5% Calorie Restriction & Longterm Dieting Make You Fat and Insulin Resistant. Plus: Model Predicts Weight Loss Based On Number, 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. 2013)

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. 2013). 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. 2013).

"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, 2013. < http://www.sciencedaily.com­ /releases/2013/08/120827074153.htm > retrieved August 29, 2013.
• 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. 2013 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. 2013; 7(8):e42858.

What's Worse: YoYo-Dieting or Constant Gluttony? What Happens During Weight Cycling? And Why Does Every Diet Make You Fatter? Lots of Questions, a Couple of Answers

Image 1: To eat or to diet, what's worse?

Despite the fact that the magazines are still full of "X pounds in Y weeks" diets, more and more people begin to realize that "diet hopping" and even "dieting" in the conventional sense, i.e. following a special, usually very strict and non-sustainable nutritional regimen for a very short amount of time, are futile. But can calling a halt before you blow up like a balloon from time to time actually be worse than letting yourself go all-day, everyday? According to the results of an experiment that has been conducted at the Institute of Biology of the State University of Rio de Janeiro, the results of which have just been published in the open access journal PLoSOne, the answer to this question must be: YES, it can! And that may be true, even when you are not starving yourself!

Even "healthy" weight cycling turns out to be profoundly unhealthy!

Now, the unfortunate news first: We are, as so often dealing with a rodent study - one that was done conducted with 80(!) 3-months old C57BL/6 mice. "Wow! 80 mice? That's plenty!" Yeah, initially it may sound like that, but in view of the fact that their number was decimated every 8 weeks, there would not have been the necessary 4x8 rodents left at the end of the 24-week study period for the final evaluation of the four experimental groups, which were

• standard chow (SC; 15kJ/g) - rodents in this group received the standard chow (76% energy from carbohydrates, 14% energy from protein, and 10% energy from fats) for the whole study period
• high fat diet (HF; 21kJ/g) - rodents in this group received a fattening hypercaloric diet (26% energy from carbohydrates, 14% energy from protein, 50% energy from animal lard and 10% energy from soy bean oil 
• SC ↔ HF - rodents in this group received standard chow for the first 8-week cycle, high fat diet for the 2nd 8-week cycle and standard chow for the third and last 8-week cycle
• HF ↔ SC - rodents in this group received high fat diet for the first 8-week cycle, standard chow for the 2nd 8-week cycle and high fat  for the third and last 8-week cycle 

If we go back to the initial question, the HF group would be our 24/7, 365 days a year eat everything the worst Western diet you can imagine has to offer, while the animals in the group SC ↔ HF and HF ↔ SC group would be representative of

• the high school football player who turns to a sedentary lifestyle and bad eating habits when he goes to college, is partying all night, bear pizza, etc. eventually, he realizes he got fat, and diets again (SC ↔ HF ↔ SC) and
• the obese kid who eventually turns to physical culture, works out, eats health and loses weight, when he starts college, to then fall back into his old bad habits and starts letting himself go, when he marries and has kids (HF ↔ SC ↔ HF)

I know this is a little far-fetched and as we are going to see later, mice are not exactly the best model to study things like that, but still, the way the weight of the rodents, who had free access to the respective chow they were on during the whole experimental period, developed is quite telling:

Figure 1: Despite intermediate fat loss the increased feed efficiency (=weight gain per kcal) that is especially pronounced in the HF phases of the weight cycling groups quashed the previous weight loss. If age effects had not become a problem this effect would have been more obvious in a 4th cycle.

And the message the data in figure 1 is sending is quite clear: Dieting, as in changing your eating habits only intermediately, is useless, at best! - "at best", because it becomes increasingly difficult to lose and constantly easier to gain weight or, as Barbosa-da-Silva et al. put it:

[...] after three consecutive WC [weight cycles], the reduction of BM is less marked during the SC cycle, as well as the increase of BM is more prominent during HF cycle (Barbosa-da-Silva. 2013).

Now, we probably would not have had to do a 24-week rodent study to know that, right? Right! Notwithstanding, though, the beauty of working with rodents - instead of Biggest Losers, for example - is that they usually don't complain much when you slaughter them, so that the scientist could not only measure the serum leptin (figure 2, left), triglycerides, cholesterol, insulin and glucose levels, but also count the number and measure the size of the adipocytes in their visceral fat pads.

Figure 2: Leptin expression and adipocyte density per area of adipose tissue mass after the 1st, 2nd and 3rd weight gain/loss cycle (data adapted from Barbosa-da-Silva. 2013)

And as you can see in figure 2 (right) the weight cycling induced quite profound effects on the adipose tissue morphology; effects that are similar to what we have seen in previous discussions on the underlying causes of the yoyo effect (see "Nasty Insights into the YoYo-Effect"). You have to keep in mind, though, that you would be comparing apples and oranges if you compare the two weight cycling groups with each other, as one group has always just lost weight, when the other has gained weight so that in one group the adipocytes will  be depleted, when they are filled to the seams in the other one. If there had been a fourth cycle in the course of which the fat cells of the SC ↔ HF group would have been repleted, we may thus safely assume that the absolute size-differences, which reached statistical significance only in the HF ↔ SC group after the third cycle (violette bar in figure 2, right), would have been similar or even more pronounced after 32 weeks and 4 cycles in the then HF dieting SC ↔ HF (note: one of the reasons the researchers did extend the experiment for another 4 weeks was that even now, age-related effects and obesity related morbidities would have reduced the significance of the data).

