Natural Migraine Prophylaxis & Treatment: Riboflavin, ALA, Magnesium, CoQ10, Feverfew, Melatonin, Butterbur & Co.

Natural migraine protection: Even if supps won't cure it, they can at least reduce the number of "bad days" and the severity of the attacks.

In the last installment of the "Short News" you've learned about the enormous costs chronic pain produces on an annual basis: Roughly $300 billion for it's treatment and another $300 billion in form of economic damage. No wonder pain killers, Cox inhibtors and & co are among the top selling and drugs in the world.

Now, migraine is unquestionably among the most debilitating forms of chronic or rather cyclic chronic pain and while women are much often hit by the pain from withing (21.8% v.s 10.0% of the US citizens suffer; NHS 2009). And while I cannot tell you how much of the $2,000 bucks each of you is "spending" on an annual base on treating the pain of his / her fellow citizens, I believe that both of you, my dear mal and female readers, may benefit from the information in today's installment of "On Short Notice" with a comprehensive, but probably not all-encompassing list of promising supplemental agents for migraine prophylaxis and "treatment":

• magnesium: I have actually mentioned that in a previous SuppVersity post already (read more), but I guess it's well worth mentioning it again. Low brain magnesium levels have been reported in a whole host of observational studies in migraineurs. There have also been a couple of respective trials with overall inconclusive, but rather positive results for acute treatment of patients with aura and, possibly, perimenstrual migraine prophylaxis.
  
  The magnesium formulation that have been used in these trials varied, and there is no large(r) scale comparison of different forms and dosing regimen as of now. Corresponding effects have been observed with 250mg of intravenous and 600mg of oral magnesium chelates (Cady. 1998; Mauskop. 1998), for example. Evans and Taylor additionally cite the following four randomized controlled trials (RCTs; my emphases):

  Take a form that does not give you diarrhea! If you look at the success rates it would appear as if  the organic formulas are superior to the inorganic ones. On the other hand, this may be a simple effect of the increased rates in diarrhea reported by many researchers using non-organic formulations. After all, this does not simply reduce magnesium absorption but will also have negative effects on the overall mineral and water balance. Both, dehydration and mineral imbalances could otherwise increase instead of decrease your risk to suffer from migraine attacks.

  "The first RCT of magnesium for migraine prevention involved only 20 subjects and was positive; the active therapy was 360 mg Mg++ pyrrolidone carboxylic acid divided TID. The second RCT, by Peikert et al, involved 81 adult women and 600 mg magnesium (trimagnesium dicitrate) daily demonstrated a 41.6% improvement with verum versus 15.8% for placebo. The third RCT for migraine prophylaxis, published by Pfafferath et al, involved 69 patients taking 486 mg magnesium; no benefit for magnesium was found; at the end of the 3-month treatment phase, the responder rate was 28.6%in the magnesium group and 29.4% in placebo subjects, according to the primary efficacy endpoint. [...] In a last trial, Wang et al gave magnesium oxide 9 mg/kg divided TID to subjects aged 3 to 17 years. Approximately three-quarters of eligible subjects completed the study, with a significant downward trend in headache days in the active treatment group versus placebo; the lack of any difference in the slope of treatment trends, however, was such that no significant superiority of magnesium over placebo could be documented." (Evans, 2006)

  While magnesium's acute effects are usually ascribed to increases in the circulating levels of Mg++ ions, it's efficacy as a prophylactic treatment is most likely a result of increasing tissue levels and requires a minimum of 3 to 4 months for measurable benefits to occur.
• CoQ10: As a student of the SuppVersity you are well aware of the beneficial (actually vital!) importance of CoQ10 on mitochondrial health. It is an endogenous enzyme cofactor that can be produced by your body. Unfortunately, there are certain conditions and medications that lead to the depletion of CoQ10 and subsequently impair the proton-electron translocation across the mitochondrial membranes.
  
