it over and over that 'magnesium is the fourth most abundant mineral in the human body', it is vital, etc., etc. - studies showing real life benefits from oral supplementation are however relatively scarce. Unfortunately, there is one caveat with this study, as well. Guerrero-Romero et al. deliberately selected only those subjects with "significant [magnesium levels ≤0·70 mM/L] hypomagnesaemia, i.e. low magnesium levels.

There were no serious adverse events or side effects because of MgCl(2) or placebo. At the beginning of the study, the AUC of the HMbCF was similar in both groups (AUC = 7·591 and 7·895 cm(2) ); at the end of follow-up, the curve of the MgCl(2) group showed a hyperbolic distribution (AUC = 18·855 cm(2) ), whereas in the placebo group, there were no changes (AUC = 7·631 cm(2) ).

So, while the above results are encouraging and back the notion that adequate magnesium intake is a necessary prerequisite for healthy blood sugar management, we do not know whether or not supplemental magnesium would render the pancreatic beta-cells of people with adequate magnesium levels even more effective - or in other words, if the common use of magnesium supplements among people with an already healthy diet is not simply a waste of monetary resources.

Reactive Oxygen Specimen (ROS) Trigger Muscle Hypertrophy via IGF-1 Signaling

I have touched on the "usefulness" of oxidation, only yesterday. Now, a very recent study appears to confirm the notion that a controlled amount of inflammation is necessary in order to achieve metabolic and muscular adaptations.

Figure 1: Eesult of the quantitative analysis of myotube diameter after IGF-I and NAC treatment (Handayaningsih. 2011)

Scientists from Division of Diabetes and Endocrinology and Division of Cellular and Molecular Medicine at the Kobe University Graduate School of Medicine published a paper (Handayaningsih. 2011) describing an investigation into the role of Reactive Oxygen Specimen (ROS) in the IGF1-signaling pathway. In this study N-Acetyl-Cystein (NAC), commonly used by recreational athletes as an "ergogenic" aid, blunted myocyte response to IGF1 and thus inhibited muscle hypertophy (cf. Figure 1):

While treatment with H2O2 significantly enhanced IGF-I-induced phosphorylation of the IGF-I receptor (IGF-IR), IGF-IR phosphorylation was markedly attenuated when cells were treated with antioxidants. The downstream signaling pathway, Akt-mTOR-p70S6K was subsequently down-regulated. Furthermore, thephosphorylationof FoxO1by IGF-I decreased concomitantly with the restoration of the expression of its target genes, Atrogin-1 and muscle RING finger 1, which are related to muscle atrophy.

Before you now go and flush all your vitamins and antioxidants down the toilette, you should consider that this is an in-vitro study with a narrow and limited ROS stimulation and not a large scale exercise supplementation study showing that the 500-1.000 mg of NAC you take on a daily basis will completely forestall muscle growth. If anything, it should remind you that excessive "inflammation" could be the "root of all evil" (cf. Super Human Radio), but excessive antioxidant supplementation certainly ain't a solution.

N3-PUFA Beneficial Only When Combined With Antioxidants

All of you who have been following this blog, lately, will have noticed that I tend to be skeptic whether fish oil and other PUFA supplements are recommendable without certain reservations. A recent study by Filaire et al. (Filaire. 2011) seems to support the view that poly-unsaturated fatty acids increase the potential for oxidative damage and should thus be combined with appropriate amounts of antioxidants to "compensate" this effect.

Over a period of 6 weeks the researchers supplemented a group of 36 judoists with either 600 mg EPA and 400 mg DHA per day or the same amount of long chain polyunsaturated fatty [LCPUFA] acids plus 30 mg vitamin E, 60 mg vitamin C and 6 mg β-carotene and measured resting and exercise-induced lipid peroxidation in their subjects. Here are the results:

At T (1) [before supplementation], there were no significant differences among treatment groups with respect to lipid peroxidation, lag phase, and levels of α-tocopherol or retinol. The consumption of an n-3 LC PUFA supplement increased oxidative stress at rest and did not attenuate the exercise-induced oxidative stress. The addition of antioxidants did not prevent the formation of oxidation products at rest. On the contrary, it seems that the combination of antioxidants added to the n-3 LCPUFA supplement led to a decrease in, CD(max) [conjugated dienes], R (max) [maximum rate of oxidation], and POOL [lipoperoxide ] and MDA [malondialdehyde] concentrations after a judo training session.

