Weight Loss, 'Metabolic Damage' and the Magic of Carbs? Human Study Probes Effects of Carbohydrate Content, GL & GI on Diet-Induced Suppression of Resting Metabolic Rate

Will slimming down from a 120 cm to a 60 cm waist always ruin your metabolic rate and set you up for weight regain or can high GI protect you from yoyoing?

Broscience tells us: "Carb up to preserve your resting metabolic rate." And in fact, there is some scientific evidence that suggests a link between high(er) carbohydrate intakes and increased thyroid function. The same amount of T3 will trigger a sign. higher stimulation of lipolysis and fat oxidation, for example, on high vs. low carb diets (Mariash. 1980). Low carb diets, on the other hand, lead to significant reductions of the active thyroid hormone and increases in the 'thyroid receptor inhibitor' rT3 - even in healthy individuals and if the energy intake is standardizes (Serog. 1982; Ullrich. 1985). So, is broscience right? Well, overfeeding studies show a similar increase in T3 in response to protein, fat and carbohydrates (Danforth Jr. 1979). So refeeds should work, irrespective of their carbohydrate content...

# Women appear to be particularly prone to # metabolic damage - more on # female fat loss:

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As you can see, it is hardly possible to confirm or reject the "carb up to prevent metabolic damage" (=prevent the diet induced over-proportional reduction in resting energy expenditure) hypothesis based on the existing evidence. A recent study by J. Philip Karl and colleagues who tried to determine "the effects of diets varying in carbohydrate and glycemic index (GI) on changes in body composition, resting metabolic rate (RMR), and metabolic adaptation during and after weight
loss" (Karl. 2015), however, may yet take us one step further towards rejecting or confirming this commonly heard of idea.

Figure 1: Overview of the key parameters of the study design and dietary composition (Karl. 2015).

In said study, Karl et al. randomly assigned adults with obesity (n = 91) to one of four diet groups for 17 weeks. As you can see in Figure 1, the diets all subjects were provided with differed in percentage energy from carbohydrate (55% or 70% | Figure 1, top-right) and GI (low or high, Figure 1, bottom-right) but were matched for protein, fiber, and energy. The study design itself comprised 5 phases:

Metabolic Damage in Biggest Losers: Will Diet & Intense Exercise Make You Fat, While Surgery Will Make You Lean? Plus: How to Avoid or Even Correct Diet-Induced REE Reductions | more

"Phase 1 was a 5-week weight maintenance phase in which weight maintenance energy needs were determined by adjusting provided energy intake to maintain stable weight. Mean Phase 1 energy intake was 12.2 MJ/day with 48% energy provided as carbohydrate, 16% as protein, and 36% as fat. Following Phase 1, participants were randomized by the study statistician to their Phase 2 dietary assignment using computer-generated randomization. The four diets differed in carbohydrate content (55%, ModCarb or 70%, HighCarb of total energy) and dietary GI (less than 60, LowGI or 80, HighGI), and were provided for 12 weeks at 67% of the weight maintenance energy intake determined in Phase 1. 

Participants were allowed to increase their energy intake during Phase 2 by requesting additional, randomization-appropriate foods from the metabolic kitchen if too hungry to be adherent. Phase 3 was a 5-week weight maintenance phase during which food was provided according to randomization. Energy intake during Phase 3 was prescribed to support weight maintenance at the new, lower body weight, and was predicted from body weight and energy intake measured at the end of Phase 2, with adjustment for self-reported physical activity. Phase 4 was a 12- month follow-up period during which participants selected and pre pared their own meals after being provided with instructions on fol lowing the diet to which they were randomized" (Karl. 2015)

To assess the effects of this sequence of induction (weight maintenance), and weight stabilization phases, the body weight, body composition, RMR, and metabolic adaptation (measured RMR vs. predicted resting metabolic rate = RMR) of the middle aged study participants (49-64 years) were measured before and after all phases of the study.

Figure 2: (A) Weight loss and (B) percentage of total weight loss attributable to fat mass and fat free mass while consuming provided-food diets differing in glycemic index (GI) and percent energy from carbohydrate (55%, ModCarb and 70%, HighCarb) for 17 weeks (n = 79). Values are mean 6 SEM. Weight loss analyzed by repeated measures ANCOVA, body composition by two-factor ANOVA. a,bMain effect of time; asignificant decrease from baseline (P < 0.001), bsignificant difference from Phase 2 end (P < 0.001). No diet effects (main effects or interactions) for any comparisons. GI, glycemic index; HighCarb, 70% energy from carbohydrate; ModCarb, 55% energy from carbohydrate (Karl. 2015).