  

  

  No headache, no problem, but not a reason not to consider CoQ10 supplementation. CoQ10 can also help if your exercise performance is what gives you headaches: "300mg CoQ10 Boost Peak Power Increases in Young Elite Athletes. Plus: 140ml of Beet Root Juice, That's all it Takes to Minimize the Oxygen Demands During a Workout" (learn more)

  Against that background and in view of the involvement of mitochondrial malfunction in the etiology of migraine, it is not surprising that Rozen et al. observed in a 2002 open label study in which 61%  of the 31 patients who consumed 150mg CoQ10 daily for 3 months had at least a 50% reduction in migraine days without experciencing any significant adverse events. Interestinly, the supplement took "only" 4 weeks to kick in (a follow up on whether or not it was necessary to stay "on" CoQ10 is not available, but I would consider it likely). In 2005 Sandor et al. conducted one of the few randomized controlled trials: In this particular study, the patients received 100mg of CoQ10 three times daily and saw significant decreases in the attack frequency, the number of headache days, and days with nausea.
  
  Interestingly the highly soluble version of CoQ10 (a liquid formulation of water dispersed nano-particles comprising a supercooled melt of CoQ10 with modified physicochemical properties; GuttaQuinone) that was used in the Sandor study had some side effects (gastrointestinal disturbances and cutaneous allergy that had not been reported in other studies). Overall, CoQ10 is yet perfectly save (even if it's nano-sized) and may even yield benefits if you don't suffer from migraine.
• Tanacetum parthenium: Also known as Feverfew, the dried chrysanthemum leaves have a long history as an analgesic and one huge problem, according to the only available peer reviewed report, preparations of feverfew have shown a >400% variation in dosage strength of the known active ingredient parthenolide (Rossi. 2005). According to evens Evans & Taylor, some experts even doubt if it can be generally assumed that parthenolide, which has some very promising research to back up its efficacy even is the active ingredient in the plant leaves.
  

  

  Feverfew does not look exactly, like powerful medicinal plant, right?

  "In a systematic review, Vogler et al reported on randomized controlled trials (RCTs) involving feverfew for migraine prophylaxis conducted prior to 1998. 11-16 Five studies qualified by Jadad score as adequate; 1 has been published in abstract form only, and only 216 subjects in total have been studied. Vogler et al concluded, “In view of the popularity of feverfew, perhaps the most striking finding was the paucity and low average quality of the existing RCTs on the subject.”

  If you wanted to cut it short you could thus say. It's popular, people swear by it, but according to our current knowledge it may as well be the placebo effect that keeps people coming back to this natural remedy for headaches.
  
  The latter would be nasty, since Feverfew does actually have a handful of side effects that range from a sore mouth and tongue (including ulcers), over swollen lips, loss of taste, abdominal pain, and GI disturbances, up to the occasional report of what Evans & Taylor call the "post-feverfew syndrome" of joint stiffness and aches that were accompanied by (guess what) increasing headaches! In the MIG-99 trials, which used an isolated and highly standardized 6.25 mg dose of parthenolide the numeber of adverse events were similar. It would thus seem very likely that many of the side effects are brought about either by the initially mentioned natural fluctuations in the active or - and this is even more likely - by other agents in the feverfew leaves.
• Riboflavin: Also and probably better known as vitamin B2, riboflavin has only few quality trials to support its efficiency with its importance in the mitochondrial energy chain and its role in the electron transport within the citric acid cycle, it does however appear to be likely that the otherwise often overlooked "yellow-green pee"-vitamin may actually help reduce the number of migraine attacks by >50% (that's 35% more than w/ 25mg/day; Schoenen. 1998), when it is consumed in doses of 400mg/day.

  

  This table shows the nutrient combination of a supplement that has been found to optimize mitochondrial function in a 2011 study (learn more) and it has not just riboflavin, but also lipoic acid and coQ10, both of which are also on the list of "anti-migraine supplements" - certainly no coincidence! Migraine is after all about mitochondrial health and disease.

