Back from my mini vacation. Had an awesome time in Bangalore, in spite of a jam packed schedule.

Spent time with the husband, window shopping at 100ft rd and Mantri mall, a great time at the Bannerghatta National Park and finally met with the very lovely Sugar. We talked about everything under the sun, but exercise, food and weight loss, was good fun. Also got to spend time with cousins, aunt,

Food for today

Food for today:

7.30 a.m BF: Coffee + 2 Slices of Healthy Masala Toast { today's version had sooji,onion, tomato,carrots,cabbage, green  chilli and coriander}
10.a.m: Snack: Half an apple and 2-3 strawberries
11.30 a.m: Snack 2: Dal soup { was ravenous and had half a bowl of dal from my lunch, thinned it out a bit and pretended I am having soup :)}
1.00p.m: Lunch: 2 chapatis, Raw banana upkari,

this, that and other things on my mind

Hey, hope everyone had a good weekend. I sure did. Nothing makes me happier than crossing off all items on my to-do list, squeezing in an unexpected workout and spending fun time with my daughter. Added bonus was lots of rest and eating well. * fingers crossed*

But before I continue, let me warn you this is a looong post. it's more like me putting down my thoughts..and believe me, I have lots of

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. 2012). 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. 2012)

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. 2012)

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. 2012) 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. 2012)

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. 2012 Dec 4;62(1):37-43.

I was staying at my mom's place for the whole of last week, to help with the wedding prep and to attend all the pre wedding functions.
Managed to run 2 days for 25 minutes each. No exercise apart from that.
Ate only 2 Gulab Jamuns, whole of last week! * patting myself on the back*. Just tasted the Sitaphal basundi on the wedding day, 2 spoons. Was not tempted by the Jalebi or Ice cream. Of

New year Challenge!

Ok, so Sugar posted this challenge on her blog, where she is aiming to lose 5 kgs by new years. Some of us are joining in, each with a different goal. I am aiming to lose 3 kgs by 31st December 2012.
Well the whole point of this challenge as mentioned by Sugar is not to wait for a certain date / time to put off your plans to change your life, eating habits and most of all to start some fitness

Adelfo Cerame: Contest Prep Update on Turkey Day! Plus: Losing Fat W/ Intermittent Fasting & 200g Carbs/Day Works

When you look at these images yo will have to concede that Adelfo brings a better conditioning to the Thanksgiving table than many a competitor to the stage ;-)

In a way it's funny how the Internet has brought us all so close together and yet we still have so little in common, when we are not "on the line". I believe it was two weeks ago, when I almost missed my own radio show on Thursday, because I assumed there wouldn't be a SuppVersity Science Round-Up on a holiday. Literally in the last minute I thought, maybe you better check whether the US guys have a holiday, as well - and what should I say? You didn't! Today, I am just back from the office and do now have an 'evening off', 'cause today it's you (or at least ~65% of you, which is the relative amount of US visitors in the last week), who have a holiday that' leaving me somewhat clueless why you are giving thanks and I am not ;-)

In the end, it does not matter for me what the deeper meaning of Thanksgiving is, as long as I know that you spend the day with your loved ones, it's a day to celebrate and that's all that counts - so HAPPY THANKSGIVING! Enjoy Adelfo's short progress update and get your share of the holiday roast - even if it will have it's share in the 0.5kg the average college student in a 2006 study by Hull et al. gained during the Thanksgiving holiday (. I will make sure there is "Get Lean and Stay Lean Quickie" either on Sunday or Monday, just in case ;-)

Happy Turkey Day SuppVersity readers! 

I’m going to make this short and sweet since I know most of you will be celebrating the Thanksgiving holiday with loved ones and eating good food, because I know I will. I’ve been getting some comments and request from a few people for an update on my progress, and I know I have not done one in a while, so this will be just a quick update on my diet, training and progress pictures… I promise that’s all!

Figure 1: Adelfo's current total caloric intake and macronutrient ratio (left); Adelfo's latest progress pics (right) comparing photos from week 2 and week 7 of this contest prep (img. Adelfo Cerame Jr. 2012).

Trainingwise, I am still following the Hybrid of P.H.A.T. training using an RPE scale with 3 to 4 workouts per week depending on what day workouts land (click here to learn more about Adelfo's routine). In addition I am doing cardio twice a week: 9 laps around a trace. Everything is pretty much the same since I started in October - the aforementioned cardio is in fact he only addition I have made to my regimen at the beginning of this month.

One thing I do notice is that my carb intake is a lot higher this year and has not yet to change. By this time last year I was probably already at 125-150g of carbs. I never realized that I was able to maintain 200g of carbohydrates (which is big for me) for a long period of time while still dropping body fat. 

When I come to think about it, it's probably less that I could not do it, but rather that I never even gave the 200g of carbs per day a chance. Ever since working with coach Alberto, I’ve learned that dieting and listening to your body is like a game of wits, and sometimes, the best move is no move, at all.

Image 1: Progress picture (backshots) comparing week 2 and week 7 of this competition (Adelfo Cerame. 2012)

With regards to my training split, it’s still kicking my ass day in day out. I’m exhausted most days every time I stroll out the gym after a training session. I feel sore more than usual nowadays, and my muscles feel tight like I’m somewhat pumped all day long. After mentioning this to Alberto and maybe second guessing myself that it was just in my head; he assures me that it’s not in my head…

“Just pushing you a bit on the frequency tip which is important for an athlete of your level. We will go back and fourth with it, and you are NOT imagining what you feel dude. Your muscle are under constant turnover now, and because of this I think you will keep a much fuller look.”

Here is another conversation between coach Alberto and I, when I mentioned still feeling sore and tight but was feeling and noticing more density in my frame especially in my chest area because I feel that the chest area is my weakest body part…

“Yep! It was about time you rode the frequency train. It’s going to pay off! This week we are going to not change a thing, since we added more cardio. I want to cruise a bit this month December push a bit, but right now it’s coming off easy. We will have some good detail in your back by the end of the month.

So far so good, and given the new frequency you are working with I think you are going to really see you keep more even though you got leaner”

But yes… I am very pleased with my training and how everything is coming along. I am confident that I will be able to outdo my old self this coming March of 2013.

Image 2: Progress picture (front double biceps) week 2 vs. week 7 of this competition (Adelfo Cerame. 2012)

That’s all I have for this Thursday edition but since it is the holidays, just in case you didn’t get to read it last year. I wrote an article on “5 simple rules to survive the feast without too much damage” So for those of you who just started following my blogs; here is the link to the respective article.

Have A blessed Holiday SuppVersity readers!


