Cholesterol Journal Articles

Record 8101 to 8120

Knockout of the cholesterol 24-hydroxylase gene in mice reveals a brain-specific mechanism of cholesterol turnover
Lund, E. G., C. Xie, et al. (2003), J Biol Chem 278(25): 22980-8.
Abstract: Most cholesterol turnover takes place in the liver and involves the conversion of cholesterol into soluble and readily excreted bile acids. The synthesis of bile acids is limited to the liver, but several enzymes in the bile acid biosynthetic pathway are expressed in extra-hepatic tissues and there also may contribute to cholesterol turnover. An example of the latter type of enzyme is cholesterol 24-hydroxylase, a cytochrome P450 (CYP46A1) that is expressed at 100-fold higher levels in the brain than in the liver. Cholesterol 24-hydroxylase catalyzes the synthesis of the oxysterol 24(S)-hydroxycholesterol. To assess the relative contribution of the 24-hydroxylation pathway to cholesterol turnover, we performed balance studies in mice lacking the cholesterol 24-hydroxylase gene (Cyp46a1-/- mice). Parameters of hepatic cholesterol and bile acid metabolism in the mutant mice remained unchanged relative to wild type controls. In contrast to the liver, the synthesis of new cholesterol was reduced by approximately 40% in the brain, despite steady-state levels of cholesterol being similar in the knockout mice. These data suggest that the synthesis of new cholesterol and the secretion of 24(S)-hydroxycholesterol are closely coupled and that at least 40% of cholesterol turnover in the brain is dependent on the action of cholesterol 24-hydroxylase. We conclude that cholesterol 24-hydroxylase constitutes a major tissue-specific pathway for cholesterol turnover in the brain.

Knowledge of blood cholesterol reduction in community residents
Stewart, D. L., B. R. DeForge, et al. (1995), J Natl Med Assoc 87(8): 533-6.
Abstract: This study examined the cholesterol knowledge of inner-city community residents, who are representative of individuals in lower socio-economic groups. "Cholesterol Pursuit," a 10-item cholesterol knowledge test distributed by the National Heart, Lung, and Blood Institute, was administered to 316 residents in eight local grocery stores. The average percentage of correct answers was 65.8%. Community residents in a large, urban city were fairly knowledgeable about blood cholesterol reduction, but there were misconceptions concerning the importance of eggs, fish oil, and olive oil, and with foods marked "no cholesterol." White community residents appeared to be slightly better informed about reducing blood cholesterol. Identification of misperceptions concerning cholesterol will guide future education programs for these specific communities.

Knowledge of cholesterol levels and targets in patients with coronary artery disease
Cheng, S., J. H. Lichtman, et al. (2005), Prev Cardiol 8(1): 11-7.
Abstract: Little is known about the extent to which patients are aware of nationally-recommended cholesterol and lipid subfraction targets. The authors interviewed 738 patients hospitalized with coronary artery disease to assess their knowledge of their low-density lipoprotein, high-density lipoprotein, and total cholesterol levels as well as corresponding national targets. Only 8%, 8%, and 43% of patients could recall their low-density lipoprotein, high-density lipoprotein, and total cholesterol values, respectively. Only 5%, 2%, and 50% could correctly name targets for these values. Knowledge of cholesterol targets was particularly poor among women, nonwhites, and patients without any college education. Patients with multiple cardiac risk factors and patients with a previous history of cardiovascular disease were no more knowledgeable about their cholesterol targets than those without these conditions. These findings suggest that current cholesterol education efforts appear inadequate, particularly for women, nonwhites, and patients without any college education.

