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. 2013)

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. 2013).
  
  

  

  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. 2013).
  
  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. 2013), 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. 2013). 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. 2013). 

  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. 2013):
  

  • 

    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. 2013)

    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. 2013 Jun;3(6):969-972. Epub 2013 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. 2013 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. 2013 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. 2013 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. 2013 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. 2013 Jul;97(7):E1229-33. Epub 2013 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. 2013. Ahead of print.

Pharmacological Starvation: 30% Increased Life Expectancy w/ Still to be Developed FGF21 Analog - The Royal Road To Longevity? Plus: Ground Yourself It's World Nutrition Day!

Do you really think this kid cares whether there is fructose in his/her banana? Think about that before you delve into the next religious discussion about whether or not food a is legit to eat, "not paleo" or "too high in carbs" *thank you*

It's World Food Day and I thought it may be nice to remind everyone about the hilariousness of such "important" first world problems as "eating X bananas a day is bad foryou", the notion of "non paleo" foods and the rest of the vitally important topics the blogosphere is so fond of, these days. Allegedly, neither the bloggers, nor the facebookers or forum posters, who spend so much time and energy debating these and similarly worldshaking issues, will be among the 24,000 human beings who are dieing each and every day from hunger, but maybe one or another of you, of whom I am sure that they don't belong to the group of real notorious nitpickers, will have a similar "grounding experience", from just being reminded of this figure, as me, when I heard it on the radio earlier this morning.

Don't get me wrong, I am not intending to point with a finger at anyone (if anything I would have to start with pointing at myself), but if one or another of you would pause for a second or two and have a similar "grounding experience" as I had, I would be happy.

From real starvation to starvation science
 
Although this prelude appears to segue quite nicely into today's science post, I am not sure if that's even a good thing... be that as it may, after listening to the news on the radio I was quite annoyed, when I read about a recent study by Zhang, Kliewer et al. on the wonderful effects of the "starvation hormone" FGF21 (fibroblast growth factor 21; the effects were observed in mutants who overexpressed FGF21, by the way) on yet another of those awful copy & paste items on Science Daily that are 99% hype and 1% science (in the scientists' defense it must be said that I am well aware of the fact that our, i.e. university or institutionalist, press offices are writing this stuff together in this way on purpose and are not really interested in the actual science background, though). With statements such as "[the mice] got the benefits of dieting without having to limit their food intake" (UT Southwestern Medical Center. 2013) the "article" tailors perfectly to the demands of the glutenous Westerner who applies his "the more the better" principle to all areas of his super sized life that people will probably already be emailing Dr. Kliever about the release date of the drug he surely must be working on.

And in fact, the actual results of the study (Zhang. 2013), the press release specifies by quoting Kliever who said "Male mice that overproduced the hormone had about a 30 percent increase in average life span and female mice had about a 40 percent increase in average life span" sound intriguing. After all this would mean that you would have a realistic chance of making it to the magic 100, when you would otherwise have died at the age of 77.

Starvation, real or hormonal is not the way to healthy longevity!

Nonetheless, the price you would have to pay to "starve yourself into this biblical age" - pharmacologically, of course since (a) otherwise no one could make money on it and (b) no one would want to do it - is high. And I am not sure any of you is willing to pay it.

Figure 1: What do you call it, when mice simply won't grow and end up as a small copy of their normal counterparts with identical body composition, but virtually no bone mass? Right! That's failure to thrive. Now, what do you call the same phenomenon, if the poor critters live 30% longer? Yeah, righ! That's a scientific break through!

I guess you could say you can cope with being a shrimpy weed (or a tiny version of yourself, which is actually what what you would be if you had half your current weight and the same totally average body composition; see figure 1), if that means that you can see your grand grand children rise, but your chances that this is going to happen outside of a wheelchair are not particularly high for men and the chance of seeing them at all is non-existent for women.

The combination of low bone mass and infertility should actually ring a bell with everyone who has been following the Athlete's Triad Series.

Why is that? Well, next to being a pathetic weed, your bone mass and density would be so low that the chances of literally breaking apart are probably way higher than the already low chance that any of these results do even translate to human beings.

And while men who like to gamble may want to make this bet with the pharmaceutical devil, the antifertility effect of FGF21 would not allow any women making the same bet to even have children. Which does obviously not make it very likely that they will ever get to see the children of their grand children - regardless of whether they become 200 years old, by the way.

