Sleeping Like an Athlete: Supplement Smart to Complement Your Diet, Periodize Your Training, Practice Sleep Hygiene

Blindfolds and earplugs can improve your sleep quality significantly. The special beauty of blindfolds is: unlike earplugs, blindfolds may also be used to refresh 'other things' you may be doing beneath or on top of your sheets, which in turn will help those who are struggling with getting restorative sleep (learn more)

While every idiot will tell you that ZMA is "the shit" (it indeed is, literally) its purported benefits are either insufficiently proven or even disproven, as it is the case for the alleged  anabolic effect of ZMA, which clearly don't exist (Wilborn 2004) outside of the "alternative facts" supplement companies use in pamphlets people call "write ups". Obviously, this won't stop the bros at the gym from telling you: "Dat ZMA gives me an amazingly anabolic sleep, bro!"

The reasons ZMA (unfortunately) hasn't disappeared, yet, is still in the TOP10 of an unfortunately high number of supplement retailers' sales-lists, though, is not only bropaganda. It's bropaganda that appears plausible, because both, B-vitamins and magnesium, play an important role in the physiology of human sleep.

Learn more about the effects of GABA & co at the SuppVersity

GABA Diabesity Treatment

Phenibut Addic- tive or Harmless?

All About GABA at SHR

Melatonin = Easy Fat Loss?

Letrozole? Use Melatonin Instead

Bone & Tooth? Melatonin Helps

It is thus only logical that they made it on a list scientists from Portugal and Spain compiled and published in "Arch Med Deporte" in form of a review. A review which does, unlike a dozen of articles on fitness websites, mislead its readers to believe that supplements were the basis or at least necessary for optimal sleep in athletes.

Figure 1: Rules of optimal sleep hygiene for athletes - Sleep hygiene measures that may contribute to improving the quantity and quality of sleep in athletes (from Ordóñez 2017).

You wouldn't have believed such bogus, anyway, would you? I mean, we all know that the basis of optimal sleep ain't different for athletes vs. couch potatoes, it's always sleep hygiene. The rules of sleep hygiene, on the other hand, may well differ. Periodization and a sensible control of one's training volume and intensity, for example, are nothing you'd find on the average couch potato's list because he's already training way too little to get optimal sleep.

Why do we care about sleep as athletes (and wanna-be athletes)? (1) Performance - not sleeping enough has direct negative effects on your cardio-respiratory capacity and possible negative effect on maximum and sub-maximum strength levels; (2) recovery - a lack of sleep will impair your recovery and predispose you to overtraining, with all its nasty symptoms, such as depression, confusion, anger, fatigue and reduced vigour, as well as increased levels of catabolic hormones, such as cortisol, in rest and reduction of anabolic hormones, like GH, IGF-1 and testosterone; (3) injury risk - you'll be more likely to get injured, because of sign. reductions in cognitive performance and proprioceptive and neuromuscular alterations (+ the aforementioned recovery deficits); (4) infections - a lack of sleep will impair your immune competence which, in turn, will make you more susceptible to infections; (5) muscle loss and fat gain - the former are direct effects of the previously mentioned changes in the hormonal balance [see (2)].

For you, who is obviously not a sedentary couch potato, my first advice to "fix your sleep" is thus: make sure you're not following the invalid "more helps more" approach and have been overtraining for weeks (that's in contrast to overreaching | learn more). When you've your sleep hygiene ducks in a row, go ahead and read the following paragraphs about supplements:

• 

  Figure 1: Changes in sleep in response to TRYP (Silber 2010).

  the serotonin precursor tryptophan - while it is unquestionably essential for optimal sleep, the amount of the serotonin precursor tryptophan in our diet is usually more than high enough to fulfill our dietary requirements;
  
  still, if your intake is low and/or your requirements are increased (e.g. low niacin intake and/or requirements of the tryptophan based-vitamin) or you've been stupid enough to block the entry of tryptophan into the brain by guzzling BCAAs all day (learn more), taking at least 1g (best consumed on empty) before going to bed may help you fall asleep and improve subjective sleep quality
• vitamins from the B-complex - yes, here it is B-vitamin, but the infamous B6 (pyridoxin) from ZMA, is required only in very low doses and together with folate as a co-factor in serotonin synthesis; in fact, taking too much (which is what you will find in most ZMA products) can ruin your sleep by giving you the weirdest kind of dreams;

  

  Figure 1: Possible mechanisms of the influence of dietary components on the synthesis of serotonin and melatonin (from Peuhkuri 2012). One thing you should remember, though: Most of us get all the necessary nutrients from our diet, accordingly you must not expect exorbitant benefits from taking supplements.

  often forgotten, but at least as important, especially for athletes, whose requirements may be significantly increased, is vitamin B3 aka niacin, the endogenous production of which will otherwise be favored by your body over the synthesis of serotonin from tryptophan (Peuhkuri 2012); some evidence also exists for B12, which is necessary for the proper synthesis of melatonin, and should thus have possible positive effect on the quantity of sleep, especially in vegetarian athletes, who often don't get enough B12 from their meatless and thus in many cases cobalamine-deficient diet
• overrated, but important magnesium - while there's little doubt that magnesium is important for the 5-Hydroxytryptamine enzyacetyltransferase to convert 5-HT into N-Acetyl-5-Hydroxytryptamine and which is then transformed into N-Acetyl-5-methoxy tryptamine aka Melatonin, there's little evidence that taking extra Mg has beneficial effects on sleep; in fact, scientists have yet to establish, if low magnesium is the cause of just a corollary factor of sleep problems (Nielsen 2010 | this could still mean that Mg supplementation will solve the underlying problems that keep you awake, though) and beneficial effects of supplementation have only been established in elderly subjects (Abbasi 2012), where it has been found to reverse the age-related neuroendocrine and sleep EEG changes (Held 2002)

No such conclusive evidence exists for zinc, the third ingredient in the supplement everybody will name when you ask for "sleep supplements for athletes". While an older rodent study suggests that a full-blown zinc deficiency goes hand in hand with reduced melatonin levels (Abbasi 2012), there's no evidence that zinc deficiency is (a) causally involved, (b) a major problem in the average athlete and (c) no human data to support improved sleep with zinc. Similarly promising, but not fully convincing evidence exists for

• GABA and phenibut, which I've discussed in detail (see "GABA - An Effective Sleep Aid W/ GH Boosting Effects that Works Within 30 Minutes - Only 100 mg Pre-Bed Will Suffice" | read it, and "Phenibut, Addictive Sleep Aid With Unhealthy Hangover? Dosages, Effects, Side Effects and Safety Concerns" | read it), ...
• plain dietary calcium and potassium, which are, much like magnesium, essential for protein encoding that facilitates sleep and regeneration, ...
• dietary (or supplemental) L-ornithine, the anti-stress effects of which I've likewise addressed in previous articles ( "L-Ornithine an Anti-Stress Agent: Lower Cortisol, Higher DHEA, Better Sleep W/ Only 400mg of Ornithine Pre-Bed" | read more) and 
• reduced intakes of palmitic acid (aka hexadecanoic acid), which have been found to be significantly associated with difficulties falling asleep (Grandner 2014).

