Hypercholesterolemia
Causes
- Genetic factors can predispose some individuals to hypercholesterolemia.3
- Secondary causes of hypercholesterolemia include obesity, diet, lifestyle, excess
alcohol, metabolic disorders, other diseases, and medications.4
Prevention and Management
- Dietary modification is recommended as the first step in the treatment of hypercholesterolemia.
Current data suggest that dietary fat should be limited to 30% of the total caloric
intake, saturated fat should be less than 10% and cholesterol less than 300mg a
day.5
- Numerous studies show the benefits of fiber in reducing serum cholesterol.6 The
American Heart Association recommends 25 to 30 grams of fiber per day along with
the above recommended intakes for fat and cholesterol.7
- Antioxidant vitamins such as beta-carotene, Vitamin C, and Vitamin E help to
reduce the susceptibility of low density lipoprotein (LDL) to oxidation.8
- Therapeutic doses of niacin have been shown to be effective in increasing high-density
lipoprotein cholesterol concentrations and reducing the Lp(a) lipoprotein level.9
- Impaired vasodilation in humans with hypercholesterolemia has been shown to improve
with Vitamin C.10
Abstracts
Crouse JR 3rd. New developments in the use of niacin for treatment
of hyperlipidemia: new considerations in the use of an old drug. Coron Artery
Dis 1996 Apr; 7(4):321-6.
Niacin has been used for many years to treat hyperlipidemia. It has been shown to
reduce coronary death and non-fatal myocardial infarction and, in a separate analysis
of long-term (15-year) follow-up, all cause mortality. It reduces total cholesterol, low density lipoprotein cholesterol (LDL-C) and triglycerides and increases high
density lipoprotein cholesterol (HDL-C). Sustained-release niacin may be associated
with more dramatic changes in LDL-C and triglyceride, whereas the short acting preparation
causes greater increases in HDL-C. The increase of HDL-C occurs at a lower dose (1500
mg/day) than the reduction of LDL-C (> 1500 mg/day). Niacin also favorably influences
other lipid parameters including lipoprotein(a) Lp(a), alimentary lipemia, familial
defective apolipoprotein B-100 and small dense LDL. Combination of niacin with a
bile acid sequestrant or a reductase inhibitor represents a powerful lipid-altering
regimen. Whereas the reductase inhibitors and bile acid binding resins primarily
affect LDL-C, the combined therapy has a synergistic effect to reduce LDL-C and,
in addition, the niacin reduces triglycerides and increases HDL-C. The major drawback
in the use of niacin is associated side effects (flushing and palpitations) and toxicity
(worsening of diabetes control, exacerbation of peptic ulcer disease, gout, hepatitis).
Niacin has a long history of use as a lipid lowering agent and has several attractive
features. Unfortunately, the side effect profile of this agent warrants its use only
in patients with marked dyslipidemia in whom side effects and potential toxicity
are closely monitored.
Rimm EB, Stampfer MJ. The role of antioxidants in preventive cardiology. Curr
Opin Cardiol 1997 Mar; 12(2):188-94.
Vitamin C, carotenoids, and vitamin E, the three main dietary sources of antioxidants,
each effect lipid peroxidation and may reduce atherogenesis and lower the risk of
coronary heart disease (CHD). Crosscultural studies of antioxidants find that regions
with relatively low dietary intake tend to have higher rates of CHD, but in these
studies it is difficult to account for other important cardiovascular risk factors.
Evidence from observational studies with more detailed information do not support
a cardiovascular benefit for vitamin C, although the cardiovascular effect of vitamin
C supplementation among populations with marginal vitamin C deficiency is not known.
Results from recent clinical trials of beta-carotene supplementation show no cardiovascular
benefit, although several observational studies have found an inverse association
between carotenoid intake or plasma levels and risk of CHD. The benefit reported
in the observational studies may be due to consumption in foods rich in beta-carotene
rather than the beta-carotene itself. The evidence for a cardiovascular benefit of
antioxidants is strongest for vitamin E.
Three large prospective studies find that
vitamin E supplement users have approximately 40% lower rates of CHD. Short durations
and doses of less than 100 IU/d (when data were available) have no significant effect.
The effect of dietary vitamin E may be more modest but still associated with lower
risk of CHD in populations in which vitamin E supplementation is infrequent. In a
large randomized trial, a nonsignificant reduction in CHD risk was reported for 50
IU/d, although the dose may have been insufficient. A secondary prevention trial
of 400 and 800 IU/day reported a strong reduction in nonfatal myocardial infarction,
further supporting the large body of evidence that suggests that high doses of vitamin
E reduce risk of CHD.
References
1 Tabers Cyclopedic Medical Dictionary. 16th ed. Philadelphia:F.A. Davis
Company;1985. P346.
2 Whitaker J. Dr. Whitakers Guide to Natural Healing. Rocklin CA: Prima
Publishing;1994. Pp.192.
3 Assouline L, Levy E, Feoli-Fonseca JC, Godbout C, Lambert M. Familial
hypercholesterolemia: molecular, biochemical, and clinical characterization of a French-Canadian
pediatric population. Pediatrics 1995 Aug; 96(2 Pt 1):239-46.
4 Stone NJ. Secondary causes of hyperlipidemia. Med Clin North Am 1994 Jan;78(1):117-41.
5 Ziegler EE, Filer LJ. Present Knowledge in Nutrition 7th ed. Washington
DC: ILSI Press; 1996. Pp.435.
6 Hunninghake DB, Miller VT, LaRosa JC, Kinosian B, Jacobson T, Brown V,
Howard WJ, Edelman DA, O'Connor RR Long-term treatment of hypercholesterolemia with
dietary fiber see comments. Am J Med 1994 Dec;97(6):504-8.
7 Van Horn L. Fiber, lipids, and coronary heart disease: A statement for
healthcare professionals from the nutrition committee, American Heart Association.
Circulation 1997;95:2701-2704.
8 Gilligan DM, Sack MN, Guetta V, Casino PR, Quyyumi AA, Rader DJ, Panza
JA,Cannon RO 3rd. Effect of antioxidant vitamins on low density lipoprotein oxidation
and impaired endothelium-dependent vasodilation in patients with hypercholesterolemia.
J Am Coll Cardiol 1994 Dec; 24(7):1611-7.
9 Crouse JR 3rd. New developments in the use of niacin for treatment of
hyperlipidemia: new considerations in the use of an old drug. Coron Artery Dis 1996
Apr;7(4):321-6.
10 Ting HH, Timimi FK, Haley EA, Roddy MA, Ganz P, Creager MA. Vitamin C
improves endothelium-dependent vasodilation in forearm resistance vessels of humans with hypercholesterolemia. Circulation 1997 Jun 17; 95(12):2617-22.
