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Green Tea & Your Thyroid: Are the T4 & T3 Reducing Effects of 250mg (HED) Green Tea Catechins Reason For Concern?

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Is there a devilish thyroid hormone eating dragon hiding out in your beloved green tea?
There is hardly a day without great, yet mostly only promising, and rarely really relevant news about green tea. With it's anti-cancer, anti-diabetes, anti-everything-that-ails our society effects it bids fair to be the elixir of life. This life, and this is the result of a recently published study, SuppVersity reader Paolo had brought to my attention a couple of days ago, could however end up being one with slightly or even profoundly compromised thyroid function. Now, before you freak out because you have been drinking green tea for the past couple of years, do me a favor, mind the conditional in the previous sentence and read the rest of today's Easterly SuppVersity article, which is not an early April fool hoax.

"You must be kiddin' green tea helps weight loss, so how can it reduce thyroid function?"

It may sound hilarious that something that is touted as a fat burner and weight loss adjuvant with tons of scientific backup is supposed to have the nasty ability of inducing (probably transient) hypothyrodism. The data Amar K. Chandra and Neela De, University of Calcutta and the University College of Science & Technology present in their most recent paper is yet unambigous: The hailed green tea catechin and flavonoids possess "potent antithyroid activity as evidenced from in vivo and in vitro studies" (Chandra. 2013)

The 20% reduction in testosterone in response to 5 cups/day of green tea (HED) researchers observed in a 2011 rodent study shows that the thyroid is not the only organ that does not like green tea catechins (learn more),
Despite the fact that this is probably news to most of you, the results of Chandra's and De's most recent experiment do actually line up pretty nicely with previous data by the same researchers (2010), as well as the goitrogenic (T3+T4 low + TSH high => abnormal growth of the thyroid) effects the daily administration of green tea extracts had on the lab animal of Y Sakamoto and his colleagues from the Tokyo Metropolitan Research Laboratory of Public Health in Japan (Sakamoto. 2001).

Moroever, their data supports the general notion that the hailed green tea flavon-3-ols (flavenols) can mess with all sort of enzymatic conversion processes in the mammalian body - including the aromatization of testosterone to estrogen (Sato. 2002).

It's not just the inhibition of iodine uptake that's the problem here. It's its release and conversion.

By acting directly on the enzymatic activities of thyroid peroxidase and 5'-deiodinase I it effectively blocks the generation of T4, by inhibiting the release of iodine (thyroid peroxidase) and subsequent conversion of the latter to thyroxine (T4), the major thyroid hormone in the mammalian body and precursor to the "metabolically active" triiodothyronine (T3).
Figure 1: Weight gain, thyroid cell morphology, enzyme activity and thyroid hormone levels after 30 days on different amounts of green tea catechins; all data expressed relative to untreated control (Chandra. 2013)
As the data in figure 1 goes to show you, the administration of pure green tea catechins at dosages of 10, 20, and 30 mg/kg body weight (intraperitoneal ~ orally, but in a way that the animal cannot puke it up) for two, respectively four weeks (15 vs. 30 days), led to statistically highly significant and dose-dependent decreases of the activity of the aforementioned enzymes and concomitant increases in Na+, K+ ATPase activity, as well as substantial decrease in serum T3 and T4 levels that went hand in hand with elevations of the thyroid stimulating hormone TSH. In view of these clearly goitrogenic effects, it's therefore not surprising that ...
"[h]istological examinations of the thyroid gland revealed marked hypertrophy and/or hyper-plasia of the thyroid follicles with depleted colloid content." (Chandra. 2013)
What we do yet  have to keep in mind is that rodents are in general more sensitive to goitrogenic agents (Döhler. 1979; Capen. 1995) so that the conclusion that dosages as low as 3-4mg/kg of a highly concentrated green tea extract could lead to fulminant reductions in thyroid function or even full blown goitre, is clearly unwarranted.
"Nutritional thyroid medication" - Sirloin of beef in smoked butter. Those plus tons of veggies and a controlled amount of fruits were the "magical" cure to low thyroid function in kids in a 2012 study shows, you may remember from the SuppVersity news (refresh your memory)
Thyroid function and body composition: Just in case you have been missing Tuesday's Facebook news on the correlation of T4 and T3 levels with total body mass, body fat, waist cirumference and more here is a brief reminder. In the 100 euthyroid men, Min Kyong Moon and his colleagues from the Department of Internal Medicine at the Seoul National University College of Medicine in Korea observed that free T3 is inversely correlated with body mass index, LDL, intramuscular fat area and the total amount of liver fat (Moon. 2013). The levels of free T4, on the other hand, also showed inverse correlations with the waist circumference and total body weight of the Koreans. In addition, both, fT3 & fT4 were negatively associated with pericardial fat.
Chandra and De are yet nevertheless right, when they point out that "human tea drinkers", and even more people who consume large amounts of the commercially available green tea extracts that have been used in the study at hand, are likely to be be "at risk", as well (Chandra. 2013). How real this risk eventually is, and which amount of green tea extracts would be necessary to induce similarly negative effects in humans would yet (as so often) require further investigation.



Bottom line: I am no friend of the notion that the consumption of large amounts isolated extracts of whatever purported health-elixir will have nothing but benefits. The current evidence is yet far from being conclusive enough to give up on your one, two or three cups of green tea per day.

Though color may matter in terms of the thyroid effects, the most important thing for anyone trying to keep his waist tight appears to be that he/she drinks tea, whether it is green, black, white or well... pu-erh (learn more ;-)
And I am not saying that, because I am afraid of going back on a previous advice, but simply because thyroid hormone abnormalities have yet never been an issue in any of the myriad of studies on the beneficial effects of regular green tea consumption, of which Crespy et al. who don't simply ignore potential downsides of green tea extracts in their 2004 review, explicitly state that it would "even [in] a very high dietary amount [...] be unlikely to cause" (Crespy. 2004) these types of effects. And if you want to make 100% sure, just exchange one or two of the cups of green tea with its fermented black cousin which has a way lower goitrogenic potential (Chandra. 2011), and still shares many of he beneficial effects of its "raw" relative (cf. Leung. 2001; Gupta. 2002; Gardner. 2007, ...)

References:
  • Capen CC. Toxic response of the endocrine system. In: Klaassen CD, Amudr MO, Doull J (eds) Casarett and Doull’s toxicology: the basic science of poisons. Barnes and Noble, McGraw-Hill, New York, 1995:617–640.
  • Chandra AK, De N. Goitrogenic/antithyroidal potential of green tea extract in relation to catechin in rats. Food Chem Toxicol. 2010 Aug-Sep;48(8-9):2304-11.
  • Chandra AK, De N, Choudhury SR. Effect of different doses of un-fractionated green and black tea extracts on thyroid physiology. Hum Exp Toxicol. 2011 Aug;30(8):884-96.
  • Chandra AK, De N. Catechin induced modulation in the activities of thyroid hormone synthesizing enzymes leading to hypothyroidism. Mol Cell Biochem. 2013 Feb;374(1-2):37-48.
  • Crespy V, Williamson G. A review of the health effects of green tea catechins in in vivo animal models. J Nutr. 2004 Dec;134(12 Suppl):3431S-3440S.
  • Döhler KD, Wong CC, von zur Mühlen A. The rat as model for the study of drug effects on thyroid function: consideration of methodological problems. Pharmacol Ther. 1979; 5:305–318. 
  • Gardner EJ, Ruxton CH, Leeds AR. Black tea--helpful or harmful? A review of the evidence. Eur J Clin Nutr. 2007 Jan;61(1):3-18.
  • Gupta S, Saha B, Giri AK. Comparative antimutagenic and anticlastogenic effects of green tea and black tea: a review. Mutat Res. 2002 Sep;512(1):37-65.
  • Leung LK, Su Y, Chen R, Zhang Z, Huang Y, Chen ZY. Theaflavins in black tea and catechins in green tea are equally effective antioxidants. J Nutr. 2001 Sep;131(9):2248-51.
  • Moon MK, Hong ES, Lim JA, Cho SW, Lim S, Choi SH, Yi KH, Park DJ, Park YJ, Jang HC. Associations between thyroid hormone levels and regional fat accumulation in euthyroid men. Eur J Endocrinol. 2013 Mar 19.
  • Sakamoto Y, Mikuriya H, Tayama K, Takahashi H, Nagasawa A, Yano N, Yuzawa K, Ogata A, Aoki N. Goitrogenic effects of green tea extract catechins by dietary administration in rats. Arch Toxicol. 2001 Dec;75(10):591-6.
  • Satoh K, Sakamoto Y, Ogata A, Nagai F, Mikuriya H, Numazawa M, Yamada K, Aoki N. Inhibition of aromatase activity by green tea extract catechins and their endocrinological effects of oral administration in rats. Food Chem Toxicol. 2002 Jul;40(7):925-33.

Concomitant Training: What's the Best Strength to "Cardio" Ratio to Become Big, Buffed and Strong? 3:1, 1:1 or No Cardio at All? Plus: Looking Back at the Latest Meta Review

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What's the best you can do after a brutal leg workout? Cardio! At least if size and not strength is your goal...
It is one of those never ending debates: "Cardio!? To do it, or not to do it!? That's the question" - especially for those of us whose main goal is to become big and buffed ... now, you know that my take on this is simple: We are not created as "either or" animals, but have the outstanding ability to make use of both our strength and endurance (just as we can eat both meat and vegetables).

If we discard these philosophical considerations and take a more scientific stance towards the topic, the question still remains: Isn't doing cardio going to interfere with your success on the bench and vice versa? I mean you can't be a marathon running, bodybuilding powerlifter, can you? Hmm... no I don't think so, at least you would be pretty bad in each of the sports - a typical Jack of All Traits, Master of None, so to say ;-)

The "big and bulky" vs. the "sinewy and weak" effect 

Not to long ago, the question of "interference" was something only meatheads would ponder. In these days, in which even women's magazines begin to incorporate the latest scientific insights into the importance of muscle mass and strength into their "shaping" and "fitness" routines, it is yet becoming increasingly interesting for "the public" and that makes it easier for scientists to get funding and get published - sometimes (yet not in today's case) even outside of the Journal of Strength and Conditioning Research.

Only a couple of weeks ago, Jacob A. Wilson and colleagues published a detailed meta-review of the interference between strength and endurance work, in which they did confirm that the often-touted interference effect between endurance and strength training exists, and that the extend of the latter latter depends on the amount, type, frequency and intensity of aerobic activity a trainee is trying to pack into his workout routine (click here for the latest on how to combine both into one routine):
Effect sizes for combined training depending on the duration of the endurance component (Wilson. 2012)
"The mean ES for power development for strength training only was 0.91; for endurance training, it was 0.11; and for concurrent training, it was 0.55. Significant differences were found between all the 3 groups. For moderator variables, resistance training concurrently with running, but not cycling, resulted in significant decrements in both hypertrophy and strength. Correlational analysis identified significant negative relationships between frequency (−0.26 to −0.35) and duration (−0.29 to −0.75) of endurance training for hypertrophy, strength, and power." (Wilson. 2012)
I would guess that the timespan between the publication of Wilson's paper in the Journal of Strength and Conditioning Research and the study by Thomas W. Jones et al. the results of which are the topic of today's SuppVersity article probably is too short to call it a "follow up" of some sort. The intention of the researchers, i.e.
"to investigate the strength, limb girth and neuromuscular responses to a variety of concurrent strength and endurance training ratios, with incremental loads in an isolated limb model." (Jones. 2013)
would yet qualify the Jones study as a follow up that could either confute of confirm the statistically derived results Wilson and his colleagues presented in their August 2012 paper.

What did the scientists do and what did they find?

Jones et al. used a balanced, randomized, between-group study design. The participants, 24 healthy recreationally resistance-trained men (25 ± 3 yrs; 82.3 ± 10.0 kg;  179 ± 7 cm; 214.2 ± 42.3 Nm; >2y of strength training experience) were randomly assigned to one of the following experimental conditions:
    True or False? "Training your legs will make
    your arms grow faster" (read more)
  • strength training, only (ST)
  • 3:1 ratio strength & endurance training (CT3) 
  • 1:1 ratio of strength & endurance training (CT1) 
  • no training (CON)
All strength and endurance training was conducted in an isolated limb model and focused on the quadriceps muscle, with the exact protocols looking like this:
  • strength training alone on all scheduled training sessions (ST)
  • strength training on every scheduled session with every third session immediately followed by an endurance training (CT3)
  • strength training immediately followed by endurance training at every scheduled session (CT1)
  • no strength or endurance training (CON)
The total duration of the intervention period was 6 weeks and all trainees, except those who had been randomized to the lazy control group, worked out three times per week with ~48h of rest in-between the sessions.

"30min of leg extensions = cardio!?"

While the resistance training consisted of 5 sets of 6 repetitions (reps) at 80±5% of unilateral leg extensions (weight was increased progressively to keep the intensity), the endurance training protocol consisted of 30 min of repeated isokinetic unilateral leg extensions at 30±5% individual maximally voluntary contraction. The frequency was set at 1s per muscle action and the tempo was standardized via electronic metronome throughout the trial. This is obviously not a realistic "cardio" program, but it has the advantage of really isolating the targeted muscle group, which would not be the case if the scientists had had their participants cycle on a classic ergometer. 
Figure 1: Effects of strength only (ST), strength + "cardio" at 3:1 (CT3) and 1:1 ratio (CT1) and not training at all (CON) on maximal voluntary contraction (strength), limb girth (size) and time to exhaustion (conditioning) - focus on the colors(!) not the figures with their hilariously large standard deviations (Jones. 2013)
As a brief peak at the data in figure 1 is going to tell you (due to the huge standard deviations, you better rely on the colors instead of the figures ;-) the researchers from the Northumbria University in Newcastle upon Tyne (UK) and the North West University in Potchefstroom (SA), the scientists did, just as they had expected, a whole host of statistically significant differences:
"Following training, ST and CT3 conditions elicited greater MVC increases than CT1 and CON conditions (P ≤ 0.05). ST resulted in significantly greater increases in limb girth than both CT1 and CON conditions (P = 0.05 and 0.004 respectively). CT3 induced significantly greater limb girth adaptations than CON condition (P = 0.04). No effect of time or intervention was observed for EMG (P > 0.05)" (Jones. 2013)
What remains to be seen, though is in how far a "saner" endurance training protocol would have produced a similarly pronounced negative effect on the training induced increases in limb girth (size) and strength (MVC), while still yielding at least some of the beneficial effects on time to exhaustion (TTE).

There may be something to higher volume for legs (learn more)
If this is not your first visit to the SuppVersity you may yet remember a couple of previous posts on leg training, all of which clearly suggested that the legs need to be hammered to grow. At first the results of the study at hand seem to contradict this assumption, but if we are honest, "a little more hammering" is not exactly doing 30 min of continuous leg extensions.

The latter takes us back to the previously mentioned methodological shortcomings of this study. In as much as the 30-min of 30% MVC leg extensions may be suitable to really isolate the muscle, they have little to nothing to do with the classic endurance protocols most people are thinking about, when the hear the term "concomitant training".

We do, on the other hand, know from previous studies, such as the Psilander study, I covered in some detail in a previous blogpost that additional cycling before a leg workout can potentially boost the growth response to a subsequent workout (learn more). Whether this means of training is sustainable over time, would obviously be a different question.



Bottom line: Due to the specific design of the "cardio" part of the study, and the exclusive focus on the quadriceps muscles, it is difficult to say something definitive about the practically more important question whether 30min of classic low to medium intensity cardio training (e.g. on a cycle ergometer) would actually hamper your gains in such a profound fashion - regardless of whether you perform it before or after your workout.

Effect of strength vs. endurance only vs. combined training on body fat loss and changes in VO2Max, power, strength and size; data expressed rel. to avg. effect sizes for each parameter (Wilson. 2012)
If I am yet looking back at the results Wilson et al. presented in their meta-review, it would seem that low-intensity, low frequency cardio training is not the no-go the study from the study at hand would suggest it was. HIIT training, obviously a whole different animal and not necessarily something you would want to perform after a strenuous leg workout, for example does provide an anabolic stimulus of its own (learn more). HIIT vs. steady state is yet only one of the any parameters that will ultimately determine, whether or not an additional aerobic component is going to hamper your strength performance.  Another interesting observation Wilson et al. made was that the equipment the subjects used (and thus probably the effective metabolic demand) had an affect on the effectiveness of the strength training, as well.

Specifically, Wilson and his colleagues were able to show that the lack of weight support during treadmill running / jogging vs. cycling increased the detrimental effects on strength, power and size gains in the 21 studies the meta-analysis was based on. More than three cardio sessions per week, and high(er) intensity aerobic activity in general were likewise associated with practically relevant reductions in effect size.


Listen to Dr. Wilson in person! My friend Carl Lanore had him on Super Human Radio a couple of weeks ago.
On the other hand, some of these effects can be mitigated by doing cardio on separate days, so that you can still benefit from the concomittant (or endurance only) exclusive improvements in conditioning and avoid the VO2Max loss the scientists observed in the strength only groups. Skipping endurance work altogether is thus probably not the ideal method for the average physical culturist.

In the end, you will yet have to answer this question for yourself. Personally, I feel a baseline of 3x30min of various forms of "cardio" training (in the broadest sense) has always served me well.

References:
  • Jones TW, Howatson G, Russell M, French DN. Performance And Neuromuscular Adaptations Following Differing Ratios Of Concurrent Strength And Endurance Training. J Strength Cond Res. 2013 Mar 21.
  • Wilson JM, Marin PJ, Rhea MR, Wilson SM, Loenneke JP, Anderson JC. Concurrent training: a meta-analysis examining interference of aerobic and resistance exercises. J Strength Cond Res. 2012 Aug;26(8):2293-307.

Coffee, Tea, Cacao, Caffeinated Sodas & Breast Cancer: 5+ Cups/Day?! Study & Meta-Analysis Show, It May Take More Coffee Than Previously Thought to Ward Off Breast Cancer

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While you don't have to bath in coffee, one cup per day is probably not enough to protect your mammary glands.
Initially today's SuppVersity post was just about coffee and breast cancer risk. Today, a couple of days and a hand full of news on other interesting papers that are piling up by dozens in my archive, I found that the paper has proliferated ;-o

Well, not exactly, but in conjunction with a recent meta-analysis on the potential anti-breast-cancer effects of coffee today's news certainly covers data from almost 380,000 women world-wide and will thus probably yield somewhat more reliable data on whatever relation may exist between a woman's coffee / caffeine consumption and her risk of developing breast cancer.

It takes Canadian women at least 5 cups of coffee to elicit significant reductions in breast cancer risk

Against that background, both the detailed 7-item sub-analysis of the data from the Women’s Diet and Health Study and the unique inclusion of information on the cytochrome P450 1A2 (CYP1A2; the enzyme that's responsible for the metabolism of caffeine) gene variant of the 25 to 74 year old women distinguish the soon-to-be-published epidemiological study by Elizabeth C. Lowcock and her Canadian (resident) who found that there is no general association with coffee and caffeine consumption on the one, and breast cancer risk on the other hand.
"[H]owever, a significant reduction in risk was observed with the highest category of coffee consumption [≥5 cups per day vs. never, multivariate-adjusted odds ratio (MVOR)=0.71, 95% confidence interval (CI): 0.51, 0.98]." (Lowcock. 2013)
Interestingly, the ~30% reduction in breast cancer risk the scientists observed in their cohort of Ontarian women, did not depend on the gene variant of the aforementioned caffeine metabolizing enzyme from the cytochrome P450 enzyme cascade. coffee consumption, but not total caffeine" (Lowcock. 2013) that's associated with a reduced risk of both estrogen receptor positive and post-menopausal breast cancers.
Figure 1: Multivariate-adjusted odds ratios for breast cancer and coffee, decaffeinated coffee and caffeine intake w/out correction for CYP1A2 (rs762551) genotype (Lowcock. 2013)
In conjunction with the actual data from the 7-item analysis, this observation supports the scientists hypothesis that it is "coffee consumption, but not total caffeine" (Lowcock. 2013) that's associated with a reduced risk of both estrogen receptor positive and post-menopausal breast cancers.

If that is true, i.e. if it's not the main active ingredient caffeine, but one of or the complete spectrum of polyphenols the dark brew has to offer, it seems logical that such an exuberant amount of coffee is necessary to benefit from the purported protective effects (remember we are still talking about associations of consumption and breast cancer incidence - not mechanisms) of coffee. Why? Well, despite the fact that a comparison on a mere weight-to-weight ratio is obviously overtly simplistic, the amount of whatever flavenoid or other ingredient may turn out to be responsible for the anti-cancer effect is almost certainly at least one, if not several magnitudes smaller than those 100-200mg of caffeine your "average" (whatever that may be today) cup of coffee has to offer.

2% risk reduction per two cups? Looks like more was really better.

The notion that "more helps more" is indeed supported by another a meta-analysis of 37 international studies, Wenjie Jiang, Yili Wu and Xiubo Jiang from the Medical College of Qingdao University in Shandong have conducted (Jiian. 2013).

Suggested read: "Only 'Real', Yet Not Decaffeinated Instant Coffee Increases Fatty Acid Oxidation. Plus: Revisited, Caffeine's Dose-Dependent Effect on the Exercise Induced Changes to the ratio of Testosterone to Cortisol" (read more)
According to the study, which is going to find it's way into one of the next issues of Gynecologic Oncology, the collective data of 966,263 study participants (59,018 breast cancer cases) does not warrant the conclusion that either coffee or caffeine consumption (yes vs. no) is associated with a significant reduction in breast cancer risk:
  • coffee -- 3% risk reduction, p = 0.09
  • decaffeinated coffee -- 2% risk reduction p = 0.55 
  • caffeine - 1% risk reduction,  p = 0.73
In fact, the p-value, i.e. the probability that a result is mere coincidence, passes the magic p < 0.05 (meaning there is a <5% chance of the observed association being mere coincidence) hurdle only in postmenopausal coffee concessionaires, whose risk of developing breast cancer is 6% lower than that of their non-coffee guzzling peers.

What's particularly intriguing, though, is the fact that Jiang, Wu & Jiang found a linear dose-response relationship for breast cancer risk with coffee and caffeine, with
"the risk of breast cancer decreas[ing] by 2% (P=0.05) for every 2 cups/day increment in coffee intake, and 1% (P= 0.52) for every 200 mg/day increment in caffeine intake, respectively." (Jiang. 2013)
If we do the math this yield a 10% reduction in breast cancer risk for the 5 cups which gave the Canadian women a 30% edge over their non-coffee drinking peers.

In view of the fact that the number of people consuming this amount of coffee on a daily base (3% in the Women's Diet & Health Study) is in epidemiological terms comparatively low, the "small" deviation of 20% is nothing that would negate the existence of a surprisingly profound protective effect of coffee on the development of breast cancer.




Bottom line: I don't want to be a spoilsport, but as a versed SuppVersity reader you should by now be aware that anything beyond 400-500mg of caffeine (for a woman, for a man maybe 500-600mg) can produce a couple of nasty heart and central nervous system related side effects in view of which the regular / chronic consumption of more than 5 cups of coffee is nothing I would suggest as a means of cancer protection. And since the currently available data does not confirm similar beneficial effects for decaffeinated coffee (see figure 1 red button for likely explanations), you should consider different means of breast cancer protection. Which means that would be? Well, ...
    Even one cup of hot chocolate per week could help reduce your risk of developing breast cancer by 15% (learn more about the health effects of cacao& chocolate)
  • cut your intake of caffeinated soft-drinks to zero and thus reduce your breast cancer risk (compared to drinking 2 cans per day) by 24% or a statistically hardly significant, but still worth mentioning -7% vs. consuming only one can per week (Lowcock. 2013)
  • drink some black tea for a change, and achieve a 13% reduction in breast cancer risk with 3-5 cups per day (Lowcock. 2013)
  • never pass on a delicious cup of cacao, even one cup of hot chocolate per week can decrease your breast cancer risk (due to the low number of cacao drinkers the -15% reduction is yet not significant, Lowcock. 2013)
  • lose weight and visceral fat to avoid the +107% increase in breast cancer risk non-hispanic white women with a BMI >30kg/m² have compared to their non-obese fellow females (Connor. 2013)
    If you work out and stick to a whole foods diet, that's about as much as you can do for the health of your mammary glands. Well,... maybe aside from taking synthetic estrogen and progestin combos to battle the symptoms of menopause (read more about this in the SuppVersity Facebook news).

    References:
    • Connor AE, Baumgartner RN, Pinkston C, Baumgartner KB. Obesity and Risk of Breast Cancer Mortality in Hispanic and Non-Hispanic White Women: The New Mexico Women's Health Study. J Womens Health (Larchmt). 2013 Mar 26.
    • Jiang W, Wu Y, Jiang X. Coffee and caffeine intake and breast cancer risk: An updated dose-response meta-analysis of 37 published studies. Gynecol Oncol. 2013 Mar 24.
    • Lowcock EC, Cotterchio M, Anderson LN, Boucher BA, El-Sohemy A. High Coffee Intake, but Not Caffeine, is Associated with Reduced Estrogen Receptor Negative and Postmenopausal Breast Cancer Risk with No Effect Modification by CYP1A2 Genotype. Nutr Cancer. 2013 Apr;65(3):398-409.

    True or False!? Glucosamine Doesn't Help Cartilage Repair. Carcacrol Based Weight Loss Products Shed Body fat. N-Acetyl-L-Glutamine Is Not Worth the Extra Bucks.

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    Compared being obese and chronically inflamed heavy squats entail a comparably low risk of "wearing off your" joints. This does yet not mean that the 2-3x increase in osteoarthritis risk of female athletes / gymrats compared with non-obese agemates (Spector. 1996)
    If I just go by the mere visitor counts the new "True or False" category appears to turn out to be one of the best innovations of the past weeks. That being said, I am happy that many of you have been submitting questions, but had to realize that even those of which I initially thought they would be easy to answer, require more research than I had expected.

    Therefore this installment contains one long and two short TOF items, which I came across more or less accidentally in the course of the past week. I hope you enjoy those as well and don't freak out that your inquiry has not been answered this week (tip: you can increase your chance of having your question answered if you pick something simple, like the two latter items in this installment).