I am therefore not so sure whether the mere fact that the FGF21 mutants' mobility was not effected is evidence enough of "living a nice, long life", as Kliewer is pointing out (UT Southwestern Medical Center. 2013).

There is no way this drug will be gluttony and thus "Western lifestyle" compatible 

Figure 2: Don't be fooled! The small "g/g body weight" makes all the difference! If you weigh half of a normal human being thanks to whatever patented FGF21 derivate you take, you better make sure you eat like half a human being, as well, if you don't want to shorten your life by 30%, instead of prolonging it!

And as far as the implicit promise of being able to eat "as much as you want" goes, it may be correct that "there were no differences in food intake, physical activity, oxygen consumption or respiratory exchange ratio" (see figure 2) but if you scrutinize the caption of the Y-axis you'll see the bad, bad letters "g/g body weight". And this label means nothing else than that whoever has written the press release has been trying to fool you, when he or she wrote

"The mice that overproduced FGF21 in this latest study were lean throughout their lives and remained lean even while eating slightly more than the wild-type mice, the researchers said." (UT Southwestern Medical Center. 2013)

The truth is, they ate almost half as much as the normal animals, so where on earth was this not a starvation diet? I mean, all of you who have read parts (better the whole) SuppVersity Athlete's Triad Series will be well aware that bone loss and infertility are hallmark features of in this case exercise induced "starvation".

And let's be honest, unless Mc Donalds is going to produce XXS Menues for people on FGF21, I can guarantee you that the only effect any future drug analog of this hormone is going to have is to make people's lives even more miserable than they already are... longevity? No way! After all, this is not going to correct the dietary induced failure of our natural satiety response that constantly drives us to overeat on all those things the people who are now probably lining up in front of Mr. Kliewer's office to be part of the earliest trial are not willing to give up, although they know that they are thus easily reducing their maximal life-expectancy by 30%!

The unsexy, since inconvenient truth is missing from the mainstream science breakdown

In view of the fact that neither the press guy (or girl) nor the scientists appear to have a wested interest to tell you that FGF21 activity is "paradoxically elevated in obese conditions" (Fletcher. 2013) and that something as awfully inconvenient (and moreover non-patentable!) as exercise is the best way to normalize not only the skewed FGF21 levels, but also to increase the expression of the "longevity factor" clotho (30-50% in a classic rodent model; cf. Fletcher. 2013), I consider it my duty to let you know that you neither have to resort to the exogenous provision of drugs, nor starve yourself and can still be sure to benefit from the effects of FGF21: Either by its modulation via exercise if you are obese as the aforementioned rodents or, more importantly, by its upregulation in normal weight individuals, like the 60 sedentary young women Cuevas-Ramos et al. put on a two week exercise regimen earlier this year, only to find that their

"[s]erum FGF21 levels significantly increased after two weeks of physical activity [and that this 66%! increment in FGF 21] correlated positively with clinical parameters related to the adrenergic and lipolytic response to exercise." (Cuevas-Ramos. 2013)

Now, I don't know about you, but I, for my part, would probably risk to make a bet with the devil (pharmacological or not) that anyone who is willing and able to appropriately fuel his workouts, get his share of anabolic and restorative sleep and refrain from overtraining, will get all the benefits, the press release aptly ties solely to the unquestionable pharmacological "separation of the hormone’s life span-extending effects", Kliever is cited for in the last paragraph of the copy & paste job, without any of the downsides.

The SuppVersity Approach to Longevity is therefore simple, cheap and 100% healthy: Work out, eat healthy and get your daily dose of SuppVersity news to know how you can optimize your training, nutrition and supplementation regimen ;-)

References:

