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828 PA R T V / Health Promotion and Disease Prevention

Table 36-3 ■ LIPID ABNORMALITIES AND ASSOCIATED MECHANISMS
Lipid Abnormality Mechanisms
Elevated total cholesterol High dietary intake of saturated fat and cholesterol
LDL receptor deficiency and other enzyme/receptor abnormalities.
Elevated LDL-cholesterol LDL receptor deficiency
Apoprotein B-100 genetic defect, other enzyme/receptor abnormalities.
High dietary intake of saturated fat and cholesterol
Elevated triglycerides Deficiency in LPL
Obesity, physical inactivity, insulin resistance, glucose intolerance
Excessive alcohol intake
Low HDL Apoprotein A-I deficiency, other enzyme/receptor abnormalities
Reduced VLDL clearance
Cigarette smoking, physical inactivity
Insulin resistance
Elevated triglycerides
Overweight and obesity
Very high carbohydrate (CHO) intake ( 60% total calories) Certain drugs
( -blockers, anabolic steroids, progestational agents)
Increased lipoprotein remnants (VLDL Defective apolipoprotein E Seen in familial combined hyperlipidemia
is a surrogate marker for Lipoprotein Level is genetically determined
remnants when triglyceride (Tg) is
200 mg/dL)
Lp(a)
2
2
A
Lipoprotein phospholipase AA (LpPLAA ) An enzyme that hydrolyzes cholesterol and initiates inflammatory processes
A
Small LDL particles Particle Size is determined by level of Triglycerides; LDL particle is denser and more atherogenic at
higher levels of TG
HDL Subspecies Low levels of HDL 2 and 3 increases CVD risk? Genetically determined versus lifestyle and other
lipid levels
Apolipoprotein B A potential marker for all atherogenic lipoprotein
Apolipoprotein A-I Increased CVD risk when apo A-I is low
Combined dyslipidemias small, dense Defects in VLDL and LDL receptor activities coexisting with environmental influences such as
LDL, high triglycerides, low HDL elevated obesity, physical inactivity, diet high in saturated fat, and cigarette smoking
LDL and triglycerides
National Cholesterol Education Program (2001).

observed abnormality. A high intake of dietary cholesterol and sat- Hypertriglyceridemia
urated fatty acids downregulates LDL receptor activity and recep-
tor synthesis, resulting in decreased LDL clearance. 63 The relationship between triglycerides and CVD is not entirely
clear. Elevated serum triglyceride levels have been associated with
CVD. However, the strength of the association is diminished
Familial (Severe) when other CVD risks are accounted for, leading some to suggest
Hypercholesterolemia that elevated triglycerides are a marker for other atherogenic fac-
tors. 65 Chylomicrons and VLDL are lipoprotein carriers of
Severe hypercholesterolemia is caused most commonly by a ge- triglyceride and, whereas chylomicrons are not considered to be
netic disorder and is known as familial hypercholesterolemia atherogenic, the remnants of VLDL catabolism are smaller parti-
65
(FH). There are two types of FH, heterozygous and homozygous. cles that are richer in cholesterol esters. These remnant particles,
Plasma LDL cholesterol normally binds to cell membrane recep- or IDL, are considered more atherogenic. 66
tors and is taken into the cell for several biologic functions. In het- Elevated triglycerides are frequently observed in people who
erozygous FH, there is one normal gene and one abnormal gene also have low HDL levels and small dense LDL particles. This
for the LDL receptor. combination of lipid abnormalities is considered an atherogenic
Because only half the normal number of LDL receptors are phenotype. 65 In addition, elevated triglycerides (and its associ-
synthesized, LDL is removed from the blood at two thirds the ated small dense LDL particle size and low HDL cholesterol
26
normal rate. The result is a two- to three-fold increase in blood level) commonly exists with insulin resistance (with or without
LDL levels. One person in 500 is thought to have this genetic dis- glucose intolerance), hypertension, obesity (particularly abdomi-
order, which eventually results in an increased risk for myocardial nal obesity pattern), and prothrombotic and proinflammatory
infarction (MI). 2,64 The homozygous form of FH develops when states. This combination of risk factors is commonly called the
two abnormal genes are inherited. The one in one million persons metabolic syndrome and is linked to increased CVD risk. 2,3 See
who have this disorder have LDL levels six times normal and may Table 36-4 for a summary of the metabolic syndrome character-
have an MI as early as age 5 to 15 years. 2,26,48,64 In addition, a ge- istics. These associations suggest that elevated triglyceride levels
netic defect related to apo B-100 results in marked elevations in may be a marker for other CVD risk factors. Diabetes also results
LDL cholesterol. in increased plasma triglyceride levels because of increased