Knowledge, attitudes, treatment practices, and health behaviors of nurses regarding blood cholesterol
Ienatsch, G. (1999), J Contin Educ Nurs 30(1): 13-9.
Abstract: BACKGROUND: This study, from a sample of west Texas RNs (n = 42), replicated a survey of New York City RNs' (n = 206) knowledge, attitudes, treatment practices, and health behaviors concerning cholesterol and cardiovascular disease. METHOD: A random sample of 42 RNs completed a 48-item questionnaire developed by the National Heart, Lung, and Blood Institute. Responses were analyzed by descriptive statistics. Differences between the present and previous study samples were analyzed by chi square. RESULTS: Nurses expressed enthusiasm for counseling clients regarding cholesterol management; yet, only approximately one eighth of respondents in either study agreed strongly they were prepared to counsel clients. Chi-square analyses showed no significant differences in most responses between the two samples. CONCLUSION: These findings suggest nurses could benefit from continuing education offerings targeted to client cholesterol management.

Konrad Bloch--a pioneer in cholesterol and fatty acid biosynthesis
Vance, D. E. and H. Goldfine (2002), Biochem Biophys Res Commun 292(5): 1117-27.

Konrad Bloch--Nobel Prize for research on cholesterol
Shampo, M. A. and R. A. Kyle (1998), Mayo Clin Proc 73(8): 764.

Labeling of the nicotinic acetylcholine receptor by a photoactivatable steroid probe: effects of cholesterol and cholinergic ligands
Fernandez, A. M., G. Fernandez-Ballester, et al. (1993), Biochim Biophys Acta 1149(1): 135-44.
Abstract: A photoactivatable steroid, p-azidophenacyl 3 alpha-hydroxy-5 beta-cholan-24- ate (APL), has been synthesized and used instead of cholesterol to functionally reconstitute purified acetylcholine receptor (AcChR) into vesicles made of asolectin phospholipids. Upon irradiation, the extent of AcChR photolabeling by APL is directly proportional to the amount of APL incorporated into the reconstituted vesicles and the maximum stoichiometry observed corresponds to approx. 50 mol of APL bound per mol of AcChR. Furthermore, all four subunits of the AcChR become labeled by APL and the observed labeling pattern resembles the 2:1:1:1 stoichiometry characteristic of these subunits within the AcChR complex. The presence of either cholesterol or neutral lipids from asolectin in the reconstituted bilayer decreases both, the incorporation of APl into the vesicles and the covalent labeling of the AcChR upon irradiation, without altering the stoichiometry of labeling in AcChR subunits stated above. This suggests that the potential interaction sites for the photoactivatable probe in the reconstituted AcChR are mostly those normally occupied by the natural neutral lipids. Carbamylcholine, a cholinergic agonist, also reduces the extent of APL photolabeling of the AcChR in a dose-dependent manner but, in contrast to the effects of cholesterol, the presence of carbamylcholine alters the stoichiometry of labeling in the AcChR subunits. This, along with the observation that such a decrease in the extent of APL photolabeling caused by carbamylcholine can be blocked by preincubation with alpha-bungarotoxin, suggest that AcChR desensitization induced by prolonged exposure to cholinergic agonists encompasses a rearrangement of transmembrane portions of the AcChR protein, which can be sensed by the photoactivatable probe. Conversely, presence of (+)-tubocurarine, a competitive cholinergic antagonist, has no effects on altering either the extent of APL photolabeling of the AcChR or the distribution of the labeling among AcChR subunits.

