Cholesterol Journal Articles

Record 521 to 540

Adenoviral overexpression of apolipoprotein A-V reduces serum levels of triglycerides and cholesterol in mice
van der Vliet, H. N., F. G. Schaap, et al. (2002), Biochem Biophys Res Commun 295(5): 1156-9.
Abstract: Mice lacking ApoA-V, a novel HDL-associated apolipoprotein identified by our group and independently by Pennacchio et al. Science 294 (2001) 169, were recently shown to be hypertriglyceridemic. To study the role of ApoA-V in triglyceride homeostasis, we compared lipid profiles in mice expressing normal and highly elevated levels of ApoA-V. For this purpose, adenoviral vectors expressing sense or antisense ApoA-V cDNA were constructed. Treatment of mice with sense adenoviral constructs resulted in circa 20-fold higher serum ApoA-V levels compared with mice injected with either PBS or antisense adenoviral constructs. ApoA-V overexpressing mice had markedly decreased (-70%) serum triglyceride levels caused primarily by lowered triglyceride content of the VLDL fraction. Furthermore, in these mice cholesterol levels were found to be lowered in all lipoprotein fractions with the largest mass decrease in the HDL fraction. This resulted in a 40% drop of serum cholesterol content. These findings suggest a role of ApoA-V in regulating levels of circulating triglycerides and cholesterol.

Adenovirus-mediated transfer of a gene encoding cholesterol 7 alpha-hydroxylase into hamsters increases hepatic enzyme activity and reduces plasma total and low density lipoprotein cholesterol
Spady, D. K., J. A. Cuthbert, et al. (1995), J Clin Invest 96(2): 700-9.
Abstract: Clinical interventions that accelerate conversion of cholesterol to bile acids reduce circulating low density lipoprotein (LDL) cholesterol concentrations. The initial and rate-limiting step in the bile acid biosynthetic pathway is catalyzed by hepatic cholesterol 7 alpha-hydroxylase. To examine the effects of transient primary overexpression of this enzyme on sterol metabolism and lipoprotein transport, we constructed a recombinant adenovirus in which a cDNA encoding rat 7 alpha-hydroxylase is expressed from the human cytomegalovirus immediate-early promoter (AdCMV7 alpha). Syrian hamsters administered AdCMV7 alpha intravenously accumulated transgene-specific mRNA in the liver and demonstrated a dose-dependent increase in hepatic microsomal 7 alpha-hydroxylase activity. The increased conversion of cholesterol to bile acids resulted in a compensatory increase in hepatic cholesterol synthesis. In addition, overexpression of 7 alpha-hydroxylase reduced the rate of LDL cholesterol entry into the plasma space and, in animals maintained on a Western-type diet, restored hepatic LDL receptor expression. As a consequence, plasma LDL concentrations fell by approximately 60% in animals maintained on control diet and by approximately 75% in animals consuming a Western-type diet. Plasma high density lipoprotein cholesterol levels were reduced to a lesser degree. These results demonstrate that transient upregulation of bile acid synthesis by direct transfer of a 7 alpha-hydroxylase gene favorably alters circulating lipoprotein profiles and suggest one potential molecular target for genetic strategies aimed at reducing cardiovascular risk.