So, in a way LCPUFA work like "exercise in a pill": At rest, they increase similar stressors as exercise does. This holds true regardless of additional anti-oxidant supplementation. When you exercise, however, a combination of LCPUFA + antioxidants appears to provide some protection from exercise induced stressors, so that overall, athletes would probably benefit from LCPUFA + antioxidants consumption.

Notice, I purposefully wrote "consumption" and not "supplementation", because let's be honest: If we have a look at the combination of nutrients a natural diet would provide, you always get your LCPUFAs with adequate amounts of antioxidants. So, keeping or switching to a healthy diet should still be your priority - if you then still see the need for additional supplementation, you may want to give a quality fish oil and some vitamins a try.

Tinospora Cordifolia as in LG Sciences' Natadrol is a Potent Antioxidant and Metal Chelator

This is only a small news-item, but unfortunately scientific background info on commercially available supplements is pretty rare - so here we go...

Scientists from India (Bhawya. 2010) investigated the antioxidant potential of various extracts of Tinospora Cordifolia (the primary ingredient in LG Sciences Test Booster Natadrol) and found that ...

Methanolic, ethanolic and water extracts showed significant antioxidant potential compared to other solvents and also possess metal chelation and reducing power activity. In the DPPH radical scavenging activity, methanolic extract  (98.13%)  showed high antioxidant potency, ethanolic  extract (90.34%) was a potent scavenger of superoxide radical. At the same time, both methanolic (97.08%) and ethanolic extracts  (95.21%)  inhibited hydroxyl radical along with other extracts. The metal chelation  in methanolic  (60.62%), ethanolic  (57.62%),   aqueous extracts  (40.89%)  and reducing of ferrous ions was significant found increasing in methanolic, ethanolic and aqueous extracts.

Although this is an in-vitro study, it may well explain the beneficial effect LG claims their product exerts on testosterone production via an antioxidant and metal-chelating pathway. Or in other words: Less oxidation and metal accumulation at the cellular level equals higher testosterone output. Interestingly, a methanolic extract would even be more potent than the "highly specialized ethanolic extract" LG uses.

What you may however be interested in, as well, is the fact (mentioned in an older blog post) that - just as many other testboosting, cortisol-lowering, etc. herbs tinospora tends to be toxic (especially in the testes) in high does in-vitro studies. This suggests that, despite all antioxidant activity, going overboard on respective supplement may not be advisable.

Calcium + Vitamin D for Breakfast Increase Dietarily Induced Thermogenesis and Fatty Acid Oxidation

Ever since the first studies suggested beneficial effects of dairy on weight loss, there have been a lot of trials that investigated the role of (supplemental) calcium in these contexts (mostly with discouraging results). A very recent study by Wendy and Soares (Wendy. 2011) took a very similar approach, but added vitamin D to the equation.

In their study, the scientists fed their 11 subjects (aged (mean ± SEM) 54 ± 1.2 y and BMI 31 ± 2.4 kg/m) a meal that was either high (HCT) or low (LCT) in vitamin D and calcium and measured diet induced thermogenesis (DIT), fat oxidation rates (FOR), serum leptin, subjective feelings of hunger/satiety hourly over a period of 8 hours. The results were far from earth-shattering; they could however solve the mystery of why most people find it easier to lose weight on a diet that is generally rich in dairy and calcium + vitamin D rich foods:

HCT resulted in lesser suppression of ΔFOR (p=0.02) and a significantly greater DIT (p=0.01). Further, the buffet to dinner interval was prolonged (p=0. 083) and reported 24h energy intake following this trial was significantly reduced (p=0.017). ∆leptin following HCT but not LCT was negatively related to 24 h fat intake (r = - 0.81, p=0.016).

