Health & Exercise Quickie: Vitamin D Deficiency, Taurine & Glycine. Multiple Sclerosis & Epstein-Barr. Paracetamol & Muscle Gains. Gender & Fatigue from Workouts. HIIT, LISS & Appetite. Plus: Scientists Debate: Light vs. Heavy Weights

While there is a positive trend in the percentage of US adults who meet the 2008 federal physical activity guidelines according to which they have to "devote at least 150 minutes/week to moderate, or 75 minutes/week to vigorous intensity exercise, or an equivalent combination", the number of people who have gotten the message that a combination of both strength and aerobic training (red line) is much more efficient than doing just aerobics (blue line) remains the same (CDC. 2013)

48%! That's the SuppVersity figure of the week and the percentage of US adults aged 18 and over who met the 2008 federal physical activity guidelines for aerobic activity in 2013 - that's 5% more than in 1997. It would be better to see it up in the 75%+ region, but it's nice to see that more and more people are devoting at least 150min/week to moderate intensity exercise, or 75 minutes/week to vigorous intensity exercise, or an equivalent combination.

What's not so nice is that people are still way too focused on aerobics and the number of US citizens that's combining resistance and aerobic training to reach their exercise goals is stagnating below 20%. Moreover, best-agers and baby boomers, who would probably benefit even more from some weight lifting than the 36% of the young men (age 18-24) who make up the lion's share of the 'real' physical culturists who know about the importance of both, 'weights' and 'cardio', are - if they work out at all - still sticking to the tried and disproven LISS only regimen.

On Short Notice, today: A Health & Exercise Quickie

Apropos "LISS" as the headline of today's On Short Notice news quickie already gave away, light intensity steady state aerobic training aka LISS is one of the exercise related topics today. We will however start out with the health related news... and don't wonder that the first post is about polar bear health. I promise you will be intrigued, when you've read it ;-)

• 'Westernized' polar bears' bones look as if they would need vitamin D supplements, in reality all they are probably missing is sufficient taurine in their diet. I don't know but maybe you've asked yourself before: "How on earth can a white bear survive in the Arctic, when his nose is the only part of his skin that's exposed to the sun and would thus be able to produce vitamin?" (Please mind that this is not a serious question ;-) He eats his vitamin D!
  
  

  

  Scientists speculate: Their cousins in captivity suffer from rickets and fractures due to secondary vitamin D deficiency in consequence of insufficient taurine intake.

  Ok, first question first answer, but what about question #2: "How come that the clubs of his brethren and cousins in captivity get rickets and fractures as if they were vitamin D deficient, although they get the exact same amount of vitamin D from mother's milk and their later diet (sometimes the latter is even supplemented) as their wild counterparts?" Answer? No idea? Well, if you ask the researchers from the The University of Tennessee Health Science Center the answer is (Cheesney. 2009): A lack of taurine in the diet.
  
  Taurine plays a fundamentally important role in the conjugation of ursodeoxycholic acid to TUDCA and facilitates the uptake of fatty acids and fat soluble vitamins. With insufficient taurine in the diet polar beers (and human beings) can probably drink as much vitamin D in olive oil or whatever other fat base they deem more appropriate then dry tabs without any effects on their 25-OHD => calcitonin levels and consequently bone health (suggested read "Fat D-Ficiency! Study Shows, Even 50.000 IU of Vitamin D3 Useless, When You Ingest It Without Fat").
  
  Moreover, a recent guinea pig study from Department of Internal Medicine at the Medical College of the National Cheng Kung University suggests that glycine could be another 'pro vitamin D amino acid' due to its beneficial effect on the liver and subsequent protection of disturbances in vitamin D metabolism and low 25-OHD levels (Chen. 2008) - now, what if any of these, i.e. taurine or glycine, or simply insufficient bile acid, which incidentally depends on the consumption of the "bad, bad" cholesterol (cf. Kern. 1994), is the actual reason of the rampant vitamin D deficiency in our meat-, fat- and cholesterol-o-phobic societies?
• "Low vitamin D and remote EBV infection may be associated with clinical MS breakthrough within 2-3 years." (Décard. 2013) Usually I don't simply copy the study titles, but this one says it all. Even before the first symptoms of multiple sclerosis occur, i.e. in the so-called pre-CIS (=clinically isolated syndrome) interval, patients with quiescent multiple sclerosis have 50% lower 25OHD levels than their healthy peers and - what could actually be the causal factor, here - three times higher Epstein-Barr specific IgG levels (EBNA1). Can these observations a group of scientists from the Department of Neurology at the St. Josef-Hospital of the Ruhr-University Bochum in Bochum, German, really be mere coincidence?
  
