Dietary Fiber - Friend or Foe? Addition of Hydroxpropyl-Methylcellulose, a Non-Fermentable Viscous Fiber, to Standard(!) Rodent Chow Reduces Fat Gain by -22%

Image 1: Just as about everything, these days, you can buy the semisynthetic non-fermentable viscous fiber Hydroxpropyl-Methylcellulose pound-wise from China - this is probably also where the producers of the junk food you hopefully are not eating get their E464 from ;-)

If the health and fitness community on the Internet was a battlefield (personally, I sometimes think it is ;-) one of the ongoing skirmishes would certainly be fought over the question whether the deliberate ingestion of great amounts of dietary fiber was a good or rather a bad thing. I must admit that I have not really made up my mind on the benefits and caveats of increasing or decreasing your fiber intake, partly because the available science appears to be quite inconclusive. This, obviously does not hinder the "ANTI faction" in the fitness and nutrition world to add "fiber" as the 1001 item on their never-ending list of ultimate dietary evils. My gut feeling does yet tells me this has more to do with the fact that mainstream dietary recommendations list dietary fiber as a "healthy food" to eat, than with a thorough research of the available literature, which has, as of lately, been extended by a particularly interesting study from scientists from the Department of Food Science and Nutrition at the University of Minnesota and the Pennington Biomedical Research Center in Baton Rouge, Louisiana (Islam. 2011).

When fiber ain't fiber, natural is not naturally better

Being aware of the partly contradictory results previous studies on the metabolic effect (as measured in the lab and not by the way your poo-poo looks or how often you have to go to the toilette, like the "experts" like to do it ;-), Ajmila Islam and her colleagues fed a group of 6 week-old male Wistar rats a standardized rodent chow (AIN-93G, composition see figure 1 in previous blogpost) with either hydroxypropyl-
methylcellulose (HPMC) or standard cellulose as a source of dietary fiber, which comprised 5% of the animals' otherwise totally identical diets. This obviously sounds nonsensical if you follow the usual black or white approach to nutrition (which btw. is propagated by the mainstream and the ANTIs, as well), after all fiber is fiber and should be good or bad!? Well, it turns out that there are more than subtle differences in

1. the viscosity of the fiber / fiber food mixture, and
2. the fermentability of different types of dietary fiber

Now, cellulose the main component in plant cell walls and "the fiber" most mainstream dietitians (and their ANTI opponents) have in mind, when they are talking about the beneficial / detrimental effects of "dietary fiber", is neither viscous nor readily fermentable. Hydroxypropyl-methylcellulose (HPMC) is also non-fermentable, but contrary to its naturally occurring cousin it has a high viscosity.

Hydroxypropyl-methylcellulose, short HPMC, is a semisynthetic, inert, viscoelastic polymer that is used as an ophthalmic lubricant, as well as an excipient and controlled-delivery component in oral medicaments, and has, under the disguise of the "E-number" E464, already found its way into a lot of commercially produced foodstuff, where it is used as an emulsifier, thickening and suspending agent, and as an alternative to animal gelatin.

While its artificial origin will obviously make the ANTI faction cry out loud, again, I suggest you first read about the effect HPMC had on the animals, before you totally discard it as being "not natural", "non paleo", "the work of Monsatan" or whatever...(btw. it is at least kosher ;-)

Figure 1: Changes in body composition (weights in g) after 6 weeks on standard diet with either non-viscous cellulose or viscous hydroxypropyl-methylcellulose as the primary source (5%) of dietary fiber (data adapted from Islam. 2011).

If you look at the data in figure 1, you will have to assert that the body composition of the lab animals did benefit from 6 weeks on the 5% HPMC diet. With a -29% reduction in the increases in purportedly "dangerous visceral fat", a -22% reduction in total adipose tissue gain and non-significant changes in lean mass accrual HMPC easily outperform the "Allis" and "Orlistats" of the pharmaceutical industry. Moreover, while the latter simply reduce the amount of dietary fat that is actually digested (an idiotic approach to weight loss, if you asked me), the non-fermentable viscous fiber in the Islam study worked its fat burning magic right via increases in AMPK, COX, citrate synthase, PGC-alpha, PPAR-delta and UCP3 expression, or, put simply: The 5% HPMC diet ramped up mitochondrial fatty acid oxidation.

Figure 2: Changes (relative to cellulose group) in gene expression in liver and soleus muscle of HMPC fed rats (data adapted from Islam. 2011).

