Saturday, April 16, 2011

Vanadium for Type II Diabetes!? Beneficial Effect of Trace Element on Blood Glucose Management in Rat Model.

Some of you may remember that vanadium has once been hailed as nutrient repartitioner (it has been shown to increase glucose uptake into muscle tissue via GLUT4-receptors) in the fitness & bodybuilding community. After reports on possible toxicity issues, which were - at least in parts - based on reports of people who dosed according to the common "more helps more" mentality of our society, vanadium supplements, stand-alone or larger doses as part of micronutrient blends, have disappeared from the market. Science, on the other hand has not given up on this promising, yet non-benign "medication".

A recent study (Kurt. 2011) published in the journal Biometals underlines that the effects of vanadium, which was named after the Scandinavian goddess of beauty and fertility, Vanadis, do in fact border on those of a pharmaceutical drug. After treating rats with streptozotocin and thus inducing a metabolic profile that is generally considered an appropriate model for human type II diabetes, the researchers from the Department of Chemistry, at the University of Istanbul, supplemented the chow of their animals (control & STZ-induced type II diabetic rats) with 100mg vanadyl sulfate per kg of body weight. For an 80kg male human this would amount to a massive dose of 1.200mg vanadium sulfate per day, the consumption of which is not advisable until definitive human data on short- and especially long-term consequences are available.
Figure 1: Blood glucose levels (mg/dl) of rats at different time-points
(data adapted from Kurt. 2011)
Regardless of the results of future studies on the effects & safety of vanadium on humans, the study results (as shown in figure 1) clearly indicate that vanadium is able to counter, maybe even reverse, the negative effects streptozotocin has on blood glucose and insulin management in rats.

Its also noteworthy that, according to the scientists, the administration of vanadium also reversed the pro-oxidative effects of streptozotocin-induced diabetes. I am yet not sure if this conclusion Kurt et al. base on a reduction of anti-oxidant activity in the tissue of the diabetic rats is valid. After all, the latter could also be a direct consequence of potential toxic effects of the trace mineral. Until further human data will be available, I would thus strongly advice against taking high dose vanadium supplements, even if you have type II diabetes.

Friday, April 15, 2011

Vitamin(S!) E, The Whole Picture: Delta Tocopherol a Rising Star in Cancer Protection

Those of you who have attentively followed my dissertation on fish oil (cf. SHR: ProfDrAndro talking on the Pros & Cons of Fish Oil) may remember that - as an aside - I mentioned that not alpha-tocopherol, which is what supplement companies add to their fish oils, but delta-tocopherol would be the anti-oxidant of choice to protect the highly oxidizable oil from going rancid.

Figure 1: Toco-8, one of the few
tocotrienol
products on the market
A very recent report (Li. 2011) on findings of scientists from The State University of New Jersey is only one out of a whole line studies that imply that the real health value of "vitamin E" (we should better start writing "the vitamins E") does not lie in one, but in the combination of the tocopherols (alpha, gamma, delta) and the naturally ocuring tocotrienols, of which both the delta-tocopherol, as well as the group of tocotrienols have long been overlooked in the course of what one should probably call the "alpha-tocopherol"-hype.

According to Li et al., of the three tocopherols (alpha, gamma, delta @ a human equivalent dose of 800IU) the scientists fed to mice, which had previously been "infected" with "human lung cancer H1299 cells", the "δ-Tocopherol inhibited tumor growth most strongly" (delta > gamma > alpha). And with reference to the underlying mechanism of the observed superiority of delta-tocopherol to the two other isomers, the scientists argue:
The higher activity of δ-T in the inhibition of tumor growth corresponded well with its ability to inhibit the formation of 8-OHdG, γ-H2AX, and nitrotyrosine as well as to induce cell apoptosis.
With 8-OHdG being a marker for oxidative stress, γ-H2AX being a marker for cellular damage and nitrotyrosine being a reactive derived from nitrogen species and tyrosines in proteins, these findings suggest that delta-tocopherol protects against oxidative stress and cellular damage, and, at the same time, facilitates apoptosis of cancerous cell lines (on a side note: a characteristic feature of cancer is that the "normal" and healthy programmed cell death does not occur). Alpha-tocopherol, on the other hand, has "little or no influence" on these parameters.

If one also takes into consideration that the tocopherols appear to displace each other...
[...] dietary γ- or δ-tocopherol, however, decreased serum α-tocopherol levels, and dietary α-tocopherol decreased serum levels of γ-tocopherol.
...it is becoming more and more obvious that supplementation with isolated tocopherols, as it has been the case in many of the inconsistent studies on the effect of "vitamin E" on cancer, is not warranted.

So, if you decide to copy the study and supplement 800IU of vitamin E, make sure it comes from a source of "natural, mixed tocopherols" or even better tocopherols & tocotrienols, of which S. Wada in a very recent review (Wada. 2011) on the effects of vitamin E on cancer writes:
Vitamin E, especially tocotrienols, seems to be a potent agent for cancer prevention, however no large-scale clinical trial on the cancer prevention effect of tocotrienols has been conducted yet. Therefore it is expected that clinical trials overcoming the lower bioavailability of tocotrienols will be conducted, and it is urgently needed to assess the safety and the efficacy of the administration of the tocotrienols as a part of a cancer prevention regimen.
Ah, and don't forget: The SuppVersity is the place where you will read about these studies first ;-)

I-Force Dexaprine Ingredient Write-Up.

Figure 1: I-Force Nutrition's
newest fat burner Dexaprine
Just received an email from the marketing guys @I-Force Nutrition informing me that "Dexaprine is finally here...". Well, to be honest, I had not been waiting for it, but the email intrigued me and I would like to give you a brief rundown on the ingredients, which are "guaranteed to give you more energy, increased appetite suppression, and insane mood enhancement than you have ever experienced!" - I don't know about you, but I think I have heard similar claims before ;-)

Ok, here we go: One bottle of Dexaprine, which is 39.99 (pre-order offer @ I-Force webshop) has 60 servings (serving size 1 capsule) of the "thermogenic powerhouse" (I love these advertisment guys) @ 600mg of the following ingredients
  • Thermophoric Amine Mood Enhancing Complex,
    which is basically just synephrine (from citrus aurantium) + geranamine (which is also known as 1,3-dimethylamylamine, 4-methyl-2-hexylamine, or as I-Force has it on the label 1,3-dimethylpentylamine)
  • Extended Release Energy Complex,
    which is a combination of caffeine and theophylline, with the latter having identical beneficial (stimulant, beta receptor agonism, etc.) as well as detrimental (e.g. temporary insulin resistance in muscle tissue, cf. Colnes. 2010, adrenal problems due to long term (over-)use etc.) effects on perceived energy and weight loss, but a longer half-life, which is even prolonged by the concomittant admistration of caffeine (Jonkman. 1991)
  • Anabolic Protein Synthesis Enhancing Complex,of which I think that it is completely mislabeled, because it is a combination of the two diiodo-L-Thyronines (also known as T2s), 3,3'-T2 and 3,5-T2, of which I have already written in a paper for a German BodyBuilding and fitness magazine (click here for Google-translation) that their impact on metabolic rate (in non-hypothyroid individuals) is probably negligible and would - according to the mice studies that are presently available - require much higher doses than those present in current "thyroid stimulating" products to up-regulate UCP significantly above "normal" levels.
So, overall this does leave us with a probably relatively long lasting stimulant that will enable you to work harder and thus burn more calories and subsequently more fat. Not bad, but nothing new or even revolutionary here.

