Determinants of urinary betaine excretion at baseline by linear regression.

<p>Abbreviations: eGFR estimated glomerular filtration rate; UACR urinary albumin/creatinine ratio.</p>a<p>Adjusted for all variables in the model.</p>b<p>Standardized beta-coefficient.</p>c<p>Log transformed.</p><p>Not significant in age and gender adjusted analysis: Acute coronary syndrome, diuretics, ACE-inhibitors, fasting blood sample, N-vessel disease, total cholesterol, low density lipoprotein, apo lipoprotein A1, apo lipoprotein B, CRP.</p

Determinants of urinary betaine excretion in diabetes by linear regression.

<p>Abbreviations: eGFR estimated glomerular filtration rate.</p>a<p>Adjusted for all variables in the model.</p>b<p>Standardized beta-coefficient.</p>c<p>Antidiabetic medication vs no antidiabetic medication.</p><p>Not significant in age and gender adjusted analysis: body mass index, smoking, hypertension, type of diabetes, total cholesterol, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apo lipoprotein A1, triglycerides, urinary albumin/creatinine ratio.</p

Density plot showing the relative distributions of urinary betaine excretion in patients with diabetes (black line), no diabetes and serum glucose ≥5.5 mmol/L (green line), and no diabetes and serum glucose <5.5 mmol/L (blue line).

<p>Density plot showing the relative distributions of urinary betaine excretion in patients with diabetes (black line), no diabetes and serum glucose ≥5.5 mmol/L (green line), and no diabetes and serum glucose <5.5 mmol/L (blue line).</p

Generalized linear models showing age and gender adjusted associations between urinary betaine excretion and estimated glomerular filtration rate (A) and plasma betaine (B).

<p>Results, with 95% confidence intervals, for patients with diabetes mellitus (black line), no diabetes and serum glucose ≥5.5 mmol/L (green line), and no diabetes and serum glucose <5.5 mmol/L (blue line) are shown. Lines at the bottom indicate distribution.</p

Generalized additive model showing the non-linear association between urinary betaine excretion and glycated hemoglobin (HbA1c).

<p>The dotted lines mark the 95% confidence interval. The line at the bottom indicates the distribution.</p

Cox regression survival models.

<p>Abbreviations: CVD cardiovascular disease.</p><p>*Covariates: age, sex, study site, participation in the WENBIT study, smoking, family history of coronary heart disease, medical history (hypertension, diabetes, acute myocardial infarction, percutaneous intervention, coronary artery bypass surgery, peripheral vascular disease, cerebrovascular disease, cured cancer, active cancer (not in the cardiovascular mortality analyses due to failure of the model to converge), deep vein thrombosis or vein surgery, pulmonary disease, atrial fibrillation, dyspnea grade 0–4), measured parameters at baseline (body mass index, ECG rhythm, left ventricular ejection fraction, number of coronary vessels with >50% stenosis), laboratory values (estimated glomerular filtration rate, uric acid, hemoglobin, potassium, sodium, C-reactive protein, glycated hemoglobin, low density lipoprotein, troponin T), medication (aspirin, adenosine diphosphate receptor inhibitor, warfarin, angiotensin converting enzyme inhibitor and/or angiotensin receptor blocker, beta-blocker, digoxin, spironolactone, thiazide, calcium antagonist, nitrate, statin, insulin, metformin, sulfonylurea, treatment for chronic obstructive pulmonary disease, non-steroid anti-inflammatory drug, corticosteroid, antidepressant, antipsychotic), and baseline revascularization.</p><p>Cox regression survival models.</p

Baseline characteristics after matching.

<p>Continuous variables are shown as means (standard deviation) and medians (interquartile range) and categorical variables as numbers (percentage). Abbreviations: WENBIT = WEstern Norway B-vitamin Trial; CAD = coronary artery disease; PCI = percutaneous coronary intervention; CABG = coronary artery bypass graft; PVD = peripheral vascular disease; DVT = deep venous thrombosis; NYHA = New York Heart Association; BP = blood pressure; eGFR = estimated glomerular filtration rate; HbA1c = glycated hemoglobin; WBC = white blood cell count; ACEI = angiotensin converting enzyme inhibitor; ARB = angiotensin receptor blocker; COPD = chronic obstructive pulmonary disease; NSAID = non-steroid anti-inflammatory drug.</p><p>Baseline characteristics after matching.</p

Circulating B-Vitamins and Smoking Habits Are Associated with Serum Polyunsaturated Fatty Acids in Patients with Suspected Coronary Heart Disease: A Cross-Sectional Study

<div><p>The long-chain polyunsaturated fatty acids are considered to be of major health importance, and recent studies indicate that their endogenous metabolism is influenced by B-vitamin status and smoking habits. We investigated the associations of circulating B-vitamins and smoking habits with serum polyunsaturated fatty acids among 1,366 patients who underwent coronary angiography due to suspected coronary heart disease at Haukeland University Hospital, Norway. Of these, 52% provided information on dietary habits by a food frequency questionnaire. Associations were assessed using partial correlation (Spearman’s rho). In the total population, the concentrations of most circulating B-vitamins were positively associated with serum n-3 polyunsaturated fatty acids, but negatively with serum n-6 polyunsaturated fatty acids. However, the associations between B-vitamins and polyunsaturated fatty acids tended to be weaker in smokers. This could not be solely explained by differences in dietary intake. Furthermore, plasma cotinine, a marker of recent nicotine exposure, showed a negative relationship with serum n-3 polyunsaturated fatty acids, but a positive relationship with serum n-6 polyunsaturated fatty acids. In conclusion, circulating B-vitamins are, in contrast to plasma cotinine, generally positively associated with serum n-3 polyunsaturated fatty acids and negatively with serum n-6 polyunsaturated fatty acids in patients with suspected coronary heart disease. Further studies should investigate whether B-vitamin status and smoking habits may modify the clinical effects of polyunsaturated fatty acid intake.</p></div

Baseline characteristics of participants regarding medical history, risk factors and medications¹.

<p>¹ Missing values: Cotinine: n = 3 (0.2%), β-blocker: n = 1 (0.1%); Fasting: n = 74 (5.4%); Hypercholesterolemia: n = 81 (5.9%); Troponin T: n = 170 (12.4%). ACE, angiotensin converting enzyme.</p><p>²<i>P</i> values for differences between smokers and non-smokers were calculated by using Mann-Whitney U test for continuous variables and chi-square tests for categorical variables.</p><p>³ n (%).</p><p>⁴ Median (25^th, 75^th percentile).</p><p>⁵ Serum total cholesterol ≥ 6.5mmol/L.</p><p>⁶ Includes diabetes types 1 and 2.</p><p>⁷ Medication prior to coronary angiography.</p><p>Baseline characteristics of participants regarding medical history, risk factors and medications<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0129049#t001fn001" target="_blank">¹</a>.</p

The relationship between cotinine and serum n-3 and n-6 PUFAs.

<p>The dose-response relationships between concentrations of plasma cotinine levels (nmol/L) and serum PUFAs (% of total fatty acids) in smokers (n = 459). Associations were modeled by GAM and adjusted for gender and age. Shaded areas indicate 95% confidence intervals. The y-axis spans 2 standard derivations of each outcome. Density plot for the distribution of cotinine are included in diagrams with 10^th, 50^th and 90^th percentile marked by dotted, vertical lines.</p