Science Round-Up Seconds: Follow-Up on Gum Arabic for Fat Loss. DMAA or Schizandra, Which Caused a Stroke in a Young Soldier? Low Doses of Resveratrol Better Than High Ones? Vitamin E Keeps Diabetic Brains Intact.

When it's served like this, Gum Arabic looks more like a healthy snack than a weight loss adjuvant.

I guess everyone who has already listened to the podcast of yesterday's show or was even able to listen live, will have noticed that the audio quality - yet not my German accent - have improved significantly, now that Carl and I did eventually switch to Skype instead of the landline. I know, you have been telling me that all along... be that as it may, unless my Internet connection hangs up for whatever reasons we will continue to do the SuppVersity Science Round-Ups via Skype from now on. Apropos, there will definitely be another show next Thursday (assuming that the world did not collapse by then ;-)

Follow up on Gum Arabic: Dosing & mechanism

In addition to that, I was actually presently surprised how much ground we were able to cover. Allegedly, we have gone way over the scheduled 60min, and I guess I could have said a couple of additional words on the Gum Arabic study and the astonishing fat loss results what I did mention was that it works astonishingly well, what I did not tell you about - or I have forgotten I did (too little caffeine I guess ;-) - is the dosage and the mechanism of action. At least as far as the former is concerned there is no debating that the fat loss magic (-2.1% from ~20% body fat to ~18% in 6 weeks; cf. Babiker. 2012) happened with just 30g of the substance that's derived  from exudates of Acacia senegal or Acacia seyal trees per day. Oher than the diarrhea and bloating, I did already mention on the show, the on average 19-year old perfectly healthy young women in the active arm of the study complained about nausea (82% in the first week) and an  "unfavourable oral viscous sensation" (100% in the first week). The latter is particularly interesting, because it does actually give us a hint on the underyling mechanism which is "not yet fully elucidated, because of a small number of conducted studies" (on its weight loss effects, but could be related to the increase in plasma leptin (without resistance obviously) as well as the increased fatty acid oxidation in muscle tissue in response to viscous fiber ingestion Islam et al. have reported only recently in Obesity (Silver Spring) earlier this year (Islam. 2012). I guess that we are going to see follow up studies on this one pretty soon and you all know that the Science Round Up and of course the SuppVersity news is where you are going to read about them first ;-)

Now that we lost the working weight loss adjuvants behind us, let's get to one which doesn't have any record of helping with weight and was still in each and every fat burner on earth before it was banned: DMAA (1,3 dimethylamylamine) aka geranium oil or geranium extract.

DMAA induced stroke in young soldier!? Or is it maybe the Schizandra that's to blame?

We all know that the job of a soldier is dangerous. A recently published case-report in Military Medicine does yet show that these dangers may not always be due to standing in the line of fire, but can also arise as a consequence of having too much DMAA supplements in your stash (Young. 2012) :

Is schizandra to blame? While the data is in fact scarce and the overall understanding of it's effects would suggest that the TCM herb would rather protect than harm the brain, it is at least worth noting that (a) schizandra has been found enhance the stimulation of the dompaminergic system (Chang. 1991) and (b) that we know that the abuse of cocaine has very similar effects on neurotransmitters (Prakash. 1993) and is associated with an increased risk of hemorrhagic stroke (Kousik. 2012)

"A 26-year-old male was presented to a military treatment facility in Afghanistan shortly after taking a weight-lifting supplement called Jack3d with a severe headache and was subsequently found to have suffered a Dejerine-Roussy variant right thalamic hemorrhagic stroke. Jack3d active ingredients include geranamine, schizandrol A, caffeine, β-alanine, creatine monohydrate, and L-arginine α-ketoglutarate. A literature search revealed case reports suggesting some of the constituent ingredients may predispose to stroke and hemorrhage and also revealed a substantial paucity of data existed regarding schizandrol A, a herb used in traditional eastern medicine." (Young. 2012)

Now, you always have to take case reports like this with an appropriate amount of skepticism - specifically, when the subject has a personal interest of not disclosing all the "supplements" he may have been taking in order not to lose is job. That being said, you know my take on DMAA from the round-table discussion with Patrick Arnold, Kurtis Frank, and one of the guys from Ergo Log. Bottom line: There really isn't any reason to be pissed of by the ban. Even if it's not to prevent stroke, it will prevent the onset of chronic fatigue syndrome in many aspiring physical culturists.

A re-appreciation of vitamin E and resveratrol

"Regular" vitamin E, i.e. alpha tocopherol, has gotten somewhat of a bad rep as of late and whenever resvertatrol is found to produce any the myriad astonishing health effects scientists have identified, it's either these effects occur either in the petri dish or in a rodent model with (often injected) mega-doses you imply couldn't afford taking on a regular basis. In this regard, a recently published paper which reports profound reductions in the fatty acid synthase, and fatty acid oxidation in the livers and adipose tissue of mice in response to a 0.005% resveratrol enriched high fat chow (this would be ~36mg/day for a human) is yet more than only an exception to the rule (Cho. 2012).

Figure 1: Metabolic effects of high fat diet (HFD) or HFD with two different doses of resveratrol; data expressed relative to mice on a standard diet (Cho. 2012)

I mean, take a look at the effects this low dose had compared to the 4x higher dosing in a second group of mice who received the human equivalent of ~142mg/day (see figure 1). Is this really another instance where more does not only yield no additional benefits, but actually reduces the effect (incidentally, de la Lastra et al. have discussed the pro-antioxidant effects of high doses of resveratrol in 2007 already; cf. de la Lastra. 2007)? Or is this just because "mice are no little human beings" and the results are therefore meaningless for us?

If you believe the latter is the case, I suggest you simply scroll down to the overview of some recent facebook news instead of reading how the adminstration of vitamin E to alloxan-induced diabetic rodents (standard model for type II diabetes) did ameliorate the shrinkage of Purkinje cells and apoptosis of cells in the granular layer, the mitochondrial defects, the splitting  of the myelin sheaths and widening axonal spaces, as well as the decrease in the number of GFAP-positive astrocytes (those that still produce a protein, namely GFAP that's responsible to keep their structure intact) in the cerebellar cortex (Mohammed. 2012)

 + + + + + + + + + + + + + +

That's it for today: You know the holiday season is coming so having too many Seconds isn't a particular good idea these days. If you still need something I suggest you pick one of the easily digestible Facebook news, for example...

