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 ;-)

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.

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.

Diet Coke & Liver Damage? Long Term Very High Dose Aspartame Consumption Impairs Antioxidant Defense of Rat Livers.

The ever-growing group of health conscious costumers is rightly very skeptical of artificial sweeteners in general and Aspartame in particular. A recent study (Abhilash. 2011) done by scientists from the Mahatma Gandhi University in Kottayam, Kerala, India, seems to rectify this attitude.

The scientists fed rats drinking water that contained either no, i.e. 0mg, 500mg or 1.000mg aspartame per kg body weight day for a period of 160days. The rats from the 1.000mg/kg group showed...

[...] a significant increase in activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and γ- glutamyl transferase (GGT). The concentration of reduced glutathione (GSH) and the activity of glutathione peroxidase (GPx), and glutathione reductase (GR) were significantly reduced in the liver of rats that had received aspartame (1000mg/kg.b.wt).

The presence of "leukocyte infiltration in aspartame-treated rats (1000mg/kg.b.wt)" further underlines that high dose aspartame consumption over a period of 160 days induced "hepatocellular injury and alterations in liver antioxidant status" by increasing the detoxification burden on the liver to supra-physiological levels.

Yet, what does that mean for the average consumer? Let us put the figures into perspective: 1 liter of diet coke contains about 390mg of aspartame. The rats in the high dose aspartame group in the study (which is the only one where anti-oxidant status fell enough to induce histological side effects) received 1.000mg/kg of aspartame per day. In human equivalent dosages (HED), this is 162mg/kg, which would be 11.35g of aspartame or 29 l diet coke for a 70kg adult. Not that I want to trivialize the possible liver toxicity due to aspartame consumption, but let's be honest: you would probably long have died from hyperhydration before you would notice any of the toxic effects induced by the consumption of an artificial sweetener, which - far from being healthy - is yet not as toxic as some health-fetishists would have it.

In spite of the fact that a diet coke here and there won't kill you, you should still ask yourselves, whether or not you really need this "spawn" of a society where we want all the convenience and (unnaturally sweet) taste of unhealthy foods without the negative consequences for our health? I mean, you obviously chose the "diet" version because you want to avoid sugar; but do you still want the sweet taste, which (at least for some artificial sweeteners, eg. Nakagawa. 2009) has been shown to increase insulin secretion even in the absence of direct beta cell stimulation!? If you are willing to accept this compromise and do not care about the other chemicals your average can of diet coke "nourishes" you with, fine! But do not tell me later on, I had told you that diet coke was good for you ;-)

Review of Intervention Studies Shows: Weight Loss Success Independent of Meal Frequency

"Eat 3 large meals à day!", "Eat smaller meals every 2 hours!", "Eat a single meal and fast the rest of the day!" If you have been trying to find information on how to lose weight effectively, you probably heard all these "expert" advises. What if I told you that a recent review of 25 weight loss interventions shows that it simply does not matter!

In an extensive review of the literature, Palmer et al. (Palmer. 2011) conclude:

Manipulating the EF [eating frequency] of a client seeking weight management is unlikely to provide any additional benefits to weight, body composition or health. The theoretical benefits of manipulating EF may not be sustained in the real life clinical setting as a change to EF may be difficult to maintain over the longer term. Current evidence does not support many of the theories that encourage manipulating EF for weight management. Focus needs to be placed on dietary weight management strategies that are achievable and sustainable over the longer term.

Better body composition? Only inconclusive evidence. Better glucose tolerance in non-diabetics? Definitely not. Decreased risk of heart disease? Unlikely. Less hunger? At least not with three vs. six meals. Bottom line: Another myth debunked!

Want to Burn More Fat During Your Cardio Training? Eat Low Carb Before Workout!

Modulation of substrate utilization is the key to effective weight loss. For years we have been told that "training in the zone" (referring to a specific heart rate) would do the trick - recent research does yet suggest otherwise: High Intensity Interval Training (HIIT) has been shown to be at least as effective in burning off unwanted body fat, as the longstanding "gold standard", Low Intensity Steady State (LISS) in the "fat burning zone".

Researchers from the Department of Exercise Science and Sports Studies at Springfield College, Springfield, MA, USA, have now found that apart from the type of exercise you chose to perform, the nutrition, especially in the hours before working out, determines whether you will predominantly burn fat or carbs to sustain the workout.

