.

.
marylin monroe
Showing posts with label skinny fat. Show all posts
Showing posts with label skinny fat. Show all posts

Leucine & Phenylalanine Enriched YoYo-Diets Ameliorate Fat Gain, Protect Muscle & Maintain T4→T3 Conversion

Too little leucine & phenylalanine in O.'s diet?
Actually it is quite counter-intuitive that the "YoYo"-diets competitive boydbuilders adhere to (diet vs. bulking phase) are capable of producing such amazing physiques. I mean, when Mr. and Mrs. Average "diet down" and "bulk", the result will usually be neither aesthetic nor healthy, right?

A recent study from the University of Sao Paulo does now provide some insights into the important role the high amount of essential amino acids (leucine and phenylalanine, to be precise) in the typical bodybuilding diets may play with respect to its moderating effects on the lean muscle loss and body fat gains of Opra-esque ups and downs in body weight.

Leucine + Phenylalanine + diet and refeed = ???

I guess the details in the headline to this paragraph are not actually detailed enough to get an idea of what Donato Jr. et al did in their latest rodent study, are they? I see. I will still try to stick to the most important facts.

Contrary to the beliefs of many mostly female victims of life-long dieting, never eating to satiety is NOT going to promote a bikini body - quite the contrary (learn more)
Donato and his colleagues fed a group of adult Wistar rats diets that differed only in their amino acid make-up. Both the control and the experimental diet were based on the same synthetic standard chow (remember what you've learned about synthetic chow lately?). What was different, though was the form of protein / amino acids the scientists used to replace 8.55g of the cornstarch (per kg) of the original diet. The final diets did thus contain either...
  • 8.55g of casein (control), or
  • 5.45g l-leucine + 3.1g l-phenylalanine (LP)
... as replacements for the cornstarch. Since both were still isocaloric and had an identical protein content (12%) this modification would allow Donato et al. to see if the different amino acid profiles would have nay effects on the weight development of the rodents.

I guess by now you may be asking yourself about the connection to Oprah and boydbuilding diets, right? Well, the 28-day experiment actually had 2 phases a dieting and a maintenance phase. Both cycles were 14 days long. In the first one, the rodents dietary intake was cut in half, while they were allowed to eat as much as they wanted (ad-libitum feeding) in the second 14-day cycle.

YoYo or not - is that the question?

Now, what would you guess happened? I mean, remember: Both diets had an absolutely identical amount of calories and protein - so, the rodents in both groups "hit their macros", right? The logical answer - at least to an increasingly popular, but over-simplistic dietary paradigm - must be: "Nothing! Both groups will end up at an identical body composition.", right!? A brief glance at the data in figure 1 does however suffice to tell you the IIFYM prognosis was not exactly correct - at least not if we take the changes in body composition into account.
Figure 1: Effects of weight cycling with casein (control) and leucine + phenylalanine (L+P) on body composition (left), feed efficiency (=how much weight do you gain per gram of food) and weight (Donato Jr. 2013)
So what can we conclude based on the results in figure 1? Firstly, the small figure on the bottom right goes to show you that weight cylcing per se does not make you "heavy" as in "having a higher BMI than somebody who does not weight cycle". The large figure on the left, on the other hand informs us that weight cycling can cost you muscle and make you fatter - 4% fatter to be precise. Skinny fat, so to say. Notwithstanding, the data from the Donato Jr. study does also tell us that the provision of a low amount of additional leucine and phenylalanine minimized the fat gain in the bulking phase and had beneficial effects on amount of lean mass the rodents maintained and build during the 4-week study. The net result is a higher body weight in the L+P group, at an almost identical body composition.

Leucine + phenylalanine also blunt the reduction of T4 → T3 conversion

If we look closer we do yet see another related, but non-negligible advantage: The typical downregulation of the conversion of the "inactive" thyroid hormone T4 to the "active" thyroid hormone T3 in response to long-term dieting was significantly reduced by the provision of leucine and (I will just go on a limb here and say "more importantly") the neurotransmitter precursor phenylalanine.
Figure 2: Effect of weight cycling of markers of glucose and thyroid metabolism (Donato Jr. 2013)
This did yet not translate into a significant amelioration of the highly significant (>50%) deterioration of the blood glucose metabolism, and the triglyceride levels (not shown) were actually 20% lower in the casein yoyo group (CON) than in the non-weight cycled control group. From a health perspective, the addition of leucine and phenylalanine is thus "only" useful, because it will help you retain or actually build muscle mass (with the data we have, it's difficult to say which effect was the dominant one, but I'd suspect it's the anti-cabatolic one).
Bottom line: You need to be careful about mis- and over-interpreting the results of the study at hand - and that's not just because it's "only a rodent study".

If there was one "take home message" from the study at hand, I guess it would be very similar to the one from the one of the December 2012 post I borrowed this figure from: "Make sure to get at least 10g of EAA with each of your meals"... ah well, "... and avoid 'classic' YoYo dieting à la Oprah, whenever possible - of course!" ;-)
The alleged "lean mass gains" on the L+P diet come at the expense of a non-negligible increase in body fat. Overall the lean mass to fat mass ratio is thus not better than in the continuously fed rodents. And unless your beauty ideal is all about being "massive", this is not necessarily going to be an improvement to your physique.

If you take another look at figure 1 you will also see that the feed efficiency, i.e. the amount of weight you gain per kcal you consume was not reduced but increased by the addition of leucine and phenylalanine. This may be a result of the pro-insulinogenic and "anabolic" (Nuttall. 2006; Iverson. 2013), as well as the anti-cabatbolic effects of these amino acids and is thus not necessarily "bad".

It would nevertheless be highly unwarranted to believe that supplementing your diet with leucine + phenylalanine on a a "lean bulk" would yield significant advantages - this hypothesis is clearly not supported by the study at hand. The same goes for the usefulness of supplementing isolated amino acids, in this case leucine and phenylalanine, on top of a high protein diet, in general. In fact, I can refer you directly to an older article of mine that confirms that you better make sure to get the full dose of 20g+ of whole protein than trying to make up for it by adding additional aminos (learn more)

References:
  • Donato, J. et al. Effects of leucine and phenylalanine supplementation during intermittent periods of food restrictionand refeeding in adult rats. Life Sciences. 2007 [epub ahead of print]
  • Iverson JF, Gannon MC, Nuttall FQ. Ingestion of leucine + phenylalanine with glucose produces an additive effect on serum insulin but less than additive effect on plasma glucose. J Amino Acids.
  • Nuttall FQ, Schweim KJ, Gannon MC. Effect of orally administered phenylalanine with and without glucose on insulin, glucagon and glucose concentrations. Horm Metab Res. 2006 Aug;38(8):518-23.