• GI, GL and cancer risk - While there are statistically significant associations, only the ones for the glycemic load, which adds another quality factor namely GI + carbs per 100g to the equation, appear to have real world significance, though (read more)
• Folic acid in pregnancy - It's not all gold that glitters in ads and carries the letters "RDA". Among the profound epigenetic effects that have been observed in rodent studies, some sound as if they were from a list of the most rampant current pathologies (read more)
• Adiposity will shrink your brain - Leptin resistance is associated with reduced brain volume, associations persist even when they are corrected for BMI (read more)

You know there is more and there is even more to come. So in case the world does not explode within the next hours you know where to go if you are bored waiting for the "Zombie Repopulation" to happen.
 
References:

• Babiker R, Merghani TH, Elmusharaf K, Badi RM, Lang F, Saeed AM. Effects of gum Arabic ingestion on body mass index and body fat percentage in healthy adult females: two-arm randomized, placebo controlled, double-blind trial. Nutr J. 2012 Dec 15;11(1):111. 
• Cho SJ, Jung UJ, Choi MS. Differential effects of low-dose resveratrol on adiposity and hepatic steatosis in diet-induced obese mice. Br J Nutr. 2012 Dec;108(12):2166-75.
• de la Lastra CA, Villegas I. Resveratrol as an anti-oxidant and pro-oxidant agent: mechanisms and clinical implications. Biochem Soc Trans. 2007;35:1156–1160.
• Islam A, Civitarese AE, Hesslink RL, Gallaher DD:  Viscous dietary fiber reduces adiposity and plasma leptin and increases muscle expression  of fat oxidation genes in rats. Obesity (Silver Spring)2012, 20(2):349–355.
• Kousik SM, Napier TC, Carvey PM. The effects of psychostimulant drugs on blood brain barrier function and neuroinflammation. Front Pharmacol. 2012;3:121.
• Prakash A, Das G. Cocaine and the nervous system. Int J Clin Pharmacol Ther Toxicol. 1993; 31:575–581.
• Young C, Oladipo O, Frasier S, Putko R, Chronister S, Marovich M. Hemorrhagic Stroke in Young Healthy Male Following Use of Sports Supplement Jack3d. Military Medicine. December 2012; 177(12): 1450-1454(5).
• Zhang L, Niu X. [Effects of schizandrol A on monoamine neurotransmitters in the central nervous system]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 1991 Feb;13(1):13-6.

Devil in the Feeding Trough: PGE-Response to "Bad" Red Meat from Grass-Fed Cattle Could Prevent not Cause Cancer, Stroke and a Whole Host of Autoimmune Diseases.

Image 1: You do not need to hunt your red meat like a paleolithic human being, just make sure it comes from grass-fed animals and you will have a "health food" that modulate the your prostaglandin response to inflammatory assaults and thusly reduce your risk of cancer, stroke and autoimmune disesases in a way no fat-free chicken breast will ever do.

I have had this in the news before, in the context of the purported health benefits of CLA, with respect to the modulation of the n3/n6 ratio in your diet and in various other context, you heard me saying, or, I should say, read me writing that rather than popping tons of fish oil caps, you should rather focus on decreasing your overall omega-6 intake by making healthy food choices at the supermarket. In this regard, choosing grass-fed over commercially raised beef (and other meat) products could turn out to be one of the most far-reaching choices you can make. While that alone will help you to concomitantly reduce the n-6 overload, as well as the overall PUFA-burden that is so characteristic of the "Western diet", a recent study shows that eating red meat, even instead of the "healthy" white fat-free chicken breasts, everyone is pounding these days, could actually have profoundly beneficial effects on your (auto-)immune health, protect you from cardivascular disease and (this is important for the ladies) get your menstrual periods and related issues back in order.

How grass-fed beef can help and why it outperforms bison, elk and chicken

In their study, the results of which were published in issue 31 of the journal Nutrition Research, K. Shane Broughton, Daniel C. Rule and Eldon Handrich did what scientists have been doing for decades now. They took mice (your usual carnivorous animal) and put them on one of those grain-based diets that was then enriched with "bad" red meat to make the animals sick. Well, ... while the design was in fact the same, the good news is that the intention was by way of exception not to show "prove" (as if mainstream dietary advice would be interested in "proof", anyway) how bad those nasty red meats are, but to evaluate whether the

[...] consumption of meat from range-fed bison vs range-fed and grain-finished cattle and grain-finished bison would lead to reductions in PGE-2 [prostaglandin E2] release without altering PGI-2 [prostacyclin] release after an infl ammatory stimulus in a mouse model.

Or put simply, the scienists wanted to check whether there was any truth to the superiority of bison compared to the "bad" red meat, when it comes to balancing out the ratio of PGE-2 and PGI-2.

Image 2: Bayer probably won't like it if everyone would start eating grass-fed beef. After all, that would probably reduce the sales of their COX-inhibitor Aspirin protect.

For those of you wondering about a) what those prostaglandins are and / or b) why you would want to modulate their ratio and not eradicate them completely, here is is brief rundown on one of my favorite topics, the Yin&Yang of life and, on a related note, the fallacy of common black-or-white thinking. As with almost everything there are also two sides (in fact there are many more ;-) to the inflammatory coin and PGE-2 and PGI-2, two acronyms that differ by only a single letter, are situated on those opposing sides. If they are expressed at the right ratio, everything is fine. The (relative) over-expression of PGE-2 that is commonly observed in people following the "Western diet", on the other hand, is associated with a host of pathologies, such as elevated risk for color ectal cancer, suppression of ovulation, and increased problems with rheumatoid arthritis and headaches. (Relative) underexperssion of PGI-2, the other hallmark result of the "food" people are poisoning themselves with on a daily basis, in turn, increases the risk of thrombosis and stroke. If any of that does ring a bell, but you do not know which one, you may want to check out the label of your Aspirin tablets - as a cyclooxygenase inhibitor Aspirin also blocks the production of PGE-2... but before you do now pop another of those tabs, I suggest you read on and learn that by paying a few extra bucks for "real meat", you will probably never have to take your daily dose of Aspirin protect.

And while the scientists were right, grass-fed bison is in fact better than grain-fed beef, a closer analysis of their results will show that the often-heard and widely believed statement that "bison is the best form of red meat you can possibly find" is nothing but another of the 1001 dietary fairy-tales of the bloggosphere.

