High Energy Flux, A New Determinant of Successful Weight Loss? Eat More, Train More, Lose More? Increased Resting Metabolic Rate & Satiety, Decreased Hunger While Dieting!

Always hungry? Can't lose weight? "Train more and eat more" (not less!) could be the solution.

A recent thesis from Rebecca Foright, highlights that a high energy flux state characterized by high daily energy expenditure (resulting from increased physical activity) with matching high energy intake (high calorie throughput) may attenuate the weight loss-induced energy gap by reducing hunger and ameliorate the otherwise diet-related reduction in resting metabolic rate.

Foright recruited recruited eleven obese study participants from the Colorado State University community and surrounding areas to test her "exercise more, eat more, lose more (easily)" hypothesis.

The enrollment criteria included: BMI between 30-43 kg/m², age 18-55 years, weight stable over the prior 12 months, desire to lose weight, and ability to exercise as assessed by electrocardiogram (ECG), resting blood pressure and a normal incremental exercise test to exhaustion with simultaneous ECG. Exclusionary criteria included: pregnancy or breastfeeding, smoking, use of medication known to affect appetite or metabolism (including but not limited to antidepressants and statins), or prior surgery for weight loss. In short, most of the participants were what we today call "healthy obese."
"The approach used in this study was a within-subjects cross-over experimental design to test the effect of high and low flux states following weight loss on resting metabolic rate and perceptions of hunger and satiety."

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The study protocol was divided into four distinct phases: (1) baseline testing phase prior to weight loss; (2) weight loss phase induced by a hypocaloric diet over the course of several months; (3) weight maintenance phase in which subjects were maintained at the reduced weight for 3 weeks; and (4) experimental phase in which measures were obtained of subjects’ resting metabolic rates, fasting and post-prandial perceived hunger and satiety, fasting and post-prandial circulating glucose, insulin, and PYY concentrations, and ad libitum food intake on the 5th day following low flux and high flux phase conditions, respectively, completed in random order with a three-day washout period in between (see Figure 1).

Figure 1: Experimental Timeline | #Order of Low Flux and High Flux were randomly assigned (Foright. 2014).

During the low flux condition subjects remained sedentary for four consecutive days. All food was provided so that energy intakes were adjusted to maintain energy balance.

• resting metabolic rate (RMR) measurements on day 1-4 of the low flux phase
• caloric intake was adjusted according to RMR everyday
• subjects were fed standardized meals with a macro composition of 50/35/15 (carbohydrate/fat/protein) and an energy intake that was 1.3x the RMR
• subjects had to refrain from physical activity (>3,000 steps per day)
• at the end of day 5 the subjects completed a hunger/satiety questionnaire used to assess general feelings of hunger/satiety over the prior four days of the low flux condition

During the high flux condition subjects exercised on four consecutive days (approximately 500 net exercise kcal expenditure at 60% V02 max) and were fed additional food necessary to maintain energy balance.

• resting metabolic rate (RMR) measurements on day 1-4 of the low flux phase
• caloric intake was adjusted according to RMR everyday
• subjects were fed standardized meals with a macro composition of 50/35/15 (carbohydrate/fat/protein) and an energy intake that was 1.7x the RMR
• subjects were given pedometers and had to achieve at least 7,500 steps per day
• subjects exercised at 60% of their VO2max to burn 500kcal
• at the end of day 5 the subjects completed a hunger/satiety questionnaire used to assess general feelings of hunger/satiety over the prior four days of the low flux condition

Overall, a testing week consisted of two baseline days and 5 high/low energy flux days. In that, three identical experimental days were used to examine possible differences in perceptions of hunger and satiety, blood glucose, insulin, and PYY in response to breakfast preload, and ad libitum intake from a meal buffet.

Note: The caloric deficit that was designed to produce a 7% weight loss over the course of the 12-16 week long weight loss phase was identical in the undulating high and low energy flux phases of the study. The results are thus not a consequence of the increase in energy intake during the high flux phase (in fact the opposite was the case in some subjects, anway). The extra calories were after all burned again during the four exercise days.

"Now what is particularly interesting about the study is that the researchers did not content themselves with measuring the acute effects of high vs. low energy fluxes. They also investigated what happened after the 12-16 week weight loss phase.

To minimize the acute effects attributable to the dynamic phase of weight loss on metabolic rate and on hunger and circulating appetitive hormone concentrations, subjects were maintained at the seven percent lower body weight for a three-week period prior to the start of the low and high flux conditions. During these three weeks subjects reported to the KANC every three days to monitor weight and minimize weight fluctuations. Subjects were instructed to consume a slightly increased kcalorie intake compared to the weight loss phase to maintain weight" (Foright. 2014).

Put simply, the scientists wanted to know, whether the effects of high vs. low energy flux dieting would influence a dieters ability to lose weight and maintain the newly achieved weight.

Figure 2: Weight loss and energy flux where exactly as the scientists had planned (Foright. 2014)

As you can see, the average weight loss was almost identical to the targeted 7% (de facto "only" 6.9%). Similarly,

[...a]s designed, the energy intake for high flux (x±SD: 3,191±587 kcal/d) was significantly greater (p < 0.001) than for low flux (x±SD: 2,449±406 kcal/d) (Figure 2, right). In accord with the study design, there was no difference in macronutrient composition between the two conditions (data not shown)" (Foright. 2014).

Now all that would be pointless if both groups lost weight similarly effortlessly. In reality, though, On the subjects were significantly more hungry and felt less satiated at the end of each of the days during low flux.

Figure 3: As you see, the mean difference was already huge. It was more than huge in in
the subject who saw the greatest benefit (Foright. 2014).

On the other hand, they were significantly more full at the end of each of the days during high flux (p=0.015). There was a strong trend for the subjects to exhibit greater hunger throughout the day during low compared to high flux (p=0.09).

RMR increases sign. in trained but not untrained subjects in a high energy flux state - no training, no difference between the two groups - the energy balance was identical in both conditions (Bullough. 1995)

No, this is not an outlier study: In 1995 Bullough et al. were already able to show that the resting metabolic rate on diet + exercise regimen that established an identical energy balance was greater in trained than in untrained subjects only when trained subjects were in HF. As Bullough et al. point out "[t]hese data indicate that RMR is influenced by exercise, energy intake, and their interaction and suggest that higher RMR in trained vs untrained individuals results from acute effects of HF rather than from a chronic adaptation to exercise training." (Bullough. 1995) Bell et al. on the other hand found that "[m]aintenance of high energy flux via regular exercise may be an effective strategy for maintaining energy expenditure and preventing age-associated obesity" (Bell. 2013).

And Goran et al. (1994) found that "RMR can be elevated during a state of energy balance when energy flux is increased," and that the "magnitude of adaptive change in RMR is similar in response to increased EI [energy intake] and/or PA [physical activity]." 

Figure 4: The subject who saw the greatest satiety benefit in the high flux phase was also the one that consumed the most energy on the low flux condition - even more than on the high flux condition (Foright. 2014)

Interestingly, the subject who saw the largest benefit (see Figure 3) was also the guy or gal who consumed the most energy in the low flux condition (orange line in Figure 4).

So what about the health markers?

The  fasting insulin decreased following weight loss and was significantly lower on the LF (8.3±1.1 µU/ml) and HF (6.4±0.8 µU/ml) experimental days compared to the pre-weight loss baseline (11.8±0.6 µU/ml). In other words, while both groups saw significant increases in insulin sensitivity due to dieting, the effects were (unsurprisingly) significantly more pronounced during the high energy flux (=exercise phase).