Adipocyte morphology, leptin expression, fat pad restructuring and body fat that sticks

Apropos significance, you ay remember from the "previously mentioned post" on this issue that one of the currently discussed hypothesis that could  (at least partly) explain why formerly obese people are not just having a really hard time to lose weight, but also, and often even more so, to keep that weight off, relates to what I have previously labeled "relative leptin defiency" (too little leptin production per adipose tissue mass) or, and this would be an alternative hypothesis, "leptin resistance" (more than enough leptin in the blood, but the signal transmission does not work).

The first thing we can say based on the data Barbosa-da-Silva acquired on the absolute fluctuations of leptin in the blood of the rodents (figure 2, left) ist that previously made conclusions about the effects of weight gain, weight loss and energy intake on leptin, like

1. weight loss and fasting are associated with reduced leptin levels, 
2. weight gain is associated with an increase in leptin concentration 
3. chronically increased leptin can lead to leptin resistance
4. meals and according to meal composition or short-term swings in energy balance such as fasting or overfeeding induce swings in systemic leptin levels

appear to be accurate. To check whether there is evidence for my "relative leptin deficiency" hypothesis, especially in weight cycling groups, I ploted the ratio of serum leptin to body fat in figure 3 (left):

Figure 3: Leptin levels in serum per body fat (left), leptin expression in adipose tissue (middle), and sectional area of adipocytes of the different groups (based on Barbosa-da-Silva. 2013)

And what is interesting is that in this calorically non-restricted scenario, the respective "relative leptin deficiency" occurs only in the SC ↔ HF group during the third and last cycle, when their relative leptin levels which should actually be identical to the SC group (we must compare them to the SC group, because the current diet will influence leptin expression as well) are 36% lower than they "should" be. In the same third cycle, the HF ↔ SC group (remember, those are our "formerly obese kids") have 21% more leptin in their blood than they "should" - given their current adipose tissue mass.

Some food for thought - Though not directly related to the topic, there is one thing pertaining to the heavily debated "CLA post" from last week (cf. "CLA Destroys Body Fat"), I want to mention. If we assume that the CLA-induced adipose tissue apoptosis Kim et al. observed in their recent study is as rodent-specific as the natural death and rejuvenation of adipose tissue Cinti et al. observed in the study I cite relating to the limited adipose tissue growth in rodents, this would not just indicate that taking copious amounts of CLA would not help to reverse the damage you may have done during previous "diets", but could also explain why conjugated linoleic acid supplements don't work in humans (or horses; see yesterday's news).

Now this segues directly into the allegedly somewhat counter-intuitive conclusion that anything that soothes the raging inflammation in your fat cells may ameliorate the downstream detrimental effects on glucose and lipid metabolism, but will, on the other hand, help your fat cells to survive or maybe even proliferate in amidst the TNF-alpha induced cytokine storm (Prins. 1997), which would otherwise kill them. Now with the current paradigm of "inflammation = bad" this may sound hilarious. In the the end, it does yet only echo the title of a 1999 paper by Hube and Hauner, "The role of TNF-alpha in human adipose tissue:  Prevention of weight gain at the expense of insulin resistance?" (Hube. 1999) and would provide us with a mechanistic explanation of several otherwise non-explicable phenomena such as the profound fat loss in rodents who lack the master antioxidant glutathion (see "Inflammation Is the True Fat Burner"),,, but as indicated: This is just some food for thought ;-)

In combination with the leptin overshoot (+153%) in the "former football players on their college binge", this data would suggest that we are not dealing with "relative deficiency" and "leptin resistance" but rather with a complex mixture of both, where the latter is probably a result of repeated overshoots like the one we see in the SC ↔ HF group after their first high fat feeding cycle (2nd cycle, 154% elevated leptin levels).

Relative leptin deficiency, systemic resistance and now local differences?

And as if things were nor already complicated enough, there are also potentially important differences between circulating leptin levels and local leptin expression in isolated fat pads figure 3 (middle; compare data to figure 2, left, 3rd cycle). Thus, the drop in leptin levels upon "fasting" in the (SC ↔ HF, 2nd cycle  and HF ↔ SC, 3nd cycle) is systemic, but does not reflect the expression of leptin in the intra-abdominal tissue. This stands in line with my previous dissertation on "relative leptin deficiency" and the differences between...

• intra-abdominal (easy to shed on a diet), and 
• subcutaneous (esp. in the lower body compartment difficult to shed on a diet)

...adipose tissue in "Nasty Insights into the YoYo-Effect" (a similar depot-specificity has been reported for pre-adipocytes, i.e. developing fat cells, as well - intriguingly only in 9 out of human subjects (=81%); cf. Niesler. 1998). Due to the fact that the expansion of adipose tissue in rodents appears to be limited and the cell-turnover high (contrary to humans, where you get the impression that obesity is only limited by death and the cell-turnover - if it exists at all - must be very slow), these effects are probably even more pronounced in humans than in mice. Consequently, it can be expected that the diet / feasting induced upward shifts of the body fat set point are more pronounced and their morphological reversal either more time-consuming (probably true for the visceral body fat) than in rodents or simply impossible (could be the case for parts of the subcutaneous body fat) in human beings.

Image 1 : Lose 20lbs now, gain 25 back and have 5 stick with every diet! We still don't understand exactly why, but by now it should be clear, diets like the "Kendra diet" are rather part of the problem than viable solutions

Implications: Despite the fact that we still don't really understand what's happening, when we are trying to shed the body fat we have acquired in times of gluttony, the few novel insights we have gained from the study at hand should make it even more obvious that "classic" dieting does not hold the answer to the obesity problem. Neither on an individual, nor on a societal level. Instead of "eat less, exercise more", the main message should read: "Don't ever think of dieting, again! Revamp your life, your activity profile and the way you eat and wait for things to fall in place." After all, the "formerly obese kids" in the HF ↔ SC group were not too bad off, when they had returned to a (for rodents!) healthy diet in the 2nd cycle. We may even speculate that the difference the rodents in the control group (SC) would not have been significant anymore, if the scientists had kept the HF ↔ SC rodents on standard chow for another 8 weeks.

