Prenatal famine exposure and cognition at age 59 years.

BACKGROUND: Despite the perceived importance of early life nutrition for mental development, few studies have related gestational undernutrition to later-life cognitive functioning. We investigated the consequences of gestational exposure to the Dutch famine of 1944-45 for cognitive functioning at the age of 59 years. METHODS: We recruited men and women who were (i) born in birth clinics in Amsterdam, Rotterdam and Leiden, between January 1945 and March 1946, whose mothers experienced famine during or immediately preceding pregnancy (n = 354); (ii) born in the same three institutions during 1943 and 1947, whose mothers did not experience famine during this pregnancy (n = 292); or (iii) same-sex siblings of those in the first two categories (n = 311). We assessed cognitive performance at the age of 59 years by means of a comprehensive test battery. RESULTS: All cognitive functioning test scores were within normal ranges for this age group. There were no differences in cognitive performance at the age of 59 years between individuals exposed to gestational undernutrition and those without this exposure. For the general cognitive index, a summary measure across six functional domains (mean 100, standard deviation (SD) 15 points), famine exposure was associated with a decrease of 0.57 points [95% confidence interval (95% CI) -2.41 to 1.28] points. Individuals exposed to famine in gestational weeks 1-10 had a cognitive functioning index 4.36 (95% CI 8.04-0.67) points lower than those without this exposure. Within-sibling-pair analyses gave consistent results. CONCLUSION: We found no overall association between maternal exposure to acute famine in pregnancy and cognitive performance of the offspring at the age of 59 years, but cannot rule out an association specific to early pregnancy exposure.

Glycemic load, glycemic index, and pancreatic cancer risk in the Netherlands Cohort Study.

BACKGROUND: Recent studies of pancreatic cancer suggest a role for hyperinsulinemia in carcinogenesis. Because insulin is secreted in response to elevated blood glucose concentrations, dietary factors that increase these concentrations may be important in pancreatic carcinogenesis. OBJECTIVE: The objective was to examine prospectively the relation between pancreatic cancer risk and dietary glycemic load (GL), overall glycemic index (GI), and intake of total carbohydrates and mono- and disaccharides. DESIGN: The Netherlands Cohort Study consisted of 120,852 men and women who completed a baseline questionnaire in 1986. After 13.3 y of follow-up, 408 pancreatic cancer cases were detected, 66% of which were microscopically confirmed. A validated 150-item food-frequency questionnaire, completed at baseline, was used to calculate carbohydrate and mono- and disaccharide intakes and the GL and GI of the diet. RESULTS: Dietary GL, GI, or intake of carbohydrates and mono- and disaccharides were not associated with pancreatic cancer risk in this cohort. Also, the associations were not modified by sex. Our results did not change after the analysis was restricted to microscopically confirmed pancreatic cancer cases or after individuals who reported a history of diabetes at baseline were excluded from the analyses. CONCLUSIONS: Overall, our findings do not support the hypothesis that GL, GI, or intake of carbohydrates and mono- and disaccharides are positively associated with pancreatic cancer risk. This is in agreement with previous prospective studies that investigated the relation between GL and GI and pancreatic cancer risk.