  

  

  Figure 1: While it would be best never to be infected with Epstein-Barr your risk of EP-related MS is more than twice as high if you are exposed late (Ascherio. 2010)

  At least as far as the Epstein-Barr relation goes the answer of a 2010 review of the literature would be 'no, probably no coincidence' (Ascherio. 2010). It appears to be established that Epstein-Barr (EB) plays a pivotal role in the etiology of MS. Based on the observation that people without EB are virtually MS free, and the fact that their own previous research has clearly shown that late infections with EP increase your risk to develop MS by more than 2x (compared to people who have been exposed in childhood; see figure 1), Ascherio et al. argue that it is very unlikely that EP is not at least the trigger, if not the ultimate cause of MS.
  
  The scientists also refer to the hygiene hypothesis which has been advanced by other authors before, unfortunately, however, getting rid of the 'cleanliness' and exposing your immune system to the training it needs by exposing yourself to the virus at an earlier age, is of little use, if not totally stupid. After all it would only reduce your risk to develop MS to a level that's still more than 1,000% higher than in people who have never been exposed to the virus in the first place (see figure 1).
  
  Due to the inconclusive data on the long and short term effects of Epstein-Barr infections on the B-cell and T lymphocyte response, the Ascherio et al. are not yet sure about the exact mechanism by which EP stimulates, triggers or drives the development of MS. All that can be said with relative certainty is that Epstein-Bar infections contribute to the increase in multiple sclerosis. Aside from the previously mentioned correlations the mere fact that those regions of the world where Epstein-Barr is quasi non-existent are virtually MS free is probably the best evidence of its involvement in autoimmune attacks on your brain. So if you want to protect yourself you better make sure you don't get infected!  Since EP is part of the herpes family and transmitted via saliva this is unfortunately not exactly easy...

• 

  Figure 2: Overall there is no statistical significant downside to chronic paracetamol supplementation, but there is a slight advantage for the NSAID free group in term of increases in lower body strength - the time course (not shown) of the strength gains was by the way identical for both groups, as well (Jankowski. 2013)

  Paracetamol does not interfere with muscle gains in elderly men. The issue whether or not NSAIDs will interfere with resistance training induced gains in skeletal muscle is certainly relevant for everyone. If there is one group of people for whom it could be of paramount importance, though, this would be the men and women in their best ages (>50 years) who have finally realized that muscle is not just metabolic currency, but a true life insurance.
  
  Against that background the most recent results from the College of Nursing at the University of Colorado Anschutz Medical Campus may be important news (Jankowski. 2013). I mean, if the use of N-acetyl-4-amniphenol (ACET) aka paracetamol would hamper or even forestall muscle gains, the training efforts of the men and women who take ACET would be to no avail.
  
  Now the good news is that the chronic use of paracetamol at a daily dose of 1,000mg did not reduce the lean mass gains in the 17 men (age >50y) who actually participated (instead of giving up) in all of the 3-5 days A/B resistance training sessions
  
  • workout A: R three sets of lateral pull down, bench ress, hip abduction and adduction, biceps curls, seated row, and ssisted chin ups
  • workout B: overhead press, leg press, triceps xtension, knee extension and flexion, heel raise, and shoulder external rotation
  • warm up / cool down: 10 min warm-up on the treadmill, a stair climing intermezzo after the first warm up sets and another 10 min cool down
  that were performed with at 80% of the 1-RM and with at least 1 day off in-between over a period of 16 weeks.
  
  
  The chronic ingestion of paracetamol is not advisable regardless of its negligible detrimental effects on skeletal muscle gain. Only recently, Kane et al. have shown that older people in are particularly prone to the hepatoxic effects of this (imho falsely OTC available) NSAID (Kane. 2013). If there is no way around it, because you cannot stand the pain, a safer (at least for the liver) and more effective medical approach could be the combination of tramadol (75 mg), a weak opioid analgesic, with low dose of paracetamol (325-650mg, max!; cf. Pergollizzi. 2013).
  In as much as the nonexistent negative effects are good news, they are likewise strange news, because according to the expression of proteins involved in the protein synthetic response to exercise, it should actually have hampered the gains:
  

  "[...] in the ACET group that the expressions of the anabolic gene p70S6K and the catabolic gene MAFbx were significantly reduced at week 16 of PRT. Given that the increases in FFM in response to PRT were not significantly different between the groups, it is possible that the suppression of catabolic signaling was sufficient to offset reductions in anabolic signaling in the ACET group." (Jankowski. 2013)

  As the authors point out future studies will have to elucidate the exact mechanism this at first sight contradictory results.
  
