Interactions between C-Reactive Protein Genotypes with Markers of Nutritional Status in Relation to Inflammation

Abstract

Inflammation, as indicated by C-reactive protein concentrations (CRP), is a risk factor for chronic diseases. Both genetic and environmental factors affect susceptibility to inflammation. As dietary interventions can influence inflammatory status, we hypothesized that dietary effects could be influenced by interactions with single nucleotide polymorphisms (SNPs) in the CRP gene. We determined 12 CRP SNPs, as well as various nutrition status markers in 2010 black South Africans and analyzed their effect on CRP. Interactions were observed for several genotypes with obesity in determining CRP. Lipid intake modulated the pro-inflammatory effects of some SNPs, i.e., an increase in both saturated fatty acid and monounsaturated fatty acid intake in those homozygous for the polymorphic allele at rs2808630 was associated with a larger increase in CRP. Those harboring the minor alleles at rs3093058 and rs3093062 presented with significantly higher CRP in the presence of increased triglyceride or cholesterol intake. When harboring the minor allele of these SNPs, a high omega-6 to -3 ratio was, however, found to be anti-inflammatory. Carbohydrate intake also modulated CRP SNPs, as HbA1C and fasting glucose levels interacted with some SNPs to influence the CRP. This investigation highlights the impact that nutritional status can have on reducing the inherent genetic susceptibility to a heightened systemic inflammatory state.

Education, Smoking and CRP Genetics in Relation to C-Reactive Protein Concentrations in Black South Africans

“…However, nicotine does increase energy expenditure [ 40 ], which may have resulted in the smaller WC observed in active tobacco users in our study. To our knowledge, we present the first indication that smoking status results in increased CRP concentrations in individuals harboring the minor allele of rs3093068, of which the major allele is associated with increased CRP concentrations [ 19 ]. Smokers with the minor allele had odds of presenting with elevated CRP concentrations statistically similar to those with the wild-type, negating the CRP-lowering effects of the minor allele.…”

“…Data from twin and family studies attribute up to 40% of heritability in CRP concentrations to heritable factors such as genetics; however, little is known about the genetics underpinning CRP in African populations [ 17 , 18 ]. Expression of a gene can be modulated by the environment and behavior of an individual, which may alter the phenotype observed [ 19 ]. To our knowledge, nothing has been reported on how different CRP single nucleotide polymorphisms (SNPs) interact with markers of SES and how this interaction could modulate CRP concentrations.…”

CRP Genotypes Predict Increased Risk to Co-Present with Low Vitamin D and Elevated CRP in a Group of Healthy Black South African Women

“…Various genetic factors have been reported to affect CRP concentrations, with twin and family studies indicating substantial heritability of between 35% and 40% [ 16 ]. Furthermore, interactions have been observed between CRP single nucleotide polymorphisms (SNPs) and dietary intake influencing circulating CRP concentrations [ 17 ]. In contrast, infection with the human immune deficiency virus (HIV) is not associated with CRP [ 18 ], an observation re-established by the present study.…”

“…African Americans, included in a meta-analysis, presented with CRP concentrations of 2.6 mg/L compared to 2.51 mg/L in Hispanics, 2.03 mg/L in white Americans, and 1.01 mg/L in East Asians [ 20 ]. Elevated CRP concentrations are also typical in black South Africans [ 17 ]; comparisons show them to be higher (3.61 mg/L) than those of their white (1.13 mg/L) compatriots [ 21 ].…”

Rheumatoid Cachexia, a Metabolic Rheumatoid Arthritis Disorder: Pathophysiological Mechanisms, Diagnostic Tools and Current Therapeutic Strategy

“…In recent decades, the concept of rheumatoid cachexia has received more consideration [5] based on the understanding of how nutritional alterations affect patient quality of life, evolution and the prognosis of rheumatologic conditions such us increased risk of cardiovascular disease and osteoporosis [8,9]. Advances have also been made in our comprehension of the pathophysiological mechanisms that mediate the nutritional impact of inflammatory diseases (acute and chronic) [10,11]. Mean while, the tools available for evaluating and staging RC have become more precise and can more adequately define the effects of inflammatory conditions on lean mass, fat mass and energy expenditure [12].…”