All these dietary links that have been outlined quite nicely by Zeng et al. a 2014 paper about their potential use in functional foods (see Figure 3):

Figure 3: Possible mechanisms of functional components in foods promote sleep (from Zeng 2014).

Certainly effective in some, but highly debated among both scientists and practitioners, is the last supplement on the list: melatonin. Useful dosages for athletes appear to range from 3-12 mg with higher doses not necessarily working better, but increasing the risk of side effects ranging from headaches over nausea and drowsiness during the day or nightmares, all of which could potentially negatively affect your performance. I would thus not necessarily call melatonin a "must have" supplement for athletes - well,... unless you're traveling over several time zones regularly. In that case, you can use it to combat jet lag and reprogram your internal clock; or, as a Cochrane Review says you could use its "remarkabl[e effectivity] in preventing or reducing jet lag [... whenever you cross] five or more time zones, particularly in an easterly direction, and especially if [you have experienced jet lag on previous journeys" (Herxheimer 2002).

Always remember: You want to control cortisol, not eradicate it if you want to melt away your belly fat, beat your personal bests and feel just great! Learn how to control cortisol.

So, what's the verdict then? I still maintain that overtraining is the #1 reason why athletes and gymrats will have trouble sleeping. It will still make sense to keep an eye on your B-vitamin, magnesium and tryptophan intake as a complement to practicing appropriate sleep hygiene (see Figure 1).

If nothing helps, a visit to the doctor who can exclude underlying physical problems like hyperthyroidism, adrenal problems, sleep apnea and a whole host of other health problems that may affect your sleep ... I can guarantee, though, in 99% of the cases not being able to fall asleep, cannot sleep through or cannot sleep at all a lack of sleep hygiene (unable to fall asleep) and/or overtraining (waking up at  1-3AM) are to blame | Comment!

References:

• Abbasi, Behnood, et al. "The effect of magnesium supplementation on primary insomnia in elderly: a double-blind placebo-controlled clinical trial." Journal of Research in Medical Sciences 17.12 (2012).
• Grandner, Michael A., et al. "Sleep symptoms associated with intake of specific dietary nutrients." Journal of sleep research 23.1 (2014): 22-34.
• Held, Katja, et al. "Oral Mg2+ supplementation reverses age-related neuroendocrine and sleep EEG changes in humans." Pharmacopsychiatry 35.04 (2002): 135-143.
• Herxheimer, Andrew, and Keith J. Petrie. "Melatonin for the prevention and treatment of jet lag." The Cochrane Library (2002).
• Ordóñez, Fernando Mata, et al. "Sleep improvement in athletes: use of nutritional supplements." Nº 135 (Murc Tlf (2017): 93.
• Nielsen, Forrest H., LuAnn K. Johnson, and Huawei Zeng. "Magnesium supplementation improves indicators of low magnesium status and inflammatory stress in adults older than 51 years with poor quality sleep." Magnesium Research 23.4 (2010): 158-168.
• Peuhkuri, Katri, Nora Sihvola, and Riitta Korpela. "Diet promotes sleep duration and quality." Nutrition Research 32.5 (2012): 309-319.
• Silber, B. Y., and J. A. J. Schmitt. "Effects of tryptophan loading on human cognition, mood, and sleep." Neuroscience & Biobehavioral Reviews 34.3 (2010): 387-407.
• Wilborn, Colin D., et al. "Effects of zinc magnesium aspartate (ZMA) supplementation on training adaptations and markers of anabolism and catabolism." Journal of the International Society of Sports Nutrition 1.2 (2004): 12.
• Zeng, Yawen, et al. "Strategies of functional foods promote sleep in human being." Current signal transduction therapy 9.3 (2014): 148-155.

Niacin (B3) & Glucose Management | Part V of the "There is More To Glucose Control Than Carbohydrates"-Series. Plus: Can You Use Niacin to Ramp Up Fat Burning During Fasts?

Some scientists speculate that the niacin could be the root cause of the diabesity epidemic. Others believe it's the solution.

After last the installments on vitamin D and calcium, I decided that it would be about time to talk about a nutrient with (purported) negative effects on blood glucose management. After some serious head-scratching I chose niacin aka nicotinic acid and it's innocent brother niacinamide for today's fifth installment of the  my choice "There is More To Glucose Control Than Carbohydrates"-Series.

Even if you haven't been following the SuppVersity articles over the last years, you will probably be aware of some of the health effects high and low vitamin B3... ha? Right! Niacin is the only vitamin with proven HDL boosting effects (van der Hoorn. 2008).

You can learn more about this topic at the SuppVersity

Proteins, Peptides & Blood Glucose

SFA, MUFA, PUFA & Blood Glucose

Vitamin D & Diabetes

Glucose Manager Calcium?

Flush & No-Flush Niacin & Diabesity

There is more to come!

The patented slow-release version "Niaspan" is often administered in conjunction with statins to patients with hypercholesteremia - quite successfully, actually... well, at least if you discard the debilitating effects both statins and slow release niacin can have on your musculature - as a series of case-reports from the Mayo Graduate School in Rochester and the Cardiovascular Institute in New York shows, even when niacin is administered without additional lipid-lowering drugs (Litin. 1989; Gharavi. 1994 | please keep in mind that all patients in these studies were well beyond 60 and high blood lipids were not their only health problems)... but I am losing sight of our actual topic.

It's not all about blood lipid management 

While the (albeit low) risk of niacin-induced myopathies have gained only minimal attention among the research community, early reports of niacin induced insulin resistance and an significant increases in fasting blood sugar in diabetes patients on Niaspan therapy (Garg. 1990), on the other hand, have lead to a marginalization of niacin as a standalone treatment of which more recent studies would suggest that they are more or less unwarranted (Grundy. 2002).

In a 16-week, double-blind, placebo-controlled trial with 148 patients who were randomized to placebo (n = 49) or 1000 (n = 45) or 1500 mg/d (n = 52) of extended release niacin (47% of the patients were on statins at the same time), Grundy et al. found that the "rates of adverse event rates other than flushing were similar for the niacin and placebo groups" and conclude that, even in type II diabetics, "[l]ow doses of ER niacin (1000 or 1500 mg/d) are a treatment option for dyslipidemia." (Grundy. 2002)

Niacin & glucose metabolism beyond metabolic syndrome

In view of the fact that I hope that only a small minority of you will (still) belong to the group of patients doctors ans scientists usually lump together as patients suffering from "metabolic syndrome", I would suggest we steer away from the niacin for cholesterol management issue and assume a more glucose-specific perspective to decide, whether or not niacin and/or niconamide supplements or fortified foods could compromise your glucose sensitivity.

