Interactions between C-reactive protein genotypes with markers of nutritional status in relation to inflammation

• Published in: Nutrients Vol. 6; no. 11; pp. 5034 - 5050
• Main Authors: Nienaber-Rousseau, Cornelie, Swanepoel, Bianca, Dolman, Robin C, Pieters, Marlien, Conradie, Karin R, Towers, G Wayne
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 11-11-2014; MDPI
• Subjects: Adult; African Continental Ancestry Group - genetics; Alleles; Blood Glucose - metabolism; Blood Pressure; C-Reactive Protein - genetics; Cholesterol, HDL - blood; Cholesterol, LDL - blood; Cross-Sectional Studies; CRP; Diet; diet-gene interactions; Dietary Carbohydrates - administration & dosage; Dietary Fats - administration & dosage; Energy Intake; Fatty acids; Fatty Acids, Unsaturated - administration & dosage; Food; Genetic Markers; Genetic Predisposition to Disease; Genotype; Glycated Hemoglobin A - analogs & derivatives; Glycated Hemoglobin A - metabolism; Households; Humans; Inflammation; Inflammation - genetics; inflammation therapy; Life Style; Lifestyles; Medical research; Middle Aged; Motor Activity; Nutrients; nutrigenetics; Nutrition Assessment; Nutrition research; Nutritional Status; Obesity - genetics; Polymorphism, Single Nucleotide; Prospective Studies; Proteins; Questionnaires; Risk Factors; South Africa; systemic inflammation; Triglycerides - blood; South Africa
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu6115034

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.