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1.  Association of apolipoprotein A1 and B with kidney function and chronic kidney disease in two multiethnic population samples 
Nephrology Dialysis Transplantation  2012;27(7):2839-2847.
lipoprotein risk factors for atherosclerosis, i.e., increased LDL cholesterol, increased triglycerides and decreased HDL cholesterol, also are associated with progression of loss of kidney function...Goek and coworkers describe the association of the apoliproteins A1 and B and eGFR in two large cohorts derived from the general polulation [the NHANES III (N=7,023) and the ARIC study (n=10,292)]. The results were similar in both cohorts...
Circulating lipoproteins and their protein constituents, apolipoproteins, are risk factors for chronic kidney disease (CKD). The associations between apolipoprotein A1, apolipoprotein B and their ratio with glomerular filtration rate estimated from the new CKD Epidemiology Collaboration (CKD-EPI) equation (eGFR) are not well studied in the general population.
Associations between apolipoprotein A1, B and their ratio with the outcomes of eGFR, CKD (eGFR <60 mL/min/1.73m2) and albuminuria were examined in the Atherosclerosis Risk in Communities study (ARIC, n = 10 292, 1996–98) and the Third National Health and Nutrition Examination Survey (NHANES III, n = 7023, 1988–91). Cross-sectional multivariable-adjusted analyses were performed using linear and logistic regression. Prospective analyses related baseline apolipoprotein levels to subsequent CKD incidence over 10 years using the ARIC Carotid MRI follow-up cohort (n = 1659).
Higher apolipoprotein A1 quartiles were associated with a lower prevalence of CKD [Q4 versus Q1: odds ratio (OR) 0.73, P-trend = 0.02 in ARIC; Q4 versus Q1: OR 0.53, P-trend <0.01 in NHANES III] as well as with higher eGFR (P-trend <0.01 in ARIC and NHANES III). No consistent significant associations were found for apolipoprotein B in either study. The apolipoprotein B/A1 ratio was significantly associated with eGFR across quartiles in both studies (P-trend <0.01) and with CKD in ARIC (Q4 versus Q1: OR 1.23, P-trend = 0.01). Prospectively, there were trends for the association of apolipoproteins with incident CKD [Q4 versus Q1: incidence rate ratio (IRR) = 0.68 for apolipoprotein A1, P-trend = 0.1; Q4 versus Q1: IRR = 1.35 for apolipoprotein B, P-trend = 0.2]. Associations were not systematically stronger when comparing traditional lipids (total cholesterol, low-density lipoprotein or high-density lipoprotein) to apolipoproteins.
Higher serum apolipoprotein A1 was associated with lower prevalence of CKD and higher eGFR estimated by the CKD-EPI equation in two large multiethnic population-based samples. While apolipoprotein B showed no consistent associations, a higher apolipoprotein B/A1 ratio was significantly associated with lower eGFR in both studies. The direction and magnitude of the longitudinal associations between apolipoproteins and CKD incidence were overall similar to those observed cross-sectionally. No consistent differences became apparent between traditional lipids and apolipoproteins.
PMCID: PMC3471548  PMID: 22287661
apolipoprotein; ARIC; chronic kidney disease; epidemiology; NHANES
2.  Comparison of High-Density Lipoprotein Cholesterol to Apolipoprotein A-I and A-II to Predict Coronary Calcium and the Effect of Insulin Resistance 
The American journal of cardiology  2011;107(3):393-398.
High-density lipoprotein (HDL) cholesterol and its apolipoproteins each capture unique lipid and cardiometabolic information important to risk quantification. It was hypothesized that metabolic factors, including insulin resistance and type 2 diabetes, would confound the association of HDL cholesterol with coronary artery calcification (CAC) and that apolipoprotein A-I (apoA-I) and/or apolipoprotein A-II (apoA-II) would add to HDL cholesterol in predicting CAC. Two community-based cross-sectional studies of white subjects were analyzed: the Penn Diabetes Heart Study (PDHS; n = 611 subjects with type 2 diabetes, 71.4% men) and the Study of Inherited Risk of Coronary Atherosclerosis (SIRCA; n = 803 subjects without diabetes, 52.8% men) using multivariable analysis of apoA-I, apoA-II, and HDL cholesterol stratified by diabetes status. HDL cholesterol was inversely associated with CAC after adjusting for age and gender in whites with type 2 diabetes (tobit ratio for a 1-SD increase in HDL cholesterol 0.58, 95% confidence interval [CI] 0.44 to 0.77, p <0.001) as well as those without diabetes (tobit ratio 0.72, 95% CI 0.59 to 0.88, p = 0.001). In contrast, apoA-I was a weaker predictor in subjects with (tobit ratio 0.64, 95% CI 0.45 to 0.90, p = 0.010) and without (tobit ratio 0.79, 95% CI 0.66 to 0.94, p = 0.010) diabetes, while apoA-II had no association with CAC. Control for metabolic variables, including triglycerides, waist circumference, and homeostasis model assessment of insulin resistance, attenuated these relations, particularly in subjects without diabetes. In likelihood ratio test analyses, HDL cholesterol added to apoA-I, apoA-II, and atherogenic apolipoprotein B lipoproteins but improved CAC prediction over metabolic factors only in subjects with diabetes. In conclusion, HDL cholesterol outperformed apoA-I and apoA-II in CAC prediction, but its association with CAC was attenuated by measures of insulin resistance.
PMCID: PMC3086062  PMID: 21257004
3.  Association of HDL Cholesterol with Incident Cardiovascular Events by LDL Cholesterol and Apolipoprotein B100 in Women 
Annals of internal medicine  2011;155(11):742-750.
Prior studies found inverse associations between high-density-lipoprotein cholesterol (HDL-C) or apolipoprotein A-1 with cardiovascular disease (CVD). Whether this is consistent across levels of low-density-lipoprotein cholesterol (LDL-C) or total atherogenic particle burden (apolipoprotein B100) is less well studied, particularly in women.
To determine the association between HDL-C or apolipoprotein A-1 with CVD across a range of LDL-C or apolipoprotein B100.
Prospective cohort study.
The Women’s Healthy Study, a cohort of US female health professionals.
26,861 initially healthy women, age ≥ 45 years at study entry (1992–1995), followed for a mean of approximately 11 years.
Baseline lipids were measured directly, and apolipoproteins with immunoassays. Outcomes were incident total CVD (N=929), coronary events (N=602), and stroke (N=319).