     Glucosamine supplements cannot help with cartilage repair

    It depends -- Like many of the true or false item the purported benefits of glucosamine supplements on cartilage health belong to those "gems" of common wisdom which have been reiterated so often that everybody is inclined to believe they must be true. Fortunately, science does not operate by the principle of majority rule, which is why you will have to spend reading the following lines if you want to know whether the use of respective supplements is going to help heal your joints.
      More often than not your pain is not (yet) the result of worn of ligaments, but simply a consequence of muscular imbalances. Your shoulder hurts, whenever you bench? Try the impingement no more protocol and reduce or even resolves shoulder pain in 6 weeks (learn more)
    • age related decline in joint health  - there is currently no convincing evidence that "glucosamine modulates ageing phenotype" (Henrotin. 2013), on the other hand the mere absense of long-term studies does not exclude that it may sill have practical value. Benefits are yet only likely to occur if the ability of human chrondocytes to produce glucosamine from glucose declines with age.
    • general prophylaxis - Aside from the by no means unambiguous evidence from animal studies a prophylactic effect of GlcN supplementation in human trials has - as of now - not been presented (Hernrotin. 2014). In this context, a specific weakness of many human studies is the use of inappropriate, often subjective measures instead of reliable MRI or other imaging methods. 
    • treatment of arthritis (OA) - While the general evidence is scarce, it appears as if GlcN could have an ameliorative effect on the progression of OA. Promising evidence that it could help, yet via a pathway much different from the original concept of "providing raw material for joint health" - comes from animal models in which the administration of high doses of glucosamine had ameliorative effects on systemic inflammation (C-reactive protein, TNF-alpha, Largo. 2009). Unfortunately, this is yet another of the many "promises" that has up to now not been reproduced in controlled human studies, in which the administration of allegedly lower amounts of GlcN (1,500 mg) did not affect any of the common markers of inflammation (Nakamura. 2007).
    I guess the previously mentioned points are all "nice to hear", but not exactly what you wanted to read about, right? So what about this one, then, ...
      • CCE the paleo glucosamine? You know that despite my frequent allusions to the (a-)buse of "paleolithic" line argumentations, I am alway open for scientific evidence that would prove any of the bazillion "paleo solutions" people are throwing around on the web (no offense to Robb Wolf, here). Therefore I don't want to miss the chance to let you know that at chicken comb extract (CCE)-containing supplement taken in dosages of 4.8g/day yielded significant improvements in pain scores for the dominant and most affected foot of 23 soccer players (Yoshimura. 2012). Aside from the "eat the whole animal" mantra, this is also interesting as far as the production of future supplements is concerned. After all CCE contains hyaluronic acid (glycosaminoglycan) and are thus themselves made up of glucosamine (or rather D-glucuronic acid and D-N-acetylglucosamine). Whether this makes them more or less effective will yet still have to be elucidated.
        prevention / strengthening of cartilage in athletes: The maintenance of joint health in conditions, where the joints are exposed to excessive loads is probably the area of application GlcN is most heavily marketed for. On the other hand, it is also the area that is the least researched. The current scientific consensus is to acknowledge the evidence from two heavily cited randomized, double-blind,
        placebo-controlled trial, of which ...
        • ... one dealt with 121 male patients who had a recent history of acute knee sport injury (Ostojic. 2007) -- the participants received either 1.5 g GlcN (n=62) per day orplacebo (cellulose; n = 59) for 28 days; despite the fact that the GlcN group demonstrated significant improvements in knee flexion and extension, neither the pain nor swelling subsided
           
        • ... the other analyzed the effect of three months 1.5g or 3.0g of GlcN on the 21 male college aged soccer players (19–22 years of age, mean 20.3) and compared the outcomes to 10 male age-matched college students (Yoshimura. 2009) -- the administration of the supplement decreased the urine levels of CTX-II, but the observed reduction of this marker of collagen turn-over was transient and disappeared after withdrawal of the administration.
        In view of the fact that the significance of the reduced CTX-II levels in the Yoshimura study is not clear these are promising, but by no means conclusive results which would suggest that strength trainees could benefit from the chronic and timely initiated supplementation of 1.5-3.0g of GlcN per day.
      Another thing to keep in mind is that therapeutic doses start at 1,500mg per day (information on optimal dosing regimen for different purposes, age groups, etc. are lacking - also because the bioavailability of glucosamine is highly species dependent and the available literature on horses has little to no value for human beings; cf. Hernrotin. 2013).

      There is still the unresolved issue of adequate vs. excessive dosages

      While the recommended dosage may be enough to achieve serum concentrations of 10µm which are 1-2x more than those the average human being will have floating around in the non-supplemented state, these are still 50x-500x lower than the concentrations scientists use in the petri-dishes of the in-vitro studies producers of respective supplements like to cite to provide evidence for the efficacy of their products (Largo. 2003; Block. 2010).

      Does glucosamine precipitate or even cause insulin resistance? While it probably ain't much of a problem with short term administration of low doses of glucosamine (1g in 2x500mg dosages is safe; cf. Muniyappa. 2005), taking glucosamine in amounts as it would be necessary to achieve serum levels similar to those that have been shown to actually work in in-vitro studies, will almost certainly induce muscular insulin resistance (Largo. 2003; Bailey. 2004; Block. 2010). Moreover, pre-existing insulin resistance (Pham. 2007), as well as diabetogenic diets (Chien. 2009) and/or systemic inflammation (Biggee. 2007) appear to increase the risk of experiencing this nasty side-effect as a consequence of the chronic ingestion (6+ weeks) of dosages of 1.5g+ per day (Dostrovsky. 2011). And let's be honest the sentence "Owing to limitations in study design, conclusions based on studies that report adverse affects of GlcN on insulin sensitivity and glucose tolerance in pre-diabetic subjects are suspect" by the means of which a 2011 review written by employees and counselors of Cargill, a major producer of respective supplements, tries to refute the aforementioned negative scientific evidence is at least as "suspect" as the studies the review is criticizing (Simon. 2011) - no?
      With all that being said, the usefulness of glucosamine supplements as a means to prevent, let alone treat cartilage degeneration is unquestionably overblown. This goes irrespective of the existing in-vitro evidence of the stimulatory effect very high concentrations of GlcN exert on their own usage and incorporation and my - at least in part - be due to another, hitherto overlooked, bottleneck that limits our bodies capacity to use the the "raw material" in the way we intend it.

      Now that you have the evidence right in front of you I'll leave it up to you to decide whether you want to take the (by no means non-existent) chance that the chronic ingestion of high dosages (at least 3g/day) of GlcN could ward of some of the wear and tear of your workouts or whether you simply stop squatting your 1-RM max for reps using a horrible technique and thus ruining not just your knees, but also your back.

      You should be aware, though, that the latter does imply that you trust the Cargill guys' judgment that the hitherto published animal and human studies have "limitations" and any "conclusions based on studies that report adverse affects of GlcN on insulin sensitivity and glucose tolerance in pre-diabetic subjects are suspect" (Simon. 2011; for more info see red box to the right).

      Carvacrol supplements will promote weight loss

      False -- Despite the fact that a recent study in mice shows that the administration of isopropyl-ortho-cresol aka cravacrol, the predominant monoterpene phenol from the essential oils of plants from the Labiatae family (Origanum, Satureja, Thymbra, Thymus, and Coridothymus), is a potent inducer of hepatic AMPK and sirtuin-1 activity (Kim. 2013), the currently available supplements are so hilariously underdosed that even the researchers could not deny themselves the following side kick:
      Cravacrol could work, if there was a supplement with adequate amounts of it on the market (data based on Kim. 2013).
      "The daily carvacrol intake of the mice in our study (100 mg/kg body weight) was equivalent to an intake of approximately 8.1 mg/kg human body weight (486 mg/60 kg person), when calculated on the basis of normalization to body surface area as recommended by Reagan-Shaw et al. and the US Food and Drug Administration.

      The daily doses of commercial dietary supplements range from 9 to 288 mg carvacrol (0.15–4.8 mg/kg body weight) for a 60 kg human." (Kim. 2013)
      This spares me to tell you that you are wasting your money, if you throw one of the carcacrol based fat burners into your virtual or real shopping basket.
      On a more general note: Irrespective of any dosage issues, it is by no means sure that any of the many "proven" anti-inflammatory weight loss agents, i.e. herbs & co that help reduce weight gain in rodents on HFD and/or help obese and metabolically deranged individuals to lose weight will do anything at all in healthy, insulin sensitive, non-inflamed, normal-weight individuals (e.g. "Epigallocatechin Gallate (EGCG), Capsaicins, Piperine & Carnitine: Rather a Health Than a Fat Loss Stack?", read more). In other words: "Not everything that's good for your obese neighbor will be beneficial for you, as well."

      Due to its stability in water N-Acetyl glutamine is way superior to regular l-glutamine

      False -- Irrespective of the never-ending debate on the usefulness of glutamine supplementation for hard-working athletes (learn more), respective supplements are still part of the most commonly used bulk-powders among bodybuilders, physique athletes and average gymrats. Contrary to the potential benefits of respective supplements, which can, despite being far from scientifically established, not be denied altogether, there is one thing that's about as sure as the eggs I had for breakfast: The allegedly more stable N-acetyl variety of glutamine (NAG) does not just taste like **** it is also a complete waste of money and probably less effective than the cheap free-form glutamine you can buy for a couple of pennies at every of the major bulk suppliers on the Internet.
      Figure 1: Glutamine content in the blood of 15 pigs (15–20 kg weight) maintained on either a 1kg/day standard diet (C) or C + 8 g L-glutamine and C + 10.5 g N-acetyl-L-glutamine provided at 1000 g/day after "breakfast" (333g of the chow) and detailed analysis of intact glutamine and glutamic acid in the jejunum mucosa, after 180min of intestinal infusion (Arnaud. 2004)
      After you have taken a look at the data in figure 1, any further elaborations that go beyond the confirmatin f the high accuracy and usefulness of porcine models for human digestion and metabolism (cf. Litten-Brown. 2010) should be dispensable... as dispensable as NAG supplements, by the way ;-)



      That's it for today: As mentioned in the introduction, I am well aware that some of you will be missing their suggestions, but I have to say that answering those inquiries in more than just a "probably no", "probably yes" fashion takes its time. No reason for the rest to keep submitting suggestions, I will keep track of them and have already done some research into the more complex stuff, which may give rise to a post of their own in the future.

      References:
      • Bailey CJ, Turner SL. Glucosamine-induced insulin resistance in L6 muscle cells. Diabetes Obes Metab. 2004 Jul;6(4):293-8. 
      • Biggee BA, Blinn CM, Nuite M, Silbert JE, McAlindon TE: Effects of oral glucosamine sulphate on serum glucose and insulin during an oral glucose tolerance test of subjects with osteoarthritis. Ann Rheum Dis 2007, 66:260-262. 
      • Block JA, Oegema TR, Sandy JD, Plaas A:  The effects of oral glucosamine on joint health: is a change in research approach needed? Osteoarthr Cartil. 2010; 18:5–11. 
      • Chen HC, Shah S, Stabler TV, Li YJ, Kraus VB: Biomarkers associated with clinical phenotypes of hand osteoarthritis in a large multigenerational family: the CARRIAGE family study. Osteoarthr Cartil. 2008; 16:1054–1059. 
      • Chien CS, Cheng SC, Wu HT, Tsao CW, Cheng JT: Insulin resistance induced by glucosamine in fructose-fed rats. Horm Metab Res 2009, 41:542-547.
      • Dostrovsky NR, Towheed TE, Hudson RW, Anastassiades TP: The effect of glucosamine on glucose metabolism in humans: a systematic review of the literature. Osteoarthritis Cartilage 2011, 19:375-380.
      • Henrotin Y, Chevalier X, Herrero-Beaumont G, McAlindon T, Mobasheri A, Pavelka K, Schön C, Weinans H, Biesalski H. Physiological effects of oral glucosamine on joint health: current status and consensus on future research priorities. BMC Res Notes. 2013 Mar 26;6(1):115.
      • Kim E, Choi Y, Jang J, Park T. Carvacrol Protects against Hepatic Steatosis in Mice Fed a High-Fat Diet by Enhancing SIRT1-AMPK Signaling. Evid Based Complement Alternat Med. 2013;2013:290104.
      • Largo R, Alvarez-Soria MA, Diez-Ortego I, Calvo E, Sanchez-Pernaute O, Egido J, Herrero-Beaumont G:  Glucosamine inhibits IL-1beta-induced NFkappaB activation in human osteoarthritic chondrocytes. Osteoarthr Cartil. 2003, 11:290–298.  
      • Litten-Brown JC, Corson AM, Clarke L. Porcine models for the metabolic syndrome, digestive and bone disorders: a general overview. Animal. 2010 Jun;4(6):899-920.
      • Muniyappa R, Karne RJ, Hall G, Crandon SK, Bronstein JA, Ver MR, Hortin GL, Quon MJ. Oral glucosamine for 6 weeks at standard doses does not cause or worsen insulin resistance or endothelial dysfunction in lean or obese subjects. Diabetes. 2006 Nov;55(11):3142-50.
      • Nakamura H, Masuko K, Yudoh K, Kato T, Kamada T, Kawahara T. Effects of glucosamine administration on patients with rheumatoid arthritis. Rheumatol Int. 2007 Jan;27(3):213-8.
      • Ostojic SM, Arsic M, Prodanovic S, Vukovic J, Zlatanovic M: Glucosamine administration in athletes: effects on recovery of acute knee injury. Res Sports Med. 2007; 15:113–124. 
      • Pham T, Cornea A, Blick KE, Jenkins A, Scofield RH: Oral glucosamine in doses used to treat osteoarthritis worsens insulin resistance. Am J Med Sci 2007, 333:333-339.
      • Simon RR, Marks V, Leeds AR, Anderson JW. A comprehensive review of oral glucosamine use and effects on glucose metabolism in normal and diabetic individuals. Diabetes Metab Res Rev. 2011 Jan;27(1):14-27.
      • Spector TD, Harris PA, Hart DJ, Cicuttini FM, Nandra D, Etherington J, Wolman RL, Doyle DV. Risk of osteoarthritis associated with long-term weight-bearing sports: a radiologic survey of the hips and knees in female ex-athletes and population controls. Arthritis Rheum. 1996 Jun;39(6):988-95.
      • Yoshimura M, Sakamoto K, Tsuruta A, Yamamoto T, Ishida K, Yamaguchi H, Nagaoka I: Evaluation of the effect of glucosamine administration on biomarkers for cartilage and bone metabolism in soccer players. Int J Mol Med. 2009; 24:487–494.
      • Yoshimura M, Aoba Y, Naito K, Watari T, Murakami S, Yoshimura K, Nakagawa T, Yamamoto T, Yamaguchi H, Nagaoka I. Effect of a chicken comb extract-containing supplement on subclinical joint pain in collegiate soccer players. Exp Ther Med. 2012 Mar;3(3):457-462.

      Adelfo Cerame - Prelude to the Off-Season: "If I can Make the Improvements I'm Striving For, I Can Be Competitive!"

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      It's not only unlikely, but probably totally counter-indicated to try ans stay in (near-)contest shape during the off season (suggested read: "Scientific Bodybuilding Coverage")
      Good news first! Despite the fact that Adelfo is probably not going to compete again before next year, his bi-monthly blogposts will keep coming. As you are going to learn in today's installment Adelfo believes in the value of an extended off-season and I am pretty sure that Adelfo is going to let participate in and learn from the one-year period of serious muscle building that's lying ahead of him... I mean, let's be honest, don't we all dream of adding some size to one or another body part?

      Before we do yet take a look what Adelfo's got in stock for you today, I'll have to tell you the bad news as well. Due to scheduling issues, the SuppVersity Science Round-Up is going to take a break today, but will be back next Thursday at 1PM EST with the regular truckload of news from the realms of exercise, nutrition and supplementation sciences.

      I am not sure how disappointed you are now, but I'd hope at least a little and would suggest you head over to the SuppVersity Facebook Page to devour a couple of the latest short news I've piled up over there (just in case you did not know that there are 6-12 exclusive items on FB every day!)...
      • premature ejaculation - suggested read (free full text, as usual) on the etiology and currently available treatment options of / for the "fast guys" (read more)
      • insulin resistance, salt intake & high blood pressure - study suggests that only insulin resistant women develop BP issues with high salt intake (read more)
      • dairy & dietary calcium in general not a problem for your kidneys - other than it is often said dairy calcium is not associated with an increased kidney stone risk (read more)
      • testosterone for body composition & health, not performance - at least in healthy older men with low-normal levels TRT is no performance enhancer (read more)
      • 5% reduced diabetes risk per 500mg/d flavenoids - regardless where you are getting them from, increasing your dietary intake of flavenoids could protect you from diabesity (read more)
      I know it's not the same, but contrary to the radio show it's even interactive: I post, you comment, I reply, ... you know the spiel, don't you?

      Is there a life after winning the pro card? Yes there is! So what’s next?

      Without a thorough understanding of the AMPK/mTOR seesaw, you will hardly find a protocol that yield 95%+ lean mass (learn more) and don't forget to complete your studies with the foundations of skeletal muscle hypertrophy (read more)
      I’ve felt that I never really had a true or solid off-season because I was always competing on a yearly basis trying to chase my pro card. Prior to this year, it was always an annual repetitive cycle of competing and falling short, then back to the drawing boards to try and chase it again, so for the past 3 years I rarely had more than three to four months in-between shows. I tried my very best to make improvements during that tie, but before those really payed off it usually was about time to diet down for the next prep, again...

      "This off-season is really going to do me some good."

      It's simply high time for a well-deserved extended off-season. I really feel as if it was time to take a break from competing it was overdue for me and I am planning to take a whole year off to fully dedicate myself to putting on the size and making the improvements I need to make in my physique in order to be competitive at the pro level.

      I’m really going to enjoy this long off-season, because I’ve finally achieved my goal at becoming an IFBB wheelchair pro and can now that the monkey is off my back finally move on and set new goals for myself to accomplish at the next level.
      This is the best of the best when it comes to wheelchair bodybuilding. As you can see, everyone brings their “A” game at this next level of competition! So, I better make sure I do the same.

      I feel that I’m really going to maximize my potential for growth which is something that I I’ve never had a chance to experience, yet. Like those guys who train day in and day out so afraid of gaining an inch on their waist that they never actually make progress, I’ve been competing and thus dieting for the major part of the past years. Under the watchful eyes of coach Alberto, I’m confident that the next 12 months are going to change this and allow me to take my physique to a level where I can stand next to the best without always being the ripped, but undermuscled light weight.

      My goal for the off season: Bringing up my back

      Did you know that prioritizing a weak body part does not necessary entail neglecting or even losing your strengths? I've talked to coach Alberto about this and we both agree that your "gifted body parts" often even grow, when you taper down on the volume and tension to devote the training resources to other less developed areas of your physique.
      Coach Alberto and I both agree that it is best for me to take advantage of this long overdue opportunity to make improvements in my physique. We both are being practical and realistic, I’m never going to be as big (muscle mass wise) as some of the biggest pros in the business, but Alberto feels I have an overall good structure and flow in my physique and since the back has a longstanding history of making the difference between victory and defeat in bodybuiling, it’s really one of my primaries to improve on this key area.

      "If I can make the improvements I am striving for in this off-season and bring in my usual conditioning, I am confident that I can be competitive."

      Aside from it's general importance in the sports of bodybuilding my back has always and still is my weakest area. That's something both, coach Alberto and I agree on. The back is therefore going to be the #1 priority in the upcoming off-season and a lot of my training will be accordingly prioritized, even if that means keeping my other body parts at maintenance.

      Post-contest/Reverse dieting

      Here was an email interaction between coach Alberto and I and a brief description of what he wanted to accomplish this off-season.
      I am about 3 weeks into my post-contest and reverse dieting and so far so smooth. As I mentioned in my previous Blog that it was a smooth transition… And it was a smooth transition because I dieted the smart and healthy way, which in turn will allow me to maintain my leanness for the long-term while still keeping my sanity. Obviously I’m not going to be maintaining my stage ready physique however I will be able to hold a sustainable body composition that my body can agree with.

      As of today my current macronutrient ranges are
      • Fats: 45-55g
      • Carbohydrates: 275-300g
      • Protein: 190-200g
      But prior to these adjustments Alberto had me on a little spurt for a couple days, which started last Wednesday, where he wanted me to increase my carbs by 25g per day until my next check-in with him which was yesterday.
      Bulking for non-bodybuilders: Adel wanted me to touch on “bulking” for non-bodybuilders and whether I feel that there is a way to really improve your physique without sacrificing your abs for a couple of weeks/months…. I touched on this before, when I was talking about being in a caloric surplus, but one thing you should never forget is that genetics plays a big part in how much of your abs, i.e. the guide I would recommend to use to judge your "body fatness", you can keep visible during the off-season. Some can hold on to a full 6-pack, while others will only have a shade of their abs remaining visible during the off-season.

      Whatever your individual genetic make up may be, once you've been there, you can definitely maintain a lean beach body physique while making improvements to your physique, you just have to be really disciplined and patient. That this "beach ready look" will never be anywhere close to the more or less cut look you may have delivered at the end of your previous prep should be obvious, though. Just don't take this as an excuse to let yourself go completely.
      The following Monday after the weekend of my show, I went back to my old dieting numbers prior to my peak week, so when I jumped back on my diet I picked up where I left off at 60fat/240carbs/200protein – I stuck to that for about a week and a half or 10 days to be exact, then that’s when I went on my 25g increase per day. So I started at 240 carbs last Wednesday and made daily 25g increases until my next check-in with coach Alberto
        Don't forget to read Adelfo's previous post on "Intermittent Carbohydrate Modulation as  Stepping Stone Towards an Anatomy Chart Physique" (go back)
      • Wednesday – 240g
      • Thursday – 265g
      • Friday – 290g
      • Saturday – 315g
      • Sunday – 350g (refeed)
      • Monday – 340g
      • Tuesday – 365g
      • Wednesday (yesterday) – leveled it back to 275g-300g
      We basically did this to get me out of the ranges of what Alberto called “non-safe body fat stores or what you would call, not a good place to make great gains from” and to also put my body at a place hormonally.

      In short, if I want to make the gains and improvements I want to make this off-season it would be counterproductive for me if I tried to stay at the body fat percentages I was at. Eventually I have to let my body adjust and find a happy and healthy body composition that my body can agree with that would benefit me in making great gains.

      Week 3 of post-contest dieting pictures
      And NO, when I say happy body composition, I do not mean being a fat ass! Lol, but I am going to have to accept the fact that in order for me to grow, I have to be at a caloric surplus and when you’re at a caloric surplus, you’re going to have to sacrifice some leanness and embrace a little bit of body fat ;-) However it can be very controlled and you can keep fat gains minimal if you approach your off-season with a mentality of making improvements rather than bulking because in my opinion bulking is just a term for being a fat ass!

      I’m close to recovering hormonally and metabolically at this point during my post contest prep. I notice my energy and strength levels climbing back up and I’m starting to supplement with d-aspartic acid to help with the process. As you as a regular reader and someone who listened to my interview on SHR will know, I started actually supplementing with d-aspartic acid two weeks out from my show when I started to notice my energy levels take a dip.

      Honestly, I am curious what the next weeks and months are going to have in stock for me and I would hope that you will enjoy following my progress. On a side note, in view of the fact that I may not have groundbreaking news or progress photos for you in every week, why don't you pose a couple of questions you want me to address in the future episodes of this series? I am looking forward to your suggestions.

      Your's truly ;-)

      Adefo Cerame

      Four Weeks "On" Two Cans of Energy Drink = 6.6% Increase in Body Fat + Other "Adaptations" in Healthy Men & Women

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      Contrary to regular coffee, the majority of energy drinks ensures that you get your daily (over-)dose of diabesity promoting sugar - so, no need for additional white poison.
      If you are following the SuppVersity news closely, I am sure you will remember the note on the carcinogenic, or rather "breast cancer risk increasing" effect a single cup of soda per week can have (read more). As a follower of the SuppVersity Facebook news, you will also remember that these effects could potentially be brought about by the hormonal chaos that's brought about by these sugar sweetened beverages (learn more; Schliep. 2013).

      Now, these results, as well as the accumulating evidence that sugar sweetened beverages in general and high fructose corn-syrup laden sodas are among the, if not simply the #1 contributer to the rise of the obesity pandemic, certainly raise the question what exactly it is that happens to us, when we consume these delicious* yet deadly elixirs on a daily basis (*personally I lost my appetite for soda years ago... along with the fat covering my abs, by the way).

      4 weeks of sugar sweetened beverages and our bodies helpless effort to adapt

      You've already gotten a first peek at what happens, when we make these unsatiating calorie-bombs a staple of our diets in a previous Suppversity article from June 30, 2012, in which I exposed the truth behind the shockingly simple formula "2 Energy Drinks per day = +1kg of Body Fat in 4 Weeks" (read more).

      Nutritional composition of the SSB
      Aside from the effects on the body weight, the 2012 study by Sartor et al. did yet not allow much insights into the corresponding metabolic changes, the bodies of their volunteers underwent. It is exactly these changes, or "metabolic adaptation" as (sounds quite positive, doesn't it) as the researchers call them, Francesco Sartor and his colleagues were now trying to elucidate in a follow-up study.

      Would you be willing to gain one kg of pure fat for $150?

      To this ends, the researchers from the College of Health and Behavioural Sciences at the Bangor University in the United Kingdom and their colleagues from Italy and the US recruited another 11 subjects who had been cherry picked for their low sugar sweetened beverage (less than 500ml SSB per week) intake from a group of 213 candidates, all of whom wanted to qualify for the £100 upon completion of testing as compensation for their time.

      Yeah, I know, obviously Sator et al. were not really honest with these 5 men and 6 women. After all, the scientists knew in advance that they would also be compensated for the ill health effect the consumption of ~760 mL/day of Lucozade Sport would have on their metabolic health.
      "Before and after the intervention, body composition, respiratory exchange ratio (RER), insulin sensitivity, muscle metabolic gene and protein expression were assessed. Adaptive responses to hyperglycaemia (7 days, 15 mM) were tested in primary human myotubes." (Sartor. 2013)
      I guess few of you will be surprised by what they are just about to see in the selected data I plotted for you in figure 1. And if you are honest, what we are seeing here is - at least in parts - actually an adaptive response.
      Figure 1: Body composition, HOMA data, glucose / insulin levels, substrate oxidation, blood lipids and skeletal muscle mRNA expression relative to pre-"supplementation" levels (Sartor. 2013)
      I mean take another look at the changes the scientists observed in vivo (11 subjects, 4 weeks on SSB) and in vitro (human muscle cells incubated with 15 mM glucose for 7 days; model of hyperglycemia). Despite all their desperate efforts, including
      • the increase in fat mass (+1kg) that's meant to stash away the glucose that would otherwise start to form a gluey lining on the cell walls and 
      • the concomitant increase in the respiratory exchange ratio (RER), which does allow for a greater oxidation of glucose (obviously at the expense of fat), 
      the subjects, or rather their bodies, were not able to to ward off the statistically significant +0.3mmol/L increase in fasting blood glucose. Moreover, the changes in protein expression scientists observed in the muscle cells they had isolated from the quadriceps muscles of the participants, namely the increased activity of the glycolytic enzyme GAPDH and the corresponding decrease of PGC-1alpha in the musculature of the previously healthy subjects are yet less "logical" (=expedient).

      The Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) induced increase in glycolysis (see schematic drawing over @Wikipedia) does not suffice to reduce the amount of glucose that's floating around while it contributes to the decrease in fatty acid oxidation that is further promoted by a decline in PGC-1a activity and thus the ability to handle the increased triglyceride load by burning the glycerol + free fatty acid ethers in the mitochondrial power plants of the subject's skeletal muscle.

      MondaA, a "bad guy" to remember?

      Against that background, it i not really surprising that the scientists did also observe an unwanted but in a way still "adaptive" (=reactive) increase in insulin resistance - an effect of which the researchers believe that it was brought about or at least facilitated by increased amounts of the glucose sensing protein MondoA:
      This may be the right time to read up on the SuppVersity article about previous study by Sartor et al. "Fat Content Per Energy Drink 0g, Body Fat Gain Per Energy Drink 18g!" (go back)
      "Glucose sensing in skeletal muscle cells, as part of a mechanism for the maintenance of cellular energy homoeostasis, has been demonstrated to be strongly dependent on the transcription factor MondoA.

      MondoA seems to be a master regulator of glycolytic genes and indeed it activates the transcription of numerous genes encoding metabolic enzymes.. Glycolytic gene expression is highly upregulated in response to MondoA recruitment from cytoplasm to nuclei, building a complex with the transcription factor max-like protein x (Mlx), in high glucose conditions. A further target of the Mond-oA:Mlx complex is the thioredoxin-interacting protein (TXNIP). TXNIP impairs peripheral glucose uptake stimulating radical oxygen species production.
      In short, the increase in MondoA protein content is directly and mechanistically involved in the etiology of a metabolic vicious circle, which is at the heart of the downward spiral that leads from "just being a somewhat chubby sedentary slob" over the "overweight pre-diabetic" right into the emergency room, where the doctors need one of those XXL operating tables, when they are trying to save the lives of people with SSB consumptions of 3-4L per day.


      Bottom line: I suppose that many of you will now be thinking. So what, I knew all that already; after all, I just got to look around and see all those SSB victims driving around in their cars. Nevertheless the details you may have learned about the enzymatic roots of the metabolic dysregulation that occurs with the consumption of "only" 2 cans of a "soda-like" sports drink per day are not the main message of the study at hand.

      As of now, there is no published in vivo evidence for the beneficial effects glutamine may have on the MondoA-induced dysregulation of glucose homeostasis, but there is an interesting 2009 paper by scientists from University of Utah suggesting that the reduction in glucose uptake due to MondoA (over-)activation in the presence of high glucose levels may be ameliorated / abolished by glutamine (Kaadige. 2009) and a study that confirms the beneficial effects of glutamine on insulin sensitivity (read more).
      From a mere scientific perspective, the news is the shockingly short time span in the course of which perfectly healthy, lean and reasonably active individuals can develop all the characteristics scientists have hitherto thought of as a result chronic hyperglycemia. A particular focus of future studies should now be on the time-course of the change in MondoA expression, as well as means to prevent and reverse the deteriorations of this "metabolic glucose sniffer".

