Aspartame's Anti-Insulinogenic Effects During a Workout; Optimal Protein Intake on a Diet is Relative. Plus: Folate Fortification, Spirulia, Succinate, Sucrose, Pork Brain & the Low Cholesterol-Suicide Connection Reviewed!

Unbelievable: The results of the latest study from the University of Western Sidney appear to suggest that you could keep your insulin levels at bay, if you mixed your sugary intra-workout supplement with aspartame-laden diet coke instead of water! The mechanism that's behind this phenomenon does yet still have to be elucidated.

You may be surprised to see a long headline, a long post and a couple of bullet points: "Looks like On Short Notice, reads like On Short Notice, but is not published on Saturday? What's that?" The answer to this question is easy. Lot's of interesting stuff I have come across as of late! And while some of them, like the study on the marginal utility of higher protein intakes on a diet would actually deserve their own post, I decided to give you the "long(er) version of a short notice" in order not to miss any of them... and yes, this means there is going to be more than today's news on the unexpected anti-insulinogenic effects of aspartame, the only partly expected outcomes of the US folic acid fortification program, the aforementioned protein study, the usefulness of spirulina, succinate and sucrose supplements for athletes and physical culturists and some brainy insights into a possible connection between low cholesterol, depression and suicide risk in men and women... ah, ok I see, you are already reading the aspartame item - well, go for it!

• The astonishing anti-insulin effects of intra-workout aspartame consumption Meanwhile even bodybuilders who are injecting and "supplementing" with all sorts of unquestionably unhealthy stuff are so afraid of the hitherto still rather vaguely established pro-carcinogenic effects of aspartame that supplement companies place huge stickers on the boxes of their products saying "ASPARTAME FREE!" Now, I am pretty sure that a recently published study that was conducted by scientists from the School of Science and Health at the University of Western Sydney in Campbelltown, Australia (Siegler. 2013), won't do much about that, but you will probably have to agree that it is still remarkable, to say the least, that the co-administration of an artificial sweetener which has not produced any glucose, insulin or whatever response in previous trials (cf. "Sweeter than your tongue allows") would do that!?

  

  Figure 1: While the mechanism is still unknown and the results need to be repeated in a second experiment, there is no question that the drop in insulin during the workout (see arrow(s)) which occurred during the carbohydrate + aspartame trial in the presence of identical glucose ingestion and blood glucose levels warrants further investigations (based on Siegler. 2013)

  During the four trials, which were separated by 7-10 days of rest, the 9 healthy, recreationally active males (age: 22±2 years; height: 180±9 cm; weight: 78.6±8.5 kg; participating in regular physical exercise at least twice per week) who had volunteered for this (in the eyes of some aspartame extremists, probably unethical undertaking ;-) cycled fasted for 60 minutes in a climate controlled laboratory. The only difference between the four sessions was the "intra-workout nutrition" the participants were fed, with...
  

  1. carbohydrate - 2% maltodextrin and 5% sucrose (figure 1, C),
  2. carbs + aspartame - 0.04% aspartame with 2% maltodextrin and 5% sucrose (figure 1, CA),
  3. water - plain water, only (figure 1, W), and
  4. aspartame + malto - 0.04% aspartame with 2% maltodextrin (figure 1, A)

  As it is common practice in studies like this, "all participants were instructed to follow the same diet and training schedule for the three days prior to each experimental trial." (Siegler. 2013, my emphasis)
  The respective intra-workout beverages were to be consumed in boluses of 4ml/kg body weight before and at 15-minute intervals throughout the trial. For the CHO groups this summed up to a total carbohydrate intake of 104.4±11.3g per participant and did - probably not to your surprise - cause a corresponding increase in insulin levels... with one exception, however: the intraworkout period in the CHO + Aspartame group (figure 1, red), when the insulin level dropped, during the exercise sessions and bumped back up to the same level as in the carbs only control afterwards (see figure 1).
  As the researchers point out, we do not yet have a mechanistic explanation for this phenomenon... nor can we even be sure that this was not some sort of strange artifact, so that
  

  "the disparity between insulin levels [does not only] warrant further investigation with a larger cohort of clinically relevant subject populations (e.g. metabolic syndrome, diabetes, etc.) [, but must also] be considered when designing nutrition-based, exercise intervention studies [in the future]" (Siegler. 2013

  That this observation could actually have very practical implications, both, in view of its potentially compromising effects on blood glucose levels in diabetics, where any insulin blocking effect of aspartame would probably reduce the already compromised glucose uptake even more, as well as in view of the anti-lipolytic (=blocks the release of fat from the cells) of insulin during a workout, which could actually be blocked with a minuscule amount of aspartame ... but alas, until the results have been confirmed and the mechanism behind this effect has been elucidated, what we are doing here is more or less intellectual masturbation - nothing to feel bad about, but still not the real deal ;-)

• 

  Figure 2: This is what the USDA expected to happen - more folic acid in food = higher intake (here in the elderly) = lower homocysteine levels; the reality looked pretty different, though, at least in adolescents the folic acid intake went up, but the homocysteine levels did not go down; moreover the B12 levels have declined as well... how much of this is related to confounding factors still has to be elucidated, but as of now it does not seem as if the fortification program was the success the USDA wanted it to be (Mc Bride. 2007).

