Healthier, Fitter & Leaner After 12-Day McDonalds Challenge Thanks to HIIT? Plus: TRX®, Fitness ↗ Fatness ↘ in Women

Short news: Sprinting & TRX 

"Have you already burned off that burger you had for lunch today?" If that's a question you're asking yourself regularly, you are at a high risk of misinterpreting a recent study by Christian Duval et al. (2017) as a license to eat how much you want, whatever you want, whenever you want. Unfortunately, a 12-week study in which young, healthy subjects were allowed to consume only three more or less energy-adequate meals is not representative of the futile "if you eat more/worse, just exercise more"-approach to diet and exercise.

Apropos exercise, if you're still looking for the right exercise to get or stay fit and healthy, TRX training, the suspension training bodyweight exercise that has purportedly been developed by/for US Navy Seals seems to actually live up to some of its promises of developing strength, balance, flexibility and core stability - overall fitness (VO2max) improvements are yet probably its greatest strength, a strength that comes with "unintended", but significant reductions in body fat in the overweight young women who participated in a recent 8-week Iranian randomized, controlled study by Dolati et al. (2017).

Read about exercise- and nutrition-related studies in the SuppVersity Short News

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• HIIT protects young, healthy individuals from fast food induced insulin resistance and reduced cardiovascular health, "in large part", study shows (Duval 2017) -- "You cannot outrun an obesogenic diet" - I guess you've heard or read that before (maybe even at the SuppVersity) and the study at hand doesn't falsify this truism. What it does, however, is to remind us that "an obesogenic diet" is any hypercaloric diet. A fast food diet, on the other hand, is not necessarily hypercaloric. In fact, you could lose a lot of weight if you ate at McDonald's every day but kept your total energy intake 30% below your baseline requirements.
  

  

  Either three McDonald's meals a day are not as bad as people think or HIIT protects young, healthy individuals from the bad effects. In the absence of a "Mc Donald's-only" control group, the study at hand cannot really answer this question. Based on previous evidence the former answer is more likely, though.

  In other words: Fast food per se is not obesogenic. It is, however, due to its high energy density, low satiety effect and nutrient density, and the pro-diabetic combination of high GI carbs and unhealthy fats that are so characteristic of Western fast foods, pro-diabetic and may deteriorate your blood lipids and other CVD-relevant blood markers in ways that have been found to be associated with an increased heart disease risk. Accordingly, the question whether high-intensity-interval training (HIIT) can counteract the deleterious effects of a fast food diet on the cardiometabolic profile of young healthy men, which was addressed in a recent study from the Université du Québec à Montréal (Duval 2017), is of fundamental importance.
  
  In the 14-day study, fifteen men, all fit, healthy and physically active (>150 min of physical activity/week), were subjected to an exclusive fast food diet from a popular fast food restaurant chain, McDonald's, where they consumed ...
  • a sandwich (e.g., Egg McMuffin®, or Sausage McMuffin®), hash browns and a small fruit drink or coffee for breakfast, and
  • a sandwich (e.g., Big Mac®, McChicken®, or Quarter Pounder with Cheese®), medium fries and a non-diet medium soft drink) for lunch and dinner and an optional snack
  Since this was a noncontrolled study, all participants were asked to perform high-intensity-interval training (HIIT) (15 × 60 sec sprint intervals (~90% of maximal heart rate) interchanged with 60 sec active recovery (walking) + 5min warm-up and 5-min cool down) on a treadmill, every day. That's a clear weakness of the study as it simply assumes that the health parameters the scientists measured, i.e. body composition (DXA), cardiometabolic profile (lipid, hepatic enzymes, glycated hemoglobin, glucose, insulin, hsC-reactive protein (hs-CRP) and blood pressure) and estimated maximal oxygen consumption (VO2 max) pre- and post-experiment would deteriorate significantly within only two weeks.

  

  Figure 1: When combined w/ HIIT the fast food diet rather improves than worsens important parameters of body composition, fitness, and glucose metabolism (Duval 2017 | all changes were stat. sign.)

  If it were not for the significant improvements of fat and lean body mass, estimated VO2 max, fasting glucose, serum lipoprotein(a) and hs-CRP after the intervention (p < 0.05), the scientists observed, the study would thus be useless. If said parameters had not improved, but worsened, it would, after all, be impossible to know whether and to which extent the worsening of the subjects body composition, metabolic and heart health would have been ameliorated by the HIIT intervention.
  

  

  Figure 2: If you look at the totality of the changes in glucose and lipid metabolism and the inflammatory status and ignore that only the changes in fasting glucose, HDL-cholesterol, and hs-CRP were statistically sign., it seems as if McDonald's + HIIT was much healthier than what the subjects usually did.

  This problem exists, however, for the significant reductions in HDL-cholesterol (p < 0.002) and the lack of change of the triglycerides/HDL-cholesterol ratio. Due to the lack of a "fast food only"-control group it's impossible to tell if the decline in HDL would have been more pronounced and the triglyceride/HDL ratio would have increased in a non-existent "fast foot only"-group. The researchers were thus lucky that their study turned out to produce results the scientists could interpret as follows: "In conclusion, in large part, insulin resistance and the cardiometabolic profile of young healthy individuals seems to be protected by HIIT from a fast food diet" (Duval 2017).
  
  Before you rejoice, jump into your car and head to the next McDonald's drive-in restaurant, remember: We are talking about a two-week study in which the energy intake was limited by certain rules, so that the average participant ended up consuming 3441 ± 337 kcal/day and expending 3503 ± 373 kcal/day (that's a 60kcal deficit |the subjects' individual energy expenditure was monitored by a portable mini SenseWear armband the validity of which has been confirmed in St-Onge 2007, Drenowatz 2011, and Ryan 2013 - needless to say that conducting the whole study in a metabolic ward would have been better ;-) - against that background it's no wonder that the sixteen young men didn't balloon up or saw significant negative effects on important health markers.
  

  

  Figure 3: The experimental diet could for sure have been worse and more obesogenic (data from Duval 2017).

  And, by the way, with a macronutrient ratio of 12%, 49% and 39% for protein, carbohydrates, and fats, their macros weren't much worse than the average Westerner does, anyway. In fact, it would be interesting to run their McDonald's diets through MyFitnessPal to compare their micronutrient intake to the one of the average American. I am not sure how much worse the McDonald's diet really was... speaking of calculations: I calculate or hope that we may see a controlled follow-up study - ideally with a longer study period ;-)
• TRX-Training an option an excellent training option for overweight (non-obese!) women (Dolati 2017) -- If you look at TRX' marketing campaign, the 24 overweight women (age of 29.41 ± 4.48, height 162.35 ± 4.97cm, weight 73.4 ± 5.47kg and BMI 27.85 ± 2.02 kg/m2) who participated in a recent study at the Islamic Azad University in Teheran clearly don't belong to the producers' target group - a big mistake? It almost looks like it.

  

  Overweight women are not yet a target of the TRX' marketing. Considering that this study shows that TRX workouts prevent a 2% increase in body fat and shed sign. 2% body fat in 8 weeks (24 sessions) this may be a mistake... or, maybe, those responsible may simply want to signal that after half a year of TRX the ladies in the study would look like the shredded girls in the campaign - unfortunately, that won't happen w/out dieting.

  Over the course of the 8-week study, all participants performed 24 workouts (three workouts per week). The training duration from the first week up to the last week increased from 12 to 30 minutes and the exercise intensity from 50 to 80 HRmax ("minimal" rest between exercises - usally it's 30s to switch from one position to the other in TRX).
  
  Prior to the implementation of the training program, the performance indicators and body composition were measured and blood test was also conducted for determining the lipid profile. After eight weeks of practicing, all of these tests were taken once more.
  

  

  Figure 4: Rel. changes in BMI and body fat % and VO2max in the TRX and control group (Dolati 2017).