In multivariable analyses, HDL-C and apolipoprotein A-1 were inversely associated with CVD and coronary events but not stroke. Adjusted coronary hazard ratios (HRs) for decreasing quintiles of HDL-C were 1.00, 1.23 (95% CI, 0.85–1.78), 1.42 (CI, 0.98–2.06), 1.90 (CI, 1.33–2.71), and 2.19 (CI, 1.51–3.19), P for linear trend<0.001; and for apolipoprotein A-1 1.00, 0.98 (CI, 0.71–1.35), 1.02 (CI, 0.72–1.44), 1.37 (CI, 0.98–1.90), and 1.58 (CI, 1.14–2.20), P for linear trend=0.005. Consistent inverse associations were found for HDL-C with coronary events across a range of LDL-C, including among women with low LDL-C. No associations were noted for HDL-C or apolipoprotein A-1 among women with low apolipoprotein B100 (<90 mg/dL).
Population of low risk women, small numbers of events in the lowest apolipoprotein B100 stratum, single baseline measurements, and potential residual confounding.
Consistent inverse associations were found for HDL-C with incident coronary events among women with a range of LDL-C. Among women with low total atherogenic particle burden (apolipoprotein B100<90 mg/dL), few events occurred and no associations were seen.
PMCID: PMC3233986  PMID: 22147713
4.  Plasma lipid and coagulation factor concentrations in insulin dependent diabetics with microalbuminuria. 
BMJ : British Medical Journal  1989;298(6672):487-490.
OBJECTIVE--To determine whether insulin dependent diabetics with microalbuminuria have significant abnormalities in concentrations of lipoproteins, apolipoproteins AI and B, fibrinogen, and clotting factor VII which could result in increased cardiovascular risk. DESIGN--Case-control study. SETTING--Outpatient department of a metabolic ward. PATIENTS--Group of 20 insulin dependent diabetics with urinary albumin excretion rates greater than 30 micrograms/min (microalbuminuria) and 20 individually matched insulin dependent diabetics with normal urinary albumin excretion rates (below 30 micrograms/min) matched for age, sex, and duration of diabetes. INTERVENTIONS--Fasting venous blood samples were taken for determination of concentrations of glucose, glycated haemoglobin, lipoproteins, apolipoproteins AI and B, fibrinogen, and factor VII. Height, weight, arterial pressure, and usual insulin dose were recorded, and each patient was given a dietary questionnaire to be completed at home. END POINT--Comparison of blood pressure and concentrations of lipoproteins, apolipoproteins AI and B, and fibrinogen in the diabetics with microalbuminuria and the controls. MEASUREMENTS AND MAIN RESULTS--Patients with microalbuminuria had significantly higher concentrations of low density lipoprotein cholesterol (mean 3.33 (SE 0.20) v 2.84 (0.12) mmol/l) and very low density lipoprotein cholesterol (0.30 (0.05) v 0.17 (0.03) mmol/l) than controls but significantly lower concentrations of high density lipoprotein 2 subfraction cholesterol (0.32 (0.04) v 0.54 (0.04) mmol/l). Concentrations of total triglyceride (1.11 (0.14) v 0.68 (0.08) mmol/l), very low density lipoprotein triglyceride (0.56 (0.10) v 0.30 (0.05) mmol/l), apolipoprotein B (0.88 (0.06) v 0.67 (0.03) g/l) and fibrinogen (2.2 (0.1) v 1.9 (0.1) g/l), and diastolic arterial pressure (80 (2) v 74 (2) mm Hg), were also higher in patients with microalbuminuria. CONCLUSIONS--Cardiovascular risk factors--namely, disturbances in lipoprotein and apolipoprotein concentrations, increased fibrinogen concentration, and increased arterial pressure--are already present in insulin dependent diabetics with microalbuminuria. The increased risk of coronary heart disease in patients with clinical proteinuria may result from prolonged exposure to these risk factors, which are present before any impairment of renal function.
PMCID: PMC1835810  PMID: 2495077
5.  Cholesterol Efflux Capacity, High-Density Lipoprotein Function, and Atherosclerosis 
The New England journal of medicine  2011;364(2):127-135.
High-density lipoprotein (HDL) may provide cardiovascular protection by promoting reverse cholesterol transport from macrophages. We hypothesized that the capacity of HDL to accept cholesterol from macrophages would serve as a predictor of atherosclerotic burden.
We measured cholesterol efflux capacity in 203 healthy volunteers who underwent assessment of carotid artery intima–media thickness, 442 patients with angiographically confirmed coronary artery disease, and 351 patients without such angiographically confirmed disease. We quantified efflux capacity by using a validated ex vivo system that involved incubation of macrophages with apolipoprotein B–depleted serum from the study participants.
The levels of HDL cholesterol and apolipoprotein A-I were significant determinants of cholesterol efflux capacity but accounted for less than 40% of the observed variation. An inverse relationship was noted between efflux capacity and carotid intima–media thickness both before and after adjustment for the HDL cholesterol level. Furthermore, efflux capacity was a strong inverse predictor of coronary disease status (adjusted odds ratio for coronary disease per 1-SD increase in efflux capacity, 0.70; 95% confidence interval [CI], 0.59 to 0.83; P<0.001). This relationship was attenuated, but remained significant, after additional adjustment for the HDL cholesterol level (odds ratio per 1-SD increase, 0.75; 95% CI, 0.63 to 0.90; P = 0.002) or apolipoprotein A-I level (odds ratio per 1-SD increase, 0.74; 95% CI, 0.61 to 0.89; P = 0.002). Additional studies showed enhanced efflux capacity in patients with the metabolic syndrome and low HDL cholesterol levels who were treated with pioglitazone, but not in patients with hypercholesterolemia who were treated with statins.
Cholesterol efflux capacity from macrophages, a metric of HDL function, has a strong inverse association with both carotid intima–media thickness and the likelihood of angiographic coronary artery disease, independently of the HDL cholesterol level. (Funded by the National Heart, Lung, and Blood Institute and others.)
PMCID: PMC3030449  PMID: 21226578
6.  The effect of ABCA1 gene polymorphisms on ischaemic stroke risk and relationship with lipid profile 
BMC Medical Genetics  2007;8:30.