  The only known side effects researchers observed in the few available randomized controlled trials, were diarrhea and polyuria - and those were pretty rare. Evans & Taylor do yet point out that despite its non-toxicity and the non-existance of a tolerable upper intake level they wouldn't recommend high dose riboflavin consumption to pregnant women, simply because the possible health effects on the unborn child are not known yet.
• Alpha lipoic acid: Certainly less known and not well-researched are the potential benefits of ALA (it is thus not necessary to buy R-ALA, which was in the formula of the supplement mentioned in the label of the table above). A double-blind, placebo-controlled trial by Magis et al. from the year 2007 was yet able to show a reduced monthly attack frequency with alpha lipoic acid at dosages of 600 mg daily after 3 months. It must be said, though that these results weere not not significantly different from those in the placebo group. Within-group analyses did yet reveal a a significant reduction in attack frequency, headache days and headache severity in patient treated with alpha lipoic acid, but not in the placebo group (Magis. 2007)
• Buttebur:
  A note of caution: The Butterbur plant contains pyrrolizidine alkaloids which are
  hepatotoxic and carcinogenic, these compounds have to be removed before you can safely use this plant from the genus of Asteraceae  to counter / prevent headaches.
  Petasites hybridus or rather extracts of its root have gotten some attention as a potential migraine treatment, as well. Petasites is thought to act through calcium channel regulation and inhibition of peptideleukotriene biosynthesis. These cells are thought to play an important role in the inflammatory cascade associated with migraine (Sheftell. 2000; Pearlman. 2001). A randomized, double-blind, placebo-controlled trial by Grossman & Schmidrams (2000) found that the consumption of 50 mg of butterbur twice daily yielded significant reduced number of migraine attacks and migraine days per month. Similar results with 50mg of Petasites extract were also reported by Lipton et al. (2004). Finally, a multicenter prospective open-label study of butterbur in 109 children and adolescents with migraine resulted in 77% of all patients reporting a reduction in migraine frequency of at least 50% (Pothmann. 2005)..
  
  Serious adverse events were not observed in any of the few hitherto published studies. Overall, butterbur was well tolerated and the most frequently reported adverse reactions were mild gastrointestinal events, predominantly eructation (burping). 
• Melatonin: Yep, you will be hard pressed to find anything melatonin the pineal sleep hormone is not good for. So it is probably not very surprising that it is on the list or rather the end of a list potential natural(*) anti-migraine supplements (some critics will probably say that supplementing with melatonin is not "natural").
  

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    Sleep is good for everything and if you look back at the past SuppVersity articles on the pineal hormone this seems to apply to melatonin, as well.

    1999, Leone et al. were among the first to report beneficial effects of 10mg of melatonin on cluster headaches; yet while this worked magically in some, other patients did not appear to benefit at all (Leone. 1999)
  • melatonin appears to be an effective alternative for indomethacine in idiopathic stabbing headache (Rozen. 2003)
  • cluster migraine which often goes hand in hand with a lack of melatonin secretion has been shown to respond to 9 mg melatonin taken at bed time (Peres. 2001)
  In a 2005 review of the literature Peres does yet point out a multitude of mechanisms by which melatonin could help alleviate headaches, including "its anti-inflammatory effect, toxic free radical scavenging, reduction of proinflammatory cytokine up-regulation, nitric oxide synthase activity and dopamine release inhibition, membrane stabilization, GABA and opioid analgesia potentiation, glutamate neurotoxicity protection, neurovascular regulation, serotonin modulation, and the similarity of chemical structure to that of indomethacin" (Peres. 2005). Despite the fact that large(r) scale randomized controlled trials are absent, up to know. I personally would certainly give it a try.

Aside from "real medications" (I wonder where you can make the distinction between a supple ment like thiotic acid aka ALA and a medicinal agent like aspirin?), there is also a "onsistent level of evidence"for the usefulness of accupuncture, which has proven to be superior to no or placebo treatment and works as an adjunct to conventional treatment (Schiaparelli. 2010).

