The Obesity Epidemic: Should We Believe What We Read and Hear?

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Note: The following has been revised to correct editing errors that appeared in the Summer, 2004 issue of Wise Traditions.
There is no question that there is an obesity epidemic in our country, as well as in some other countries. One cannot avoid awareness of this problem. The subject of obesity is regularly covered in newspapers and on radio and television. It is reported in the United States alone that obesity is responsible for $90 billion in medical costs and 300,000 premature deaths every year. According to some sources, one third of the adults in our country are obese, and another one third of our population is overweight.¹

If you stand on a street corner used by many pedestrians or at the entrance of a high school at the beginning or end of the day, you will observe not only what would be considered to be obese people, but a number of people, including the young, who would be considered grotesquely obese.

If one is to believe the reports of the media,^2-3 often based on the findings of researchers,⁴ obesity is mainly the result of poor nutrition and lack of adequate exercise. Psychological problems, poor parenting, and genetics are also reported as contributing factors.

Although what we read and hear through the media seems logical, one must ask whether the perceived reasons for obesity are, in fact, the actual causes, and whether researchers are looking in the right places for the causes of obesity and a possible resolution of the problem.

The purpose of this paper is to raise awareness of a more likely cause of the obesity epidemic than you have read and heard of, and to encourage researchers, including those at the Centers for Disease Control and Prevention (CDC) and the National Institutes of Health, to consider the points raised in this paper. Also, if the reader feels that the material in this paper makes sense, it is hoped that the reader will take time to write to his or her representatives in Washington to request that the Food and Drug Administration (FDA) be forced to be responsive to the facts they already know about obesity, and take appropriate action. (See conclusion of this article.)

A New Phenomenon

The fact is that the obesity epidemic is a relatively new phenomenon. Prior to the 1950s, there were overweight people, but it was relatively rare to find an individual who was grotesquely obese. I graduated from college in the 1950s, and do not recall one person in high school or college who approached 300 pounds, not even members of the football team. I can also relate that as recently as 2003, when I visited Spain, a country that does not heavily rely on processed foods, or that has just recently begun to use processed foods, I never saw a grotesquely obese person.

What has changed through the years?

Simply stated, our food supply has changed along with the changes in our lives brought about by the demands of our fast-paced society. We are depending more and more on processed foods, and with each year, the FDA approves more and more chemicals for use in foods. With each year, the food industry is using more and more chemicals in their products. These chemicals increase shelf life, kill bacteria, improve taste, replace fats, replace carbohydrates, even replace meat in some vegetarian preparations, and more. Most important to food producers, chemical use can increase profits. Most important to the consumer is the fact that some of the chemicals are neurotoxic and/or carcinogenic.

For purposes of this paper, we will report on the neurotoxins MSG (glutamic acid that has been freed from protein through a manufacturing process – what many MSG-sensitive people refer to as processed free glutamic acid) and aspartic acid (about 40% of the sugar substitute aspartame).

In 1968, John W. Olney, M.D., a respected researcher at Washington University Medical School, St. Louis, Missouri, and member of the National Academy of Science, found that mice in his laboratory that were being used to replicate a 1957 study by Lucas and Newhouse, in which the administration of MSG had resulted in retinal damage,⁵ had become grotesquely obese. Dr. Olney decided to sacrifice some of the mice and found lesions in the hypothalamus portion of the brain, the portion of the brain, as defined in Stedman’s Online Medical Dictionary, that is “…prominently involved in the functions of the autonomic (visceral motor) nervous system and, through its vascular link with the anterior lobe of the hypophysis, in endocrine mechanisms; it also appears to play a role in neural mechanisms underlying moods and motivational states.”⁶

Dr. Olney published a paper on his findings in 1969, in which he described the hypothalamic lesions, stunted skeletal development, and obesity in maturing mice which had been given the food ingredient “monosodium glutamate” as neonates. Olney also commented on observed pathological changes found in several brain regions associated with endocrine function in maturing mice.⁷

Confirmation

Since 1969, many scientists have confirmed Dr. Olney’s findings of damage to the hypothalamus from MSG with resulting obesity. Go to the National Library of Medicine website, www.pubmed.gov, and type in “monosodium glutamate, obesity” (without the quotation marks). As of May 13, 2004, you’ll find 151 studies listed in addition to Dr. Olney’s study. Fewer studies come up with “aspartic acid, obesity” (without the quotation marks).^8-9 More research has been done on the effects of MSG on the hypothalamus leading to obesity than on the effects of aspartic acid.

