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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 can happen 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 or any other ingredient that contains manufactured free glutamate, the toxic component in monosodium glutamate (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 glutamate-induced obesity can thrive. In the first, free glutamate 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 and satiety. In other words, when delivered to the fetus in utero and/or fed to the very young, free glutamate causes brain damage that destroys the neurons that would have regulated appetite and satiety had they not been obliterated by excitotoxic free glutamate.

Diet and exercise will do little of a permanent nature for a person whose endocrine system has been damaged in this way.

Second, in both children and adults, continuous ingestion of free glutamate will raise various 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 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...
Findings 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 nonhuman primates; and, as noted elsewhere, 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 a research tool used 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.
Free glutamate is readily available to the unborn, neonates, and infants...
It is now recognized the fetus can receive free glutamate in utero through the mother's diet if the mother is consuming processed food that contains free glutamate and after birth, the infant can receive free glutamate through the mother's milk if the mother is consuming processed food that contains free glutamate, and/or the infant can receive free glutamate in infant formula. Free glutamate is invariably present in infant formula. The greatest amounts of free glutamate in infant formula will be found in hypoallergenic formulas--which are typically soy based.

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

Studies have demonstrated that free glutamate 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 the young are particularly at risk from ingestion of free glutamate. The blood brain barrier, once thought to prevent glutamate from entering the brain, is not fully developed until puberty.

Free glutamate has an effect on at least some hormone levels...
The extent of free glutamate's effect(s) on hormone levels is as yet unknown. It is known, however, that continuous ingestion of free glutamate 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 free glutamate 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 2008 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.

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

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