Complete Meals & GI (Non-)Sense, Glutamine & GLP-1, Low Thyroid & High Trigs, N-3 vs. N-6 Interactions, Optimal DHA Dosage in Kids W/ NAFLD, Selenium vs. Aluminum Toxicity

While this is not the exact combination of chicken breast, mashed potatoes and salad in the first one of today's news items, it's more than likely that the predicted GI (and thus probably what you would find if you looked it up in a table) overestimates the postprandial glucose response to this meal by ~50% and says absolutely nothing about the insulin response. It looks like complex meals and over-simplified theories, don't mix well, at all ;-)

78% that's the SuppVersity Figure of the Week and actually part of the additional information I provided on one of today's On Short Notice items. It's the increase in coronary heart disease risk women with subclinical hypothyroidism have compared to their peers with spot on TSH levels of 0.5-1.5mU/L (Asvold. 2013). In conjunction with other more or less recent studies, such as Mitchel's, Hsu's and Sahai's paper confirming the previously often talked about but not well-established 2-fold increase in congenital hypothyroidism from the early 1990s to the first years of the new millennium (Mitchel 2011), the predictive value of high TSH levels in the first trimester (early pregnancy hypothyroidism) for adverse pregnancy outcomes (Schneuer. 2013), the 30% risk increase in all-cause mortality in both women and men with subclinical hypothyroidism Tseng et al. reported in their paper earlier this year or the impairment of spatial working memory (Yin. 2013), Asvold's results only add to the evidence that the potential pitfalls of an increasingly prevalent metabolic dysfunction may have been ignored way too long.

• More GI lovin' - On the menu today: Mashed potaoes with chicken, rapeseed oil or both (Hätönen. 2011) - I thought a mini-follow-up on Friday's post on the GI would be nice, 'cause some of you have not without reason been complaining that not everyone would eat pure white bread, like my students do.
  
  

  

  Figure 1: The real (=measured) GI of a meal does differ significantly from the theoretical prediction. So, even if the concept was worth bothering, the GIs of complete meals simply wrong, if they are not measured (Hötönen. 2011).

  Moreover, the mere fact that the scientists from the Department of Lifestyles and Participation at the National Institute for Health and Welfare in Helsinki, Finland, found that the addition of chicken breast, rapeseed oil and a salad, individually and in combination, had the GI of a meal containing six mashed potatoes (this was the parameter that was held constant) induced more than twofold changes in GI, with the addition of chicken breast having the greatest deviation from the predicted value in this group of 11 (initially 12) healthy subjects, three men and nine women, aged 36.2 (SD 14.1) years with a BMI of 21.3 (SD 1.7) kg/m² and normal glucose tolerance (see figure 1).
  
  Now given the fact that most data on the GI of complete meals has never been measured, but is actually based on the same predictions the scientists used, it stands to reason that...
  

  [...] this highlights the problems encountered when predicting the GI values of mixed meals. The protein com-ponent of the mixed meal evoked the largest insulinaemic responses and markedly increased the II of the mixed meal containing protein. However, introducing fat into the meal decreased the effect of protein on the insulinaemic responses (Hätönen. 2011)

  So, this does not simply bust the idea that you could calculate the GI, it does likewise show you that people who are still overtly scared of insulin (which is hillarious as long as you are insulin sensitive) are doing he exact wrong thing, when they make food-choices based on GI: Whey protein would in that case be in as much a no-go as simply eating a chicken breast with your mashed potatoes would be, because other than what most people believe, it does increase the insulin spike and thus reduce the glycemic index by allowing your body to clear the glucose more efficiently from the circulation.
  
  Suggested reads: The red box in the "Whey is More Insulinogenic than White Bread" post on the partitioning effects of BCAAs and yesterday's Facebook post on the anti-Alzheimer's effects of insulin.

• 

  Suggested read: Amino Acids for Super Humans the purported ergogenic effects of l-glutamine

  30g of oral glutamine have similar effects on GLP-1 as 75g of glucose (Greenfield. 2008) - Still a follow up on the GI discussion, I think you may be interested in. If you are someone who follows the questionable practice of ingesting large boluses of glutamine in the futile believe that this would increase your gains or speed up recovery, you may be pleased to hear that only 30g of oral l-glutamine produced an increase in the "Fat Burning Satiety Hormone GLP-1" (read more on GLP-1) that's on a gram to gram basis more pronounced than in response to insulin (0.41pmol/L per gram glucose vs. 0.75pmol/L per gram of glutamine; in 8 healthy subjects).
  
  Before you go and buy tons of glutamine, you should however consider that GIP, the pro-insulinogenic peptide and glucagon (ramps up gluconeogenesis in the liver) were likewise increased by the ingestion of this bolus of glutamine. It is therefore no wonder that glutamine has never been shown to be a "fat burner". Nonetheless, a 1999 study by Bowtell et al. would suggest that it may come handy to replenish liver and muscle glycogen after a workout (8g alone did increase glucose storage after a workout to a similar degree as a 18.5% glucose polymer solution and additional 25% glucose storage mostly in the liver, when both were coingested; cf. Bowtell. 1999). And if you don't care about that - your gut integrity could also be a reason to consider supplementation in the vicinity of particular strenuous or length workouts (see "Shedding Some Light on the Leaky Gut <> Exercise Connection") 

• Practical relevance? Based on data from a 12-year longitudinal study, even women with subclinical hypothyroidism have 76% risk for coronary heart disease (p = 0.005), than women with spot on TSH levels of 0.5-1.5mU/L (Asvold. 2013). And even women well within in the "normal range" (TSH of 1.5-2.4mU/l) have a 41% higher risk of heart disease, although this is only borderline significant (p = 0.08). For men the TSH level alone had not predictive value. Spec. w/ regards to T3, there are also reports of increased incidence of ventricular disfuntion (Cassetti. 2009), increased cardiac death in CVD patients (Iervasi. 2003) and impaired recovery after a stroke (Alevizaki. 2007). We do yet have to be cautious, here as "low T3" syndrome could as well be the consequence of overall inflammation and the association does not tell us anything about what's the chicken and the egg.
  Low thyroid, high triglyceride (Hashimoto. 2013) -- If you are wondering why on earth your trigs won't come down, it may well be that it's the absence of sufficient amounts of thyroid hormone. I a soon-to-be-published paper in Endocrinology scientists from the Gunma University in Maebashi, Gunma, Japan, report that thyroid hormone regulates the expression of a Stearoyl-CoA desaturase-1 (SCD-1) which controls the production of trigs from carbohydrates.
  
  Surprisingly the 75% increase due to hypothyroidism and the 75% decrease in SCD-1 mRNA expression (both compared to a euthyroid state) the scientists observed in rodents in response to the administration of T3 were not mediated by receptor binding, but simply as a down-stream effect of direct modifications of the SCD-1 gene promoter between -124 and -92 bp by T3.
  
  On a related side note: It is actually the last mentioned mechanism which is the major new finding in the study at hand and not the fact that T3 can reduce the conversion of carbohydrates to triglicerides that is the actual news here. After all, the latter is something scientist should know, but obviously like to forget about ever since the late 1999s (Waters. 1997)

• Omega-6 intake and not low omega-3 intake is the problem (Liou. 2007) -- Another older study, but one I am posting in response to a discussion some of you are having about omega-3 (ALA) intake in the post about safflower oil and DHT, because I simply feel that it's necessary to shed some light  on the erroneous assumption that by simply upping your intake of omega-3s or fish oil intake you could get away without decreasing your omega-6 intake, which in and out of itself will already increase the amount of anti-inflammatory omega-3 fatty acids (supplementation of DHA can still be advisable, specifically if you are a vegetarian).
  