To this ends, it may make sense to take a close look at the mechanism that's responsible for the previously described increase in blood glucose in type II diabetics and the significant reductions in of the glucose infusion rate Kelly et al. measured in a study with healthy 7 healthy volunteers who had been consuming 500 mg daily nicotinic acid (=regular niacin) for 7 days then 1 g daily for a further 7 days in euglycemic clamp scenario (Kelly. 2002).

What's the mechanism?

It is generally accepted that the negative effects of niacin are mediated by its interaction with the GPR109A receptor. What scientists still argue about is, whether the effects of the ingestion of high amounts of niacin (not niacinamide, by the way!) are of direct or indirect nature. 

Now, contrary to common believe, science is actually a very simple business. In physics, specifically, history has told us that it's usually the simpler of two competing hypothesis that's the right one. Against that background it's not unlikely that the negative effects of niacin aka nicotinic acid (pyridine-3-carboxylic acid, cf. Guyton. 2007) are nothing but the mechanistic profound changes in the amount and handling of blood lipids.

Figure 1: Illustration of the niacin induced changes in FFA (initial drop and rebound after 2h); levels were measured in healthy normolipidemic volunteers after the ingestion of 2g of regular niacin (Wang. 2000)

For you as a diligent reader of the SuppVersity it should not be too difficult to see that it's the FFA / TG pin-pong that's brought up by niacin's ability to suppress the release of free fatty acids via its interaction with the GPR109A receptor which is at the heart of the acute impairments in glucose uptake (Offermanns. 2006 | recent studies have shown that this effect is accompanied by a stimulation of adiponectin production, an adipokine with beneficial effects on glucose metabolism; cf. Plaisance. 2009).

Figure 2: Consider the growth hormone release in response to the administration of niacin and the drop of free fatty acids an "added bonus" - not a growth bonus, but certainly one that will increase the liberation of bound and oxidation of free fatty acids (data based on Quabbe. 1983).

Can you (ab-)use niacin during (intermittent) fasts? Actually, I have been thinking about ways to (ab-)use the rebound effect that occurs with large (>1,000mg of niacin - in people at risk of developing type II diabetes, even niacinamide; cf. Greenbaum. 1996) for quite some time now. Someone who is "intermittent fasting", for example, should be able to ingest a large amount of niacin before a low(-ish) fat, high carb meal (e.g. after a workout) should actually benefit from the low free fatty acid & triglyceride levels in the blood (Usman. 2012) and the corresponding increase in insulin sensitivity / glucose uptake (Boden. 1997) and give a damn about the free fatty acid rebound that occurs a couple of hours later (Kamanna. 2008). In healthy individuals, the sudden appearance of large amounts of free fatty acids in the blood stream would even ramp up fatty oxidation and thus increase the energy availability during the fast - wouldn't be too bad, don't you thinks so?

Blood lipids up, glucose tolerance down! It's as easy as that and in the end a result of the way our bodies react to the overabundance of a certain type of energy source by prioritizing its usage of that of another one; and during the free fatty acid rebound that occurs ~2-3h after the ingestion of nicotinic acid the overabundant energy source if fat.

As the words "temporary" and "adaptation" in the previous sentence already suggest, this does not necessarily have to be a bad thing. I mean, as long as you don't stuff yourself with carbs during this 3h+ "fat flood" (the actual length depends on the dosage and will vary from person to person), your fasting blood glucose levels will remain stable.

Figure 3: Correlation between diabetes & obesity prevalence (left) and per capita niacin intake (mg/day) and obesity prevalence in US adults (right) from 1920 to 2000 (Zhou. 2010)

Against that background it is in my humble opinion unwarranted to speculate about a causal nature of the the correlation between the increased diabetes and obesity ratesm on the one hand, and the average per capita niacin intake of the average American you can see in Figure 3 - and that in spite of rodent studies by the same researchers which suggest that "long-term high nicotinamide intake (e.g. induced by niacin fortification) may be a risk factor for methylation- and insulin resistance-related metabolic abnormalities" (Li. 2013).

In view of the fact that grains (flour and cereals) are the most widely used vehicles for niacin-fortification, it should be obvious that the over-consumption of over-processed, but fortified junk foods, and not the relatively small amounts of extra niacin in this "foods" are much more likely to explain the increased prevalence of obesity in US adults and children, Zhou et al. and Li et al.seek to explain by a "chronic niacin overload" in their 2010 papers in BMC Public Health (Zhou. 2010) and the World Journal of Gastroenerology (Li. 2010).

On the other hand...

Moreover, we are, as usual, dealing with conflicting evidence, some of you may actually remember from the SuppVersity Facebook News (like www.suppversity.com/facebook and make sure you always stay ahead of the game | read the corresponding news item on niacin). In a rodent model of obesity and type II diabetes, a group of scientists from South Korea observed small, albeit significant increases in glucose tolerance in response to the administration of both high dose niacin (NA) and niacinamide (with niacinamide > niacin; Yang. 2014).

Figure 4: Changes in blood glucose, insulin, HOMA-IR and triglyceride levels in response to 10/100mg of niacin (NA) or niacinamide (NAM) in a rodent model of obesity and type II diabetes (Yang. 2014)

And while both nicotinic acid (niacin) and niacinamide led to improvements in insulin sensitivity (= reduced HOMA-IR), the latter lead to significant increases in triglycerides which stand in contrast to the triglyceride lowering effects of nicotinic acid.

In addition to that, there is evidence that niacin and nicotinamide decreases high glucose-dependent oxidative stress (Ye. 2011; Torres-Ramírez. 2013). What we don't have though, is reliable evidence from controlled human studies to support this Janus-faced nature of "niacin" and the purported benefits of high dose niacinamide supplementation:

• Reduced incidence of type I diabetes: Although this would appear to be rather an auto-immune issue, the net consequences of the results of a population‑based diabetes prevention trial that was conducted on school children aged 5‑7.9 years are obviously of utmost importance for glucose control (Elliott. 1996). The kids who received sustained‑release
  niacinamide 1.2 grams/m² (body surface area) per day for an average of 7.1 years had a
  lower incidence of T1DM versus controls.
• Niacinamide may also have protective benefits in T2DM. A single blind study of 18 diabetic patients found that niacinamide improves C‑peptide release leading to a metabolic control similar to patients treated with insulin (Pozzilli. 1996).
  
  The patients had been assigned for 6‑month to either: (1) insulin plus nicotinamide (500 mg three tablets/day); (2) insulin plus placebo (3 tablets/day) and (3) current sulphonylureas plus nicotinamide (500 mg three tablets/day). Compared to the placebo group, C‑peptide release increased in both the insulin/niacinamide and sulphonylureas/niacinamide groups, while HbA1C, fasting and mean daily blood glucose levels improved in the three groups to the same extent.