References:

• Hull HR, Hester CN, Fields DA. The effect of the holiday season on body weight and composition in college students. Nutr Metab (Lond). 2006 Dec 28;3:44.

Gene-ial or Dan-Gene-rous? Better Make Sure You Are Made For Every Other Day Fasting, If You Don't Want to Ruin Your Glucose + Lipid Metabolism and Become Viscerally Obese

Yes! I freely admit that I do have a problem with the subliminal "binge and starve" of the popular every other day fast, because it paves the not so royal road to binge eating disorders.

Only 2 years ago, there was hardly anyone but the followers of Martin Berkhan's "Lean Gains" regimen who knew what intermittent fasting would be. Ironically, now that mainstream is catching on, the hype within the fitness community is slowly abating  - maybe part of the reason is that it's no longer "cool" enough now that your fat neighbor does it ;-).

It goes without saying that the mainstream version comes without an obligatory exercise component and - what's probably even worse - in the absence of macronutrient, let alone food prescriptions that would make sure that the every other day fasts that are becoming increasingly popular these days become "binge and starve" protocols.

The every other day fast, a gateway to eating disorders?

I could probably write a whole article about the potential of feast and fast strategies to function as a gateway to binge-eating disorders, but I know that most of you will discard that by stating: "Pah, that's happening only to the psychologically labile person who can't control his-/herself"... I will argue against that in another article, but I want to let you know here and now, that you could hardly be more off.

Did you know that eggs can improve the lipid profile of most of us?

Stay calm! In view of the fact that rodents in the wild-type control group, who had fully functional LDL receptors did not show a similar negative response to the well-meant dietary intervention, the results of the study at hand are hopefully irrelevant for most of you. If you do have friends and relatives with inexplicably high cholesterol levels, you would however be ill-advised to encourage them to battle their problems with every other day fasting.

Anyway... What this article is actually about is a paper from the British Journal of Nutrition. It was written by Dorighello et al. and has been published online ahead of print. The corresponding study was designed to test the hypothesis that alternate day fasting, which has previously been shown ... 

• to decrease established metabolic risk factors of CVD and diabetes in human subjects and rodents (Varady. 2007),
• to reduce the production of liver mitochondrial reactive oxygen in mice (Caro. 2008), and 
• to increases the lifespan of rodents (Martin. 2006)

would ameliorate tissue mitochondrial oxidative stress and glucose intolerancr in LDL-receptor knockout mice. The LDL-receptor negative mouse is a common, or rather the scientific model of familial high cholesterol (these are the people who are put on a statin the very moment, they enter their doctor's office).

What the scientists expected and what they found were two pair of shoes

I guess you don't have to be a rocket scientists to see what the data in Figure 1 is telling us: In spite of a 20% reduction in energy intake (over the whole week), the rodents in the Dorighello study did not benefit from their every other day fasting regimen (EODF)

Figure 1: Changes in lipid and blood glucose levels (relative to control on ad libitum diet; left) and carcass composition in % of total weight (right; data based on Dorighello. 2013)

Accordingly, the Brazilian scientists who had expected that the fasting induced energy restriction, (-20%), alone, should ameliorate the metabolic disturbances in LDL-receptor knockout mice, and reduce their susceptibility to atherosclerosis, had to acknowledge that their clever every other day fasting regimen can have unexpected and, in the last consequence, eventually fatal effects on the heart health of the laboratory mice:

• Epididymal and carcass fat depots and adipocyte size were significantly enlarged by 15, 72 and 68 %, respectively.
• Pasma levels of leptin were 50 % higher in the EODF mice than in the ad libitum-fed mice.
• EODF mice showed increased plasma levels of cholesterol -  total cholesterol (37 %), VLDL-cholesterol (195 %) and LDL-cholesterol (50 %). 
• The glucose homeostasis of the "EODF mice" also disturbed. The scientists observed a +40 % increase in glycemia and a +50% increase in insulinaemia. In short, the mice became glucose intolerant and insulin resistant.
• The significant increases in systemic inflammatory markers, TNF-a and C-reactive protein, only topped the list of negative side effects of the every other day fast off.

Overall this lead to a 3-fold increase in spontaneous atherosclerosis development, an effect of which it cannot be said often enough that it was observed exclusively in the LDL-receptor negative mice.

Practically speaking... In spite of the fact that the main take home message of the study at hand may be relevant only for those who harbor a certain genetic disposition, I do not recommend a zero calorie every other day fast to anyone - irrespective of whether he or she does or doesn't have LDL receptors  ;-)

If you are not aware of cases of familiar hyper-cholesteraemia and want to improve your lipid metabolism by fasting and eating clean, I suggest you re-read my previous article about the "Two Day High-Protein, Low-Carb Fast" and try this, or a classic intermittent fasting routine with a 6-8h feeding window to shed some body fat and get in better metabolic shape.

So what does this mean? The results of the study at hand are exemplary of something regular SuppVersity readers have encountered a dozen of times, already. A fact that vindicates the often-heard, but rarely understood notion that "we are all different". As the study at  hand clearly shows, our gene's and their consequences on our physiology determine not just what we should eat, but also when we shoult eat it. 

You got to be wary, though! Contrary to what you may read in some shiny magazines and on banners on the Internet, the often advertized "gene type diet" is not even on the horizon, yet.

Yes, we can (theoretically) identify each and every gene in our bodies, but in contrast to a general LDL receptor dysfunction, many of the more subtle genetic differences are as of yet totally unknown. Any list of foods, or, as this study shows, suggest food frequency rules you may get are up to know about as accurate as the names of the man or woman of your dreams you will get if you follow the friendly advice the music television advertisement gives you and "send an SMS with the keyword 'love' and your name" to a random number. Even for the well-studied APO-E polymorphisms, scientists are time and again surprised to find that their results are not in line with data from previous studies. Contemporary accepted implications, such as "people whose apolipoproteins belong to the APO-E4 class will do more harm than good if they consume larg(er) amounts of fish oil" could thus be as flawed as the idea that only fat can make you fat - likewise the result of premature conclusions that seemed logical in view of the contemporarily available, highly insufficient data, by the way.

References:

• Caro P, Gómez J, López-Torres M, Sánchez I, Naudi A, Portero-Otín M, Pamplona R, Barja G. Effect of every other day feeding on mitochondrial free radical production and oxidative stress in mouse liver. Rejuvenation Res. 2008 Jun;11(3):621-9.
• Martin B, Mattson MP, Maudsley S. Caloric restriction and intermittent fasting: two potential diets for successful brain aging. Ageing Res Rev. 2006 Aug;5(3):332-53.
• Varady KA, Hellerstein MK. Alternate-day fasting and chronic disease prevention: a review of human and animal trials. Am J Clin Nutr. 2007 Jul;86(1):7-13. Review.

