[Presentation of a medical and nutritional study of the Spanish Armed Forces of 1958 conducted by the Interdepartamental Committee on Nutrition for National Defense of the United States of America]. / Presentación del estudio médico y nutricional de las Fuerzas Armadas españolas realizado en 1958 por el Interdepartamental Commitee on Nutrition for National Defense de Estados Unidos.

INTRODUCTION: studies of the nutritional and epidemiologic transition in Spain do not seem to have used the report "Spain: Nutrition Survey of the Armed Forces" (SNSAF)" conducted in 1958 by the Interdepartamental Committee on Nutrition for National Defence (ICNND) of the United States of America. OBJECTIVE: this article provides an introduction to this report with an assessment of its methodology and results. MATERIALS AND METHODS: examine the objectives, approach and process of implementation of the survey conducted on a sample of 10,727 Spanish soldiers from April to June in 1958. In the first place, it will be assessed its representativeness and, secondly, the published results of three clinical examinations and one biochemical examination practiced to the soldiers will be analysed. RESULTS: the correspondence between the diagnosed diseases and the estimated micronutrient levels, both in the biochemical examination and in the analysis of diets, show that the military population examined was not affected by any serious deficiency condition. Except in vitamin A and riboflavin, in the other micronutrients no deficient levels were observed according to the ICNND standards. CONCLUSION: the final conclusion of SNAF report was that the nutrition of the Armed Forces of Spain was satisfactory. But, such statement should be qualified taking into account four possible factors of bias: the geographical distribution and the allocation of soldiers from the sample between the three armies. The improvement in the nutritional condition during the military service period and the proportion of youngsters called to the military service excluded from the service and declared fugitives.

Introducción: los estudios de la transición nutricional y epidemiológica en España no parece que hayan utilizado el informe sobre el estado nutricional del Ejército español realizado en 1958 por el Interdepartamental Commitee on Nutririon for National Defense (ICNND) de Estados Unidos.Objetivo: el objetivo de este trabajo es presentar y examinar la metodología y resultados del Spain: Nutrition Survey of the Armed Forces (SNSAF). Materiales y métodos: examinar el planteamiento y el proceso de ejecución de la encuesta realizada a una muestra de 10.727 soldados españoles entre abril y junio de 1958. Analizar, en primer lugar, su representatividad y, en segundo, los resultados de los tres exámenes médicos y de los análisis bioquímicos practicados.Resultados: la correspondencia entre las enfermedades diagnosticadas y los niveles de micronutrientes estimados muestran que la población militar examinada no estaba afectada por ningún estado carencial grave. Excepto de vitamina A y de riboflavina, no se detectaron niveles deficientes de acuerdo a los estándares de valoración del ICNND.Conclusión: la conclusión del informe de que la nutrición de las Fuerzas Armadas españolas a finales de los años cincuenta era satisfactoria debería matizarse teniendo en cuenta cuatro potenciales factores de sesgo: la distribución geográfica y entre los tres Ejércitos de los soldados de la muestra, la mejora del estado nutricional producida durante el periodo del servicio militar y la proporción de jóvenes de las correspondientes generaciones excluidos del servicio y declarados prófugos.

Global Update and Trends of Hidden Hunger, 1995-2011: The Hidden Hunger Index.

