Diet Deoptimization with Rice Protein: Less Weight Gain, Lower Cholesterol and Fatty Acid Synthesis - So What?

Image 1: Rice protein power - I'd bet a pouch of casein protein that this Chinese "body builder" must have eaten plenty of rice protein. I mean, check out how ripped he is! Update: Garymar informed me that this is a Japanese comedian called Yoshiaki Yamane - sorry, my mistake ;-)

The "real" supplement news have been pretty slow as of late - there have not been any, to be precise. Unless you are interested in yet another study on an exotic African or Asian root or herb and its "antioxidative activity" in the petri-dish, you would probably have been as bored as I was by the latest articles in respective journals. And if Stephen Watt had not asked my opinion on a study my colleagues over at ergo-log had in the news, as of late, I would probably have ignored a "rodents on rice protein" study from the Department of Food Science at the School of Food Science and Engineering of the Harbin Institute of Technology in Harbin, China (Yang. 2012) - the headline ergo-log headline "Fat percentage too high? Add rice protein to your shake", did however look too intriguing not to take another look at a study, the abstract of which I did not really suggest that rice protein would actually help you burn body fat.

Rice for lactose intolerant vegetarians and poor Chinese farmers ...

What the scientists from the Middle Kingdom had done, was to feed three groups of 7-week (adolescent*) male Wistar rats on diets containing either

• 22.9% casein - could the one in your cheap protein blend, after all it was from China ;-),
• 23.2% rice protein A - extracted from Oryza sativa L. cv. Longijng by alkaline / acid extraction, or
• 23.2% rice protein E - extracted by sigma aldrich via heat stable starch degradation

The total experiment lasted two weeks and aside from the protein faction, the composition of the chow, to which the rodents had ad-libitum (=whenever they wanted) access was identical.

Figure 1: Blood amino acid concentrations in rodents fed casein or rice protein (the figures in % represent the relative level of the given amino acid in the RP-A group compared to the casein group, e.g. RP-A rats had 92% of the amount of Alanine, the casein rats had in blood; left; data adapted from Yang. 2012) and absolute and relative amounts of amino acids in casein and rice protein (open pars indicate relative amount of the given amino acid in rice compared to casein, eg. 172% more alanine in rice than in casein protein; data adapted from Morita. 1997)

The latter, i.e. the being identical, cannot be said of either of the amino acid structure of the casein and rice protein (figure 1, right), nor the amino acid contents and ratios in the plasma of the lab animals (cf. figure 1, left), though.

... yet not necessarily for aspiring physical culturists!

The muscle head and fitness fanatic that you probably are, you will certainly already have realized that the level of BCAAs in the blood of the animals on the rice protein diets was 26% and 29% (RP-A and RP-E, respectively) lower than that of the rodents receiving the casein chow. An observation which was to be expected in view of the -27% lower BCAA concentration in rice compared to the casein protein (Morita. 1997; figure 1, right). Astonishingly, this does not hold true for all other amino acids, for glycine, for example, the amino acid content in the source was 2x higher, the serum levels were yet only 15% higher than in the casein group (note: the casein chow was enriched with cysteine, in this particular case a comparison of source vs. serum levels would thus be futile).

Figure 2: Fecal analysis (left) and changes in body weight, as well as absolute body fat percentage and food intake  (right) of adolescent male Wistar rats (data calculated based on Yang. 2012.

If you also take into account that a 7-week old male rat has just become fertile (at about the 6th week of its life), think of yourself, your brother or son at the age of 16y, of what you / he ate and how much weight he gained and then take another, closer look at the data in figure 2 I would say that the question whether switching from casein to rice protein would actually help you lose fat appears more than warranted. After all, we are looking at weight (not fat!) gain in a period of growth (the body fat levels of the rodents, were 2.1%, 1.9% and 1.8%, respectively, cf. figure 2, right). If the latter were totally absent, you would call that "failure to thrive" - a term that would not strictly apply in the situation at hand, though.