  In the mean time Jankowski et al. do yet speculate that the loss of prostaglandin signalling and supsequent increases in p70S6K, the protein that's responsible for muscle protein synthesis may be countered by the normalizing effects paracetamol exerts on the expression of Akt, the ameliorative effect on the overexpression of nitric oxide synthase (iNOS) and the reduction of the age-relatedly increased myocyte apoptosis.
  

• 

  Compared to Hope Solo or Serena Williams Olympian Brian Lochte, is probably a weakling - of course only as far as the fatigabilty of his skeletal muscle is concerned - as far as the risk do develop the Athlete's Triad is concerned, this may yet be advantage.

  Men and women tire differently - men (once more ;-) the weaker sex Let's face it guys,  we are weaklings. At least this is what Beth W. Glace and her colleagues from the Nicholas Institute of Sports Medicine and Athletic Trauma at the Lenox Hill Hospital in New York report in their latest paper. Other than the quadriceps muscles of our significant others, our muscles fatigue after 2h of cycling with intermittent one minute sprints every 20 minutes.
  
  In women, in this particular case just like their male counterparts trained cyclists or triathletes with a training load of at least 100km per week, on the other hand, it's solely the central nervous system fatigue that will keep them from cycling 'forever'. Unfair, right? Us men have to battle both, central as well as local muscular (=peripheral) fatigue.
  
  Now what seems nothing but advantageous can however turn against you. In a way the low fatigability of female muscle is also part of the reason why are way more susceptible to the athlete's triad (click here to learn more) than men: They are simply able to work their CNS into the ground, because their peripheral musculature is less prone to exhaustion.
• Recent study puts question mark behind assumed appetite reducing benefit of HIIT sprints vs. classic aerobics - but does that mean that aerobics is the way to go? Not yet in press, but already intriguing are the results of a recent study by  Kevin Deighton et al. from the School of Sport at the Loughborough University who say that they found that ...
  

  "[a]n acute bout of endurance exercise resulted in lower appetite perceptions in the hours after exercise than sprint interval exercise and induced a greater 24 h energy deficit due to higher energy expenditure during exercise" (Deighton. 2013)

  

  Figure 3: Intentionally or not, based on the conclusion of the abstract you would probably not have expected to see these results (data adapted from Deighton. 2013)

  Now this sentence from the abstract certainly suggests that sprinting would have nothing but negative effects. The actual data you see in figure 3 does yet tell you something different. The sprinters may have had increased ghrelin and lower PYY levels with the expected downstream effects on perceived hunger, but this did not translate into significant differences in food intake. In other words, even longish sprint exercises like the ones in the study at hand won't put you at danger of overeating - despite transient increases in ghrelin levels.
  
  In fact, the increased ghrelin amplitude can actually be an advantage (see August 04, 2013) and the calories in vs. out calculation the scientists do is so irrelevant to the real world health and body composition effects of exercise that I refuse to repeat it here ("No, you cannot eat that extra piece of layer cake because you ran on the treadmill earlier today" ;-)
  
  In the end, comparisons like this always suggest you had to choose between doing one or another mode of "cardio", when a combination of both, i.e. cycling HIIT and LISS, yet not both in one session, would be the most productive way to go. And no, Mr. Taubes, none of them is "just going to make you hungry" (see "Every Dog Has His Day: Dr. Oz Was Right, Exercise Does Not "Just Make You Hungry", But Reduces Energy Intake!")
  
• Researchers debate the "low vs. high weight" conundrum. In the editorial to the next issue of the Journal of Applied Physiology Mark D. Schuenke, Jennifer Herman, and Robert S. Staron reject the criticism they received from Nicolas Burd et al. for the pro heavy weights arguments they put forward in their recently published study on the effects of high vs. low weight training (Schuenke. 2013a; covered on the SuppVersity on October 01, 2013). Now while this back and forth between the two groups does not deliver any new data, I believe that it is still interesting and highly educative to see how science is actually a matter of negotiated not set truths. So, let's see how Schuenke et al. respond to Burd's assertion that ...
  

  

  Figure 4: Changes in body composition (left) and changes in muscle fiber cross-sectional area in response do different training regimen (Schuenke. 2013a; this study was discussed here on the SuppVersity on October 01, 2013)

  "[t]he authors’ views continue to contribute to a resistance training doctrine that is incorrect, most notably the belief that heavier weights are better concept. This conclusion is likely due to the relative dearth of quality studies assessing the hypertrophy potential of lower load resistance training paradigms, in contrast to the large number of studies employing ‘traditional’ resistance training intensities (*70 % of maximal strength).