So, the underlying mechanism is actually threefold and much different from the commonly heard hypothesis that dietary caclium would "bind fat in the intestine" and thus reduce caloric intake:

1. greater postprandial fat oxidation
2. significantly greater thermogenesis
3. beneficial effect on leptin and thus decrease in hunger

What else would you want? If there was not the issue with lactose intolerance, eating as much dairy as possible could actually become a general recommendation for everyone who intends to lose weight and/or improve body composition

6 Weeks of 400mcg Chromium per Day Improve Insulin Sensitivity and Lean Body Mass in Obese Children over Lifestyle Intervention Alone

Chromium, once hyped as a next generation anti-diabetes and lean mass agent, has disappeared from the best-selling lists of supplement vendors. Too few studies were able to confirm the encouraging results from rodent experiments. Possible toxicity issues put the icing on the cake and people just stopped buying it.

A very recent study published in the Journal of Nutritional Biochemistry (Kim .2010) took another look at whether chromium, which irrefutably is a vital co-factor in insulin production and secretion, may not yet be beneficial for patients with pre-diabetes. The scientists supplemented a group of 25 obese children (age 9-12y) who participated in a 6-week diet and lifestyle intervention with 400mcg chromium chlorid a day and monitored changes in body mass index (BMI; kg/m²), BMI Z-score, waist circumference, body composition and fasting plasma glucose. The results were positive- body composition and insulin sensitivity improved:

[...] children who received chromium chloride demonstrated more positive changes versus the placebo group in HOMA (−1.84±1.07 vs. 0.05±0.42, P=.05), QUICKI (0.02±0.01 vs. −0.002±0.01, P=.05), lean body mass (2.43±0.68kg vs. 1.36±1.61kg, P=.02) and percentage body fat (−3.32±1.29% vs. 0.65±1.05%, P=.04)

Once again, chromium did not prove to be the panacea of the age of obesity, but supplemental chromium can be a beneficial co-factor in the treatment of metabolic disorders in general and diabetic complications in particular. Without appropriate life-style interventions it will however prove similarly useless as many other supplements which have been "proven in clinical studies to do XYZ"...

The Great Feast: Overeating With a Macronutrient Emphasis on Carbs Suppresses GH Levels Via Hyperinsulinemia

An interesting study done by scientists from the Department of Internal Medicine (A.L.B.) at the University of Michigan (Cornfold. 2011) reveals a direct influence of overeating (+75% over maintenance) and the associated rise in insulin on growth hormone levels.

Cornfold et al. found that GH levels of seven (formerly ;-) healthy, nonobese men (body mass index, 24 ± 1 kg/m²; age, 25 ± 1 yr) "declined nearly 80% by d 3 of overeating".

Figure 1: Mean plasma GH concentration every 20 min for 24 h before overeating
(baseline), ond3of overeating, and at the end of the 2-wk overeating period. Inset,
The average plasma GH concentration at baseline, d 3, and 2 wk of overeating.

In view of some people's "eat all that cannot run away fast enough" mass gain diets, it is noteworthy that the decline in GH concentration is not an initial reaction. As it is shown in figure 1, GH response stayed way below baseline for the whole 2 weeks the subjects ate their standardized meals containing 70 kcal/kg fat-free mass/d (~4000 kcal/d; 50% carbohydrate, 35% fat, and 15% protein).

So, what can we conclude from that? A dirty / extreme bulk with a high carb intake will ruin your GH levels, spike your insulin levels and set the stage for fantastic, or should I say "fatastic", mass or rather fat gains.

Lower Protein to Carb Ratio Impairs Akt/TOR Signaling Pathway after Fasting in Rainbow Trout

"Boy, you need your carbs post workout!" This cornerstone of conventional bodybuilding wisdom is crumbling and a new study, if it had been done in humans, not in rainbow trout, would potentially refute this myth once and for all - at least, if one follows the popular (but false) assumption that it is because you are in a carb depleted or overall fasted state after a strenuous workouts.

A group of European scientists (Seiliez. 2011) investigated the effect of diets with different protein to carbohydrate ratios on the Akt/TOR Signaling Pathway after fasting for 48h. What they found contradicts conventional wisdom:

Activation of the Akt/TOR signaling pathway by refeeding was severely impaired by decreasing the proteins/carbohydrates ratio. Similarly, post-prandial regulation of several genes related to glucose (Glut4, glucose-6-phosphatase isoform 1), lipid (fatty acid synthase, ATP-citrate lyase, sterol responsive element binding protein, carnitine palmitoyltransferase 1 and 3-hydroxyacyl-CoA dehydrogenase) and amino acid metabolism (serine dehydratase and branched chain α-keto acid dehydrogenase E2 subunit) only occurred when fish were fed the high protein diet. On the other hand, diet composition had a low impact on the expression of genes related to muscle protein degradation.