In view of the huge fecal loss of dietary fat (+60% over casein) and dietary protein (+145% in the RP-A and +217% in the RP-E group), the 5% lower fat free mass in the rodents on the rice protein diets and the reduced ALT and AST levels, which are not necessarily indicative of "improved liver function", but rather of a reduced hepatic protein turnover, it seems as if "Rice protein reduces body weight gain, energy availability and storage in adolescent rodents due to its lower digestibility" would have been a more appropriate title for the study than "Rice protein improves adiposity, body weight and reduces lipids level in rats through modification of triglyceride metabolism" - and alas, a very similar study, yet without the data on the "body weight gain", has already been published by the same research group in 2011 (Yang. 2011).

Diet-deoptimization a novel weight loss strategy?

Image 2: I guess the Chinese have heard how the Americans got rid of their corn and soy and do now try to pull off a similar "it's good for your health"-stunt with rice protein as the US did with their "healthy" vegetable oils and soy proteins.

Personally, I would yet suggest to call the study "diet-deoptimization by the provision of less palatable, less digestible chow to rodents", but I guess in that case the results would never have made it to ergo-log and subsequently to the SuppVersity. It was thus pretty clever to disguise what could simply be a natural (side) effects of a reduced energy intake (-5%) and reduced energy absorption (-60% from fat and -145% or -217% from protein), i.e. a reduction in fatty acid synthesis and an increase in breakdown (you may remember that even rodents need fat, right?), as evidence that (I quote from the conclusion) "rice protein can modify triglyceride metabolism, leading to an improvement of body weight and adiposity" - wouldn't you agree?

In the end, the protein and fat wasting effects of the rice protein diets could even explain the advertised "beneficial" impact on the lipid profile with VLDL/HDL ratios of 0.19 and 0.16 vs. 0.24 in the RP-A and RP-E groups vs. the casein group. Whether similar effects could be observed in a human trial and whether these "improvement" (from one end of the normal range to another) would decrease the risk of heart disease, is yet questionable. Moreover, the reduction (or replacement; not necessarily the complete elimination) of the whopping ~60% carbohydrate content (488g cornstarch and 100g succrose per kg of chow) in the diet and/or the replacement of the pro-inflammatory soy-bean oil with e.g. olive oil would probably elicit way more beneficial effects on the triglyceride and blood glucose level in humans than a switch from casein to indigestible and in rodent-terms obviously non-palatable rice protein.

Three Servings of Grapefruit /Day Have No Effect on Weight Loss, But Increase Triglycerides and Make a Potentially Deadly Cocktail With A Whole Host of Prescription Meds!

Image 1: Grapefruit does not help with weight loss and, as it turns out, is not even healthy. On the contrary, in conjunction with your favorite statin it is even potentially deadly.

Do you remember the "grapefruit diet" (WebMD)? No? Well, then you are probably male and have always been satisfied with your weight. Otherwise, you would probably have heard how a "magical ingredient" in the subtropical citrus fruit is going kill all those unaesthetic adypocytes, which have made themselves at home on your hips and buttocks, in no time... What do you say? Bullsh*t? Well, I guess you have been reading to much of my stuff already, after all this purported short-cut to six-pack abs is also known as the Hollywood Diet and that alone will have people fall for it by the dozen... I mean, if Brooke Shields and Kylie Minogue got in shape with it, it must be working, right?