Adenovirus-mediated transfer of a gene encoding human apolipoprotein A-I into normal mice increases circulating high-density lipoprotein cholesterol
Kopfler, W. P., M. Willard, et al. (1994), Circulation 90(3): 1319-27.
Abstract: BACKGROUND: In animal models of atherosclerosis, augmentation of circulating high-density lipoprotein (HDL) cholesterol exerts a protective effect against development of fatty streaks and promotes plaque regression. METHODS AND RESULTS: To investigate the potential of gene transfer to increase HDL cholesterol, a fusion gene encoding human apolipoprotein A-I (apo A-I) under the control of the human cytomegalovirus (CMV) immediate-early promoter was packaged into a recombinant adenovirus (AdCMV apo A-I). BALB/c mice infected with AdCMV apo A-I by intravenous injection accumulate immunoreactive apo A-I in serum; levels 5 days after infection averaged 168 mg/dL. A 35% increase in HDL cholesterol and a 47% increase in total cholesterol were observed in mice infected with AdCMV apo A-I compared with control viruses. Analysis of size-fractionated lipoproteins revealed that human apo A-I is incorporated into murine HDL particles. Expression of human apo A-I declined to < 10% of maximum after 12 days and mRNA encoding apo A-I, prevalent 5 days after infection, was undetectable in the livers of infected mice after 12 days. CONCLUSIONS: We conclude that adenovirus-mediated transfer of a gene encoding apo A-I produces transient elevations of circulating HDL cholesterol of a magnitude correlated with important physiological effects. These observations suggest the potential for gene-based therapeutic strategies to reduce cardiovascular risk.

Adenovirus-mediated transfer of low density lipoprotein receptor gene acutely accelerates cholesterol clearance in normal mice
Herz, J. and R. D. Gerard (1993), Proc Natl Acad Sci U S A 90(7): 2812-6.
Abstract: We have explored the use of adenovirus-mediated gene transfer to transiently elicit production of low density lipoprotein (LDL) receptors in mice. A recombinant adenovirus carrying the human LDL receptor cDNA restored LDL receptor function in receptor-deficient cultured cells. Intravenous injection of recombinant virus acutely lowered plasma cholesterol levels and increased the rate of 125I-labeled LDL clearance from the circulation in normal mice. At 4 days after virus injection, the t1/2 of plasma LDL was reduced up to 10-fold. An estimated 90% of the parenchymal cells in liver expressed the adenovirus-transferred genes as judged by immunofluorescence of LDL receptors or by beta-galactosidase staining. These results demonstrate that adenovirus-mediated transfer of the LDL receptor gene provides an efficient way of augmenting LDL receptor gene function in the liver over the short term.

Adequacy of NCEP recommendations for total cholesterol, triglycerides, HDLC, and LDLC measurements
Caudill, S. P., S. J. Smith, et al. (1998), Clin Chem 44(5): 1063-6.

Adherence to National Cholesterol Education Program Treatment goals in postmenopausal women with heart disease. The Heart and Estrogen/Progestin Replacement Study (HERS). The HERS Research Group
Schrott, H. G., V. Bittner, et al. (1997), Jama 277(16): 1281-6.
Abstract: OBJECTIVES: To determine the proportion of volunteer women with established heart disease who have low-density lipoprotein cholesterol (LDL-C) levels at or below the National Cholesterol Education Program Adult Treatment Panel goals and to determine what factors are associated with levels above goal or not receiving lipid-lowering medication when indicated. DESIGN: Cross-sectional measurement of lipids and lipoproteins, blood pressure, height, weight, and other demographic and cardiovascular risk factors in 2763 postmenopausal women with heart disease. SETTING: At 18 centers throughout the United States, participants were recruited by means of lists of women with coronary heart disease from coronary units and catheterization laboratories, direct mail to age-eligible women, and advertisements. PATIENTS: Mean age of the cohort was 66.7 years (range, 44-79 years) and the distribution by race/ethnicity was 88.7% white, 7.9% African American, 2.0% Hispanic/Latina, 0.8% Asian/Pacific Islander, and 0.7% other. INTERVENTION: We report cross-sectional analysis of the cohort at baseline. OUTCOME MEASURES: We measured the frequency of achieving 1988 and 1993 Adult Treatment Panel treatment goals, and of being on a regimen of lipid-lowering medication. RESULTS: Although 47% of participants were taking a lipid-lowering medication, 63% did not meet the 1988 treatment goal of LDL-C level less than 3.4 mmol/L (130 mg/dL) and 91% did not meet the 1993 goal of LDL-C level less than 2.6 mmol/L (100 mg/dL). Factors independently associated with achieving the earlier goal were use of lipid-lowering medication, marital status, education, body mass index, exercise, hypertension, diabetes, gallbladder disease, and first diagnosis of coronary heart disease after 1990. Failure to use lipid-lowering medication was associated with age, being African American, marital status, body mass index, lack of exercise, alcohol consumption, current smoking, and first diagnosis of coronary heart disease before 1985. CONCLUSION: The majority of women enrolled in the trial had LDL-C levels that significantly exceeded the treatment goals set by the 1988 and 1993 Adult Treatment Panel guidelines. Better implementation of these guidelines among women with coronary disease would be highly desirable.