On a side note: As it is quite often the case in the supplement industry, Dexaprine is deliberately named to sound similar to a potent drug, the synthetic amphetamine Dexedrine (has up to 15 mg dextro-Amphetamin per cap). This practice is about as shabby as calling a product XYZ-"drol". The latter, i.e. the "drols", have incidentally been banned by bodybuilding.com - good idea, guys ;-)

    Thursday, April 14, 2011

    Algae Cake: Delicious & Healthy!? Wait Until You Learn that it is a Waste Product of Biofuel Production

    Despite the Fukushima disaster and the possible contamination of seafood and algae from the pacific ocean, seaweed still has a very good reputation among the health & longevity "experts" (especially those who happen to sell respective supplements).
    Figure 1: Algae cake (left) and differently processed algae (right);
    pictures as they appear on homepage of Dr V Sivasubramanian
    And though I do not want to argue that there are lots of studies that indicate beneficial effects of eating whole algae or supplementing with certain constituents, I must say that I was somewhat puzzled, when I read about the "terrific" idea, a group of Indian scientists (Singh. 2011) has recently come up with. They want to use algal cake (basically a waste product of the production of biofuel from algae) as ...
    [...] extremely valuable, high protein by-product of our system that will be used for the production of nutritional food additives, vitamin supplements, animal/fish feed and other valuable consumer products.
    Somehow that reminds me of the economically clever, yet from a health perspective questionable practice of feeding cows and other cattle with fishmeal, another "by-product"  which has traditionally been produced from the waste products of the fishery industry and has - among other health problems - been implicated as a contributing factor to the rise of BSE infection, everyone seems to have forgotten about, these days... But, hey, these are just my 2 cents. If anyone of you has the chance to taste one of these outstanding "cakes" let me know how it did you ;-)

    Wednesday, April 13, 2011

    Save Our Children: No more "Obeldickses" - Lifestyle Intervention, Not Rigorous Dieting Key to Solving Childhood Obesity

    What is good for adults cannot be bad for children!? Right so in the case of turning a sedentary life upside down: Changing the lifestyle, i.e. eating and exercise habits of overweight children (8 year olds) produced profound and above all persistent (>12 month) improvements in body weight, fat mass, waist circumference, and blood pressure!

    In a recent report (Schaefer. 2011) on what the German scientists felicitously called the "Obeldicks" program (with reference to the obese Gaul from the famous comic book series),  Schaefer et. al. report the results of a large scale intervention program with 76 obese children and their parents. The program was based on three-pillar-strategy:
    • physical activity training, 
    • nutrition education, 
    • and behavior counseling 
    And the beneficial and more importantly lasting (>12 month follow up) effects it had on the participants should make it pretty clear that in a society, where pathological eating & movement patterns (driving to McDonalds, eating the SuperSizeMenue right in your car) become the norm, profound lifestyle changes are the only sustainable way to lose weight, improve or maintain health and promote long jeopardy.

    So, if you want to die from diabetes, cancer or heart disease (you chose your favorite) in 10 years from now, that is your choice, BUT be fair and give your children the education and advice they need to get their acts together, they probably still have the chance.

    Fukushima & You: Understand What's Going On & How to Protect Yourself.

    I am back on SHR - this time talking about a very serious topic: The meltdown at the nuclear power plant(s) in Fukushima.

    "What the Fukushima Is Going On?"

    Listen live @ 9:00AM AM/12:00PM ET
    Tune in live and listen to some solid background info that will help you understand what's going on in Japan, California and the rest of the world.

    Tuesday, April 12, 2011

    Calorie Restriction vs. Exercise for Optimal Body Composition? Exercise Preserves Muscle Tissue and Prevents Metabolic Downregulation.

    Those of you who listened to my comments on set points and reasonable weight loss on Super Human Radio, will already know that - other than Gary Taubes, for example - I am a huge advocate of exercise, when it comes to weight loss, -maintenance and overall improvements in body composition. Data from a recently published study (Soare. 2011), despite being evaluated from an anti-aging perspective, confirms the adequacy of approaching your body composition goals, by dietary modifications and exercise induced increases in energy expenditure, instead of just "eating less calories".

    In their study, Soare et al compared 24 subjects who had been on a calorically restricted diet (CR, 1769±348 kcal/d) for an average of 6 years to 24 age- and sex-matched sedentary individuals (control, WD, 2302±668 kcal/d) and 24 body fat-matched exercise-trained (EX, 2798±760 kcal/d) volunteers, who were eating Western diets.
    Figure 1: Total body weight, lean mass & fat mass in sendentary control, calorie restricted (CR) and exercise (EX) group. (Data adapted from Soare. 2011)

    Although the researchers found that both, "the CR and EX groups were significantly leaner than the control (WD) group" both the greater amount of lean body mass (cf. figure 1) as well as their finding that...
    Mean 24-hour, day-time and night-time core body temperatures were all significantly lower in the CR group than in the WD and EX groups (P≤0.01).
    ...underline the futility of every effort to achieve improved body composition, i.e, to maximize muscle (lean mass), while shedding as much body fat, as possible via (even moderate) caloric restriction.

    Two other things are noteworthy, as well. Firstly, the reduction in body temperature, which is indicative of a downregulation of the metabolic rate, may be favorable for a longer, but that does not equate into more livable life. And secondly, the "Taubes-Hypothesis" that exercise is "useless", because "it makes you hungry" (the subjects in the EX group in fact consumed more calories) and you would compensate by eating more, anyway, would be relevant, only, if in fact "a calorie was a calorie" and "only calories" counted; the superior body composition of the exercise group, on the other hand, speaks for itself and does suggest that even Garry himself may benefit from one or another training session in the gym ;-)

    Edit: As I hear in an anonymous comment Taubes is supposed to do resistance training. When he was talking to doctor Oz, he did however propose the hypothesis I refer to above and this really bothered me.

    Monday, April 11, 2011

    TARFU: LaBrada Nutrition Financed Study Finds no Effect of Super Charge Xtreme N.O. on Training Induced Increases in Muscle Size. Minor Effects on 1RM Max.

    As mentioned in previous blogposts, I highly credit all supplement companies which - instead of just putting out untenable claims about the "steroid-like" effects of their products - spend a few bucks of their immense marketing budgets on research on how fantastic their products actually are. In the case of LaBrada Nutrition's Super Charge Xtreme N.O. it does yet seem that it would have been wiser to do some research before formulating their new "NO booster".

    Other than the guys over at LaBrada Nutrition probably have hoped or even expected, the study (JSCR. 2011) that was published in the March issue of the well-known Journal of Strength & Conditioning Research found no "significant improvements in LBM over the placebo drink" and only minor increases in bench press 1RM and squat power, which may well be attributed to CNS stimulation due to the hefty 450mg load of caffeine each serving of Super Charge Xtreme N.O. contains.

    Other than that, the "15 physically active, resistance trained, college age (19.5 +/- 0.269 yr) males" in the placebo group attained the same changes in body weight, body [as measured via dual-energy X-ray absorptiometry (DEXA)] and maximal strength in the rest of the 8 different exercises of their 3-day/week exercise regimen:
    A main effect for time was identified for each of the 1RM strength measures tested (p<0.05) except biceps curls (p = 0.34). [....] Significant main effects were found for lean body mass (F1/22 = 20.32, p<0.001), but there were no significant group x time interactions for changes in LBM (F1/22 = 0.142 p = 0.710).
    But let's be honest. Did you still believe an NO booster will improve your gains? I, for my part, take them for the feeling of being pumped up. And although I have not yet had the chance to test this particular product, I am inclined to believe that it will provide similar results as the classics like NO Xplode & Co - that kind of cosmetic pump you either love or hate.

    Sunday, April 10, 2011

    Beet Root Juice Supplementation Improves Exercise Performance. Nitrate Content of the Beets Decreases ATP Turnover in High Intensity Exercise.

    Nitrates have long been decried as toxic and dangerous and I bet, before their latest appearance to the supplement market, none of you would even have remotely considered to consciously increase his/her dietary nitrate supply. Yet, recent scientific studies confirm that nitrate (in moderate doses) is not only safe, but also has, its effects on vasodilation aside, quantifiable effects on exercise performance.

    A group of scientists from the UK tried to find out the underlying mechanisms of the ergodicity of supplemental nitrate (Baily. 2011). Following a six day supplementation period in the course of which seven males (aged 19-38 yr) consumed 500 mL per day of either nitrate-rich beetroot juice (~300mg nitrate content) or placebo (PL, with negligible nitrate content). What they observed is best described as a "tuning effect" that was observable both, in the course of high, as well as in the course of low intensity exercise training.

