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.

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.

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.

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.

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!

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.

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.

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?

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.”

Protein's Effects on Gene Expression: Higher Protein Lower Carbohydrate Diet Spares Gylcogen, Lowers Insulin and Reduces Lipogenesis

High protein diets have become the "gold standard" within the fitness community. On the countless bodybuilding, fitness and weight loss related bulletin boards on the Internet, athletes, gymrats and even overweight house-wives report outstanding benefits of a higher than normal protein intake on weight gain and/or fat loss. French scientists (Stepien. 2011) have now taken a closer look at the mechanism behind these success stories and found a strong (epi)genetic component (for an introduction to epigenetics, I recommend listening to Dr Rouse's interview series on Carl Lenore's Super Human Radio).

 Figure 1: Effect of high protein diet on genes regulating lipogenesis [lipo = fat; genesis = production] in the liver (Stepien. 2011)

Stepien et al. fed 80 male winstar rats either a normal or a high protein (50% protein) diet for 1,3,6 or 14 days and evaluated the mRNA levels [indicators of how active these genes are] of genes "involved in carbohydrate and lipid metabolism", energy expenditure (EE) and substrate oxidation, as well as liver glycogen, plasma glucose and hormones. What they observed stands in line with the positive anecdotal evidence you will find if you google muscle gain or fat loss "success stories":

    In liver, HP feeding 1) decreased mRNA encoding glycolysis enzymes (GK, L-PK) and lipogenesis enzymes(ACC, FAS), 2) increased mRNA encoding gluconeogenesis enzymes (PEPCK), 3) first lowered, then restored mRNA encoding glycogen synthesis enzyme (GS), 4) did not change mRNA encoding b-oxidation enzymes (CPT1, ACOX1, bHAD).

So, interestingly, with the exception of the 1st day of the experiment (where the increase in protein intake resulted in a short-term increase in fat oxidation), fat oxidation was stable (cf. 4) The "fat burning" effect, which is often ascribed to high protein diets, thus is not existent - or let's say its not a direct one, but a result of the synergy of other genetic and metabolic adaptations and the calorie restriction all weight loss regimens have in common.

Figure 2: Postprandial macronutrient balance as assessed during a 4 h period after the intake of a calibrated meal consisting of 4 g of an adequate diet.  (Stepien. 2011)

Here is where the insulin lowering effect, the reduced hepatic glucose uptake and the reduction in lipogenesis (cf. fig. 1) come into play. Combined with an overall increase in postprandial energy expenditure (observed only under long term high protein feeding conditions, cf. fig 2, HP14) and a slight but significant increase in the percentage of fat (LOX, fig. 2) that is used to fuel these demands, these genetic and metabolic adaption (most prominently the lower insulin levels and the reduction in lipogenesis) are the most probable mechanisms to explain the reduced fat gains and increases in fat loss on high protein weight gain and weight loss diets, respectively.

Supplemental (!) Coconut Diet Reduces Waist Circumference in Men more Than in Women While Leaving Lipid Profiles Unchanged

I take the recent New York Times Article on coconut oil as clear evidence of the fact that the health benefit of tropical oils is getting more and more public attention. Studies that establish the many anecdotal reports you can find all over the Internet may even speed up this process and thus I am happy to report the findings of a Malasian study (Liau. 2011) that clearly underlines that the "bad" saturated fat cannot be so "bad" after all.

The scientists had a group of 20 healthy, but obese Malay volunteers consume an additional 30 mL of coconut oil (approx 2 tablespoons) per day taken in three divided doses, half an hour before each meal (as far as digestive side effects are concerned, this was the best tolerated dose as assessed before the actual study) and found...

that only waist circumference [WC] was significantly reduced after one month of VCO with a mean reduction of 2.87 +/-4.95 cm.

The high standard deviation of this data may well be attributed to the fact that there was no additional control of the dietary habits of the volunteers. The study says subjects "continued their weight loss efforts", but you probably know these "efforts" often turn out to be hardly comparable. I also feel that the real-world significance of the scientists statistical assessment "WC reduction was only seen in males" must be reevaluated, especially in view of the fact that "the reduction [meaning in cm WC] was larger in females" and the reduction in females with BMI <30 (4.8 +/-6.1 cm), other than in females with BMI >30 2.61 +/-2.17) was statistically significant (for more data cf. figure 1).