  The body fat percentage of the subjects in the treatment group dropped from 39.8 to 36.97% (p = 0.001), their body fat mass decreased from 28.22 to 26.32 (p = 0.001), their upper-body muscle strength increased from 13.85 to 15.21 kg (p=0.001), and their the lower body muscle strength from 126.78 to 132.24 (p=0.001). The women in the control group, on the other hand, saw no such improvements - in fact, their body fat percentage increased from 36.67 to 38.22% while their muscle mass and strength remained virtually identical.
  
  In the absence of additional cardio training the subjects in the TRX group also saw a highly significant increase in VO2max from 55.05 to 61.89 ml/kg/min (p= 0.002) - probably a consequence of the fact that TRX training is, in contrast to strength training, not standardized by 1-RMs, but by heart rate. With the target heart rate for the study at hand being increased from 50-60% to 80% of the maximal heart rate from the first to the last week of the study, the intervention obviously provided an effective stimulus for VO2max gains (note: there was no change in the non-exercised control | see Figure 4).
  
  If you look at the results, TRX is neither an efficient mass/strength builder nor the best tool to shed body fat (if you hate "weights" want a strong aerobic component and still build mass/strength and lose body fat, check out kettlebells). The significant VO2-gains and the proven increase in muscle activity during core training still make it attractive - even if it's only as a means to diversify your training program.

Be a glutton from time to time! Believe it or not, three days of overfeeding won't make you fat, even with 1,500 extra-calories per day and more than 50% of the energy coming from carbohydrates | more. 

Bottom line: Trying to outrun a bad diet is, unfortunately, still a common practice ... a practice you don't want to follow; that does not mean, though, that the Duval study was irrelevant. It does, after all, confirm that you don't have to be afraid to get fat or, even worse, sick from the occasional fast food meal. I've written about the futility of the idea that every 'nutritional mistake' is punished with obesity, diabetes, or both (e.g. "Can You Get Fat in Just Three Days?" | read it)... let's be honest: the stress you may experience after "sinning" if you hold such beliefs is going to be worse for your physique, overall and metabolic health than the occasional burger with fries - at least, if you (a) understand that "calories count" and (b) do not fall completely off the wagon and subscribe to the "as much of everything I want at anytime I want it"-dietary approach a significant number of our fellow human beings subscribe to.

And in case things go south, anyway, remember: you don't have to wait for new years eve to start a new - whether this restart involves TRX, is obviously up to you. If we go by the results of Dolati et al. (2017), however, this is maybe not the worst exercise equipment to use. Whether it's right for you, though, is something only you can answer: if you like it, fine; if you hate it, find something else - enjoyment is, after all, a key determinants of exercise adherence (Richard 1997) and adherence is the key to success in both diet (Alhassan 2008) and training (e.g. Van Gool 2005) | Comment!

References:

• Alhassan, S., et al. "Dietary adherence and weight loss success among overweight women: results from the A TO Z weight loss study." International journal of obesity (2005) 32.6 (2008): 985.
• Dolati, Mahya, Farshad Ghazalian, and Hossein Abednatanzi. "The Effect of a Period of TRX Training on Lipid Profile and Body Composition in Overweight Women." International Journal of Sports Science 7.3 (2017): 151-158.
• Duval, Christian, et al. "High Intensity Exercise: Can It Protect You from A Fast Food Diet?." Nutrients 9.9 (2017): 943.
• Drenowatz, Clemens, and Joey C. Eisenmann. "Validation of the SenseWear Armband at high intensity exercise." European journal of applied physiology 111.5 (2011): 883-887.
• Richard, M., et al. "Intrinsic motivation and exercise adherence." Int J Sport Psychol 28.4 (1997): 335-354.
• Ryan, Jennifer, and John Gormley. "An evaluation of energy expenditure estimation by three activity monitors." European journal of sport science 13.6 (2013): 681-688.
• St-Onge, Maxime, et al. "Evaluation of a portable device to measure daily energy expenditure in free-living adults." The American journal of clinical nutrition 85.3 (2007): 742-749.
• Van Gool, Coen H., et al. "Effects of exercise adherence on physical function among overweight older adults with knee osteoarthritis." Arthritis care & research 53.1 (2005): 24-32.

Low Carb(-ing) Reduces Fat & Fast Food (10-20%) Cravings Plus 60% Less Hunger After Meals in Obese Men/Women

You always crave the foods you must not eat, right? No, ... a recent study finds decreases in sweet and starch cravings in obese individuals on low-carb diets.

If the calorie intake is standardized, low-carb dieting has no proven metabolic weight loss benefit compared to any other dietary weight loss intervention. In the real-world, as well as less tightly controlled studies in obese individuals, however, they tend to outperform their American Heart Association inspired bogus low fat, low protein, high carbohydrate counterparts.

The reason? No, still no "metabolic advantage": reduced hunger and food cravings and the subsequently increased adherence and reduced energy intake - an assumption that isn't proven, but at least supported by Colette Heimowitz' latest paper. A paper based on a study that was sponsored by Atkins Nutritionals and smells of bias, but a study that's in line with millions of N=1 reports on the internet.

Would be interesting to compare keto to high-protein, not western diets, right?

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As the authors explain, "[...m]any individuals entering weight loss programs may believe that restriction of a certain type of food (e.g., carbohydrate, CHO) may increase their cravings for that food" (Heimowitz 2017). With their vested interest in making the low-carb diet and their low-carb convenience food look good, the scientists' goal was to prove that these carbohydrate cravings don't exist. Obviously, that's not what you will read in the paper which phrases things significantly less suspiciously stating that "the present study was to assess motivation for entry into a weight loss program, acceptability of low-CHO commercially-prepared foods, and changes in food cravings during rapid weight loss associated with high-fat, low-CHO dietary consumption" (Heimowitz 2017). "The foods provided for the first 2 wks included Atkin’s products (frozen dinners, bars and shakes), and some freshly-prepared meals (total fat was 54±4% of energy (%E), protein, 28±2 %E, and CHO 14±1 %E; fiber intake, 26±8 g/d) and resulted in an energy deficit of 1198 ± 655 kcal/d, then...

Figure 1: Macronutrient composition of the energy-reduced diets (intended deficit of ~1200kcal/day | Heimowitz 2017)

"[f]or the next 2 wks, subjects prepared their own meals with the goal of achieving a similar food intake. Subjects were surveyed regarding reasons for enrolling in the program, and at baseline (BL) and 4 wks, completed the Food Craving Inventory (cravings for foods that were fatty, sweet, high in CHO (starches), or categorized as fast foods), and the Three Factor Eating Questionnaire (TFEQ) to assess food intake motivation" (Heimowitz 2017).

All N=20 subjects (10 men and 10 women with a mean age o 40±8y, and a BMI in the red obesity zone of 34±3 kg/m²) completed the study with their main goal being to look better - not to be healthier, which ran as a poor second, along with family issues.

Figure 2: Plot of the most relevant anthropological and psychological study outcomes (Heimowitz 2017).

Over the course of the intervention, of which you should by now have realized that its non-controlled nature significantly reduces its meaningfulness, the subjects lost a highly significant amount of bod weight (5.7±0.6 kg, P<0.00001) and, more importantly, were able to reduce their waist circumference by 5.6±0.9 cm (P<0.00001). Unsurprisingly, "subjects stated that consumption of [the authors' company's] pre-made meals aided them in meeting their weight-loss goals" (Heimowitz 2017).

• 95% of subjects reported being somewhat satisfied to very satisfied with the meals, 
• 60% felt less hunger after meals, and 
• 75% reported reduced 'eating when bored'

With regard to the underlying research question, the scientists' statistical analysis of the data from the questionnaires, the authors observed a high baseline craving for sweet foods (45% of subjects reported frequent cravings for sweets) that did not increase with low-carb dieting. In fact, after weight loss, cravings for sweets and starchy foods were reduced by significant 12±10% (P=0.02 | low effect size, though) and 12±6% (P<0.01 | medium effect size), respectively.