• Cuevas-Ramos D, Almeda-Valdés P, Meza-Arana CE, Brito-Córdova G, Gómez-Pérez FJ, Mehta R, Oseguera-Moguel J, Aguilar-Salinas CA. Exercise increases serum fibroblast growth factor 21 (FGF21) levels. PLoS One. 2013;7(5):e38022.
• Fletcher JA, Meers GM, Laughlin MH, Ibdah JA, Thyfault JP, Rector RS. Modulating fibroblast growth factor 21 in hyperphagic OLETF rats with daily exercise and caloric restriction. Appl Physiol Nutr Metab.
• UT Southwestern Medical Center. Newsroom. Starvation hormone markedly extends mouse life span, without need for calorie restriction. Oct 16, 2013. < http://www.utsouthwestern.edu/newsroom/news-releases/year-2013/october/starvation-hormone-mangelsdorf-kliewer.html > retrieved Oct 16, 2013.
• Zhang Y, Xie Y, Berglund ED, Coate KC, He TT, Katafuchi T, Xiao G, Potthoff MJ, Wei W, Wan Y, Yu RT, Evans RM, Kliewer SA, Mangelsdorf DJ. The starvation hormone, fibroblast growth factor-21, extends lifespan in mice. elife. 2013;1:e00065. doi: 10.7554/eLife.00065.

On Short Notice: Oxytocin to Boost Testosterone & Block Cortisol? Exercise for Life-Extension? Which Tea for Metal-Chelation? Which Fat to Reduce Calorie Intake by ~30%?

Image 1: This is still my preferred way to boost oxytocin - regardless of possible ergolytic effects ;-)

Due to the sudden heat-wave over here in good old Germany I thought, I'd use these early morning hours to get another installment of "On Short Notice" on it's way before my brain dries out (or I drown in the public swimming pool ;-). I hope you enjoy the four items on the recent interest in intranasal the hormone modulating effects of oxytocin, it's effect on cortisol and progesterone, estradiol and (I know you were waiting for that ;-) testosterone, my early morning / late evening (depending on whether you see this from my or Wyatt's perspective) 'intellectual' exchange on the potential longevity effects of exercise and why it probably is not life-extending in the literal sense, the different antioxidant potency of green, black and white tea and their ability to chelate metals (=help to remove all not just "bad" metals from the body) and the best fat, DHA or MUFA to blunt appetite and help you stick to your diet.

Don't forget to come back later today (or maybe early tomorrow for some of you ;-), for a third installment of "On Short Notice", which will hopefully suffice to "get rid" of the stock I have... ah, I did not forget about the Circadian Rhythm Series, by the way, it's just that the SuppVersity rhythm got slightly out of sync ;-)

• 

  Figure 1: Effects of 26IU of intranasal oxytocin at rest on progesterone, estradiol and testosterone in healthy men (large; based on Gossen. 2013); effects of 24IU or 48IU of intranasal oxytocin administered before a steady state cardio session on cortisol levels in healthy young men (small; from Cardoso. 2013)

  Intranasal oxytocin to block cortisol & boost testosterone A whole series of studies has been published recently; all of them have one thing in common, they investigate the various physiological and psychological effects of oxytocin. Of these, the two studies by Gossen et al. and Cardoso et al. are yet probably of greatest interest for the average physical culturist. After all, the researchers from the Centre for Research in Human Development at the Concordia University in Quebec (Canada) were able to show that the administration of 24IU (not the higher dose of 48IU, though;see figure 1) effectively reduced the increase in cortisol in a 70% HRmax steady-state cardio session in 17 healthy young men (aged 18–3; mean ± SD; 23.1 ± 3.5), in the experiment they describe in their Aug 2013 paper in Psychoneuroendocrinology (Cardoso. 2013).
  And even though the German scientists from the University of Aachen report minimal, but statistically significant increases in testosterone in 8 young men (mean age 26.4 ± 2.6 years) at rest, 210min after the (likewise) intranasal administration of a minimally higher dose (26IU) of oxytocin (Gossen. 2013). Both of these observations are not just very similar to what your average natty test booster is supposed to do, their real-world effects are probably also as insignificant. Also, did you ever try to tear down the gym and rep out a couple of PRs a couple of minutes after having sexual intercourse? If so, you should actually be aware why oxytocin probably ain't the ideal pre-workout supplement - in this regard it is also somewhat unfortunate that Cardoso et al. did not do a real performance test (suggested read: "Will Sex Before A Competition Hamper Your Performance"; note: this is not about sex minutes before the competition ;-).
  And when it comes to building muscle, previous research from Phillips lab at McMasters University appears to suggest that blocking cortisol is a hilarious idea, anyway. After tall, cortisol was the only endocrine hormone the elevation of which in the vicinity of resistance training sessions showed a positive correlation (r=0.29, P=0.03 cf. West. 2011) with increases in lean muscle mass in the large-scale by West et a.
• Exercise gets rid of the junk in your body, but will it help increase your lifespan? Basically this could be the headline to an interesting exchange of thoughts, I just had with Wyatt Brown on the SuppVersity facebook wall - one I believe is well worth being "recorded" as a short news item. The discussion came about in response to me posting the link to a study by He et al. who found that the way exercise induces autophagy (=natural, healthy cell death) contributes to its beneficial effects in the prevention of all sort of ailments, above all cancer and neurological problems such as Alzeimer's & co, because it allows your body to get rid of the debris and junk that's accumulating from just living your life (no matter how healthy or unhealthy that may be). Since exercise is not the only thing that can ramp up autophagy, and caloric restriction (as in starving yourself to live longer) can do the same, Wyatt mused about whether or not you could achieve the same (more or less; for animals vs. humans) proven benefits of life-long caloric restriction by exercise.