Nevertheless, the slight, yet statistically significant smaller increases in bone density in the HPMC group (+6.4g vs. +7.4g) do suggest that in addition to these inert metabolic effect, the mere excretion of parts of the diets (with respect to bone density probably minerals like calcium and phosphorus), of which the animals in both groups consumed about identical amounts, could also have contributed to the otherwise beneficial effects of HPMC feeding, which, as the profound decrease (-41%) in liver PEPCK expression suggests, also included reductions in the hepatic rate of gluconeogenesis.

Figure 3: Changes (relative to cellulose group) in glucose metablism and adipokine expression of HMPC fed rats (data adapted from Islam. 2011).

The overall beneficial effects on glucose and fatty acid metabolism, by the way, are also reflected in the changes in blood glucose and adipokine concentrations I plotted in figure 3. The lower insulin and leptin levels in the presence of reduced body fat stores indicate increased insulin and leptin sensitivity and could be partly mediated by the marked increase in adiponectin expression, as the latter, as Islam et al. point out, has been found to have an "insulin sensitizing effect in both muscle and liver and a thermogenic effect (enhanced lipid metabolism) in skeletal muscle".

"Fiber is good, then! Right?"

Contrary to cellulose and fermentable viscous fiber, such as guar gum, of which a 2010 study by Isken et al. (Isken. 2010) found that it had, fed at 10% of the diet of mice, no effect on body fat levels in the short term (15 weeks) and even increased adiposity in the long-term (from 27 weeks to 43 weeks), short term feeding with 5% hydroxypropyl-methylcellulose (HPMC) exhibited unexpectedly profound beneficial effects on the metabolism of these otherwise healthy and normally fed (this is important, because we usually see fiber supplementation in the context of "high fat" diets) rodents.

Whether it would be advisable to deliberately look for the number E464 on the foods you consume is yet still highly questionable. For one, every food with an "E -number" on its ingredient list should disappear from your grocery list, anyways. I do not care which number it is, but if food has "E"'s in it chances that this is highly processed garbage are 99% and in that case the supposedly insignificant amount of HPMC will not turn junk into health food. And secondly, and certainly more importantly, we are just beginning to understand how the viscosity of the foods we eat and their susceptibility to fermentation interact and which impact(s) these characteristics have on our digestion and metabolism. After all, it could well be possible that, just as in the Isken study, this beneficial short term effects eventually fire back and the formerly lean HMPC rats suddenly start gaining weight (and body fat) like crazy... you see, as usual things are more complicated than the innocent (yet actually invalid) question "Is fiber good or bad?" might suggest.

Sodium Bicarbonate (NaHCO3) Increases PGC1-A & Speeds Up Mitochondrial Adaptation - HIIT + Bicarb = Perfect Match

Study suggests, significant increases in mitochondrial builder PGC1-a with HIIT + bicarbonate

If this is not your first visit to the SuppVersity, I am confident you've read about the ergogenic effects of sodium bicarbonate aka baking soda before. If you haven't here is the short version: Sodium bicarbonate will act as a systemic acid buffer during workouts. That's in contrast to beta-alanine which works exclusively in the muscle, but has very similar, in some studies albeit significantly more pronounced and first and foremost acute beneficial effects on exercise performance.

No loading, no waiting, no hoping. You simply wash down 20g of bicarbonate (better 0.3g/kg body weight) before the race of your life and - as long as your tummy can stomach it - see / feel the benefits during the race.

You can learn more about bicarbonate and pH-buffers at the SuppVersity

The Hazards of Acidosis

Build Bigger Legs W/ Bicarbonate

HIIT it Hard W/ NaCHO3

Creatine + BA = Perfect Match

Bicarb Buffers Creatine

Beta Alanine Fails to HIIT Back

In his thesis paper, Michael E. Percival investigated the effects of bicarbonate supplementation on the cellular adaptation process in response to high intensity interval training (HIIT).

"Acute and chronic high-intensity interval exercise is a potent stimulus to influence a number of physiological adaptations with implications for health and athletic performance. [...] Due to the intense nature of this training modality and associated disturbance to muscle pH, which has been implicated in fatigue, it has been hypothesized that augmenting the body’s natural buffering capacity through nutritional means may be a strategy to augment training adaptations. One way of doing this is through the ingestion of NaHCO 3 prior to exercise, which has shown to have ergogenic effects allowing athletes to perform more work with each training session. In addition, greater mitochondrial and performance adaptations are seen when HIIT is preceded by NaHCO3 ingestion even when work is matched (Edge. 2006; Thomas. 2007; Bishop. 2010)."