Eventually, I would thus be hesitant to recommend using amounts of 1,500mg of niacinamide or niacin / nicotinic acid (the terms are used inter-changeably) per day as a strategy to prevent the development of type II diabetes. If you stay active and stay away from the niacin-fortified junk Zhou and Li failed to recognize as the common denominator of the increases in niacin intake, obesity and diabetes, you don't need it anyway.

Figure 5: The increases in HOMA-IR Westphal et al. observed in response to the administration of 1g/1.5g of niacin in patients with high LDL and low HDL levels look more severe than they actually are - in fact, they did not even achieve statistical significance. In contrast to the beneficial effects on adiponectin and HDL (Westphal. 2006)

Bottom line: Our regular niacin intake, as well as the comparatively low amounts of niacin and niacinamide in multi-vitamins and other useless supplements are not going to push you over the diabetic edge. As far as high dose supplements are concerned, we will probably have to distinguish between extended release (ET) preparations, which would be used for lipid management and immediate release forms of niacin and nicotinamide.

The extended release (ET) preparations appear to be useful as lipid lowering drugs. Their effects on blood glucose management are yet either neutral or negative (). High amounts of the "regular", flush-niacin, will produce a free fatty acid rebound and transient impairments in insulin sensitivity, of which I would like to see if you they cannot be used to your advantage (see infobox "Can you (ab-)use niacin during fasts?". Unlike ET and "flush" niacin, nicotinamide does not interact with the GPR109A receptor (Soga. 2003; Tunaru. 2003; Wise. 2003) and will thus neither produce free fatty acid rebounds nor will it raise your HDL, adiponectin and leptin levels (Westphal. 2006 & 2007; see Figure 5). In other words, it's benign, but useless - this is at least what we have to assume until there is convincing evidence from human studies outside of type-I-diabetes scenarios as they were described by Elliott (1996) or Pozzilli (1995).

References:

• Boden, Guenther. "Role of fatty acids in the pathogenesis of insulin resistance and NIDDM." Diabetes 46.1 (1997): 3-10.
• Elliott, Robert B., et al. "A population based strategy to prevent insulin-dependent diabetes using nicotinamide." Journal of Pediatric Endocrinology and Metabolism 9.5 (1996): 501-510.
• Fernandez-Mejia, Cristina. "Pharmacological effects of biotin." The Journal of nutritional biochemistry 16.7 (2005): 424-427. 
• Garg, Abhimanyu, and Scott M. Grundy. "Nicotinic acid as therapy for dyslipidemia in non—insulin-dependent diabetes mellitus." Jama 264.6 (1990): 723-726.
• Gharavi, Ali G., et al. "Niacin-induced myopathy." The American journal of cardiology 74.8 (1994): 841-842.
• Greenbaum, Carla J., Steven E. Kahn, and Jerry P. Palmer. "Nicotinamide's effects on glucose metabolism in subjects at risk for IDDM." Diabetes 45.11 (1996): 1631-1634.
• Guyton, John R. "Niacin in cardiovascular prevention: mechanisms, efficacy, and safety." Current opinion in lipidology 18.4 (2007): 415-420.
• Grundy, Scott M., et al. "Efficacy, safety, and tolerability of once-daily niacin for the treatment of dyslipidemia associated with type 2 diabetes: results of the assessment of diabetes control and evaluation of the efficacy of niaspan trial." Archives of internal medicine 162.14 (2002): 1568-1576.
• Kamanna, Vaijinath S., and Moti L. Kashyap. "Mechanism of action of niacin." The American journal of cardiology 101.8 (2008): S20-S26. 
• Kelly, J. J., et al. "Effects of nicotinic acid on insulin sensitivity and blood pressure in healthy subjects." Journal of human hypertension 14.9 (2000).
• Lauring, Brett, et al. "Niacin lipid efficacy is independent of both the niacin receptor GPR109A and free fatty acid suppression." Science translational medicine 4.148 (2012): 148ra115-148ra115. 
• Li, Da, et al. "Chronic niacin overload may be involved in the increased prevalence of obesity in US children." World journal of gastroenterology: WJG 16.19 (2010): 2378. 
• Li, Da, et al. "Nicotinamide supplementation induces detrimental metabolic and epigenetic changes in developing rats." British Journal of Nutrition 110.12 (2013): 2156-2164.
• Litin, Scott C., and Carl F. Anderson. "Nicotinic acid-associated myopathy: a report of three cases." The American journal of medicine 86.4 (1989): 481-483.
• McCarty, M. F. "High-dose biotin, an inducer of glucokinase expression, may synergize with chromium picolinate to enable a definitive nutritional therapy for type II diabetes." Medical hypotheses 52.5 (1999): 401-406. 
• Offermanns, Stefan. "The nicotinic acid receptor GPR109A (HM74A or PUMA-G) as a new therapeutic target." Trends in pharmacological sciences 27.7 (2006): 384-390.
• Plaisance, Eric P., et al. "Niacin stimulates adiponectin secretion through the GPR109A receptor." American Journal of Physiology-Endocrinology and Metabolism 296.3 (2009): E549-E558.
• Pozzilli, P., et al. "Adjuvant therapy in recent onset type 1 diabetes at diagnosis and insulin requirement after 2 years." Diabete & metabolisme 21.1 (1995): 47-49.
• Pozzilli, Paolo, Peter D. Browne, and Hubert Kolb. "Meta-analysis of nicotinamide treatment in patients with recent-onset IDDM." Diabetes Care 19.12 (1996): 1357-1363.
• Quabbe, Hans-Jürgen, et al. "Growth Hormone, Cortisol, and Glucagon Concentrations during Plasma Free Fatty Acid Depression: Different Effects of Nicotinic Acid and an Adenosine Derivative (BM 11.189)*." The Journal of Clinical Endocrinology & Metabolism 57.2 (1983): 410-414. 
• Soga, Takatoshi, et al. "Molecular identification of nicotinic acid receptor." Biochemical and biophysical research communications 303.1 (2003): 364-369. 
• Torres-Ramírez, Nayeli, et al. "Nicotinamide, a glucose-6-phosphate dehydrogenase non-competitive mixed inhibitor, modifies redox balance and lipid accumulation in 3T3-L1 cells." Life sciences 93.25 (2013): 975-985.
• Tunaru, Sorin, et al. "PUMA-G and HM74 are receptors for nicotinic acid and mediate its anti-lipolytic effect." Nature medicine 9.3 (2003): 352-355.
• Usman, M. Haris U., et al. "Extended-release Niacin Acutely Suppresses Postprandial Triglyceridemia." The American journal of medicine 125.10 (2012): 1026-1035.
• van der Hoorn, José WA, et al. "Niacin increases HDL by reducing hepatic expression and plasma levels of cholesteryl ester transfer protein in APOE* 3Leiden. CETP mice." Arteriosclerosis, thrombosis, and vascular biology 28.11 (2008): 2016-2022.
• Wang, Wei, et al. "Effects of nicotinic acid on fatty acid kinetics, fuel selection, and pathways of glucose production in women." American Journal of Physiology-Endocrinology And Metabolism 279.1 (2000): E50-E59.
• Westphal, Sabine, et al. "Extended-release niacin raises adiponectin and leptin." Atherosclerosis 193.2 (2007): 361-365. 
• Wise, Alan, et al. "Molecular identification of high and low affinity receptors for nicotinic acid." Journal of Biological Chemistry 278.11 (2003): 9869-9874.
• Yang, Soo Jin, et al. "Nicotinamide improves glucose metabolism and affects the hepatic NAD-sirtuin pathway in a rodent model of obesity and type 2 diabetes." The Journal of nutritional biochemistry 25.1 (2014): 66-72.
• Ye, X., et al. "Niaspan reduces high-mobility group box 1/receptor for advanced glycation endproducts after stroke in type-1 diabetic rats." Neuroscience 190 (2011): 339-345.
• Zhou, Shi-Sheng, et al. "B-vitamin consumption and the prevalence of diabetes and obesity among the US adults: population based ecological study." BMC public health 10.1 (2010): 746.