The same group is however living (now dead ;-) proof that the notion that you could diet today, look better tomorrow and then return to what has gotten you into misery before is not just illusive, but outright life-threatening. Since caloric restrictions, which are still at the heart of 99% of the mainstream diets, will probably magnify the amplitude (i.e. the up and down) of the yoyo effect and its negative metabolic consequences, it appears reasonable to assume that the yoyo-dieter will eventually be worse off than the "happy fatso" who has been eating whatever he wanted for all his life and dropped dead morbidly obese with a heart attack at 45. After all, it seems likely that he (or she!) will not even live to the 45th year before he falls victim to the very same fate and that after not despite, but rather because of all the temporary austerities... now, this may be like choosing between pest and cholera, and the third option, i.e. following the path of physical culture would alway be my first choice, but honestly, if I had to choose, I'd rather be the fatso who enjoyed his 45 years of pizza, pasta and chocolate pie than the frustrated yoyo dieter.

References

• Barbosa-da-Silva S, Fraulob-Aquino JC, Lopes JR, Mandarim-de-Lacerda CA, Aguila MB. Weight Cycling Enhances Adipose Tissue Inflammatory Responses in Male Mice. PLoS ONE 2013; 7(7): e39837.
• Cinti S, Mitchell G, Barbatelli G, Murano I, Ceresi E. Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans. J Lipid Res 2005; 46: 2347–2355.
• Hube F, Hauner H. The role of TNF-alpha in human adipose tissue: prevention of weight gain at the expense of insulin resistance? Horm Metab Res. 1999 Dec;31(12):626-31.
• Kim JH, Kim J, Park Y. trans-10,cis-12 Conjugated Linoleic Acid Enhances Endurance Capacity by Increasing Fatty Acid Oxidation and Reducing Glycogen Utilization in Mice. Lipids. 2013 Jul 11.
• Niesler CU, Siddle K, Prins JB. Human preadipocytes display a depot-specific susceptibility to apoptosis. Diabetes. 1998 Aug;47(8):1365-8.  
• Prins JB, Niesler CU, Winterford CM, Bright NA, Siddle K, O'Rahilly S, Walker NI, Cameron DP. Tumor necrosis factor-alpha induces apoptosis of human adipose cells. Diabetes. 1997 Dec;46(12):1939-44.
• Zhu. Ncb5or in Fatty Acid Desaturation and Metabolic Diseases. Zhu Diabetes Research Group. University of Kansas School of Health Professionals. < http://www.alliedhealth.kumc.edu/school/research/zhu/more_info.html > retrieved July 22, 2013

On Short Notice: Insanity vs. TurboFire - What's the Best HIIT Regimen? Plus: USA vs. China, Chews vs. Raisins, Epi-Sesamine vs. Body Fat, Exercise vs. Neurotoxins & More

Figure 1: The latest medal prognosis for Olympia 2013 by researchers at the Department of Economics at the Ruhr-Universität Bochum in Germany (Otten. 2013) - I must admit I am curious how accurate this prognosis will be... what's your take? The US or China? Who's going to take the lead?

The Queen has officially opened the Olympic Games 2013 and the games have their first doping case - those of you who followed yesterday's advice to subscribe to the SuppVersity Facebook page are already in the know... anyways, this is not the place for one of my hypocrisy rants, but for the weekly installment of "On Short Notice". Still, in the "honor" of the Olympics *rofl* and the spirit of the SuppVersity - which is, as you all know, the place you will get the news first! - I have compiled the TOP15 from the latest medal prognosis by Sebastian Otten, the chair of the Department of Economics at the Ruhr-Universität Bochum in Germany, for you as an appetizer (figure 1). Moreover, I picked more sports and less health, weight-loss, supplementation and nutrition related topics from my ever-growing collection of "On Short Notice" items, which is by the way already so exuberant that there will be another episode of this series either tomorrow or early next week, mostly because otherwise the latest news would come in late... so, let's go for it!

Insanity vs. TurboFire Interval - What's the optimal HIIT regimen?

As part of her recently published master thesis, Sarah A. McGlinchy investigated the differential effects two commercial fitness programs had on the heart rate pulmonary O2 uptake, CO2 output, caloric expenditure and substrate utilization during exercise and recovery, as well as the subjective satisfaction and physical exertion of trained individuals (N=15, four males and 11 females, aged 22.3 ± 1.6 years McGlinchy. 2013).

• 

  Image 1: Insanity (top) vs. Turbo Fire (bottom) - My HIIT workouts look profoundly different, but this does not mean that those workouts cannot be effective; specifically if you enjoy stuff like this and don't do it alone in front of your TV, but with friends & new friends at the gym. And trust me, I don't even need a study to be able to tell you that a workout you enjoy will be more productive than the "objectively" best workout you hate

  Insanity® Interval Training Protocol - A plyometric cardio circuit workout that is performed after a 9 min warum-up and followed by a 5 min stretch. It revolves around different drills (performed at progressively increasing intensity) that are separated by 30s water breaks, the drills last about 1 min each - the total length of the workout is 41 minutes and 35 seconds (click here to watch a promo video on YouTube)
• Turbo Fire® Interval Training Protocol - The HIIT 30 variety of a series of DVDs that comes from the same company that sells the P90X DVDs includes a 3 min warm-up, a 3 min cool down with stretching and slow movements to get the heart rate back to normal and a series of five drills of which the first four are repeated twice and the last one three times. Drills last about 1 min and are supposed to be performed with maximum effort each is followed by one minute of active recovery (walking, jogging in place, etc.). Water breaks are allowed during the active recovery. The total length of the workout is 30 minutes and 36 seconds (click here to watch a private workout video on YouTube).

