What's the Optimal Dose of Vitamin D3 for Lean, Normal-, Overweight & Obese Women With Established Vitamin D Deficiency to Get 25OHD Back into the Normal Range?

Both ladies are D-ficient, but will probably need profoundly different amounts of D3 to get their 25OHD back in range.

Actually, I guess, I don't really have to tell you that there is not going to be guest post by Adelfo Cerame, today. Adelfo is busy with the last weeks of school, but will be back as soon as he has passed all the tests. And while I am not sure, whether or not you would call the latest on vitamin D supplementation an adequate replacement for a contest prep update from "your's truly", I suppose that it's better than nothing to bridge the time that still remains until the SuppVersity  Science Round-Up on the Super Human Radio Network is going to air (the show starts at 12PM, EST; the Science-Round-Up airs in the 2nd hour and will thus begin at 1PM, EST; click here to listen live or wait for the podcast // update: now available).

I am honestly not yet sure what exactly we will cover today, but among the things I am still thinking about how we can squeeze them into a 1h show are...

• methylxanthines caffeine, theobromine and theophylline can bind to human DNA - what does that tell us about the purported health benefits of caffeine & co?
• caffeine prevents memory impairment - in this case in a model of sporadic Alzheimer's disease
• anti-Alzheimer's effect of CLA - plus a list of supplements that have been implicated in the prevention of Alzheimer's and other amyloid diseases such as Parkinson's, Cerebellar Ataxis, Amyotrophic lateral sclerosis and (hardly recognized as an amyloid disease) diabetes type II
• the effect of body weight on the benefits of circuit training in older women - turns out that those who need it the most, namely the obese, also see the greatest benefits
• Gum arabicum to ward off holiday weight gain - that this could actually work is at least what a recent human study would suggest
• more on vitamin E, resveratrol, soldiers don't get hurt in battle, but by geranium (DMAA), ...

I think there should be something for everyone of you. Plus: If everything works out, this is going to be the first show to air live via Skype, so no nagging land line echoes and noise any more.

Let's get to the D-news, now

The general consensus among the vitamin D advocates currently is that 2,000 IU of vitamin D3/day is the minimum you need to bring low levels of 25OHD back into the normal range. A soon-to-be-published study by Gallagher, Yalamanchili and Smith that's available ahead of print on the website of the Journal of Steroid Biochemistry and Molecular Biology does yet contradict this notion - at least for women with a body mass <25kg/m² even the meager RDA of 400IU would be enough (Gallagher. 2013). That said the concise paper actually describes the results of two, not just one experiment, with

• study 1 (ViDOS) being a one-year randomized, double-blind placebo controlled study (ViDOS – Vitamin D supplementation in Older Subjects) of increasing doses of vitamin D3 (400,  800, 1600, 2400, 3200, 4000 or 4800 IU/day vitamin D3 vs. placebo + calcium supplements to maintain calcium intake between 1,200-1,400mg/day) in 163 Caucasians, age 57–90 years; all vitamin D insufficienty, i.e. serum 25OHD ≤ 20 ng/ml (50 nmol/l), and 
• study 2 (STOP IT) being a 3-year intervention study of calcitriol 0.25 mcg (the active form of vitamin D) twice daily, conjugated estrogens 0.625 mg  daily, a combination of both and placebo in 488 elderly women, age 65–77 years

Body composition indices for the studies at hand (i.e. percentages of total and regional fat and fat-free mass) were measured by dual energy X-ray absorptiometry (DEXA Hologic Delphi) at baseline and after 12 months.

Figure 1: Mean total body weight, total body lean mass, total body fat mass and serum 25OHD in different BMI subgroups of study 2 (STOPIT); right, corresponding calculated ratios (based on Gallagher. 2013).

Even the baseline data in figure 1 does actually yield some insights into the relation of BMI, adiposity and 25OHD levels. While the data on the left already shows that the fat mass increases almost linearly across the BMI levels, while the lean mass remains relatively stable (with the highest value in the overweight group, though), the ratios I calculated and plotted on the right-hand side of figure 1 make it even more obvious clear: The lean / fat mass ratio scales with the BMI. With identical levels in the normal- and overweight individuals and significant increases and declines in the lightest and heaviest study participants. Moreover, the 25OHD vitamin D to fat mass ratio drops most significantly between the low BMI and the upper normal zone, where I suppose even most of the "healthy" individuals will be hovering around these days.

Being lean is a positive predictor of increases in 25OHD with supplementation

That this latent "chubbiness" of the average Westerner may be of particular significance in view of the negative / non-significant outcomes in many of the vitamin D supplementation trials, becomes self-evident, when you take a closer look at the data in figure 2, however you will have to realize that my plot which comprises above all the highly relevant relative changes (middle, marked in red) tells a different story than the original plot from the study showing only the absolute changes (left, but in form of a line graph).

Absolute, relative (compared to baseline) changes and total 25OHD levels (ng/ml) after supplementation with low, medium and high amounts of vitamin D3 in lean, normal, overweight and obese women (based on Gallagher. 2013)

Accordingly, the conclusion of the abstract, which says that "the response to vitamin D is dependent on body weight" and that "women with BMI <25 kg/m² develop much higher levels of serum 25OHD after vitamin D supplementation compared to those with BMI of >25 kg/m²" (Gallagher. 2013) may be correct, but is somewhat misleading as it is open to be interpreted as 'lean women respond most favorably to vitamin D supplementation' - an interpretation that is not really sustainable in view of the relative changes I calculated for figure 2  (middle), yet by no means as incredible as the abstract of another vitamin D study, I dessicated back in September (see "Stronger & Leaner or Fatter & Less Muscular W/ 4,000IU Vitamin D3 - What if Abstract and Data Tell Different Stories?")

Bottom line: The data from this most recent investigation into the differential response of lean, normal, overweight and obese women to vitamin D3 supplementation shows that the absolute increases appear on BMI and that...

• 

  Always take vitamin D with fatty foods! (see "A Fat D-Ficiency")

  low dose supplementation (400 or 800IU/day) is probably only sufficient to rise and maintain adequate vitamin D levels in lean women,
• medium dose supplementation (1,400 or 2,400IU/day) yields the most favorable outcomes in total 25OHD levels and 
• high dose supplementation (3,200, 4,000 or 4,800IU/day) does not yield additional benefits in either the the normal-, overweight and obese subgroup and only marginally higher levels in the lean women.

Overall the study at hand would thus support the notion that a daily vitamin D supplement containing ~2,000IU is the best way to get deficient levels back up, esp. for lean women it should be no problem to cut back to 2x the RDA, i.e. 800IU after normal vitamin D levels are achieved. For the rest, future studies will have to show if low dose supplementation is enough.

These longissimus dorsi slices of mice on a normal and a vitamin D3 supplemented diet show that supplemental vitamin D3 can be used as a fat synthesizer and meat tenderizer in "meat-producing animals". (learn more)

The often-heard hypothesis that the decreased response to vitamin D supplementation in the obese would be a result of the preferential storage of vitamin D in the adipose tissue was not supported by data of the Ghallagher study "there is no evidence from the dose response curves that in obesity serum 25OHD is being deposited in fat" (Gallagher. 2013). In view of the fact that contrary to total vitamin D, which is in fact preferentially stored in adipose tissue (78%) over lean muscle (14%), 25OHD stores are distributed much more evenly with 33% being stored in body fat and 20% in muscle tissue in omnivores like humans and swine (the data is in fact based on a study in pigs; cf. Jakobsen. 2007).

Lastly, a beneficial effect of increase / normalized vitamin D levels on lean or fat mass was (once again) not observed in any of the studies; and that despite the fact that "body fat was an independent predictor of serum PTH", which decreased in response to calcitriol supplementation in study 2 (which is actually more of an adjunct for correlative analysis and as a data source to compare the results of study 1 to). In other words, normalizing your vitamin D levels without taking appropriate measures to counter what's probably behind both, the nasty body fat and the low vitamin D level is not going to make you lean or musclar - at least as of now, it rather appears as if this was yet another instance, where we are - if anything - treating isolated symptoms instead of the root causes of the obesity epidemic.

