Sidney Udenfriend

Bio: Sidney Udenfriend is an academic researcher from Nagoya University. The author has contributed to research in topics: Scurvy & Ascorbic acid. The author has an hindex of 1, co-authored 1 publications receiving 17 citations.

Skeletal manifestations of infantile scurvy.

Abstract: Recent investigations of human skeletal material from the historic St. Martin's cemetery, England, found a range of abnormal lesions in six infants that are almost certainly related to scurvy. Porous and proliferative bone lesions affecting the cranial bones and scapulae were found, and this paper presents images obtained using both macroscopic and scanning electron microscope examination of the lesions. Previous work on infantile scurvy (Ortner et al., 1997-2001) relied heavily on changes at the sphenoid, which is often missing in archaeological bone, so the identification of changes attributable to scurvy on other cranial bones and the scapulae is encouraging. The ability to recognize changes related to scurvy on a range of bones will ensure an enhanced potential for recognition of this disease in future research involving archaeological bone. Research on historical documents from Birmingham dating to the eighteenth and nineteenth centuries, combined with the probable cases of scurvy identified, supports the view that the paucity of cases of infantile scurvy from the archaeological record reflects a lack of understanding and recognition of bone manifestations, rather than a lack of occurrence in this period. Changes linked to scurvy were only found in infants from the poorer sections of the community from St. Martin's, and this is almost certainly linked to patterns of food consumption and may be related to shortages of potatoes, due to blight, experienced during this period.

Biochemistry and Molecular Biology of Ascorbic Acid Biosynthesis

Abstract: Ascorbic acid is synthesized by a variety of organisms of the animal and plant kingdoms Among mammals, however, humans, other primates, and guinea pigs cannot exceptionally produce this vitamin, and as a consequence, they are subject to a vitamin C—deficiency disease, scurvy, if the supply of vitamin C from their diet is not sufficient The genetic defect causing the inability to synthesize ascorbic acid in these animals arose as a result of a mutation that had occurred during their evolution, and this trait is currently carried in all individuals of the scurvy-prone species In this sense, scurvy is an unusual type of inborn error of metabolism (Nishikimi and Udenfriend, 1977; Stone, 1967) Besides the above-mentioned scurvy-prone animals, there is a mutant rat strain that suffers from scurvy when fed a vitamin C—deficient diet (Mizushima et al, 1984) In this chapter we will focus on the genetic basis of the incapability of humans, guinea pigs, and the scurvy-prone mutant rat to biosynthesize ascorbic acid In fact, elucidation of the human genetic defect at the gene level has long been a subject of interest for ascorbic acid research We will also deal with the recent studies related to biosynthesis of ascorbic acid, including the terminal enzymes of the biosynthetic pathways of ascorbic acid

Vitamins and cancer prevention: Issues and dilemmas

Abstract: Vitamins are a class of organic compounds that are components of an adequate diet. They or their derivatives function as coenzymes, cellular antioxidants, and/or regulators of gene expression. Fourteen vitamins are recognized in human nutrition (Vitamins A, D, E, K, B1, B2, B6, B12, C, niacin, folacin, pantothenic acid, biotin, choline), with deficiencies or excesses in intake leading to changes in protein, nucleic acid, carbohydrates, fat and/or mineral metabolism. Thus, the integrity of physiological systems, including those associated with detoxification, cellular repair, immune processes, and neural and endocrine function, depends upon the nutritional and vitamin status of the host. For these reasons, it may be anticipated that the adequacy of the vitamin supply to cells and tissues would affect the development, progress, and outcome of cancers. In this review, the definition and functions of and requirements and recommended allowance for vitamins are discussed briefly before exploring the evidence, largely from studies in experimental animals, that indicates the nature of the link between vitamins and cancer. Although evidence based on studies in animal systems reveals that vitamin intake and status can modulate the outcome of experimental carcinogenesis, the findings are often conflicting and difficult to interpret. Furthermore, it is not yet possible to develop a suitable prediction of the role of the individual vitamins in tumor development. The significance of these observations for human nutrition and cancer prevention, particularly in reference to ascorbic acid (vitamin C), vitamin E, and B-complex vitamins is considered. Vitamin A and retinoid compounds are discussed elsewhere in the symposium. The many popular misconceptions and unsound advice concerning vitamins and health, including "fake" vitamins-pangamic acid ("vitamin B15") and laetrile ("vitamin B17")-are also discussed. On the basis of current evidence, it would be inappropriate to recommend either substantial changes in habitual vitamin intakes, as provided by an adequate, well-balanced diet, or promotion of megavitamin intakes, as a means of reducing risk from cancers in the human population. However, a prudent approach toward diet and food habits, as a means of better optimizing the health consequences of our complex lifestyle is to be recommended.