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There is one thing left to mention that may even work better than any of the previously enumerated supplements: Prevention! While many people don't really know the cause of their migraine attacks there are a couple of known food triggers you may want to avoid or even test (Peatfield. 1984; Scharff. 1995):

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  MSG in fast food is a problem (learn more about MSG)

  Alcohol -- 29-35% of people with migraine are sensitive to mankind's most consumed poison
• Chocolate -- 19-22% of the migraine sufferers worldwide are sensitive to the sweet superfood
• Cheese -- 9-18% don't tolerate the tyramine which can also be found in other fermented foods
• Caffeine -- 14% of the patients report that the vasoconstrictive effects of caffeine make the headaches significantly worse
• MSG -- 12% of the migraine sufferers report that eating high mono-sodium glutamate foods gives them the "Chinese Restaurant Migraine"

Theoretically each and every food item could trigger migraine attacks, therefore I would not suggest to rely on this list all too much. Instead of just testing those 5 and resigning, when you are unable to trigger / avoid migraines by consuming / abstaining from them, I'd strongly advise to start a food diary, in which you log everything you eat, drink and supplement (nitrates are by the way notorious for triggering headaches, as well) + your migraine symptoms. Once you go through the notes you should be able to identify what causes the problem, if it has any dietary cause at all.

References:

• Cady RK, Farmer K, Altura BT, et al. The effect of magnesium on the responsiveness of migraineurs to a 5-HT1 agonist.Neurology.1998;50(suppl 4):A340. 
• Evans RW, Taylor FR. "Natural" or alternative medications for migraine prevention. Headache. 2006 Jun;46(6):1012-8. Review.
• Grossman M, Schmidrams H. An extract of Petasites hybridus is effective in the prophylaxis of migraine.Int J Clin Pharmacol Ther.2000;38:430–435.
• Leone M, D'Amico D, Moschiano F, Fraschini F, Bussone G. Melatonin versus placebo in the prophylaxis of cluster headache: a double-blind pilot study with parallel groups. Cephalalgia. 1996 Nov;16(7):494-6.  
• Lipton RB, Gobel H, Einhaupl KM, et al. Petsites hybridus root (butterbur) is an effective preventive treatment for migraine.Neurology.2004;63:2240–2244.
• Magis D, Ambrosini A, Sándor P, Jacquy J, Laloux P, Schoenen J. A randomized double-blind placebo-controlled trial of thioctic acid in migraine prophylaxis. Headache. 2007 Jan;47(1):52-7.
• Mauskop A, Altura BM. Role of magnesium in the pathogenesis and treatment of migraines.Clin Neurosci.1998;5:24-27.
• Pearlman EM, Fisher S. Preventive treatment for childhood and adolescent headache: role of once-daily montelukast sodium.Cephalalgia.2001;21:461
• Peatfield RC, Glover V, Littlewood JT, et al. The prevalence of diet-induced migraine.Cephalalgia.1984;4:179–183.
• Peres MF, Rozen TD. Melatonin in the preventive treatment of chronic cluster headache. Cephalalgia. 2001 Dec;21(10):993-5.
• Peres MF. Melatonin, the pineal gland and their implications for headache disorders. Cephalalgia. 2005 Jun;25(6):403-11. 
• Pothmann R, Danesch U. Migraine prevention in children and adolescents: results of an open study with a special butterbur root extract.Headache.2005;45:196–203.  
• Rossi P, Di Lorenzo G, Malpezzi MG, et al. Prevalence, pattern and predictors of use of complementary and alternative medicine (CAM) in migraine patients attending a headache clinic in Italy.Cephalalgia.2005;25:493-506. 
• Rozen TD, OshinskyML, Gebeline CA, et al. Open label trial of Coenzyme Q10 as a migraine preventive. Cephalalgia. 2002;22:137–141.
• Rozen TD. Melatonin as treatment for idiopathic stabbing headache. Neurology. 2003 Sep 23;61(6):865-6. 
• Sandor PS, DiClemente L, Coppola G, et al. Efficacy of coenzyme Q10 in migraine prophylaxis: a randomized controlled trial. Neurology. 2005;64:713–715.
• Scharff L, Turk DC, Marcus DA. Triggers of headache episodes and coping response of headache diagnostic groups. Headache.1995;35:397–403. 
• Schiapparelli P, Allais G, Castagnoli Gabellari I, Rolando S, Terzi MG, Benedetto C. Non-pharmacological approach to migraine prophylaxis: part II. Neurol Sci. 2010 Jun;31 Suppl 1:S137-9.
• Schoenen J, Jacquy J, Lenaerts M. Effectiveness of high-dose riboflavin in migraine prophylaxis. A randomized controlled trial.Neurology.1998;50:466-470 
• Sheftell F, Rapoport A, Weeks R, et al. Montelukast in the prophylaxis of migraine: a potential role for leukotriene modifiers.Headache.2000;40:158–163. 
• Srivastava KC, Mustafa T. Ginger (Zingziber officinale) in rheumatism and musculoskeletal disorder. Med Hypotheses.1992;33:342–348.
• Sun-Edelstein C, Mauskop A. Foods and supplements in the management of migraine headaches. Clin J Pain. 2009 Jun;25(5):446-52.