References

• Gallagher JC, Yalamanchili V, Smith LM. The Effect Of Vitamin D Supplementation On Serum 25OHD In Thin And Obese Women. J Steroid Biochem Mol Biol. 2013 Dec 11.
• Jakobsen H, Maribo A, Bysted HM, Sommer OH. 25-Hydroxyvitamin D3 affects vitamin D status similar to vitamin D3 in pigs – but the meat produced has a lower content of vitamin D. British Journal of Nutrition. 2007; 98 908–913.
• Shephard RJ. Limits to the measurement of habitual physical activity by questionnaires. Br J Sports Med. 2003 Jun;37(3):197-206; discussion 206.

Whey or Casein, Pulse or Spread Evenly Across the Day? Does it Even Make a Difference in Terms of Fat Loss and Lean Mass Retention on a Diet? New + Old Empirical Data!

Image 1: Instinctively right? Milk contains soluble (=whey) proteins and casein. Are we overthinking things, when we rip them apart and does it even make a difference? Or is timing all that counts?

It's funny "overthinking", right next to overtraining and overdieting, has become one of the most common problems among the health and fitness enthusiasts who spend equal (or even more) time online as in the gym. "Would it be better if I take my BCAAs at a 3:1:1 or 2:1:1 ratio?", "Does it matter if my protein powder is 10% hydrosolate, 50% isolate and 40% concentrate or has a 30/50/20 ratio?" All that may well make a difference, but let's be honest: Look at the things 80% of these people are eating day in and day out and the way they throw the weights around in the gym and contrast that to a question like "Will my post-workout protein synthesis be 5% greater, when I switch from concentrates to hydrosolates?" ... enough of the ranting, though. After all this post is actually about one of the more sensible among these world-shattering questions:

Q

Will it make a difference, whether I use casein or whey protein on a diet and... what's the significance of having my daily allotment of protein spread evenly across the day vs. mostly (80%) in one sitting, when I am dieting?

In order to find the answer to this question a group of French scientists recruited 41 healthy, but chubby subjects (BMI ~32kg/m²; age ~33y) and put them on a relatively moderate caloric deficit that was calculated based on their basal energy requirement (what you would need lying around all day). In all four arms of the study, the macro-nutrient composition (25% as proteins, 25% as lipids, and 50% as carbohydrates) and energy content per pound of lean body weight (average energy intake 5.87 MJ per day) of the meals, which were prepared according to personalized menus the subjects received from trained dietitians, were identical.

Figure 1: It did not make a difference if the protein was ingested either spread equally across the day or as a pulse mostly (80%) in one sitting (top), fat and weight loss after the 6 week study period were virtually identical (data based on Adechian. 2013)

The little information on the exact menu choices the scientists offers includes a list of stable foods, such as various proportions of spinaches, broccoli, lentils, or green beans, butter, bread, fruits, soy yogurt, rice cakes and gingerbread and suggest that we are dealing with the typical "your dietitian recommends diet", here. With one exception, of course, the main protein source of all four experimental diets were dairy proteins (~80g; >80% of total protein). Casein and whey aka "milk soluble protein"* (see red box above), which were to be ingested either spread equally across or in a "pulsed" fashion (see figure 1, left):

*Note: the scientists refer to whey as "milk soluble protein, I stuck to the terminology in the graphs, but in essence these are mainly β-lactoglobulin, α-lactalbumin, as well as serum albumin, immunoglobulins, lactoferrin, and other minor fractions and thus the same you would find in your average whey concentrate which is, as you may have notices "more soluble" than casein (cf. Lacroix. 2006)

• casein spread- subjects consumed ~20g of a casein protein supplement 4x a day
• milk spread - subjects consumed ~20g of milk protein supplement 4x a day
• casein pulse - subjects consumed the lions share, i.e. 80% of their ~80g of casein, as part of their 2nd meal, so that the protein intake over the day was 6.4g / 64g / 3.2g / 6.4g (see figure 1)
• milk pulse - same as above, but with milk instead of casein protein

In view of the overemphasisze nutrient timing has gotten as of late withing the physical culture and the assumption that you would expect to see profound differences based on when you consume how much of fast or slow, high (milk) or average (casein) leucine protein etc., it may be disappointing that the weight loss was absolutely identical in all four arms of the study (-7.5 ± 0.4 kg).

Differences are few and far between: Weight loss, fat loss, muscle loss - NOT different! 

What may yet surprise even you, a seasons SuppVersity veteran, who will probably already have expected the non-significant (in fact non-existent) differences in terms of weight loss, could be surprised that the changes in body composition (see figure 1, bottom), i.e. -5.1 ± 0.2 kg reduction in body fat mass and -2.2 ± 0.2 kg reduction in lean body mass, were identical.

Since the same goes for the changes in the fat "liberating" proteins lipoprotein lipase (LPL) and adipose triacylglycerol lipase (AGTL), the fat "forming" protein fatty acid synthase (FAS), and three of the usual subjects, i.e. leptin, the adipoQ gene which is responsible for encoding adiponectin, of which recent research suggests it may be even more important than leptin for your metabolic health (Li. 2013; Hickman. 2013), and the reduction in the pro-inflammatory monocyte chemotactic protein-1  (MPC-1), the slightly more pronounced meal-induced postprandial protein synthetic response in the casein group at the end of the study period is actually the only difference based on which you could argue for one over the other protein source:

Figure 2: While the changes in LPL, AGTL, FAS, leptin, AdipoQ and MCP expression were identical (left); the post 6-week protein synthetic response to identical meals was slightly more pronounced in the casein group (right), the overall significance of this finding is yet questionable in view of identical lean mass losses - it could yet become important on a diet + exercise regimen as in the Demling study discussed in the bottom line box  (data based on Adechian. 2013).

Whether the measurable advantage of casein during this test (the evaluation was carried out by leucine tracer infusion, by the way) is just an experimental artifact or

Adherence is the key to success: While there was no difference in terms of the hunger the subjects felt when they were on the diet, the fact that only 23 of the initially 41 subjects did make it through the 6- week on ~ 1,500kcal/day is quite telling, also in view of the perceived inability to lose weight - if you can't stick to a by no means crazy caloric restriction for 6 weeks, how can you expect to get lean and stay lean, when the inevitable prerequisite for the latter is that you totally revamp your dietary habits for the rest of your life not just six, eight, or twelve weeks.

• maybe something like "leucine resistance" in response to the higher leucine concentrations after the ingestion of the milk protein supplement in the course of the study period, or
• alternatively, the greater IGF-1 response to casein (cf. Hoppe. 2009, a study which compares whey vs. casein, but would obviously suggest an advantage of casein over milk = whey + casein, as well); unfortunately IGF-1 wasn't measured, but the insulin levels which were minimally higher in the casein group could support that hypothesis,

... is questionable. Since the same is true for the practical relevance of the ~10-13% larger leucine balance during the postprandial phase of the post-diet whole body protein metabolism test in week 6, I would not fret about this difference too much, though.

Maybe, just maybe, the adipocyte morphology could make a difference

What I would consider significant, though it did not reach that status (probably due to the low number of participant that actually made it to the end of the study, see red box on the right), is the slight but in my eyes potentially important superiority of the equally spread protein ingestion in terms with respect to the before vs. after adipocyte diameter in the casein group:

Figure 3: The difference did not reach statistical significance, but if we take for granted that greater reductions in adopcyte sizes are associated with healthier metabolic profiles, you would be better advised to take your casein protein equally spaced across (15% reduction in adipocyte size vs. 7%, only, for pulsed casein intake) the day... for whey, aka "milk soluble protein", on the other hand it does not seem to matter (data calculated base on Adechian. 2013)

Now, even if we assume that this made a difference and a greater reduction in adipocyte size was a significant advantage, which it probably is from a health perspective, as Skurk et al. state that there is

"[...] a differential expression of pro- and antiinflammatory factors with increasing adipocyte size resulting in a shift toward dominance of proinflammatory adipokines largely as a result of a dysregulation of hypertrophic, very large cells." (Skurk. 2006)

and a recently conducted human trial, by Rizkalla et al. the main message this study should be sending out is not that it does not make a difference whether you use casein or milk protein as your main protein source on a diet, but that a high protein diet with a mediocre caloric reduction of ~20-25% and supplemented with high quality dairy protein (whey or casein) works: After all, more than -1kg of weight loss per week, 68% of the weight loss from fat in the absence of exercise is more than your average celebrity XYZ diet will do for you ;-)

Whey or casein? It's high cysteine content that can help to replenish your glutathione (=the master antioxidant) pools would be another factor that speaks in favor of whey. Whether normal-weight individuals on an already optimized dietary regimen would benefit to the same extend as the obese young men in the 6-week whey supplementation trial, Vatani et al. describe in the August issue of Appetite, is however questionable. After all, the increases in HDL the total antioxidant capacity and glutathione is as questionable as any possible negative influence of the starchy placebo the researchers used in that study (some of you may have seen the link on the SuppVersity Facebook Wall, already).