What is particularly interesting is that the reduction in sweet cravings tended to be associated with a reduction with significant reductions in disinhibition and increases in cognitive restrained: over time, the subjects were thus more and more able to control their food intake and less susceptible to fall victim to their (now reduced) cravings - reduced cravings for sweets and starches and reduced cravings for fatty foods (11±7% | P<0.03) and fast food cravings (19±5% | P=0.0006), all without the often-heard-of difference between men and women (you know how women are supposed to crave sweets, and men fatty foods).

Different Study Population = Different Goals, Different Outcome: "Low Carb Diets and Physical Performance - Recent Studies Show Performance Decrements in Average Joes + Athletes" | read  more

Bottom line: The study provides valid evidence for the commonly heard claim that low-carbing would reduce food cravings. It does not, however, prove that a similar effect wouldn't have been observed simply due to weight loss with other diets. Do the scientists mention that in the conclusion to the abstract, the only part of a paper many people read? Obviously not.

Without a follow-up study that compares the effects of a low-carb to an energy-equivalent control diet (ideally one that's high(er) in satiating proteins), the study at hand must be considered preliminary evidence.

Evidence that is, however, in line with the reports of many (formerly) obese low-carb fans all around the world - reports from lean individuals and athletes, as well as the results of studies comparing low- and high-carb diets head to head (e.g. Brehm 2003; ), on the other and, are much more inconsistent and suggest that metabolic, genetic and/or lifestyle differences may determine whether low-carbing will curb your appetite | Comment!

References:

• Brehm, Bonnie J., et al. "A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women." The Journal of Clinical Endocrinology & Metabolism 88.4 (2003): 1617-1623.
• Heimowitz, Colette, et al. "Changes in Food Cravings during Dietary Carbohydrate-restriction." The FASEB Journal 31.1 Supplement (2017): 643-23.

Glutamate: Can It Be Use To Your Advantage? Study Shows Insulin Sensitizing Effects of Dreaded Food Additive

"Now you've got me confused!"

In the context of MSG scare, glutamate has gotten such a bad rep that it seems highly counterintuitive to assume that there was anything good about the major excitatory amino acid in the human body and still, a recent study from the Department of Kinesiology at the University of Waterloo clearly suggests that "MSG and carbohydrate supplementation can be used to manipulate plasma glutamate" (Sebastiano. 2013)... and no, we are not talking about an in-vitro or rodent study here.

With 9 perfectly healthy, recreationally active men aged 23.9+/-1.9y and a BMI of 25kg/m² the results can however be taken as being representative for at least large parts of the ever-decreasing number of "normal-weight" individuals.

There is a potential string attached

Usually, the "on the other hands", are something I am talking about at the end of the article, but in this case, of which I expect that it's going to become pretty controversial it appears prudent to address them right away: there was a hitherto unexplained dichotomy in the insulin response of the 9 subjects after the ingestion of the 150 mg/kg body weight MSG or placebo capsules, the subjects ingested after an overnight fast and 30 minutes before they consumed a 75 g carbohydrate or a non-energy placebo drink.

Figure 1: AUC for glucose and insulin across the trials (left); serum insulin and glucose concentrations in the post-prandial period during the glutamate and no-glutamate trials (Sebastiano. 2013)

What looks like a Taubs'ian nightmare is actually nothing but a perfectly normal insulin response to the ingestion of 75g of carbohydrates. In a healthy individual, the insulin response is proportional to the influx of glucose from the digestive tract and ensures that the latter is getting stored in muscle, liver and fat (with the former being topped of first, cf. figure 3 in previous article).

On average, we do the the same if not less insulin with a greater reduction in glucose

That being said, there is no debating that contrary to the scientists' working hypothesis, the average insulin secretion was not on augmented in the GLU+CHO, while the onslaught of glucose was significantly reduced (see figure 1, bottom right) compared with the CHO only trial.

Epidemiology paints a different picture of MSG (learn more)

"[I]t appears that glutamate, when combined with carbohydrate, elicits one of two insulin responses, depending on the individual.

Although the present study was not designed to explore this question, we did remark that the differences between these two groups of participants were not explained by factors associated with glucose handling, such as habitual activity levels (assessed using the Baecke questionnaire), fasting glucose, available glutamate or insulin sensitivity." (Sebastiano. 2013)

Now this is quite astonishing as it would suggest that the co-ingestion of glutamate does actually improve the insulin sensitivity only in some. In those the effect must yet have been so pronounced, though, that the "non-responders" didn't carry any weight...

---

Apropos weight, in order to confirm whether or not you can use glutamate to your advantage, we would need at least two follow up studies:

Will the additional butter on top of the potatoes reduce the insulin response? Learn the answer to this other questions in one of the famous installments of the "True or False?" Series on the SuppVersity (learn more)

• One study to elucidate the long-term consequence of the addition of glutamate to every (high) carbohydrate meal in healthy human subjects (the hypothesis would be that we should lower HOMA-IR and HbA1C levels as a sign of improved glucose metabolism).

• And another study to make sure that the obvious insulin-sensitizing effects glutamate appears to exert in at least some subjects are not adipose-tissue specific - or, in other words, that it is not an increase in fatty acid synthethase and subsequent storage of glucose as fat that's behind the significantly reduced glycemia the scientists observed.

What? You think all that is bullocks, because "we all know" that glutamate is going to make you fat? Well, in a non-calorically controlled scenario this may still be the case.

YamYol: Yeast extract = MSG

Did you know that almost all producers of convenience "food" are tricking their consumers by claiming their products were free of added flavor enhancer, MSG-free or at least free of artificial flavor enhancers only to add yeast extract as an ingredient. Now being an ingredient it's no longer an additive and in view of the fact that most consumers are not aware that it is basically MSG, nobody will complain... besides you, obviously ;-)

To understand that you will however have to get rid of your false prejudices against insulin, the release of which also acts as a satiety signal (in the insulin sensitive individual) and will have you stop eating (Verdich. 2001). With your glutamate laden super size fast food menu, your body may not even recognize that you have just been downing a Big Mac, XXL French fries and an XXL Coke, estimating that the stuff you ate was probably a Happy Meal with only 50% of the calories. In other words, in the real world, McGlutamate and ChinaMSG are probably still not the best places to dine regularly ;-)

References:

• Di Sebastiano KM, Bell KE, Barnes T, Weeraratne A, Premji T, Mourtzakis M. Glutamate supplementation is associated with improved glucose metabolism following carbohydrate ingestion in healthy males. Br J Nutr. 2013 Jun 11:1-8. [Epub ahead of print] 
• Verdich C, Toubro S, Buemann B, Lysgård Madsen J, Juul Holst J, Astrup A. The role of postprandial releases of insulin and incretin hormones in meal-induced satiety--effect of obesity and weight reduction. Int J Obes Relat Metab Disord. 2001 Aug;25(8):1206-14.

2.1kg Muscle From Fast Food Supplement; No Prolactin, No Fat; Oleic Acid Counters CLA's Inflammatory Effect; Spicy Marinades vs. Salmonella; Flaxseed, Estrogen & Penis Size; TTA in the Emergency Room; Alcohol & Binge Eating

Image 1: Scientifically proven muscle builder - 2.1kg lean mass in 3 months, no post-cycle therapy necessary!

I was just about to write another one of my artistic introductions, trying to incorporate all the exciting On Short Notice news I've piled up for you into a brief narrative, when I realized that you probably don't really appreciate those introductions (I guess, I would skip them myself, so don't worry, this is more of an objective assessment than an accusation). So, I listened to my gut and decided to skip this part of this series, today, and rather spend the time to edit another item I did actually not want to post today. It's the one on the "IIFYM slightly gone wrong fast food bulk" in the Hambre study, to be precise; and I would venture the guess that you won't mind taking that instead of a longer introduction, once you've read and digested the impossible: You cannot only gain muscle with "fast food supplements", you won't even get fatter than you would if you just used a classic whey protein... oh my, I see, you are already scrolling down: What I said, I would have been wasting my time, had I written a longer introduction. But dare you, if you don't at least read the other items, as well!

