Inflammation is thought to play a central role in the etiology and outcome of atherosclerosis.
Animal studies as well as in vitro and in vivo human studies suggest that host factors
modulate the magnitude and extent of inflammatory responses. We investigated familial
aggregation of three systemic markers of inflammation (C-reactive protein (CRP), white
blood cell count (WBC), and albumin) in a large, cross-sectional study conducted in
four US communities. We found evidence of substantial heritability (35-40%) for CRP
levels as well as for WBC and albumin levels. Negligible spouse correlations suggested
little influence of shared household environment on these traits. The combination
of sociodemographic factors (age, center, education), behavioral and lifestyle factors
(cigarette smoking, alcohol intake, hormone replacement therapy), obesity and fat
patterning, and prevalent diabetes explained 13-30% the interindividual variability
of these traits. There was no evidence that these inflammation phenotypes were linked
to a microsatellite marker in the interleukin-1 gene cluster on chromosome 2q, a region
that includes several candidate genes for chronic inflammatory diseases. Our findings
suggest that CRP levels, albumin levels, and WBC are determined at least partially
by genetic factors. Further efforts to identify gene loci affecting these traits are
warranted.