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.

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.

Gadgetry & Caffeine a Dynamic Duo for Sleep Deprivation and, Consequently, Obesity in School-Aged Children

Ever wondered what your children do, when you send them to bed in the evening? According to the results of a study from the Department of Family and Community Health at the University of Maryland School of Nursing, they probably drink Coke and watch TV or play video-games. Does not sound too bad? Well, Calamaro et al. found that children who

drank caffeinated beverages had 15 fewer minutes of sleep per night than did children who did not drink such beverages (b = –0.27, P = .002). Children with three technology items in their bedroom received 45 fewer minutes of sleep than did children without these items in their bedroom (b = –0.75, P = .010).

Still not impressed? What if I told you that these kids missed out on 15 to 60 minutes of what - to my mind - is the most healthiest, most anabolic and most lipolytic time of the day (sleep), and that the study provides evidence for the hypothesis that the immediate consequence of caffeine induced sleep deprivation is obesity? If you do now reconsider whether your 7 year old really needs his own TV-set and whether plain water ain't no viable alternative for Red Bull and Coca Cola, you've already taken the first step to make a change that could - in the years to come - save your children from turning from the "fat guy / girl" in elementary school into the fat and diabetic guy / girl at high school.

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 ;-)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

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

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

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

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

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

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

Exercise at the Anaerobic Threshold Increases GH Release and Burns Fat in Obese Patients with Type 2 Diabetes

Scientists still argue about the most important contributing factor to the ever increasing obesity epidemic in the Western World: Is it bad dietary habits or our sedentary lifestyle - honestly, I don't care... you got to work on both if you want to stay healthy.

The results of a recent study published by scientists from the Toho University Sakura Medical Center (Yamaguchi. 2010) do yet underline the importance of exercise (and I mean exercise, as in sweating and panting, not just walking to your car!) in the "health equation", i.e. "diet + exercise = health". The scientists had their 19 obese type 2 diabetics either keep their sedentary lifestyle or performed 2× 30-min bouts of exercise (treadmill walking) everyday in the morning and evening during the 4-week study period. What is of particular importance is that the exercise intensity was determined by pretesting the exercise capacity of each participant, so that all patients exercised at their individual anaerobic threshold. The results of this regimen (cf. table 1) were quite remarkable:

Table 1: Baseline characteristics and changes in clinical and biochemical variables.BMI: body mass index, VFA: visceral fat area, SFA: subcutaneous fat area, BP: blood pressure, FPG: fasting plasma glucose, HbA_1C: hemoglobin A_1C, HOMA-IR: homeostasis model assessment of insulin resistance, TC: total cholesterol, TG: triglyceride, HDL-C: HDL-cholesterol, LDL-C: LDL-cholesterol, IGF-1: insulin-like growth factor-1, LPL mass: LPL mass in preheparin serum.

In view of recent research findings about the relation of visceral fat (VFA) and metabolic derangements, the remarkable reduction of VFA by -21.7% vs. -5.5% in the control group is of paramount importance for the subjects' health. The researchers attribute this success mainly increases in growth hormone which were elicited by the exercise intervention. In that, it is important to note that we are talking about a 100% increase in growth hormone after a 30-min bout of exercise.

Although this is just speculation on my part, I think it is questionable whether walking for more than 30 minutes, but at a lower intensity would have provided similar results. Or in other words: If the key is to trigger metabolic changes (via natural hormonal pathways) intensity (not overexerting oneself, though) is key.

Anti-obesity & Anti-diabetic effect of Trehalose in Rats on a High Fat Diet

I know, I know, rats on a high fat diet are a topic on their own: "Are they a valid model for metabolic disease in man?" etc. - Be that as it may, the findings of scientists from the Biomedical Institute, Research Center, Hayashibara Biochemical Laboratories in Okayama (Arai. 2010) suggest that, of all things, a sugar(!) molecule may help prevent the negative effects of a high fat diet on fat mass and insulin resistance, which are commonly observed in the rat-model of the typical western-world high-fat diet.

