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MSG and ObesityStudies are regularly showing the likely link between the almost ubiquitous use of MSG and obesity levels. It's undeniable that obesity has grown as a major problem in western developed countries throughout the same period that has seen a proliferation of convenience foods, fast foods, snack foods and the widespread use of the flavor enhancer Monosodiumglutamate, commonly referred to as MSG. Naturally this may just be coincidence and there may well be (indeed are most likely) a number of factors that have influenced the rise in obesity levels in countries such as the US, UK, Australia and in fact most of the more affluent nations... The fact is that MSG provides what is called the 5th-taste, umami, which is a sort of 'lip smacking' flavor that almost all of us will recognize, yet probably don't think of as being attributable to a flavoring chemical. MSG is undoubtedly exploited because that umami flovor has the kind of tongue-stimulating effect that leads you to desire -- "ooh, just one more" -- be that crisps, extruded snacks, portions of food of almost every kind (almost ALL processed foods contain this enhancer). The manufacturers of MSG are 'keen' to sell the 'benefit ' of this effect and have produced research to show that such factorings encourage elderly people to 'consume large amounts of food' -- which may be beneficial when appetite becomes impaired and nutritional profile suffers. What is less 'played up' is that this flavor component is so widely used that encourages all age groups to eat more -- it's a great ploy as it means that that tube of 'crisps' just MUST be finished in one sitting, those packs of snack food MUST be consumed every day; that packet of 'whatever' never seems to last more than a day or two... and that 'recommended' portion size is NEVER enough! So beware of this 'addictive' flavor that encourages additional food consumption. It doesn't take a scientist to work out that if you are encouraged to eat more you'll 'pile on the pounds'... Even so, science is revealing (see below) that MSG and obesity might be only one of the worries reltaed to the widespread use, and consumption, of this questionable chemical... AND BY THE WAY: If you're asking how to avoid MSG when it seems to be in almost everthing! Well the answer is actually simple! GO BACK TO eating freshly prepared food and 'ban' all processed foods from your diet! It takes a little trouble but the health benefits are more than worth it... Healing Gourmet  Here are just a few summaries of research papers published in reputable journals and available via PubMed the online medical research papers resources (note: we added the emphasis/underlines where included in summaries below): Obesity (Silver Spring). 2010 Jan 14. [Epub ahead of print] Obese Women Have Lower Monosodium Glutamate Taste Sensitivity and Prefer Higher Concentrations Than Do Normal-weight Women. Pepino MY, Finkbeiner S, Beauchamp GK, Mennella JA. [1] Monell Chemical Senses Center, Philadelphia, Pennsylvania, USA [2] Department of Internal Medicine, School of Medicine, Washington University, St. Louis, Missouri, USA [3] Department of Psychiatry, School of Medicine, Washington University, St. Louis, Missouri, USA. The goal of this study was to determine whether obese women exhibit altered umami and sweet taste perception compared to normal-weight women. A total of 57 subjects (23 obese and 34 normal weight) participated in a 2-day study separated by 1 week. Half of the women in each group were evaluated using monosodium glutamate (MSG; prototypical umami stimulus) on the first test day and sucrose on the second test day; the order was reversed for the remaining women. We used two-alternative forced-choice staircase procedures to measure taste detection thresholds, forced-choice tracking technique to measure preferences, the general Labeled Magnitude Scale (gLMS) to measure perceived intensity of suprathreshold concentrations, and a triangle test to measure discrimination between 29 mmol/l MSG and 29 mmol/l NaCl. Obese women required higher MSG concentrations to detect a taste and preferred significantly higher MSG concentrations in a soup-like vehicle. However, their perception of MSG at suprathreshold concentrations, their ability to discriminate MSG from salt, and their preference for sucrose were similar to that observed in normal-weight women. Regardless of their body weight category, 28% of the women did not discriminate 29 mmol/l MSG from 29 mmol/l NaCl (nondiscriminators). Surprisingly, we found that, relative to discriminators, nondiscriminators perceived less savoriness when tasting suprathreshold MSG concentrations and less sweetness from suprathreshold sucrose concentrations but had similar MSG and sucrose detection thresholds. Taken together, these data suggest that body weight is related to some components of umami taste and that different mechanisms are involved in the perception of threshold and suprathreshold MSG concentrations. PMID: 20075854 [PubMed - as supplied by publisher] J Autoimmun. 2008 Feb-Mar;30(1-2):42-50. Monosodium glutamate (MSG): a villain and promoter of liver inflammation and dysplasia. Nakanishi Y, Tsuneyama K, Fujimoto M, Salunga TL, Nomoto K, An JL, Takano Y, Iizuka S, Nagata M, Suzuki W, Shimada T, Aburada M, Nakano M, Selmi C, Gershwin ME. Department of Diagnostic Pathology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan. Chronic inflammation is a common theme in a variety of disease pathways, including autoimmune diseases. The pathways of chronic inflammation are well illustrated by nonalcoholic steatohepatitis (NASH), which is of a serious concern due to its increasing prevalence in the westernized world and its direct correlation with lifestyle factors, particularly diet. Importantly, NASH may ultimately lead to the development of hepatocellular carcinoma. We previously reported that injection of monosodium glutamate (MSG) in ICR mice leads to the development of significant inflammation, central