Grape Seed Extract Protects EPA & DHA From Intestinal Oxidation. Niacin Shifts Muscle Fiber Type. Cholesterol & Sialic Acid Build Babies' Brains. Pro-Diabetic GUMPs 4 Kids

"What? Don't gimme that look. I did walk to the fast-food outlet. I swear!" - When it comes to how much they sit around, people love to lie... ah, I mean they often overestimate their activity level - especially the really lazy ones ;-)

It's not always easy to find a "figure of the week" and actually the on I am going to present you today is not "week specific". It is rather related to yesterday's post on the statistics of the diabesity epidemic. That said, you may remember that the gap between "more" and "less" active individuals was widening, but on average the NHANES stats would suggest that the average US citizen is not sitting around much longer today (or rather in 2004) than 40 years ago. Now, the NHANES data is based on a questionnaire of which Healy et al., who have analyzed the accuracy of these self-reported activity levels in a 2010 paper (Healy. 2011), found that the difference between the real and the claimed sedentary time increases by one hour for every 3h of sedentary time (at least for people with a sedentary time of >7h)

In other words, someone who actually sits on his booty for 10h will be telling you that he would be sitting around for 9 hours. It should be said though that there are outlier on both sides so that it may well be that the guy will boldly lie to you and tell you he would sit around max. 7h per day. The chances that he underestimates his activity level, on the other hand, are slim; and if he does it's by no more than 1h.

Now that we have already been talking about health, why don't we simply keep on this track and take a look at a handful of recently published studies which may help you to do what it takes to keep "healthy, happy and lean" (cf. "bottom line" of yesterday's post): learn what's good for you (and your family) and take responsibility for your own well-being.

Grape seed extract to protect and deliver unoxidized omega-3 fatty acids

(Maestre. 2013) -- If we assume that you want your omega-3 fatty acids unoxidized (this is by no means sure, see link beneath the image on the right), it would be prudent to ingest your fish, but even more so the unprotected fish oil from caps with some grape seed extract.

Surströmming, a Swedish delicates that's essentially rancid fish. Can't be healthy? Well, even with pure, yet oxidized fish oils did not have any negative health effects in previously healthy individuals in (read more)

That's at least what a recent study by scientists from the Department of Seafood Chemistry at the Instituto de Investigaciones Marina in Vigo, Spain and their US colleagues from the Department of Nutritional Sciences at the Rutgers University in New Brunswick, NJ, would suggest.

In their latest paper that has been published in the last issue of the Journal of Nutrition the scientists report that the addition polyphenol-rich grape seed extract (GSE) during the in-vitro digestion of omega-3 fatty decreased the amounts of oxidation products in the stomach compartment and intestinal dialysate and would thus facilitate a higher uptake of intact omega-3 fatty acids in the intestine.

Want more type I and less type II fibers? Niacin is your friend, then

(Ringseis. 2013) -- Hard do believe but after one months of niacin supplementation (750 mg/kg diet niacin aka vitamin B3, also "nicotinic acid") the obese Zucker rats in a recent study by Robert Ringseis, Susann Rosenbaum, Denise K. Gessner et al. exhibited a statistically significant shift towards a more oxidative (type I) muscle type.

Is there a connection between niacin and the diabesity epidemic or is the increase in niacin intake (also due do fortification) and the explosion of the obesity and diabetes rates coincidence?
(Figure from Zhou. 2010)

Unfortunately the latter are not without side effects - especially for those who don't really need to lower their blood lipids, where the administration of high dosages of nicotinic acid will induce transient insulin resistance (Poynten. 2003). And contrary to hyperlipidemic obese individuals the he increased use of fatty acids by the skeletal muscle is a cold comfort for healthy people like (I hope) you, especially in view of the fact that it adds to already existent negative modulators of insulin sensitivity such as aging (Chang. 2006)

And while these "pro-diabetic" effects may not be as pronounced from nicotinamide (the stuff that's usually in supps, because it won't make you flush), the latter has also been shown to reduce insulin sensitivity in people with at high risk of insulin dependent diabetes mellitus (Greenbaum. 1996).The increased oxidative capacity went hand in hand with the well-known lipid lowering effects of niacin (Creider. 2012).

The main difference being that the 2g of nicotineamide the subjects in that study received lack most of the beneficial effects of "real" niacin. So is the common practice to "fortify" foods with this stuff turning all of us into diabetics (cf. Li. 2012)? I tend to agree with Paul Jaminet who wrote an excellent article on that matter back in the day that it is - on it's own - probably not a problem, but if you add tons of multivitamins and other niacin / nicotinamide laden supps on top, you could in fact risk running into trouble without even the slightest chance to see any benefits.

Sialic acid and cholesterol two vitally important bad guys

Low (or insufficient?) sialic acid (in mmol/L), another reason for the inferiority of formula vs. breast milk (Wang. 2001) - use your brain and make sure your kids will be able to use theirs, as well (Wang. 2001).

(Scholtz. 2013) -- I guess you are by now over the "dietary cholesterol is bad for you" mantra and probably did not even know that sialic acid (SA) is another of those supposedly bad guys, which do eventually turn out to be as bad as the jacketed metal bullets are made of.