Other than rats on a glucose [Glc], a maltose [Mal], a high-fructose corn syrup, or a fructose [Fru] rich high-fat-diet [HFD], the rats which were fed the natural alpha-linked disaccharide trehalose did not exhibit the typical signs and symptoms subsumed under the keyword "metabolic syndrome":

After 7 weeks of HFD and saccharide intake, fasting serum insulin levels in the Tre/HFD group were significantly lower than in the Mal/HFD and Glc/HFD groups (P < .05). Furthermore, the Tre/HFD group showed a significantly suppressed elevation of homeostasis model assessment–insulin resistance compared with the Mal/HFD group (P < .05) and showed a trend toward lower homeostasis model assessment–insulin resistance than the Glc/HFD group. After 8 weeks of feeding, mesenteric adipocyte size in the Tre/HFD group showed significantly less [fat] hypertrophy than the Glc/HFD, Mal/HFD, high-fructose corn syrup/HFD, or Fru/HFD group. Analysis of gene expression in mesenteric adipocytes showed that no statistically significant difference in the expression of monocyte chemoattractant protein–1 (MCP-1) messenger RNA (mRNA) was observed between the Tre/HFD group and the distilled water/standard diet group, whereas a significant increase in the MCP-1 mRNA expression was observed in the Glc/HFD, Mal/HFD, Fru/HFD, and distilled water/HFD groups.

While these results certainly appear promising, I better add that the laboratory that did the study is financed by the Hayashibara company, the same company which recently developed a new technique to produce or rather to extract trehalose commercially. So treat these results with a grain of skepticism, if you understand what I mean ;-)

BAT: Brown Adipose Tissue in Humans - An Update

In the latest edition of Current Opinion in Lipidology we find a mini-summary (COL. 2010) on current findings on the existence and metabolic purpose of brown adipose tissue (BAT) in human beings. These days the previously accepted position that adults have little to no BAT is put into question by the results of PET, where brown fat becomes especially visible upon cold exposure, when its metabolic activity is increased as a result of thermogenesis.

The author points out that adipocytes (fat cells) and myocytes (muscle cells) do not only share the same origin, the metabolically active BAT exhibits other similarities to muscle cells, as well - it is a metabollically active tissue and of particular importance in the context of insulin sensitivity and glucose disposal:

BAT glucose uptake rate is 10-15-fold higher in cold than in normal room temperature. Other factors that may increase the activity of sympathetic nervous system and uncoupling protein 1 are several including the complex network of hormonal and neuronal signals. Preliminary results suggest that BAT resembles skeletal muscle not only by origin but also by the effect of insulin on the tissue.

Doubtlessly, more research has to be done on the issue of BAT vs. WAT (white adipose tissue) and their relation to obesity, diabetes and the metabolic syndrome. In spite of that, even what we know today suggests that a better understanding of this hitherto overlooked remainder from the days when our ancestors ran around naked could help to find a solution for some of the "fat" health problems of the western societies.

Hydroxycitrate (HCA) for Weight Loss - Revisited

The hype around hydroxycitrate (HCA) as a remedy for obesity and general weight problems has long abated. Nevertheless, in a recent review (Onakpoya. 2010), scientists from the Peninsula Medical School at the University of Exeter reexamine past studies and come to the (surprising?) conclusion that

The evidence from RCTs suggests that Garcinia extracts/HCA generate weight loss on the short term. However, the magnitude of this effect is small, is no longer statistically significant when only rigorous RCTs are considered, and its clinical relevance seems questionable.

So, although the data from the study shows that there is a minor improvement in weight loss in the supplemented groups (cf. fig. 1, below)

Figure 1: Forest plot of comparison showing the effect of hydroxycitrate on body weight. The vertical line represents no difference in weight loss between HCA and placebo. (Onakpoya. 2010)

buying a pure HCA supplement for weight loss purposes is probably not worth it. There are certainly better fat-burners out there.

Leptin & AMPK Activation in Muscle - Did Scientists Investigate the Wrong Species?

Actually, this is something I have been reminding people of for years: Human beigns are no mice and although some people may be rats, genetically they are still very different. Usually I put this argument forward if anyone presents me with a study done on rodents that "shows" how bad dietary protein, especially from meat, is for you - thin of it: when was the last time you saw a mouse eating a cow? This time the issue is a little more sophisticated, though...

Australian scientists (Laker. 2010) have recently investigated the effect of leptin on AMP-activated protein kinase (AMPK) in muscle of sheep and (I do not know if to their, but maybe to some of the proclaimed experts surprise) they found that...

