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At least 19 recordsLinked to original sources

PubMed1991

Linoleic acid lowers LDL cholesterol without a proportionate displacement of saturated fatty acid.

We tested the specificity of the plasma cholesterol-lowering effect of linoleic acid in a comparison of linoleate-rich and saturated fatty acid-rich foods. Twelve mildly hypercholesterolemic men and women ate the two diets for three weeks each in a random cross-over design, after a two-week baseline period. A linoleic acid-rich supplement was added to the baseline diet so that the saturated and monounsaturated fatty acid content did not change significantly. Despite the consequent increase in total fat intake, the linoleate-rich diet (23 per cent energy from polyunsaturated fatty acids) significantly lowered plasma total and low-density lipoprotein (LDL) cholesterol (-8 per cent and -14 per cent respectively), while high-density lipoprotein (HDL) cholesterol rose 8 per cent. The direction of these changes was similar in all 12 subjects. Compared with a supplement that raised dietary saturated fatty acids to 30 per cent energy, the linoleate acid-rich diet gave lower total cholesterol (-14 per cent), LDL cholesterol (-18 per cent) and HDL cholesterol (-12 per cent) concentrations. Linoleic acid lowers LDL cholesterol even when saturated fatty acids are not significantly displaced and substantially more when there is such displacement.

Adult↗

PubMed1992

Intense dietary counseling lowers LDL cholesterol in the recruitment phase of a clinical trial of men who had coronary artery bypass grafts.

Intense dietary counseling lowered low-density-lipoprotein (LDL) cholesterol levels during the recruitment phase of a 5-year clinical trial of men who had undergone coronary artery bypass grafts. At visit 1, a 24-hour dietary recall was obtained and analyzed for intakes of total energy; total, saturated, monounsaturated, and polyunsaturated fat; and dietary cholesterol. Participants were then instructed to follow the National Cholesterol Education Program (NCEP) Step I diet. Additional dietary counseling was provided at 1-month intervals during visits 2 and 3. At visit 3, another 24-hour dietary recall was obtained and analyzed similarly. Of 59 men with an LDL cholesterol level greater than 4.5 mmol/L at visit 1, 52 decreased their level to 4.5 mmol/L or less to qualify for the 5-year study. Between visits 1 and 3, mean LDL cholesterol levels decreased significantly from 4.86 +/- 0.04 mmol/L to 4.27 +/- 0.05 mmol/L, which coincided with significant mean decreases in dietary intake of total fat from 33.4 +/- 1.3% to 25.2 +/- 1.4%, saturated fat from 11.1 +/- 0.6% to 7.0 +/- 0.4%, and dietary cholesterol from 122 +/- 6.1 to 90 +/- 6.3 mg/1,000 kcal. Overall, the dietary intake improved to more closely follow the NCEP Step II diet and resulted in a 10.7% decrease in total cholesterol level and a 12.4% decrease in LDL cholesterol level.

Adult↗

PubMed1989

Hypertriglyceridemia and lower LDL cholesterol concentration in relation to apolipoprotein E phenotypes in myotonic dystrophy.

Plasma lipid, lipoprotein levels and apolipoprotein apo E phenotypes were determined in 70 patients with myotonic dystrophy (MyD) and 81 controls. Marked differences were noticed in the apo E phenotype frequencies between the two groups. Plasma triglycerides and VLDL cholesterol were higher in MyD than controls, but only the latter was related to differences in the apo E phenotypes between two groups. Accordingly, the ratio of VLDL cholesterol/plasma triglycerides was increased significantly in MyD, suggesting accumulation of intermediary density particles due to lower affinity of E2 containing lipoproteins for lipoprotein cell receptors. The LDL cholesterol concentration was lower in MyD than controls and was related to differences in the apo E phenotype frequencies between the two groups. These results indicate increased removal of LDL particles in the apo E2 phenotypes, perhaps due to upregulation of LDL (B, E) receptor activity. Plasma cholesterol and HDL cholesterol concentrations were similar in both groups. Another feature of the study was lower levels of plasma cholesterol, triglycerides, VLDL and LDL cholesterol in the homozygous E4:E4 phenotype. These results suggest increased clearance rate of both VLDL and LDL particles and support the concept that apo E4-containing lipoproteins have higher in vivo affinity for ape E and/or B, E receptors.