Increasing Adolescent Obesity Among Girls: How School Stress is the New Scapegoat When the Skinny Fat Phenomenon and Twinkie Diets Really are to Blame.

Image 1: Was it school stress that cost Michelle Obama her famous "guns" (=muscular upper arms)? Probably not - and despite contrary conclusions in the study at hand, I doubt that it is school stress that leaves our daughters fat, but undermuscled. What do you say?
According to the results of a recent evaluation of the data from the European HELENA trial, school, or rather the stress your children are exposed to within the educational system, may be one of the reasons for the increasing number of obese adolescents (age 12-18 years) - at least if we trust the statistical finesse of Tineke De Vriendt, Els Clays and 10 other scientists who recently published a paper on European adolescents’ level of perceived stress and its relationship with body adiposity in the European Journal of Public Health (DeVriendt. 2011). The study was part of the Healthy Lifestyle in Europe by Nutrition in Adolescence cross-sectional study (HELENA-CSS), the aim of which is to obtain "reliable and comparable data from a selected cohort of European adolescents concerning a broad variety of parameters related to nutrition, health, physical activity and fitness", or in other words, to provide the epidemiological back-bone for the formulation of more or less mainstream hypotheses on "why we are getting sick and obese"... be that as it may, with a sample size that allows for a confidence level of 95% and <0.3 error and 3865 adolescents from more than 10 European cities, the data from the HELENA study is probably the best we can get at the moment and thus you may nonetheless be interested to hear that ...
School-related stress was demonstrated to be a main source of stress in European adolescents, [...and] in adolescent girls (but not in boys), a positive association was observed between their level of perceived stress and measures of general and abdominal obesity.
If you have a closer look at the stress data, expressed on a 6-scale Likert scale from 1 = ‘Not at all stressful’ over  2 = ‘A little stressful’, 3 = ‘Moderately stressful’, 4 = ‘Quite stressful’ to 5 = ‘Very
stressful’ (with 6 indicating ‘Is irrelevant to me’), you will notice that school and the closely related fear of an "uncertain future" are in fact the major stressors in the life of our adolescent children (and you may safely assume that the results won't be very different in the US).
Figure 1: Overview of perceived stressors; values expressed on a Likert-scale from 1 to 5 (data adapted from DeVriendt. 2011)
In that, it is yet interesting to observe that none of the stressors is on average perceived as "quite stressful" or even "very stressful". It is also noteworthy that on 5 out of 10 scales and on the summary scores girls experienced more stress than boys. In view of the scientists previously cited conclusion (of which I do not have to tell you that it is based on one of those sophisticated *cough* statistical models) that only "in adolescent girls (but not in boys), a positive association was observed between their level of perceived stress and measures of general and abdominal obesity", it may thus surprise you to hear that the obesity rate among boys is more than 2x higher than among adolescent girls (cf. figure 2). So how is that?
Figure 2: Body adiposity characteristic of study sample (n=1121) of adolescents from the HELENA trial (data adapted from DeVriendt. 2011)
Well, we all know that even with a perfectly "normal" BMI, you can easily be "skinny fat". A phenomenon of which I feel that it is becoming the norm, not the exception, among adolescent girls, who - after their nth an-apple-a-day diets have lost nothing but muscle and thus have a very high body-fat percentage with a low overall body-weight.

This hypothesis would be confirmed by the regression coefficients of the statistical models from the study, according to which the association of perceived stress with the body fat level of the girls is 7x higher than the association of perceived stress and BMI, which is something that should you make reconsider, whether
  1. body weight and BMI is an important biological measure, at all,
  2. the real "obesity" rate, including skinny fats, among girls is not way higher than the 1.9% reported in the study would suggest, and
  3. in how far school-stress, despite being the "major stressor" in this survey and not a misguided beauty-ideal is to blame for the increasingly unbalanced ratio of lean to fat mass in adolescent girls
The importance of the latter, i.e. a questionably beauty-ideal, in the etiology of (and this would be ironic if it was not so unfortunate) diet-induced obesity could also explain that the pubertal stage the girls were in and not stress or their diet had the greatest "explanatory value" (remember: we are talking of associations here) in regard of their body fat levels (cf. figure 3).
Image 2: Low self-esteem and false beauty-ideals pave the way into disordered eating and life-long misery. Something you want to spare your daughter and son, don't you?
Did you know that according to a 2000 national survey 45% of the girls, but only 20% of the boys from 5th to 12th grade reported to have tried one or more diets at some point in the past (Neumark-Sztainer)? And would you have guessed that 17% did even consider their own eating behavior as already "distorted"? Needless to say that both of these factors showed a high correlation with overweight status, low self-esteem, depression, suicidal ideation, and substance use; and certainly reason enough for you to help our children (girls and boys) not to fall victim to ill-advised beauty-ideals and false dietary recommendations.
And from the fact that the same variable had 7x less predictive value in boys, who obviously do not want to be skinny fat and refrain from Twinkie-style low calorie, low fat dieting, we can with some caution (due to hormonal effects on fat accumulation) conclude that it is not just a time factor, meaning that the older girls have more time to accumulate body fat...
Figure 3: Regression coefficients (=associative strength*100) of stress or pubertal stage with body-fat percentage in adolescent boys and girls from the HELENA trial - mind the logarithmic scaling! (data adapted from DeVriendt. 2011)
Now, what can you do about that? Well, without even knowing you probably have already done something! Assuming that you (just like every other reader of the SuppVersity ;-) are of above-average intelligence, your education has already provided your daughter, but not your son, with a better chance of staying lean than her peers from less educated parents (~80x higher explanatory value than stress!). All that is left now to make absolutely fat-proof, is to tell her that strong, not skinny fat is the new beautiful ;-)

5% Calorie Restriction & Longterm Dieting Make You Fat & Insulin Resistant. Plus: Model Predicts Weight Loss Based On Number of Weight Lost & Diet Pill Use On Previous Diets

Image 1: "Bikini Body Now!", headlines like this and the unfair suggestion that by following diet X or taking supplement Y you would make it onto the cover of a magazine like that are part of the problem why diets fail, people get discouraged and caught in the diet trap.
The issue of yoyo dieting and the existence and non-existence of a body weight or body fat set-point has been an issue in more than a handful of SuppVersity posts, already (click here to read more). None of the studies I cited (and not even one of those I have read) did yet provide a conclusive and experimentally verifiable answer to the question whether or not there is such a thing as a "set point" and how or even if dieting influences the latter. What common "wisdom" would suggest, though, is that dieting will ruin your metabolism, so that both the post-dieting weight rebound, as well as future problems with losing weight would be programmed.