[...] leptin infusion reduced (P<0.05) food intake and body weight and it also increased plasma adrenaline concentration at 6 h and 7 days, suggesting increased sympathetic nerve activity. Despite this, and in contrast to rodent studies, central leptin infusion did not increase skeletal muscle AMPKα Thr172phosphorylation or ACCβ Ser221 phosphorylation.

With sheep being genetically closer to human beings than mice, this is an interesting finding and could possible lead into new insights into why leptin, once proclaimed as possible panacea for the obesity epidemic, does work on rodents, but has little positive effect on obese human beings. Hitherto, the most accepted theory is "leptin resistance", which, similar to insulin resistance, is supposed to prevent leptin from doing its magic. This study, however, suggests that there might be genetic issues involved, as well. As always, I will keep you posted...

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

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

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

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

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

B-Vitamins & Diabetes: Protective or Causative?

In a very interesting study, scientists from China and Japan (Zhou. 2010) found that "long-term exposure to high level of the B vitamins may be involved in the increased prevalence of obesity and diabetes in the US in the past 50 years". At first this appears to be counterintuitive, since we have been told over and over that B-Vitamins are not only good for our health, but that we could not even "overdose" them. While the latter has been questioned for years and certainly is not the case for e.g. B6 and niacin, even the former seems questionable, if you read the results from the above mentioned study:

The prevalences of diabetes and adult obesity were highly correlated with per capita consumption of niacin, thiamin and riboflavin with a 26- and 10-year lag, respectively (R2 = 0.952, 0.917 and 0.83 for diabetes, respectively, and R2  = 0.964, 0.975 and 0.935 for obesity, respectively). [...] The relationships between the diabetes or obesity prevalence and per capita niacin consumption were´similar both in different age groups and in male and female populations. The prevalence of adult obesity and diabetes was highly correlated with the grain contribution to niacin (R2 = 0.925 and  0.901, respectively), with a 10- and 26-year lag, respectively.

These results (especially those referring to the detrimental effect of niacin) confirm test-tube studies conducted by a group of scientists from South Korea earlier this year (Choi. 2010), who found that

NA [nicotinic acid] alters gene expression in insulin-sensitive tissues by various mechanisms. Some of the NA-induced changes in gene expression are discussed as potential mechanisms underlying wanted and unwanted effects of NA treatment.

Just anecdotal: My personal perspective on B-vitamins has changed since my overall energy and well being, as well as my physique have largely improved after stopping to take those B-vitamin (over-)loaden mulit-vitamin preparations like Now ADAM, CL Orange Triad, Animal Pak, ON Opti-Men etc. But remember: it is mere speculation that this could in fact be related to their high B-vitamin contents - could be any other constituent, as well.

Chromium Ain't Dead Yet: Positive Effects of Chromium Glycinate on Glucose Metabolism and Memory Acquisition in Rats Fed High-Fat Diet

"Chromium"? Sounds familiar, eh? Not too long ago, everybody was all over supplementing with chromium picolloniate to improve insulin sensitivity, to lose fat and to gain muscle. Most human studies, however, failed to reproduce the encouraging results from rodent studies. From todays perspective fat loss and muscle gain, if they occurred would probably have to be considered an indirect effect due to improvements in insulin management, the latter, on the other hand appear to be very real and may even benefit your cognitive performance.

When an international team of scientists supplemented male Wistar rats (n = 60; weighing 200–220 g) on a high-fat (40%, high-fat diet (HFD)) diet with either chromium-glycinate (CrGly) or chromium-acetate (CrAc) at doses of 0, 40, or 80 μg/kg body weight (BW) for 12 weeks, chromium supplementation ameliorated the detrimental effects of HFD on GLUTs, and Memory (32% reduction in expressions of glucose transporters 1 and 3 (GLUTs) in brain tissue and a 27% reduction in mean percentage time spent in the target quadrant and a 38% increase in spatial memory acquisition phase (SMAP)):

Compared with supplemental Cr as CrAc, CrGly was more effective to ameliorate response variables (i.e., restoration of tissue Cr concentration, enhancement of cerebral GLUTs expressions, and reduction of the glucose/insulin ratio and SMAP) in a dose–response manner, especially in rats fed HFD. Supplemental Cr as CrGly may have therapeutic potential to enhance insulin action and alleviate memory acquisition in a dose-dependent manner, through restoring tissue Cr reserve and enhancing cerebral GLUTs expressions.