Interestingly, the analysis of this data revealed no significant inter-group differences in terms of any of the relevant study outcomes. Yes, you read me right: This means that neither the GI, nor the GL, nor the carbohydrate content of the diet had statistically significant effects on weight loss, body composition, RMR, or the metabolic adaptation aka "metabolic damage" due to weight loss.

Figure 3: Measured resting metabolic rate as a function of predicted metabolic rate (Karl. 2015). Note: If there was no "metabolic damage", the solid line which represents the ideal body-weight dependent decline of energy expenditure and the dashed line which represents the actual ratio of the measured to the predicted RMR should be congruent.

While there were no inter-group differences and neither the amount or the type of carbohydrates had an effect on the reduction of the metabolic rate, there is still one interesting result you can see in the right graph in Figure 3. Said graph depicts the ratio of the measured to the predicted metabolic rate during the 5-week weight maintenance phase. If you look closely, you will realize that it suggests that having a high predicted RMR, i.e. being heavier, being taller and being more muscular, is associated with a non-significant decline of the non-predicted reduction of the energy expenditure (=metabolic damage) and thus a narrowing of the gap between the solid and dashed line.

"Solid and dashed? I don't get it!"

You're asking how I can support this hypothesis? Well, the dashed line that represents the true ratio of the actual to the predicted RMR approaches the theoretical one (the solid line) for higher RMR values. If this was more than a trend, it would suggest that two things: (a) Losing less weight and thus maintaining a higher predicted metabolic rate protects against metabolic damage (that would be useless). And (b) being tall and muscular and thus having a naturally high(er) predicted RMR can protect you from suffering metabolic damage when you lose weight.

Unfortunately, it's not possible to tell which (if any) of the two options is correct. If I had to make an educated guess, though, I would say it's a combination of both: The weight change of an average 5.5 kg did not wary too much and was withing 95% confidence intervals of [-7.1 kg, -4.6 kg]. In conjunction with individual physiological qualities of people with higher baseline RMRs, it could still explain the narrowing of the gap between predicted and true RMR after dieting.

Figure 4: Changes in body composition (absolute value in kg) after 20 weeks and after weight loss phase 2 (Karl. 2015).

Bottom line: As Karl et al. point out, "neither low-GI relative to high-GI diets nor moderate-carbohydrate relative to high-carbohydrate diets showed differences with respect to effects on changes in body composition or resting metabolism during weight loss when confounding dietary factors were tightly controlled in a study providing all food for 22 weeks" (Karl. 2015).

This does not just go against the mainstream assumption that low GI and/or low(er) carbohydrate diets facilitate weight loss, fat loss and weight maintenance (see data in Figure 4 for an overview of these parameters, it also contradicts the initially mentioned broscientific assumption that carbohydrates, in general, and high GI carbs, in particular, have a protective effect against the unexpected diet-induced reduction of basal energy expenditure many people know as "metabolic damage". If there's anything of which the study at hand suggests that it could protect you from such unexpectedly large decrease in RMR, it's not high GI carby, but rather an already high(er) baseline RMR (see Figure 3).

And what does that tell us? Right! Since a high predicted RMR is a function of (a) being male, (b) being tall, and (c) being muscular, all three attributes may protect you from diet-induced "metabolic damage" | Let me know your thoughts and comment on Facebook!

References:

• Danforth Jr, Elliot, et al. "Dietary-induced alterations in thyroid hormone metabolism during overnutrition." Journal of Clinical Investigation 64.5 (1979): 1336.
• Karl, J. Philip, et al. "Effects of carbohydrate quantity and glycemic index on resting metabolic rate and body composition during weight loss." Obesity 23.11 (2015): 2190-2198.
• Mariash, C. N., et al. "Synergism of thyroid hormone and high carbohydrate diet in the induction of lipogenic enzymes in the rat. Mechanisms and implications." Journal of Clinical Investigation 65.5 (1980): 1126.
• Serog, P., et al. "Effects of slimming and composition of diets on VO2 and thyroid hormones in healthy subjects." The American journal of clinical nutrition 35.1 (1982): 24-35.
• Ullrich, Irma H., Philip J. Peters, and M. J. Albrink. "Effect of low-carbohydrate diets high in either fat or protein on thyroid function, plasma insulin, glucose, and triglycerides in healthy young adults." Journal of the American College of Nutrition 4.4 (1985): 451-459.