  

  Image 2: Twin studies are one of the ways to identify whether genes or lifestyle are the fundamental determinants of how old we get. One of the consistent findings of the numerous pertinent studies is that lifestyle factors (diet, exercise, but also our outlook on life, friends and family!) determine how well we are able to use the time that our genes (or whoever you want) has granted us on earth. Not more, but not less, either: If 100 years are what we got, all exercise and healthy eating will allow us to make it to that age with great ease, not more... and let's be honest, if that was the biblical age of 100y, wouldn't it be ungrateful to ask for more?

  A very good question, indeed and one I do not have a definite answer to. In view of recent reviews of the role of exercise in the longevity of centenarians (the oldest of the old; cf. Venturelli. 2013), it does however seem more likely that exercise does not have direct effects on the life-span, but, as Huffman states, "[e]pidemiologic evidence in humans supports exercise as a strategy to reduce the risk of morbidity and mortality" (Hufmann. 2010). Unfortunately, a low mortality won't help you to make it past the 100 ± X years your genes have in stock for you. The insights into the genetic determinants from pertinent studies into single-nucleotide polymorphisms (SNPs ~ single gene variations) does support this notion (Sorensen. 2013): The oldest of the old don't stick out, because their genes protect them from premature death, but simply because their genes allow for more cell cycles to occur before the 'natural reserve'. We already know that telomere length is a fundamental determinant of this 'reserve', so that it is not really surprising that telomere length at birth is one of the most reliable predictors of longevity (Heidinger. 2013)!
  Now, if we just use a totally random number to use basic math to make us understand, what this means, we could say that your telemore length at birth may be sufficient to make it to age 100, assuming that it is not prematurely shortened or you are dying from whatever other "natural" (not accidents etc.) cause, such as cancer, metabolic syndrome, CVD etc., exercise will of course help you to make it to those 100 years, but when the say 100,000 total turn overs that your telomeres allow for are done, you are done as well - no matter how "healthy" you eat and how much you exercise in the 99.99 years before. If you complement this "preventive" (=mortality reducing) effect by literally living on the slow lane, i.e. downregulating all your metabolic processes by starving yourself, you will obviously slow down the turn-over rate, as well. For simplicity of the calculation we assume that all these processes are linear (which I can guarantee they are not) and you are eating so little that you achieve a 50% slow down. That would mean that your turn-over rate would be reduced from 1,000 / year to 500 / year. Your reserves would last 2x longer and, assuming you eat and exercise and thus decrease your mortality risk, will allow you to make it to the ueber-biblical age of 200years! Great? Well you decide...

• 

  Image 3: If you want to get rid of metals, white tea should be your tea of choice, if you are already low on iron, copper, zinc & co. you should at least drink it away from your meals, though.

  Different tea preparations different effects antioxidant activity and metal chelation ability  It is nothing new that green and black tea will have differential effects on your physiology. What is yet a novelty is a comparison of the antioxidant and metal chelating activity the exact same hand plucked leaves of a specific cultivar (in this case PC108, bred in Malawi, typically used for black CTC tea production) will have when it is used for the production of either white, two black (Orthodox and CTC; both methods produce leaves of fannings or dust grades that are commonly used in tea bags, CTC = crush + tear + curl is processed by machines, while orthodox usually involves a mixture of mashine and manual processing) or two green (w/ and w/out caffeine) teas - a comparison like the one Patricia Carloni and her colleagues present in their latest paper in Food Research International (Carloni. 2013).
  As you will probably have expected the least processed green tea exhibited the greatest, while the most processed CTC black tea the least antioxidant activity (green ≥ low-caffeine green > white ≥ black Orthodox > black CTC), what may come as a surprise though is the superiority of white tea in the metal chelation essay the scientists performed. Closely followed by the orthodox black tea, the CTC tea (<50% of the white tea metal chelating activity) and the two green teas (<25% of the white tea metal chelating activity).