Leucine & Leptin, Two "L"s for More Muscle & Less Fat? "I'll Get There, When I Can!" How Important is it to Stick to the Plan? Is Organ Growth Inevitable for the Big Guys?

With annual costs of $560-$635 billion chronic pain is going to bankrupt the US before the diabesity epidemic can. After all the $146 billion obesity cost the US economy in 2008 is pretty cheap compared to the ~$300 due to chronic pain, wouldn't you agree?

$560-$635 billion that's the SuppVersity Figure of the Week and it quantifies the annual amount of money that is spent for treating chronic pain in the US (Institute of Medicine (US) Committee on Advancing Pain Research, Care, and Education. 2011). According to the latest data (2011) each US citizen is thus paying $2,000.00 to relieve the pain of 100 million chronic pain patients in the US alone.

Obviously you are not  paying those two grands to your sick neighbor, directly. In fact, the $2,000 consist of the total incremental cost of health care due to pain which ranges from $261 to $300 billion and a $297-$336 billion "penalty" due to lost productivity (that's more than 2x more than the $147 economic costs of obesity; CDC data from 2008)... what? Now, you are in pain, as well? Ah, never mind. At least a few cents of the two grand are now going to be spend on yourself.

Leucine & leptin: There is more than the "L" they have in common

(Mao. 2013) Yep, that's right there is more than the "L" that links leucine and leptin and that's not the fact that both are two-syllabled words. If the results, Xiangbing Mao and his colleagues from the State Key Laboratory on Animal Nutrition in China translate from the rodent model to human beings, the physiological relation between the two may turn leucine into an important tool in our war against diabesity, because the special thing about leucine is that ... leucine increases leptin and leptin receptor expression.

Figure 1: Protein synthesis, degradation and leptin mRNA expression of mice on alanine or leucine supplemented diets (Mao. 2013)

In the C57BL/6 mice the researchers used for their experiment, Mao et al. also observed significant reductions in plasma urea and protein degradation in skeletal muscle. What's also interesting is that both treating the mice with leucine and injecting them with leptin lead to similar increased weight of the gastrocnemius and soleus muscles in ob/ob mice (rodent model of diabesity). In that,

"[t]here were interactions (P 0.05) between the leucine and leptin treatments with regard to protein metabolism in C2C12 myotubes and soleus muscles [predomintantly oxidative] of ob/obmice but not in the gastrocnemius muscles [pred. glycolytic] of ob/ob mice." (Mao. 2013)

So that it can be assumed that the "anti-obesity" hormone which has as of late acquired somewhat of a bad rep is also a "muscle builder" that supports the muscle building prowess of leucine.

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Suggested read: "Leucine + Resveratrol - Synergistic Sirtuin Boosters: +118% Fatty Acid Oxidation, 60% Increase In Muscular Glucose Uptake, -30% Visceral Fat & More" (read more)

Now the bad news is that these results would suggest that both people starving themselves, as well as the victims of years of gluttony are not going to benefit from this synergy, because their leptin levels will either border zero (starvation) or the receptor expression will be so downregulated that even the 100% increase the researchers observed in the high leucine diet (compared to a high alanine diet) would not matter.

For the rest of us, it may yet be another research to keep an eye on the quality of each of the 30g+ protein servings you are supposed to have with every meal (learn why), after all you want your body to know that there is not need to store it as fat, don't you?