Adolescent↗

PubMed1989

HMG CoA reductase inhibitors lower LDL cholesterol without reducing Lp(a) levels.

Lp(a) is a plasma lipoprotein particle consisting of a plasminogenlike protein [apo(a)] disulfide bonded to the apo B moiety of low-density lipoprotein (LDL). Increased plasma levels of Lp(a), either independently or interactively with LDL levels, have been shown to be a risk factor for atherosclerosis. Recently, a new class of lipid-lowering drugs, HMG CoA reductase inhibitors, have been introduced. These drugs act by decreasing liver cholesterol synthesis resulting in up-regulation of LDL receptors, increased clearance of LDL from plasma, and diminution of plasma LDL levels. In this study, we examined the effect of HMG CoA reductase inhibitors on Lp(a) levels in three groups of subjects, five volunteers and two groups of five and 14 patients. In all 24 subjects, mean decreases were observed in total cholesterol (43 +/- 5%), total triglyceride (35 +/- 8%), very low-density lipoprotein (45 +/- 9%), and LDL cholesterol (43 +/- 5%). The mean change in high-density lipoprotein cholesterol was an increase of 7 +/- 8%. Despite the very significant decrease in LDL cholesterol levels (p less than 0.001), Lp(a) levels increased by 33 +/- 12% (p less than 0.005). This was not associated with a measurable change in the chemical composition or size of the Lp(a) particle. This emphatically suggests that Lp(a) particles, despite consisting principally of LDL, are cleared from plasma differently than LDL. The surprising finding of an increase in Lp(a) levels suggests this class of drugs may have a direct effect on Lp(a) synthesis or clearance independent of its effect on LDL receptors.

Adult↗

PubMed2026

Current and Future Perspectives of LDL-C Lowering Therapies 2026.

LDL cholesterol (LDL-C) is the central causal factor for atherosclerotic cardiovascular disease (ASCVD), and its reduction is a cornerstone of both primary and secondary prevention. Since the introduction of statins more than three decades ago, LDL-C-lowering therapy has expanded substantially, now encompassing ezetimibe, proprotein convertase subtilisin/kexin type 9 (PCSK9)-targeting agents, bempedoic acid, and other emerging modalities. This expanding therapeutic landscape has improved the feasibility of achieving guideline-recommended LDL-C targets, but it has also increased the complexity of clinical decision making. This review provides a contemporary and practical overview of the LDL-C-lowering strategies, beginning with the initial evaluation of patients with elevated LDL-C, including differentiation between primary and secondary causes and the identification of familial hypercholesterolemia (FH). We summarize the current treatment targets for primary and secondary prevention, highlight the optimal selection and use of statins, and discuss the assessment and management of statin intolerance, including the role of the nocebo effect. Non-statin therapies, including ezetimibe, bile acid sequestrants, PCSK9 inhibitors, inclisiran, and bempedoic acid, are reviewed with an emphasis on their mechanisms, efficacy, and clinical positioning. Advanced therapies for severe dyslipidemia, such as lipoprotein apheresis, lomitapide, and evinacumab, are also discussed in this review. Finally, we outline the future directions, including oral PCSK9 inhibitors, next-generation cholesteryl ester transfer protein (CETP) inhibitors, lipoprotein(a)-lowering agents, and genome-editing approaches. Collectively, these developments offer new opportunities to address unmet clinical needs, particularly in patients with FH, statin intolerance, and residual cardiovascular risk. A comprehensive understanding of these therapies is essential for further reducing the burden of ASCVD in the coming decades.