      Theoretically glutamine could be a potential candidate, as it has the ability to block the MondoA induced, glucose dependent activation of the thioredoxin-interacting proteinin and the subsequent blockade of glucose uptake. And while respective research on this mechanism is not yet available, those of you who have been around ever since the early beginnings of the SuppVersit, may remember the 2010 post on the "Positive Effect of L-Glutamine on Insulin Sensitivity" (read more) - who knows, maybe it is mediated by the blockade of the transcriptional activity of MondoA at the TXNIP promoter (see figure on the right)!?

      References:
      • Kaadige MR, Looper RE, Kamalanaadhan S, Ayer DE. Glutamine-dependent anapleurosis dictates glucose uptake and cell growth by regulating MondoA transcriptional activity. Proc Natl Acad Sci U S A. 2009 Sep 1;106(35):14878-83.
      • Schliep KC, Schisterman EF, Mumford SL, Pollack AZ, Perkins NJ, Ye A, Zhang CJ, Stanford JB, Porucznik CA, Hammoud AO, Wactawski-Wende J. Energy-containing beverages: reproductive hormones and ovarian function in the BioCycle Study. Am J Clin Nutr. 2013 Mar;97(3):621-30.
      • 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.

      Leucine & HMB - Similar, Yet Different. BCAA, B6 & NAFLD - It's About Ratios. Eccentrics, Mitochondria & GLUT-4 - No Pain, No Fat Gain. Fiber & Diabesity - Useful, But Not Magic.

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      "Potatoes" have the "pot-" from "potassium" not just in their name, they also got plenty of it in them. A medium sized potato (147g) contains 926mg of highly bioavailable potassium and covers ~26% of your daily requirements... and no, normal potatoes are not pro-diabetic unless you over-process them (learn more in the Potato Manifesto)
      5.93 mm and 3.7 millimeters those are the SuppVersity Figures of the Week and the average heights by which the systolic and diastolic blood pressure of dropped in 21 controlled trials in the course of which the subjects simply increased their daily potassium intake (Aburto. 2013). Results like these, which were published in the latest issue of the British Medical Journal rarely make it to the mainstream news and if they do than just as a marginal note to the paradigmatically blinded message that we all had to dramatically reduce our salt intakes if we did not want to end up in the emergency room.

      Now, aside from the fact that Maillott et al. have demonstrated only recently, that "the 2010 Dietary Guidelines for sodium were incompatible with potassium guidelines and with nutritionally adequate diets, even after reducing the sodium content of all US foods by 10%" (Mailott. 2013), both a dramatic reduction in salt and significant increase in potassium intake could be achieved if people simply stopped eating convenient, but blatant and thus salt- and sugar-laden products of the food industry and bought fresh products instead.

      Leucine and HMB both work, but they work via different pathways / mechanisms.

      If you want to learn more about the usefulness of HMB, check I suggest take (another) look at my article about the results of a 2012 dissertation (read more)! And in case you feel you need to learn more, browse the SuppVersity archive for the key-words leucine and HMB and educate yourself.
      (Wilkinson. 2013) A group of researchers from the UK and Canada has recently found that "leucine (Leu) possesses the most marked anabolic characteristics in acting as a trigger element for the initiation of protein synthesis". In that it is even superior to its best-known metabolite β-hydroxy-β-methylbutyrate (HMB), which has a 40% less pronounced stimulatory effect on protein synthesis (110% leucine; 70% HMB; after oral supplementation).

      The reason there may still be merit supplementing with (additional?) HMB is its non-insulin depended effects on skeletal muscle breakdown (-57%), which would up the rate of protein retention, i.e. the difference of protein synthesis (70%) and protein breakdown (-57%) to 127% and should thus result in superior net gains in skeletal muscle protein compared to pure leucine.

      Bottom line: Whether you actually "need" HMB, is a whole different question, though. After all studies comparing a simple 30g whey protein shake and an HMB supplement are missing and whether the addition of HMB to the whey would yield benefits is questionable. Doing just that with leucine has, after all, already been shown not to yield any additional benefits.

      Fatty liver from 50%+ of the currently available dietary supplements? 

      (Kaimoto. 2013) If we go by the results of a soon-to-be-published rodent study from Japan the chronic consumption of BCAA containing supplements could in fact result in an increased hepatic lipid and cholesterol deposition and would thus pave the way to non-alcoholic fatty liver disease (Kaimoto. 2013).
      Figure 1: Changes in body composition & organ weight, serum and liver measures after 21 days on BCAA (BCAA(+)) and/or pyridoxin (B6(+)) enriched diets (Kaimoto. 2013)
      If you take a look at the data in figure 1, you will yet also realize that the triglyceride and cholesterol deposition in the liver the scientists observed, when the rats were fed with a show that contained comparatively low supplemental amounts of 2%, 1.5% and 1.25% leucine, valineand isoleucineand thus the human equivalent of ~3-4g of BCAAs, was ameliorated when the diet contained sufficient amounts of vitamin B6 aka pyridoxin. Since the corresponding human equivalent dosages for B6 were ~3-4x higher than the RDA of 1.3mg/day but still way below the amount of B6 almost every currently available BCAA supplement contains, you probably don't have to worry about fatty liver or a shrinking thymus and compromised immune system.

      Tired, exhausted, had to cut your workout short today? Is it the flu, or just too much BCAAs?
      As a seasoned SuppVersity reader you will however be aware that the hailed anti.catabolic muscle builder is by no means free of nasty side effects, when consumed in excess - suggested reads:
      • High Dose BCAA Supplementation Can Inhibit Serotonin Metabolism & Cause Anxiety (read more)
      • Chronic High Dose BCAA Supplementation Reduces Endurance Performance by 43% Plus: How Ammonia, Glutamine, Arginine & Low Carbing Could be Involved (read more)
      If you want to know more about the established benefits of leucine, valine and isoleucine, I suggest you simply go through the archives and pick whatever yo are interested in.

      Bottom line: The latest BCAA news don't negate their established ergogenic effects, but they do support the notion that the "more is more" and "better take them with every meal" principles are not worth following - even if you get your BCAAs for free, by the way.

      More dietary fibre lovin' ... but rightly so?  

      (Dall'Alba. 2013) A recent study from the Universidade Federal do Rio Grande do Sul in Brazil confirms that the consumption of additional 10g of soluble dietary fiber (/-re) in the form of partially hydrolysed guar gum can have beneficial effects on some of the markers of metabolic syndrome.
      Figure 2: Relative changes compared to baseline in 44 patients with type 2 diabetes (males 38·6 %, mean age 62 years, diabetes duration 14.2y) after 4 and 6 weeks on diets w/ or w/out 10g of additional guar gum (Dall'Alba. 2013)
      The results of the study (figure 1) do yet also show that the benefits are modest at best. Even the statistically highly significant increase in HDL after 6 weeks on the guar gum diet is not necessarily physiologically relevant and if it was not for the higher baseline energy intake in the supplementation group, and the greater reduction in HbA1c (indicating a better blood glucose stability), you could even argue that the addition of the 10g/day of dietary fiber was totally useless (suggested read: previous articles about fiber).

      Bottom line: While dietary fiber has its merit. It's not much different from veggies. If you just add it / them on top of you junkfood diet, the effects you can expect are modest - if not non-existent.

      Eccentric exercise it's not all productive that induces damage

      More reasons for a GLUT-4 boosting EAA smoothie post workout (learn why)
      (Magalhães. 2013) According to a study that has been published ahead of print in the online version of the Journal of Applied of Physiology, eccentric exercise (downhill running) did not jst lead to highly significantly increases in plasma creatine kinase activity, myoglobin and interleukin-6 content of the muscle of 12-week old mice, it also impaired state 3 and respiratory control ratio of the mitochondria and increased their susceptibility to mitochondrial permeability transition pore (MPTP) which can lead to cell sqelling and eventually cell death. Accordingly, Mangalhães et al. observed an increase in cell swelling amplitude, lower time to maximal swelling velocity, and calcium release immediately after the end of exercise annd conclude that
      "prolonged EE [eccentric exercise] transiently impaired mice skeletal muscle mitochondrial function and increased susceptibility to calcium-induced MPTP opening"
      Now you can certainly argue that this is the necessary training effect your cells need in order to adapt, in view of previous findings from human studies (just randomly selected examples, here)...
      • Figure 3: Glycogen snythase  (in mmol/mg protein per min) 4h after postexercise (10 x 10 eccentric or concentric isokinetic leg extensions after previous glucose depleting cycling exercise) carbohydrate feeding depening on G6Pase levels (Doyle. 1993)
        -37% reduction in insulin-mediated glucose disposal rate in 6 healthy, but untrained men after 30min downhill running (Kirwan. 1992)
      • -11% reduced glucose uptake and glucose necessary to maintain euglycemia during maximal insulin stimulation, as well as -39% lower basal = non-insulin triggered GLUT-4 expression and in seven healthy subjects even 48h after one-legged eccentric exercise (Asp. 1996)
      • significantly reduced glycogen synthase after eccentric vs. concentric training in ten moderately trained subjects after 10 sets of 10 repetitions of either concentric or eccentric contractions in opposite legs and the ingestion of 0.4g carbohydrate/kg body wt every 15min (Doyle. 1993; see figure 3).
      ... you should yet reconsider to which extend the "no pain no gain" principle is going to yield the healthy lean mass and performance gains you are probably looking for.

      Bottom line: While the broscientific wisdom "You won't grow, if you're training like a puss'!" may have its limited merit, the equation "maximal damage = maximal growth" many of the bros derive from this supposition is not just unsustainable and counterproductive, but potentially unhealthy and fattening.... How's that? Just imagine bulking while you are constantly insulin resistant for daily eccentric exercise.



      Aside from the obligatory Facebook news that's it for today's installment of On Short Notice!  So once, you've checked out the following news over @ www.facebook.com/SuppVersity ...
        Aside from coffee and nutrition in general, vitamin A is another potential regulator of the peripheral  (non-light regulated) circadian clock - especially in the liver (learn more)
      • Some light exercise can shed some heavy fat -- Weight loss success of healthy, but sedentary women demonstrates: as long as you are not fixated on what the scale says you will be surprised by how powerful even moderate physical activity is (read more
      • Treating type I diabetes with GABA -- In a 2011 rodent study the administration of the amino acid and neurotransmitter helped repair damaged pancreatic beta cells (read more)
      • Undereating + (over-)training is the most effective endocrine disruptor -- At least among natural stressors, the aforementioned combination is far "superior" to regular stress (read more)
      • Don't forget about vitamin A -- Scientists identify the mechanism behind the anti-Alzheimer's effect of retinoic acid (read more).
      ...it's high time to get your behind off the couch or computer chair and enjoy a well-deserved active and social, yet regenerative weekend.

      References:
      • Aburto NJ, Hanson S, Gutierrez H, Hooper L, Elliott P, Cappuccio FP. Effect of increased potassium intake on cardiovascular risk factors and disease: Systematic review and meta-analyses. BMJ 2013;346:f1378.
      • Asp S, Daugaard JR, Kristiansen S, Kiens B, Richter EA. Eccentric exercise decreases maximal insulin action in humans: muscle and systemic effects. J Physiol. 1996 Aug 1;494 ( Pt 3):891-8.
      • Dall'Alba V, Silva FM, Antonio JP, Steemburgo T, Royer CP, Almeida JC, Gross JL, Azevedo MJ. Improvement of the metabolic syndrome profile by soluble fibre – guar gum – in patients with type 2 diabetes: a randomised clinical trial. British Journal of Nutrition. April 2013. [Epub ahead of print]
      • oyle JA, Sherman WM, Strauss RL. Effects of eccentric and concentric exercise on muscle glycogen replenishment. J Appl Physiol. 1993 Apr;74(4):1848-55.
      • Kaimoto T, Shibuya M, Nishikawa K, Maeda H. High Incidence of Lipid Deposition in the Liver of Rats Fed a Diet Supplemented with Branched-Chain Amino Acids under Vitamin B6 Deficiency. J Nutr Sci Vitaminol (Tokyo). 2013;59(1):73-8.
      • Kirwan JP, Hickner RC, Yarasheski KE, Kohrt WM, Wiethop BV, Holloszy JO. Eccentric exercise induces transient insulin resistance in healthy individuals. J Appl Physiol. 1992 Jun;72(6):2197-202.
      • Magalhães J, Fraga M, Lumini-Oliveira J, Gonçalves I, Costa M, Ferreira R, Oliveira PJ, Ascensãoa A. Eccentric exercise transiently affects mice skeletal muscle mitochondrial function. Applied Physiology, Nutrition, and Metabolism, 10.1139/apnm-2012-0226. 
      • Maillot M, Monsivais P, Drewnowski A. Food pattern modeling shows that the 2010 Dietary Guidelines for sodium and potassium cannot be met simultaneously. Nutr Res. 2013 Mar;33(3):188-94.
      • Wilkinson DJ, Hossain T, Hill DS, Phillips BE, Crossland H, Williams J, Loughna P, Churchward-Venne TA, Breen L, Phillips SM, Etheridge T, Rathmacher JA, Smith K, Szewczyk NJ, Atherton PJ. Effects of Leucine and its metabolite, β-hydroxy-β-methylbutyrate (HMB) on human skeletal muscle protein metabolism. J Physiol. 2013 Apr 3. 

      Cardio or Weights? What's The Best Tool For a Non-Obese Active Individual to Lose 20% of Abdominal Fat in 10 Weeks?

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      Slowly, painfully slowly the message transpires: Men and women are different, but the means by which they achieve the physique many of us desire are the virtually the same: Diet and exercise. Needless to say hat both lifting weight & doing "cardio" (LISS& HIIT) are obligatory for either sex. But is that true for fats and carbs, as well (learn more)?
      If you are not one of those people who simply  ignore the fact that SuppVersity articles have "telling" titles, you will already have realized that the subject selection is one of the greatest strengths of the 10-week experiment Jorge Perez-Gomes and his Spanish colleagues have conducted recently. While we are bombarded with information on how walking in the park strips tons of body fat off the bodies of morbidly obese "big losers", detailed information on what works for people like the 26 healthy young men (age 22.5 ± 1.9 yr) who participated in the study at hand is surprisingly scarce.

      "Dieting" does not necessary imply "eating less"

      The participants, whose body composition was measured by the means of dual-energy X-ray absorptiometry (DXA) were all healthy and physically active and with an average BMI ~22kg/m² and body fat levels of  ~17% at a level comparable to that of the average gymrat striving "to [eventually?] look good naked" ;-) According to the research design, all participants were required to keep their dietary habits unchanged during the 10-week study period.

      Since they were free to eat as much as they wanted, you can however safely assume, that the subjects in the endurance and strength training groups did increase their caloric intake in response to the energetic demands of their workouts (the subjects trained three times per week).
        Table 1: Detailed outline of the strength training protocol. The scientists had used the exact same protocol in a previous study in the course of which 18 male physical education students lost a whopping 7% BF in 6 weeks (Ara. 2006).
      • endurance training group (EG) - "The EG performed running and cycling sessions with a load intensities ranging between the ventilatory threshold 1 (VT1) and 2 (VT2), during 90 minutes per
        session. The VT were calculated from the cardiorespiratory tests that were performed at the same time of the day (16:00-19:00 h) under similar environmental conditions (20º C; relative humidity, 45-55%, 720 mmHg) on an electrically braked cycle-ergometer" (Perez-Gomez. 2013)
      • strength training group (ST) - "Briefly, RG trained with 5 different exercises (parallel squat, leg extension, inclined leg press, leg curl and hip flexors), for which 1RM was assessed before and after 10-week training. The ranged between 50-90% of 1RM values obtained were used for the training. A 90-s rest period was taken between exercise sets." (Perez-Gomez. 2013)
      With the nutritional aspect off the table, you may be asking yourselves: "Why on earth we are we seeing a lower-body-only-workout, here?" Obviously, I cannot ask the scientists directly, but I would guess that it is a combination of (a) the proven efficiacy of the workout, which has been used by the same group of researchers in a previous study, in the course of which the 18 male physical education students had lost a whopping an statistically highly significant 7% body fat (Ara. 2006), and (b) the fact that it would be unfair to compare a whole body strength workout to a "leg only" endurance workout on a cycle ergometer.
      Figure 1: Relative changes in body composition compared to baseline (Perez-Gomez. 2013)
      Still, the advantage of the endurance training as far as overall fat loss is concerned is not a simple result of not training the upper body. You can even argue that the overall energy expenditure on a classic body part split would have been even  lower. With the latter, as well as the degree of dietary compensation for the "used" energy in the time between the workouts being the main determinant of the amount of weight you'll lose it should thus  not surprise you that a 90min of pretty intense cardio had an edge over a classic resistance training regimen (slow paced, progressive; cf. table 1)

      Exercise doesn't just make you hungry

      Don't trust anyone who wants to tell you that "exercise will just make you hungry" or that calories didn't count at all - regardless of how prominent he/she may be (learn why)
      Now, you will probably remember that a fast paced, more versatile CrossFit-esque workout (learn more) would have been a better option for someone whose main goal is to shed that belly fat of his (or hers!), but could you honestly say that the 10 weeks of training on either protocol didn't server their purpose? I don't think so.

      Moreover, the differential effects the two "types" of exercise had on the body composition of the subjects, as well as the observed correlations between improved HDL levels and increases in lean muscle mass (EG) and trunk fat (ST), and lower LDL levels with waist circumference (EG) do actually confirm that there is something healthy about striving to be lean and muscular.



      Sometimes it also takes doing less, less of "dieting" and less of "training" to make progress again. I know it sounds like something only women who need a psychologist would fall for, but the Athlete's Triad (learn more) is neither a female thing, nor something only psychos would get trapped in. On the contrary! My personal experience tells me that it's often the smartest and most determined physical culturists who fall victim to their own burning ambition... much contrary to their often prominent role-models they don't have a team of shrinks and trainers to help them get back on track. So you better make sure not to sacrifice your friendships on your quest for perfection!
      Bottom line: You don't have to reinvent the wheel. The simple combination of endurance and resistance training that has worked for the fathers of physical culture still works, today. If you need some inspirations on how you can combine them into a training program that matches your individual needs, professional schedule & social life and will take your physique another step closer to where you want it to be, check out the SuppVersity "Step by Step Guide to Your Own Workout Routine" (learn more)...

      I guess, I don't have to tell you that 90min of LISS may be one way but certainly not the best way to improve on your physique - specifically if you are way past the "Homer Simpson" stage. You can learn more about training & dieting for your type and measuring your progress in one of the previous installments of the Intermittent Thoughts.

      Ah, and one last word of wisdom: Don't forget that looking and feeling great is not all about having a cover model physique.

      So, once you've got rid of the unhealthy blubber, it's often time to re-think whether taking the next and for the "non-genetic freaks" among us not necessary healthy step to being totally jacked is really what you want, or if the desire to look like X,Y or Z does not have much different roots.

      References:
      • Ara I, Perez-Gomez J, Vicente-Rodriguez G, Chavarren J, Dorado C, Calbet JA. Serum free testosterone, leptin and soluble leptin receptor changes in a 6-week strength-training programme. Br J Nutr. 2006 Dec;96(6):1053-9.
      • Perez-Gomez J, Vicente-Rodríguez G, Ara Royo I, Martínez-Redondo D, Puzo Foncillas J, Moreno LA, Díez-Sánchez C, Casajús YJA. Effect Of Endurance And Resistance Training On Regional Fat Mass And Lipid Profile. Nutr Hop. 2013;28(2):340-346.

      Antioxidants For Lazy Rodents: Alpha Lipoic Acid + CoQ10 + Vitamin E Work Mitochondrial Wonders On Untrained Female Mice... And ONLY On Untrained Female Mice!

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      ACE!? Are alpha lipoic acid, coQ10 and vitamin E good for them or not?
      With all the bad press on anti-oxidants, you could actually get the impression that performance and longevity should be a function of the amount of oxidative stress you're exposed to.

      Despite the fact that this hypothesis may have it's merit, the "True or False" item on the negative side effects of eccentric training should probably have reminded you that keeping a balance between the constant oxidative assault from our environment (in the broadest sense) on the one hand and our bodies' continuously evolving defense system is what we should actually be aiming for.

      Whether or not we will benefit from an increase in exogenous anti-oxidants like vitamins, will therefore always depend on both the stressor and the state and performance of our anti-oxidant defense system.A recent paper that has just been published in the peer-reviewed online journal PLOS-ONE does actually appear to confirm this notion of "stress management". In other words:

      Adaptation occurs, when you expose yourself to stressors which are taxing, but won't obliterate your defense system = the "i + 1" / hormesis principle


      We know from previous human studies that vitamin C and vitamin E (1g Vit C, 400IU Vit E; about as much as you will find in any of the useless "high performance multis") can blunt the hormetic effects of exercise-induced oxidative stress on insulin sensitivity and the concomitant adaptive response of the endogenous antioxidant defense system (Ristow. 2009).
      Figure 1: TBARS in the supplemented (no improve in insulin sensitivity) and non-supplemented trainees (Ristow. 2009)
      A quick note on how to interpret study results: Whenever you take a look at one of the "pro-antioxidant studies", you got to make sure the scientists don't base their assessment that the use of the respective molecule was beneficial on the observation of a reduction in exercise induced stress.

      If the (mito-)hormesis theory holds, the amelioration of the latter in the 2009 study by Ristow (see figure 1) is in fact to blame for the absence of increases in insulin sensitivity, adiponectin, etc.
      The results of the Ristow study have caused quite an upset within the scientific community and the world of physical culture. Especially within the latter the results of the researchers from the University of Jena were often misinterpreted as "all anti-oxidants are bad for you" and then prematurely dismissed on the basis of studies in which the researchers were able to observe mostly marginal and in terms of the explanations in the red info box above, highly questionable "beneficial" effects of anti-oxidant supplements.

      Not all "antioxidants" are created equal

      Suggested read: In a 2012 letter to the proponents of the mitohormesis hypothesis pick the results of a paper by Higishada et al. that's often cited in support of vitamin C + E supplementation to pieces and conclude "The vast majority of experimental evidence clearly advises against this supplementation. Thus, we unreservedly confirm the conclusions derived from our previous research and disagree with Higashida et al. In our opinion, antioxidant supplements are, at the least, useless" (Gomez-Cabrera. 2012). The letter should be accessible for all of you, so feel free to read up on the evidence they provide to support this conclusion... keep in mind, though no honest scientist will claim he would tell you the one and only truth. What they will give you is their assessment of the facts and the conclusion they believe should be drawn based on these facts.
      In fact, the actual number of exercise interventions in which scientists observed real-world benefits from vitamin C and vitamin E, in particular, is often overestimated. Therefore neither of these most prominent members of a very broad class of molecules that carries the label "antioxidant" can be considered a "proven ergogenic" and it is therefore not very surprising that Nikolaidis et al. conclude their 2012 review of the literature on the words:
      "Based on the contradictory evidence regarding the effects of higher intakes of vitamin C and/or E on exercise performance and redox homeostasis, a permanent intake of non-physiological dosages of vitamin C and/or E cannot be recommended to healthy, exercising individuals." (Nikolaidis. 2012)
      Now, despite the fact that the acronym may be the same (ACE usually stands for beta carotene, vitamin C and vitamin E), the "antioxidant" supplement in the study at hand has a different makeup. While it does contain vitamin E, it does not contain the additional "kamikaze vitamin" ascorbic acid, which cannot distinguish between "good" and "bad" ROS formation and will - much like a fire extinguisher - quench both "smoke signal" that's telling your boy "the mitochondrial engine is running at full speed, it may be time for an upgrade", as well as the not so beneficial "sparking" that occurs when the engines are overheating.

      Does the mix make the difference?

      CoQ10 on the other hand, is more or less specialized on protecting the mitochondria. It is not a "fire extinguisher", but rather a fire-proof coating that protects the mitochondria from "leaking" reactive oxygen specimen into the circulation. In conjunction with the cell-membrane protecting effects of vitamin E and the "vitamin recycler" alpha lipoic acid, we get a highly specialized antioxidant stack of which the results of the study at hand show that it is beneficial in those situations, where the baseline protection against an imposed stressor is insufficient.
      Figure 2: Differential effect of anti-oxidant supplementation on trained (8 wks treadmill running) (n = 12/group) and untrained (n = 24/group) male and female rodents' endurance performance; data presented in meters (Abadi. 2013)
      If you do now take a peak at the data in figure 2 you will realize that the latter was the case in the female rodents who were not exposed to the chronic exercise regimen. Correspondingly the provision of the ALA + CoQ10 + vitamin E stack did improve the exercise performance and mitochondrial respiratory chain protein capacity. The same data plot does yet also reveal that these effects were sex and training specific and generally absent in the trained rodents.
      Figure 3: Questionable (female) and non-existant (male) "benefits" of antioxidant supplementation on the relative expression of the mitochondrial builder PGC-1a, the satellite cell recruiting "stress" kinase p-38 MAPK and the well known glucose sensitizing AMPK (Abadi. 2013)
      One of the many things, Abadi et al. don't mention, though, is the fact that the "reduced the activation of the stress kinase p38-MAPK following acute exercise in untrained" (Abadi. 2013, cf. figure 3) could also decrease the "repair" and supercompensation process that will take place after the unaccustomed (remember the data in figure 3 is from untrained animals after the 2nd exercise test). After all, the "stress kinase" is at the same time "a molecularswitch for satellite cell activation" (Jones. 2005) and thus heavily involved in the recruitement of satellite cells.

      "Voilà it works.... ahm, ok only in one out of four groups, but it works!"

      Similarly, Arkan Abadi and his colleagues unfortunately forgot to mention is that they did not measure "THE" training-induced adaptations in the sense of "all training induced adaptations", but only a couple of mitrochondrial protein expressions. Against that background we cannot exclude that the insulin sensitizing effects of exercise Ristow et al. have been missing in their human subjects was not blunted in Abadi's C57Bl/J6 mice, as well.

      Remember the case is not yet settled: This is an analysis of a single study and the fact that this suggests that CoQ10, ALA and vitamin E are worthless for the majority of trainees does neither negate that the provision of only on of them, e.g. 200mg/day CoQ10 in athletes taking statins (Deichmann. 2012), or the provision of respective supplements during specifically stressful training periods can have ergogenic effects.
      The absence of more comprehensive data on the actual metabolic effects of the supplement regimen, as well as the unexplained confounding effects of gender and training status, specifically the non-significant, yet paradoxically opposed effects the scientist observed in the male rodents certainly warrant the question, why the abstract focuses almost exclusively on the already moderate benefits they observed in the untrained females. After all, the scientists declare that the
      "study was undertaken to investigate the effects of dietary supplementation with vitamin E, a-lipoic acid, and CoQ10 in combination on basal and training-induced mitochondrial adaptations in mice." (Abadi. 2013)
      In other words, their interest was in the effectiveness in mice in general and not in untrained female mice. Against that background, the most significant finding of the study would actually have been that there are confounding factors rendering the combination of these three mitochondrial antioxidants useless.



      Figure 4: Health and longevity as a function of mitochondrial reactive oxygen species (ROS) formation.
      Both too much and too little ROS are detrimental, due to either insufficient stimulus for or overtaxing of hormetic processes (this graph is a mere illustration and is not based on any existing experimental data and was first published in a previous SuppVersity article from May 2011)
      Bottom line: I bet you will soon see the results, or rather excerpts of the results of this study referenced on the bottles and shiny adverts of the supplement industry. "Most recent studies show that the combination of alpha lipoic acid, CoQ10 and vitamin E in RippYouOffSupplements (ROS) newest product increases ..." You know the whole spiel and are probably not fooled by pseudo-scientific nonsense like that anyway.

      Take a look at the data and use your gray matter: Are you rather an untrained female mouse? Or would you rather describe yourself as a devoted physical culturist?  If choose the 2nd option, you don't have to rack your brain any longer about the what ifs and maybes pertaining to potential reductions in the exercise induced increase in insulin sensitivity, because the "scientific evidence" ROS presents in favor of the efficacy of their newest "blockbuster product" is not relevant for you, anyway.

      Now that I am done ranting, I should maybe add that I sill like this study. Not just as an educative example of how easily scientifically valid data can be abused to provide proof for whatever you want, by simply skipping on parts of the results, but also because it adds sex as a new confounding factor you have to keep in mind, when you compare studies on the useful an uselessness of antioxidant supplements. And that's not just in an exercise, but also in any other scenario (e.g. longevity, metabolic syndrome, etc.) - after all, the gender-difference was present only in the non-exercised rodents.

