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Saturday, November 15, 2014

The Truth About Monosodium Glutamate (MSG) - Part 1

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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
  1. "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?
  2. "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 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)
  3. "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)
  4. "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)
  5. "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.
  6. "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.
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COMPLETE LINKS FOR THIS ARTICLE:
  1. The Truth About Monosodium Glutamate (MSG) - Part 1
  2. The Truth About Monosodium Glutamate (MSG) - Part 2
  3. The Truth About Monosodium Glutamate (MSG) - Part 3

SOURCE: http://suppversity.blogspot.com/2012/06/fat-thais-monosodium-glutamate-msg.html

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