  Clearly, evidence exists to support the concept that light(er) loads can support training-induced muscle hypertrophy both independently and by comparison to heavy loads. We would propose that so long as the stimulus is an overload, performed with high effort (fatigue), and progressive then even the most seasoned lifters would see progression,  at the very least no regression, in strength or muscle mass." (Burd. 2013)

  I will briefly summarize the most important points the researchers from the University of New England College of Osteopathic bring forward to defend their "go heavy or go home" argumentation:
  
  • The list of previous studies which confirm the the efficacy of training with high(er) weight for "optimal" gains in hypertrophy and strength is extensive.
  • Low load training is not as Burd et al. suggest "simply a milder form of low-load blood flow restrictive exercise", of which the researchers state that it is "interesting".
  • Schuenke et al. specifically refer to a Y2k study by Takadara et al. which shows that without the cuffs light loads don't build anything (Takadara. 2000).
  • The researchers point out that the claim by Burd et al. that "maximal muscle fiber activation can be achieved in any circumstance as long as the effort is to failure is unwarranted and unsubstantiated".
  • The study by Mitchel et al. Bird et al. cite to prove their hypothesis may not report significant differences between knee extensions performed at 30 % of 1RM for 3 sets, 80 % of 1RM for 1 set, or 80 % of 1RM for 3 sets as far as the isometric strength and hypertrophy between the three types of training are concerned, but
    

    "[t]his result is not surprising considering the following: (1) no control group was used, (2) each subject trained each limb using a different protocol (cross-over effect), (3) only one single-joint exercise was used (low volume versus a much higher volume of training used, for example, in Schuenke et al.: 3 sets each of leg press, squat, and knee extension), and (4) only fiber types I and II were delineated (severely limiting interpretation of the results).

    In that the last parentheses is obviously another direct criticism of what Schuenke would probably call "cherry picking" studies and specific results to support an unwarranted hypothesis.
  Based on this line of argumentation, Schuenke et al. conclude their deliberations on the note:
  

  

  One should not forget that it's not only about light vs. heavy, but in as much about appropriate and inappropriate weights. If you go by the quantity of the evidence there is however no debating that those weights are too light - probably even for a Lady in her best years.

  "Low-load training appears to have some merit. How-ever, our data support the use of high-load, high-intensity resistance training to maximize fiber hypertrophy and strength. In addition, heavy loading of the muscle has an impact on bone and other connective tissues which are minimized/lacking using low-load training. Finally, Burd et al. appear to oversimplify the field of exercise physiol-ogy. To claim that any training load (light or heavy) con-fers the same physiological adaptations as long as the end point is volitional failure is shortsighted and similar to claiming that running for any distance or time will elicit the same effects as long as fatigue is reached." (Schuenke. 2013)

  If you asked me, both are right. While I personally tend to agree with Schuenke, the main reason that I do is that the heavy weights approach is tried and proven, while - just as Burd says - the sceintific evidence pertaining to low weights is scarce and ambiguous and the anecdotal evidence from 'big guys' is non-existent. I am still curious about the next move(s) on both sides of this divide. And by the way, conflicts like these have always been among the driving forces of scientific progress, so I am pretty sure that we as trainees can only benefit from this debate as well as potential follow-up studies, both groups will feel inclined to conduct in order to 'prove' their point.

That's all for today! I hope you enjoyed the stay, all have electricity and an intact water supply ... I mean it's nice if you have a fully charged iPhone to get your daily dose of SuppVersity news, but even I have to concede that some other things in live are way more elementary.

