There are actually two separate and possibly distinct paths through which MfG-induced obesity can thrive. In the first, MfG 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, MfG 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 MfG 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.
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.
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.
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).
The newborn and young children are also introduced to MfG through vaccines. All live virus vaccines, and some, if not all of the others, contain MfG. The MfG in vaccines will typically be contained in one or more ingredients that give no clue to the fact that they contain MfG.
Studies have demonstrated that MfG 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 MfG. The blood brain barrier, once thought to prevent glutamate from entering the brain, is not fully developed until puberty.
There is evidence (from the FDA's own laboratory) that MfG 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 MSG exerts an important effect on glucose metabolism and insulin action in adipocytes of adult animals (9).
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