Decrease In Total Cholesterol Levels Research Articles

Resistance Exercise Training Is Associated With Decreases in Serum Low-Density Lipoprotein Cholesterol Levels in Premenopausal Women

Aerobic exercise training is associated with reduced serum concentrations of triglycerides, increased concentrations of high-density lipoprotein cholesterol, and minimal changes in serum levels of total cholesterol or low-density lipoprotein cholesterol. There are few data on the effects of resistance exercise on blood lipid levels. Premenopausal women were randomly assigned to a supervised resistance exercise training program (n = 46) or a control group (n = 42) for 5 months. Serum was analyzed for levels of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides. Body composition and dietary intake were also measured. The exercise group showed a 0.33 +/- 0.03-mmol/L (mean +/- SE) decrease in total cholesterol level and a 0.36 +/- 0.001-mmol/L decrease in low-density lipoprotein cholesterol level that was significantly different from the control group. No significant changes were noted in serum high-density lipoprotein cholesterol or triglyceride levels in either group. Changes in body composition showed no significant correlations with changes in total cholesterol or low-density lipoprotein cholesterol. There were no significant differences in nutrient intake between the groups. In healthy, premenopausal women, with normal baseline lipid profiles, 5 months of resistance exercise training was associated with significant decreases in serum total cholesterol and low-density lipoprotein cholesterol concentrations.

Saturated Fats, Cholesterol, and Dietary Compliance

Lack of response to a cholesterol-lowering diet can be caused by physiological nonresponsiveness, inadequate knowledge, or inability to change dietary habits (poor compliance). The purpose of this study was to evaluate the dietary compliance of hyperlipidemic individuals who received intensive initial dietary education and followup, and who showed an initial reduction of their plasma cholesterol levels. One hundred five individuals with fasting cholesterol levels of 5.17 mmol/L (200 mg/dL) or greater received intensive education and follow-up on the American Heart Association Step I diet during an initial 12-week period. The participants provided 3-day dietary records every week, and fasting lipoprotein analysis was performed biweekly. Six months after termination of this period, the subjects were requested to return for a follow-up evaluation of their lipoprotein profile and dietary adherence. Seventy-three (70%) of the subjects returned for a follow-up evaluation of lipoprotein cholesterol levels. Of these, 42 (58%) had a 10% or greater average initial decrease in total cholesterol levels at weeks 3 and 4 ("baseline"), and they were considered to be "high responders." At the 6-month follow up, the average plasma cholesterol level in these responders remained 6.4% below that at entry level, but it had increased by 19% compared with baseline values (6.30 mmol/L [244 mg/dL] vs 5.43 mmol/L [210 mg/dL], respectively). Corresponding significant increases at 6 months were found in high-density lipoprotein cholesterol (8%), low-density lipoprotein cholesterol (16%), and very-low-density lipoprotein cholesterol (66%) levels. Analysis of dietary histories revealed that dietary cholesterol and percent calories from fat increased significantly, but remained within the recommended guidelines. However, the increase in percent calories from saturated fat (from 10.0% +/- 0.5% to 14.4% +/- 1.0% [mean +/- SEM]) deviated markedly from these guidelines. The results suggest the long-term compliance to the reduction of dietary saturated fat remains a problem, even in individuals who receive intensive initial training and show an early favorable response. Follow-up evaluation of hyperlipidemic patients who are receiving dietary therapy should take into account this behavioral pattern. It remains to be determined whether continuing supervision and better nutritional labeling will facilitate dietary compliance.

Effectiveness of Low-Dose Lovastatin in Lowering Serum Cholesterol

This study reviews the progress of 56 consecutive patients with type IIa and IIb hyperlipoproteinemia following treatment with lovastatin. Lovastatin, a potent inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, has been shown to have a cholesterol-lowering effect in doses ranging from 10 to 80 mg/d. Thus far, however, no large study has been performed to show the effectiveness of low-dose lovastatin (20 mg/d) for more than a 6-week duration. Fifty-six patients with known coronary artery disease were prospectively studied, with fasting lipid values being measured at baseline and after 6, 12, 18, and 24 weeks of 20-mg/d lovastatin therapy given as a single evening dose. The total cholesterol level fell 26% from a mean baseline of 8.12 mmol/L (314 mg/dL) and triglyceride levels fell by 12% from a mean baseline of 2.46 mmol/L. The high-density lipoprotein levels increased 7.6%. One patient with known preexisting liver disease was withdrawn from the study owing to an asymptomatic significant rise in liver function test results; one subject complaining of proximal muscle weakness was also withdrawn. The maximal decrease in total cholesterol level occurred within 6 weeks of initiation of therapy. We conclude that low-dose (20-mg/d) lovastatin was effective in lowering serum cholesterol levels in patients with primary type IIa or IIb hyperlipoproteinemia with minimal short-term side effects. Further studies are needed to establish the long-term safety and effectiveness of this drug.

Fenofibrate affects the compositions of lipoproteins

This study assessed the effects of fenofibrate on lipoprotein levels and lipoprotein compositions in a subgroup of patients who participated in a multicenter fenofibrate study. Eleven men and 10 women aged 29 to 63 were studied, 12 with type II A and nine with type II B hyperlipoproteinemia. Fasting blood samples were obtained every four to six weeks. Lipoprotein lipids were quantified by procedures of the Lipid Research Clinics, and apolipoproteins by radioimmunoassay. Fenofibrate decreased mean triglyceride and cholesterol levels of the type II A patients from 130 to 99 and from 286 to 237 mg/dl, respectively. Levels of very low-density lipoprotein triglycerides, low-density lipoprotein cholesterol, and very low-density lipoprotein cholesterol decreased and high-density lipoprotein cholesterol levels rose. Apolipoprotein B and apolipoprotein E levels decreased, whereas apolipoprotein AI and apolipoprotein All levels rose. The mean very low-density lipoprotein cholesterol:very low-density lipoprotein triglyceride ratio and low-density lipoprotein cholesterol:low-density lipoprotein triglyceride ratio decreased. The low-density lipoprotein cholesterol:apolipoprotein B ratio and high-density lipoprotein cholesterol:apolipoprotein All ratio decreased as did the apolipoprotein AI:apolipoprotein AII ratio. In patients with type II B hyperlipoproteinemia, triglyceride and cholesterol levels decreased with fenofibrate therapy with most of the decrease in triglyceride levels due to very low-density lipoprotein triglycerides, whereas the decrease in total cholesterol levels was due to decreases in very low-density lipoprotein and low-density lipoprotein cholesterol. High-density lipoprotein cholesterol levels rose. The decrease in low-density lipoprotein cholesterol levels was not significant in this group. Apolipoprotein E levels decreased and apolipoprotein AI and apolipoprotein AII levels rose. Indices of composition in type II B patients were similar to those in type II A patients but the changes were less dramatic. Very low-density lipoprotein cholesterol:very low-density lipoprotein triglyceride ratios decreased significantly, but low-density lipoprotein cholesterol:low-density lipoprotein triglyceride ratios did not change significantly with treatment. The mean low-density lipoprotein cholesterol:apolipoprotein B ratio, high-density lipoprotein cholesterol: apolipoprotein AII ratio, and apolipoprotein AI:apolipoprotein AII ratio all were lowered by therapy. Thus, very low-density lipoprotein and low-density lipoprotein lost cholesterol in response to fenofibrate therapy and high-density lipoprotein particles became enriched in cholesterol.