References

• Ascherio A, Munger KL. Epstein-barr virus infection and multiple sclerosis: a review. J Neuroimmune Pharmacol. 2010 Sep;5(3):271-7.
• Burd NA, Moore DR, Mitchell CJ, Phillips SM. Big claims for big weights but with little evidence. Eur J Appl Physiol. 2013 Oct 20. 
• CDC. Early Release of Selected Estimates Based on Data From the January–March 2013 National Health Interview Survey. September 2013
• Chen CY, Wang BT, Wu ZC, Yu WT, Lin PJ, Tsai WL, Shiesh SC. Glycine ameliorates liver injury and vitamin D deficiency induced by bile duct ligation. Clin Chim Acta. 2013 Oct 23-
• Chesney RW, Hedberg GE, Rogers QR, Dierenfeld ES, Hollis BE, Derocher A, Andersen M. Does taurine deficiency cause metabolic bone disease and rickets in polar bear cubs raised in captivity? Adv Exp Med Biol. 2009;643:325-31.
• Deighton K, Barry R, Connon CE, Stensel DJ. Appetite, gut hormone and energy intake responses to low volume sprint interval and traditional endurance exercise. Eur J Appl Physiol. 2013 Oct 31.
• Décard BF, von Ahsen N, Grunwald T, Streit F, Stroet A, Niggemeier P, Schottstedt V, Riggert J, Gold R, Chan A. Low vitamin D and elevated immunoreactivity against Epstein-Barr virus before first clinical manifestation of multiple sclerosis. J Neurol Neurosurg Psychiatry. 2013 Aug 11.
• Kane A, Mitchell SJ, Carroll PR, Matthews S, Hilmer SN. Characteristics of older and younger patients with suspected paracetamol toxicity. Australas J Ageing. 2013 Sep;31(3):190-3.
• Kern F Jr. Effects of dietary cholesterol on cholesterol and bile acid homeostasis in patients with cholesterol gallstones. J Clin Invest. 1994 Mar;93(3):1186-94.
• Kappenstein O, Vieth B, Luch A, Pfaff K. Toxicologically relevant phthalates in food. EXS. 2013;101:87-106.
• Pergolizzi JV Jr, van de Laar M, Langford R, Mellinghoff HU, Merchante IM, Nalamachu S, O'Brien J, Perrot S, Raffa RB. Tramadol/paracetamol fixed-dose combination in the treatment of moderate to severe pain. J Pain Res. 2013;5:327-46.
• Schuenke MD, Herman JR, Gliders RM, Hagerman FC, Hikida RS, Rana SR, Ragg KE, Staron RS. Early-phase muscular adaptations in response to slow-speed versus traditional resistance-training regimens. Eur J Appl Physiol. 2013a Oct;112(10):3585-95.
• Schuenke MD, Herman J, Staron RS. Preponderance of evidence proves "big" weights optimize hypertrophic and strength adaptations. Eur J Appl Physiol. 2013b Oct 25.
• Sioen I, Fierens T, Van Holderbeke M, Geerts L, Bellemans M, De Maeyer M, Servaes K, Vanermen G, Boon PE, De Henauw S. Phthalates dietary exposure and food sources for Belgian preschool children and adults. Environ Int. 2013 Nov 1;48:102-8.
• Takarada Y, Takazawa H, Sato Y, Takebayashi S, Tanaka Y, Ishii N. Effects of resistance exercise combined with moderate vascular occlusion on muscular function in humans. J Appl Physiol. 2000; 88:2097–2106.

Fat From Serotonin. MS Despite Vitamin D. DHA & DPA Feel at Home in Your Cellwalls. Weightloss Obstacle Late Lunch? Wrist Predicts Diabetes Risk. Viagra Detoxes the Brain. Acetyl Cysteine Battles Acne. Propolis Increases GLUT-4

Yet another reason why calorie counting is not good for your sanity: The "average" sexual intercourse burns only 14 kcal more than watching TV.  and significantly less than a fast paced walk on the inclined treadmill. Luckily weight loss & maintenance is more complex than calories in vs. out, anyway ;-)

"14" that's the SuppVersity figure of the number of extra calories you will expend when you and your significant other decide to have sex instead of sitting on the couch watching TV tonight. I got that figure from a paper my buddy Sean Casey from CasePerformance has brought to my attention. Published in the latest issue of the prestigious New England Journal of Medicine (Casazza. 2013), it discusses the 7 most commonly held "false and scientifically unsupported beliefs about obesity" the scientists identified in a thorough analysis of popular media and scientific literature.

"The scientific community needs some more honesty"

While the sex-myth, which originally states that you would burn at least 100kcal, with a little more action"" even 300kcal per intercourse, is obviously my favorite, there are also a couple of  less sexy "presumptions about obesity" (e.g. simply eat more veggies and fruit and you lose weight) and "facts about obesity" (e.g.  the scientists dug up and debunked in a paper that ends with the wise words:

"While we work to generate additional useful knowledge, we may in some cases justifiably move forward with hypothesized, but not proved, strategies. However, as a scientific community we must always be open and honest with the public about the state of our knowledge and should rigorously evaluate unproved strategies." (Casazza. 2013)

Actually the term "the state of our knowledge" is an ideal segue to what follows - the "short" news! Originally the On Short Notice column was actually intended as a very brief overview over what has been going on in the "community" as of late. And since we are talking about honesty, I must admit that I have failed miserably in the past installments as far as the tiny word "short" in the column's title is concerned. 

The new short news are short again ;-)

So, as of now, I will be doing my very best to bring the On Short Notice column back on the short track, so to say. I guess, we will see in a couple of paragraphs, how successful my efforts will be ;-)

• Does serotonin make you fat? It's pro-fat storage effects would suggest so
  
  

  

  If 5-HT can make you fat and creatine blunts its increase PWO (learn more), what does that tell us about creatine? Nothing, but it leaves room for speculations.

