Parental and offspring associations of the metabolic syndrome in the Fels Longitudinal Study123

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Background: Evidence shows that some causes of the metabolic syndrome (MS) begin in childhood, which could indicate a familial association, through either genetic inheritance or cohabitation.

Objective: This study examined associations between parents and adult offspring diagnoses of the MS and its risk factors.

Design: Measurements were obtained from adult participants and their adult offspring enrolled in the Fels Longitudinal Study, with simultaneous waist circumference, systolic blood pressure (SBP), diastolic blood pressure (DBP), triglycerides, HDL, and glucose observations used for diagnosis. On the basis of repeated measurements (in some cases), adult participants were classified as having the MS at least once or as never having the MS. Chi-square tests, ORs, and mixed-effects models were used to study familial associations.

Results: Maternal (OR: 2.5; 95% CI: 1.1, 5.5) and paternal (OR: 4.1; 95% CI: 1.4, 12.1) MS classifications were significantly associated with MS classification in sons. MS classification in mothers and daughters (OR: 2.7; 95% CI: 0.9, 8.7; P = 0.08) was similar to that in sons but was not significant, whereas fathers and daughters were not associated (OR: 1.1; 95% CI: 0.4, 3.5). Maternal MS diagnoses were significantly and positively associated with triglycerides in male offspring and were significantly associated with SBP, DBP, and triglycerides in females. Paternal diagnoses were significantly associated only with DBP and HDL in male offspring.

Conclusions: Parental MS diagnosis is significantly associated with MS diagnosis in adult male offspring, and adverse levels of certain risk factors are associated between offspring and parents, although these associations vary across risk factors and child sex.

Abbreviations:

BP
blood pressure
DBP
diastolic blood pressure
FLS
Fels Longitudinal Study
MS
metabolic syndrome
SBP
systolic blood pressure
WC
waist circumference

Cited by (0)

1

From the Department of Biostatistics, School of Medicine, Virginia Commonwealth University, Richmond, VA (RTS, ZL, XD, CR, and SSS); the Department of Pediatrics, School of Medicine, University of Colorado, Aurora, CO (SD); and the Department of Pediatrics, School of Medicine, University of Pittsburgh, Pittsburgh, PA (SA).

2

Supported by an investigator-initiated grant from the National Institute of Diabetes and Digestive and Kidney Diseases and the NIH (grant 5R01DK071485).

3

Address correspondence and reprint requests to RT Sabo, One Capitol Square, Room 737, 830 East Main Street, PO Box 980032, Richmond, VA 23298-0032. E-mail: [email protected].