    During low intensity exercise, the pulmonary VO2 amplitude and thus the oxygen need during this kind of aerobic exercise decreased by -7%. An even more profound effect of nitrate supplementation was observed during high intensity activity (knee extensor exercises) where the ATP turnover decreased by -25%. These results stand in line with an overall increase in exercise tolerance of +25% in the nitrate supplemented group over placebo.

    Other than a some other researchers had speculated, Baily et al. did not find any indications of a changed phosphate vs. oxygen (P/O) ratio in the muscle. The changes in ATP turnover a 6-day loading phase with dietary nitrate from beet root juice triggers, must thus be considered the underlying mechanism of the ergogenic effect of nitrates, which, as you may have notices, appear in various forms (amino acid nitrates, creatine nitrates, etc.) in recently released supplements - not without reason, as it turns out.

    Saturday, April 9, 2011

    Taking a Week Off? Sudden 7-Day Exercise Cessation Perceived as a Strain by Highly Trained Athletes. Overtraining is the Culprit!

    Did you ever decide to take a week off and felt like hell? Did you feel how the gym, a place of which, only two days before, you thought you would be happy not to see for at least a month, suddenly seemed to draw you in as a giant magnet? Yes? Then you are either an exercise addict or just a highly trained athlete (probably you are both), of whom a recent study (Zeller. 2011) published in the Israel Medical Journal reports that
    exercise deprivation is associated with change in non-articular tenderness threshold and reduction in quality of life scores. 
    I already hear the exercise junkie within you jubilating: "24/7, 365 days a year! That's the way to go. That's my way." Before you do fall for this misunderstanding, you'd better thing about possible underlying reasons for the sudden tenderness and the decrease in perceived overall health (-4pts out of 100) the 26 asymptomatic healthy athletes who regularly exercise 6.75 ± 3.65 hours a week reported after the 7 days intervention.
    In fact, the scientists conclude that it is not the resting that fatigued them, but rather the constant exercise that prevented them from feeling their ever-increasing level of fatigue (keyword: overtraining):
    [...] healthy individuals who have hypoactive function of the biological stress response systems unknowingly exercise regularly to augment the function of these systems
    Aside from falling victim to the mainstream believe in the "more helps more"-principle, this almost pathological behavior, i.e. to blunt exhaustion by exhausting oneself even more, is unquestionably the central mechanism behind the commonly observed tendency of athletes, who are already severly overtrained, to 'naturally' ramp up training volume and/or intensity in order to achieve the short term satisfaction the increased nervous system stimulus provides. In the long run, however, this will inevitably lead to performance declines, total exhaustion, susceptibility to infections and injuries, and so on.

    Bottom line: Take a week or two off every now and then. If you crash badly, you know it was about time ;-)

    Friday, April 8, 2011

    Confusing Study Results: Saliva Testing "Adequate" For Free Testosterone, Yet Way Off For Cortisol!?

    Many of us spend a fortune on "hormone optimization", but when it comes to actually testing our levels, most of us are pretty cheap: "200$ for labs? No way I rather buy another test booster for that money - won't hurt, I guess!" And even, if we finally decide to test our testosterone levels, we will usually choose the cheapest and most convenient testing method: saliva testing. But is this an adequate way of assessing one's hormonal status? Although these tests have been around forever, nobody appears to be sure how reliable they actually are. A recent study (Caenegem. 2011) from the University Hospital of Ghent, Belgium, attempts to provide answers.

    The researchers tested two saliva collection methods, chewing on a cotton swab (Salivette, Sarstedt) and passive drooling on 30 healthy males with a median age of 27 years (range 19–65 years) and compared their findings against serum levels, which were measured on the same occasion. Here are their results:
    For cortisol, we observed a mean positive bias of 65% for passive drooling versus Salivette. In addition, cortisol determined on passive drooling samples correlated much worse with calculated free cortisol than cortisol analyzed on the cotton samples (respectively r=0.34 versus r=0.70). However, for testosterone passive drooling correlated well with the calculated free fraction (r=0.66). A positive bias of 21% for testosterone collected by passive drooling versus Salivette was observed. In contrast to earlier reports, we found no artefactually high testosterone results with the cotton-based collection method.

    Obviously, these results seem to indicate that saliva testing for testosterone is a good, while saliva testing for cortisol is a bad idea, BUT these results are in fact intrinsically flawed. By just calculating free serum values instead of using equilibrium dialysis to actually measure them, the scientists' control values and with them their assessment of the "appropriateness" and "inappropriateness" of salivary testosterone, respectively cortisol testing are questionable. 

    From what I hear from practitioners like Dr Crisler, it is highly advisable to spend the extra cash to have measured (not calculated) serum testosterone levels as reliable baseline and 4x saliva cortisol profiles to see where your levels are at throughout a 24h period. Arguably, this is yet another case in which a questionable study design leads to results which refute common practice and aggravate a confusion around hormonal testing procedures which affects practitioners and patients, alike.

    Thursday, April 7, 2011

    DHEA the Slimming Hormone? Study Finds: Dehydroepiandrosterone Directly Inhibits Cortisol Synthesis in Rodent Adipocytes

    After initially being hailed as the fountain of youth, the pharma-financed medical sciences dropped DHEA, when investors realized that a naturally occurring hormone would not be patentable. This and some discouraging and/or inconclusive results from long-term studies had DHEA literally disappear from the research scene for quite some time. Therefore, I am positively surprised that on the forthcoming European Congress of Endocrinology 2011 researchers from the Kobe University in Japan are going to present a paper (Tagawa. 2011) that shows that there may in fact be more to the initial findings of DHEA induced weight loss than follow-up studies would have it.

    Tagawa et al. investigated the possible mechanism behind the weight loss effects of DHEA and found that there is a direct inhibitory effect of DHEA on glucocorticoid (re-)synthesis in adipose tissue:
    Using differentiated 3T3-L1 adipocytes, we demonstrated that DHEA inhibited 11β-HSD1 activity at a concentration of 1 μM within 10 min. Inhibition was also observed in a cell-free system comprised of microsomes prepared from rat adipose tissue and NADPH, a coenzyme of 11β-HSD1. A kinetic study revealed that DHEA acted as a non-competitive inhibitor of 11β-HSD1. Further, DHEA did not inhibit 11β-HSD type 2, which inactivates cortisol or corticosterone in tissues involved in water and electrolyte metabolism, in rat kidney microsomes at a concentration <25 μM. Moreover, no conversion from DHEA to other sex steroid hormones or their precursors was observed under the present experimental conditions.
    These are three significant observations. Firstly, the presence of DHEA inhibits the synthesis of cortisol via 11Beta-HSD1. Secondly, it does not prevent exogenous cortisol to be converted to the "inactive" cortisone via 11Beta-HSD2 and thirdly, the dreaded conversion into estrogen, testosterone or DHT does not take place. All this would make the naturally occurring hormone DHEA a perfect selective 11β-HSD1 inhibitor, of which Stewart et al. from the University of Birmingham write (Stewart. 2011):
    Selective 11β-HSD1 inhibitors lower blood glucose, improve insulin sensitivity and cause weight loss in animal models. Biomarkers have been validated to confirm target inhibition in primate and human studies. Recent clinical trials show reduction in HbA1c and blood pressure in obese patients with diabetes mellitus who have failed on metformin therapy. Potentially the therapy offers a ‘magic bullet’ for patients with Metabolic syndrome with reduced blood glucose accompanying improved insulin sensitivity, lower lipids and blood pressure and reversal of hepatic steatosis secondary to reduced autocrine generation of cortisol in liver, adipose tissue, pancreas and muscle. Liabilities include activation of the HPA axis secondary to increased cortisol clearance with hyperandrogenism, though the extent and significance of this is debated.
    One thing, though, before you now go about eradicating cortisol to zero. Your body needs a healthy level of cortisol to function. It goes hand in hand with thyroid hormone, helps you manage stress, perform in the gym and is even necessary to "burn" body fat. Again, moderation is key and you certainly want to know where you stand before you start tweaking your cortisol levels into the wrong direction.