The myth and the truth about grapefruits

I know that you would never be so stupid to start eating nothing but grapefruit (you would not, right?), but despite the fact that the Grapefruit Diet has rightly gotten a bad rep within the (self-)educated members and followers of the wealth of good and not-so-good blogs and websites dealing with nutrition and weight loss, many people still believe that there must be something about this fruit that will help you lose weight. And in view of the fact that I myself know a couple of these (interestingly all female) unfortunate critters, I believe that it is still worth to take a closer look at the results of a recently published study on the effects of 1.5 fresh Rio-Red grapefruit per day on the outcomes of a 6-week dietary intervention (Dow. 2012). The study involved 74 male and female subjects (age: 41y; BMI: 32kg/m²; Bodyfat: 35.7%) who, despite having problems with their weight, had been weight-stable in the past 6 months (or more). After an initial 3-week "wash out period" in the course of which the subjects had to follow a diet that was restricted in bioactive-rich fruits and vegetables (the intention, here, was to get all to a baseline level as far as the purported "magic fat loss ingredient" in citrus fruits is concerned), the subjects were randomized to one of two groups:

1. intervention group (n=42) continued eating the "wash-out diet" and supplemented with their 3x0.5 Rio-Red grapefruit per day 15 minutes prior to their regular three meals
    
2. control group (n=32) continued eating the "wash-out diet"

The dietary intake of the subjects, was evaluated with your usual (unreliable, but in want of alternatives obligatory) repeated 24-hour diet recalls (3x during the washout phase and 3x during the intervention phase). Things like the total caloric intake (1800-1900kcal) or the macronutrient composition did not really differ between diets - in other words: The scientists did a pretty good job to isolate the grapefruit intake and the (obviously) correlating vitamin C intake (cf. figure 1) as the single confounding factors in their study.

Figure 1: Total caloric intake, the number of vegetable servings, the overall macronutrient ratio etc. all were identical between the two groups, except the fruit and (consequently) the vitamin C intake (data based on Dow. 2012)

With a subject pool of 74 men and women and virtually identical diets, we should thusly well be able to see an effect on body weight, body fat, lipid or glucose metablism, if there was one, but as the data in figure 2 indicates, "the magic just did not happen":

Figure 2: Relative changes in anthropometric data in the course of the 6-week study period; no statistically significant inter-group differences, not even statistical significant pre-post changes (data based on Dow. 2012)

Aside from the fact that grapefruit does not make you lose fat, the graph in figure 2 carries another important message, which is: Never use a body impedance device to track your progress. And this goes for all those stupid things, and not only the Omron Body Fat Analyzer HBF-306 which was used in the study. Why? Well, take a look at the body fat and the waist circumference data: How can your gut become smaller, when your body fat percentage increases? The answer is easy, because the grapefruit eaters lost water, they lost ~1% more of their waist circumference. This did yet change the impedance of their bodies so that the stupid for the Omron was tricked to believe that the body fat percentage of the study participants had increased (if you are at a loss how you can track your progress, make sure you read the Intermittent Thoughts on "Stocktaking, Goalsetting, -Tracking & -Resetting").

"But, Dr. Andro, weight loss is not everything" - Correct! And another reason not to eat huge amounts of grapefruits

Another argument of the "grapefruit fanatics" is that, although the weight loss effects of the fruit may be negligible, it still is a healthy superfood that will improve your overall and metabolic health... now, if we take a look at what (unfortunately) is still considered the "gold-standard" as far as the assessment of CVD risk is concerned, i.e. the allmighty lipid profile (imagine a fanfare, here), I guess that only those of you who still believe in the black-and-white version of the lipid hypothesis (HDL = good guy; LDL = bad guy; nothing else counts) will wholeheartedly agree with Dow et al. conclusion that ...

grapefruit consumption does elicit beneficial effects compared with baseline values that are
associated with CVD risk reduction.

If you take a look at the actual data in figure 3 you can hardly argue that the 1.5 grapefruits à day gave the "bad guy" (LDL) a slightly more thorough beating than the "wash out diet" with its quasi non-existent polyphenol content, but...

