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From The December 2001 Issue of Nutrition Science News
The Evolution of Orthomolecular Medicine
Jack Challem
In the 1940s and 1950s, physicians discovered that large doses of vitamins benefited patients with heart disease, infections, and mental illness. In 1954, a group of physicians published the first double-blind study with evidence that vitamins B3 and C helped patients with acute schizophrenia.1
Many physicians dismissed the study results because the prevailing belief at the time was that vitamins were effective only in the treatment of classic deficiency diseases, such as pellagra and scurvy. Today, a growing number of physicians recognize the vital roles vitamins play in preventing and treating disease.
The rationale for vitamin therapy was developed in the 1960s by the late Nobel laureate, Linus Pauling, Ph.D. Although Pauling was a controversial figure, he also was regarded by many as the 20th century's second most brilliant scientist, after Einstein. Pauling was intrigued with the phenomenon that most mammals produce large quantities of vitamin C, whereas humans and some other primates, because of their genetic makeup, do not produce any. Pauling studied the research of Abram Hoffer, M.D., Ph.D., and Humphry Osmond, M.D., who used large vitamin doses to successfully, and safely, treat schizophrenia.
It was a natural progression for Pauling—who had identified sickle-cell anemia as the first molecular disease and subsequently laid the foundation for molecular biology—to then develop a theory that explained the molecular basis of vitamin therapy.
In a 1968 edition of the journal Science, Pauling coined the term "orthomolecular" (meaning "to straighten out molecules") to describe nutritional medicine. He explained how health could be improved by straightening out the body's molecules, specifically by using "the optimum concentrations of substances normally present in the human body."2 (See Pauling's entire article at www.orthomed.org/pauling2.htm.)
Pauling's underlying hypothesis was that people require at least 40 vitamins, minerals, and amino acids. Because these nutrients are the substrates for all bodily biochemicals, low levels become rate-limiting factors that interfere with biochemical reactions. In addition, said Pauling, because of genetic variations and subtle biochemical defects in the population, some people have high requirements for specific nutrients.
New insights into molecular biology and biochemistry have clarified vitamin benefits and confirmed Pauling's theories of orthomolecular medicine. For example, free radicals trigger two gene transcription factors, NFkB and AP-1, which cause inflammation and stimulate cancer cells. Vitamin E has the ability to override these processes.3
On the clinical side, many physicians who prescribe vitamins to their patients refer to this treatment as "precursor therapy." Vitamins, minerals, amino acids, and other micronutrients help build thousands of biochemicals. For reasons not entirely understood, supplements can enhance biochemical reactions and, in some cases, even override genetic defects.4,5
This year marked the 100th anniversary of Pauling's birth. His legacy clearly lives on.
Jack Challem, known as the The Nutrition Reporter™, has been writing about vitamin research for 25 years and is the author of Syndrome X: The Complete Nutritional Program to Prevent and Reverse Insulin Resistance (Wiley, 2000).
References
1. Clancy J, et al. Design and planning in psychiatric research as illustrated by the Weyburn Chronic Nucleotide Project. Bulletin of the Menninger Clinic 1954;18:147-53.
2. Pauling L. Orthomolecular psychiatry. Science 1968;160:265-71.
3. Davies CA, et al. Radicals and inflammation: mediators and modulators. Fuches J, Packer L, editors. Environmental stressors in health and disease. New York: Marcel Dekker; 2001. p. 17-52.
4. Whitehead AS, et al. A genetic defect in 5,10 methylenetetrahydrofolate reductase in neural tube defects. QJM 1995;88:763-6.
5. van der Put NMJ, et al. Mutated methylenetetrahydrofolate reductase as a risk factor for spina bifida. Lancet 1995;346:1070-1.
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