In contrast to what the significant differences in hunger ratings would suggest, there were no general differences in fasting PYY (the satiety hormone) concentrations among pre-weight loss, low and high flux conditions respectively.

Figure 5: Insulin and PYY levels of the subjects in the high and low flux phases over the course of the day (2014).

If you look at the data in Figure 5, it's obvious that the PYY levels were in fact lower in the high flux condition - from 180-360 minutes in the high flux condition compared to the baseline (pre-weight loss) and low flux, to be precise.

Figure 6: Average resting metabolic rate at baseline and across 5 days of low and high flux (Foright. 2014)

So what? Beneficial, not beneficial, or not sure? In spite of the absence of significant differences in PYY, the post-diet response of the subjects clearly indicates that the energy deficit was easier to tolerate in the high flux phases.

The slightly, but significantly higher resting metabolic rate during the high flux phases further underlines that there is a benefit of eating more and training more and the absence of corresponding evidence from any of the hormonal markers measured may simply be related to a "bad" choice of markers. If the researchers had determined the level of the hunger hormone ghrelin, instes, it may well have been that we would have had a physiological explanation for the "hunger difference".

The way it is, we still have the decreased subjective hunger, increased subjective satiety and increased RMR which speak in favor of the high flux state dieting. What we do not know, though, is whether the effects will be the same in athletic (vs. sedentary) subjects [based on my personal experience we will!] and whether they can be maintained for say 4 weeks instead of four days | Comment on Facebook!

References:

• Bell, Christopher, et al. "High energy flux mediates the tonically augmented β-adrenergic support of resting metabolic rate in habitually exercising older adults." The Journal of Clinical Endocrinology & Metabolism 89.7 (2004): 3573-3578.
• Bullough, Richard C., et al. "Interaction of acute changes in exercise energy expenditure and energy intake on resting metabolic rate." The American journal of clinical nutrition 61.3 (1995): 473-481.
• Foright, Rebecca. A high energy flux state attenuates the weight loss-induced energy gap by acutely decreasing hunger and increasing satiety and resting metabolic rate. Diss. Colorado State University, 2014.
• Goran, Miachel I., et al. "Effects of increased energy intake and/or physical activity on energy expenditure in young healthy men." Journal of Applied Physiology 77.1 (1994): 366-372.
• Rarick, Kevin R., et al. "Energy flux, more so than energy balance, protein intake, or fitness level, influences insulin-like growth factor-I system responses during 7 days of increased physical activity." Journal of Applied Physiology 103.5 (2007): 1613-1621.

Health & Exercise Quickie: Vitamin D Deficiency, Taurine & Glycine. Multiple Sclerosis & Epstein-Barr. Paracetamol & Muscle Gains. Gender & Fatigue from Workouts. HIIT, LISS & Appetite. Plus: Scientists Debate: Light vs. Heavy Weights

While there is a positive trend in the percentage of US adults who meet the 2008 federal physical activity guidelines according to which they have to "devote at least 150 minutes/week to moderate, or 75 minutes/week to vigorous intensity exercise, or an equivalent combination", the number of people who have gotten the message that a combination of both strength and aerobic training (red line) is much more efficient than doing just aerobics (blue line) remains the same (CDC. 2012)

48%! That's the SuppVersity figure of the week and the percentage of US adults aged 18 and over who met the 2008 federal physical activity guidelines for aerobic activity in 2012 - that's 5% more than in 1997. It would be better to see it up in the 75%+ region, but it's nice to see that more and more people are devoting at least 150min/week to moderate intensity exercise, or 75 minutes/week to vigorous intensity exercise, or an equivalent combination.

What's not so nice is that people are still way too focused on aerobics and the number of US citizens that's combining resistance and aerobic training to reach their exercise goals is stagnating below 20%. Moreover, best-agers and baby boomers, who would probably benefit even more from some weight lifting than the 36% of the young men (age 18-24) who make up the lion's share of the 'real' physical culturists who know about the importance of both, 'weights' and 'cardio', are - if they work out at all - still sticking to the tried and disproven LISS only regimen.

On Short Notice, today: A Health & Exercise Quickie

Apropos "LISS" as the headline of today's On Short Notice news quickie already gave away, light intensity steady state aerobic training aka LISS is one of the exercise related topics today. We will however start out with the health related news... and don't wonder that the first post is about polar bear health. I promise you will be intrigued, when you've read it ;-)

• 'Westernized' polar bears' bones look as if they would need vitamin D supplements, in reality all they are probably missing is sufficient taurine in their diet. I don't know but maybe you've asked yourself before: "How on earth can a white bear survive in the Arctic, when his nose is the only part of his skin that's exposed to the sun and would thus be able to produce vitamin?" (Please mind that this is not a serious question ;-) He eats his vitamin D!
  
  

  

  Scientists speculate: Their cousins in captivity suffer from rickets and fractures due to secondary vitamin D deficiency in consequence of insufficient taurine intake.

  Ok, first question first answer, but what about question #2: "How come that the clubs of his brethren and cousins in captivity get rickets and fractures as if they were vitamin D deficient, although they get the exact same amount of vitamin D from mother's milk and their later diet (sometimes the latter is even supplemented) as their wild counterparts?" Answer? No idea? Well, if you ask the researchers from the The University of Tennessee Health Science Center the answer is (Cheesney. 2009): A lack of taurine in the diet.
  
  Taurine plays a fundamentally important role in the conjugation of ursodeoxycholic acid to TUDCA and facilitates the uptake of fatty acids and fat soluble vitamins. With insufficient taurine in the diet polar beers (and human beings) can probably drink as much vitamin D in olive oil or whatever other fat base they deem more appropriate then dry tabs without any effects on their 25-OHD => calcitonin levels and consequently bone health (suggested read "Fat D-Ficiency! Study Shows, Even 50.000 IU of Vitamin D3 Useless, When You Ingest It Without Fat").
  
  Moreover, a recent guinea pig study from Department of Internal Medicine at the Medical College of the National Cheng Kung University suggests that glycine could be another 'pro vitamin D amino acid' due to its beneficial effect on the liver and subsequent protection of disturbances in vitamin D metabolism and low 25-OHD levels (Chen. 2008) - now, what if any of these, i.e. taurine or glycine, or simply insufficient bile acid, which incidentally depends on the consumption of the "bad, bad" cholesterol (cf. Kern. 1994), is the actual reason of the rampant vitamin D deficiency in our meat-, fat- and cholesterol-o-phobic societies?
• "Low vitamin D and remote EBV infection may be associated with clinical MS breakthrough within 2-3 years." (Décard. 2012) Usually I don't simply copy the study titles, but this one says it all. Even before the first symptoms of multiple sclerosis occur, i.e. in the so-called pre-CIS (=clinically isolated syndrome) interval, patients with quiescent multiple sclerosis have 50% lower 25OHD levels than their healthy peers and - what could actually be the causal factor, here - three times higher Epstein-Barr specific IgG levels (EBNA1). Can these observations a group of scientists from the Department of Neurology at the St. Josef-Hospital of the Ruhr-University Bochum in Bochum, German, really be mere coincidence?
  
  

  

  Figure 1: While it would be best never to be infected with Epstein-Barr your risk of EP-related MS is more than twice as high if you are exposed late (Ascherio. 2010)

  At least as far as the Epstein-Barr relation goes the answer of a 2010 review of the literature would be 'no, probably no coincidence' (Ascherio. 2010). It appears to be established that Epstein-Barr (EB) plays a pivotal role in the etiology of MS. Based on the observation that people without EB are virtually MS free, and the fact that their own previous research has clearly shown that late infections with EP increase your risk to develop MS by more than 2x (compared to people who have been exposed in childhood; see figure 1), Ascherio et al. argue that it is very unlikely that EP is not at least the trigger, if not the ultimate cause of MS.
  