      References:
      • Abadi A, Crane JD, Ogborn D, Hettinga B, Akhtar M, Stokl A, MacNeil L, Safdar A, Tarnopolsky, M. Supplementation with a-Lipoic Acid, CoQ10, and Vitamin E Augments Running Performance and Mitochondrial Function in Female Mice.
      • Deichmann RE, Lavie CJ, Dornelles AC. Impact of coenzyme Q-10 on parameters of cardiorespiratory fitness and muscle performance in older athletes taking statins. Phys Sportsmed. 2012 Nov;40(4):88-95.
      • Gomez-Cabrera MC, Ristow M, Viña J. Antioxidant supplements in exercise: worse than useless? Am J Physiol Endocrinol Metab. 2012 Feb 15;302(4):E476-7; author reply E478-9.
      • Higashida K, Kim SH, Higuchi M, Holloszy JO, Han DH. Normal adaptations to exercise despite protection against oxidative stress. Am J Physiol Endocrinol Metab. 2011 Nov;301(5):E779-84.
      • Jones NC, Tyner KJ, Nibarger L, Stanley HM, Cornelison DD, Fedorov YV, Olwin BB. The p38alpha/beta MAPK functions as a molecular switch to activate the quiescent satellite cell. J Cell Biol. 2005 Apr 11;169(1):105-16.
      • Nikolaidis MG, Kerksick CM, Lamprecht M, McAnulty SR. Does vitamin C and E supplementation impair the favorable adaptations of regular exercise? Oxid Med Cell Longev. 2012;2012:707941.
      • Ristow M, Zarse K, Oberbach A, Klöting N, Birringer M, Kiehntopf M, Stumvoll M, Kahn CR, Blüher M. Antioxidants prevent health-promoting effects of physical exercise in humans. Proc Natl Acad Sci U S A. 2009 May 26;106(21):8665-70.

      Meaty "News": Choline, Carnitine & "Bacteria Poop" Make (Red) Meat Unhealthy. Learn Why the Latest Revelations Are Neither New, Nor Meat-Specific And Still Made the News

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      Personally, I eat meat and will continue to do so, but the above is not meat. That's junk, for which there is evidence that it precipitates heart disease (Micha. 2012).
      Actually I did not really want to "blog" about the latest hypothesis on a mechanism by which red meat could give contribute to atherosclerosis and heart disease, but since it's all over the news I feel inclined to provide you with some information to (a) find the happy medium between the scaremongering media hype and the similarly misplaced assessment that "we have been made to eat meat, so it cannot be bad for us" and (b) understand how science news are made.

      I am not 100% sure which approach would be most appropriate, but I guess, it would be prudent to start the whole discussion by taking a peak at the actual paper, the publication, or rather the media coverage of which has sparked the whole turmoil.

      Why does everybody and his mama talk about the study?

      As a SuppVersity reader you probably belong to small number of people who actually care about scientific research. Being such a person myself, I know that people like us are hard-pressed to find anyone who will not answer questions like "have you heard about the latest results from the XYZ study" with a blank stare. So why on earth are there studies like the one Robert A Koeth et. al. just published (in fact the study is not even officially published, as of now it's only an e-paper!) that spread faster than the Hollywood-caliber flu scenarios that are supposed to "encourage" you to get vaccinated? Personally I feel like there are a couple of factors coming together here:
      • Familiarity & ostensible tangibility: The concept that red meat was bad for your heart is something everyone has heard about. You just have to add the words "bacteria poop" and even the average consumer of the Oz-show will feel like he/she knew all about the latest scientific evidence.
      • Personal concernment: Whether we do, or don't eat meat, news like these concern all of us. The meat-eaters will question, whether they may be hurting their health and/or get upset about the "vegan propaganda", while the vegetarians and vegans will celebrate how smart they are not to eat meat and point with a finger at the dumb omnivores, who will soon be suffering the consequences of their "unsustainable and cruel" dietary habits ;-)
      • The vegetarian / vegan lobby: Despite the fact that the "paleo movement" has gathered some momentum, vegetarianism and veganism still have a huge lobbying with sympathizers at many key positions of the society - esp. in the media business. With all "bad news about meat" being "good news for vegetarianism", it should be obvious that the "hurdle" a press release like the one Laura Ambro wrote for the Cleveland Clinic (read what all the "science mags" just copied and pasted here) does not have to pass a similarly high hurdle as the press release from the Michigan Diabetes Research and Training Center which does assert that lifting weights could help keep blood glucose levels under control (read it)
      • The Nature factor: Before I started reading scientific papers on a regular basis I would have been impressed by the words "a recent article published in the prestigious journal Nature", these days I ignore statements like that. Good science will prevail, whether it is published in Nature or in an open journal like PLOS-1.
      •  "Only bad news are good news" Let's be honest, we all know that bad news spread way more rapidly than good news. Imagine the study would have found that "no risk [increase of coronary arthery disease in type II diabetics] is seen with unprocessed meat consumption" (as a 2012 review of the evidence says; cf. Micha. 2012), who would have cared?
        "[...] the generally recognized tendency of the popular media to publish mostly negative aspects of news items is driven by the demand of their audience, rather than by inherent preferences of the media itself. To understand this, consider for a moment that there are two types of stories: positive stories or “good news” (and negative stories or “bad news”. Think of good news as stories about happy endings, in which people made the right choices. Bad news stories are about unhappy endings, in which people made the wrong choices. When consumers read good news stories, they can make similar choices to increase their incomes. When they read bad news stories, they can choose to avoid bad outcomes and the resulting income losses." (Swinnen. 2005)
        You see, according to science it's your own fault that you are fooled by the media... and let's be honest, it in fact is. If people did not click on the "bad news" first, those would generate lower page impressions and ad revenues and the media would have to revise their policy.
      Now these are five reasons that may explain why you've already heard about the study. There is yet at least another sixth reason that's missing from the list above - and that despite the fact that I already mentioned it in the introduction.
      • The more publicity a study receives the more idiots like me will deem it necessary to blog about it, so that after bazillions of shares on Facebook (I got three on my Facebook, alone) and a couple of thousand blogposts, all the world knows exactly what the study is about (why are you laughing?)
      In essence these would be 5 + 1 good reasons not to delve any deeper into the matter, but now that I am at it, I won't let you go without at least some additional rambling. 

      What's the main message of the article?

      Apropos evidence: I wonder how the "choline is the bad guy hypothesis" that's at the heart (all puns intended) of the new "red meat causes heart disease" hypothesis is compatible with statements like "the long-term consumption of [dietary choline and betaine] have been shown to prevent CVD mortality by decreasing inflammation and other risk factors." (Rajaie. 2011) And why are they going after red meat specifically, if soy and particularly Miso have been shown to have similar effects on TMAO concentrations and - in human beings, by the way (Solanky. 2005). Plus: Isn't it surprising that the exact same (or almost the same) results have been reported by Wang et al. for phosphatidylcholine (best dietary source = soy lecithin!) and without the words "red meat" in the title in 2011 already and nobody cared? Just sayin'...
      Choline and choline-like/-based substances such as l-carnitine and phosphatidylcholine that are found at comparably high concentrations in (red) meat, eggs and all the other usual subjects are converted to trimethylamine by certain bacteria in your gut and metabolized to trimethylamine-N-oxide (TMAO) in your liver.
      • Epidemiological evidence -- Concomitant elevations of serum l-increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events carnitine and TMAO levels.
      • Experimental evidence --Tthe chronic administration of l-carnitine to rodents increased the incidence atherosclerosis. A process that was probably mediated by the reduction of reverse cholesterol transport from the arteries to the liver the scientists observed, when they kept their rodents on a carnitine, choline or TMAO supplemented chow. The extent to which the TMAO load explains variations in the risk of heart disease in rodent studieshas been estimated by Bennett et al. in another recently published study to be 11% (Bennett. 2013)
      As mentioned before these are valid scientific findings that cannot be "discussed away" by stating that "we evolved to eat meat" or "that's just rodents, and I am no rodent!"

      Which bacteria are to blame?

      In view of the fact that scientists usually have a genuine interest in developing means to prevent (in this case) heart disease and not like the media and certain lobbyists to generate hype, acquire readers or rather advertisement consumers or reduce the consumption of meat, the most significant finding of the study at hand actually is that the use of a broad spectrum antibiotic does not only kill all bacteria, it also prevents the ill-health effects that come with the ingestion of large amounts of choline and l-carnitine (please mind my wording: "ill health effects of dietary choline and carnitine - not red meat).
      "Discovery of a link between l-carnitine ingestion, gut microbiota metabolism and CVD risk has broad health-related implications. Our studies reveal a new pathway potentially linking dietary red meat ingestion with atherosclerosis pathogenesis. The role of gut microbiota in this pathway suggests new potential therapeutic targets for preventing CVD." (Koeth. 2013)
      Against that background it is pretty intruiging that none of the articles I have read mentions that the scientists do already have preliminary evidence of who exactly those bad guys may be (only stat. sign. associations):
        sign. associations with high TMAO concentrations 
        • Tenericutes Mollicutes
        • Tenericutes Mollicutes Anaeroplasmatales
        • Tenericutes Mollicutes Anaeroplasmatales Anaeroplasmataceae
        sign. associations with high TMA concentrations  >
        • Bacteroidetes Bacteroidia Bacteroidales Prevotellaceae
        • Bacteroidetes Bacteroidia Bacteroidales Prevotellaceae Unclassified
        • Bacteroidetes Bacteroidia Bacteroidales Prevotellaceae Prevotella
        • Deferribacteres Deferribacteres
        • Deferribacteres Deferribacteres Deferribacterales
        • Deferribacteres Deferribacteres Deferribacterales Deferribacteraceae
      But things get even better there is more than a handful of potential "good guys" who appear to be associated with lower than average levels of TMAO in the blood on the scientists' radar, already. Fostering the growth or directly supplementing with each of the following bacterial strains could thus mitigate if not nullify the ill health effects of carnitine & co. These potentially protective bacteria are bacteriodetes and firmicutes certain strains of protobacteria (* denotes statistical signficance)
        If the connection of choline, meat & co and a certain enterotype is news to you, you can learn more about it in a previous post
      • Bacteroidetes Bacteroidia
        • Bacteroidia Bacteroidales
        • Bacteroidales Porphyromonadaceae*
      • Firmicutes Erysipelotrichi
        • Erysipelotrichales
        • Erysipelotrichales Erysipelotrichaceae
      • Proteobacteria Betaproteobacteria
        • Proteobacteria Deltaproteobacteria
        • Deltaproteobacteria Desulfovibrionales
      It is still preliminary to say, whether or not it would be a viable and more importantly practical strategy to constantly suppress the nutrient-dependent (see article referenced in the image above) rise in "bad bacteria" by using antibiotics or probiotics, but it would certainly be good to see the research zoning in on that instead of trying to find new explanations for epidemiologically non-sustainable claims such as "all red meat is bad for you".

      A final word on the potential involvemend of the liver, bile and dietary fiber?

      Another totally neglected yet potentially important factor, I personally feel would be worth investigating is the role of the liver. If you take a look at my slightly modified version of the proposed mechanism in Illustration 1 and remember my elaborations on the TMA => TMOA conversion in the liver, the brown metabolic "waste dump" certainly appears to be at an absolutely crucial position within the proposed etiology of TMAO-induced cardiovascular disease. 
      Illustration 1: Modified sketch of the potential mechanism behind the pro-artherogenic effects of dietary carnitine and choline (adapted from Koeth. 2013)
      I mean, what is the most common reason for heart disease? Meat consumption? No, if anything it is something that oftentimes correlates with the #1 reason, or I should say reasons for heart disease: the metabolic syndrome. You are very likely to give studies the abstracts of which include statements such as...
      "The bile acid receptors farnesoid X receptor (FXR) and TGR5 both regulate lipid, glucose, and energy metabolism, rendering them potential pharmacological targets for MS therapy." (Porez. 2012)
      "[Bile acid sequestrants] reduce atherosclerosis in Ldlr-deficient mice, coinciding with a switch from body cholesterol accumulation to cholesterol loss. RUN slightly modulated atherosclerotic lesion formation but the combination of BAS and RUN had no clear additive effects in this respect." (Maissner. 2013)
      ... a more thorough reading in the future. Especially in view of the fact that the -26% reduction in bile acids (Taurodeoxycholate, Tauroursodeoxycholate, Tauro-β-muricholate, Taurocholate) the scientists observed in the TMAO fed rodents suggest that the provision of bile acid sequestrants that promote the natural adaptation process and lower the intestinal cholesterol absorption even further could at least ameliorate the problem.

      Moreover, the natural ability of dietary fiber to bind bile acids leads us back to things of which we already know that they are beneficial for the heart. Things that target both the gut microbiome and the absorption / excretion of cholesterol via bile... oats, for example! A 2010 study by Andersson et al. for example, shows quite conclusively that the bran of the fiber, protein, carb and fat laden powerfood will increase the faecal excretion of cholesterol and bile acids, lower blood lipids and reduce atherosclerotic lesion areas in the descending aorta (-77%) and aortic root (-33%) of LDR(-/-) mice, i.e. mice who lack the ability to "recycle" cholesterol due to the absence of the respective receptors on the liver.



      You cannot handpick the several billion lodgers in your intestine, but you can attract the right ones by providing them with the foods they like. Contrary to the current probiotic hype, scientific evidence suggests the key to gut and metabolic health lies in the prebiotics you are stuffing down your piehole (learn more).
      Bottom line: The main reason for mentioning the involvement of the liver and the potential role of the FXR (=bile acid receptor) in the etiology of the problem in the end of this post which got much longer than I had intended it to be is to point you to the hilarious over-generalizations that are taking place when the results and implications of studies like these are passed from one person to another before they finally end up at the "Mr. Joe Average Level" in the form of either Meat Kills! or The Vegan Lobby is at it again!

      What's lost in all the hysteria is the fact that the study at hand could in fact provide insights into the often-touted involvement of the gut microbiome in the etiology of all sorts of diseases... this, and not the "red meat is fill in whatever you like for you" debate, is what could actually help us to reduce the number of CVD related deaths on both an the large nation- and world-wide, as well as on a personal level.

      Ah, and in the mean time, you probably don't have to be all too worried, as long as you eat a varied whole foods diet that's includes different sources of dietary fiber, vegetables and a rational amount of fruits, you can easily keep your gut microbiome in a state where real (=unprocessed meat) is not a problem.

      References:
      • Andersson KE, Svedberg KA, Lindholm MW, Oste R, Hellstrand P. Oats (Avena sativa) reduce atherogenesis in LDL-receptor-deficient mice. Atherosclerosis. 2010 Sep;212(1):93-9.
      • Bennett BJ, de Aguiar Vallim TQ, Wang Z, Shih DM, Meng Y, Gregory J, Allayee H, Lee R, Graham M, Crooke R, Edwards PA, Hazen SL, Lusis AJ. Trimethylamine-N-oxide, a metabolite associated with atherosclerosis, exhibits complex genetic and dietary regulation. Cell Metab. 2013 Jan 8;17(1):49-60.
      • Meissner M, Wolters H, de Boer RA, Havinga R, Boverhof R, Bloks VW, Kuipers F, Groen AK. Bile acid sequestration normalizes plasma cholesterol and reduces atherosclerosis in hypercholesterolemic mice. No additional effect of physical activity. Atherosclerosis. 2013 Feb 26.
      • Micha R, Michas G, Mozaffarian D. Unprocessed red and processed meats and risk of coronary artery disease and type 2 diabetes--an updated review of the evidence. Curr Atheroscler Rep. 2012 Dec;14(6):515-24.
      • Koeth RA, Wang Z, Levison BS, Buffa JA, Org E, Sheehy BT, Britt EB, Fu X, Wu Y, Li L, Smith JD, Didonato JA, Chen J, Li H, Wu GD, Lewis JD, Warrier M, Brown JM, Krauss RM, Tang WH, Bushman FD, Lusis AJ, Hazen SL. Intestinal microbiota metabolism of l-carnitine, a nutrient in red meat, promotes atherosclerosis. Nat Med. 2013 Apr 7.
      • Porez G, Prawitt J, Gross B, Staels B. Bile acid receptors as targets for the treatment of dyslipidemia and cardiovascular disease. J Lipid Res. 2012 Sep;53(9):1723-37.
      • Rajaie S, Esmaillzadeh A. Dietary choline and betaine intakes and risk of cardiovascular diseases: review of epidemiological evidence. ARYA Atheroscler. 2011 Summer;7(2):78-86.
      • Solanky KS, Bailey NJ, Beckwith-Hall BM, Bingham S, Davis A, Holmes E, Nicholson JK, Cassidy A. Biofluid 1H NMR-based metabonomic techniques in nutrition research - metabolic effects of dietary isoflavones in humans. J Nutr Biochem. 2005 Apr;16(4):236-44.
      • Swinnen, J. F. M., McCluskey, J. and Francken, N. Food safety, the media, and the information market. Agricultural Economics. 2005; 32: 175–188.

      True or False: Vinegar Reduces Postprandial Glycemia And Insulin Response. Vitamin D Must Be Taken With Fat or It Won't Work. Chewing Gum Will Help You Get & Stay Lean

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      This is quite an extraordinary Wednesday! To make sure that you don't have to go without your beloved Science Round Up, Carl and I are doing the show one day early, which means that you better make sure to make some room for listening to the show at 1PM EST (listen live!), if you want to be the first to learn the truth about the
        Is it possible that your significant other outpaces you on all cardio activities, because she has the hormonal edge?
      • effects of soy protein supplementation on the endocrine effects of exercise
      • psychological effects of performance enhancing drugs & supplements
      • interaction between dietary salt & your bodies ability to store magnesium
      • vitamin D "dosage equivalent" of two tanning bed sessions per week
      • estrogen's fat burning prowess
      • better (?) alternatives to testosterone gel
      ... and all the other great topics, you will be able to listen to after you've witnessed Alex aka Primalkid's premier (what an alliteration) as SuppVersity guest author. I suppose that most of you will already have noticed that he helps me more than just "a lot" by answering questions in the comment section. Oftentimes these are pretty individual things, but sometimes they are downright "True or False"-compatible - just as the mini-article on Vinegar, Alex sent me a couple of days ago.

      Vinegar Helps Reduce Postprandial Glycemia and Insulin Spike

      True (minimally edited answer written by Alex aka Primalkid) Recently, apple cider vinegar has earned merit as a health tonic. No longer sold solely as a condiment in grocery stores, more and more people see apple cider vinegar as a remedy. Its wide availability and affordability make it appealing to those who have browsed the Internet, read various diet books, or even read the label on the bottle, all of which make fame of its weight loss ability. But is there any truth about those "rumors" or do they belong to the same class of "repeat it until everyone believes it must be true" gems of dietary wisdom like the notion that "fat will reduce the insulin spike from a carby meal" (learn more about this one in the previous of "True or False")

      The discussion following last week's installment of "True or False", particularly about the way generations of dieters have been fooled to believe that it was a good idea to drown your carbs in fat in order to minimize the insulin spike was probably the incentive for Alex to author his first (and maybe not last) SuppVersity article... well, a part of an article ;-)
      A 2006 review of all relevant epidemiologic studies and clinical trials found that "many recent scientific investigations have documented that vinegar ingestion reduces the glucose response to a carbohydrate load in healthy adults and in individuals with diabetes" (Alex' emphasis in Johnston. 2006). The review also concluded that "vinegar ingestion increases short-term satiety."

      A fairly recent randomized controlled trial seeking to investigate if a combination of cinnamon and vinegar would have an additive blood glucose-lowering or satiety-enhancing effect compared to the substances in isolation, however, "did not see an effect of acetic acid on blood glucose" (Mettler. 2009). The study consisted of 27 non-smokers 20 to 30 years old with normal BMI and fasting blood glucose. In other words, they may be considered healthy adults. The control meal consisted of 194g vanilla milk rice and 33g glucose dissolved in water, providing a total of 75g carbohydrates, 5g fats, and 7g protein, and was consumed after an overnight fast of at least ten hours.

      The researchers concluded that "the most apparent difference between the studies was the food matrix with which the acetic acid or vinegar was ingested," and admit ignorance as to why the vinegar might work more or less in different contexts.
      Table 1: Tabular overview of the design of the four trials in the 2010 study by Johnston et al.
      Fortunately, the answer comes three months later when a group of researchers at The College of Nursing and Health Innovation sought to investigate the dosage, timing and application of vinegar for reducing postprandial glycemia (PPG) (Johnston. 2010). This study recruited both healthy and type-2 diabetic individuals, and had them consume either a meal (white bagel, 20g butter, 200g juice) or a glucose drink after a ten to 12 hour fast in four different trials.
      • Trial one examined whether small amounts (2 – 20g) of vinegar had any glycemic effects.
      • Trial two sought whether this effect persisted for five hours after consumption of the vinegar.
      • Trial three looked at whether the type of carbohydrate influenced vinegar’s antiglycemic effect.
      • Trial four looked at whether the neutralized salt of acetic acid was effective in diabetics.  
      One detail I want to bring to your attention pertains trial 3 and could in fact explain why other studies failed to observe an antiglycemic effect of vinegar: In Mettler’s study, the control meal consisted of milk rice and a dextrose solution, both of which can safely be classified as "simple" sugars.

      So, Johnston’s research suggests that the antiglycemic effect of vinegar is best realized when ingested with foods composed of complex carbohydrates and that vinegar may not attenuate PPG following the consumption of foods sweetened with corn syrups or dextrose, as is the case for many processed beverages and foods.


      Bottom line: Aside from the fact that the last mentioned limitation implies that taking your vinegar with junk food is pointless, it appears that apple cider vinegar may in fact earn a place among the list of truly "functional" foods. And while the real-world benefits may be more pronounced for people who do already have slightly suboptimal (or worse ;-) insulin sensitivity, a small amounts of vinegar (2tsp - doesn't really matter which type) taken with a whole foods based meal may be considered one out of many proven dietary manipulations for reducing PPG. 

      No Fat No Vitamin D - Fat's Necessary to Benefit from High Dose Vitamin D

      Probably false. I know that you will now be citing an older post of mine discussing a study that showed quite conclusively that the usage of supplemental vitamin D is hampered, if it is not ingested with a significant amount of dietary fat (see "A Fat D-Ficiency").

      Now, a soon-to-be-published paper by a group of scientists from the Human Nutrition Research Center on Aging at Tufts University and the Division of Endocrinology, Diabetes, and Metabolism at the Tufts Medical Center put a huge question mark after the results of the 2011 study by Raimundo et al. who had used an almost identical protocol in 20 likewise healthy subjects.
      Figure 1: Changes in serum vitamin D3 and storage form of D3 (25OHD, small grey-scale graph) in response to 50,000 IU of vitamin D with / without a meal with high or low fat content (Dawson-Hughes. 2013)
      As you can see in figure 1, the low fat meal did yield an even more rapid incline in plasma vitamin D3 levels, after the 90-day follow-up period the net "gain" in terms of serum 25OHD was yet identical in all three groups and brought the sixty-two 50-69 yrs subjects who were enrolled in this 3-month study well into the >70 nmol/L range for 25OHD - and that irrespective of whether they had ingested their D3 tablet** on empty or with an egg or egg white frittata with low or high amounts of olive oil and vegetables, turkey bacon, and Parmesan cheese topping, a slice of toast with either jelly (low-fat meal group) or butter, and a mango milk smoothie (mango, milk, ginger ale) with or without cream.
      Foods & the Sun are the natural vitamin D sources, listen to today's Science Round Up to learn more about the latter.
      ** Note: I mentioned this before on the Science Round-Up: You better don't put too much faith into what the label of your D3 supplement says. Even with the supplement used in the study (50,000 IU vitamin D3 tablets that were purchased from BioTech Pharmacal) there was a >10% difference between what the label said the tabs would contain (obviously 50,000IU) and the measured amount of 57,000 IU of vitamin D3 the tabs actually contained. In the aforementioned study by Garg et al,. one of the tested vitamin D3 tabs contained more than twice of the labeled amount (Garg. 2013).
      Just like Dawson-Hughes and colleagues, I can only speculate about the underlying reasons for the differences between the study at hand and the Raymundo study. The scientists' hypothesis that the unexpectedly high and early increase in the high fat (25.6g) group of the study by Raimundo et al. could be attributable to "inadvertent sun exposure or supplemental vitamin D ingestion in the second half of that study", would yet be a plausible explanation. Another one could be the use of cabs instead of tabs, as they were used in the study at hand. After all, the content of the 50,000IU vitamin D cap Raimundo et al. have used is like to be released much more rapidly so that the fat may have been necessary to slow the gastric emptying and thus facilitate absorption.



      Bottom line: For you it does not really matter if you can ingest your vitamin D without fat. It's not the "better" alternative, so why would you bother anyway? So have it with a fatty meal, but don't forget that testing is not optional, but obligatory - I mean you do not even know how much vitamin D your Vitamin D product actually provides.

      Chewing gum Helps to Get & Stay Lean (Note: This is just about regular chewing gum!)

      True.  I know it may sound hilarious, but in view of the fact that research has shown "gum chewing is sufficiently exothermic that if a person chewed gum during waking hours and changed no other components of energy balance, a yearly loss of more than 5 kg of body fat might be anticipated." You can certainly argue that chewing of calorie-free gum, of which James Levin points out that it "can be readily carried out throughout the day", the "potential effect on energy balance should not be discounted" (Levin. 1999).
      Mint chewing gums are incompatible to the "6x Bananas a Day!?" approach to lowering your glucose, insulin and HbA1c levels (learn more)
      Chewing mint gums will reduce fruit consumption (Swobody. 2013) -- Why? Give it a try, I bet you will not recognize the delicious pineapple when you try to eat it right after you've been through a packet of Orbit Mint ;-) This may sound like it was not important, but it could in fact diminish or even blunt the effects of chewing gum... I mean think of Mr. Average Obese American at a barbecue. If he had not been chewing mint-flavored gum all the time, he may well have had his share of filling, refreshing & libido enhancing water melon before the barbecue was even ready to be served. Now that he missed on that, he will stick to the meat (+) and tons of salty junk (-). Not a good bargain, right?
      Now, all of you know that I am no fan of the "calories in vs. calories out"-hypothesis Levin is referring to, here, but in view of the fact that chewing (sugar free!) gum has also been shown to
      • 8% reduced food intake on a "snack break" and generally reduced cravings and perceived likelihood of snacking on sweet foods in 40 women and 20 men (21.7+/-4 years; BMI=22.7+/-3.4) who participated in a 2007 study at the Glasgow Caledonian University) who came to the laboratory four times for lunch and then returned 3 h later for a snack after either chewing gum or not chewing gum for 15 minutes before the snack break (Hetherington. 2007). 
      • chewing gum will reduce the size of snacks even in moderately restraint eaters, although the effect is not as pronounced as it is in people who are not thinking about what and how much they are eating all day (Hetherington. 2011)
      So, in general, it is probably advantageous to chew gum. The probability that it will result in significant weight loss is however small. A 2012 one of those pathetic randomized controlled trials, in the course of which the researchers provide their subjects with dietary advice and expect something to happen, the 102 of the 201 overweight and obese adults who were furthermore required to chew gum for at least 90min/day did not lose significantly more body weight or inches off their waist. Contrary to their non chewing gum chewing peers in the control group there was a greater heterogeneity so that only the difference to baseline reached statistical significance only in the chewing gum group.

      If there is anything bad to say about chewing gums it would probably pertain to the (imho) not fully elucidated side effects xylitolm a proven "antimicrobial" (Mäkeläinen. 2007), could theoretically have on the gut microbiome, but since we do not know if that would be a detrimental and not even a beneficial effect (initial evidence exists, cf. Salminen. 1985), I just want to mention it as an "would be interesting to see more research in this direction". Possible artificial sweetener related distortions of the hedonic response to sweet foods, on the other hand, are not very likely... well, as long as you stick to the spearmint and peppermint varieties and refrain from those disgustingly sweet fruit gums.



