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MSG and OBESITY

The human body is a wonderful thing.  There are systems working together that create checks and balances to keep us well – or to fight disease should we encounter it.  Obesity happens when one or more of those systems is not working.  It can happen when stress or depression throw the endocrine system off balance, and there is loss of appetite control.  It can happen when there is an injury (a blow to the head for example), that disrupts the endocrine system.  And it can happen when MSG is fed to the unborn and the very young – fed to them before their blood brain barriers are well enough developed to protect the brain cells destined to control endocrine function later in life.

There are actually two separate and possibly distinct paths through which MSG-induced obesity can thrive.  In the first, MSG moves through the incomplete (immature) blood-brain-barrier in the arcuate nucleus of the hypothalamus of the unborn and very young, and kills brain cells (neurons), causing permanent damage to the endocrine system that controls appetite.  In other words, when delivered to the fetus in utero and/or fed to the very young, MSG produces brain damage that damages the endocrine system and causes obesity as children approach maturity. Diet and exercise will do little of a permanent nature for a person whose endocrine system has been damaged in this way.


If that isn't bad enough, in both children and adults continuous ingestion of MSG will raise some hormone levels, including levels of the hormone insulin.  When the insulin level is raised, the glucose level is lowered, which is the body’s signal to eat more food in order to raise (balance) the glucose level.  With the brain signaling the body to consume more food, diet and exercise have little chance of controlling weight gain without a permanent highly restrictive diet.

 

Data: MSG kills brain cells...

In 1957, Lucas and Newhouse(26) first noticed that severe retinal lesions could be produced in suckling mice (and to some extent in adult mice) by a single injection of monosodium glutamate. In the late 60s, Olney(59) became suspicious that obesity in mice, which was observed after neonatal mice were treated with monosodium glutamate for purposes of inducing and studying retinal pathology, might be associated with hypothalamic lesions caused by monosodium glutamate treatment; and in 1969 Olney first reported that monosodium glutamate treatment did indeed cause brain lesions, particularly acute neuronal necrosis in several regions of the developing brain of neonatal mice, and acute lesions in the brains of adult mice given 5 to 7 mg/g of glutamate subcutaneously(59).  

Research that followed confirmed that glutamate, which was routinely given as the sodium salt, monosodium glutamate (brand name Accent), induces hypothalamic damage when given to immature animals after either subcutaneous (60,61,62,63,64,66,67,68,69,70,71,72,73,74,75,76,77,78,81) or oral(67,73,74,76,82,83,84,85,86) doses.

Data: Brain cells damaged by MSG lead to endocrine disorders…

Olney found not only hypothalamic lesions in 1969, but described stunted skeletal development, obesity, and female sterility, as well as a spate of observed pathological changes found in several brain regions associated with endocrine function in maturing mice which had been given monosodium glutamate as neonates(59).

Longitudinal studies in which neonatal/infant animals were given doses of monosodium glutamate and then observed over a period of time before being sacrificed for brain examination, repeatedly supported Olney's early findings of abnormal development, behavioral aberration, and neuroendocrine disorder. Animals treated with monosodium glutamate as neonates or in the first 12 days of life were shown to suffer neuroendocrine disturbances including obesity and stunting, abnormalities of the reproductive system, and underdevelopment of certain endocrine glands (59,68,70,86,88,89,90, 92,93,94,95,96,97,98,99,100,101,102,103,104,105,106) and possible learning deficits either immediately or in later life (92,95,96,107,108,109,110,112,113). In addition, there were reports of behavioral reactions including somnolence and seizures (114,115,116,117,119,120,121); tail automutilation (94,108); and learned taste aversion(110). Irritability to touch was interpreted as conspicuous emotional change by Nemeroff(94). Lynch(14) reported hyperglycemia along with growth suppression. He noted that hyperglycemia did not occur when subjects were given intact protein containing a large amount of glutamate. 

Olney et al. (122,123,124) have written a number of review articles which summarize the data on neuroendocrine dysfunction following monosodium glutamate treatment. Nemeroff (125) has written another.

Relating animal studies to humans…


Finding of neurotoxicity and neuroendocrine dysfunction in laboratory animals raised questions about the effects that monosodium glutamate might have on humans. Since it would be unthinkable to administer doses of monosodium glutamate that might produce the same sorts of neurotoxicity and neuroendocrine dysfunction as found in laboratory animals, researchers had no alternative but to make decisions based on the best of the animal studies. "Best," in this case, would be studies that would most closely parallel the true human condition.

At the time, a seemingly logical first step was to study the effects of monosodium glutamate on subhuman primates; and, as already noted, hypothalamic lesions had been demonstrated in monkeys as early as 1969(61). A seemingly logical second step was to study  "normal" ingestion of monosodium glutamate as opposed to some kind of forced feeding. Many felt that ad libitum feeding of laboratory animals parallels the human situation more closely than either subcutaneous or gavage administration of monosodium glutamate, and that ad libitum feeding studies were, therefore, the vehicle of choice. Ad libitum feeding would give animals free access to feed or water thereby allowing the animal to self-regulate intake. Some tended to disagree, feeling that the ad libitum feeding studies were, by and large, studies that had the greatest potential for minimizing the amount of monosodium glutamate actually ingested while registering the irrelevant amount of monosodium glutamate available.