Things that matter: Sticking to the plan

No schedule? No routine?  No clue? No Problem! Read the SuppVersity Step By Step Guide to Your Own Workout Routine and find a plan to stick to (learn more)

(Gentil. 2013) It should actually go without saying that showing up at every training session and sticking to a plan is the primary parameter of training success. Unfortunately, the camp of fitness and physique enthusiasts is a pack of notorious "I'll get there, when I can"-s, "Just another set"-s and "Rest days suck I'll just do some bicep curls"... we have been discussing the counterproductive effects of the two latter strategies, which will usually lead to overtraining often enough (read up on overtraining). What I am not so sure about, though is whether or not we have ever taken a look at whether there is actually good evidence that the former group, the "I'll get there, when I can"-s actually don't see the results they are striving for.

Against that background I decided to take the very recent publication of a paper by Paulo Gentil and Martim Bottaro as an incentive to pose the question: "Does sticking to the plan make a difference?" Ok, ok, it probably won't come as a surprise that those of the 92 resistance training noobs (21.7 ± 2.7 years; 175.4 ± 6.7 cm; 74.1 ± 15.0  kg) who simply did not show up got what they deserved: nothing.

On the other hand, I would guess that some of you  may be surprised to hear that the XX% of the subjects who skipped 10-20% of their resistance training sessions, which consisted of

• five exercises -  leg  press,  knee  flexion,  bench  press,  pull down and sit ups 
• performed for two sets of 8-12 repetitions, with 90-120 s rest between sets
• for 11 weeks with two training sessions per week

did actually show (100% non-significant) greater increases in 1-RM strength on the bench than their more reliable peers (18% vs. 17.6%).

Figure 2: Scatter plot of 1-RM bech pres gains according to training attendance (in % on the x-axis; left); mean bench press and leg extension strength gains (right) expressed relative to mean levels of all three groups at baseline (Gentil. 2013)

As you can see in figure 2 there are still significant inter-individual differences, but the trend is clear - if you skip more than one out of 10 workouts on a 2x per week training schedule your gains suffer. Even Gentil and Bottaro were yet surprised that there was not a more distinct statistically significant correlation between  training attendance and strength gains after RT in these previously untrained young men and conclude that it "is not possible to suggest that, in the initial training phase, a higher attendance would lead to better results" (Gentil. 2013) At the same time, the authors do yet acknowledge that

"[...] there seems to  exist a cutting point, from  where  the  lack  of  compliance  starts  to  hinder upper  body  strength  gains.  In  the  present  study,  the group  of  subjects  with  less  than  80%  of  training attendance showed less gains in 1RM bench press [but not leg strength; my note] than the other groups." (Gentil. 2013)

Against that background the experiment was not totally useless. In conjunction with a previous study by Chin et al. who found a similar cut off level (75% non-attendance) in their 2006 study of the effects and feasibility of controlled exercise in long-term care facilities, it does yet confirm the notion that some lesser-fair ain't detrimental.

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Bottom line: In view of the results of the study at hand and the 2006 study by Chin et al. it appears that the non-athlete who must manage his workouts around his professional and social life won't hamper his progress, if he skips a workout once in a while. On the contrary, listening to your body (not your lazy weaker self, though) may even be something many of the most dedicated trainees could benefit from. When I think about the stubborn, frustrated faces of the vast majority of trainees who are simply always there, when I hit the gym, I don't need a study to tell you that doing the opposite, i.e. training when you actually have a rest day scheduled is much more detrimental to your physical development and psychological well-being than vice versa. 

Organ growth without drug abuse

(Miyauchi. 2013) The GH gut, i.e. the protruded abdomen many professional bodybuilders and strength athletes have, is a pretty nasty and unaesthetic abnormality and certainly not completely unrelated to the (ab-)use of all sorts of growth promoting "supplements". According to a very recent paper from the Waseda University in Saitama, Japan, it is however perfectly normal that increases in lean mass are accompanied by organ growth.