Ischaemic stroke is a common disorder with genetic and environmental components contributing to overall risk. Atherothromboembolic abnormalities, which play a crucial role in the pathogenesis of ischaemic stroke, are often the end result of dysregulation of lipid metabolism. The ATP Binding Cassette Transporter (ABCA1) is a key gene involved in lipid metabolism. It encodes the cholesterol regulatory efflux protein which mediates the transfer of cellular phospholipids and cholesterol to acceptor apolipoproteins such as apolipoprotein A-I (ApoA-I). Common polymorphisms in this gene affect High Density Lipoprotein Cholesterol (HDL-C) and Apolipoprotein A-I levels and so influence the risk of atherosclerosis. This study has assessed the distribution of ABCA1 polymorphisms and haplotype arrangements in patients with ischaemic stroke and compared them to an appropriate control group. It also examined the relationship of these polymorphisms with serum lipid profiles in cases and controls.
We studied four common polymorphisms in ABCA1 gene: G/A-L158L, G/A-R219K, G/A-G316G and G/A-R1587K in 400 Caucasian ischaemic stroke patients and 487 controls. Dynamic Allele Specific Hybridisation (DASH) was used as the genotyping assay.
Genotype and allele frequencies of all polymorphisms were similar in cases and controls, except for a modest difference in the ABCA1 R219K allele frequency (P-value = 0.05). Using the PHASE2 program, haplotype frequencies for the four loci (158, 219, 316, and 1587) were estimated in cases and controls. There was no significant difference in overall haplotypes arrangement in patients group compared to controls (p = 0.27). 2211 and 1211 haplotypes (1 = common allele, 2 = rare allele) were more frequent in cases (p = 0.05). Adjusted ORs indicated 40% and 46% excess risk of stroke for these haplotypes respectively. However, none of the adjusted ORs were statistically significant. Individuals who had R219K "22" genotype had a higher LDL level (p = 0.001).
Our study does not support a major role for the ABCA1 gene as a risk factor for ischaemic stroke. Some haplotypes may confer a minor amount of increased risk or protection. Polymorphisms in this gene may influence serum lipid profile.
PMCID: PMC1894956  PMID: 17553166
7.  Serum lipoproteins and apolipoproteins in young normocholesterolaemic, non-diabetic Indian men with myocardial infarction. 
Postgraduate Medical Journal  1991;67(784):159-164.
Serum total cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoprotein A-I and apolipoprotein B were evaluated as potential indicators of the risk of coronary artery disease in young (less than 46 years) normocholesterolaemic, non-diabetic men who had previously sustained a myocardial infarction (n = 50) and in healthy age and sex matched controls (n = 122) with a similar socioeconomic background. Significant differences were observed between patients and controls in the mean concentrations of serum total cholesterol, triglycerides, low density lipoprotein cholesterol, high density lipoprotein cholesterol and apolipoprotein B, as well as in the ratios of total cholesterol to high density lipoprotein cholesterol and apolipoprotein A-I to apolipoprotein B. No significant difference was demonstrated in the concentration of apolipoprotein A-I between the two groups. Stepwise discriminant analysis indicated that apolipoprotein B was the best discriminant between patients and controls. The percentage of exact classification was 74% in patients and 66% in controls. When the patients were compared to a subset of controls (n = 50) matched for age and total cholesterol, significant differences were demonstrated only in the mean concentrations of apolipoprotein B. Discriminant analysis confirmed that the best single discriminating variable was apolipoprotein B. The results therefore indicate that in young normocholesterolaemic, non-diabetic Indian men with myocardial infarction, apolipoprotein B is superior to other lipid parameters studied, as a marker for coronary artery disease.
PMCID: PMC2398973  PMID: 2041847
8.  Resolving the Relationship between Apolipoprotein E and Depression 
Neuroscience letters  2009;455(2):116-119.
Several studies have reported an association between the ApolipoproteinE-ε4 (APOE4) allele and depression among elders. However others have failed to find an association. Since APOE4 is a well recognized risk factor for Alzheimer dementia, cognitive status may represent an important confounder between APOE4 and depression. In this investigation, we examined the relationship between the ApolipoproteinE-ε4 allele and depression among elders accounting for cognitive status.
Using a case-control design (n=1052), we investigated the association between ApolipoproteinE-ε4 and depression in Alzheimer disease patients (n=528) and in cognitively intact controls (n=524).
We demonstrated an apparent association between the APOE4 allele and depression in the combined dataset (p=0.001) when not controlling for cognitive status. However, once stratified by the presence of Alzheimer disease, there was no association in either the Alzheimer group (p=0.290) or the cognitively intact controls (p=0.494).
In this dataset there is no association between the ApolipoproteinE-ε4 allele and depression among those with Alzheimer disease or among cognitively intact elders. However there is a significant association between female gender and depression in the cognitively intact (p=0.003) but not among those with Alzheimer disease. Additionally, individuals with Alzheimer disease and depression had a significantly younger age of onset for their Alzheimer disease than those without depression (p=0.017).
PMCID: PMC2945257  PMID: 19368858
9.  Indicators of the atherogenic lipoprotein phenotype measured with density gradient ultracentrifugation predict changes in carotid intima-media thickness in men and women 
Progression of carotid intima-media thickness (CIMT) is a surrogate indicator for the early stages of atherosclerosis.
The study investigated relationships between baseline lipoprotein cholesterol, triglyceride (TG), and apolipoprotein (Apo) B levels assessed with density gradient ultracentrifugation (DGU) and progression of posterior wall common CIMT in men (45–75 years of age) and women (55–74 years of age) in the control arm of a clinical trial. Participants had baseline posterior wall CIMT 0.7–2.0 mm, without significant stenosis. CIMT was assessed using B-mode ultrasound at baseline, and 12 and ~18 months. A DGU cholesterol panel that assessed the major lipoprotein classes and subclasses, plus triglycerides, lipoprotein (a) cholesterol, low-density lipoprotein (LDL) peak time (inversely related to LDL particle density), and Apo B were performed on fasting baseline samples. Apo B was also measured using an enzyme linked immunosorbent assay.
Baseline CIMT was inversely associated (P < 0.001) with CIMT progression. After adjustment for baseline CIMT, significant predictors of posterior wall CIMT progression in linear regression analyses included LDL peak time (inverse, P = 0.045), total high-density lipoprotein cholesterol (HDL-C) (inverse, P = 0.001), HDL2-C (inverse, P = 0.005), HDL3-C (inverse, P = 0.003), very low-density lipoprotein (VLDL)-C (P = 0.037), and VLDL1+2-C (P = 0.016).