Lability of serum low-density lipoprotein cholesterol levels during screening in subgroup of Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS) cohort
Clearfield, M. B., S. E. Weis, et al. (2002), J Am Osteopath Assoc 102(7): 377-84.
Abstract: In the enrollment phase of the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS), a number of heart disease-free potential subjects did not qualify to participate in the study because their low-density lipoprotein cholesterol (LDL-C) levels fluctuated. This report looks at the incidence of lability of LDL-C levels and premature coronary heart disease (CHD) in the nuclear family based on data collected on a group excluded primarily based on lipid levels during the enrollment phase at the TexCAPS site. Lipid inclusion criteria were total cholesterol (TC), 180 mg/dL to 264 mg/dL; low-density lipoprotein cholesterol (LDL-C), 130 mg/dL to 190 mg/dL; high-density lipoprotein cholesterol (HDL-C), less than or equal to 45 mg/dL for men and less than or equal to 47 mg/dL for women; and triglyceride (TG) concentrations, less than or equal to 400 mg/dL. After participants had been on the American Heart Association (AHA) step 1 diet for 8 to 10 weeks, lipid parameters were again tested in a total of 4257 individuals. Both lipid screening measurements at 8 and 10 weeks were required to be within 15% of each other for inclusion in subsequent study. A total of 2868 individuals met the study criteria and were randomly assigned to groups; 1389 failed to qualify for a variety of reasons. Of these, 1070 (25.1% of those who initially qualified based on lipid levels) were excluded because of unacceptable lipid levels on the evaluations repeated at 8 and 10 weeks. This excluded subpopulation (n = 1070) was stratified into three groups based on changes of LDL-C between 8 and 10 weeks on the AHA step 1 diet. One group had a less than 15% fluctuation in LDL-C (LN group, n = 637, 15.0% of cohort, n = 4257). Of those with LDL-C variability, 177 had a greater than 15% increase in LDL-C (LI group, n = 177, 4.2% of cohort); and 256 had a greater than 15% decrease in LDL-C (LD, n = 256, 6.0% of cohort). At week 8, TC and LDL-C levels were lower and the HDL-C level was higher in the LN group compared with both groups having labile lipid levels (LI and LD groups). Changes by gender showed similar trends; however, HDL-C was 5 mg/dL lower at 8 weeks in both groups of women with labile LDL-C levels (groups LI and LD) when compared with the women in the LN group (P <.01). The frequency of TG concentrations greater than 150 mg/dL was greater in men having labile LDL-C level when compared with the control group. The trend was similar for women. In assessing the incidence of CHD in the nuclear family, parents of probands with labile LDL-C levels (LI and LD groups) had a higher frequency (P =.0044) of premature CHD than parents of probands with stable LDL-C (LN). The following conclusions can be drawn: (1) within the general population, there is a substantial number (10%, 433 of 4257) of individuals with labile LDL-C levels; (2) labile LDL-C levels in the probands were found to be associated with an increased familial frequency of premature CHD in their parents. Definition of the molecular basis for this lability of LDL-C could reveal new opportunities to regulate plasma cholesterol levels and thus have an impact on CHD-associated morbidity and mortality in a substantial portion of the general population.

Laboratory process specifications for assuring quality in the U.S. National Cholesterol Education Program
Westgard, J. O., P. H. Petersen, et al. (1991), Clin Chem 37(5): 656-61.
Abstract: We have assessed the laboratory specifications necessary for ensuring that cholesterol testing processes satisfy the quality required by the U.S. National Cholesterol Education Program (NCEP). A model for setting process specifications has been developed to relate the NCEP guidelines for medical interpretation of a cholesterol test to the pre-analytical and analytical variables that can affect a test result. Using this model, we derived specifications for the imprecision (coefficient of variation, CV, or standard deviation, s) and inaccuracy (bias) that are allowable under stable operation, as well as the quality-control procedures (control rules and number of control measurements) that are necessary to detect unstable operation. The NCEP goals of an allowable CV less than or equal to 3% and an allowable bias no greater than +/- 3% are inadequate for assuring the quality of an individual or single cholesterol test when monitoring performance with many of the statistical quality-control procedures currently used in the U.S. With quality-control procedures having two control measurements per run, a CV of 3% is allowable only when bias is zero; a CV less than or equal to 2% is necessary if bias is +/- 3%. With quality-control procedures having four control measurements per run, a CV of 3% is allowable when bias is +/- 1.5%; a CV less than or equal to 2.5% is required if bias is as large as +/- 3%. For two serial tests, the NCEP 3% goals are adequate for current quality-control procedures having four control measurements per run.

Lack of agreement of homogeneous assays with the reference method for LDL-cholesterol may not indicate unreliable prediction of risk for cardiovascular disease
Warnick, G. R. (2002), Clin Chem 48(10): 1812-4; author reply 1814-5.

Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years
Krumholz, H. M., T. E. Seeman, et al. (1994), Jama 272(17): 1335-40.
Abstract: OBJECTIVES--To determine whether elevated serum cholesterol level is associated with all-cause mortality, mortality from coronary heart disease, or hospitalization for acute myocardial infarction and unstable angina in persons older than 70 years. Also, to evaluate the association between low levels of high-density lipoprotein cholesterol (HDL-C) and elevated ratio of serum cholesterol to HDL-C with these outcomes. DESIGN--Prospective, community-based cohort study with yearly interviews. PARTICIPANTS--A total of 997 subjects who were interviewed in 1988 as part of the New Haven, Conn, cohort of the Established Population for the Epidemiologic Study of the Elderly (EPESE) and consented to have blood drawn. MAIN OUTCOME MEASURES--The risk factor-adjusted odds ratios of the 4-year incidence of all-cause mortality, mortality from coronary heart disease, and hospitalization for myocardial infarction or unstable angina were calculated for the following: subjects with total serum cholesterol levels greater than or equal to 6.20 mmol/L (> or = 240 mg/dL) compared with subjects with cholesterol levels less than 5.20 mmol/L (< 200 mg/dL); subjects in the lowest tertile of HDL-C level compared with those in the highest tertile; and subjects in the highest tertile of the ratio of total serum cholesterol to HDL-C level compared with those in the lowest tertile. RESULTS--Elevated total serum cholesterol level, low HDL-C, and high total serum cholesterol to HDL-C ratio were not associated with a significantly higher rate of all-cause mortality, coronary heart disease mortality, or hospitalization for myocardial infarction or unstable angina after adjustment for cardiovascular risk factors. The risk factor-adjusted odds ratio for all-cause mortality was 0.99 (95% confidence interval CI, 0.56 to 2.69) for the group who had cholesterol levels greater than or equal to 6.20 mmol/L (> or = 240 mg/dL) compared with the group that had levels less than 5.20 mmol/L (< 200 mg/dL); 1.00 (95% CI, 0.59 to 1.70) for the group in the lowest tertile of HDL-C compared with those in the highest tertile; and 1.03 (95% CK, 0.62 to 1.71) for subjects in the highest tertile of the ratio of total serum cholesterol to HDL-C compared with those in the lowest tertile. CONCLUSIONS--Our findings do not support the hypothesis that hypercholesterolemia or low HDL-C are important risk factors for all-cause mortality, coronary heart disease mortality, or hospitalization for myocardial infarction or unstable angina in this cohort of persons older than 70 years.

Lack of association between dietary alcohol and HDL-cholesterol concentrations in obese women
Fricker, J., F. Fumeron, et al. (1990), Atherosclerosis 81(2): 119-25.
Abstract: The relationships of alcohol intake and corpulence to HDL-cholesterol were studied in 653 women taking medical advice about body weight. The body mass index (BMI) was positively correlated with triglyceride and negatively with HDL-cholesterol. The relation between BMI and HDL-cholesterol was discontinuous. Total cholesterol, triglycerides and diastolic blood pressure were increased for alcohol intakes greater than 10 g/d regardless of body weight. Alcohol intake was associated with higher concentrations of HDL-cholesterol (P = 0.006) in non obese (BMI = 25.2 +/- 1.5 kg/m2) subjects, but not in mildly (27.3 less than or equal to BMI less than 32.3) or massively (BMI greater than or equal to 32.3) obese subjects. The fact that HDL concentrations were not associated with alcohol intake in obese patients suggests that (1) alcohol acts on the HDL pool through one of the pathways which are perturbed in obesity, possibly lipolysis, (2) obesity is one of the reasons for the differences in individual responses of HDL-cholesterol to alcohol, (3) myocardial infarction might not be inversely correlated with alcohol intake in the obese as it is in the non-obese population.