  

  

  Figure 2: Effect of 4 weeks of high (red) vs. 4 weeks of low (green) linoleic acid (n-6) intake on short and long-chain omega-3 plasma phospholipid content in healthy men (Liou. 2007)

  In 2007, already Liu et al. conducted a very interesting experiment in the course of which they fed healthy men diets with identical amounts of omega-3 fatty acids (1% of the total energy intake), but two different amounts of linoleic acid (omega-6) and found that the high omega-6 intake (10.1% vs. 3.8% of the total energy intake) alone decreased the total amount of EPA among the plasma phospholipids (the major long-chain omega-3 fatty acid in fish oil), not just the ratio of omega-3 to omega-6, in the blood of their 29-45 year-old subjects by more than 25% (see figure 2). The paradoxical effect on DHA, on the other hand, would warrant further investigation, and underlines how reliant we are - if anything on the intake of pure DHA, which dropped in consequence to the test diet, which was devoid of fatty fish, while the original diet of the non-vegetarian subjects had fish in it.
  
  In this context, I would also like to point out that DHA is exactly where real fish is far superior to fish oil caps, because it has a way more favorable EPA:DHA ratio than fish oil caps. Salmon fillets for example have - depending on the fatty acid source in the diet 8.5g : 13.8g, 4.4g : 7.8g and 1.5g : 2.9g (all values per 100g) when the feed contains fish oil, fish and rapeseed and fish + rapeseed and rapeseed, only.
  
  And while the ratios are similar regardless of the chow, the data from the Seierstad et al. clearly shows that the fatty acid content of the diets can induce almost 5-fold differences in terms of the total DHA content and the omega-3 to omega 6 ratio (fish oil diet: 6.5, fish oil + rapeseed: 1.7, rapeseed: 0.6) of salmon fillets (Seierstad. 2003). 

• It does not take much: 500mg DHA not more effective than 250mg  (Nobili. 2013) -- At least if it comes to its beneficial effects against liver steatosis in children  (mean age 11 years; BMI 26.6kg/m² and 24.4kg/m², in the low and high dose groups respectively with with NAFLD, the amount of DHA does not appear to be so important. According to the results of their 2-year registered controlled trial, both 250mg and 500mg of Docosahexaenoic acid lead to identical and profound reductions in the odds ratio of developing more severe steatosis during the study period.
  
  

  

  Figure 3: Odds ratio (comparing DHA supplement vs. placebo) of more severe vs. less severe liver steatosis determined every 6 months during the 24-month study period (Nobili. 2013)

  If you take a closer look at the data in figure 3, you will even have to concede that the lower dosage did a better job - while the mean odds ratios were only marginally lower in the 250mg DHA group, the extremely high standard deviations in the 500mg DHA would suggest that the 250mg dose appears to be more reliable. In this regard it may be interesting that the increase in serum DHA did mirror the dosages. With a 0.65% and 1.15% increase in DHA those were about 2x higher in the 20 boys and girls in the high dose group compared to the 20 kids in the control group who received a 290 mg linoleic acid germ oil supplement "placebo" (by the way, a monosaturated fatty acid placebo would have been more of a placebo than 290mg of omega-6)
  
  In view of the fact that the changes in triglycerides, ALT, HOMA-IR and BMI (which was not even different from the placebo group) were likewise identical, it does not appear as if anything that goes beyond the amount you will find in 2x cheap fish oil caps, or 10g even of the cheapest salmon fillet (see last paragraph of previous item) would be necessary to ellicit the anti-steatosis effect of fish oil - since those kids weight on average 55kg, an adult may want to add in another fish oil cap to get up to 360mg DHA per day or simply eat his fatty fish once or twice a week.

• Selenium ameliorates aluminum toxicity (Viezeliene. 2013) -- With the whole upheaval about the potential negative side effects of the aluminum in vaccines, the formerly overlooked yet well-known neurotoxic (Exley. 1992; Gupta. 2005), hepatotoxic (Abubakar. 2003; Perez. 2005) and nephrotoxic metal (Geyikoglu. 2013) has all of a sudden returned to the center of public interest.
  
  Therefore I thought that you will be interested in the results of a study that's going to be published in the next issue of the Journal of Trace Elements in Medicine and Biology - irrespective of whether you believe, like Tomljenovic and Shaw that
  

  "the possibility that vaccine benefits may have been overrated and the risk of potential adverse effects underestimated, has not been rigorously evaluated in the medical and scientific community"(Tomljenovic. 2011)

  After all, vaccines are not the only potential source of aluminum in our environment, so that the ameliorative effects (all values remained normal in the aluminum exposed group, while there were 30%, 55% and 42% increases in GSH in the animals who received only the selenium injection) the co-administration of supplemental selenium had on the GSH reductions in liver, kidney and brain of Balb/c mice weighing 20–25g who were exposed (by i.p. injection)to AlCl3 (25 mg Al(3+)/kg body mass) for 16h could be important, regardless of whether you do or don't intend to get vaccinated.
  
  

  

  There is more about selenium at the SuppVersity, for example on its pro-fertility effects, and its anti-corrosive effects in the brain.

  That said, the dosage requirements necessary to maintain healthy GSH levels are probably much lower than the hillarious (for a healthy individual) in the study at hand 1,250µg/kg body weight of sodium selenite (Na2SeO3). Considering the elemental selenium content in Na2SeO3, the latter would equal to ~3,650µg - unquestionably WAY too much (remember this was a one-time dosage that was specifically co-administered w/ the aluminum). Even the 'no observed adverse effect' level for a 70kg man of intake which is ~1000µg/d (Whanger. 1999) appears unnecessarily high, so that the consumption of a handful of brazil nuts once or twice a week and/or other high selenium foods such as tuna, cod, oysters, shrimp, but also eggs, meats, poultry, mushroom and onions on a regular should suffice to get what you need, to fortify yourself against the constant assault of heavy metals.
  
  What would be interesting, though, is a study into the effects of adding selenium to the "safe" aluminum in vaccines. I mean, you cannot seriously tell me that we could not afford doing that and if it reduced any toxicity issues, why not?

That's about it for today, I did not post all too many new facebook news as of yet (I mean, come on, it's Saturday ;-), but if you are into medicinal horror-stories, you will certainly like the story about the flesh eating killer fungus. If you prefer microbes over fungi, you are probably better off with the latest insights into the associations of certain gutbacteria with the incidence of stroke. And if you are more into other aspects of the digestive tract you may be interested in the effects of gastric emptying time on postprandial gylcemia and insulin release.

If none of those news is to your liking, I suggest you either wait for me to post something else (could be happening within the next hours at www.facebook.com/SuppVersity), or simply enjoy the weekend and come back tomorrow when you are rested for another (hopefully) enlightening SuppVersity post.

References:

• Abubakar  MG,  Taylor  A,  Ferns  GA.  Aluminium  administration  is  associated  with enhanced  hepatic  oxidant  stress  that  may  be  offset  by  dietary  vitamin  E  in  the rat. Int J Exp Pathol 2003;84:49–54.
• Asvold BO, Bjøro T, Platou C, Vatten LJ. Thyroid function and the risk of coronary heart disease: 12-year follow-up of the HUNT Study in Norway. Clin Endocrinol (Oxf). 2013 Dec;77(6):911-7.
• Bowtell JL, Gelly K, Jackman ML, Patel A, Simeoni M, Rennie MJ. Effect of oral glutamine on whole body carbohydrate storage during recovery from exhaustive exercise. J Appl Physiol. 1999 Jun;86(6):1770-7.
• Cassetti G, Pinelli M, Bindi M, Bianchi M, Castiglioni M. [Low T3 syndrome and left ventricular diastolic function]. G Ital Cardiol (Rome). 2009 Aug;10(8):553-7. 
• Exley  C,  Birchall  JD.  The  cellular  toxicity  of  aluminium.  J  Theor  Biol 1992;159:83–98.
• Geyikoglu  F,  Turkez  H,  Ozhan  Bakir  T,  Cicek  M.  The  genotoxic,  hepa- totoxic,  nephrotoxic,  haematotoxic  and  histopathological  effects  in  rats after aluminium chronic intoxication. Toxicol Ind Health 2013;15.
• Greenfield JR, Farooqi IS, Keogh JM, Henning E, Habib AM, Blackwood A, Reimann F, Holst JJ, Gribble FM. Oral glutamine increases circulating glucagon-like peptide 1, glucagon, and insulin concentrations in lean, obese, and type 2 diabetic subjects. Am J Clin Nutr. 2009 Jan;89(1):106-13.
• Gupta  VB,  Anitha  S,  Hegde  ML,  Zecca  L,  Garruto  RM,  Ravid  R,  et  al.  Alu- minium  in  Alzheimer’s  disease:  are  we  still  at  a  crossroad?  Cell  Mol  Life  Sci 2005;62:143–58.
• Hashimoto K, Ishida E, Miura A, Ozawa A, Shibusawa N, Satoh T, Okada S, Yamada M, Mori M. Human Stearoyl-CoA Desaturase 1 (SCD-1) Gene Expression Is Negatively Regulated by Thyroid Hormone without Direct Binding of Thyroid Hormone Receptor to the Gene Promoter. Endocrinology. 2013 Dec 7.
• Hätönen KA, Virtamo J, Eriksson JG, Sinkko HK, Sundvall JE, Valsta LM. Protein and fat modify the glycaemic and insulinaemic responses to a mashed potato-based meal. Br J Nutr. 2011 Jul;106(2):248-53. 
• Iervasi G, Pingitore A, Landi P, Raciti M, Ripoli A, Scarlattini M, L'Abbate A, Donato L. Low-T3 syndrome: a strong prognostic predictor of death in patients with heart disease. Circulation. 2003 Feb 11;107(5):708-13.
• Liou YA, King DJ, Zibrik D, Innis SM. Decreasing linoleic acid with constant alpha-linolenic acid in dietary fats increases (n-3) eicosapentaenoic acid in plasma phospholipids in healthy men. J Nutr. 2007 Apr;137(4):945-52. 
• Mitchell ML, Hsu HW, Sahai I; Massachusetts Pediatric Endocrine Work Group. The increased incidence of congenital hypothyroidism: fact or fancy? Clin Endocrinol (Oxf). 2011 Dec;75(6):806-10.
• Perez  G,  Pregi  N,  Vittori  D,  Di  Risio  C,  Garbossa  G,  Nesse  A.  Aluminium  expo- sure  affects  transferrin-dependent  and  -independent  iron  uptake  by  K562  cells. Biochim  Biophys  Acta  2005;1745:124–30. 
• Schneuer FJ, Nassar N, Tasevski V, Morris JM, Roberts CL. Association and predictive accuracy of high TSH serum levels in first trimester and adverse pregnancy outcomes. J Clin Endocrinol Metab. 2013 Sep;97(9):3115-22.
• Seierstad SL, Seljeflot I, Johansen O, Hansen R, Haugen M, Rosenlund G, Frøyland L, Arnesen H. Dietary intake of differently fed salmon; the influence on markers of human atherosclerosis. Eur J Clin Invest. 2005 Jan;35(1):52-9.
• Waters KM, Miller CW, Ntambi JM. Localization of a negative thyroid hormone-response region in hepatic stearoyl-CoA desaturase gene 1. Biochem Biophys Res Commun. 1997 Apr 28;233(3):838-43. 
• Whanger P, Vendeland S, Park Y-C & Xia Y. Metabolism of sub-toxic levels of selenium in animals and humans. Annals of Clinical Laboratory Science. 1996;26, 99-113.

The Starch Satiety Shootout: Potatoes, Baked or Mashed, Pasta, Brown Rice or Even White Bread? What's the Best After a 12h Fast? Plus: Science Round-Up Preview!

Pasta! From a satiety perspective even white bread would be a better choice for breakfast.

It's one of those Thursday's where I am alone here at the SuppVersity - no Adelfo Cerame Jr. guest lecture today. But don't worry, there will not only be another guest post next Thursday, but both, today's SuppVersity post, which is actually related to Adelfo's "Carbophobia" post from last week, as well as the SuppVersity Science Round-Up  with Carl Lanore (live at 1PM EST on the Super Human Radio Network), will compensate at least somewhat for Adelfo's absence.

Apropos Science Round-Up, I am absolutely not sure where today's show will be heading to, but I can tell you that by now it looks as if we would start out with a very recent study on the leucine <> leptin connection and it's role in getting big and ripped.

It stands to reason that the big "L"s are not going to get the job done without some sort of workout, we will then segue into the acute hormonal effects of doing cardio before vs. after a workout - something I suppose many of you who have listened to the last installment and read the follow-ups (the Seconds and the post on PGC-1 alpha-4), here at the SuppVersity, will be intrigued to hear and something on which I want to provide a little more background information with respect to the role of fasting, overall energy intake, glyogen depletion, stress and a couple of other things that will primarily effect your luteinizing hormone levels and are thus equally important for male and female SuppVersity students.

I am honestly not sure how much time will be left, afterwards, but either live at 1PM EST, or as part of tomorrows "Seconds" you will also get the chance to learn something about the little known link between nicotine (as in cigarettes) and brain aromatase, the muscle building effects of exercise induced nNOS and the certainly not advisable, but probably likewise anabolic effects of capsaicin injections. And while there is more on the list, I guess this is enough for a preview... unless you were waiting for me to mention the endocrine disrupting effects of bottled water? No!? Well, then let's finally get to the actual post ;-)

Judging carbohydrates by their GI is like adopting another man's prejudice

As I already mentioned today's post is in a way an indirect follow up on Adelfo's confession that his love-and-hate affair with carbohydrates turned into a true friendship now. I mean starches are carbs and though Adelfo explicitly said that he says a place (in moderation) for all of them in his diet, it would be nice to know a little more about the differences between the dreaded potatoes, of which I have argued before that it is in your own hands whether they will (French fries, meshed potatoes, puree, etc.; "The Potato Manifesto") turn into a problem, or not, the demonized white bread and the "healthy" - since organic and brown - starch from pasta and rice.

I guess Allan Geliebter Michelle, I.-Ching Lee, Mariane Abdillahi and James Jones from the New York Obesity Nutrition Research Center at the St. Luke’s-Roosevelt Hospital Center that's part of the Columbia University College of Physicians and Surgeons in New York, when they devised the experimental procedures for their latest study (Geliebter. 2013). And in fact their approach to the problem appears to be pretty down to earth. Instead of just measuring insulin, glucose and what-not - we have had other scientists do that before - they simply fed their twelve healthy normal-weight participants (6 male, 6 female; mean age 25.6 years,  mean BMI 22.4kg/m², mean percent body fat 19.0%) who were recruited from the Columbia University community equienergetic portions (240kcal) of starch-rich side dishes:

• baked potato, no skin - nutrient composition as
• mashed potato, instant - Betty Crocker Idaho potato buds
• brown rice - Carolina natural whole grain brown rice
• pasta - Bionature organic pasta
• white bread - Wonder Classic Giant*

As the (*) indicates, the white bread was in there mainly as a GI standard (you usually supply GI values w/ reference to either glucose or white bread) and in order to make sure that it had it's 50g of carbs, just like all the other meals, the scientists needed so much that the overall caloric value of this "standard" meal was 33kcal higher (keep that in mind, thats ~12.5% and could therefore very well make a difference). In order to exclude any confounding variables, the water content (400g) and salt content were likewise standardized - both were added if necessary.

Pasta, rice and potatoes for breakfast?

In know, its not realistic that you have only pasta, rice, potatoes or white bread ... hold on, I know a couple of people in fact a large amount of my students eats nothing but white bread right from the baker for breakfast in their first lecture of the day :-( So it's not that unrealistic: At least we could ask ourselves would they be better off, if they ate potatoes, pasta or rice as their first meal after a 12h overnight fast, when maximal satiety is what we are looking for?