Get Lean & Stay Lean Quickie: Add Cinnamon to Cereals. NPY Detrimental? Melatonin Beneficial! 50,000IU Vitamin D3 Useless. Phtalate DHEP Dangerous! PPAR, AKT & GLUT-4 Agonist From False Black Pepper Surprisingly Potent!

In 1998 the Consumer Union wrote a letter to the FDA complaining about the occurrence of DEHP and other "endocrine disrupting chemicals" in cheese and dairy of which they suspected that they were partially emitted from the plastic wrappings (read more)

Those of you who are following the SuppVersity news on Facebook very closely, will be aware that I announced yesterday, already that there was going to be another installment of On Short Notice, today... another "Quickie", so to say with a couple of selected news on getting and staying lean. Something I know is pretty much a pain in the a** of most of us and if you take a closer look at the news about phtalates it is actually no wonder. I guess on their own those nasty plasticizers would probably not even be a problem, but together will all the other byproducts of our convenient lives, they form a perfect storm.

And you know what's worst, simply wrapping all those plastics that 'infect' even organic foods with the 'P-Virus' around your waist while you're working out will probably make things worse, not better.

Let's get down  to business ;-)

Enough of that! Are you ready for today's quickie -- Note: The next installment of the Athletes' Triad is scheduled for next week. I am honestly sorry for these delays, but I just have "real" work to do on the weekends at the moment and no time to do the respective research that would be necessary to provide you with not just any, but actually useful information. In the mean time I hope you like this post, as well.

• 6g of cinnamon stretch postprandial glucose response to cereals over more than 2h. That's the result of the latest study from the Ball State University in Muncie (Magistrelli. 2012). Interestingly the effects of 6g of ground Cassia Cinnamon were independent of the body weight and metabolic health of the thirty-seven 18 to 30 year-old normal-weight and obese study participants.
  
  

  

  Figure 1: Postprandial blood glucose with plain cereal containing 50g  carbs and the same cereal with cinnamon in all subjects, normal-weight and obese; by the way if you go by the AUC I doubt there is a benefit, after all the glucose does not drop base to baseline within 120min (Magistrelli. 2012).

  There is however one slight downside to this study: The scientists measured the blood glucose response for only 120min. If you take a look at the graph in figure 1 you will immediately notice that the co-ingestion of 75g of "Cream of Wheat", an instant farina cereal, with 6g of regular cinnamon did lead to a 24% reduction in the area under the glucose curve, but only if you discard what happened after the 120-min period the scientists used to measure. After all, the co-administration of Cassia cinnamon did not do anything that could not be ascribed to a mere reduction in glucose uptake - there is no evidence for an improvement of insulin sensitivity here. On the other hand, the absence of spikes in blood glucose will protective effects against the development of type II diabetes, esp. in the presence of a diet that's overall high in carbohydrates where one blood sugar spike chases the other.
  

  "To date, no study has documented cinnamon's influence on postprandial blood glucose after a mixed meal. Although preliminary in nature, the available research suggests cinnamon supplementation can significantly reduce short-term glycemic response in healthy adults." (Magistrelli. 2012)

  The last information is actually pretty surprising. Personally I expect the effects to be less pronounced with mixed meals, but since we still don't really know the underlying mechanism it's difficult to predict what exactly is going to happen, when you eat a spoon full of cinnamon right before your steak with rice. This as well as the previously discussed prolonged elevation of blood glucose (see figure 1)  actually raise some doubts about the real-world usefulness of eating tons of cinnamon if you don't actually like it, just as a way to manage blood glucose - specifically if you are not a type II diabetic (or on your way to become one) and avoid "food" like cereals and similar junk, anyways.
• Neurpeptide Y (NPY) does not protect against obesity -- Based on the results of a recent rodent study from the University of Turku in Finland, it seems that the exact opposite is the case. In that it does not seem as if it would fail to make you satiated and happy. Rather than that it appears to put your metabolism in "high efficacy" mode, so that you gain weight despite the fact that you are not eating more.
  
  The Finish researchers exposed two strains of mice to a typical Western type diet (high energy, high fat, high carbohydrate) for seven weeks. One strain, the OE-NPY(DBH) mice, had 'naturally' high amounts of NPY in the noradrenergic neurons of the brain, the other were normal wild type mouse. Actually, the scientists had expected that the high NPY expressing mice would gain less weight than their wild-type peers, but much to their surprise, the exact opposite was the case.
  
  

  

  In 1990 Kaye et al. conducted post-mortem analyses on the brains of patients with anorexia nervosa and found highly elevated levels of NPY. These results do actually stand in line with those of the study at hand, after all anorexic patients don't feel any exuberant hunger (in the later stages of the disease) and their bodies are running in a mode that is meant to conserve even the smallest amount of energy they consume.

  And as if that was not already strange enough, the scientists also found that female OE-NPY(DBH) were much more prone to gain significantly more weight and larger white and brown fat depots with no difference in UCP-1 levels, hyperphagia (=overeating) or decreased activity. And the weight gain was not without consequence, as these mice
  

  "...also displayed impaired glucose tolerance and decreased insulin sensitivity. OE-NPY (DBH) and WT males gained weight robustly, but no difference in the degree of adiposity was observed." (Ruohonen. 2012)

  Now what's interesting is that similar effects were only observed in 40% of their male counterparts and in exactly none of the wild type males on the Western type diets. These observations lead Ruhonen et al. to the conclusion that ...
  

  "[...] increased NPY release may predispose females to a greater risk of weight gain under high caloric conditions." (Ruhonen. 2012)

  And if you asked me this must be mediated by whatever gender-specific direct effect on feed efficacy and the changes in brown adipose tissue morphology the researchers observed in the NPY overexpressing mice. This would be good news, since brown fat figure much less in human beings than in rodents. Unfortunately, with identical body temperatures and UCP-1 expression in all animals that is at best one of the causative factors. It can hardly explain all the profound weight and fat gains in the non-hyperphagic (not overeating) OE-NPY mice.
  
  Now, at least for me this raises the question if this is not yet another instance, where the artificially increased NPY levels in the absence of the natural confounding factors, such as increased GLP-1 levels, for example (click here to learn more about GLP-1), couldn't be the actual reason and any conclusions with respect to pro- or anti-obesogenic effect of NPY based on the results at hand would be as unwarranted as the usage of drugs that target this and other neuropeptides in isolation.