So the question is: Can you diet yourself fat?

As I have pointed out in previous posts, as well, the hypothesis that you cannot only diet yourself fat, but also make it practically impossible ro reverse the damage is supported by a myriad of N=1 reports on the Internet, objective evidence, on the other hand, is very rare, often inconclusive and mostly either of epidemiological or experimental nature.

In the case of the most recent study from the Pennington Biomedical Research Center at the Louisiana State University, this is yet somewhat different, as it is one of the few studies to combine a controlled dietary intervention with a focus on lifestyle changes that went beyond just telling participants to cut calories (and fats ;-) and a detailed epidemiological analysis of the weight loss history of the subjects to produce a model that would actually allow predictions of future weight loss based on specific aspects of the weightloss history of a given individual.
Figure 1: Based on the diet history and the weight loss success during the 6-month weight loss intervention, the scientists developed a model to predict future weight loss - I would take the exact quantities with a grain of salt, but the qualitative trend, as well as the confounding factors are interesting (data based on Myers. 2012)
As you can see in figure 1, there is something like a "breaking point" at the 10+ diets margin, when it comes to the ability to lose weight. Aside from the fact that you will have all dieters with more than 10 diets packed in there (people could have dieted 100 times or more!), this is by no means evidence for the existence of negative physiological / metabolic side effects of dieting.

In view of another important finding of the study, which is the prognostic validity of previous successful weight loss (figure 1, left) as a positive indicator of future weight loss success, it is much more likely that people who failed 10 or more times, simply make the same mistake(s) over and over again - and while most of them are probably falling victim to one or another of the following culprits
Did you know that a reanalysis of data from the DiOGENES study, a large scale dietary intervention with participants all across Europe, yielded an astonishing result which is yet pretty much in line with the weight loss success of the biggest losers Myers et al. report?

According to Monica H.T. Wong and her colleagues, who scrutinized the weight loss and subsequent weight maintenance of 502 study subjects from 8 different study centers, those participants who lost the most weight during the initial 8-week weight loss phase on a very low calorie diet (800kcal/day) were also the ones who did best in staving the weight off!

Moreover, neither the starting weight nor the glucose sensitivity were significantly associated with the ability to weight and to avoid the dreaded weight rebound, in the course of the 6-months follow up (Wong. 2012). After the weight loss, on the other hand, those participants who lost the most weight also saw the greatest improvements in insulin resistance - ex-post, this could therefore at least be one physiological factor contributing to the long-term success of the biggest losers.
  • following an unbalanced, single-sided / fad diet (e.g. cabbage diet, etc.)
  • starving themselves for X weeks and falling off the wagon, before lasting results can even be achieve
  • cheating too often / not cheating at all
  • overexercising (and undereating)
  • doing no exercise at all
  • meticulously counting  calories and grossing up energy expenditure (as measure with a heart rate monitor and pieces of cake eaten after the workout)
  • eating too little protein to ever be satiated and keep your muscles from being cannibalized 
  • eating too much protein (and no carbs or fats) and running on cortisol and catecholamines until you crach
  • (ab-)using fat burners (esp. stims) and burning out (cf. figure 1, right)
  • seeking for the magic pill, both in supplement and diet form
  • sticking to a diet, because it worked so well for X months, when your body has long changed and the previously optimal diet is now inappropriate for your novel you (e.g. following Atkins diet when you got rid of most of the blubber and turned to physical culture)
an older study by Xi et al. appears to suggest that one item that's not usually on lists like the above could pose a similar, if not even more pronounced thread even to the "educated" dieter.

Being in a very mild caloric deficit, is no solution, but a potential cause of the problem. In fact, "not dieting hard enough" could be just as detrimental, as any of the previously mentioned self-imposed obstacles.

Figure 2: Total and resting energy expenditure of mice that were exposed to a -5% reduction in energy intake for 21 days (graph from Xi. 2010)
This is at least what the results of a study from the Department of Nutrition Sciences at the University of Alabama at Birmingham, Birmingham in Alabama, would suggest.

In 2010, already, Xi et al. have shown that a mild (=5%) reduction in energy intake is probably the worst approach to dieting rodents (and probably humans, as well ;-) can take, as it triggered...
  • increases in fat mass (p < 0.01) 
  • decreases in lean mass (p < 0.01),
  • decreases in total energy expenditure (p < 0.05) and  
  • resting energy expenditure (p < 0.05) 
and all that within no more than 3 weeks and in the absence of reduction in locomotor activity (Xi. 2010) - which means that you cannot exercise these detrimental effects away!

The HIID solution: High Intensity Interval Dieting to get ripped and stay ripped?

You may now certainly complain that biggest losers and mice are nothing you want to go by and you are certainly right; yet still, the notion that slow and steady is not the way to go is also corroborated by results of another 2010 study, this time done in humans and not from Alabama, but from the Washington University School of Medicine, where Fontan et al. conducted an ex-post analysis of the effects of really long-term moderate caloric restriction (and endurance exercise) on insulin-sensitivity and glucose management.