Adherence to statin therapy and LDL cholesterol goal attainment by patients with diabetes and dyslipidemia
Parris, E. S., D. B. Lawrence, et al. (2005), Diabetes Care 28(3): 595-9.
Abstract: OBJECTIVE: The purpose of this study was to assess the relationship between adherence to statin therapy and LDL cholesterol goal achievement in patients with diabetes and dyslipidemia. RESEARCH DESIGN AND METHODS: The records of patients being medically treated for dyslipidemia in a managed care diabetes program from January 2001 to December 2002 were used to assess LDL cholesterol goal attainment (<100 mg/dl) and to compute a 9-month medication possession ratio (percentage of days when medication was available MPR, beginning with the first prescription in the database). RESULTS: A total of 653 patient records was analyzed. The average MPR was significantly higher for men than for women (0.75 vs. 0.66, P < 0.05). Overall, 44% (n = 290) of the patients achieved an LDL cholesterol level <100 mg/dl (52% of men and 37% of women, P < 0.05). A significant correlation emerged between MPR and plasma LDL cholesterol (P < 0.001), and MPR was significantly higher in patients who achieved the LDL cholesterol target than in those who did not (0.82 vs. 0.61, P < 0.05). CONCLUSIONS: Although statins are highly effective for decreasing LDL cholesterol levels in patients with dyslipidemia, including those with diabetes, failure to reach LDL cholesterol targets remains common. Adherence to statin therapy, as reflected by MPR, is closely related to LDL cholesterol goal attainment in patients with diabetes and dyslipidemia. The probability of goal achievement appears to increase substantially when the MPR is >0.80. Pharmacy records can be used to identify patients who are poorly compliant with statin therapy and at high risk for failure to attain LDL cholesterol goals. Because outcomes are directly related to patients' medication-taking behavior, when clinical goals (such as serum cholesterol levels) are not being reached, adherence should be the first item assessed by the clinician.

Adherence to trizivir and tenofovir as a simplified salvage regimen is associated with suppression of viraemia and a decreased cholesterol
Latham, V., J. Stebbing, et al. (2005), J Antimicrob Chemother 56(1): 186-9.
Abstract: BACKGROUND: Treatment failure during highly active antiretroviral therapy (HAART) is ultimately common and associated with the development of resistance mutations. Trizivir (zidovudine/lamivudine/abacavir) and tenofovir disoproxil fumarate may improve adherence and enhance virological suppression in individuals who have failed previous regimens. METHODS: Individuals were identified who had failed previous HAART and who were then prescribed trizivir and tenofovir. Viral load and genotypic information were obtained to assess virological response. RESULTS: One hundred and twenty-two individuals were identified from a database containing 5883 patients. In a last observation carried forward intention to treat analysis, 34% of individuals achieved an undetectable viral load of <50 copies/mL at 1 year. Of those who were able to remain on treatment for 1 year, 65% achieved undetectability. We observed no effect regarding previous regimens on viral outcome. Accumulation of TAMs (thymidine analogue mutations) was associated with a decrease in the number of patients achieving an undetectable viral load (with <2 TAMs present 38% of patients developed undetectable viral loads, > or =1;2 TAMs 17% undetectable; P = 0.03). Using the mean cell volume as a measure of compliance, those with higher values were more likely to achieve a viral load <50 copies/mL (P = 0.04). A beneficial effect on cholesterol was noted regardless of virological outcome. CONCLUSIONS: In compliant heavily pre-treated individuals with less than 2 TAMs, salvage therapy with trizivir and tenofovir is associated with suppression of viraemia and an improved lipid profile.