• 

  Just in case you have missed the Circadian Rhythm Series, this would be the right time to read about how to boost / not hamper melatonin, live by your internal clock and get healthy and lean (and stay the same) - light and foods timing are key, here (learn more).

  Thiazolidinediones + melatonin, a dynamic duo vs. insulin resistance -- A group of researchers from the Indira College of Pharmacy in Tathawade, India, have just published a study on the combined effects of PPAR agonists and melatonin as a means to ameliorate dexmethasone (artificial cortisol) induced insulin resistance in rodents (Ghaisas. 2012).
  
  The data of the study casts a particularly good light on melatonin which does, contrary to the potentially fattening PPAR agonists pioglitazone and rosiglitazone, not entail a simple increase in glucose storage within the adipose tissue. The combination treatment did also normalize the levels of superoxide dismutase, catalase, glutathione reductase and lipid peroxidation in liver homogenates, an effect the scientists partly ascribe to the antioxidant effects of melatonin , as well (the reduced blood glucose is obviously another factor) 
• 50,000 IU of vitamin D per week improve 25OHD in previously vitamin D deficient subjects but don't produce the expected improvements in insulin sensitivity. Contrary to one of the most underrated dietary supplement, namely melatonin (see previous news item), the most overrated, namely vitamin D3, does not do anything for insulin sensitivity -- even when the subjects are deficient to begin with and their 25OHD levels do actually respond to supplementation (Simha. 2012).
  
  Despite a weekly dose of 50,000 IU of vitamin D3 and a + 42% increase in 25-OHD levels (to be fair it must be said that the levels were still relatively low and nowhere near where some experts want to see it), the researchers from the Department of Internal Medicine at the Texas Tech University Health Sciences Center at Permian Basin did not observe any improvements in glucose uptake after 8 weeks of supplementation in their 12 healthy subjects with baseline plasma 25-hydroxy vitamin D (25OH-D) levels of less than 20 ng/mL.
• More about DEHP and its occurrence in your environment: Prepackaged foods are among your best sources to get your detrimental dose of DEHP every day. Belgian children have been shown to get up to 80% of their DEHP and other phtalates from school lunch. And bread was the worst offender (Sioen. 2012) - probably because it's packed 'sandwich style' in plastic containers of which Cirillo et al. were able to demonstrate that these and other plastic packagings leech the phtalates right into the food (Cirillo. 2011). It is therefore no wonder that the packaged hopsital foods are full of it (Teresa. 2012).
  

  Apropos, having a venyl flooring in either schools or hospitals will only increase the DEHP load due to the emission of the plasticizer into the air (Yu. 2012) and the DEHP content of the bags with blood transfusions are so high that the anti-doping agencies use it as a marker of illegal blood transfusions (Monfort. 2012). Moreover, phtalates leech into milk and dietary products fat-enriched food such as cheese and cream during processing and storage (Kappenstein. 2012); vegetable oils in plastic containers are likewise full of it (Wu. 2012).

  Cooking seems to remove some of the phatalates, but that does not work for vegetables for example (Fierens. 2012). No wonder foods are still the #1 source, followed by bottled water and indoor air of phatalate exposure in Westerners (Martine. 2012).
  

  Unfortunately, the negative effects of DEHP and its metabolites are not restricted to obesity or the prenatal period, they also induce insulin resistance and metabolic syndrome later in life (Rajesh. 2012) - effects which can be ameliorated by increased vitamin C + E intakes. DEHP has also been shown to reduce progesterone and lead to apoptosis of the ovarian granulosa cells and subsequent infertility (Li. 2012a). Similar detrimental effects have been seen in male rodents (Li. 2012b).
  Natural metabolite of ubiquitous plasticizer DEHP sets you and your unborn kids up for obesity DEHP is used in a wide range of soft PVC products ranging from lifesaving medical devices such as medical tubing and blood bags, to footwear, electrical cables, packaging, tarpaulins for lorries, flooring, stationery and roofing. According to a recent study that's been published in Bioscience Reports its natural metabolite MEHP [mono-(2-ethylhexyl) phthalate] has the potential of turning you into a fat, sick slob:
  

  "In the present study, we show the dose-dependent effects of MEHP on adipocyte differentiation and GPDH (glycerol-3-phosphate dehydrogenase) activity in the murine 3T3-L1 cell model. MEHP induced the expression of PPARγ as well as its target genes required for adipogenesis in vitro. Moreover, MEHP perturbed key regulators of adipogenesis and lipogenic pathway in vivo. In utero exposure to a low dose of MEHP significantly increased b.w. (body weight) and fat pad weight in male offspring at PND (postnatal day) 60. In addition, serum cholesterol, TAG (triacylglycerol) and glucose levels were also significantly elevated. These results suggest that perinatal exposure to MEHP may be expected to increase the incidence of obesity in a sex-dependent manner and can act as a potential chemical stressor for obesity and obesity-related disorders." (Hao. 2012)

  In the latest risk assessment of the EU and the DEHP Information Center it is of course 100% save... which bags the question, whether the guys working there simply consider being obese normal, so that anything that makes you even fatter is "save" and does not pose any more of a health threat than life in general, or if they just deliberately ignore that molecules rarely go in and out of our bodies unmetabolized and thus settled for a set of totally meaningless petri dish experiments, before they concluded:
  

  "The use of DEHP has been carefully considered by EU scientists and it is already well regulated by European legislation relating to toys and childcare articles, cosmetics, food contact materials and medical devices." (DEHP Information Center. 2009)

  Hallelujah! Unfortunately it's metabolite MEHP [mono-(2-ethylhexyl) phthalate] obviously is not such a nice guy :-/  

• 

  Figure 2: Serum markers and adiposity, as well as mRNA expression in adipose tissue of male and female mice after 14 weeks on "high fat" diets (based on Estrany. 2012)

  High fat diets (Western style) for women only? I know, this is once again a rodent study, but it is still intriguing that scientists from the Universitat de les Illes Balears in Palma de Mallorca and the Instituto de Salud Carlos III in Madrid, Spain, found that male rodents become insulin resistant and obese, when they are fed a high fat diet (30% fat, in other words high fat + high carb), the female rodents, on the other hand, switch to a 'fat burning mode' or as the scientists state they ...

  "[...] counteract excessive fat intake by improving their ability to use lipid fuels, which limits adiposity and maintains insulin sensitivity." (Estrany. 2012)

  Just as in a previous study neither the male nor the female rats showed the usual symptoms of hyperphagia (overeating), and the body weight gains in all groups were normal.
  