In their study (Gregory. 2011), Gregory et al. compared the metabolic responses of a group of 8 "active, pre-menopausal" women to a 30 minute exercise regimen performed after either a low carbohydrate (LC: 392 kcal @ 15% carbohydrate, 68% fat, and 18% protein) or a low fat (LF: 396 kcal @ 78% carbohydrate, 7% fat, and 15% protein) meal. Respiratory gas exchange (RER), blood glucose (G), insulin (IN), triglycerides (TG), and free fatty acids (FFA) were measured. While "no significant differences existed between test meals for fasting blood measurements", the post-exercise results showed significant differences:

Postexercise (PE) FFA (mEq·L-1) levels were significantly greater following LC [1.1 (0.3) vs. 0.5 (0.3)]. PE TG (mg·dL-1) levels were significantly greater following LC [152.0 (53.1) vs. 114.4 (40.9)]. RER was significantly lower at all time points following LC compared to LF.

With the respiratory gas exchange being a measure of the relative contribution of fatty acids to fulfill the exercise-induced energy demand (Chessex. 1995), the researchers rightly conclude "ingestion of a single LC meal resulted in greater lipid oxidation at rest and during exercise as compared to a single LF meal." But, let's be honest - did you expect anything else?

Low Dose Caffeine Ameliorates Catabolic Effects and Increases AMPK and PPAR Expression During Reduced Food Intake in Mice

Caffeine, "the mother of all stimulants", has lately developed a bad reputation. Stress, Cortisol, Adrenal Fatique, Insulin Resistance etc. are only the most recognized buzzwords occurring within the context of caffeine consumption. A very recent paper (Shermann. 2011) coming from scientists from the University of Jerusalem draws a wholly different picture.

Shermann et al. investigated the effect of caffeine consumption (3.5 mg/kg/day or 7 mg/kg/day) on circadian rhythms and expression of disease and metabolic markers in mice under two distinct dietary conditions over a period of sixteen weeks. When the rats were fed an ad libitum diet (meaning they could consume as much food as they wanted), ...

caffeine reduced the average daily mRNA levels of certain disease and inflammatory markers, such as liver alpha fetoprotein (Afp), C-reactive protein (Crp), jejunum alanine aminotransferase (Alt), growth arrest and DNA damage 45β (Gadd45β), Interleukin 1α (Il-1α), Il-1β mRNA and serum plasminogen activator inhibitor 1 (PAI-1).

For those of you who still want to shed some pounds of fat, it may yet be even more interesting to read that "caffeine supplementation led to decreased expression of catabolic factors under RF". With the RF = restricted feeding condition being comparable to what is known as "intermittent fasting" in the fitness community, this finding is highly significant.

Figure 1: Metabolic markers PPAR-Gamma (above) and PPAR-Alpha (below) in mice fed an ad libitum (AL) or a restricted diet (RF) (Shermann. 2011)

This is particularly valid given the fact that there was a highly significant increase in PPAR-Gamma, PPAR-Alpha (cf. figure 1) and AMPK (not shown) activities in the group receiving "high dose" (7mg/kg; for humans this would equal a pretty low dose of about 0.6mg/kg) caffeine. Both, peroxisome proliferator activated receptor (PPAR), as well as AMPK are regarded as master metabolic regulators that have been implicated in the physiology of fat loss. A moderate caffeine consumption, i.e. about one cup of coffee, in the course of an intermittent fast, may thus well spare muscle protein and burn body fat, at the same time.

Life-Long Endurance Exercise and Myocardial Fibrosis - A Potential Danger for Endurance Athletes

Habitual aerobic exercise has long been the cornerstone of what was considered a "healthy" lifestyle. Yet, lately, scientists are not only questioning the time-efficacy of these training regimens (there are studies showing that one can achieve similar metabolic adaptations with short high intensity interval training), there is also cumulative evidence that indicates that life-long engagement in endurance exercises may even be detrimental to your health.