Adipocyte cholesterol balance in obesity
Le Lay, S., P. Ferre, et al. (2004), Biochem Soc Trans 32(Pt 1): 103-6.
Abstract: Adipose tissue is specialized in the storage of energy in the form of triacylglycerol. Within the fat cell, triacylglycerols are found in a well-defined structural compartment called the lipid droplet, which occupies the vast majority of the fat cell volume. However, many other lipids are present in the lipid droplet. These include sterols, carotenoids, cholecalciferol and lipophilic toxic pollutants of the environment such as dioxins and tocopherols. The topic of this article is the role of fat cell cholesterol in adipose tissue physiology and its potential implication in pathological states such as obesity.

Adiponectin represents an independent cardiovascular risk factor predicting serum HDL-cholesterol levels in type 2 diabetes
Zietz, B., H. Herfarth, et al. (2003), FEBS Lett 545(2-3): 103-4.
Abstract: Low levels of high-density lipoprotein (HDL)-cholesterol represent an independent cardiovascular risk factor and, besides reduced physical activity, mechanisms leading to decreased HDL-cholesterol levels are not known. We aimed to test the hypothesis, that adiponectin provides a missing link between type 2 diabetes and low levels of HDL-cholesterol, independent from common metabolic risk factors. 523 patients with type 2 diabetes were investigated for adiponectin serum levels and parameters of lipid metabolism. Even after correction for age, gender, BMI and fasting insulin concentration, serum levels of adiponectin were highly significant (P<0.0001) and positively (regression analysis: r=0.86) associated with HDL-cholesterol levels in type 2 diabetes. CONCLUSION: adiponectin seems to predict HDL-cholesterol levels in patients with diabetes mellitus type 2. Low levels of adiponectin are associated with low levels of HDL-cholesterol independently from common metabolic risk factors and therefore represent an independent cardiovascular risk factor in type 2 diabetes. Thus, adiponectin is a potentially new drug target in the treatment of dyslipidaemia.

Adipose tissue cholesteryl ester transfer protein mRNA in response to probucol treatment: cholesterol and species dependence
Quinet, E. M., P. Huerta, et al. (1993), J Lipid Res 34(5): 845-52.
Abstract: Probucol treatment results in an increase in plasma concentrations of cholesteryl ester transfer protein (CETP) which may account, in part, for the effects of this agent on plasma concentrations of HDL cholesterol. We have examined the mechanism by which probucol increases plasma CETP and have determined the associated changes in the plasma distribution of high density lipoprotein (HDL) particles. Studies were carried out in nine hypercholesterolemic subjects and five normal volunteers. Probucol treatment resulted in a 31% increase in plasma concentrations of CETP and a 23% decrease in HDL cholesterol (P < 0.01). The plasma concentration of LpA-I decreased by 40% (P < 0.01) whereas no change occurred in the LpA-I/A-II subclass of HDL. Plasma CETP increased significantly by 1 week of therapy and remained stable over 10 to 14 weeks of therapy. In spite of the significant increase in plasma concentrations of CETP, the abundance of CETP mRNA in peripheral adipose tissue decreased markedly (P < 0.001). These results suggested that probucol may alter CETP synthesis in another tissue such as liver or, alternatively, may have other effects on CETP secretion into or catabolism out of the plasma pool. Further studies were carried out in hamsters because, in this species, adipose tissue is a major site and liver is a negligible site for CETP synthesis. Hamsters were fed probucol with or without dietary cholesterol because this species was previously shown to respond to dietary cholesterol with an increase in adipose tissue mRNA levels and in plasma CETP concentrations, thus providing the opportunity to determine whether probucol would alter these parameters independently of the dietary cholesterol effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration of phosphatidylcholine-cholesterol liposomes partially reconstitutes fat absorption in chronically bile-diverted rats
Nishioka, T., R. Having, et al. (2004), Biochim Biophys Acta 1636(2-3): 90-8.
Abstract: BACKGROUND AND AIMS: Intestinal bile deficiency in cholestatic patients leads to fat malabsorption. We addressed the potency of model bile, bile salts and phosphatidylcholine (PC)-cholesterol (CH) liposomes to reconstitute fat absorption in permanently bile-diverted (BD) rats. METHODS: The plasma appearance of 13C-labeled palmitic acid (13C-16:0) and linoleic acid (13C-18:2) was determined after their enteral administration to BD or to control rats with an intact enterohepatic circulation (EHC) (13C-16:0 and 13C-18:2 dissolved in 25% olive oil-75% medium chain triacylglycerol oil mixture). BD rats were intraduodenally infused with buffer, model bile consisting of 60 mM taurocholate (TC), 8 mM PC and 1 mM CH, buffer with TC, buffer with PC and CH liposomes, or buffer with lyso-PC and CH. RESULTS: Plasma concentrations of 13C-16:0 and 13C-18:2 were consistently three- to eightfold higher in control rats than those in buffer-infused BD rats (P < 0.01). ID administration of either model bile or TC to BD rats restored plasma appearance of 13C-fatty acids at least to concentrations observed in control rats. Administration of PC + CH liposomes to BD rats partially reconstituted the plasma appearance of 13C-16:0, but did not affect that of 13C-18:2. Compared with control rats, the area under the curve (AUC) of plasma 13C-16:0 concentrations was 13.0 +/- 6.9% in buffer-infused rats and 40.9 +/- 3.1% in liposome-infused rats (P < 0.005). CONCLUSIONS: Enteral administration of PC + CH liposomes to BD rats partially corrects the absorption of palmitic acid. Present data suggest that administration of PC + CH liposomes could enhance fat absorption in clinical conditions of cholestasis in which bile salt supplemention is contraindicated.