So, chronic overfeeding + exercise grows muscle, liver, heart, kidney & more, but it ain't going to grow your brain... no, I don't think this part of your body is going to grow. It's not exactly an organ and the corpus cavernosum is no muscle, either ;-)

"Fat-free mass (FFM), skeletal muscle, and adipose tissue mass were obtained using dual-energy X-ray absorptiometry. Liver, kidney, brain, and heart volumes were calculated using magnetic resonance imaging or echocardiography. Compared to the freshman players, the senior players had 10.8 kg more FFM, and 0.29 kg, 0.08 kg, and 0.09 kg greater liver, heart, and kidney mass, respectively. In the longitudinal study, FFM, liver, heart, and kidney mass of the freshman players increased by 5.2 kg, 0.2 kg, 0.04 kg, and 0.04 kg, respectively, after one year of overfeeding and physical training. On the other hand, the organ-tissue mass to FFM ratio did not change except for the brain in neither the cross-sectional or longitudinal studies." (Miyauchi. 2013; my emphasis)

Ok, admittedly, their subjects, collegiate male American football players (10 freshmen vs. 17 senior players in their second and third years of college) are certainly not 100% drug free study objects. The results are yet probably still relevant for the average trainee who will thus have to cope with some protrusion of the abdomen if he wants to compete with the heavy weights. After all, according to the results of the study at hand a 30% increase in lean muscle mass would yield a 30% increase in organ mass without a concomitant growth of the rib-cage, so that a slight protrusion of the abdomen is not unlikely to become visible even if you don't do drugs.

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Bottom line: Being big is a "whole body issue" and organ growth (as nasty as it may look) obviously a normal result of overfeeding and chronic training. In the end you can even argue that it's functionally important. I mean how is a heart that is used to fuel say 60kg of lean mass continue to supply a 90kg lean mass body with enough blood, just by increases in effectiveness? Well, that's like buying a VW Golf to which you then add extra after extra until it weighs as much as a Royce Royce Phantom and trying to compensate for that with nothing but chip tuning... sooner or later your Golf engine is going to get winded ;-)

Happy weekend everyone

If we discard the Facebook news that's it for today's installment of "On Short Notice", the "Short News" and all the funky names I have been giving these mini-items which will by the way no longer exists, whenI will finally find two weeks time to get the blog over into the new design. So, once you've checked out..

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  Don't worry, sweet & regular potatoes are equally suited for human consumption. And if they increase the risk of diabetes at all it is in the form of  French fries, potato chips & co, or in response to the effects of juicing, which is not only 100% unpaleo but notorious to produce exorbitant increases in the glycemic load of otherwhise healthy foods... You don't believe a word? In that case I'd suggest you (re?)read parts I & part II of the the SuppVersity Potato manifesto.

  ... how creatine can activate the alpha-1 adrenoreceptor according to a recent study from the  Universidade Federal de Santa Catarina in Brazil | read more...
• ... how endurance training leeches the salt from the bones and may thus increase the risk of osteopenia | read more... 
• ... how the molecular weight is the main determinant of the glucose blunting effects of beta-glucans and not, as it was previously thought the viscosity | read more... 
• ... how the antinutrient content of sweet potatoes and yams will put some inhabitants of the blogosphere at the verge of extinction, once they get wind that those two items are now also on the never-ending list of items "you are not supposed to eat" | read more...

I hope all of you are going to have a nice, painless weekend. Enjoy it, if you've been eating too many sweet potatoes in the past it may be your last ... just kiddin' folks ;-)

References:

• Chin APMJ, van Poppel MN, Twisk JW, et al. Once a week not enough, twice a week not feasible? A randomised controlled exercise trial in long-term care facilities. Patient Educ Couns. 2006;63:205-14.
• Gentil P, Bottaro M. Effects of training attendance on muscle strength of young men after 11 weeks of resistance training. Asian J Sports Med. 2013 Jun;4(2):101-6. 
• Institute of Medicine (US) Committee on Advancing Pain Research, Care, and Education. Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research. Washington (DC): National Academies Press (US); 2011. 
• Mao X, Zeng X, Huang Z, Wang J, Qiao S. Leptin and leucine synergistically regulate protein metabolism in C2C12 myotubes and mouse skeletal muscles. Br J Nutr. 2013 Jul;110(2):256-64.
• Miyauchi S, Oshima S, Asaka M, Kawano H, Torii S, Higuchi M. Organ Size Increases With Weight Gain in Power-Trained Athletes. Int J Sport Nutr Exerc Metab. 2013 Jun 24.