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Historical Aspects of the Major Neurological Vitamin Deficiency Disorders: Overview and Fat-Soluble Vitamin A

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Historical Aspects of the Major Neurological Vitamin Deficiency Disorders: Overview and Fat-Soluble Vitamin A Comp. by: GVasenthanProof0000876233 Date:16/11/08 Time:01:50:23 Stage:First Proof File Path://spiina1001z/Womat/Production/PRODENV/0000000001/0000011393/0000000016/ 0000876233.3D Proof by: QC by: ProjectAcronym:BS:FINGER Volume:02129 Handbook of Clinical Neurology, Vol. 95 (3rd series) History of Neurology S. Finger, F. Boller, K.L. Tyler, Editors # 2009 Elsevier B.V. All rights reserved Chapter 29 Historical aspects of the major neurological vitamin deficiency disorders: overview and fat-soluble vitamin A DOUGLAS J. LANSKA* Veterans Affairs Medical Center, Tomah, Wisconsin, and University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA VITAMINS AND DIETARY importantly are able to prevent these disorders in the DEFICIENCY DISEASES first place by targeted supplementation and food fortification. As a result, incidence, prevalence, case Introduction fatality, and mortality of neurological vitamin Vitamins are organic micronutrients that are essential deficiency disorders have declined dramatically in to normal growth and metabolism, and are present developed countries since the middle of the 20th cen- in only minute amounts in natural foodstuffs. Histori- tury. Endemic forms of these disorders have been cally, vitamin deficiency disorders have been major either eliminated from or greatly curtailed in causes of neurological morbidity and mortality developed countries, and the relatively rare residual throughout the world, often affecting large segments cases generally reflect individual predispositions of malnourished populations. The neurological presen- because of altered intake (e.g., alcoholics, food fad- tations vary with the deficiencies involved, but dists, total parenteral nutrition), malabsorption (e.g., included dementia, amnestic confabulatory states, pernicious anemia, chronic diarrhea, iatrogenic causes, delirium, acute psychosis, blindness, eye movement alcoholism), and altered metabolism or abnormal utili- abnormalities, ataxia, myelopathy, polyneuropathy, zation.(e.g., medications, coincident disease). Unfortu- and congenital neural tube defects. nately, high rates of many neurological vitamin Although diseases that are now recognizable as vita- deficiency disorders persist in developing countries min deficiency disorders have been known for millen- and other populations besought with war, famine, nia, the “vitamin doctrine” was not developed until and poverty. the early 20th century (Hopkins, 1929/1965). Prior to This chapter begins a historical review of vitamin this development, vitamin deficiency disorders were deficiency disorders causing neurological illness, generally attributed to toxic or infectious causes, the and includes a general overview of the historical most powerful pathophysiological paradigms of the origins of the vitamin doctrine and an historical review late-19th and early-20th centuries. of fat-soluble vitamin A. Study of the history of Since the initial development of the vitamin doc- neurological vitamin deficiency disorders can be trine, there has been an explosive growth in our under- rewarding from several vantage points, and can aug- standing of cellular metabolism, including the ment understanding of normal neurochemistry and coenzyme functions of many of the vitamins. In some neurophysiology, neuropathophysiology, the interrela- cases we now possess a fairly complete pathophysiolo- tionships between neurological and systemic illness, gical understanding of the development of specific neurotherapeutics, neuroepidemiology, and neurologi- neurological vitamin deficiency disorders, are able to cally-oriented social medicine and public health. identify such disorders early, are able to treat and Seldom in the case of neurological disorders is such a often cure people with such disorders when identified breadth and depth of medical understanding available early using synthetic forms of the vitamins, and most to help prevention and treatment efforts. *Correspondence to: Douglas J. Lanska MD, VA Medical Center, 500 E Veterans St., Tomah, WI 54660, USA. E-mail: [email protected], Tel: +1-608-372-1772, Fax: +1-608-372-1240. Comp. by: GVasenthanProof0000876233 Date:16/11/08 Time:01:50:23 Stage:First Proof File Path://spiina1001z/Womat/Production/PRODENV/0000000001/0000011393/0000000016/ 0000876233.3D Proof by: QC by: ProjectAcronym:BS:FINGER Volume:02129 436 D.J. LANSKA Components of a physiologically From Funk’s “vitamine” to vitamin complete diet and Hopkins’ In 1911 and 1912 Polish chemist Casimir Funk (1884– “accessory food factors” 1967), then working at the Lister Institute for Preven- In the late-19th century, a physiologically