Figure 4: Fat loss and lean mass gains in formerly overweight police officers after 12 weeks of training and dieting with or without casein / whey hydrosolate (Demling. 2000)

Moreover, one of the few long-term (=non acute protein synthesis) studies investigating the differential effects of concomitant whey vs. casein hydrosolate protein supplementation, found statistically significant higher body fat reductions and lean mass gains in those 33-34 year-old police officers who supplemented their 12-week diet + strength training regimen with 2x37g of casein hydrosolate (8h apart; for the exact data see figure 4; Demling. 2000).

Note: since both the whey (Pro-Score Champion Nutrition) and the casein protein (MET-Rx USA) in this study were hydrosolates the differences in lean mass gains and fat loss are depend primarily on the amino acid composition of the proteins, and not, as it would be with micelle casein vs. whey, the absorption kinetics!

Bottom Line: Against that background the study at hand supports previous findings of the importance of a threshold intake of protein. Interestingly, it did not confirm the notion that this threshold intake should be spread equally across the day, which is something most commenters (me included) read into the seminal paper by Loenneke et al., which found a statistically significant negative correlation not between total protein intake, but between the number of meals with 10g or more essential amino acids in them and abdominal obesity (Loenneke. 2013). So, does timing matter, or does it not? 

1. It does matter, when you work out, there is ample evidence to support that the ingestion of protein in the vicinity of the workout cannot just amplify the protein synthetic response but will also results in an increase in real world muscle gains.
2. It appears that it does not matter, when you are dieting (only), though; not just the study at hand, but also the success many people report on intermittent fasting regimen, would support the notion that the more sustained anabolism you may be able to achieve by ingesting say 4x25g of protein instead of 1x80 + 2x10g has, compared to the total amount of protein you eat, relatively little influence on the conservation of lean body mass, when you are dieting.

And as far as the choice between casein and milk soluble protein, aka whey (see first red box), is concerned (see box on the right, as well), it would appear prudent to assume that a combination of both - just like nature intended it - would be the best choice as a "standalone" protein source (cf. "Whey and Casein Work Hand in Hand for Protein Anabolism, but Scientists Overlook Fat, When They Reassemble Milk"), while the higher leucine content and faster digestibility render whey the better candidate for classic "supplementation", as in having an additional shake before you start preparing your whole-foods post-workout meal, which should - and I hope it's not really necessary that I say that - obviously include a significant amount of protein (fish, eggs, meats, and if you will even more dairy ;-), as well. The usefulness (again, not necessarily the superiority!)  of slow digesting protein is something you should be aware of, anyway, right? If not re-read the "3.2kg of Lean Mass Over Night W/ 40g of Slow Digesting Protein 30min Before Bed!?" post from February 22, 2013.

References:

• Adechian S, Balage M, Remond D, Migné C, Quignard-Boulange A, Marset-Baglieri A, Rousset S, Boirie Y, Gaudichon C, Dardevet D, Mosoni L. Protein feeding pattern, casein feeding or milk soluble protein feeding did not change the evolution of body composition during a short-term weight loss program. Am J Physiol Endocrinol Metab. 2013 Aug 14.
• Demling RH, DeSanti L. Effect of a hypocaloric diet, increased protein intake and resistance training on lean mass gains and fat mass loss in overweight police officers. Ann Nutr Metab. 2000;44(1):21-9.
• Hickman IJ, Whitehead JP. Structure, signalling and physiologic role of adiponectin - dietary and exercise-related variations. Curr Med Chem. 2013 Aug 9.
• Hoppe C, Mølgaard C, Dalum C, Vaag A, Michaelsen KF. Differential effects of casein versus whey on fasting plasma levels of insulin, IGF-1 and IGF-1/IGFBP-3: results from a randomized 7-day supplementation study in prepubertal boys. Eur J Clin Nutr. 2009 Sep;63(9):1076-83. 
• Lacroix M, Bos C, Léonil J, Airinei G, Luengo C, Daré S, Benamouzig R, Fouillet H, Fauquant J, Tomé D, Gaudichon C. Compared with casein or total milk protein, digestion of milk soluble proteins is too rapid to sustain the anabolic postprandial amino acid requirement. Am J Clin Nutr. 2006 Nov;84(5):1070-9.
• Li FY, Lam KS, Xu A. Therapeutic perspectives for adiponectin: an update. Curr Med Chem. 2013 Aug 9.
• Loenneke JP, Wilson JM, Manninen AH, Wray ME, Barnes JT, Pujol TJ. Quality protein intake is inversely related with abdominal fat. Nutr Metab (Lond). 2013 Jan 27;9(1):5. 
• Rizkalla SW, Prifti E, Cotillard A, Pelloux V, Rouault C, Allouche R, Laromiguière M, Kong L, Darakhshan F, Massiera F, Clement K. Differential effects of macronutrient content in 2 energy-restricted diets on cardiovascular risk factors and adipose tissue cell size in moderately obese individuals: a randomized controlled trial. Am J Clin Nutr. 2013 Jan;95(1):49-63.
• Skurk T, Alberti-Huber C, Herder C, Hauner H. Relationship between adipocyte size and adipokine expression and secretion. J Clin Endocrinol Metab. 2007 Mar;92(3):1023-33.
• Vatani DS, Golzar FA. Changes in Antioxidant Status and Cardiovascular Risk Factors of Overweight Young Men after Six Weeks Supplementation of Whey Protein Isolate and Resistance Training. Appetite. 2013 Aug 10.

3x15g/Day E401, Sodium-Alginate, Increase Weight Loss and Reduction in Body Fat % on Mild Caloric Deficit by 30-40%! The GPA (Gut-Brain Axis) Makes it Possible.

Image 1: The small amounts of sodium-alginate, aka E401 many chocolates and commercially produced foods contain is obviously not enough to ward off obesity. Otherwise the obesity rates should have fallen not risen with the increase in crappy foods.

Aside from the ubiquitous stimulant based fatburners there is another class of weight loss supplements emerging as of late. Those of you who have read Adelfo's Thursday post, here at the SuppVersity, may have seen his plug for Myotropics' WM-HDP based "new Fat Burning Carbohydrate" ThermiCarb(TM). Now as hilarious as it may sound, this resistant starch is in fact as much of a "fat burner" as any of the 1001 currently available stims is. After all, none of those products actively burns fat. What still makes them effective, though, is their ability to shift substrate utilization away from glucose and towards fat, to curb appetite and to deliver the energy you need to do what it takes to shed body fat, i.e. to function normally while eating slightly less and working out.

Contrary to the good old (and certainly not obsolete) stims, these new "fat burners" act on the gut-brain axis, instead of HPA (the hypothalamus-pituatary-adrenal axis), by stimulating the release of a whole host of peptides from the gut. Among those, the  incretin hormones GLP-1 & co. (cf. "Eat More, Burn More and Lose Fat Like on Crack with GLP-1!?") are probably the best understood among these mis-understood "satiety hormones" with their profound  downstream effects on overall energy expenditure, glucose and fatty acid metabolism (Mudaliar. 2013). 

Is alginate, a polysaccharide from marine brown algae, a novel "fat burning fiber"?