The subjects of the study were 28 volunteers, who had been eating a calorically restricted diet for an average of 6.9 +/- 5.5 years, (mean age 53.0 +/- 11 years), 28 age-, sex-, and body fat-matched endurance runners (EX), and 28 age- and sex-matched sedentary controls eating the SAD or standard Western diet (WD). (Fontana. 2010):
Figure 3:  Parameters of glucose management in 23 subjects who have been following a calorically restricted diet for ~7y  (range 3–20 years; CR) and 28 endurance runners who had been training for an an average of 21 years (range 5–35y; 20 to 90miles/week) relative to 28 sedentary (regular exercise <1 h per week) age and sex matched individuals eating typical Western diets (WD); data calculated based on Fontana. 2010.
Probably much to the surprise to all researchers who love their worms and fruit flies and still believe that starving was the solution to all your problems, Fontana et al. found that long-term caloric restriction in the absence of exercise had statistically highly significant negative consequences on glucose tolerance, as measure in a standardized oral glucose tolerance test (figure 2, small graphs). What's particularly interesting though is that
  1. the non-exercising long-term calorie restricters were practically insulin resistant and still had perfect HOMA-IR values, and that
  2. among long-term dieters there were only 11 subjects (CR-IGT subgroup) who were so glucose intolerant that the result was still statistically significant, though the other 12 subjects' (CR-NGT subgroup) ability to clear the glucose from the bloodstream was in the normal range
Now, while former (1) does tell you much about the validity of HOMA-IR values as a marker of insulin resistance in people on long-term calorie restriction, the latter (2) observation flies right into the face of the "cut your calories to live longer and healthier" paradigm - after all, those 11 calorically restricted subjects had apparently become (or maintained?) glucose intolerant despite having lower BMIs and lower caloric intakes than their peers (1,858 kcal/day, BMI 18.6 vs. 1,729kcal/day, BMI 20 in glucose tolerant caloric restriction subjects, CR-NGT).

Due to the size of the two subgroups in the calorie-restricted group on which Fontana et al. conducted a sub-analysis, we cannot come to any clear-cut conclusions with respect to physical mechanisms that would  explain the general tendency towards a reduced glucose tolerance and the intra-group differences between those who stayed glucose tolerant and those who are now underweight, malnourished and still glucose intolerant:
Dont fall for the false believe that being "normal weight" or even skinny means being healthy! Researchers from the Mayo Clinic in Rochester have found only recently that subjects with normal BMI but central obesity as defined by a high waist-to-hip ratio had the highest cardiovascular death risk and the highest death risk from all causes among the six subgroups (normal weight / overweight / obese x normal waist-to-hip ratio / high waist-to-hip ratio). The risk of cardiovascular death was 2.75 times higher and the risk of death from all causes was 2.08 times higher in normal weight obese people as compared with subjects with normal BMI and normal waist-to-hip ratio. And Dr Lopez-Jimenez points out: "Our research shows that if a person has a normal BMI, this by itself should not reassure them that their risk for heart disease is low. Where their fat is distributed on their body can mean a lot, and that can be determined easily by getting a waist-to-hip measurement, even if their body weight is within normal limits." In lights of the increased fat deposition in the aforementioned rodent study by Xi et al., constant calorie restriction is thus probably not the way to lead a healthy, let alone happy life (ESC. 2012).
"To try to obtain some insight regarding the mechanism responsible for this difference, we did a post hoc evaluation of the data. There were no significant differences between the CR-NGT and CR-IGT groups in either the HOMA-IR (0.32±0.20 versus 0.24±0.10) or the ISI (19.6±7.6 versus 16.8±4.7). Fasting plasma glucose, insulin, and C-peptide concentrations were similarly low in the two CR subgroups. Plasma 30-, 60-, 90-, and 120-min glucose concentrations were significantly higher in the CR-IGT subgroup than in the CR-NGT subgroup. Glucose AUC was significantly higher in the CR-IGT group than in the CR-NGT subgroup. Plasma insulin and C-peptide concentrations after the glucose load were not significantly different between the two CR subgroups except for the 120-min C-peptide value, which was higher in the CR-IGT groups. Insulin AUC and C-peptide AUC were not significantly different between the CR-IGT group and the NGT-CR group." (Fontana. 2010)
If you take closer look at the actual data there are however certain parameters that could at least point into the right directions for future research and provide us with some clues that may help us in setting up our own dietary regimen.

Though not statistically significant (mostly a result of the small size of the dataset for this sub-analysis with N=11 and N=12 subjects in each group), there are a couple of things, it cannot be negated that the insulin tolerant subjects had ...
  • 33% higher IGF-1 + 78% higher testosterone levels,
  • 36% lower fiber intakes + 28% greater VO2MAX
  • 8% higher BMIs
than their insulin resistant peers. Now, you tell me what does "Lower fiber intake, higher IGF-1, higher testosterone, higher BMI" sound like?

Yeah, exactly the nightmare of every physician and exactly what the medical orthodoxy would consider to be indicators of a skewed metabolism and would be trying to solve by putting you on a fiber-laden energy, fat, nutrient and often even protein deficient diet that may work as long as you are morbidly obese and every pound less on the scale takes you one step away from dying from a heart attack but will make you, an already (more or less) lean physically active individual starve yourself into an asexual catabolic state, of which I do not believe and do not even care if it will allow me to live 2 or maybe even 10 years longer...
So what? Conventional wisdom will tell you that the first diet is always the most successful one, that you will regain weight after dieting, no matter what, and that it will become increasingly difficult to get rid of the fat and avoid the yoyo effect.

And in fact, all this will become true, as long as you do your very best to make it become a self-fulfilling prophecy by setting yourself unattainable goals (e.g. "by tomorrow everything will be different") and regarding your "diet" as a temporary step to get from A to B (e.g. "I lost 50 pounds! Hurray, let's party for the rest of the year...")
Implications: Before I get into an essentially pointless rant, let's briefly recapitulate what main, or I should say most relevant outcomes of the individual studies were:
  • Myers' and Wong's studies "proof" only one thing: You got to be prepared to and actually make lifestyle changes! If you do, you will have success, huge success, in fact, in losing and staving off the weight.
  • Xi's and Fontana's studies, as well as the recent results from the Mayo Clinic, on the other hand, underline the fallacy of lifelong dieting. If anything, it is this, i.e. never eating to satiety, always counting calories and disregarding the mandatory nature of exercise, that's underlying reason of "diet resistance" and "diet induced obesity"
None of the studies, however provides significant evidence, let alone "proves", that there was a general physiological response to intentional weight loss that would make subsequent reductions in body weight harder and maintaining your weight (assuming this is not already in the skinny / anorexic zone) near to impossible!
The general message should thus be clear: A "diet" (as in restricted eating) is always just a temporary tool to be used within the broader context of lifestyle changes that are designed to maintain a healthy weight and improve the cardiovascular, and metabolic fitness that is the cornerstone of every goal in the SuppVersity's navigation bar, i.e. staying healthy & improving longevity, boosting performance, building muscle, losing fat and even having a fulfilled sex life... and don't fool yourself and take any of those for granted!