  The scientists also refer to the hygiene hypothesis which has been advanced by other authors before, unfortunately, however, getting rid of the 'cleanliness' and exposing your immune system to the training it needs by exposing yourself to the virus at an earlier age, is of little use, if not totally stupid. After all it would only reduce your risk to develop MS to a level that's still more than 1,000% higher than in people who have never been exposed to the virus in the first place (see figure 1).
  
  Due to the inconclusive data on the long and short term effects of Epstein-Barr infections on the B-cell and T lymphocyte response, the Ascherio et al. are not yet sure about the exact mechanism by which EP stimulates, triggers or drives the development of MS. All that can be said with relative certainty is that Epstein-Bar infections contribute to the increase in multiple sclerosis. Aside from the previously mentioned correlations the mere fact that those regions of the world where Epstein-Barr is quasi non-existent are virtually MS free is probably the best evidence of its involvement in autoimmune attacks on your brain. So if you want to protect yourself you better make sure you don't get infected!  Since EP is part of the herpes family and transmitted via saliva this is unfortunately not exactly easy...

• 

  Figure 2: Overall there is no statistical significant downside to chronic paracetamol supplementation, but there is a slight advantage for the NSAID free group in term of increases in lower body strength - the time course (not shown) of the strength gains was by the way identical for both groups, as well (Jankowski. 2012)

  Paracetamol does not interfere with muscle gains in elderly men. The issue whether or not NSAIDs will interfere with resistance training induced gains in skeletal muscle is certainly relevant for everyone. If there is one group of people for whom it could be of paramount importance, though, this would be the men and women in their best ages (>50 years) who have finally realized that muscle is not just metabolic currency, but a true life insurance.
  
  Against that background the most recent results from the College of Nursing at the University of Colorado Anschutz Medical Campus may be important news (Jankowski. 2012). I mean, if the use of N-acetyl-4-amniphenol (ACET) aka paracetamol would hamper or even forestall muscle gains, the training efforts of the men and women who take ACET would be to no avail.
  
  Now the good news is that the chronic use of paracetamol at a daily dose of 1,000mg did not reduce the lean mass gains in the 17 men (age >50y) who actually participated (instead of giving up) in all of the 3-5 days A/B resistance training sessions
  
  • workout A: R three sets of lateral pull down, bench ress, hip abduction and adduction, biceps curls, seated row, and ssisted chin ups
  • workout B: overhead press, leg press, triceps xtension, knee extension and flexion, heel raise, and shoulder external rotation
  • warm up / cool down: 10 min warm-up on the treadmill, a stair climing intermezzo after the first warm up sets and another 10 min cool down
  that were performed with at 80% of the 1-RM and with at least 1 day off in-between over a period of 16 weeks.
  
  
  The chronic ingestion of paracetamol is not advisable regardless of its negligible detrimental effects on skeletal muscle gain. Only recently, Kane et al. have shown that older people in are particularly prone to the hepatoxic effects of this (imho falsely OTC available) NSAID (Kane. 2012). If there is no way around it, because you cannot stand the pain, a safer (at least for the liver) and more effective medical approach could be the combination of tramadol (75 mg), a weak opioid analgesic, with low dose of paracetamol (325-650mg, max!; cf. Pergollizzi. 2012).
  In as much as the nonexistent negative effects are good news, they are likewise strange news, because according to the expression of proteins involved in the protein synthetic response to exercise, it should actually have hampered the gains:
  

  "[...] in the ACET group that the expressions of the anabolic gene p70S6K and the catabolic gene MAFbx were significantly reduced at week 16 of PRT. Given that the increases in FFM in response to PRT were not significantly different between the groups, it is possible that the suppression of catabolic signaling was sufficient to offset reductions in anabolic signaling in the ACET group." (Jankowski. 2012)

  As the authors point out future studies will have to elucidate the exact mechanism this at first sight contradictory results.
  
  In the mean time Jankowski et al. do yet speculate that the loss of prostaglandin signalling and supsequent increases in p70S6K, the protein that's responsible for muscle protein synthesis may be countered by the normalizing effects paracetamol exerts on the expression of Akt, the ameliorative effect on the overexpression of nitric oxide synthase (iNOS) and the reduction of the age-relatedly increased myocyte apoptosis.
  

• 

  Compared to Hope Solo or Serena Williams Olympian Brian Lochte, is probably a weakling - of course only as far as the fatigabilty of his skeletal muscle is concerned - as far as the risk do develop the Athlete's Triad is concerned, this may yet be advantage.

  Men and women tire differently - men (once more ;-) the weaker sex Let's face it guys,  we are weaklings. At least this is what Beth W. Glace and her colleagues from the Nicholas Institute of Sports Medicine and Athletic Trauma at the Lenox Hill Hospital in New York report in their latest paper. Other than the quadriceps muscles of our significant others, our muscles fatigue after 2h of cycling with intermittent one minute sprints every 20 minutes.
  
  In women, in this particular case just like their male counterparts trained cyclists or triathletes with a training load of at least 100km per week, on the other hand, it's solely the central nervous system fatigue that will keep them from cycling 'forever'. Unfair, right? Us men have to battle both, central as well as local muscular (=peripheral) fatigue.
  
  Now what seems nothing but advantageous can however turn against you. In a way the low fatigability of female muscle is also part of the reason why are way more susceptible to the athlete's triad (click here to learn more) than men: They are simply able to work their CNS into the ground, because their peripheral musculature is less prone to exhaustion.
• Recent study puts question mark behind assumed appetite reducing benefit of HIIT sprints vs. classic aerobics - but does that mean that aerobics is the way to go? Not yet in press, but already intriguing are the results of a recent study by  Kevin Deighton et al. from the School of Sport at the Loughborough University who say that they found that ...
  

  "[a]n acute bout of endurance exercise resulted in lower appetite perceptions in the hours after exercise than sprint interval exercise and induced a greater 24 h energy deficit due to higher energy expenditure during exercise" (Deighton. 2012)

  

  Figure 3: Intentionally or not, based on the conclusion of the abstract you would probably not have expected to see these results (data adapted from Deighton. 2012)

  Now this sentence from the abstract certainly suggests that sprinting would have nothing but negative effects. The actual data you see in figure 3 does yet tell you something different. The sprinters may have had increased ghrelin and lower PYY levels with the expected downstream effects on perceived hunger, but this did not translate into significant differences in food intake. In other words, even longish sprint exercises like the ones in the study at hand won't put you at danger of overeating - despite transient increases in ghrelin levels.
  
  In fact, the increased ghrelin amplitude can actually be an advantage (see August 04, 2012) and the calories in vs. out calculation the scientists do is so irrelevant to the real world health and body composition effects of exercise that I refuse to repeat it here ("No, you cannot eat that extra piece of layer cake because you ran on the treadmill earlier today" ;-)
  
  In the end, comparisons like this always suggest you had to choose between doing one or another mode of "cardio", when a combination of both, i.e. cycling HIIT and LISS, yet not both in one session, would be the most productive way to go. And no, Mr. Taubes, none of them is "just going to make you hungry" (see "Every Dog Has His Day: Dr. Oz Was Right, Exercise Does Not "Just Make You Hungry", But Reduces Energy Intake!")
  
• Researchers debate the "low vs. high weight" conundrum. In the editorial to the next issue of the Journal of Applied Physiology Mark D. Schuenke, Jennifer Herman, and Robert S. Staron reject the criticism they received from Nicolas Burd et al. for the pro heavy weights arguments they put forward in their recently published study on the effects of high vs. low weight training (Schuenke. 2012a; covered on the SuppVersity on October 01, 2012). Now while this back and forth between the two groups does not deliver any new data, I believe that it is still interesting and highly educative to see how science is actually a matter of negotiated not set truths. So, let's see how Schuenke et al. respond to Burd's assertion that ...
  