These data indicate that DGU-derived indicators of the “atherogenic lipoprotein phenotype,” including increased TG-rich lipoprotein cholesterol, lower HDL-C and HDL-C subfractions, and a greater proportion of LDL-C carried by more dense LDL particles, are associated with CIMT progression in men and women at moderate risk for coronary heart disease.
PMCID: PMC3262484  PMID: 22272073
carotid intima media thickness; density gradient ultracentrifugation; coronary heart disease risk; lipids; atherosclerosis; lipoprotein subfractions
10.  Relationship of Oxidized Phospholipids on Apolipoprotein B-100 Particles to Race, Apolipoprotein(a) Isoform Size and Cardiovascular Risk Factors: Results from the Dallas Heart Study 
Circulation  2009;119(13):1711-1719.
Elevated levels of oxidized phospholipids (OxPL) on apolipoprotein B-100 particles (OxPL/apoB) are associated with cardiovascular disease and predict new cardiovascular events. Elevated lipoprotein (a) [Lp(a)] levels are a risk factor for cardiovascular disease in Whites, and in Blacks if they also carry small apolipoprotein (a) [apo(a)] isoforms. The relationship of OxPL/apoB levels to race, cardiovascular risk factors and apolipoprotein(a) isoforms is not established.
Methods and Results
OxPL/apoB levels were measured in 3481 subjects (1831 Black, 1047 White and 603 Hispanic) in the Dallas Heart Study and correlated with age, gender, cardiovascular risk factors, lipoprotein (a) [Lp(a)] and apolipoprotein(a) isoforms. Significant differences in OxPL/apoB levels were noted among racial subgroups, with Blacks having the highest levels, compared to Whites and Hispanics (p<0.001 for each comparison). OxPL/apoB levels generally did not correlate with age, gender or risk factors. In the overall cohort, OxPL/apoB levels strongly correlated with lipoprotein (a) [Lp(a)] (r=0.85, p<0.001), with the shape of the relationship demonstrating a “reverse L” shape for log-transformed values. The highest correlation was present in Blacks followed by Whites and Hispanics, was dependent on apo(a) isoform size, and became progressively weaker with larger isoforms. The size of the major apolipoprotein(a) isoform (number of kringle type-IV repeats) was negatively associated with OxPL/apoB (r=-0.49, p<0.001) and Lp(a) (r=-0.61, p<0.001), irrespective of racial group. After adjusting for apolipoprotein(a) isoform size, the relationship between OxPL/apoB and Lp(a) remained significant (r=0.67, p<0.001).
OxPL/apoB levels vary according to race, are largely independent of cardiovascular risk factors, and are inversely associated with apolipoprotein(a) isoform size. The association of OxPL with small apolipoprotein(a) isoforms, where a similar relationship is present among all racial subgroups despite differences in Lp(a) levels, may be a key determinant of cardiovascular risk.
PMCID: PMC2782388  PMID: 19307470
lipoproteins; oxidation; atherosclerosis; lipoprotein (a); oxidized phospholipids; risk factors
11.  Apolipoprotein B–Containing Lipoprotein Subclasses as Risk Factors for Cardiovascular Disease in Patients With Rheumatoid Arthritis 
Arthritis care & research  2012;64(7):993-1000.
The purpose of this study was to explore whether nontraditional risk factors, such as apolipoprotein C-III (Apo C-III) and its corresponding Apo B lipoprotein (Lp) subclasses, contribute to the risk of cardiovascular disease in rheumatoid arthritis (RA) patients.
Apolipoprotein and lipoproteins were measured in 152 RA patients by immunoturbidimetric procedures, electroimmunoassay, and immunoprecipitation. Patients had a coronary artery calcium (CAC) score assessed at baseline and at year 3. Differences in the CAC scores between baseline and year 3 were calculated and dichotomized at 0, where patients with a difference score >0 were denoted as progressors and the rest were denoted as nonprogressors. Differences between means were tested with a 2-sided independent Student’s t-test with Satterthwaite’s adjustment. Proportion differences were tested with a chi-square test. Multiple logistic regression was performed to assess the relationship between apolipoprotein and lipoprotein levels and the dichotomized CAC score.
Progressors accounted for almost 60% of the cohort. Progressors had significantly higher levels of triglycerides, very low-density lipoprotein (VLDL) cholesterol, total cholesterol/high-density lipoprotein (HDL), triglycerides/HDL, Apo B, LpA-II:B:C:D:E, LpB:C, Apo B/Apo A-I, Apo C-III, and Apo C-III–heparin precipitate than the nonprogressors. After adjusting for age, sex, statin use (yes/no), and hypertension (yes/no), significant risk factors of progressors were total cholesterol, triglycerides, VLDL cholesterol, LDL cholesterol, Apo B, LpB:C, Apo C-III, and Apo B/Apo A-I.
Apo C-III–containing Apo B lipoprotein subclasses were found to be significantly elevated in progressors compared to nonprogressors. Many of these same lipoproteins were found to be associated with an increase in CAC scores among progressors. These lipoproteins may be considered new risk factors for progression of atherosclerosis in RA patients.
PMCID: PMC3552355  PMID: 22337612
12.  Insulin resistance syndrome in postmenopausal women with cardiological syndrome X. 
British Heart Journal  1995;74(1):47-52.
OBJECTIVE--To determine whether postmenopausal women with cardiological syndrome X (chest pain and abnormal exercise electrocardiogram despite normal coronary angiography) exhibit disturbances in the full range of proposed components of the putative "insulin resistance syndrome". PATIENTS AND METHODS--20 postmenopausal women with syndrome X and 20 healthy controls each underwent measurement of insulin resistance (by minimal model analysis of the intravenous glucose tolerance test), lipid, lipoprotein, and apolipoprotein concentrations, a range of haemostatic variables, serum uric acid concentration, and centrality of body fat distribution (by dual energy x ray absorptiometry). RESULTS--Women with syndrome X had higher fasting triglyceride concentrations than controls (median: 1.60 v 1.02 mmol/l, P < 0.05). Concentrations of high density lipoprotein cholesterol were lower (1.33 v 1.61 mmol/l, P < 0.05) as were those of the high density lipoprotein apolipoproteins AI and AII. Insulin and C peptide responses to the intravenous glucose tolerance test were higher (27.6 v 19.8 microU/ml/min, P < 0.01; 101 v 72 pmol/ml/min, P < 0.05, respectively), and insulin sensitivity was lower (1.89 v 3.09 min/microU/ml, P < 0.05). There were, however, no significant differences between other proposed components of the insulin resistance syndrome (blood pressure, glucose tolerance, proportion of central body fat, serum uric acid concentration, and plasminogen activator inhibitor-1 activity). Antithrombin III activity was higher in women with syndrome X (121 v 113%, P < 0.01). CONCLUSIONS--Women with syndrome X tend to be insulin resistant and have lipid and lipoprotein abnormalities, but do not exhibit all characteristics of the insulin resistance syndrome. Such variation in correlated risk factors is consistent with underlying heterogeneity in the insulin resistance syndrome and cardiological syndrome X.
