Egg consumption and high-density-lipoprotein cholesterol

Abstract. Objectives . To examine if increased egg consumption raises serum high-density-lipoprotein (HDL) cholesterol in healthy individuals. Design . A cross-over study. Setting . A private clinic for preventive health examinations in Copenhagen. Subjects . Twenty-four healthy adults, 12 men and 12 women, aged 23–52 (median 40) years. Interventions . After a 1-week control period each person added two bolled eggs to the usual daily diet for 6 weeks. All persons were instructed not to change the lifestyle in other ways during the whole study period. Main outcome measures . Serum HDL cholesterol, total cholesterol and triglycerides were measured before, during and after 6 weeks of extra egg consumption. The corresponding serum Iow-density-lipoprotein (LDL) cholesterol was calculated from the Friedewald formula. Results . After 6 weeks of extra egg consumption serum HDL cholesterol increased by 10% (P < 0.05) and total cholesterol increased 4% (P < 0.05), whereas the ratio total cholesterol/HDL cholesterol did not change significantly. Serum triglycerides and LDL cholesterol were also unchanged. Conclusions . A moderate egg intake should not be rigorously restricted in healthy individuals.     

Low density lipoprotein particle diameter in young,nonobese, normolipidemic Japanese men

Background: prospective studies have demonstrated that a predominance of small, dense LDL particles (pattern B) precedes the clinical onset of coronary heart disease. Prevalence and characteristics of subjects with this LDL size abnormality were studied in young, nonobese, Japanese normolipidemic men. Methods and results: LDL peak particle diameter (PPD) was measured by continuous disc polyacrylamide gel electrophoresis in 223 nonobese normolipidemic men aged 18–20 years (mean±S.D. body mass index: 21.9±3.7 kg/m², total cholesterol: 180±29 mg/dl, triglyceride: 62±34 mg/dl, HDL cholesterol: 58±12 mg/dl). Men with small LDL (PPD <25.8 nm) were found in only 5.4% (n=12) whereas 197 men (88.3%) had a preponderance of large LDL (PPD 26.3 nm). As compared with men in a top tertile (PPD 27.5 nm) those in a low tertile (PPD <26.9 nm) had higher serum levels of LDL cholesterol (120±31 vs 104±24 mg/dl), triglyceride (72±39 vs 49±16 mg/dl) and apolipoprotein (apo) B (84±21 vs 68±14 mg/dl), and lower HDL cholesterol (54±10 vs 60±12 mg/dl). They also had greater body mass index (23.2±4.6 vs 20.9 3.1 kg/m²) and percent body fat (21.5±7.7 vs 17.5±4.9%). LDL-PPD was positively correlated with HDL cholesterol (R=0.20, P=0.002) and was negatively correlated with apoB (R=0.34, P<0.001), triglyceride (R=0.32, P<0.001), percent body fat (R=0.26, P<0.001), body mass index (R=0.24, P<0.001), fat mass (R=0.23, P=0.001), total cholesterol (R=0.20, P=0.002). In multiple regression analysis, apoB, triglyceride, HDL cholesterol, apoAI and percent body fat explained 18% of LDLPPD variability. Conclusion: even in young, nonobese, normolipidemic men, LDL size appears to be associated with triglyceride-rich lipoprotein metabolism and body fat.     

Elevated plasma phospholipid transfer protein activity is a determinant of carotid intima-media thickness in type 2 diabetes mellitus

Aim/hypothesis The plasma activity of phospholipid transfer protein (PLTP), which has putative pro- and anti-atherogenic roles in lipoprotein metabolism, is increased in type 2 diabetes mellitus. We analysed the relationship between carotid artery intima–media thickness (IMT), an established marker of atherosclerosis, and PLTP activity in diabetic patients and control subjects. Methods The IMT (mean of three segments in both carotid arteries by ultrasonography), clinical variables, plasma PLTP activity (phospholipid vesicle–HDL system), lipoproteins, C-reactive protein and insulin were measured in 87 non-smoking men and women, who had type 2 diabetes mellitus, no cardiovascular disease, and were not on insulin or lipid-lowering medication, and in 83 age-matched control subjects. Results In diabetic patients, carotid IMT (p=0.02), pulse pressure (p=0.003), plasma PLTP activity (p<0.001), triglycerides (p=0.01), C-reactive protein (p<0.01) and insulin (p<0.001) were higher, whereas HDL cholesterol was lower (p<0.001) than in control subjects. Multiple stepwise linear regression analysis demonstrated that in type 2 diabetic patients IMT was independently associated with age (p<0.001), sex (p=0.001), pulse pressure (p=0.003), plasma PLTP activity (p=0.03) and HDL cholesterol (p=0.03), but not with very low density lipoprotein+LDL cholesterol, triglycerides, C-reactive protein and insulin (all p>0.20). The relationship between plasma PLTP activity and IMT was not significant in control subjects. Conclusions/interpretation Plasma PLTP activity is a positive determinant of IMT in type 2 diabetes mellitus, suggesting that high PLTP activity is involved in accelerated atherosclerosis in this disease.     