Net Protein Retention and Dietary Protein: When It Comes to Steaks, More Helps More - By Inhibiting Protein Breakdown

Want to maximize net protein retention? Order another one... another steak ;-)

In view of the WHO's recent epidemiological bogus publication, ... ah I mean their review of the epidemiological research that said that "red meat kills", it is quite surprising that the study Il-Young Kim and colleagues conducted in healthy young adults was even approved by the ethics committee of their respective research institutions. After all, the study involved measuring the whole body protein kinetics of young men and women after the consumption of ~40g (moderate protein, or MP) or, even "worse", ~70g (higher protein, HP) of protein in form of red meat (85% lean ground beef) in a regular food matrix (=as part of a normal meal | see Table 1 for an exact overview of the macronutrient content).

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Whole protein kinetics? Yes, that's different from what you see in the average "whey protein builds muscle study", in which the researchers measure only the fractional protein synthesis. Kim et al. went one step further and measured the protein synthesis (PS), breakdown (PB), and net balance (NB) in their subjects, twenty-three healthy subjects [18 – 40 yrs] who were recruited from the Little Rock area using local newspaper advertisements and flyers posted around the University of Arkansas for Medical Sciences (UAMS) campus and the Little Rock area. Now, it's not like humans had a display you can use to read these variables, so eventually, they were still calculated based on the determinations of the rate of appearance (Ra) into the plasma of phenylalanine and tyrosine, and the fractional Ra of endogenous tyrosine converted from phenylalanine as in a previous study by the same team of researchers (Kim. 2015a). Since this technique is unable to distinguish between the different sites of protein breakdown.and storage, the results of the study at hand could describe increases or decreases in splachnic (=organ) protein synthesis or breakdown, too. It is thus not possible to exclude a null effect on skeletal muscle protein synthesis and breakdown based on the available data.

Whole protein kinetics, two different amounts of protein, with and without exercise

There were yet other things Kim's study had in common with many of the aforementioned "whey protein studies": The study had a run-in that was included to minimize any potential effects of the protein content of the subjects' baseline diets. The subjects ate their high or medium protein meals in the fasted state and the participants - or at least some of them - also trained. To be more specific, the subjects were randomly assigned into an exercise group (X, n=12) protocol consisting of 3 sets of 10 repetitions of bench press, lateralis pull-down, leg press, and leg extension each at 80% of 1 repetition maximum (1 RM, the maximum weight that can be lifted for one repetition) at a pace of 30 sec per set (rest interval between sets was less than 2 min, and the entire exercise bout was completed in ~45 – 50 min), or a resting group (R, n=11).

Table 1: Overview of the macronutrient intake during the 4-day run-in and the actual experiment (Kim. 2015b)

So much for the study design. Let's take a look at the results now: When the scientists analyzed the data from the 7-h stable isotope tracer infusion protocol that was used to determine the rate of protein synthesis (PS), breakdown (PB) and net protein balance (NP), they realized that...

• exercise did not significantly affect protein kinetics and blood chemistry, while 
• feeding, in general, resulted in a positive net protein balance at both levels of protein intake,

Boring? You're right. This would hardly be a 'SuppVersity newsworthy' study if the researchers had not also confirmed what most of you probably already suspected: The high protein meal lead to a significantly greater increase in net protein balance than the medium protein meal.

Figure 1: It's the decrease in protein breakdown, not the marginal increase in protein synthesis that makes the difference between the net protein balance after the high and medium protein meals (Kim. 2015b).

Interestingly enough, this increase in net protein balance was achieved primarily through a greater reduction in PB and to a lesser extent stimulation of protein synthesis (for all, p<0.0001). This is an important results, because it suggests that all previously reported ceiling effects for protein synthesis could be irrelevant when we are talking about a potential limit of protein intake beyond which you won't be able to see further beneficial effects on body composition in general and the accrual of lean mas in particular.

Figure 2: The analysis of the inter-group differences in EAAs, glucose and insulin suggest that the difference is meadiated mainly by the increase in serum EAAs and not a "side effect" of increased, highly anticatabolic (Fukagawa. 1985) insulin.

Bottom line: When it comes to interpreting the results, two things are important. Firstly, it is worth mentioning that the previously described decrease in protein breakdown was achieved in response to a greater increase in plasma EAAs (p<0.01) - not in response to increased insulin levels (inter-group differences were non-significant over time). That's important because it means that you wouldn't see the same effect by simply adding more insulinogenic carbs to the meal in order to increase the levels of one of the most powerful inhibitors of protein breakdown: insulin (Fukagawa. 1985)!