Figure 1: Hunger ratings and desire to eat from 10min before to 120min after the breakfast (Geliebter. 2013)

Well let's see, what do we have here? First off, one thing that's not in any of the graphs is the statistically significant gender bias, with the women experienced greater fullness across the test meals than men (p < 0.01). As far as the rest is concerned, the ...

• AUC of the appetite ratings from 10 minutes before to 120min after the ingestion of the meal did not differ, and still there was a...
• lower ‘desire to eat’ AUC following bakedpotato compared to pasta (p = 0.027) and brown rice (p = 0.004) and a much less significant advantage for rice over pasta (p = 0.041);
• changes in fullness, however, did not differ between test meals (not shown in figure 1)

So, obviously the baked potato, which was incidentally the only food that had no nutrition label (all the rest was packaged branded and labeled), was the subjectively most satiating starch source, followed by rice and trailed by the mashed potatoe and the distant (given the overall difference) "healthy" pasta.

So, to get back to my research question, whether my real students (not you, but those at the University), would be better off eating another bland starch instead of their buns, the answer would be yes - in the long run, both brown rice and baked potatoes would qualify. 

Potato-ish insulin spikes and low GI white bread

What is interesting though, is that the spike in the "How much food could you eat now?" graph in figure 2 coincides with the early insulin spike in response to the potato meals. If you are into grazing like a cow, i.e. if you like to eat bazillions of small meals, all day long, potatoes may therefore be not your best choice.

Figure 2: Insulin after breakfast,estimation how much the participants believe the could eat and calculated GI values (based on the measured glucose response; Geliebter. 2013)

What could be downright surprising for some of you, I guess, is yet probably the fact that anyone adhering to a low GI diet, would actually have to copy my students and eat the white bread, which had the lowest GI of all the test meals ... but I guess this and the fact that pasta by far the least satiating of the 4 meals had an only 7.6% higher GI should be the nail to the real-world relevance of the glycemic index, anyway.

The non-significance of the glycemic index  was also evident during the following lunch, where the subjects were allowed to chose or simply eat both of an on an individual base already non-manageable amount of chicken or tuna salad with mayonnaise, celery, salt, and pepper that were served "in covered serving containers with openings on top to reduce visual feedback" (Geliebter. 2013) and bundled with six slices of wheat bread and six slices of seedless rye bread:

"The group mean IAUC glucose and GI using the white bread standard and adjusted for the glucose load standard are listed in table 2 . Mashed potato had the highest GI of the side dishes. The correlation between the group mean fullness AUC and the group mean GI was 0.59. The correlation between the group mean fullness AUC and the group mean lunch energy intake was –0.21. These corrrlations are not significant." (Geliebter. 2013)

Remember Peter Czerwinski, aka Furious Pete's 900g of protein in 3:30min binge (Furios Pete, 2010)? No? In that case the fact that whey is more insulinogenic than white bread is probably news to you, as well, after all, the video was part of the SuppVersity post discussing that.

So, if you intend to become friends with starches and other carbohydrates, just like Adelfo did, don't judge them by the GI value you've found in whatever online or print source. Don't fear potatoes and if you need something to count to satisfy your OCD tendencies, count total amount carbohydrates (not the rice crumbs), keep the simple sugars in check and match both of them to your personal preferences / needs.

The GI is not the "unit of food quality"

And if that's not enough counting for you, what about counting the nutritional labels on the stuff you buy? The less you have, the better your diet - after all, whole foods you buy at the farmer's market or wherever else you can still get non-industrialized real food, does not have nutritional labels ;-)

References:

• Geliebter A, Lee MI, Abdillahi M, Jones J. Satiety following Intake of Potatoes and Other Carbohydrate Test Meals. Ann Nutr Metab. 2013 Dec 4;62(1):37-43.

Is Hypoglycemia Obesogenic? Is the GI Totally Worthless? Is Mild, But Chronic Stress Behind the Diabesity Pandemic? Is Leptin Obesogenic? And How Do You Calculate the Energy Requirements of Diabetics?

One of the mistakes researchers and dieters make time and again, using the scale as their only guide

Since I had a couple of interesting, but not earth-shatteringly exciting studies on obesity, body weight gain, the GI, leptin and a couple of other things lying around, I thought I'd compile a brief potpourri for you to get you on par with the helplessness with which researchers are still facing the diabesity pandemic. So don't expect any of the one-size-fits-it-all solutions the scientists still appear to be looking for from any of the following items. What you may find, however, is some inspiration when you read between the lines or follow up on the suggested reads, I mention. And if that's not the case, you can still browse previous articles on fat loss or simply go to the gym and try the fat loss example routine from the SuppVersity "Step By Step Guide for Your Own Workout Routine" or simply go to be early to preserve your circadian rhythm.

• Going "Hypo" time and again will make you fat (McNay. 2013) -- Usually you think of hyogylcemia as a sign of a lack of energy, yet despite the fact that this may well be the case this very lack in energy has recently been shown to exert obesogenic effects in a rodent model.
  
  

  

  Often a picture says more than 1000 words: Normal (left) and repeatedly hypoglycemic rodents after 8 months of weekly insulin injections (McNay. 2013)

  The weekly injections Ewan C McNay and his colleagues administered to their rodents and the subsequent episodes of hypoglycemia lead to profound weight gain in the absence of diabetes, hyperphagia, changes in hypothalamic NPY or POMC mRNA expression and  the other usual suspects that could explain this phenomenon. The one thing that's left is therefore what the researchers call a "multi-faceted deficit in metabolic regulation" (McNay. 2013) - interestingly enough the 69.5% higher body weight at 12 months went hand in hand with the usual laziness (-25% activity) of people whose brains are starving in abundance (e.g. type II diabetics).
  
  What remains to be seen, though, is whether similar effects would occur in response to "regular" non-insulin induced hypoglycemia. In view of the easy with which crash dieters and people with roller-coaster blood glucose levels gain weight, it is yet not unlikely that it is actually the avoidance of (reactive) hypoglycemia and not so so much the prevention of hyperglycemia that makes low GI diets successful for weight maintenance (for weight loss the picture is more complicated, since this will require a energy deficit and that's a game changer).

• Dietary glycemic index and load are not associated with type II diabetes risk in 12,403 Europeans (Sluijs. 2013) -- Apropos GI, scientists from the University Medical Center in Utrecht did not find statistical significant correlations dietary glycemic index and/or glycemic load and the risk to develop type II diabetes in in a subcohort of the European Prospective Investigation into Cancer and Nutrition Study (n = 12,403 participants).
  
  Even when they compared participants in the highest and lowest quantiles, the increase in risk was only 5% and 7% for GI and GL respectively. Since this is by no means the first study that suggests that the still propagated concept of the beneficial health effects "low GI diets" is faulty, I would suggest you rather watch the actual food items, than their respective glycemic indexes if you intend to ward off obesity and diabetes. Potatoes for example may have a high GI (including sweet potatoes, by the way), but their high potassium and overall mineral content, as well as the mere fact that you can hardly eat the same amount of total carbohydrates you can easily annihilate, when you are eating pasta still makes them one of the best sources of starchy carbs you have (learn more in the Potato Manifesto, Part I & II).

• 

  Figure 1: There were no statistically significant difference in terms of weight gain or loss, but the 2-week re-feed had a greater impact on blood glucose and insulin levels in the high GI group (Lagerpusch. 2013)

  There is use for the GI on a bulk or after a diet, but only if you are concerned about insulin sensitivity (Lagerpusch. 2013) -- While the general value of the GI as a means to distinguish good from bad carbohydrate sources is certainly questionable, the recently published results from a study that was conducted at the Institute of Human Nutrition and Food Science, of the -Albrechts University in Kiel, Germany, does suggest that monitoring the GI of your diet and adding additional fiber to reduce the insulin response to your meals can come quite handy, in phases, where you are particularly prone to store body fat. On a bulk, for example, or even more so when you have been dieting and are trying to return to a normal caloric intake.
  