Percival's goal was now to finally establish what exactly it is that gives bicarbonate the adaptational edge, so to say. To this ends, Michael E. Percival had his subjects, nine active men (22 ± 2 y; 78 ± 13 kg, VO²peak = 48 ± 8 mL/kg/min; mean ± SD) perform the same 10 x 60 s HIIT cycling protocol on two occasions, either with

• 0.2 g/kg body weight sodium bicarbonate (BICARB) or 
• an equimolar dose of a placebo, sodium chloride (PLAC),

both ingested in two equally sized doses that were ingested 30 minutes after the breakfast - a means to minimize gastrointestinal distress | and in the study at hand it worked: There was not difference in gastrointestinal complaints between placebo and bicarbonate trial.

Figure 1: Pre vs. post PGC1a and muscular glycogen content (Percival. 2014)

The two trials were separated by 1 week, the subjects had to perform their 10 all out cycling bouts at an intensity of ~263 ± 40 W - more than enough to bring all of them up to the 90%+ heart rate zone. , interspersed by 60 s of recovery. Total work during each trial was identical for a given subject.

A brief reminder of the benefits of bicarbonate: Regulation of hydrogen ions (H + ) or pH within homeostatic concentrations is critical for proper physiological function. The factors contributing to the change in muscle pH seen during intense exercise are numerous and the role of each factor remains hotly debated. However, classically it is believed that a large contributor of H + is through the accumulation of lactate produced from glycolysis. Next to internal buffers, which are exhausted relatively quickly, the shuttling of H + and lactate across the sarcolemma is also believed to play an important role in the maintenance of pH during intense exercise. This is due to the extracellular buffering capacity HCO3 - which is believed to promote the efflux of H + from active muscles ( Hollidge-Horvat. 2000; Bishop. 2004).

Table 1: Overview of the studies Carr et al. reviewed in their meta-analysis (Carr. 2011)

One way to facilitate this process is obviously the provision of exogenous bicarbonate in form of NaHCO3. According to the most recent meta-analysis by Carr et al. (2011), even acute dosing will lead to performance enhancements of 1.7% during short high intensity activities as sprinting. As Percival points out, it does eventually not matter how "sodium bicarbonate imposes its ergogenic effects, the ability to allow athletes to work harder may enhance the exercise stimulus", anyways, and thus contribute to faster / greater size and strength gains. There is yet also accumulating evidence "that NaHCO3 supplementation can improve adaptations independent of greater work output." One of the underlying factors, i.e. the increase in the mitochondrial builder protein PGC-1a has been identified in the study at hand.

Figure 2: Bicarbonate increases mitochondrial respiration specifically during longer-duration exercise (Bishop. 2010) - the study at hand does not just confirm the results of the previous rodent study, it does also provide information about the underlying mechanism that's responsible for the accelerated mitochondrial adaptation w/ sodium bicarbonate.

The latter is important, because otherwise the significant differences in PGC1-a expression (see Figure 1), of which the study at hand indicates that they are the most probably reason for the previously cited significant adapational benefits from bicarbonate supplementation (compare Figure 2), could be a mere function of the training volume.

Based on the data from blood draws and needle biopsies from the vastus lateralis we can now conclude that it is the increase in PGC-1α mRNA, which was increased after 3 h of recovery to a greater extent in BICARB vs. PLAC (~7- vs. 5-fold, p < 0.05) that is responsible for the enhanced adaptations after chronic supplementation.

Speaking of which, as I've previously pointed out, I truly believe that the serial loading protocol, as described by Driller et al. (2012) is the most promising dosing scheme for the long(er)-term use of sodium bicarbonate supplements (read my write-up for more information). Issues with increasing blood pressure or calcium loss as they have been reported for very high sodium chloride intakes in susceptible individuals should, as I repeatedly pointed out, not be an issue (Luft. 1990). In pre- and post-menopausal women on high-protein diets, the addition of small amounts of sodium bicarbonate is in fact an effective way to increase calcium retention and thus any potential negative effects on bone health that may arise as a consequence of protein-induced hypercalciuria (Lutz. 1984).