  

  Figure 4: Changes in body composition (left) and changes in muscle fiber cross-sectional area in response do different training regimen (Schuenke. 2012a; this study was discussed here on the SuppVersity on October 01, 2012)

  "[t]he authors’ views continue to contribute to a resistance training doctrine that is incorrect, most notably the belief that heavier weights are better concept. This conclusion is likely due to the relative dearth of quality studies assessing the hypertrophy potential of lower load resistance training paradigms, in contrast to the large number of studies employing ‘traditional’ resistance training intensities (*70 % of maximal strength).

  Clearly, evidence exists to support the concept that light(er) loads can support training-induced muscle hypertrophy both independently and by comparison to heavy loads. We would propose that so long as the stimulus is an overload, performed with high effort (fatigue), and progressive then even the most seasoned lifters would see progression,  at the very least no regression, in strength or muscle mass." (Burd. 2012)

  I will briefly summarize the most important points the researchers from the University of New England College of Osteopathic bring forward to defend their "go heavy or go home" argumentation:
  
  • The list of previous studies which confirm the the efficacy of training with high(er) weight for "optimal" gains in hypertrophy and strength is extensive.
  • Low load training is not as Burd et al. suggest "simply a milder form of low-load blood flow restrictive exercise", of which the researchers state that it is "interesting".
  • Schuenke et al. specifically refer to a Y2k study by Takadara et al. which shows that without the cuffs light loads don't build anything (Takadara. 2000).
  • The researchers point out that the claim by Burd et al. that "maximal muscle fiber activation can be achieved in any circumstance as long as the effort is to failure is unwarranted and unsubstantiated".
  • The study by Mitchel et al. Bird et al. cite to prove their hypothesis may not report significant differences between knee extensions performed at 30 % of 1RM for 3 sets, 80 % of 1RM for 1 set, or 80 % of 1RM for 3 sets as far as the isometric strength and hypertrophy between the three types of training are concerned, but
    

    "[t]his result is not surprising considering the following: (1) no control group was used, (2) each subject trained each limb using a different protocol (cross-over effect), (3) only one single-joint exercise was used (low volume versus a much higher volume of training used, for example, in Schuenke et al.: 3 sets each of leg press, squat, and knee extension), and (4) only fiber types I and II were delineated (severely limiting interpretation of the results).

    In that the last parentheses is obviously another direct criticism of what Schuenke would probably call "cherry picking" studies and specific results to support an unwarranted hypothesis.
  Based on this line of argumentation, Schuenke et al. conclude their deliberations on the note:
  

  

  One should not forget that it's not only about light vs. heavy, but in as much about appropriate and inappropriate weights. If you go by the quantity of the evidence there is however no debating that those weights are too light - probably even for a Lady in her best years.

  "Low-load training appears to have some merit. How-ever, our data support the use of high-load, high-intensity resistance training to maximize fiber hypertrophy and strength. In addition, heavy loading of the muscle has an impact on bone and other connective tissues which are minimized/lacking using low-load training. Finally, Burd et al. appear to oversimplify the field of exercise physiol-ogy. To claim that any training load (light or heavy) con-fers the same physiological adaptations as long as the end point is volitional failure is shortsighted and similar to claiming that running for any distance or time will elicit the same effects as long as fatigue is reached." (Schuenke. 2012)

  If you asked me, both are right. While I personally tend to agree with Schuenke, the main reason that I do is that the heavy weights approach is tried and proven, while - just as Burd says - the sceintific evidence pertaining to low weights is scarce and ambiguous and the anecdotal evidence from 'big guys' is non-existent. I am still curious about the next move(s) on both sides of this divide. And by the way, conflicts like these have always been among the driving forces of scientific progress, so I am pretty sure that we as trainees can only benefit from this debate as well as potential follow-up studies, both groups will feel inclined to conduct in order to 'prove' their point.

That's all for today! I hope you enjoyed the stay, all have electricity and an intact water supply ... I mean it's nice if you have a fully charged iPhone to get your daily dose of SuppVersity news, but even I have to concede that some other things in live are way more elementary.

References

• Ascherio A, Munger KL. Epstein-barr virus infection and multiple sclerosis: a review. J Neuroimmune Pharmacol. 2010 Sep;5(3):271-7.
• Burd NA, Moore DR, Mitchell CJ, Phillips SM. Big claims for big weights but with little evidence. Eur J Appl Physiol. 2012 Oct 20. 
• CDC. Early Release of Selected Estimates Based on Data From the January–March 2012 National Health Interview Survey. September 2012
• Chen CY, Wang BT, Wu ZC, Yu WT, Lin PJ, Tsai WL, Shiesh SC. Glycine ameliorates liver injury and vitamin D deficiency induced by bile duct ligation. Clin Chim Acta. 2012 Oct 23-
• Chesney RW, Hedberg GE, Rogers QR, Dierenfeld ES, Hollis BE, Derocher A, Andersen M. Does taurine deficiency cause metabolic bone disease and rickets in polar bear cubs raised in captivity? Adv Exp Med Biol. 2009;643:325-31.
• Deighton K, Barry R, Connon CE, Stensel DJ. Appetite, gut hormone and energy intake responses to low volume sprint interval and traditional endurance exercise. Eur J Appl Physiol. 2012 Oct 31.
• Décard BF, von Ahsen N, Grunwald T, Streit F, Stroet A, Niggemeier P, Schottstedt V, Riggert J, Gold R, Chan A. Low vitamin D and elevated immunoreactivity against Epstein-Barr virus before first clinical manifestation of multiple sclerosis. J Neurol Neurosurg Psychiatry. 2012 Aug 11.
• Kane A, Mitchell SJ, Carroll PR, Matthews S, Hilmer SN. Characteristics of older and younger patients with suspected paracetamol toxicity. Australas J Ageing. 2012 Sep;31(3):190-3.
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• Schuenke MD, Herman JR, Gliders RM, Hagerman FC, Hikida RS, Rana SR, Ragg KE, Staron RS. Early-phase muscular adaptations in response to slow-speed versus traditional resistance-training regimens. Eur J Appl Physiol. 2012a Oct;112(10):3585-95.
• Schuenke MD, Herman J, Staron RS. Preponderance of evidence proves "big" weights optimize hypertrophic and strength adaptations. Eur J Appl Physiol. 2012b Oct 25.
• Sioen I, Fierens T, Van Holderbeke M, Geerts L, Bellemans M, De Maeyer M, Servaes K, Vanermen G, Boon PE, De Henauw S. Phthalates dietary exposure and food sources for Belgian preschool children and adults. Environ Int. 2012 Nov 1;48:102-8.
• Takarada Y, Takazawa H, Sato Y, Takebayashi S, Tanaka Y, Ishii N. Effects of resistance exercise combined with moderate vascular occlusion on muscular function in humans. J Appl Physiol. 2000; 88:2097–2106.

Skipping Breakfast Decreases Energy Intake, Water Before Meal Trick Works, Food Addiction Self-Diagnosis, Eating Speed & Obesity, Chilled Water as a Nootropic & More

Food addiction is a self-diagnosed disease that befalls preferentially those people who spend hours and days on the Internet seeking for an excuse for their inability to lose weight.

It has been a while since I have published the last installment of the short news. Today, however, the publication of the latest edition of the scientific journal Appetite appears to be a good opportunity to finally put out another of the short news potpourris.