Figure 1: Fatty acid content of the diet (in g per 100g of the whole chow) - saturated, mono- and polyunsaturated fatty acids (n3, n6), left; CLA content, right (data adapted from Broughton. 2011)

But let's first take a look at the experimental diets, the male CD-1 mice were fed for 14 days. What is interesting about these, is that, due to the inclusion of standard rodent chow, the differences in fatty acid composition between the grass-fed vs. corn-fed bison and beef diets and the diets that were based on (wild-type) elk and commercial chicken breast meat were actually not very pronounced (cf. figure 1). And while the inclusion of corn oil in every diet may sound blasphemic in the ears of the hard-core anti-grain croud (I know you are out there ;-), the addition of grass-fed meat to an otherwise standardized (and probably suboptimal) diet is actually a strength of the study. Thusly, the study does reflect pretty well, what could happen, if the average Joe or Jane did nothing else, but replace the corn-fed meat in his/her diet with meat from range-fed animals - and wouldn't you agree that this is a much more realistic scenario than living on nothing but grass-fed beef or bison?

Figure 2: Modulatory effect of 2 weeks on prostaglandin expression of mice after two weeks on diets enriched with range-fed, or feedlot fed meat of different sources (data adapted from adapted from Broughton. 2011)

And, if we focus solely on the PGE-2 to PGI-2 ratio (you can read up on its importance in the red box above), it is obvious that a small dietary change from grain- to grass-fed meets could actually have pretty profound effects on your (auto-)immune health. The data also shows that the "healthy" lean chicken breast your nutritionist has probably told you to eat actually should not be your first choice, when it comes to establishing a healthier prostaglandin milieu - and if you don't believe me, maybe you want to trust Broughton et al.'s judgement:

[...] chicken is promoted for its health benefits, yet in our study, it was no better for possible prevention of PGE 2-associated immune pathophysiology. Furthermore, chicken would not be as beneficial as grain-fed beef and elk consumption in reducing thrombos is and stroke potential.

So, while eating (commercially raised) chicken won't harm you, it will not help you steer your inflammatory response into either the PGE or the PGI direction. Broughton, Rule and Handrich are thusly right, when they conclude that

Based on results of the present study, consumption of any of the range-fed meat sources examined would be better at reducing the possibility of immune-related pathophysiologies than meat from grain-fed cattle. [...] Although range-fed beef and bison consumption would be equivalent for their immune-based role, consumption of range-fed beef would be better for the prevention of thrombosis and stroke.

Now, isn't that surprising? Chicken not the best thing you can eat? The "healthy alternative to beef" that has been pimped in the mass media lately only on par with plain beef and superior as far as reduction in the risk of stroke and thrombosis are concerned? Could it really be possible that the "bad red meat" is not so bad, after all? Is there the remote possibility that it's not red meat per se, but sick meat, or I should say the meat of animals we have been making sick by feeding them the same "healthy whole grains" with which we have been poisoning... ah, I mean nurturing *rofl* ourselves over all these years that is giving us migraines, arthritic joints, cancer, strokes and a whole host of nasty autoimmune diseases? I guess, I will leave it up to you to find and answer to that question ... and I am confident that you are smart to one and one, or rather grain-fed meat and (auto-)immune disease together ;-)

Chloride & Heart Disease - Overlooked & Misunderstood? Low Chloride Levels (Below 100meq/L) Are Associated W/ 20% Increased All Cause Mortality in Hypertensive Subjects

Salt is a four-letter-word today - literally and figuratively; and so would be NaCl, if it was a word and not the combination of the acronyms for natrium, or as Americans like to all it "sodium", and chloride and that despite the fact that low Cl may put your life at risk.

From my previous articles and Facebook posts on the questionable usefulness of dietary salt restriction you will remember that several epidemiological studies have already shown that a very low salt intake can be associated with increases in cardiovascular and all cause mortality. In NHANES I, for example, total sodium intake was inversely associated with all-cause (p=0·0069) and CVD mortality (Alderman. 1998)

You may also have heard me say and write that some scientists have suggested that we should better focus on the chloride rather than the sodium atom in NaCl, if we wanted to rid ourselves of the hypertension problem we are facing these days. Against that background, it sounds somewhat surprising that Linsay McCallum and her colleagues from the BHF Glasgow Cardiovascular Research Centre at the University of Glasgow found that low (not as other scientists suggested high) chloride levels are associated with a +20% increase in all-cause, cardiovascular and noncardiovascular mortality in patients with (pre-)hypertension.

Na(+) >135 & Cl(−) >100 = best survival rate

Among the study subjects, those with Na+ values of more than 135mEq/L, but lower Cl- levels of less than 100mEq/L in the blood, were the ones with the highest (+21%) mortality risk:

Figure 1: Associations of serum chloride, natrium, potassium and HCO2 with systolic and diastolic blood pressure as well as risk of all-cause, cardiovascular disease, ischemic heart disease, stroke and non-CVD mortality risk (McCallum. 2013)

If you take a closer look at the data in figure 1, you as a well-versed SuppVersity reader will albeit also recognize that the main, because only correlate of both systolic (that's the upper value that's supposed to be below 130) and diastolic (that's the lower level that's supposed to be around 80) is neither sodium, nor chloride. It's  HCO3 - or bicarbonate!

Did you know that soccer players lose ~3.4g of chloride (ca. 6g NaCl = salt) and less than 500mg of potassium during a 90 minute pre-season training session (Maughn. 2004)?

Not surprising for you, I know, but still worth highlighting, also because it has been a couple of weeks since I have been writing about the benefits of sodium-bicarbonate and maintaining a healthy acid-base ratio.

There are still many questions to be answered

Excerpt from the researchers' press release: "Sodium is cast as the villain for the central role it plays in increasing the risk of high blood pressure, with chloride little more than a silent extra in the background. [...] However, our study has put the spotlight on this under-studied chemical to reveal an association between low levels of chloride serum in the blood and a higher mortality rate, and surprisingly this is in the opposite direction to the risks associated with high sodium [...] It is likely that chloride plays an important part in the physiology of the body and we need to investigate this further." (co-author Jeemon Panniyammakal)

As Mc Callum et al. point out, there is still a lot of research to be done (including whether similar associations can be observed in hitherto healthy individuals), but as of know it does in fact appear as if ...

"[...s]erum Cl − is a marker of risk that appears to be dissociated from serum Na +and HCO 3 − levels. The underlying mechanism for this risk is unclear. A simple explanation would be that serum Cl − reflects abnormal physiology better than serum Na + , levels of which are perhaps more homeostatically regulated than Cl−" (McCallum. 2013)

Against that background, it is somehwat unsettling that serum chloride levels are not part of the current routine clinical screening (not even in patients with hypertension), so that levels in the "danger zone" between the current lower limit of 95 mEq/L and 100mEq/L could go unnoticed unnoticed for years.

---

So what do these findings tell us? While the study has been done in hypertensive individuals, I personally feel that the results still support what I have been telling you before about the salt requirements of people who belong to the minority of those who are not yet living on convenience and fast food and work out (and sweat) regularly.