Lack of association between increased carotid intima-media thickening and decreased HDL-cholesterol in a family with a novel ABCA1 variant, G2265T
Hong, S. H., W. Riley, et al. (2002), Clin Chem 48(11): 2066-70.
Abstract: Low HDL-cholesterol (HDL-C) concentrations are inversely correlated with cardiovascular disease, and previous studies have demonstrated that variants in the ATP-binding cassette transporter, ABCA1, are responsible for a proportion of HDL-C deficiency states. We identified a novel variant in ABCA1 in a kindred with decreased HDL-C. This variant was not identified in >200 chromosomes of healthy individuals. The proband, a heterozygote for G2265T, developed premature coronary artery disease. In addition to low HDL-C, six biological family members heterozygous for the ABCA1 variant exhibited low HDL-C concentrations compared with unaffected family members (0.83 +/- 0.32 vs 1.33 +/- 0.36 mmol/L; P = 0.009). Despite the decreased HDL-C, carotid artery B-mode ultrasound studies failed to reveal increased intima-media thickening in affected individuals compared with age- and sex-matched controls. Although these data extend previous observations that a single defective ABCA1 allele may lead to decreased HDL-C, associated evidence of early atherosclerosis was not confirmed.

Lack of cholesterol-lowering effect of graded doses of cholestyramine in children with Alagille syndrome: a pilot study
Larrosa-Haro, A., C. Saenz-Rivera, et al. (2003), J Pediatr Gastroenterol Nutr 36(1): 50-3.
Abstract: BACKGROUND: There is controversy about the potential risk of sustained high concentrations of cholesterol and triglyceride in patients with cholestatic chronic liver disease. However, it is currently accepted that cholesterol-lowering therapy may reduce morbidity and mortality rates in hypercholesterolemic patients without preexisting coronary heart disease, as well as in those with coronary heart disease. The objective of this study was to evaluate the effect of cholestyramine on the serum lipid profile of a group of children with Alagille syndrome and hypercholesterolemia. METHODS: Five children with Alagille syndrome and basal serum cholesterol concentrations greater than 230 mg/dL were included. Total serum cholesterol, triglyceride, low-density, and high-density lipoprotein cholesterol concentrations were measured on days 0, 10, 20, and 30 after the administration of oral cholestyramine 100, 250, and 500 mg(kg.d), respectively. Lipid fractions were reported as mean +/- 1 SD. Statistical analysis was performed with Friedman analysis of variance. RESULTS: The basal values and those of the three 10-day subsequent 100-, 250-, and 500-mg(kg.d) cholestyramine periods were as follows: total cholesterol: 327.6 +/- 77.1, 305.4 +/- 52.1, 290.6 +/- 24.1, and 320.6 +/- 32.3, respectively (P = 0.668); triglyceride: 136.4 +/- 14.6, 144.8 +/- 41.3, 161 +/- 30.9, and 165.4 +/- 40.7, respectively (P = 0.356); low-density lipoprotein cholesterol: 245.4 +/- 57.8, 239.8 +/- 48.6, 242.2 +/- 68.6, and 246.4 +/- 49.5, respectively (P = 0.782); and high-density lipoprotein cholesterol: 44.4 +/- 11.2, 41.8 +/- 12.8, 44.6.2 +/- 13.2, and 47 +/- 8.5, respectively (P = 0.431). CONCLUSION: Under the conditions of the current study, no significant effect of variable doses of cholestyramine could be demonstrated on the serum lipid profile of a series of children with Alagille syndrome. While the controversy on the potential atherogenic risk of low-density lipoprotein hypercholesterolemia in patients with chronic liver disease persists, new, prospective pharmacologic or nutritional trials are required.