I mean, one of the study shows that it may be essential for your well-being to listen to what scientists say and eat healthy, not unhealthy, which is associated with below average well-being in undergraduate students at the Cardiff University (Richards. 2014). But the study by Richards et al. is by no means the only one with highly health-relevant and surprisingly interesting information you will find in today's short news potpourri.

Learn more about the effects of your diet on your body composition at the SuppVersity

Only Whey, Not Soy Works for Wheytloss

Taste Matters - Role of the Taste Receptors

Dairy Protein Satiety Shoot-Out: Casein vs. Whey

How Much Carbs Before Fat is Unhealthy?

5 Tips to Improve & Maintain Insulin Sensitivity

Carbohydrate Shortage in Paleo Land

I mean, who would have guessed that we have a built-in apathy against being too close to obese individuals? No? Well, me neither, but this is just what L.D. Stafford and K. Banks found in their latest study: "[T]he mere proximity effect", which occurs, when normal-weight individuals stand close to obese ones, "can be influenced positively or negatively depending on the perceived status of the non-target individual and that implicit attitudes act to modulate this effect" (Stafford. 2014).

And there is more than just exotic study results in the latest edition of Appetite - examples? Well, here you go:

• 

  Another recent study indicates: Having a small breakfast (118kcal) before morning can benefit 5h post-exercise mood and appetite control in the time between breakfast and lunch and will avoid the cognitive decline associated with consuming a larger breakfast (Vasey. 2014)

  Another breakfast-omitting study (Plekhanova. 2014) shows that high energy intakes at breakfast increase the total daily energy intake compared to both no breakfast and a regular breakfast. Interestingly, though, the energy intake between 9:00-14:00 and 14:00-bedtime was similar between conditions (P>0.05).
  
  Overall, the most important message of the study is thus, the subjects of the UK study at hand indicates that normal- and overweight 2 to 14 year-old girls do not appear to compensate by consuming more energy over the remainder of the day during three days of breakfast omission compared with habitual or high-energy breakfast consumption.
  
  "The lack of compensation in terms of energy intake indicates that energy expenditure may be more important in explaining the higher obesity risk in girls who do not regularly consume breakfast," the scientists who are still analyzing the effects on physical activity point out.
• Scientists find what makes the British fat (Stewart-Knox. 2014) and it's the spit image of the sedentary, meat eating, oil omitting, non-resilient man with higher mood valance and sick relatives. Of these indirect pathways to dietary habits, physical activity level, higher resilience and mood valance were directly related to negative life events, which are thus another determinant of increased waist circumference in middle-aged British adults.
  
  Sounds crazy? Well, but that's exactly what scientists from the University of Bradford found to be associated with increased weight circumference in a representative samples of middle-aged adults aged >43 years were recruited in Great Britain (GB) (n = 1182). 

Think of energy containing foods as fluids... and bang! they become more satiating! A recent study from the University of Sussex (McCrickerd. 2014) confirms once again that satiety is triggered in the brain. In a small scale study the researchers observed that the satiating effects of one and the same calorie containing beverage increased when it was served as a "filling snack" instead of a fluid that was designed to "quench the thirst".

• The water-trick works (Corney. 2014) you all know that common wisdom is commonly bullsh*t, but in the case of the "water-preload reduces food intake" myth, scientists from the Loughborough University have recently been able to show that "consumption of 568 ml water immediately before a meal reduces energy intake in non-obese young males and might therefore be an effective strategy to suppress energy intake in this population."
  
  When the participants arrived at the laboratory fasted (7–10 am) all consumed an ad-libitum porridge breakfast, with either 568 ml water (PRE) or no water (NO-PRE) consumed immediately before the meal. Subjective feelings questionnaires to assess hunger, fullness and satisfaction were completed before (pre-trial) and after (post-trial) the meal in both trials and after the water preload (post-PRE) during PRE.
  
  

  

  Figure 1: Energy intake w/ and w/out water preload (Corney. 2014)

  As you can see in Figure 1, the subjects who didn't receive the water preload consumed statistically significantly more energy than those who didn't.
  
  Immediately after the water preload the subjects in the PRE group also experienced an increase in fullness and satisfaction and a decrease in  hunger compared to pre-trial.
  
  After the meal, on the other hand, the fullness and satisfaction ratings in both groups were identical.
  
  Thus, "[t]his study demonstrates that consumption of 568 ml water immediately before a meal reduces energy intake in non-obese young males and might therefore be an effective strategy to suppress energy intake in this population." (Corney. 2014) Drinking water with the meal, by the way has previously been shown to be not effective to reduce the food intake in lean women (Rollls. 1999); in obese older individuals, on the other hand, it worked (Davy. 2008)

  

  Figure 2: Weight loss (left) and energy intake (right) in a 12-week study investigating the effects of
  pre-meal water intake (500ml) on weight loss (Dennis. 2014)

  Moreover, a study by Dennis et al. shows that consuming 500 ml water prior to each daily meal helped subjects on a hypocaloric diet lose an extra ∼2 kg over the course of a 12-week study (Dennis. 2010).
• We buy & eat the packages we know and like (Gutjar. 2014), study shows. While in a blinded condition liking was the only determinant of food choice in a recent study from the Wageningen University, food choice in the "familiar package session", where the subjects had to pick from a bunch of unhealthy breakfast drinks and dessert products, lay between the blind and naïve package session.

Question: Can advertising make us choose certain foods? At least in preschool children it takes just 30 seconds of ad-exposure to influence their food preferences (Borzekowski. 2001). "Nutritionists and health educators should advise parents to limit their preschooler's exposure to television advertisements," scientists say.

• The scientists interpret their results as being indicative of the guiding effect of extrinsic factors, in this case the packaging, which can have a similar impact on food choices as intrinsic (sensory) properties.

• 

  Figure 3: Previous studies show that chewing your food 40x vs. 15x will significantly reduce the food intake in lean and obese subjects. Sign. effects on hunger and satiety will yet be apparent only in the obese (Li. 2011)

  Fast eaters have higher BMI, waist circumference and body fat! Scientists from the Wageningen University analyzed data from 311 men and 551 women from the Dutch NQplus cohort. What they found was that (a) 17.4% of the women described themselves as being slow, 54.3% as average and 28.3% as fast eaters and that (b) fast eating women had higher weight, BMI, waist circumference and body fat (p<0.05).
  
  Similar results were observed for the male participants of whom 8.7% of reported to be slow, 44.7% average and 46.6% fast eaters. A result that supports previous evidence indicating that a reduction in eating speed / increase in chewing frequency decreases food intake.
• Chilled water as a nootropic! You've read previously that 500ml water can help you lose weight. Interestingly enough the same 500ml chilled water may also help you master your next exams.
  
  According to a study from the University of Reading the consumption of 500ml of chilled water before a set of standardized cognitive tests will improve performance in several of the tests in young and older individuals (Masento. 2014).
• High flavenol cacao drink increases cerebral perfusion in older individuals (Lamport. 2014) One of the latest studies from the University of Reading investigated the effect of a single acute dose of flavanols on cerebral blood flow and fount that the flavenol-rich (494 mg vs. 23mg) drinks  lead to significant increases in regional perfusion across.

• 

  Figure 4: In contrast to whole fruit which increase the risk of diabetes, fruit juices increase T2DM risk sign. (Muraki. 2014)

  If it contains fruits or a lot of water it must be healthy (Bucher. 2014). Parents and children's health perception of beverages are highly susceptible to marketing gabberish. Worst of all, while "water is good", "fruit is even better".
  