Figure 1: Comparison of mean differences in anthropometric measurements and lipid profile values in 7 males and 13 females after VCO consumption. (Liau. 2011)

I refrain from commenting on the reasons and invite readers to come up with their own theories, why someone who has gotten to a BMI of >30 (!!) may have problems losing weight on an uncontrolled intervention. What this should tell you, however, is that you may safely assume that 2 x tablespoons of coconut oil (~30ml) à day may be a worthwhile addition to your well-planned diet & exercise regimen.

On a side note: Who knows how much centimeters the volunteers had lost if the had just replaced some of the "good" seed oils in their diets? Well, I guess in view of the fact that the scientists seemed surprised that the bad saturated fats in coconut oil did not ruin their volunteers fatty acid profiles, they probably considered it unethical to ask their participants to completely replace corn with coconut oil ;-)

Energy Drinks Increase Resting Metabolic Rate, But Do Not Influence Energy Expenditure During Exercise

Ever wondered, whether the drink that was once rumored to contain "taurine from bull sperm" and similar fashionable "energy drinks" are of any use? Well, a recent study (Nienhuesser. 2011) coming from an international team of scientists showed that the consumption of each and every of the three energy drinks used in this study lead to a statistically significant increase in resting metabolic rate (RMR).

[...] in a randomly assigned cross-over design, the subjects consumed 473 ml of one of three commercially available energy drinks or a placebo and then RMR and RER [respiratory exchange ratio; i.e. a measure of the relative amount of fat/carbs that is used as fuel] were measured 1 hour later.  The subjects then engaged in 15 minutes of treadmill exercise at 50% of V02max, during which RER and oxygen consumption (VO2) were measured. RMR was not changed by placebo, but increased (P<0.05, means ± se) above baseline by 10 ± 2.5%, 15.0 ± 2.9%, and 15.3 ± 2.9%, following Energy Drink One, Energy Drink Two, and Energy Drink Three (respectively) [...]

In view of the stimulating effect, some of the ingredients (cf. Table 1) of these chemical containing beverages exhibit, these results do not come as a surprise.

Table 1: Listing of ingredients according to Nienhuesser. 2011

What may be surprising, however, is that the study results suggest that - at least from a "calorie expenditure" point of view - the consumption of an energy drink before exercise appears to be less effective than drinking it after exercise or at your desk at the office...

Carbohydrate Restriction Reduces Liver Triglycerides More Effectively Than Calorie Restriction - With Equal Weight Loss Outcomes.

A calorie is not a calorie, I hope you knew that even before Garry Taubes published his famous NY Times best-seller. Yet, in case you are still looking for respective studies to show to medially indoctrinated family members or friends, who still believe that - even if fat is not the enemy - half ratios would be the key to health & longevity, you might be interested in the results of a very recent investigation by Browning et al. (Browning. 2011).

The scientists put a group 18 non-alcoholic-fatty-liver patients on either a carbohydrate-restricted (<20g/day) or a calorie restricted (1200-1500kcal/day) diet - just to make sure you get this right: the carb-restricted group ate as much calories as they wanted! - and measured hepatic triglyceride levels before and after the 2 week dietary intervention. Probably to the surprise of many members of the medical orthodoxy, both groups lost about the same amount of weight (in fact the low-carb group lost -4.6kg, while the low-calorie group lost only -4.0kg!), yet the low-carb group had a much greater reduction in hepatic triglyceride levels:

Liver triglycerides decreased significantly with weight loss (P , 0.001) but decreased significantly more (P = 0.008) in carbohydrate-restricted subjects (-55.6%) than in calorie-restricted subjects (-28.6%).

So, even if you are not particularly interested in your liver health, the fact that by eating to satiety and just dropping your carb intake to <20g/day you can lose the same ~4.5kg you would lose if you starved yourself for 14 days should prick your ears.

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!

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.

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?

Acquittal: Anti-Oxidants do not Blunt the Beneficial Effect of Endurance Training on Insulin Sensitivity!

Regular visitors of the SuppVersity will remember that there has been and still is a controversy about whether or not athletes and average gymrats benefit from antioxidants or whether this may even blunt training induced adaptation effects. Other than a 2009 study by Ristow et al. (Ristow. 2009), a more recent investigation into the effects of antioxidant supplementation (Yfanti. 2011), coming from my northern neighbors from Denmark, did not find any negative effects of antioxidants on the exercise induced rise in insulin sensitivity.