In this regard, the study at hand provides further evidence that falling for the "salt" (=NaCl) restriction propaganda you are exposed to on a daily basis will do more harm than good to someone like you, whose "paleo-ish" diet may cover your bicarbonate needs, but may put you in a similar position as our ancestors, when it comes to the availability of dietary salt - a scarcity that is at the heart of the "salty tooth" we have conserved till today.

Suggested reads:

• 

  It is probably due to the HCO3 in Sodium bicarbonate (NaHCO3) that baking soda lowers blood pressure | see red box in previous article

  "No Pump + Insulin Resistant? Maybe It's Your Healthy Low Salt Diet. Low Sodium Induced Increase in Aldosterone Has Direct Negative Impact on GLUT4 Mediated Glucose Uptake" | read more
• "The SuppVersity Science Round Up on Super Human Radio - Seconds: 3g Salt/Day = 33% Lower Magnesium Retention" | learn more
• "Calcium, Magnesium, Potassium & Co in Food, Water & Supps - Getting Enough is Easy, Knowing How Much Is Not!" | read more

References:

• Alderman MH, Cohen H, Madhavan S. Dietary sodium intake and mortality: the National Health and Nutrition Examination Survey (NHANES I). Lancet. 1998 Mar 14;351(9105):781-5.
• Maughan RJ, Merson SJ, Broad NP, Shirreffs SM. Fluid and electrolyte intake and loss in elite soccer players during training. Int J Sport Nutr Exerc Metab. 2004 Jun;14(3):333-46.
• McCallum L, Jeemon P, Hastie CE, Patel RK, Williamson C, Redzuan AM, Dawson J, Sloan W, Muir S, Morrison D, McInnes GT, Freel EM, Walters M, Dominiczak AF, Sattar N, Padmanabhan S. Serum Chloride Is an Independent Predictor of Mortality in Hypertensive Patients. Hypertension. 2013 Aug 26. [Epub ahead of print] 

2.1kg Muscle From Fast Food Supplement; No Prolactin, No Fat; Oleic Acid Counters CLA's Inflammatory Effect; Spicy Marinades vs. Salmonella; Flaxseed, Estrogen & Penis Size; TTA in the Emergency Room; Alcohol & Binge Eating

Image 1: Scientifically proven muscle builder - 2.1kg lean mass in 3 months, no post-cycle therapy necessary!

I was just about to write another one of my artistic introductions, trying to incorporate all the exciting On Short Notice news I've piled up for you into a brief narrative, when I realized that you probably don't really appreciate those introductions (I guess, I would skip them myself, so don't worry, this is more of an objective assessment than an accusation). So, I listened to my gut and decided to skip this part of this series, today, and rather spend the time to edit another item I did actually not want to post today. It's the one on the "IIFYM slightly gone wrong fast food bulk" in the Hambre study, to be precise; and I would venture the guess that you won't mind taking that instead of a longer introduction, once you've read and digested the impossible: You cannot only gain muscle with "fast food supplements", you won't even get fatter than you would if you just used a classic whey protein... oh my, I see, you are already scrolling down: What I said, I would have been wasting my time, had I written a longer introduction. But dare you, if you don't at least read the other items, as well!

• 

  Figure 1: Food intake (top, lef) and energy expenditure (bottom, left) as well as body fat % (top, right) and body weight development of the normal vs. prolactin negative mice after 14 weeks on standard chow (SC) or high fat diet (HFD; Auffret. 2012); btw: taking super-doses of vit. B6 will induce nerve damage, not fat loss!

  Without prolactin mice can't get fat! If that is true for humans as well, this would mean that Julien Auffret and his colleagues would have made a very important finding that could help us solve at least part of the diabesity pandemic, if we found a way to mimick the effects the "beigening" (=making white adipose tissue behae similar to the fact burning brown adipose tissue) effect the genetic ablation of the prolactin receptor on the fat cells of the mice in the Auffret study had on their susceptibility to diet induced obesity (Auffret. 2012).
  In particular, the scientists found that the ablation of the prolactin receptor gene in the mice results in profound increases in the expression of master genes controlling brown adipocyte fate (PRDM16) and mitochondrial function (PGC1α, UCP1), which allow - and this is the actual caveat,, here - for an inrease in thermogenesis.
  The latter, in turn, allows the rodents to burn off a major part of the fat they would otherwise store and thus keeps them relatively lean despite HFD feeding. Aside from the fact that the hyperphagic rodents on the high fat diet were still fat (there is no debating that!), you may savely assume that the effects will be way less pronounced in human beings, where 9/10 "thermogenic" agents that have been successfully tested in rodents do nothing at all, anyway. Against that background the hunger-promoting effects of the prolactin recetor ablation would suggest that it is almost as likely that a drug that block prolactin completely would make obese individiuals even fatter, since that's usually what happens if you eat more - like the mice in the prolactin (-/-) group did (see figure figure 1), without burning more.

• 

  Figure 2: Comparison of MUFA : CLA ratios in steak and mince from grass fed or conventional beef and milk from mares, sows, women (human milk ;-), goats and cows (based on Dhiman. 1999; Jahreis. 1999; McAfee. 2011); higher values indicate more MUFA per unit of CLA, but more must not necessarily be better - in fact too much MUFA could completely block the fat loss effects of CLA and thus maybe explain why it rarely works in humans - our diets are pretty high in oleic acid and thus the ratio will be much lower, than in the high dose CLA rodent trials

  Conjugated linoleic acid needs oleic acid to work without side effects. That's the main take-home message from a recent study conducted by researchers at the at the University of North Carolina at Greensboro, who found that oleic acid, the mono-unsaturated fatty acid from olive oil & co, does prevent the expression of inflammatory genes in adipocytes treated with the "anti-fat fat CLA"..
  So, until my friends from the supplement industry read this post and come out with yet another SuppVersity science powered product with CLA in olive oil* you simply make sure to have a spoon of the liquid gold from time to time, when you feel that you need to take CLA to burn more fat. Unfortunately, this could not just mean that you can rid yourself of the nasty side-effects as discussed in "CLA Destroys Body Fat! But at Which Costs?", but also that the "body fat destruction" will at least be ameliorated if not totally absent :-(
  * I had hardly written this post, when I browsed the web and found that a certain newcomer and as of late very succesful "yellowish green" company has already a CLA + Olive Oil + Avocado Oil combination on the market, for them this would mean that they didn't even have to change their formula

• 

  Image 2: It's funny how so many things people (or at least chefs) have been doing forever, here marinating meats, simply make sense, isn't it?