Plasma triglycerides related decrease in high-density lipoprotein cholesterol and its association with myocardial infarction in heterozygous familial hypercholesterolemia

Recent studies suggest that decreased levels of high-density liopoprotein (HDL) may contribute to the risk of premature occlusive atherosclerosis in familial hypercholesterolemia (FH). To investigate further, we have analyzed the concentration as well as distribution of HDL cholesterol in relation to plasma triglycerides and their influence on ischaemic heart disease in FH subjects. The study was carried out in 71 men with heterozygous FH and 46 matched controls. FH subjects were relatively young with a mean age of 38 ± 11 years. Tendon xanthomatas were observed in 57% of the subjects, whereas ischemic heart disease was identified in 33%. Compared to normals, the mean value of HDL cholesterol is significantly reduced by 21% in FH heterozygotes (42 ± 12 v 33 ± 9 mg/dL, P < 0.001). The decrease in HDL cholesterol is highly correlated to the levels of plasma triglycerides (r = −0.50, P < 0.001) and VLDL cholesterol (r = −0.53, P < 0.001). Moreover, HDL cholesterol decrease is not associated with elevated levels of LDL cholesterol (r = −0.20, NS), which is the primary characteristic feature of FH subjects. However, HDL cholesterol decrease is weakly related to total plasma cholesterol concentration (r = −0.24, P < 0.05). The body weight is also contributory to the reduction of HDL cholesterol (r = −0.42, P < 0.01), probably due to its strong positive correlation to plasma triglycerides (r = +0.54, P < 0.001). Grouping of subjects on the basis of triglyceride levels of less than 200 mg/dL (IIa phenotype) and more than 200 mg/dL (IIb phenotype) shows that the concentration of HDL cholesterol undergoes a further significant decrease in the latter group (36 ± 9 v 30 ± 11 mg/dL, P < 0.001). Since the level of LDL cholesterol is similar in both groups (314 ± 68 v 316 ± 76 mg/dL, NS), a further reduction in HDL cholesterol concentration results in an increased LDL/HDL ratio in IIb phenotypes. Although HDL cholesterol is normally distributed in controls and type IIa phenotypes, its distribution is skewed to lower values in type IIb. In addition to similar levels of LDL cholesterol, the presence of tendon xanthomatas is equally observed in both type IIa and type IIb subjects (51.1% and 62.5%, respectively). Similarly, the incidence of angina pectoris (19.2% and 12.5% in type IIa and type IIb, respectively) is also approximately the same in both groups. However, the differences are striking in the incidence of myocardial infarction (MI), which is increased three-fold (25% v 8.5%) in type IIb subjects, as compared to type IIa. These findings indicate that in addition to LDL excess, HDL deficiency associated with elevated plasma triglycerides contributes to the severity of ischemic heart disease, as revealed from the manifestation of MI in some FH heterozygotes.     

Influence of polyunsaturated fats and fat restriction on serum lipoproteins in humans

This study was designed to determine the effects of polyunsaturated fats and of reducing intake of total fat on serum lipids, lipoproteins, and apolipoproteins. Twenty-two normolipidemic women living in a nunnery were given a reference diet (fat/carbohydrate $\text{42}\text{46\%}$ of energy, $\text{P}\text{S}$ ratio 0.16), a polyunsaturated diet ($\text{42}\text{46\%}\text{,}\text{P}\text{S}\text{1.0}$), and a low-fat, polyunsaturated diet ($\text{32}\text{56\%}\text{,}\text{P}\text{S}\text{1.0}$) for 6 weeks each. Serum and lipoprotein lipids were determined by standard procedures, apolipoproteins either by laser immunonephelometry or by rocket immunoelectrophoresis. Consumption of the polyunsaturated diet decreased cholesterol and apolipoprotein B levels in VLDL (?33.1% and ?23.8%) and in LDL (?13.5% and ?8.8%) without affecting HDL. Consumption of the low-fat, polyunsaturated diet resulted in a reincrease of VLDL triglycerides, but not of VLDL cholesterol. Concentration of VLDL apolipoprotein B further fell (?41.6%) and that of apolipoprotein E decreased (?25.9%), resulting in an increased VLDL lipid/apolipoprotein mass ratio. This study indicates that responses to therapeutic polyunsaturated diet are lowered levels of VLDL and LDL, but unchanged levels of HDL. Additional restriction of dietary fat intake alters the VLDL composition with a decrement in apolipoprotein E enriched VLDL particles.     

