, 2005), our research did not find a significant association betw

, 2005), our research did not find a significant association between the

CRP gene and the metabolic syndrome. However, we showed an interaction between CRP rs1205 and affective status on the risk of the metabolic syndrome. Our finding of adolescent emotional problems being associated with elevated risk for the metabolic syndrome only in rs1205 CC homozygotes may be linked to their higher CRP levels. According the study by Halder et al., C allele carriers had a higher mean CRP level than the TT genotype ( Halder et al., 2010). Consistently with this finding, we showed that depressive symptoms were associated with higher risk Z-VAD-FMK clinical trial of the metabolic syndrome only in CC homozygotes, possibly through higher level of inflammation. The same study also reported interaction effect between three-marker haplotype (A–G–T, rs1417938–rs1800947–rs1205) and depressive symptoms on the higher level of CRP ( Halder et al., 2010). Unfortunately, our results are not directly comparable with these findings, since we do not have the information on the two other SNPs. It is possible that this three-marker haplotype, with T allele of rs1205, captures another functional significant variant within CRP gene. Our findings are in line with

the following hypothesis explaining the association Veliparib in vitro between depression and the metabolic syndrome: that depression dysregulates immune system pathways in ways that promote inflammation and through inflammation lead to higher risk of the metabolic syndrome. Recent studies have shown that early life trauma, with or without clinical depression, is associated with clinically significant levels of inflammation in adulthood (Danese

et al., 2007 and Pace et al., 2006). Stress system activation might promote inflammation process through several mechanisms: through activation of the sympathetic nervous system, through vagal withdrawal or through the development of glucocorticoid resistance associated with increased cytokine production (Raison et al., 2006). Thus, HPA axis hyperactivity and autonomic nervous system dysfunction could be one Clomifene plausible mechanism that explains how emotional problems in adolescence affect the metabolic syndrome in adulthood via the inflammation process (Kop and Gottdiener, 2005). In conclusion, we find that adolescent emotional problems are associated with the metabolic syndrome 40 years later, in women but not in men, although this sex difference was not statistically significant. We also show that a CRP polymorphism modifies the association between adolescent affective status and the metabolic syndrome. This suggests that inflammatory system genes could provide a link between depression and the metabolic syndrome but through more complex interactions than simple associations. Funding organisations had no role in design and conduct of the study or in preparation of the manuscript. The authors have no conflict of interests to disclosure.

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