PMCID: PMC483945  PMID: 7662453
13.  Transport of Apolipoproteins A-I and A-II by Human Thoracic Duct Lymph 
Journal of Clinical Investigation  1981;67(3):857-866.
The daily transport of human plasma apolipoproteins A-I and A-II, triglyceride, and total cholesterol from the thoracic duct lymph into plasma was measured in two subjects before and three subjects after renal transplantation. Lymph triglyceride transport was ∼83% of the daily ingested fat loads, whereas lymph cholesterol transport was consistently greater than the amount of daily ingested cholesterol. Lymph apolipoprotein transport significantly (P < 0.05) exceeded the predicted apolipoprotein synthesis rate by an average of 659±578 mg/d for apolipoprotein A-I and 109±59 mg/d for apolipoprotein A-II among the five subjects. It is estimated that 22-77% (apolipoprotein A-I) and 28-82% (apolipoprotein A-II) of daily total body apolipoprotein synthesis takes place in the intestine.
Lymph high density lipoprotein particles are mostly high density lipoprotein2b and high density lipoprotein2a and have a greater overall relative triglyceride content and a smaller relative cholesteryl ester content when compared with homologous plasma high density lipoproteins. The major quantity of both lymph apolipoprotein A-I (81±8%) and apolipoprotein A-II (90±11%) was found within high density lipoproteins with almost all of the remainder found in chylomicrons and very low density lipoproteins.
The combined results are consistent with a major contribution of the intestine to total body synthesis of apolipoprotein A-I and apolipoprotein A-II. An important role of lymph in returning filtered apolipoprotein to plasma in association with high density lipoproteins is proposed. Accompanying the return of filtered apolipoprotein to the plasma is a probable transformation, both in size and composition, of at least some of the lymph high density lipoprotein2b and high density lipoprotein2a particles into high density lipoprotein3.
PMCID: PMC370637  PMID: 7204560
14.  Major Lipids, Apolipoproteins, and Risk of Vascular Disease 
Associations of major lipids and apolipoproteins with the risk of vascular disease have not been reliably quantified.
To assess major lipids and apolipoproteins in vascular risk.
Design, Setting, and Participants
Individual records were supplied on 302 430 people without initial vascular disease from 68 long-term prospective studies, mostly in Europe and North America. During 2.79 million person-years of follow-up, there were 8857 nonfatal myocardial infarctions, 3928 coronary heart disease [CHD] deaths, 2534 ischemic strokes, 513 hemorrhagic strokes, and 2536 unclassified strokes.
Main Outcome Measures
Hazard ratios (HRs), adjusted for several conventional factors, were calculated for 1-SD higher values: 0.52 loge triglyceride, 15 mg/dL high-density lipoprotein cholesterol (HDL-C), 43 mg/dL non-HDL-C, 29 mg/dL apolipoprotein AI, 29 mg/dL apolipoprotein B, and 33 mg/dL directly measured low-density lipoprotein cholesterol (LDL-C). Within-study regression analyses were adjusted for within-person variation and combined using meta-analysis.
The rates of CHD per 1000 person-years in the bottom and top thirds of baseline lipid distributions, respectively, were 2.6 and 6.2 with triglyceride, 6.4 and 2.4 with HDL-C, and 2.3 and 6.7 with non-HDL-C. Adjusted HRs for CHD were 0.99 (95% CI, 0.94-1.05) with triglyceride, 0.78 (95% CI, 0.74-0.82) with HDL-C, and 1.50 (95% CI, 1.39-1.61) with non-HDL-C. Hazard ratios were at least as strong in participants who did not fast as in those who did. The HR for CHD was 0.35 (95% CI, 0.30-0.42) with a combination of 80 mg/dL lower non-HDL-C and 15 mg/dL higher HDL-C. For the subset with apolipoproteins or directly measured LDL-C, HRs were 1.50 (95% CI, 1.38-1.62) with the ratio non-HDL-C/HDL-C, 1.49 (95% CI, 1.39-1.60) with the ratio apo B/apo AI, 1.42 (95% CI, 1.06-1.91) with non-HDL-C, and 1.38 (95% CI, 1.09-1.73) with directly measured LDL-C. Hazard ratios for ischemic stroke were 1.02 (95% CI, 0.94-1.11) with triglyceride, 0.93 (95% CI, 0.84-1.02) with HDL-C, and 1.12 (95% CI, 1.04-1.20) with non-HDL-C.
Lipid assessment in vascular disease can be simplified by measurement of either total and HDL cholesterol levels or apolipoproteins without the need to fast and without regard to triglyceride.
PMCID: PMC3284229  PMID: 19903920
15.  High prevalence of hypertriglyceridaemia and apolipoprotein abnormalities in coronary artery disease. 
British Heart Journal  1988;60(5):397-403.
Serum lipids and apolipoproteins A-I and B were measured in 174 men aged less than 60 with angiographically confirmed coronary artery disease and in 572 healthy control men. Two thirds of the patients had raised age-corrected values of fasting serum cholesterol and/or triglyceride and/or a low high density lipoprotein (HDL) cholesterol compared with the controls. Eighteen (30%) of the 61 normolipidaemic patients had a concentration of serum apolipoprotein A-I below the 5th percentile of 233 controls. In normolipidaemic patients on beta blockers the relative prevalence of serum low density lipoprotein (LDL)-apolipoprotein B values above the 95th percentile of 339 controls was significantly increased. Discriminant function analysis showed that a raised concentration of serum triglyceride was the best discriminant between patients and controls, with raised LDL-apolipoprotein B and reduced apolipoprotein A-I coming second only to triglyceride in analyses where each was separately compared with all the lipid variables. These associations were highly significant and were independent of other influences, including beta blockade. These findings re-emphasise the importance of hypertriglyceridaemia as a risk factor and confirm that apolipoprotein abnormalities occur frequently in coronary disease, even in normolipidaemic patients.
