Four families highly clustered for extreme longevity are described here, representing the first report of clustering for this phenotype. Families such as these may prove to be helpful in the further understanding of the genetic contribution to achieving exceptional longevity.
Family studies of exceptional longevity can potentially identify genetic and other factors contributing to long life and healthy aging. Although such studies seek families that are exceptionally long lived, they also need living members who can provide DNA and phenotype information. On the basis of these considerations, the authors developed a metric to rank families for selection into a family study of longevity.
While there is evidence that longevity runs in families, the study of long-lived families is complicated by the fact that longevity-related information is available only for the oldest old, many of whom may be deceased and unavailable for testing, and information on other living family members, primarily descendents, is censored. This situation requires a creative approach for analyzing determinants of longevity in families.
The Journal of Clinical Endocrinology and Metabolism
CONTEXT: A relation between low thyroid activity and prolonged life span in humans has been observed. Several studies have demonstrated hereditary and genetic influences on thyroid function. OBJECTIVE: The objective of the study was to test whether low thyroid activity associated with extreme longevity constitutes a heritable phenotype, which could contribute to the familial longevity observed in the Leiden Longevity Study. DESIGN: This was a cross-sectional study. SETTING: The study was conducted at a university hospital in the city of Leiden, The Netherlands.
The pathogenetic links between diet and diseases such as hypertension and atherosclerosis remain the subject of much controversy. This article reviews the evidence about the relationship between diet and these two widespread adult conditions, proposes an approach for their early recognition, examines the rationale and safety of dietary changes, and formulates specific recommendations.
NIDDM appears to be a disease of complex aetiology. Although specific genetic markers for the disease have yet to be defined, there is clear evidence for genetic predisposition, with high concordance in monozygous twins. However, concordance is incomplete, and there are therefore additional, non-genetic, mechanisms which are responsible for increasing the risk of the disease in susceptible subjects. At the present time, the most plausible environmental precipitants appear to be the inter-related triad of obesity, low levels of habitual physical exercise and diet.
