Relatively little is known about the mechanisms underlying carcinogenesis in humans. Caloric restriction strongly inhibits the development of neoplasia in rodents, and there is evidence of a positive relationship between cancer and body weight in humans. Caloric restriction early in life is also known to permanently diminish organ cellularity. A recent link between adult stature and cancer incidence similarly implicates a lasting effect for growth and possibly for early nutrition in carcinogenesis. It is postulated that cancer risk is proportional to the number of proliferating cells, which in turn depends on both the number of cells and the rate of cell division within the tissue. This hypothesis is consistent with several aspects of human carcinogenesis, including multistage models and the epithelial origin of most cancers.
Nutrition support for the patient with cancer is an important part of the overall treatment regimen. Nutrition support for the child with cancer poses a special challenge. For the purpose of reviewing the special nutritional needs of children with cancer, a Task Force was formed by the American Academy of Pediatrics to review the current state of knowledge. The work of the Task Force was supported by the Food and Drug Administration through its Liaison Representative, Joginder Chopra, M.D., Staff support from the Academy was provided by Jean D. Lockhart, M.D., This review is prepared from the Task Force Report to the FDA. It is designed to review factors enhancing nutritional risks for the child with cancer and to discuss nutritional intervention strategies and their efficacies.
Studies were conducted to examine in detail the effects of vitamin A deficiency on fetal growth and development in the rat. The gradations of deficiency were examined in two studies. The first included total vitamin A depletion followed by retinoic acid supplements, and the second included three different levels of restricted intake of retinyl acetate (42, 16, or 8 mug of retinol equivalents/day/kg of body weight) in vitamin A-depleted rats. In the first study, extensive fetal resorption and death were observed in retinoic acid-fed females after day 14 of gestation. These findings confirmed the morphological studies of Thompson and associates (Proc. Roy. Soc. London, Ser. B 159, 510-535, 1964) who found the earliest Detectable histological lesions to be in the placentas at days 15-16 of pregnancy. Analyses were carried out of the total weight, the DNA, RNA, and protein contents of fetuses and placentas of different gestational ages in retinyl ester-fed and retinoic acid-fed females. Biochemical changes indicative of a reduced rate of cell division were observed in both fetus and placenta by day 14 in the retinoic acid-fed rats. The few live fetuses in this group maintained a growth rate of only 60-70% of that of the fetuses of retinyl ester-fed dams after day 14. By contrast, the growth rate of the placentas (of live fetuses) after day 14 of gestation was not as consistently affected by retinol deficiency. Restriction of retinyl acetate intake (in the second study) significantly reduced both the total litter size and the number of live pups per litter. Most of the females in the retinyl acetate-restricted groups delivered pups that had normal body weight and appeared normal on visual inspection. Significant differences from normal controls were seen only in the neonates from dams given 8 mug of retinol equivalents (per kg of body weight per day), which had smaller livers and kidneys than the control neonates. In contrast, the weights of the brains of the neonates in all three retinyl acetate-restricted groups showed no differences from control values. Vitamin A assays on maternal and neonatal sera and livers indicated that the transport of vitamin A across the placenta was well regulated, and suggested that this transport is maintained with high priority in the presence of maternal deficiency. The effects of vitamin A deficiency on fetal growth and development might reflect primary effects on the placenta, with secondary effects on the fetus, or primary direct effects on the fetus itself. The mechanisms of the observed effects remain to be explained.
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