Sounds great, right? More helps more! True, there's yet (a) the previously hinted at problem that we can't tell if what the scientists measured was muscle or splachnic protein. Furthermore, the results of the study are (b) valid only if the protein comes from slow-digesting meat. From previous research, I discussed in detail back in 2013, already, we know that the ingestion of similarly high amounts of fast digesting proteins, like whey, does not inhibit, but rather trigger an increase in protein breakdown and gluconeogenesis that uses the ingested protein as a substrate. Now, that doesn't mean that using too much whey protein will cost you muscle mass. What it does mean, though, is that you'll be "Protein Wheysting" if you mistakenly believe that the results of Kim's study apply with a very slow digesting protein source apply turbo-proteins, as well.

So what's the verdict?  Don't economize on protein, but don't fool yourself to believe that with protein more is always always better. Maybe I should also remind you that when you're dieting a high protein intake can yield better results than a very high one and that's a conclusion from a metabolic ward study | Tell me and others what you think on Facebook!

References:

• Fukagawa, N. K., et al. "Insulin-mediated reduction of whole body protein breakdown. Dose-response effects on leucine metabolism in postabsorptive men." Journal of Clinical Investigation 76.6 (1985): 2306.
• Kim, Il-Young, et al. "Quantity of dietary protein intake, but not pattern of intake, affects net protein balance primarily through differences in protein synthesis in older adults." American Journal of Physiology-Endocrinology and Metabolism 308.1 (2015): E21-E28.
• Kim, et al. "The anabolic response to a meal containing different amounts of protein is not limited by the maximal stimulation of protein synthesis in healthy young adults." Am J Physiol Endocrinol Metab (November 3, 2015b). doi:10.1152/ajpendo.00365.2015.

Many Probiotics Contain Antibiotic Resistant Bacteria. Plus: Number of Live Bacteria is up to 95% Below Label Claims

Probiotics under urgently needed scrutiny - This is the first study to test for antibiotic resistances and to highlight the discrepan- cy between label claims and the actual number of live bacteria in supplements.

There have been plenty of good news about probiotic supplements in the news (including the SuppVersity News), lately. One thing that is often forgotten, though, is that the effect of the supplements depends on (a) the exact type of bacteria that are in the pills, (b) the ratio of the different strains and (c) the number of bacteria that are still alive.

Unfortunately, this important truth is rarely mentioned in the edutainment articles on probiotics in the laypress and sales pitches you will find all over the Internet.

Another thing, even you may not have thought about yet is however the potential occurrence of antibiotic resistances among the bazillions of bacteria in your allegedly healthy probiotic supplements.

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A group of people who thought of this hitherto overlooked problem are researchers from the  King Abdullah University of Science and Technology in Saudi Arabia and the UCSI University in Malaysia (Wong. 2015). In their recent paper in the scientific journal Nutrition Journal, the international group of researchers are the first to highlight a previously ignored problem i.e. the possibility that certain genes that make bacteria resistant to antibiotics "could transfer to pathogens sharing the same intestinal habitat" - an event that is, as the scientists rightly point out, "conceivable considering the fact that dietary supplements contain high amounts of often heterogeneous populations of probiotics" and could thus "confer pathogens protection against commonly-used drugs" (Wong. 2015).

MRSA in your probiotic supplements? 

Against that background and in view of the numerous reports of antibiotic resistant probiotics in food and biological sources, the antibiogram of probiotics from dietary supplements remains elusive.

Figure 1: Petri dishes from the antibiotic test (top). If the antibiotics still worked on the bacteria in the probiotics, they all should be dead. As you can see (in the graph, as well), that's by no means the case (Wong. 2015).

In fact, Wong et al. are apparently the first researchers to screen five commercially available dietary supplements (the full names were not disclosed) for resistance towards antibiotics of different classes - with somewhat disconcerting results, namely:

• 

  Even probiotics that help weight loss, could transfer antibiotic resistances.

  Probiotics of all batches of products were resistant towards vancomycin.
• Several batches of probiotics from four different brands were also resistant towards streptomycin, aztreonam, gentamycin and / or ciprofloxacin antibiotics (this includes the US and Austrian products, i.e. Cn and Bn, respectively)
• The fifth brand showed a unique resistance towards gentamycin, strepto- mycin and ciprofloxacin antibiotics. 

Now, as previously pointed out, this does not mean that "bad" bacteria which will always be present in your gut, will automatically acquire the same resistances, but the mere fact that it is possible should tell you that the current hype over probiotics as the "go-to supplement" everyone should take is unwarranted, or at least premature.

You're not getting what you're paying for!

The problem with antibiotic resistances is yet not the only intriguing result of Wang's study. The researchers analyses also revealed that you're not just getting more (albeit unwanted) ingredients that you're paying for, they also found a significant discrepancy between the enumerated viable bacteria amounts and the claims of the manufacturers.