BACKGROUND: Deficiencies in essential vitamins and minerals-also termed hidden hunger-are pervasive and hold negative consequences for the cognitive and physical development of children. METHODS: This analysis evaluates the change in hidden hunger over time in the form of one composite indicator-the Hidden Hunger Index (HHI)-using an unweighted average of prevalence estimates from the Nutrition Impact Model Study for anemia due to iron deficiency, vitamin A deficiency, and stunting (used as a proxy indicator for zinc deficiency). Net changes from 1995-2011 and population weighted regional means for various time periods are measured. FINDINGS: Globally, hidden hunger improved (-6.7 net change in HHI) from 1995-2011. Africa was the only region to see a deterioration in hidden hunger (+1.9) over the studied time period; East Asia and the Pacific performed exceptionally well (-13.0), while other regions improved only slightly. Improvements in HHI were mostly due to reductions in zinc and vitamin A deficiencies, while anemia due to iron deficiency persisted and even increased. INTERPRETATION: This analysis is critical for informing and tracking the impact of policy and programmatic efforts to reduce micronutrient deficiencies, to advance the global nutrition agenda, and to achieve the Millennium Development Goals (MDGs). However, there remains an unmet need to invest in gathering frequent, nationally representative, high-quality micronutrient data as we renew our efforts to scale up nutrition, and as we enter the post-2015 development agenda. FUNDING: Preparation of this manuscript was funded by Sight and Life. There was no funding involved in the study design, data collection, analysis, or decision to publish.

[Carl Arthur Scheunert's experiments on human nutrition, 1938-1943: boundary transgressions of a scientist under national socialism]. / Carl Arthur Scheunerts Ernährungsversuche am Menschen 1938-1943: Grenzüberschreitungen eines Wissenschaftlers im Nationalsozialismus.

Carl Arthur Scheunert (1879-1957) was a German scientist who supervised several studies with prisoners that were designed to assess the optimal vitamin and nutrient supply, and were conducted by his associate Karl-Heinz Wagner (1911-2007) from 1938 to 1943. This contribution describes the aims, results and conclusions of Scheunert's research 1923 to 1945 in comparison with the national and international vitamin research and its consequences for public health measures. Conditions and results of the human experiments are reconstructed and compared with similar studies performed in other countries. Burden as well as health risks for the study participants are assessed. In addition, it is discussed whether general rules for human experimentation were followed (e.g. informed consent and minimizing of health risks). Although the available documents support the conclusion that no deaths or lasting injuries were caused, the experiments violated ethical standards, in particular because of the conditions in the Waldheim prison including progressive deterioration of nutrition and health.

The discovery of the vitamins.

The discovery of the vitamins was a major scientific achievement in our understanding of health and disease. In 1912, Casimir Funk originally coined the term "vitamine". The major period of discovery began in the early nineteenth century and ended at the mid-twentieth century. The puzzle of each vitamin was solved through the work and contributions of epidemiologists, physicians, physiologists, and chemists. Rather than a mythical story of crowning scientific breakthroughs, the reality was a slow, stepwise progress that included setbacks, contradictions, refutations, and some chicanery. Research on the vitamins that are related to major deficiency syndromes began when the germ theory of disease was dominant and dogma held that only four nutritional factors were essential: proteins, carbohydrates, fats, and minerals. Clinicians soon recognized scurvy, beriberi, rickets, pellagra, and xerophthalmia as specific vitamin deficiencies, rather than diseases due to infections or toxins. Experimental physiology with animal models played a fundamental role in nutrition research and greatly shortened the period of human suffering from vitamin deficiencies. Ultimately it was the chemists who isolated the various vitamins, deduced their chemical structure, and developed methods for synthesis of vitamins. Our understanding of the vitamins continues to evolve from the initial period of discovery.

Chapter 29: historical aspects of the major neurological vitamin deficiency disorders: overview and fat-soluble vitamin A.