    Wednesday, April 6, 2011

    There Are Two Sides to Each Coin: Vitamin D Increases Insulin Sensitivity in Obese, Yet Decreases it in Lean Mice

    I am probably repeating myself, but I cannot emphasize enough that a common fallacy of medical research is the focus on pathologies. A recent example with respect to the "omnipotency" (that's what the Internet news could make you believe) of vitamin D comes from researchers at George Town University (GU. Press Release).

    The scientists were able to replicate the results of previous studies, where high dose vitamin D supplementation had "significantly reduced development of estrogen receptor-positive (ER+) breast cancer", but for estrogen receptor-negative (ER-) breast cancer they found either no effect (lean mice) or even an increased rate of cancerous growth in the group of obese mice.

    What's yet even more interesting that a similar contradiction was evident with respect to vitamin D's widely perpetuated beneficial effects on insulin resistance. In the pathologic model of the obese mice, vitamin D @ 15-25k IU per day was in fact able to ameliorate insulin resistance, in the lean, naturally insulin sensitive mice, however, insulin sensitivity was reduced by supplemental vitamin D.

    As I've discussed it in the context of the most recent fish oil study (and will probably repeat for other "super nutrients"), in 99.9% of the cases the effect of - especially high dose - supplementation with ostensibly harmless "vitamins" or "nutrients" vary enormously depending on the subjects current nutritional and health status. To derive one-size-fits-it-all recommendations from individual studies and to transfer results obtained from a pathological model without further scientific investigations to a healthy one is careless and may turn out to be very dangerous.

    Tuesday, April 5, 2011

    Victorious Veteran: Creatine Monohydrate Still First Class! Usefulness & Safety of “Innovative” Creatine Formulas Questionable.

    If we discount a high protein intake as a regular constituent of a healthy diet, creatine is unquestionable the King of Natural Ergogenics. Its impact on athletics way beyond the Gold’s Gyms of the bodybuilding world is evident from its being cited as “effective and safe” in almost each and every “position stand” published in one of the journals of the various sports & nutritional societies all over the world in regular intervals. Thus, with the (nephro-)toxity myth being finally dispelled, creatine has become a stable in the supplement regimen of both recreational, as well as professional athletes.

    Now, the financial revenue you can make from a non-patentable amino acid that is commonly found in fish and meat products is obviously limited. Thus, the steadily increasing number of players on the supplement market is continuously trying to “reinvent the wheel”, by putting forward a new, better-absorbed, more effect, side-effect free or whatever else the marketing guys had on their minds forms of N-(aminoiminomethyl)-N-methyl glycine (=chemical formula of creatine). These “superior” forms of creatine are then put forward as the must have for every seriously training athlete and/or creatine non-responders (these are people, where – due to various not fully understood mechanisms – creatine has no measurable effect on performance, (intracellular) water retention and body weight) and usually disappear from the market just about at the same time, the first batch has been sold and disappointed customers begin to vent their anger on the blogs and bulletin boards of the fitness world.

    With reference to the purported superiority of novel forms of creatine R. Jäger, one of the leading researchers in the field writes in a recently published paper (Jaeger. 2011), the results of which have previously been presented at the 2010 Creatine in Health and Sports conference:
    […] the efficacy, safety, and regulatory status of most of the newer forms of creatine found in dietary supplements have not been well established. Additionally, there is little to no evidence supporting marketing claims that these newer forms of creatine are more stable, digested faster, and more effective in increasing muscle creatine levels and/or associated with fewer side effects than CM.
    In their extensive review of the literature Jäger et al. dissect many of the commonly held views on the purported “instability” and “low absorbtion rate” of creatine monohydrate, evaluate the different creatine contents of various supplemental forms and their individual solubility, stability and bioavailability. And while some other forms are in fact more soluble…
    Creatine monohydrate dissolves at 14 g/L at 20°C resulting in a neutral pH of 7. A saturated solution of tricreatine citrate in water has a pH of 3.2; whereas a saturated solution of creatine pyruvate even has a pH of 2.6 (pyruvic acid is a stronger acid than citric acid). The decrease in pH results in an increase in solubility: 29 g/L creatine citrate at 20°C, and 54 g/L creatine pyruvate at 20°C. Normalized by the relative amount of creatine per molecule (monohydrate 87.9%, citrate 66%, pyruvate 60%), creatine citrate (19.14 g/L) shows a 1.55-fold and creatine pyruvate (32.4 g/L) a 2.63-fold better solubility when compared with the monohydrate (12.3 g/L).
    The acidity of your stomach is high enough, anyway, so that even if you just swallow the powder it will eventually dissolve, when it comes in contact with your gastric acid - for monohydrate [CM] Jaeger reports the absorption to be as high as 99%.

    Furthermore, pre-solving of creatine in water is counter-indicated, because, as Jaeger et al. write, …
    […] solution precludes the manufacture of shelf-stable standard ingredient. If creatine is not consumed immediately after it has been dissolved in water, it should be stored at a low temperature to retard the degradation.
    So you better throw away your liquid creatine - chances are its 99% degraded even before you bought it from your retailer.

    The instability is even more of concern in the case of Creatine Ethyl Ester (CEE) which has been found to be “actually less stable than CM.” (Child & Tallon. 2007).
    CEE is mostly converted into creatinine under physiological conditions encountered during transit through the various tissues, suggesting no ergogenic effect is to be expected from supplementation of CEE.
    The latter, i.e. creatine ethyl esther, is also less bioavailable
    Figure 1:Changes in total muscle creatine content in response to placebo (PLA), creatine monohydrate (CRT), and creatine ethyl ester(CEE) supplementation (Spillane et al. 2009, cf, fig. 1).
    and studies (Spillane. 2009) suggest that its higher rate of degradation to creatinine may pose a possible health risk.

    Also, while Jaeger et al. report some evidence for the beneficial effects of co-supplementation with glucose, protein or (low dose) D-pinitol, I personally doubt that either of them is necessary to take advantage of the repeatedly proven ergogenic effects you can get from the cheapest, most researches, safest and easiest to obtain form of creatine – creatine monohydrate.

    On a side note: My friends @ironmagazine.com have found an interesting study on the effect of creatine + nitrate, which is currently hyped as “the next big thing”. Although, I suppose that the amount of the carcinogen N-nitrososarcosine, which is a byproduct of their reaction, is hardly high enough to trigger cancerous growth, the lack of direct scientific evidence that creatine nitrate has any beneficial effect over the individual use of nitrates (for pump) and creatine (for performance) at least makes me wonder if you could not eat a buckload of beet roots (high in nitrate) with your creatine monohydrate to achieve the same effect ;-)

    Monday, April 4, 2011

    Green Tea Inhibits Fat Gain, But Will It Also Hinder Muscle Gain? Decreased Protein Absorption in Rats Supplemented With Green Tea Extract

    It has gotten relatively quiet around green tea within the past weeks. Everybody knows about its anti-oxidant effects, its modest efficacy as a weight loss supplement and the relaxing effect of taking a time-out from the stressors of daily life with a good cup of freshly brewed tea. Now, scientists from Poland (Bajerska. 2011) found another interesting, yet not so beneficial property of green tea extract.

    The scientists fed laboratory rats on a high fat diet chow with either 0%, 1.1% or 2.2% of green tea extract [GTAE] added and found that only the chow containing 2.0% GTAE had significant effects on body weight gain (5.6% less than control) and visceral fat accumulation (-17.8% vs. control). Yet, they observed a
    [...] considerably (P < .05), reduction in the digestion of protein (but not fat) was observed in both GTAE groups (1.1% GTAE: 82.6% ± 1.8%; 2.0% GTAE: 84.3% ± 0.8%) when compared to the control (93.3% ± 1.5%).
    This novel finding appears to stand in line with previous studies, in which green tea supplementation decreased fat absorption in the intestine. Interestingly, this effect was absent / non-significant in the current study (cf. figure 1).
    Figure 1: Daily food intake, FER, apparent digestion of protein and fat, energy value of feces, and visceral fat content of treatment and control groups (Bajerska. 2011)
    These findings have yet to be put into perspective, in order to assess how significant these results are for you, as a potential consumer of green tea supplements. Do you have to increase your protein intake if you consume one or two caps of green tea extract or the occasional cup of freshly brewed tea? Probably not. The rats in the study consumed 11g/kg, respectively, 20g/kg body weight of the extract. For a 80kg human being this would be a daily GTAE consumption of roughly 260g. Personally, even a teaspoon of GTAE makes me nauseous within minutes, so I guess none of you will even come close to this (over-)dose of supplemental green tea.

