Commentary on: "Further studies are necessary in order to conclude a causal association between the consumption of monosodium L-glutamate (MSG) and the prevalence of the metabolic syndrome in the rural Thai population"
© Collison; licensee BioMed Central Ltd. 2013
Received: 5 January 2013
Accepted: 11 January 2013
Published: 22 January 2013
See related article: http://www.nutritionandmetabolism.com/content/10/1/14
I read with considerable interest the epidemiological study by Insawang et al., which demonstrates an association between monosodium glutamate (MSG) intake and the prevalence of the Metabolic Syndrome in a rural Thai population . It is important to point out that Insawang et al. did not claim that MSG causes the Metabolic Syndrome, they did however concluded that “elevated dietary MSG consumption is significantly associated with having the Metabolic Syndrome and being overweight in a Thai rural population”.
Hypertension, defined as elevated blood pressure defined as = 130/85 mmHg.
Abdominal obesity defined as waist circumference = 102 cm or 40 inches (male), or = 88 cm or 36 inches (female).
Hyperglycemia, defined as elevated Fasting plasma glucose = 110 mg/dl.
Dyslipidemia, defined as elevated triglycerides = 150mg/dL.
Dyslipidemia, defined as presence of high-density lipoprotein cholesterol (HDL-C) = 40 mg/dL (male), or = 50 mg/dL (female).
Importantly, elevated body weight is not one of the criteria for the presence of the Metabolic Syndrome; and indeed, animal model systems indicate that MSG-obese rodents exhibit either lower body weights [7–10], or similar body weights compared to control animals [11, 12], depending on the species and experimental conditions. However, impaired cardiovascular autonomic function, elevated arterial pressure, insulin resistance and dyslipidemia have all been documented in rodents exposed to MSG during the neonatal period at a time when the blood brain barrier is immature and vulnerable to excitotoxicity [13, 14]. Moreover, neonatal exposure to non-physiological levels of MSG is a proven experimental methodology for inducing Metabolic Syndrome in rodents [15–18]; and sometimes referred to as “hypothalamic obesity” [19, 20] due to the fact that high levels of glutamate may damage the hypothalamus and other areas of the brain which are rich in glutamate receptors [11, 12]. Interestingly, increased hypothalamic inflammatory signaling and neuronal injury can also be induced in rodents consuming high fat diets [21–24]; and recent data also provides evidence of hypothalamic low-grade inflammation and gliosis in obese humans [24, 25], which may impair the regulation of food intake and energy expenditure.
 The authors of the epidemiological study associating MSG consumption with the prevalence of Metabolic Syndrome were under no obligation to provide a causal relationship between the two.  Under experimental conditions in rodents, non-physiological levels of MSG, or high levels of dietary fat may promote damage to the hypothalamus and other areas of the brain regulating energy expenditure.  In humans, obesity may be associated with hypothalamic damage. The commentary by Rogers has provided several interesting points of discussion.
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