In a recent study by Wilson et al. (Wilson. 2011)  "twelve lifelong veteran male endurance athletes (mean ± SD [range] age: 56 ± 6 yr [50-67]), 20 age-matched veteran controls (60 ± 5 y; [52 - 69]) and 17 younger male endurance athletes (31 ± 5 years [26-40]) without significant co-morbidities underwent cardiac magnetic resonance (CMR) imaging to assess cardiac morphology and function." The results of the CMR were disquieting - to say the least:

In 6 (50%) of the veteran athletes LGE [late gadolinium enhancement, short LGE indicates the presence of fibroses as a consequence of minor tissue ruptures] of CMR indicated the presence of myocardial fibrosis (4 veteran athletes with LGE of non-specific cause, 1 probable previous myocarditis and 1 probable previous silent myocardial infarction). There was no LGE in the veteran controls or young athletes. The prevalence of LGE in veteran athletes was not associated with age, height, weight or BSA (p>0.05), but was significantly associated with the number of years spent training (p<0.001), number of competitive marathons (p<0.001) and ultra-endurance (>50 miles) marathons (p<0.007) completed.

In fact, this study is only part of the accumulating evidence against the health benefits of (ultra-)endurance and or excessive aerobic training. Weight lifting and intense, but short sprint-intervals, on the other hand, turn out to be a healthier and much more effective way of keeping lean and healthy up into the older ages.

From Subclinical to Full-Blown Hypothyroidism by Soy Supplementation. 3-Fold Risk with Just 15mg Soy Phytoestrogens per Day.

"Soy is healthy!" At least the majority of women in the western hemisphere still seems to believe this. Interestingly, it is this group of individuals who is most susceptible to subclinical and clinical hypothyroidism. A recent study may reveal why...

A group of scientists from the UK (Sathaypalan. 2011) investigated the effect an 8 weeks dietary intervention with "high-dose phytoestrogens (30 g soy protein with 16mg phytoestrogens, representative of a vegetarian diet)" on thyroid function in sixty patients with subclinical hypothyroidism. The results were unequivocal - high dose phytoestrogens put your thyroid over the edge:

Six patients (10%) developed overt hypothyroidism after high-dose phytoestrogen, and none after low-dose phytoestrogen supplementation. [...] All six subjects were diagnosed as having overt hyothyroidism during their end-of-study visit after the 8-wk high-dose phytoestrogen supplementation period, when they were found to have raised TSH of more than 10 mU/liter and a low fT4 of less than 9 pmol/liter, i.e. overt hypothyroidism.

Even in view of the fact that some "health markers" such as insulin resistance, hsCRP, and blood pressure improved in the 16mg (high dose) phytoestrogen group, the question remains, whether lifelong levothyroxin medication and the possible subsequent damage due to hypothyrodism (even with "adequate" medication, cf. stopthethyroidmadness.com) is worth it!?

Low Fat Dairy no more! Milk Fat Protects Women from Myocardial Infarction.

Do you like your 0.1% yogurt? No? Well, what if I told you that it ain't even healthy? A recent study from Sweden (Warensjö. 2011) shows that milk fat is heart healthy! Particularly in women.

The study population comprised roughly 1000 Swedish men and women, whose anthropometric, biomarker fatty acid, physical activity, and dietary data were collected and comparisons were made between people with previous myocardial infarctions (cases) and healthy age-mates (controls).

In women, proportions of milk fat biomarkers in plasma phospholipids were significantly higher (P < 0.05) in controls [i.e. healthy individuals] than in cases and were, in general, negatively, albeit weakly, correlated with risk factors for metabolic syndrome. [...] After multivariable adjustment for confounders, the inverse association remained in both sexes and was significant in women. In agreement with biomarker data, quartiles of reported intake of cheese (men and women) and fermented milk products (men) were inversely related to a first MI [myocardial infarction] (P for trend < 0.05 for all).

So, you better ditch your low fat diary products and grab some full-fat cheese and yogurt (preferably from grass-fed cows). Believe me, they also taste much better!

Hungry? Better Eat Whey than Soy! Rats Receiving Soy Supplement Consume More Calories.

Lately, whey protein is all the rage. Rightly, as it seems! A recent study on the effect of protein supplementation on appetite and calorie consumption in rats showed that whey is way superior to soy protein in inducing satiety and reducing caloric intake.

For 10 weeks rats were fed a standard diet (control), or a high protein diet, with either 24% whey or isoflavone-free soy protein added to the chow. Both dietary interventions, i.e. the increase in protein intake, led to significantly reduced body weight and body fat gains, but ...

[...] cumulative food intake measured over the 10-week study period was lower in the HP-W vs. control and HP-S groups (P < 0.01).[...] Plasma concentrations of total GLP-1 [glucagon-like peptide 1] were higher in HP-W and HP-S vs. control group (P < 0.05), whereas plasma CCK, PYY, and leptin did not differ among the three groups.