Figure 3: Changes in lipid profile (unadjusted and adjusted with ANCOVA for BMI, age, sex, and washout-phase p-values) for the control and grapefruit group (left) and the questionable conclusion the scientists draw based on the observed reduction in LDL and statistically likewise non-significantly greater reductions in blood pressure in the grapefruit group (right) (based on Dow. 2012)

...with a p-value (indicating the probability that this is mere coincidence; p < 0.05 is considered "statistically significant) of p = 0.871 for the inter-group difference this difference did not only fail to reach statistical significance, it must also be seen in the context of an increase in triglyceride levels (instead of a decrease in the control group), of which a 2009 study by Kannel et al. states that

[...n]onfasting triglycerides maintained an independent graded relationship with CVD in fully adjusted analyses, with elevated 4 h postprandial triglyceride imposing a 4.5-fold increment relative to lower levels [...and that] triglyceride-associated CVD risk occurs even in patients with low low-density lipoprotein cholesterol (Kannel. 2009)

Just to make sure nobody is missing the point here, neither the inter-group differences in LDL reduction nor the different outcomes as far as the trigs are concerned, reached statistical significance, but against the background of the results of the meta-analysis of Kannel and Vasan from 2009 and recent findings on the contribution of elevated triglyceride levels to the etiology of cardiovascular and metabolic diseases, I personally feel that beyond not helping with weight / fat loss, eating grapefruit could potentially even contribute to, or aggravate existing metabolic disturbances.

If you are on any medication grapefruit is a no-go, anyway!

Image 2: If you are healthy eating grapefruits from time to time won't hurt. If you are taking medication, however, it can potentially be fatal - although I's say that the meds, not the fruit are to blame for this

Yet even if you don't care about the pro-diabetic effects of triglycerides and discard the non-existent effect of grapefruits on weight loss / body composition, there is another, probably more important, because potentially fatal side-effects of eating grapefruit (or drinking its juice / taking respective supplements), which relates to the inhibitory effects it exerts on a hitherto not fully elucidated number of liver enzymes in the cytochrome cascade (CYP), which is heavily involved in drug and hormone metabolism. So, even if you don't take a statin, of which Dreier et al. have shown that it can induce profound rhabdamyolysis (=total break down of muscle protein, which can lead to kidney failure and death), when the grapfruit flavenoids and polyphenols block its metabolism in the liver (Dreier. 2004), or any other of the countless drugs the effects of which are profoundly modulated by the ingestion of grapfruit or grapefruit juice (Hanley. 2011), you better stick to no more than a single grape-fruit once in a while... I mean, it has no beneficial health / weight loss effect, anyway.

Eat Whole Eggs All Day and Throw Your Statins Away? 375x Increased Dietary Cholesterol Intake From Eggs Reduces Visceral Fat & Promotes Healthy Cholesterol Metabolism

Image 1: You better make sure you don't miss out on these delicious heart- and brain-healthy cholesterol bombs.

Most of you will probably be familiar with the good old saying "An apple a day, keeps the doctor away!", right? And if you are an otherwise healthy individual the micronutrients from the apple will probably really help you maintain this status. But what if the doctor was already there to put you on the healthy low fat diet, the negative health consequences of which I have addressed in yesterday's blogpost? In that case, whole eggs probably provide a more promising escape route from that low-fat, high-carb trap - at least this is what the the results of a soon to be published study from the Huazhong Agricultural University in Wuhan, China would suggest (Yang. 2012).

Surprising(?) -9% belly-fat reduction on whole egg diet

In their 60 to 90 day experiment, the Chinese researchers put a group of 8-week old Sprague-Dawley rats (n=18 for each group) on dietary regimen which differed in either cholesterol content (control vs. experimental groups) or the source of dietary cholesterol, i.e. 17.5% lard + synthetic cholesterol, 31.25% freeze dried egg yolk or 55.56% whole egg powder.

