Plasma fatty acids: Biomarkers of dietary intake?

OBJECTIVE: To our knowledge, there is currently no consensus in the literature on the association between dietary fatty acids and circulating levels in plasma. The aim of this study was to assess the association of the intake of fatty acids with their relative plasma concentrations. METHODS: We conducted a study with 300 adults from the population-based health survey in São Paulo city (ISA-Capital 2008). We assessed demographic, lifestyle and anthropometric data, biochemical measurements, and two 24-h dietary recalls collected on non-consecutive days. Intake distribution was adjusted for intrapersonal variance to give usual dietary intake using the multiple source method (MSM). Percentage of fatty acids in plasma were analyzed by gas chromatography. The κ statistic, Spearman's correlation, and multiple linear regression (adjusted for confounders) and ratio limits of agreement were employed to determine the relationship between plasma and dietary measurements. RESULTS: Low correlation and agreement were found between dietary and plasma fatty acids. Docosahexaenoic acid (ß = 0.25; P < 0.001) and saturated (ß = 0.19; P = 0.048) fatty acids exhibited an association for means of intake adjusted by the MSM and for confounding variables. A large mean difference, with a large variation of "ratio limits," were observed between the measurements. CONCLUSION: Plasma and dietary polyunsaturated and saturated fatty acids exhibited low correlation and agreement, as well as weak association between each other. No association between intake and plasma concentrations of monounsaturated fat was found. Plasma fatty acids are not good biomarkers of food intake.

Dairy consumption and inflammatory profile: A cross-sectional population-based study, São Paulo, Brazil.

OBJECTIVES: The aim of this study was to investigate the association between dairy product consumption and plasma inflammatory biomarkers levels among a representative sample of Brazilian adults from São Paulo City. METHODS: Data were acquired from the Health Survey for São Paulo, a cross-sectional population-based study. All individuals 20 to 59 y of age with complete food consumption information (24-h dietary recall and food frequency questionnaire) and blood sample analysis were included (N = 259). The sample was separated into two groups according to systemic inflammatory pattern considering plasma levels of C-reactive protein; tumor necrosis factor-α; soluble intracellular adhesion molecule; soluble vascular cell adhesion molecule, monocyte chemoattractant protein; interleukin-1ß, -6, -8, -10, and -12; adiponectin; leptin; and homocysteine. Multiple logistic regression tests were conducted to estimate the odds ratio for the inflammatory cluster across tertiles of dairy consumption. RESULTS: When adjusted by age, smoking status, and energy intake the odds ratio for the inflammatory cluster group in the highest tertile of yogurt consumption was 0.34 (95% confidence interval [CI], 0.14-0.81) relative to the reference tertile, demonstrating also a linear effect (Ptrend = 0.015). Cheese consumption exhibited an odds ratio of 2.49 (95% CI, 1.09-5.75) relative to the reference. CONCLUSIONS: Increasing yogurt consumption might have a protective effect on inflammation, whereas cheese consumption appears to be associated with a proinflammatory status. The results of the present study aggregate a new perspective on existing evidence demonstrating the importance of assessing the contribution of dairy products on diet and their effect on the development of non-communicable diseases and associated risk factors.

Influence of IL1B, IL6 and IL10 gene variants and plasma fatty acid interaction on metabolic syndrome risk in a cross-sectional population-based study.

BACKGROUND & AIMS: Metabolic syndrome (MetS) is a cluster of interrelated risk factors for type 2 diabetes mellitus, and cardiovascular disease, with underlying inflammatory pathophysiology. Genetic variations and diet are well-known risk factor for MetS, but the interaction between these two factors is less explored. The aim of the study was to evaluate the influence of interaction between SNP of inflammatory genes (encoding interleukin (IL)-6, IL-1ß and IL-10) and plasma fatty acids on the odds of MetS, in a population-based cross-sectional study. METHODS: Among participants of the Health Survey - São Paulo, 301 adults (19-59 y) from whom a blood sample was collected were included. Individuals with and without MetS were compared according to their plasma inflammatory biomarkers, fatty acid profile, and genotype frequency of the IL1B (rs16944, rs1143623, rs1143627, rs1143634 and rs1143643), IL6 (rs1800795, rs1800796 and rs1800797) and IL10 (rs1554286, rs1800871, rs1800872, rs1800890 and rs3024490) genes SNP. The influence of gene-fatty acids interaction on MetS risk was investigated. RESULTS: IL6 gene SNP rs1800795 G allele was associated with higher odds for MetS (OR = 1.88; p = 0.017). Gene-fatty acid interaction was found between the IL1B gene SNP rs116944 and stearic acid (p inter = 0.043), and between rs1143634 and EPA (p inter = 0.017). For the IL10 gene SNP rs1800896, an interaction was found for arachidonic acid (p inter = 0.007) and estimated D5D activity (p inter = 0.019). CONCLUSION: The IL6 gene SNP rs1800795 G allele is associated with increased odds for MetS. Plasma fatty acid profile interacts with the IL1B and IL10 gene variants to modulate the odds for MetS. This and other interactions of risk factors can account for the unexplained heritability of MetS, and their elucidation can lead to new strategies for genome-customized prevention of MetS.