PMCID: PMC1216597  PMID: 3203033
16.  Moderate alcohol intake and lower risk of coronary heart disease: meta-analysis of effects on lipids and haemostatic factors 
BMJ : British Medical Journal  1999;319(7224):1523-1528.
To summarise quantitatively the association between moderate alcohol intake and biological markers of risk of coronary heart disease and to predict how these changes would lower the risk.
Meta-analysis of all experimental studies that assessed the effects of moderate alcohol intake on concentrations of high density lipoprotein cholesterol, apolipoprotein A I, fibrinogen, triglycerides, and other biological markers previously found to be associated with risk of coronary heart disease.
Men and women free of previous chronic disease and who were not dependent on alcohol. Studies were included in which biomarkers were assessed before and after participants consumed up to 100 g of alcohol a day.
Alcohol as ethanol, beer, wine, or spirits.
Main outcome measures
Changes in concentrations of high density lipoprotein cholesterol, apolipoprotein A I, Lp(a) lipoprotein, triglycerides, tissue type plasminogen activator activity, tissue type plasminogen activator antigen, insulin, and glucose after consuming an experimental dose of alcohol for 1 to 9 weeks; a shorter period was accepted for studies of change in concentrations of fibrinogen, factor VII, von Willebrand factor, tissue type plasminogen activator activity, and tissue type plasminogen activator antigen.
61 data records were abstracted from 42 eligible studies with information on change in biological markers of risk of coronary heart disease. An experimental dose of 30 g of ethanol a day increased concentrations of high density lipoprotein cholesterol by 3.99 mg/dl (95% confidence interval 3.25 to 4.73), apolipoprotein A I by 8.82 mg/dl (7.79 to 9.86), and triglyceride by 5.69 mg/dl (2.49 to 8.89). Several haemostatic factors related to a thrombolytic profile were modestly affected by alcohol. On the basis of published associations between these biomarkers and risk of coronary heart disease 30 g of alcohol a day would cause an estimated reduction of 24.7% in risk of coronary heart disease.
Alcohol intake is causally related to lower risk of coronary heart disease through changes in lipids and haemostatic factors.
Key messagesResults from observational studies provide strong evidence that moderate alcohol intake lowers risk of coronary heart diseaseShort term trials of alcohol intake show significant changes in concentrations of lipids and clotting factorsThe changes in concentrations of high density lipoprotein cholesterol, fibrinogen, and triglycerides associated with an intake of 30 g of alcohol a day should reduce risk of coronary disease by 24.7%Alcohol intake may be causally related to lower risk of coronary heart disease through changes in lipids and haemostatic factors
PMCID: PMC28294  PMID: 10591709
17.  Relationship between Hyperuricemia and Lipid Profiles in US Adults 
BioMed Research International  2015;2015:127596.
Background. Although the link between hyperuricemia and metabolic syndrome had been recognized, the association of the dyslipidemia among individuals with hyperuricemia remains not comprehensively assessed. Methods. Using NHANES III study, we examined the relation between serum lipid profiles and different serum uric acid levels, including serum total cholesterol, LDL cholesterol, triglycerides, HDL cholesterol, apolipoprotein-B, lipoprotein (a), apolipoprotein AI, ratio of triglycerides to HDL cholesterol, and ratio of apolipoprotein-B to AI. Results. After adjusting for potential confounders, average differences (95% confidence interval) comparing the top to the bottom (reference) serum uric acid were 0.29 (0.19, 0.39) mmol/L for total cholesterol, 0.33 (0.26, 0.41) mmol/L for triglycerides, 0.14 (0.01, 0.27) mmol/L for LDL cholesterol, −0.08 (−0.11, −0.05) mmol/L for HDL, and 0.09 (0.05, 0.12) g/L for serum apolipoprotein-B. Notably, ratios of triglycerides to HDL cholesterol and apolipoprotein-B to AI were also linearly associated with uric acid levels (P for trend < 0.001). Conclusions. This study suggested that serum LDL cholesterol, triglycerides, total cholesterol, apolipoprotein-B levels, ratio of triglycerides to HDL cholesterol, and ratio of apolipoprotein-B to AI are strongly associated with serum uric acid levels, whereas serum HDL cholesterol levels are significantly inversely associated. In the clinical practice, the more comprehensive strategic management to deal with dyslipidemia and hyperuricemia deserves further investigation.
PMCID: PMC4299312  PMID: 25629033
18.  Paradoxical Association of Enhanced Cholesterol Efflux With Increased Incident Cardiovascular Risks 
Diminished cholesterol efflux activity of apolipoprotein B (apoB)–depleted serum is associated with prevalent coronary artery disease, but its prognostic value for incident cardiovascular events is unclear. We investigated the relationship of cholesterol efflux activity with both prevalent coronary artery disease and incident development of major adverse cardiovascular events (death, myocardial infarction, or stroke).
Approach and Results
Cholesterol efflux activity from free cholesterol–enriched macrophages was measured in 2 case– control cohorts: (1) an angiographic cohort (n=1150) comprising stable subjects undergoing elective diagnostic coronary angiography and (2) an outpatient cohort (n=577). Analysis of media from cholesterol efflux assays revealed that the high-density lipoprotein fraction (1.063
Heightened cholesterol efflux to apoB-depleted serum was paradoxically associated with increased prospective risk for myocardial infarction, stroke, and death. The majority of released radiolabeled cholesterol from macrophages in cholesterol efflux activity assays does not reside within a high-density lipoprotein particle.
PMCID: PMC3743250  PMID: 23520163
cholesterol efflux; high-density lipoprotein-cholesterol; macrophage; prognosis
Major cardiovascular disorders are being recognized earlier in life. In this study we examined the effects of swimming and soccer training on male adolescent lipid-lipoprotein profiles relative to a maturity matched control group to determine the effects of these exercises on specific cardiovascular risk and anti-risk factors.
Forty five adolescent males (11.81 ± 1.38 yr) including swimmers (SW), soccer players (SO), and non-athlete, physically active individuals as controls (C), participated in this study. Training groups completed 12-wk exercise programs on three non-consecutive days per week. Plasma low-density lipoprotein (LDL), very low density lipoprotein (VLDL), high density lipoprotein (HDL), apolipoprotein A-I (apoA-I), apolipoprotein B (apoB), total cholesterol (TC), and triglyceride (TG) levels were measured in control, pre-training, during-training, and post-training.
