Health Professional Resources
Natural Cholesterol Management
Alice H. Lichtenstein, Lawrence J. Appel, Michael Brands et al Diet and Lifestyle Recommendations Revision 2006: A Scientific Statement From the American Heart Association Nutrition Committee
Circulation http://circ.ahajournals.org/cgi/content/full/114/1/82
David JA Jenkins, et al Direct comparison of a dietary portfolio of cholesterol-lowering foods with a statin in hypercholesterolemic participants American Journal of Clinical Nutrition, Vol. 81, No. 2, 380-387, February 2005.
http://www.ajcn.org/cgi/content/abstract/81/2/380
Integrating Complementary Medicine Into Cardiovascular Medicine
Journal of the American College of Cardiology Vol 46, No. 1 July 5, 2005: 184-221.
http://www.acc.org/qualityandscience/clinical/consensus/complementary/index.pdf
Detection, Evaluation & Treatment of High Blood Cholesterol in Adults
Third Report of the National Cholesterol Education Program Expert Panel
National Institute of Heart, Lung and Blood Institute, Natitonal Institutes of Health
www.nhlbi.nih.gov/guidelines/cholesterol/atp3full.pdf
Combination Diet and Exercise Interventions for the Treatment of Dyslipidemia: an Effective Preliminary Strategy to Lower Cholesterol Levels?
Krista A. Varady and Peter J. H. Jones
Journal of Nutrition August, 2005. 135: 1829-1835.
http://jn.nutrition.org/cgi/content/abstract/135/8/1829
Plant Sterols
MARTIJN B. KATAN, PHD, ET AL “Efficacy and Safety of Plant Stanols and Sterols in the Management of Blood Cholesterol Levels”
Mayo Clinic Proceedings, 2003;78: pages 965-978.
Abstract: Foods with plant stanol or sterol esters lower serum cholesterol levels. We summarize the deliberations of 32 experts on the efficacy and safety of sterols and stanols. A meta-analysis of 41 trials showed that intake of 2 g/d of stanols or sterols reduced low-density lipoprotein (LDL) by 10%; higher intakes added little. Efficacy is similar for sterols and stanols, but the food form may substantially affect LDL reduction. Effects are additive with diet or drug interventions: eating foods low in saturated fat and cholesterol and high in stanols or sterols can reduce LDL by 20%; adding sterols or stanols to statin medication is more effective than doubling the statin dose. A meta-analysis of 10 to 15 trials per vitamin showed that plasma levels of vitamins A and D are not affected by stanols or sterols. Alpha carotene, lycopene, and vitamin E levels remained stable relative to their carrier molecule, LDL. Beta carotene levels declined, but adverse health outcomes were not expected. Sterol-enriched foods increased plasma sterol levels, and workshop participants discussed whether this would increase risk, in view of the marked increase of atherosclerosis in patients with homozygous phytosterolemia. This risk is believed to be largely hypothetical, and any increase due to the small increase in plasma plant sterols may be more than offset by the decrease in plasma LDL. There are insufficient data to suggest that plant stanols or sterols either prevent or promote colon carcinogenesis. Safety of sterols and stanols is being monitored by follow-up of samples from the general population; however, the power of such studies to pick up infrequent increases in common diseases, if any exist, is limited. A trial with clinical outcomes probably would not answer remaining questions about infrequent adverse effects. Trials with surrogate end points such as intima-media thickness might corroborate the expected efficacy in reducing atherosclerosis. However, present evidence is sufficient to promote use of sterols and stanols for lowering LDL cholesterol levels in persons at increased risk for coronary heart disease.
Available on-line at www.mayoclinicproceedings.com
Viscous Soluble Fiber
Soluble fiber and nondigestible carbohydrate effects on plasma lipids and cardiovascular risk
Current Opinion in Lipidology. 12(1):35-40, February 2001.
http://www.co-lipidology.com/pt/re/colipidology/abstract.00041433-200102000-00007.htm
James W Anderson Et Al Cholesterol-lowering effects of psyllium intake adjunctive to diet therapy in men and women with hypercholesterolemia: meta-analysis of 8 controlled trials
American Journal of Clinical Nutrition, Vol. 71, No. 2, 472-479, February 2000
http://www.ajcn.org/cgi/content/abstract/71/2/472
Niacin
M.J. Chapman, et al Raising high-density lipoprotein cholesterol
with reduction of cardiovascular risk: the role of nicotinic acid--a position
paper developed by the European Consensus Panel on HDL-C.
2004 Aug;20(8):1253-68.
Curr
Med Res Opin.
Anne Goldberg, MD et al Multiple-Dose Efficacy and
Safety of an Extended-Rleease Form of Niacin in the Management of Hyperlipidemia.
The American Journal of Cardiology, Vol 85, May 1, 2000.