References:
  • Anderson JW, Konz EC, Frederich RC, Wood CL. Long-term weight-loss maintenance: a meta-analysis of US studies. The American Journal of Clinical Nutrition. 2001; 74: 579–584.
  • European Society of Cardiology (ESC). Normal weight individuals with belly fat at highest CVD risk. ScienceDaily. August 27, 2012. < http://www.sciencedaily.com­ /releases/2012/08/120827074153.htm > retrieved August 29, 2012.
  • Fontana L, Klein S, Holloszy JO. Effects of long-term calorie restriction and endurance exercise on glucose tolerance, insulin action, and adipokine production. Age (Dordr). 2010 Mar;32(1):97-108.
  • Li X, Cope MB, Johnson MS, Smith DL Jr, Nagy TR. Mild calorie restriction induces fat accumulation in female C57BL/6J mice. Obesity (Silver Spring). 2010 Mar;18(3):456-62. 
  • Myers VH, McVay MA, Champagne CM, Hollis JF, Coughlin JW, Funk KL, Gullion CM, Jerome GJ, Loria CM, Samuel-Hodge CD, Stevens VJ, Svetkey LP, Brantley PJ. Weight loss history as a predictor of weight loss: results from Phase I of the weight loss maintenance trial. J Behav Med. 2012 Aug 21.
  • Wong MHT, Holst C, Astrup A, Handjieva-Darlenska T, Jebb SA.Caloric Restriction Induces Changes in Insulin and Body Weight Measurements That Are Inversely Associated with Subsequent Weight Regain.PLoS ONE. 2012; 7(8):e42858.

Do Chronic Energy Deficits Make Athletes Fat? The Longer & More Severe You Starve, the Fatter You Are. Irrespective of What the Calories-in-VS-Calories-Out Formula May Say

This is not an "anti-gymanstics" or "anti-runners" article, this is an anti-ruin-your-life-post for the average female and male gymrat.
Maybe you've read about the results Deutz, Bernardot, Martin and Cody published in their 1999 paper on the "Relationship between energy deficits and body composition in elite female gymnasts and runners"... in fact, it may be possible that I already mentioned it in the "Athletes Triad Series" (read more), but even if I did, the fact that I get messages like "I eat 1,100kcal/day and still gain, not lose fat" or "my girlfriend eats 900kcal/day and maintains that this is normal", tells me it does not matter if I mention one or two of the figures the authors compiled in this unfortunately highly "under-cited" paper (only 72 citations are referencing this article) twice.

If that makes just one of the victims of their own ambition rethink what he or she is doing, it was well worth... wouldn't you agree?

Can the elite be wrong?

Usually you would assume that elite athletes are doing everything right, they are the epitome of our modern understanding of "health". As a SuppVersity reader you are yet well aware that there is a disconnect between optimal health and performance and with the latter being in part dependent on having a certain look as it is the case for bodybuilding, figure competitions and the like this disconnect can be so huge that being successful may eventually require a non-genetically gifted athlete to sacrifice his or her health on the altar of a misinterpretation of "physical culture".

That being said there is a way more traditional and, contrary to bodybuilding, officially Olympic sport where similar rules apply: Gymnastics! Especially among the female competitors the paradigm still is - the thinner the better. And to make things even worse, in this case "thin" actually means "thin" as in "being able to hide behind a straw". Now, this is obviously not the case in any of the aforementioned disciplines and yet they claim way more victims of life-long dieting than those sports, where "being thin" is actually part of the game - and what's almost sarcastic, the tortures some professional and many hobby athletes subject themselves to are not even rewarded.
You will have to take the following figures with two grains of skepticism! One for the scientifically established bias due to under-reporting in female gymnasts (Jonnalagadda. 2000), and the other one for the discrepancy between factual and calculated energy expenditures, which is, due to the negative feedback chronic dieting exerts on the total energy expenditure, much narrower than the formulas suggest. And another thing, remember that we are talking about body-fat % not total body fat masses here!
Against that background you will probably not be surprised to hear that the vast majority of the elate female artistic (N=32) and rhythmic (N=11) gymnasts in the study at hand is consuming 1,002kcal less than they would actually need to satisfy their caloric demands.
Figure 1: Comparison of within-day energy balance in the four groups of elite athletes (left); largest energy deficit per hour and average 24h energy deficit in all athletes, gymnasts and runners (Deutz. 2000).
If you take a closer look at the data in figure 1 you will yet realize that the average medium- and long-distance runner is not much better off. Now, whether the latter is a necessary prerequisite to make it to the top or simply a result of being unable (for physical or psychological reasons) to compensate for the training induced increase in energy expenditure, is beyond the scope of this post and essentially irrelevant to the statistically highly relevant acorrelation between between energy balance and body fatness, I've plotted for you in figure 2.
Figure 2: Relationships (Pearson correlations) between energy balance factors and body fat percentage in all athletes, gymnasts, and runners (Deutz. 2000)
I hope that these results do not come as a surprise for the vast majority of those for whom this is not the first visit to the SuppVersity. After all, I have been trying my very best for years (hard to believe I am doing this "chronically" ;-) to scare you away from the chronic and towards the cyclic calorie reduction as a means to cut body fat and maintain muscle mass (note: with the relatively small study size not all effects reached statistical significance; for the parameters pertaining to the "energy out vs. energy in"-calculations the average dieter is so fond of, this was yet particularly noteworthy).

In athletes chronic "dieting" results in an increase in body fat percentage

The message is simple and so is the underlying mechanism. The chronic provision of an insufficient amount of energy leads to a metabolic downregulation that goes hand in hand with an increased disposition to store and a decreased disposition to let go of body fat.
Another note: This is not an anti-intermittent fasting article either. If you do IF to cut weight you will have an overall negative energy balance, just like on every other diet, but if you are doing it for life (for whatever reason), you should be meeting your daily energy demands. This means you would have a much higher energy surplus on the other hours - in essence the data simply don't apply to someone who is doing intermittent fasting on a maintenance diet.
The concomitant exercise induced physical stress lulls your body to believe that you are amidst a starvation period, where building muscle and/or maintaining more muscle than is absolutely necessary to sustain the regular exercise routines is a no go and each and every energy unit that that is not necessary to keep you from passing out will get stored to cover those hours with a per hour deficit of 750kcal (which is the average maximal deficit per hour in the rhythmic gymnast group).