Alcohol intake and dyslipidemia in male patients with hypertension and diabetes enrolled in a China multicenter registry

Alcohol consumption is a proven risk factor of dyslipidemia. In the present analysis, we investigated the association of alcohol intake with dyslipidemia, an emerging epidemic in China, in male patients with hypertension and diabetes mellitus. Our study participants were from a nationwide registry (n = 1181). A questionnaire was administered to collect information on alcohol intake. Dyslipidemia was defined as an elevated concentration of serum triglycerides (≥2.3 mmol/L), total (≥6.2 mmol/L) or low-density lipoprotein (LDL) cholesterol (≥4.1 mmol/L), or a reduced high-density lipoprotein (HDL) cholesterol (< 1.0 mmol/L). Serum concentrations of triglycerides (1.60 mmol/L) and total (4.93 mmol/L) and LDL cholesterol (2.95 mmol/L) were highest with current usual drinking, with a significant P value for trend from never (n = 679) to ever (n = 107) and to rare (n = 187) and usual drinkers (n = 208, P ≤ .002). Serum HDL cholesterol (1.13 mmol/L) was lowest in ever drinkers, with a nonsignificant P value for trend (P = .22). The prevalence was highest in usual drinkers for hypertriglyceridemia (27.4%) and total (12.5%) and LDL hypercholesterolemia (8.7%), and in ever drinkers for low HDL cholesterol (34.6%). The P value for trend was significant for hypertriglyceridemia and total hypercholesterolemia (P ≤ .01), but not for LDL hypercholesterolemia or low HDL cholesterol (P ≥ .26). The between-province ecological analysis showed that the proportion of usual drinking was significantly associated with the prevalence of any dyslipidemia across 10 China provinces (r = .42, P < .0001). In conclusion, alcohol drinkers showed a worse lipid profile in patients with hypertension and diabetes mellitus. Usual drinking ecologically explained the between-province variation in the prevalence of dyslipidemia.     

Change in lipid profile in celiac disease: beneficial effect of gluten-free diet

Purpose

Celiac disease is associated with hypocholesterolemia, which is thought to contribute to a favorable cardiovascular risk profile. This led to suggestions that the diagnosis of celiac disease and its treatment with a gluten-free diet may result in elevation of the serum cholesterol level and worsen this risk profile. However, no study proves this in adults. We therefore examined the effect of a gluten-free diet on the lipid profile in patients with celiac disease.

Subjects and methods

We identified 132 patients with celiac disease who adhered to a gluten-free diet and had lipid profiles performed before and after a median of 20.5 months on the diet. The patients lacked diseases that may affect serum lipids.

Results

There were significant increases in total cholesterol and high-density lipoprotein (HDL) cholesterol (P < .0001) but not low-density lipoprotein (LDL) cholesterol (P = .06). The LDL/HDL ratio decreased by 0.36 ± 0.7 (P < .0001). Both men and women had a significant increase in total cholesterol and HDL and a significant decrease in the LDL/HDL ratio. Only men had increases in LDL (P = .02). The greatest increase in lipid values was seen in those with the lowest initial values. The largest increase in HDL was seen in subjects with more severe disease as indicated by low albumin level and presence of total villous atrophy.

Conclusions

Diagnosis of celiac disease and its treatment with a gluten-free diet resulted in improvement in the lipoprotein profile, which included an increase in HDL and a decrease in the LDL/HDL ratio.     