    It is also noteworthy that, in view of the dose-response relationship between the amount of extract the rats consumed and its effect on their body weight, these results do also indicate that the amounts of GTAE you usually find in so-called "fat burners" will hardly have any direct effect on your body weight or fat, no matter what the respective supplement companies are telling you.

    Sunday, April 3, 2011

    Follow Up on Set-Point Theories: Could Royal Jelly Help With Obesity / Diet Induced Structural Brain Changes?

    The colleagues over at ergo-log.com dug up a 2009 study (Narita. 2009) on the endocrine effects of royal jelly supplementation on rats. You may now wonder "Why is he suddenly beginning to writing off information about old studies on other sites?" Well, my interest in this study relates to my recent appearance on Carl Lenore's Super Human Radio show (I know, I promised a write-up /just have to find the time ;-) and diverges from the original interpretation the anonymous author over at ergo-log provided.

    As you may have heard on the podcast, the most significant finding of the Ravussin study (Ravussin. 2011) was the down-regulation of pro-opiomelanocortin [POMC] neurons in the hypothalamus, which went hand in hand with weight gain and weight loss and is associated with a reduction of the metabolic rate to levels at which further weight loss or even weight maintenance become a significant challenge. Here, the findings of the aforementioned study on royal jelly, "a honey bee secretion that is used in the nutrition of larvae, as well as adult queens" (Wikipedia), come into play. As can be seen from in figure 1, 7 months supplementation with 5% Royal Jelly produced profound effects on the expression of the rats' pituitary hormone genes, one of which (you will have guessed that) is POMC.
    Figure 1: Expression of Pituitary Hormone Genes in Middle-Aged Female Rats Fed a 5% Royal Jelly Diet for 7 Months. (Narita. 2009)
    Now, one could speculate that despite the fact that a ~10% increase in POMC expression could not compensate for the obesity induced loss of 50% of excitatory POMC neurons observed by Ravussin et al., the combined effect of increased POMC expression and a rise in thyroid stimulating hormone TSH could eventually turn out to be beneficial for someone, who has maneuvered him or herself in a metabolic state, where effective weight loss, i.e. the loss of body fat and conservation of muscle mass, is nigh on impossible.
    Yet, before you break into the next beeyard, you should consider that...
    1. the amount of royal jelly the rats consumed in the study, i.e. 5% of their daily food intake is almost impossible to achieve without plundering beeyards all over the country (for the same reason it is no practical alternative to medications for "rejuvinating the pituitary" which the author of the ergo-log post seems to imply in the headline of his post)
    2. an upregulation in gene expression alone does not guarantee an increase in metabolic rate (the increase in the thyroid (pre-)hormone T4, for example, was non-significant, despite a significant increase in TSH related gene expression)
    Basically, this means that you should get accustomed to the idea that the damage years of overeating and/or crash- & yoyo-dieting has inflicted to your body are unlikely to be repaired within weeks or even months by just popping pills or eating some kind of superfood, no matter how "royal" it may be. In the end, it will come down to making a decision to change your life (nutrition and exercise) and to stick to this decision, no matter how hard it may seem.

    Saturday, April 2, 2011

    Ironclad Liver Hampers Insulin Sensitivity: Association Between Hepatic Iron Load and Insulin Resistance Discovered

    "Insulin resistance", "insulin sensitivity", etc. Type in these key words and find 4.000.000 +1 results on Google. I want to focus on the +1 here and briefly report the results of a study (Haap. 2011) coming from the University of Thübingen, Germany.

    Via magnetic resonance gradient echo imaging technique Michael Haap and his colleges assessed the iron load in the livers of of 113 healthy nondiabetic subjects [69 females, 44 males; age 47 ± 1 yr; body mass index (BMI) = 28.9 ± 0.5 kg/m2], who were "at increased risk for type 2 diabetes". Various statistical analysis of their data revealed that:
    [Hepatic iron levels] adjusted for age negatively associated with serum ferritin levels (P < 0.0001) and positively associated with IS [insulin resistance] (P = 0.009). In addition, T2* values [indicator of hepatic iron load] associated with LF [liver fat] (P = 0.008) but not with BMI (P = 0.6). In a multivariate model, IS adjusted for gender, age, and BMI was associated with T2* values (P = 0.015). IS adjusted for gender and age was independently associated with LF (P = 0.033) and T2* values (P = 0.004). In a stepwise regression analysis, LF explained 13.5% (P < 0.01) of the variation in IS, and HIL [hepatic iron load] explained an additional 4.1% (P = 0.03).
    With 4.1% the contribution of iron to the development of type II diabetes is certainly only one out of a multitude of factors. I would yet still be interested in further information on the interplay of iron, insulin and blood glucose, also because low ferritin levels, which, according to the study, go hand in hand with high hepatic iron loads, have also been implicated in other metabolic disorders such as hypothyroidism, which in and out of itself would further aggravate existing blood sugar and weight issues within the pre-diabetic study population.

    Friday, April 1, 2011

    Something Fishy: Leucine-Rich Protein + Fish Oil Supplement Boosts White Blood Cell EPA Content and Immune Response

    Regular readers of the SuppVersity, as well as people who religiously follow Carl Lenore's Super Human Radio and happened to listen to my 1st appearance on the show, will know that I am generally skeptic about the usefulness of unwarranted high dose (>1-2g of combined EPA + DHA) fish oil supplementation. This is not because I think fish oil is poison, but rather out of my awareness that its pharmacological effects have more similarity to those of a drug than to those of a "common food" (including possible side effects).

    Now, a group of scientists from the Netherlands and the United Kingdom published the results of a study (Faber. 2011) which found another interesting stone from the fragmented mosaic our current understanding of the effects and nutritional interactions of fish oil, in general, and EPA, in particular, resembles. While the aim of the study, which was to quantify the incorporation of EPA and DHA into white blood cells, was nothing new, the nutritional supplement they used for this purpose, a mixture of 2.4 g EPA, 1.2 g DHA, 39.7 g protein (including 4.4 g L-leucine), and 5.6 g oligosaccharides was innovative and the results were astounding. After 1 week of 2x200ml of what the scientists label a "medical food" (beware there is probably somebody patenting the formula already ;-), ...
    [... from 0.5% at baseline] the percentage of EPA [in white blood cell phospholipids] rose to 2.8% (P < 0.001). Additionally, the production of proinflammatory cytokines in LPS-stimulated whole blood cultures was significantly increased within 1 wk.
    It appears that the addition of protein has a positive influence on the incorporation of EPA into white blood cells, which, in turn, boosts the natural immune response to lipopolysaccharides stimulation. This, however, brings me back to my initial comment about "pharmacological" effects of fish oil: While for a cancer patient with lowered immunity, the consumption of the "medical food" or, what I would consider equivalent, a combination of whey + fish oil, would unquestionably be beneficial - but what about someone with allergies or even auto-immune issues? I assume you would agree that to further boost an immune system that is already running havoc does not seem to be a good idea!? In the end, and here I do not mind repeating myself, it again all comes back to considering who you are and what your current medical and nutritional condition is, before you start taking a supplement of which the whole Internet community seems to believe that its the healthiest (if not the only healthy) fat on earth...

    Connelly, Andrich, Norton, Arnold, Lenore, Andro - BodyRX #17: Carbohydrate Intake For People Who Will NEVER Settle for Being "Normal"

    BodyRX guest: Pete Ciccone, 
    national-level NPC
    competitive bodybuilder
    For those who missed out on yesterday's episode of the new, totally revamped BodyRX Radio Show, episode #17 "Carbohydrate Intake For People Who Will NEVER Settle for Being 'Normal'" is now available for download.


    I will compile a write up of the most significant facts and include links to some research on the coming weekend. So stay tuned!