  Antibacterial marinades for your meat! Don't worry this is not yet another dysfunctional functional food that's going to make you sick, but an all-natural mixture of green tea, lemon and turmeric you will have to smear onto your chicken meat if you want to make sure to get rid of the C. jejuni and S. enteritidis it may be contaminated with.
  All it takes are 24h of "incubation", but that's nothing else than leaving your meat lying in the marinade in your fridge and thus something you would do anyway, right? That's what I would call a convenient, effective and above all totally natural and healthy way of gettting rid of Samonella and Campylobacter :-)
• Tons Flaxseed flour in your diet will increase estrogen, but won't decrease the size of your penis, well at least not visible ;-) That's probably the most straight-forward summary of the results, Ludmila Ferreira Medeiros de França Cardozo and her colleagues present in the latest issue of Food and Chemical Toxicology after analyzing the effect of a flaxseed flour containing diet on the expression of hormone levels and penis morphology of male rats (de Franca. 2012)

  

  Image 3: Flaxseed bread won't turn you into an hermaphrodite overnight, don't worry.

  While the rats that were maintained on a diet containing 25g of flaxseed flour per 100g for 250days had significantly elevated estrogen levels in the blood 39.5 vs. 32.5 pg/mL (+22%), the minor drop in testosterone did not reach statistical significance and the reduced diameter of the corpus spongiosum, which helps to maintain the urethea as a viable channel for the ejaculation was obviously no problem for the fertility, either - at least the scientist don't mention anything in this regard; unfortunately, they did not really test it, either, as the poor male Wistar rats that were abused in this experiment were bachelors against their will.
  In view of the fact that flaxseed ain't the best source of omega-3s, anyway, and there appears no other good reason (for men and women!) why you would eat them in large quantities (I am not talking about the occasional tablespoon of flaxseed, here), I would still suggest to stay away from it.

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  Image 4: In farm-raised salmon chronic TTA administration has been shown to improve cardiac function and immune activity; it does however also lead to cardiac growth during viral infections, so that the benefits of chronic administration are still by no means certain (Grammes. 2012a & 2012b); long-term human studies, on the other hand, are not yet available.

  Acute TTA administration soothes the flames and keeps the coronary vessel open You will unquestionably remember my previous posts about the fat burning fatty acid tetradecylthioacetic acid (TTA) and how it's ability to accumulate in various tissues of your body could potentially become problematic. In the short term however, it's anti-inflammatory effects can come very handy. So handy, in fact, that the a recently published study by Pettersen et al. would suggest that we are soon going to see TTA balloons being inserted into coronary vessel walls, in order to deliver the sulfur-containing fatty acid right to an obstructed vessel that's being operated on, in order to suppress the local expression of inflammatory cytokines, as well as the subsequent macrophage infiltration and the unwanted collagen formation, which would precipitate restenosis (=further clogging) of the very heart vessel that has only just been opened operatively.
  You may now rightly ask yourself what this has got to do with you? Well, if it works locally, it could work similarly systemically and other studies such as Bjørndal (2012) do confirm just that: 0.4% TTA reduce TNF-α, IL-1β, and IL-6 in an experimental model of colitis and render the rodents guts more of less bullet..., ah, pardon, dextran sulfate sodium (DSS; a chemical used to induce cholitis) proof. The long-term effects of the continous consumption of ~3g of TTA, which would be the human equavalent of those 0.4% TTA in the rodent diets is yet still not fully established (re-read: "TTA & Fish Oil" and "TTA & Fish Oil - Revisited").

• 

  Figure 3: Alcohol overrides the inhibitory control over food intake (Chapman. 2012)

  Of TV watching, sleep deprivation and alcohol consumption, booze has the most pronounced negative effect on reward saliency and inhibitory control of food intake! That's the conclusion Colin Daniel Chapman, Christian Benedict, Samantha Jane Brooks, and Helgi Birgir Schiöth mkae based on their latest meta-review of pertinent studies from pubmed (N=23). With an impact factor of 1.03 on a scale from -4 to 4, alcohol is by far the worst the greatest effect on food intake and shows the highest correlation with obesity (Chapman. 2012).
  Compared to booze, both sleep deprivation (50% less) and TV watching (20% less) appear almost harmless. Their contribution in the non-drinking part of the population may yet still not be underestimated, also because the urge to do the latter, i.e. watch TV, when you ought tho sleep, precipitates the former and subsequent derangements in the circadian rhythm (suggested read: "The SuppVersity Circadian Rhythm Series").
• IIFYM was yesterday, ROWFYM is today, but what's going to be tomorrow? If that's all Greek to you, let me first bring you in the loop on the acronyms. While IIFYM designates "If It Fits Your Macros", implies (in the most extreme case) that you give a sh*t about what you eat, as long as you hit your macronutrient ratios for the day ("Carbs? Gimme that pizza!") and is getting increasingly popular among those who are fed up with broccoli and chicken breast and either unwilling or unable to see that those are not the only, and I would say, by far not the most healthy foods you can eat, ROWFYM is my own invention, means "Regardless Of Whether It Fits Your Macros" and would probably end up for way too many trainees in a protocol similar to the one 12 of the 24 subjects in a recent study from the Linköping University in Sweden were following for 12 weeks (Hambre. 2012).

  

  Image 5: "WTF do you want, I am doing ROWIFYM, here! That's serious bulking, man. Scientifically validated." If you want to follow his example, go ahead... but 3 months really is the absolute max and only if you are still healthy - regardless of whether the blood markers return to normal in the course of your next diet.

  While those lucky (?) twelve healthy young men (aged 19–32 years) in what I will from now on call the "fast-food arm" of the study had to add a delicious (???) fast food menu (1350 kcal, 41 g protein) on top of their diets, the other twelve participants had to contend themselves with a blatant protein shake (33g of whey) as their bulking supplement of choice. The reasoning behind this at first sight unquestionably highly questionable experiment was that the Swedish scientists wanted to elucidate, whether it would really make a difference whether you are eating "clean" (=adding a whey protein shake) or simply stuffing yourself with the next best, allegedly protein-laden fast food you can find during a 3-months bulking cycle (at least three lifting sessions per week) and the results were, ... well, let's say surprising.
  As you would expect, subjects in both groups managed to gain some weight. The first surprise is that subjects in both groups gained identical amounts of weight, namely 3.6kg. That's not all, however. Even the lean mass increases 2.1kg did not differ between the groups (measure by DEXA scans) and the sophisticated (compared to a similar calories in vs. calories out calculation) measurement of the resting metabolic rate, the scientists had conducted yielded that both groups had compensated for the overeating by a statistically highly significant (p < 0.0001!) + 10% increase in resting metabolic rate!