Humans↗

PubMed1991

Pravastatin in heterozygous familial hypercholesterolemia: low-density lipoprotein (LDL) cholesterol-lowering effect and LDL receptor activity on skin fibroblastS.

The cholesterol-lowering effect of provastatin, a new competitive inhibitor of 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase, was studied in 10 patients with heterozygous familial hypercholesterolemia (FH). Residual low-density lipoprotein receptor (LDL-R) activity was also evaluated in cultured skin fibroblasts prior to treatment, and showed a wide range of reduction from 30% to 70% of the normal value. Treatment with pravastatin 40 mg once daily reduced total and LDL cholesterol (LDL-C) after 6 months by 19.7% and 25.4%, respectively (P less than .001). Serum apolipoprotein (apo) B levels decreased significantly by 29.1% (P less than .001). No significant changes were observed in mean serum total triglycerides or high-density lipoprotein cholesterol (HDL-C) levels. A positive correlation between residual LDL-R activity and maximum percent reduction of LDL-C levels was observed (r = .676, P less than .05). No clinically important side effects were recorded and the treatment was well tolerated. Thus, pravastatin effectively reduces LDL in heterozygous FH, and this effect appears to be related to LDL-R status.

Cholesterol, LDL↗

PubMed1989

Intensive combination drug therapy of familial hypercholesterolemia with lovastatin, probucol, and colestipol hydrochloride.

Patients with familial hypercholesterolemia (FH) have had a life-long sustained elevation of low-density lipoprotein (LDL) cholesterol levels. Consequently, there is a need to maximally lower their elevated levels, and this usually requires lowering LDL levels more than 50%. Because no single hypolipidemic drug will consistently produce such degrees of lowering, combination drug therapy with two or even three agents is required to produce the desired degree of cholesterol lowering. A prospective trial was designed to determine if combination therapy using three hypolipidemic agents could effectively lower LDL levels in 17 severely affected FH subjects. Colestipol hydrochloride (10 g b.i.d.), probucol (500 mg b.i.d.), and lovastatin (20 or 40 mg b.i.d.) were given to each patient, in varying combinations, over a 25-month period. Lovastatin (40 mg/day) uniformly lowered LDL levels 36%. Probucol lowered LDL only 14% and in a variable manner. The combination of lovastatin and probucol lowered LDL no better than lovastatin alone. Lovastatin plus colestipol lowered LDL 52%; probucol added as a third agent produced no further lowering. Lovastatin (80 mg/day) plus colestipol lowered LDL 56%. Lovastatin increased high-density lipoprotein (HDL) cholesterol levels 6%, whereas probucol decreased HDL 29%. In all patients there was an effective lowering of LDL levels, ranging from 40% to 70%. Thus, lovastatin plus colestipol is an effective hypolipidemic regimen for producing marked decreases in LDL levels in FH subjects. The addition of probucol as a third hypolipidemic agent adds little to the therapeutic regimen as measured by lowering of LDL levels.

Cholesterol↗

PubMed2026

Comparative efficacy of LDL-C-lowering therapies in first-time vs. recurrent myocardial infarction prevention: a meta-analysis of large-scale randomized controlled trials.