Polymorphisms of the TNF-α gene interact with plasma fatty acids on inflammatory biomarker profile: a population-based, cross-sectional study in São Paulo, Brazil.

The aim of the present study was to investigate the relationship of four TNF-α SNP with inflammatory biomarkers and plasma fatty acids (FA), and the interaction among them in a population-based, cross-sectional study in São Paulo, Brazil. A total of 281 subjects, aged >19 and <60 years, participated in a cross-sectional, population-based study performed in Brazil. The following SNP spanning the TNF-α gene were genotyped: -238G/A (rs361525), -308G/A (rs1800629), -857C/T (rs1799724) and -1031T/C (rs1799964). In all, eleven plasma inflammatory biomarkers and plasma FA profile were determined. To analyse the interaction between TNF-α SNP and plasma FA, a cluster analysis was performed to stratify individuals based on eleven inflammatory biomarkers into two groups used as outcome: inflammatory (INF) and non-inflammatory clusters. The -238A allele carriers had higher TNF-α (P=0·033), IL-6 (P=0·013), IL-1ß (P=0·037), IL-12 (0·048) and IL-10 (P=0·010) than the GG genotype. The -308A allele carriers also had lower levels of plasma palmitoleic acid (P=0·009), oleic acid (P=0·039), total MUFA (P=0·014), stearoyl-CoA desaturase (SCD) activity index-16 (P=0·007), SCD-18 (P=0·020) and higher levels of PUFA (P=0·046) and DHA (P=0·044). Significant interactions modifying the risk of belonging to the INF cluster were observed with inflammatory cluster as outcome between -857C/T and plasma α-linolenic acid (P=0·026), and also between -308G/A and plasma stearic acid (P=0·044) and total SFA (P=0·040). Our study contributes to knowledge on TNF-α SNP and their association with inflammatory biomarker levels, plasma FA and the interaction among them, of particular interest for the Brazilian population.

Influence of toll-like receptor 4 gene variants and plasma fatty acid profile on systemic inflammation: A population-based cross-sectional study.

OBJECTIVE: The aim of this study was to investigate the interaction of toll-like receptor 4 (TLR4) gene single nucleotide polymorphism (SNP) and plasma fatty acid (FA) profile in modulating risk for systemic inflammation. METHODS: In all, 262 adult (19-59 y) participants of the Health Survey of São Paulo met the inclusion criteria. Anthropometric parameters, blood pressure, plasma inflammatory biomarker concentration, and fatty acid profile were measured and four SNPs of the TLR4 gene (rs4986790, rs4986791, rs11536889, and rs5030728) were genotyped. Multivariate cluster analysis was performed to stratify individuals based on levels of 11 plasma inflammatory biomarkers into two groups: inflammatory (INF) and noninflammatory (NINF). RESULTS: No association was found between any of the SNPs studied and systemic inflammation. The INF cluster had higher palmitic acid levels (P = 0.039) and estimated stearoyl coenzyme A desaturase activity (P = 0.045) and lower polyunsaturated fatty acid (P = 0.011), ω-6 fatty acid (P = 0.018), arachidonic acid (P = 0.002) levels, and estimated δ-5 desaturase activity (P = 0.025) compared with the NINF cluster. Statistically significant interaction between rs11536889 and arachidonic acid/eicosapentaenoic acid (AA/EPA) ratio (P = 0.034) was found to increase the odds of belonging to the INF cluster when individuals had the variant allele C and were at the higher percentile of AA/EPA plasma ratio. CONCLUSION: Plasma fatty acid profile modulated the odds of belonging to the INF cluster depending on genotypes of TRL4 gene polymorphisms.

Association between 25-hydroxyvitamin D and inflammatory biomarker levels in a cross-sectional population-based study, São Paulo, Brazil.

