PubMed · 8829572
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S Skrzypczyk. 1995. "Overzealous" recommendations causing concern.. https://pubmed.ncbi.nlm.nih.gov/8829572/
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In 1996, more than 300,000 new cases of bladder cancer were diagnosed worldwide. Besides tobacco smoking, occupation, and other factors, diet may play a role in causation of this illness. The authors performed a meta-analytical review of epidemiologic studies linking six dietary factors to bladder cancer. These factors include retinol, beta-carotene, fruits, vegetables, meat, and fat. Increased risks of bladder cancer were associated with diets low in fruit intake (relative risk (RR) = 1.40, 95% confidence interval (CI): 1.08, 1.83), and slightly increased risks were associated with diets low in vegetable intake (RR = 1.16, 95% CI: 1.01, 1.34). Elevated risks were identified for diets high in fat intake (RR = 1.37, 95% CI: 1.16, 1.62) but not for diets high in meat intake (RR = 1.08, 95% CI: 0.82, 1.42). No increased risks were found for diets low in retinol (RR = 1.01, 95% CI: 0.83, 1.23) or beta-carotene (RR = 1.10, 95% CI: 0.93, 1.30) intake. These results suggest that a diet high in fruits and vegetables and low in fat intake may help prevent bladder cancer, but the individual dietary constituents that reduce the risks remain unknown.
BACKGROUND: For term infants, human milk provides adequate nutrition to facilitate growth, as well as potential beneficial effects on immunity and the maternal-infant emotional state. However, the role of human milk in premature infants is less well defined as it contains insufficient quantities of some nutrients to meet the estimated needs of the infant. There are potential short term and long term benefits from human milk, although observational studies have suggested that infants fed formula have a higher rate of growth than infants who are breast fed. OBJECTIVES: The main objective is to determine if addition of supplemental fat to human milk leads to improved growth and neurodevelopmental outcomes without significant adverse effects in preterm infants. SEARCH STRATEGY: The standard search strategy of the Cochrane Neonatal Collaborative Review Group was used. This includes searches of the Oxford Database of Perinatal Trials, MEDLINE, previous reviews including cross references, abstracts, conferences and symposia proceedings, expert informants, journal handsearching mainly in the English language. SELECTION CRITERIA: All trials utilizing random or quasi-random allocation to supplementation of human milk with fat or no supplementation in preterm infants within a hospital were eligible. DATA COLLECTION AND ANALYSIS: Data were extracted using the standard methods of the Cochrane Neonatal Collaborative Review Group, with separate evaluation of trial quality and data extraction by each author and synthesis of data using relative risk and weighted mean difference. MAIN RESULTS: Results are available for only one small study evaluating the effects of fat supplementation. There are insufficient data to evaluate short term or long term growth outcomes and neurodevelopmental outcomes. There are insufficient data to comment on potential adverse effects. REVIEWER'S CONCLUSIONS: There is insufficient evidence to make recommendations for practice. Further research should evaluate the practice of supplementation of human milk with fat. This may best be done in the context of the development of multicomponent fortifiers. Both short term growth outcomes and long term growth and neurodevelopmental outcomes should be evaluated. Adverse effects should be evaluated.
This review addresses the hypothesis that polyunsaturated fatty acids (PUFA), particularly those of the n-3 family, play essential roles in the maintenance of energy balance and glucose metabolism. The data discussed indicate that dietary PUFA function as fuel partitioners in that they direct glucose toward glycogen storage, and direct fatty acids away from triglyceride synthesis and assimilation and toward fatty acid oxidation. In addition, the n-3 family of PUFA appear to have the unique ability to enhance thermogenesis and thereby reduce the efficiency of body fat deposition. PUFA exert their effects on lipid metabolism and thermogenesis by upregulating the transcription of the mitochondrial uncoupling protein-3, and inducing genes encoding proteins involved in fatty acid oxidation (e.g. carnitine palmitoyltransferase and acyl-CoA oxidase) while simultaneously down-regulating the transcription of genes encoding proteins involved in lipid synthesis (e.g. fatty acid synthase). The potential transcriptional mechanism and the transcription factors affected by PUFA are discussed. Moreover, the data are interpreted in the context of the role that PUFA may play as dietary factors in the development of obesity and insulin resistance. Collectively the results of these studies suggest that the metabolic functions governed by PUFA should be considered as part of the criteria utilized in defining the dietary needs for n-6 and n-3 PUFA, and in establishing the optimum dietary ratio for n-6:n-3 fatty acids.