  In the eyes of the parents and kids who participated in a recent study at the ETH Zürich fruit content seemed to be a more important criterion specifically for children to rate a certan food as "healthy". Bad news, in view of the fact that fruit juice - in contrast to whole fruit - consumption is associated with an 8% increase in type II diabetes risk according to a 2013 Harvard study (Muraki. 2013).

Food addicts - what do they say about themselves? A recent study (Ruddock. 2014) found that those who identified as a ‘food addict’ reported frequent food cravings, a preoccupation with food, unhealthy eating patterns, a lack of dietary self-control, and the tendency to eat in the absence of hunger. Furthermore, food addicts reported a problem controlling their intake of foods high in fat and/or sugar. Non-addicts reported the opposite to these behaviours, thus indicating that self- perceived addicts and non- addicts share similar beliefs about what characterizes food addiction.

And last but not least, I want to conclude this installment of the short news with a primer on food addiction. An Internet-based disease... well, sort of. The latest data from the University of Liverpool (Hardman. 2014) would at least suggest that having read on the Internet (or elsewhere) about food addiction and the subsequent belief in the existence of this pathology increases the prevalence of being a “food addict” on both the self-diagnosed measure (57% vs. 27%, respectively, p = .018) and the Yale Scale (16% vs. 0%, p = .02).

As Herbert points out, "[t]hese findings suggest that people readily endorse the concept of food addiction as an explanation for their behaviour." (Herbert. 2014) What will have to be determined in future studies, however, is whether one's belief in his / her own food addiction will also affect the actual food intake -- in other words: Is there a "I am a food addict, so I can't but eat until I die" phenomenon | Comment on Facebook.

References:

• Borzekowski, Dina LG, and Thomas N. Robinson. "The 30-second effect: an experiment revealing the impact of television commercials on food preferences of preschoolers." Journal of the American Dietetic Association 101.1 (2001): 42-46. 
• Bucher, T., M. Siegrist. "If it contains fruits or a lot of water it must be healthy. Parents and children's health perception of beverages." Appetite 83 (2014):347.
• Corney, R.A., C. Sunderland, L.J. James. "Effect of an immediate pre-meal water preload on voluntary energy intake in non-obese young males." Appetite 83 (2014):361.
• Davy, Brenda M., et al. "Water consumption reduces energy intake at a breakfast meal in obese older adults." Journal of the American Dietetic Association 108.7 (2008): 1236-1239.
• Dennis, Elizabeth A., et al. "Water Consumption Increases Weight Loss During a Hypocaloric Diet Intervention in Middle‐aged and Older Adults." Obesity 18.2 (2010): 300-307.
• Gutjar, S., C. de Graaf, G. Jager. "Food choice. The battle between package, taste and consumption situation." Appetite 83 (2014):358 
• Hardman, C.A., H.K. Ruddock, R. Dallas, J. Scott, P.J. Rogers, E. Robinson. "Food addiction, myth or reality? The effects of priming beliefs about food addiction on self-diagnosis and consumption." Appetite 83 (2014): 355.
• Lamport, D., D. Pal, C. Moutsiana, D.T. Field, C.M. Williams, J.P.E. Spencer, L.T. Butler. "The effect of flavanol rich cocoa on cerebral perfusion in older adults during conscious resting state." Appetite 83 (2014):351.
• Li, Jie, et al. "Improvement in chewing activity reduces energy intake in one meal and modulates plasma gut hormone concentrations in obese and lean young Chinese men." The American journal of clinical nutrition 94.3 (2011): 709-716. 
• Masento, N.A., A. John, V. Wilton, V. Benzesin, D.T. Field, L.T. Butler, C.M. van Reekum. "Investigating the effects of acute water supplementation on cognitive performance and mood in young and older adults." Appetite 83 (2014):355.
• McCrickerd, K. L. Chambers, M.R. Yeomans. "Food or fluid? The context of consuming a beverage influences satiety." Appetite 83 (2014):348.
• Muraki, Isao, et al. "Fruit consumption and risk of type 2 diabetes: results from three prospective longitudinal cohort studies." BMJ: British Medical Journal 347 (2013).
• Plekhanova, T., J.K. Zakrzewski, Effect of consuming compared with omitting breakfast on free-living energy intake and eating patterns in overweight and non-overweight adolescent girls, Appetite 83 (2014):361.
• Richards, G., A.P. Smith. "Diet and wellbeing in undergraduate students." Appetite 83 (2014): 362.
• Rolls, Barbara J., Elizabeth A. Bell, and Michelle L. Thorwart. "Water incorporated into a food but not served with a food decreases energy intake in lean women." The American journal of clinical nutrition. 70.1 (1999): 448-455. 
• Ruddock, H.K., C.A. Hardman, M. Field. "'I perceive myself to be a food addict'. A qualitative exploration of the ‘food addiction’ concept." Appetite 83 (2014):355.
• Stafford, L.D., K. Banks. "Don't (do) stand so close to me. Mere proximity effects in overweight and underweight contexts." Appetite 83 (2014): 362.
• Stewart-Knox, B., M. Duffy, B. Bunting, D. Almeida, M. Gibney. "Psychological pathways to central obesity in healthy middle-aged British." Appetite 83 (2014):361.

The Fallacy of Working Out To "Burn Calories" + Exercise Shuts Down the Carb Cravings: Bench Press, Leg Press HIIT & LISS Are Not Meant to Incinerate the Junk You Eat

If you work out to be able to allow yourself to eat, you know you have a serious problem.

So, what was that about the bench pressing consuming as much energy as leg presses and the "exercise just makes you hungry myth" on the last installment of the Science Round-Up? If that's what you have been asking yourself this morning, when you showered I am impressed - or should I be worried?

If you have not done so already, this would be the right time to download + listen to the Science Round-Up - I promise there is much to learn and not all of it is going to be repeated here.

Whatever... in the end it does not matter how urgent you were waiting to take a look at the data that supports my argument that (a) exercise does not just make you hungry, and that (b) the notion to work out primarily to burn energy is hilarious.

Chest vs. legs what's energetically more costly?

While I could imagine that the comparison would have yielded a different result if the 10 healthy young men (>1 year of resistance training experience; BMI ~24kg/m²) had performed squats instead of regular leg presses, I have to admit that I was still surprised to see that Magossoa et al. actually found no difference in the total energy expenditure between 3 sets of 10 reps (70% 1RM) of bench vs. leg presses (Note: The researchers determined the total energy expenditure using the oxygen uptake (aerobic component) the EPOC and lactate production (anaerobic component)).

Table 1: Workload, energy expenditure total, per minute per weight lifted (Magosso. 2013)

If you look at the data in Table 1, you will have to concede: The only difference between the energy expenditure during the leg and the leg press was the inferior energy consumption per kg of weight on 'the bench'.

If you were one of the lazy (and mostly ignorant) buggers who "already have big enough legs", you could probably use these results to argue that leg presses and the rest of the leg workout was a pretty unnecessary undertaking - I mean, if you don't want bigger legs it should at least help you with that sixpack by burning a couple of calories, right?

Only a fool will work out to "burn energy"

Suggested Read: "Busting the 3,500kcal = 1lbs Weight Loss Myth! Debunking the rule of thumb with the power of science" | read more

Once they're there, it does usually you not take very long until people will remember this ingeniously simply (and about s flawed) rule of thumb that says: To lose 1lbs of fat you got to burn 3,5000kcal. Here, in our concrete example, that would mean that it would not matter if you did another 228 sets of bench presses or leg presses to lose 1lbs of pure body fat.

Once you've gotten caught in calculations such as the above, i.e. 229 sets x 46kcal / 3 sets  > 3500kcal, or in words "I got to do 228 sets of bench presses to burn one pound of body fat!", you are lost.