I don't know about you, but based on the part of the videos I saw, before I felt I had seen enough, I would probably prefer the Insanity (Ins) over the Turbo Fire (TF) protocol; not so the study participants, though: After having performed both workouts in a randomized order, their "positive engagement" was slightly more pronounced after the TF protocol (see figure 2, left). It should however be mentioned that neither the the pre- to post- nor the inter-workout differences were statistically significant (with a total number of subjects of N=15, the difference could well have been 7/8, had the subjects been asked to pick one or the other).

Figure 2: Physical exhaustion, tranquility and pos. engagement after workouts (left), respiratory exchange ratio at rest and from min. 5-60 (middle), and time (in s) during the workout, when the heart rate was within the given percentages of the calculated personal HR_max(data adapted from McGlinchy. 2013)

My gut tells me that the part of the preference for the TurboFire (TF) protocol could be due to from a) the shorter overall duration and b) the greater exhaustion the subjects in experienced during the Insanity trial -I mean "insanity"? What else do you expect???

Ignore fatty acid oxidation and total calorie expenditure - pick the one you like!

The significantly less pronounced at the end of the TurboFire Intervals stand in contrast to the total the subjects were working out in the 81-90% HR_max, though. With 1000 seconds (vs. 580s) the latter was significantly longer during the Turbo Fire session. Accordingly, the subjects' respiratory exchange ratio (RER), a measure for the relation of glucose to fatty acid oxidation was significantly higher, as well.

SuppTensity Workout Perform 3 cycles of these 5 drills, each drill lasts 1 min, 45s active recovery  between drills, 2 min between cycles

• Squats*
• Push ups
• Lunges**
• Clean & press*
• Rope skipping

use adequately loaded *barbell or **dumbbell

While the former was to be expected, it may appear somewhat odd at first, though, is the higher and longer-lasting post-exercise energy expenditure in the Insanity group (p < 0.05), which could yet be explained by an overall slightly more demanding (figure 1, left > exhaustion) workout, which - and this is just based on what I saw in the videos - appears to have more "complete" drills - or did you see things like push-ups in the Turbo Fire workout? Against the background that the minimal differences in intra- and post-workout energy expenditure and substrate utilization won't have any noticeable effect on the desired outcome variable, i.e. a leaner, still muscular physique, and in view of the fact that"EPOC comprises only 6-15% of the net total oxygen cost of the exercise" (LaForgia. 2006), anyway, I would fully subscribe to Sarah McGlinchy's recommendation to simply pick the workout you like - based on McGlinchy's interpration of her subjects' feedback that would be the ...

• Turbo Fire® for people who are "looking for more variety of movements with fun music"
• Insanity® for people for whom "music isn’t a priority", but who look for "intense motivation"

Before I conclude this pretty longish and therefore single "on short notice" item with the implications and go ahead to the promised truckload of "on very short notice" items, I would yet like to add one thing to this recommendation: You don't actually need to buy a DVD to do HIIT. It's actually pretty straight forward to compile your own personal HIIT 1min on, 30s off (alternatively 1min active rest) workout by handcrafting your drills from from simple sprints on the grass or beach, intense rope skipping, push-ups, pull-ups, squats, kettlebell swings, stair climbers and everything else you can think of - if you are at a loss now, check out my botchy sample workout on the upper right - took me ~1min to put that together and I know that each one of you can do better!

Image 2: I am not saying everyone needs one of those workout DVDs, but for those of you (or friends of yours) who are not already fed up with "motivational pics + statements" like the one above, which are handed around on facebook like the WWF cards 20y ago on my schoolyard, it my be worth looking into either of these.

Implications: I don't care whether you like it or not (I don't like those workouts either), but I am 2x more inclined to believe the numerous success stories the producers of these workout DVDs use to plaster the Internet than any of the reports on how great supplement X is working for Mr. Y on bodybuilding.com and the like.

Do I suggest you buy a DVD or hop around like a jackass in the gym, let alone in front of your TV, when you prefer going to the next best park or beach doing sprints and combine those with your regular strength training program in the gym? Certainly not! Would I rather see you, your friends or family perform any of these workouts than doing exclusively strength training (let alone ultra low volume 1-rep max style) or hours of steady state aerobics if your goal is to get jacked? Abs(!)olutely ;-)

On very short notice

• 

  Image 3: Not everything that's golden is good - the "golden" raisins for example have been treated with sulfur dioxide, to prevent them from darkening. At least in susceptible persons SO2 can lead to serious allergic reactions, 4-8% of asthmatics are (also) allergic to dietary sulfites and its general safety is still a matter of constant debate - commonly associated health effects are Urticaria, angioedema, and IgE-mediated anaphylaxis (Rangan. 2009).