Adolescent erythrocytes: influence of high density lipoproteins-cholesterol (HDL-c) plasmatic levels on Na+/Li+ exchange kinetics
Serrani, R., D. Taborda, et al. (2003), Acta Physiol Pharmacol Bulg 27(2-3): 39-42.
Abstract: An inverse relationship between HDL-c plasmatic levels and Li+ flux (Na+-Li+ exchange mediated) has been reported in normotensive individuals with hypertensive ancestors as well as in essential hypertensive subjects. This lipoprotein reaction with plasmatic membrane components induces modifications in membrane transport mechanisms as well as in cellular enzymes. In this paper we present data on Li+ flux (Na+-Li+ exchange mediated) in red blood cells from normotensive individuals without hypertensive ancestors. Kinetic analysis of Li+ efflux as a function of Na+(extracell) concentration was carried out. Vmax and Km values were determined. HDL-c plasmatic levels were also determined. Vmax showed a significant inverse correlation with HDL-c levels. No significant correlation of Km values with HDL-c levels was observed. The data presented support previous data showing that variable Vmax is sensitive to cellular environmental factors. Otherwise the Km variable not influenced by these factors is sensitive to hereditary influences.

ADP-ribosylation factor (ARF)-like 7 (ARL7) is induced by cholesterol loading and participates in apolipoprotein AI-dependent cholesterol export
Engel, T., A. Lueken, et al. (2004), FEBS Lett 566(1-3): 241-6.
Abstract: Here, we identify ADP-ribosylation factor (ARF)-like 7 (ARL7) as the only ARF- and ARL-family member whose mRNA-expression is induced by liver X-receptor/retinoid X-receptor agonists or cholesterol loading in human macrophages. Moreover, subcellular distribution of mutant and wild type ARL7-enhanced green fluorescent protein (EGFP) supports that ARL7 may be involved in a vesicular transport step between a perinuclear compartment and the plasma membrane. Therefore, we investigated the effect of ARL7 over-expression on the cholesterol secretory pathway. We found that expression of wild type and dominant active ARL7-EGFP stimulated the rate of apolipoprotein AI-specific cholesterol efflux 1.7- and 2.8-fold. In contrast, expression of the dominant negative form of ARL7-EGFP led to approximately 50% inhibition of cholesterol efflux. This data is consistent with a model in which ARL7 is involved in transport between a perinuclear compartment and the plasma membrane apparently linked to the ABCA1-mediated cholesterol secretion pathway.