In the study 21 young, healthy men, who received 500 mg vitamin C and 400 IU vitamin E (α-tocopherol) daily, completed a 5-days-a-week supervised intense endurance-training (interval training on Tuesday & Thursday; steady-state cardio on Wednesday & Friday). Insulin response, maximal oxygen consumption (VO_2max), maximal power output (P_max) and body composition (fat mass, fat-free mass) were measured and "muscle biopsies were obtained for determination of the concentration and activity of proteins regulating glucose metabolism". The scientists summarize their results as follows:

Although plasma levels of vitamin C (P < 0.05) and α-tocopherol (P < 0.05) increased markedly in the AO group, insulin-stimulated glucose uptake increased similarly in both the AO (17.2%, P < 0.05) and the PL (18.9%, P < 0.05) group in response to training. VO_2max and P_max also increased similarly in both groups (time effect: P < 0.0001 for both) as well as protein content of GLUT4, hexokinase 2 and total Akt (time effect: P ≤ 0.05 for all).

I don't know if you consider this "good" or "bad" news, but in any case, I suspect you will want to know what happened to the participants body composition (at least I would want). Well, the scientists say, there were no significant pre-post changes and from a statistic point of view, this is unquestionably right. I find it interesting, nevertheless that the average decline in fat mass was somewhat larger in the placebo (-21%)  vs. the anti-oxidant group (-8%); the intra-group differences are however so large that, with the given count of subjects, this is hardly meaningful.

L-Arginine Biscuits Exhibit Ameliorated Insulin Response. A Viable Alternative for People with Metabolic Syndrome!?

"L-Arginine ameliorates insulin resistance and has beneficial effects on blood pressure", "Fat people love cookies and tend to develop insulin resistance!" - if these two thoughts get together in the head of an Italian scientists, a new product is born: the L-Arginine Biscuit!

In a recent study Emanuela Setola (Setola. 2011) investigated the effect of a biscuit with 6.6g arginine on selected metabolic parameters of 7 healthy subjects. The results are encouraging:

A significant increase of nitric oxide (NOx) and cGMP levels were significantly increased with Biscuit +L-ARG 6.6 g and Powdered L-ARG as compared to Biscuit. AUC NOx and cGMP were significantly increased (p<0.04vs Biscuit). Percentage incremental increase of post-ischemic blood flow significantly increased with Biscuit +L-ARG 6.6 g and Powdered L-ARG, suggesting a functional effect of L-ARG added to the food preparation. Further, at 240 minute mean arterial blood pressure and peripheral vascular resistances slightly declined with Biscuit +L-ARG 6.6 g without reaching a statistical significance. At metabolic levels, the addition of L-ARG to a biscuit decreased insulin levels in the presence of similar glycemic levels, in particular a significant decrease of AUCinsulin during the test with Biscuit +L-ARG 6.6 g in comparison to Biscuit alone was found (p<0.05).

The last result, i.e. the decreased insulin release is probably the most interesting finding of this study and was further investigated by the researcher:

From the results of glucose and insulin, two indices were derived: a Modified Matsuda, (index of whole-body insulin sensitivity) and the Disposition Index (index of the product of insulin sensitivity and first phase insulin secretion). We were able to define that both indices were significantly increased with 6 Biscuits having 6.6 g of L-Arginine while intermediate values were found when 3 Biscuits (3.3 g) were eaten as compared to Biscuits without L-Arginine addition.

After all, I think it would be better to avoid cookies and biscuits completely, but if you just cannot resist, you may well add some arginine to the dough for this years Christmas baking.

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.

Lose More than 2 Pounds of Fat-Mass in Less than 30 Minutes: The Illusiveness of Bioelectrical Impedance Analysis

Wouldn't it be nice to burn more than 2 pounds of body-fat within 30 minutes of exercise? Well, according to your body impedance scale this is easily possible! You would even gain 1 pound of solid muscle...

In a recent study Selma Civar Yavuz (Yavuz. 2011) had 52 healthy volunteers perform an exhaustive treadmill exercise (Bruce test) and evaluated the body composition changes by the means of bioelectrical impedance analysis. The results summarized in Table 1 are amazing:

Table 1: Comparison of the body mass index (BMI), fat mass (FTM), fat free mass (FFM), total body water (TBW) and bioelectrical impedance measurements taken before and after the exercises.

What is amazing about these results is yet not the amount of fat the subjects burned in <30 min of running. Its rather the inaccuracy of the impedance analysis. In view of the results of this study you better throw your expensive body-fat scale out of the window and revert to using an old fashioned tape measure to evaluate your dieting / exercise success.