The increase of PGC1-a is significant, because the signaling protein has previously been shown to exert "IGF-1 Promoting, Myostatin Reducing, Muscle Building Effects" | learn more

Bottom line: While I am pretty sure that many people will still be more attracted by the shiny ads for beta alanine containing supplements, there is little doubt that baking soda is the cheaper and at least acutely more effective buffering supplement.

That being said, the elevated PGC1-a levels in the study at hand add to the existing evidence that bicarb is more than a pre-/intra-workout acid buffer. And while it's still not 100% clear if it is a result of an increased use of intra-muscular glycogen or a consequnce of a reduced acid level during exercise, the increase in PGC1-a of which SuppVersity readers know that it has "IGF-1 Promoting, Myostatin Reducing, Muscle Building Effects" (learn more) make chronic sodium bicarbonate supplementation regimen even more interesting than they've been before | Comment on FB!

References:

• Bishop, David, et al. "Induced metabolic alkalosis affects muscle metabolism and repeated-sprint ability." Medicine and science in sports and exercise 36.5 (2004): 807-813.
• Bishop, David J., et al. "Sodium bicarbonate ingestion prior to training improves mitochondrial adaptations in rats." American Journal of Physiology-Endocrinology and Metabolism 299.2 (2010): E225-E233. 
• Carr, Amelia J., Will G. Hopkins, and Christopher J. Gore. "Effects of acute alkalosis and acidosis on performance." Sports medicine 41.10 (2011): 801-814. 
• Driller, Matthew W., et al. "The effects of serial and acute NaHCO3 loading in well-trained cyclists." The Journal of Strength & Conditioning Research 26.10 (2012): 2791-2797.
• Edge, Johann, David Bishop, and Carmel Goodman. "Effects of chronic NaHCO3 ingestion during interval training on changes to muscle buffer capacity, metabolism, and short-term endurance performance." Journal of applied physiology 101.3 (2006): 918-925.
• Hollidge-Horvat, M. G., et al. "Effect of induced metabolic alkalosis on human skeletal muscle metabolism during exercise." American Journal of Physiology-Endocrinology And Metabolism 278.2 (2000): E316-E329. 
• Luft, Friedrich C., et al. "Sodium bicarbonate and sodium chloride: effects on blood pressure and electrolyte homeostasis in normal and hypertensive man." Journal of hypertension 8.7 (1990): 663-670. 
• Lutz, Josephine. "Calcium balance and acid-base status of women as affected by increased protein intake and by sodium bicarbonate ingestion." The American journal of clinical nutrition 39.2 (1984): 281-288.
• Percival, Michael E. "Sodium bicarbonate ingestion augments the increase in PGC-1α mRNA expression during recovery from intense interval exercise in human skeletal muscle." Diss. McMaster University, 2014.
• Thomas, Claire, et al. "Effects of high-intensity training on MCT1, MCT4, and NBC expressions in rat skeletal muscles: influence of chronic metabolic alkalosis." American Journal of Physiology-Endocrinology and Metabolism 293.4 (2007): E916-E922.

Build a Bigger Mitochondrial Engine and Double Your Endurance With Chitooligosaccharides! Glucosamine Mix from Chitosan Acts on Sirt1 & AMPK, Similar to Resveratrol

Figure 1: Glucosamine composition of the chitooligosaccharide used in the study (data adapted from Jeong. 2012).

Usually I try to avoid this term, as it seems to imply that there is, or at least soon will be a pill that would allow you to stay the lazy bastard you are now and still make it into your old age, healthy lean, attractive and vigorous, but in this case the word "exercise mimetic" is unquestionably what describes the effects of 6 weeks of oral supplementation with chitooligosaccharide described in a recently published paper by scientists from the Amorepacific Corporation Research & Development Center and the Kyung Hee University in South Korea best. I have to give props to my friend Carl Lanore the voice (and brain) of Super Human Radio who shot me an email on this issue, yesterday.

A brief glance at the full-text was enough to realize that Carl who likes to pretend he was the idiomatic "blind man" with no scientific degree (I could hardly care less, by the way ;-) who hits upon things like this only perchance was up to something - those who now the show, will be aware that he is smarter than many of the experts he interviews, anyways... but I am getting derailed, here. Where was I? Ah yeah, the study...