  According to the results Lagerpusch et al. present in the November issue of the British Journal of Nutrition even healthy young men who were subjected to a 3-week diet phase (-50% in caloric intake) and subsequent overfeeding (+50% in caloric intake) the subjects in the high GI study arm had a 135% higher increase in fasting insulin levels during the refeed than those in the low GI group. In view of the fact that the glucose clearance (measured in an oral glucose tolerance test) was identical, it is not only no wonder that the weight gain did not differ either (see figure 1), but also unlikely that we would see significant differences as far as the fat gains are concerned (the latter were unfortunately not measured in the study at hand). At the same time, longer hyper-caloric high GI diets are certainly a risk factor for both insulin resistance and obesity, so that you are probably still at lower risk with 65g instead of 27g of fibre per day and a mean GI of 40 vs. 74.
  
  If you are interested in the influence of different diets on weight gain and health during overfeeding, I suggest you check out the following two SuppVersity posts: "194 Bananas in Three Weeks" and "A Tale of Macro- and Micronutrient Modifications".

• 

  Figure 2: Chronic mild stress leads to an overactivation of the HTPA and subsequen metabolic dysregulations (Takahashi. 2013)

  Further evidence that chronic mild stress is to blame for the obesity pandemic (Takahashi. 2013) -- As researchers from the Tohoku University Graduate School of Medicine in Japan report in the latest issue of the  American Journal of Physiology - Endocrinology & Metabolism, the localized re-setting of the clock genes in the liver, yet not the hypothalamic suprachiasmatic nuculeus (SCN), of BALB/c mice in response to chronic mild stress exposure elevated and phase-shifted serum corticosterone levels (see figure 2).
  
  Takahashi et al. argue that the observed changes are indicative of an overactivation of the HPA axis, which induced disturbances in the rhythmic expressions of core clock genes, e.g. Clock, Npas2, Bmal1, Per1 and Cry1 in the liver and subsequently circadian patterns of glucose and lipid metabolism-related genes such as the proliferator activated receptor (PPAR) family which favor the storage and hamper the oxidation of fatty acids.
  
  If you want to learn more about clock genes and how you can modify them, (re-)read the SuppVersity Circadian Rhythm Series!

• Scientists develop improved formula to calculate the resting energy expenditure of diabetics (Ikeda. 2013) -- While I would hope that you don't belong to the group who would have to use the new and improved formula scientists from the Department of Diabetes and Clinical Nutrition at the Kyoto University in Japan have now proposed, you may have clients or relatives who could benefit from its high predictive validity (78% +/- 103kcal vs. 50% for Harris-Benedict; 38% for Oxford, 42% for Liuand 63% for Ganpule):
  
  
  What you should keep in mind though, is that this equation was tested on Japanese individuals. Since we know from other studies that there are certain metabolic differences between people with different ethnic backgrounds I would remain a "healthy skeptic" as far as the outcomes of this equation are concerned - the same obviously goes for any other equation, e.g. the ones for athletes I provided in part III of the Female Athlete Triad series.

• 

  If you are interested in ways to modulate your leptin levels that may facilitate weight gain, I suggest you take a look at my second "Carbs Past 6PM Won't Make You Fat" post.

  Leptin induced weight gain? 13% more body fat in 2 weeks, when it hits the wrong part of the brain (Harris. 2013) -- With the mixed results from intervention trials, the enthusiasm around leptin has abated over the past months, the general consensus is yet still that leptin and leptin resistance loom large in the metabolic dysregulation that's at the heart of the diabesity pandemic. Against that background, the results Ruth B.S: Harris presents in her latest paper in the American Journal of Physiology - Endocrinology & Metabolism are unquestionably surprising.
  
  When Harris injected twice the amount of leptin (0.6 µg leptin/day) that had previously been shown to decreased 24 food intake, body fat and lean tissue, when it was injected into the third ventricle of the hindbrain, into the fourth ventricle of her lab rats, the rodents gained an almost incredible amount of 13% body fat within only 2 weeks! And that in the absence of statistically significant change in daily food intake, suggests an "increase in efficiency of energy utilization" (Harris. 2013). Fortunately, further experiments showed that the pro-obesogenic effects of leptin in the 4th ventricle was antagonized when both the 3rd and the 4th ventricle were exposed to leptin. In this scenario the leptin exposure of the 4th ventricle did even protect the lean mass of the rodents from the negative effects the exclusive exposure of the 3rd ventricle had. Overall, the study is yet somewhat chaotic and a clearcut message aside from "look people things are even more complex than we already thought", is probably not going to contribute to a solution of the obesity dilemma in the near future. 

There are, as usual more news on Facebook, some of them, such as the relation between hypothyroidism during pregnancy and the diabetes risk of the offspring later in life, are even related to the topic at hand. And if that's nothing you are interested, you may want to read about ...

• the non-existent effects of coffee consumption before bed on the sleep quality of habitual coffee drinkers (read more),
• the problem with inaccurate vitamin D tests and the absence of a reliable and scientifically sound definition of "vitamin D deficiency" (read more), or
• the strength promoting in-vitro effects of sodium bicarbonate, or in other words, a rather alkaline milieu on muscular force production (read more)

... and if neither of those can satisfy your thirst for more information from the realms of exercise and nutrition sciences, you can still wait for the next serving of facebook news or tomorrow's SuppVersity article :-)


References:

• Harris RB. Leptin-induced increase in body fat content of rats. Am J Physiol Endocrinol Metab. 2013 Dec 4.
• Ikeda K, et al. A new equation to estimate basal energy expenditure of patients with diabetes. Clinical Nutrition. 2013 [article in press] 
• Lagerpusch M, Enderle J, Later W, Eggeling B, Pape D, Müller MJ, Bosy-Westphal A. Impact of glycaemic index and dietary fibre on insulin sensitivity during the refeeding phase of a weight cycle in young healthy men. Br J Nutr. 2013 Nov 28:1-11.
• McNay EC, Teske JA, Kotz CM, Dunn-Meynell A, Levin BE, McCrimmon RJ, Sherwin RS. Long-term, intermittent, insulin-induced hypoglycemia produces obesity without hyperphagia or insulin resistance: a model for weight gain with insulin therapy. Am J Physiol Endocrinol Metab. 2013 Nov 20.
• Sluijs I, Beulens JW, van der Schouw YT, van der A DL, Buckland G, Kuijsten A, Schulze MB, Amiano P, Ardanaz E, Balkau B, Boeing H, Gavrila D, Grote VA, Key TJ, Li K, Nilsson P, Overvad K, Palli D, Panico S, Quirós JR, Rolandsson O, Roswall N, Sacerdote C, Sánchez MJ, Sieri S, Slimani N, Spijkerman AM, Tjønneland A, Tumino R, Sharp SJ, Langenberg C, Feskens EJ, Forouhi NG, Riboli E, Wareham NJ; on behalf of the InterAct consortium. Dietary Glycemic Index, Glycemic Load, and Digestible Carbohydrate Intake Are Not Associated with Risk of Type 2 Diabetes in Eight European Countries. J Nutr. 2013 Nov 28.
• Takahashi K, Yamada T, Tsukita S, Kaneko K, Shirai Y, Munakata Y, Ishigaki Y, Imai J, Uno K, Hasegawa Y, Sawada S, Oka Y, Katagiri H. Chronic mild stress alters circadian expressions of molecular clock genes in the liver. Am J Physiol Endocrinol Metab. 2013 Dec 4.

Meal Timing, Glycemic Index & Load: Human Study Probes Whether "Hitting Your Macros" Really is All That Counts

High or low GI, carbs in the morning or in the evning, cookies and dingdongs or all bran. So many questions and way too many answers from rodent studies or studies in obese diabetics... but what are Mr. and Mrs. Healthy Average Joe supposed to do?