Low HDL‐cholesterol is common in European Type 2 diabetic patients receiving treatment for dyslipidaemia: data from a pan‐European survey

Aims To measure the prevalence of low high‐density lipoprotein (HDL)‐cholesterol (men < 1.03 mmol/l; women < 1.29 mmol/l) in European Type 2 diabetic patients receiving treatment for dyslipidaemia. Methods The pan‐European Survey of HDL‐cholesterol measured lipids and other cardiovascular risk factors in 3866 patients with Type 2 diabetes and 4436 non‐diabetic patients undergoing treatment for dyslipidaemia in 11 European countries. Results Diabetic patients were more likely to be obese or hypertensive than non‐diabetic patients. Most patients received lifestyle interventions (87%) and/or a statin (89%); treatment patterns were similar between groups. Diabetic patients had [means (SD)] lower HDL‐cholesterol [1.22 (0.37) vs. 1.35 mmol/l (0.44) vs. non‐diabetic patients, P < 0.001] and higher triglycerides [2.32 (2.10) vs. 1.85 mmol/l (1.60), P < 0.001]. More diabetic vs. non‐diabetic patients had low HDL‐cholesterol (45% vs. 30%), high triglycerides (≥ 1.7 mmol/l; 57% vs. 42%) or both (32% vs. 19%). HDL‐cholesterol < 0.9 mmol/l was observed in 18% of diabetic and 12% of non‐diabetic subjects. Differences between diabetic and non‐diabetic groups were slightly greater for women. LDL‐ and total cholesterol were lower in the diabetic group [3.02 (1.05) vs. 3.30 mmol/l (1.14) and 5.12 (1.32) vs. 5.38 mmol/l (1.34), respectively, P < 0.001 for each]. Conclusions Low HDL‐cholesterol is common in diabetes: one in two diabetic women has low HDL‐cholesterol and one diabetic man in four has very low HDL‐cholesterol. Management strategies should include correction of low HDL‐cholesterol to optimize cardiovascular risk in diabetes.     

Comparison of Bezafibrate and Simvastatin in the Treatment of Dyslipidaemia in Patients with NIDDM

Fibrates and HMG CoA reductase inhibitors are commonly used in the treatment of diabetic dyslipidaemia. However, these two groups of drugs have not been compared in diabetic patients in a randomized controlled trial. Therefore, a multicentre study was performed in 73 subjects with non-insulin-dependent (Type 2) diabetes mellitus (NIDDM) and combined hyperlipidaemia (serum cholesterol 6.2–10.0 mmol l⁻¹, serum triglycerides 2.3–10.0 mmol l⁻¹), comparing the efficacy of 400 mg bezafibrate with 10 mg simvastatin in a double-blind fashion. Treatment with bezafibrate during 12 weeks reduced serum triglycerides significantly more than simvastatin (−41 % vs −22 %, p < 0.001) and increased HDL cholesterol more (bezafibrate: + 17 % vs simvastatin: + 9 %, p < 0.05). LDL cholesterol levels decreased by 14 % (p < 0.001) during simvastatin and increased by 21 % (p < 0.01) during bezafibrate. This increase in LDL cholesterol was positively correlated with fasting serum triglycerides (p < 0.001) and was associated with a reduction of the serum apolipoprotein B concentration, suggesting an increase in LDL particle size. Metabolic control of diabetes (fasting glycaemia; HbA_1c) and insulin secretion (C-peptide levels) were unaffected by both treatments. The incidence of side-effects during treatment was similar for both drugs. Thus, 400 mg bezafibrate mainly increases HDL cholesterol and lowers serum triglycerides but at the expense of an increase in LDL cholesterol; 10 mg simvastatin lowers LDL cholesterin more effectively but has a smaller effect on HDL cholesterol and triglycerides. © 1997 John Wiley & Sons, Ltd.     

Plasma Lipoproteins and Fatty Acid Composition during a Moderate Eicosapentaenoic Acid Diet