Firstly, the equation 3,500kcal caloric deficit = 1lbs fat loss if flawed (learn more).

Secondly, and even more importantly, doing more, which is what all the "I workout to lose fat" weekend warriors do, is not going to yield superior results. If you don't believe that, I suggest you go back to my "How to Burn 27,300 Kcal Extra W/out Losing a Single Extra Pound of Fat!"-article and take a look at the results of the Rosenkild study from 2012 (figure 3).

Gary is ... no, not a fool, but he is still wrong

Now, I obviously cannot forbid workout extra and luckily even Gary Taubes can't because even if you insisted to burn 600kcal, instead of just 300kcal, you can at least console yourself that this is not going to increase your appetite (learn more). Especially if we are talking about relatively intense exercise for similarly "relatively obese" individuals, working out will not only reduce your window of opportunity to eat (for some people even that may make a difference, believe me), but rather work like a gastric bypass - one that won't allow you to hit your obesogenic macros on the subsequent meals.

Figure 1: Macronutrient intake (lunch + dinner in g) on control vs. exercise day (David. 2013)

Those of you who have not listened to the podcast yet will now probably be wondering what I am talking about, right? Well, take a look at the 3D bars in Figure 1. They represent the results of a study David et al. conducted earlier this year. A study that involved both lean and obese kids and a study that demonstrates that a relatively short (3x10 min) but comparably hard workout (75% VO2max) is not going to make the sugar junkies crave for more - quite the opposite, it will reduce their apperite for carb(age) to a normal level [similar appetite-reducing effect were observed by Sim et al. (2013) in adult men and Rosenkilde (2013; already discussed at the SuppVersity].

I mean, a voluntary 35% reduction in carbohydrate intake during lunch and dinner and a total reduction in energy intake of 475kcal are impressive ballpark figures considering the fact that exercise is often said to "just make you hungry" - wouldn't you agree?

EPOC should not determine your choice of exercise either

If you are sprinting because of the increase in EPOC, you are a fool.

From the article I referenced in yesterday's write-up ("More Than 3x Higher EPOC Induced Energy Expenditure With HIIT vs. LISS! But Does That Really Matter?" | read more) you already know that  HIITing it hard on Wingate tests will yield a pretty pathetic increase in EPOC of ~20kcal over a casual 30min jog.

So even if it was about burning calories the jog would be far superior because the increase in Excess Post-Exercise Oxygen Consumption (EPOC) is not going to compensate the additional kcal the subjects in the Townsend study burned during the steady state exercise.

The latter is by the way not much different if you compare two different HIIT regimen - a very intense short one (HIIT1) and a somewhat longer slightly less intense alternative regimen (HIIT2):

• HIIT1: 10 x 1min, 1min pause between intervals; cycling at 80-90RPM at 90% of the HRmax

• HIIT2: 10 x 4min, 2min pause; cycling at 60-80RPM and without a prescribed minimal heart rate

In their trial that involved 9 lean, healthy male subjects, Kelly et al. obeserved that the HIIT2 trial was more than two times more energetically costly (675kcal vs. 275kcal) - the EPOC effect on the other hand did not lead to any significant differences in post-exercise energy expenditure, so that the HIIT1 group was stuck with their ~400kcal inferior energy expenditure... now, that sounds as if it was a bad thing, but if we consider that they spent less time on the ergometer and were rewarded with a greater stimulus for mitochondrial expansion and even muscle growth (see "The Anablic Effects of HIIT" | read more), I would not say that they came off second best - would you?

Practical suggestions for your workout week...

• health focus - 2-3x resistance training + daily LISS as in walking (min. 30-60min)
• performance focus - 3x resistance training + 1-2x HIIT + 6x LISS as in walking (30-40min)
• physique focus - 3-4x resistance training + 1x HIIT +  6x LISS as in walking (30-40min)

Don't forget that the reason you do the LISS training is not because you want to burn calories, but rather because you want to spend some time doing what you actually would have to do everyday: Walking from place A to B; and if you belong to the few of us who don't sit on a desk all day, you may skip the walk in the park.

So what's a good reason to work out, then? Health! I know that does not sound as sexy as six-pack abs and bigger sleeves, but there is not denying it: Exercise is your vaccine and magic pill. It's what's going to make you feel good, look good and age well and unless you want to end up debilitated in a nursing home it is not optional even if you follow an energy restricted diet for the rest of your life. What is optional, though, is exercise as a means to increase athletic performance or influence the shape of you body withing your individual very specific limits.

Within this health ↔ performance ↔ looks triangle you will often encounter conflicts, where the optimization of one compromises the realization of another. I am nevertheless convinced that classic light intensity steady state (to make up for our modern sedentary lifestyle), en vogue high intensity interval training (to increase your VO2max) and classic and modern forms of resistance training (to build and maintain muscle mass) all have their place in a routine that does not lose sight of any of the vertices of the triangle.

What? How you can ever lose weight without doing endless hours of cardio? Well what about dieting?

References:

• David T, et al. Obese but not lean adolescents spontaneously decrease energy intake after intensive exercise. Physiol Behav. 2013 [epub ahead of print]
• Kelly B, King JA, Goerlach J, Nimmo MA. The impact of high-intensity intermittent exercise on resting metabolic rate in healthy males. Eur J Appl Physiol. 2013 Oct 6. [Epub ahead of print]
• Magosso et al. Energy Expenditure during Multiple Sets of Leg Press and Bench Press. Journal of Exercise Physiology online. October 2013.
• Rosenkilde M, Auerbach P, Reichkendler MH, Ploug T, Stallknecht BM, Sjödin A. Body fat loss and compensatory mechanisms in response to different doses of aerobic exercise--a randomized controlled trial in overweight sedentary males. Am J Physiol Regul Integr Comp Physiol. 2012 Sep 15;303(6):R571-9.
• Rosenkilde M, Reichkendler MH, Auerbach P, Toräng S, Gram AS, Ploug T, Holst JJ, Sjödin A, Stallknecht BM. Appetite regulation in overweight, sedentary men after different amounts of endurance exercise - a randomized controlled trial. J Appl Physiol (1985). 2013 Sep 19. [Epub ahead of print]
• Sim AY, Wallman KE, Fairchild TJ, Guelfi KJ. High-intensity intermittent exercise attenuates ad-libitum energy intake. Int J Obes (Lond). 2013 Jun 4. doi: 10.1038/ijo.2013.102. [Epub ahead of print]

Pharmacological Starvation: 30% Increased Life Expectancy w/ Still to be Developed FGF21 Analog - The Royal Road To Longevity? Plus: Ground Yourself It's World Nutrition Day!

Do you really think this kid cares whether there is fructose in his/her banana? Think about that before you delve into the next religious discussion about whether or not food a is legit to eat, "not paleo" or "too high in carbs" *thank you*

It's World Food Day and I thought it may be nice to remind everyone about the hilariousness of such "important" first world problems as "eating X bananas a day is bad foryou", the notion of "non paleo" foods and the rest of the vitally important topics the blogosphere is so fond of, these days. Allegedly, neither the bloggers, nor the facebookers or forum posters, who spend so much time and energy debating these and similarly worldshaking issues, will be among the 24,000 human beings who are dieing each and every day from hunger, but maybe one or another of you, of whom I am sure that they don't belong to the group of real notorious nitpickers, will have a similar "grounding experience", from just being reminded of this figure, as me, when I heard it on the radio earlier this morning.

Don't get me wrong, I am not intending to point with a finger at anyone (if anything I would have to start with pointing at myself), but if one or another of you would pause for a second or two and have a similar "grounding experience" as I had, I would be happy.