In how far the reduced caloric intake is retractable to the GLP-1 (exclusively?) is questionable. What is certain is that GLP-1 has for quite some time been investigated as a potential treatment of diabetes. It plays a major role in insulin release and blood glucose management induces satiety and increases insulin sensitivity.

If you still think this is no reason to spend the additional bucks on whey, I suggest you listen to last weeks interview with Dr. Scott Connelly on Super Human Radio - I bet you won't have joy with soy, anymore ;-)

High MUFA Diets are (Heart-)Healthy and Probably Superior to High PUFA Diets

Ever since the "Mediterranean Diet" was/is the talk of the town, more and more people become aware of the potential benefits of the formerly largely ignored mono-unsaturated fatty acids (MUFAs). In spite of that, the majority of consumers (probably due to the misinformation coming from the marketing machinery of the food industry) still focuses on avoiding the "bad" saturated fats and consuming as much "healthy" polyunsaturated fats (PUFAs) as possible in order not to fall victim to an obesity epidemic which is inseparably intertwined with these kind of black-and-white approaches to nutrition.

In an extensive review (Jones. 2011) scientists from the Department of Human Nutritional Sciences at the Richardson Centre for Functional Foods and Nutraceuticals (University of Manitoba, Canada) evaluated data from over 50 years of research to come to the conclusion:

Consumption of dietary MUFA promotes healthy blood lipid profiles, mediates blood pressure, improves insulin sensitivity and regulates glucose levels. Moreover, provocative newer data suggest a role for preferential oxidation and metabolism of dietary MUFA, influencing body composition and ameliorating the risk of obesity. Mounting epidemiological and human clinical trial data continue to demonstrate the cardioprotective activity of the MUFA content of dietary fat.

In fact, they found MUFA rich diets to be superior even to diets enriched in PUFAs, which have lately oftentimes been hailed as the saviors of the fat and unhealthy:

When PUFA and MUFA rich diets were compared for replacement of dietary SFA in healthy adult subjects, those consuming MUFA rich diets demonstrated a preservation of HDL-C levels to a greater extent with only a 4% decrease in HDL-C levels compared to those consuming PUFA rich diets, which decreased HDL-C levels by 14%.

What is interesting, however, is that there still seems to be an initial bias against saturated fatty acids. This can also be seen from the fact that the general questions the authors pose throughout their review always come back to the idea of replacing saturated fatty acids by either carbs or MUFA, PUFA or MUFA etc. I would be interested to see a study or a review without this initial bias against saturated fats - the results could be very interesting... what do you think?

Overweight Korean Adults Benefit from Protein Rich "Oriental" Diet - More than from Conventional Diet Program.

Americans and Europeans are by no means the only people with unhealthy weight problems. Korea, where the traditional diet is gradually replaced by an Americanized fast-food diet, faces a similar obesity epidemia. The solution, on both sides, appears to be the same: a significant increase in protein intake.

Compared to a 2006 conventional dieting regime the subjects who participated in the 12 week high protein dietary intervention described in a recent study (Joo. 2011) lost more weight (- 4.7 kg vs. -2.3 kg), had a greater reduction in waist circumference (- 6.8 cm vs. 3.3 cm) and lost more body-fat (- 4.2 kg vs. -2.0 kg). In view of the obesity related health issues it is also noteworthy, that...

... the triglyceride reduction was significantly greater (- 30.16 mg/dL, p < 0.001) in the PRO Diet group after intervention compared to the conventional group.

Unfortunately, the original study is missing the dietary guidelines the subjects were provided (the file is not on the server), so you have to content yourselves with the following short summary as to what a "PRO Diet" looks like:

The PRO Diet aims to reduce consumption of refined starches (cooked rice, noodles, white bread) and to encourage the consumption of high protein. Additionally, the PRO Diet encourages the intake of "favorable" carbohydrates with a low glycemic index (GI) and "favorable" fats with high unsaturated fatty acids, while avoiding "unfavorable" carbohydrates with high GI and "unfavorable" fats such as high saturated fatty acids or trans fats.

The old adage of "bad saturated fats" and the hilarous concept of the glycemic index aside, regular visitors of the SuppVersity will recognize these dietary recommendations - certainly no coincidence ;-)

Want to Stay Lean on a High-Fat Diet? Consume Whey Protein Everyday.

