Familial history of metabolic disorders and the Multiple Metabolic Syndrome: The NHLBI Family Heart Study

Citation
Kj. Hunt et al., Familial history of metabolic disorders and the Multiple Metabolic Syndrome: The NHLBI Family Heart Study, GENET EPID, 19(4), 2000, pp. 395-409
Citations number
41
Categorie Soggetti
Molecular Biology & Genetics
Journal title
GENETIC EPIDEMIOLOGY
ISSN journal
07410395 → ACNP
Volume
19
Issue
4
Year of publication
2000
Pages
395 - 409
Database
ISI
SICI code
0741-0395(200012)19:4<395:FHOMDA>2.0.ZU;2-2
Abstract
A case-control study was conducted to investigate the association between f amily history of obesity, hypertension, and diabetes and the co-occurrence of metabolic disorders associated with the multiple metabolic syndrome (MMS ). Included were 1,448 African and European American men and women aged 48- 71 who participated in both the third cohort examination of the Atheroscler osis Risk in Communities study, 1992-1994, and phase I of the Family Heart Study 1993-1995. The joint occurrence of hypertension, dyslipidemia, and di abetes or impaired fasting glucose in an individual determined his/her stat us of "affected" (MMS: n = 97), while the absence of these three metabolic disorders determined his/her status of "unaffected" (Control: n = 527). Fir st-degree relatives provided the information to calculate family risk score s (FRSs) for the phenotypes under study: obesity, diabetes and hypertension . Although the majority of cases were obese (76.3%), family history of obes ity was associated only weakly with the MMS, while family history of diabet es, or hypertension was associated significantly with the MMS (controlling for age, race, gender, and sampling group). Obesity of cases and controls m odified the strength of these associations-odds ratios were 2.5 (95% CI:1.1 -6.1) and 2.9 (95% CI:1.2-7.0) for the diabetes and hypertension FRSs in th e non-obese, while in obese individuals the respective odds ratios were 1.6 (95% CI:0.9-2.8) and 1.7 (95% CI:0.9-3.1). These results may imply that ob esity, whether familial or environmental in nature, is associated with the development of the MMS. while in non-obese individuals a family history of diabetes, hypertension, or obesity is a marker of genetic predisposition to components of the MMS. (C) 2000 Wiley-Liss. Inc.