obesity, and type 2 diabetes. To directly address the long-term consequences of MSG on inflammation, we have performed serial analysis of MSG-injected mice and focused in particular on liver pathology. By 6 and 12 months of age, all MSG-treated mice developed NAFLD and NASH-like histology, respectively. In particular, the murine steatohepatitis at 12 months was virtually undistinguishable from human NASH. Further, dysplastic nodular lesions were detected in some cases within the fibrotic liver parenchyma. We submit that MSG treatment of mice induces obesity and diabetes with steatosis and steatohepatitis resembling human NAFLD and NASH with pre-neoplastic lesions. These results take on considerable significance in light of the widespread usage of dietary MSG and we suggest that MSG should have its safety profile re-examined and be potentially withdrawn from the food chain. Eur J Clin Nutr. 2006 Jan;60(1):25-31. Obesity, voracity, and short stature: the impact of glutamate on the regulation of appetite. Hermanussen M, García AP, Sunder M, Voigt M, Salazar V, Tresguerres JA. Aschauhof Altenhof Germany. hermanussen.aschauhof@t-online.de BACKGROUND: World-wide obesity has risen to alarming levels. We present experimental support for a new and very challenging hypothesis linking obesity, voracity, and growth hormone (GH) deficiency, to the consumption of elevated amounts of the amino-acid glutamate (GLU). Supraphysiological doses of GLU are toxic for neuronal cells. METHODS: Human data were obtained from 807,592 German conscripts born between 1974 and 1978, and from 1,432,368 women of the German birth statistics (deutsche Perinatalerhebung) 1995-1997. The effects of orally administered monosodium glutamate (MSG) were investigated in 30 pregnant Wistar rats and their offspring. Pregnant animals either received no extra MSG, or 2.5 g MSG, or 5 g MSG per day, up to the end of the weaning period. In all, 2.5 g, respectively 5 g, MSG accounted for some 10%, respectively 20%, of dry weight of the average daily food ration. After weaning, MSG feeding was continued in the offspring. FINDINGS: Morbid obesity associates with short stature. Average stature of conscripts progressively declines when body mass index increases above 38 kg/m2. Also morbidly obese young women are shorter than average though to a lesser extent than conscripts. Oral administration of MSG to pregnant rats affects birth weight of the offspring. Maternal feeding with 5 g MSG per day results in severe birth weight reduction (P<0.01). Weight increments remain subnormal when MSG feeding to the mothers is maintained during weaning (P < 0.01). GH serum levels are affected in animals that received MSG during prenatal life via maternal feeding. Animals that are kept on high MSG diet (5 g MSG per day) continue to show serum GH levels that are as low or even lower than those of MSG injected animals (P < 0.05), both at day 30 and at day 90 of life. Animals that were kept on medium MSG diet (2.5 g MSG per day) showed low serum GH levels at day 30 of life (P < 0.01), but seemed to partially recover before day 90. Almost identical results were observed in IGF-1 serum levels. Oral MSG resulted in dose dependent voracity. The animals fed 5 g MSG per day increased water uptake by threefold (P < 0.01), and food uptake by almost two-fold (P < 0.01). The influence of MSG is in general more marked in males than in females. Interpretation: GLU is a widely used nutritional substance that potentially exhibits significant neuronal toxicity. Voracity, and impaired GH secretion are the two major characteristics of parenterally administered GLU-induced neuronal damage. GLU maintains its toxicity in animals even when administered orally. Males appear to be more sensitive than females. The present study for the first time demonstrates, that a widely used nutritional monosubstance--the flavouring agent MSG--at concentrations that only slightly surpass those found in everyday human food, exhibits significant potential for damaging the hypothalamic regulation of appetite, and thereby determines the propensity of world-wide obesity. We suggest to reconsider the recommended daily allowances of amino acids and nutritional protein, and to abstain from the popular protein-rich diets, and particularly from adding the flavouring agents MSG. PMID: 16132059 [PubMed - indexed for MEDLINE] J Pediatr Endocrinol Metab. 2003 Sep;16(7):965-8. Does high glutamate intake cause obesity? Hermanussen M, Tresguerres JA. Aschauhof, Altenhof, Germany. hermanussen.aschauhof@t-online.de World-wide obesity has risen to alarming levels. The average weight of German conscripts now increases by almost 400 g/year. Similar data were obtained in Austria, Norway and the UK. The rising prevalence of obesity coincides with a rising popularity of protein-rich diets. On average, Germans consume meat at 100 kg/year. Children eat some threefold more protein than recommended; infants of 6 to 12 months receive daily up to 5 g/kg body weight of protein. We hypothesise that it is not the protein, but the amino acid glutamate that determines the propensity of obesity. Chronic hyperglutamataemia may intoxicate arcuate nucleus (AN) neurons, thereby disrupting the hypothalamic signalling cascade of leptin action, causing hyperphagia, obesity and hyperleptinaemia. Hyperleptinaemia also exerts sympathetic effects including blood pressure elevation that are mediated via mechanisms different from the hypothalamic system, and other symptoms of the 'metabolic syndrome'. This may happen even before birth when in small-for-gestational-age foetuses with impaired umbilical plasma flow, foetal hyperglutamataemia induces AN damage followed by later impairment of feeding regulation, hyperleptinaemia and symptoms that characterise the 'thrifty phenotype'. We suggest abandoning the flavouring agent monosodium glutamate and reconsidering the recommended daily allowances of protein and amino acids, particularly during pregnancy. PMID: 14513871 [PubMed - indexed for MEDLINE] |
