A recent study has revealed that regulation of eating and smoking habit, instead of an autoimmune genetic predisposition, drives the alleged contribution of genes to an increased inflammation in depression.
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Moreover, linkage between depression and increased
inflammation even after full adjustment reveals either the presence of yet unknown
or unmeasured psychosocial and clinical confounding factors or that a core
biological relationship between the two exists independently from confounders,
according to researchers.
Case-controlled study covered 26,894 individuals with
a lifetime diagnosis of major depressive disorder from the Composite
International Diagnostic Interview and 59,001 controls with no mental disorder
and had not taken any antidepressant treatment.
Researchers then fitted linear regression models of
log C-reactive protein or CRP to regress out the effects of age, gender, body
mass index, and smoking, as well as to test whether the polygenic risk scores
or PRS for major depression associated with log CRP level and whether the
correlation between log CRP and major depression persisted following adjustment
for early-life trauma, socioeconomic status, and self-reported health matters.
The participants with depression had significantly
higher CRP levels than control participants (2.4 vs 2.1 mg/L). Additionally, more
participants than controls had CRP levels >3 mg/L (21.2% vs 16.8%), which
indicated low-grade inflammation.
PRS for depression significantly associated with log
CRP levels; however, this correlation did not remain significant following the
adjustment for BMI and smoking. Moreover, the correlation between depression
and increased log CRP level markedly reduced but remained significant following
the adjustment for clinical and sociodemographic factors.
Source: Am J Psychiatry 2021;178:522-529