    If you wanna be Super Human,
    the SuppVersity is the place to read

    and SHR and BodyRX the shows to listen to ;-)

    Thursday, March 31, 2011

    Exhaustive Aerobic Exercise Increases Serum Calcium Levels and Dietary Requirements

    You probably have heard of the fundamental importance of calcium as a structural component of bones. Yet, calcium is way more than the building block of our bone structure and the concrete the of the hopefully non-existent plaque in your arteries. It is also one of the major players in muscle contraction. Thus, it is not very surprising that a group of Iranian Scientists (Pourvaghar. 2011) found major effects of pro-longed (15min) high intensity aerobic exercise on serum calcium levels of 12 randomly selected student athletes (22.36y; 75kg @ 1.76m):
    […] the participants' mean of serum calcium concentration in the first stage and before Balke exhausting aerobic exercise was measured 98.38 ng/mic L. In the second stage, i.e. after the exhausting aerobic activity, it increased to 114.96 ng/mic L. Research results indicated that the difference in serum calcium concentration between the first and second stages is significant (P= 0.0001).
    With the calcium that is appearing in the blood of the athletes being leeched from bones, organs to fulfill the increased calcium needs of active muscle tissue. Due to calcium “consumption” and urinary losses, the scientists speculate, the overall result to be a negative calcium balance.
    Figure 1: Serum Calcium levels of athletes before, immediately after and 24h after exhaustive aerobic exercise. (Pourvaghar. 2011)
    In view of the fact that, in the 24h after exercise, there is no sudden falloff (only -9.13%) of blood calcium, I would yet advice against extensive calcium supplementation. Previous works from other researchers have conclusively shown that a nutritionally dense, calorically adequate, diverse, calcium-rich diet satisfies the needs of both, the average gymrat and the hard training endurance athletes.

    For athletes on a weight-reduction diet, or active gym-goers who – due to whatever other reasons – consume a diet that is low (<1.000mg/d) in calcium supplementing with a bio-available form of calcium, like calcium citrate, could yet be a viable strategy to prevent bone loss and sustain exercise performance.

    Wednesday, March 30, 2011

    An Old Dog Learns New Tricks: "Fatloss Fat" Tetradecylthioacetic Acid (TTA) Cardioprotective in Diabetic Rats

    Do you remember the acronym TTA? Tetradecylthioacetic Acid? No. Well, I guess then you were not into fat burners in the early 2000s. TTA, a thia-fatty acid, was all the rage back in the day: Supplement producers claimed it would literally melt fat away and it actually turned out that some users had outstanding results megadosing respective supplements. Others, however, got bloated and/or started cramping. In view of these nasty side effects, most companies decided to reformulate their products and - with the exception of a few so-called "non-thermogenic" fat burners - TTA has almost disappeared from the market.

    An international team of scientists from Norway and Canada (Khalid. 2011) has now discovered that the artificial fatty acid tetradecylthioacetic acid, which was originally intended as a drug for the treatment of the metabolic syndrome, might have the potential to protect type II diabetics from heart attacks.
    In a previous study (Hafstad. 2009) the scientists had already shown that TTA does increase myocardial fatty acid oxidation in normal mice, a finding that would generally suggest impaired cardiac efficiency and thus be considered detrimental. In the current study on hyperlipidemic [high blood lipid levels] type 2 diabetic mice, however, TTA-treatment (0.5%, 8 days) had almost opposite effects on on cardiac metabolism and function
    We found that TTA treatment increased myocardial FA oxidation, not only in non-diabetic (db/+) mice, but also in diabetic (db/db) mice, despite a clear lipid-lowering effect. While TTA had deleterious effects in hearts from non-diabetic mice (decreased efficiency and impaired mitochondrial respiratory capacity), these effects were not observed in db/db hearts. In db/db hearts TTA improved ischemic tolerance, an effect that is most likely related to TTA's antioxidant property.
    Being a specifically designed (Pan-)PPAR-ligand [TTA seems to activate all PPAR-receptors] the lipid lowering effect of TTA was to be expected. The differential effect on heart function in healthy and diabetic rats, however, comes as a surprise and reminds us, again, that not all that has been shown to help sick people is beneficial - and sometimes its not even safe! - for the healthy part of the population.
    Figure 1: Myocardial fatty acid and glucose oxidation in hearts of db/+ (white  545
    bars) and db/db (gray bars) mice. Results are mean of 8-9 hearts in each group. (Khalid. 2011)
    So, regardless how promising the shift in substrate metabolism from carbohydrates to fats, as it is visualized in figure 1 may appear, if you just want to shed a few pounds of unaesthetic, but healthy subcutaneous body fat, stay away from tetradecylthioacetic acid - for your heart's sake!

    More on Putting Carbs to Good Use: Scott Connelly's BodyRX Show - Tune in Live at 12:00pm PDT

    Who listened to my interview on Super Human Radio, yesterday, may have heard my advice to tune in to today's BodyRX Show with Dr. Scott Connelly, Vince Andrich, Layne Norton, Patrick Arnold and (this is new) me, ProfDrAndro, being the brains behind a completely overhauled show concept, I promise you won't be disappointed.

    BodyRx Radio Show #017

    Tune in Live @ 12pm PDT

    Here is a short glimpse onto what is waiting for you:
    On our last BodyRx Radio show (#016) we learned that by reducing carb intake from levels at the top of the food pyramid (>60% of energy) to a modest 35-40% of energy, you can effectively “teach” your body to preferentially store the carbs you eat into muscle cells and NOT your fat cells [cf. Effect of Macronutrient Composition]. But, when does reducing carb intake negatively impact your performance in the gym, where the work to build muscle takes place? More importantly, does that number change if you alter your training program? We take this age old question head on with:
    • A revealing interview with renowned researcher Dr. Kevin Tipton by our very own Dr. Scott Connelly.
    • Next, Vince Andrich taps into the minds of two of the industries top physique competitors and personal trainer/coaches; Pete Ciccone and his wife Meriza Deguzman––listen for their practical advice that men and women can use right NOW!
    • Lastly,  renowned chemist Patrick Arnold will take on a list of hard hitting questions that will give listeners an inside look at the popular diet and energy compound; geranium. We know you’ll agree this is a one-of-a-kind interview since it was Patrick Arnold himself who brought this compound to the market several years ago, and is now the darling of the supplement world.
    The prominent line-up alone makes it worth listening - no doubts about that, folks!

    Tuesday, March 29, 2011

    ProfDrAndro @ Super Human Radio: Set to Be Obese? Of Set & Settle Points on Your Way to a Super Human Physique

    Just in case you got nothing else to do: Tune in live and listen to some more (probably Carl) or less (probably me ;-) intelligent Supp-Talk on Carl Lenore's Super Human Radio!

    Topic: Set & settle points and how contemporary science
    may contribute & explain your personal weight loss success


    Listen live @ 9:00AM AM/12:00PM ET

    Putting Carbs to Good Use: Meta-Review Reports Ergogenic Effect of Carbohydrates in Endurance Athletes

    One of the leitmotifs, many of my posts here at the SuppVersity share, is the idea that (almost) everything works for someone. From the feedback I am receiving, from the crowd this blog is attracting, I gather that my general advice against high carbohydrate intake is (as human as that may be) often misinterpreted as "carbs are evil, beware of all carbs"! For the average pizza eating fast-food junkie, this certainly is an adequate message, because even if he believes that carbs are the root of all disease, without a MAJOR change in his dietary habits (I am not talking of ordering the normal, instead of the super size menu at McDonalds, here) he will probably still get way more carbs out of his diet than it would fit his sedentary lifestyle.
    If, however you are an athlete or avid gym-goer you may probably already start to notice that following what you took to be a one-solution-fits-it-all recommendation lead to performance decreases, laziness, brainfog, lack of sexual desire, bad sleep and many of the other symptoms you would find, when you googled one of the ambiguous terms "adrenal fatigue" or "general fatigue syndrome"... Carbs are more than just insulin triggers, and fatteners. Glucose is the gasoline in your fuel tank and - most importantly - its the substrate your nervous system thrives on. And while it might not be necessary to eat them, very active (and lean) individuals may derive similar benefits from a moderate carb consumption as the athletes from the 50 studies included in a meta-review by Themesi et al. (Themesi. 2011).