Bottom line: Don't get fooled by the "Don't worry. That's not you, starve yourself! It's good for you - don't you feel it?" the little gal or guy in your shoulder is now whispering into your ear. The rule "chronic starvation = increase in body fat percentage" applies to male and female athletes, gymnasts, runners, sprinters, cyclists, fitness junkies, bodybuilders, footballers, ... and across a wide range of energy deficits.

You don't have to eat burgers and French fries all day, to meet your energy requirements. Living on chicken breast & broccoli for the rest of your life is neither necessary nor conducive to your goals, and that's even true for such profane goals as "staying lean"! And by the way - how much do you need (learn more)?
So say good buy to the little guy with the hunger high and use your brains and acknowledge to yourself: "I am a junky. A starvation junky!"  You are not? Well then check this out:
Addiction is a persistent, compulsive dependence on a behavior or substance. [...] Addiction has been extended [...] to include mood-altering behaviors or activities." (Livingston. 2008; my emphases)
And the main criteria for being addicted are a loss of willpower, fear of harmful consequences, an unmanageable lifestyle, tolerance or escalation of use and withdrawal symptoms upon quitting. Well if all that is not you and you. Stop working out like mad and return to eating normal without going crazy whenever you feel satiated, now!

References:
  • Deutz RC, Benardot D, Martin DE, Cody MM. Relationship between energy deficits and body composition in elite female gymnasts and runners. Med Sci Sports Exerc. 2000 Mar;32(3):659-68. 
  • Jonnalagadda SS, Benardot D, Dill MN. Assessment of under-reporting of energy intake by elite female gymnast. Int J Sport Nutr Exerc Metab. 2000 Sep;10(3):315-25.
  • Livingstone, C. "addiction." Dictionary of Sport and Exercise Science and Medicine. 2008. Elsevier Limited 14 Jul. 2013 http://medical-dictionary.thefreedictionary.com/addiction

Pre-Hypertension Ain't Benign: Up to 80% Increased Risk of Cardiovascular Morbidity W/ "High Normal" Blood Pressure and Less! Plus: Foods & Supps to Reduce Your BP

"High normal" is misleading - there is no such thing as a "high normal" BP
"Ah, that's not so bad!" If that's what your doctor said, when he last measured your blood pressure and said "129/84" when he looked at the display of the Sphygmomanometer he must have been living beneath a rock for the past decades.

If that sounds familiar, it may be useful to show him a recent meta-analysis of pertinent papers from the early 2000s - a metapa-analysis like the one Yuli Huang and her colleagues from the Department of Cardiology at the Nanfang Hospital at the Southern Medical University in Guangzhou, China, published in BMC Medicine a couple of days ago (Huang. 2014).
"Pre-hyper-tensive? Pah that's not me!" If you just thought that, I'd hope that you are right, but honestly... in view of the fact that 3 out of 10 US citizens have a blood pressure in the 129-139 / 84-95 mmHg and against the background that the latter has long been considered as "high normal" I am afraid that some of you may qualify for the >50% increase in heart disease risk as a result of "suboptimal" blood pressure values.
In said paper Huang et al. present the results of an extensive database search in the course of  two independent reviewers identified 18 prospective cohort studies with a total of 468,561 participants the researchers used to evaluate the cardiovascular and coronary heart disease (CVD and CHD) risk in prehypertensive individuals.
Figure 1: Risk increases for cardiovascular morbidity (all subjects, left), stroke and cardiovascular heart disease (right); difference expressed relative to subjects w/ normal BP (Huang. 2014)
According to data from the Centers for Disease Control and Prevention in Atlanta, "[a]lmost 30% of American adults have prehypertension" (CDC website). What the CDC website does not tell you, though, is that being prehypertensive and not just the correspondingly increased "risk of developing hypertension" the authors of the info-document on www.cdc.gov mention in the next sentence is a problem.

If you look at the data, the Chinese researchers present in their latest paper, it turns out that even a blood pressure below what is usually considered "high normal", i.e. a systolic blood pressure between 130 and 139 in concert with a diastolic blood pressure of 85 to 89 mm Hg. In fact, Huang et al. report at statistically significant increase in cardiovascular morbidity of 46% even in those of the almost 5000,000 study participants with "below high normal" levels of 120-129 / 80-84 and thus in a BP range where your doctor may even say: "Hey that's pretty good!"

If you happen to be lucky enough to be a women, the risk will be slightly reduced. If, on the other hand, you are a man, your CVD morbidity risk will increase by 80% - irrespective of your age, by the way.
Not on the list on the left, but in the SuppVersity News: " Olive Leave Extract Equally Effective at Lowering Blood Pressure as ACE Inhibitor Captopril" | read more
Men or not, you better do something about it: Usually I would summarize the misery in this last paragraph, but in this case, it appears more appropriate to remind you of the beneficial effects of regular physical activity (walking, running, lifting) and the usefulness of a whole foods, high nut (Casas-Agustench. 2011), high magnesium (Rosanoff. 2010; Kass. 2012), high potassium diet (Geleijnse. 1994; use supplements only if you can't get enough from your diet).