• 

  Figure 2: Reduction in calorie intake on standardized breakfast 20min after the ingestion of 6ml of a lemon flavored oil emulsion and in the course of the day compared to no oil control (based on Harden. 2013)

  Fat satiety effects: DHA > Olive Oil (MUFA) > regular diet That would be the ranking according to the satiety effects of the different fatty acids, as elucidated in a recently published study in the British Journal of Nutrition (Harden. 2013). For their study, the researchers had recruited 18 healthy normal-weight men. In a single-blind, three-way crossover study design the subjects received a single 6ml dose of either DHA or oleic acid (olive oil is 60-80% oleic acid, alternatives would macadamia ~60% and high-oleic acid sunflower oil >82%) with lemon flavor. The day before, the subjects had consumed standardized diets. 20min after the ingestion of the emulsion, they had a standardized breakfast, went home and went about their regular daily business for the rest of the day.
  The telephone interviews the researchers conducted on the next day showed that the ingestion of the DHA emulsion had exerted an, as the researchers argue cholecystokinin (CCK) dependent, decrease in energy intake of -20% and -29% for the breakfast and the total daily energy intake, respectively. That would make DHA a pretty effective tool to stick to my often-suggested -20% caloric deficit when you're dieting - at least for healthy individuals. Whether this will work for the obese, let alone morbidly obese with their deranged satiety signaling remains to be seen, though.

As I mentioned in the introduction, already. This was not the last "On Short Notice" item for this weekend. So, digest this, have some sex to calm down (unless you are about to work out, obviously), and drink a cup of tea to increase your chance to make sure that your end is not arriving before it's time and you can come back for more ;-)

References

• Cardoso C, Ellenbogen MA, Orlando MA, Bacon SL, Joober R. Intranasal oxytocin attenuates the cortisol response to physical stress: A dose-response study. Psychoneuroendocrinology. 2013 Aug 10. 
• Carloni P, Tianob L, Padellab L, Bacchettic T, Customud C, Kayd A, Damian E. Antioxidant activity of white, green and black tea obtained from the same tea cultivar. Food Research International. 2013.
• Gossen A, Hahn A, Westphal L, Prinz S, Schultz RT, Gründer G, Spreckelmeyer KN. Oxytocin plasma concentrations after single intranasal oxytocin administration - A study in healthy men. Neuropeptides. 2013 Aug 9. 
• Harden CJ, Jones AN, Maya­Jimenez T, Barker ME, Hepburn NJ, Garaiova I, Plummer SF, Corfe BM. Effect of different long­chain fatty acids on cholecystokinin release in vitro and energy intake in free­living healthy males. British Journal of Nutrition. 2013; 108:755­-758
• He C, Sumpter R Jr, Levine B. Exercise induces autophagy in peripheral tissues and in the brain. Autophagy. 2013 Oct 1;8(10).
• Heidinger BJ, Blount JD, Boner W, Griffiths K, Metcalfe NB, Monaghan P. Telomere length in early life predicts lifespan. Proc Natl Acad Sci U S A. 2013 Jan 31;109(5):1743-8. Epub 2013 Jan 9.
• Huffman DM. Exercise as a calorie restriction mimetic: implications for improving healthy aging and longevity. Interdiscip Top Gerontol. 2010;37:157-74. Epub 2010 Aug 10. 
• Soerensen M. Genetic variation and human longevity. Dan Med J. 2013 May;59(5):B4454.
• Venturelli M, Schena F, Richardson RS. The role of exercise capacity in the health and longevity of centenarians. Maturitas. 2013 Aug 7.
• West DW, Phillips SM. Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. Eur J Appl Physiol. 2013 Jul;112(7):2693-702. Epub 2011 Nov 22.

