Parent-offspring association of metabolic syndrome in the Framingham Heart Study.

Pubmed ID: 25584075

Pubmed Central ID: PMC4290436

Journal: Diabetology & metabolic syndrome

Publication Date: Dec. 15, 2014

Affiliation: Cardiovascular Section, Genomics of Metabolic, Cardiovascular and Inflammatory Disease Branch, Social Epidemiology Research Unit, National Human Genome Research Institute, 10 Center Drive, Room 7 N316 MSC 1644, Bethesda, MD 20892 USA.

Authors: Khan RJ, Gebreab SY, Riestra P, Xu R, Davis SK

Cite As: Khan RJ, Gebreab SY, Riestra P, Xu R, Davis SK. Parent-offspring association of metabolic syndrome in the Framingham Heart Study. Diabetol Metab Syndr 2014 Dec 15;6(1):140. doi: 10.1186/1758-5996-6-140. eCollection 2014.

Studies:

Abstract

BACKGROUND: Metabolic syndrome (MetS) is a clustering of five metabolic risk factors including abdominal obesity, elevated blood pressure, hypertriglyceridemia, low high-density lipoprotein cholesterol (HDL-C), and impaired fasting glucose. Few studies have fully reported the strength of clustering of these risk factors in a parent-offspring relationship. This analysis describes the associations between parents and their adult offspring in regard to MetS. It also estimates the association between each risk factor in parents and the presence of MetS in their offspring. METHODS: We analyzed data for 1193 offspring (565 sons, and 628 daughters) from the Framingham Offspring Study who attended examinations 5, 6, and 7. Information about their parents was collected from examinations 13, 14 and 15 of the Framingham Original Cohort study. We used pedigree file to combine parental and offspring's data. Participants were classified as having the MetS according to the Adult Treatment Panel III criteria. Analyses were conducted separately for mothers and fathers. Logistic regression was used to estimate the associations. RESULTS: After adjusting for age, education, smoking, alcohol consumption and physical activity level of offspring, no significant association was found between father's and their offspring's MetS. Mother's MetS was significantly and positively associated with their daughter's MetS (adjusted odds ratio or adj OR: 1.63; 95% confidence Interval, CI:1.02-2.61), but not with their sons' MetS. When analyzed by individual components, maternal impaired glucose (adj OR: 2.03; 95% CI: 1.02- 9.31), abdominal obesity (adj OR: 1.56; 95% CI: 0.98- 2.55) and low HDL-C (adj OR: 2.12; 95% CI: 1.36-3.32) were associated daughter's MetS. Maternal low HDL-C and raised total cholesterol showed marginal association with son's MetS. For fathers, only impaired glucose (adj OR: 4.91; 95% CI: 2.07- 11.68) was associated with their daughter's MetS. CONCLUSIONS: Using the data from Framingham Heart Study, we demonstrate differential association of MetS and its components between parents and offspring. Mother's MetS was strongly related with daughter's MetS, but the association was inconsistent with son's MetS. No association was found between father's MetS and offspring's Mets. These results provide evidence that daughters with mother's MetS are in higher risk than daughters or sons with father's MetS.