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DYSLIPIDEMIA AND LIPID SUBPARTICLES CHARACTERIZATION

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BIO-MONITORS

  • The lipid panel is a well-established group of tests that aids in identifying patients at risk for cardiovascular disease.
  • The lipid panel identifies patients with lipid abnormalities and guides therapeutic lifestyle changes and pharmacological therapy.
  • The lipid panel measures the total amount of plasma cholesterol and triglycerides but does not measure the size of the particles. Knowing the size of the subparticles that contain cholesterol aids in determining a person’s risk for cardiovascular disease and guides pharmacological therapy and lifestyle considerations. Medication classes to consider when treating specific abnormal values are statins, fenofibrates, nicotinic acid, and cholesterol absorbing agents.
  • Repeat abnormal results 6 weeks after initiating or changing therapy, then quarterly until treatment goal is met. Monitor stable patients annually.
  • Direct LDL is a measure of LDL in the blood. It’s not a calculated value therefore not affected by the triglyceride content. Measurements are accurate even if triglycerides are > 400 mg/dl.
  • Direct LDL can be measured in fasting and non-fasting conditions.
  • Use Direct LDL to determine risk of heart disease and to monitor lipid-lowering lifestyle changes and drug therapies especially in patients with insulin resistance, metabolic syndrome and diabetes.
  • Repeat abnormal results 6 weeks after initiating or changing therapy, then quarterly until treatment goal is met. Monitor stable patients annually.
  • Individuals with an elevated apoB value are 3 times more likely to have a heart attack.
  • ApoB is the primary apolipoprotein on LDLand other non-HDL lipoproteins allowing them to attach to cells and release cholesterol into tissues.
  • Because LDL-C in a lipid panel is a calculated value with some individual variance, apoB is a better metric of the number of atherogenic particles.
  • Individuals with a high apoB, even with a normal LDL-C, are at higher risk of heart disease.
  • Use apoB to guide decisions for pharmacological therapy or lifestyle changes. The same medi- cations that lower LDL should be considered for improving apoB. Assess CoQ10 levels as recent evidence suggests that low ApoA1 and/or HDL-C levels are associated with low CoQ10 levels.
  • Repeat abnormal results 6 weeks after initiating or changing therapy then quarterly until treatment goal is met. Monitor stable patients annually.
  • Direct LDL is a measure of LDL in the blood. It’s not a calculated value therefore not affected by the triglyceride content. Measurements are accurate even if triglycerides are > 400 mg/dl.
  • Direct LDL can be measured in fasting and non-fasting conditions.
  • Use Direct LDL to determine risk of heart disease and to monitor lipid-lowering lifestyle changes and drug therapies especially in patients with insulin resistance, metabolic syndrome and diabetes.
  • Repeat abnormal results 6 weeks after initiating or changing therapy, then quarterly until treatment goal is met. Monitor stable patients annually.
Lipoprotein fractionation
  • Individuals with cardiovascular disease and high levels of sd-LDL are 3 times more likely to have disease progression.
  • This smaller, denser version of LDL is more atherogenic. Due to its size, it has a higher affinity for vessel wall penetration, and it oxidizes readily in the cell wall, accelerating the atherosclerotic process.
  • sd-LDL IV particles are more cholesterol depleted and triglyceride enriched than sd-LDL III creating more lipid content for macrophage cells and promoting rupture prone plaque.
  • Individuals with high sd-LDL IV respond well to lipid modifying medications, but are not as responsive to lifestyle changes. Individuals with high sd-LDL III respond well to both lifestyle and lipid improving medications including, nicotinic acid and fenofibrate.
  • Monitor individuals with increased levels of sd-LDL for increased triglycerides and reduced HDL-C as seen in patients with metabolic syndrome. Consider more aggressive drug and lifestyle therapy in those at risk of metabolic syndrome. Addressing insulin resistance with medications or lifestyle will improve the small dense LDL trait.
  • Repeat abnormal results 6 weeks after initiating or changing therapy, then quarterly until treatment goal is met. Monitor stable patients annually.
  • Low levels of HDL2b indicate impaired “reverse cholesterol transport” or cholesterol clearance by the liver.
  • HDL2b promotes cholesterol exporting from macrophages thus promoting an anti-inflammatory state and cardio protective properties. It is an indicator of how well lipids are removed.
  • High triglyceride levels can increase the degradation of HDL through hepatic lipase and “CETP” activity resulting in low HDL levels. Consider more aggressive drug (nicotinic acid) and lifestyle therapy for individuals with low HDL2b.
  • Repeat abnormal results 6 weeks after initiating or changing therapy, then quarterly until treat- ment goal is met. Monitor stable patients annually.
  • More than 30% of the population has cholesterol-depleted LDL, a condition in which a patient’s cholesterol may be “normal” but their lipoprotein particle number, and hence their actual risk, could be much higher than expected.
  • LDL particles carry cholesterol into various cells; excess particles enter the arteries and the cholesterol becomes plaque or atherosclerosis. With a higher LDL particle number the probability of particle penetration of the arterial wall rises and risk for heart disease increases.
  • Cholesterol-depleted LDL is especially common in persons whose triglycerides are high or HDL low.
  • If LDL-P# is not at goal, consider statins, ezetimibe or combination therapy if not contraindicated. Add niacin, omega-3 fatty acid, fenofibrates to lower triglycerides or increase HDL-C.
  • Consider diet, exercise and weight reduction efforts if appropriate
  • Repeat abnormal results 6 weeks after initiating or changing therapy, then quarterly until treatment goal is met. Monitor stable patients annually.
  • Individuals with elevated Lp(a) are twice as likely to experience a cardiovascular event than those without elevated levels.
  • Lp(a) is a LDL particle with an additional apo(a) attached. This structure has a higher affinity to cell wall penetration than LDL & has prothrombotic qualities promoting cerebrovascular or cardiovascular events.
  • Lp(a) can rise after females go through menopause, as estrogen aids in keeping Lp(a) levels lower.
  • When elevated, treat other risk factors more aggressively with drug and lifestyle response. Nicotinic acid will help improve Lp(a) levels, but may not completely correct them.
  • Repeat abnormal results 6 weeks after initiating or changing therapy, then quarterly until treatment goal is met. Some individuals, especially African Americans and Asian Indians, may genetically remain above goal. Monitor stable patients annually.
  • Low CoQ10 levels are associated with lowHDL levels and, potentially, poor CVD outcomes.
  • CoQ10 is a fat soluble vitamin-like substance critical for cellular energy and is a powerful antioxidant.
  • Levels of CoQ10 decline with age, statin therapy and low intake of specific nutrients.
  • ApoA1 may be involved in CoQ10 absorption. Consider dietary sources or CoQ10 supplementation if on statin therapy, has low apo-A1, or low HDL. Depending on the CoQ10 level, doses should range between 50 – 200 mg each day.
  • Repeat abnormal CoQ10 levels quarterly until treatment goal is met and then annually.