    The scientists' results suggest that intake of a <8% carbohydrate beverage (~50-80g) [TT] in the course of an endurance event (≥1 h) significantly "enhances endurance exercise performance in adults" as measured by submaximal exercise performance and time to exhaustion [TTE]:
    The ES [effect size] for submaximal exercise followed by TT was significant (ES = 0.53; 95% CI = 0.37–0.69; P < 0.001) as was the ES for TT (ES = 0.30; 95% CI = 0.07–0.53; P = 0.011). The weighted mean improvement in exercise performance favored CHO ingestion (7.5 and 2.0%, respectively). TTE (ES = 0.47; 95% CI = 0.32–0.62; P < 0.001) and submaximal exercise followed by TTE (ES = 0.44; 95% CI = 0.08–0.80; P = 0.017) also showed significant effects, with weighted mean improvements of 15.1 and 54.2%, respectively, with CHO ingestion. Similar trends were evident for subanalyses of studies using only male or trained participants, for exercise of 1–3 h duration, and where CHO and PLA beverages were matched for electrolyte content.
    Against this background, can the relevant question really be: "To carb or not to carb?" Probably not. You better follow Vince Andrich's recent advice and ask yourself "Are you working your sugar-bags (muscles) hard enough to earn your fair share of carb intake?" in order to make sure that you use just as much carbs as it takes to optimize performance without compromising health and body composition.

    Monday, March 28, 2011

    Epidemiological Study Shows Correlation Between Anti-Oxidant Intake and C-Reactive Protein & Homocystein

    After a sudden onset of discussions around the beneficial or even detrimental effects of vitamin supplements in general and antioxidants in particular in the mid to late 2000s, vitamins and, even more, other anti-oxidants have been put back on the map, lately.

    A recent epidemiological study from the University of Connecticut (Floegel. 2011) provides further evidence for the hypothesis that, after all, consumption of adequate amounts of vitamins C and E, beta carotene, flavonoids and selenium would be beneficial to your overall health
    Intakes of vitamins C and E and carotene were inversely associated with the probability of having serum CRP concentrations >3 mg/l in multivariate logistic regression models. Flavonoid and Se intakes were not associated with the odds of elevated serum CRP concentrations. The mean plasma Hcy concentration was 8·61 (95 % CI 8·48, 8·74) μmol/l. Intakes of vitamins C, E, carotenes and Se were inversely associated with the odds of plasma Hcy [Homocysteine] concentrations >13 μmol/l after adjusting for covariates
    While all these results appear to be quite unambiguous, you still have to keep in mind that they support the interpretation "antioxidants are healthy" only, if we assume that the relation between high C-Reactive Protein [CRP], inflammation and the metabolic syndrome, as well as the relation between homocysteine and heart disease is more than just a correlative one; and, to my best knowledge, no study has yet been able to show that injection of homocysteine caused heart disease or an increase in CRP increases inflammation or causes tissue damage. In this context, for example, the hitherto hardly understood involvement of "positive inflammation", such as an exercise induced rise in IL-6 levels, come to mind. In this context, studies such as Ristow et al. (2009) that found the positive effects of exercise being blocked by antioxidant supplementation would warrant further research into what - irrespective of reductions in purported markers of inflammation and cardiac disease - the actual health outcome of higher antioxidant intakes are.


    Note: Don't get me wrong. I do not want to argue against a diet rich in natural antioxidants. I just want YOU to be aware that the proven health benefits from eating healthy, antioxidant-rich foods cannot be extrapolated to high (or even mega-dose) vitamin & flavonoid supplements and that taking megadoses of isolated antioxidants such as alpha-tocopherol (especially in its synthetic form and without the complementary tocopherols and -trienols), which is the most commonly sold form of vitamin E, may in fact do more harm than good.

    Sunday, March 27, 2011

    Now Its Official: Propecia Drug Finasteride Kills Male Libido Permanently

    Image 1: Chemical structure of finasteride
    Other than the FDA some European medicine and health care agencies, such as the Swedish Medical Products Agency and the Medicines and Healthcare Products Regulatory Agency of the United Kingdom already had the guts to declare in their patient informations that "persistence of erectile dysfunction after discontinuation of treatment with Propecia has been reported in post-marketing use." While this was obviously no reason for the all-mighty FDA to correct or re-evaluate their own documents, two it did intrigue Michael S. Irwig and Swapna Kolukula, two US scientists from Washington and Baltimore, respectively.

    In their study (Irwig. 2011), the scientists conducted standardized interviews with 71 otherwise healthy men (age: 21–46y), who experienced permanent (>3 months) sexual side effects after temporary use of Finasteride. Their reports are staggering:
    94% developed low libido, 92% developed erectile dysfunction, 92% developed decreased arousal, and 69% developed problems with orgasm. The mean number of sexual episodes per month dropped and the total sexual dysfunction score increased for before and after finasteride use according to the Arizona Sexual Experience Scale (P < 0.0001 for both).
    These sexual side effects occurred after a "mean duration of finasteride use [of] 28 months" and they were persistent up to the interview date. For the study population this meant that they had already been suffering 40 months, on average, when the interviews took place; and chances are that many of them will suffer the consequences of an insufficient (or should I say incompetent or corrupted?) drug approval process and consequent indoctrination of medical practitioners for the rest of their lives.

    Note: After receiving some critical feedback via facebook, I feel that it is necessary to point out that the result of the study may not be misinterpreted as "Every Finasteride user will experience persistent decreases in libido, erectile disfunction etc.", but as "In those percentage of Finasteride users, where such side effects occur, they can potentially be permanent." So the news is neither that Finasteride will cause these effects in each and every user, nor that it may cause such side effects (that is in fact mentioned in the package insert, I suppose), but that IF side effects occur, it is possible that they are persistent.

    Saturday, March 26, 2011

    Fat or Fire, What Comes First? Scientists Answer: Obesity Alone Triggers Inflammatory Signaling in Mice

    The metabolic syndrome, i.e. the combination of obesity, inflammation and insulin resistance, is at the center of contemporary medical research. In my appearance on Carl Lenore's Super Human Radio, I already mentioned that from a logical perspective the mainstream belief, inflammation was the root of all evil, must be flawed. How should the reaction to a problem be the cause of the very problem itself? A recent study coming from a group of Korean scientists strengthens my conviction that out of the triad that not inflammation, but rather obesity or - one step further up in the genesis of the pathology - the combination of an unhealthy diet and a sedentary lifestyle is at the heart of the triad we now call the "metabolic syndrome".

    Kim et al. investigated the pro-inflammatory signaling cascade in either diet-induced (DIO) or leptin gene deficient (ob/ob) obese mice and found that obesity alone ...
    [...] up-regulated the expression of TLR1–9 and TLR11–13 in murine adipose tissues, a phenomenon linked with downstream nuclear factor κB [inflammatory protein linked to linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection, and improper immune development], interferon regulatory factors, and STAT-1 activation, and up-regulated the expression of cytokines and chemokines via MyD88-dependent and MyD88-independent cascades [activate NF-κB].
    Thus, obesity sets the scene for inflammation and inflammation in turn triggers a cascade of unfavorable metabolic and hormonal changes which in and out of themselves result in further weight gain...

    Here, we have a self-enhancing pathologic circle, which - and this is probably an even more important result of the study - was especially "effective" in the group of diet-induced obese mice:
    The magnitudes of the obesity-induced up-regulation of the TLR1, TLR4, TLR5, TLR8, TLR9 and TLR12 genes in the visceral adipose tissue were greater in the DIO mice than in the ob/ob mice. Similarly, the expression of the IFNα and IFNβ genes significantly increased in the adipose tissues of the DIO mice but did not change in the adipose tissues of the ob/ob mice.
    So, its not in your genes, but in your hands, feet and mouth to ward off the plague of the 21st century: Exercise and eat healthy to get lean and/or stay lean and stave off inflammation and diabetes.