The vitamine doctrine: Although diseases resulting from vitamin deficiencies have been known for millennia, such disorders were generally attributed to toxic or infectious causes until the "vitamin doctrine" was developed in the early 20th century. In the late-19th century, a physiologically complete diet was believed to require only sufficient proteins, carbohydrates, fats, inorganic salts, and water. From 1880-1912, Lunin, Pekelharing, and Hopkins found that animals fed purified mixtures of known food components failed to grow or even lost weight and died, unless the diet was supplemented with small amounts of milk, suggesting that "accessory food factors" are required in trace amounts for normal growth. By this time, Funk suggested that deficiencies of trace dietary factors, which he labeled "vitamines" on the mistaken notion that they were "vital amines," were responsible for such diseases as beriberi, scurvy, rickets, and pellagra. Vitamin A deficiency eye disease: Night blindness was recognized by the ancient Egyptians and Greeks, and many authorities from Galen onward advocated liver as a curative. Outbreaks of night blindness were linked to nutritional causes in the 18th and 19th centuries by von Bergen, Schwarz, and others. Corneal ulceration was reported in 1817 by Magendie among vitamin A-deficient dogs fed for several weeks on a diet limited to sugar and water, although he erroneously attributed this to a deficiency of dietary nitrogen (i.e. protein). Subsequently, corneal epithelial defects, often in association with night blindness, were recognized in malnourished individuals subsisting on diets now recognizable as deficient in vitamin A by Budd, Livingstone, von Hubbenet, Bitot, Mori, Ishihari, and others. During World War I, Bloch conducted a controlled clinical trial of different diets among malnourished Danish children with night blindness and keratomalacia and concluded that whole milk, butter, and cod-liver oil contain a fat-soluble substance that protects against xerophthalmia. Early retinal photochemistry: In the 1870s, Boll found that light causes bleaching of the retinal pigment, and suggested that the outer segments of the rods contain a substance that conveys an impression of light to the brain by a photochemical process. Shortly thereafter, Kühne demonstrated that the bleaching process depends upon light, and was reversible if the retinal pigment epithelium was intact. Kühne proposed an "optochemical hypothesis," a prescient concept of photochemical transduction, attributing vision to a photochemical change in visual purple (rhodopsin) with resulting chemical products stimulating the visual cells and thereby conveying a visual image. Vitamin A: In 1913, Ishihara proposed that a "fatty substance" in blood is necessary for synthesis of both rhodopsin and the surface layer of the cornea, and that night blindness and keratomalacia develop when this substance is deficient. That year McCollum and Davis (and almost simultaneously Mendel and Osborne) discovered a fat-soluble accessory food factor (later called "fat-soluble A") distinct from the water-soluble anti-beriberi factor (later called "fat-soluble B"). By 1922 McCollum and colleagues distinguished two vitamins within the fat-soluble fraction, later named vitamins A and D. In 1925 Fridericia and Holm directly linked vitamin A to night blindness in animal experiments using rats, and in 1929 Holm demonstrated the presence of vitamin A in retinal tissue. In the 1930s, Moore, Karrer, Wald, and others established the provitamin role of beta-carotene. Karrer and colleagues isolated beta-carotene (the main dietary precursor of vitamin A) and retinol (vitamin A), and determined their chemical structures. In 1947, Isler and colleagues completed the full chemical synthesis of vitamin A. Modern retinal photochemistry: Beginning in the 1930s, Wald and colleagues greatly elaborated the photochemistry of vision, with the discovery of the visual cycle of vitamin A, demonstration that rhodopsin is decomposed by light into retinal (the aldehyde form of vitamin A) and a protein (opsin), elaboration of the enzymatic conversions of various elements in the rhodopsin system, and discovery that the rhodopsin system is dependent on a photoisomerization of retinal. In 1942, Hecht and colleagues demonstrated that a single photon could trigger excitation in a rod. In 1965, Wald suggested that a large chemical amplification was necessary for this degree of light sensitivity, likely by a cascade of enzymatic reactions. Later studies elaborated this cascade and found that an intermediary in the photoisomerization of retinal interacts with transducin, a G-protein, to activate phosphodiesterases that control cyclic GMP levels, which in turn modulate the release of neurotransmitter from the rod cell. Public health: Although the availability of vitamin A through food fortification and medicinal supplements virtually eliminated ocular vitamin A deficiency from developed countries by the second half of the 20th century, vitamin A deficiency remains a serious problem in developing countries as indicated by global surveys beginning in the 1960s. Millions of children were shown to be vitamin A deficient, with resultant blindness, increased susceptibility to infection, and increased childhood mortality. Beginning in the 1960s, intervention trials showed that vitamin A deficiency disorders could be prevented in developing countries with periodic vitamin A dosing, and in the 1980s and 1990s, large randomized, double-blind, placebo-controlled clinical trials demonstrated the marked efficacy of vitamin A supplementation in reducing childhood mortality.