  "Normal" body weight gain and insulin resistance? That should actually ring a bell. Correct! "Normal-weigh obesity" or being skinny fat! And in fact, the underlying reason for Estrany et al.'s observations seems to be that the diet increased the inflammation in the male rats, while it did not do so in the female rodents. What exactly it was that made the difference here, will yet still have to be elucidated, but my best bet is estrogen, which is by no means just the bad guy as which it is portrayed within the fitness community.
• Molecule in false black pepper aka Embelia ribes turns out to be natural GLUT-4 + PI3K/AKT activator, PPAR-gamma agonist and anti-diabetic. What's particularly exciting about the embelin the active ingredient in Embelia ribes Burm, a member of the species Myrsinaceae, which is widely distributed in India and and has a documented history of being used as a diabetes 'medication' in the Ayurvedian traditional medicine system, is that it increases insulin sensitivity without predisposing to further weight gain and adiposity, as the standard Thiazolidinediones (TZDs) such as rosiglitazone and pioglitazone do.
  
  Using the same streptozotocin (STZ) induced rodent model of type II diabetes you have encountered in numerous other studies that have been covered here at the SuppVersity a group of researchers from the Loyola College in Chennai and the University of Madras (Gandhi. 2012), have found that 50mg/kg body weight of embelin that had been extracted from fresh E. ribes fruits by drying and eluting the raw material in benzene...
  

  • 

    Figure 3: Effects of embelin vs. rosiglitazone on insulin levels and rel. expression of antioxidant enzyme activity (Gandhi. 2012)

    reduced body weight gain, blood glucose and plasma insulin in treated diabetic rats,
  • modulated the altered lipid profiles and antioxidant enzymes,
  • exerted cytoprotective effects on the β-cells of the pancreas,
     
  • increased the PPARγ expression in epididymal adipose tissue,
  • inhibited adipogenic activity (=fat gain),
  • mildly activated PPARγ levels in the liver and skeletal muscle, and
     
  • regulated insulin mediated glucose uptake in epididymal adipose tissue through translocation and activation of GLUT4 in PI3K/p-Akt signaling cascade.
  And best of all, contrary to most natural anti-diabetes, these effects were no mere downstream effects of the antioxidant effects of Embelin, but can be ascribed to direct receptor binding: The active ingredient from false black pepper does not only show a high binding affinity for PPARγ, in the experiments Gandhi et al. condcted, it also had stable binding affinities for the active sites of PI3K, p-Akt and GLUT.
  
  
  Embelia ribes in Ayurveda The false black pepper is no newcomer to the scene of natural medicine / health supplements. Embelia ribes has been used in Ayruveda for centuries as an appetiser, laxative, carminative, anti tape-worm cure, to ameliorate / protect from snake bites, against skin deseases, bronchitis and urinary discharges, versus dyspepsia, liver ailments, jaundice, and glatulence.
  The results certainly are exciting, specifically in view of the fact that emeblin could be interesting not just for type II diabetics and individuals with insulin resistance, but also for lean mean women who are looking for a tool that would optimize their insulin sensitivity without the pro-obesogenic effects that render most other "insulin sensitizer" at best useless. And if we assume that similar effects on PI3K and p-AKT do occur in skeletal muscle, as well (this was unfortunately not measured in the study at hand), embelin could even help you build some muscle. Just as its general efficacy in human beings the last hypothesis does of course still require experimental verification... but don't worry, you know that I will keep you posted on any future studies!

That's it! What? You want more? But that's what a quickie is supposed to be it's the frequency that makes it worthwile not the length... ah, I guess I better wish everyone a happy Sunday before I am starting to go into further details here ;-)


References:

• Cirillo T, Fasano E, Castaldi E, Montuori P, Amodio Cocchieri R. Children's exposure to Di(2-ethylhexyl)phthalate and dibutylphthalate plasticizers from school meals. J Agric Food Chem. 2011 Oct 12;59(19):10532-8.
• DEHP Information Center. DEHP Fact Sheet (revised). June 14, 2012. <  www.dehp-facts.com/upload/documents/webpage/ECPI%20-%20factsheet%20DEHP%20revised%20-%20140609.pdf > retrieved on Nov. 03, 2012.
• Estrany ME, Proenza AM, Gianotti M, Lladó I. High-fat diet feeding induces sex-dependent changes in inflammatory and insulin sensitivity profiles of rat adipose tissue. Cell Biochem Funct. 2012 Oct 30.
• Fierens T, Vanermen G, Van Holderbeke M, De Henauw S, Sioen I. Effect of cooking at home on the levels of eight phthalates in foods. Food Chem Toxicol. 2012 Sep 14;50(12):4428-4435.
• Ghaisas MM, Ahire YS, Dandawate PR, Gandhi SP, Mule M. Effects of Combination of Thiazolidinediones with Melatonin in Dexamethasone-induced Insulin Resistance in Mice. Indian J Pharm Sci. 2011 Nov;73(6):601-7.
• Gandhi GR, Stalin A, Balakrishna K, Ignacimuthu S, Paulraj MG, Vishal R. Insulin sensitization via partial agonism of PPARγ and glucose uptake through translocation and activation of GLUT4 in PI3K/p-Akt signaling pathway by embelin in type 2 diabetic rats. Biochim Biophys Acta. 2012 Oct 24. doi:pii: S0304-4165(12)00302-9.
• Hao C, Cheng X, Xia H, Ma X. The endocrine disruptor mono-(2-ethylhexyl) phthalate promotes adipocyte differentiation and induces obesity in mice. Bioscience Reports. 2012; 32:619–629.
• Kaye WH, Berrettini W, Gwirtsman H, George DT. Altered cerebrospinal fluid neuropeptide Y and peptide YY immunoreactivity in anorexia and bulimia nervosa. Arch Gen Psychiatry. 1990 Jun;47(6):548-56.
• Li N, Liu T, Zhou L, He J, Ye L. Di-(2-ethylhcxyl) phthalate reduces progesterone levels and induces apoptosis of ovarian granulosa cell in adult female ICR mice. Environ Toxicol Pharmacol. 2012 Sep 1
• Li XW, Liang Y, Su Y, Deng H, Li XH, Guo J, Lian QQ, Ge RS. Adverse effects of di-(2-ethylhexyl) phthalate on Leydig cell regeneration in the adult rat testis. Toxicol Lett. 2012 Oct 11. 
• Martine B, Marie-Jeanne T, Cendrine D, Fabrice A, Marc C. Assessment of Adult Human Exposure to Phthalate Esters in the Urban Centre of Paris (France). Bull Environ Contam Toxicol. 2012 Oct 23.
• Magistrelli A, Chezem JC. Effect of ground cinnamon on postprandial blood glucose concentration in normal-weight and obese adults. J Acad Nutr Diet. 2012 Nov;112(11):1806-9. 
• Monfort N, Ventura R, Balcells G, Segura J. Determination of five di-(2-ethylhexyl)phthalate metabolites in urine by UPLC-MS/MS, markers of blood transfusion misuse in sports. J Chromatogr B Analyt Technol Biomed Life Sci. 2012 Sep 21. doi:pii: S1570-0232(12)00560-0.
• Rajesh P, Sathish S, Srinivasan C, Selvaraj J, Balasubramanian K. Exposure to diethyl hexyl phthalate (DEHP) to adult male rat is associated with insulin resistance in adipose tisssue: Protective role of antioxidant vitamins (C & E). J Cell Biochem. 2012 Sep 18.
• Ruohonen ST, Vähätalo LH, Savontaus E. Diet-induced obesity in mice overexpressing neuropeptide y in noradrenergic neurons. Int J Pept. 2012;2012:452524. doi: 10.1155/2012/452524. Epub 2012 Oct 18. 
• Simha V, Mahmood M, Ansari M, Spellman CW, Shah P. Effect of Vitamin D Replacement on Insulin Sensitivity in Subjects With Vitamin D Deficiency. J Investig Med. 2012 Oct 29.
• Wu P, Yang D, Zhang L, Shen X, Pan X, Wang L, Zhang J, Tan Y, Feng L, Ying Y. Simultaneous determination of 17 phthalate esters in edible vegetable oils by GC-MS with silica/PSA-mixed solid-phase extraction. J Sep Sci. 2012 Nov;35(21):2932-9.
• Xu Y, Liu Z, Park J, Clausen PA, Benning JL, Little JC. Measuring and Predicting the Emission Rate of Phthalate Plasticizer from Vinyl Flooring in a Specially-Designed Chamber. Environ Sci Technol. 2012 Oct 23.