Adrenocorticotrophic hormone lowers serum Lp(a) and LDL cholesterol concentrations in hemodialysis patients
Arnadottir, M., A. L. Berg, et al. (1997), Kidney Int 52(6): 1651-5.
Abstract: Previously, we have shown that short-term administration of adrenocorticotrophic hormone (ACTH) results in reduced concentrations of apolipoprotein B-containing lipoproteins, including lipoprotein(a), and reduced activities of hepatic lipase. These effects were observed in steroid-treated patients suffering from iatrogenic ACTH deficiency and in healthy individuals. The direct nature of the influence of ACTH on hepatic lipoprotein metabolism was confirmed by in vitro experiments. The aim of the present investigation was to study the effects of ACTH treatment on uremic patients, who exhibit disturbed lipoprotein pattern due to the slow removal of triglyceride-rich lipoproteins and who probably are ACTH resistant. Eight patients on chronic hemodialysis were studied. After one intramuscular injection of Synacthen Depot (a synthetic ACTH1-24 preparation from Ciba Geigy AG, Basel, Switzerland) 1 mg, the only change noted was a significant reduction of 26% in median lipoprotein(a) concentration. After five injections, a further decrease (65%) was found in the lipoprotein(a) concentration. Also, reductions in median concentrations of total cholesterol, low density lipoprotein cholesterol and apolipoprotein B were observed. The magnitude of these changes was 15 to 30%. In contrast to previously studied groups, no changes were observed regarding triglyceride metabolism. Significantly increased median concentration of apolipoprotein CIII was found. However, the excess apolipoprotein CIII was confined to the fraction that was not associated with apolipoprotein B. Thus, administration of ACTH to uremic patients improved their atherogenic lipoprotein profile, a fact that may have future therapeutic implications. In comparison to previously studied groups, the uremic patients responded rather slowly and not at all regarding triglyceride metabolism.

Adsorption of bile acids and cholesterol from model solutions and biological liquids modified with charcoal enterosorbents
Gerasimenko, N. V., S. S. Stavitskaia, et al. (1995), Biokhimiia 60(4): 533-40.
Abstract: Adsorption of some bile acids and cholesterol from simulated solutions and body fluids by medical carbons of different origin has been studied in order to elucidate the role of adsorption in cholesterol reduction as well as in prophylaxis and treatment of atherosclerosis by orally applied carbon adsorbents. Oxidized carbons modified by different metal cations were tested for the first time for their ability to correct the saline composition of body fluids.

Adsorption of mixtures of bile salt taurine conjugates to lecithin-cholesterol membranes: implications for bile salt toxicity and cytoprotection
Heuman, D. M., R. S. Bajaj, et al. (1996), J Lipid Res 37(3): 562-73.
Abstract: Tauroursodeoxycholate (TUDC), a relatively hydrophilic bile salt, reduces disruption of cholesterol-rich membranes by more hydrophobic bile salts such as taurocholate (TC), taurochenodeoxycholate (TCDC), or taurodeoxycholate (TDC). We examined the interactions of these bile salts in adsorption to large unilamellar vesicles to determine whether TUDC may stabilize membranes by preventing adsorption of more toxic bile salts. Fractional adsorption was quantified by rapid ultrafiltration. Adsorption coefficient Ai was defined for each bile salt i as (bound i/free i)/lecithin. Affinity of different bile salts for lecithin vesicles varied with their relative hydrophobicity, increasing in the order TUDC < TC << TCDC < or = TDC. Ai of each bile salt fell with its accumulation on membranes, reaching a minimum at bound bile salt/lecithin mole ratio (B:L) between 0.05 and 0.1, then increasing with formation of higher-affinity mixed micelles. Inclusion of cholesterol in vesicles reduced Ai of all bile salts. In heterologous binding studies at submicellar concentrations, Ai of each bile salt varied with total B:L but was independent of the specific bile salts present on the membrane. Addition of TUDC to TDC reduced binding of TDC to membranes only slightly and lowered the threshold TDC concentration associated with transition to mixed micelles. However, above this threshold, TUDC markedly altered the adsorption of TDC to lecithin-containing phases. We conclude that TUDC does not directly stabilize membranes; rather, reduced permeabilization and dissolution of cholesterol-rich membranes after addition of TUDC to TDC may result from effects on the formation and structure of simple and mixed micelles.