Next to designer-starches such as WM-HDP there is also an increasing interest in the effects natural fiber / fiber extracts, such as the 15g alginate from brown algae the obese subjects (0–55y; BMI 30-45kg/m²) in a recent study from the University of Copenhagen in Denmark had to consume before each of their three meals in the course of a 12-week double-blind randomized parallel-intervention (Jenson. 2013), exert on the endocrine signals from your gut.

Image 2: Popsticles are not the only products containing sodium alginate (E401) as a thickener and stabilizer. If you take a closer look at the ingredients of the stuff in the supermarkets, you will notice that  many commercially produced low fat dairy products, ready made sauces, gravies, dressings, puddings, pies and pastry fillings contain it, as well.

What is alginate? Alginate is a gelling polysaccharide (gelling = it forms a gel which passes slowly through your digestive tract) that is extracted from marine brown algae. In seaweed the mannuronic and guluronic acid based components are responsible for the mechanical strength and flexibility. During the regular extraction process alginate is bound to sodium. The result, sodium alginate, has been used a E401 in various foodstuffs to stabilize, gel or viscosify it for years now (Brownlee. 2005). The appetite reducing effects of sodium alginate and other marine-derived fiber are widely known, but the underlying mechanism is still not completely elucidated. According to the current paradigm, it is related to the interaction of sodium-alginate and calcium during the digestive process and the subsequent changes in viscosity of the gastric content, which has been associated with slowed gastric emptying and a reduction of postprandial glucose and insulin response. Of these the latter, i.e. the prolonged influx of glucose, the absence of blood glucose spikes and the overall reduction in insulin levels is currently believed to be at the heart of the observed satiety effects (Cani. 2009).

What is interesting about this study is that according to the self-set goals of the scientists, which lay at the ground of their "Intention-To-Treat analysis" (ITT), which evaluated the changes in body weight and overall body composition, as well as the improvements of metabolic risk factors as a whole, yielded no differences between the two study arms.

Figure 1: Changes in body weight and body composition in response to caloric reduction (-300kcal/day) with or without supplemental alginate (15g/day) after 12 weeks (large graph); actual weight development over the whole 12-week study period (small graph; directly from Jenson. 2013)

If you do yet take a closer look at the actual study data (see figure 1), you will see that there were very important differences between those dieters who simply consumed 300kcal/per day less (control group) and those who followed the exact same calorically reduced dietary regimen yet with an additional 15g of fiber from sodium alginate before every meal (alginate group)!

Lose more weight, more fat and do this at a constant rate beyond week 9!

Despite the fact that onlye the differences between the reduction in total weight and body fat percentage reached statistical significance, this and the absence of the "weight loss plateau" in week 9+ (see figure 1, right) in the alginate group clearly suggest that much contrary to what Jenson et al. had apprehended, the previously demonstrated short-term weight loss benefits of fibrous algae extract and other dietary fiber (Paxman. 2008; Odunsi. 2010; Peters. 2011; Wanders. 2011) did not disappear after an initial adaptation phase. On the contrary! The 40% greater reduction in body weight, as well as the 36% greater reduction in body fat percentage would be of little value if the body weight stagnated after only -6.78kg weight loss in week 9 and left the dieters with an average BMI of 32kg/m² well in the obesity / danger zone.

Figure 2: Changes in glucose metabolism and ghrelin (left) and lipid metabolism (right) in response to caloric reduction (-300kcal/day) with or without supplemental alginate (15g/day) after 12 weeks (large graph); actual weight development over the whole 12-week study period (small graph; directly from Jenson. 2013)

Looking back at the exact weight development in figure 1 (right), we may thus speculate that the observed improvements of the measured markers of blood glucose management and lipid metabolism of which only the HbA1c (not shown in figure 2) showed a statistically significant inter-group difference (+0.01% in control -0.01% in alginate; p < 0.024) would have reached statistical significance after 16-20 weeks. This is particularly true for the insulin levels, for which the difference between control and alginate group is already borderline significant (p < 0.062) after 12 weeks of alginate supported dieting.

Bottom line useful for the obese, safe, well tolerated, but...

Image 3: Duong Nguyen from the first installment of the SuppVersity Student Spotlight at the beginning and end of his amazing 12-week transformation!

As usual we do however have to remember that the subjects in this study were more than just a little chubby, with body fat percentages in the >40% range a reduction of -5.8% (control) and -8.2% (alginate) is easier achieved than a (from a merely mathematical standpoint) equal -12% of the body fat content from 12% to 10%. So, while healthy dieters don't have to care about the minimal, but statistically significantly lower reduction in blood pressure in response to weight loss with sodium-alginate (the scientists ascribe this to the relatively high sodium content of the alginate supplement), the will probably not benefit in the same way as Jenson's obese subjects from the additional 45g of fiber per day. Well, unless, it exerts similar effects effects as they have been observed for hydroxypropyl-distarches (cf. "Waxy Maize Reloaded") on the expression of GIP, GLP-1 and the whole host of the initially mentioned incretin hormones, and adipokines (Sánchez. 2013) and don't just curb appetite and slow digestion.

If it had all those GBA (gut brain axis ;-) effects, seaweed derived sodium-alginate supplements could however make an ideal adjunct to a ~20% reduction in food intake, a reasonable fat loss workout (e.g. "Step By Step Guide to Your Own Workout Routine - Part V: Example Routines - Round 2: Fat Loss Support Routine") and a stimulant-based fat burner of your choice, whenever you strive to cut a few pounds of body weight. I mean, just imagine if Duong (see image 3), who likewise dieted for 12 weeks would have lost 35% more fat mass - yeah you're right, he would probably have been "disgustingly" lean, as Adelfo likes to call it ;-)

References:

1. Brownlee IA, Allen A, Pearson JP, Dettmar PW, Havler ME, Atherton MR, Onsøyen E. Alginate as a source of dietary fiber. Crit Rev Food Sci Nutr 2005;45:497–510.
2. Cani PD, Lecourt E, Dewulf EM, Sohet FM, Pachikian BD, Naslain D, De Backer F, Neyrinck AM, Delzenne NM. Gut microbiota fermentation of prebiotics increases satietogenic and incretin gut peptide production with consequences for appetite sensation and glucose response after a meal. Am J Clin Nutr 2009;90:1236–43
3. Jensen GM, Kristensen M, Astrup A. Effect of alginate supplementation on weight loss in obese subjects completing a 12-wk energy-restricted diet: a randomized controlled trial. Am J Clin Nutr. 2013 Jul;96(1):5-13. Epub 2013 May 30.
4. Mudaliar S, Henry RR. The incretin hormones: from scientific discovery to practical therapeutics. Diabetologia. 2013 Jul;55(7):1865-8. Epub 2013 May 4.
5. Odunsi ST, Vazquez-Roque MI, Camilleri M, Papathanasopoulos A, Clark MM, Wodrich L, Lempke M, McKinzie S, Ryks M, Burton D, et al. Effect of alginate on satiation, appetite, gastric function, and selected gut satiety hormones in overweight and obesity. Obesity (Silver Spring) 2010;18:1579–84.
6. Paxman JR, Richardson JC, Dettmar PW, Corfe BM. Daily ingestion of alginate reduces energy intake in free-living subjects. Appetite 2008; 51:713–9.
7. Peters HP, Koppert RJ, Boers HM, Stro ¨m A, Melnikov SM, Haddeman E, Schuring EAH, Mela DJ,Wiseman SA. Dose-dependent suppression of hunger by a specific alginate in a low-viscosity drink formulation. Obesity (Silver Spring) 2011;19:1171–6.
8. Sánchez D, Miguel M, Aleixandre A. Dietary fiber, gut peptides, and adipocytokines. J Med Food. 2013 Mar;15(3):223-30. 
9. Wanders AJ, van den Borne JJGC, Graaf EJMF. Effects of three dietary fiber on food in real life setting. Appetite 2011;57:544.

More Muscles For Old Chaps, Less Fat for Baby Boomers: The Age Specific Anabolic Anti-Obesity Effect of HMB

Image 1: Nutrition, exercise and most importantly the right mindset will always be the foundation of leading a long, strong and healthy life - irrespective of how many supplements you take - you cannot out-supplement a bad diet, laziness and a lack of motivation and determination.