AIMS: Reducing elevated low-density lipoprotein cholesterol (LDL-C) is central to global efforts to prevent myocardial infarction (MI). While many studies have evaluated LDL-C-lowering therapies in first-time and recurrent MI prevention, direct comparisons of their relative efficacy are lacking. Therefore, we conducted a systematic review and meta-analysis to compare the efficacy of LDL-C-lowering therapies in first-time vs. recurrent MI prevention. METHODS AND RESULTS: We searched three databases until 30 November 2024, for randomized controlled trials (RCTs) with at least 1000 patient-years of follow-up. Efficacy was quantified as relative risk (RR) with 95% confidence intervals (CIs). Differences in benefit magnitude were assessed using Cochran's Q test. Data were pooled with a random-effects model, and heterogeneity was measured using the I2 statistic. Additionally, we applied the Cochrane Risk of Bias Tool to evaluate study quality and utilized the GRADE method to assess the certainty of the evidence. This study included 22 large-scale RCTs involving 180 304 participants. In first-time MI prevention, LDL-C-lowering therapies achieved a remarkable 38% reduction in MI risk [12 RCTs; 79 604 participants; RR, 0.62 (95% CI, 0.55-0.69); P < 0.001]. In recurrent MI prevention, these therapies were associated with a more modest but significant 16% risk reduction [11 RCTs; 100 700 participants; RR, 0.84 (95% CI, 0.80-0.88); P < 0.001]. Importantly, the benefit magnitude between the two groups was significantly different (Q = 22.63; P < 0.001), highlighting the greater relative benefit in first-time MI prevention. Furthermore, the robustness of our findings was consistently supported by leave-one-out analyses, the absence of publication bias, high-quality GRADE evidence, and subgroup and sensitivity analyses. CONCLUSION: Our findings suggest that LDL-C-lowering therapies may offer a greater benefit in preventing first-time MI compared with recurrent MI.

Humans↗

PubMed1990

Why women live longer than men: the biologic mechanism of the sex differential in longevity.

1. Exogenous sex steroids appear to influence lipoproteins in a manner that is a caricature of the effects of endogenous sex steroids: Estrogens raise HDL (selectively HDL2) and lower LDL; Androgens lower HDL (selectively HDL2), while raising LDL. 2. Exogenous sex steroids are likely to affect LDL metabolism via effects on the LDL receptor; Estrogens increase LDL receptor activity (in non-human species at both the hepatic cellular and mRNA levels, though this is yet to be confirmed in humans); ??Androgens decrease LDL receptor activity (yet to be tested in either human or non-human species). 3. Exogenous sex steroids appear to alter HDL levels predominantly via modulation of HDL catabolism; Estrogens retard HDL catabolism (33) (and may also increase apo A-I synthesis and HDL production); Androgens accelerate HDL catabolism (30). 4. Modulation of HDL (and possibly LDL) metabolism by sex steroids may be mediated by alterations in hepatic triglyceride lipase (HTGL) activity.

Adolescent↗

PubMed1992

Plasma cholesterol-lowering potential of edible-oil blends suitable for commercial use.

We tested semihardened blends of edible oils, suitable for commercial food manufacture, with a lower-than-conventional saturated fatty acid content, for their effects on plasma cholesterol. Twenty-six mildly hypercholesterolemic men took part in a double-blind crossover experiment in which two test blends were compared with two control dietary periods [which resembled the Australian fat intake: proportions of polyunsaturated, monounsaturated, and saturated fatty acids (PMS) 0.4:0.9:1]. PMS in the test diets was approximately 0.8:1.3:1 and resulted in significantly lower LDL-cholesterol concentrations (reductions of less than or equal to 7.7%). HDL cholesterol and plasma triglyceride were unchanged. The trans fatty acid (mainly elaidic) content of the blends was 16%, raising its contribution to energy by 4% but without apparent effect on LDL and HDL concentrations. Provided the overall ratio of linoleic acid to palmitic acid in commercial edible-oil blends exceeds that in the prevailing national diet, partial hydrogenation will not negate the LDL-lowering potential.

Adult↗

PubMed1991

Plasma estradiol and lipid profile in perimenopausal women.

This study was conducted to examine the estradiol level and plasma lipid profile in perimenopausal women. The estradiol and HDL levels were higher and LDL levels lower in premenopausal women than in postmenopausal women of the same age group. Higher HDL and lower LDL levels in premenopausal women are likely to protect them against atherosclerosis, and the difference may be casually related to estradiol levels.