Listeners of Carl Lenore's Super Human Radio already know: Dr. Paul Arciero of Skidmore College is going to publish a study the results of which confirm that obese individuals can lose weight and improve markers of metabolic health by just adding a 20g shake of whey protein 3x a day.

While you still have to wait for the detailed results of this study to be published, another group of scientists (Shertzer. 2011) derived similar results from a study on mice. Despite being on a high fat diet, mice who received 100mg of whey protein isolate (WPI) per liter of their drinking water (WPI group) ...

had lower rates of body weight gain and percent body fat and greater lean body mass, although energy consumption was unchanged. These results were consistent with WPI mice having higher basal metabolic rates, respiratory quotients, and hepatic mitochondrial respiration. [...] Livers from WPI mice had significantly fewer hepatic lipid droplet numbers and less deposition of nonpolar lipids. Furthermore, WPI improved glucose tolerance and insulin sensitivity.

While you are waiting for the human study to be published (the SuppVersity will have it first ;-), get yourself some tasty whey protein and listen to Dr Arciero on Super Human Radio!

Burn Additional 27 kcal with 6mg/kg Caffeine Pre-Workout

Caffeine is the cornerstone of almost each and every fat-burner on the market. But how effective is it in raising your energy expenditure? A study (Astorino. 2011) conducted at the Department of Kinesiology of the California State University provides an answer: Not very effective.

Astorino et al. had 14 strength-trained men who were regular caffeine consumers perform a strength workout with either 6mg/kg (thanks to Ezhan who pointed me to a type here. It's 6mg not 0.6 as it said before) caffeine or placebo supplement pre-workout. What they found was that

Caffeine intake increased total energy expenditure by 15% (P<0.05), but the additional calories burned was minimal (+27 kcal).

Well, I suppose this is about the amount of calories of a small carrot and not really what you would expect from a fat burner.

Vitamin K for Healthy Bones & a Lean Physique: Rat Study Finds Phylloquinone (K1) & Menaquinone (K2) Ward off Fat Gain and Cut Triglycerides by Half

Until not too long ago, scientists thought vitamin D was all about bone. Every follower of this blog knows that this is a way too narrow perspective on what turned out to be more of a hormone than a vitamin. A recent study (Sogabe. 2011) on the effects of vitamin K supplementation in mice does now suggest that vitamin D's "cofactors" phylloquinone (PK, vitamin K1) and menaquinone-4 (MK-4, vitamin K2) have been similarly mistaken.

Figure 1: Weight of visceral fat pad in g after 85 days of  phylloquinone (PK, vitamin K1) or menaquinone-4 (MK-4, vitamin K2) supplementation (Sogabe. 2011)

Japanese scientists, who wanted to investigate the effect of 85 days of vitamin K supplementation (PK: 600 mg/kg; MK-4: 600 mg/kg) on bone development in mice, were surprised to find that vitamin K did not only improve bone mass and structure, but that...

the addition of PK or MK-4 significantly decreased the total fat accumulation (p < 0.01 and p < 0.05, respectively), and serum triglycerides were reduced by 48% in the PK group and 29% in the MK group compared with the control.

This is an interesting result, which is not related to increases in growth hormone release, as one might expect in view of the bone-building effects of vitamin K. The scientists speculate: "The effect of vitamin K on fat mass could be mediated through adiponectin regulation which itself has been found to be associated with fat mass." This, as well as the dose response relationship (the human equivalence dose for the amount of PK and MK-4 used in the study would be about 7.5g!) warrant further investigation - and, as always, the SuppVersity is the place to read about it, first!

Glycogen-Depleted Athletes may Benefit from 0.3g/kg BCAA Supplementation: Improved Endurance & Lipid Oxidation

If you have ever read up on the general recommendations concerning "cardio on an empty stomach" you will most likely have encountered the advice to supplement with branched-chained amino acids (BCAA) before or in the course of the workout. I have always considered this to be a solid advice, up to now, I had yet not seen a study underpinning the common sense reasoning behind the suggestion.

Now, Gualano et al. (Gualano. 2011) published a study that investigated the effect of BCAA supplementation on exercise performance and energy metabolism in glycogen-depleted athletes (let's assume by now that an athlete following a low carb diet is in fact glycogen-depleted when he wakes up). In a double-blind placebo controlled fashion the scientists provided their subjects with either 0.3g/kg BCAA or placebo for 3 days...