      There may be more advantages of chewing gum. People with GERD / reflux disease, for example have been shown to benefit from chewing gum for 1 h after the meal. The effect lasted for up to 3 h and occured in both patients with and without chronic reflux disease (Avidan. 2001). Chewing gum has also been shown to reduce the symptoms of depression (Erbay. 2013), alleviate acute psychological stress (Scholey. 2009), and increase alertness on "intellectual" performance during regular intelligence tests (Smith. 2009; similar effects in previous studies with sugar- and artificially sweetened gums, cf. Stephens. 2004)
      Bottom line: The Shikany study is actually a perfect example of what chewing gum can do for the average dieter. Although it overall effects on caloric expenditure are non-significant the act of chewing and what my friend Carl Lanore once aptly called "cleaning one's pallet" with a sugar-free peppermint gum can help you (a) not to return to the buffet, once you've decided that you've had enough and started chewing gum and (b) not grab another snack between your main meals.

      Against that background, the statement "chewing gum can help you lose weight" is actually correct. What is yet a hilariously unrealistic expectation is that you would - just like Levin mentioned it in the initially cited letter to the editor - be able to lose X pounds of pure body fat per year, because chewing gum increased the caloric expenditure of the subjects in the Levine study by 12kcal per hour.

      That's what people in Germany call a "Milchmädchenrechnung" or as you would call it, my dear American friends, "naive fallacy" - a type of naive fallacy which is unfortunately still pretty common especially among people who make not one, but two major mistakes and don't read the SuppVersity and listen to Super Human Radio ;-)



      That's it for the written part (don't miss the Science Round Up at 1PM EST, though!), I hope you enjoyed this installment of True or False and though I will be hard pressed to answer all the questions, just keep the suggestions coming. I will take the weekend to compile a detailed list to make sure I don't overlook any of them, when I tackle at least one of your suggestions in the future installments of this series.

      References:
      • Avidan B, Sonnenberg A, Schnell TG, Sontag SJ. Walking and chewing reduce postprandial acid reflux. Aliment Pharmacol Ther. 2001 Feb;15(2):151-5.
      • Dawson-Hughes B, Harris SS, Palermo NJ, Ceglia L, Rasmussen H. Meal conditions affect the absorption of supplemental vitamin D(3) but not the plasma 25-hydroxyvitamin D response to supplementation. J Bone Miner Res. 2013 Feb 20.
      • Erbay FM, Aydın N, Satı-Kırkan T. Chewing gum may be an effective complementary therapy in patients with mild to moderate depression. Appetite. 2013 Jun;65:31-4.
      • Garg S, Sabri D, Kanji J, Rakkar PS, Lee Y, Naidoo N, Svirskis D. Evaluation of vitamin D medicines and dietary supplements and the physicochemical analysis of selected formulations. J Nutr Health Aging. 2013 Feb;17(2):158-61.
      • Hetherington MM, Boyland E. Short-term effects of chewing gum on snack intake and appetite. Appetite. 2007 May;48(3):397-401.
      • Hetherington MM, Regan MF. Effects of chewing gum on short-term appetite regulation in moderately restrained eaters. Appetite. 2011 Oct;57(2):475-82.
      • Johnston CS, Steplewska I, Long CA, Harris LN, Ryals RH. Examination of the antiglycemic properties of vinegar in healthy adults. Ann Nutr Metab. 2010;56(1):74-9. 
      • Johnston CS, Gaas CA. Vinegar: medicinal uses and antiglycemic effect. MedGenMed. 2006 May 30;8(2):61.
      • Levine J, Baukol P, Pavlidis I. The energy expended in chewing gum. N Engl J Med. 1999 Dec 30;341(27):2100.
      • Mäkeläinen HS, Mäkivuokko HA, Salminen SJ, Rautonen NE, Ouwehand AC. The effects of polydextrose and xylitol on microbial community and activity in a 4-stage colon simulator. J Food Sci. 2007 Jun;72(5):M153-9. 
      • Mettler S, Schwarz I, Colombani PC. Additive postprandial blood glucose-attenuating and satiety-enhancing effect of cinnamon and acetic acid. Nutr Res. 2009 Oct;29(10):723-7. 
      • Salminen S, Salminen E, Koivistoinen P, Bridges J, Marks V. Gut microflora interactions with xylitol in the mouse, rat and man. Food Chem Toxicol. 1985 Nov;23(11):985-90.
      • Scholey A, Haskell C, Robertson B, Kennedy D, Milne A, Wetherell M. Chewing gum alleviates negative mood and reduces cortisol during acute laboratory psychological stress. Physiol Behav. 2009 Jun 22;97(3-4):304-12. 
      • Smith A. Effects of chewing gum on mood, learning, memory and performance of an intelligence test. Nutr Neurosci. 2009 Apr;12(2):81-8.
      • Shikany JM, Thomas AS, McCubrey RO, Beasley TM, Allison DB. Randomized controlled trial of chewing gum for weight loss. Obesity (Silver Spring). 2012 Mar;20(3):547-52.
      • Stephens R, Tunney RJ. How does chewing gum affect cognitive function? Reply to Scholey (2004). Appetite. 2004 Oct;43(2):217-8; discussion 221-3.
      • Swoboda C, Temple JL. Acute and chronic effects of gum chewing on food reinforcement and energy intake. Eat Behav. 2013 Apr;14(2):149-56.

      Science Round Up Seconds: 2x10-15Min Of Tanning Per Week Equal 2,000IU Vitamin D3/Day. Low GI Diet Adds 9.4 Years to Your Life. Estrogen + Progestin = Bad Choice For ERT. 3g Salt/Day = 33% Lower Magnesium Retention

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      It has not always been this way, but these days our beauty ideal has at least one potentially healthy feat: The tan!
      I don't know if you have been able to listen live to yesterday's in many ways "extraordinary" episode of the SuppVersity Science Round Up on Super Human Radio(click here to download the podcast), but if you were, you may have made the same observation I did: Whenever you feel that you got more than enough time to get a task done or, in this case, a list of topics discussed, you start loiter, to go on tangents and to end up in interesting, yet in the end "off-topic" discussions about all and sundry or "Gott und die Welt" as people in Germany woul say (literally translated: "God and the world").

      Personally, I enjoyed the less packed format of yesterday's show, though. What about you? Shall we aim to discuss less news items in the future and thus have time to discuss those we picked in more detail or do you prefer the classic "short" over the long version?
      This show is for you, so tell us what you want! We could also have a "motto show" once a months - something like "what's the news about fat burners" or "low carb dieting, what does the latest science say", ... I am doing this show for two reasons. Reason #1: I want to spread the word about the latest scientific studies and #2 I want you and other people to enjoy the show.

      Now, it should be obvious that #1 and #2 are not independent from each other. In other words, I will reach more people if you like the show and I don't have to force you to listen to my painful accent ;-) So ... "where do you want to go", not today, but maybe next Thursday?
      I guess these were more than enough questions for a single installment of the Seconds now and you are starving for the news items that did not make it into yesterday's show. Well, let's see what we've got here, then:

      Tan Yourself into the >75nmol Range For Vitamin D 

      Actually it is obvious that it should be possible to use a tanning bed (in the study at hand a type 3 sunbed w/ 2,15% UVB: 280-320nm; note: as Tim informed me in the comment area most sunbeds in the EU have max. 1% UVB, so you better make sure what type you are using) to boost and keep your vitamin D levels in the >75nmol range, of which current research suggests that this is where the magic happens (click here learn more also about Vitamin D and my own skepticism towards the "vitamin D solves all your problems" hype).

      Figure 1: Graphical outline of the cross over design (Lagunova. 2013)
      The same thought obviously occurred to a group of scientists from Norway, where the latitude, respectively the incidence angle of radiation and the scattering of short wave radiation in the atmosphere allows for effective vitamin D synthesis only in the summer months from April to October. To find out how long you'd have to stay on the "Asitoaster" (an only in some cases inappropriate derogative German term for the "sunbed", which denotes that only the less educated lower class uses the regularly) the scientists recruited 31 healthy Oslo (59°N) residents. The men and women were 23-61 and only one of them had already 25OHD levels in the >75nmol/L range.

      As the graphical outline (see figure 1) of the study protocol goes to show you, the 8 men and 23 women were assigned to two different groups. Both groups underwent both the tanning bed, as well as the vitamin D3 supplement intervention (cross over design) with the only difference being that one group started out taking 2,000IU vitamin D (Carlson's brand), while group II jumped right onto the tanning bed, ...

      ...well, actually no one "jumped right onto the tanning bed"

      For both groups the tanning bed intervention had a similar built-in progression as you would expect it from any beginner workout: Starting with a weekly exposure of 2 x 1-1.3 SED (7 min; this is what even the most fairly skinned individuals can do), the subject slowly accustomed their body to the radiation by extending their stay on the tanning bed to 1.9 SED (10 min) in weeks 2 + 3 over 2.4 SED (13 min; warning: according to Fitzpatrick et al. "light tanned" people with a greater risk of developing skin cancer can get a sunburn from this dose already; Fitzpatrick. 1995) in weeks 4 + 5 to a maximal exposure of 2.8 SED (15 min) in weeks 6-10.
      Figure 2: Serum vitamin D (25OHD) levels during the supplementation / tanning bed phase in the two arms of the study (Lagunova. 2013)
      As the data in figure 2 goes to show you, both protocols were equally effective in building and + or maintaining vitamin D levels in the >75nmol/L range.

      In case you missed yesterday's "True or False" click here to learn whether or not you have to take your D3 supps with fatty foods.
      For "the average" study participant that was a >40% increase over baseline, for the 9 volunteers who began with baseline vitamin D levels below the 50nmol/L margin, the increase was correspondingly higher.

      The scientists do therefore have good reason to head the manuscript of their soon-to-be-published study with the following statement about what the study adds to our knowledge about the relative efficiency of supplemental and natural vitamin D sources, with respect to efficiency to increase serum 25-hydroxyvitamin:
      "Two weekly whole body UV exposures to a total dose of 4.8 SED for 5 weeks to a total dose of  23.8 SED are equal to 2000 IU/d of oral vitamin D supplementation for 30 days and enough to achieve and maintain serum 25(OH)D concentrations above 75 nmol/L in ~ 55% of the cases." (Lagunova. 2013).
      In the end, it does therefore not appear to matter, whether you take the natural or supplemental approach to keep your vitamin D levels in the upper tertile of the (revised) normal range - personally I would yet prefer the ultra-natural route (at least for the summer months).

      Bottom line: There is little to add to the title of another recently published study "Make Vitamin D While the Sun Shines, Take Supplements When It Doesn't". Although,... when I come to thing about it, I guess there still is one thing to add: Don't be too cheap to test where you're at!

      Additional news and follow ups

      • Can you add 9.4 years to your live by following a low GI diet? Maybe... at least if the recent data from a rodent study that was conducted at the School of Medicine of the Deakin University in Geelong (Australia) would translate to human beings (Nankervis. 2013). Especially in those of us (or the others) who still live on the garbage that's called food, when it's part of the standard American diet, I am yet pretty confident that it would.

        Over the course of their 24-months experiment the scientists had provided their mice with either the normal rodent chow or (GI 70) or a low GI alternative (GI 27), did a whole series and tests and waited for the animals to pass away.
        Figure 3: Relative telomere length of the mice and diet composition (Nankervis. 2013)
        Much to my personal surprise this one set-screw (=low GI diet) was potent enough to extend the average lifespan by 12%.

        I doubt it's a coincidence that the purported telomerase activator Astragalus is also a potent anti-diabetic and anti-inflamatory - in the end glycemia and inflammation are the determinants of longevity, telomerase length only an indicator (learn more)
        If we take into consideration that the life-expectancy of the average American is 78.7 years (CDC. 2013), this would mean that he / she would live almost 10 years longer if he simply stayed away from all the processed junk to reduce the average GI of his / her diet to the sub 30pts region.

        And while it is probably not even necessary to say that this increased life-expectancy went hand in hand with improved glucose tolerance up into the old age and an "impressive [...] amelioration of oxidative damage to DNA in white blood cells." (Nankervis. 2013), it is imho important to point out that this longevity bonus came in the absence of improved telomere lengths in quadriceps muscle and/or the reactivation of telomerase.

        Bottom line: Contrary to overpriced and from a science perspective highly questionable "telomerase promoters"  a simple reduction of the sugary onslaught on your metabolism will not just improve some exotic markers of which we still don't know exactly how they figure in the aging process, but actually extend the life of a relatively complex species. How beneficial a similar dietary protocol would be in humans
      • Pre- or post-menopausal, Drinking coffee, tea or cacao could protect you from breast cancer (learn more)
        Estrogen therapy for women -- Everyone who's following the SuppVersity Facebook news closely, will probably remember my recent post on the latest scientific spin-off from the Women's Health Initiative (WHI) dataset which suggests that the combination treatment of estrogen + artificial progesterone (=progestin) was associated with a 55%+ higher risk of breast cancer. Even more when the drug treatment was initiated in the early phase of menopause (Chlebowski. 2013). Against that background.

        And as if that was not enough, the same wicked drug cocktail (equine estrogen + progestin) has also been shown to increase the risk of dementia, although you would expect that ERT (estrogen replacement therapy) should do the opposite (Shumaker. 2003).

        Way before the publication of the troublesome data from the large scale WHI study, the perspective on HRT for women has been changing, with the current concept suggesting that estrogen plus progestin useincreases breast cancer risk and the effect on risk may be greater in women who initiate therapy closer to menopause, broadly increases breast cancer risk with the increase in risk not limited to hormone receptor–positive cancer, interferes with breast cancer mammographic detection resulting in cancers diagnosed at more advanced stage and increases breast cancer mortality. Estrogen only use on the other hand is currently understood to reduce breast cancer risk and does not interfere with breast cancer detection by mammography (cf. Chlebowsky. 2012).

        Bottom line:If you consider hormone therapy ladies, don't let your Dr. tell you that the "new" (when he went to medical school) estrogen + progestin drugs were the way to go.
      • Figure 4: Relative magnesium absorption and retention in black and white girls (11–15 y old) after 3 weeks on a high sodium diet (3.8 g/d); neither calcium intake nor vitamin D levels influenced the detrimental effects of the high sodium diet (Palacios. 2013)
        Too much NaCl or too little Mg is that the question? It actually could be the question, after all a recent study from the School of Public Health at the University of Puerto Rico would suggest that magnesium deficiency, which is in and out of itself associated with most if not all the bad things salt is usually blamed can come about much easier if you consume a high salt diet.

        As the data in figure 4 goes to show you, the amount of magnesium that's actually retained (not the amount you absorb!) is reduced by 33%, when the salt intake approaches the 4g/day mark. With a dietary intake of ca. 230mg/day (RDA for 11-15y old girls) the participants were "grams away" of a daily intake level that would require the body to get rid of excess magnesium.

        Bottom line: If you don't eat processed foods, you are not really at risk of getting too much NaCl or too little magnesium. Plus, as an aspiring physical culturist you lose tons salt, but almost no magnesium (the NaCl:Mg ratio in sweat is >682:1; cf. Montain. 2007) with your sweat, but don't we all have friends and family who are still pretty "average"? Well, in that case you already have a present for them: 1-2lbs of cheap magnesium citrate powder... but beware, never use this as a birthday, anniversary or Valentin's present for your significant other ;-)
      Actually I could go on forever with notes on stuff Carl and I have been talking about, but you would not be interested in it anyways, right? Plus, let's be honest if you have listened to the podcast, read and digested the Seconds it's about time for some Intermittent SuppVersity Fasting. You know the whole thing about the cyclicity of life? This is not much different with the latest science news: If you were not forced to be without them for some time, you would lose sight of how extraordinary the daily SuppVersity news actually are ;-)

      References:
      • CDC. FastStats - Life Expectancy. March 04 2013. < http://www.cdc.gov/nchs/fastats/lifexpec.htm > retrieved on April 11, 2013. 
      • Chlebowski RT, Manson JE, Anderson GL, Cauley JA, Aragaki AK, Stefanick ML, Lane DS, Johnson KC, Wactawski-Wende J, Chen C, Qi L, Yasmeen S, Newcomb PA, Prentice RL. Estrogen Plus Progestin and Breast Cancer Incidence and Mortality in the Women's Health Initiative Observational Study. J Natl Cancer Inst. 2013 Mar 29.
      • Chlebowski RT, Anderson GL. Changing concepts: Menopausal hormone therapy and breast cancer. J Natl Cancer Inst. 2012 Apr 4;104(7):517-27.
      • Fitzpatrick TB, Cesarini JP, Young A, Kollias N, Pathak MA. Reported in Fitzpatrick TB, Bolognia JL. Human melanin pigmentation: Role in pathogenesis of cutaneous melanoma. In: Zeise L, Chedekel MR, Fitzpatrick B, eds. Melanin: Its Role in Human Photoprotection. Overland Park, KS: Val-denmarPublishing Co; 1995: 177-182.
      • Lagunova Z, Porojnicu AC, Aksnes L, Holick MF, Iani V, Bruland OS, Moan J. Effect of vitamin D supplementation and ultraviolet B exposure on serum 25-hydroxyvitamin D concentrations in healthy volunteers: a randomized, crossover clinical trial. Br J Dermatol. 2013 Apr 1.
      • Montain SJ, Cheuvront SN, Lukaski HC. Sweat mineral-element responses during 7 h of exercise-heat stress. Int J Sport Nutr Exerc Metab. 2007 Dec;17(6):574-82.
      • Nankervis SA, Mitchell JM, Charchar FJ, McGlynn MA, Lewandowski PA. Consumption of a low glycaemic index diet in late life extends lifespan of Balb/c mice with differential effects on DNA damage.  Longevity & Healthspan. 2013; 2(4).
      • Palacios C, Wigertz K, Braun M, Martin BR, McCabe GP, McCabe L, Pratt JH, Peacock M, Weaver CM. Magnesium retention from metabolic-balance studies in female adolescents: impact of race, dietary salt, and calcium. Am J Clin Nutr. 2013 Apr 3.
      • Pittaway JK, Ahuja KD, Beckett JM, Bird ML, Robertson IK, Ball MJ. Make Vitamin D While the Sun Shines, Take Supplements When It Doesn't: A Longitudinal, Observational Study of Older Adults in Tasmania, Australia. PLoS One. 2013;8(3):e59063. 
      • Shumaker SA, Legault C, Rapp SR, Thal L, Wallace RB, Ockene JK, Hendrix SL, Jones BN 3rd, Assaf AR, Jackson RD, Kotchen JM, Wassertheil-Smoller S, Wactawski-Wende J; WHIMS Investigators. Estrogen plus progestin and the incidence of dementia and mild cognitive impairment in postmenopausal women: the Women's Health Initiative Memory Study: a randomized controlled trial. JAMA. 2003 May 28;289(20):2651-62.

      Foam Rolling For Cardiovascular Health. Propolis For Muscle Protection. Melatonin For Insulin Sensitivity. Plus: Bananas, Pineapples, Oranges & Beer to Boost Your Melatonin Levels!

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      Among 18-35 year-old Canadians 80% present with premature hardening of the arteries that could potentially lead to an ischaemic event (LLSA).
      Despite the fact that it ain't Saturday, yet, I decided to compile a couple of short news for you, also to make sure you re-appreciate the value of melatonin as a prerequisite to be and stay healthy and beautiful. It should therefore not come as a surprise to you that the SuppVersity Figure of the Week comes from the exact same context.

      The exact serum value is 51.5 pg/ml melatonin and it is the cut-off point for decreased nocturnal melatonin as a significant marker of an increased risk of stroke (Atanassova. 2009). Accordingly, every 1.0 pg/ml  decrease in melatonin would be associated with a >2% increase in stroke risk with a 50% risk suffering from an ischaemic stroke for people of all ages with a 3 a.m. value for melatonin of approx. 25pg/ml.

       Foam roll yourself towards a healthier cardiovascular system

      Who would have thought that: Foam rolling is good for something beside making fun of it! And if the results of the recent study from Nippon Sports University are applicable to everyone, it could be something as vital as the function of our arteries that will benefit from foam rolling the the adductor, hamstrings, quadriceps, iliotibial band and trapezius.

      The Japanese scientists had a group of  seven men and three women (age, 19.9 ± 0.3 y; height, 162.7 ± 8.1 cm; weight, 60.6 ± 11.2 kg, means ± SD), all healthy and free of any overt chronic disease performed the self-myofascial release (SMR) with a 15 × 91-cm (diameter × length) uniform polystyrene roller.
      Figure 1: Acute brachial-ankle pulse wave velocity and plasma NO concentration in healthy individuals before and after foam rolling aka self-myofascial release (Okamuto. 2013)
      The upper and lower extremities and the trunk were moved across the roller, pressure (direct force) was directed at the lower sacrum, mid thoracic spine and posterior head.
      "Pressure was adjusted by applying body weight to the roller and using the hands and feet to offset weight as required. The roller was placed under the target tissue area and the body was moved back and forth across the roller. Briefly, to accomplish SMR of the adductor, the thigh is extended and the roller is placed in the groin region with body prone on the floor. For SMR of the hamstrings, the lower extremities are extended and the roller is placed on the hamstrings with the hips unsupported.

      For SMR of the quadriceps, the thigh is extended and the roller is placed on the quadriceps with the body prone on the floor. For SMR of the iliotibial band, the roller is placed on the iliotibial band with the body lateral on the floor.

      You don't feel comfortable foam rolling? It's awkward? Yes, it is, but that's probably something you will get used to.
      For SMR of the upper back, the hands are placed behind the head and the roller is positioned on the trapezius with the hips unsupported. The head is maintained in a neutral position with the ears and shoulders aligned. The bottom leg is raised slightly off floor. The hips are raised until they are unsupported and the head is stabilized in the neutral position.

      The SMR proceeded in the order of adductors, hamstrings, quadriceps, iliotibial band and trapezius.

      Each participant practiced two or three times to learn the correct foam rolling technique with the guidance of a trainer and performed 20 SMR repetitions on each muscle group at 1-min intervals." (Okamuto. 2013)
      As you can see this protocol is a pretty time-consuming undertaking, which was however rewarded with significant

      Bottom line: With this being the first study to examine the effects of foam rolling or to say it the sexy way "Self-Myofascial Release" we cannot tell whether or not the benficial effects on brachial-ankle pulse wave velocity and plasma NO concentration are (a) replicable in sick and old people who would certainly benefit to a greater extent than the healthy young adults in the study at hand, and whether these changes would (b) persist / reoccur, if you practiced foam-rolling on a regular basis. Therefore Oakmuto et al. may be right that their results suggest that "repeated long-term SMR might decrease baseline arterial stiffness" (Okamuto. 2013), but if you had the choice of taking a walk and foam rolling for 30min, I bet the former will be WAY superior to waddling around with higgledy-piggledy 100% paleo incompatible polystyrene ;-)

      More evidence that propolis could promote muscle gain - at least in the elderly

      With all the rage about protein anabolism we often tend to overlook that pumping air into a balloon with hundreds of holes in it is not the wisest thing to do... or to say it in plain English, we tend to underestimate the importance of anti-catabolic substances. And while this is particularly true for elderly individuals, in whom the catabolic side effects of exercise tend to eat away their gains, even younger folks could benefit from a reduction in the as of now exclusively detrimental effects of TNF-alpha.

      Learn more about inflammation and skeletal muscle hypertrophy
      A recent study from nowhere else than the Department of Chinese Martial Arts at the Chinese Culture University did now elucidate that the provision of 5 and 10 mg/kg of caffeic acid phenethyl ester (CAPE, HED 50-150mg per day), a phenolic compound isolated from propolis (the honey beehive propolis, not the fungus) effectively blunts the inflammatory assault in response to downhill running and could thus "protect [...] against eccentric exercise-induced skeletal muscle damage" and avert (a) over exertion and (b) potential atrophy (Shen. 2013).

      It is however problematic that the TNF-alpha decline goes hand in hand with concomittant declines in OX2, iNOS, and production of IL-1β and MCP-1, all of which have been implicated as an integral part of the beneficial adaptive response to exercise. Genetic ablation of the MCP-1 gene for example lead to persistent macrophage accumulation in association with residual necrotic tissue and impaired muscle regeneration (Shireman. 2007).

      Bottom line: As mentioned before a propolis supplement is probably more beneficial for older people or other trainees with health conditions that make them more susceptible to skeletal muscle catabolism. Whether this will be beneficial in young people is yet about as questionable as the whole COX-inhibitor for or against muscle growth conundrum, of which Trappe et al. wrote in a very recent review that they probably won't hamper muscular adaption in young and middle aged individuals and showed some promise in promoting the adaptation process in the older guys and gals (Trappe. 2013). For both "regular" COX inhibitors like aspirin, but also "exotic" supplements like propolis extracts it may thus depend on both timing & dosage  and age / baseline inflammation & ability to cope with it  - whether or not supplementing with respective compounds makes sense.

      Melatonin supplementation doubles insulin sensitivity in old obese rodents

      I know another rodent study, but if you look at the sleep problems your own older relatives have and the way similar patterns have become prevalent in ever-increasing parts of the younger generation, as well, even the mere possibility that the 2.1x increase in insulin sensitivity researchers fro the Department of Physiology and Biophysics at the Institute of Biomedical Sciences of the University of São Paulo describe in their soon-to-be published paper would warrant an N=1 experiment with melatonin (Zanuto. 2013). mesenchymalstemcells from oxidative damage and can be temporarily doubled by simply consuming tropical fruits even (pineapple < orange < banana, see figure 2; Sae-Teaw. 2012)
      Figure 2: KITT–Glucose disappearance rate (%/min), weight change from week 0, periepididimal fat weight (left; Zanuto. 2013); effect of fruit extract from 1kg pineapples, 1kg oranges or two ripe bananas on serum melatonin in 12 healthy male healthy volunteers (left; Sae-Teaw. 2012)
      This is all the more true, in view of the fact that the pineal hormone, of which you do find 60-170µg/l in beer (with higher values in beers with high alcohol content; cf. Garcia-Moreno ), has also been shown to protect rodents from ischaemic heart disease (at high doses of ~1.5mg/kg ; cf. Sehirli. 2013) and to be inversely associated with the incidence of stroke in humans (Atanassova. 2009).

      Bottom line: Don't discount the value of natural and supplemental melatonin. If it was patentable it would maybe be the #1 prescription drug in the stressful an restless world of the 21st century. You think that's an exaggeration? Maybe, but if you just check out the few SuppVersity news on the matter, you will realize that it's only a minor exaggeration.

      And in case you don't want to supplement. A decent amount of sleep, some testosterone boosting high alcohol beer as a "Post Workout Booze" (not really recommended) and the insulin sensitizing "6x Bananas à Day Protocol" you can also boost it the natural way ;-)

      References:
      • Atanassova PA, Terzieva DD, Dimitrov BD. Impaired nocturnal melatonin in acute phase of ischaemic stroke: cross-sectional matched case-control analysis. J Neuroendocrinol. 2009 Jul;21(7):657-63.
      • Garcia-Moreno H, Calvo J, Maldonado M. High levels of melatonin generated during the brewing process. J Pineal Res. 2012 Aug 1.
      • LLSA - Stroke at a Young Ag. < http://www.lifelinescreening.com/health-updates/healthy-you/stroke/stroke-at-a-young-age.aspx > retrieved April 12, 2013.
      • Liu X, Gong Y, Xiong K, Ye Y, Xiong Y, Zhuang Z, Luo Y, Jiang Q, He F. Melatonin mediates protective effects on inflammatory response induced by interleukin-1 beta in human mesenchymal stem cells. J Pineal Res. 2013 Jan 30.
      • Okamoto T, Masuhara M, Ikuta K. Self-Myofascial Release and Arterial Function. Journal of Strength and Conditioning Research. April 2013 [ahead of print]
      • Sae-Teaw M, Johns J, Johns NP, Subongkot S. Serum melatonin levels and antioxidant capacities after consumption of pineapple, orange, or banana by healthy male volunteers. J Pineal Res. 2012 Oct 5.
      • Sehirli AO, Koyun D, Tetik S, Ozsavcı D, Yiğiner O, Cetinel S, Tok OE, Kaya Z, Akkiprik M, Kılıç E, Sener G. Melatonin protects against ischemic heart failure in rats. J Pineal Res. 2013 Mar 15.
      • Shen YC, Yen JC, Liou KT. Ameliorative Effects of Caffeic Acid Phenethyl Ester on an Eccentric Exercise-Induced Skeletal Muscle Injury by Down-Regulating NF-κB Mediated Inflammation. Pharmacology. 2013 Apr 3;91(3-4):219-228. 
      • Shireman PK, Contreras-Shannon V, Ochoa O, Karia BP, Michalek JE, McManus LM. MCP-1 deficiency causes altered inflammation with impaired skeletal muscle regeneration. J Leukoc Biol. 2007 Mar;81(3):775-85.
      • Trappe TA, Liu SZ. Effects of Prostaglandins and COX Inhibiting Drugs on Skeletal Muscle Adaptations to Exercise. J Appl Physiol. 2013 Mar 28. 
      • Zanuto R, Siqueira-Filho MA, Caperuto LC, Bacurau RF, Hirata E, Peliciari-Garcia RA, do Amaral FG, Marçal AC, Ribeiro LM, Camporez JP, Carpinelli AR, Bordin S, Cipolla-Neto J, Carvalho CR. Melatonin improves insulin sensitivity independently of weight loss in old obese rats. J Pineal Res. 2013 Mar 30.