Lack of concordance in classification of coronary heart disease risk: high-risk HDL cholesterol less than 35 mg/dl in subjects with desirable total serum cholesterol, less than 200 mg/dl
Glueck, C. J., V. R. Sanghvi, et al. (1990), J Lab Clin Med 116(3): 377-85.
Abstract: In using National Cholesterol Education Program guidelines (for desirable low risk, a total cholesterol level less than 200 mg/dl, and for high risk, a level of high-density lipoprotein cholesterol (HDLC) less than 35 mg/dl), our specific aim was to examine lack of concordance in classification of coronary heart disease (CHD) risk by HDLC less than 35 mg/dl in subjects with total cholesterol less than 200 and to determine whether lack of concordance increased as group CHD risk increased. We studied four cohorts ranging from putatively low to high CHD risk. These included self-referred subjects in a public urban total cholesterol screening (n = 897), hospitalized patients with depression (n = 144), Cholesterol Center referrals at presumed high CHD risk (n = 1120), and patients having coronary arteriography (n = 145) because of presumed coronary artery disease. Total cholesterol was less than 200 mg/dl in 25% of subjects from the urban sampling, in 54% of hospitalized patients with depression, in 27% of Cholesterol Center referrals, and in 41% of those undergoing cardiac catheterization. In these four cohorts, of subjects with total cholesterol less than 200, 7%, 26%, 25%, and 48%, respectively, had HDLC less than 35 mg/dl. The likelihood of having total cholesterol less than 200 and HDLC less than 35 mg/dl was 1.7% in urban public subjects, 6.8% in Cholesterol Center referrals, 13.9% in depressed patients, and 20% in cardiac catheterization patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Lack of correlation between ACAT mRNA expression and cholesterol esterification in primary liver cells
Rea, T. J., R. B. DeMattos, et al. (1996), Biochim Biophys Acta 1299(1): 67-74.
Abstract: A partial rabbit cDNA clone (14b) for ACAT has been characterized and used to demonstrate that hepatic and aortic ACAT mRNA14b abundance increased 2-3-fold in rabbits receiving a high fat/high cholesterol-diet compared to chow fed animals (Pape et al. (1995) J. Lipid Res. 36, 823-838). Because of those data we hypothesized that increased hepatic cholesteryl ester mass and synthesis rates in rabbit liver cells are associated with an increase in ACAT mRNA14b levels. To test this hypothesis we altered cellular cholesteryl ester mass and synthesis rates in primary parenchymal and nonparenchymal cells using various extracellular agents and measured the accumulated mass of ACAT mRNA14b. Parenchymal cells incubated with rabbit beta VLDL or mevalonolactone displayed a 6-10-fold increase in cellular cholesteryl ester mass over a three day treatment with no significant changes in cellular free cholesterol, triacylglycerols, or ACAT mRNA14b levels; HMG CoA reductase and LDL receptor mRNA mass decreased initially as a result of cholesteryl ester loading. Treatment of parenchymal cells with CI-976, an ACAT inhibitor, showed a marked reduction in cholesteryl ester synthetic rate compared to beta VLDL controls but displayed no change in ACAT mRNA14b levels. A mixed population of rabbit hepatic nonparenchymal cells was incubated with beta VLDL for 24 h in culture which resulted in a 6-fold increase in cellular cholesteryl ester mass; there was no change in ACAT mRNA14b levels. In an in vivo study, rabbits consuming a high fat/high cholesterol-diet for three weeks showed a 10-fold increase in hepatic cholesteryl ester with no significant changes in ACAT mRNA14b levels. Together these data indicate that rabbit liver cellular cholesteryl ester mass increases of up to 10-fold are not correlated with ACAT mRNA14b changes. Thus, hepatic ACAT mRNA14b expression and cellular cholesterol esterification do not appear to be coordinately regulated at this level of cholesteryl ester loading.

Lack of effect of cholesterol esterase inhibitor CVT-1 on cholesterol absorption and LDL cholesterol in humans
Bosner, M. S., A. A. Wolff, et al. (1999), Cardiovasc Drugs Ther 13(5): 449-54.
Abstract: Two clinical trials were performed to test the hypothesis that CVT-1, a potent inhibitor of pancreatic cholesterol esterase, reduces percent cholesterol absorption and LDL cholesterol in humans. Measurements of cholesterol absorption were made with deuterated cholesterol tracers given orally and intravenously and detected in plasma by a new technique using negative ion mass spectrometry. Study 1 was a randomized, double-blind parallel study of CVT-1 treatment at doses of 0, 300, 1500, and 3000 mg/day in 19 subjects. Percent cholesterol absorption measured at baseline and again after 2 and 6 weeks showed no treatment effect and LDL cholesterol was unchanged. Study II was a randomized open-label crossover comparison between CVT-1 given as 1000 mg three times daily for 2 weeks and 187.5 mg hourly 16 hours/day for 2 weeks. Percent cholesterol absorption and plasma LDL cholesterol were not different between periods. We conclude that cholesterol esterase is not required for unesterified cholesterol absorption in human subjects.