Chapter 30: historical aspects of the major neurological vitamin deficiency disorders: the water-soluble B vitamins.

This historical review addresses major neurological disorders associated with deficiencies of water-soluble B vitamins: beriberi, Wernicke-Korsakoff syndrome, pellagra, neural tube defects, and subacute combined degeneration of the spinal cord. Beriberi: Beriberi was known for millennia in Asia, but was not described by a European until the 17th century when Brontius in the Dutch East Indies reported the progressive sensorimotor polyneuropathy. The prevalence of beriberi increased greatly in Asia with a change in the milling process for rice in the late 19th century. In the 1880s, Takaki demonstrated the benefits of dietary modification in sailors, and later instituted dietary reforms in the Japanese Navy, which largely eradicated beriberi from the Japanese Navy by 1887. In 1889 Eijkman in Java serendipitously identified dietary factors as a major contributor to "chicken polyneuritis," which he took to be an animal model for beriberi; the polyneuritis could be cured or prevented by feeding the chickens either unpolished rice or rice polishings. By 1901, Grijns, while continuing studies of beriberi in Java, suggested a dietary deficiency explanation for beriberi after systematically eliminating deficiencies of known dietary components and excluding a toxic effect. Wernicke-Korsakoff syndrome: In the late 1870s, Wernicke identified a clinicopathological condition with ophthalmoparesis, nystagmus, ataxia, and encephalopathy, associated with punctate hemorrhages symmetrically arranged in the grey matter around the third and fourth ventricles and the aqueduct of Sylvius. In the late 1880s, Korsakoff described a spectrum of cognitive disorders, including a confabulatory amnestic state following an agitated delirium, occurring in conjunction with peripheral polyneuropathy. Beginning around 1900, investigators recognized the close relationship between Korsakoff's psychosis, delirium tremens, and Wernicke's encephalopathy, but not until several decades later were Wernicke's encephalopathy, Korsakoff's psychosis, and beriberi all linked to the deficiency of a specific dietary factor, i.e. thiamin. Thiamin: Thiamin was crystallized from rice polishings by Jansen and Donath in 1926, and synthesized by Williams and Cline in 1936. In the late 1930s and early 1940s, characteristic pathological changes of Wernicke-Korsakoff syndrome were produced in animal models, the biochemical roles of thiamin in intermediary carbohydrate metabolism were elaborated by Peters and others, and the therapeutic benefits of thiamin for Wernicke-Korsakoff syndrome and beriberi were demonstrated. By the 1950s synthetic forms of the vitamin were produced cheaply, allowing both therapeutic administration and prevention with food enrichment. Pellagra and niacin: Pellagra was unknown prior to the introduction of maize into Europe from the New World. In the 18th century, Casàl and Frapolli described the clinical features of pellagra in Europe, and linked it with poverty and subsistence on nutritionally marginal corn-based diets. In the United States, pellagra became epidemic among poor Southerners in the early 20th century, in part because of economically-driven reliance on monotonous, nutritionally inadequate diets, combined with new manufacturing methods that removed vitamins from processed grain. From 1914-1929, Goldberger completed well-designed epidemiologic investigations, tested theories with human experiments, and utilized an animal model ("black tongue" in dogs) - all strongly supporting a dietary deficiency explanation for pellagra over prevailing toxic and infectious theories. Initial prevention and treatment approaches proved inadequate because of complex social issues linked to poverty, even after Goldberger and colleagues established that dried brewer's yeast could cure or prevent pellagra less expensively than dietary modification. During the depression, the collapse of cotton as an economically viable crop facilitated crop diversification, which contributed to an abrupt decline in pellagra mortality in the early 1930s. In 1937 Elvehjem isolated the P-P (pellagra preventive) factor, identified it as nicotinic acid (niacin), and demonstrated that nicotinic acid and nicotinic acid amide cure black tongue in dogs. Although