In response to the 12-wk training period, the SO group demonstrated a decrease in the mean LDL level compared to the SW and C (SW: 0.15%; SO: −9.51%; C: 19.59%; p < 0.001) groups. There was an increase in both the SW and SO groups vs. the control in mean HDL (SW: 5.66%; SO: 3.07%; C: −7.21%; p < 0.05) and apoA-I (SW: 3.86%; SO: 5.48%; C: −1.01%; p < 0.05). ApoB was considerably lower in the training groups vs. control (SW: −9.52%; SO: −13.87%; C: 21.09%; p < 0.05). ApoA-I/apoB ratio was significantly higher in training groups vs. control (SW: 16.74%; SO: 23.71%; C: −17.35%; p < 0.001). There were no significant differences between groups for other factors.
The favorable alterations in LDL, HDL, apoA-I, and apoB observed in the training groups suggest that both regular swimming or soccer exercise can potentially mitigate cardiovascular risk in adolescent males.
PMCID: PMC4064523  PMID: 24912476
Cardiovascular risk; Anti-risk factors; Cholesterol; Lipids
Coronary heart disease (CHD) has been considered as a multifactorial disorder with the involvement of both environmental and genetic factors. The advent of tools to investigate individual variability of DNA has allowed us to perform the association studies of candidate genes. However, an association between genetic trait and phenotypic variations is not easy to demonstrate and several reported association between genetic markers and risk factors or overt CHD have gone unconfirmed. It should not be assumed that for a given genetic trait, the impact on risk will be similar in all populations. In particular, most studies of the molecular bases of CHD have involved Caucasian subjects, so much more work with the Korean population is needed before genetic testing for susceptibility to CHD can be offered to Koreans as a clinical service. In this review, we discuss two aspects of the molecular bases of CHD: i) Molecular bases of the candidate gene related to lipoprotein metabolism including apolipoprotein AI-CIII-AIV gene duster, apolipoprotein B, apolipoprotein E-CI-CII gene cluster, apolipoprotein(a), LDL receptors, lipoprotein lipase, cholesteryl ester transfer protein, and apo B editing protein; ii) Molecular bases of the candidate gene related to thrombotic and other factors including fibrinogen, factor VII, plasminogen activator inhibitor 1, homocysteine, stromelysin, paraoxonase, and angiotensin converting enzyme. Studies involving the Korean population, especially those performed by our teams, are also summarized.
PMCID: PMC3054341  PMID: 9539312
British Heart Journal  1994;72(6):542-547.
OBJECTIVE--To compare risk factors in two populations of patients with advanced atheroma requiring coronary or femoropopliteal artery bypass grafting to try to account for the different localisations of vascular disease. DESIGN--Cross sectional epidemiological study. SETTING--Cardiovascular surgery department of a university hospital. SUBJECTS--464 men (mean age 59.25 (SD 8.57) years) undergoing coronary artery bypass grafting; 74 men (mean age 56.28 (13.3) years) undergoing femoropopliteal artery bypass grafting; and 204 control men (mean age 45.07 (6.59) years) who had been recruited in a preventive medicine department. INTERVENTIONS--Blood samples were drawn 24 hours before surgery. METHODS--Lipid and lipoprotein concentrations were measured for each patient and with adjustment for age were compared by analysis of covariance. The main risk factors (smoking, arterial hypertension, obesity, and diabetes) were determined by a standardised history, and the chi 2 test was used to compare the results in the two patient groups. Pairwise comparisons between the three populations were performed by logistic discriminant analysis. RESULTS--Both patient groups showed a significant rise in triglyceride concentration and in the ratio of total cholesterol to high density lipoprotein cholesterol (R1) and a drop in apolipoprotein AI and high density lipoprotein cholesterol concentrations. Disturbances were greater in patients undergoing coronary artery bypass grafting than in those undergoing femoropopliteal artery bypass grafting for the R1 ratio, apolipoprotein B concentration, and the ratio of apolipoprotein AI to apolipoprotein B (R2). A higher proportion of smokers was found in the femoropopliteal bypass group than in the coronary bypass group, whereas were often obese. Logistic discriminant analysis with adjustment for age and with the coronary bypass as the reference group selected three factors: smoking, the R2 ratio, and obesity. CONCLUSION--Disturbances in lipid and apoprotein concentrations varied with respect to bypass site. Other risk factors played a part in accelerating the atherogenic process, especially smoking in patients undergoing femoropopliteal artery bypass grafting and, to a lesser degree, obesity in patients undergoing coronary artery bypass grafting.
PMCID: PMC1025640  PMID: 7857737
The fasting plasma lipid, lipoprotein and apolipoprotein profiles were determined in 14 healthy Nigerian male athletes and controls matched for sex and anthropometric parameters. The mean levels of total cholesterol (P < 0.05), low-density lipoprotein (LDL) cholesterol, apolipoprotein (apo) AII and E were significantly lower (P < 0.01) in the athletes than in the controls. However, there were no statistically significant differences (P > 0.05) between the mean values of the plasma triglycerides, high-density lipoprotein (HDL), very low-density lipoprotein (VLDL) cholesterol, apo AI, B, Lp(a), LpA1 and CIII:NonB respectively for the athletes and controls. A priori, the potential effect on cardiovascular disease (CVD) risk was also compared using three predictor ratios - total cholesterol: HDL cholesterol (TC:HDL), LDL cholesterol: HDL cholesterol and apo B:AI. The mean of the three ratios was lower in the athletes than in the controls; however, the differences were not statistically significant (P > 0.05). Based on our data, exercise appears to decrease the TC:HDL ratio in the athletes by lowering LDL-cholesterol, while the HDL-cholesterol is unaffected. We conclude that physical activity has salutary effects on the lipid, lipoprotein and apolipoprotein profiles of healthy Nigerian men.
PMCID: PMC1332019  PMID: 8130968
Arteriosclerosis and Thrombosis  1993;13(6):842-851.