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  Figure 1: Food intake (top, lef) and energy expenditure (bottom, left) as well as body fat % (top, right) and body weight development of the normal vs. prolactin negative mice after 14 weeks on standard chow (SC) or high fat diet (HFD; Auffret. 2012); btw: taking super-doses of vit. B6 will induce nerve damage, not fat loss!

  Without prolactin mice can't get fat! If that is true for humans as well, this would mean that Julien Auffret and his colleagues would have made a very important finding that could help us solve at least part of the diabesity pandemic, if we found a way to mimick the effects the "beigening" (=making white adipose tissue behae similar to the fact burning brown adipose tissue) effect the genetic ablation of the prolactin receptor on the fat cells of the mice in the Auffret study had on their susceptibility to diet induced obesity (Auffret. 2012).
  In particular, the scientists found that the ablation of the prolactin receptor gene in the mice results in profound increases in the expression of master genes controlling brown adipocyte fate (PRDM16) and mitochondrial function (PGC1α, UCP1), which allow - and this is the actual caveat,, here - for an inrease in thermogenesis.
  The latter, in turn, allows the rodents to burn off a major part of the fat they would otherwise store and thus keeps them relatively lean despite HFD feeding. Aside from the fact that the hyperphagic rodents on the high fat diet were still fat (there is no debating that!), you may savely assume that the effects will be way less pronounced in human beings, where 9/10 "thermogenic" agents that have been successfully tested in rodents do nothing at all, anyway. Against that background the hunger-promoting effects of the prolactin recetor ablation would suggest that it is almost as likely that a drug that block prolactin completely would make obese individiuals even fatter, since that's usually what happens if you eat more - like the mice in the prolactin (-/-) group did (see figure figure 1), without burning more.

• 

  Figure 2: Comparison of MUFA : CLA ratios in steak and mince from grass fed or conventional beef and milk from mares, sows, women (human milk ;-), goats and cows (based on Dhiman. 1999; Jahreis. 1999; McAfee. 2011); higher values indicate more MUFA per unit of CLA, but more must not necessarily be better - in fact too much MUFA could completely block the fat loss effects of CLA and thus maybe explain why it rarely works in humans - our diets are pretty high in oleic acid and thus the ratio will be much lower, than in the high dose CLA rodent trials

  Conjugated linoleic acid needs oleic acid to work without side effects. That's the main take-home message from a recent study conducted by researchers at the at the University of North Carolina at Greensboro, who found that oleic acid, the mono-unsaturated fatty acid from olive oil & co, does prevent the expression of inflammatory genes in adipocytes treated with the "anti-fat fat CLA"..
  So, until my friends from the supplement industry read this post and come out with yet another SuppVersity science powered product with CLA in olive oil* you simply make sure to have a spoon of the liquid gold from time to time, when you feel that you need to take CLA to burn more fat. Unfortunately, this could not just mean that you can rid yourself of the nasty side-effects as discussed in "CLA Destroys Body Fat! But at Which Costs?", but also that the "body fat destruction" will at least be ameliorated if not totally absent :-(
  * I had hardly written this post, when I browsed the web and found that a certain newcomer and as of late very succesful "yellowish green" company has already a CLA + Olive Oil + Avocado Oil combination on the market, for them this would mean that they didn't even have to change their formula

• 

  Image 2: It's funny how so many things people (or at least chefs) have been doing forever, here marinating meats, simply make sense, isn't it?

  Antibacterial marinades for your meat! Don't worry this is not yet another dysfunctional functional food that's going to make you sick, but an all-natural mixture of green tea, lemon and turmeric you will have to smear onto your chicken meat if you want to make sure to get rid of the C. jejuni and S. enteritidis it may be contaminated with.
  All it takes are 24h of "incubation", but that's nothing else than leaving your meat lying in the marinade in your fridge and thus something you would do anyway, right? That's what I would call a convenient, effective and above all totally natural and healthy way of gettting rid of Samonella and Campylobacter :-)
• Tons Flaxseed flour in your diet will increase estrogen, but won't decrease the size of your penis, well at least not visible ;-) That's probably the most straight-forward summary of the results, Ludmila Ferreira Medeiros de França Cardozo and her colleagues present in the latest issue of Food and Chemical Toxicology after analyzing the effect of a flaxseed flour containing diet on the expression of hormone levels and penis morphology of male rats (de Franca. 2012)

  

  Image 3: Flaxseed bread won't turn you into an hermaphrodite overnight, don't worry.

  While the rats that were maintained on a diet containing 25g of flaxseed flour per 100g for 250days had significantly elevated estrogen levels in the blood 39.5 vs. 32.5 pg/mL (+22%), the minor drop in testosterone did not reach statistical significance and the reduced diameter of the corpus spongiosum, which helps to maintain the urethea as a viable channel for the ejaculation was obviously no problem for the fertility, either - at least the scientist don't mention anything in this regard; unfortunately, they did not really test it, either, as the poor male Wistar rats that were abused in this experiment were bachelors against their will.
  In view of the fact that flaxseed ain't the best source of omega-3s, anyway, and there appears no other good reason (for men and women!) why you would eat them in large quantities (I am not talking about the occasional tablespoon of flaxseed, here), I would still suggest to stay away from it.

• 

  Image 4: In farm-raised salmon chronic TTA administration has been shown to improve cardiac function and immune activity; it does however also lead to cardiac growth during viral infections, so that the benefits of chronic administration are still by no means certain (Grammes. 2012a & 2012b); long-term human studies, on the other hand, are not yet available.

  Acute TTA administration soothes the flames and keeps the coronary vessel open You will unquestionably remember my previous posts about the fat burning fatty acid tetradecylthioacetic acid (TTA) and how it's ability to accumulate in various tissues of your body could potentially become problematic. In the short term however, it's anti-inflammatory effects can come very handy. So handy, in fact, that the a recently published study by Pettersen et al. would suggest that we are soon going to see TTA balloons being inserted into coronary vessel walls, in order to deliver the sulfur-containing fatty acid right to an obstructed vessel that's being operated on, in order to suppress the local expression of inflammatory cytokines, as well as the subsequent macrophage infiltration and the unwanted collagen formation, which would precipitate restenosis (=further clogging) of the very heart vessel that has only just been opened operatively.
  You may now rightly ask yourself what this has got to do with you? Well, if it works locally, it could work similarly systemically and other studies such as Bjørndal (2012) do confirm just that: 0.4% TTA reduce TNF-α, IL-1β, and IL-6 in an experimental model of colitis and render the rodents guts more of less bullet..., ah, pardon, dextran sulfate sodium (DSS; a chemical used to induce cholitis) proof. The long-term effects of the continous consumption of ~3g of TTA, which would be the human equavalent of those 0.4% TTA in the rodent diets is yet still not fully established (re-read: "TTA & Fish Oil" and "TTA & Fish Oil - Revisited").

• 

  Figure 3: Alcohol overrides the inhibitory control over food intake (Chapman. 2012)

  Of TV watching, sleep deprivation and alcohol consumption, booze has the most pronounced negative effect on reward saliency and inhibitory control of food intake! That's the conclusion Colin Daniel Chapman, Christian Benedict, Samantha Jane Brooks, and Helgi Birgir Schiöth mkae based on their latest meta-review of pertinent studies from pubmed (N=23). With an impact factor of 1.03 on a scale from -4 to 4, alcohol is by far the worst the greatest effect on food intake and shows the highest correlation with obesity (Chapman. 2012).
  Compared to booze, both sleep deprivation (50% less) and TV watching (20% less) appear almost harmless. Their contribution in the non-drinking part of the population may yet still not be underestimated, also because the urge to do the latter, i.e. watch TV, when you ought tho sleep, precipitates the former and subsequent derangements in the circadian rhythm (suggested read: "The SuppVersity Circadian Rhythm Series").
• IIFYM was yesterday, ROWFYM is today, but what's going to be tomorrow? If that's all Greek to you, let me first bring you in the loop on the acronyms. While IIFYM designates "If It Fits Your Macros", implies (in the most extreme case) that you give a sh*t about what you eat, as long as you hit your macronutrient ratios for the day ("Carbs? Gimme that pizza!") and is getting increasingly popular among those who are fed up with broccoli and chicken breast and either unwilling or unable to see that those are not the only, and I would say, by far not the most healthy foods you can eat, ROWFYM is my own invention, means "Regardless Of Whether It Fits Your Macros" and would probably end up for way too many trainees in a protocol similar to the one 12 of the 24 subjects in a recent study from the Linköping University in Sweden were following for 12 weeks (Hambre. 2012).