Natural Resistant Starch Reduces Body Fat & Weight Gain in Obesity Prone & Lean Rodents. 8% RS2 Necessary for Weight Loss Effect, Only 4% for Increases in GLP-1 and PYY

Potatoes! I don't suggest you eat them raw, but if you did they would make a good source of resistant starch. You don't eat potatoes at all? Read the Potato Manifesto and learn why regular potatoes are not as black as they are portrait!

I guess, you will remember my post on WM-HDP from back in the day. As usual you, as a SuppVersity reader were in the know, way before the ThermiCarbs and its identical clones hit the supplement market. It has however gotten relatively quiet around these purported super starches, which bypass enzymatic breakdown in the small intestine and get converted to short-chain fatty acids (SFCA) in the colon. Why? Well, my best bet is that people expected some sweet junk of which they could eat as much as they wanted with the only side effect being increased muscularity and decreased body fat levels. I am well aware that you knew better than that, but you know how people are: Always on the look-out for the magc pill... or in this case, the magic starch ;-)

Cutting fat by eating more: The old adage of the "fat burning foods"

Be that as it may, a soon to be published study by researchers from the Commonwealth Scientific & Industrial Research Organization in Australia confirms: If you exchange a high enough amount of regular carbohydrates with resistant starches (even regular ones, lower resistance to enzymatic breakdown that WM-HPD), this can be a viable tool to shed some body fat.

Unfortunately, though, the results of the very this study do also suggest that the effectiveness of this regimen will largely depend on (a) your phenotype and (b) your willingness to follow your hopefully not totally messed up satiety response and decrease your caloric intake voluntarily, just as the male Sprague-Dawley, the 'subjects in this study by Belobrajdic, King, Christophersen and Bird.

Figure 1: Energy intake and final body weight (left) and relative changes in fat mass and total liver weight after 6 weeks on diets with different resistant starch content (based on data from Belobrajdic. 2012)

Both (a) and (b) could however be major caveats when it comes to the practical realization of similar results in human beings, to whom I would not suggest that they follow a standardized diet with ~15% fat, 19% protein and ~66% carbohydrate, either - regardless of whether they exchange 0%, 4%, 8%, 12% and 16% of the mostly high GI carbs in their diets by resistant starch or not (the values are relative to the weight of the chow).

Just as raw potatoes, green bananas contain RS-2, the natural form of fermentable resistant starch. When you cook them, the RS2 content is continuously reduced.

Note: The "2" in "RS2", indicates that RS2 is, contrary to WM-HDP, which belongs to the "RS4" variety of resistant starches, a naturally occurring molecule. And though this is the case for WM-HDP vs. high amylase maize starch, the latter does not necessarily mean that one is more resistant to enzymatic breakdown than the other. You could for example think of special applications, where you want to have a starch that of which roughly 75% will be broken down into glucose in the small intestine, while the other 25% are fermented further down in the large intestine. This would be a synthetic molecule and therefore categorized as RS4, but still relatively easily "digested".

What I consider especially problematic, though is the fact that people who like to eat, let alone those, who use food as a, if not the only way to experience pleasure in their lives (eating for reward), are going to have a very hard time to satisfy their cravings with this blatant "food". I mean, we all know that "satiety" is not really an issue for most people with weight problems, so it remains questionable to which degree those who actually need a crouch like this will eventually benefit from a resistant starch which exerts its fat loss effect in rodent experiments at least partly via dose-dependent decreases in food intake -- 3%, 6%, 9% and 11% in the 4%, 8%, 12% and 16% resistant starch groups, respectively.

Ok, I have to admit there is more to it than just eating less

Figure 2: For the lean rodents, body weight gain and feed efficacy (weight gain per gram of chow) favor different "optimal" RS2 levels.

Allegedly, the reduction in food intake alone cannot explain the decrease in weight gain in either the obese or lean rodents, but if you take a closer look at the data I plotted in figure 2, it does still become obvious that  the ameliorative effects weight gain in the obesity resistant (i.e. naturally lean) rodents don't obey the "more is more" rule, as the scientists would have it in their abstract:

"Obesity prone rats (OB) gained less weight with 4, 12 and 16% RS compared to 0% RS, but the effect in obesity resistant [lean] animals was significant only at 16% RS. Irrespective of phenotype, diets  containing ≥8% RS reduced adiposity compared to 0% RS. Energy intake decreased by 9.8 kJ/d for every 4% increase in RS. [...] Insulin sensitivity was not affected by RS." (Belobrajdic. 2012)

In the naturally lean animals, the "optimal", i.e. the lowest feed efficacy would be achieved with 8% of RS2 in the chow and not as the "≥8% RS" implies with 16% of resistant starch in the diet.