ABSTRACT. The effect of a diet rich in marine fatty acids, especially eicosapentaenoic acid, on plasma lipids (total plasma cholesterol, HDL cholesterol, total triglycerides and apolipoproteins A and B) and fatty acid composition in plasma phosphatidylcholine (PC) was studied in 10 healthy men. They were maintained for 11 weeks on their normal diet which was partly replaced by 150–200 g of fatty fish per day. In the same individuals this diet had previously caused a delay in primary haemostasis and a decrease in platelet aggregability similar to that caused by acetylsalicylic acid, a known inhibitor of thromboxane A₂ formation. Apart from its effect on haemostasis, the fish diet substantially reduced serum triglycerides (by 43%, p < 0.01) but caused no changes in total plasma or HDL cholesterol or apolipoproteins A and B. After three weeks on the diet the proportion of plasma PC ω-3 polyunsaturated fatty acids increased (C20: 5 and C22: 6) and ω-6 fatty acids decreased (C18: 2 and C20:3). The relative plasma PC content of arachidonic acid was unaffected throughout. These alterations in plasma PC fatty acid composition were principally in accordance with those seen in platelet membrane PC. There was a linear correlation between the content of ω-3 and of ω-6 fatty acids in plasma PC with that of platelet PC as well as in predominate individual fatty acids of the two series. Six weeks after the volunteers had resumed their usual diet, total triglycerides and the fatty acid composition of plasma PC had returned to the original state.     

Long-term effects of a reduced fat diet intervention on cardiovascular disease risk factors in individuals with glucose intolerance

The long-term effects on cardiovascular disease risk factors of a reduced fat (RF), ad libitum diet were compared with usual diet (control, CD) in glucose intolerance individuals. Participants were 136 adults aged > or =40 years with 'glucose intolerance' (2h blood glucose 7-11.0 mmol/l) detected at a Diabetes Survey who completed at 1 year intervention study of reduced fat, ad libitum diet versus usual diet. They were re-assessed at 2, 3 and 5 years. Main outcome measures were blood pressure, serum concentrations of total cholesterol, HDL and LDL cholesterol, total cholesterol:HDL ratio, triglycerides and body weight. The reduced fat diet lowered total cholesterol (P<0.01), LDL cholesterol (P< or =0.05), total cholesterol:HDL ratio (P< or =0.05), body weight (P<0.01) and systolic blood pressure (P< or =0.05) initially and diastolic blood pressure (P<0.01) long-term. No significant changes occurred in HDL cholesterol or triglycerides. In the more compliant 50% of the intervention group, systolic and diastolic blood pressure levels and body weight were lower at 1, 2 and 3 years (P<0.05). It was concluded that a reduced fat ad libitum diet has short-term benefits for cholesterol, body weight and systolic blood pressure and long-term benefits for diastolic blood pressure without significantly effecting HDL cholesterol and triglycerides despite participants regaining their lost weight.     

Long-term effects of a ketogenic diet in obese patients

BACKGROUND:

Although various studies have examined the short-term effects of a ketogenic diet in reducing weight in obese patients, its long-term effects on various physical and biochemical parameters are not known.

OBJECTIVE:

To determine the effects of a 24-week ketogenic diet (consisting of 30 g carbohydrate, 1 g/kg body weight protein, 20% saturated fat, and 80% polyunsaturated and monounsaturated fat) in obese patients.

PATIENTS AND METHODS:

In the present study, 83 obese patients (39 men and 44 women) with a body mass index greater than 35 kg/m², and high glucose and cholesterol levels were selected. The body weight, body mass index, total cholesterol, low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol, triglycerides, fasting blood sugar, urea and creatinine levels were determined before and after the administration of the ketogenic diet. Changes in these parameters were monitored after eight, 16 and 24 weeks of treatment.

RESULTS:

The weight and body mass index of the patients decreased significantly (P<0.0001). The level of total cholesterol decreased from week 1 to week 24. HDL cholesterol levels significantly increased, whereas LDL cholesterol levels significantly decreased after treatment. The level of triglycerides decreased significantly following 24 weeks of treatment. The level of blood glucose significantly decreased. The changes in the level of urea and creatinine were not statistically significant.

CONCLUSIONS:

The present study shows the beneficial effects of a long-term ketogenic diet. It significantly reduced the body weight and body mass index of the patients. Furthermore, it decreased the level of triglycerides, LDL cholesterol and blood glucose, and increased the level of HDL cholesterol. Administering a ketogenic diet for a relatively longer period of time did not produce any significant side effects in the patients. Therefore, the present study confirms that it is safe to use a ketogenic diet for a longer period of time than previously demonstrated.     

The effect of dietary changes on high density lipoprotein cholesterol. The Oslo Study.