Besides the classic vitamin D function on bone homeostasis, there are bodies of evidence showing that adequate status of vitamin D can modulate inflammation. We hypothesized that higher plasma levels of 25-hydroxyvitamin D (25[OH]D) would correlate with lower plasma levels of proinflammatory cytokines, acute-phase proteins, and soluble adhesion molecules and higher plasma levels of anti-inflammatory cytokines. We included all adults (age, 20-59 years) of the population-based, cross-sectional study, Health Survey-São Paulo, conducted in São Paulo (Brazil) in the study (n = 281). Anthropometric parameters, blood pressure measurements, and a fasting blood sample were collected by trained fieldworkers. Serum 25(OH)D concentration, plasma inflammatory biomarker levels (C-reactive protein, interleukin [IL]-1ß, IL-6, IL-8, IL-10, tumor necrosis factor [TNF] α, IL-12p70, adiponectin, monocyte chemoattractant protein-1, soluble intercellular adhesion molecule-1, and soluble vascular cell adhesion molecule-1), and plasma blood lipid parameters were evaluated. The prevalence of vitamin D inadequacy (<50 nmol/L) was 65.5%. Inadequate participants were younger, with lower body mass index (BMI), systolic and diastolic blood pressures, triglyceride, and total cholesterol levels as well as low-density lipoprotein cholesterol, compared with individuals adequate for vitamin D status. After adjustment, plasma concentration of soluble intercellular adhesion molecule-1 was statistically higher among adequate participants. Stratifying for BMI categories, a negative association was observed between plasma IL-6 and TNF-α levels and serum 25(OH)D concentration in normal-weight participants, whereas a negative association was detected between plasma adiponectin level and serum 25(OH)D concentration in overweight participants. The present findings suggest that BMI interacts with serum 25(OH)D levels, modulating inflammatory response and affecting plasma IL-6, TNF-α, and adiponectin levels. These data indicate that BMI plays a determinant role in the vitamin D-inflammation axis.

Influence of adiponectin gene variants and plasma fatty acids on systemic inflammation state association-A cross-sectional population-based study, São Paulo, Brazil.

SCOPE: Interactions between adiponectin genetic variants and plasma fatty acid profile can modulate plasma inflammatory biomarker concentration and the risk for metabolic diseases. The aim of this study was to investigate the interaction between single nucleotide polymorphisms of the adiponectin gene and plasma fatty acid profile in modulating the odds for systemic inflammation in a cross-sectional population-based study. METHODS AND RESULTS: Inflammatory patterns comprised 11 inflammatory biomarkers. Among participants of the Health Survey of São Paulo, 262 adults (19-59 years) met the inclusion criteria. Anthropometric parameters, blood pressure, plasma inflammatory biomarker concentration, and fatty acid profile were measured and five single nucleotide polymorphisms of the adiponectin gene (rs2241766, rs1501299, rs16861209, rs17300539, and rs266729) genotyped. Individuals in the upper 50th percentile for plasma araquidonic acid, n-3 highly unsaturated fatty acid and estimated delta-5-desaturase activity, had reduced odds of being in the inflammatory cluster (OR (95% CI) = 0.55 (0.32-0.95), 0.50 (0.28-0.88) and 0.48 (0.28-0.83), respectively). Gene-plasma fatty acid profile interaction was found between rs2241766 and n-3 (p = 0.019), rs16861209 and araquidonic acid and docosapentaenoic acid (p = 0.044, p = 0.037, respectively), and rs17300539 and saturated fatty acid (p = 0.019). CONCLUSION: Plasma fatty acid profile can interact with adiponectin gene variants to modulate the risk for systemic inflammatory state.

Interaction of SNP in the CRP gene and plasma fatty acid profile in inflammatory pattern: A cross-sectional population-based study.