Neuroscientists have found in animal studies that glutamic acid and aspartic acid load on the same receptors in the brain, cause identical brain lesions and neuroendocrine disorders, and act in an additive fashion.¹⁰

Research indicating that MSG causes damage to the hypothalamus has been carried out mostly on small laboratory animals, primarily the mouse and the rat. In the 1960s, a few studies looked at the effects of MSG on primates, using rhesus monkeys. The findings were the same for rhesus monkeys as they were for rodents.^11-12 Although research designed to produce brain lesions cannot be carried out on humans, neuroscientists have determined that humans are 5 times more sensitive to MSG than the mouse and 20 times more sensitive to MSG than the monkey, based on blood plasma levels of glutamate following an oral dose of 150 mg/kg of glutamic acid.¹³ Furthermore, individual variability in plasma response to glutamate loading is more extreme in humans than in the mouse or monkey.¹⁴

Neuroscientists have known that MSG and aspartic acid cause lesions in the hypothalamus since 1969, but only recently has a possible explanation for the mechanism by which this occurs come to light. In 1994, researchers discovered the appetite-suppressing hormone, leptin. As described in many articles, leptin regulates, among other things, energy, control of appetite, and body weight. Leptin acts by altering neuropeptide circuits in the hypothalamus.^15-20

While there is abundant literature demonstrating that MSG and aspartic acid cause hypothalmic lesions which, in turn, can cause gross obesity, I know of no research that has examined a possible relationship between the hypothalamic damage caused by MSG and/or aspartame, and the leptin abnormalities found in obese individuals. Research is needed in this area.

Blood-Brain Barrier

The glutamate industry would like us to believe that MSG is not a problem for humans because the human brain is protected from MSG by the blood-brain barrier. However, that is not true. The blood-brain barrier is not fully developed in newborns, and although there is some evidence that it is not fully developed in some children until puberty, when it reaches full maturity is unknown.²¹ It is definitely not fully developed in any fetus. Furthermore, throughout life, certain regions of the brain, known as the circumventricular organs, lack a blood brain barrier,^22-24 and the blood brain barrier can be damaged from, among other things, high fever, stroke, trauma to the head, seizures, repeated ingestion of MSG, and the normal process of aging.^21,25-26 The developing fetus is at particular risk since the placental barrier is not impervious to MSG;^27-29 and we can assume the same is true for the aspartic acid contained in aspartame. Since most of the processed foods we eat contain MSG, as do many personal care items, supplements, and pharmaceuticals, it is almost impossible for an expectant mother to avoid it. (See list of common food ingredients that contain MSG at www.truthinlabeling.org/hiddensources.html.) She may also be using aspartame in diet soda or as a sweetener in coffee and/or ingesting free glutamic acid or free aspartic acid as a chelating agent in the minerals included in her multi-vitamin preparation.

Infant Exposure

Following birth, an infant is exposed to MSG in most, if not all of the vaccines it is given, and in most cases, is also exposed to free aspartic acid in vaccines.³⁰ The effect of the glutamic acid in vaccines is intensified by any mercury that is also present.³¹ All infant formulas contain some free glutamic acid and free aspartic acid. An infant on a hypoallergenic soy-based formula will ingest more excitotoxic amino acids (glutamic acid, aspartic acid, and L-cysteine) per day than is contained in any serving of food that this writer has seen on grocery store shelves.³² (We understand hypoallergenic soy formulas are now being used by 25% of mothers because they have been led to believe that soy formulas are better for their babies than are milk based formulas, even if their children are not lactose intolerant.) If an infant is breast fed, it appears likely that the MSG and/or aspartame ingested by the mother will pass into her milk. If the infant becomes ill, he/she may receive a medication sweetened with aspartame. As soon as the infant begins to eat table foods, the infant will be ingesting free glutamic acid, and, in many cases, free aspartic acid.

Industry Response

The glutamate industry claims that glutamic acid and aspartic acid are natural components of protein and, therefore, cannot be harmful. What they fail to mention is that when glutamic acid and aspartic acid are freed from protein through a manufacturing process, they will invariably be accompanied by contaminants. If the manufacturing process used to free amino acids from protein is acid hydrolysis, carcinogenic propanols will be included as contaminants. In a speech before The Celiac Sprue Association in 2000, an FDA researcher reported that in freeing L-tryptophan from protein, certain contaminants are produced, and it is now believed that those who died or became ill from L-tryptophan in the late 1980s, were people who were intolerant to those contaminants. (The FDA has suppressed that finding.)

In July, 1992, the Federation of American Societies for Experimental Biology (FASEB) issued its findings on an FDA-funded study entitled “Safety of Amino Acids Used as Dietary Supplements.” In the section on glutamic acid (the reactive component of the food ingredient “monosodium glutamate”), the report concluded, in part, that “The continuing controversy over the potential effects of glutamate on growth and development of neonatal animal models suggests that it is prudent to avoid the use of dietary supplements of L-glutamic acid by pregnant women, infants and children. The existence of evidence of potential endocrine responses, i.e. elevated cortisol and prolactin, … would also suggest a neuroendocrine link and that supplemental L-glutamic acid should be avoided by women of child bearing age and individuals with affective disorders.”