COS - What we already know

• Ameliorates weight gain (-15%) and high blood lipids on HFD in mice in the absence of reduced energy intake (Choi. 2012)
• Promotes cytokine release in intestinal epithelial cells (Bahar. 2012)
• Inhibits pancreatic lipase and thus breakdown and subsequent uptake of dietary fat (Kang. 2012)
• Suppresses TNF-alpha induced collagen breakdown in-vitro (Ryu. 2012)
• Has neuroprotective effects (Joodi. 2011)

Promising in vivo rodent + in vitro cell line data: Very promising, but not yet field-tested

Hyun Woo Jeong and his colleagues fed 39 female Sprague-Dawley rats either normal or 0.05% chitooligosaccharide (COS produced by Bioland Korea Co. Briefly from chitosan by enzyme digestion, followed by deacetylation of chitin; cf. Hirano. 1989) enriched rodent chow for 6 weeks.

At the end of the study period, 50% of the rodents had performed an exercise test on the treadmill, in the course of which they had to run at a pace of 20m/min until exhaustion, while the rest of the animals were sacrificed before this final workout to assess their pre-exercise plasma profiles including ALT, AST, triglyceride, total cholesterol, lactate, and free fatty acid levels (none of which showed significant changes over the course of the 6-week study period).

Despite the fact that the scientists did not measure the total lean and fat mass of the rodents, the collective data in figure 2 clearly suggests that the -72% reduction in weight gain was not at the expense metabollically active muscle tissue.

Figure 2: Body weight and energy intake (left) and muscle weight vs. body weight (right) data at the end of the 6-week trial (data adapted from Jeong. 2012).

Despite a statistically non-signficant reduction in food intake (-6%) the chitooligosaccharide treated rodents had heavier soleus (slow twitch, type II fiber dominant muscle) muscles and a more favoreable plantaris (fast twitch, type II-X fiber dominant muscle) to total body weight ratio (indicative of a lower body fat percentage), than their non-supplemented peers. Moreover, a cursory glance at figure 3 does also reveal why this is the case.

Figure 3: Electron microscopic image of muscle tissue (top; small arrows and green areas indicate the presence of mytochondria), mitochondrial density in in-vitro control experiment after exposre to different doses of  resveratrol vs. chitooligosaccharide (bottom, left) and time to exhaustion during treadmill test (adapted from Jeong. 2012)

Even as a non-expert it is easy to see that the chitooligosaccharides had profound "anabolic" effects on the mitochondria of the lab animals.

COS activated AMPK and increased the cellular NAD+ / NADH ratio to induce Sirt1 activation. The activation of AMPK and Sirt1 increased the expression and activity of PGC1 and augmented the expression of mitochondrial genes. As a result of activation of AMPK, Sirt1, and PGC1, COS facilitated mitochondrial biogenesis. In rodents, the administration of COS significantly increased intramuscular mitochondrial content, resulting in enhanced exercise endurance and reduced plasma lipid profiles. (Jeong. 2012)

In the Petri-dish, it may be less potent than resveratrol on a per mg base (figure 3, bottom-left), but the real world effects in terms of both, increased mitochondrial biogenesis (see green mitochondria in the electron microscopic image of skeletal muscle; figure 3, top) and subsequent increases in average running time to exhaustion (+96%; figure 3, bottom right) speak for themselves.

Implications: Other than resveratrol, which has an oral biovailability that is hardly high enough to be quantified (Walle. 2004), chitooligosaccharide could actually be suitable for oral supplementation - at least if we assume similar pharmacokinetics in humans as in rats (which is likely, but not necessarily the case).

• especially sedentary individuals or people who rarely train could benefit from the exercise-mimicking effects 
• in a previous study by Cho et al. chitooligosaccharide lactate has been found to be superior to chitooligosaccharide HCL (Cho. 2010)
• the optimal dosage and, more importantly, whether trained and well-conditioned individuals would benefit to a similar extend / at all, would yet require further studies. 
• the human equivalent dosages for the study at hand would be 600-900mg/day depending on the individuals body weight

Image 1: COS is rather something for the "old" Mr C. than for Adelfo

Aside from the fact that there are (at least to my knowledge) no over-the-counter chitooligosaccharide supplements on the market, so that you would probably have to order a metric ton right from China at Alibaba.com, I would not expect too much from it, anyways. Firstly, the chances that it turns out to be another supplemental non-starter like resveratrol are high. And second- and more importantly, the beneficial effects will be less pronounced for well-conditioned individuals and could even be close to zero (and certainly not practically relevant) for people who go to the gym to train and not to pose, to chat or to flirt. People like you and me and Adelfo Cerame, whose new client Mr. C. is soon going to join the ever-growing community of physical culturists, who don't need a "mimetic" for something they love: Exercise!