So, not only did an increase in carbohydrates negatively impact muscle protein synthesis stimulated by the Akt/TOR signaling pathway, interestingly it also failed to reduce muscle protein degradation, which is the second reason people use in favor of a high carb meal after workouts (/fasting). 

For people following the research and writings of low carb proponents such as Mauro di Pasquale these results may not be surprising. However, before flushing your weight gainer down the toilette, you should really reevaluate your personal and training goals. For an athlete whose exercise bouts are long and frequent, carbohydrate repletion may well turn out to be beneficial. If not for muscle growth, then for performance maintenance. A general demonization of carbs would thus be similarly inappropriate as the "fat scare" of the late 20th century. It all depends on who you are and what your athletic and aesthetic goals are.

Rat Study: High Carb Diet Induces Hepatic Steatosis and Increases Heart Fat by 43%

For a large part of the 1980s and 1990s fats have been considered the "source of all evil". Now, it is our carbohydrate consumption which is held to be responsible for diabetes, obesity and the other ugly faces of "the metabolic syndrom". A recent study by a group of scientists from Sao Paulo (Haubert. 2010) seems to confirm this "revised" hypothesis.

Over a period of 21 days, the scientists fed a group of rats (experimental) a 70% carbohydrate diet with astonishing or rather shocking results (cf. table 1)

 

Within three weeks the rats developed a fatty liver and their heart fat mass increased by 43%. While the scientists did not provide much information about the overall underlying mechanism of these changes, they emphasize the pronounced decline in tissue vitamin E produced by the high carb consumption. In how far additional vitamin E may have prevented some of the fat accumulation yet remains unknown and would warrant further investigation.

AKG as in Arginine Alpha-Ketoglutarate for GI Health

For many of us, our gut is like our feet. We ignore it as long as it appears to be working properly. I think, I do not have to tell you that this is a mistake. Just like you cannot run without healthy feed, you cannot digest and use all the good food and supplements you consume without a healthy gut. This is why you should be interested in the findings of a recent review by scientists from the Hubei key Laboratory of Animal Nutrition and Feed Science in Wuhan 430023, China (Hou. 2011).


The scientists evaluation of related studies lead them to conclude that the conversion of Alpha-ketoglutarate (AKG), which is an intermediate of the Krebs cycle and bridges amino acid metabolism with glucose oxidation, into glutamate in the gastrointestinal tract of humans and animals is of particular interest in view of overall gastric functioning, "including regulation of cell function, neurotransmission, and gastric emptying".

Translating the basic research into practice, results of recent studies indicate that dietary supplementation with AKG alleviates oxidative stress and injury in intestinal mucosal cells, while improving intestinal mucosal integrity and absorption of nutrients in endotoxin-challenged pigs.

If you do not find that exciting, you might be interested in AKG's effect on mTOR-signaling (largely regarded as one of the fundamental triggers of protein synthesis and "muscle growth"):

The beneficial effects of AKG are associated with increased activation of the mTOR signaling pathway and net protein synthesis.

So, in view of the disappointing news on the inability of Arginine-AKG to raise nitric oxide levels, it may come as a surprise that it may have a distinct value far apart from muscle pumps and popping veins.

Tired of Being Obese? Walk Like a Bodybuilder! Study Confirms Effectivity of Incline Treadmill-Walking

Are you obese or just generally concerned about your joint health? Forget jogging and ramp up your treadmill. According to the results of a study published in the latest issue of the Journal of the American College of Sports Medicine (MSSE. 2011) slow walking on an incline produces a similar metabolic workload as running while concomitantly reducing loading rates on lower extremities:

Metabolic rates were similar across trials and were moderate intensity (48.5-59.8% of VO2max). Walking slower uphill significantly reduced loading rates and lower extremity net muscle moments compared to faster level walking. Peak knee extension and adduction moments were reduced by ~ 19% and 26%, respectively, when subjects walked up a 6[degrees] incline at 0.75m/s vs. level walking at 1.50m/s.

So, ramp up your incline and walk, but please do me a favor and do not hold on to the handle in front of you, like some of the overweight mamas at my gym do. This will not only reduce the work-intensity and thus diminish the metabolic effect, it may as well ruin your back.