  Commercial carbohydrate chews not better than plain raisins - I guess this one falls into the "Olympia tribute" category, aside from Albanian weightlifters, wo obviously prefer Stanozolol, most of the athletes probably use carbohydrate supplements in one form or another. Whether anybody relies on resins as is intra-competition carbohydrate supplement is yet questionable and that despite the fact that the dried grapes can easily compete with the far more expensive Cliff blocks carbohydrate chews. Aside from nonsignificantly faster time-trial performances, the fourteen healthy competitive runners from the University of California who consumed raisins instead of chews, also felt slightly less sore after and had lower insulin levels and greater fatty acid oxidation rates during the run.
  Reason enough for Brandon W Too and his colleagues to conclude "that consuming a natural CHO source (raisins) [..] is well tolerated and maintains blood glucose levels and running performance similar to a commercial CHO product (sport chews)" (Too. 2013). Did you hear that Michael Phelps?
• Epi-sesamine from Lindera obtusiloba could be novel source for potent anti-obesity drug - This is at least what a recently published study that was conducted by scientists from the German Charité Universitätsklinikum in Berlin would suggest (Freise. 2013). In their in-vitro tests the active ingredient of the Japanese spice bush, which has traditionally been used for treatment of inflammation and the prevention of liver damage in Oriental Medicine, did not just prevent the accumulation of lipid droplets, it also activated the pro-apoptotic enzymes caspases-3/-7, which initiated programmed cell-death in the treated fat cells. In view of my recent blogpost on the nasty persistence of lower body fat, the latter could turn out to be of extreme importance - especially for those of you who have already lost a significant amount of body fat and are now suffering from "relative leptin deficiency" (see "Nasty Insights into the Yo-Yo-Effect" for more on how this relates to the YoYo-Effect and weight loss plateaus).

• 

  Figure 3: Mild exercise (5x 30 min / week, treadmill) boosts brain 5a- reductase and neurogenesis (Okamoto. 2013)

  Mild exercise and the brain: Is DHT what builds new neurons? If there was one hormone that really has gotten a bad rep over the past 50 years, it certainly is DHT: All of you who've read the respective installment of the Intermittent Thoughts (cf. "DHT - The All Things Male Hormone") or the latest news on the DHEA <> DHT muscle generation connection will be aware that the myth of the dangerous, carcinogenic bigger brother of testosterone is at least overtly simplistic if not totally devoid any scientific bases.
  Recently published data from the Laboratory of Exercise Biochemistry and Neuroendocrinology at the University of Tsukuba, in Japan does now add another piece to the "DHT is not bad" puzzle - one even women could come to appreciate (Okamoto. 2013): According to Masahiro Okamoto and colleagues, the exercise induced increase in 5-alpha reductase activity (5-ar converts testosterone to dihydrotestosterone) and the subsequent rise in neuronal DHT appears to be the driving force of neurogenesis (the generation of new neuronal networks / brain tissue and wiring).

• 

  Image 4: Those of you who have made the transition to physical culture too late or have friends or relatives who missed the boat completely may be interested to hear that researchers from the RIKEN Center for Developmental Biology successfully used stem cells to replete Purkinje neurons two years ago, already (Maguruma. 2010)

  Chronic exercise renders Purkinje neurons bullet proof - In a way unquestionably related to the previous "On Very Short Notice" item are the findings from Huang et al. have just published in Journal of Applied Physiology. In their paper the researchers describe the 8-weeks of moderate treadmill running had on the toxin resistance of 6-week old rodents. Specifically, Huang et al. observed that the "exercised rats not only performed better in the rotarod task [skilled behavior test, see video] but also showed finer Purkinje cell structure (higher dendritic volume and spine density)" (Huang. 2013). And while this is unquestionably reminiscent of the aforementioned neuron-building effects of DHT (which is, as you should know increased with aerobic / volume training; cf. "Intermittent Thoughts on DHT"), the big news is that the neurons of the exercised rodents were also protected against the immunotoxin OX7-saporin.
  If these results translate (I personally believe that this is not a question of yes or no, but only one of the extend to which these results translate) to any of the bazillion other toxins we are exposed to on a daily basis, this would imply that regular exercise may not just protect us from the "classic" neurodegenerative diseases such as Alzheimer's or Parkinson, but also from autoimmune diseases which have a neuronal component and often involve damage to the very Purkinje neurons the researchers found to be "bullet proof" in the study at hand.
• Children of diabetic parents benefit most from hitting the weights - "The offspring" of type II diabetics that's the somewhat surprising result of a 9-week training + 9-week detraining experiment Katherine Schofield and her colleagues from New Zealand and Denmark conducted respond particularly favorable to resistance training programs (Schofield. 2013). At the end of the initial 9 week training period, the insulin response of the children with diabetic parents was still worse than thatof their peers in the control group, but with improvements of roughly 30% they were already approaching what you may call the "normal zone", when the detraining phase begun. Contrary to the kids in the control group, whose insulin sensitivity did not change over the 9 weeks of laziness, the children of type II diabetics lost all their previously achieved improvements. Now, you could certainly argue how those poor kids are at such a disadvantage, but unless you want to feed them metformin for the rest of their lives, I suggest we should rather think of ways to teach them how to resist the bad eating habits of their parents and stick to a workout routine that will make the diabetes medication obsolete - don't you agree?

• 

  Suggested reads for everyone interested in some background info on nitrates: (1) Ask Dr. Andro: Is Creatine Nitrate Worth it? (2) Nitrates Work! First NO2 Victim in ER

  Nitrate supplements don't work for athletes and could mess with blood pressure regulation - At least if you are a trained athlete who wants to improve his/her performance, the use of sodium nitrate is a waste of time and money - this is at least what the soon to be published results of a randomized, double-blind cross-over study by Spanish scientists would suggest. For their experiment, Bescós et al. recruited 13 trained athletes and had them perform a 40-min ergometer distance-trial test after a 3-day supplementation regimen with either sodium nitrate (10mg/kg body weight) or placebo (Bescós. 2013).
  Contrary to earlier trials in non-trained subjects, the athletes' performance did not benefit from the supplemental nitrate - despite statistically significant increases in plasma nitrate (+17%) and nitrite (+56%), by the way. Moreover, the concommitant increase in endothelin-1, a protein that constricts blood vessels, raises blood pressure and thus counters the vasodilating effects of the nitrates raises concerns regarding potential side effects that could occur once you drop the supplement.