Reduced plasma levels of high density lipoprotein (HDL) cholesterol are associated with increased risk for coronary heart disease. Although plasma HDL levels are, in general, inversely related to plasma triglyceride (TG) concentrations, a small proportion of individuals with low HDL cholesterol concentrations have normal plasma TG levels. We wished to determine whether subjects with low plasma levels of HDL cholesterol could be characterized by common abnormalities of lipoprotein metabolism independent of plasma TGs. Therefore, we studied the metabolism of low density lipoprotein (LDL) apolipoprotein B (apo B) and HDL apolipoprotein A-I (apo A-I) in subjects with low plasma HDL cholesterol concentrations with or without hypertriglyceridemia. Nine subjects with low plasma HDL cholesterol levels and normal levels of plasma TGs and LDL cholesterol were studied. Autologous 131I-LDL and 125I-HDL were injected intravenously, and blood samples were collected for 2 weeks. LDL apo B and HDL apo A-I levels were measured by specific radioimmunoassays. Fractional catabolic rates (FCRs, pools per day) and production rates (PRs, milligrams/kilogram · day) for each apolipoprotein were determined. The results were compared with those obtained previously in nine subjects with low plasma HDL cholesterol levels and hypertriglyceridemia and in seven normal subjects. The normal subjects had an HDL apo A-I FCR (mean±SD) of 0.21±0.04. Despite large differences in plasma TG levels, the HDL apo A-I FCRs were similar in the low-HDL, normal-TG group (0.30±0.09) and the low-HDL, high-TG group (0.033±0.10), although only the latter value was significantly increased versus control subjects (p<0.03). Increased apo A-I FCRs were associated with reduced HDL apo A-I levels in both groups of patients. Apo A-I PRs were similar in all groups. In contrast, LDL apo B PR was increased approximately 50% in the low-HDL, normal-TG group (19.3±6.6; p<0.01) compared with normal subjects (12.5±2.6). There was a strong trend toward a greater LDL apo B PR in the low-HDL, high-TG group (17.6±4.5;p=0.06 versus normal subjects) as well. LDL apo B FCRs were similar in all three groups. LDL apo B concentrations were also increased in the group with low HDL cholesterol and normal TG levels. Both groups with low HDL cholesterol levels had cholesterol-depleted LDL and HDL particles. In summary, reduced levels of plasma HDL cholesterol were generally associated with accelerated fractional removal of HDL apo A-I from plasma, increased production of plasma LDL apo B, and evidence of increased cholesteryl ester transfer out of LDL and HDL. The presence of these similar metabolic abnormalities whether or not plasma TG levels were increased suggests that increased apo B production may be a central defect in these patients and that low plasma HDL levels may be closely linked to increased plasma levels of apo B–containing lipoproteins independent of circulating levels of plasma TG.
PMCID: PMC3277740  PMID: 8499404
coronary heart disease; HDL; LDL; apolipoprotein B; apolipoprotein A-I; cholesteryl ester transfer protein; reverse cholesterol transport
There is little data on the relationship between novel cardiovascular risk factors and silent coronary artery disease (CAD) in diabetic patients. We investigated whether Lipoprotein(a), homocysteine and apolipoprotein(a) polymorphism are associated with angiographically assessed asymptomatic coronary artery disease (CAD) in diabetic patients.
1,971 type 2 diabetic patients without clinical signs of cardiovascular diseases and with a negative history of CAD were consecutively evaluated. Among them, 179 patients showed electrocardiographic abnormalities suggestive of ischemia or previous asymptomatic myocardial infarction. These 179 patients were subjected to a non-invasive test for CAD (ECG stress testing and/or scintigraphy). Among patients with a highly positive stress testing (n = 19) or a positive scintigraphy (n = 74), 75 showed an angiographically documented CAD (CAD group). Seventy-five patients without CAD (NO CAD group) were matched by age, sex and duration of diabetes to CAD patients. In NO CAD patients an exercise ECG test, a 48-hour ambulatory ECG and a stress echocardiogram were negative for CAD.
Lipoprotein(a) levels (22.0 ± 18.9 versus 16.0 ± 19.4 mg/dl; p < 0.05), homocysteine levels (13.6 ± 6.6 versus 11.4 ± 4.9 mmol/l; p < 0.05) and the percentage of subjects with at least one small apolipoprotein(a) isoform (70.7% versus 29.3%; p < 0.0001) were higher in CAD than NO CAD group. Logistic regression analysis showed that apolipoprotein(a) polymorphism (OR:8.65; 95%CI:3.05–24.55), microalbuminuria (OR:6.16; 95%CI:2.21–17.18), smoking (OR:2.53; 95%CI:1.05–6.08), HDL (OR:3.16; 95%CI:1.28–7.81), homocysteine (OR:2.25; 95%CI:1.14–4.43) and Lipoprotein(a) (OR:2.62; 95%CI:1.01–6.79) were independent predictors of asymptomatic CAD.
The present investigation shows an independent association of Lipoprotein(a), homocysteine and apo(a) polymorphism with silent CAD. Other studies are needed to establish whether these parameters are suitable for CAD screening in diabetic patients.
PMCID: PMC149426  PMID: 12473160
European journal of epidemiology  2010;25(6):403-409.
Depression and cardiovascular disease (CVD) are closely associated, but the mechanisms underlying this connection are unclear. Regardless of the low cholesterol levels observed in depression, a small particle size of low-density lipoproteins (LDL), as well as elevated apolipoprotein B (ApoB) levels, are related to increased CVD risk, even when levels of LDL cholesterol are low. We examined the association between elevated depressive symptoms and compositional changes in serum LDL particles in a sample of 2456 middle-aged Finnish men. Depressive symptoms were assessed with the 18-item Human Population Laboratory Depression Scale, and the study population was divided into two groups (elevated depressive symptoms, n=269; non-depressed, n=2187). The levels of serum total cholesterol (TC), low-and high-density lipoprotein cholesterol (LDL-C, HDL-C), triglycerides (TG), and ApoB were determined. The LDL-C/ApoB ratio, a marker of compositional changes in LDL particle size, was calculated. The group with elevated depressive symptoms had lowered levels of serum TC (p=0.028) and LDL-C (p=0.008). No differences were observed in the LDL-C/ApoB ratio. The likelihood for belonging to the group with elevated depressive symptoms increased 10% for each 0.5 mmol/L decrease in the levels of TC (p=0.002) or LDL-C (p=0.001) in regression models adjusted for age, examination years, marital and socioeconomic status, energy expenditure, body mass index, CVD history, alcohol consumption, smoking, and the use of lipid-lowering, antidepressant and antipsychotic medications. Our findings suggest that greater small-particle LDL levels are not associated with depression, and are thus unlikely to underlie the association between cardiovascular risk and depression.
PMCID: PMC3249261  PMID: 20414796
Apolipoprotein B; Cholesterol; Depression; Low-density lipoprotein cholesterol

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