The hype was, as usual, huge, when back in the day Beta-Hydroxy-Beta-Methl-Butyrate (HMB), marketed as the natural alternative to Deca (Nandrolone; update: thx to anonymous for the heads-up that it was not just Anavar, as I original thought ;-), hit the market. What was yet even bigger than the hype, though, was the disappointment of customers who felt ripped off; and that not without reason, because the early HMB supplements were not only touted to be as effective as the previously mentioned anabolic steroid, they were also sold at similarly high prices and low doses, of which every scientists could easily have told you that the one thing that would grow were the purses of the manufacturers.When the marketing bubble eventually burst, the (at that time) pretty expensive and incredibly disgustingly tasting (no way you put a working amount of that stuff into a tasty pre- or postworkout amount without ruining the taste!) supplement disappeared from the market, literally overnight. Today, HMB is, if at all, sold as a standalone in 250mg-500mg capsule form or 250-1,000g pouches from bulk suppliers and leads an overall miserable existence being perceived as a probably useful, but simply unnecessary metabolite of the contemporary "natural Deca", leucine.

HMB - More than expensive leucine for old folks!?

The astonishing results of a recently published study from Jacob M Wilson's lab at the Department of Nutrition, Food and Exercise Sciences at The Florida State University in Tallahassee do yet suggest that at least the best-agers among the SuppVersity students, beta-hydroxy-beta-methl-butyrate could derive  undeniable advantages from the almost forgotten leucine metabolite (5% of a normal dietary leucine intake from food sources are metabolized into HMB; cf. Van Koevering et al.1993, according to Wilson. 2013). In what was allegedly "only another rodent study" (before you start complaining, please acknowledge that as long as you don't have your rodents "work out", those studies usually elicit pretty accurate results), the scientists enriched the diets of twelve young (44 wk.), 6 middle-aged (60 wk.), 10 old (86 wk.), and 5 very old (102 wk.) male rats with ~500mg/kg body weight HMB per day, which, using the standard conversion chart (cf. "Ask Dr. Andro: What Are Human Equivalent Doses "), yields a human equivalent of ~81mg/kg or 6.5g for a person who weighs 80kg.

Figure 1: Changes in body composition (left) and strength (right) during 16-week transition from young to middle age and old to very old age with and without supplementation in male Fisher rats (data adapted from Wilson. 2013)

As the data in figure 1 clearly shows this supplementation protocol (16 weeks, transition from young to middle aged and from old to very old) did not only prevent the decline in muscle strength, it had also pretty profound effects on the body composition of the aging animals. In case of the very old rodents, those effects were so profound (-56% body fat!) that it is questionable whether they were actually able to eat or rather metabolize enough food (food intake was not different) to accommodate for the +10% increase in lean mass.

HMB shuts down atrophic and ramps up myogenic factors, but why does it burn fat?

The late, but profound increase in lean mass in the very old animals (102wk) was brought about by a totally blunted increase in the "catabolic" Atrogin-1 signaling, the expression of which is so characteristic of aging skeletal muscle, and (and this is actually surprising) an increase of the "anabolic" myogenin expression that yielded myogenin levels which exceed those of the young (44 week) control group by +40%!

Although these changes in Atrogin-1 and myogenin expression can explain the anti-sarcopenic (=working against the age-induced decline in muscle mass) effects of HMB and would even suggest tat it is a very useful "muscle builder" in the elderly population, where similar amounts of leucine (7.5g) have hitherto not yielded not the desired results (Verhoeven. 2009), they do not explain the unquestionably profound effect on the total fat mass of the animals, which reached statistical significance during both, the transition from young to a middle age (HMB body fat change not significant vs. +49% body fat mass in control) and the transition from the old to the very old age (HMB body fat -56%, control -8% n.s.) and of which Wilson et al. say (Wilson. 2013):

To date, the underlying mechanisms that HMB exerts its effects on adipose remain to be elucidated. It may be that HMB directly increases oxidative capacity in myofibers, as exposure of cultured myotubes to the leucine metabolite increased palmitate oxidation by 30%.

If the latter, i.e. the increase in palmitate oxidation transfers to human studies, Skelton et al. observed in their in-vitro studies (Skelton. 1994, according to Wilson. 2013), was dose dependent, I would be interested to see studies on the effect of twice the amount of the 3.0g/day HMB per day that did already produce greater increases in lean and decreases in fat mass over the course of a four week resistance training program in a twelve-year-old study in young (Panton. 2000), as well as an eleven-year-old study in 70-year old individuals (Vukovic. 2001), in younger and older trainees, and sedentary individuals.

Something to think about

Also, what if HMB was in fact one of the rare cases, where "more" actually yields "more". I mean, wouldn't it be remotely possible that our body's ability to convert leucine to HMB is not just rate limited, but that the rate decreases with age (this would explain why leucine works much better in younger folks) and saturates, when a certain concentration of HMB is achieved (if that was the case even the 5% conversion could be questionable, because you could have an upper limit of say 500mg, which would be 5% of 10g leucine and just 1% of 50g)? The latter would mean that you could not produce more than x grams of HMB total per day and would imply that the "old natural Deca" could in fact turn out to be superior to the "new natural Deca" for trainees (and maybe even non-trainees) from all age groups - as long as the dosage was appropriate, i.e. beyond what your body would produce from dietary leucine.

References:

1. Panton LB, Rathmacher JA, Baier S, Nissen S. Nutritional supplementation of the leucine metabolite beta-hydroxy-beta-methylbutyrate (hmb) during resistance training.Nutrition 2000,16(9):734-739.
2. Skelton DA, Greig CA, Davies JM, Young A. Strength, power and related functional ability of healthy people aged 65-89 years. Age Ageing 1994, 23(5):371-377
3. Van Koevering M, Gill DR, Smith RA, Owens F, Nissen S, Ball R. Effect of β-hydroxy-β-methyl butyrate on the health and performance of shipping-stressed calves.Oklahoma State Univ Res Rep; 1993, 312-331.
4. Vukovich MD, Stubbs NB, Bohlken RM. Body composition in 70-year-old adults responds to dietary beta-hydroxy-beta-methylbutyrate similarly to that of young adults. J Nutr. 2001 Jul;131(7):2049-52.
5. Wilson JM, Grant SC, Lee SR, Masad IS, Park YM, Henning PC, Stout JR, Loenneke JP, Arjmandi BH, Panton LB, Kim JS. Beta-hydroxy-beta-methyl-butyrate blunts negative age-related changes in body composition, functionality and myofiber dimensions in rats. J Int Soc Sports Nutr. 2013 Apr 18;9(1):18.

Scientific BB Contest Prep Coverage: Six Months of Dieting, Daily Workouts & Hormonal + Metabolic Shutdown Pave the Natural Way to the Sub 5% Body Fat Zone

Dexter Jackson was not the 26-year old natural bodybuilder in the study at hand, but he is the Winner of the Arnold '13 (Photo bb.com)

Who would have thought that!? Dexter Jackson won the Arnold Classic 2013. "The Blade" as Jackson is also called has been competing ever since 1999 and will thus probably be able to tell you one thing or another about the hardships bodybuilders have to go through during the pre-contest phase. It is these hardships today's SuppVersity post will be dealing with - the hardships of those who do (almost) everything to "peak" (=achieve the best conditioning possible) at day 0 and in this particular case without resorting to all the readily and less readily  available "helpers" from the arsenal of the "big guys".

People like the 26 year-old caucasian, natural, professional bodybuilder, whose latest contest prep has been monitored by Lindy M. Rossow and her colleagues from the Department of Health and Exercise Science at the University of Oklahoma and her colleagues from the Creighton University and the University of Central Florida (note: the whole study period comprised 12 months, 6 months prep and 6 months follow-up and the data on diet and training volume were derived from the subjects meticulous food and workout logs).

Diet, meal planning and nutrient timing

With 5 meals per day and occasional week-by-week reductions in fat and carbohydrate intake (5-10g), whenever he felt he stagnated, neither the meal pattern nor the total energy intake (~2,500kcal/day) of the subject changed dramatically over the course of the pre-contest period.