Figure 1: Composition of the control and the three experimental diets (adapted from Yang. 2012)

If you take a closer look at the exact composition of the diets in figure 1 the you will probably notice that macronutrient-wise the three standard-chow + lard/yolk/whole egg "high cholesterol" diets are miles-apart from what the average "low carber" would consider a healthy high fat diet. Still, the idea of choosing whole eggs as a major constituent (>55%) of one's diet should ring a bell for everyone who is familiar with the practical realization of the so-called "induction phase" of the purportedly (from the perspective of the same people who recommend the purportedly "heart-healthy low-fat diet") artery-clogging Atkins diet.

Figure 2: Body weight gain, food intake, food efficiency (food intake / weight gain) and relative visceral fat weight (per body weight) in Sprague Dawley rats after 60 and 90 days on experimental diets; data expressed relative to control group on standard rodent chow (data calculated based on Yang. 2012)

Interestingly, the data in figure 2 shows that even this version of "Atkins gone wrong", with a 40% carbohydrate content in the whole egg group (cf. figure 1) lead to significant reductions in weight gain and food efficiency (weight gain per gram of chow) and, more importantly, produced statistically significant reductions in the visceral fat / total body weight ratio at the end of the 90day study period (at 60 days there were no statistical significant inter-group differences).

55.56% whole egg diet kickstarts healthy cholesterol metabolism

In view of the fact that it has never been the notion that eggs would make you fat, but rather their purported negative effect on cholesterol levels due to which eggs, in general, and yolks, in particular, have gotten a bad rep over the last years, I guess that the visceral fat argument, alone, won't suffice to convince the egg-white consumer that they are missing out on the best part of the egg. After all, it was and unfortunately still is their purported negative effect on cholesterol that is literally at the heart of the egg(yolk)-scare.

Figure 3: Triglyceride, total, low density (LDL) and high desnity (HDL) cholesterol in Sprague Dawley rats after 60 and 90 days on experimental diets; data expressed relative to control group on standard rodent chow (data calculated based on Yang. 2012)

If you do yet take a look at the actual effects the natural cholesterol from the egg-containing diets had on the blood lipids of the rodents (cf figure 3), you will notice that those were statistically non-existent. In other words, only the lard + synthetic cholesterol diet had a statistically significant negative impact on the plasma lipids of the rats.

Figure 4: mRNA expression of hydroxymethylglutaryl CoA reductase (HMG-CoA R), LDL receptor (LDL-r), cholesterol 7a -hydroxylase (CYP71A), acyl-CoA:cholesterol acyltransferase (ACAT) lecithin cholesterol acyltransferase (LCAT) expressed relative to control (data adapted from Yang. 2012)

The 375x higher dietary cholesterol intake in the egg-groups, on the other hand, did not only shut down the endogenous cholesterol synthesis, as evidenced by the reduction in hydroxymethylglutaryl CoA reductase expression (HMG-CoA R, cf. figure 4) and increase its metabolization into bile acid via cholesterol 7a -hydroxylase (CYP71A), it also increased the LDL receptor expression in the liver (lack of LDL-r expression in the brain is associated with increased plaque formation in Alzheimer's, cf. Katsouri. 2011), lowered the formation and storage of cholesterol esterified cholesterol in the tissue by reducing acyl-CoA:cholesterol acyltransferase (ACAT) and increased the maturation of HDL and peripheral tissue cholesterol efflux via increased lecithin cholesterol acyltransferase (LCAT) expression.

In case you doubt that this rodent data has any significance for human beings, I just want to remind you that a 2008 study by Mayurasakorn et al., which found that "[i]n the majority of healthy adults" the addition of one egg per day to a "normal fat diet" lead to increases in HDL-c and decreases of the total cholesterol to HDL ratio (Mayurasakorn. 2008). Their conclusion that "egg consumption might benefit blood cholesterol" was however similarly ignored as the absence of scientific data to support the "eggs = increased risk of heart disease"-myth.

