PubMed · 13826530
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
K E GARDNER. 1960. Problems in troop feeding.. https://pubmed.ncbi.nlm.nih.gov/13826530/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Nutrition has long been suspected to play an important role in cancer etiology. The biologic properties of nutrients make them prime candidates to aid in cancer prevention. Indeed, early epidemiologic cancer studies seemed to confirm the relevance of diet. These studies, however, were plagued by recall bias and confounding and may have thus been misleading. The results from large, prospective cohorts do not support a strong relation between nutrition and cancer. Given the difficulties in precisely assessing habitual diet, modest associations may exist, which may be impossible to capture when relying on self-reported dietary information. Energy balance, reflected in a low body weight and high level of physical activity, has been more convincingly related to lower cancer rates. The potential importance of more extreme dietary regimens and of nutrition during earlier periods of life remains to be explored. Finally, epigenetic research is likely to contribute to the understanding of nutritional regulation of gene expression.
The yellow color of the macula lutea is due to the presence of the carotenoid pigments lutein and zeaxanthin. In contrast to human blood and tissues, no other major carotenoids including Beta-carotene or lycopene are found in this tissue. The macular carotenoids are suggested to play a role in the protection of the retina against light-induced damage. Epidemiological studies provide some evidence that an increased consumption of lutein and zeaxanthin with the diet is associated with a lowered risk for age-related macular degeneration, a disease with increasing incidence in the elderly. Protecting ocular tissue against photooxidative damage carotenoids may act in two ways: first as filters for damaging blue light, and second as antioxidants quenching excited triplet state molecules or singlet molecular oxygen and scavenge further reactive oxygen species like lipid peroxides or the superoxide radical anion.
Selenium biochemistry is reviewed in respect to its presumed relevance to age-related ocular diseases. Selenium is an essential trace element that exerts its physiological role as selenocysteine residue in at least 25 distinct selenoenzymes in mammals. Lack of GPx-1 due to alimentary selenium deprivation has been inferred to induce cataract in rats and was demonstrated to cause cataracts in mice by targeted gene disruption. The role of other selenoproteins in the eye remains to be worked out. Selenium in excess of the tiny amounts required for selenoprotein synthesis is toxic in general and causes cataracts in experimental animals. Clinical evidence for a protective role of selenium in the development of cataract, macula degeneration, retinitis pigmentosa or any other ocular disease is not available, likely because suboptimum selenium intake, as it may result from unbalanced diet, does not cause any pathologically relevant selenium deficiency in the eye. At present, there is neither theoretical nor an empirical basis to expect beneficial effects of selenium supplementation beyond the dietary reference intakes of 55 microg/day in the context of ocular diseases.