I know something you don’t know. I know that man-made free glutamic acid (free glutamate), the active ingredient in monosodium glutamate (MSG), caused and maintains the obesity epidemic.
Evidence? Some things are easy to understand.
1. Anyone who was reading medical journals in 1969 and the 1970s knew that monosodium glutamate (which contains manufactured free glutamate) fed in large amounts to newborn animals causes brain damage in a particular area of the hypothalamus — brain damage that is aways followed by gross obesity, infertility, behavior disorders and other abnormalities (1).
2. The obesity epidemic materialized in the 1960s. Prior to 1957, there were people who had problems with obesity, but not in numbers so significant that they couldn’t be explained (2,3).
3. In 1957 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 – brain damaging (4).
Studies done over the years leave no question that there are three requirements for glutamate-induced brain damage, and that humans can meet them all:
A vulnerable brain –
The vulnerable brain in humans is the immature brain of a fetus or newborn, never protected by a blood-brain barrier.
Sufficient free glutamate to cause the free glutamate to become excitotoxic –
Virtually unlimited amounts of free glutamate became available in 1957 when production of free glutamate for use in food changed from extraction of glutamate from protein to production of free glutamate by bacterial fermentation (4).
A way to deliver the toxin to the vulnerable brain –
You couldn’t feed glutamate-containing ingredients to a newborn with a fork or a spoon. But if a pregnant woman consumes enough glutamate during the course of a day (which she will do if she is eating processed and ultra-processed foods), she will pass that glutamate through the placenta to her fetus, damaging the fetuses’ vulnerable brain.
It’s the timing that tells the story of the obesity epidemic.
Prior to 1957, there was obesity, but not in such amounts that it would be called an epidemic. During that time, glutamate was produced using a slow and costly method.
After 1957, there was sufficient production of glutamate to cause it to be excitotoxic – brain damaging. And sales of products containing free glutamate, not just MSG, were vigorously promoted.
Increases in the incidence of obesity began to be noticed in the early 1970s, when the first glutamate-induced brain damaged fetuses reached maturity as obese adults.
1. The first study to address the possibility that glutamate from outside the body (from eating for example) might cause brain damage followed by obesity and reproductive dysfunction was published in 1969. At the time, researchers were administering glutamate to laboratory animals subcutaneously using Accent brand MSG because it had been observed that MSG was as effective for inflicting brain damage as more expensive pharmaceutical grade L-glutamate (7).
In the decade that followed, research confirmed that glutamate given as monosodium glutamate administered or fed to neonatal animals causes hypothalamic damage, endocrine disruption, and behavior disorders when given to immature animals after either subcutaneous (8-29) or oral (15,21,22,24,30-34) doses.
15. Olney, J.W. Glutamate-induced neuronal necrosis in the infant mouse hypothalamus. J Neuropathol Exp Neurol 30: 75-90, 1971.
21. Burde, R.M., Schainker, B., and Kayes, J. Acute effect of oral and subcutaneous administration of monosodium glutamate on the arcuate nucleus of the hypothalamus in mice and rats. Nature(Lond) 233: 58-60, 1971.
22. Olney, J.W. Sharpe, L.G., Feigin, R.D. Glutamate-induced brain damage in infant primates. J Neuropathol Exp Neurol 31: 464-488, 1972.
24. Burde, R.M., Schainker, B., and Kayes, J. Monosodium glutamate: necrosis of hypothalamic neurons in infant rats and mice following either oral or subcutaneous administration. J Neuropathol Exp Neurol 31: 181, 1972.
30. Olney, J.W., Ho, O.L. Brain damage in infant mice following oral intake of glutamate, aspartate or cystine. Nature(Lond) 227: 609-611, 1970.
31. Lemkey-Johnston, N., and Reynolds, W.A. Incidence and extent of brain lesions in mice following ingestion of monosodium glutamate (MSG). Anat Rec 172: 354, 1972.
32. Takasaki, Y. Protective effect of mono- and disaccharides on glutamate-induced brain damage in mice. Toxicol Lett 4: 205-210, 1979.
33. Takasaki, Y. Protective effect of arginine, leucine, and preinjection of insulin on glutamate neurotoxicity in mice.Toxicol Lett 5: 39-44, 1980.
34. Lemkey-Johnston, N., and Reynolds, W.A. Nature and extent of brain lesions in mice related to ingestion of monosodium glutamate: a light and electron microscope study. J Neuropath Exp Neurol33: 74-97, 1974.
2. Monitoring Human Tissues for Toxic Substances (https://www.ncbi.nlm.nih.gov/books/NBK234172/)
3. Overweight and Obesity in the United States, 1960–2000 https://www.infoplease.com/math-science/health/fitness-nutrition/overweight-and-obesity-in-the-united-states-1960-2000
4. Sano C. History of glutamate production. Am J Clin Nutr. 2009 Sep;90(3):728S-732S. doi: 10.3945/ajcn.2009.27462F. Epub 2009 Jul 29. PMID: 19640955.