In some good responders to dietary treatment of hyperlipidemia followed for four years (the Oslo Study of men aged 40 to 49 years), a significantly increased high density lipoprotein (HDL) cholesterol concentration was found in the treated men as compared to an untreated control group, well matched for pretreatment values of HDL cholesterol, triglycerides and other relevant variables.In the treated group, diet analysis at four years revealed an isocaloric diet, with 27.9 per cent of total calories from fats, 8.2 per cent of total calories from saturated fatty acids and a polyunsaturated to saturated ratio (P:S ratio) of 1.01—as compared to 44.1, 18.3 and 0.39, respectively, in the control group.After four years of observation the mean total cholesterol in the treated group was 263 mg/dl versus 341 mg/dl in the control group, mean fasting triglycerides 129 mg/dl versus 200 mg/dl, whereas mean HDL cholesterol was approximately 20 per cent higher in the treated group than in the control group (50.09 mg/dl versus 42.22). The “HDL ratio” (HDL cholesterol × 100 to total cholesterol — HDL cholesterol) was 69 per cent higher in the treated group. HDL cholesterol was significantly and positively correlated with the P:S ratio in the diet.In this investigation only good diet responders have been studied. On the other hand, a clearly significant increased HDL cholesterol has been demonstrated in the dieters as compared to well matched control subjects. These results might be of interest in the view of HDL cholesterol as a well documented and independent “antirisk factor” for coronary heart disease.     

Effects of dietary cholesterol on plasma lipoproteins and their subclasses in IDDM patients

Summary To compare the effects of dietary cholesterol supplementation in insulin-dependent diabetic (IDDM) patients and normal subjects, 10 male IDDM patients in good glycaemic control (HbA_{1 c} 7.3 ± 0.9 %) (mean ± SD) and normal plasma lipid levels, and 11 control male subjects of similar age, body mass index and lipid plasma levels underwent a double blind, cross-over, sequential study. Cholesterol supplementation of 800 mg/day or placebo were given for consecutive periods of 3 weeks. The concentration of plasma total cholesterol increased significantly with the dietary cholesterol supplementation compared to placebo in IDDM patients by 6 % (p < 0.05) and in control subjects by 9 % (p < 0.05). No changes were observed in the concentration of plasma triglycerides in either group. The LDL cholesterol level increased by 12 % (p < 0.01) in patients and by 7 % (p < 0.05) in control subjects. In patients plasma HDL cholesterol concentration remained the same, while in control subjects it tended to increase after cholesterol supplementation (from 1.14 ± 0.26 to 1.23 ± 0.27 mmol/l, p = 0.06). During the cholesterol intake period the mean concentration of LDL1, LDL2 and LDL3 subclasses in patients showed a significant increase by 21.0 (p < 0.05), 20.4 (p < 0.001) and 11.1 % (p < 0.05), respectively, resulting in an 18.0 % increase in mean total LDL mass (p < 0.001) without major changes in LDL composition. In the control subjects the changes in the concentrations of LDL subclasses during cholesterol intake were less and not significant. In the IDDM patients the cholesterol intake did not affect the concentration or composition of HDL subclasses or total HDL mass. In contrast, in control subjects cholesterol intake increased the mean concentration of HDL2 a by 12.2.% (p < 0.05) and this increase was significantly different if compared to changes obtained in the patients. In conclusion, compared to normal subjects, in IDDM patients, dietary cholesterol intake increased the LDL particle mass significantly and had no positive effect on HDL. [Diabetologia (1998) 41: 193–200] Received: 4 July 1997 and in revised form: 12 September 1997     

Link between traditional cardiovascular risk factors and inflammation in patients with early arthritis: Results from a French Multicenter Cohort

Objective

To compare the characteristics of traditional cardiovascular risk factors for untreated patients with early arthritis (EA) and healthy subjects, and to look for a link between cardiovascular risk factors and inflammation in EA patients.

Methods

This multicenter case–control study enrolled 607 patients with EA (ESPOIR cohort) and 1,821 age‐ and sex‐matched controls (World Health Organization MONICA survey). Lipid levels, blood pressure, glucose levels, and exposure to smoking were characterized in patients and controls. Systemic inflammation was quantified in EA patients. Traditional cardiovascular risk factor characteristics were compared between patients with EA and controls. The link between cardiovascular risk factors and inflammation was assessed in EA patients.