The latter is what a recent study from the University of Kansas Medical Center clearly indicated for both of them cholesterol, as well as sialic acid, a monosaccharide with a nine-carbon backbones that's a derivate of neuroaminic acids. While it has been implicated in cancer development, influenza infection or bacterial infections (as a food for the bacteria), the recent paper by Scholtz and her coworkers clearly shows that it's high presence in human milk is just like that of cholesterol necessary for optimal brain development:

"Cholesterol exposure from conception to P32 increased cortex weight (P = 0.003) and the concentrations of cortical cholesterol (P = 0.006), protein (P = 0.034), and ganglioside SA (P = 0.02). Independent of cholesterol feeding, SA fed from P17 to P32 [post natal day 17 to 32] increased the cortical ganglioside SA concentration (P-trend = 0.007)."

Their conclusion that "[d]ietary cholesterol and SA independently contribute to brain cortex composition during early brain development." (Scholtz. 2013) also puts a huge question mark behind the current nutrient composition of infant formulas which are significantly lower in both these "bad" nutrients than mother's milk. And I guess I don't have to mention that the "healthy" soy "milk" is almost devoid of both this vital nutrients.

Pro-Diabetic formula - "Growing Up Milk Powders" today, insulin therapy tomorrow?

(Brand-Miller. 2013) -- It's really amazing how parents are fooled by the industry to believe they would do their kids a favor, when they buy "milk products" that have been specifically formulated for kids: Sweet and delicious, just like kids like it, so that parents who are worried about the health of their kids don't have fret, when the little ones refuse to drink their milk. If only they knew,...

What to make of this study? The study was sponsored by the Fonterra Research Centre, who certainly have a vested interest in pointing out the weaknesses of the sugary "dairy" products of their competition. And the "milk replacements" that have been tested in the study are mainly used in Asia (in fact, all products are sold and were purchased in Malaysia and Indonesia), but that does not nullify the results and the validity of the scientists conclusion that "there is the potential for the risks to outweigh the benefits if manufacturers do not take a responsible approach in formulation" (Brand-Miller. 2013)

Yeah, if only the knew about the results of a recent study by Jennie Brand-Miller, Fiona Atkinson and Angela Rowan who studied the glycemic index and glycemic load of 7 products that had been specifically selected to represent the full spectrum of 58 previously analyzed so-called "Growing Up Milk Powders" (GUMPs) and found that:

"[Milk p]roducts containing maltodextrins, corn or glucose syrups increased the GI by more than 2-fold, and glycemic load (GL) by 7-fold compared to milk powders with no added  carbohydrates." (Brand-Miller. 2013)

Just to make sure no one misses the crucial point here. Even products that contain maltodextrin or corn syrup and could thus carry a label like "no added sugar" will raise the insulin level 2x more than regular milk and an even 7x higher glycemic load.

---

That's it for today, but obviously there is more for those of you who feel the weight of the initially mentioned responsibility on their shoulders and want to make sure they don't mess up on the SuppVersity's facebook wall. Let's see, what do we have?

"Strong is the Better Sexy!" Study Shows: Athletes Are Better Role Models for Women Than Sexualized Cover Models for young women (read more)
.

• Healthy marathon running - if at all, only for women!? Men 5.7x more likely to suffer from sudden cardiac arrest (SCA) during a marathon. 11/13 men with SCA are 40+ (read more)
• Sex differences in body dissatisfaction and its effects on eating behavior in athletes: Women hate themselves for each lbs of body fat. Men are more complex (also consider BMI) and don't change their diet if they feel they are too fat / skinny (read more)
• Common CoQ10 wisdom debunked: CoQ10 + Selenium do not reduce statin induced myopathy (read more)
• Woman with slimmer waistlines improve their significant other's sexual performance... or if your girlfriend has a 120er waist your chances of having erectile dysfunction increase significantly (read more)
• There is more & still more to come in the course of the next 24h @ www.facebook.com/SuppVersity

Assuming you are still hungry for more, I suggest you head over to CasePerformance to learn why supplements are so freaking expensive and price is no indicator of quality let alone efficacy in the 2nd installment of the CasePerformance New Year's Resolution Series.

References:

• Brand-Miller J, Atkinson F, Rowan A. Effect of added carbohydrates on glycemic and insulin responses to children’s milk products. Nutrients. 2013 Jan 10;5(1):23-31.
• Chang AM, Smith MJ, Galecki AT, Bloem CJ, Halter JB. Impaired beta-cell function in human aging: response to nicotinic acid-induced insulin resistance. J Clin Endocrinol Metab. 2006 Sep;91(9):3303-9. Epub 2006 Jun 6.
• Creider JC, Hegele RA, Joy TR. Niacin: another look at an underutilized lipid-lowering medication. Nat Rev Endocrinol. 2012 Sep;8(9):517-28.
• Greenbaum CJ, Kahn SE, Palmer JP. Nicotinamide's effects on glucose metabolism in subjects at risk for IDDM. Diabetes. 1996 Nov;45(11):1631-4. 
• Healy GN, Clark BK, Winkler EA, Gardiner PA, Brown WJ, Matthews CE. Measurement of adults' sedentary time in population-based studies. Am J Prev Med. 2011 Aug;41(2):216-27.
• Li D, Sun WP, Zhou YM, Liu QG, Zhou SS, Luo N, Bian FN, Zhao ZG, Guo M. Chronic niacin overload may be involved in the increased prevalence of obesity in US children. World J Gastroenterol. 2010 May 21;16(19):2378-87.
• Maestre R, Douglass JD, Kodukula S, Medina I, Storch J. Alterations in the Intestinal Assimilation of Oxidized PUFAs Are Ameliorated by a Polyphenol-Rich Grape Seed Extract in an In Vitro Model and CACO-2 Cells. J Nutr. 2013 Jan 16.
• Poynten AM, Gan SK, Kriketos AD, O'Sullivan A, Kelly JJ, Ellis BA, Chisholm DJ, Campbell LV. Nicotinic acid-induced insulin resistance is related to increased circulating fatty acids and fat oxidation but not muscle lipid content. Metabolism. 2003 Jun;52(6):699-704.
• Ringseis R, Rosenbaum S, Gessner DK, Herges L, Kubens JF, Mooren FC, Krüger K, Eder K. Supplementing Obese Zucker Rats with Niacin Induces the Transition of Glycolytic to Oxidative in Skeletal Muscle Fibers. J. Nutr. 2013; 143: 125-131.
• Scholtz SA, Gottipati BS, Gajewski BJ, Carlson SE. Dietary Sialic Acid and Cholesterol Influence Cortical Composition in Developing Rats. J Nutr. February 1, 2013; 143(2):132-135.
• Wang B, Brand-Miller J, McVeagh P, Petocz P. Concentration and distribution of sialic acid in human milk and infant formulas. Am J Clin Nutr. 2001 Oct;74(4):510-5.
• Zhou SS, Li D, Zhou YM, Sun WP, Liu QG. B-vitamin consumption and the prevalence of diabetes and obesity among the US adults: population based ecological study. BMC Public Health. 2010 Dec 2;10:746.