Two studies that demonstrate neurotoxic reactions after ad libitum feeding of monosodium glutamate are reported here. In a 1979 study done as part of a project designed to evaluate a developmental test battery for neurobehavioral toxicity in rats, in which rats were exposed to monosodium glutamate and other food additives mixed with ground Purina rat chow beginning five days after arrival at the laboratory(109), it was demonstrated that high doses of dietary monosodium glutamate produce behavioral variations. Monosodium glutamate was mixed with food as opposed to being administered subcutaneously or by gavage. A year later, dietary studies demonstrated that weanling mice will voluntarily ingest monosodium glutamate and that such voluntary ingestion results in readily detectable brain damage(127).

MSG is now used as a research tool to produce obesity…

 

By the early 1980s, evidence of monosodium glutamate induced brain lesions and resultant endocrine disorders, including obesity, were so well documented that researchers interested in brain function and/or development of drugs with which to treat disease conditions in which glutamate played a role, began to use monosodium glutamate as an ablative or provocative tool with which to kill selected brain cells and induce obesity.

MSG is readily available to the unborn, neonates, and infants…


It is now recognized the fetus can receive MSG in utero through the mother's diet if the mother is consuming processed food that contains MSG; and, after birth, the infant can receive MSG through the mother's milk if the mother is consuming processed food that contains MSG, and/or can receive MSG which is invariably present in infant formula. The greatest amounts of MSG in infant formula will be found in hypoallergenic formulas--which are typically soy based. 

The newborn and young children are also introduced to MSG through vaccines.  All live virus vaccines, and some, if not all of the others, contain MSG.  The MSG in vaccines will typically be contained in one or more of the ingredients that give no clue to the fact that they contain MSG.

Studies have demonstrated that MSG can cross the placenta during pregnancy(1-2), can cross the blood brain barrier in an unregulated manner during development, and can pass through the five circumventricular organs, which are "leaky" at best at any stage of life(3-5).  Moreover, the blood brain barrier is easily damaged by fever, stroke, trauma to the head, seizures, ingestion of processed free glutamic acid, and the normal process of aging(5-6).  It is generally accepted that, given the lack of full development of the blood-brain barriers in some infants and children, the young are particularly at risk from ingestion of MSG.

 

MSG has an effect on at least some hormone levels…

 

The extent of MSG's effect(s) on hormone levels is as yet unknown.  It is known, however, that continuous ingestion of MSG raises some hormone levels, including the hormone insulin.  When you raise the insulin level, you lower the glucose level, which is the body’s signal to eat more food in order to raise (balance) the glucose level. 

There is evidence (from the FDA's own laboratory) that MSG in the general human diet can disrupt normal metabolism and affect insulin function. Lynch reported hyperglycemia along with growth suppression. He noted that hyperglycemia did not occur when subjects were given intact protein containing a large amount of glutamate(7).


A recent study by He et al. demonstrated that in a rural area of China, persons who ingested more monosodium glutamate were heavier than persons who ingested less monosodium glutamate.  In the journal Obesity, it was reported that monosodium glutamate used in food may be associated with increased risk of obesity independent of physical activity and total food intake(8).  The study is available online at: http://www.nature.com/oby/journal/v16/n8/full/oby2008274a.html.

 

In 2000, Macho, Fickova, and Jezova found that early postnatal administration of MSG exerts an important effect on glucose metabolism and insulin action in adipocytes of adult animals(9).

 

Abstracts of three articles of interest…

Does high glutamate intake cause obesity?

Hermanussen M, Tresguerres JA.
Aschauhof, Altenhof, Germany. hermanussen.aschauhof@t-online.de

J Pediatr Endocrinol Metab. 2003 Sep;16(7):965-8

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.

 

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

 

Eur J Clin Nutr. 2006 Jan;60(1):25-31.

 

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

 

 

[Effect of monosodium glutamate given orally on appetite control (a new theory for the obesity epidemic)]

[Article in Spanish]

 

Fernandez-Tresguerres Hernández JA.

An R Acad Nac Med (Madr). 2005;122(2):341-55; discussion 355-60.

 

Monosodium glutamate is a substance widely used as flavouring agent in the whole world. It is considered to be innocuos by the health agencies of North America and Europe. The effects of the oral administration of two dosages of MSG during the second half of pregnancy and all The developmental process of pups on appetite control and various hormones has been analysed in rats. Effects have been compared with the neonatal parenteral administration of the same compound. The structure of the arcuate nucleus of the hypothalamus has been investigated as well as plasma levels of GH, IGF-1 and leptin and its influence on food consumption. Measurements were performed at 30 and 90 days of life. A nearly total destruction of the arcuate nucleus can be observed with the parenteral administration of MSG but also with the highest oral dose. Significant reductions can be seen in plasma GH and IGF 1 levels at 30 days of life, that are partially recovered at 90 days. Plasma leptin levels are significantly reduced at 90 days of life with the two oral doses together with a significant increase in food intake. In conclussion, oral administration of MSG during pregnancy and development in rats is able to significantly affect hypothalamic control of various hormones and increases appetite.

PMID: 16463577

 

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