The FDA appears to have suppressed this FASEB finding. When asked how the FDA can allow MSG to be used in food, FDA officials stated that one cannot compare the free glutamic acid in supplements to the free glutamic acid in food. Of course, this position is completely untenable since food products contain far more free glutamic acid than supplements.

Following issuance of the FASEB report on supplements, the FDA contracted with FASEB for over $500,000 to conduct a study on the safety of MSG in food. In July, 1995, FASEB published its report entitled “Analysis of Adverse Reactions to Monosodium Glutamate (MSG).” Most people who inquired, and the media, received a 20 page “Executive Summary,” primarily made up of questions developed by the FDA and the answers to those questions. The carefully crafted summary left readers with the impression that MSG was essentially safe.

What is not generally known about the FASEB report on the safety of MSG in food is that the original draft final report was issued to the FDA in September, 1994, and leaked to the glutamate industry. The glutamate industry was not happy with FASEB’s report and the FDA rejected it. The FDA paid FASEB over $100,000 in additional money to “clarify” the report, leading to the final report, dated July, 1995. A reading of the entire July, 1995, FASEB report (over 350 pages long rather than the 20 pages making up the Executive Summary), will not give the reader the impression that MSG is safe.

Conclusion

Although there are a number of causes for obesity, there is no question in this writer’s mind that the main cause for the obesity epidemic is the ever increasing use of MSG and aspartame – free glutamic acid and free aspartic acid – in our food supply. MSG, is most often found in food as a component of food ingredients with names that give consumers no clue to its presence. It was not used in our country to any extent until the late 1940s, and not used widely until the 1960s, when the Ajinomoto Company introduced MSG made by bacterial fermentation. (Ajinomoto Company is the world’s largest producer of the food ingredient monosodium glutamate.) Aspartame was approved by the FDA in 1981. Today, most processed foods contain MSG, and it is even found in personal care items and pharmaceuticals. According to The NutraSweet Company, aspartame is used in over 5,000 products. As the use of MSG and aspartame grows, the incidence of obesity appears to be growing.

Since there is no question that MSG and aspartame cause lesions in the hypothalamus, the portion of the brain that is recognized to affect weight, I call upon scientists to consider the destructive qualities of glutamic acid and aspartic acid as they expand their search into the reasons for obesity. In particular, I urge those who are exploring the role of leptin in obesity to consider that it may be the relationship of leptin to a hypothalamus damaged by MSG and aspartame that results in the inability of some people to control food intake, and resulting obesity.

What can be done to stem the obesity epidemic? I would start by identifying the sources of MSG in processed food. MSG should be fully disclosed on processed food labels. I ask that all processed food be measured for “free glutamic acid,” post production, and when free glutamic acid is found to be present, it be disclosed on the product label as “MSG,” with the amount present stated in milligrams. Such an action would stop the accelerating use of MSG, and likely cause its current use to drop because some people would recognize their intolerance for MSG. Others, realizing its toxicity, will choose to avoid it.

Aspartame should be withdrawn from the market. There is no need for aspartame or the recently approved sweetener, neotame, described by some as a super aspartame.

Your thoughts on this matter should be submitted to your representatives in Washington, to the FDA, and to the CDC. Your submission might include the suggestion that all MSG should be disclosed on processed food labels and that all aspartame products be withdrawn from the market.

Suggested Reading

1. A book by Russell L. Blaylock, M.D., a neurosurgeon, entitled Excitotxins: the Taste that Kills. Health Press, 1995
2. A published paper by John W. Olney, M.D. It is entitled Excitatory Neurotoxins as Food Additives: An Evaluation of Risk. The paper was published in Neurotoxicity in 1980. It will be found in volume 2 on pages 163 to 192
3. Website of the Truth in Labeling Campaign regarding MSG (www.truthinlabeling.org)
4. Website regarding aspartame (www.dorway.com)