clinical trials soon confirmed dramatic therapeutic effects in individual people, therapeutic administration of niacin had relatively little impact on population-level morbidity and mortality. Vitamin fortification of foodstuffs during World War II ultimately eradicated endemic pellagra in the United States. In the 1940s and 1950s, with expanded biochemical knowledge, pellagra was reformulated as a deficiency disease due to inadequate niacin and its amino acid precursor tryptophan. Neural tube defects and folate: Folate deficiency was initially recognized clinically as a macrocytic anemia in the 1920s, and only clearly separated from pernicious anemia by the mid-20th century. When folic acid was isolated and synthesized in the 1940s, it was shown to correct the macrocytic anemia associated with pernicious anemia, while the neurological manifestations progressed. In the 1950s and 1960s, the biochemical role of folates in transferring single carbon units was elucidated. Beginning in the 1960s, folate deficiency was increasingly recognized as the major cause of preventable neural tube defects. In the early 1990s well-designed randomized trials established that folate supplementation could prevent neural tube defects. Trial data, collectively indicating that periconceptual folate administration reduces both the occurrence and recurrence risks of neural tube defects by at least 70%, helped establish governmental recommendations concerning folic acid intake and health policy concerning vitamin fortification of foodstuffs. When dietary modification and supplementation strategies proved inadequate, folic acid food fortification was legally mandated in the US in the late 1990s, which significantly improved population folate status and produced an abrupt decline (20%-27%) in the prevalence of neural tube defects at birth. Recent studies have established genetic predispositions for neural tube defects, including both infant and maternal gene polymorphisms for enzymes involved in folate-dependent homocysteine metabolism, which help explain how the genotype of the mother, the genotype of the unborn child, and environmental factors (e.g. folate intake) can all impact on the risk of neural tube defects. Subacute combined degeneration and B(12) deficiency: Pernicious anemia was recognized clinically in the mid-19th century by Addison, but the most important neurological manifestation - subacute combined degeneration of the spinal cord - was not recognized clinically and linked with pernicious anemia until the end of the 19th century, particularly by Lichtheim, Putnam, and Dana. At the beginning of the 20th century, pernicious anemia and the associated subacute combined degeneration of the spinal cord were considered, by many investigators, to result from infectious or toxic causes. During the first quarter of the 20th century, various therapies were employed, but, with the possible exception of transfusion, were largely ineffective. In the 1920s, Minot and Murphy showed that large quantities of ingested liver could be used to effectively treat pernicious anemia, and specifically could improve or prevent progression of neurological manifestations, and could extend life expectancy beyond 2 years. Beginning in the late 1920s, Castle demonstrated that a substance elaborated by the gastric mucosa ("intrinsic factor") was essential for the absorption of a dietary factor ("extrinsic factor," later shown to be vitamin B(12)) needed to prevent pernicious anemia. Over two decades, from the late 1920s until the late 1940s, increasingly potent liver extracts were manufactured that could be given either intramuscularly or intravenously. In 1947, vitamin B(12) was isolated by Folkers and colleagues, and nearly simultaneously by Smith. Shortly thereafter the therapeutic efficacy of vitamin B(12) on subacute combined degeneration was demonstrated by West and Reisner and others. By 1955, Hodgkin determined the molecular structure of cyanocobalamin using computer-assisted x-ray crystallography, allowing complete chemical synthesis of vitamin B(12) in 1960 by an international consortium. Beginning in the late 1950s, the absorption and biochemistry of vitamin B(12) were elaborated, and several lines of evidence converged to support an autoimmune basis for pernicious anemia.

Impact of the discovery of human zinc deficiency on health.