• 

  Image 5: Mineral supplements are usually not necessary, as long as you pick the right foods and drinks! What's much more likely in the Western hemisphere than deficiencies, though, are imbalances - and weekend warriors and gymbros are even more likely than your average obese pre-diabetic to run into oftentimes self-inflicted problems... there is going to be a Super Human University seminar Carl Lanore and I are currently working on - and let me tell you this, this is a topic that is literally very dear to Carl's heart.

  Decrease your risk of heart disease by 5% with each mg/L of Magnesium in your drinking water! - I am certainly not among the magnesium enthusiast who propose supplementation with whichever form of oral mg supplement (let alone the scientifically hitherto not verified use of oils) as the latest panacea, but as you may have heard on Super Human Radio on Wednesday, July 25, 2013 (click here for the podcast), I do believe in the overlooked importance of getting your ratios straight; and that, i.e. having the right ratio of Ca:Mg begins at the most fundamental level - with the mineral ratios in your drinking water! Finish scientists who recorded the mineral intake of 14,495 male subjects (aged 35-74), for example, found that with a constant and roughly two times too high mean Ca / Mg ratio of 5.39 / 1 in the drinking water of the area, every additional milligram of magnesium per liter drinking water (e.g. from 2.61mg/L to 3.61mg/L), would help to reduce the risk of acute myocardial infarction by 4.9% (Kousa. 2006)!
  This is an impressive figure and yet, the real beauty of this study is that it emphasizes the need to re-evaluate your nutritional mineral intake, instead / before considering using dietary (let alone oily ;-) supplements!

References:

• Bescós R, Ferrer-Roca V, Galilea PA, Roig A, Drobnic F, Sureda A, Martorell M, Cordova A, Tur JA, Pons A. Sodium Nitrate Supplementation Does Not Enhance Performance of Endurance Athletes. Med Sci Sports Exerc. 2013 Jul 17.
• Freise C, Trowitzsch-Kienast W, Erben U, Seehofer D, Kim KY, Zeitz M, Ruehl M, Somasundaram R. (+)-Episesamin inhibits adipogenesis and exerts anti-inflammatory effects in 3T3-L1 (pre)adipocytes by sustained Wnt signaling, down-regulation of PPARγ and induction of iNOS. J Nutr Biochem. 2013 Jul 18.
• Huang TY, Lin LS, Cho KC, Chen SJ, Kuo YM, Yu L, Wu FS, Chuang JI, Chen HI, Jen CJ. Chronic treadmill exercise in rats delicately alters the Purkinje cell structure to improve motor performance and toxin-resistance in the cerebellum. J Appl Physiol. 2013 Jul 26.
• Kousa A, Havulinna AS, Moltchanova E, Taskinen O, Nikkarinen M, Eriksson J, Karvonen M. Calcium:magnesium ratio in local groundwater and incidence of acute myocardial infarction among males in rural Finland. Environ Health Perspect. 2006 May;114(5):730-4.
• LaForgia J, Withers RT, Gore CJ. Effects of exercise intensity and duration on the excess post-exercise oxygen consumption. J Sports Sci. 2006 Dec;24(12):1247-64.
• Muguruma K, Nishiyama A, Ono Y, Miyawaki H, Mizuhara E, Hori S, Kakizuka A, Obata K, Yanagawa Y, Hirano T, Sasai Y. Ontogeny-recapitulating generation and tissue integration of ES cell-derived Purkinje cells. Nat Neurosci. 2010 Oct;13(10):1171-80.
• McGlinchy SA. The Effect of Two High Intensity Interval Training Protocols on Heart Rate, Caloric Expenditure, and Substrate Utilization During Exercise and Recovery. University of Toledo - Submitted to the Graduate Faculty as partial fulfillment of the requirements for The Master of Science Degree in Exercise Science. 2013.
• Okamoto M, Hojo Y, Inoue K, Matsui T, Kawato S, McEwen BS, Soya H. Mild exercise increases dihydrotestosterone in hippocampus providing evidence for androgenic mediation of neurogenesis. Proc Natl Acad Sci U S A. 2013 Jul 17.
• Schofield KL, Rehrer NJ, Perry TL, Ross A, Andersen JL, Osborne H. Insulin and Fiber Type in Offspring of T2DM with Resistance Training and Detraining. Med Sci Sports Exerc. 2013 Jul 17.
• Rangan C, Barceloux DG. Food additives and sensitivities. Dis Mon. 2009 May;55(5):292-311.
• Too BW, Cicai S, Hockett KR, Applegate E, Davis BA, Casazza GA. Natural versus Commercial Carbohydrate Supplementation and Endurance Running Performance. J Int Soc Sports Nutr. 2013 Jun 15;9(1):27.

Fiber Up Your Foods, Omega-3 Preload For Female Fat Loss, 50+ Ways to Treat Constipation, Serotonergic Peptides in Milk, Weight Cycling & Reduced Metabolic Rates, Exercise & 102% Weight Loss From Fat - Plus: More Short News

Inulin enriched foods are good for your gut, your waistline and your pancreas (anti-diabesity effect) and what's more inulin is also on the list of anti-constipation agents,

100g that's this week's SuppVersity figure of the week and that despite the fact that it is the amount of fat you are going to gain within one year when your metabolic rate is 100kcal below where it should be (Piaggi. 2013)... Where it should be? Yeah, ok I know that's idiotic, but if you read today's news-item about the down-regulation of the metabolic rate due to YoYo-dieting the picture that emerges is that of yet another vicious cycle that leads directly into a weight spiral that knows but one direction: upwards!