  (Gres. 2013) -- If you trust in TV wisdom the reason women eat chocolate, whenever they feel sad or alone is it's ability to boost serotonin (5-HT). The latter is yet not the reason Sandra Grès et al. say that serotonin could make you fat. Rather than that, it's the ability of 5-HT to stimulate the obesogenic peroxisome proliferator-activated receptor γ (PPAR-γ, learn more), on adipose cells, which will increase fat storage and the recruitment of new fat cells from the stem cell reservoir.
  
  These effects happen in the periphery (vs. the brain) and are totally unrelated to the centrally mediated effects of serotonin.

• MS patients benefit from the sun, not vitamin D
  
  (Zivadinov. 2013) -- Where is your vitamin D supposed to come from? From your skin, right. And where does your skin get it from? From tablets? No. It manufactures it from the "bad" cholesterol, when it's  exposed to the "bad" sunlight.
  
  

  

  In the upper left of this image you see, where the magic is - the rest is just a nice bonus.

  With all those supposedly bad, but in fact vital things being important for much more than vitamin D synthesis it is therefore not surprising that a recently published paper on the asociations of sun-exposure and/or vitamin D with MRI measures in multiple-sclerosis patterns revealed that
  

  "[...] sun exposure was associated with increased grey matter volume (GMV, r_p=0.16, p=0.019) and whole brain volume (WBV, r_p=0.20, p=0.004)" (Zivadinov. 2013).

  ...and that totally irrespective of whether the subjects had high or low vitamin D levels. If you wanted to say it fancily, you'd say the beneficial effects of sun exposure on the brain volume in MS patients was found to be disassociated from the effect the sun has on vitamin D levels (suggested read: Vitamin D, Epstein Bar & MS)

• If you want to up the omega-3 levels in your tissue, pick DHA and / or its precursor DPA over EPA
  
  

  

  Figure 1: Incorporation various lipid fractions in different tissues (Kaur. 2013)

  (Kaur. 2013) -- According to a very recent rodent study docosahexaenoic acid (DHA) and docosapentaenoic acid (DPA) are much more readily incorporated into two of your most vital organs, namely your brain and liver and likewise the preferred phospholipid in the cell walls of your kidneys and muscle tissue. Only your fat cells don't really like these long(est) chain omega-3s the incorporation of which was ~50% lower than that of oleic acid (OA; that's the mono-unsuaturated fatty acid in olive oil), which was used as a "neutral" control.
  
  The one question I would still like to have an answer to is how beneficial it actually is, if the phospholipids (PL, figure 1) in your cell membranes are full of easily oxidizable fatty acids.
  
  Also, what do we make of the other lipid fractions? Cholesterol (CHOL), diacylglycerol (DGL) and NEFAs + triglycerides (NE+TG)? Where do we actually want those good omega-3 fatty acids to accumulate? ... just some food for thought  for your DPA and DHA lovin' brains ;-)

• 
  On a side note: If you like GMO, you won't have to eat fish any longer to get your omega-3 PUFAs
  
  (Petrie. 2013) -- Researchers from the CSIRO Food Futures National Research Flagship have already engineered the first GMO brassica species with a higher DHA yield >11% than fish. The invention is hailed as "a breakthrough in the development of sustainable alternative sources of DHA as this technology should be applicable in oilseed crops" (Petrie. 2013)

• When late eating (spec. lunch) and certain genes come together weight loss can become pretty difficult - reasons still not fully understood, though
  
  (Garaulet. 2013) -- Late lunch and certain genotypes appear to make weight loss difficult for some. And the relation holds even after possible confounding factors like energy intake and even appetite hormones, were measured.
  

  

  Skipping breakfast. Yay or Nay? (read more)

  "Late lunch eaters lost less weight and displayed a slower weight-loss rate during the 20 weeks of treatment than early eaters (P=0.002). Surprisingly, energy intake, dietary composition, estimated energy expenditure, appetite hormones and sleep duration was similar between both groups." (Garaulet. 2013)

  While this is not a general argument against intermittent fasting, skipping breakfast and thelike, it does still go to show you that we are not all created exactly equal and any cookie cutter approach to weight loss therefore counter-indicated. 

• Show me your wrist and I'll tell you something about your glucose metabolism.
  
  (Nudeh. 2013) -- A study that was published in the latest issue of the The Journal of Clinical Endocrinology & Metabolism reveals: Wrist circumference is a significant predictor of diabetes in both genders of adult population.

  

  Figure 2: Incidence of diabetes during 8.8 years of follow-up in different tertiles of baseline
  wrist circumference among male and female populations (significant trend in both genders; Noudeh. 2013)

  What's particularly interesting is that this association which was observed in cohort of 6393 subjects (2716 males and 3677 females), who had been subjected to a standard 2-hour postchallenge plasma glucose, test holds independent of BMI and waist circumference - allegedly in women, only. 