Does Your Diet Fail, 'cause You Sleep Too Little? 40 Minutes Extra Sleep Will Shed an Additional Pound of Fat in 6 Months

Image 1: Blindfolds are cheaper than light-tight curtains or shutters and they are more versatile ;-)

I have repeatedly emphasized the importance of quality sleep, here at the SuppVersity. Based on my own experience sleeping should be your your #1 priority if you want to look good, feel good and perform at your personal best on the cognitive and physiological level into your old age. Unfortunately, the number of controlled long(er)-term studies on the issue is quite small and the epidemiological data either unreliable, inconclusive or both (in most of the cases, the latter is the case; for a review see Nielsen. 2011). I was therefore happy to see that the results of one of the comparatively tightly controlled study from the Healthy Active Living and Obesity Research Group at the Children’s Hospital of Eastern Ontario Research Institute in Canada confirm my personal experience - even if the effect-size was not as pronounced as I would have expected. But let's take one thing after the other...

Take 123 overweight men and women and reduce their caloric intake by 600-700kcal ... 

... what is going to happen? Well, the answer to that question should be straight forward, right? These obese men and women, whose mean age was 41.1 years and who had an average BMI of 33.2kg/m², should begin losing weight, right? According to my previous post on "Busting the 3,500kcal = 1lbs Weight Loss Myth!" not necessarily 1lbs in 5-6 days but 1lbs in say 10 days should be the minimum. So, after the 24-week study period of trial Jean-Philippe Chaput and Angelo Tremblay conducted, the 90% of the participants who reported that they actually complied to the dietary prescription should be ~16.8lbs or 8.4kg lighter.

Figure 1: Lean mass and fat mass loss over the 24-week study period (left, calculated based on data + the information that the mean ratio of lean to fat mass loss was 3:10; Chaput. 2013); illustration of what min. and maximal weight loss would mean, if the data was normally distributed (right)

In view of the fallacy of the "calories-in-vs-calories-out" hypothesis and its logical consquence, the "eat less, lose more" diet trap, it should not come as a surprise that the average weight loss across all participants fell short of the expectations. In that, it is however interesting to remark that the expected 8.4kg are identical to the mean weight loss + one standard deviation of the same; now, if we assume a normal distribution (warning: scientific jargon! see figure 1, right for some illustrations ;-) of the data, this implies that ~16% of the subjects lost even more than my conservative prediction of 8.4kg would have suggested.

Never underestimate the fat-burning prowess of a good night's sleep!

The reasons the other 84% "underperformed", however, are manifold (keep in mind: Against the background that many obese people simply get more obese year by year even stagnation may have been progress for some). Those I consider the most important / likely ones are:

Table 1 (Chaput. 2013): This is the original table from the study and while it says "baseline characteristics" it is actually no wonder that the subjects did not lose more weight if their baseline energy intake was already as low as 1,310kcal (=5242kJ/day). After all, that would be what I would suggest as a good energy deficit (~20-30%) to lose weight, already.

• reporting to be compliant, when you actually are not - a 24h food recalls done every 2 weeks as in the study at hand are notoriously unreliable, even if subjects don't fake them intentionally.
• eating way too little - in view of the fact that the reported baseline calorie intake was only 1,310kcal the additional reduction of 600-700kcal put them in starvation mode; no wonder they hardly lost weight (I wonder if the authors did maybe enter the reduced energy intake into the "baseline characteristics table, accidentally; cf. table 1)
• not eating the right whole foods - people tend to think "if I go to starve I better starve on chocolate and pie than on broccoli and chicken filet", so that - in the absence of concrete meal plans - subjects would eat cream cake every day and still comply to their goal wrt to total energy intake

Non-compliance (suggested read: "High Carb vs. High Fat for Obese Type II Diabetics and What Really Happens, When Science Meets Real Life), over-dieting and food quality aside, there is a fourth factor which would have been on my list, as well, if it had not been on Chaput's and Tremblay's the research agend, anyways: SLEEP! Duration and quality.

Figure 2: Fat loss as a function of sleep duration (left) and sleep quality (middle; both based on Chaput. 2013); as well as the "normal" distribution of PSQI (sleep quality scores) among healthy people (right; from Buysse. 1998)

Interestingly enough, the total sleep duration remained a better predictor of dietary success, as defined by loss of pure body fat (r =0.26), than the actual sleep quality (r = -0.20; note: -1 or 1 would indicate perfect negative or perfect positive correlations) even after adjustment or age, sex, baseline BMI and the
change in total energy intake (r _Duration = 0.34 vs. r _Quality = -0.31; data not shown in figure 2). This may be surprising at first, but in view of the fact that only PSQI score greater than 5 are highly sensitive to determine whether you are or aren't a "good sleeper" it appears reasonable.