It is thusly not surprising that the Chinese scientists conclude that contrary to the "conventional approach to weight reduction", of which the scientists state that it is "a high-carbohydrate, low-fat, energy-deficient diet" that "has not proven to be very effective for many obese and over-weight individuals [I am not making that up, it is the exact wording from the study ;-]", an "egg diet", which "theoretically [...] would be more likely to cause obesity", could not only help those individuals finally shed unhealthy visceral fat, it could also lead to significant improvements in their lipid metabolism. If it were not for the statement that

[...] the mechanisms by which an egg diet lowers plasma cholesterol need to be further characterized and the special functional factors in egg need to be identified

one could be led to believe that Yang et al. had finally grasped the notion that just eating the right (whole) foods could solve the problem... the term "functional factors" does yet tell me that they are probably just trying to developing an "egg in a pill" that will soon be patented and sold as an adjunct to the standard statin therapy,

Brown Algae Extract Reduces Body Fat Without Dieting or Exercise. Ecklonia Cava Polyphenols Help Shed Weight Even in The Presence of a Slight Caloric Surplus.

Image 1: If that were a peace of meat, I'd
say its roadkill, in the case of these
Ecklonia  cava algae the term "floatsam"
would probably be more  fitting,
though (photo by Nikemoto2511)

With obesity being among, if not the major promoter of all modern diseases, researchers around the world are constantly trying to find magic bullet against, a condition of which hardly anyone argues that it could not be prevented in 99.9% of the cases by diet and lifestyle changes, or even better, leading an active and healthy life from early childhood to old age, alone. Be that as it may, if the horse has already bolted, the help of a side effect free dietary supplement, to promote and accelerate the results of consistent life style interventions, would unquestionably come handy. In a recently published study (Shin. 2011) a polyphenol extract from Ecklonia cava, a brown algae that has long been used in traditional foodstuff and folk medicine in Asian countries, turned out to be a another potential candidate in the long list of natural diet aids in the arsenal of holistic medicine.

For 12 weeks, a group of 97 overweight (not obese; BMI 24-29kg/m²) Koreans (mean age 40.5yr) consumed a test liquid containing 0 g of fructose, 0.65 g of dextrin, 12mg of sucralose, 0.15 g of sodium chloride, 0.6 g of citric acid, 0.15 g of vitamin C and lemon flavor. Depending on which group (C, LD, HD) the respective subject had been assigned to, the content of the otherwise identical cans held had been enriched by 0mg (C), 72mg (LD) or 142mg (HD) of an Ecklonia cava extract with a total polyphenol content of 98.5% (measured in phloroglucinol equivalents). The subjects were adviced to consume the drink in between meals, but otherwise to maintain "their usual dietary intake and physical activity", so that any changes in antropometric measurements, dietary intakes and biochemical and hematologic parameters would be attributable to the Ecklonia cava polyphenol (ECP) supplementation.

Figure 1: Anthropometric changes in 97 overweight Koreans after 12 weeks of 0mg=control, 72mg=ECP(72) and 144mg=ECP(144) supplemtal Ecklonia cava polyphenols (data calculated based on Shin. 2011)

The anthropometric data taken after 12 weeks of supplementation makes it quite clear, that the polyphenols from the brown algae found in the ocean off Japan and Korea do in fact hold some potential as an adjunct to a well planned weight loss regimen. In that, two things are particularly intriguing:

1. In contrast to some other natural weight loss supplements (cf. yesterday's news on green tea extract), the dose response curve does not seem to flatten out. At least within the range that has been tested in this study, doubling the dosage even produced a 2.25-fold increase in body fat loss.
2. The polyphenol extract does not seem to work its magic by appetite suppression. As the data in figure 1 shows, the difference between calorie intake and estimated calorie expenditure did even rise by 4.7% and 5.5% in the ECP(72) and the ECP(144) group respectively (judged by the estimated calorie-expenditures both groups had a minimal caloric surplus of 79 and 106kcal).