  

  Image 5: "WTF do you want, I am doing ROWIFYM, here! That's serious bulking, man. Scientifically validated." If you want to follow his example, go ahead... but 3 months really is the absolute max and only if you are still healthy - regardless of whether the blood markers return to normal in the course of your next diet.

  While those lucky (?) twelve healthy young men (aged 19–32 years) in what I will from now on call the "fast-food arm" of the study had to add a delicious (???) fast food menu (1350 kcal, 41 g protein) on top of their diets, the other twelve participants had to contend themselves with a blatant protein shake (33g of whey) as their bulking supplement of choice. The reasoning behind this at first sight unquestionably highly questionable experiment was that the Swedish scientists wanted to elucidate, whether it would really make a difference whether you are eating "clean" (=adding a whey protein shake) or simply stuffing yourself with the next best, allegedly protein-laden fast food you can find during a 3-months bulking cycle (at least three lifting sessions per week) and the results were, ... well, let's say surprising.
  As you would expect, subjects in both groups managed to gain some weight. The first surprise is that subjects in both groups gained identical amounts of weight, namely 3.6kg. That's not all, however. Even the lean mass increases 2.1kg did not differ between the groups (measure by DEXA scans) and the sophisticated (compared to a similar calories in vs. calories out calculation) measurement of the resting metabolic rate, the scientists had conducted yielded that both groups had compensated for the overeating by a statistically highly significant (p < 0.0001!) + 10% increase in resting metabolic rate!

  

  Figure 4: Kaplan-Meier plots indicating the percentage of patients that made it to time-point X (see horizontal axes) without adverse event after their first coronary event - patients w/ (thin line) vs. w/out (bold line) metabolic syndrome (top), patients with high (thin line) vs. low (bold line) ApoB leves (bottom; based on Corsetti. 2005); ApoB turns out to be a way better risk predictor than having metabolic syndrome

  Before you do now jump into your car and head for the next drive-in "restaurant" with a big yellow "M" in front of it, you may want to take into consideration that this extended ROWIFYM version of the IIFYM approach, where you may hit the protein but overshoot on the carbs and fats (and certainly not  the good ones), did lead to statistically significant increases in fasting insulin and ApoB, a building block of LDL that has been associated with increased risk of arterial plaque formation (Gebel. 2008), compared to the "clean bulk" (= whey only) group. And while those changes (as well as the increase in RMR) were reversed on the 12 months follow-up, I am not sure if especially those people, who are most fond of bulking approaches like that, i.e. men (and very rarely women) who have been following a junk food diet for way too long already, should take the results of this study as an incentive to do a 3-month fast food bulk during the winter. After all, it could be that one additional LDL molecule that nests in the already existent arterial plaque which will eventually break the camel's, no your neck - or for those who like it more explicitly, which won't let the next mini blood clot pass by and causes a stroke, which could, in the worst case, end deadly!

That's it as far as the official On Short Notice items go, for today. If you don't have enough yet, I suggest you take a glance at the 6-10 news-items I've piled up on the SuppVersity Facebook Wall for you to review. Maybe you've read that sleeping with wife and children in a room would decrease your testosterone levels? False! Maybe it decreases the intellectual capacity of the reporter who wrote the respective news-item you may have read, but what really happens, is an increase in the amplitude of the circadian pattern with higher morning and lower evening testosterone levels (click here to read more). And if you neither have or plan to have children or don't care about your or your significant other's testosterone levels, you may be interested in a study that debunks the use of a "slim belt" for weight loss purposes, the idiotic idea to counter BPA toxicity with soy, the way working out can make depressed old people happy again, and more... ah, I almost forgot, there will also be an exercise special of On Short Notice very soon - and I am not talking about next Saturday, here - so stay tuned, it could be published anytime (Tip: If you subscribe to the SuppVersity Facebook Page you won't miss it ;-)

 References:

• Auffret J, Viengchareun S, Carré N, Denis RG, Magnan C, Marie PY, Muscat A, Fève B, Lombès M, Binart N. Beige differentiation of adipose depots in mice lacking prolactin receptor protects against high-fat-diet-induced obesity. FASEB J. 2012 Sep;26(9):3728-37. 
• Bjørndal B, Grimstad T, Cacabelos D, Nylund K, Aasprong OG, Omdal R, Portero-Otin M, Pamplona R, Lied GA, Hausken T, Berge RK. Tetradecylthioacetic Acid Attenuates Inflammation and Has Antioxidative Potential During Experimental Colitis in Rats. Dig Dis Sci. 2012 Aug 2.
• Chapman CD, Benedict C, Brooks SJ, Birgir Schiöth H. Lifestyle determinants of the drive to eat: a meta-analysis. Am J Clin Nutr. 2012 Sep;96(3):492-7. Epub 2012 Jul 25.  
• Corsetti JP, Zareba W, Moss AJ, Sparks CE. Apolipoprotein B determines risk for recurrent coronary events in postinfarction patients with metabolic syndrome. Atherosclerosis. 2004 Dec;177(2):367-73.
• de França Cardozo LF, Boaventura GT, Brant LH, Pereira VA, Velarde LG, Chagas MA. Prolonged consumption of flaxseed flour increases the 17β-estradiol hormone without causing adverse effects on the histomorphology of Wistar rats' penis. Food Chem Toxicol. 2012 Aug 25.
• Dhiman TR, Anand GR, Satter LD, Pariza MW. Conjugated linoleic acid content of milk from cows fed different diets. J Dairy Sci. 1999 Oct;82(10):2146-56.
• Gebel E. Meet LDL's partner in plaque. ApoB puts the "bad" in bad cholesterol. Diabetes Forecast. 2008 May;61(5):39-40.
• Grammes F, Rørvik KA, Takle H. Tetradecylthioacetic acid modulates cardiac transcription in Atlantic salmon, Salmo salar L., suffering heart and skeletalmuscle inflammation. J Fish Dis. 2012a Feb;35(2):109-17. 
• Grammes F, Rørvik KA, Thomassen MS, Berge RK, Takle H. Genome wide response to dietary tetradecylthioacetic acid supplementation in the heart of Atlantic Salmon (Salmo salar L.). BMC Genomics. 2012n May 11;13(1):180.
• Hambre D, Vergara M, Lood Y, Bachrach-Lindström M, Lindström T, Nystrom FH. A randomized trial of protein supplementation compared with extra fast food on the effects of resistance training to increase metabolism. Scand J Clin Lab Invest. 2012 Aug 30.
• Jahreis G, Fritsche J, Möckel P, Schöne F, Möller U, Steinhart H. The potential anticarcinogenic conjugated linoleic acid, cis-9,trans-11 C18:2, in milk of different species: Cow, goat, ewe, sow, mare, woman. Nutrition Research. October 1999; 19:10. 1541–1549.
• McAfee AJ, McSorley EM, Cuskelly GJ, Fearon AM, Moss BW, Beattie JA, Wallace JM, Bonham MP, Strain JJ. Red meat from animals offered a grass diet increases plasma and platelet n-3 PUFA in healthy consumers. Br J Nutr. 2011 Jan;105(1):80-9.
• Murali N, Kumar-Phillips NS, Rath NC, Marcy J, Slavik MF. Effect of Marinating Chicken Meat with Lemon, Green Tea and Turmeric Against Foodborne Bacterial Pathogens.International Journal of Poultry Science. 2012; 11(5): 326-332.
• Pettersen RJ, Salem M, Rotevatn S, Kuiper KK, Larsen TH, Bohov P, Berge RK, Nordrehaug JE. Effects of local delivery of Tetradecylthioacetic acid within the injured coronary vessel wall. Scand Cardiovasc J. 2012 Aug 30.
• Reardon M, Gobern S, Martinez K, Shen W, Reid T, McIntosh M. Oleic Acid Attenuates trans-10,cis-12 Conjugated Linoleic Acid-Mediated Inflammatory Gene Expression in Human Adipocytes. Lipids. 2012 Sep 2.

