Manual of Clinical Nutrition

(Brent) #1
Medical Nutrition Therapy for Disorders of Lipid Metabolism

Manual of Clinical Nutrition Management C- 49 Copyright © 20 13 Compass Group, Inc.


cholesterol levels (1). Lowering total cholesterol and saturated fat intake (less than 7% to 8% of total energy)
reduces total cholesterol and LDL cholesterol by 13% and 16%, respectively (59). For every 1% decrease in
energy consumed from saturated fat, total cholesterol levels and LDL cholesterol levels may each decrease by
approximately 2 mg/dL (59). Studies of MNT provided by a registered dietitian indicate that with two to six
planned visits patients reported a 15% to 22% reduction in total dietary fat (from 32% to 33% of energy to
25% to 28% of energy) and a 22% to 36% reduction in saturated fat (from 11% to 12% of energy to 7% to 9%
of energy). These dietary changes were accompanied by a 6% to 13% reduction in total plasma cholesterol
levels and a 7% to 14% reduction in LDL cholesterol levels (Grade I) (5).


Management of Specific Dyslipidemias and Special Considerations
Because the LDL cholesterol level offers more precise risk assessment and is the primary target of medical
interventions, treatment decisions are primarily based on LDL cholesterol levels. However, the NCEP ATP III
recommends the evaluation of a comprehensive lipoprotein panel that includes fasting blood LDL cholesterol,
HDL cholesterol, triglycerides, and total cholesterol. A comprehensive panel provides a more accurate picture
so that the Therapeutic Lifestyle Changes Diet and drug therapy can be individualized based on a patient’s
metabolic characteristics.


Low HDL cholesterol (<40 mg/dL): Low HDL cholesterol levels are a significant risk factor for CHD,
independent of LDL cholesterol levels and other risk factors (1). A reduced serum level of HDL cholesterol is
defined as a concentration less than 40 mg/dL. For every 1 mg/dL decrease in HDL cholesterol level, the risk of
CHD is increased by 2% to 3% (60). Likewise, higher HDL cholesterol levels appear to afford a degree of
protection against CHD. This protection warrants considering a high HDL cholesterol level (60 mg/dL) as a
negative risk factor. HDL cholesterol is measured as part of the lipoprotein analyses for primary prevention in
adults without CHD. For secondary prevention in adults with evidence of CHD, lipoprotein analysis is required
in all patients, and classification is based on only LDL cholesterol. Appropriate advice in treatment includes
smoking cessation, weight reduction, and increased physical activity. Avoidance of certain drugs that reduce
HDL cholesterol, such as beta-adrenergic blocking agents (beta-blockers), anabolic steroids, and progestational
agents, should also be considered (1).


Very high LDL cholesterol (>190 mg/dL): Persons with very high LDL cholesterol levels usually have genetic
forms of hypercholesterolemia (eg, familial hypercholesterolemia, familial defective apolipoprotein B, and
polygenic hypercholesterolemia). Early detection should be completed in young adults to prevent premature
CHD. These disorders often require combined drug therapy (statin and bile acid sequestrant) to achieve the
goals of LDL-lowering therapy (1).


Elevated serum triglycerides levels (>200 mg/dL): According to the NCEP ATP III, meta-analyses of
prospective studies indicate that elevated triglycerides levels are an independent risk factor for CHD. Factors


that contribute to elevated triglycerides levels include obesity and overweight, physical inactivity, cigarette
smoking, excess alcohol intake, high-carbohydrate diets (more than 60% of energy intake), certain diseases (eg,
type 2 diabetes mellitus, chronic renal failure, and nephrotic syndrome), certain drugs (eg, corticosteroids,
estrogens, retinoids, and higher doses of beta-adrenergic blocking agents), and genetic disorders (1). Generally,
elevated serum triglycerides levels are most often observed in persons with metabolic syndrome (1). The NCEP
ATP III adopts the following classification of serum triglycerides levels:


Normal triglycerides <150 mg/dL
Borderline high triglycerides 150 to 199 mg/dL
High triglycerides 200 to 499 mg/dL
Very high triglycerides >500 mg/dL

The VLDL level is the most readily available measure of atherogenic remnant lipoproteins. The ATP III
identifies the sum of LDL and VLDL cholesterol (termed non-HDL cholesterol, which can also be calculated by
taking total cholesterol minus HDL cholesterol) as a secondary target of therapy in persons with high
triglycerides levels (more than 200 mg/dL) (1). The goal for non-HDL cholesterol in persons with high serum
triglycerides levels can be set at 30 mg/dL higher than that for LDL cholesterol (eg, if LDL goal is less than 100
mg/dL, non-HDL goal would be less than 130 mg/dL) (1).


The treatment for elevated triglycerides level depends on the causes and severity (1). The primary aim of
therapy is to achieve the target goal of LDL cholesterol. Fibrates and nicotinic acid can be used in combination
with LDL-lowering drugs to lower triglycerides and achieve lipid goals (1,4). The ideal macronutrient

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