1957 was the year that mass produced free glutamate was first consumed by pregnant women, causing brain damage followed by irreversible obesity in their fetuses.\u00a0<\/p>\n\n\n\n
1957 was the year that Lucas and Newhouse demonstrated that manufactured free glutamate (the toxic component of monosodium glutamate) damaged the inner layers of the retina, causing macular degeneration.<\/p>\n\n\n\n
I957 was the year that the major U.S. producer of MSG and the free glutamate contained in it started producing free glutamate in sufficient amounts to cause that free glutamate to be excitotoxic \u2013 brain damaging.<\/p>\n\n\n\n
Prior to 1957, there was not very much in the way of free amino acids to be found in food in the American diet, and ultra-processed food hadn\u2019t been invented.<\/p>\n\n\n\n
Prior to a 1957 change in glutamate production, it would have been rare for there to be enough free glutamate in food to cause it to be excitotoxic – brain damaging.<\/p>\n\n\n\n
Today there\u2019s more than enough free glutamate to become brain damaging if multiple servings are consumed during the course of a day.<\/p>\n\n\n\n
Glutamic acid. On the one hand, it\u2019s essential to life itself, but in 1957 it became a deadly killer. <\/strong><\/p>\n\n\n\n Monosodium glutamate, the food additive, was invented in 1908 at which time the glutamate component was produced by extracting glutamate from protein — a slow and costly method.<\/p>\n\n\n\n It was reinvented in 1957 using genetically modified bacteria to produce glutamate. Following reinvention, virtually unlimited amounts of free glutamate became available, and great quantities of free glutamate, often in monosodium glutamate, were poured into processed foods. For the first time in history, there existed the excessive amounts of free glutamate needed to produce excitotoxicity.<\/p>\n\n\n\n In 1968, John Olney published the first of many studies that demonstrated that large (excessive) amounts of glutamic acid delivered in monosodium glutamate destroyed neurons in the arcuate nucleus of the hypothalamus, destroying the subject\u2019s capacity for managing appetite and satiety, and also destroying neurons essential to reproductive function (fertility).<\/p>\n\n\n\n In the 1970s, Olney and others established that immature animals fed large amounts of free glutamate suffered brain damage followed by intractable obesity, behavior disturbances, and\/or reproductive disorders including infertility<\/p>\n\n\n\n By 1980, glutamate-associated disorders such as headaches, asthma, diabetes, muscle pain, atrial fibrillation, ischemia, trauma, seizures, stroke, Alzheimer’s disease, amyotrophic lateral sclerosis (ALS), Huntington’s disease, Parkinson\u2019s disease, depression, multiple sclerosis, schizophrenia, obsessive-compulsive disorder (OCD), epilepsy, addiction, attention-deficit\/hyperactivity disorder (ADHD), frontotemporal dementia and autism were on the rise, and evidence of the toxic effects of glutamate were generally accepted by the scientific community.<\/p>\n\n\n\n The obesity epidemic was set in motion following the 1957 introduction of unlimited amounts of excitotoxic \u2013brain damaging — free glutamate in processed foods, dietary supplements, snacks, protein powders and protein drinks, protein substitutes, enteral care products, and pharmaceuticals. <\/p>\n\n\n\n In 2022 Samuels demonstrated that the abnormalities first seen in 1969 by Olney in animals fed free glutamate were being replicated in humans. This happens when a pregnant woman ingests large amounts of free glutamate and \u201cshares\u201d it though the umbilical cord with her fetus.<\/p>\n\n\n\n It\u2019s only since 1957 that manufactured free glutamate has been a deadly killer.<\/p>\n