, 2004). Much less attention, however, has been paid to the association between anxiety and the metabolic syndrome, with the few existing cross-sectional studies reporting mixed

findings (Carroll et al., 2009 and Dunbar et al., 2008). So far, the biological mechanisms underlying the association between depression and anxiety and later metabolic syndrome remain poorly understood. One biological factor receiving increased attention as a potential mechanism for this association is inflammation. C-reactive protein (CRP) is a non-specific marker of systemic Venetoclax cost inflammation. Its concentration rises as much as 2000-fold during the first 24–48 h after the onset of tissue injury or inflammation. Higher CRP plasma levels have been shown to be associated with both the metabolic syndrome (Devaraj Selleck Wortmannin et al., 2009) and depression

(Raison et al., 2006, Gimeno et al., 2009 and Howren et al., 2009) and anxiety (Bankier et al., 2009 and Pitsavos et al., 2006), although some studies failed to confirm these associations (Douglas et al., 2004, O’Donovan et al., 2010 and Whooley et al., 2007). Among the possible reasons for these inconsistent findings is the potential confounding of the relationship by factors such as lifestyle and socioeconomic conditions. Genetic studies have the potential to shed light on the role of CRP in the relationship

between depression and anxiety and the metabolic syndrome, since genes influencing CRP levels will not be influenced by these potential confounding factors. It has been estimated that the interindividual variability in blood CRP level is 35–52% heritable (Pankow et al., 2001 and MacGregor et al., 2004) and certain single nucleotide polymorphisms (SNPs) of the Resminostat CRP gene have been found to strongly influence the blood level of CRP ( Kolz et al., 2008, Almeida et al., 2009 and Lee et al., 2009). Two CRP SNPs, rs3093068 and rs1205, have been associated with variation in CRP level, with the C allele of rs3093068 and the C allele of rs1205 being associated with higher level of plasma CRP ( Kolz et al., 2008 and Halder et al., 2010). To date, only a few studies have investigated CRP variations in relation to the metabolic syndrome, with some providing null results ( Evrim et al., 2009 and Timpson et al., 2005), and the most recent reporting a significant association ( Hsu et al., 2010). Similarly, only two studies have evaluated associations between CRP polymorphisms and depression: one study reported a significant association between CRP rs1205 polymorphism and clinically significant depression in men ( Almeida et al., 2009), while another found no effect of three CRP polymorphisms or haplotypes on depressive scores ( Halder et al., 2010).