From real starvation to starvation science
 
Although this prelude appears to segue quite nicely into today's science post, I am not sure if that's even a good thing... be that as it may, after listening to the news on the radio I was quite annoyed, when I read about a recent study by Zhang, Kliewer et al. on the wonderful effects of the "starvation hormone" FGF21 (fibroblast growth factor 21; the effects were observed in mutants who overexpressed FGF21, by the way) on yet another of those awful copy & paste items on Science Daily that are 99% hype and 1% science (in the scientists' defense it must be said that I am well aware of the fact that our, i.e. university or institutionalist, press offices are writing this stuff together in this way on purpose and are not really interested in the actual science background, though). With statements such as "[the mice] got the benefits of dieting without having to limit their food intake" (UT Southwestern Medical Center. 2012) the "article" tailors perfectly to the demands of the glutenous Westerner who applies his "the more the better" principle to all areas of his super sized life that people will probably already be emailing Dr. Kliever about the release date of the drug he surely must be working on.

And in fact, the actual results of the study (Zhang. 2012), the press release specifies by quoting Kliever who said "Male mice that overproduced the hormone had about a 30 percent increase in average life span and female mice had about a 40 percent increase in average life span" sound intriguing. After all this would mean that you would have a realistic chance of making it to the magic 100, when you would otherwise have died at the age of 77.

Starvation, real or hormonal is not the way to healthy longevity!

Nonetheless, the price you would have to pay to "starve yourself into this biblical age" - pharmacologically, of course since (a) otherwise no one could make money on it and (b) no one would want to do it - is high. And I am not sure any of you is willing to pay it.

Figure 1: What do you call it, when mice simply won't grow and end up as a small copy of their normal counterparts with identical body composition, but virtually no bone mass? Right! That's failure to thrive. Now, what do you call the same phenomenon, if the poor critters live 30% longer? Yeah, righ! That's a scientific break through!

I guess you could say you can cope with being a shrimpy weed (or a tiny version of yourself, which is actually what what you would be if you had half your current weight and the same totally average body composition; see figure 1), if that means that you can see your grand grand children rise, but your chances that this is going to happen outside of a wheelchair are not particularly high for men and the chance of seeing them at all is non-existent for women.

The combination of low bone mass and infertility should actually ring a bell with everyone who has been following the Athlete's Triad Series.

Why is that? Well, next to being a pathetic weed, your bone mass and density would be so low that the chances of literally breaking apart are probably way higher than the already low chance that any of these results do even translate to human beings.

And while men who like to gamble may want to make this bet with the pharmaceutical devil, the antifertility effect of FGF21 would not allow any women making the same bet to even have children. Which does obviously not make it very likely that they will ever get to see the children of their grand children - regardless of whether they become 200 years old, by the way.

I am therefore not so sure whether the mere fact that the FGF21 mutants' mobility was not effected is evidence enough of "living a nice, long life", as Kliewer is pointing out (UT Southwestern Medical Center. 2012).

There is no way this drug will be gluttony and thus "Western lifestyle" compatible 

Figure 2: Don't be fooled! The small "g/g body weight" makes all the difference! If you weigh half of a normal human being thanks to whatever patented FGF21 derivate you take, you better make sure you eat like half a human being, as well, if you don't want to shorten your life by 30%, instead of prolonging it!

And as far as the implicit promise of being able to eat "as much as you want" goes, it may be correct that "there were no differences in food intake, physical activity, oxygen consumption or respiratory exchange ratio" (see figure 2) but if you scrutinize the caption of the Y-axis you'll see the bad, bad letters "g/g body weight". And this label means nothing else than that whoever has written the press release has been trying to fool you, when he or she wrote

"The mice that overproduced FGF21 in this latest study were lean throughout their lives and remained lean even while eating slightly more than the wild-type mice, the researchers said." (UT Southwestern Medical Center. 2012)

The truth is, they ate almost half as much as the normal animals, so where on earth was this not a starvation diet? I mean, all of you who have read parts (better the whole) SuppVersity Athlete's Triad Series will be well aware that bone loss and infertility are hallmark features of in this case exercise induced "starvation".

And let's be honest, unless Mc Donalds is going to produce XXS Menues for people on FGF21, I can guarantee you that the only effect any future drug analog of this hormone is going to have is to make people's lives even more miserable than they already are... longevity? No way! After all, this is not going to correct the dietary induced failure of our natural satiety response that constantly drives us to overeat on all those things the people who are now probably lining up in front of Mr. Kliewer's office to be part of the earliest trial are not willing to give up, although they know that they are thus easily reducing their maximal life-expectancy by 30%!

The unsexy, since inconvenient truth is missing from the mainstream science breakdown

In view of the fact that neither the press guy (or girl) nor the scientists appear to have a wested interest to tell you that FGF21 activity is "paradoxically elevated in obese conditions" (Fletcher. 2012) and that something as awfully inconvenient (and moreover non-patentable!) as exercise is the best way to normalize not only the skewed FGF21 levels, but also to increase the expression of the "longevity factor" clotho (30-50% in a classic rodent model; cf. Fletcher. 2012), I consider it my duty to let you know that you neither have to resort to the exogenous provision of drugs, nor starve yourself and can still be sure to benefit from the effects of FGF21: Either by its modulation via exercise if you are obese as the aforementioned rodents or, more importantly, by its upregulation in normal weight individuals, like the 60 sedentary young women Cuevas-Ramos et al. put on a two week exercise regimen earlier this year, only to find that their

"[s]erum FGF21 levels significantly increased after two weeks of physical activity [and that this 66%! increment in FGF 21] correlated positively with clinical parameters related to the adrenergic and lipolytic response to exercise." (Cuevas-Ramos. 2012)

Now, I don't know about you, but I, for my part, would probably risk to make a bet with the devil (pharmacological or not) that anyone who is willing and able to appropriately fuel his workouts, get his share of anabolic and restorative sleep and refrain from overtraining, will get all the benefits, the press release aptly ties solely to the unquestionable pharmacological "separation of the hormone’s life span-extending effects", Kliever is cited for in the last paragraph of the copy & paste job, without any of the downsides.

The SuppVersity Approach to Longevity is therefore simple, cheap and 100% healthy: Work out, eat healthy and get your daily dose of SuppVersity news to know how you can optimize your training, nutrition and supplementation regimen ;-)

References:

• Cuevas-Ramos D, Almeda-Valdés P, Meza-Arana CE, Brito-Córdova G, Gómez-Pérez FJ, Mehta R, Oseguera-Moguel J, Aguilar-Salinas CA. Exercise increases serum fibroblast growth factor 21 (FGF21) levels. PLoS One. 2012;7(5):e38022.
• Fletcher JA, Meers GM, Laughlin MH, Ibdah JA, Thyfault JP, Rector RS. Modulating fibroblast growth factor 21 in hyperphagic OLETF rats with daily exercise and caloric restriction. Appl Physiol Nutr Metab.
• UT Southwestern Medical Center. Newsroom. Starvation hormone markedly extends mouse life span, without need for calorie restriction. Oct 16, 2012. < http://www.utsouthwestern.edu/newsroom/news-releases/year-2012/october/starvation-hormone-mangelsdorf-kliewer.html > retrieved Oct 16, 2012.
• Zhang Y, Xie Y, Berglund ED, Coate KC, He TT, Katafuchi T, Xiao G, Potthoff MJ, Wei W, Wan Y, Yu RT, Evans RM, Kliewer SA, Mangelsdorf DJ. The starvation hormone, fibroblast growth factor-21, extends lifespan in mice. elife. 2012;1:e00065. doi: 10.7554/eLife.00065.