  

  Figure 4: Kaplan-Meier plots indicating the percentage of patients that made it to time-point X (see horizontal axes) without adverse event after their first coronary event - patients w/ (thin line) vs. w/out (bold line) metabolic syndrome (top), patients with high (thin line) vs. low (bold line) ApoB leves (bottom; based on Corsetti. 2005); ApoB turns out to be a way better risk predictor than having metabolic syndrome

  Before you do now jump into your car and head for the next drive-in "restaurant" with a big yellow "M" in front of it, you may want to take into consideration that this extended ROWIFYM version of the IIFYM approach, where you may hit the protein but overshoot on the carbs and fats (and certainly not  the good ones), did lead to statistically significant increases in fasting insulin and ApoB, a building block of LDL that has been associated with increased risk of arterial plaque formation (Gebel. 2008), compared to the "clean bulk" (= whey only) group. And while those changes (as well as the increase in RMR) were reversed on the 12 months follow-up, I am not sure if especially those people, who are most fond of bulking approaches like that, i.e. men (and very rarely women) who have been following a junk food diet for way too long already, should take the results of this study as an incentive to do a 3-month fast food bulk during the winter. After all, it could be that one additional LDL molecule that nests in the already existent arterial plaque which will eventually break the camel's, no your neck - or for those who like it more explicitly, which won't let the next mini blood clot pass by and causes a stroke, which could, in the worst case, end deadly!

That's it as far as the official On Short Notice items go, for today. If you don't have enough yet, I suggest you take a glance at the 6-10 news-items I've piled up on the SuppVersity Facebook Wall for you to review. Maybe you've read that sleeping with wife and children in a room would decrease your testosterone levels? False! Maybe it decreases the intellectual capacity of the reporter who wrote the respective news-item you may have read, but what really happens, is an increase in the amplitude of the circadian pattern with higher morning and lower evening testosterone levels (click here to read more). And if you neither have or plan to have children or don't care about your or your significant other's testosterone levels, you may be interested in a study that debunks the use of a "slim belt" for weight loss purposes, the idiotic idea to counter BPA toxicity with soy, the way working out can make depressed old people happy again, and more... ah, I almost forgot, there will also be an exercise special of On Short Notice very soon - and I am not talking about next Saturday, here - so stay tuned, it could be published anytime (Tip: If you subscribe to the SuppVersity Facebook Page you won't miss it ;-)

 References:

• Auffret J, Viengchareun S, Carré N, Denis RG, Magnan C, Marie PY, Muscat A, Fève B, Lombès M, Binart N. Beige differentiation of adipose depots in mice lacking prolactin receptor protects against high-fat-diet-induced obesity. FASEB J. 2012 Sep;26(9):3728-37. 
• Bjørndal B, Grimstad T, Cacabelos D, Nylund K, Aasprong OG, Omdal R, Portero-Otin M, Pamplona R, Lied GA, Hausken T, Berge RK. Tetradecylthioacetic Acid Attenuates Inflammation and Has Antioxidative Potential During Experimental Colitis in Rats. Dig Dis Sci. 2012 Aug 2.
• Chapman CD, Benedict C, Brooks SJ, Birgir Schiöth H. Lifestyle determinants of the drive to eat: a meta-analysis. Am J Clin Nutr. 2012 Sep;96(3):492-7. Epub 2012 Jul 25.  
• Corsetti JP, Zareba W, Moss AJ, Sparks CE. Apolipoprotein B determines risk for recurrent coronary events in postinfarction patients with metabolic syndrome. Atherosclerosis. 2004 Dec;177(2):367-73.
• de França Cardozo LF, Boaventura GT, Brant LH, Pereira VA, Velarde LG, Chagas MA. Prolonged consumption of flaxseed flour increases the 17β-estradiol hormone without causing adverse effects on the histomorphology of Wistar rats' penis. Food Chem Toxicol. 2012 Aug 25.
• Dhiman TR, Anand GR, Satter LD, Pariza MW. Conjugated linoleic acid content of milk from cows fed different diets. J Dairy Sci. 1999 Oct;82(10):2146-56.
• Gebel E. Meet LDL's partner in plaque. ApoB puts the "bad" in bad cholesterol. Diabetes Forecast. 2008 May;61(5):39-40.
• Grammes F, Rørvik KA, Takle H. Tetradecylthioacetic acid modulates cardiac transcription in Atlantic salmon, Salmo salar L., suffering heart and skeletalmuscle inflammation. J Fish Dis. 2012a Feb;35(2):109-17. 
• Grammes F, Rørvik KA, Thomassen MS, Berge RK, Takle H. Genome wide response to dietary tetradecylthioacetic acid supplementation in the heart of Atlantic Salmon (Salmo salar L.). BMC Genomics. 2012n May 11;13(1):180.
• Hambre D, Vergara M, Lood Y, Bachrach-Lindström M, Lindström T, Nystrom FH. A randomized trial of protein supplementation compared with extra fast food on the effects of resistance training to increase metabolism. Scand J Clin Lab Invest. 2012 Aug 30.
• Jahreis G, Fritsche J, Möckel P, Schöne F, Möller U, Steinhart H. The potential anticarcinogenic conjugated linoleic acid, cis-9,trans-11 C18:2, in milk of different species: Cow, goat, ewe, sow, mare, woman. Nutrition Research. October 1999; 19:10. 1541–1549.
• McAfee AJ, McSorley EM, Cuskelly GJ, Fearon AM, Moss BW, Beattie JA, Wallace JM, Bonham MP, Strain JJ. Red meat from animals offered a grass diet increases plasma and platelet n-3 PUFA in healthy consumers. Br J Nutr. 2011 Jan;105(1):80-9.
• Murali N, Kumar-Phillips NS, Rath NC, Marcy J, Slavik MF. Effect of Marinating Chicken Meat with Lemon, Green Tea and Turmeric Against Foodborne Bacterial Pathogens.International Journal of Poultry Science. 2012; 11(5): 326-332.
• Pettersen RJ, Salem M, Rotevatn S, Kuiper KK, Larsen TH, Bohov P, Berge RK, Nordrehaug JE. Effects of local delivery of Tetradecylthioacetic acid within the injured coronary vessel wall. Scand Cardiovasc J. 2012 Aug 30.
• Reardon M, Gobern S, Martinez K, Shen W, Reid T, McIntosh M. Oleic Acid Attenuates trans-10,cis-12 Conjugated Linoleic Acid-Mediated Inflammatory Gene Expression in Human Adipocytes. Lipids. 2012 Sep 2.