• Sildenafil Citrate Attenuates the Deleterious Effects of Elevated Ammonia
  
  (Arafa. 2013) -- You will probably remember the problems with ammonia accumulation due to huge BCAA and protein intakes (learn more). If you trust the latest results of two Egyptian researchers from the Zagazi University it would look as if a solution to that problem (which shouldn't be one, if your liver is healthy and you don't go overboard on pro-ammonia foods, anyway) would already exist: Sildenafil citrate aka Viagra can help.
  
  In their study the researcher administered 10mg/kg sildenafil to rats that were treated with daily intraperitoneal (i.p.) injection of ammonium chloride (100 mg/kg body weight) for eight weeks. This treatment resulted in a significant reduction in serum liver enzymes, lipid profile and - maybe most importantly - brain lipid peroxidation and caspase-3 mRNA. It also increased the nitric oxide (NO) levels in the blood and lead to a significant increase in cGMP, antioxidants and endothelial nitric oxide synthase (eNOS) gene expression in the brains of hyperammonemic rats.
  

  

  List of various foods and their ammonia content (Rudnan. 1973)

  "Our results showed that sildenafil exerts a protective effect on the brain by reversing oxidative stress during hyperammonemia and this could be due to (i) cytoprotective, antioxidant and anti-apoptotic effects ii) increasing cGMP and enhancing the proper metabolism of fats which could suppress oxygen radical generation and thus preventing oxidative damage in the brain."

  Until now, the scientists cannot tell how exactly the human equivalent of 1.62mg/kg sildenafil citrate work, but its modulatory effect on the NO/cGMP pathway is the most likely candidate. That these effects are of real world significance has incidentally been shown, already. In 2003, for example, the learning abilities of rats with hyperammonia was restored by a similar regimen (Erceg. 2003) 

• Acetyl cysteine - don't swallow, but rub it... onto your skin, if you have acne
  
  (

  

  The comedo count is a measure of the number of comedones, i.e. the open black "pores" like those on the forehead of the person shown on this photo

  Montes. 2013) -- According to a study published in the latest issue of Skinmed, the application of a 5% acetylcysteine topical gel proved to be "significantly superior to placebo (P = .04)" in reducing the comedo counts. The results were comparable in  male and female participants and would suggest that "acetylcysteine is an effective therapeutic option for the treatment of mild to moderate acne". Whether it is an alternative to the retinoid based standard drugs, is yet still questionable.
  
  By the way, the latter, or rather the most prescribed of these retinol-like drugs, namely tretinoin has only recently been found to synergize with Aloe vera for even better results (Saeedi. 2013).

• Brazilian propolis ethanol extract promotes glucose uptake and translocation of insulin-sensitive glucose transporter (GLUT) 4 in skeletal muscle
   
  

  

  In the unfortunate case you missed the news: The commonly ignored BCAA Isoleucine also boosts GLUT4 (read more)

  (Ueda. 2013) I guess you will have heard about the miracles "royal jelly" is supposed to work on your health, right? Well, the cheap "packaging" material bees use to seal the smaller gaps in their hives (the larger ones are usually filled with beeswax) seems to have similarly outstanding - and in this case scientifically backed effects.
  
  When propolis was administered at a human equivalent dose of 20mg/kg to mice, those rodents saw increases in both PI3 and AMPK modulated increase in the glucose transporter 4 activity and skeletal glucose uptake.
  
  The main active polyphenols were artepillin C, coumaric acid, and kaempferide. All of them promoted GLUT4 translocation in a subsequent ex-vivo analysis using L6 myotubes, but kaempferide, which can also be found in acovado seeds (Pahua-Ramos. 2013) and cordia sinensis aka  grey-leaved saucer berry extracts (Martinetti. 2010), was the most potent one.

Now you are surprised, right? Me too. Nine individual items and all of them still qualify as "short news". I guess in view of the sheer abundance of news you won't need anything else till tomorrow, but in case you do, I have a couple of suggestions to check out on the SuppVersity Facebook Wall:

• Lycopene works as an anti-cancer agent, because some of it's metabolites "look" like retinol (vitamin A) and dock to the retinol receptor (read more)
  
• Curcumin is a hormetic agent (learn more about hormesis), but not all curcuminoids are created equally effective (read more)
• White poison!? Low sugar diet does not improve insulin sensitivity but decreases glucose levels in obese subjects (read more)
• Myostatin knockout mice have increased brown fat - Does this mean that myostatin suppression will increase browning of fat in man, as well? The recent SuppVersity article on PGC-1A4 already confirmed that (read more) 
• Fish oil for alcohol withdrawal - Only three weeks on low dose EPA (60 mg/day) and high dose DHA (252 mg/day) supplement yielded significant decreases in distress symptoms and basal cortisol secretion in abstinent alcoholics (read more)
• SuppVersity Suggested Read: The Hunter-Gatherer Within: Health and the Natural Human Diet - "Don't get your food from the same place your car does" (read more)

There are going to be a couple of more news before the official next SuppVersity post will be posted in ~24h - so "like" the SuppVersity on Facebook and make sure you don't miss any of them. Have a nice weekend!