With a ratio of 36/36/28 % the macronutrient ratio of the pro-bobyduilder who started out with a body-fat percentage of 14.8% (4-C model based on DXA and BOD POD data vs. 8.9% when measured by chest, abs and thigh skinfolds), was very balanced and actually pretty close to what I suggested in my interview with Sean for CasePerformance for both average Joes and Janes and aspiring gymrats alike (read the whole interview here).

Figure 1: Overview of the key aspects of the nutritional regimen in the pre-contest (Prep), immediately pre-contest (last wee before the show) and the subsequent recovery period (based on data from Rossow. 2013)

With two moderate carb-refeeds per week during which he increased his carbohydrate intake to 48% (see figure 1), the subject, who had won his pro-card two years before he agreed to participate in this study, stuck to the above macronutrient ratios until "just prior" to competition, when he dropped the carbohydrate intake to <30% and increased the protein intake to 46% keeping fats almost stable at 25%. When we do the math in order to calculate the corresponding nutrient intakes in grams we get ~207g of protein (, 130g of carbohydrates and 112g in the last phase of the contest prep.

There is evidence that a high carb bulk works best the classic way, i.e. with almost zero fat (read more)

"I don't want to gain fat too quickly afterwards": While the subjects declared goal for the post-competition phase was "not to regain body fat too quickly", his irregular and unquestionable ravenous eating habits tell us that he must have forgotten about that ;-)

No wonder his body fat levels shot up to 15.5% (higher than precontest) within 5 months, then stabilized and despite constant overeating began to drop again. What is an interesting side-note that over the whole study period, but especially in the off season, the often hailed skin-fold measurements hilariously underestimating the body fat content (the values were up to 8% off).

The only supplements the subject took were 5g/day of creatine and whey protein, which was already part of the regular diet and thus included in the macro-breakdown in figure 1 and the ~200g/day of protein I calculated based on the not exactly exhausting information about the exact macronutrient and energy content of the diet.

Strength and cardio - working out every day is key

A key contributer to the sustained weight- and, as we are going to see in figure 3 further below, fat loss at a relatively high energy intake (2,500kcal at a starting weight of ~100kg is obviously below maintenance, but no starvation diet) is probably the versatile workout routine with daily workouts, except on days before the exercise tests at the lab were conducted.

"During competitive preparation, per week on average, the subject performed four days of resistance training (5 hourst total per week), two days of high intensity interval training (HIIT, 40 minutes total per week), and one day of low-intensity, steady-state, aerobic exercise (30 minutes per week). This resistance training split allowed for the athlete to train each major muscle group twice per week."

This training regimen, as well as the often underestimated 30-60s isometric contractions during the 15-30 min posing practices the subject performed only once in the initial 1-6 weeks and 2-4 times per week during weeks 20-26, will have done one last thing to propel the fat loss in face of a constantly declining resting metabolic rate. The latter, as well as the hormonal changes, the dropping blood pressure and the - for a non-athlete - dangerously low heart rate all point towards one thing: Metabolic shutdown (see figure 2):

Figure 2: If you want to know about the hormonal / metabolic consequences of cutting down to sub-natural body fat levels (4.5% for the guy in the study) this is the graph to look at (data expressed relative to pre-prep values; based on Rossow. 2013).

As I have already hinted at in one of the infoboxes in figure 2 the resting metabolic rate the scientists measured only thrice during the 12-months observation phase, i.e. twice before and once after the contest  dropped by >1,000kcal from week -25 to week -1 (=one week before the contest) and did not fully recover within the 12 weeks up to the subject's last REE assessment with a metabolic cart.

A note to the desperate haters out there:  No, I did not check the guy's urine for additional "supplements", so I cannot know for sure whether he was indeed natural. What I do however know is that you were just about to post something along the lines of "you cannot achieve this level of conditioning without drugs" - obviously, without daring to do so under your own name. Do me and yourself a favor and spend the time and energy in the gym instead - thank you!

Starvation mode without starvation = continuous fat loss?

In view of these metabolic changes the drastic reduction in body fat (%) from 14.8% to 4.5% appears surprising. Likewise, common sense would tell you that the cortisol increase (more than +100%) would (a) burn away your muscles in no time and (b) stop your fat loss in tracks. The data in figure 3 does yet speak a very different language.

Figure 3: Body mass, fat free mass and body fat % over the 12-months study period (Rossow. 2013)

What the increase in cortisol did, was saving our dieter's brain from starving while getting him shredded by facilitating the catecholamine induced lipolysis (=squeezing the fat out of the cells) and bugging the liver to produce more glucose (Exton. 1972; Lamberts. 1975). That the substrate for the increased hepatic gluconeogenesis was not exclusively fat, but also protein should be obvious. As obvious as the fact the contribution of muscle protein was still negligible compared to the energy that came from the adipose tissue. Otherwise you could hardly explain that the subject lost not even 3kg of lean mass, while he dropped 14kg of body weight and kept the hydration level constant (62.6% at the beginning and 62.12% on contest day).

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Chronically fatigued? Taking a meditative time-out with qigong twice weekly will improve mental + physical symptoms by ~50% & increase telomere-length by 75%! (learn more)

Bottom line: If you look at the time it took the subject of the study to get down to the <5% body fat range and at how his body reacted (cf. The Athlete's Triad), I probably don't have to mention that the notion that any of these guys, drugged or not, is running around like you see him on stage or in the magazines all year is hilarious.

This does also mean that any training program that aims at running around at real (and not caliper measured) single-digit body fat levels year round is destined to fail and will go hand in hand with hypogonadism, low thyroid levels, 6-7x elevated fatigue levels, confusion, anger, hostility and overall 7x higher levels of mood disturbances. I bet your significant other will like neither the former nor the latter symptoms and let's be honest, even if you are single, would this be worth it?

"So are natural bodybuilders stupid idiots?" 

Certainly not! The exact opposite is the case, people like the subject in the study at hand have a goal and the plan, the determination and the guts to achieve it. They want to show up on stage in the best form possible, never knowing whether this will be enough to take the trophy home. They are sportsmen like so many other athletes; and while it may be debatable how healthy these ups and downs in body weight eventually are, I would venture the guess that natural bodybuilding is not unhealthier than American football.

So, if there is anything "idiotic" about bodybuilding, it would probably be its unintended downstream effects on some of the gymrats who believe they can have the upsides, i.e. the hyper-muscular contest-ready sub 5% body fat look, without the downside, i.e. the time spend at a normal body fat level of ~12-15%.

Moreover, if you look at the way the guy in the study broke through the 5% body fat wall, there is just one thing that sticks out: persistence! Patience and a stubborn persistence. No low-to-no-carb diets, no no-fat interventions, no protein only days, not even intermittent fasting or thermogenics and certainly no natural test boosters.  If you feel that you have the persistence and want to step on stage, go for it, but be aware that it's not going to be an easy ride.

References:

• Exton JH, Friedmann N, Wong EH, Brineaux JP, Corbin JD, Park CR. Interaction of glucocorticoids with glucagon and epinephrine in the control of gluconeogenesis and glycogenolysis in liver and of lipolysis in adipose tissue. J Biol Chem. 1972 Jun 10;247(11):3579-88.
• Lamberts SW, Timmermans HA, Kramer-Blankestijn M, Birkenhäger JC. The mechanism of the potentiating effect of glucocorticoids on catecholamine-induced lipolysis. Metabolism. 1975 Jun;24(6):681-89.
• Rossow LM, Fukuda DH, Fahs CA, Loenneke JP, Stout JR. Natural Bodybuilding Competition Preparation and Recovery: A 12-Month Case Study. Int J Sports Physiol Perform. 2013 Feb 14.

Science Round-Up Seconds: Rare Sugar Syrup, HFCS 2.0? Body Recomposition W/ 7 Marathons in 7 Days!? Reduced REM Sleep With Intense Workouts in the Evening.

99% of the guys & gals on this photo are not going to see anywhere similar improvements in body composition from marathon running as the highly trained 7x7 runners in the Karstoft study.