Edit: Dr. Rouse was kind enough to remind me that there is a world beyond the gym (cf. my Facebook page) and that just walking outside would be a better alternative - thanks Peter ;-)

L-Carnitine Works! At Least if it's L-Carnitine L-Tartrate.

Initially, carnitine was considered the super-supplement for both, the athlete seeking the ergogenic edge, as well as for the obese trying to shed unhealthy body fat. Surprisingly, however, study after study showed no to little effect on exercise performance and/or fat loss. Ultimately, it became clear that, even at very high doses, only very little of the orally delivered l-carnitine actually makes it to the muscle. Consequently, its effects on performance and body composition where negligible. Now, a very recent study by Wall et. al. (Wall. 2011) found that adding a transporter, in this case l-tartrate, to the molecule does not only help to increase muscle carnitine levels, it eventually produces exactly those effects on exercise performance and substrate metabolism one would have expected from l-carnitine supplementation in the first place.

The scientists had their 14 healthy male volunteers ingest either 80 g of CHO (Control) or 2 g of L-carnitine L-tartrate and 80 g of CHO (Carnitine) twice daily for 24 weeks in a randomised, double blind manner. Other than in previous studies with plain l-carnitine (minus the l-tartrate) there was a significant increase of muscle carnitine content with all the downstream metabolic benefits on exercise performance one would expect:

Muscle TC increased from basal by 21% in Carnitine (P<0.05), and was unchanged in Control. At 50% VO2max, the Carnitine group utilised 55% less muscle glycogen compared to Control (P<0.05) and 31% less pyruvate dehydrogenase complex activation (PDCa) compared to before supplementation (P<0.05). Conversely, at 80% VO2max, muscle PDCa was 38% higher (P<0.05), acetylcarnitine content showed a trend to be 16% greater (P<0.10), muscle lactate content was 44% lower (P<0.05) and the muscle PCr/ATP ratio was better maintained (P<0.05) in Carnitine compared to Control. The Carnitine group increased work output 11% from baseline in the performance trial, while Control showed no change.

So, after all, it was not the wrong the substance previous investigations used, but rather the wrong form - l-carnitine l-tartrate - though expensive - is the way to go to burn fat and increase athletic performance. If you do not want to buy it in bulk, I suggest you at least buy a product like MAN Sports Body Octane, where you actually know how much (here 1g) of the carnitine you're getting per serving.

Creatine + Caffeine = No-Go? Still Nothing but a Myth

You probably have heard both that a) caffeine would negate the ergogenic effects of creatine loading and b) that the latter is nothing but one of those gym-myths which just won't disappear.

A recent study by scientists from the Department of Recreational Sports Management, Yu Da University, Miaoli, Taiwan (Lee. 2011) provides practical evidence that "the no caffeine when on creatine"-advice is garbage. The scientists investigated the effects of acute caffeine ingestion on intermittent high-intensity sprint performance after 5 days of creatine loading and found no detrimental effects of 0.6mg/kg caffeine on the creatine induced increase in exercise performance. What's more the ergogenic effect of caffeine added to that of creatine, so that ...

[...] the mean and peak power observed in the CRE + CAF were significantly higher than those found in the CON during Sprints 1 and 3; and the CRE + CAF showed significantly higher mean and peak power than that in the CRE + PLA during Sprints 1 and 2. [...] Heart rates, plasma lactate, and glucose increased significantly with CRE + CAF during most sprints.

On the other hand, one has to consider that this does not ultimately refute that "caffeine loading", or rather binging on caffeine day by day, may well exhaust your adrenal reserves in a way that after a few weeks of epinephrine overload, you are so drained that it becomes hard to drag yourself to the gym. In this situation all the creatine in the world probably won't help you.

Protein Supplementation in Heavy Resistance Training: "A case for whey protein"

"Protein builds muscle!" < this is a sentence you will read pretty often in the advertisements - sorry, I meant "scientific explanations" supplement producers print onto their product labels to make you buy their newest "invention". In the end, however, it mostly comes down to a blend of different forms of whey protein with added vitamins minerals and digestive enzymes. But do you really need all that? Do you even need whey?

