Genetic factors are commonly assumed to play a more important role in generalized than in partial epilepsy. This study tested this hypothesis by comparing risks of unprovoked seizures in offspring of individuals with generalized versus partial epilepsy. Overall, seizure incidence was no higher in offspring of persons with generalized epilepsy than in offspring of those with partial epilepsy. The number of affected offspring was about three times that expected from population incidence rates, regardless of whether the parent had partial or generalized epilepsy. For the subgroup of generalized cases with absence seizures, however, seizure incidence in offspring was about three times as high as for partial cases. The higher incidence in offspring of absence cases was only partly explained by a higher proportion of absence than partial cases with two factors associated with high risk in relatives, namely early age at onset and idiopathic epilepsy. Offspring of absence cases had higher risk than offspring of other cases not only for absence seizures, but for other seizure types as well, suggesting that absence epilepsy is not genetically distinct from other seizure types of epilepsy. These results suggest that the higher incidence sometimes observed in relatives of patients with generalized epilepsy is due to a small proportion of generalized cases with extremely high familial risks--most generalized epilepsies are no more likely than partial epilepsies to have a genetic basis.
Future research should focus on the understanding of the role of cigarette smoking and alcohol consumption as these two factors relate to the evolution of colorectal adenomatous polyps and subsequent carcinogenesis.
We conducted a case-control study to investigate the relation between dietary fiber, calcium, and total fat and the risk of colorectal adenomatous polyps. We used a food frequency questionnaire to assess the usual diet for 157 cases and 480 controls. In multivariate analyses, dietary fiber was inversely associated with risk of adenomatous polyps. The odds ratio (OR) for individuals in the highest vs the lowest quartile was 0.5 [95% confidence interval (CI) = 0.3-0.9]. We found an inverse association between dietary calcium and risk of adenomatous polyps, but the protective effect was present only for individuals in the fourth vs the first quartile (OR = 0.7; 95% CI = 0.3-1.3). Intake of total fat was positively associated with risk of adenomatous polyps, but we saw no consistent trend. Calcium intake appeared to modify the effect of total fat intake on the risk of adenomatous polyps.
As a means of examining the virus-relatedness of acute lymphoblastic leukemia (ALL) in children, we investigated the association between month-of-birth and the occurrence of ALL in 1487 children aged 0-15 years at the time of diagnosis. Our hypothesis being that evidence of seasonal variation in births of ALL cases would suggest exposure to a transmissible etiologic agent during the perinatal period. The data were obtained from the Surveillance, Epidemiology, and End Results (SEER) Program and consisted of children diagnosed during the years 1973-1986. Aggregate monthly incidence rates of ALL stratified by month-of-birth, for each SEER site, all sites combined, and for broad geographic regions were calculated. No evidence for an association between month-of-birth and childhood ALL was found.
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