      True Or False: Alpha Lipoic Acid Promotes Creatine Uptake. Using Non-Stick Teflon Pans Causes Colorectal Cancer. Locusts, Beetles & Moths Can Easily Compete With Whey

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      As a SuppVersity reader you already know that eggs are not going to give you cancer (learn more about eggs), but with the recent Facebook News on the correlation between non-stick pans and colorectal cancer in a Greek study, the question is, whether this changes, when you prepare your eggs in a Teflon coated pan.
      Since the really interesting news are a bit slow these days and you've got your weekly serving of short-news yesterday, already I thought it would be nice if I tackled one of the "True or False" suggestions I have - as promised - started to collect and file for future episodes, mix that with two things I just had on my mind and serve the gray-matter enhancing mixture as an extraordinary installment of "True or False".

      I am, by the way, still open for suggestions, although I suppose I should come up with a better way to submit them... well, I guess that's something to keep in mind for the re-design, which is slowly but steadily progressing.

      Apropos, any other suggestions (aside from a better archive, which is already on the list) you believe could make the SuppVersity even better, are highly appreciated :-)

      Alpha lipoic acid increases creatine uptake

      True. The only human study I know of which investigated the effect of alpha lipoic acid (ALA) on the efficiacy of creatine supplementation shows that the addition of 1g of alpha lipoic acid to the baseline 20g/day + 100g/day sucrose supplement the 16 male subjects (18-32 y) in the 2003 study from the Department of Human Kinetics at the St. Francis Xavier University in Antigonish, Nova Scotia, Canada received in the course of a 5-day loading phase lead to a significantly faster increase in phosphocreatine and total creatine in the skelatal muscle of the vastus lateralis muscle (Burke. 2003)

      It is however about questionable how relevant this effect actually is, after all the whole notion of the benefits, let alone the necessity of a "loading phase" has been revised over the past decade. Outside of scenarios, where the immediate supercompensation of the PCr stores is of utmost importance the use of ALA as a to promote creatine uptake is thusly probably unwarranted.
      Figure 1: Relative 10th-rib fat depth, 10th-rib longissimus muscle area and intramuscular fat in pigs finished on diets containing 24g/day of creatine, 600mg of alpha lipoic acid or a combination of both; data expressed relative to unsupplemented control (Berg. 2003)
      As far as its effects on body composition and metabolic health are concerned the data in figure 1 clearly shows that the additional provision of alpha lipoic acid must not necessarily translate into visible (muscle size & body fat) or unvisible (intramuscular fat) improvements - especially during a bulk. This is at least what the higher body fat and lower muscle size of the pigs in the the 2003 study by Berg et al. would suggest (Berg. 2003; it should be said, though, that the differences did not reach statistical significance!).

      Bottom line: There is hardly any dietary supplement, where the good old saying "never change a winning team" is so to the point as with the good old creatine monohydrate. Whether it is one of the bazillion "advanced creatine formulas" or the myriad of different supplementation protocols or uptake promoters, time and again the simple, the "boring", yet proven and effective chronic ingestion 3-5g of creatine monohydrate per day produced equal or, as it was / still is the case of the die hard supplement scam creatine ethyl esther (CEE; learn more), even superior results.

       The Teflon coating of non-stick pans will give you cancer

      False. While the average American carries 4–5ppb of Perfluorooctanoic acid (PFOA), the potentially carcinogenic synthetic perfluorinated carboxylic acid and fluorosurfactant that's used in the production process of teflon pans & co is not the main, most likely not even a source of the PFAO in your blood.
      Coffee-Chile-Cocoa Rubbed Sirloin, Creamed Kale (recipe) - The perfect way to eat your red meats and avoid potentially carcinogenic effects of more than well-done meats? Or is it enough if you drink an Espresso afterwards? Lot's of additional questions and a handful of answers in previous SuppVersity posts.
      "[T]he coated cookware tested here do not appear to be a significant source of PFOA which will migrate due to cookware’s low µg/kg initial residual level of PFOA. Furthermore, an extreme heating test (abusive) of the cookware did not appear to increase the residual amount of PFOA in the cookware. That is, additional PFOA does not appear to form during the normal use or misuse of these products.

      [...]  This conclusion also assumes that all cookware has the same highest initial concentration of PFOA. In fact, a number of cookware items had at least ten times less PFOA. [...] Eventually because the cookware is a repeat use item, the amount of PFOA in cookware should approach zero provided that no PFOA is generated over time." (Begley. 2005)
      Much more likely candidates for PFOA in your blood are papers with fluorochemical coatings/additives such as popcorn bags which emit a 100x higher amount of fluorochemical (e.g. PFOA) than even high PFOA cookware at 175°C during its first use.
      Figure 2: Serum fluorochemical levels in Greeks with and without cancer (Vassiliadou. 2013)
      And while the Kontou study, which spiked my interest in this topic (Kontou. 2013), showed correlation between colorectal cancer patients and the use of non-stick cooking ware. Another study, likewise done in Greece, shows that there is no correlation between cancer and the serum PFOA levels in Greek citizens (Vassiliadou. 2010; see figure 2).

      Which confounding factors? The fact that you tend to overheat and burn the foods (learn more), when you don't have to clean the mess later on, for example, or the simple correlation that exists between the use of non-stick pans and the frequency of fried food consumption which has repeatedly been shown to increase the risk of colorectal cancer (e.g. Miller. 2013).
      Bottom line: In view of the current scientific evidence wrt to the total amount of potentially carcinogenic fluorochemicals leeching from non-stick coated cookware, I want to reemphasize my previously voiced hypotheses that the use of non-sick cookware was associated with an increased risk of colorecteral cancer in a recently published study from Greece is probably the result of confounding factors as those I mentioned in the original facebook post and in the box on the right.

      Yet although I suspect that it's really about eating too much "burnt" foods (if the stuff burns in a sticking pan it will remain in the pan and not be eaten!) is the best explanation I cannot exclude that something else than the fluorochemical that the could be responsible for the observations in the Kontou study.

      Whey was yesterday, maggots, locusts & co are the future

      *Yamyoll* As in the case of meat, it may be a good idea not to panfry your insects for too long; see "True or False" item on Teflon pans and burnt meats above
      True. It may sound disgusting, but from what I gather it (a) isn't and (b) is pretty realistic that we are going to see more and more insect proteins in our food-chain in the future. So why shouldn't he protein powder of the future also be an "insect protein isloate"?

      I mean, ISI sounds much cooler than WPI, as in whey protein isolate...Well, not so much for the whey was yesterday, as I believe it will take at least a couple of day for whey to be overtaken by insect protein (isolates?), but the current scientific evidence clearly suggests that insect protein is not only a nutritionally complete protein source, but offers similar if not superior additional health benefits as whey.

      You don't believe a word I am saying? You want examples? While there are no controlled trials with insect protein isolates (ISI) + resistance training as of yet, there is good evidence that ISIs would be competitive.
        The insect protein cheat sheet: Grass hoppers are the chicken (high protein, low fat; 362–427kcal per 100g), beetles the eggs (high protein, high fat; 410–574kcal) and butterflies and moths the meats (high protein medium fat content; 293–762kcal) of insect nutrition.
      • high digestibility -- insect protein is of high quality and has a high digestibility (77-98%; cf. Verkerk. 2007)
      • high protein content  -- 0-75 g/100g of the dry weight of most of the critters is pure protein (Verkerk. 2007)
      • high essential amino acid content -- the concentration of essential amino acids ranges from 46-96% of the nutritional profile (Verkerk. 2007)
      • ACE inhibition -- just like whey protein hydrolysates, insect protein hydrolysates have been shown to contain enzymes that can reduce blood pressure (Vercruysse. 2005 & 2010) 
      Aside from simply eating insect proteins, various proteins and cell lines have already been tested for the manufacturing of vaccines and functional molecules (Altmann. 1999; Drugmand. 2012).

      Table 1: EAA content of various insect proteins (Verkerk. 2007) and a a standard whey protein concentrate (Met+Cys, Phe+Tyr not measured individually)
      Bottom line:  As so often, it appears as if we were once again racing the tortoise. Whenever we think we have invented the "optimal" *put whatever you like here* it doesn't take long until we realize that nature has already been there or has topped our latest invention millions of years ago, already.

      Allegedly, nature's way of "inventing" things may not comply to the strict standards of natural science, but still, insect proteins are only one example for the unexploited bio-ressources that slumber in the Brazilian rain forests and also and even more so the deepest dephts of the oceans.



      That's it for today and since it's Saturday, I guess I will have to close this post with the obligatory reminder of the SuppVersity Facebook News you can find at www.facebook.com/SuppVersity ... why you should go there? Well,... maybe you want to learn the latest about how...
        Days ago the carnitine in them was bad for our heart, now it saves the lives of patients with heart disease?
      • TV watching "dissolves" the trunk muscles of adolescents, so that each hour/day costs them ~20lbs of muscle power (read more)
      • being "somewhat diabetic" is not just "somewhat of a problem", but will effectively increase your risk of cardiovascular disease (read more)
      • carnitine in red meat saves not threatens lives, those of people with heart disease, to be precise (read more)
      Just don't forget that sitting in front of the computer or with your shiny iPhone on the sofa is not going to (re-)build your trunk musculature either and the fact that you did not have junkfood today is not an excuse to skip on your workout ;-) Have a nice weekend!


      References:
      • Altmann F, Staudacher E, Wilson IB, März L. Insect cells as hosts for the expression of recombinant glycoproteins. Glycoconj J. 1999 Feb;16(2):109-23.
      • Begley TH, White K, Honigfort P, Twaroski ML, Neches R, Walker RA. Perfluorochemicals: potential sources of and migration from food packaging. Food Addit Contam. 2005 Oct;22(10):1023-31. 
      • Berg EP, Maddock KR, Linville ML. Creatine monohydrate supplemented in swine finishing diets and fresh pork quality: III. Evaluating the cumulative effect of creatine monohydrate and alpha-lipoic acid. J Anim Sci. 2003 Oct;81(10):2469-74.
      • Burke DG, Chilibeck PD, Parise G, Tarnopolsky MA, Candow DG. Effect of alpha-lipoic acid combined with creatine monohydrate on human skeletal muscle creatine and phosphagen concentration. Int J Sport Nutr Exerc Metab. 2003 Sep;13(3):294-302.
      • Drugmand JC, Schneider YJ, Agathos SN. Insect cells as factories for biomanufacturing. Biotechnol Adv. 2012 Sep-Oct;30(5):1140-57.
      • Miller PE, Lazarus P, Lesko SM, Cross AJ, Sinha R, Laio J, Zhu J, Harper G, Muscat JE, Hartman TJ. Meat-related compounds and colorectal cancer risk by anatomical subsite. Nutr Cancer. 2013 Feb;65(2):202-26.
      • Vassiliadou I, Costopoulou D, Ferderigou A, Leondiadis L. Levels of perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) in blood samples from different groups of adults living in Greece. Chemosphere. 2010 Aug;80(10):1199-206. 
      • Vercruysse L, Smagghe G, Herregods G, Van Camp J. ACE inhibitory activity in enzymatic hydrolysates of insect protein. J Agric Food Chem. 2005 Jun 29;53(13):5207-11.
      • Vercruysse L, Van Camp J, Morel N, Rougé P, Herregods G, Smagghe G. Ala-Val-Phe and Val-Phe: ACE inhibitory peptides derived from insect protein with antihypertensive activity in spontaneously hypertensive rats. Peptides. 2010 Mar;31(3):482-8.
      • Verkerk MC, Tramper J, van Trijp JC, Martens DE. Insect cells for human food. Biotechnol Adv. 2007 Mar-Apr;25(2):198-202.

      Fighting to Stay Lean? These 20+ Anti-Obesity Agents Have the Potential to Inhibit Fat Gain Right at the Cellular Level

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      No, none of the 20 agents in the list below is going to do the work for you, but they could help you "conserve" the results, keep you lean on a bulk and/or avoid the hazardous Yoyo effect when you go off a die.
      It's actually normal that the introduction is the last part of an article I write. What's special about today's SuppVersity article is thus not that I write the introduction at the end, but that I did not really know what I would be writing here, when I set out to compile the unsorted (but not chaotic) list of potential anti-obesity agents below. All of them act by pathway(s) you as a SuppVersity reader will have read about before, most prominently AMPK, and the peroxisome proliferator receptors (PPARs), of which the blockade of the obesogenic PPAR-gamma pathway, which is the main working principle of CLA turned out to be the go-to explanation for the ability of these agents to block both the differentiation of adipocytes and the storage of triglycerides in existing fat cells.

      20 more or less proven anti-obesity agents for the weekend

      As you are about to see, the list, which was never intended to be complete, got pretty and I guess I could add a couple of additional items, if I spent more time digging. In order not to steal your and waste more of my precious time on this sunny (finally!) Sunday, I did yet decide to call it a day, when I hit the 20-items mark. Now it's up to you to invest some of your sunny Sunday time, to read up on the details. 
      • On a side note: The "holy" vitamin D does the exact opposite, if you incubate preadipocytes with 25(OH)D(3) this will lead to a significant increase in the active 1,25(OH)(2)D(3) and enhanced adipogenesis in primary mouse. Reason enough for a group of Thai researchers to conclcude that "vitamin D status may [actually] regulate human adipose tissue growth and remodeling." (Nimitphong . 2012)
        Vitamin A - Retinoic acid upregulates the expression of the adipogenesis inhibitors Pref-1, Sox9, and Kruppel-like factor 2 (KLF2) to "suppress adipogenesis in vivo and that the activity significantly contributes to the ability of the hormone to counteract diet-induced obesity." (Berry. 2012) Previous studies have also shown that all-trans-retionic acid directly increases the activity of PPARbeta/delta and so that Berry & Noy conclude "RA may be a uniquely efficacious agent in the therapy and prevention of the metabolic syndrome." (Berry. 2009) Similar results have been reported and conclusions have been drawn by Brun et al. and Sagara et al. (Brun. 2012; Sagara. 2013). Finally, Hisada et al report that - just like testosterone (learn more) - retinoic acid ensures that mesenchymal stem cells (MSCs) become osteoblasts (bone precursor cells), not fat cells (Hisada. 2013).
      • Bromocriptine - If you do know it at all, then probably for it's ability to decrease the "milk hormone" prolaction. If you take a look at the broad spectrum of physiological effects of prolactin, the effect it has on the mammalian mammary gland is really negligible. A recent study from the Department of Biotechnology at the Daegu University in The Republic of Korea does now suggest that the inhibition of adipogenesis (formation of new fat cells) and lipogenesis (storage of lipids in existing fat cells) via decreased expressions of the adipogenic activators Pparα, Pparγ, and Cebpα, as well as major lipogenic target genes, including Me1, Acc1, 6Pgd, Fasn, and Prkaa1 is one of these "auxiliary functions" (Mukherjee. 2013)
      • EC also boosts erectile performance and testosterone (learn more)
        Ecklonia cava (EC) - or rather the dioxinodehydroeckol (DHE) molecules that are contained in this type of brown seaweed "exert[s] its anti-adipogenic effect on adipocyte differentiation through the activation and modulation of the AMPK signaling pathway" (Kim. 2010a). As a SuppVersity reader, you will be aware that this effect has been confirmed in in-vivo studies, later on (learn more).

        What's probably Interestingly DHE is not the only anti-adipogenic agent in brown sea algae, Fucoidan, a sulfated polysaccharide from brown seaweeds has likewise been reported to affect the development of adipocytes. In 2010, Kim et al. were able to show that it targets the MAPK kinase pathway by inhibiting the the expression of both early CCAAT-enhancer-binding proteins alpha (C/EBPalpha) and peroxisome proliferator-activated receptors gamma (PPARgamma), as well as the late activating protein 2 (aP2) adipogenic transcription factors (Kim. 2010b).
      • Curcumin - While you my get the impression there was nothing curcumin cannot do (learn more), I am not whether the anti-PPAR gamma effects of curcumin are a result of it's anti-inflammatory effects or not... be that as it may, Lee et al. have demonstrated in 2009 already that the stimulatory effect curcumin exerts on the AMPK expression of adipocytes results in a down-regulation of PPAR-gamma in 3T3-L1 adipocytes (Lee. 2009).
      • Resveratrol - Similar popularity, similar "cures it all" status and similar effects on AMPK and downstream PPAR-gamma expression in 3T3-L1 adipocytes... actually I would not need another bulletin point for resveratrol which acts by the exact same pathway(s) s curcumin to inhibit fat cell differentiation (Chen. 2011)
        • Creatine RT by Athletic Edge Nutrition; contains a cousin of ASL and is supposed to be another "super creatine" -  True or False? The 2011 SuppVersity article has the answer (read it!).
          Artemisia sacrorum Ledeb. (ASL) - Extracts from the small shrub have been used in Oriental Medicine for centuries, in 2011 Yuan et al. were able to show that ASL "down-regulate[s] the adipogenesis-related gene expression of the sterol regulatory element-binding protein 1c (SREBP1c) and its target genes, such as fatty acid synthase (FAS), stearoyl-CoA desaturase 1 (SCD1) and glycerol-3-phosphate acyltransferase (GPAT) in a concentration-dependent manner" (Yuan. 2011) The effects are meediated by a reduced expression of the peroxisome proliferator-activated receptor γ (PPARγ) and of the CCAAT/enhancer binding protein-α (C/EBPα), both of which are key transcription factors in adipogenesis.

          With the concomitant reduction in adipocyte fatty acid binding protein (aP2) gene expression, ASL is another potential anti-obesity agent of which Yuan et al. propose that it works its  anti-adipogenic magic via AMPK activation. In view of the fact that the same is true for the fat accumulation in human liver cells, it could serve a viable tool "in the prevention of serious diseases such as fatty liver and type-2 diabetic mellitus" (Yuan. 2010). Related increases in fatty acid oxidation have been observed in a rodent study by Hong later in 2009 with another variety of Aertemisia, namely Artemesia Capillaris (Hong. 2010). The human equivalent dosage in this trial wast 8mg/kg of the ethyl acetate fraction of the shrub.
        • Phosphorylated glucosamine - While you will probably remember that large doses of regular glucosamine have been associated with insulin resistance (see previous installment of "True Or False"), it's phosphorylated variety glucosamine-6-phosphat (PGlc), Kong et al. synthesized using methanesulfonic acid, phosphorus pentoxide (P(2)O(5)), NH(2)NH(2) and DMF "significantly reduced lipid accumulation during adipocyte differentiation and induced down-regulation of peroxisome proliferator-activated receptor-gamma, sterol regulatory element binding protein 1 and CCAAT/enhancer binding protein-alpha in a dose-dependent manner." (Kong. 2010)
          Phosphorylated glucosamine works (like most of the anti-obesity agents, including the well-known conjugated linoleic acid by reducing the expression of PPAR-gamma (left). It's dose-dependent effects are yet not restricted to the peroxisome proliferator receptor, but affect the pro-adipogenic genes C/EBP-alpha and SREBP1, as well (right; Kong. 2010)
          What's also worth mentioning is that the in-vitro study from the Marine Bioprocess Research Center at the Pukyong National University in South Korea also revealed that PGcl also hampered the maturation of pre-adipocytes by down-regulating adipocyte-specific gene promoters such as adipocyte fatty acid binding protein, fatty acid synthase, lipoprotein lipase and leptin. In conjunction "[t]hese results suggest that the inhibitory effect of PGlc on adipocyte differentiation might be mediated through the down-regulation of adipogenic transcription factors, such as peroxisome proliferator-activated receptor-gamma, sterol regulatory element binding protein 1 and CCAAT/enhancer binding protein-alpha, which are related to the downstream adipocyte-specific gene promoters" (Kong. 2010) 
        • Add. reads: "Temporary +100kcal/Day Cold Thermogenesis Response W/ Exotic Ginger Extract" (more) "250-1000mg of Freeze-Dried Ginger Reduce Visceral Fat Even When Rodents Are Fed an Obesogenic High Fat Diet" (more).
          6-gingerol (6G) - The active ingredient in ginger has just been shown to block the obesity effects of the anti-diabetes med rosiglitazone (Tzeng. 2013). It does so by blocking the PPAR-gamma mediated effects of the "store the superfluous energy as body fat"-drug and was thus able to suppress the oil droplet accumulation and reduce the sizes of the droplets in the course rosiglitazone(RSG)-induced adipocyte differentiation in 3T3-L1 cells. Since it also blunted the increased levels of mRNA and protein in adipocyte-specific fatty acid binding protein 4 and fatty acid synthase induced by RGZ, it can be expected that 6G will not only inhibit the accrual of new, but also the (re-)filling of existing fat cells. 
        • Piperine and capsaicin - In view of the fact that piperine is a "quasi-cousins" of 6-gingerol, it is actually not really surprising that it shares similar effects on the expression of PPAR-gamma (Park. 2012). It is therefore not surprising that the third member of this spicy triumvirate, i.e. capsaicin, shares the exact same PPAR-gamma reducing effects (Joo. 2010).
            • Berberin - Contrary to many other items on the list, berberin's anti-PPAR-gamma effects are actually pretty well-known. There is ample evidence from in-vitro (Huang. 2006; Liu. 2009) and in-vivo (Lee. 2006) evidence that it blunts fat gain by increasing the catabolism of high energy intermediates, upregulating AMPK, modulating the expression of the GATA-2 and 3 gene and reducing the expression of (you guessed it) PPAR-gamma (Hu. 2009).
              Table 1: Berberine content of various commercially available supplements (Brown 2008)
              Berberine has also been shown to improve endothelial function in man (Wang. 2009) and promote the "longevity and mitochondrial health gene" SIRT1 in obesity ridden, insulin resistant skeletal muscle (Gomes. 2012).
            • Ginsenosides (spec. ginsenosideRg3) - Just like ginereol (see above) ginsenosideRg3 has been shown to block the adipogenic effects of the anditiabetic drug rosiglitazone via an AMPK/PPAR-gamma dependent pathway (Hwang. 2009). It may be worth mentioning that at least the effect triglyceride storage was not dose-dependent. Once  a threshold amount of 40µM was reached, the adipocytes that were incubated with Rg3 did not "lose" any additional triglycerides, when the dosage was increased to 80µM.
            • On a side note: Although promoted in the same health and longevity circles as CAPE, the hailed "telomerase lengthener" Astraglaus is a PPAR-gamma promoter and will thus "enhance the accumulation of lipid drops, and increase the terminal differentiation of preadipocytes" (Liu. 2007)
              Caffeic acid phenethyl ester (CAPE) - You've heard about the anti-inflammatory, muscle protective ability of this compound from bee propolis only recently (go back). In addition to being a potent anti-inflammatory, the natural phenolic compound that's also found in a variety of plants, has also been found to block the conversion of mouse fibroblasts into fat cells (Juman. 2010). As for most of the other agents the effects of CAPE appear to be mediated by a reduction inperoxisome proliferator-activated receptor (PPAR) gamma and CCAAT/enhancer-binding protein (C/EBPalpha) and concomittant reduction isn fatty acid synthetase and the expression of adipocyte-specific fatty acid binding protein (aP2). 
            • Lysimachia foenum-graecum (LFE) - LFE is a Chinese herb and well-known anti-inflammatory from Oriental Medicine. The anti-obesity effect of L. foenum-graecum extract was first discovered by Seo et al., when they simply screened a whole host of potential natural agents for their anti-adipogenic effects. In 2011 the researchers found that "LFE blocked the differentiation of 3T3-L1 preadipocyte in a dose-dependent manner with an IC50 of 2.5 μg/ml". The underlying mechanism which has also been observed in an in-vivo rodent study with 100 mg/kg/day, are - how else could it be - mediated by the inhibition of PPARγ and C/EBPα expression.
              Effects of the administration of an lysimachia foenum-graecum ethanol extract on lipid and glucose metabolism and adipokine signalling in mice on an obesogenic diet (Seo. 2011)
              Moreover, LFE stimulated fatty acid oxidation in an AMPK-dependent manner, greatly improved serum levels of obesity-related biomarkers such as glucose, triglycerides, and adipocytokines leptin, adiponectin, and resistin and lead to an effective decrease in total body weight gain in mice who received 30, 100, and 300 mg/kg/day of an Lysimachia foenum-graecum ethanol extract (50:6; LFE) in addition to their obesogenic high fat diet (see figure above). The mice in the HFD + LFE group did simply have lower body weights, they also had a reduced amount of adipose tissues especially within the metabolically active and highly unhealthy abdominal subcutaneous, epididymal, and perirenal adipose tissue.
            • Photos of the lean (A and D), HFD-fed (B and E) and HFD-fed + SRLE supplemented (C and F) mice in the Thounaojam study (2011).
              Sida rhomboidea. Roxb leaf extract (SRLE) - SRLE does only sound like the stuff many supplement companies used after the ban of mua huang (natural source of ephedrine). It is however a different variety of Sida (Batyάlaka, Sida cordifolia)... well, at least it is from the same family which lacks the CNS stimulating activity of mua huang. With its ability to prevent high fat diet (HFD) induced visceral adiposity by down-regulation of PPARγ2 and leptin gene expression it could in fact work synergistically with ephedrine, though. After all the HED of the 24% w/w water extract Thounaojam et al. used to prevent the obesogenic effects of a hypercaloric high fat diet in their rodent study amounts to no more than ~40mg/kg and since SRLE has been shown to be non-toxic up to 3g/kg (in mice; HED ~240mg/kg) it would be interesting to see studies that probe whether it works in humans (Thounaojam. 2011).
            • SH21B is an anti-obesity composition composed of seven herbs: Scutellaria baicalensis Georgi, Prunus armeniaca Maxim, Ephedra sinica Stapf, Acorus gramineus Soland, Typha orientalis Presl, Polygala tenuifolia Willd and Nelumbo nucifera Gaertner (active ingredients; see figure below) that has been used for the treatment of obesity in traditional medical clinics in Korea and has recently been shown to decrease the expression of major transcription factors of the adipogenesis pathway and result in the down-regulation of lipid metabolizing enzymes involved in the transport, uptake and synthesis of lipids - unfortunatedly, only in vitro (Lee. 2009)
              Effects of SH21B on fat droplet formation in 3T3-L1 cells (top) and size of adipocytes in adipose tissue. (bottom), as well as active ingredients in SH21B (based on Lee. 2009)
              As you can see in the stains from the adipose tissue of the above, the effects are clearly mediated by both an inhibition of the maturation of preadipocytes (top) and the inhibition of fat storage... now you tell me the world needs "new" anti-obesity agents!? I mean, it's quite obvious that the Koreans knew all along what keeps you lean ;-)
            • Lactobacillus plantarum KY1032 cell extract - Before you begin to jubilee about the triumph march of probiotics, let me tell you this: I am not sure how on earth the remnants of a gut bacterium are supposed to reach your adipocyte tissue in a healthy individual without a leaky gut. Against that background I am not sure, whether it is even necessary to mention that Park et al. observed in 2011 that a cell exctract of the KY1032 strain of lactobacilli is another compound that can down-regulate the expression of peroxisome proliferator-activated receptor-γ2, CCAAT/enhancer binding protein-α, fatty acid synthase, and adipocyte-fatty acid binding protein and thus blunt fat gains in vitro... ah, now I wrote it down, so I'll just leave it here ;-) 
            • Irvingia gabonensis seed extract - Likewise not a newcomer to the supplement the African / Southeast Asian tree, respectively an extract from its seeds has been shown to dose-dependently decrease the expression of PPAR-gamma in murine adipose cells in the petri dish in a 2008 study by scientists from  Faculty of Science, University of Yaoundé in Cameroon and the Wake Forest University School of Medicine in Winston-Salem, USA (Oben. 2008).
              The in-vitro study shows, CAF may inhibit fat storage, but it does not "squeeze" the fat out of the cells (data based on Kim. 2012)
              • Citrus aurantium falvenoids (CAF)- Despite the fact that most of you will probably have realized in N=1 experiments that citrus aurantium is a supplemental non-starter as a fatburner. It has (in-vitro) the ability to reduce the epxression of C/EBPβ and subsequently inhibit the activation of PPARγ and C/EBPα. So unless you have taken tons of pure CAF supplements during your last bulk, it is no wonder that you did not realize any effect from the fat burner you bought last summer. After all you are not storing any fat when you are dieting anyway... and I guess you have been dieting, when you took that product, right?