Dietary Zinc & Copper Improve Glucose & Lipid Metabolism. High Cortisol Amplitudes Counter Belly Fat. Hypoxic Hearts Love Creatine + Ribose. Apples Counter Cancer & Obesity

I guess this is about as close as we have hitherto gotten to understand why we got fat. Wrt to the hilarious pace at which we got fat and are still getting fatter, we are much better informed though.

After you've learned about the general importance of exercise for your health and a couple of tweaks that may or, as in the case of sugary "energy drink", may not help you maximize the benefits and performance gains on Saturday. The focus of today's SuppVersity article is on the results of non-exercise related studies that highlight non-exercise related confounders of your health.

Before we get to the actual news, I would yet like to invite all of you to take a look back at the increasingly obese history of the US... I suppose those of you who have not yet seen the link on my Facebook wall, will enjoy the animated obesity map in the Atlantic article from April 11. I mean, even if we still don't have anything but over-simplistic cookie-cutter "explanations" of why we get fat, the map shows that we do at least know how fast we got fat!

You don't feel knowing about how fast we got fat is good news? Ok, maybe you'll like one the following results from recent studies better:

• Dietary zinc & copper influence glucose & lipid metabolism in women (Shab-Bidar. 2013) According to a recent study from the Obesity Research Center at Shahid Beheshti University of Medical Sciences in Tehran, Iran, there is a gender specific effect of copper and zinc in the diet on glucose and lipid metabolism of men and women in Iran - statistical significant effects were observed only in women with...

  

  Odds ratios for the MetS and low HDL across quartiles of copper intake (Shab-Bidar. 2013)

  • higher zinc intakes being associated with higher HDL-C, lower triglycerides (TG) and lower 2-hour blood glucose, and 
  • higher copper intake correlating with higher HDL-C, lower fasting blood glucose (FBG), significantly lower TG and a huge 81% reduction in the risk for suffering from metabolic syndrome (highest vs. lowest copper intakes)
  These observations stand in contrast with the current notion of the "bad" copper and the "good" zinc and reamphasize the importance of both nutrients for metabolic health.

  ---

  Remember: Two questions that will still have to be resolved pertain to (a) the gender-specificity of the effects and (b) confounding effects of food quality / choice and thus whether the same beneficial effects would be observed with the standard American diet.
  For both, but espicially for copper a little more than the RDA does not appear to hurt: What's particularly interesting, is that contrary to the zinc intakes in quartile 4 (>14mg/day; RDA 9mg/day) the copper intake in quartile 4 was more than 3x higher than the current RDA for women (0.9 mg). In fact, even the copper intake in the lowest quartile ~1.5mg/day was way above the RDA. If that's something we have to be surprised about is yet questionable, after all, there is not exactly much research on "optimal copper nutrition" (much contrary to zinc, by the way) and the RDA is based on age-old depletion-repletion studies and will thus probably reflect the absolute minimum to maintain "normal" serum levels.

• Evidence from human study: Flat cortisol profile not averages or spikes are associated with increased adiposity and visceral obesity (Sharp. 2013) In their most recent paper that's soon going to be published in the American Journal of Human Biology Dan S. Sharp and his colleagues from the Center for Disease Control and the State University of New York provide conclusive evidence for the irrelevance of mean cortisol levels with respect to the purported negative effects of cortisol on visceral obesity.

  

  Associations between sextiles of within-subjects cortisol standard deviation (SD) in 217 Buffalo policemen and adjusted lean-mass trunk index (Sharp. 2013)

  As the data in the figure above clearly shows, the police officers with the greatest cortisol fluctuations (spikes and troughs) had the highest ratio of lean body mass to trunk mass. It is thus, as the scientists phrase it,
  

  "not the average level of salivary cortisol among 18 specimens on each officer that drives the association; it is the variation among specimens."

  The oral cortisol measures were taken on 3 subsequent days in standardized procedures that involved a venipuncture and a standardized high protein meal as "challenges", on day 1, six measures that were taken by the police officers over the course of the day, on day 2, and series of tests that was taken after a dexamethasone challenge after waking on day 3 (the subjects had ingested 0.5mg of dexamethasone the night before).

  ---

  Bottom line: While the scientists are careful in pointing out that it will still have to be established that the results translate to other populations. The results corroborate the uselessness (if not potential detrimental effects) of "cortisol blockers", I've discussed in my previous in the Science Round Up Seconds on March 29, 2013 (read more).

• Combination of creatine and d-ribose heals damaged, but unscarred rodent-hearts (Caretti. 2013) While the many of the "daggered" claims* on the boxes of various "advanced" creatine products (learn more about their uselessness) are probably a little overblown (*the dagger refers to the "not verified by the FDA"), that's nothing compared to the absolutely disappointing results trainees had with d-ribose. Meanwhile, it seems as if even the last jerk knew that the unbearably sweet simple sugar is nothing worth spending his/her money on.
  
  

  

  Ribose regulates the novo synthesis and restoration nucleotides, can relieve the energy toll of ischemia  and its usefulness in the context of CVD is backed by rodent and human studies (Shecterle. 2011)

  In view of it's physiological role in the recovery of ATP levels (Helsten. 2004), it was assumed that supplementatal D-ribose would ameliorate the ATP depleting effects on exercise and improve endurance in glycolytic and/or long endurance activities, yet...
  

  "[...s]tudies examining the effect of ribose on performance during intense intermittent exercise and rowing have not been able to demonstrate improved performance in humans." (King. 2012)

  Other than the non-existence of side-effects, pertaining studies, which used up to ∼40 g/day, as well as acute and chronic supplementation regimen did  yet not yield any positive results
  
  Now, the aforementioned studies on the ergogenic effects of d-ribose were conducted in healthy individuals, in whom the ATP re-synthesis obviously does not depend (and not even benefit) from the provision of the monosaccharid that was discovered by Emil Fischer in 1891, when he analyzed the carbon structure of gum arabic (Prince. 2012). "Healthy" would yet not be the correct term to describe the rodents in the recently conducted study by Caretti et al. who observed that five week-old mice who were exposed to an atmosphere containing 10% O2 for 10 days in order to induce right ventricle hypertrophy and left ventricle apoptosis did not show any signs of cardiac damage, when they were gavaged creatine + D-ribose, every day.
  
  And while both phenotypes, i.e. the hypertrophy of the right and apoptosis of the left ventricle, were blunted to a certain degree by creatine or d-ribose, only their reversed the pathogenic changes to the heart muscle "almost" completely, by normalizing the expression of AMPK and Akt signaling in the hearts of the rodents.