Supplements that may be useful are taurine (Militante. 2002), fish oil (Campbell. 2013), dark chocolate / cacao (Desideri. 2012), vitamin C (short term; Juraschek. 2012), green tea extracts (Bogdanski. 2012), pomegrenate (Asgary. 2013; juice), melatonin (Scheer. 2004) and - as on every list of suggested supplements - whey protein (Lee. 2007) ;-)
References:
  • Asgary, Sedigheh, et al. "Clinical Evaluation of Blood Pressure Lowering, Endothelial Function Improving, Hypolipidemic and Anti‐Inflammatory Effects of Pomegranate Juice in Hypertensive Subjects." Phytotherapy Research (2013).
  • Bogdanski, Pawel, et al. "Green tea extract reduces blood pressure, inflammatory biomarkers, and oxidative stress and improves parameters associated with insulin resistance in obese, hypertensive patients." Nutrition Research 32.6 (2012): 421-427.
  • Campbell, Fiona, et al. "A systematic review of fish-oil supplements for the prevention and treatment of hypertension." European journal of preventive cardiology 20.1 (2013): 107-120.
  • Desideri, Giovambattista, et al. "Benefits in Cognitive Function, Blood Pressure, and Insulin Resistance Through Cocoa Flavanol Consumption in Elderly Subjects With Mild Cognitive Impairment The Cocoa, Cognition, and Aging (CoCoA) Study." Hypertension 60.3 (2012): 794-801.
  • Geleijnse, J. M., et al. "Reduction in blood pressure with a low sodium, high potassium, high magnesium salt in older subjects with mild to moderate hypertension." Bmj 309.6952 (1994): 436-440. 
  • Juraschek, Stephen P., et al. "Effects of vitamin C supplementation on blood pressure: a meta-analysis of randomized controlled trials." The American journal of clinical nutrition 95.5 (2012): 1079-1088.
  • Kass, Lindsy, J. Weekes, and Lewis Carpenter. "Effect of magnesium supplementation on blood pressure: a meta-analysis." European journal of clinical nutrition 66.4 (2012): 411-418.
  • Militante, J. D., and J. B. Lombardini. "Treatment of hypertension with oral taurine: experimental and clinical studies." Amino Acids 23.4 (2002): 381-393.
  • Rosanoff, Andrea. "Magnesium supplements may enhance the effect of antihypertensive medications in stage 1 hypertensive subjects." Magnesium Research 23.1 (2010): 27-40.
  • Scheer, Frank AJL, et al. "Daily nighttime melatonin reduces blood pressure in male patients with essential hypertension." Hypertension 43.2 (2004): 192-197.

True or False? Caffeine is The Main Main Stroke Protectant in Tea & Coffee. High MCT Diets Are the Key to Longterm Fat Loss. Soybean Oil Makes You Fat not Heavy.

Adelfo Cerame Jr. after winning his weight class, the overall and the pro-card (leave him a message).
The first "True or False?" today, does not really pertain to diet and nutrition science, but it is still highly relevant for the SuppVersity:

Adelfo Cerame Jr. did eventually win his well deserved pro-card at the Wheelchair Nationals in Florida, yesterday. - True!

Ok, I have to admit that this may have been too easy with the picture of Adelfo holding the trophies for his weight class and the overall in his hands on the right, but it was the best way to include this important news "seamlessly" *rofl* into today's SuppVersity article.

You want some more difficult stuff? Well, let's see what you know about tea, coffee, MCTs and heated soy bean oil, then.

Caffeine (probably) is the main stroke protectant in coffee and tea

True. As a recent study from the Universidade Federal de Santa Maria in Brazil clearly indicates, the "bad" caffeine is at least one, if not the main anti-oxidants that's responsible for the neuroprotective effects of coffee, tea and co (Souza. 2013).

Caffeine is also part of the classic CCC fat loss stack (learn more)
According to the results of the paper MA Souza et al. are about to publish in one of the future issues of  Neurochemistry International, a 2-weeks front-load with 6mg/kg caffeine per day increases the glutathione (=master antioxidant of the mammalian body) levels in the brain and protects rats from the oxidative damage and subsequent seizures in response to the administration of pentylenetetrazol-induced seizures (pentylenetetrazol is a circulatory and respiratory stimulant that overtaxes the brain, when it is administered in high doses).

What you should keep in mind, though, is the fact that Souza et al. used a dosage that was way lower than the amount of caffeine the average stim-junkie is consuming. It is thus not unlikely (in fact it is quite the opposite ;-) that we are dealing with a hormetic effect that occurs at human equivalent doses of 0.97mg/kg (~1 small cup of coffee) and turn against you when you escalate the doses to four or five MonterBullDrinks(TM) per day... I mean, the mere willingness of spending money on products like this goes to show you that drinking them compromises people's brain function, doesn't it? No, well I guess you have to reread the "Fat Content Per Energy Drink 0g. Fat Gain Per Energy Drink Drink 18g Study", then (reread it).

Most recent epidemiological human data supports these findings

And in case you don't believe this was relevant, check out the latest study in Stroke, in which Kokubo et al. which does not only confirm the stroke protective effects of green tea and coffee (Kokubo. 2013), but also yields some insights into what may be the "optimal" intake. After all, it takes 2x more green tea to achieve the effect you get from >2x cups of coffee per day, which is another hint at caffeine as the major driving force behind the anti-stroke effects of tea and coffee. Why? Well a large cup of Starbucks' green tea has 80mg of caffeine, the same amount of their regular coffee has roughly 290mg of caffeine in it.
Figure 1: Age and multivariable-adjusted hazard ratios of cardiovascular disease and its subtypes according to coffee (left) and green tea consumption in 82 369 Japanese (aged 45-74 years; without cardiovascular disease [CVD] or cancer in 1995 and 1998 for Cohort I and II, respectively) who received 13 years of mean follow-up through the end of 2007 (Kokubo. 2013)
Yet despite the validity of the "more caffeine = more brain protection" eqation the catecholamine surge of high amounts of green tea, but even more so coffee is not what you would call "heart healthy" (see figure 1; I would love to tell you the caffeine equivalents, but the scientist don't disclose the serving size). Just another reason to take it easy on stims in pill and drink form and keep your daily caffeine intake in the < 400 mg range (suggested read especially for the smokers: "Putting an "N" as in "nicotine" into "EC" amplifies the negative effects of ephedrine and caffeine on your heart";  read more)

Eating tons of medium chain triglycerides (MCTs) will make you lean

Are we, or rather you, my American friend eating too much fat or simply the wrong type of fats? According to a study that was in the SuppVersity news in Nov. 2012, it's the latter the "SAD Diet Has the Optimal Ratio to Induce Diabesity" (learn more)
It depends. While it may be that you can derive certain benefits by kicking out junkfood from your diet and replacing it with MCTs the "fat-burning" effects of medium chain triglycerides (MCTs) wear off after one to two weeks (White. 1999). Unfortunately, this is way longer than the usually cited studies on the direct metabolic effects lasted, so that a cursory look at the research easily fools you to believe that you could effectively burn fat by simply using MCT oils instead of whatever "bad" fat you had been using before.

Moreover, in the aforementioned study that was published in the American Jorunal of Nutrition roughly 14 years ago the postprandial total energy expenditure was already only 3% higher after the MCT meal in the first week. And it's not only that this advantage disappeared within the next 7 days, the respiratory ratio, a measure of the ratio of carbohydrate to fat oxidation, total fatty acid oxidation and carbohydrate oxidation were also identical in the  32% MCT and 32% LCT diets (both diets contained additional 8% of fat from other sources).