    Friday, March 25, 2011

    Effects of Macronutrient Composition on Metabolic Signaling: Higher Protein Diet Favors Glycogen Storage in Muscle Over Adipose Tissue

    Those of you who have already listened to the latest, revamped (and improved) episode of Dr Scott Connelly's BodyRx Show will already have heard of Suzanne Devkota's and Donald K Layman's study (Devkota. 2011) on the effects of different meal compositions on the postprandial glucose disposal. For the rest of you who have missed the episode and those of you who like their info white-on-black, here are the main results...

    For 10 days, Devkota and Layman fed 60 rats a diet containing either 60% of energy from carbohydrates, 12% protein, 28% fat (CHO) or 35% carbohydrate, 35% protein, 30% fat (PRO) and evaluated plasma levels of insulin, glucose and C-peptide, as well as muscle and adipose tissue Akt, p70S6K and Erk 1/2 (markers of glucose and protein metabolism and cellular growth, respectively).

    The graphs in figure 1 illustrate their most significant finding quite nicely. Other than in the case of the protein-fed rats, blood glucose is preferentially stored in fat tissue in the 30-90 min time window upon the ingestion of a meal in the high carb (CHO) group
    Figure 1: Muscle and adipose tissue Akt expression (marker of glucose metabolism) after "high" protein (PRO) and high carbohydrate (CHO) meal, respectively (Devkota. 2011
    The authors summarize this effect of macronutrient partitioning on metabolic signaling that is supported by the rest of their data as follows:
    Animals chronically consuming the CHO diet produced greater metabolic signaling in adipose tissue to handle excess glucose and blunted signaling in skeletal muscle consistent with interpretation of insulin resistance. Conversely, animals consuming the PRO diet produced greater metabolic signaling in skeletal muscle with little signaling in adipose.
    To fuel your workouts, it thus seems not only unnecessary, but even detrimental, to consume high amounts of carbohydrates. A "lower"  [note: even the high protein diet that was matched to the USDA's acceptable macronutrient distribution ranges (AMDR) had a carbohydrate content of 35% and thus a 1:1 protein to carb ratio!] carbohydrate intake, on the other hand, appears to prime your body to store glycogen primarily in muscle tissue. On a "high" protein, "lower" carb diet, you thus get the performance benefit without the unwanted fat gain and isn't this what we all are looking for?

    Thursday, March 24, 2011

    Got a Pot Belly? Stubborn Belly Fat? Unhandy Love Handles? Massage Them Away!

    "Massage away your pot belly!" Sounds hillarious, doesn't it. Well, a small study (Rahimi. 2011) coming from scientists from the University of Mashhad in Iran suggests that massaging your love handles could actually facilitate localized fatloss.

    In their study, Rahimi and Javahery put 16 healthy - I quote - "non-sportsperson male students"  ;-), aged 20-27y on a 5x a week massage regimen (15-20 min) that had, if not outstanding, then at least statistically significant results:
    The results of correlated t test show that the mean values of skin fold fat of the stomach are of the participants before and after the massage program was 36.81 and 36.12 respectively, which shows a significant decrease after 30 sessions of massage (p=0.036).
    - 2% skin fold: You are not impressed? Well, me neither. Although the increased blood flow to the subcutaneous fat pads may, as the scientists speculate, have a beneficial effect on local fat mobilization, I would suggest you better spend the time in the gym or doing sprints on the track to not only mobilize, but also oxidize these stubborn and unaesthetic fat pads and simultaneously improve your cardiac and metabolic health.

    On a side note: If there is anything significant to learn from this study, it is that sometimes, even scientists try to trick you into believing that what they found (similar to what supplement companies sell) is a great thing. Look at the following graph from the study:
    Figure 1: pretest (1) and posttest (2) mean values of the subcutaneous fat of the stomach area of the participants (Rahimi. 2011)
    Just by selecting a very narrow scaling on the Y-axis of the graph, the scientist create the impression that their massage therapy was a huge success. If, however, you take a closer look, you inevitably notice the figures and the bluff is exposed. Remember tricks like that, when you look at the colorful graphs in supplement ads all over the Internet. Or as Churchill is said to have put it (in fact this is another myth) “Never trust any statistics that you didn’t forge yourself.”

    Wednesday, March 23, 2011

    NAC + Zinc + Selen = Silver Bullett Against Mercury Poisoning

    Mercury certainly is among the most dangerous and, at the same time, most ubiquitous heavy metals, we are exposed to. In a recent article (thanks to Dominique for raising my awareness of its publication) strength coach Charles Poliquin references a 2010 study from Michigan State (Wirth. 2010) :
    Looking at several well-designed studies, they determined that even low exposures from cadmium, lead and mercury had an impact on semen quality and reproductive hormone levels in men.
    As far as solutions to this problem are concerned, Polliquin refers somewhat dubiously to "a specific herbal combination" of "andrographis paniculata, zinc citrate, humulus lupulus, and curcuma longa" without providing scientific evidence for why he thinks this specific formula would work (guess what, Charles sells it ;-). Chances would have it, though, that Joshi et al., in a very recent study (Joshi. 2011, still ahead of print) report the beneficial effects of another, from my perspective, probably even more potent combination of nutrients/antioxidants in experimentally induced mercury poisoning:
    Exposure to DMM [dimethylmercury] caused significant alterations in cytochrome P450 (CYP) activity, microsomal lipid peroxidation, and proteins [in rats]. Activities of transaminases (aspartate aminotransferase/alanine aminotransferase), alkaline phosphatase, and lactate dehydrogenase in serum, as well as activities of CYP enzymes aniline hydroxylase (AH), amidopyrine-N-demethylase (AND) in liver microsomes and activities of acid phosphatase, alkaline phosphatase, glucose-6-phophatase, and succinic dehydrogenase in the liver and kidney, were significantly altered after DMM administration. DMM exposure also induced severe hepato-renal alterations at the histopathological level. NAC, along with Zn and Se, dramatically reversed the alterations in all of the variables more toward control.
    Actually these results do not come as a surprise, as all three of these nutrients/antioxidants are well-known for their beneficial effects on (liver) enzyme activity and thus heavy metal clearance. Those of you, who read Tim Ferris' book The 4 Hour Body may also remember that his Brazil nut consumption (he ate them for their high selenium content, 1 ounce contains 544µg, i.e. 780% DV) along with other nutritional changes tripled his testosterone levels from low normal levels to the upper quartile of the range. In that, it is of secondary importance whether this was a mercury related effect, or not, since an increase in the detoxification abilities of the liver, as it was achieved in the study by twice a week supplementation with NAC (360mg/kg; human equivalent dose [HED] ~ 52mg/kg)  + Zn (130mg(kg; HED ~ 26mg/kg) + Se 0.5mg/kg; HED ~0.08mg/kg), will benefit the hormonal millieu via multiple pathways (increased estrogen clearance being one of them).

    A word of caution: I advice against using the dosing scheme applied in the study, i.e. twice a week mega-dosing of supplements. Spread across a whole week, the human equivalent doses (for an 80kg human being) would equal roughly 600mg NAC, 300mg Zinc and 1mg* Selenium per day, which - apart from the exorbitant amount of zinc (I would not take more than 100-150mg/day even for short term interventions) - constitutes a quite reasonable nutrient stack for shorter detox protocols (4-6 weeks) for mercury, cadmium (cf. eg. Said. 2010) and other heavy metals with an increase in testosterone being one of the possible positive "side effects".

    *Note on selenium toxicity: Rumors have it that selenium is toxic even at doses of >400µg. Most of these reports yet turned out to be based on anecdotal evidence from people who poisoned themselves with supplements that contained up to 200x the labeled dose (e.g. >40mg! selenium in MacFarquhar. 2010). It is thus very unfortunate that current data on the ‘Lowest Adverse Effect Level’ (LOAEL) is lacking. A 1989 study by Yang et al. give1.5mg/day as a threshold beyond which longterm supplementation may produce adverse side effects. And though this is below the 1g derived from the results of the rat study, I recommend to better err on the side of caution and to stick to max. 200-400µg supplemental selenium + a handfull of Brazil nuts from time to time as part of a safe antioxidant supplement stack.