  US adolescents and their "healthy grains" are now folic acid fortified, but are they also healthier? According to a study that has just been published in the Journal of Public Health, the great idea to put another artificial vitamin into our the food chain and fortify "healthy" cereal-grain products with folic acid, was so "successful" that the average US teen (14y at the time the fortification program began, 18y now) does now have 16% higher folate and 14% higher B6 concentrations.
  Instead of the expected decrease in homocysteine levels, of which scientists still believe that it plays in imminently important role in the development of heart disease, its serum levels did likewise increase by 17%, while the serum concentrations of vitamin B₁₂ decreased by 11 % post-fortification. The additional ~118 μg folate/d the subjects ingested from the fortified food products, appeared to be particularly useless (or even detrimental?) for boys / young men whose total homocysteine (tHcy) levels increased by 24%  to a much greater extent than in the girls / young women.
  Honestly, I don't really know what to make of these results at the moment, ... at least nothing better than to shake my head over the hilariousness of trying to turn junk(-food) into (good) food by simply enriching it with artificial vitamins. On the other hand, I am happy that even Daniel A. Enquobahrie and his colleagues feel that it is "warranted to investigate the significance of these improvements in folate status on clinical outcomes, in the post-fortification era." (Enquobahrie. 2013) - and that not just because the fortification program did not produce the desired results, but also because the folic acid intake already started to exceed the RDA in many of the subjects. This, and the alarming decrease in B12 levels of which Katherine L. Tucker had cautioned in the 2007 interview with Judy Mc Bride, already, that "better diagnosis for B12 deficiency should be given high priority"(Mc Bride. 2007) do not "warrant", imho, they rather make it imperative to follow the effect of this "nationwide health program" very closely.

• 

  Figure 3: The principle of relativity for protein based body recompositioning diets - When it comes to weight los, the word "high" in high protein diets must always be seen in the context of habitual protein intake and to whom we are comparing our dieters; or put simply: The average SAD dieter benefits from every gram, the average bodybuilder will hardly benefit from the 7th whey shake.

  Effectiveness of high(er) protein diets for weight loss depends on spread / change vs. baseline not on total protein intake That's basically how you could summarize the conclusion of the latest review of the existing data on the influnece of (high) protein intakes on changes in body composition by John D. Bosse and his colleagues from the University of Utah. To find out whether either the protein change (=high protein diets are only effective when the change in protein intake from baseline to intervention is large enough) or the protein spread theory (=those dieters within a cohort with the highest protein intake will see the most beneficial changes in body comosition) could explain the different outcomes of previous studies best, the researches collected an impressive dataset comprising 51 peer-review studies the analysis of which yielded the following two main results (Bosse. 2013):
  1. The 35 successful dietary interventions had on average 58.4% higher average protein intakes than those trials in which the authors had not been able to observe an additional beneficial of going high protein over the standard calorical restriction approach
  2. The 17 successful (=greater anthropomorphic changes than with calorie restriction alone) of the 25 studies, where the baseline protein intake of the subjects was available, the increase in protein intake was 28.6% (if you ate 100g protein per day before, that would mean you would eat 128.6g while you are dieting), minimal increases in 4.7% range, on the other hand, did not provide any additional benefit over energy reduction, alone.
  Overall, the review does therefore support the original hypothesis of the researchers that there are certain thresholds which have to be surpassed before dieters will see any benefits from an increase in protein intake. This does yet also mean, that for someone who is already eating 200g of protein on a daily basis, the addition of a protein shake with 20g of protein is probably not going to make so much of a difference as it would be way below the 28.6% change in protein intake, the protein change theory would prescribe (see [2] in the list above). As a matter of fact going higher and higher (e.g. like eating 300g of protein per day), will, if anything stall, not propel your progress, after all, there will be too little room for other nutrients, when you are already getting the lions share of your daily energy intake from protein... and NO you cannot lose weight without being in a caloric deficit, even if that is not readily calculable by the idiotic "calories-in-vs-calories-out" equation.
• The BMJ Supplement Review says: Thumbs up for sucrose, thumbs down for succinate and undecided  for spirulina In installment #36 of the A-Z of Nutritional Supplement Supplements, a series dedicated to review the pros and cons of purported ergogenic aids, the authors conclude that ...