In a recently published paper, Linda M. Morgan, JiangWen Shi, Shelagh M. Hampton and Gary Frost take yet another look on a concept that has lost much of the momentum it had only a decade ago: The GI and / or GL paradigm (GI: glycemic index (abstract unit); GL: glycemic load, i.e. GI / actual amount of food) and combines another paradigm, which is still gathering momentum within the medical science community - the issue of nutrient timing, in order to answer the following questions:

• Will a large evening energy and carbohydrate load cause an increase in postprandial glucose that is comparable to the same amount of energy and carbohydrates in the morning?
• Will a high glycaemic excursions in the evening be ameliorated by decreasing the glycaemic index (GI) of the meal?

Or put simply: Does carbohydrate and energy timing make a difference and can this difference be mitigated by chosing the "right", i.e. low glycemic carbs (e.g. sweet potato vs. white bread)?

White bread king or all-bran pauper - is that  the question?

To answer this world-shattering question and actually prove their hypothesis that both, i.e. having carbs in the evening and having those in the form of high glycemic index foods, will have negative consequences on postprandial glycemia, the scientists picked six healthy volunteers (four females, two males; mean age 30 +/- 4.3 years, BMI 21·6 +/- 1.3 kg/m²) and randomly assigned them to a follow one of the four following dietary protocols:

• Low GI (average GI = 34), with the majority of energy load consumed in the morning (LGI-am)
• Low GI, with the majority of energy load consumed in the evening (LGI-pm)
• High GI (average GI = 84), with the majority of energy load consumed in the morning (HGI-am)
• High GI, with the majority of energy load consumed in the evening (HGI-pm)

with identical energy content of approx. 8368 kJ (2000 kcal) for the whole day on four individual intervention days with a minimum of 7 days between each of the tests. Breakfast was given at 09.30 hours, lunch at 13.30 hours and the evening meal at 20.30 hours - subjects were at the laboratory for the whole day. Blood samples were taken 2h postprandial and blood glucose levels were monitored continuously via a "MiniMed continuous glucose monitoring system" that senses interstitial glucose by electrochemical detection in subcutaneous interstitial fluid in 5 min intervals.

Figure 1: Composition of the two test diets (low GI, blue; high GI read) and individual macronutrient breakdown of the test meals the subjects consumed on two seperate occasions (based on Morgan. 2013)

It does not take a nutrition expert to see that despite the obvious differences with respect to the glycemic index and load, even the allegedly healthy low GI diet with all-bran for dinner* and a macronutrient composition 72% carbohydrates 14% protein and 14% fat is not exactly what the latest research would suggest to be a healthy, let alone a "physique enhancing" diet.

*note: The scientists probably chose similar foods for breakfast and dinner, because the study design required those to be exchangeable.

Against that background it is still astonishing how much of a difference...

• 99% higher fiber content,
• -60% lower glycemic index (GI), and
• -63% lower glycemic load (GL)

... actually make when it comes to the effect of isocaloric meals with identical macronutrient compositions (see figure 1, right):

Figure 2: Total area under the curve for interstitial glucose (0–20 h), postprandial plasma insulin, TAG (**mind the text for info a potential typo, here) and NEFA (0–2 h after each meal) in six healthy volunteers following either a high-glycaemic index (HGI) or a low-glycaemic index (LGI) diet, with most of the energy consumed either early (LGI-am, HGI-am) or late (LGI-pm, HGI-pm); all values expressed relative to respective statistical mean (data calculated based on Morgan. 2013)

I guess I don't have to tell you that the image that emerges here stands in line with the as of late largely ignored glycemic index paradigm the underlying message of which is: It is not simply the amount of sugar you eat,  but rather how fast / hard it hits your blood stream that determines it's impact of on your glucose metabolism. And with respect to the latter, the researchers remark:

"Glucose and insulin responses showed broadly similar patterns. Both meal timing and quality of carbohydrate affected postprandial glucose and insulin responses (P < 0.01). The area under the glucose and insulin response curves was greatest for the HGI-pm meal regimen. The HGI-pm meal regimen produced a significantly greater postprandial area under the glucose curve than for any of the other three meal regimens (P < 0.05). The postprandial area under the insulin curve was significantly greater than both the LGI regimens (P < 0•05). Postprandial insulin resistance measured by homeostatic model assessment was also significantly greater for the HGI-pm meal than for the two LGI meals (P < 0•05)."

However, since Morgan, Shi, Hampton and Frost also state that "[p]ostprandial TAG and NEFA levels were not affected by meal timing or carbohydrate quality", I do suspect that there is a typo in table 3 of the original study, where it says that the TAG would be 5.04 mmol/l x h (probably is 6.04) and thus more than 15% lower than the average (TAG levels and insulin resistance usually go hand in hand, so it is really very unlikely that the 5.04 mmol/l x h is correct).

So what's the take home message here?

The only question that still has to be answered would be "King or pauper? At least with regard to the former, the best thing I can to is to suggest you read both the posts on "Breaking the Fast" and the "Carbs Past 6PM Posts"  (Part 1 & Part 2). When you have done that your perspective on the importance of breakfast and the purported fallacy of having a large dinner should already have changed. The things that are still left to do is not fool yourself into the false belief that you can pound whatever junk you want (as long as it fits your macros). As the glucose curve of the high GI arms (light color) in the figure above goes to show you, your body won't be happy when you get your "carb macros" from sugary junk.

Stick to starchy (or "save carbs", if you will) and fruit. Use veggies to fill you up. Use coconut & olive oil and the fats that are already in your meats, fish and dairy products to achieve baseline fat intake of at least 40-50g (all together). Aim for a 100-120g carbohydrate basis, diverge towards the lower side, when your body fat is high, you can't train or you're dieting and towards the higher side, when you are already very lean, have a high training volume, or are trying to build muscle. Complement that with min. 20g of quality protein with each meal. Don't deprive yourself on any nutrient completely and ramp up the total amount of food (at the given ratio) to fulfill your energy requirements.

In that, avoid processed food sand rely on whole foods, whenever possible (>90%),. Use food supplements* only where it makes sense, e.g. a protein shake post workout (*creatine for example would not be a "food supplement", since you can NEVER get the amounts that are necessary to supersaturate your stores from meat alone) and don't forget to live about all that "dieting" and thinking about the best ways to eat, please!

So if we assume that my assumption with respect to the triglyceride values in the originally published study are correct and we are simply dealing with a typo here, the next questions which arise here, are...

1. What is / are the reason/s that the lipid metabolism did not suffer?
2. How reliable is the HOMA-PP, i.e. the postprandial assessment of insulin sensitivity via the homeostasis model assessment? 
3. What does all this mean for you? Does meal timing not make a difference and are macros all that counts? 

As far as (1) goes, the answer is pretty simple: With a diet that was that low in fat and not overabundant in energy (2,000kcal for both diets) any potential the negative downsides on lipid metabolism will take their time to show. The acute ingestion of three high GI meals on a single day or modifications in their distribution across the day won't have much of an effect in healthy individuals, such as the four women and two men in the study at hand (in diabetics and especially patients with NAFLD things will probably look different, though).

The absence of changes in lipid metabolism after one day on high vs. low GI diets w/ different meal timing patterns yields answer #1 to question (3): If you are healthy the occasional day with junk food won't hurt you as long as you keep the total amount of energy at bay and jump back on the "healthy diet" wagon the very next day.

On the other hand, if only a single day of high GI food consumption can have such a pronounced impact on the postprandial HOMA levels, this raises the question how reliable this "long term measure" of glucose sensitivity actually is. Obviously, you should not go to the doctor's office and have your HOMA measured, at a morning after a day with three SuperSize Meals from McDonalds (even if you have been fasting after supper at night before, as the participants in the study at hand did) - unless you want a prescription for meformin, of course ;-)

It would however be likewise unwise to "do everything right" for three (maybe even just one day) before you head to the doctor to get blood drawn, just to be able to rejoice over a HOMA reading that does by no means represent your "normal" insulin sensitivity. This may make your doctor happy and spare you getting ticked off, but could have you run around pre-diabetic unnoticed for months if not years - maybe so long until the first irreversible damage has already been done.