Ok, I have to admit there is more to it than "minimal feed efficiency"

In the scientists defense, it must however be mentioned that the plasma lipid and gut / satiety regulating hormone levels they measured did in fact show an almost linear increase with the amount of fermentable resistant starch in the diets (see figure 3). Since Belobrajdic et al. do not provide individual data from the two groups, but settle for a table that will tell you that there were no treatment x group interactions  (this means that the outcome was not different for obesity resistant and prone animals) and a phenotype interaction with the overall outcome was only present for leptin, there is no way to tell for sure.

Figure 3: Inter-group comparison (not differentiated for lean vs. obese, because there were no significant interactions, except for leptin) of plasma lipid and gut derived hormone levels (data adapted from Belobrajdic. 2012)

So, with all these "admission" (as in "I have to admit..."), I have to admit *lol* that using high-amyolse starch as a part of your contest prep, maybe to bake pancakes or use it in another food, where the "taste" does not matter that much is could in fact be a viable dietary tool. It won't get you stage ready on its own, though and has one major caveat I have not even mentioned yet: You better make sure you always know where the next clean toilette is. Assuming that those 16% RS2 have the same effect on the volume of your feces as they had on that of the rodents in the study at hand, you may be spending 5-times more time on the loo thhan usually ;-)

If you can't remember what WM-HDP was, click on the image to go back to the article. Regardless of whether you pick up a natural or an artificial starch, this stuff is not "zero calories"! The high amylose maize starch in the study at hand has 10.45kJ (WM-HDP should be similar), i.e. 2.5kcal/g you will have to make up for by cutting out real foods.

Bottom line: Assuming that the results from the study at hand translate to human beings the incorporation of resistant starches in your diet seems - at least to a degree at which your bowel can handle it - to entail a lot of health benefits. The problem I see, is that you will have to force down these empty calories instead of eating healthy foods if you want to benefit.

If you simply add resistant starches (natural or artificial) to your diet, without cutting back on calories, elsewhere, you will become fatter, not leaner.

You will also have to take into account that adding resistant starch to the high sucrose diet of the rodents in this study will necessarily entail greater benefits than exchanging some tubers, rice, fruit and other non-sugary carbohydrate sources from a healthy diet with resistant starch powder - not to speak of all the beneficial micro-nutrients you will be missing!

References:

• Belobrajdic DP, King RA, Christophersen CT, Bird AR. Dietary resistant starch dose-dependently reduces adiposity in obesity-prone and obesity-resistant male rats. Nutr Metab (Lond). 2012 Oct 25;9(1):93.

High Reps vs. 5x5 - Revisiting the "High(er) Reps for Fat Loss"-Myth: Do You Really Believe that "Burning" +13 Extra Calories Will Make a Difference?

Image 1: Vince Andrich, here at the 1988 Nevada State Bodybuilding Competition, knew it all along: Hard work, not high reps will get you the stage-ready physique everybody aspires... and I mean look at him are you seriously questioning Vince's expertise?

If you have listened to the latest installments of BodyRX Radio, the idea that strength (and HIIT) training, not calorie restriction and endless cardio sessions pave the way to a leaner, more muscular physique. And although it may be of secondary importance whether you are burning 100kcal or 200kcal during those workouts, it stands out of question that you won't get rid of those damn spare tire, if you do not exert yourself in the gym (something Layne Norton is notorious for, as you may have seen in one of his workout videos or heard on BodyRX, lately) - because, after all, energy expenditure does count, even if the energy equation is much more complex than the simplistic calories in vs. calories out paradigm that is still upheld by mainstream dietitians. The results of a recent study from scientists from the Departments of Health and Sport Sciences at the Salisbury University and the University of South Carolina are may thus come handy to decide, to which extent workout intensity and volume influence acute and post-exercise energy expenditure (Mazetti. 2011). Or, to make it simple, does the good old bro-scientific high volume, high rep, low-weight training during a contest prep make any sense at all?

Exposed! The absurdity of going to the gym to "burn calories"

Scott A. Mazetti and his colleagues recruited 10 resistance trained young men (22+/-3.6 years) with an average body mass of 84+/-6.4kg, a height of 180+/-5.1cm, and a body fat percentage of 13+/-3.8% - an adequate model of the "average gymrat", if you asked me. After a 3-week familiarization and testing period, all participants performed every of the following four different explosive strength training regimen in a randomly assigned, but counterbalanced order (cf. figure 1)

Figure 1: The four training protocols all trainees performed after an initial 3-week familiarization and testing period in a randomly assigned, but counterbalanced order (Mazetti. 2011)

Now, you may complain that there is neither a "high rep" nor a "heavy group" in the conventional sense of 15+ pump training with an endless amount of sets, or the minimalist 1-2 rep approach of the hardcore HIT faction... granted, you are right. Nevertheless, we should see a significant difference in energy expenditure between a 5x5 and a 4x10 (both normally considered as "hypertrophy training) regimen, already, if the good old saying "high(er) reps" for increased energy expenditure and subsequent fat loss had any merit.

Figure 2: Energy expenditure (kcal/min) during and after squatting, and bench pressing in the four training groups and total energy expenditure during the whole workout and 60min post-workout window (data adapted from Mazetti. 2011)

As figure 2 goes to show, there are differences in energy expenditure between the different protocols, during the squat, the deadlift and up to 5 minutes post exercise, nevertheless, the "the differences in total energy expenditure among protocols were not significant". So, even if there were any merit in exercising primarily to burn calories during your workout (a ridiculous way of trying to lose weight, which is predestined to fail, anyway), the -6kcal difference between the -13kcal difference between the least energy consuming form of training, i.e. 5x5 and the one with the highest energy demand, i.e. 4x10, would not even suffice to "make up" (another hilarious idea) for proverbial "apple à day", which keeps the doctor away.

Image 2: Don't let your lazy love handles decide what type of "cardio" you are doing!

A brief note on what Lane already pointed out in the last installment of Body RX Radio: Classic low-intensity cardio training may "burn" calories for a week or two. Afterwards, this type of chronic low-grade stressor is yet notorious for shutting down your metabolism and reducing your resting energy expenditure. Of high intensity aerobic exercise with intensities way beyond the 70% VO2max limit (YES! This is aerobic, two - cf. "HIIT is the Hit! Even for Patients with Myocardial Infarctions!"), we have known for decades that it increases your resting energy expenditure by "5 ±15% for 24 ± 48 h" (Hunter. 1998). So, I suggest you get off the stationary bike you are just riding while browsing the web, get your running shoes out and do a couple of sprints. Your spare tire won't like that, but I bet you will like the effect it's going to have on the person you see in the mirror, each morning ;-)

In view of these results, it appears prudent to reassess the often-heard advice of doing high reps for fat loss. Even if you insist that you need to "burn calories" in the gym, it is very unlikely that those few extra calories would make a noticeable difference in terms of how you look on stage - or just in front of your private mirror. Moreover, even this small advantage vanishes as soon, as you increase the workload by doing 2x7 + 2x6 with a heavy weight, or put simply: Identical workload identical calorie expenditure.