References:

• Bahar B, O'Doherty JV, Maher S, McMorrow J, Sweeney T. Chitooligosaccharide elicits acute inflammatory cytokine response through AP-1 pathway in human intestinal epithelial-like (Caco-2) cells. Mol Immunol. 2012 Jul;51(3-4):283-91. Epub 2012 Apr 16.
• Cho SY, Lee JH, Song MJ, Park PJ, Shin ES, Sohn JH, Seo DB, Lim KM, Kim WG, Lee SJ. Effects of chitooligosaccharide lactate salt on sleep deprivation-induced fatigue in mice. Biol Pharm Bull. 2010;33(7):1128-32.
• Choi EH, Yang HP, Chun HS. Chitooligosaccharide ameliorates diet-induced obesity in mice and affects adipose gene expression involved in adipogenesis and inflammation. Nutr Res. 2012 Mar;32(3):218-28.
• Hirano S, Tsuchida H, Nagao N. N-acetylation in chitosan and the rate of its enzymic hydrolysis. Biomaterials. 1989;10: 574–576.
• Jeong HW, Cho SY, Kim S, Shin ES, Kim JM, Song MJ, Park PJ, Sohn JH, Park H, Seo DB, Kim WG, Lee SJ. Chitooligosaccharide Induces Mitochondrial Biogenesis and Increases Exercise Endurance through the Activation of Sirt1 and AMPK in Rats. PLoS One. 2012;7(7):e40073.
• Joodi G, Ansari N, Khodagholi F. Chitooligosaccharide-mediated neuroprotection is associated with modulation of Hsps expression and reduction of MAPK phosphorylation. Int J Biol Macromol. 2011 Jun 1;48(5):726-35.
• Kang NH, Lee WK, Yi BR, Park MA, Lee HR, Park SK, Hwang KA, Park HK, Choi KC. Modulation of lipid metabolism by mixtures of protamine and chitooligosaccharide through pancreatic lipase inhibitory activity in a rat model. Lab Anim Res. 2012 Mar;28(1):31-8. Epub 2012 Mar 21.
• Ryu B, Himaya SW, Napitupulu RJ, Eom TK, Kim SK. Sulfated chitooligosaccharide II (SCOS II) suppress collagen degradation in TNF-induced chondrosarcoma cells via NF-κB pathway. Carbohydr Res. 2012 Mar 1;350:55-61.
• Walle T, Hsieh F, DeLegge MH, Oatis JE Jr, Walle UK. High absorption but very low bioavailability of oral resveratrol in humans. Drug Metab Dispos. 2004 Dec;32(12):1377-82. Epub 2004 Aug 27.

Fat Content Per Energy Drink 0g, Body Fat Gain Per Energy Drink 18g! Human Trial Confirms: +1kg of Body Fat in 4 Weeks From Less than 2x Energy Drinks per Day!

Image 1 (NYC Dept. of Health & Mental Hygiene): The words on this poster from a 2009 campaign in the NY subway must be taken literally!

There is a reason for me to always begin my "dietary advice" with the statement "there is NO WAY that you ever again drink any soft, energy drinks or fruit juices on a daily basis". And though I would not have needed a study to confirm skipping, lemonade, coke & co is one of the simplest, for many people yet not easiest steps to a healthier and leaner physique, I must admit that I was pretty surprised how rapid both your health and body composition deteriorate, once you reintroduce this junk into your diet. +1kg of pure body fat in 4 weeks, that was the amount of weight the 11 healthy men and women in a recently published study by scientists from the UK, Italy and the US gained within just 4 weeks in the course of which they drank on average two more or less tasty Lucozade Energy drinks per day (Sartor. 2012).

Fat content of energy drink 0g, body fat gain per energy drink 18g!

Figure 1 (gsk): Nutritional information of the energy drink the subjects drank during the 4-week study period

Sartor et al. about whose study on the "habituation effects" of sweet beverage you may already have read in one of the installments of the Insulin Resistance Saga (cf. "Where Has All the Sweetness Gone? Plus: Bullied to Eat Twinkies") had recruited 11 healthy young men (n=5) and women (n=6) with a mean age of 26 years, who were handed a month's supply of GlaxoSmith Kline's yummy Lucozade Energy of which they had to drink ~2 bottles per day (2x 380ml; in fact the average intake was only 760ml and was matched to deliver 2g carbohydrates per kg body weight; for detailed "nutritional" information based see figure 1) - just to make that clear, I suspect the results would not have been much different if this had not been Lucozade, but plain Coke, if the daily consumption (1.2l) had delivered the same amount of sugary carbs.