Adult↗

PubMed1992

Effects of psyllium hydrophilic mucilloid on LDL-cholesterol and bile acid synthesis in hypercholesterolemic men.

The goal of the current study was to determine the mechanism of the hypocholesterolemic effect of psyllium using a randomized, double-blind, crossover design. Twenty males (age 44 +/- 4 yr, weight 79 +/- 10 kg) with moderate hypercholesterolemia (total 265 +/- 17 mg/dl, low density lipoprotein (LDL) 184 +/- 15 mg/dl) were studied at baseline (B) and after randomization to receive a 40-day course of 15 g/day of either psyllium (Ps) or placebo (Pl) (cellulose). After a washout period (11 +/- 2 days), subjects were crossed over to the other fiber treatment for an additional 40 days and restudied. Intestinal cholesterol absorption, cholesterol synthesis in isolated peripheral blood mononuclear cells, bile acid kinetics, gallbladder motility, and intestinal transit were measured at each study period. Psyllium lowered LDL cholesterol (x:184 (B), 169 (Ps), and 179 (Pl) mg/dl; Ps vs. B,Pl: P less than 0.004, P less than 0.02), decreased relative cholesterol absorption (x:51 (B), 45 (Ps), and 49 (Pl) %; Ps vs. B,Pl: P less than 0.03, P less than 0.03), did not alter absolute cholesterol absorption, and increased the fractional turnover of both chenodeoxycholic acid (x:0.176 (B), 0.203 (Ps), and 0.170 (Pl) day-1; Ps vs. B,Pl: P less than 0.0001, P less than 0.01) and cholic acid (x:0.303 (B), 0.411 (Ps), and 0.301 (Pl) d-1; Ps vs. B, Pl: P less than 0.006, P less than 0.002). Bile acid synthesis increased in subjects whose LDL cholesterol was lowered by more than 10% (Ps vs. B: 1304 +/- 489 vs 992 +/- 307 mumol/day, P less than 0.006; Ps vs. PI: 1304 +/- 489 vs. 914 +/- 321 mumol/day, P less than 0.0002). We conclude that psyllium lowers LDL cholesterol primarily via stimulation of bile acid synthesis.

Adult↗

PubMedDate not supplied

Effect of dietary fat saturation and cholesterol on low density lipoprotein degradation by mononuclear cells of Cebus monkeys.

The mechanism by which dietary unsaturated fatty acids lower low density lipoprotein (LDL) cholesterol is unknown. Unsaturated fatty acids incorporated into the cell membrane can increase membrane fluidity and, as a result, dramatically alter membrane-dependent cell functions. Therefore, we examined the effect of long-term dietary consumption of corn oil and coconut oil with and without cholesterol in amounts equivalent to those of a typical Western diet on the degradation of human LDL by peripheral blood mononuclear cells in Cebus albifrons monkeys. Cellular LDL degradation was dramatically enhanced in the mononuclear cells isolated from animals fed corn oil in comparison with those from animals fed coconut oil. The addition of cholesterol to the diets resulted in a slight attenuation of LDL degradation in the corn oil group while no effect was noted in the coconut oil group. Crossover LDL binding and degradation experiments with LDL isolated from animals fed corn oil diets and coconut oil diets demonstrated increased binding and degradation of LDL in mononuclear cells from animals fed corn oil diets. Enhanced mononuclear cell LDL degradation was accompanied by increased cellular cis-unsaturated fatty acyl content, increased membrane fluidity, and decreased plasma cholesterol. Increased cellular cis-unsaturated fatty acyl content with its concomitant increase in membrane fluidity mirrored the dietary lipid profile of the host animal. A linear relationship was observed between cellular LDL degradation and both cellular cis-unsaturated fatty acyl content and membrane fluidity. These observations parallel results noted in whole-animal LDL catabolic studies with these same animals described elsewhere. These data suggest a novel mechanism by which dietary unsaturated fatty acids exert their LDL-lowering effect.