It's Friday and that means its time for the wrap-up of yesterday's installment of the Science Round-Up on SHR. Well, let's see then what this weeks Round-Up of the Round-Up has to offer. Somehow I felt like picking up something we did actually cover in the live-show yesterday (download the podcast here). I guess I want to give everyone the chance to look at the data himself in order to decide whether "rare sugar syrup" (RSS) is going to be the savior of the Western world and the unfortunate rest who's currently "westernized" by the big Ms, the big As and the rest of the corporate alphabet soup with a vested interest in the prosperity of mankind, or - to be precise - that the part of mankind who owns their shares ;-)

Rare Sugar Syrup has 90% of the sweetness of regular sugar + "cleaner taste" than HFCS

(IIda. 2013) -- Assuming that you've by now all listened to the podcast, I will stick to some additional explanations, citations and graphs in this follow up.

While D-psicose is not the only fructose epimer in rare sugar syrup, it is probable the one with the most potent beneficial effects on blood glucose management (learn more). One potential caveats of RSS is that its d-psycose content is only 5% with te rest being other hexoses including D-allose, D-sorbose, and D-mannose,

As the scientists point out, the main intention of their study was to assess whether their rare sugar syrups would suppress

"body weight gain and abdominal fat accumulation in rats fed on diets composed of different carbohydrate sources: starch, starch + HFCS (50:50), and starch + RSS (50:50) were examined. (Iida. 2013)"

Accordingly, they maintained their rodents on otherwise identical diets containing (on a per weight not per kcal basis!) 57% carbs, 18% protein, 4% fat, cellulose, added methionine and a couple of vitamin and trace elements with either plain corn starch, corn starch and HFCS or cornstarch and rare sugar syrup (see figure 1, left).

Now, as mentioned in the show, there is no debating that this feeding regimen worked and with "90% of the sweetness of sucrose, and a more rich and clean taste than HFCS" replacing HFCS with RSS could even improve the taste of respective products, but let's be honest: How likely is it that we are going to see products without HFCS and 50% of rare sugar syrup actually making up the lion's share of the processed junk in the super market anytime soon?

Figure 1: Carbohyrate content of the diets and weight of different visceral fat pads after the 8-week dietary intervention in otherwise healthy rodents on a cornstarch only, cornstarch + HFCS or cornstarch + RSS diet (Iida. 2013)

Isn't it more likely that you will see labels like "now with rare sugars" on the front of the packaging and the hardly legible figure "contains 3% carbohydrates from rare sugars" hidden on its back? I would think so and the fact that neither this study nor the general existence of this HFCS substitution did as of now hit the media certainly doesn't refute contradict this hypothesis.

7 marathons (!) in 7 days - A marathon a day keeps the fat stores at bay?

(Karstoft. 2013) -- I probably don't have to preface this part of the seconds with a "don't do this at home" (or anywhere else ;-), but I think it's nevertheless newsworthy that accordingly trained people can actually run 7 marathons  in 7 days without the dreaded negative effects the average bro is expecting when he is just walking for 40min on a treadmill.

Figure 2: Body composition before and after the race (left) and changes in markers of muscle damage as well as hormonal changes and differences in markers of blood glucose management (right) in 8 experienced recreational runners participating in a multiple-marathon running event in which 7 marathons were completed on consecutive days (Karstoft. 2013)

Doesn't look so bad, ha? The reason I still stick to the initially voiced recommendation not to copy this protocol if you intend to lose body fat is pretty simple. The main reason "nothing" happened here is that the subjects were conditioned to run marathons.

That's the same "repeated bout effect, we have seen only a couple of days ago in the "No Pain No Gain" post (click here to go back) and the ~2kg of "muscle mass" are (despite being measured with DEXA) probably rather a result of glycogen hyper-compensation from tons of energy gels and pasta (the subjects did not follow a prescribed diet, but simply ate, drank and supplemented what had helped them on previous marathons), than structural increases in muscle tissue.

No high intensity training before a good night's sleep

Unless you have read the SuppVersity Circadian Rhythm Series, you have no right to complain about being overweight or undermuscled (read it ;-)

(Wong. 2013) -- After listening to the show, you know what you got to do once you got out of the bed, namely to switch on your bright light therapy lamp, but what do you have to do before you go to bed? I did actually discuss most of the things you should do (curtains, ear-plugs, turn the temperature down, etc.) in the Circadian Rhythm Series, but with the recent publication of a study by Wong et al. there is another thing you should - or in this case should not do and that's working out at a high intensity.

According to the results the researchers present in their soon-to-be-published paper in the Journal of Sports Science, a cycling exercise at intensities of  65% and 75% VO2Max lead to significant increases in light sleep and reductions in the recuperative REM sleep from 22.5% to 19& and 18.7% of the total sleep time.

Light exercise, in this study done at 45% and 55% of the VO2max, on the other hand did not have these side effects it did however not improve sleep, which is by the way an urban myth of which Driver and Taylor wrote in a Y2k paper in the Sleep Medicine Review that it "has yet to be established empirically" (Driver & Tailor. 2000).

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That's it for today, unless you want to head over to the SuppVersity Facebook Wall and check out some of the news that are already available over there, e.g.

• 

  Newsweek title from the year 2000 - "Fat for Life?"; did his mother love her soy protein more than her son's health? (learn more)

  "High" dose supplementation with vitamin C and/or E increases cataract risk - 1,000mg of vitamin C increase the risk +36% and 100mg of vitamin E by 57% (read more)
• Aerobic fitness could have greater impact on academic achievement than obesity -- Although obesity is a concern for children, this study shows that aerobic fitness can have a greater effect on academic performance than weigh (read more) 
• Aqua Mel, Portuguese "folk medicine" works for the alleviation of simple symptoms of upper respiratory tract -- Effect probably mitigated by the phenols in the honey this product is made of (read more).
• Serum albumin carries cholesterol out of the cells -- Hitherto scientists thought that this was a prerogative of HDL (read more)

If you don't like these or the other ones I did not mention just wait for further news to be posted. Alternatively switch of the computer and your mobile devices and head off into a well deserved weekend!

Don't worry, there is going to be a whole heap of short news tomorrow, you won't get bored... ah, you don't get bored on the weekend, anyway - do you?

References:

• Driver H.S., Taylor SR. Exercise and sleep. Sleep Medicine Reviews. 2000; 4(4):387–402
• Iida T, Yamada T, Hayashi N, Okuma K, Izumori K, Ishii R, Matsuo T. Reduction of abdominal fat accumulation in rats by 8-week ingestion of a newly developed sweetener made from high fructose corn syrup. Food Chem. 2013 Jun 1;138(2-3):781-5.
• Karstoft K, James Solomon TP, Laye MJ, Pedersen BK. Daily Marathon Running for a Week - the Biochemical and Body Compositional Effects of Participation. J Strength Cond Res. 2013 Feb 25.
• Wong SN, Halaki M, Chow CM. The effects of moderate to vigorous aerobic exercise on the sleep need of sedentary young adults. J Sports Sci. 2013 Feb;31(4):381-6.

Buffered Alternate Day Fasting + Light Aerobics Cut Body Fat, Maintain Lean Mass & Improve LDL Particle Size. Plus: Conventional Alternate Day Fasting Detrimental for Fertility

This is how the "buffered" alternate day fast works: You eat 1/4 of the White Choc Banana Cream Pie on your fasting day and a whole pie on the next one - well, not really, but the ratios would be right ;-)

I guess at least the SuppVersity facebook friends are probably going to remember the study today's article is dealing with: "Alternate day fasting and endurance exercise combine to reduce body weight and favorably alter plasma lipids in obese humans." To me that sounded like Intermittent Fasting Done Wrong Does Still Produce Great Results, When You Combine It With an Aerobic Exercise Regimen", when I first read the abstract. After taking a brief look at the full-text (thx John!),  however, my perspective on the study changed from "even a dog has its day" to "that oes look interesting, let's see whether this kind of buffered alternate day fasting" is able to take bear up with a classic intermittent fast. 


A brief warning with respect to the data in figure 1: I know that a couple of you are too lazy to actually read the article and do headline + figure hopping. If you intend to to that, please keep in mind that the data in figure 1 is from another recent study, I used to illustrate the negative effects of "real" alternate day fasting.