MICRONUTRIENT TESTS ASSOCIATED WITH DYSLIPIDEMIA

Nutri meter
Manganese
Cofactor to an antioxidant (superoxide dismutase) that repairs damage to blood vessels caused by oxidized LDL (low density lipoprotein).

Magnesium
Deficiency causes pro-atherogenic (heart-disease causing) changes in lipoprotein metabolism; Protects LDL (low density lipoprotein) from being oxidized.

Vitamin C
Protects LDL from oxidation, thus making it less “sticky” and prone to atherosclerosis (clogging of arteries); Prevents white blood cells (monocytes) and oxidized LDL from sticking to blood vessel wall; Lowers Lp(a) in some people.

Vitamin D
Suppresses foam cell formation thus reducing risk of lipid-related arterial blockages; Deficiency linked to dyslipidemia.

Vitamin B3
Niacin (B3) effectively lowers the highly atherogenic Lp(a) by decreasing its rate of synthesis in the liver.

Vitamin B5
Favorably alters low density lipoprotein metabolism and reduces triglycerides; Full benefit of lipid lowering effects may not be seen for up to four months.

Carnitine
In supplementation trials, carnitine lowers triglycerides, oxidized LDL and the atherogenic Lp(a); This effect is likely due to its role in transporting fatty acids into cells so they can be used as fuel.
Lipoic Acid
Imrpoves lipid profile by reducing small, dense LDL (dangerous type); Protects vascular lining from oxidized cholesterol.

Inositol
Decreases small, dense LDL especially in patients with metabolic syndrome; Lowers triglycerides.

Choline
Regulates HDL metabolism; Part of the enzyme lecithin-cholesterol acyltransferase that has a major impact on lipoprotein metabolism.

Chromium
Specifically improves the dyslipidemia that accompanies insulin resistance; May increase HDL; Synergistic effect with niacin (B3) for dyslipidemia.

Coenzyme Q10
It is well established that statins, often prescribed for dyslipidemia, deplete CoQ10; Lowers Lp(a) and improves efficacy of some dyslipidemia meds.

Copper
Several copper-dependent enzymes affect lipoprotein metabolism; Deficiency contributes to fatty buildup in arteries caused by dyslipidemia.

Selenium
Prevents post-prandial (after a meal) changes in lipoproteins that make them susceptible to oxidation and thus harmful.

Zinc
Suboptimal zinc raises dangerous lipoproteins that promote vascular inflammation and arterial plaque formation; Cellular zinc controls the gene that makes heart-protective HDL (high density lipoprotein).