The high susceptibility of HOMA measures to acute dietary modifications yields answer #2 to question (3): If you want know where you stand, don't make last minute changes to your diet before you get blood drawn. After all, the 90:10 rule (better 95:5 rule ;-) applies both ways - the 90/95 days of consistent eating patterns will decide whether you are lean, muscular and above all healthy or fat, undermuscled and sick.


References:

• Morgan LM, Shi JW, Hampton SM, Frost G. Effect of meal timing and glycaemic index on glucose control and insulin secretion in healthy volunteers. Br J Nutr. 2013 Oct;108(7):1286-91.

Jump Squats 80% Type-II Fiber Activity, Cold Thermogenesis Better Fasted, Tuned Swiss Ball Crunch, 5-HTP vs. Asthma, HIIT Before Strength & High vs. Low GI Meal Pre Workout

Image 1: Few of the things the average trainee does in places that call themselves "fitness studios" has little to do have will actually promote fitness, as in being athletic. "Mr. check out my biceps", for example would be similarly lost ding this as the sedentary computer nerd "Mr. biceps" loves to laugh about.

I know from time to time I am not 100% in time when it comes to delivering promised articles, but after an exhaustingly hot day, I am pretty much in-time with the 2nd installment of "On Short Notice" for today and the third for this weekend. Since I felt that it looked awkward to have three posts with the "On Short Notice" in front posted one after the other, I did however decide to ditch that (at least for today) and get straight down to ... well, "business" with posts on the revealing type II fiber specific muscle-damage from jump squats, the reason why you better sit in your ice-tub fasted if you want to practice cold thermogenesis, the superiority of Swiss Ball Crunches with resistance bands over the classic ab machine, the surprising anti-asthmatic effects of super high doses of 5-HTP, the way women benefit equally from a progressive strength training regimen with or without HIIT or steady state cardio before the strength workout, and, lastly, the futility of fretting about the acute effects of high vs. low GI meals before a workout and how that relates to childhood obesity. And while I do, believe it or not, have material for at least another episode, I am not going to bore you with even more short news pieces for this weekend. Don't worry ;-)

• Plyometrics for type II muscle fiber(-damage) It probably depends on your individual take on the usefulness of muscle damage, if the headline to this "On Short Notice" got you excited about plyometric training or not. When I am now telling you that the participants in the recently conducted trial by Macaluso et al. were previously untrained (N=8; age = 22 ± 1 years, height = 179.2 ± 6.4 cm, weight = 78.9 ± 5.9 kg) and the creatine kinase levels (a marker of muscle damage and the subsequent leakage of the creatine kinase enzyme into the blood) peaked at only 529.0 ± 317.8 U/L (that's high, but way below the 1,000er range you often see in untrained subjects after nothing but a couple of eccentric biceps curls being performed to failure) after the exercise intervention, I'd guess that most of you will appreciate that the researchers observed significantly more severely damaged type II than type I fibers (on average 85% vs. 27% of the respective fiber type).

  

  Image 2: The effect of plyomtetrics on your fitness & physique is still  underrated by the most fitness enthusiasts; and that despite the facts that plyos are the bread and butter of many athletes whose physical feats they are admiring.

  If we now make the reasonable assumption that the ~60% higher rate of muscle damage in both the glycolytic and oxidative subtypes of the type II fibers was indicative of the fact that they were the ones which shouldered the main workload of the 10 x 10 jump squat regimen the young men had to perform, this is unquestionable good news for everyone trying to get big and buffed. After all, these fibers, which are also known as type IIa (86% severely damaged) and type IIx fibers (84.% severely damaged vs. just 27% of type I fibers), are the ones that allow bodybuilders to get lean and muscular - not just one or the other... if that got you intrigued about what plyometrics are and if there is more research on it, I suggest you take a(nother) look at my previous posts on "ploys", such as "Building the Jack-of-All-Traits Legs Workout With Squats, Jump Squats and Body Weight Plyometrics?" or even the "Turbo-Fire vs. Insanity ShootOut" from one of the previous installments of "On Short Notice".
• Cold thermogenesis is not for everyone, but if it works for you, better do it fasted! That the amount and in many cases even the presence of the metabolically active brown adipose tissue and with it the thermogenic response to cold exposure is a very individual thing, is something you, as a diligent SuppVersity student will be aware of after all you have already read my previous post of the matter (cf. "Cold Thermogenesis vs. Ephedra").

  

  Figure 1: Cold thermogenesis in postprandial (PP) vs. fasted state (FF); dark areas indicate high 18F-FDG uptake (=high metabolic activity; Vrieze. 2013)

  Since there are still way too many people who actually seem to believe that sitting in a cold bathtub for a couple of minutes everyday would be all it takes to get you ripped and jacked, I thought it prudent to give them the chance to make it actually work and advice them to do it fasted! According to a recently published study from the Department of Internal Medicine at the Academic Medical Center in Amsterdam, in the Netherlands (Vrieze. 2013), the metabolic activity of the brown fat in all 6/10 of the 10 healthy, lean male volunteers (18-32 y; body mass index, 20-24 kg/m²) who participated in the study was about twice as high when they sat in a room which was cooled down to 16-18°C for 2h fasted (13.1 g/mL glucose uptake) vs. in the postprandial state (6.8 g/mL).
  Aside from the usual non-responders (40%) and the huge heterogenity with respect to the thermogenic response (6.1 - 27.6g/L), which are typical for these experiments there is a similarly large intra-individual difference with respect to the increase in BAT activity in the fasted state with the highest responder going from 11g/L in the post-prandial to 27.6g/L in the fasted state and the "fasting non responder" with a statistically non-existent (the term "non-significant" would not be bold enough ;-) "increase" in cold induced thermogenesis from 5g/L to 6g/L.

• 

  Video 1 (askthetrainer.com): The Swiss ball crunch with resistance bands takes some "tweaking" to be done correctly. After all you usually don't have the equipment set up in the way you would need it at your gym (click image to watch).

  Swiss ball crunch with resistance bands effective and saver than ab machine While I am not sure how "effective" the ab-machine in the study by Sundstrup et al. actually was, I can tell you that done with resistance bands the allegedly hilariously looking swiss ball crunch is not just at least as effective in recruiting the musculature of the rectus abdominus (104±3.8 vs 84±3.8% nEMG, respectively) as one of those machines, where your legs are locked in a way that the rectus femoris will do take do way too much of the work (2x more activity than in the swiss ball crunch with resistance bands) and you thus set yourself up for future lower back (=lumbar pain).
  Against that background and in view of the fact that Sundstrup et al. found that "both men and women, younger and elderly, and individuals with and without pain benefitted equally from the exercises" (Sundstrup. 2013), it is probably well worth taking the 2-3 min to get the equipment in position and do 3-4 sets of this unquestionably unconventional exercise (check out the SuppVersity EMG Series and my post on "Integrated Core Exercises For 6-Pack Abs" for additional ab exercises).
• 

  A couple of statistics on the current asthma rates in the US
  

  • asthmatic adults: 18.7 million (8.2%)
  • asthmatic children: 7.0 million (9.4%)