  

  Figure 4: In view of the fact that the TCA or citric acid cycle is one of the #1 aerobic source of cellular energy (APT) and succinate is one of its intermediates it makes sense that supplementation could improve exercise performance, but hitherto this has not been confirmed.

  • ...the studies on spirulina fail to "study well-trained individuals", to use appropriate standardization regimen with relevance for physical culturists and athletes, identify the active ingredients and their effect on the antioxidant status, of which the respective scientists speculate that it would be the underlying mechanism of the observed ergogenic effects on chronic low-intensity exercise regimen
  • ...the research on succinate (only) supplementation is basically non-existent and claims with respect to its permanence enhancing effects is mostly based on theoretical considerations about its role in the TCA cycle 
  • ...despite the general trend within our society, where the overconsumption of sucrose (table sugar) is one of the major offenders to public health, "there may be value in, or at least room for, its inclusion in sports products targeting the provision of carbohydrate fuel during exercise"
  Nothing exciting, but a realistic and educative analysis, which has all the classic elements you should keep in mind, whenever you try to find out whether a product is worth its money: What research is there? What are the results? Are the positive results significant for me as a person? And... in the case of succrose: Could the use of this ergogenic aid be an obstacle for another goal of mine? I mean, you can benefit from guzzling tons of sugary drinks during your workouts, but if "looking good naked" is your primary goal and your performance only a means to an end - it is probably not wise to do so ;-)

• 

  Figure 5: Suicide risk in psychiatric patients /w (SA) or w/out (PS) prev. suicide attempt and surgical control (SC) in lowest, 2nd and 3rd cmp. to highest quartiles (Olié. 2011)

  Can pork brain in milk tell us something about suicide? Those of you who are on the SuppVersity Facebook news RSS channel will already know the image on the right. I only saw it today, but as Mark mentioned on my Facebook wall, he has used it (the image not the brain) in lectures before... be that as it may, that reminded me of an older study on the highly significant correlation between cholesterol levels and suicide attempts Emilie Olié and her colleagues observed in a 2010 study on the reliability of serum cholesterol levels as a predictor of the suicide risk in 3207 subjects [510 patients with a history of suicidal attempts (SA), 275 patients with no history of suicidal attempts (PC), and 2422 surgical controls (SC); Olié. 2011].
  The exact mechanism for the highly significant increase in suicide risk, esp. among women with previous suicide attempts in the lowest (1st quartile) is still not fully elucidated, Olié et al reference previous studies which suggest that low serum cholesterol levels, a "potentialmarker of central nervous systemcholesterol", impair the serotoninergic activity and" increase impulsivity" and thus precipitate to severe depression and the tendency and ability to pot a premature end to your life.
  In view of the fact that this and similar results were derived exclusively from analysis of psychiatric patients and considering that the cholesterol levels in the SA group were already significantly lower that in the PC and SC control (178±36 mg/dL vs. 217±43 mg/dL and 219±52 mg/dL, respectively) we should be very wary of transferring these results 1:1 to the "normal" people. 

I guess this is enough for today. After all, news are not so different than protein, it's the relative intake that makes all the difference - in other words: If I keep flooding you with those awesome posts, you won't appreciate each and every of them the same way you do now... and we don't want that to happen, do we? 

References:

• Bosse JD, Dixon BM. Dietary protein in weight management: a review proposing protein spread and change theories. Nutr Metab (Lond). 2013 Sep 12;9(1):81.
• Enquobahrie DA, Feldman HA, Hoelscher DH, Steffen LM, Webber LS, Zive MM, Rimm EB, Stampfer MJ, Osganian SK. Serum homocysteine and folate concentrations among a US cohort of adolescents before and after folic acid fortification. Public Health Nutrition. 2013; 15: 1818-1826.
• Mc Bride. Foods To Be Fortified With Folic Acid. USDA ARS. News. February 7, 2007. < http://www.ars.usda.gov/is/ar/archive/jun97/folate0697.htm > retrieved on September 14, 2013.
• Olié E, Picot MC, Guillaume S, Abbar M, Courtet P. Measurement of total serum cholesterol in the evaluation of suicidal risk. J Affect Disord. 2011 Sep;133(1-2):234-8.
• Siegler J, Howell K, Vince R, Bray J, Towlson C, Peart D, Mellor D, Atkin S. Aspartame in conjunction with carbohydrate reduces insulin levels during endurance exercise. J Int Soc Sports Nutr. 2013 Aug 1;9(1):36.
• Zemski AJ, Quinlivan RM, Gibala M, Burke LM, Stear SJ, Castell LM. A-Z of nutritional supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance: Part 36. Br J Sports Med. 2013 Sep;46(12):893-4. 

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 . 2013). 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. 2013)
• "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. 2013 Apr;7(2):265-80. Epub 2011 Dec 6. 
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