Another one of today's news-items does however hint at a solution: Just lose 102% fat! What? I see I got you interested. So what are you waiting for? Lot's of good stuff today. So much in fact that let's spend no time and get right to the news-business ;-)

"Fiber up" you foods with prebiotics (inulin in particular)

Pretty obvious that these Spanish Christmas confections take a toll on your HbA1c ;-)

(Capriles. 2013; Garcia-Garcia. 2013) -- You've read about the benefits of "feeding the good guys" a couple of days ago. Now, aside from being a substrate for the purportedly beneficial gut bacteria fiber also changes the feel, taste and most importantly digestive properties of foods. A couple of recently published studies confirm that this can have pretty profound and in most cases highly desirable consequences.

Garcia-Garcia, for example, added some inulin (5%) to Turon, a traditional Spanish sweet treat that's made of toasted almonds, honey and sugar and fed 30g of the Christmas nougat-type confection to 32 healthy, normal-weight volunteers.

While the subjects in the "regular" Turon group had a slight but significant increase in HbA1c (long-term measure of blood glucose management) the blood glucose management of the 17 subjects in the active group did not budge. And while most subjects (64%, specifically those who conumed Turon as a Christmas snack on a regular basis) preferred the "classic" variety, at least 24% did actually like the inulin Turon better (Garcia-Garcia. 2013)

Gluten will interact with PPARs & gut bacteria and can thus precipitate insulin resistance (read more).

In a similar study, scientists were able to show that the addition of prebiotic inulin-type fructans to gluten-free bread (4 g of fructans per 50 g bread serving size) did

"[...] provide structure and gas retention during baking, thus improving GFB quality by yielding better specific volume, softer crumb, improved crust and crumb browning with enhanced sensory acceptance" (Capriles. 2013)

 and decreased the glycemic index and glycemic load of the gluten-free bread by 34% (from 71 to 48) and 33% (from 12 to 8), respectively.

Omega-3 loading improves weight loss in obese women

(Munro. 2013) -- According to a recently published study, a 4-week preload with 6 × 1 g capsules per day LC ω-3PUFA (fish oil) each comprising 70 mg EPA and 270 mg DHA, increased the amount of weight the female (and only the female!) participants of a very low calorie weight loss intervention lost in the subsequent 8-weeks.

Despite being statistically significant, the 1.4% increase in bod weight loss is yet not so pronounced that anyone whose been dieint with LC-PUFA preload in the past should now be fretting about having missed out on this great chance of getting ripped. If you are a man, the protocol would have been useless, anyways.

Constipated? Review offers three types of "solutions" - in some cases a literal sense

(Gelinas. 2013) -- If you are one out of five, chances are you belong to the 20% of the world's population who suffer from constipation on a regular base. If that's the case, you may want to consider one of the following "treatment" strategies, Pierre Galinas mentions in his latest review of the literature:

• 

  Table 1: Relative laxative potential of 50 food ingredients for the prevention of constipation

  Bulking agents  - They soften the stool by binding water; examples are psyllium seed husk, wheat bran, methylcellulose, calcium polycarbophil; are considered "mild" and are not habit forming, but may cause abdominal pain and bloating because of gas formation
• Osmotic agents - They also soften the stool but ba a dfferent mechanism than the bulk fiber, they create an osmotic gradient, which will distend the intestines and stimulates a contractile response; examples are lactulose, sorbitol, mannitol, polyethylene glycol (PEG), magnesium hydroxide (milk of magnesia), sodium phosphate; side effects are gas, and the offensive taste (of some)
• Softeners and lubricants  - They  lubricate (oil) and soften (detergent) the stool; examples are sodium docusate and various mineral oils; pretty milk
• Stimulants - Just like the stims in a fat burner get you going, these get your colon going; examples are epson salts (magnesium sulphate heptahydrate), bisacodyl, sodium picosulphate, sodium sulphate, magnesium oxide, phenolphthalein; they taste offensive, but don't produce gas
• Herbal teas - Provide water and can increase bowel frequency; examples are anthracenes derivatives (senna; aloe; cascara, Frangula bark); unfortunately they taste offensive and work almost immediately; moreover tolerance builds up pretty fast

As you can see there are different ways to get going with the bulk agent aka an increase in fiber intake being the only healthy long-term solution.

Even unhappy cows produce "Happy Milk"

"Mutant Milk" is homogenized milk a potential threat to your health (learn more)?

(Nongonierma. 2013) -- Three days ago a paper by Alice Nongonierma and her colleagues was published ahead of print on the website of the Journal of Food & Function. In the said paper, the researchers describe an experiment, in the course of which they were able to proof that hydrolyzed milk proteins contain a peptides that "behave as serotonin 2C (5-HT2c) receptor agonists" (Nongenierma. 2013). According to the scientists, the bioactive peptides have a relatively low molecular mass (< 1 kDa) and are hydrophobic in nature. With the 5-HT2c receptor being more than just a pharmacological target for the treatment of depression and anxiety, but also a trigger of neurogenesis (growth of new neurons) in the hippocampus (Millan. 2005), this certainly is good news for all the milk junkies out there - or could the serotonine-like effects make you fat?

Magic anti-diabetic mushrooms

(Su. 2013) -- Not what you are thinking now, folks! That's Traditional Chinese Medicine. After all, mushrooms such as Coriolus versicolor and Grifola frondosa have been used in TCM for centuries now. As a recent study by Scientsts from Kang Jien BioTech confirms rightly, so. Extracts from both mushroom had potent inhibitory effects on the carbohydrate digesting enzymes α-amylase and α-glucosidase. With Coriolus being a better inhibitor of the former and Grifola a more potent inhibitor of the latter enzymes.

How this relates to glucose control? Easy: If you don't disentangle the complex carbs your body cannot access their sugar content and if you do it only very slowly even "high" GI starches suddenly turn into low GI foods.