SuppVersity Science Round Up Seconds: Wheat Gluten Hydrolysates Fail, Exposure to Air Pollutants During Workout Reduces Brain Benefits, Homocysteine, B-Vitamins, Cognitive Impairment and Mortality

Before the profound weight loss (A) you don't see any of the glucose sucking and fad burning brown fat depots (black spots in B) on the neck of the in (B) 'foermerly obese', now only 'overweight' subject (also take a look at how the visceral fat in the abdominal region in (A) is actually pushing the organs upwards; img Vijgen. 2012)

Those of you who have listened to yesterday's show will have noticed that despite its flow the number of things you can discuss in a 1h podcast is simply very limited, to say the least. This is also why these Friday posts are probably never going to be simple summaries of the SuppVersity Science Round Up of the day before. The same is true for today and still I decided not to use the allegedly lame logo I did for the first two installments, but provide you with some 'real science' evidence of the absence of brown adipose tissue on the obese and it's magical reappearance after shedding 100lbs+ subsequent to a gastric bypass operation, instead (see image on the right).

Assuming that you have no idea what this "evidence" is for, I would suspect that you missed the live show yesterday and also did not find the time to download and listen to the podcast, yet -- right? Well, you should either download and listen to the show now and digest the Seconds later, or you read the following paragraphs first and download the podcast later.

What is not an option, however, is to miss one or another - I mean you can hardly want to eat the seconds if you have not had the main dish yet... and after listening to the podcast, I cannot imagine you don't want at least some seconds. Apropos seconds, here are today's seconds...

• Wheat gluten hydrolysate is not the new goto protein supplement - certainly not for female distance runners and probably not for anyone else, either! These are the kinds of studies that really annoy me. Studies that start out with blatant statements like "WGH [Wheat gluten hydrolysate] has been reported to suppress post-exercise rises in serum creatine kinase in male distance runners" (Hirao. 2012).
  
  

  

  Figure 1: CK, AST, ALT response in the "success trial" with men. In women even the miniscule beneficial effect on CK was not there. No reason to even think about buying a gluten hydrolysate as you new go-to protein supplement with only 5.6g of leucine/100g (whey has 50% more) and almost no GSH replenishing cysteine in it (0.9g vs. 3g+ in whey, which is more than +200% more).

  Sentences like that make the null-results of the study they precede look like the exception to the rule and are still nothing but a concession to a bias (let's hope not due to the grant from Nisshin Pharma Inc. which was the manufacturer of the wheat gluten hydrolysate used in this study). A bias, due to which an isolated observation as the slightly blunted increase in CK is blown up as if a slightly lower CK level was what could turn a sedentary pencil pusher into the next Hussein Bolt (Aoki. 2012).
  
  So, even if you are not afraid of the evil in gluten (which I believe not everyone has to), I strongly caution against making the switch from a high EAA protein with ton's of GSH boosting cysteine in it like whey to a mediocre grain protein, which is a potential allergen and contains tons of glutamine your body will readily turn into glucose, once it passes through the portal veign into the liver (I bet a large part won't even make it into systemic circulation).
  
  And as far as the purported "gender difference" goes the study at hand tries to blame the null result on (Hiriao. 2012), I suspect that it is rather the indisputable difference between the long-distance running at a continuous pace the women in the study at hand did, versus the totally different strains the guys in the previous study were exposed to during a soccer training + mini-match, which made the difference.
• Working out next to a street takes away some of the beneficial cognitive effects due to ultrafine particulate matter (UFPM) exposure. "Working out in the fresh air will promote weight loss more than working out inside." You heard me state that in one of the previous installments of the SuppVersity Science Round Up on Super Human Radio. Now this is still correct and based on sientific evidence, but at least as far as the cognitive benefits are concerned, working out outside does also have its downsides - at least for those of you who live in the inner city area.
  
  

  

  You better watch what you breath while you run.

  During a 12-week program the researchers from the Universiteit Brussel, the Hasselt University and the Royal Military Academy measured the improvements in physical performance, changes in serum markers and corresponding ultrafine particulate matter (UFPM) concentrations in the enviromnent in which their 15 previously untrained subjects conducted their aerobic training program thrice a week (Bos. 2012). What Bos et al. found was that the UFPM levels were signfificantly higher in the urban compared to the rural environment and that the higher UFPM exposures correlated with increases in leukocyte counts (p = 0.02), neutrophil counts (p = 0.04), and eNO levels (p = 0.002) that were exclusively observed in the group that trained in the urban environment.
  
  With the latter being markers of inflammation which exert their effects systemically, i.e. not just in the lung or musculature of which you may be thinking now, but also in the brain, it is no wonder that
  

  "reaction times on the Stroop task improved in the rural group (p = 0.001), but not in the urban group" (Bos. 2012). 

  What's comforting, though, is that the physical fitness did increase to a similar extend in both arms of the study.
• Homocysteine levels, mortality, cognitive impairment and which nutrients can offer some protection. I am not sure about what your impression is, but for whatever reason homocystein seems to be 'out of vogue' -- probably no room for it on the research agenda with all the hype surrounding vitamin D. It used to be all the rage in CVD risk research and today's news item is actually ain't about cardiovascular health, either.
  
  What the researchers from China and Taiwan actually were interested in was the correlation of high and low homocysteine levels with cognitive impairment and the corresponding nutrient intakes. In that Xiu et al. paid particular attention to the "B-vitamins" and found the following correlations between the mortality, cognitive status, homocystein levels and nutrient intake of their 1412 study participants (Xiu. 2012):
  

  • 

    Figure 2: Unadjusted mortality in the four quartiles of homocysteine levels (top); mortality according to homocysteine levels in subjects with different degrees of cognitive impairment (based on Xiu. 2012)

    if you go by the unadjusted data in figure 2, it's plain obvious that the all-cause mortality increases linearly from one quartile to the other 
  • this relation between plasma homocysteine levels and all mortality remained statistically significant after adjustments for age, sex, smoking status, BMI, physical function and general health were made
  • of the general foods, the scientists assessed, only regular fish intake had a statistically significant effect on homocysteine levels, with higher intakes being associated with lower homocysteine levels
  • of the b-vitamins choline was the only one with a significant association with plasma homocysteine levels (suggested read "Old School Supplement Choline Could Save Your Live and Liver!") 
  • neither betaine, nor vitamin B1, B2, B3 or B6 intakes did show statistically significant correlations with plasma homocysteine (not even "borderline significant; p > 0.15 for all, most way hither)
  • of the plasma markers, folate showed a highly significant correlation with homocysteine (14.4 nmol/L in the lowest HCY and 8.70 nnmol/L in the highest HCY group)
  • PLP, the active form of vitamin B6, came in close second with 70.3 nmol/l in the lowest HCY quantile and only 44.4 nmol / l in the highest quantile.
  Now, if you consider the fact that higher intakes of B-vitamins are probably not doing much to lower homocysteine levels int he elderly (at least not dose-dependently, when they are already getting enough) oddity #1, another look at the data in figure 2 will reveal oddity #2: The surprisingly high mortality in the lowest homocysteine quartiles in the patients with severe cognitive decline - how come? I mean, with low homocysteine they should not be at risk of having severe cognitive decline, anyway - right?
  