Table 1: Approximate Essential Amino Acid Profile of Various Protein Sources

A group of scientists from Finland (Hulmi. 2010) would probably say "YES!". In a very recent review they come to conclusions which sound pretty similar to what you can read all over the web:

Most, but not all studies have shown that supplementation of whey alone or with carbohydrates immediately after and possibly before and during resistance exercise can enhance the muscle hypertrophy response to resistance training in healthy adults. Such a response seems to at least be the case when comparing the effects of whey versus a non-energetic, or carbohydrate or soy protein alternative. Some studies also suggest that whey may enhance recovery from heavy exercise and possibly decrease muscle damage and soreness. This could, over time, enhance training adaptations by way of increasing training volume or reducing the potential for over-reaching/over-training.

There is another point, where Hulmi et al. reasoning is pretty much in line with main-stream "bro-science" and this is the extraordinary role of leucine in terms of muscle protein synthesis and hypertrophy:

[Leucine] is probable that the most important component in whey, for increasing protein synthesis and skeletal muscle size, is its high concentration of the BCAA, leucine (see
Table 1). Leucine, acting as a signaling molecule in the mTOR cascade, has been shown to be a critical amino acid for increasing skeletal muscle protein synthesis, both in vitro and in vivo in humans and rats. Leucine may also be involved in suppressing muscle protein degradation.

Their perspective is yet a little more differentiated:

However, if recent data involving rodents can be duplicated in humans, leucine concentrations from whey may only affect peak activation of skeletal MPS but not the duration of MPS or duration of mTOR signaling. Similarly, despite the positive effects of leucine per se, it likely is not the sole factor responsible for whey-induced adaptations to resistance training. For example, adding leucine to intact protein has been shown to offer little, if any, effect on protein synthesis and protein balance when consumed after resistance exercise.

Bottom line: If you go for muscle, go for whey and get drag yourself to the gym ;-)

Low Iron Still an Issue in Professional Athletes

Despite the fact that most of you are probably weekend-warriors or recreational athletes, I suspect that some of you expose their bodies to similar stressors as professional athletes do. Therefore, I assume you'd be interested in a recent study coming from German scientists (Reinke. 2011) who found that "although recuperation seems to allow a certain recovery of iron storage, particularly in athletes with initially low ferritin levels, this retrieval was insufficient to fully normalise reduced iron levels."

The scientists had previously examined the iron metabolism in 20 elite rowing athletes and 10 professional soccer players at the end of a competitive season, after recuperation and during pre-season training and found:

At the end of season, 27% of all athletes had absolute ID [iron deficiency] and 70% showed functional ID. Absolute iron depletion was not generally restored after recuperation and observed at all time points in 14% of the athletes. Although athletes with initially low ferritin levels showed a slight increase during recuperation (p < 0.09), these increases remained within borderline levels. Furthermore, 10% showed borderline haemoglobin levels, suggestive of mild anaemia, as defined by the World Health Organisation.

While I would not suggest supplementing with iron without due reason, this study should remind you to have your levels checked, at least once a year in order to intervene before you actually feel the negative effects of low iron and anemia.

Taurine Decreases Oxidative Stress After Eccentric Exercise in Rats: Human Equivalent Dose ca. 3.5g-4g

Regular readers of the SuppVersity will certainly be familiar with the sulfur-amino-acid taurine and its various benefits on exercise performance, insulin sensitivity and weight management. So, it may not come as a surprise that a recent study conducted by young scientists from the Postgraduate Program in Health Sciences at the Universidade do Extremo Sul Catarinense in Brazil found that 14-days "preloading" with 300mg/kg taurine per day reduced the exercise induced increase in oxidative stress in rats.

Taurine supplementation was found to decrease superoxide radical production, CK [creatine kinase], lipoperoxidation and carbonylation levels and increased total thiol content in skeletal muscle, but it did not affect antioxidant enzyme activity after EE [excentric exercise].

It is rather speculative, whether standard dose equivalent calculations apply to one situation or another - IF they did, you could probably get away with as little as 3.5-4.0g of taurine per day to achieve similar results. It would however warrant further investigations to find out, how, for example, the consumption of beta-alanine (cf. News on the Taurine vs. Beta Alanine Antagonism) would increase the need for supplemental taurine.