Figure 2: Non-strain specific essay that evaluated the number of live bacteria in the products. The products from producers Bi, Bg, and L didn't just contain significantly less living bacteria than the manufacturers claim, the number is even so low that it is absolutely certain that they are 100% useless. The good news may be that the low dose supplements from the Austria(BN) and USA (CN) contained either more or at least roughly the amount of bacteria on the label (Wong. 2015).

In other words, while the scientists claim that you would get more than enough viable bacteria from their product to have a significant impact on your intestinal microbiome, the reality is that many of the good bacteria are dead before you even open the package.

The "live bacteria"-problem can be solved by eating probiotic foods like yogurt. The problem with potential antibiotic resistances, on the other hand, is rampant with foods, too. Even meat (especially chicken) and allegedly extra-healthy products like veggies from the farmers market may be tainted (the latter due to natural fertilizers of animal origin aka slurry).

Bottom line: The transfer of genes that could make bad gut bugs resistant to antibiotic is only a possibility, but it's one with literally fatal consequences. If bacterial strains in your gut have become resistant to antibiotics and you end up - for whatever reason - with an infection, i.e. a rapid multiplication of these bacteria, you could probably find yourself in the emergency room ... or worse.

In conjunction with the proven lack of viable bacteria in the five products from the US, Malaysia and Austria this study casts a shadow on a class of supplements with rapidly increasing sales - a shadow that becomes even darker if you remember my previous warning that we know literally nothing about the far-reaching interactions between the billion of different bacteria in our gut to even know the "good" from the "bad" guys | Comment on Facebook!

References:

• Wong, Aloysius, et al. "Detection of antibiotic resistance in probiotics of dietary supplements." Nutrition journal 14.1 (2015): 1-6.

Muscle Regeneration & Hypertrophy Update: Vitamin D and Super-Slow Training - What Are They Good For?

Is it worth to replete vitamin D, but not to train super-slow, right?

No, I haven't dug up a study that deals with vitamin D and super-slow training at once, but I've found two very recent studies that are in one way or another related to muscle regeneration and hypertrophy and the way/s vitamin D and different training methods affect these outcomes. More specifically, the researchers investigated the effects of vitamin D (20OHD) repletion and the use of higher times-under-tension (TUT) and super-slow training.

Before I go ahead, though, I would like to point out that the long-term implications of some of the results are not totally obvious - a fact I will therefore (re-)address in the bottom line.

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• (Super-)slow training and its inferior effects on early-phase satellite cell and myonuclear domain adaptation (Herman-Montemayor. 2015) -- The purpose of one of the latest studies from the Rocky Vista University was to identify adaptations in satellite cell (SC) content and myonuclear domain (MND) after 6-week slow-speed vs. “normal-speed” resistance training programs.
  
  To this ends, thirty-four untrained women were divided into slow speed (SS), traditional strength (TS), traditional muscular endurance (TE), and nontraining control (C) groups. The ladies performed a leg work consisting of three sets of each of the following exercises twice per week in the first and thrice per week in the fifth week: Leg press, squat, and knee extensions. To investigate how the way these workouts were performed would affect the adaptive response, the scientists randomly assigned their subjects to four different groups:
  • The Super-Slow (SS) group performed 6– 10 repetition maximum (6–10RM) for each set with 10-second concentric (con) and 4-second eccentric (ecc) contractions for each repetition.
  • The Traditional Strength (TS) group and the Traditional Muscular Endurance (TE) group who performed 6–10RM and 20–30RM, respectively, at “normal” speed (1–2 seconds per con and ecc contractions).
  • The sedentary control group (C) which did not work out at all.
  To allow for a similar number of reps in the TS and SS group, the intensity (=weight used) in the SS group was reduced to the same 40–60% of the 1RM that was also used in the TE group. The TS group, on the other hand trained at 80–85% 1RM.

What do the changes in fiber type satellite cell increases actually tell us? Unfortunately, the answer to this question is by no means straight forward. In conjunction with the overall increase in domain sizes, cross sectional fiber size and myonuclear domain numbers (see Figure 1) the increased satellite cell recruitement in the traditional training group does yet support its superiority over super-slow training (learn more about satellite cells).

• I know that this is not ideal, but there's no way you do 6-10 reps with a time-under-tension (TUT) of 10-0-4 with the same weight you'd do 6-10 reps at a normal TUT of 1-0-1 or 2-0-2, accordingly, the results the scientists' analysis of the pretraining and posttraining muscle biopsies the authors analyzed for fiber cross-sectional area, fiber type, SC content, myonuclear number, and MND still have practical relevance.
  