OBJECTIVE: To assess the interaction of three single nucleotide polymorphisms in the C-reactive protein (CRP) gene and plasma fatty acid (FA) levels in modulating inflammatory profile. METHODS: A total of 262 subjects, aged >19 y and <60 y, participated in a cross-sectional, population-based study performed in Brazil. Three single nucleotide polymorphisms (rs1205, rs1417938, and rs2808630) spanning the CRP gene were genotyped. Eleven plasma inflammatory biomarkers and plasma FA profile were determined. Cluster analysis was performed to stratify individuals based on eleven inflammatory biomarkers into two groups: an inflammatory (INF) and a noninflammatory group. RESULTS: The INF cluster had higher age, waist circumference, systolic blood pressure, and diastolic blood pressure; higher levels of triacylglycerol, high-sensitivity CRP, tumor necrosis factor-α, interleukin (IL)-8, IL-6, IL-1ß, IL-12, IL-10, soluble monocyte chemoattractant protein-1, soluble intercellular adhesion molecule-1, C16:0, polyunsaturated fatty acid, and omega (n)-6 polyunsaturated fatty acid; and greater C20:4n-6, C18:1/18:0, and C20:4/20:3 ratios than the noninflammatory group. Statistically significant gene-plasma C16:1n-7 interaction was detected for rs1417938 (P = 0.047). Those with a dominant homozygous rs2808630 had a lower risk of belonging to the INF group with the upper 50th percentile of C20:4n-6, n-3 highly unsaturated FA, and C20:4/20:3 ratio. Regarding rs1205, A allele carriers had lower risk of being in the INF group when C20:5n-3 and n-3 highly unsaturated FA levels were greater than the median. CONCLUSIONS: The INF group exhibited changes in metabolic parameters that predispose this group to chronic disease, where polymorphisms in the CRP gene modulated the risk of being in the INF group depending on individual plasma fatty acid and lipid profile.

Associação entre polimorfismos de nucleotídeo único relacionados aos genes da proteína C reativa, TNF- e IL-10 e ácidos graxos plasmáticos e seus efeitos sobre um padrão inflamatório sistêmico em estudo de base populacional - ISA / Association between single nucleotide polymorphism in genes of CRP, TNF- and IL-10 and plasma fatty acids and their effect to a systemic inflammatory patter at a population-based study ISA-Capital

Variações genéticas podem influenciar a relação entre ácidos graxos (AG) do plasma e concentração plasmática de biomarcadores inflamatórios. Objetivo: Verificar a associação entre polimorfismos de nucleotídeo único (SNP) presentes nos genes da proteína C reativa (PCR), fator de necrose tumoral (TNF) e interleucina (IL)-10 e AG do plasma e seus efeitos sobre a concentração plasmática de biomarcadores inflamatórios em um estudo de base populacional ISACapital. Métodos: Foram coletadas informações sociodemográficas, de estilo de vida, de atividade física (IPAQ longo), hábito de fumar e beber, bem como amostras de sangue de 281 indivíduos (20 a 59 anos), oriundos de um estudo de base populacional (ISA-Capital). A partir do plasma, foram determinadas as concentrações de IL1, IL6, IL8, IL10, TNF, IL12p70, adiponectina, PCR, proteína quimiotática para macrófagos solúvel (sMCP)1, molécula de adesão intercelular solúvel (sICAM)1 e molécula de adesão celular vascular solúvel (sVCAM)1 por meio da técnica multiplex de imunoensaio e o perfil de ácidos graxos por cromatografia gasosa. O DNA genômico foi extraído e realizada a genotipagem dos SNP presentes no gene da PCR (rs1205, rs1417938, rs2808630), TNF (rs1799964, rs1799724, rs1800629 e rs361525) e IL10 (rs1800871, rs1800896 e rs1800872) pela ténica TaqMan Open Array. Foi realizada análise multivariada de cluster com base nos 11 biomarcadores inflamatórios, permitindo agrupar os indivíduos em grupo inflamado e cluster não inflamado...

Genetics variation can influence the relation between fatty acids (FA) and inflammatory biomarkers levels. Objective: To verify the association between Single Nucleotide Polymorphisms (SNP) in adiponectin, C-Reactive Protein (CRP), Tumor Necrosis Factor (TNF)- and Interleukin (IL)-10 genes and plasma fatty acids and their effects to a systemic inflammatory pattern at a population-based study. Methods: Sociodemographics information, life style, physical activity (IPAQ long form), smoking and drinking habits, as well as blood samples of 281 individuals (20 years 59 years) participants of a population based study (ISA-Capital). Plasma IL1, IL6, IL8, IL10, TNF, IL12p70, adiponectin, CRP, soluble monocyte chemoattractant protein-1 (sMCP-1), soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule 1 (sVCAM-1) levels were measured using a multiplex immunoassay and the fatty acid profile was measured by gas chromatography. The DNA was extracted and genotyping of SNP in CPR gene (rs1205, rs1417938, rs2808630), TNF (rs1799964, rs1799724, rs1800629 e rs361525) and IL10 (rs1800871, rs1800896 e rs1800872) was analyzed by TaqMan Open Array. Multivariate cluster analysis was applied on 11 inflammatory biomarkers, allowing to group individuals in inflammatory (INF) or non-inflammatory (NINF) group...