So, after all chromium certainly ain't no magic bullet, it is likely, however, that patients who suffer from obesity and diabetes, as well as athletes who have been found to be at risk of chromium deficiency, may in fact benefit from your occasional dose of supplemental chromium.

Eat Rice, Stay Healthy!?

A recently published study (Fulgoni. 2010) analyzing data from 25 374 eligible participants identified as rice consumers study on the correlation of rice-eating to several markers of metabolic health showed that people who ate at least one serving of rice (white or brown) a day tend to have

better health and diet parameters including less total fat, saturated fat, and added sugars; higher amounts of more than 12 essential vitamins and minerals, including iron, folate, and other B vitamins; more fruit and legumes; nearly 4 tsp (16 g) less added sugar; and 7 g less solid fats. For the 19- to 50-year-old subgroup, main results (P < .05) also showed rice consumption associated with reduced likelihood of being overweight or obese, 34% reduced risk of high blood pressure, 27% reduced likelihood of having an increased waist circumference, and 21% reduced risk of metabolic syndrome.

This, however, should not encourage you to just add one serving of rice to your bad diet habits, because the most important information coming from the study is the first one: Rice eaters tend to have better diet parameters. In other words their general dietary regimen is more healthy, no wonder they have a reduced likelihood of obesity and health issues. Overall, rice is still a very dense source of energy and overeating on it would not be advisable, both from a caloric, as well as (this is more important) from a nutritious point of view - with its high amount of carbohydrate one serving of rice may well amount to all the carbs you may eat, if you follow a heart healthy low carbohydrate diet. Bottom line: Moderation is the key!

An In-Depth Look at How You Get Fat: You Acquire More Rather than Bigger Fat Cells

Scientists from the National Institute of Health in Bethesda, Maryland (Jo. 2010) have investigated the exact cellular pathways of weight or rather fat gain. They report:

We found a qualitatively universal adipose tissue remodeling process in all four fat depots: 1), There is continuous recruitment of new cells under weight gain; 2), the growth and shrinkage of larger cells (diameter >50 μm) is proportional to cell surface area; and 3), cell loss occurs under prolonged weight gain, with larger cells more susceptible.

It needs some interpretation of the results to understand their significance in view of staying lean in the first place. Normally, you would mean it does not depend if one fat cell holds a certain amount of fat or if this fat is held by two different cells. Unfortunately, it is a) much easier to "empty" one big fat cell which is about to burst anyway than two smaller cells and b) even if you emptied them completely that would leave you with more fat in the case of two cells than in the case of just one. In the end, by continuously multiplying the amount of fat cells you carry, you end up in a state, when even with all of them being empty you look either still obese or carry leaps of "empty fat" which has to be removed surgically. Consider that before you go onto your next 6 week "bulk" Mr BodyBuilder ;-)

Viscous Circle: Low Testosterone > Increased Visceral Fat > Insulin Resistance > Even Lower Testosterone

E.J. Hamilton and colleges (Hamilton. 2010) investigated the effect of androgen deprivation therapy (ADT) in prostate cancer patients on subcutaneous and visceral fat. There results are far from being surprising:

Twelve months ADT increased visceral abdominal fat area by 22% (from 160.8 ± 61.7 to 195.9 ± 69.7 cm²; p<0.01) and subcutaneous abdominal fat area by 13% (from 240.7 ± 107.5 to 271.3 ± 92.8 cm²; p<0.01). Fat mass increased by 14% (+3.4 kg; p<0.001) and lean tissue mass decreased by 3.6% (-1.9 kg; p<0.001). Insulin resistance (HOMA-IR) increased by 12% (2.50 ± 1.12 to 2.79 ± 1.31, p<0.05).

All that by itself is bad enough, but in the end, by the medical suppression of androgens doctors put their poor patients in a viscous circle, from which it will be very difficult to escape, as obesity and insulin resistance will further reduce testosterone production and overall metabolic health regardless of whether they are secondary to low testosterone, come from bad eating habits or whatever.