  

  Figure 1: Percentage change (%) in mean fiber cross-sectional area, myonuclear domain size (domain), and number of myonuclei per fiber cross-section (myonuclear number) from pretraining to posttraining for each group (TS, SS, TE, and C). *Significant increase after training, p , 0.001. §Significant increase after training, p # 0.05. #Significantly greater increase after training compared with all other groups (SS, TE, C), p , 0.01. TS = traditional strength (Herman-Montemayor. 2015).

  And what does the scientists' analysis tell us? Well, along with the data in Figure 1, the exclusive increase in satellite cell content of type I, IIA, fibers (IIX and IIAX increased in both SS and TS, but not TE or control) that was observed in the traditional strength (TS) training group appears to confirm the superiority of this way of training when it comes to lying the foundations of further myonuclear domain growth (learn more in the "Muscle Hypertrophy 101").
  
  The fact that myonuclear domain increases of type I, IIAX, and IIX fibers occurred exclusively in the TS, yet not in the SS group, where only the domains of the type IIA fibers increased, does still appear to confirm the common prejudice that - for the average trainee - training at higher times under tension (TUTs) does not offer benefits that suggest faster or more robust size gains. Compared to strength-endurance training, however, super-slow training is still the better option. On a "per load basis" it is thus more effective to do fewer reps slower vs. more reps at a normal speed if your goal is to "grow" muscle.
• Vitamin D affects muscle recovery directly (Owen. 2015) -- We already know that vitamin D figures in one way or another in (a) the adaptive response to exercise and (b) the recovery process after strenuous workouts. Unfortunately our "knowledge" is based mostly on correlations and associations and can thus hardly be considered reliable evidence. That's something researchers from the Liverpool John Moores University, the Charité in Berlin, the Norwich Medical School and other European labs weren't happy with, either. Accordingly, they designed a randomised, placebo-controlled trial that involved twenty males with low serum 25[OH]D (45 ± 25 nmol.L-1) who performed 20×10 damaging eccentric contractions of the knee extensors with peak torque measured over the following 7 days of recovery prior to and following 6-weeks of supplemental Vitamin D3 (4,000 IU.day-1) or placebo (50 mg cellulose).
  
  To complement the results of this human trial, the authors conducted a parallel experimentation using isolated human skeletal muscle derived myoblast cells from biopsies of 14 males with insufficient serum 25[OH]D (37 ± 11 nmol.L-1) that were subjected to mechanical wound injury. Thus, the scientists tried to emulate the process of muscle repair, regeneration and hypertrophy in the presence and absence of 10 nmol or 100 nmol 1α,25[OH]2D3 in the petri dish.
  

  

  Figure 2: In view of the fact that the scientists used active vitamin D3 (calcitriol) in the in-vitro study, the improved recovery in the human trial is all the more the more relevant results of the study. It does yet pose the question whether similar or any effects had been observed in subjects with sufficient vitamin D levels in whom the provision of extra vitamin D3 may have increased 25OHD, but not the systemic calcitriol levels of which the scientists' in-vitro dta shows that it is responsible for the effects (Owens. 2015).

  What the results of both studies have in common is that they support the previously claimed role of vitamin D in muscle repair and regeneration. How's that? Well, the supplemental Vitamin D3 the D-ficient human subjects received didn't just increase the serum 25[OH]D levels. It also lead to measurable improvements of the recovery of peak torque at 48 hours and 7 days post-exercise. In conjunction with the observation that 10 nmol 1α,25[OH]2D3 aka calcitriol (=active vitamin D3, not the supplement you consume) improved muscle cell migration dynamics and resulted in improved myotube fusion/differentiation at the biochemical, morphological and molecular level in the cell study, where it also increased the myotube hypertrophy at 7 and 10 days post-damage, these preliminary data do just as the scientists say "characterise a role for Vitamin D in human skeletal muscle regeneration and suggest that maintaining serum 25[OH]D may be beneficial for enhancing reparative processes and potentially for facilitating subsequent hypertrophy" (Owens. 2015).

"Explosive Reps May Pay Off - At Least on the Bench: Fast Reps = Higher Muscle Activity, Higher Volume... Gains?" Find the answer to this question from a previous SuppVersity article here.

So what? Yes and no! Those are the answers to the questions you are probably about to ask. Yes, it does make sense to keep an eye on your vitamin D (25OHD in serum) levels, to do blood tests regularly and to supplement according to your personal needs. Yes, it does also make sense to get 1,000 IU of vitamin D3 per day even if you don't know you're deficient. And yes, all that may actually help you to recover faster.