The essentiality of zinc was recognized 46 years ago. Zinc deficiency resulting in growth retardation, hypogonadism, immune dysfunction and cognitive impairment affects nearly 2 billion subjects in the developing world. High phytate content of the cereal proteins consumed in the developing world, results in decreased availability of zinc for absorption. Zinc therapy has been very successful and life saving measure in patients with acrodermatitis enteropathica and Wilson's disease. Beneficial therapeutic responses of zinc supplementation have been ovserved in acute diarrhea in children, chronic hepatitis C, shigellosis, leprosy, leishmaniasis, and common cold. Zinc supplementation was effective in decreasing incidences of infection in elderly and patients with sickle cell disease. Zinc supplementation was effective in preventing blindness in 25% of the elderly with dry type of age related macular degeneration. Zinc supplementation in the elderly decreased oxidative stress and decreased generation of inflammatory cytokines. Zinc is an intracellular signaling molecule in monocytes, dendritic cells and macrophages and it plays an important role in cell-mediated immune functions and oxidative stress. Zinc is also an anti-inflammatory agent. These unique properties of zinc may have significant therapeutic benefits in several diseases in humans. In many diseases concurrent zinc deficiency may complicate the clinical features, affect adversely immunological status, increase oxidative stress and increase generation of inflammatory cytokines. Oxidative stress and chronic inflammation may play important causative roles in many chronic diseases, including atherosclerosis, several malignancies, neurological disorders, and auto-immune diseases. It is therefore, important that status of zinc is assessed and zinc deficiency corrected in these chronic diseases. A controlled clinical trial of zinc supplementation in these disorders in order to document the preventive and therapeutic effects of zinc is warranted.

Eduardo Cruz-Coke: la vitamina D / Eduardo Cruz-Coke: the D vitamin

Presenta una abordagen sobre el término vitamina, que fue creado por el bioquímico polaco Casimir Funk en 1912. Por ese entonces, se había probrado que cierras patologías como el beriberi, el escorbuto y el raquitismo se debían a la carencia de ciertos 'factores alimenticios acesorios' en la dieta que, aunque en catidades íntimas, son esenciales para la salud del organismo. Funk propuso designar a estos factores alimenticios eccesorios, a la sazón desconocidos, con el nombre de vitaminas, creyendo que eran 'aminas de la vida'. La identificación de aquellos factores alimenticios con las aminas resultó errada, pero el término vitamina se impuso definitivamente a partir de aquel año. Poco más tarde, un bioquímico estadunidense comprobó en experimentos con ratas que la alimentación de éstás contenía al menos dos sustancias imprescindibiles para su desarrollo, la que llamó 'A-liposolubles' y 'B-hidrosolubles'. Como el término vitamina ya estaba en boga, combinó ambas denominaciones, llamándolas respectivamente vitamina C, D, E, F, una lista que sigue prolongándose.

Eduardo Cruz-Coke: la vitamina D / Eduardo Cruz-Coke: the D vitamin

Presenta una abordagen sobre el término vitamina, que fue creado por el bioquímico polaco Casimir Funk en 1912. Por ese entonces, se había probrado que cierras patologías como el beriberi, el escorbuto y el raquitismo se debían a la carencia de ciertos 'factores alimenticios acesorios' en la dieta que, aunque en catidades íntimas, son esenciales para la salud del organismo. Funk propuso designar a estos factores alimenticios eccesorios, a la sazón desconocidos, con el nombre de vitaminas, creyendo que eran 'aminas de la vida'. La identificación de aquellos factores alimenticios con las aminas resultó errada, pero el término vitamina se impuso definitivamente a partir de aquel año. Poco más tarde, un bioquímico estadunidense comprobó en experimentos con ratas que la alimentación de éstás contenía al menos dos sustancias imprescindibiles para su desarrollo, la que llamó 'A-liposolubles' y 'B-hidrosolubles'. Como el término vitamina ya estaba en boga, combinó ambas denominaciones, llamándolas respectivamente vitamina C, D, E, F, una lista que sigue prolongándose. [AU]