Mono-Sodium Glutamate (MSG), NAFLD, Leptin Resistance, Trans-Fats, HFCS, Gluttony, Leaky Gut & Brain, the Vagus Nerve and the Chinese Restaurant Syndrome - Bon Appetit!

Image 1 (msg-exposed.com): Is obesity the inevitable, unnatural metabolic long-term equivalent of the dreaded "Chinese Restaurant Syndrome"?

Earlier today, I posted a blurb from a recently published epidemiological study on the effects of mono-sodium glutamate, aka MSG, an umami = all taste receptor activator that is commonly found in all sorts of ready made foods that would otherwise taste as lame as their individual fake ingredients, on the SuppVersity facebook wall (Insawang . 2012). The scientists had evaluated the data from 324 families (349 adult subjects, age 35–55 years) from a rural area of Thailand and found that the prevalence of metabolic syndrome was not just significantly higher in the tertile with the highest MSG intake, but that the "odds ratio", i.e. the chance that a certain parameter, in this case "obese, yes/no" would be found to be true, increased with every 1 g increase in total MSG intake irrespective of  the total energy intake and the level of physical activity.It took roughly 2 minutes for the first sharp-witted "SuppVersity student", in this case that was Wyatt Brown, to spot that post and ask what I believed could explain this observation.

Honestly, I had not really thought about that before, but simply assumed that the effects were probably mediated via not yet fully elucidated effects of dietary glutamate on the balance of excitatory and inhibitory neurotransmitters... after thinking about that for a moment I realized that in the absence of hyperphagia (i.e. extreme hunger and subsequently higher caloric intake), which was obviously not the case for the obese Thais with high MSG intakes, this explanation was not really satisfactory.

Does it all come back to food quality once again?

My next thought was that this could yet again be an issue of food quality vs. food quantity. After all, junk food and all sorts of foodstuff that's made with tons of food-additives to disguise their inferior, nutrient-poor and thus "tasteless" ingredients are the most likely candidates with respect to the MSG exposure in the Western and Eastern "developed" *rofl* world are concerned. In view of the fact that "diet quality" was (as so often) not among the variables Insawang et al. had assessed, their study did not allow for any conclusions in this respect, so that I had to dig deeper and came up with a couple of interesting findings,  I did not want to hold back from me (sorry, Stephen, for postponing the "HIIT Manual"-post, once again, but think about it like that, what's the use of working out if your MSG intake would quash your results anyway ;-)

• * See figure 2 for exact data on the average daily human intake of MSG - with 91mg MSG /kg body weight, an amount that would translate to a daily intake of ~500+mg MSG in humans, the mice in the Collison were representative of the average American, yet not the Thai, Japanese and Korean MSG intake; against that background it is  important to note that MSG ingestion alone did not result in microscopic fat deposits in the liver. These effects were exclusively observed upon co-ingestion of the MSG with a diet with ~9% TFA content!
  "MSG intake at doses similar to human average daily intake[*] caused hepatic microsteatosis and the expression of beta-oxidative genes." - in a 2009 study, Collison confirmed the negative effects of even moderate MSG intake on liver health in a rodent model; only the common combination of trans-fatty acids (TFA) + MSG that is one of the main characteristics of modern "convenience" foods, did yet induce statistically significant increases in liver weight and hepatic triglyceride content; the increases in total, but also HDL cholesterol due to MSG + TFA were accompanied by profound increases in circulating leptin levels, probably in response to developing leptin resistance and increased storage of lipids in the white adipose tissue stores of the nine-week old C57BL/6J mice (Collison. 2009); in a follow up study Collison et al. confirmed that the double-whammy of trans-fatty acids + MSG becomes even more toxic if a third villain is added to the mixture, high fructose corn syrup (Collison. 2011) - and I don't have to tell you where in the human food chain you will find this unholy trinity, do I?
• "MSG ingestion reduces weight gain, body fat mass, and plasma leptin levels" - in a 2008 trial Kondoh and Torii observed a very different and in fact surprisingly pronounced beneficial effect of the ingestion of a 1% solution (in biology this means 1g per 100ml) MSG resulted in decreases in weight gain, body fat mass and plasma leptin levels in male Sprague-Dawley rats irrespective of the energy content of their diets (!) and without effecting total energy intake or food intake, but in the presence of a profound decrease in 24h-water intake (2g vs. 9g); these effects were observed in both adult and young animals, in the latter without any negative side effects on the normal development of body length

  

  Figure 1: Leptin levels (ng/ml) on diets with different energy density and macronturient composition with or without MSG added to the water (data based on Kondoh. 2008)

  this leaves more than enough room to speculate about centrally mediated increases in energy expenditure in response to the ~20mg total MSG (equivalent to 33mg/kg for a rodent and a human equivalent dose of ~5.5mg/kg) intake of which Kondoh and Torii speculate that they may be "mediated via gut [glutamate] receptors functionally linked to the afferent branches of the vagus." (Kondoh. 2008); subsequent studies into the effects of MSG on the "gut brain axis" appear to support this hypothesis (cf. Kondoh. 2009a,b; Otsubo. 2011)
• " MSG, in spite of mild hypophagia [reduced food intake], caused severe increase in fat body weight ratio, via leptin resistance" - in 2011 Afifi and Abbas, two researchers from the Department of Biochemistry at the Zagazig University in Egypt, report that feeding high amounts of MSG to pregnant rat dams had similar negative effects on body composition and leptin sensitivity as a hypercaloric diet and that despite an overall reduction in total food intake; moreover, despite similar gains in body fat, the negative effects on the offspring of those pregnant rats was more pronounced than in the rats on the "normal" hypercaloric diet (Afifi. 2011)
• If you suffer from "Chinese Restaurant Syndrome", you should check whether increased gastrointestinal permeability could be the root cause of your problems and avoid all foods with any of the following "ingredients": E620 Glutamic acid, E621 Mono-sodium glutamate, E622 Mono-potassium glutamate, E623 Calcium diglutamate, E624 Mono-ammonium glutamate, E625 Magnesium diglutamate!
  "Findings from the literature indicate that there is no consistent evidence to suggest that individuals may be uniquely sensitive to MSG" - in one of the few reviews evaluating exclusively human studies, Freeman did not find any placebo controlled research that would confirm the universal existence of side-effects (e.g. headaches, chest pain, flushing, numbness or burning in or around the mouth, sense of facial pressure or swelling and sweating) as a direct consequence of the consumption of food-borne mono-sodium glutamate; e.g.
  