  Actually if you follow this rationale you can almost answer the question yourself. If you have low homocysteine and severe cognitive decline, the severe cognitive decline can hardly be from high homocysteine levels, so it must have another obviously pathological reason, or as the scientists have it
  

  "The joint effects of the 2 variables [homocysteine and cognitive decline] were most pronounced with severe cognitive impairment where mortality HRs ranged from 5- to 18-fold across a wide range of homocysteine concentrations. The findings with hypohomocysteinemia provide some insight into what might be an optimal range for this analyte in peripheral blood and tissues. The low concentrations may be seen with severe illness and malnutrition, and our study population comprises the health-vulnerable aged. For these reasons, we adjusted these associations for BMI (using the World Health Organization chronic energy deficiency category of, 18.5 kg/m 2 ), and we excluded those who died in the first year of follow-up. The findings were unchanged. Because mortality among the very old may have skewed the joint effects, these are presented for those ≤75 years and over, but again with similar findings." (

  A sarcastic person would now probably say: "We all have to go some time!" and just wave his hands at these results. True! And I am the last to advice you to become over-anxious. Yet in the mean time it would appear prudent to make sure to get your homocysteine levels checked from time to time, not to forget that choline is a b-vitamin as well and not to fall for the idea that you cannot overdose on B-vitamins - I don't have to remind you of the negative effects, specifically folic acid supplementation can have on all sorts of cancer (e.g. breast cancer, where a high folic acid intake from foods and supplements is associated with a +30% risk of cancerous growth; cf. Kim. 2006).

In case you are looking for the post on "ammonia accumulation brain-fog, toxicity, liver 'pathologies' and workout performance", yeah it was on the list, but I decided it would be a shame to tackle that within a short two paragraph seconds items. Don't worry I am not going to forget about it, after all its in my humble opinion one of the main reasons the diets and workout regimen of the many ambitious physical culturists fail. If you are still looking for more and have not listened to the podcast, yet, this would be the right moment to download the file from the Super Human Radio Network server (click here to download), otherwise the latest short news on the SuppVersity Facebook Wall may offer some diversion ;-)

References:

• Aoki K, Kohmura Y, Suzuki Y, Koikawa N, Yoshimura M, Aoba Y, Fukushi N, Sakuraba K, Nagaoka I, Sawaki K. Post-training consumption of wheat gluten hydrolysate suppresses the delayed onset of muscle injury in soccer players. Exp Ther Med. 2012 Jun;3(6):969-972. Epub 2012 Apr 3.
• Bos I, De Boever P, Vanparijs J, Pattyn N, Panis LI, Meeusen R. Subclinical Effects of Aerobic Training in Urban Environment. Med Sci Sports Exerc. 2012 Oct 15.
• Cankurtaran M, Yesil Y, Kuyumcu ME, Oztürk ZA, Yavuz BB, Halil M, Ulger Z, Cankurtaran ES, Arıoğul S. Altered Levels of Homocysteine and Serum Natural Antioxidants Links Oxidative Damage to Alzheimer's Disease. J Alzheimers Dis. 2012 Oct 29.
• Guest PC, Urday S, Ma D, Stelzhammer V, Harris LW, Amess B, Pietsch S, Oheim C, Ozanne SE, Bahn S. Proteomic analysis of the maternal protein restriction rat model for schizophrenia: Identification of translational changes in hormonal signalling pathways and glutamate neurotransmission. Proteomics. 2012 Oct 16.
• Hirao T, Koikawa N, Aoki K, Sakuraba K, Shimmura Y, Suzuki Y, Sawaki K. Female distance runners show a different response to post-workout consumption of wheat gluten hydrolysate compared to their male counterparts. Exp Ther Med. 2012 Apr;3(4):641-644.
• Kim YI. Does a high folate intake increase the risk of breast cancer? Nutr Rev. 2006 Oct;64(10 Pt 1):468-75.
• Vijgen GH, Bouvy ND, Teule GJ, Brans B, Hoeks J, Schrauwen P, van Marken Lichtenbelt WD. Increase in brown adipose tissue activity after weight loss in morbidly obese subjects. J Clin Endocrinol Metab. 2012 Jul;97(7):E1229-33. Epub 2012 Apr 24.
• Xiu LL, Lee MS, Wahlqvist ML, Chia-Yu Chen R, Huang YC, Chen KJ, Li D. Low and high homocysteine are associated with mortality independent of B group vitamins but interactive with cognitive status in a free-living elderly cohort. Nutr Res. 2012. Ahead of print.

B-Vitamins & Diabetes: Protective or Causative?

In a very interesting study, scientists from China and Japan (Zhou. 2010) found that "long-term exposure to high level of the B vitamins may be involved in the increased prevalence of obesity and diabetes in the US in the past 50 years". At first this appears to be counterintuitive, since we have been told over and over that B-Vitamins are not only good for our health, but that we could not even "overdose" them. While the latter has been questioned for years and certainly is not the case for e.g. B6 and niacin, even the former seems questionable, if you read the results from the above mentioned study:

The prevalences of diabetes and adult obesity were highly correlated with per capita consumption of niacin, thiamin and riboflavin with a 26- and 10-year lag, respectively (R2 = 0.952, 0.917 and 0.83 for diabetes, respectively, and R2  = 0.964, 0.975 and 0.935 for obesity, respectively). [...] The relationships between the diabetes or obesity prevalence and per capita niacin consumption were´similar both in different age groups and in male and female populations. The prevalence of adult obesity and diabetes was highly correlated with the grain contribution to niacin (R2 = 0.925 and  0.901, respectively), with a 10- and 26-year lag, respectively.

These results (especially those referring to the detrimental effect of niacin) confirm test-tube studies conducted by a group of scientists from South Korea earlier this year (Choi. 2010), who found that

NA [nicotinic acid] alters gene expression in insulin-sensitive tissues by various mechanisms. Some of the NA-induced changes in gene expression are discussed as potential mechanisms underlying wanted and unwanted effects of NA treatment.

Just anecdotal: My personal perspective on B-vitamins has changed since my overall energy and well being, as well as my physique have largely improved after stopping to take those B-vitamin (over-)loaden mulit-vitamin preparations like Now ADAM, CL Orange Triad, Animal Pak, ON Opti-Men etc. But remember: it is mere speculation that this could in fact be related to their high B-vitamin contents - could be any other constituent, as well.