On the second day, subjects were submitted to an exercise-induced glycogen depletion protocol. They then performed an exhaustive exercise test on the third day, after which time to exhaustion, respiratory exchange ratio (RER), plasma glucose, free fatty acids (FFA), blood ketones and lactate were determined. BCAA supplementation promoted a greater resistance to fatigue when compared to the placebo (+17.2%). Moreover, subjects supplemented with BCAA showed reduced RER and higher plasma glucose levels during the exhaustive exercise test.

For all of you who are now asking themselves, what validates the claim of increased fatty acid oxidation, its the reduced respiratory exchange ratio. Although its arguable how reliable a measure the ratio between O2 in and CO2 out is in terms of fatty acid metabolism, these results support the hypothesis and real world observation that BCAA-supplemented cardio on an empty stomach reliably promotes fat loss.

A Natural Cure for Obesity and Insulin Resistance!? Promising Results from Animal Experiments with Bitter Melon Bioactives

In a very recent investigation, researchers from the Pennington Biomedical Research Center (Wang. 2011) found that high-fat diet fed mice gained less weight and had less compromised insulin response, if they received an (unfortunately) unspecified amount of an aquaeus extract from bitter melon:

Body weight, plasma glucose, insulin, leptin levels and HOMA-IR values were significantly lower in the BM-fed HFD group when compared to the HFD group. BM supplementation significantly increased IRS-2, IR β, PI 3K and GLUT4 protein abundance in skeletal muscle, as well as phosphorylation of IRS-1, Akt1 and Akt2 when compared with HFD (P<.05 and P<.01). BM also significantly reduced muscle lipid content in the HFD mice. BM extract greatly increased glucose uptake and enhanced insulin signaling in L6 myotubes. 

There is however two major caveat to these findings. Firstly, mice ain't a particularly good model for predictions concerning the effect of supplements that are added to a high fat diet. And secondly, even if we would see similar results in human beings, the most obvious conclusion one MUST (but obviously nobody does) draw from the results of this study is that without supplementation the low fat diet, i.e. the group of mice that consumed a diet that is appropriate to their genetic make-up, gained the least amount of weight, had the lowest leptin levels and the best insulin sensitivity.

Figure 1: Insulin levels of the mice on a low fat diet (LFD), a high fat diet (HFD) and a high fat diet supplemented with bitter melon extract (BM)

Does this tell you that you should revert to a low fat diet? No, at least not if you ain't a mouse. What it should tell you, however, is that revamping your diet, making correct food choices and eating according to what our bodies are made for is the key to health and long jeopardy - the "natural cure for obesity and insulin resistance", it's already out there. Don't even think about dietary supplements before you've got that in check...

The (Re-)Discovery of 17{beta}-hydroxyestra-4,9,11-trien-3-one: Low Dose Trenbolone Safely Promotes Myotrophic Actions in Skeletal Muscle and Provides Partial Protection Against Bone Loss and Visceral Fat Accumulation

Sometimes it is interesting to see how agents that have been around all along reappear back on the medical scene, all of a sudden. A recent study conducted by a group of scientists from Florida (Yarrow. 2011) that compared the effect of different doses of 17{beta}-hydroxyestra-4,9,11-trien-3-one aka Trenbolone on muscle hypertrophy and prostate health of testosterone seems to have the potential to trigger such a "revival":

In both intact and orchiectomized animals, all TREN doses and supraphysiologic testosterone-enanthate augmented androgen-sensitive levator ani/bulbocavernosus muscle mass by 35-40% above Shams (p≤0.001), and produced a dose-dependent partial protection against orchiectomy-induced total and trabecular bone mineral density losses (<0.05) and visceral fat accumulation (<0.05). The lowest doses of TREN successfully maintained prostate mass and hemoglobin concentrations at Sham levels in both intact and orchiectomized animals; whereas supraphysiologic testosterone-enanthate and high-dose TREN elevated prostate mass by 84% and 68%, respectively (<0.01). 

Whether this indicates that "trenbolone therapy" in men would actually be an alternative to the traditional androgen therapy to counter muscle wasting and other medical conditions remains to be elucidated. This is especially valid in view of the fact that the variables controlled in this study did not encompass any of the side-effects steroid (ab-)users tend to report on injectable trenbolone. In other words: Just because it does not enlarge your prostate, this does not mean that it is safe.

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.