Adult changes in body composition are associated with changes in cholesterol levels: the Fels longitudinal study
Siervogel, R. M., W. Wisemandle, et al. (1998), Appl Radiat Isot 49(5-6): 727-9.
Abstract: Serial data from 507 adult participants in the Fels Longitudinal Study were used to study relationships between average annual changes in serum cholesterol levels and annual changes in total body fat, fat-free mass, percent body fat or body mass index in men and women aged 18-45 years or 45-65 years. Average annual changes in adiposity before and after 45 years of age for men and women show statistically significant, strong, positive relationships with corresponding changes in cholesterol levels.

Adult Treatment Panel III: do we really need another set of cholesterol guidelines?
Clearfield, M. B. (2002), J Am Osteopath Assoc 102(5 Suppl 1): S6-11.
Abstract: Reducing high levels of plasma low-density lipoprotein cholesterol (LDL-C) is still the primary focus of the Adult Treatment Panel III (ATP III) guidelines developed by the National Cholesterol Education Program. The LDL-C goal of less than 100 mg/dL for those with coronary heart disease (CHD) is now extended to patients with diabetes and those with a Framingham risk score of greater than 20% in 10 years, both of which are now considered "CHD risk equivalents." Consequently, many more people will be considered candidates for aggressive lipid-lowering therapy under the new ATP III guidelines. Other prominent features in the new guidelines include determining an individual's absolute risk category by using a nine-step process, instituting therapeutic lifestyle changes to reduce LDL-C levels, and strategies for treating patients with other forms of dyslipidemia such as metabolic syndrome.

Adults aged 20 and older should have their cholesterol measured
Cleeman, J. I. (1997), Am J Med 102(2A): 31-6.
Abstract: The guidelines of the National Cholesterol Education Program recommend that adults > or = 20 years of age should have their total and high-density lipoprotein cholesterol measured. This recommendation, which has been endorsed by representatives of > 40 medical and health organizations, is based on a large and diverse body of scientific evidence derived from animal, pathologic, genetic, biochemical, metabolic, and epidemiologic studies and clinical trials. Elevated cholesterol levels raise the risk of coronary heart disease (CHD) in men and women and in younger and older adults. Recent clinical trials have confirmed that cholesterol lowering reduces CHD morbidity and mortality and total mortality, without an increase in noncardiovascular mortality, in patients with and without CHD. Measuring cholesterol levels in adults > or = 20 years of age is necessary to provide an accurate assessment of CHD risk to an individual; to identify individuals who should lower their cholesterol levels, using diet and lifestyle changes as the primary treatment; and to reinforce population recommendations. Atherosclerosis begins early in life, and cholesterol levels in young adults predict CHD risk 30-40 years later. Cholesterol measurement can be used to motivate lifestyle changes that will reduce the long-term risk for CHD. Waiting until mid-life to find an elevated cholesterol loses a significant portion of the benefit. Cholesterol is a CHD risk factor in women and older adults, and recent trials show significant CHD risk reduction in these groups. While drug treatment is properly directed to patients with high CHD risk, in whom drugs are cost-effective, cholesterol measurement and lifestyle-based cholesterol lowering are necessary on a broader scale to reduce long-term CHD risk in adults aged > or = 20 years.

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Cholesterol Journal Articles