But what about all the other research?

While the transient benefits of the MCT feeding on energy expenditure alone are unlikely to have practical relevance there are a good handful of trials, which show some real world benefits in various dieting scenarios. Unfortunately, they are usually too short (Alexandrou. 2007), compare MCTs to beef tallow & co only diets, observe increases in fatty oxidation, which don't translate into changes in body composition (St-Onge. 2003), or have the subjects in the control group use relatively fragile control oils, such as olive oil for frying and cooking (St-Onge. 2008).

Accordingly, you should not be too surprised that the latest review of the effects of dietary intake of medium chain triglycerides on body composition, energy expenditure and satiety concludes: "
Curried Carrot Soup w/ coconut oil certainly qualifies as a good food choice, also bc. it's made with coconut oil, not plain MCTs (more).
"In the present review it was possible to verify that data related to increased satiety after consumption of MCT are quite controversial. Most studies showed no significant difference as to increased satiety and/or satiation related to lipid consumption. [...] A relevant fact in the lack of consensus among the studies concerns the large variation in the amount of MCT provided in different studies due to lack of reference values for a minimum, ideal and maximum consumption in literature. Moreover, there isn’t enough to long-term studies to identify either beneficial effects or potential harmful effects." (Souza. 2013)
If you go through the list of studies included in the review there are a couple other interesting patterns emerging: (a) the effects - if there were any - originated from the gut (mostly greater satiety effects), (b) if there were effects on body composition those often reached statistical significance in the obese individuals, only, (c) the benefits were more pronounced the less the subjects ate (esp. on those 800kcal hunger diets), (d) when the control was not nasty corn oil, or saturated long chain triglycerides (Atkins diet style), the effects were non-existent.

So, if your are lean, your current diet is balanced and your main fat source is neither corn oil nor beef tallow, the chances that you will be better off with expensive MCT oils than with a couple of spoons of coconut oil in your diet probably border zero. You see, it's just as so often not so much about "adding something in", as it is about leaving something else out / replacing it with a better food choice.

Soy bean oil offers a shortcut to metabolic disease even in the absence of obesity

True. I guess that this "true or false" item was actually way too easy to answer, but the recently published study by Potu et al. is simply too intriguing not to add it to the huge heap of existing evidence that the overabundance of "healthy" polyunsaturated fats from purportedly healthy plant oils is a major contributer to the fat mess we are dealing with.
Figure 2: Effects of 16 weeks on non-heated and heated soybean oil diets rodent food intake, weight gain and body fat (EWAT & IWAT) levels (Penumetcha. 2013)
Now, pro-obesity and pro-diabetic effects of corn oil, soy oil & co are actually no news. Penumetcha et al. do yet emphasize that they are the first to observe that soybean oil which has been heated on a hot plate at 190°C for 3 hours (think of the huge pots, frying pans & co that are used to produce convenient and fast foods) before it was added to the rodent chow has the unique ability to increase its consumers body fat levels without increasing their total body weight. Excellent, right?



Thats it for today! Ok, I guess that was too easy, as well. Still, it's true and I hope you enjoyed the last week and are already looking forward to the next week of exercise and nutrition science news here at the SuppVersity.

In the mean time you can kill some time by surfing over to the Suppversity Facebook Wall, where you will find news such as
  • Even if you align them like that, it is at least debatable whether capped fish oil is much more natural than the structurally modified 16 -carbon saturated fatty acid tetradecylthioacetic acid (TTA). And the usefulness of the longterm use of both remains questionable (learn more). 
    Beware of omega-3s unless you have the right genes -- New Inuit study confirms: If n-3 fatty acids are good or bad for you is in your genes (read more)
  • Muscular imbalances commonly overlooked factor in lower extremity sports injuries -- Scientists observe significant relationship of the coordination between muscle strength (ankle plantar flexor/ dorsi flexor), (hip addactor/abdactor), (knee flexor/ extensor) with muscle injuries (read more)
  • Arteriosclerosis is not a "neolithic" disease that occurred with the advent of agriculture -- Lancet paper debunks the myth of the "agricultural origin" of atherosclerosis (read more)
and when you are at it, don't forget to congratulate the one and only Adelfo Cerame Jr for finally bringing home those two small muscular statues you see in the image on the top of the page.

References:
  • Alexandrou E, Herzberg GR, White MD. High-level medium-chain triglyceride feeding and energy expenditure in normal-weight women. Can J Physiol Pharmacol. 2007 May;85(5):507-13.
  • Kokubo Y, Iso H, Saito I, Yamagishi K, Yatsuya H, Ishihara J, Inoue M, Tsugane S. The Impact of Green Tea and Coffee Consumption on the Reduced Risk of Stroke Incidence in Japanese Population: The Japan Public Health Center-Based Study Cohort. Stroke. 2013 Mar 14.
  • Rego Costa AC, Rosado EL, Soares-Mota M. Influence of the dietary intake of medium chain triglycerides on body composition, energy expenditure and satiety: a systematic review. Nutr Hosp. 2012 Jan-Feb;27(1):103-8. 
  • Souza MA, Mota BC, Gerbatin RR, Rodrigues FS, Castro M, Fighera MR, Royes LF. Antioxidant activity elicited by low dose of caffeine attenuates pentylenetetrazol-induced seizures and oxidative damage in rats. Neurochem Int. 2013 Feb 26.
  • St-Onge MP, Bourque C, Jones PJ, Ross R, Parsons WE. Medium- versus long-chain triglycerides for 27 days increases fat oxidation and energy expenditure without resulting in changes in body composition in overweight women. Int J Obes Relat Metab Disord. 2003 Jan;27(1):95-102.
  • St-Onge MP, Bosarge A. Weight-loss diet that includes consumption of medium-chain triacylglycerol oil leads to a greater rate of weight and fat mass loss than does olive oil. Am J Clin Nutr. 2008 Mar;87(3):621-6.
  • White MD, Papamandjaris AA, Jones PJ. Enhanced postprandial energy expenditure with medium-chain fatty acid feeding is attenuated after 14 d in premenopausal women. Am J Clin Nutr. 1999 May;69(5):883-9.