complete diet tive Medicine in London, proposed that the active diet- was believed to require only a sufficient amount of ary factor that was effective in the treatment of animal proteins, carbohydrates, fats, inorganic salts, and models of beriberi was a specific organic substance water. However, as early as 1880 and 1881, in studies present in trace amounts—one of several trace dietary for a doctoral thesis, Russian physician Nicolai I. Lunin factors that were essential for life and which, when (1853–1937) in Dorpat (now Tartu, Estonia) found that deficient, resulted in such diseases as beriberi, scurvy, mice did not thrive or grow when fed on purified diets rickets, and pellagra (Funk, 1911, 1912, 1922; Harrow, containing only these constituents, although he made 1955). Funk had isolated a concentrate from rice polish- no effort at identifying any missing essential factors ings that seemed to be curative for polyneuritis in in the inadequate diets (Hopkins, 1929/1965; Voss, pigeons, and that his chemical analyses suggested was 1956; Rosenfeld, 1997). probably an amine. Because this substance appeared In 1905, Cornelius Pekelharing (1848–1922) in to be vital for life, Funk named it “vitamine” for “vital Utrecht performed similar experiments and achieved amine” (Funk, 1912). similar results, but found that animals that received Funk supposed that vitamines would all belong to milk instead of water thrived. Pekelharing suggested the same chemical class, just as amino acids as the con- that there was an unrecognized substance in milk, stituents of proteins are chemically related. However, present in very small amounts, which was necessary Funk’s concentrates were primarily nicotinic acid, for the animals to adequately utilize the other dietary which was contaminated with small amounts of the components—a clear statement of what would later anti-beriberi factor (thiamin). Nevertheless, Funk’s be called the “vitamin doctrine” (Hopkins, 1929/1965; term was widely adopted and applied to a series of Rosenfeld, 1997). food substances, regardless of their chemical struc- Unfortunately, the early reports by Lunin, Pekelhar- tures. Indeed, the introduction of the term and its ing, and others attracted little attention until the work popularization led to further research efforts interna- of British biochemist Frederick Hopkins (1861–1947) tionally, as these dietary substances became recognized at Cambridge University was published in 1912. From as clinically important beyond the prevention of some 1906 to 1912 Hopkins conducted similar feeding experi- distant tropical diseases. In 1920, Jack Drummond ments with young mice and rats (Hopkins, 1929/1965). (1891–1952) proposed that the “e” be dropped from Hopkins’ experiments were notable for providing care- “vitamine,” because there was no evidence that the ful observations under controlled laboratory conditions essential dietary factors are amines; the revised with “analytical control of materials, for the meticu- term “vitamin” would then conform to a standard lous weighing and measurement of the quantities of nomenclature convention, one in which substances of food consumed, for the many days over which animals undefined composition end with the suffix “-in” were studied ..., for consistent recording of the weight (Drummond, 1920; Rosenfeld, 1997). and growth of the rats, and for ...independence from current dogma” (Weatherall, 1990, p. 123). Hopkins VITAMIN A DEFICIENCY: NIGHT found that rats fed purified mixtures of protein BLINDNESS AND KERATOMALACIA (casein) or amino acids, carbohydrates (sucrose, Introduction starch), fats (butter or lard), mineral salts, and water failed to grow or even lost weight and died, unless Vitamin A is integral to sensory transduction and spe- the diet was supplemented with small amounts of milk cifically the transduction of light for visual perception. (Hopkins, 1906, 1912, 1929/1965). Hopkins concluded Vitamin A is the precursor of the visual pigments that milk contained “accessory food factors” that are within the rods and cones of the retina. In particular, required in trace amounts for normal growth (Hopkins, a derivative of vitamin A, 11-cis retinal, is the chromo- 1912, 1929/1965). Although there were clearly others phore within the G protein-coupled photoreceptor pro- who anticipated this work, and although other investi- tein, rhodopsin, which is localized to the outer gators had difficulty reproducing and confirming segments of rod cells in the retina. This transmem- Hopkins’ results, Hopkins shared the 1929 Nobel Prize brane detector undergoes a conformational change in in Physiology or Medicine for his contributions to response to light, which activates an intracellular the “discovery of the growth-stimulating vitamins” G-protein-coupled transduction cascade, and ultimately (Hopkins, 1929/1965). cellular responses that lead to visual perception.
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