100 calorie snacks

‘Weight loss is 70% food and 30% exercise” seems to be the widespread conclusion of people who have successfully lost weight. The numerous blogs that I follow and articles that I read, all say the same thing. I believe it too. My initial weight loss attempts more or less involved controlling what I eat and how much I eat and the strategy has proved to be somewhat effective, but not completely

Increasing Adolescent Obesity Among Girls: How School Stress is the New Scapegoat When the Skinny Fat Phenomenon and Twinkie Diets Really are to Blame.

Image 1: Was it school stress that cost Michelle Obama her famous "guns" (=muscular upper arms)? Probably not - and despite contrary conclusions in the study at hand, I doubt that it is school stress that leaves our daughters fat, but undermuscled. What do you say?

According to the results of a recent evaluation of the data from the European HELENA trial, school, or rather the stress your children are exposed to within the educational system, may be one of the reasons for the increasing number of obese adolescents (age 12-18 years) - at least if we trust the statistical finesse of Tineke De Vriendt, Els Clays and 10 other scientists who recently published a paper on European adolescents’ level of perceived stress and its relationship with body adiposity in the European Journal of Public Health (DeVriendt. 2011). The study was part of the Healthy Lifestyle in Europe by Nutrition in Adolescence cross-sectional study (HELENA-CSS), the aim of which is to obtain "reliable and comparable data from a selected cohort of European adolescents concerning a broad variety of parameters related to nutrition, health, physical activity and fitness", or in other words, to provide the epidemiological back-bone for the formulation of more or less mainstream hypotheses on "why we are getting sick and obese"... be that as it may, with a sample size that allows for a confidence level of 95% and <0.3 error and 3865 adolescents from more than 10 European cities, the data from the HELENA study is probably the best we can get at the moment and thus you may nonetheless be interested to hear that ...

School-related stress was demonstrated to be a main source of stress in European adolescents, [...and] in adolescent girls (but not in boys), a positive association was observed between their level of perceived stress and measures of general and abdominal obesity.

If you have a closer look at the stress data, expressed on a 6-scale Likert scale from 1 = ‘Not at all stressful’ over  2 = ‘A little stressful’, 3 = ‘Moderately stressful’, 4 = ‘Quite stressful’ to 5 = ‘Very
stressful’ (with 6 indicating ‘Is irrelevant to me’), you will notice that school and the closely related fear of an "uncertain future" are in fact the major stressors in the life of our adolescent children (and you may safely assume that the results won't be very different in the US).

Figure 1: Overview of perceived stressors; values expressed on a Likert-scale from 1 to 5 (data adapted from DeVriendt. 2011)

In that, it is yet interesting to observe that none of the stressors is on average perceived as "quite stressful" or even "very stressful". It is also noteworthy that on 5 out of 10 scales and on the summary scores girls experienced more stress than boys. In view of the scientists previously cited conclusion (of which I do not have to tell you that it is based on one of those sophisticated *cough* statistical models) that only "in adolescent girls (but not in boys), a positive association was observed between their level of perceived stress and measures of general and abdominal obesity", it may thus surprise you to hear that the obesity rate among boys is more than 2x higher than among adolescent girls (cf. figure 2). So how is that?

Figure 2: Body adiposity characteristic of study sample (n=1121) of adolescents from the HELENA trial (data adapted from DeVriendt. 2011)

Well, we all know that even with a perfectly "normal" BMI, you can easily be "skinny fat". A phenomenon of which I feel that it is becoming the norm, not the exception, among adolescent girls, who - after their nth an-apple-a-day diets have lost nothing but muscle and thus have a very high body-fat percentage with a low overall body-weight.

This hypothesis would be confirmed by the regression coefficients of the statistical models from the study, according to which the association of perceived stress with the body fat level of the girls is 7x higher than the association of perceived stress and BMI, which is something that should you make reconsider, whether

1. body weight and BMI is an important biological measure, at all,
2. the real "obesity" rate, including skinny fats, among girls is not way higher than the 1.9% reported in the study would suggest, and
3. in how far school-stress, despite being the "major stressor" in this survey and not a misguided beauty-ideal is to blame for the increasingly unbalanced ratio of lean to fat mass in adolescent girls

The importance of the latter, i.e. a questionably beauty-ideal, in the etiology of (and this would be ironic if it was not so unfortunate) diet-induced obesity could also explain that the pubertal stage the girls were in and not stress or their diet had the greatest "explanatory value" (remember: we are talking of associations here) in regard of their body fat levels (cf. figure 3).

Image 2: Low self-esteem and false beauty-ideals pave the way into disordered eating and life-long misery. Something you want to spare your daughter and son, don't you?

Did you know that according to a 2000 national survey 45% of the girls, but only 20% of the boys from 5th to 12th grade reported to have tried one or more diets at some point in the past (Neumark-Sztainer)? And would you have guessed that 17% did even consider their own eating behavior as already "distorted"? Needless to say that both of these factors showed a high correlation with overweight status, low self-esteem, depression, suicidal ideation, and substance use; and certainly reason enough for you to help our children (girls and boys) not to fall victim to ill-advised beauty-ideals and false dietary recommendations.

And from the fact that the same variable had 7x less predictive value in boys, who obviously do not want to be skinny fat and refrain from Twinkie-style low calorie, low fat dieting, we can with some caution (due to hormonal effects on fat accumulation) conclude that it is not just a time factor, meaning that the older girls have more time to accumulate body fat...

Figure 3: Regression coefficients (=associative strength*100) of stress or pubertal stage with body-fat percentage in adolescent boys and girls from the HELENA trial - mind the logarithmic scaling! (data adapted from DeVriendt. 2011)

Now, what can you do about that? Well, without even knowing you probably have already done something! Assuming that you (just like every other reader of the SuppVersity ;-) are of above-average intelligence, your education has already provided your daughter, but not your son, with a better chance of staying lean than her peers from less educated parents (~80x higher explanatory value than stress!). All that is left now to make absolutely fat-proof, is to tell her that strong, not skinny fat is the new beautiful ;-)