References:

• Arafa MH, Atteia HH. Sildenafil Citrate Attenuates the Deleterious Effects of Elevated Ammonia. Toxicol Mech Methods. 2013 Jan 23. 
• Casazza K, Fontaine KR, Astrup A, Birch LL, Brown AW, Bohan Brown MM, Durant N, Dutton G, Foster EM, Heymsfield SB, McIver K, Mehta T, Menachemi N, Newby PK, Pate R, Rolls BJ, Sen B, Smith DL Jr, Thomas DM, Allison DB. Myths, presumptions, and facts about obesity. N Engl J Med. 2013 Jan 31;368(5):446-54.
• Erceg S, Monfort P, Hernández-Viadel M, Rodrigo R, Montoliu C, Felipo V. Oral administration of sildenafil restores learning ability in rats with hyperammonemia and with portacaval shunts. Hepatology. 2005 Feb;41(2):299-306.
• Garaulet M, Gómez-Abellán P, Alburquerque-Béjar JJ, Lee YC, Ordovás JM, Scheer FA. Timing of food intake predicts weight loss effectiveness. Int J Obes (Lond). 2013 Jan 29.
• Grès S, Canteiro S, Mercader J, Carpéné C. Oxidation of high doses of serotonin favors lipid accumulation in mouse and human fat cells. Mol Nutr Food Res. 2013 Feb 6.
• Jahangiri Noudeh Y, Hadaegh F, Vatankhah N, Momenan AA, Saadat N, Khalili D, Azizi F. Wrist Circumference as a Novel Predictor of Diabetes and Prediabetes: Results of Cross-Sectional and 8.8-Year Follow-up Studies. J Clin Endocrinol Metab. 2013 Feb;98(2):777-84.
• Kaur G, Molero JC, Weisinger HS, Sinclair AJ. Orally administered [14C]DPA and [14C]DHA are metabolised differently to [14C]EPA in rats. British Journal of Nutrition. 2013; 109, pp 441-448. 
• Martineti V, Tognarini I, Azzari C, Carbonell Sala S, Clematis F, Dolci M, Lanzotti V, Tonelli F, Brandi ML, Curir P. Inhibition of in vitro growth and arrest in the G0/G1 phase of HCT8 line human colon cancer cells by kaempferide triglycoside from Dianthus caryophyllus. Phytother Res. 2010 Sep;24(9):1302-8.
• Montes LF, Wilborn WH, Montes CM. Topical acne treatment with acetylcysteine: clinical and experimental effects. Skinmed. 2013 Nov-Dec;10(6):348-51.
• Pahua-Ramos ME, Ortiz-Moreno A, Chamorro-Cevallos G, Hernández-Navarro MD, Garduño-Siciliano L, Necoechea-Mondragón H, Hernández-Ortega M. Hypolipidemic effect of avocado (Persea americana Mill) seed in a hypercholesterolemic mouse model. Plant Foods Hum Nutr. 2013 Mar;67(1):10-6.
• Petrie JR, Shrestha P, Zhou XR, Mansour MP, Liu Q, Belide S, Nichols PD, Singh SP. Metabolic engineering plant seeds with fish oil-like levels of DHA. PLoS One. 2013;7(11):e49165. 
• Rudnan D, Smith RB 3rd, Salam AA, Warren WD, Galambos JT, Wenger J. Ammonia content of food. Am J Clin Nutr. 1973 May;26(5):487-90.
• Ueda M, Hayashibara K, Ashida H. Propolis extract promotes translocation of glucose transporter 4 and glucose uptake through both PI3K- and AMPK-dependent pathways in skeletal muscle. Biofactors. 2013 Jan 28.
• Zivadinov R, Treu CN, Weinstock-Guttman B, Turner C, Bergsland N, O'Connor K, Dwyer MG, Carl E, Ramasamy DP, Qu J, Ramanathan M. Interdependence and contributions of sun exposure and vitamin D to MRI measures in multiple sclerosis. J Neurol Neurosurg Psychiatry. 2013 Feb 5.