Apropos effects, if you take a look at the actual data in figure 2 it is quite obvious that the increase in body fat did not occur in the absence of the rise of other characteristic features of the metabolic syndrome, i.e. changes in blood glucose and lipid metabolism.

Figure 2: Changes in body composition, HOMA markers of insulin resistance, sensitivity and pancreatic function, as well as blood lipids after 4 weeks of sugar-sweetened beverage consumption (based on Sartor. 2012)

A particular reason of concern - at least in my humble opinion - are the rapid (remember these deteriorations occurred within only 4 weeks!) reductions in HOMA measure insulin sensitivity / increases in HOMA based insulin resistance measures. Which would only exponentiate the detrimental effects of the daily glucose overload.

High blood glucose, high RER, high insulin, but no increase in energy intake

Together with the significantly increased fasting glucose (+6%) and fasting insulin levels (+25%) and the accompanying reversal of the fat-to-carbohydrate oxidation rates from 2:1 to 1:3 in the fasted state this does already suggest that this is once more not solely an effect of an increase in energy intake as conventional wisdom would have it!

Figure 3: Changes in macronutrient composition and non-existent changes in total caloric intake over the course of the 4 weeks of sugar-sweetened beverage consumption (based on Sartor. 2012)

If you take a closer look at the data in figure 3 you can even drop the "solely" from the previous sentence and state: "the obesogenic effect of sugary beverages has no relation whatsoever to an increase in overall energy intake!"

Its not so much about how much, its about what and which!

It stands to reason that this increasingly accepted "violation" of the rules of thermodynamics *rofl* did not go unnoticed by Sartor et al., who had also analyzed the expression of several genes in samples of the skeletal muscle tissue of their subjects and found that there were statistically significant

• increases in glyceraldehyde-3-phosphate dehydrogenase (GAPH), acetyl-CoA carboxylase alpha (ACC) and MonodA mRNA expression, which are indicative of increased glycolysis, decreased fatty acid oxidation and an increased cellular awareness of blood sugar abundance, respectively, as well as a significant
• decrease in peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC-1a), of which you have read in relation to Irisin in "If a High Fat Diet was a Pill, the Lay Press Would Celebrate it as Exercise in a Pill!" that it is responsible for increases in mitochondrial firepower and fatty oxidation capacity

Much more so than the 1kg of body fat, which should be relatively easy to shed by simply pouring energy-, soft-drinks & co down the sink, instead of downing them with a gulp, these transcriptional (epigenetic) changes and the previously reported deteriorations in taste perception in response to the consumption of sugar (not fructose!) sweetened beverages (Sartor. 2011), are the real alarming results of this 4-week trial. After all, they are the ones that predispose to future fat gain, diabetes and hyperlipidemia!

So, what can be done?

Image 2: OTC solution to the problem? Water + Workout

Luckily there is a tried and proven non-pharmacological solution to this problem, an OTC double-whammy, if you will that is not just free, but will actually save you truckloads of money! Initially for all the energy drinks and soft-drinks you are not buying anymore and for all the medication the medical bill's and the XXL coffin for your funeral in the weeks, months, years and decades to come. What? You want to know what this OTC double-whammy is? Plain water and regular exercise! While the former is equally if not more thirst-quenching than the differently colored sugar waters, the latter will help to gradually reverse the epigenitic changes and restore a healthy glucose and fatty acid metabolism.

References:

1. GlaxoSmithKline (gsk). Lucozade Official Shop. Lucozade Energy - Original. 2012 < http://www.lucozadeshop.com/lucozadeenergy/lucozadeenergyoriginal > Received on June 30, 2012.
2. Sartor F, Donaldson LF, Markland DA, Loveday H, Jackson MJ, Kubis HP. Taste perception and implicit attitude toward sweet related to body mass index and soft drink supplementation. Appetite. 2011 Aug;57(1):237-46. 
3. Sartor F, Jackson MJ, Squillace C, Shepherd A, Moore JP, Ayer DE, Kubis HP. Adaptive metabolic response to 4 weeks of sugar-sweetened beverage consumption in healthy, lightly active individuals and chronic high glucose availability in primary human myotubes. Eur J Nutr. 2012 Jun 26.