What neither vitamin D3 nor super-slow training will do, though, is to turn you into a ripped super-muscular freak. In fact, the answer to the rarely asked question whether it makes sense to switch from a regular hypertrophy training regimen with a TUT of 1-0-1 or 2-0-2 to a super-slow regiment, is "no". Or more precisely: No, it is not generally recommendable to do super-slow training instead of regular resistance training if your goal is max. muscle hypertrophy.

A question the study by Herman-Montemayor cannot answer, however, is whether doing super-slow training only least temporarily (as part of a perdiodization scheme, for example) would help pro-athletes to make further or faster progress. Even without a study, though, it can be said that someone who has been training with a TUT of 1-0-1 and weights corresponding to his/her 6-10RM (=80-85% of 1RM) for years and for whom the super-slow training would constitute a novel training stimulus is probably more likely to benefit from intermediate super-slow training than the subjects in the study at hand for whom this was the first 6-week gym experience | Comment on Facebook!

References:

• Herman-Montemayor, Jennifer R., et al. "Early-phase satellite cell and myonuclear domain adaptations to slow-speed versus traditional resistance training programs." Journal of strength and conditioning research/National Strength & Conditioning Association (2015).
• Owens, Daniel J., et al. "A Systems Based Investigation into Vitamin D and Skeletal Muscle Repair, Regeneration and Hypertrophy." American Journal of Physiology-Endocrinology and Metabolism (2015): ajpendo-00375.

Is »BAIBA« the Next Big Thing in Fat Loss Supplements? 24% Reduction in Fat Gain is an Impressive Number, But...

Could BIBA be the active ingredient in a pill that solves your weight problems once and for all? Or is that too good be true?

Beta-aminoisobutyric acid, aka BAIBA, is a natural catabolite of thymine. As with many other purported "next big things in fat loss supplements", early rodent studies suggest that it can significantly reduce body fatness through a mechanism that appears to involve increases in fatty acid oxidation (FAO) and reductions in de novo lipogenesis - in particular in the liver (Maisonneuve. 2003 & 2004; Begriche. 2008).

As Karima Begrich et al. point out in a more recent review of the literature, "experimental evidence [... also] suggested that BAIBA could reduce body adiposity through increased leptin expression and secretion" (Begriche. 2010).

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Caffeine Resis- tance - Does It Even Exist?

Against that background, it is only logical to ask whether we have overlooked a potent natural fat burner with a mechanism of cation that may be beneficial for both losing fat (increase in fat oxidation and decrease in fat storage) and keeping it off (modulation of leptin expression and secretion).

Unfortunately, it does not take long to find the first evidence that blows a hole into the neat "BAIBA could solve the diabesity epidemic"-theory. It comes right from one of the previously cited studies.
In their 2008 study, Begriche et al. were able to confirm that the provision of 100mg/kg per day (for humans that would be ~8mg/kg per day) of Beta-aminoisobutyric acid triggers significant reductions in body fat gain in lean mice (Figure 1, left).

Figure 1: 100mg/kg/day BAIBA may be an anti-weight gain supplement The data from obese rodents (rights) does yet suggest that it is not a weight loss supplement (Maisonneuve. 2004) | Anti-obesity, but not weight loss effects were also observed in obesity prone rodents in a 2008 study by Begrich et al. at the same dosage of BAIBA.

What the same amount of BAIBA did not do, though, was to prevent the weight gain in already obese mice (Figure 1, right). In view of the fact that the same discrepancies were observed for liver fat and total body weight (not shown in Figure 1), the currently available evidence clearly doesn't support the use of BAIBA as a classic "fat burner".

In obesity prone mice, BAIBA (100mg/kg) did not just ameliorate the body fat gain, it also reduced (c,d) the number of fibrotic leasons (a,b) of the liver that occured when the ob +/+ mice got fat (Begrich. 2008).

Is BAIBA even safe? In the absence of human studies that's difficult to say, but in rodents it had no ill effects on mtDNA replication (Mainonneuve. 2004) and displays a generally low toxicity. As Begrich et al. point out, their "further investigations are [still] requested to determine whether BAIBA could induce deleterious effects," even though, "it seems that this endogenous derivative could have a favourable safety profile that might be attractive for pharmacological usage" (Begrich. 2010). Deteriorations of the lipid or glucose metabolism, were not observed in any of the currently published studies and at a dosage of 100mg/kg BAIBA reduced the fibrotic leasons in the livers of obesity prone mice and improved the level of lactate dehydrogenase, a potential marker of liver problems (Begrich. 2008).