Weight cycling does not forestall future weight loss, but it makes it harder

Geoffrey Cannon's "Dieting Makes You Fat" was first published in 1983 but is that true? Does dieting always make you fatter and would it be better so simply surrender   (learn more)?

(Bosy-Westphal. 2013) -- While the ups and downs in body weight so many dieters are experiencing on a regular basis do not, as it was long suspected, ruin your body composition. A paper that has been published roughly a week ago in the International Journal of Obesitysuggests that another often touted downside, namely the long-term creeping down-regulation of the basal energy expenditure is unfortunately very real.

According to the analysis of the researchers from the Christian-Albrecht University in Kiel, Germany, the 27 "weight regainers" (after ~30% of loss) showed a reduced REE adjusted for changes in organ and tissue masses after weight loss that was not present in the 20 previously weight stable, yet likewise overweight / obese subjects in the control group of the researchers' 13-week dietary intervention study.

It is however not sure, whether this actually is a result of previous weight cycling or vice versa; meaning that the people with the ups and downs in body weight are the ones whose metabolism shuts down the easiest. The study at hand was obviously not able to exclude this possibility.

More than 100% weight loss from fat? How is that supposed to work?

(Hall. 2013) -- Actually this study was published late in the year 2013, that it still made it to On Short Notice has two reasons. Reason #1 is that it was an Epub way ahead of print. Reason #2 is that the figures the author reports appear to be pretty nonsensical. I mean how on earth can the projection K.. Hall from the National Institute of Health in Bethesda made based on data from the Biggest Loser camp yield a net weight loss of 24kg of which more than 100% (102% to be precise) came from the exuberant body fat stores of the (>70kg for the average participant) of the "big losers"?

For the researchers who worked with the Biggest Losers the highly successful TV show was a fluke. Having a TV station pay for their "research" certainly is something extraordinary and against and the study at hand is only the latest publication based on data from the Biggest Loser camp (read up on a previous news item)

The answer is actually pretty straight forward and underlines the efficacy of exercise as a weight loss tool that won't leave you skinny fat, but lean and more muscular. After all, the initially counter-intuitive +2% extra came from the increase in lean mass the Big Losers experienced despite being on a 1,300kcal-1,600kcal diet and working out at a "vigorous intensity" for 3.1h and 1.1h per day in phase 1 and phase 2 of the boot-camp intervention (the simulation of a diet only intervention yielded a slightly larger total weight loss yet with only 65% of the weight coming from the fat stores).

The one thing I am a bit skeptical about is whether Hall's prediction that the weight loss will be sustainable with no more than 20min/day of, once again, "vigorous" exercise per day. I mean that probably would be true in the sheltered environment of the weight loss camp. In a real life scenario, on the other hand, the super size menus, family pizzas and cosy TV couches are probably too much of a temptation for the many of the Big Losers.

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Wine was yesterday! Chocolate liqueur is the future of healthy alcohol consumption (learn more)

That's all for today, at least as far as On Short Notice is concerned. By now the majority of you should yet be aware that there's always more... correct, the Facebook News - not sure if you notices, but you can actually see the latest items in the side-bar of the SuppVersity. To make sure you don't miss any of them it would yet be wise to simply "like" the SuppVersity on Facebook and/or register as a follower to my Twitter Account. It's hard-wired to the Facebook page, so if you are into tweeting.. maybe you prefer being notified this way.

Whatever your social media service provide of choice may be, I am pretty sure that you don't want to miss news such as the one on the total phenols, flavonoids, flavan-3-ols and proanthocyanidins of chocolate liqueur and how this may make it a better choice for your daily dose of "healthy" alcohol than wine ;-)

References:

• Carpiles VD, Aréas JADG. Effects of prebiotic inulin-type fructans on structure, quality, sensory acceptance and glycemic response of gluten-free breads. Food & Function. 03 Oct 2013 [Epub] 
• Garcia-Garcia E., Narbona E, Carbonell-Barrachina AA, Sanchez-Soriano J, Roche E. The effect of consumption of inulin-enriched Turrón upon blood serum lipids over a 5-week period. International Journal of Food Science & Technology. 2013; 48(2):405–411.
• Gelinas P. Preventing constipation: a review of the laxative potential of food ingredients. International Journal of Food Science & Technology. 2013; 48(3):445–467. 
• Hall KD. Diet versus exercise in "The Biggest Loser" weight loss competition. Obesity (Silver Spring). 2013 Oct 3. doi: 10.1002/oby.20065. [Epub ahead of print]
• Lai MN, Ng LT. Inhibitory effects of medicinal mushrooms on α-amylase and α-glucosidase – enzymes related to hyperglycemia. Food & Function. 2013 [Epub ahead of print].
  
• Millan MJ. Serotonin 5-HT2C receptors as a target for the treatment of depressive and anxious states: focus on novel therapeutic strategies. Therapie. 2005 Sep-Oct;60(5):441-60.
• Munro IA, Garg ML. Prior supplementation with long chain omega-3 polyunsaturated fatty acids promotes weight loss in obese adults: a double-blinded randomised controlled trial. Food & Function. February 2013 [Epub ahead of print].
• Nongonierma A,  Schellekens H, Dinan T,  Cryan JF, Fitzgerald D. Milk protein hydrolysates activate 5-HT2c serotonin receptors: influence of the starting substrate and isolation of bioactive fractions. Food & Function. 2013 [Epub ahead of print]
• Piaggi P, Thearle MS, Bogardus C, Krakoff J. Lower Energy Expenditure Predicts Long-Term Increases in Weight and Fat Mass. JCEM. 2013; jc.2013-3529;