REFERENCES

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2. Diabetic Gourmet Magazine. Why Is Obesity A Growing Problem in America? http://diabeticgourmet.com/bin/info.cgi?ID=192
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4. Centers for Disease Control, National Center for Chronic Disease Prevention and Health Promotion. Physical activity and good nutrition: essential elements to prevent chronic diseases and obesity 2003. Nutr Clin Care. 6(3):135-8. Review.,Oct – Dec, 2003
5. Lucas, DR and Newhouse, JP, The toxic effect of sodium-L-glutamate on the inner layers of the retina. AMA Arch Opthalmof. 58: 193-201, 1957
6. Stedman’s Online Medical Dictionary, 27th Edition, (www.onelook.com)
7. Olney JW. Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate. Science. 164(880):719-21, May 9, 1969
8. Burbach JA, Schlenker EH, Goldman M. Characterization of muscles from aspartic acid obese rats. Am J Physiol. 249(1 Pt 2):R106-10, July, 1985 9. Schainker B, Olney JW. Glutamate-type hypothalamic-pituitary syndrome in mice treated with aspartate or cysteate in infancy. J Neural Transm. 35(3):207-15, 1974
9. Olney, JW and Ho, OL. Brain damage in infant mice following oral intake of glutamate, aspartate, or cysteine. Nature (Lond). 227: 609-611, 1970
10. Olney, JW and Sharpe, LG. Brain lesions in an infant rhesus monkey treated with monosodium glutamate. Science. 166:386-388, 1969
11. Olney, JW, Sharpe, LG, and Feigin, RD. Glutamate-induced brain damage in infant primates. J Neuropath Exp Neurol. 31: 464-488, 1972
12. Stegink, LD, Reynolds, WA, Filer, LJ Jr., Baker, GL, and Daabees, T. Comparative metabolism of glutamate in the mouse, monkey and man. In Advances in Biochemistry and Physiology. Edited by Filer, LJ Jr., Garatttini, S, Kare,MR, Reynods, WA, and Wurtman, RJ. New York: Raven Press, 85-102, 1979
13. Himwhich, WA, Peterson, IM, and Graves, IP. Ingested glutamate plasma levels of glutamic acid. J Appl Physiol. 7: 196-201, 1954
14. Bouret, SG and Simerly, RD. Minireview: leptin and development of hypothalamic feeding circuits. Endocrinology. 145 (6), 2621-2626, June, 2004
15. Bouret, SG, Draper, SJ, and Simley, RB. Trophic action of leptin on hypothalamus neurons that regulate feeding. Science. 2; 304 (5667), 108-110, April, 2, 2004
16. Small, CJ, Stanley, SA, and Bloom, SR. appetite control and reproduction: leptin and beyond. Semin Reprod Med. 20 (4): 389-398, Nov 2002
17. Dadoun, F. Food intake: who controls what? Ann Endocrinol (Paris). 63 (6 Pt 2): S15- S24, Dec, 2002
18. Simon, E and Barrio, AS. Leptin and obesity. An Sist Sanit Navar. 25 Suppl 1: 53-64, 2002 -Translated from Spanish
19. Bjorbaek, C and Kahn, BB. Leptin signaling in the central nervous system and periphery. Recent Prog Horm Res. 59: 305-331, 2004
20. Blaylock, Russell L, MD. Excitotoxins: The Taste that Kills. Health Press , 1995
21. Brightman, MN and Broadwell, BD. The morphological approach to the study of normal and abnormal brain permeability. Adv Exptl Med Biol 69. 41, 1976
22. Weindel, A. Neuroendocrine aspects of circumventricular organs. In Frontiers in Neuroendocrinology, edited by Maretini, L and Ganong, WF, London: Oxford University Press, 1-32, 1973 24. Broadwell, RD and Sofroniew, MV. Serum proteins bypass the blood-brain fluid barriers for extracellular entry to the central nervous system. Exp neurol.120: 245-263. 1993
23. Nemeroff, CB and Crisley, FD. Monosodium L-glutamate induced convulsions: temporary alteration in blood-brain barrier permeability to plasma proteins. Environ Physiol Biochem 5: 389-395, 1975
24. Toth, E and Lajtha. A. Neurochem Res. 6: 1309- 1317, 1981
25. Yu T, Zhao Y, Shi W, Ma R, and Yu L. Effects of maternal oral administration of monosodium glutamate at a late stage of pregnancy on developing mouse fetal brain. Brain Res. 747(2):195-206, Feb 7, 1997
26. Gao J, Wu J, Zhao XN, Zhang WN, Zhang YY, and Zhang ZX. Transplacental neurotoxic effects of monosodium glutamate on structures and functions of specific brain areas of filial mice. Sheng Li Xue Bao. 46(1): 44-51, Feb 1994. Translated from Chinese
27. Frieder, B and Grimm, VE. Prenatal monosodium glutamate (MSG) treatment given through the mother’s diet causes behavioral deficits in rat offspring. Intern J Neurosci. 23: 117-126, 1984
28. Truth in Labeling Campaign. ( www.truthinlabeling.org/Mercury&MSGinVaccines.html) 31. Aschner M, Yao CP, Allen JW, Tan KH. Methylmercury alters glutamate transport in astrocytes. Neurochem Int. 2000 Aug-Sep;37(2-3):199-206. Review.
29. Truth in Labeling Campaign. (www.truthinlabeling.org/formulacopy.html)
30. Truth in Labeling Campaign. (www.truthinlabeling.org/manufac.html)

This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Summer 2004.

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