Background: Cardiovascular diseases are the major health problem worldwide and the understanding of genetic contributions on the development of cardiovascular diseases is increasing significantly. The CD36 is a protein associated with uptake of oxidized forms of LDL and the single nucleotide polymorphism (SNP) rs1761667 A/G in the CD36 gene is correlated with increased consumption of total fat. The transcription factor STAT3 is released during the inflammatory acute phase response and the SNP rs8069645 G/A in the STAT3 gene is associated with abdominal obesity and higher intake of saturated fat. Studies have been shown the benefits of the Mediterranean diet in secondary prevention of cardiovascular disease and these dietary patterns have been often studied with nutrigenetic approach; these studies, however, are often limited to European populations, making it difficult to generalize to different populations. Hypothesis: Different dietary approaches may similarly influence in modifying metabolic, inflammatory and anthropometric profile, especially among patients with coronary arterial disease (CAD). The genetic interaction with environmental factors such as the nutrient intake, and the prescription of a different diet according to individual genotype, could influence the development and/or the treatment of cardiovascular diseases. Objective: To evaluate the effect of three dietary approaches on metabolic, inflammatory and anthropometric profile in patients with CAD and possible interactions with polymorphisms in CD36 and STAT3 genes.
A randomized clinical trial with a nutrigenetic approach among patients ≥ 40 years diagnosed with CAD. Randomization will be made in blocks from a list of random numbers generated by site www.randomization.org (sealed opaque envelopes). A questionnaire with demographic and clinical data will be applied; systolic and diastolic blood pressure, waist, hip and neck circumferences, height and weight will be assessed. Nutrients intake will be assessed through a food diary. Laboratory evaluation will consist of lipid profile (LDL-cholesterol, HDL-cholesterol and total cholesterol, serum triglycerides), glycemic profile (fasting plasma glucose, glycated hemoglobin) and inflammatory profile (high-sensitivity C-reactive protein, fibrinogen, TNF-alpha, interleukin-6 and interleukin-10). Genotyping will be made by TaqMan SNP Genotyping Assay®. Patients will be randomized in three groups: Group 1 Intervention \[Supplementation with nuts (SN)\]: standard dietary guidelines + 30g of nuts a day; Group 2 Intervention \[Supplementation with olive oil (SAO)\]: standard dietary guidelines + 30ml of olive oil a day; Group 3 \[Control diet (CO)\]: standard dietary guidelines. Patients will be followed for three months (12 weeks) and the primary endpoint will be the change in LDL-cholesterol. The follow-up visits will be made at 30 days, 60 days and 90 days (final visit).
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
SINGLE
Enrollment
204
30ml a day of olive oil
30g a day of nuts
Diet based on standard guidelines
Instituto de Cardiologia/Fundação Universitária de Cardiologia (IC/FUC)
Porto Alegre, Rio Grande do Sul, Brazil
LDL
LDL-cholesterol, in mg/dL
Time frame: twelve weeks
TC
total cholesterol (TC), in mg/dL)
Time frame: twelve weeks
NHDL
non-HDL-cholesterol, in mg/dL
Time frame: twelve weeks
HDL
HDL-cholesterol, in mg/dL
Time frame: twelve weeks
TG
serum triglyceride, in mg/dL
Time frame: twelve weeks
TyG index
Triglycerides/fasting glucose index, calculated according to (fasting triglycerides \[mg/dL\] x fasting glucose \[mg/dL\])/2
Time frame: twelve weeks
HbA1C
glycated hemoglobin (HbA1C), in %
Time frame: twelve weeks
FG
fasting glucose, in mg/dL
Time frame: twelve weeks
Insulin
serum insulin, in UI/mL
Time frame: twelve weeks
HOMA-IR
Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), calculated according to fasting insulin (microU/L) x fasting glucose (nmol/L)/22.5
Time frame: twelve weeks
inflammatory profile
CRP-us, in mg/dL; IL-6, in mg/dL; IL-10, in mg/dL
Time frame: twelve weeks
BW
body weight, in kg;
Time frame: twelve weeks
BMI
body mass index (BMI), in kg/m2, calculated according to weight (kg)/height\*height (m)
Time frame: twelve weeks
WC
waist circumference, in cm
Time frame: twelve weeks
NC
neck circumference, in cm
Time frame: twelve weeks
LAP index
Lipid Accumulation Product Index (in cm.mmol.l), calculated for men: men (waist circumference \[WC\] - 65) x triglycerides (TG), and women (WC - 58) x TG
Time frame: twelve weeks
DAAT index
Deep-Abdominal-Adipose-Tissue Index (in cm2), calculated for men (- 382.9 + \[1.09 x weight\] + \[6.04 x waist circumference (WC)\] + \[- 2.29 x body mass index (BMI)\]) and women (- 278 + \[- 0.86 x weight\] + \[5.19 x WC\])
Time frame: twelve weeks
VAI index
Visceral Adiposity Index (log), calculated for men (waist circumference (WC)/\[39 + (1.88 x body mass index (BMI)) x (triglycerides (TG)/1.03) x (1.31/HDL)\]) and women (WC/\[36.58 + (1.89 x BMI) x (TG/0.81) x (1.53/HDL)\])
Time frame: twelve weeks
PFA
plasma fatty acids, in percentage
Time frame: twelve weeks
Mon
plasma monocytes, in percentage
Time frame: twelve weeks
rs1761667 G>A
Polymorphism rs1761667 G\>A in the CD36 gene
Time frame: baseline
rs8069645 A>G
Polymorphism rs8069645 A\>G in the STAT3 gene
Time frame: baseline
Interaction diet * genotype
Interaction between dietary intervention, rs1761667 and rs8069645
Time frame: twelve weeks
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