If you also take into account that subjects in the ECP groups, "showed significant decreases in total cholesterol level after 12 weeks by 7.1% [ECP(72)] (p < 0.01) and 9.3% [ECP(144)] (p < 0.001), [...] significantly reduced serum total cholesterol levels (p < 0.05 and p < 0.01, respectively)" and 10.0% and 14.3% lower LDL and 8.6% and 13.3% higher HDL levels, the slimy sea food from the Far East does already appear more appetizing, doesn't it? To eat your way through >10kg of sea weed (this is what the yield of the extraction process described by Lo et al. (Lo. 2009) would suggest to be needed as "basis" of a high quality extract), would nevertheless be pretty hard, which is why I tend to think that this is one of the few cases, where you should prefer the highly processed over the unprocessed variety of a natural superfood.

As far as the mechanism of action, responsible for the highly appreciable effects on body composition, blood lipids and, at high doses, glucose management (-4.9% blood glucose in the ECP(144) group) are concerned the scientists are yet still in the dark:

The antidyslipidemic mechanism of the phlorotannins is not clear. Based on the moderate inhibition of cholesterol esterase (IC50 = ~100 μg/mL on porcine pancreatic cholesterol esterase, unpublished result) by ECP, inhibition of cholesterol absorption may partly contribute to this effect. Other mechanistic speculations include protection of liver function from chronic exposure to high‐fat or high‐glycemic diet. [...] In the present study, significant reduction was observed of serum ALT and AST levels in ECP‐supplemented groups compared with the placebo group. Therefore, based on its antioxidant, antiinflammatory, and hepatoprotective (Kim et al., 2005) activities, ECP might possibly contribute to normalization of blood lipids by
suppressing fat‐induced damage of liver tissue.

Be that as is may, as long as it entails small, but statistically significant, side-effect-free improvements in body-composition, lipid profile and glucose management, I doubt any overweight end-consumer will give a damn about the underlying molecular mechanisms which certainly won't make the necessary lifestyle changes obsolete, but could potentially multiply and accelerate their effects.

Overweight Boys More at Risk of Obesity Related Health Problems than Girls

In a recent study from Egypt, Hassan et.al. took anthropometric measures of adiposity from 150 pupils between the ages of 7 to 18. Along with data on body composition and serum total lipids profiles the scientists intended to find correlation between obesity and adverse health effects at younger age. The results are interesting in that no correlation was found between lipid profile and body composition in the adolescent group (12-18 years). On the other hand, in the younger children , ...

For young age [7-11 years], triglycerides and HDL-C are correlated to most of the body composition and anthropometric parameters in boys and not in girls.

The scientists speculate on whether the different fat distribution pattern in young boys (centrally dominant) could be one of the underlying reasons for this observation. Be that as it may, I consider this another good reason to encourage boys (and girls, alike) to act out their natural desire to move and exercise before they  become PlayStation cambling couch potatoes.

Neptune Krill Oil Effective for Athletes, as well

As a reader of the SuppVersity, you already know about the positive effects of Krill Oil on blood lipids and glucose homeostasis. A very recent investigation into its effect in trained athletes (rowers) revealed significant effects on exercise recovery at only 1g/day. The polish scientists (Scarpansca. 2010) report:

Exercise significantly increased values of SOD, TNF-α and TBARS in both groups, but recovery levels of TBARS were significantly lower in athletes receiving Krill oil compared with the control group.

Figure 1: Training schedule in the week preceding blood sample collection before, and after the supplementation period; volume in minutes per day (Scarpansca. 2010)

Interestingly, supplementation had no effect on antioxidant enzymes, TNF-α and serum lipid profiles. So, there appear to be various reasons for very different parts of the public to consume, or rather supplement, with Krill Oil: Of yet, we know it does improve blood lipids for the ordinary couch potato or severely sick and it speeds up exercise recovery in professional athletes, who obviously have rock bottom blood lipids to begin with (a further reduction could even impair their performance).