  "The present study led to the conclusion that 'Chinese Restaurant Syndrome' is an anecdote applied to a variety of postprandial illnesses; rigorous and realistic scientific evidence linking the syndrome to MSG could not be found." (Tarasov. 1993)

  instead, the author suggests that "unique sensitivities" could explain the documented case reports (Freeman. 2008 // see also Walker. 2000; Geha. 2000); given the emerging evidence of the existence of something you could call a "leaky brain" (in analogy to "leaky gut"), it appears likely that an unnaturally increased permeability of the blood-brain-barrier and subsequent penetration of large amounts of glutamate into the brain even at lower serum concentrations could well explain those differences (although not directly related to MSG, I would still like to point you to the results of a recently released study, which found a profound decrease in the permeability of the BBB in response to an oral 1mg/kg (HED ~0.16mg/kg) Lycium barbarum extract in an experimental stroke model; Yang. 2012)
• "dietary antioxidants have protective potential against oxidative stress induced by MSG" - in 2006 Faromby and Onyema observed that previously described oxidative damage to the liver and subsequent steatosis (lipid accumulation) in response to the intra-peritoneal administration of ridiculously high amounts of MSG (4g/kg body weight) could be ameliorated by vitamin C + vitamin E + quercitin; these results suggest that exorbitantly high doses of MSG (human equivalent ~51g/day) are probably a result of an increase in reactive oxygen species
• "after intragastric administration of MSG, the MSG is preferentially metabolized through gluconeogenesis in B6 mice, whereas thermogenesis is the predominant process for 129 mice" - in previous studies scientists had observed profound differences in terms of the effects of MSG on food intake and preference; in 2009 Bachmanov et al. traced those differences back to genetic polymorphisms and respective differences in the metabolic response to / utilization of MSG - if we assume that similar differences exist in human beings, those would provide another explanation for the different incarnations of the "Chinese Restaurant Syndrome" with the classic headaches, high blood pressure and sweating in people who would be long to the human equivalent of the 129 mice and the highly rewarding and appetite stimulating gluconeogenic (hepatic production of glucose from the glutamate) effects in those humans with a similar genetic programming as the B6 mice

I could certainly go on for hours, citing study after study with "evidence" and "counter-evidence", or rather what the respective authors consider as such, but I believe that you have read enough to see a couple of basic patterns emerge, here.

So what about those differences? Genes, dosages, or what?

One of these patterns is also brought up by Kondoha and Torii in the discussion of the results of their study (remember: decrease in body fat and increase in energy expenditure; purported mechanism = activation of glutamate receptors that are linked to the vagus nerve), in which the researchers state that they believe that the diametrically opposed results of their, compared to other studies (most of which report an increase not a decrease in body fat that is accompanied by increases in circulating leptin and decreases in leptin sensitivity and not vice versa as in the Kondoh study), may well be explained by

[previous] studies [being] designed specifically to produce toxic effects in the brain (where GLU is an excitatory neurotransmitter), through the administration of extremely high doses (2000 mg/kg or more, administered repeatedly) to infant animals, either by single, direct injection or intubation (Kondoh. 2008).

Those high dosages could in fact have lead to blood glutamate concentrations that would allow the flux of the excitatory amino acid even across intact blood-brain-barriers. The more realistic, orally administered dosages  Kondoh and Torii used in their experiment, on the other hand, did not induce any (not even statistically non-significant) elevations of serum glutamate levels.

Hence, the effects seen in the present study, as discussed above, are probably linked via a physiologic mechanism, to a local action of GLU in the gut, rather than via a pharmacologic/toxicologic mechanism to a distant action of exogenous GLU forced on the brain (Kondoh. 2008).

If you review the brief rundown of the literature I've provided in the previous paragraphs you will have to acknowledge the validity of this remark (remember: the steatosis in the Collison study required co-administration of trans-fatty acids /TFA/ and even then the increase solely due to MSG was marginal compared to that of the TFAs, alone).

Without a leaky gut, you would probably have to eat pure MSG all day to do harm

If you also take into account, that in healthy individuals only <5% of the dietary glutamate are actually absorbed into systemic circulation, while the rest is used as an oxidative substrate by the intestinal mucosa (Smriga. 2007), the difference between thhe orally consumed 33mg/kg MSG that helped the rodents in the study by Kondoh and Torii to lean out and the intraperitoneally injected 4,000mg/kg that were necessary to induce the touted hepatic side effects in the study by Faromby and Onyema are way above the average intake even the worst offenders among the MSG abusers are exposed to (cf. figure 2):

Figure 1: Average per capita daily MSG intake in different countries (adapted from Löliger. 2000)

Even if we discard the oxidative loss within the intestine, those 4,000mg/kg for a rodent (in previous studies Onyema et al. had even used 6,000mg/kg to elicit the hepatic damage; Onyema. 2006) would translate to ~650mg/kg in humans and would mean that you would have to shovel down anywhere between 32g and 64g of pure MSG (depending on whether you weigh 50 or 100kg), i.e. 20-40x more than the average daily intake of a Korean (note: The "rodent model of MSG induced obesity" is induced by injection of 10,000mg/kg body weight; cf. Bunyan. 1976) and the whopping MSG equivalent of 400-800ml of soy sauce (avg. MSG content 80mg/ml), which is probably the worst offender in the E-number-laden ingredient arsenal of the Asian cuisine.

Figure 3: Protein-bound and free glutamate content of "high" glutamate foods (left) and total glutamate content of selected plant proteins (right; data adapted from Loliger. 2000)

Your best bet to ingest similar amounts of free glutamate from real foods is, as the data from a review by Loliger suggests (cf. figure 3), would be parmesan cheeese, but in all honesty, in view of the fact that you would have to consume 2.6kg of the Italian delicacy, it is pretty unlikely that the glutamate and not the sheer amount of pure energy in the cheese would be the underlying reason for subsequent weight gain. Against that background it should not be surprising that negative side-effects as they occur as a result of high to unrealistically high MSG intakes and or in especially susceptible individuals, are not exactly common in people who don't eat out and/or consume pre-packaged convenient foods on a regular, if not daily basis.

Too much of a vitally important thing at the wrong time and as part of the wrong foods...

The mere presence of non-negligible amounts of glutamate in all sorts of "real" foods, should yet remind you that glutamate is not a toxin, or a "foreign substance" we are not evolutionary adapted to, but an amino acid that is of utmost importance for the health of your central nervous system (Platt. 2005). So that at the end of this analysis we may not be back at square one, but still have to concede that it brought us back to a set of very common motifs here at the SuppVersity:

• When consumed in excess, substances that are good, healthy, beneficial and even "vitally" (=vitamin ;-) important can easily turn against you
• When substances do not have to pass the gut, the dose-response relationship can differ so substantially that results that are acquired using route A (e.g. intraperitoneal injection) cannot simply be transfered to scenarios employing different administration routes (e.g. oral ingestion)
• Inter-individual/-species differences and differences between healthy and unhealthy individuals / animals, warrant utmost caution, when it comes to interpreting data - the "Chinese Restaurant Syndrome", for example, could be a result of increased gut and blood-brain-barrier permeability that would lead to an increased absorption of glutamate from the intestine into the blood and from there across the blood-brain-barrier right into the brain.
• Oftentimes, differences due to the aforementioned factors are not of simple quantitative, but of qualitative nature, in the case of MSG this would be the difference between the metabolic activation in response to the local activation of glutamate receptors in the gut that are connected to the vagus nerve, on the one hand, and the systemic / central obesogenic (fattening) effects of glutamate that leaks from the gut into the blood and from there into the brain.

And lastly, to eventually come full circle and remind you of the results of Collison et al., we cannot ignore that MSG is one of those substances that is usually found in foods with a whole host of other nutrient-poor ingredients, anti-nutrients and proven obesogenic, pro-inflammatory and otherwise unhealthy substances and food additives. They are wrapped in plastics have an extended shelf life due to tons of preservatives and highly adorned with stickers and labels saying "low this", "extra that", "only X amounts of calories", etc. - as long as you avoid those foods on 360+ days of the year, prepare your meals from whole foods, don't dine at cheap restaurants, fast-food outlets and snack bars too often or try to find the "optimal amount of supplemental MSG to stimulate your vagus nerve and help you shed fat" *lol*, you can calmly watch the ever-recurring MSG scares on the Internet and other mass media ;-)

References:

1. Afifi MM, Abbas AM. Monosodium glutamate versus diet induced obesity in pregnant rats and their offspring. Acta Physiol Hung. 2011 Jun;98(2):177-88.
2. Bachmanov AA, Inoue M, Ji H, Murata Y, Tordoff MG, Beauchamp GK. Glutamate taste and appetite in laboratory mice: physiologic and genetic analyses. Am J Clin Nutr. 2009 Sep;90(3):756S-763S. Epub 2009 Jul 1.
3. Bachmanov AA, Inoue M, Ji H, Murata Y, Tordoff MG, Beauchamp GK. Glutamate taste and appetite in laboratory mice: physiologic and genetic analyses. Am J Clin Nutr. 2009 Sep;90(3):756S-763S. Epub 2009 Jul 1.  
4. Bunyan J, Murrell EA, Shah PP. The induction of obesity in rodents by means of monosodium glutamate. Br J Nutr. 1976 Jan;35(1):25-39.
5. Collison KS, Maqbool Z, Saleh SM, Inglis A, Makhoul NJ, Bakheet R, Al-Johi M, Al-Rabiah R, Zaidi MZ, Al-Mohanna FA. Effect of dietary monosodium glutamate on trans fat-induced nonalcoholic fatty liver disease. J Lipid Res. 2009 Aug;50(8):1521-37. Epub 2008 Nov 11.  
6. Collison KS, Zaidi MZ, Saleh SM, Makhoul NJ, Inglis A, Burrows J, Araujo JA, Al-Mohanna FA. Nutrigenomics of hepatic steatosis in a feline model: effect of monosodium glutamate, fructose, and Trans-fat feeding. Genes Nutr. 2012 Apr;7(2):265-80. Epub 2011 Dec 6. 
7. Farombi EO, Onyema OO. Monosodium glutamate-induced oxidative damage and genotoxicity in the rat: modulatory role of vitamin C, vitamin E and quercetin. Hum Exp Toxicol. 2006 May;25(5):251-9.
8. Freeman M. Reconsidering the effects of monosodium glutamate: a literature review. J Am Acad Nurse Pract. 2006 Oct;18(10):482-6.nonalcoholic fatty liver disease. J Lipid Res. 2009 Aug;50(8):1521-37. Epub 2008 Nov 11.
9. Geha RS, Beiser A, Ren C, Patterson R, Greenberger PA, Grammer LC, Ditto AM, Harris KE, Shaughnessy MA, Yarnold PR, Corren J, Saxon A. Review of alleged reaction to monosodium glutamate and outcome of a multicenter double-blind placebo-controlled study. J Nutr. 2000 Apr;130(4S Suppl):1058S-62S.
10. Hermanussen M, García AP, Sunder M, Voigt M, Salazar V, Tresguerres JA. Obesity, voracity, and short stature: the impact of glutamate on the regulation of appetite. Eur J Clin Nutr. 2006 Jan;60(1):25-31. 
11. Insawang T, Selmi C, CHa'on U et al. Monosodium glutamate (MSG) intake is associated with the prevalence of metabolic syndrome in a rural Thai population. Nutrition & Metabolism 2012, 9:50 doi:10.1186/1743-7075-9-50
12. Iwase M, Ichikawa K, Tashiro K, Iino K, Shinohara N, Ibayashi S, Yoshinari M, Fujishima M. Effects of monosodium glutamate-induced obesity in spontaneously hypertensive rats vs. Wistar Kyoto rats: serum leptin and blood flow to brown adipose tissue. Hypertens Res. 2000 Sep;23(5):503-10.
13. Kondoh T, Torii K. MSG intake suppresses weight gain, fat deposition, and plasma leptin levels in male Sprague-Dawley rats. Physiol Behav. 2008 Sep 3;95(1-2):135-44. 
14. Kondoh T, Tsurugizawa T, Torii K. Brain functional changes in rats administered with monosodium L-glutamate in the stomach. Ann N Y Acad Sci. 2009a Jul;1170:77-81.
15. Kondoh T, Mallick HN, Torii K. Activation of the gut-brain axis by dietary glutamate and physiologic significance in energy homeostasis. Am J Clin Nutr. 2009b Sep;90(3):832S-837S.
16. Loliger J. Function and importance of glutamate for savory foods. J Nutr. 2000 Apr;130(4S Suppl):915S-20S. 
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Is it Your Neighbor(hood)'s Fault That You are an Obese Couch Potato? Plus: Higher Incomes Increase Obesity Risk in Men, Better Education Decreases Risk in Men & Women

Image 1: If this photo looks as if it was taken in your neighborhood, statistics say that you will have a harder time than others warding off obesity.

If you have not already been aware that the major weightloss obstacles are not so much of physio- than of psychological, or I should say behavioral natural, Monday's blogpost on the inability or unwillingness of the majority of the study participants in the Krebs study should have reminded you that there is more to losing weight than having an "optimal" diet plan. In this context, the results of a recently published paper from the University of Ottawa, Canada (Prince. 2012), comes to mind, in which Stepanie A. Prince and her colleagues report the results of a large-scale cross-sectional multi-level analysis of the association between neighborhoods, physical activity and obesity in Ottawa.

Mislead and misfed, but by no means unable to afford leading a healthier life-style

Although obviously of epidemiological nature, the study is remarkable in that it relies on relatively recent data (2006-2008) from 494,000 residents from 86 neighborhoods in Ottawa, who were part of the Ottawa Neighborhood Study (ONS). My usual advice not to confuse correlation (no matter how "significant") and causation, does yet still apply. A statement like "for each additional km² of park area per 1,000 inhabitants, the odds of being physically active increased by 17% in the female inhabitants of the respective neighborhood" (cf. figure 1, left; respective value: 1.17) does thusly signify that readily available parks areas seem to encourage women to be more physically active in their leisure time. It does not mean that moving to an apartment from which you can see the joggers doing their rounds in Central Park will turn a couch potato into a sporting ace. After all, it is at least as likely that people who like to jog try to make sure that they move to an area, where they can easily pursue their hobby.

Figure 1: Model predictions for the influence of environmental, social and contextual parameters on physical activity (left) and overweight/obesity rate (right) in men and women; * p < 0.05 (data based on Prince. 2012)

Against that background, I decided to include only factors which showed a statistically significant association with either obesity or physical activity in at least one of the two sexes in the data in figure 1. Now, you rarely have a rule without exception, and in this case, I also included the associative strength with the so-called census-based socio-economic status (SES) index, because the non-existent influence of social status on obesity rates goes just about as nicely against the notion that you cannot eat healthy if you are on a budget, as the +39% increased obesity risk of men in households with incomes >30,000$ (cf. figure 2)

Figure 2: Model predictions for the influence of the individual parameters household income and education overweight/obesity rate in men and women; * p < 0.05 (data based on Prince. 2012)

Moreover, the strong negative association -44% for men and -45% for women between having at least a college degree and being overweight/obese, would would support the argument that it is less about not being able to afford a "healthy lifestyle" than about not having learned / not being able to teach oneself to do so... or, if you will, being more susceptible to the misleading information from the food industry and less aware of the pitfalls of shopping in convenience stores (+17% increased risk of obesity in women per additional convenience store for 1,000 inhabitants) and eating at fast food outlets.

Note: Neither the age nor parameters, such as the number of indoor or outdoor recreational facilities, grocery stores, specialty stores and (normal) restaurants which, at least taken in isolation, had no statistically significant influence on either physical activity or obesity rates.

With respect to the +22% and +39% increased obesity risk per additional fast-food outlet (per 1,000 inhabitants), it should also be mentioned that this is only one out of several of the environmental factors, which had statistically significant influence only on obesity rates in women from the respective neighborhoods - a phenomenon, which could yet be a consequence of the fact that men are less likely to be in their respective neighborhood during working hours than women, so that the susceptibility to fast food stores is probably not gender-specific ;-)

The bitter or delighting truth about your neighbor(-hood ;-)

It is nevertheless quite remarkable that the associative strength of individual criteria such as age, income, education etc. showed an overall much more pronounced variation (0.98, p<0.05), than one of the area-specific variables, the variance of which did not reach statistical significance for either of the two study outcomes, i.e. physical activity level or overweight/obesity (cf. figure 1). This would suggest that environmental influences in the area we live in is in fact a more reliable indicator of our likelihood of ending up as an overweight couch potato or lean physical culturist than our incomes, education or say our age. A finding, which I would say is actually quite remarkable, don't you think so?