                Apropos dieting, the data in the figure on the right also shows that citrus aurantium, alone, won't help with that. After all it lacks the ability to increase LPL and thus the release of free fatty acids from the triglyceride stores in your fat stores.
              • Silibinin (from milk thistle) - You will probably have heard that milk thistle can help replenish the antioxidative defenses of your liver and thus prevent all sorts of systemic toxicities (learn more). At least in-vitro silibinin (aka silybin), the major active ingredient in silymarin, can also prevent the accumulation of triglycerides in existing, as well as the formation / maturation of future adipocytes. From a mechanistic point of view, the effect is mediated by the usual suspects respectively their downregulation (CAAT/enhancer binding protein-alpha, fatty acid synthase, sterol response element binding protein 1c, adipocyte-specific lipid binding protein, peroxisome proliferator-activated receptor gamma and lipoprotein lipase; cf. Ka. 2009).
              • Stem bromelain (SBM) - Just as so many of the previously mentioned agents, SBM, a specific member of the bromelain family you may know as "pineapple enzyme", is by no means a "new kid on the anti-fatloss block". Rather than that it has been used for centuries in traditional medicine as - guess what? - an anti-obesity agent. Now, I would never suggest that all TCM medicines work, but for stem bromelain it does at least seem as if the in-vitro studies, Dave et al. conducted about a year ago would support the notion that the ingestion of respective supplements can in fact exert beneficial effects on the accumulation of body fat (Dave. 2012).
                Illustration of the mechanism and selected downstream effects of stem bromelain (SBM) on fat cells in the petri dish (compiled based on data from Dave. 2012)
                At the molecular level, SBM targets the same adipogenesic genes as (almost all) of the previous agents. What's interesting though, is the fact that the scsientists also found that "SBM's ability to repress PPARγ expression seems to stem from its ability to inhibit Akt and augment the TNFα pathway." (Dave. 2012) In other words, it's the increase in "bad" TNF-alpha and the decrease in the purportedly muscle, but in fact simply "mass building" Akt-TSC2-mTORC1 pathway that entails the apoptosis (controlled cell death) of mature adipocytes and lipolysis.
              With the stem bromelain this comprehensive, but by no means all-encompassing list of "proven" (mostly only in vitro) anti-adipogenic agents, has come full circle. After all, Dave et al. point out that their data would indicate that stem bromelain, together with all-trans retinoic-acid (atRA), which is a metabolite of vitamin A, the first item on our list "may be a potent modulator of obesity by repressing the PPARγ-regulated adipogenesis pathway at all stages and by augmenting TNFα-induced lipolysis and apoptosis in mature adipocytes." (Dave. 2010).

              It's not just beyond the scope of this article, but - in the majority of the cases simply not known - whether or not the TNFα increase is an integral part of the anti-obesity effects of all of the aforementioned compounds. As far as the inhibition of PPAR-gamma is concerned things are different, though. With PPAR-gamma being the central "fat storage" switch, its deactivation and the entailing blockade of adipocyte differentiation, pre-adipocyte maturation and triglyceride storage is currently probably the most effective anti-obesity  mechanism we know. A mechanism that is way more fundamental than the diet-induced and stimulant / alpha/beta-agaonist (caffeine, ephedra, clenbuterol, yohimine) supported emptying of existing adipocyte triglyceride stores.



              I know it's not popular, but in the case of vitamin D we already have evidence of it's obesity promoting effects (read more). It's straight forward experimental evidence, much contrary to the epidemiological guesswork on the basis of which people are popping vitamin D pills, these days.
              Keep in mind: Most of the data is derived from in-vitro studies. Few compounds do have actual evidence from rodent studies and the number of substances that showed beneficial effects in human studies is even smaller.

              Nevertheless, the above list harbors a number of compounds which could be of great interest for the lean physical culturist, for whom (at least physique-wise) stuff like vitamin D (note: the effects could be dose-dependent with benefits at low, and detrimental effects at high levels), astragalus and the rest of the healthy, but pro-adipogenic agents that can help obese individuals to stash away the tons of sugar and fat floating through their arteries are of little use.

              Against that background I want to close this post with a warning, or I should say a reminder of the the fact that the effects of PPAR-gamma are physiologically important (e.g. prevention of lipotoxicity, Medina-Gomez. 2007) and go beyond "just making you fat" in how it would be worth striving to suppress it altogether is thus questionable (suggested read: CLA Destroys Body Fat). Since for all of the previously discussed agents that have in-vivo data to support their efficacy have postivite, not negative "side effects" (think of curcumin, gingerol, ginseng, etc.), it is yet unlikely that the use of reasonable amounts of one or a stack of many of them is going to harm you.

              Just keep in mind: The goal should be to keep the PPAR-gamma activity in check, not to annihilate it. Consequently you should not and cannot expect to be able to "eat whatever you want and still stay lean" by supplementing with any of the agents above. On the other hand, they can hardly be even less useful than the vast majority of currently available arsenal of OTC "fat burners" ;-)

              References:
              • Berry DC, Noy N. All-trans-retinoic acid represses obesity and insulin resistance by activating both peroxisome proliferation-activated receptor beta/delta and retinoic acid receptor. Mol Cell Biol. 2009 Jun;29(12):3286-96.
              • Berry DC, DeSantis D, Soltanian H, Croniger CM, Noy N. Retinoic acid upregulates preadipocyte genes to block adipogenesis and suppress diet-induced obesity. Diabetes. 2012 May;61(5):1112-21. 
              • Brown PN, Roman MC. Determination of hydrastine and berberine in goldenseal raw materials, extracts, and dietary supplements by high-performance liquid chromatography with UV: collaborative study. J AOAC Int. 2008 Jul-Aug;91(4):694-701.
              • Brun PJ, Yang KJ, Lee SA, Yuen JJ, Blaner WS. Retinoids: Potent regulators of metabolism. Biofactors. 2012 Dec 22. doi: 10.1002/biof.1056. 
              • Chen S, Li Z, Li W, Shan Z, Zhu W. Resveratrol inhibits cell differentiation in 3T3-L1 adipocytes via activation of AMPK. Can J Physiol Pharmacol. 2011 Nov;89(11):793-9.
              • Gomes AP, Duarte FV, Nunes P, Hubbard BP, Teodoro JS, Varela AT, Jones JG, Sinclair DA, Palmeira CM, Rolo AP. Berberine protects against high fat diet-induced dysfunction in muscle mitochondria by inducing SIRT1-dependent mitochondrial biogenesis. Biochim Biophys Acta. 2012 Feb;1822(2):185-95.
              • Hisada K, Hata K, Ichida F, Matsubara T, Orimo H, Nakano T, Yatani H, Nishimura R, Yoneda T. Retinoic acid regulates commitment of undifferentiated mesenchymal stem cells into osteoblasts and adipocytes. J Bone Miner Metab. 2013 Jan;31(1):53-63.
              • Hong JH, Hwang EY, Kim HJ, Jeong YJ, Lee IS. Artemisia capillaris inhibits lipid accumulation in 3T3-L1 adipocytes and obesity in C57BL/6J mice fed a high fat diet. J Med Food. 2009 Aug;12(4):736-45.
              • Hu Y, Davies GE. Berberine increases expression of GATA-2 and GATA-3 during inhibition of adipocyte differentiation. Phytomedicine. 2009 Sep;16(9):864-73. doi: 10.1016/j.phymed.2009.03.002. Epub 2009 Apr 28.
              • Huang C, Zhang Y, Gong Z, Sheng X, Li Z, Zhang W, Qin Y. Berberine inhibits 3T3-L1 adipocyte differentiation through the PPARgamma pathway. Biochem Biophys Res Commun. 2006;348:571–578.
              • Hwang JT, Lee MS, Kim HJ, Sung MJ, Kim HY, Kim MS, Kwon DY. Antiobesity effect of ginsenoside Rg3 involves the AMPK and PPAR-gamma signal pathways. Phytother Res. 2009 Feb;23(2):262-6.
              • Joo JI, Kim DH, Choi JW, Yun JW. Proteomic analysis for antiobesity potential of capsaicin on white adipose tissue in rats fed with a high fat diet. J Proteome Res. 2010 Jun 4;9(6):2977-87.
              • Juman S, Yasui N, Okuda H, Ueda A, Negishi H, Miki T, Ikeda K. Caffeic acid phenethyl ester inhibits differentiation to adipocytes in 3T3-L1 mouse fibroblasts. Biol Pharm Bull. 2010;33(9):1484-8.
              • Ka SO, Kim KA, Kwon KB, Park JW, Park BH. Silibinin attenuates adipogenesis in 3T3-L1 preadipocytes through a potential upregulation of the insig pathway. Int J Mol Med. 2009 May;23(5):633-7.
              • Kim SK, Kong CS. Anti-adipogenic effect of dioxinodehydroeckol via AMPK activation in 3T3-L1 adipocytes. Chem Biol Interact. 2010a Jun 7;186(1):24-9.
              • Kim KJ, Lee OH, Lee BY. Fucoidan, a sulfated polysaccharide, inhibits adipogenesis through the mitogen-activated protein kinase pathway in 3T3-L1 preadipocytes. Life Sci. 2010b May 22;86(21-22):791-7.
              • Kim GS, Park HJ, Woo JH, Kim MK, Koh PO, Min W, Ko YG, Kim CH, Won CK, Cho JH. Citrus aurantium flavonoids inhibit adipogenesis through the Akt signaling pathway in 3T3-L1 cells. BMC Complement Altern Med. 2012 Apr 3;12:31.
              • Kong CS, Kim JA, Eom TK, Kim SK. Phosphorylated glucosamine inhibits adipogenesis in 3T3-L1 adipocytes. J Nutr Biochem. 2010 May;21(5):438-43. 
              • Lee YS, Kim WS, Kim KH, Yoon MJ, Cho HJ, Shen Y, Ye JM, Lee CH, Oh WK, Kim CT, et al. Berberine, a natural plant product, activates AMP-activated protein kinase with beneficial metabolic effects in diabetic and insulin-resistant states. Diabetes. 2006;55:2256–2264. 
              • Lee YK, Lee WS, Hwang JT, Kwon DY, Surh YJ, Park OJ. Curcumin exerts antidifferentiation effect through AMPKalpha-PPAR-gamma in 3T3-L1 adipocytes and antiproliferatory effect through AMPKalpha-COX-2 in cancer cells. J Agric Food Chem. 2009 Jan 14;57(1):305-10.
              • Lee H, Kang R, Yoon Y. SH21B, an anti-obesity herbal composition, inhibits fat accumulation in 3T3-L1 adipocytes and high fat diet-induced obese mice through the modulation of the adipogenesis pathway. J Ethnopharmacol. 2010 Feb 17;127(3):709-17.
              • Liu Y, Wang WJ, Chen WH, Yin J. [Effects of Astragalus polysaccharides on proliferation and differentiation of 3T3-L1 preadipocytes]. Zhong Xi Yi Jie He Xue Bao. 2007 Jul;5(4):421-6.
              • Liu Y, Lou SY, He YM. [Effects of berberine on cell proliferation, peroxisome proliferation activated receptor gamma, CAAT/enhancer binding protein mRNA and protein expression in 3T3-L1 pre-adipocytes]. Zhongguo Zhong Xi Yi Jie He Za Zhi. 2008 Nov;28(11):1005-9.
              • Medina-Gomez G, Gray SL, Yetukuri L, Shimomura K, Virtue S, Campbell M, Curtis RK, Jimenez-Linan M, Blount M, Yeo GS, Lopez M, Seppänen-Laakso T, Ashcroft FM, Oresic M, Vidal-Puig A. PPAR gamma 2 prevents lipotoxicity by controlling adipose tissue expandability and peripheral lipid metabolism. PLoS Genet. 2007 Apr 27;3(4):e64.
              • Mukherjee R, Yun JW. Bromocriptine inhibits adipogenesis and lipogenesis by agonistic action on α2-adrenergic receptor in 3T3-L1 adipocyte cells. Mol Biol Rep. 2013 May;40(5):3783-92.
              • Nimitphong H, Holick MF, Fried SK, Lee MJ. 25-hydroxyvitamin D₃ and 1,25-dihydroxyvitamin D₃ promote the differentiation of human subcutaneous preadipocytes. PLoS One. 2012;7(12):e52171.
              • Oben JE, Ngondi JL, Blum K. Inhibition of Irvingia gabonensis seed extract (OB131) on adipogenesis as mediated via down regulation of the PPARgamma and leptin genes and up-regulation of the adiponectin gene. Lipids Health Dis. 2008 Nov 13;7:44.
              • Park DY, Ahn YT, Huh CS, Jeon SM, Choi MS. The inhibitory effect of Lactobacillus plantarum KY1032 cell extract on the adipogenesis of 3T3-L1 Cells. J Med Food. 2011 Jun;14(6):670-5.
              • Park UH, Jeong HS, Jo EY, Park T, Yoon SK, Kim EJ, Jeong JC, Um SJ. Piperine, a component of black pepper, inhibits adipogenesis by antagonizing PPARγ activity in 3T3-L1 cells. J Agric Food Chem. 2012 Apr 18;60(15):3853-60.
              • Sagara C, Takahashi K, Kagechika H, Takahashi N. Molecular mechanism of 9-cis-retinoic acid inhibition of adipogenesis in 3T3-L1 cells. Biochem Biophys Res Commun. 2013 Mar 29;433(1):102-7. 
              • Seo JB, Choe SS, Jeong HW, Park SW, Shin HJ, Choi SM, Park JY, Choi EW, Kim JB, Seen DS, Jeong JY, Lee TG. Anti-obesity effects of Lysimachia foenum-graecum characterized by decreased adipogenesis and regulated lipid metabolism. Exp Mol Med. 2011 Apr 30;43(4):205-15.
              • Thounaojam MC, Jadeja RN, Ramani UV, Devkar RV, Ramachandran AV. Sida rhomboidea. Roxb Leaf Extract Down-Regulates Expression of PPARγ2 and Leptin Genes in High Fat Diet Fed C57BL/6J Mice and Retards in Vitro 3T3L1 Pre-Adipocyte Differentiation. Int J Mol Sci. 2011;12(7):4661-77.
              • Tzeng TF, Chang CJ, Liu IM. 6-Gingerol Inhibits Rosiglitazone-Induced Adipogenesis in 3T3-L1 Adipocytes. Phytother Res. 2013 Mar 21.
              • Wang JM, Yang Z, Xu MG, Chen L, Wang Y, Su C, Tao J. Berberine-induced decline in circulating CD31+/CD42- microparticles is associated with improvement of endothelial function in humans. Eur J Pharmacol. 2009;614:77–83.
              • Yuan HD, Yuan HY, Chung SH, Jin GZ, Piao GC. An active part of Artemisia sacrorum Ledeb. attenuates hepatic lipid accumulation through activating AMP-activated protein kinase in human HepG2 cells. Biosci Biotechnol Biochem. 2010;74(2):322-8.
              • Yuan HD, Piao GC. An active part of Artemisia sacrorum Ledeb. inhibits adipogenesis via the AMPK signaling pathway in 3T3-L1 adipocytes. Int J Mol Med. 2011 Apr;27(4):531-6.

              Shock Your Calves to Grow Stronger & Recover Faster: $650 Electromyostimulation Device Works, But Is It Worth It?

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              You will have heard about "calf shocker" routines, but would you have imagined that it takes electro shocks?
              I don't know how often I've been writing about the truth and fallacy of the good old saying "no pain, no gain", here at the SuppVersity. And while it certainly has its merit for the faint-hearted, the notion that "pain" will entail "gain" is fallacious, also because it suggests that allowing for adequate recovery would be inferior to digging a deep black "hole of pain" (suggested read: "The SuppVersity Athlete's Triad Series").

              And while I know that you know that this ain't the way to go, I am also honest enough to admit that I often catch myself pondering the incorporation of intensity techniques, additional exercises or some fat burning minutes of HIIT, but rarely thinks about the undeniable benefits of things like the hot baths for pre-regeneration and other means to speed up recovery (learn more) ...

              Recovery, ceratinly not the #1 topic for gym-conversations

              I am not sure, whether or not today's SuppVersity article on the surprising benefits of electrical muscle stimulation (EMS) during the recovery period is going to change that, but it certainly adds another interesting option to my toolbox. After all, the improvements in strength and the researchers from the Quincy College the University of Texas at San Antonio, the Hospital  of the University of Pennsylvania, the National Strength and Conditioning Association and the University of Florida present in their most recent paper in the April issue of Official Research Journal of the American Society of Exercise Physiologists would suggest that it will not just allow me to return to the gym earlier, but will also make me stronger.
              The "Marc Pro(TM)" is not just the $650 device used in the study, it is also one of most frequently used words in the study at hand... what? No, there is no conflict of interest declared, but I believe the Journal of the American Society of Exercise Physiologists does not even require that.
              The study of which I'd better tell you in advance that is has a slight smack of "product pimping", because it mentions the specific EMS device, the Marc Pro(TM) not just in the methods section, but also in the title (Westcott. 2013), involved two trials with comparably large groups (n=43 / n=62) of male and female subjects in their best years (mean age: 61.3 / 61.7 years).

              10 weeks 2x per week full body + 4x per week EMS

              Suggested read: "Fast Paced High-Resistant Explosive Circuit Training Burns More Fat and Builds More Muscle Than Classical Weight Training. Trainees Dropped 1.5% Body Fat and Gained 3 Pounds of Lean Mass in 8 Weeks." - Don't discard the value of a fast paced full body resistance training (read more).
              During both 10-week trials all participants trained twice a week for 60 minutes. The training comprised a medium-paced circuit training on 13 Nautilus machines including leg extension, leg curl, leg press, hip abduction/adduction, chest press, seated row, shoulder press, lat pull down, low back extension, abdominal flexion, torso rotation, neck flexion/extension and calf press. Each exercise was performed only once and the weight was progressively increased by 1% whenever the subjects were able to perform more than the prescribed number of 8-12 reps at a well-controlled pace of 3s for both the concentric and eccentric portion of the exercise. In addition to the standard strength workout, the subjects performed ~20 min of recumbent cycling at 70 to 80% of predicted maximum heart rate) and ~5 min of major muscle group stretching exercises towards the end of each workout. 

              While all subjects underwent the same supervised workout program, only 50% of them were assigned to the EMS group, and instructed to self-administer 1h of electrical muscle stimulation to the calf muscles of both legs four times a week. With the two obligatory exercise sessions, this allowed for two "recovery sessions" in-between workouts.
              Figure 1: Changes (rel. to baseline) in the EMS and control groups after 10-weeks of training (Westcott. 2013)
              As the data from the pre- and post strength 3-RM tests and the results of the fatigue questionnaire, a 9-point rating scale with anchors of 1 (never experience feelings of calf muscle fatigue) and 9 (always experience feelings of calf muscle fatigue) in figure 1 goes to show you this routine was surprisingly effective in both increasing the effective gains in calf muscle strength and decreasing the workout induced fatigue.

              So what's the mechanism here?

              It is not exactly likely that the medium intensity EMS targets the IGF-1 + muscle growth promoting PGC-1 a4 isoform (learn more)
              The exact mechanism for the benefits, the researchers observed in both experiments, is not fully understood, they stand in line with previous research mostly by members of the same research group (Parker. 2003; Kemmler. 2010; Wescott. 2012; DiNubile. 2011; Girold. 2012) which suggests that the application of electical muscle stimulation "causes positive cellular responses such as nitric oxide (NO) production, fluid shifts, protein clearance, and angiogenesis" and allow for the hypothesis that additional, isokinetic contractive stimulus has the potential to induce mRNA transcriptional proteins such as PPAR gamma co-activator (PGC)-1 alpha (learn more) and the vascular endothelial growth factor VEGF.

              Against that background, the scientists assumption that [...]the enhanced muscle recovery associated with [...] electrical stimulation may be due to increased microcirculation, muscle loading, and angiogenesis." (my emphasis in Westcott. 2013) appears reasonable and would warrant their conclusion that EMS which is hitherto used mainly by professional athletes (esp. football players) "may also be beneficial for less fit individuals who experience  prolonged periods of recovery or uncomfortable levels of muscle fatigue after exercising." (Westcott. 2013)




              I openly admit: Hot baths are still not a part or my "pre-recovery" routine, but I like some cheap and effective walking on an incline on the day after a leg workout.
              Bottom line: Depite the overall promosing results of the study at hand, I'd still have a few questions as far as (a) the usefulness, (b) the alternatives and (c) the superiority of EMS therapy as a means to accelerate recovery and adaptation actually is. A handful of studies, a shiny website and the argument that it does works in recreational, or as the scientists write "less fit" trainees, as well as in pro-athletes won't make me pay approx. $650 for an "electro shocker".  This is all the more true in view of the fact that regular aerobic exercise and HIIT (learn how to set up a routine) will also promote PGC1-alpha and VEGF and could - appropriately dosed - probably elicit similar effects.

              Apropos "effects" you should not forget that the parameters the scientists measured are actually both performance parameters. Regardless of the fact that the latter is called "fatigue", the fatigue after a standardized workout is mainly determined by your central and peripheral conditioning. It is thus obvious that you should be able to reduce the post-workout fatigue by any means of additional exercise that does not overtax the system - this may also involve enhanced recovery, but the enhancement is a function of physiological adaptations and not externally applied electrical stimuli.

              Against that background, the only advantage of EMS over "conscious", i.e. brain-controlled contractions such as a 3x3min (x2 for each leg) session of single-legged body-weight calf-raises or even a simple walk in the park with a deliberate emphasis on calf-involvement would produce, appears to be that it would ease the burden on the central nervous system. Whether that's essentially necessary for the average trainee is however questionable; and though I would probably be slightly irritated, if you called me "an average trainee", I for my part will stick to some recuperative walking on an incline to promote calf-recovery.

              References:
              • DiNubile N, Westcott W, Reinl G, et al. The Marc  Pro TM device is a novel paradigm shift in muscle conditioning, recovery and performance:  Induction of nitric oxide (NO) dependent enhanced microcirculation coupled with angiogenesis mechanisms. JEPonline. 2011;14(5): 10-19.
              • Girold S, Jalab C, Bernard O, et al. Dry-land strength training vs. electrical stimulation in sprint swimming performance. J Strength Cond Res. 2012;26(2):497-505.
              • Kemmler W, Schliffka R, Mayhew JL, von Stengel S.  Effects of whole-body electromyostimulation on resting metabolic rate, body composition, and maximum strength in postmenopausal women:  The training and electrostimulation  trial. J Strength Cond Res. 2010;24(7):1880-1887.
              • Parker MG, Bennett MJ, Hieb MA, et al. Strength response in human femoris muscle during 2 neuromuscular electrical stimulation programs.  J Orthop Sports PhysTher. 2003:33(12): 719-726.
              • Westcott WL, Chen T, Neric FB, et al.  The Marc Pro TM device improves muscle performance and recovery from concentric and eccentric exercise in duced muscle fatigue in humans: A pilot study.  JEPonline. 2011;14(2):55-67. 
              • Westcott W, Han D, DiNubile N, Neric F, Loud RLR, Whitehead S, Blum K. Effects of Electrical Stimulation Using the Marc Pro(TM) Device during the Recovery Period on Calf Muscle Strength and Fatigue in Adult Fitness Participants. JEPOnline. April 2013; 16(2): 40-49.

              Triphasic Nutrient Supplement W/ Caffeine, Aminos, Carbs, Creatine & All the Usual Suspects Allows For Higher Training Volume, Lowers Cortisol & Dampens Muscle Damage

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              Do you really need the whole pre-, intra-, post workout supp-arsenal to benefit from your workouts?
              Finally, another workout supplementation study! Yeah, I know you are already suffering the side-effects of withdrawl, but it's just a couple of lines and you will feel relieve - thanks to Stephen P. Bird and his colleagues from the Charles Sturt University in Bathurst, Australia, whose latest paper is about to be published in one of the upcoming issues of Nutrition Research (Bird. 2013). And as if that was not already enough, the participants were strength trained athletes, the  physical activity and diet were standardized according to pre-recorded habits and the supplementation protocol was extensive! With pre-, intra- and post-workout supplements it was exactly what many people today seem to believe was necessary to see any gains

              ... but is that true? Do you really need all that stuff?

              The Australian researchers probably had a similar question in their minds, when they recruited their 15 strength-trained male field and court sport athletes (mean age 21.7years; 1-RM squat 133.0kg, bench press, 94.7 and 3.1 ± 0.3 years of strength training experience) and randomized them to ingest either a placebo supplement or a supplement "stack" consisting of 15g of Musashi Reactivate Hardcore before, 30g of Musashi Elevator during and 50g of Musashi SPORTS after the workout.
              Table 1: Ingredient profile of the "tri-phasic" peri-workout supplement;  the placebo contained an aspartame based flavor that matched the taste of the active supplement (based on data from Bird. 2013)
              In view of the fact that this probably sounds similarly "Chinese" to you as to me, I've provided you with a tabular overview of the ingredient profile of what the scientists call a "triphasic multinutrient supplement". Basically nothing you would not find in the line-up of every major supplement company: Some carbs, EAAs, creatine, beta alanine and AAKG, caffeine and b-vitamins (not listed in table 1) before workout, carbs, EAAs and creatine intra-workout and the obligatory protein- (whey/casein mix), carb-combination garnished with some creatine and glutamine after the workout. Add in some salt, magnesium and potassium and you can even at the as of late obligatory "contains electrolytes" blend and you are good to go.

              Acute effects = stat. significant, long-term physiological significance = ?

              Caffeine (pre, only), creatine, EAAs, whey (post, only) and even beta alanine and AAKG, the additional carbhydrates, ... all that should do something right? Yep, you are of course right it should. After all people are paying with their hard-earned money for it!
              Figure 1: Serum markers glucose, AST, CRP, CK, cortisol and testosterone before, during, right after, 30min after and 24h after the workouts with the active (SUPP) or placebo beverage (PLA); data expressed relative to group-specific pre-values (Bird. 2013)
              That being said, the data in figure 1 provides at least initial relieve. There are statistically significant effects for almost all measured hormonal parameters,  if we compare the supplemented with the non-supplemented trials in this double-blind, placebo (PLA)-controlled, crossover study.

              Figure 2: Supplement & blood draws (top); overview of the exercises, set x rep scheme and equipment used in the lower body workout (Bird. 2013)
              The study design allowed for a 7-day washout before the "crossing" took place and those participants who had been randomized to the supplement group after an obligatory 28-day washout to clear all previously used supplements (and what not ;-) from the system had to perform the test workout (4 sets of 8 to 15 repetitions for 5 lower-body exercises; see figure 2) with/without the "triphasic nutrient supplement" on top of their 33.6 ± 1.8 kcal/kg body mass diet (macros: 3.8g/kg, 1.5g/kg carbs and protein, respectively.

              The supplement, or rather the supplements, had to be ingested 15 minutes preexercise, in small, regular doses during the exercise, and the whole 300ml of their post-workout drink right after the workout. and thus according to the manufacturers suggestions.