Not all alternate day fasting is created equal

For the course of this 12-week, randomized, controlled, parallel-arm feeding trial the participants, 61 women and only 3 men aged 25 to 65 years, overweight / obese (BMI 30-39.9kg/m²) and weight stable for at least 3 months were randomized to one of the four study arms (unfortunately the data does not allow for any conclusions, whether the men and women reacted differently to the intervention or "real" alternate day fasting the data from the rodent study I discuss in the interlude surrounding figure 1 shows that this is the case, though):

• control group (C): sedentary, no diet

• exercise group (E): 25, 30, 35, 40min at intensities of 60, 65, 70, 56% of the calculated HRmax (intensity and duration were increased in week 4, 7 and 10)

• alternate day fasting group (ADF): after 4-week controlled feeding period the study concluded with an 8-week self-selected feeding period.
  

  

  As long as study subjects just have to eat what scientists serve them, every diet works. When they are however told to eat a high protein diet, for example, even the reported nutrient intake diverges massively from what the scientists had in mind, when they devised the protocol - you don't believe me? Well, then read for yourself, "What Really Happens, When Science Meets the Real World"

  "During the controlled feeding period (week 1-4) participants consumed 25% of their baseline energy needs on the "fast day” (24 h) and consumed food ad libitum on each "feed day” (24 h). [...] The diet consisted of a 3-day rotating menu plan, and all fast day meals were prepared in the metabolic kitchen of the Human Nutrition Research Unit (HNRU). Fast day meals were consumed between 12.00 pm and 2.00 pm to ensure that each subject was undergoing the same duration of fasting.[...] During the self-selected feeding period (week 8-12) subjects continued with the ADF regimen but no the fast day food was provided to them. Instead, each subject met with a dietician at the beginning of each week to learn how to maintain the ADF regimen on his or her own at home." (Bhuatin. 2013)

  During the counseling sessions the participants were also instructed to make (I quote) "healthy foodchoices on the ad libitum feed days by choosing low fat meat and dairy options and
  increasing fruit and vegetable intake." (Bhutani. 2013)

• combination group (ADF + E): combination of alternate day fasting and exercise protocol

Table 1: Nutrient composition of the fast day diet provided to the combination and ADF groups (Bhutani. 2013)

So, as you've learned from the above overview this was no "alternate day fast", as I had expected it to be, when I read the term "Alternate Day Fasting (ADF)" in the abstract of the study. With 450kcal/day and a nutrient composition providing 50% of the energy in form of carbohydrates, and 25% (each) from fat and protein the "fasting days" were characterized by a low caloric intake (see table 1), but should not have triggered a similar starvation response as the classic alternate day fasting regimen in a recently published rodent study by Kamur et al. from which the data in figure 1 is derived.

Let's briefly take a look why "real" alternate day fasting may not be a good idea

As you can see the effect of the alternate day fasting regimen in the Kumar study, in the course of which the rodents simply did not receive any food for a whole day, had profound negative effects on the hypothalamo-gypophysial-gonadal axis - especially in the female rodents.

Figure 1: Effects of every-other day fasting vs.ad libitum feeding on ovarian weight, estradiol, lutenizing hormone, leptin, and testosterone in female and male rodents (Kumar. 2013)

Now the first thing that will jump your eye is certainly the profound increase in serum estrogen in the IF group. Looks strange and certainly not anywhere near what you would have expected right? If you think that this cannot be that bad, you are probably a man, is that right? I see... so what really is bad about the estrogen explosion is actually that it is "living proof" of the total disruption of the cyclic interplay between estrogen and progesterone that's at the heart of female (in-)fertility (on a side note: the male rodents simply got skinny fat on that regimen).

Now why didn't these adverse events occur in the study at hand?

Actually I am only assuming that there were not similar negative effects in the study at hand. After all, we don't have the respective hormonal and even in the rodents it took it's time (2 cycles) until the females were totally infertile. Changes like these would thus probably have gone unrecognized. I do however suspect that the major factors contributing to the overall hormonal decline in the rodent study were the extendended time-span without food and the overall caloric deficit, which is usually ~30-40% of the habitual intake in rodents on alternate day fasting regimen, as they do not compensate for the fasting day on the subsequent day.

Figure 2: Changes in body composition in the combined, ADF, exercise and control groups (Bhutani. 2013)

With the extended fast being absent and a ~75% reduction in calorie intake on the fasting days, only (humans are unfortunately much better in "compensating" for a lack of food on a fasting day, anyway ;-) and the huge amount of adipose tissue the rodents in the Kumar study obviously did not have as an "emergency reserve", it is therefore unlikely that the beneficial changes in body composition Bhutani and his colleagues observed in their 64 subjects (see figure 2) were accompanied by hormonal deteriorations (although 61 of them were, as previously mentioned, female).

Figure 3: Changes in lipid profile (left) and glucose metabolism in the combined, ADF, exercise and control groups (Bhutani. 2013)

It is nevertheless interesting to see that there were no significant improvements in fasting glucose, insulin or HOMA-IR (the measure of long-term blood glucose levels; not shown in figure 3) in any of the groups. Moreover, the improvements in total LDL and HDL cholesterol were only significant in the combined group and that the total amount of the inflammatory marker CRP remained essentially the same in all four arms of the 12-week intervention study.

Image 2: Ramadan fasting can serve as a relatively well studied "model" of intermittent fasting. With the additional restriction of water intake and the common practice of rising early to have breakfast there are yet non-negligible differences. You can find more information about the strengths and limitations of this model in Part 2 and Part 3 of the IF series.

A brief reminder for everyone who missed the Intermittent Thoughts on Intermittent fasting series back in the day: If there is one thing we can take away from studies investigating the effects Ramadan fasting (a Muslim fasting ritual, where you eat only when the sun goes down) it is that eating the same amount of food at different times of the day alone is not going to make you lose weight. If you do intermittent fasting in order to lose weight you still have to achieve a caloric deficit. Plus, when you are doing it during a bulk, I personally suspect that you are more likely to gain body fat, simply because your body cannot make "good use" (=muscle glycogen and skeletal muscle protein) from all the food you will be cramming down in a small fasting window. So, if you insist on IF on a bulk, do at least increase your feeding window to 8h to be able to spread your energy intake more evenly.

Based on a comparison of the data from all three groups, we can yet also conclude that it is the alternate day fasting (or probably rather the caloric deficit) that exerts the beneficial effects on what the scientists subsume under the umbrella term "CHD risk indicators":

"the combinationof ADF plus exercise decreased LDL cholesterol (12% from baseline) while increasing HDL cholesterol (18% from baseline); a change that was not noted for any other intervention. The combination group also experienced an increase in LDL particle size, and a  reduction in the proportion of small LDL and HDL particles." (Bhutani. 2013)

Only later in the discussion of their results do they mention that those "CHD risk indicators" improved to the same extend in the ADF only group - with even more significant changes in the particle profile.

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Learn why breakfast is probably not the "most", but rather the least "important meal of the day" (read more).

Bottom line: The weight and fat loss are certainly intriguing. The regimen appears to be reasonably easy to follow and the fact that the improvements in glucose metabolism were marginal could well be related to the fact that the subjects were - despite being seriously overweight (!) - not diabetic.

Keeping all that in mind I am still not convinced that a regular intermittent fasting routine (16-18h fasting window on every day; learn more about intermittent fasting here at the SuppVersity) and a combined aerobic + strength training regimen would not have yielded even superior results. The average physical culturist probably will be better of with this by now almost "classic" diet routine.

References:

• Bhutani S, Klempel MC, Kroeger CM, Trepanowski JF, Varady KA. Alternate day fasting and endurance exercise combine to reduce body weight and favorably alter plasma lipids in obese humans. Obesity (Silver Spring). 2013 Feb 14.
• Kumar S, Kaur G. Intermittent Fasting Dietary Restriction Regimen Negatively Influences Reproduction in Young Rats: A Study of Hypothalamo-Hypophysial-Gonadal Axis. PLoS ONE. 2013; 8(1): e52416.