Additional advice: Do not buy your taurine in caps. Rather go for some bulk powder. It is cheap as hell and, at the suggested dose of 4.0g, a 500g pot will last you 125 days. And just another thing: Better take your taurine in divided doses. I've heard of people getting severe diarrhea from doses greater than 2g.

2g Spirulina à Day Enhance Quadriceps Strength in Trained and Untrained Individuals

Hitherto, most of you may have considered algae such as spirulina mostly as a source of anti-oxidants or a pretty useless weight-loss supplement. What you probably did not know is that taking 2g of spirulina each day might noticeably increase your strength gains in the gym.

Scientists from the Department of Sports Medicine and Physiotherapy at the Guru Nanak Dev University, in Punjab, India supplemented the diet of a group of 40 healthy volunteers (20 trained, 20 untrained) with 2g of spirulina per day and measured peak force, average force and fatigue index of dominant quadriceps muscle before and after 8 week of supplementation.

Table 1: Comparisons of effect of spirulina supplementation on peak force, average force, and fatigue index of dominant quadriceps muscle in supplemented and placebo trained and untrained groups.
Values are shown as mean values with standard deviation

The data in table 1 shows the astonishing results: While supplementation did not improve time to exhaustion spirulina supplementation did in fact produce a 30% increases in peak force production even in the untrained group.

Unfortunately, the scientists refrain from speculations about the underlying mechanism of action, but maybe you are satisfied to know that it works and do not care about the how's and why's? No? Well, as soon as there is further information available, you'll find it here at the SuppVersity.

Even Individuals on a "Healthy" Diet May Benefit from Supplemental Fiber

Fiber has been advertised for years as a universal health promoter. It curves appetite, reduces cholesterol and improves digestion - but is it really necessary to supplement with additional fiber, if your intake in fibrous veggies etc. is already high? A recent study by scientists from Australia (Pal. 2010) suggests that it may not be necessary, yet beneficial.

Figure 1: Changes in body weight (A); BMI (B); % body fat (C) and waist circumference (D).
From left to right: Control, FIB, HLT, HLT-FIB

Studying a cohort of 72 overweight and obese individuals with a BMI between 25 and 40 kg/m² and age between 18 and 65 years, the researchers found that over a time period of 12 weeks in which the subjects either practiced their "normal" eating habits or changed to a healthy food diet (HFT), supplemented with fiber (FIB) or switched to a healthy food diet that was supplemented with fiber (HFT-FIB)...

[...] weight, BMI and % total body fat were significantly reduced in FIB and HLT–FIB groups, with weight and BMI significantly reduced in the HLT group compared with control at 12 weeks. HLT–FIB and HLT groups had significant reductions in TAG and insulin compared with control at 6 and 12 weeks, and in insulin compared with the FIB group at 12 weeks. The HLT–FIB, HLT and FIB groups all had significant reductions in total cholesterol and LDL-cholesterol compared with control after 6 and 12 weeks.

As can be seen from figure 1 (above) the addition of fiber to an already healthy diet did in fact improve the overall beneficial results of the change in dietary habits. Bottom line: Firstly, eat healthy! Secondly, consider using a fiber supplement only if your diet is already in check.

Oral ATP Supplementation Proves Completely Ineffective Even at Very High Doses

I think most supplement companies have hitherto given up on convincing you of the use of oral ATP supplements. About 2 month ago, I did however notice a new "high dosed" product (I cannot remember the figures out of my head, but the daily dose was far below 1.000mg) was released to be bought by the in-educated public ;-)

Just to discourage you from wasting your money on any such products, here is a very recent study (Coolen. 2010) on the futility of attempting to rise ATP levels via oral supplementation:

Thirty-two healthy subjects were randomised to receive 0, 250, 1250 or 5000 mg ATP per d for 28 d by means of enteric-coated pellets. In addition, on days 0 and 28, all thirty-two subjects received 5000 mg ATP to determine whether prolonged administration would induce adaptations in the bioavailability of ATP. ATP supplementation for 4 weeks did not lead to changes in blood or plasma ATP concentrations. Of all ATP metabolites, only plasma uric acid levels increased significantly after the administration of 5000 mg of ATP.

If you are an athlete and really intend to raise ATP levels orally, creatine supplementation (and thus increased ATP resynthesis) would be one way to go.