Results

Mean ± SEM total cholesterol (2.14 ± 0.022 versus 2.34 ± 0.017 gm/liter; P < 0.001), high‐density lipoprotein (HDL) cholesterol (0.60 ± 0.011 versus 0.63 ± 0.007 gm/liter; P = 0.020), and low‐density lipoprotein (LDL) cholesterol (1.28 ± 0.025 versus 1.51 ± 0.016 gm/liter; P < 0.001) were lower in EA patients than in controls. Triglycerides, triglycerides/HDL ratio, and pulse pressure were higher in patients with EA. Diastolic blood pressure and glucose levels were lower in EA patients. Former or current smokers were more frequent in patients with EA. Total and HDL cholesterol levels were negatively associated with C‐reactive protein or serum interleukin‐6 levels.

Conclusion

Total, HDL, and LDL cholesterol, triglycerides, diastolic blood pressure, pulse pressure, glucose, and triglycerides/HDL ratio differ between patients with EA and controls. Some of these risk factors appear to be linked to systemic inflammation. Such initial differences could modulate the risk of cardiovascular events later in the course of arthritis.     

Effect of colestipol and clofibrate,singly and in combination,on plasma lipid and lipoproteins in Type IIb hyperlipoproteinemia

The effect of colestipol, clofibrate and a combination of these two drugs on plasma lipid and lipoprotein levels was evaluated in 14 adult male patients with Type IIb hyperlipoproteinemia. A crossover design with each patient receiving all three treatments was utilized. Twenty g of colestipol per day reduced total and LDL cholesterol by 39.1 and 51.5 mg/dl, respectively (p < 0.001). There was an associated rise in total triglycerides of 63.5 mg/dl (p < 0.01) with no significant change in HDL cholesterol. Clofibrate, 2.0 g per day, did not significantly lower either total (?7.9 mg/dl) or LDL cholesterol (+8.7 mg/dl). There was marked interpatient variability in terms of the LDL cholesterol response to clofibrate, but the majority of patients demonstrated an increase. HDL cholesterol levels increased by 6.7 mg/dl (p < 0.01) and total triglycerides were reduced by 94.6 mg/dl (p < 0.001). Utilizing the same dosages of both drugs, the combination of colestipol and clofibrate was less effective in lowering total and LDL cholesterol than colestipol therapy alone, and increases in HDL cholesterol and decreases in triglycerides similar to those obtained with clofibrate were observed.     

Treating patients with documented atherosclerosis to national cholesterol education program-recommended low-density-lipoprotein cholesterol goals with atorvastatin,fluvastatin, lovastatin and simvastatin

Objectives. This study compared the efficacy and safety of atorvastatin, fluvastatin, lovastatin, and simvastatin in patients with documented atherosclerosis treated to U.S. National Cholesterol Education Program (NCEP) recommended low-density-lipoprotein (LDL) cholesterol concentration (≤100 mg/dl [2.59 mmol/liter]).Background. For patients with advanced atherosclerosis, NCEP recommends lipid-lowering drug therapy if LDL cholesterol remains ≥130 mg/dl (3.36 mmol/liter).Methods. A total of 318 men or women with documented atherosclerosis and LDL cholesterol ≥130 mg/dl (3.36 mmol/liter) and ≤250 mg/dl (6.5 mmol/liter), and triglycerides ≤400 mg/dl (4.5 mmol/liter) participated in this 54-week, multicenter, open-label, randomized, parallel-group, active-controlled, treat-to-target study. Patients were titrated at 12-week intervals until the LDL cholesterol goal was reached. Number of patients reaching target LDL cholesterol levels and dose to reach target were evaluated.Results. At the starting doses, atorvastatin 10 mg produced significantly greater decreases (p < 0.05) in plasma LDL cholesterol than the other treatments. Subsequently, the percentage of patients reaching goal at the starting dose was 32% for atorvastatin, 1% for fluvastatin, 10% for lovastatin and 22% for simvastatin. Atorvastatin-treated patients required a lower median dose than other treatments. Median doses at week 54 with the last available visit carried forward were atorvastatin 20 mg/day, fluvastatin 40 mg/day + colestipol 20 g/day, lovastatin 80 mg/day, simvastatin 40 mg/day.Conclusions. A significantly greater number (p < 0.05) of patients with confirmed atherosclerosis treated with atorvastatin reached the target LDL cholesterol concentration at the starting dose than patients treated with fluvastatin or lovastatin, and significantly fewer (p < 0.05) patients treated with atorvastatin required combination therapy with colestipol to achieve target LDL cholesterol concentrations than all other statins tested.     

Influence of oral polyunsaturated and saturated phospholipid treatment on the lipid composition and fatty acid profile of chimpanzee lipoproteins.