  In 2010, most U.S. children aged 17 years and under had excellent or very good health (82%). However, 8% of children had no health insurance coverage, and 5% of children had no usual place of health care. Seven percent of children had unmet dental need because their families could not afford dental care. Fourteen percent of children had ever been diagnosed with asthma. An estimated 8% of children aged 3–17 years had a learning disability, and an estimated 8% of children had ADHD. (Bloom. 2011; based on data from 2010)
  5-HTP switches allergic asthma off No good news for the average Olympian athlete who would then lose his script for his beta-agonists (clenbuterol & co, see also SuppVersity Facebook news from Aug 01, 2013), but probably something those of you who suffer from allergic rhinitis or full-blown asthma will appreciate: The administration of 5-hydroxy-tryptophan an orally available precursor to serotonin over the course of  led to a profound reduction (70-90%!) reduction in allergic lung inflammation in a rodent model (Abdala-Valencia. 2013). While the supplement left all sorts of side-effect related parameters unchanged and did not lead to weight gain, which is an often touted side effect of SSRIs - mostly unjustly, by the way! - the hilariously high dosage of 5mg 5-HTP per kg body weight the rodents received did reduce the allergen-induced transglutaminase 2 (TG2) expression, the migration of immune cells into the lung tissue, the local synthesis of serotonin and the subsequent serotonylation of proteins (serotonin conjugation of proteins) which is a key feature of allergic asthma.
  Regardless of the fact that Abdala-Valencia explicitly point out that these effects "occured without systemic increases in serotonin" (Abdala-Valencia. 2013), which could have led to vasoconstriction and other negative side-effects, I strongly caution against the ingestion of a whole bottle of 5-HTP tabs per day... when the researchers from the Northwestern University Feinberg School of Medicine publish a follow up study on humans, I'll let you know, though - in view of the ever-increasing asthma (see infobox on the right) research in this area could not just offer a valuable new treatment strategy, but also insights into the underlying reasons of this epidemic.
• Young women can combine strength training with either steady state or HIIT and still make progress - Somewhat related to my post earlier this week on doing cardio before instead of after your strength workout are the results of a recent study by Silva et al. who found that young women (age ~23y) make identical strength gains, regardless of whether and which type (HIIT sprinting or steady state cardio on the cycle ergometer or classic jogging) they perform before with their twice a week full-body training (Silva. 2013). Just as in the Di Blasio study, the "cardio" sessions, which were performed in a 1 min all-out vs. 1 min active recovery (HIIT) or 95% of the ventilatory threshold (SST) fashion for 20-30min (progressing from 20-30 over the course of the 11 weeks), were performed before the weight training (note: changes in body composition were not evaluated in detail, but I would be very surprised, if the concomitant training regimen, and in that specifically the HIIT protocol, did not outperform the resistance training only protocol in this respect).

  

  Image 3 (rippedfitness.com): You will certainly remember Wednesday's news on doing cardio before weights, well, here you have more evidence that even doing 20-30 min of HIIT won't hamper the gains of fit female beginners on a twice a week full-body regimen with built-in progression regimen - neither will steady state cardio "in the zone", by the way.

  If you are a young, fit woman (or man) without years of competitive athletics under your belt and don't train all too often (~2-3 times per week), it does thus obviously not harm your strength gains on a classic strength training program with built in linear progression from 15-18RM to 8-10RM, if you concomitantly work on your conditioning - whether the results would be identical if the subjects were not just fit and healthy but had been training for years and were working out 5x instead of 2x a week, is yet questionable. On the other hand, it is very unlikely that seasoned athletes (and this goes out to the gentlemen, in particular) will lose muscle and ruin their strength gains, whenever they move further than the bench to the squat rack - it's all a matter of total volume and running out of puff due to bad conditioning can just as well keep you from pulling those additional 10kg off the floor as the exhaustion from doing too much cardio.
  This, by the way, brings me back to the notion of "fitness" vs. "being fit", I alluded to in the caption of image 1, already: If you want to exploit the 100 year credit your genes have granted you (see "Exercise for Life Extension" in today's first installment of "On Short Notice"), you better focus on "being fit". Try different things and don't get stuck in a rut.
• High GI, low GI, ... f*** GI! When you, a healthy, more or less well-conditioned individual are about to engage in a high intensity exercise protocol that simulates a football match (bouts of walking (31-39 s), jogging (41-46 s), cruising (41-45 s), sprinting (16-21 s) and standing), it make absolutely no difference whether you ingest a high (=80) or low (=44) pre-workout meal (total energy=377 kcal; CHO=79 g; Fat=3 g; Protein=13 g) 3.5h before your workout (Hulton. 2013).

  

  Image 4: Add Lucozade + Akash rice for high GI (80) or apple juice and basmati for low GI (44) and you have two isocaloric test pre-workout meals

  That's at least what the results of a recent study by Hulton et al. which did not find any differences in blood glucose, fatty acids (FA), glycerol, β-hydroxybutyrate, lactate and insulin (assessed before, during, and after the exercise bout), rates of CHO and fat oxidation (determined at 4 time points during the protocol) or 1 km time trial performance. It should be mentioned, though, that this was not a liquid meal, but consisted of either Lucozade + akash rice (high GI) or apple juice + basmati rice (low GI) with an identical chicken breast + tomato sauce "base" and identical macro-nutrient and calorie content.
  That the long-term consequences on your body composition may still be different is a different cattle of fish though and how "beneficial" liquid sugar, ah... I mean energy drinks, such as Lucozade are is something at least those of you who read my "Fat Content Per Energy Drink 0g, Body Fat Gain Per Energy Drink 18g!" post from June 30, 2013. Whether apple juice is much better is still debatable, though. Wojcicki & Heyman, for example, argue (finally, as I would like to add) in their latest paper that "excessive fruit juice consumption is associated with increased risk for obesity" and the ingestion of "sucrose [...]without the corresponding fiber, as is commonly present in fruit juice, is associated with the metabolic syndrome, liver injury, and obesity". Reason enough for the two pediatrics from the University of California to recommend that the "US Department of Agriculture's Child and Adult Food Care Program, which manages the meal patterns in childcare centers such as Head Start, promote the elimination of fruit juice in favor of whole fruit for children." (Wojcicki. 2013)

Before I eventually call it a week, I would like to remind everyone of the daily mini-news on the SuppVersity Facebook wall. Only few of them will also make it into the "On Short Notice" column (actually the "Exercise for Life Extension" in today's first installment was an exception), so that even the few of you who don't suffer acute short news withdrawal symptoms, may want to stop by from time to time ;-)

References

• Abdala-Valencia H, Berdnikovs S, McCary CA, Urick D, Mahadevia R, Marchese ME, Swartz K, Wright L, Mutlu GM, Cook-Mills JM. Inhibition of Allergic Inflammation  by Supplementation with 5-hydroxytryptophan. Am J Physiol Lung Cell Mol Physiol. 2013 Jul 27.  
• Bloom B, Cohen RA, Freeman G. Division of Health Interview Statistics Summary Health Statistics for U.S. Children: National Health Interview Survey, 2010. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Centers for Disease Control and Prevention National Center for Health Statistics. Hyattsville, Maryland December 2011. DHHS Publication No. (PHS) 2013–1578.
• Hulton AT, Gregson W, Maclaren D, Doran DA. Effects of GI Meals on Intermittent Exercise. Int J Sports Med. 2013 Jun 15.
• Macaluso F, Isaacs AW, Myburgh KH. Preferential Type II Muscle Fiber Damage From Plyometric Exercise. J Athl Train. 2013;47(4):414-20.
• Silva RF, Cadore EL, Kothe G, Guedes M, Alberton CL, Pinto SS, Pinto RS, Trindade G, Kruel LF. Concurrent training with different aerobic exercises. Int J Sports Med. 2013 Aug;33(8):627-34. Epub 2013 May 4.
• Sundstrup E, Jakobsen MD, Andersen CH, Jay K, Andersen LL. Swiss ball abdominal crunch with added elastic resistance is an effective alternative to training machines. Int J Sports Phys Ther. 2013 Aug;7(4):372-80.
• Vrieze A, Schopman JE, Admiraal WM, Soeters MR, Nieuwdorp M, Verberne HJ, Holleman F. Fasting and Postprandial Activity of Brown Adipose Tissue in Healthy Men. J Nucl Med. 2013 Jul 31. 
• Wojcicki JM, Heyman MB. Reducing childhood obesity by eliminating 100% fruit juice. Am J Public Health. 2013 Sep;102(9):1630-3. Epub 2013 Jul 19.