And still, my personal experience tells me that without a reasonably good sleep quality you will rather feel worse than better if you simply stayed in bed for another 83min. So my suggestion remains (see implications for more): Get yourself a blindfold and earplugs - it will make a huge change to your sleep quality and you ability to sleep longer and wake up more refreshed and don't worry about either the alarm clock or your partner. While you will hear the former anyway, your partner certainly won't mind if you are better rested and physically more attractive than ever, although that may mean that he or she will be nudging you more often to put the blindfolds to an alternative and certainly not less enjoyable use ;-)

Implications: The results of this study put another emphasis on the importance of good sleep (7-9h every night) in the context of losing weight, building a better physique and living an overall healthier and happier life. Aside from the previously mentioned ear-plugs and blindfolds, there are yet a couple of other things you can / should do to get the sleep your body needs

• go to bed with or as closely after sundown, whenever this is possible - don't worry if you are "up early" this is how life is supposed to be, not the other way around (note: alarm clocks are 100% non-paleo ;-)
• don't sacrifice your social life for sleep, but don't persuade yourself that you have to party everyday and thus cannot go to bed in time
• don't use your computer / mobile phone / social media in the vicinity of going to bed; it will delay your ability to fall asleep and the light of the small (often blueish) LCD screens will interfere with your circadian rhythm
• if anything have a shake or other readily digestible food before bed, otherwise digestion may interfere with  your sleep quality in the first 2h and losing 2 out of 8 hours of sleep could already cost you 1.4kg of body fat you would otherwise have lost (you know the figure is mere statistical shenanigan, right?)
• plan your TV consumption and set a deadline for when the boob tube must be off; even consider buying a timer switch to make sure it will be off
• consider using melatonin and light therapy for a short period of time (or strategically, when you are a shift worker) to get into the new rhythm (dosing 3-10 mg melatonin before bed, 15-45min bright light therapy when you wake up or strategically during night shifts; eg. Sharkey. 2001; Bjorvatn. 2007; Sadeghniiat-Haghighi. 2008)

There will be way more on this in the future, as I am - as some of the SuppVersity Facebook friends know - still working on a post / series of posts on the circadian rhythm and a couple of past experiences of my own - including the use of light therapy to tweak my biorhythm. For the time being I suggest that you go to the official PSQI website, download the test (click on "PSQI instrument"), fill out and evaluate the questionnaire, take the first 5 steps I have outlined above, and see if that's not already enough to get an even better night's sleep in the next two weeks to come. And just in case that's not enough or your partner has gotten so fond of the blindfolds that there simply is too little time left for sleeping during the night hours, you will soon find more information on the 6th bullet point and the whole theoretical background of circadian rhythmicity and how it can work for, but also against your... until then, good night!

References:

• Bjorvatn B, Stangenes K, Oyane N, Forberg K, Lowden A, Holsten F, Akerstedt T. Randomized placebo-controlled field study of the effects of bright light and melatonin in adaptation to night work. Scand J Work Environ Health. 2007 Jun;33(3):204-14. 
• Buysse DJ, Reynolds CF 3rd, Monk TH, Berman SR, Kupfer DJ. The Pittsburgh Sleep Quality Index: a new instrument for psychiatric practice and research. Psychiatry Res. 1989 May;28(2):193-213.
• Chaput JP, Tremblay A. Sleeping Habits Predict the Magnitude of Fat Loss in Adults Exposed to Moderate Caloric Restriction. Obes Facts 2013;5:561–566.
• Nielsen LS, Danielsen KV, Sørensen TI: Short sleep duration as a possible cause of obesity: critical analysis of the epidemiological evidence. Obes Rev 2011; 12: 78–92.
• Sadeghniiat-Haghighi K, Aminian O, Pouryaghoub G, Yazdi Z. Efficacy and hypnotic effects of melatonin in shift-work nurses: double-blind, placebo-controlled crossover trial. J Circadian Rhythms. 2008 Oct 29;6:10.
• Sharkey KM, Fogg LF, Eastman CI. Effects of melatonin administration on daytime sleep after simulated night shift work. J Sleep Res. 2001 Sep;10(3):181-92.