The influence of treatment with polyunsaturated lecithin (EPL) and with saturated lecithin on the lipoprotein composition and fatty acid profile was investigated in 4 male chimpanzees. The animals were successively given 3 isocaloric diets containing the same amount of fat with a degree of saturation varying from 1 in the control diet to 0.2 in the diet enriched with polyunsaturated lecithin, to 4 in the diet enrich with saturated lecithin. The VLDL, LDL and HDL3 fractions were isolated by ultracentrifugal flotation; changes in their lipid and fatty acid composition were followed and their microviscosity was measured. The treatment with polyunsaturated lecithin increases the cholesterol esters and lysolecithin content in HDL3, presumably via activation of the enzyme LCAT. These modified HDL particles have a more fluid surface and a denser core and are susceptible to act as better cholesterol carriers. A complementary effect of this treatment is a decrease of the plasma triglycerides and VLDL concentration, an increase in the unsaturation ratio of the triglycerides which might take place via activation of triglyceride lipase. The saturated lecithin treatment increases the plasma VLDL and LDL concentrations and the triglyceride levels and increases mostly the saturation ratio of the cholesterol esters. These effects are likely to enhance the progression of atherosclerosis.     

Lowering LDL cholesterol in adults: a prospective, community-based practice initiative

Purpose

The purpose of our study was to see if a clinic-wide initiative, with low-density lipoprotein cholesterol (LDL)-lowering interventions, could be an effective health maintenance strategy to decrease LDL levels to <100 mg/dL in a community-based, internal medicine outpatient setting.

Methods

There were 1375 patients screened with an initial/baseline LDL (LDL₁) measurement. Patients whose LDL₁ levels were >100 mg/dL were put on a lipid-lowering action plan and re-evaluated with a follow-up LDL (LDL₂) in 3-4 months. An additional action plan was given to patients whose LDL₂ values were still too high, and their values retested in 3-4 months for a third LDL (LDL₃). LDL₁ levels versus postintervention LDL measurement (LDL₂ or LDL₃) levels were the primary endpoints, with secondary endpoints of total cholesterol, total triglyceride, and high-density lipoprotein cholesterol (HDL) levels over the 3 measurement periods.

Results

Of 514 patients who were given action plans, 443 returned for their follow-up lipid assessment. LDL levels in this group fell from 140.7 ± 29.2 (mean ± 1 SD) mg/dL (LDL₁) to 110.9 (29.6) mg/dL (LDL₂) (P <.05). Of these 443 patients, 167 individuals had LDL₂ levels that now met National Cholesterol Education Program/Third Adult Treatment Panel III guidelines (<100 mg/dL) and 87 were now considered by their primary care provider as controlled (LDL 100-130 mg/dL). However, 158 individuals had LDL₂ levels that were either not controlled or not meeting National Cholesterol Education Program/Third Adult Treatment Panel guidelines. These 158 patients were provided with a second action plan, and of these, 50 (32%) returned to the clinic for a third lipid panel. Their LDLs, as a group, subsequently fell from an LDL₂ of 139.9 (24.4) mg/dL to 112.5 (28.2) mg/dL (LDL₃) (P <.05). Sixteen of 50 now had LDLs <100 mg/dL, and 26 of 50 were considered controlled. Initial HDL (HDL₁) levels rose from 55.4 (17.2) mg/dL to 57.3 (14.6) mg/dL (HDL₂) (n = 443). Blood levels of triglycerides and cholesterol also decreased in our returning patients over this time period (P <.05).

Conclusions

Community-based physicians can help their patients realize significant reductions in low-density lipoprotein cholesterol levels by implementing and closely monitoring lipid-lowering initiatives for their patients, resulting in potentially large positive impacts on the long-term health and well-being of their patients.     

The Effect of Acebutolol on Plasma Lipids,Blood Glucose and Serum Insulin Levels

Abstract The effect on plasma lipids of acebutolol given orally over a 6-month period to 18 patients with essential hypertension was studied. There were no significant changes in the concentrations of plasma total cholesterol, LDL cholesterol, VLDL cholesterol and triglycerides during treatment. The level of HDL cholesterol decreased slightly but not significantly during treatment. Plasma free fatty acids decreased significantly (p<0.05) during treatment with acebutolol. During an oral glucose tolerance test, blood glucose values were elevated after acebutolol therapy at 60 (p<0.05) and 120 min (p<0.05). No impairment of insulin release was observed after acebutolol therapy.