Lack of effect of chronic administration of oral beta-carotene on serum cholesterol and triglyceride concentrations
Nierenberg, D. W., G. T. Bayrd, et al. (1991), Am J Clin Nutr 53(3): 652-4.
Abstract: Previous studies suggest that chronic oral administration of retinol and other retinoids causes elevation of plasma triglyceride concentrations. The effects of chronic oral administration of beta-carotene, a carotenoid partially metabolized to retinol, on plasma lipid concentrations have not been well studied; therefore, we studied 61 subjects over 12 mo while they were enrolled in a skin-cancer-prevention study in which patients were randomly assigned to receive either placebo (n = 30) or 50 mg beta-carotene/d orally (n = 31). At study entry and 1 y later, fasting blood samples were obtained for measurement of triglycerides, total cholesterol, HDL cholesterol, retinol, and beta-carotene. Retinol concentrations changed minimally in both groups; beta-carotene concentration increased an average of 12.1 +/- 47 nmol/L in the placebo group and 4279 +/- 657 nmol/L in the active-treatment group. Both groups experienced similar small increases in triglyceride and total cholesterol concentrations and small decreases in HDL cholesterol. Daily oral administration of 50 mg beta-carotene/d did not affect plasma lipid concentrations.

Lack of effect of hydrocholorthiazide on total cholesterol
Jones, D. W. and C. D. Sands (1994), Clin Exp Hypertens 16(5): 675-89.
Abstract: To determine the effect of hydrochlorothiazide on total cholesterol, baseline total cholesterol and blood pressure were determined in 618 hypertensive subjects in a hypertension clinic in Pusan, Korea. After 12-24 months (mean follow-up time 14 months), total cholesterol and blood pressure measurements were repeated. In the group whose therapy included hydrochlorothiazide (n = 436), total cholesterol fell by 8 +/- 39 mg/dL. Those not treated with a diuretic (n = 182) had an identical fall in total cholesterol of 8 +/- 42 mg/dL (P < 0.001 for change from baseline). Patients with a baseline total cholesterol > 200 mg/dL were asked to reduce intake of saturated fat. Change in total cholesterol for 180 patients on this diet and hydrochlorothiazide was -24 +/- 31 mg/dL (P < 0.0001); for 71 patients on the diet and non-diuretic therapy, change was -22 +/- 35 mg/dL (P < 0.0001). There was no change in total cholesterol in either drug group for those with a baseline value < or = 200 mg/dL. It is concluded that in this group of Korean patients on a relatively low-fat diet, a low dose of hydrochlorothiazide had no adverse effect on total cholesterol at 14 months, and hydrochlorothiazide nor other agents prevented a beneficial effect of further reduction of saturated fat on total cholesterol.

Lack of effect of linoleic acid on the high-density-lipoprotein-cholesterol fraction of plasma lipoproteins
Iacono, J. M. and R. M. Dougherty (1991), Am J Clin Nutr 53(3): 660-4.
Abstract: Low-fat, natural diets were fed to 11 middle-aged, healthy male subjects for two 40-d periods to determine effects on plasma lipoproteins. The diets were designed to maintain saturated and monounsaturated fatty acids at 10 en% and linoleic acid (LA) at 3.8 and 10.8 en%. When compared with baseline concentrations, total cholesterol decreased 10% at the end of the lower LA diet and 15% at the end of the higher LA diet. Low-density-lipoprotein cholesterol (LDL-C) decreased 18% and 22%, respectively, during the same periods. Plasma high-density-lipoprotein cholesterol (HDL-C) at the end of each dietary period was not significantly different but the midpoint values were lower by 12.5% on the lower LA diet and 7.3% on the higher LA diet. Apolipoprotein B decreased 27% at the end of the lower LA diet and 37% at the end of the higher LA diet whereas apolipoprotein A-I increased 18% and 24%, respectively. HDL-C was not reduced by dietary LA over a 6-wk period.

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