Animals↗

PubMed1990

Dietary recommendations to prevent coronary heart disease.

The evidence that limiting dietary saturated fat and cholesterol will lower LDL cholesterol and contribute to the reduction in risk of cardiovascular disease is adequate for sound dietary recommendations to patients and to the public at large. Reduction of intake of all saturated fats to less than 10% of calories is a practical and achievable goal for Western man. Further reduction to less than 7% of calories is possible with a motivated and well instructed patient. The mechanism by which saturated fatty acids, particularly palmitate and laurate raise LDL cholesterol need detailed biochemical and physiologic study. Dietary cholesterol is unnecessary and clearly contributes to vascular disease in Western man. This vascular effect appears to be only partially explained by its effect on LDL cholesterol. Reduction to less than 300 mg per day for men of average size is achievable. Women and those eating fewer calories should strive for even less. Monounsaturated fats (oleic acid) can be consumed at levels of 20% of calories without significant concern if total calories are within limits to maintain desirable weight. Omega-6 polyunsaturated fats do not offer a significant health concern and need not be limited below the current intake of 7% of calories in the United States. Populations eating higher levels should be monitored to determine if such intakes are associated with either improved health or long-term ill effects since this level of intake has not been a long-standing tradition in any known culture. Omega-3 fatty acids might be increased to 2 or 3% of calories with potential benefit. Eating fish and marine animals is the most clearly documented safe method for achieving this. Larger intakes and particularly the use of fish oil supplements is unproven therapy for vascular disease prevention and needs much further study as a medical treatment for a variety of disorders. Protein intake is more than adequate in the USA and further increases could have negative effects on the prevalence of renal disease and osteoporosis. Although these issues are of hypothetical interest at the moment, they are worthy of considerable investigation. Complex carbohydrates consumed as components of vegetables, fruits and grains should be considered proven safe and healthful. Increasing calories from these sources at the expense of saturated fats and simple sugars should prove highly beneficial to Western populations. Fiber from these sources may have beneficial effects on blood cholesterol and intestinal function. Soluble fiber is documented to lower LDL cholesterol but the mechanism of this effect is not established and is worthy of considerable study.(ABSTRACT TRUNCATED AT 400 WORDS)

Alcohol Drinking↗

PubMed1988

The fractional catabolic rate of low density lipoprotein in normal individuals is influenced by variation in the apolipoprotein B gene: a preliminary study.

In a random sample of 22 normolipidaemic male Caucasian individuals, 35-49 years old, homozygosity for the X2 allele (cutting site) of the XbaI RFLP of the apo B gene was associated with higher mean total cholesterol and LDL-cholesterol concentration. These individuals also had significantly lower LDL fractional catabolic rate (P less than 0.03) and a lower degradation of LDL by mononuclear cells in vitro. We propose that the XbaI polymorphism is associated with amino acid changes in the apo B protein which influences LDL binding to the LDL-receptor. This modulates catabolism of this lipoprotein and so contributes to variability of plasma cholesterol levels.

Adult↗

PubMed1991

THP-1 cells form foam cells in response to coculture with lipoproteins but not platelets.