              Aside from the hormonal and inflammatory response (see figure 1) to the workout the scientists also measured the muscular performance and perceptual response during the workouts:
              Figure 3: Perceptual measures of exertion & muscle soreness (Bird. 2013)
              • the total training volume was higher for SUPP (15 836 ± 518 kg⋅repetitions) compared with PLA (14 390 ± 491 kg⋅repetitions) (P <.05;d = 0.70); 
              • countermovement jump peak power(CMJ) did not differ between groups at any timepoint (P> .05;d= 0.05-0.18); in the SUPP group there was however a trend (P= .08;d= 0.32) for increased countermovement jump peak power was yet observed on the third of the four tests 30min after the workout (exact timing see figure 2, top)
              • the global rate of perceived exertion (RPE) did increase after the workout in both groups, and was higher 30min after the supplement trial (P < .01; d= 0.89)
              • the perceptual responses for muscle soreness was elevated and did not differ between treatments
                after the workouts
              However, even for the statistical significant inter-group difference in msucle perceived exertion, the overall effect size is pretty small. It is therefore by no means "obvious", whether the 10% lower perceived exertion during the placebo trial which is probably a direct result of the +10% increase in total training volume, anyways, is of physiological relevance.



              So what do we make of these results? On the one hand it is unquestionably true, that the peri-workout supplementation (I refuse to keep using the hilarious sciency expression "triphasic") did increase the total workout volume, It is also true that it did lower the cortisol increase and produced lower areas under the curve for creatine kinase, but it also lowered the testosterone response to the workout (that the post-workout increase in testosterone is not a legitimate predictor of muscle growth is something you should now, after countless articles on the matter, be aware of; read more about testosterone).

              Whey is more insulinogenic than white bread and creatine could make you fatt True for the 1st, remotely possible for the 2nd! And still both simply work....
              Much ado about nothing? No, not really. While the hormonal changes are more or less irrelevant an increase in total volue that does not entail greater muscle damage could in fact make a difference that's not just statistically, but also physiologically significant.

              What I do yet doubt is that the same results could not have been achieved with a cup of oatmeal, water and protein powder 1h before the workout, a coffee right before the workout and 3-5g of creatine, two bananas and a regular whey protein afterward. All you would have to buy then is a pouch of whey and a 500g jar of creatine monohydrate, which will last you for months. Both SuppVersity supplement staples, as you know and actually among the few supps with physiologically significant effects almost every trainee can benefit from... and did I mention that they are dirt cheap and can be combined with real foods?

              References:
              • Bird SP, Mabon T, Pryde M, Feebrey S, Cannon J. Triphasic multinutrient supplementation during acute resistance exercise improves session volume load and reduces muscle damage in strength-trained athletes. Nutrition Research. April 2013 [EPub ahead of print].

              2-3g of β-hydroxy-β-methylbutyrate (HMB) Slam the Brake on Muscle Damage and Hit the Gas Paddle on Muscle Growth, Race Performance & Fat Loss in Elite Canoeists

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              With their intense strength + endurance training in the pre-contest phase canoeists may be among those athletes who benefit most from the muscle protectant anti-catabolic advantage of HMB.
              It's funny how the leucine metabolite β-hydroxy-β-methylbutyrate (HMB) disappeared into oblivion in the early 2000s, only to rise like Phoenix from the ashes, now that the 21st century is in its teenage years (Thomson. 2009; Wilson. 2013a,b) From previous SuppVersity news (read more about HMB), you know that β-hydroxy-β-methylbutyrate has slightly less pronounced anabolic, yet better anti-catabolic effects than its precursor leucine. You may also remember that many of the studies with beneficial outcome have been conducted on elderly or sick subjects (e.g. May. 2002; Vukovich. 2001) and that these studies showed (more or less across the board) favorable effects that could not be replicated in younger and/or trained subjects (e.g. Slater. 2001).

              Now, despite the fact that it seems logical that HMB would have a greater "muscle building effect" for those of us who are - due to their age or other confounding factors - more prone to muscle protein catabolism than for someone like a competing elite canoeist in the strength phase of his seasonal training cycle - or, without further beating around the bush, the average 78.5kg, 11% body fat male participant of a study, the results of which have recently been published in the online edition of the Journal of Exercise Physiology (Ferreira. 2013).   

              "Old school", but neither out-of-date nor "for the oldies only"

              To "determine whether HMB supplementation at 37.5 mg·kg/d during intense endurance training affects markers of catabolism, body composition, and sports performance in kayak athletes’ high performance sprints" (Ferreira. 2013), the scientists from the Laboratory Cell Metabolism (LABMETAB) and the Laboratory Motor Behavior at the Federal University of Parana in Curiba, Brazil, randomized their 20 subjects to receive either a placebo (n = 6) or the active treatment dose of 37.5 mg·kg (2.5-3.0g; depending on body weight) "classic" powdered calcium HMB per day during the six strength training weeks of their prep. To minimize any non-supplementation-related influences, ...
              HMB & leucine could also help you shed fat & live longer (learn more)
              "[a]ll meals were kept under strict control by the nutritionist. None of the subjects was allowed the use of creatine and/or beta-agonists for at least 8 wks prior to the study. [Furthermore, a]ll subjects (i.e., athletes) were instructed to not ingest other dietary supplements with ergogenic effects during the study." (Ferreiara. 2013)
              As the data in figure 1 goes to show you, the use of the supplement, which was to be taken in three seperate doses equally spread across the day (morning, afternoon, and evening), had statistical significant effects on the the results of the subjects’ training sessions.

              Training like the "pros": Frequent high volume training

              The workloads of the latter had been individualized and averaged ~ 6 hr/wk of resistance training (1 to 3 sets of 2 to 8 repetitions at intensities ranging from 80 to 95% of 1 RM) on Monday, Wednesday, and Friday plus 10 hr//wk of specific sprint technique training in the boat. Overall, the subjects were thus training two times a day for a total of 11 training sessions a week (bear that in mind, because it will be important in the bottom line). All trainings sessions ha been conducted under the supervision of certified coaches by CBC and subjects who missed a training session were required to make them up in accordance with the procedures of the study.
              Figure 1: Relative changes in body composition, blood lipids, race performance, creatine kinase (CK), lactate dihydrogenase and creatinine (Ferreira. 2013)
               All subjects underwent monthly testing of venous blood samples, body composition analysis, and specific testing for performance in the water (boat) in the course of which the scientists observed that the paddlers in the HMB group showed...
              • significantly more pronounced improvements in body composition than the subjects who had been randomized to the placebo group (-10.26% reduction in body fat % vs. +0.21% in the placebo group), and
              • likewise highly significant -34.4% decreases in the skeletal muscle specific iso-form of the "muscle damage gauge" creatine kinase (CK-MM; -34.44% vs. + 40.42% in the placebo and
              • pronounced reductions in lactate dehydrogenase (LDH; -20.92% vs. -1% in the placebo group), as well as
              Moreover, the race-times of the participants in the active arm of the study improved by 2%, while the elite paddlers who consumed the placebo supplement increased their race-performance by only 1%



              The green dots on the left and right of the blue myonuclei are satellite cells that thrive on high(er) volume routines (learn more)
              Bottom line: The overall image that emerges is clear. β-Hydroxy-β-Melthylbutyrate (HMB) works! And the improvements the Brazilian researchers observed in their 20 highly trained subjects were so pronounced that there is no debating with their conclusion that the "improvement in strength and development of muscular hypertrophy [may help] not only athletes but the general population".

              For us, all devoted trainees who are well-versed in the previous literature on HMB, the most important conclusion to be drawn is yet that the early Y2K "muscle builder of the elderly" works for everyone, if - an this is the hypothetical part of the conclusion - the training regimen is intense enough to generate similar muscle damage as the relatively low volume, medium intensity resistance training protocols that were used in previous studies with older and mostly untrained subjects (e.g. Baier. 2009).

              Whether training twice a day and 10+ times a week is the way to go for everyone, does still remain questionable. After all, the fundamental rule that you cannot 'out-supplement' insufficient regeneration is still valid (learn more). This is particularly true in view of the fact that the majority of trainees is not as well-conditioned as the elite athletes in the study at hand. This does yet also mean that they will suffer similar eustress from lower volume / intensity / density workouts and could still benefit from 2-3g of HMB... I am yet still waiting for study to investigate how significant this effect is, when the subjects already use a pre-/post workout protein supplementation strategy as outlined in yesterday's post, but alas - this is no research request program.

              References:
              • Baier S, Johannsen D, Abumrad N, Rathmacher JA, Nissen S, Flakoll P. Year-long changes in protein metabolism in elderly men and women supplemented with a nutrition cocktail of beta-hydroxy-beta-methylbutyrate (HMB), L-arginine, and L-lysine. JPEN J Parenter Enteral Nutr. 2009 Jan-Feb;33(1):71-82. 
              • Ferreira HR, Rodacki ALF, Gill P, Tanhoffer R, Filho JF, Cláudio L.The Effects of Supplementation of β-Hydroxy-β-Melthylbutyrate on Inflammatory Markers in High Performance Athletes. Journal of Exercise Physiology. 2013; 2:53-63.
              • May PE, Barber A, D'Olimpio JT, Hourihane A, Abumrad NN. Reversal of cancer-related wasting using oral supplementation with a combination of beta-hydroxy-beta-methylbutyrate, arginine, and glutamine. Am J Surg. 2002 Apr;183(4):471-9.
              • Slater G, Jenkins D, Logan P, Lee H, Vukovich M, Rathmacher JA, Hahn AG. Beta-hydroxy-beta-methylbutyrate (HMB) supplementation does not affect changes in strength or body composition during resistance training in trained men. Int J Sport Nutr Exerc Metab. 2001 Sep;11(3):384-96. 
              • Slater GJ, Jenkins D. Beta-hydroxy-beta-methylbutyrate (HMB) supplementation and the promotion of muscle growth and strength. Sports Med. 2000 Aug;30(2):105-16. 
              • Thomson JS, Watson PE, Rowlands DS. Effects of nine weeks of beta-hydroxy-beta- methylbutyrate supplementation on strength and body composition in resistance trained men. J Strength Cond Res. 2009 May;23(3):827-35. 
              • 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.
              • Wilson JM, Lowery RP, Joy JM, Walters JA, Baier SM, Fuller JC, Stout JR, Norton LE, Sikorski EM, Wilson SM, Duncan NM, Zanchi NE, Rathmacher J. β-Hydroxy-β-methylbutyrate free acid reduces markers of exercise-induced muscle damage and improves recovery in resistance-trained men. Br J Nutr. 2013a Jan 3:1-7.
              • Wilson JM, Fitschen PJ, Campbell B, Wilson GJ, Zanchi N, Taylor L, Wilborn C, Kalman DS, Stout JR, Hoffman JR, Ziegenfuss TN, Lopez HL, Kreider RB, Smith-Ryan AE, Antonio J. International Society of Sports Nutrition Position Stand: beta-hydroxy-beta-methylbutyrate (HMB). J Int Soc Sports Nutr. 2013b Feb 2;10(1):6.

              Adelfo Cerame's Beach Ready Program: A Blueprint to Shed The Winterfat in Time. Sample Workout + Diet Guide

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              The beach season is almost at the ready... what about you?
              It's another of those "every other Thursdays" and after realizing that even after months of the same routine not everyone out there has gotten that these are the days, when Wheelchair IFBB Pro Adelfo Cerame is doing the lion's share of the work here at the SuppVersity and I (=Adel) am just editing the stuff Adelfo shot me via email earlier today. I write an introduction (the words you are are reading just now) and add a short preview on what you can expect from the thursdaily 1PM (ET) Science Round Up on the Super Human Radio Network (listen live!) and hit the "publish" button.

              Adelfo Cerame's Beach Ready Program: A Blueprint to Shed The Winterfat in Time

              Summer is just around the corner, and I’m positive that the majority of you will be preparing those beach bodies within the next couple of months. So while you guys and gals are trying to get lean and mean and shredded for the summer, I will be fighting the inevitable and doing the opposite. Lol!

              Adelfo's current off-season form is probably better than the 2beach body" of most of the posers on Jersey Shore ;-)
              So I thought it would be a good idea to share my thoughts and opinions on how you can set up a sensible training and nutrition regimen to get you ready for those upcoming hot summer nights!

              I. Training - Keep it simple. 

              There really is no need to over-analyze or overthink your training routine, just because you are now "cutting". "K.I.S.S." (=keep it stupidly simple) the tried and proven:
              Focus on core/compound exercises such as your bench, squats, dead lifts, and horizontal rows like a bent-over BB row and maybe 2-3 other exercises to supplement those core exercises depending on the focal point on that day.
              Here’s a sensible training regimen I’ve put together that’s simple and straightforward. It has a sensible volume (no more than 5-6 exercise), but is condensed enough to be challenging and help you maintain your muscles while your diet is taking care of the midriff bulge you can't seriously want to be carrying along the shore:
              As you can see you will be kicking your training week off with two "volume workout" and follow them up with workout 3 and 4, both of which have a strength focus.
              It goes without saying that adequate rest is imperatively needed before and in-between the 5x5 strength day - after all, you're going to be doing some heavy lifting on those days.

              Do you do (additional) cardio? If you have been following my posts here at the SuppVersity for quite some time, now, you will be aware that I am not a fan of cardio.

              With cardio more ain't more. If you do too much you can actually hamper not promote your progress (learn more)
              Especially the notion that you can "run away" from dietary mistakes, or "outtrain a crappy diet" as Adel likes to call it is simply hilarious and will inevitably lead to failure. In other words, you should actually be able to answer the cardio question, yourself.

              With cardio for fat loss, doing less is more. Therefore you'll do the least amount that will allow you to make continuous progress towards your beach body goal. Reevaluate your progress on a weekly basis and decide whether it is really necessary to up your cardio volume.

              I would start with 0-1 cardio sessions per week and just make adjustments depending on your progress week by week. (Weight, food intake…) but don’t run yourself to the dirt neither.

              How much weight so you pick? Since we’re trying to K.I.S.S. the chubbiness goodbey, you're simply going by how you feel: Pick a weight heavy enough that you can bang out the given reps yet challenging enough… So how do we do that?
              • high volume days - pick a weight heavy enough that you probably will have 2-3 reps left in the tank - obviously after you've completed the number of prescribed reps
              • strength days: pick a weight heavy enough that you probably will have 1 more rep left in the tank or will be able to exactly do just the given rep range.
              In a way, it is like using an RPE scale (learn more) - with a lot more leeway, though and without the constant revision of RPE-numbers from workout to workout or even exercise to exercise.

              A brief note to those looking for detailed diet + training counseling: Adelfo also offers coaching services via email. You know that he happily answers all general questions in the comments, here at the SuppVersity, but I guess you will also understand that he cannot write an individual training plan for everyone who asks politely. So, if you want more than just "rules of thumbs" and "general guidelines", reach out to him via Facebook.
              Why does the routine look like that?

              I’ve become a real fan of high volume/strength training splits nowadays, and in my opinion they can be very beneficial whenever you are trying to improve your body composition while maintaining or even building your baseline strength and muscular endurance. To put it in simpler terms, you need to be strong in order for your body to handle the workload and in turn your body will have to compensate for the increased workload by building new muscle tissue, so it kind of makes sense to me that by combining a hypertrophy style training regimen with a strength split you can get the best of both worlds.

              A typical BB style workout combined with a simple strength training protocol like 5x5 is a pretty simple model/split to follow. It's self explanatory and you don't have to put much thought into it. Just pick a heavy weight that you can lift for the prescribed 5 sets of 5 reps (5x5), and when that load begins to feel "light", you increase the weight - it's as simple as that, but guess what: It's about as effective ;-)

              Again this workout is not set in stone, you can make tweaks as you see fit but this is just to give you an idea of how simple it can be to structure a training regimen for yourself without have to over analyze and out think yourself

              II. Diet - Nutritional guidelines to lose fat not just weight

              You can lose weight on just about any type of diet just as long as you are in a negative energy balance. However, if you are trying to lose fat, not just weight, want to maintain/build muscle and keep your gym performance and overall energy levels up, a sensible macronutrient composition is key.

              The latter entails that you get adequate amounts of protein, adequate amounts of fats and adequate amounts of carbohydrates in your diet and top that off with a reasonable amount of fiber. It stands to reason that this won't work, if you don't track your macronutrient & fiber intake and keep an eye on the micronutrients.

              A. Determine your overall calorie intake for the dieting phase

              Firstly, you will have to find identify your baseline energy requirements. This is best done by logging your food intake for 1-2 weeks and subtract ~20% from that to determine initial caloric intake for this cutting phase. Alternatively, you can use the following rule of thumb as a basic guideline to estimate your starting energy requirements: Multiply your body weight in lbs 9-12 kcal. If you’re already fairly lean it’s fine to just use your overall body weight. If you are on the heavier or obese end of the scale, you'd want to get as close to your lean body mass as possible

              While you are dieting your goal should always be to keep the maximal caloric intake that allows you to achieve a slow and gradual weight loss of around 1 lb./ week if you are a man and .5-1 pound/ week if you are a women. Don't beat yourself up if you don’t lose that pound on a given week and by don't make any drastic changes – remember everyone's body is different and we have to allow our bodies to adjust and adapt. That this process takes one week for some, while two or even three for others is only natural.

              What else do you have to take into account? A brief summary of the most important things to keep in mind as far asyour actual diet composition is concerned:

              (1) prioritize protein and fiber over carbs and fats

              (2) eat at least 2-3 servings of veggies/ day, and at least 1-2 servings of fruits/day

              (3) eat a variety of whole “nutrient dense” foods and limit your intake energy dense, but non-nutritive foods

              (4) use an 80/20 ratio of whole to processed "fun/cheat" foods

              Don't forget: Deviating from these rules ain't a good idea, but it's even worse to give up, once you've fallen off the wagon. You can take it for granted that it's going to happen. It's part of the game and as long as you get back on track asap, it won't break your neck ;-)
              B. Set a baseline protein intake - ca. 0.8-1g /lbs lean body mass
              You will have to consume roughly 1g of protein per 1lbs lean body weight. Again, if you are fairly lean, it does not really matter if you use your total body weight, but if you are still on the heavier side of the divide, try to estimate your lean mass or you will end up consuming way too much protein.

              C. Set a baseline fat intake - ca. 0.3-0.5g /lbs lean body mass

              If you’re on the higher BF% or on the heavier or obese end of the scale you'll probably benefit more of a high to moderate fat intake with low(ish) carbs (never go below 50g, though; more around the 100-150ish range). If you've already come a long way or have never had any real weight problems, though, low carb is not the way to go for you and you'd better go with a high(er) carbohydrate intake while keeping the fats on the low(er) to moderate end.

              D. Fill the rest of your macros up with carbs 

              Your daily carbohyrate intake can now easily be calculate by dividing the rest of your energy intake, i.e. total energy (A) minus protein intake (B x 4kcal) minus fat intake (C x 9kcal), by four, which is the kcal-content of 1g of carbohydrates. If you've calculated a 2,400kcal baseline energy intake for your "beach body diet", have a baseline protein intake of 200g and a baseline fat intake of 60g, this means that you have 2,400kcal -200g x 4kcal - 60g x 9kcal = 1080kcal, or 265g of carbs "left"

              E. Make sure to get your dietary fiber

              Actually you are almost done, now. The only thing that's left to consider is a baseline fiber intake of 35-50g/ day for men and 25-50g/ day for women.



              That's it: If you have never been counting your macros it may appear complicated, but if you compare this protocol to the complicated prescriptions of other "diets", you will see that you it's actually pretty easy. After you've done the math, the "only" thing you still got to do is being patient and consistent. As long as you do that, allow your body to adjust and adapt and don't pull the trigger to make adjustments too quickly, when all it would have taken was another week of consistent dieting, you will achieve your goal - and if you don't get to the "ridiculously ripped" zone this summer, you still have the next year to make further improvements ;-)

              Science Round-Up Seconds: A Focus on Intra-/Post Workout Stims, Carbs & Protein and Their Effects on Performance, Hydration, GH, Cortisol, Testosterone & Fatty Acid Oxidation

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              As mentioned on yesterday's show, small 100kcal packets are as much of a problem as large dinner plates and XXL meals (data based on Coelho do Vale. 2008)
              I want to start today's Seconds with a question: How did you like that Carl and I did not rush through the news-lineup as it was the case in previous episodes, but simply took our time to discuss the topics in depth an breadth, yesterday?

              Personally, I believe that this is much better than the accumulation of "buzzword" the show had become in the previous weeks due to my "study hunter and gatherer" drive - or, in other words, the mere mass of studies I wanted to pack into the show and Carl's desperate effort to cover them all.

              Would you agree? And what other changes / improvements would you like to see in the future? We are open for constructive criticism. You can't improve your game without it.

              Let's get to what did not fit into the show, then...

              The net result of the spending more time on each and every of the single items, or, to say it in the spirit of yesterday's show, a bit more mindfulness was obviously a much larger amount of Seconds for you to devour today. So, let's not waste any time and get right down to business:

              • Is 200mg of caffeine the optimum!?A 2008 study by Beavan et al., which involved 24 professional rugby players who were randomly assigned to receive 0, 200, 400 or 800mg of caffeine 1h before performing a standardized resistance training protocol (Beavan. 2008), found that contrary to what bro-science has been suggesting for years, the ingestion of the high amounts of caffeine (800mg) lead to a profound drop in the testosterone-to-cortisol ratio, while the lower doses of 200mg and 400mg of caffeine only blunted the performance hampering decline of cortisol half-way into the workout, while increasing the testosterone levels by 15%
                Caffeine or pseudoephedrine for performance enhancement? As far as improving you game is concerned, a recent study from the School of Sports Science at the department of Exercise and Health of the University of Western Australia was able to show that you are only wasting your time an money, if you are trying to up your cycling-time trial and thus probably every other HIT performance by ingesting the purported CNS stimulant pseudoephedrine (not to be confused with the "real deal"; cf Spence. 2013).

                Contrary to the comparatively low amount of 200mg caffeine, which allowed the 10 well-trained cyclists and triathletes who participated in the study improve their TT times in trial 2 of 3, all of which were performed on th same day, by statistically significant 57s, the ingestion of the WADA banned substance pseudoephedrine at a dosage of 180g would have cost them their license for nothing.
                Bottom line: Spare yourselves pseudoephedrine and other nasal/sinus decongestant belonging to the the class of phenethylamines and amphetamines (e.g. geranium). Even if others worked (for 1,3-dimethylamine this has never been proven in isolation), the long(er)-term detrimental effects they'll have on your central nervous system really isn't worth it.

              • Protein-enhanced Gatorade ain't worth your money -- If you are no ultra-endurance runner or at least marathon runner, you don't need, because you don't benefit intra-workout carbohydrate + electrolyte + protein (CEP) drinks for hydration.

                The results of a recent study from the Chinese University of Hong Kong show: A CEP solution containing 42g/L carbohydrate, 21g/L whey protein and 15.3 mmol/L sodium and 2.3 mmol/L potassium does not show "extra benefits for the maintenance of hydration status during 60 min cycling" (Sun. 2013)

                • Carbohydrate + protein drinks maximizes GH response to exercise -- Now that you know that it's not worth to guzzle on carbohydrate + electrolyte + protein drinks during a workout for hydration purposes, I guess I should tell you that doing the same (w/out the electrolytes, though), may still provide an athletic / anabolic edge. After all, another recently published study that was conducted at the School of Sport at the Department of Exercise and Health Sciences of the Loughborough University in Leicestershire, U.K (Betts.  2013) shows that the ingestion of a carbohydrate + protein mixture (CHO+PRO: 0.8 g sucrose per kg bod weight per hour + 0.3 g/kg/h whey protein isolate) in the 4h recovery period between two exhaustive treadmill runs at the same intensity augmented the growth hormone response by 60%(!) compared to the ingestion carbohydrate only (0.8 or 1.1g of sucrose /kg per hour).
                  Figure 1: Growth hormone (GH) and cortisol response to 2nd bout of exhaustive treadmill running with either 0.8 or 1.1g of sucrose /kg per hour (CHO, CHO-CHO) or  0.8 g/kg/h sucrose per kg bod weight per hour + 0.3 g/kg/h whey protein isolate (CHO+PRO; cf.
                  As the data in figure 1 goes to show you this increase in GH was accompanied by a 23% reduction in cortisol. With both, GH and cortisol being released in response to the depletion of muscle glycogen and impeding low blood glucose levels (Galbo. 1977), you could thus argue that protein (probably by its glucagon promting effects; cf. Claessens. 2008) programs the "anabolic glucose procurement plan".

                  Bottom line: Yet another reason for the often touted, yet tried and proven "Bananas + whey" = WIN! And that's not true wrt to the protein anabolic response after a workout, but also in view of the "anabolic" or I should probably say generally more favorable way of glucose procurement during subsequent workouts.

                • No, no and no! The ingestion of carbs before a HIIT workout will only increase, not blunt the fatty acid oxidation in the post-workout period.
                  Pre-workout carb ingestion does not blunt, but promote fatty acid oxidation after the workout -- In as much as this result may go against common bro-science that you must never consume any carbs before your workout if you are trying to lose body fat, it is actually in line with what I have been preaching before. The beneficial effects of AMPK come with the depletion of ATP and the rise in ADP (~used ATP), not with the constantly depleted ATP stores of a no-carbohydrate + protein only starvation diet. Or put more simply - a constant over-expression of AMPK negates all the benefits of it's cyclic up and down (cf. "The mTOR/AMPK Seesaw"; read more)

                  While the scientists from the Department of Nutrition & Metabolism at the Faculty of Health and Medical Sciences of the University of Surrey in Guildford, UK, did not observe statistically significant improvements in fatty oxidation due to the small study size (10 healthy untrained females; age 18–22 yr; BMI 22kg/m²), the pronounced decrease in RQ after 8-10x 60 second cycling bouts at 95 % VO2peak separated by 90 seconds recovery at 50 watts in 9 out of 10 participants (see figure 2) does speak itself: "In women, consuming carbohydrate before exercise may potentially be more beneficial for fat oxidation than consuming carbohydrate post-exercise" (Honnor. 2013).

                  Bottom line: The results of the study at hand, which stand in line with previous research by Fuchs et al. who presented their research in the Proceedings of the Nutrition Society one year before, re-emphasis the fallacious over-reliance of high fatty oxidation rates during a workout. The max. 60-90min in which you may burn slightly more fat, are simply negligible compared to the much longer post-workout period, where the ingestion of 59 g CHO before a HIIT workout did not blunt but promote fatty acid oxidation.



                Believe it or not, but that's it for today! If you are hungry for more, I suggest you either go to the SuppVersity Facebook Wall or listen to Casual Friday later today... actually, I found Gabriel's name, i.e.  "The Alisa Profumo Show", for the Friday edition of Super Human Radio show quite fitting ;-)

                      References:
                      • Beaven CM, Hopkins WG, Hansen KT, Wood MR, Cronin JB, Lowe TE. Dose effect of caffeine on testosterone and cortisol responses to resistance exercise. Int J Sport Nutr Exerc Metab. 2008
                        Apr;18(2):131-41.
                      • Betts JA, Stokes KA, Toone RJ, Williams C. Growth Hormone Responses to Consecutive Exercise Bouts with Ingestion of Carbohydrate plus Protein. Int J Sport Nutr Exerc Metab. 2013 April. 
                      • Claessens M, Saris WH, van Baak MA. Glucagon and insulin responses after ingestion of different amounts of intact and hydrolysed proteins. Br J Nutr. 2008 Jul;100(1):61-9.
                      • Coelho do Vale R, Pieters R, Zeelenberg. Flying under the Radar: Perverse Package Size Effects on Consumption Self‐Regulation. Journal of Consumer Research. 2008; 35(3):380-39.
                      • Fuchs, A. & Young, H. Investigation into gender differences in the effects of feeding around exercise on exercise performance, energy expenditure and substrate utilisation. Proceedings of the Nutrition Society. 2011; 70 (OCE6), E380.
                      • Galbo H, Richter EA, Hilsted J, Holst JJ, Christensen NJ, Henriksson J. Hormonal regulation during prolonged exercise. Ann N Y Acad Sci. 1977;301:72-80. Review.
                      • Honnor M, Herdsman M, Collins AL.The effect of food timing on fat oxidation during exercise and resting recovery. Proceedings of the Nutrition Society. 2012; 71 (OCE3), E236 
                      • Spence A, Sim M, Landers G, Peeling P. A Comparison of Caffeine versus Pseudoephedrine on Cycling Time-Trial Performance. Int J Sport Nutr Exerc Metab. 2013 Apr 9. 
                      • Sun, F; Li, L; O’Reilly, J; Wong, SH. Effect of carbohydrate-electrolyte-protein solution on hydration. International Journal of Sport Nutrition and Exercise Metabolism. 2013; 23: S1-S15
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