Cardiovascular and diabetes mortality determined by nutrition during parents' and grandparents' slow growth period.

Overfeeding and overeating in families are traditions that are often transferred from generation to generation. Irrespective of these family traditions, food availability might lead to overfeeding, in its turn leading to metabolic adaptations. Apart from selection, could these adaptations to the social environment have transgenerational effects? This study will attempt to answer the following question: Can overeating during a child's slow growth period (SGP), before their prepubertal peak in growth velocity influence descendants' risk of death from cardiovascular disease and diabetes? Data were collected by following three cohorts born in 1890, 1905 and 1920 in Overkalix parish in northern Sweden up until death or 1995. The parents' or grandparents' access to food during their SGP was determined by referring to historical data on harvests and food prices, records of local community meetings and general historical facts. If food was not readily available during the father's slow growth period, then cardiovascular disease mortality of the proband was low. Diabetes mortality increased if the paternal grandfather was exposed to a surfeit of food during his slow growth period. (Odds Ratio 4.1, 95% confidence interval 1.33-12.93, P=0.01). Selection bias seemed to be unlikely. A nutrition-linked mechanism through the male line seems to have influenced the risk for cardiovascular and diabetes mellitus mortality.

Longevity determined by paternal ancestors' nutrition during their slow growth period.

Social circumstances often impinge on later generations in a socio-economic manner, giving children an uneven start in life. Overfeeding and overeating might not be an exception. The pathways might be complex but one direct mechanism could be genomic imprinting and loss of imprinting. An intergenerational "feedforward" control loop has been proposed, that links grandparental nutrition with the grandchild's growth. The mechanism has been speculated to be a specific response, e.g. to their nutritional state, directly modifying the setting of the gametic imprint on one or more genes. This study raises the question: Can overnutrition during a child's slow growth period trigger such direct mechanisms and partly determine mortality? Data were collected by following-up a cohort born in 1905 in Overkalix parish, northernmost Sweden. The probands were characterised by their parents' or grandparents' access to food during their own slow growth period. Availability of food in the area was defined by referring to historical data on harvests and food prices, records of local community meetings and general historical facts. If there was a surfeit of food in the environment when the paternal grandfather was a 9-12 year old boy a shortening of the proband survival could be demonstrated. The influence of parents', maternal grandparents' and paternal grandmothers' access to food during their slow growth period was discounted in a multivariable analysis. The results are indicative of very early programming mechanisms in human adaptation to the social environment.

Influence of epilepsy on mortality in mental retardation: an epidemiologic study.

PURPOSE: A cohort consisting of all persons with known mental retardation (MR) and living in a Swedish province on December 31, 1985, was followed for 7 years (1987-1992) to study the mortality pattern. METHODS: A file of the cohort was linked to the cause-of-death pattern of the general population in the study area. RESULTS: One hundred twenty-four deaths (8.4%) occurred among the 1,478 persons with MR. Thirty deaths (10.1%) occurred among the 296 persons with epilepsy and MR. The standardized mortality ratio (SMR) in those with only MR was significantly increased as compared with that of the general population: 1.6 [95% confidence interval (CI) 1.3-2.0]; MR and epilepsy, 5.0 (CI 3.3-7.5); and MR, epilepsy, and cerebral palsy (CP), 5.8 (CI 3.4-9.7). Mortality was increased both in patients with partial seizures without seizures secondarily generalized (SMR 3.7, CI 1.0-13.6) and in patients with seizures secondarily generalized (5.0, CI 2.3-11.0). The highest mortality occurred in patients who had seizures that were always generalized from the onset: 8.1 (CI 5.7-11.5). Mortality increased with increasing seizure frequency during the year preceding the prevalence date. In patients with epilepsy and MR, pneumonia was the most common cause of death and a seizure was the probable cause of death in 6.7%. CONCLUSIONS: Epilepsy is associated with a significantly increased mortality in persons with MR. The increase is related to seizure type and seizure frequency. Death in persons with epilepsy and MR is seldom directly due to seizures. Other impairments associated with epilepsy and MR are important causes of death.

Epilepsy in a population of mentally retarded children and adults.

All mentally retarded (MR) subjects in a northern Swedish county were assessed for the occurrence of active epilepsy on a prevalence day. Active epilepsy was found in 299 subjects (20.2% of those with MR) corresponding to a crude prevalence rate of 1.2/1000 inhabitants. The age-specific prevalence for 0-9 years was higher for females than for males, while in other age groups it was slightly higher for males or showed no difference between the sexes. Epilepsy and MR were the only disorders in 129 subjects (43.1%). Cerebral palsy was the most common associated disorder and occurred in 100 (33.4%). A presumable etiology for epilepsy and MR was identified in 73.2% and 71.9%, respectively. The presumable etiological factors which caused MR occurred prenatally in 35%, perinatally in 10% and postnatally in 9%. The pathogenetic period was unknown in 31%. In 15%, the etiological events occurred during more than one of the above periods. The presumable causes were responsible for both epilepsy and MR in all except 7 cases. MR individuals with epilepsy were significantly more retarded than those without epilepsy. The first seizure occurred during the neonatal period in 11.6% and before 1 year of age in 27.7%. Generalized tonic-clonic seizures were the most common type and occurred in 204 subjects (68.2%). Seventy-one of these also had partial seizure manifestations. Daily to weekly seizures occurred in 26.8% and 32.0% had been seizure-free for the past year.

Frequency of the fragile X syndrome in infantile autism. A Swedish multicenter study.

In a Swedish multicenter study, 102 cases of infantile autism (I.A.) were examined for fragile X (q27). The fragile X syndrome was observed in 13 of the 83 (16%) boys with I.A., but in none of the 19 girls with I.A.