Abstract: This multicenter trial evaluated the safety and efficacy of escalating doses of Niaspan (niacin extended-release tablets) and placebo (administered once-a-day at bedtime) in patients with primary hyperlipidemia on the percent change from baseline in levels of low-density lipoprotein (LDL) cholesterol and apolipoprotein B. Extended-release niacin was initiated at a dose of 375 mg/day, raised to 500 mg/day, and further increased in 500-mg increments at 4-week intervals to a maximum of 3,000 mg/day. A total of 131 patients (n = 87, extended-release niacin; n = 44, placebo) were treated for 25 weeks with study medication after a 6-week diet lead-in/drug washout phase and 2-week baseline LDL cholesterol stability phase. Significant decreases from baseline in levels of LDL cholesterol and apolipoprotein B became apparent with the 500-mg/day dose and were consistent at all subsequent doses (p < or =0. 05), reaching 21% and 20%, respectively, at the 3,000-mg/day dose. Significant increases from baseline in levels of high-density lipoprotein cholesterol became apparent with the 500-mg/day dose and were consistent at all subsequent doses (p < or = 0.05), reaching 30% at the 3,000-mg dose. Significant decreases from baseline in triglycerides and lipoprotein(a) occurred at the 1,000-mg dose and were apparent at all subsequent doses (p < or =0.05), reaching 44% and 26%, respectively, at the 3,000-mg dose. The most common adverse events were flushing and gastrointestinal disturbance. Transaminase increases were relatively small, and the proportion of patients who developed liver function abnormalities on extended-release niacin was not significantly different from placebo. Thus, extended-release niacin was generally well tolerated and demonstrated a dose-related ability to alter favorably most elements of the lipid profile.
Goldberg AC. A meta-analysis of randomized controlled studies on the effects of extended-release niacin in women. Am J Cardiol.
2004 Jul 1;94(1):121-4
The present meta-analysis pooled data from 5 double-blind, placebo-controlled studies in 432 patients with dyslipidemia treated with various doses of extended-release niacin. Data were analyzed for possible gender differences in response to treatment. At all doses, mean decreases in low-density lipoprotein cholesterol were greater in women than in men; differences were significant at doses of 1,000 mg (6.8% vs 0.2%, p = 0.006), 1,500 mg (11.3% vs 5.6%, p = 0.013), 2,000 mg (14.8% vs 6.9%, p = 0.010), and 3,000 mg (28.7% vs 17.7%, p = 0.006). Decreases in triglyceride levels also tended to be greater in women than in men but reached significance only at the 1,500-mg dose (28.6% vs 20.4%, p = 0.040). No similar trends or significant gender differences were noted in levels of lipoprotein(a) and high-density lipoprotein cholesterol. This meta-analysis confirms that women respond as well as men, and possibly slightly better, to treatment with extended-release niacin and that it is a safe and effective treatment option for women with dyslipidemia.
S. F. Gardner, et al Combination therapy with low-dose lovastatin and niacin is as effective as higher-dose Lovastatin.
1996 May-Jun;16(3):419-23.
Pharmacotherapy.
Jennifer Wink, MD, et al Effect of Very Low-Dose Niacin on High-Density
Lipoprotein in Patients Undergoing Long-Term Statin Therapy
143(3):514-518, 2002.
Abstract: A low level of high-density lipoprotein (HDLC) is a proven risk factor for coronary artery disease. Niacin raises HDLC levels, but it is infrequently used because of its side effect profile. Niacin's side effects are dose related. This study tests the hypothesis that very low-dose niacin, in conjunction with long-term statin therapy, will improve the lipid profile by significantly raising the level of HDLC, with fewer side effects than traditional doses of niacin. METHODS: Fifty patients undergoing stable statin therapy for 3 months were blindly randomized to receive either placebo or niacin 50 mg administered by mouth 2 times daily for 3 months. Patients with diabetes and active smokers were excluded. Each patient completed a questionnaire regarding current medical problems, medications, and lifestyle before and after the therapy. Patients were questioned about any possible side effects that occurred during the medication trial. The primary end points were change in HDLC level and patient-reported side effects. RESULTS: Thirty-nine patients completed the study. Very low-dose niacin added to statin therapy increased the mean HDLC, 2.1 mg/dL in niacin group (standard error of the mean, 0.767) versus -0.56 mg/dL for placebo group (standard error of the mean-.816, P =.0246 by analysis of variance). Five patients receiving niacin, versus 2 patients receiving placebo, had episodes of flushing. No major side effects were noted. No patients stopped the study medication as a result of side effects. CONCLUSIONS: The addition of very low-dose niacin to statin therapy increased HDLC cholesterol significantly, while avoiding the side effects that are associated with traditional doses of niacin therapy.
American
Heart Journal
Conclusions The addition of very low–dose niacin (50mg 2x per day) to
statin therapy increased HDLC cholesterol significantly, while avoiding the
side effects that are associated with traditional doses of niacin therapy
Varying Cost and Free Nicotinic Acid Content in Over-the-Counter Niacin Preparations for Dyslipidemia
Annals of Internal Medicine December 16, 2003, Volume 139, Issue 12, pages 996-1002.
C. Daniel Meyers, MD
http://www.annals.org/cgi/reprint/139/12/996.pdf
Omega-3s
Penny M. Kris-Etherton, PhD, RD Et Al AHA Scientific Statement: Fish
Consumption, Fish Oil, Omega-3 Fatty Acids, and Cardiovascular Disease
Circulation. 2002;106:2747.
http://circ.ahajournals.org/cgi/reprint/106/21/2747
From Inuit to Implementation: Omega-3 Fatty Acids Come of Age
Mayo Clinic Proceedings, 2000.
http://www.mayoclinicproceedings.com/inside.asp?AID=1472&UID