The human monocytic leukemia cell line, THP-1, shares many properties with human monocyte-derived macrophages and might be a useful model for studying foam cell formation in vitro. Therefore, we examined the ability of THP-1 cells to accumulate cholesteryl esters, the hallmark feature of foam cells, in response to culture with native low density lipoprotein (LDL), modified LDL, and platelets. THP-1 cells stored more cholesteryl esters than macrophages in response to 200 micrograms/ml of LDL. Down-regulation of LDL receptors occurred in macrophages at lower LDL concentrations than in THP-1 cells. Phorbol ester-treated THP-1 cells stored more cholesteryl esters than human macrophages in response to 25-200 micrograms/ml of acetylated LDL. Because we have previously demonstrated that activated platelets enhanced macrophage cholesteryl ester storage, we examined the ability of THP-1 cells to store cholesteryl esters in response to coculture with platelets. Compared with macrophages, dividing THP-1 cells and phorbol ester-treated THP-1 cells accumulated only 50% and 33% as much cholesteryl esters, respectively. Furthermore, although platelets induced a 90% reduction in cholesterol synthesis in macrophages by day 5, cholesterol synthesis in THP-1 cells and phorbol ester-treated THP-1 cells was inhibited less than 50% by platelets. Nevertheless, both THP-1 cells and macrophages responded to platelets by increasing their secretion of apolipoprotein E. Therefore, we conclude that dividing THP-1 cells and phorbol ester-treated THP-1 cells are capable of forming foam cells in response to physiologic doses of both LDL and acetylated LDL, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoproteins E↗

PubMed1990

Lovastatin therapy reduces low density lipoprotein apoB levels in subjects with combined hyperlipidemia by reducing the production of apoB-containing lipoproteins: implications for the pathophysiology of apoB production.

We investigated the metabolism of very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), and low density lipoprotein (LDL) apolipoprotein B (apoB) in seven patients with combined hyperlipidemia (CHL), using 125I-labeled VLDL and 131I-labeled LDL and compartmental modeling, before and during lovastatin treatment. Lovastatin therapy significantly reduced plasma levels of LDL cholesterol (142 vs 93 mg/dl, P less than 0.0005) and apoB (1328 vs 797 micrograms/ml, P less than 0.001). Before treatment, CHL patients had high production rates (PR) of LDL apoB. Three-fourths of this LDL apoB flux was derived from sources other than circulating VLDL and was, therefore, defined as "cold" LDL apoB flux. Compared to baseline, treatment with lovastatin was associated with a significant reduction in the total rate of entry of apoB-containing lipoproteins into plasma in all seven CHL subjects (40.7 vs. 25.7 mg/kg.day, P less than 0.003). This reduction was associated with a fall in total LDL apoB PR and in "cold" LDL apoB PR in six out of seven CHL subjects. VLDL apoB PR fell in five out of seven CHL subjects. Treatment with lovastatin did not significantly alter VLDL apoB conversion to LDL apoB or LDL apoB fractional catabolic rate (FCR) in CHL patients. In three patients with familial hypercholesterolemia who were studied for comparison, lovastatin treatment increased LDL apoB FCR but did not consistently alter LDL apoB PR. We conclude that lovastatin lowers LDL cholesterol and apoB concentrations in CHL patients by reducing the rate of entry of apoB-containing lipoproteins into plasma, either as VLDL or as directly secreted LDL.

Adult↗

PubMed1989

Lovastatin reduces postprandial lipoprotein levels in hypercholesterolaemic patients with mild hypertriglyceridaemia.

Drugs that inhibit cholesterol synthesis have recently been released for lowering LDL-cholesterol levels. The current study examines the effect of one of these drugs, lovastatin, alone and in combination with cholestyramine on postprandial fat metabolism in five patients with severely elevated LDL-cholesterol and normal triglyceride levels (less than 1.8 mmol l-1) and in five patients with similarly elevated LDL-cholesterol and mildly elevated triglyceride levels (1.8 to 2.7 mmol l-1). In the group of patients with normal triglyceride levels, neither lovastatin alone nor in combination with cholestyramine had any effect on postprandial lipoprotein levels, while profoundly decreasing LDL-cholesterol levels. This provides evidence that LDL and postprandial lipoproteins are cleared by different mechanisms. In the group of five patients with mildly elevated triglyceride levels, in addition to LDL-cholesterol lowering, lovastatin significantly lowered VLDL-cholesterol, fasting triglyceride and postprandial lipoprotein levels. Thus in patients with mild hypertriglyceridaemia, lovastatin may have another favourable effect on the lipoprotein system in addition to LDL-cholesterol lowering.

Adult↗