Overall, it does thus appear as if Begrich's own conclusion that BAIBA supplements "may be indeed an attractive pharmacological strategy in order to prevent (and/or treat) obesity" (Begrich. 2010) is only partly warranted:

• While BAIBA may be useful to ameliorate the body fat gain in lean individuals and would thus in fact be an "attractive pharmacological strategy in order to prevent [...] obesity" (ibid.) in an obesogenic environment,
• it appears to be more than just 'a little too early' to assume that BAIBA supplements could also be used to "treat" (ibid.) obesity in individuals who are already carrying >50% more body fat on their frame than the average lean person.

It is however more than the fact that many of you are probably (still) lean that keeps BAIBA in the game: If you look at the data in Figure 2, it becomes obvious that BAIBA may do more than to prevent the body fat gain in people who have always been lean: its effect on leptin, in particular, could be of even greater use for people who have lost a significant amount of body fat and are now struggling with the nasty yoyo effect.

Figure 2: The increase in adipocyte (=fat cell) leptin and adiponectin production that was observed in the petri dish is particularly interesting for people who have already lost a significant amount of body fat (Begrich. 2010). If it translates into in vivo human studies, it may help those people to stay lean and reverse "metabolic damage".

As you can see in Figure 2, in vitro data shows that the direct exposure of fat cells (adipocytes) of mice, which are at a particularly high risk of becoming obese, will trigger a significant increase in leptin and adiponectin production. Why's that important? Well, of these...

• 

  Metabolic Damage, Energy Intake & the Human "Energy Thermostat" - An Update Based on Recent Studies | read it!

  the increase in adiponectin that is produced by one's fat cells has been linked to important health markers, like increased insulin sensitivity and improved markers of lipid management.
• the increase in leptin production, however, may be of greater importance, because the diet- or rather fat-loss induced remodelling of the adipose tissue (many small empty fat cells) will reduce the production of the "you're fat enough" signal leptin and thus increase the risk of formerly obese individuals to regain every pound (or even more) of body fat they have painfully lost over months of hard dieting.

With that being said, the possibility that BAIBA may be able to reverse a potential cause of something that is often referred to as "metabolic damage" of which it appears as if it was at least partly triggered by a reduction in relative leptin production (i.e. the amount of leptin that is produced at a certain level of body fat) brings BAIBA back into the game. 

Bottom line: Whether an increase in leptin production is, as Figure 3 from Begrich's previously cited review suggests, the only (or at least the most important) mechanism of the beta-aminoisobutyric acid induced anti-obesity effect will yet have to be confirmed in future studies.

Figure 3: If Begrich et al. (2010) are right, the beneficial effects of BAIBA are mediated mostly, if not exclusively by leptin. Due to a lack of human data, BAIBA must - as of now - still be classified as "promising, but unproven" anti-obesity supplement.

Of even greater importance than investigations into what I would like to call the "leptin hypothesis of BAIBA's anti-obesity effects", though, is the simple confirmation of its effects in independent human studies. I mean, rodents are (often) a good model of human metabolism, but there are instances where slight metabolic differences between man and mouse can have a huge impact on several practically relevant research outcomes. It is thus well possible that unexpected human-specific "side effects" like an extreme increase in appetite and energy intake could reduce or blunt the purported anti-obesity prowess of BAIBA. Before the aforementioned human studies have not been conducted, peer-reviewed and published, I recommend to stay skeptical about BAIBA being the "next big thing in fat loss supplements." | Comment on Facebook!

References:

• Begriche, Karima, et al. "β‐Aminoisobutyric Acid Prevents Diet‐induced Obesity in Mice With Partial Leptin Deficiency." Obesity 16.9 (2008): 2053-2067.
• Begriche, Karima, Julie Massart, and Bernard Fromenty. "Effects of β‐aminoisobutyric acid on leptin production and lipid homeostasis: mechanisms and possible relevance for the prevention of obesity." Fundamental & clinical pharmacology 24.3 (2010): 269-282.
• Maisonneuve, Caroline, et al. "Mitochondrial and metabolic effects of nucleoside reverse transcriptase inhibitors (NRTIs) in mice receiving one of five single-and three dual-NRTI treatments." Antimicrobial agents and chemotherapy 47.11 (2003): 3384-3392.
• Maisonneuve, Caroline, et al. "Effects of zidovudine, stavudine and beta-aminoisobutyric acid on lipid homeostasis in mice: possible role in human fat wasting." Antiviral therapy 9.5 (2004): 801-810.