Unfavorable socioeconomic conditions in early life presage expression of proinflammatory phenotype in adolescence.
OBJECTIVE
Unfavorable socioeconomic status (SES) circumstances early in life are associated with heightened vulnerability to respiratory and cardiovascular diseases in adulthood. However, little is known about mechanisms underlying this phenomenon.


METHODS
This study examined whether early-life SES predicts future activity of two genes involved in regulating inflammation. An ethnically diverse cohort of 136 adolescent females was enrolled in the study. SES was measured by home ownership. The messenger ribonucleic acid (mRNA) for glucocorticoid receptor (GR) and toll-like receptor 4 (TLR4) was quantified in peripheral blood leukocytes using real-time reverse transcriptase polymerase chain reaction (RT-PCR).


RESULTS
Three findings emerged: a) Years 2 to 3 of life were a critical period: the participants whose families owned homes during these childhood years showed higher GR mRNA and lower TLR4 mRNA during adolescence, a profile that suggests better regulation of inflammatory responses. b) These effects were not mediated through current economic circumstances, life stress, or health practices. C) Changes in SES during later years were unable to "undo" these effects.


CONCLUSIONS
These findings suggest that unfavorable SES circumstances in the early years of life presage the expression of a proinflammatory phenotype in adolescence. To the extent that this proclivity toward inflammation persists over one's lifespan it could explain the heightened incidence of respiratory and cardiovascular disease in low SES populations.
Miller
Gregory
G
Department of Psychology, University of British Columbia, Vancouver, BC, Canada. gemiller@psych.ubc.ca
Chen
Edith
E
D000293:Adolescent; D041923:Adolescent Development; D000328:Adult; D002318:Cardiovascular Diseases / Q000191:economics / Q000235:genetics; D002648:Child; D002675:Child, Preschool; D015331:Cohort Studies; D005260:Female; D006798:Housing / Q000191:economics; D006801:Humans; D007223:Infant; D007249:Inflammation / Q000235:genetics*; D010067:Ownership; D010641:Phenotype; D012333:RNA, Messenger / Q000032:analysis / Q000378:metabolism; D011965:Receptors, Glucocorticoid / Q000378:metabolism*; D012140:Respiratory Tract Diseases / Q000191:economics / Q000235:genetics; D012307:Risk Factors; D012923:Social Class; D051197:Toll-Like Receptor 4 / Q000378:metabolism*
D012333:RNA, Messenger; D011965:Receptors, Glucocorticoid; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4