  ---

  

  Light micrograph of representative nuclear pro-files (background, red = atypical, green = normal nuclei; my emphasis) and volume (%) of atypical cardiac cells in anterior left ventricle of rodents on caffeine + nicotine + ephedrine combo (learn more)

  Bottom line: While they may not be beneficial for the average trainee, people "on" the literally heart-breaking combination of nicotine + caffeine and ephedrine, could be able to reduce their detrimental effects on the heart (learn more), by adding this combination of proven (creatine) and disproven (d-ribose) ergogenics to their supplement regimen. People with sleep-apnea and other conditions which will leave the heart poorly oxygenized for longer time-periods should obviously benefit, as well.
  
  Based on the likewise promising results of previous studies in (human!) subjects with congestive heart failure (e.g. Omran. 2003), a daily dose of 5g d-ribose, along with the tried an proven chronic ingestion of 5g of creatine appears to be a good starting point, until respective human trials have been conducted.

• Further evidence for the "An apple a day..." theory (Rago. 2013) In an allegedly methodically complicated, but very comprehensive analysis of the effects of raw, whole apples on the plasma metabolome of rodents, researchers from the University of Copenhagen found
  

  

  Total antioxidant activity (µmol vitamin C equivalents/g) of various fruits (Boyer. 2004)

  "that the intake of fresh apple in rats has a considerable and specific impact on the plasma metabolite profile, reflecting altered gut microbial metabolism, retarded lipid- and protein catabolism, and lowered metabolic, oxidative and steroid-related stress". (Rago. 2013)

  These results stand in line with the recent observations a group of Spanish researchers made, when they added a polyphenol extract from apples to the chow of rodents on an obesogenic high-fat + high sugar (HFS) diet:
  

  "Our results from histological studies demonstrated that supplementation of HFS with AP markedly reversed the enlargement of adipocyte volume induced by HFS diet intake in the epididymal fat pad, reducing it by almost 28% [...it also] reversed the increase in the population of large epididymal adipocytes, especially with diameters higher than 130m." (Boqu. 2013)

  The visceral specific effects of the apple polyphenols in the Boqué study could thus be interpreted as supportive evidence for the real-world significance of the metabolomic changes Rago et al. observed in the afore-cited study.

  ---

  Bottom line: No reason to be scared of the "high fructose fruit" apple. It comes with all HFCS sweetened beverages don't have. Polyphenols, vitamins, minerals and most importantly a flesh from which the fructose is extracted only slowly. Still, I have to warn you: Apple consumption can have profound beneficial effects on your health, such as (random examples)
  
  •  - 17% colorectal cancer risk (Michels. 2006)
  •  - 37% wheeze risk in your offspring (Willers. 2007)
  •  - 21% reduced risk for cancers of the oral cavity and pharynx (Gallus. 2005)
  •  - 25% reduced risk for oesophagus (Gallus. 2005) 
  •  - 18% / -15% / -9% risk red. for breast / ovary / prostate cancer (Gallus. 2005)
  and obviously the - 15% reduced breast cancer risk, the if you want to avoid these, you should thus better keep obsessing about the high fructose content of apples and stick to sausages and lard ;-)

References:

• Boqué N, de la Iglesia R, de la Garza AL, Milagro FI, Olivares M, Bañuelos O, Soria AC, Rodríguez-Sánchez S, Martínez JA, Campión J. Prevention of diet-induced obesity by apple polyphenols in Wistar rats through regulation of adipocyte gene expression and DNA methylation patterns. Mol Nutr Food Res. 2013 Mar 25.
• Boyer J, Liu RH. Apple phytochemicals and their health benefits. Nutr J. 2004 May 12;3:5.
• Caretti A, Bianciardi P, Marini M, Abruzzo PM, Bolotta A, Terruzzi C, Lucchina F, Samaja M. Supplementation of creatine and ribose prevents apoptosis and right ventricle hypertrophy in hypoxic hearts. Curr Pharm Des. 2013 Apr 10. [Epub ahead of print]  
• Gallus S, Talamini R, Giacosa A, Montella M, Ramazzotti V, Franceschi S, Negri E, La Vecchia C. Does an apple a day keep the oncologist away? Ann Oncol. 2005 Nov;16(11):1841-4. 
• Hellsten Y, Skadhauge L, Bangsbo J. Effect of ribose supplementation on resynthesis of adenine nucleotides after intense intermittent training in humans. Am J Physiol Regul Integr Comp Physiol 2004;286:R182–8.
• Michels KB, Giovannucci E, Chan AT, Singhania R, Fuchs CS, Willett WC. Fruit and vegetable consumption and colorectal adenomas in the Nurses' Health Study. Cancer Res. 2006 Apr 1;66(7):3942-53. PubMed PMID: 16585224.  
• Omran H, Illien S, MacCarter D, St Cyr J, Lüderitz B. D-Ribose improves diastolic function and quality of life in congestive heart failure patients: a prospective feasibility study. Eur J Heart Fail. 2003 Oct;5(5):615-9.  
• Price, NPJ. The Name of the–ose: An Editorial on Carbohydrate Nomenclature. J Glycobiol. 2012; 1(e105).
• Rago D, Kristensen M, Gözde G, Federico M, Morten P, LarsOve D. LC–MS metabolomics approach to investigate the effect of raw apple intake in the rat plasma metabolome. Metabolomics. 2013; 1573-3882.
• Shab-Bidar S, Hosseini-Esfahani F, Mirmiran P, Mehran M, Azizi F. Dietary intakes of zinc and copper and cardiovascular risk factors in Tehranian adults: Tehran Lipid and Glucose Study. Nutrition & Dietetics. 2013
• Sharp DS, Andrew ME, Fekedulegn DB, Burchfiel CM, Violanti JM, Wactawski-Wende J, Miller DB. The cortisol response in policemen: Intraindividual variation, not concentration level, predicts truncal obesity. Am J Hum Biol. 2013 Apr 20.
• Shecterle LM, Wagner S, St Cyr JA. A sugar for congestive heart failure patients. Ther Adv Cardiovasc Dis. 2011 Apr;5(2):95-7.
• Willers SM, Devereux G, Craig LC, McNeill G, Wijga AH, Abou El-Magd W, Turner SW, Helms PJ, Seaton A. Maternal food consumption during pregnancy and asthma, respiratory and atopic symptoms in 5-year-old children. Thorax. 2007 Sep;62(9):773-9. Epub 2007 Mar 27.
   

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

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

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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).

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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). mesenchymal stem cells 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).

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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.