High-density lipoprotein/ja: Difference between revisions

|+ Total HDL particle Table

! MESA Percentile

! Total HDL particles [[mole (unit)|μmol]]/L

! Interpretation

| Those with highest (Optimal) total HDL particle concentrations & lowest rates of cardiovascular disease events

| Those with moderately high total HDL particle concentrations & moderate rates of cardiovascular disease events

| Those with lower total HDL particle concentrations & Borderline-High rates of cardiovascular disease

| Those with lowest total HDL particle concentrations & Highest rates of cardiovascular disease events

|+ Large (protective) HDL particle Table

! MESA Percentile

! Large HDL particles [[mole (unit)|μmol]]/L

! Interpretation

| Those with highest (Optimal) Large HDL particle concentrations & lowest rates of cardiovascular disease events

| Those with moderately high Large HDL particle concentrations & moderate rates of cardiovascular disease events

| Those with lower Large HDL particle concentrations & Borderline-High rates of cardiovascular disease

| Those with lowest Large HDL particle concentrations & Highest rates of cardiovascular disease events

The lowest incidence of atherosclerotic events over time occurs within those with both the highest concentrations of total HDL particles (the top quarter, >75%) and the highest concentrations of large HDL particles. Multiple additional measures, including LDL particle concentrations, small LDL particle concentrations, VLDL concentrations, estimations of [[insulin resistance]] and standard cholesterol lipid measurements (for comparison of the plasma data with the estimation methods discussed above) are routinely provided in clinical testing.

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== Increasing HDL levels ==

HDL lipoprotein particles that bear [[apolipoprotein C3]] are associated with increased, rather than decreased, risk for [[coronary heart disease]].

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=== Diet and exercise ===

* Decreased intake of [[simple carbohydrates]].

* [[Aerobic exercise]]

* [[Weight loss]]

* [[Avocado]] consumption

* [[Magnesium]] supplements raise HDL-C.

* Addition of [[Dietary fiber|soluble fiber]] to diet

* Consumption of [[omega-3 fatty acids]] such as fish oil or [[Linseed oil#Nutritional supplement|flax oil]]

* Increased intake of [[unsaturated fat]]s

* Removal of [[trans fat]]ty acids from the diet

Most [[saturated fats]] increase HDL cholesterol to varying degrees but also raise total and LDL cholesterol.

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=== Recreational drugs ===

HDL levels can be increased by [[smoking cessation]], or mild to moderate [[Alcohol and cardiovascular disease|alcohol]] intake.

[[Cannabis (drug)|Cannabis]] in unadjusted analyses, past and current cannabis use was not associated with higher HDL-C levels.  A study performed in 4635 patients demonstrated no effect on the HDL-C levels (P=0.78) [the mean (standard error) HDL-C values in control subjects (never used), past users and current users were 53.4 (0.4), 53.9 (0.6) and 53.9 (0.7) mg/dL, respectively].

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Exogenous [[anabolic androgenic steroids]], particularly [[17α-alkylated anabolic steroid]]s and others administered orally, can reduce HDL-C by 50 percent or more. Other [[androgen receptor]] agonists such as [[selective androgen receptor modulators]] can also lower HDL. As there is some evidence that the HDL reduction is caused by increased [[reverse cholesterol transport]], it is unknown if AR agonists' HDL-lowering effect is pro- or anti-atherogenic.

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=== Pharmaceutical drugs and niacin ===

[[Pharmacological therapy]] to increase the level of HDL cholesterol includes use of [[fibrate]]s and [[Niacin (substance)|niacin]]. Fibrates have not been proven to have an effect on overall deaths from all causes, despite their effects on lipids.

[[Niacin (substance)|Niacin]] (nicotinic acid, a form of [[vitamin B3]]) increases HDL by selectively inhibiting hepatic [[diacylglycerol acyltransferase]] 2, reducing [[triglyceride]] synthesis and [[VLDL]] secretion through a receptor HM74 otherwise known as  [[niacin receptor 2]] and HM74A / GPR109A, [[niacin receptor 1]].

Pharmacologic (1- to 3-gram/day) niacin doses increase HDL levels by 10–30%, making it the most powerful agent to increase HDL-cholesterol. A randomized clinical trial demonstrated that treatment with niacin can significantly reduce atherosclerosis progression and cardiovascular events. Niacin products sold as "no-flush", ''i.e.'' not having side-effects such as "niacin [[Flushing (physiology)|flush]]", do not, however, contain free nicotinic acid and are therefore ineffective at raising HDL, while products sold as "sustained-release" may contain free nicotinic acid, but "some brands are hepatotoxic"; therefore the recommended form of niacin for raising HDL is the cheapest, immediate-release preparation. Both fibrates and niacin increase artery toxic [[homocysteine]], an effect that can be counteracted by also consuming a multivitamin with relatively high amounts of the B-vitamins, but multiple European trials of the most popular B-vitamin cocktails, trial showing 30% average reduction in homocysteine, while not showing problems have also not shown any benefit in reducing cardiovascular event rates.  A 2011 extended-release niacin (Niaspan) study was halted early because patients adding niacin to their statin treatment showed no increase in heart health, but did experience an increase in the risk of stroke.

In contrast, while the use of [[statins]] is effective against high levels of LDL cholesterol, most have little or no effect in raising HDL cholesterol.

[[Lovaza]] has been shown to increase HDL-C. However, the best evidence to date suggests it has no benefit for primary or secondary prevention of cardiovascular disease.

The [[peroxisome proliferator-activated receptor|PPAR]] modulator [[GW501516]] has shown a positive effect on HDL-C and an antiatherogenic where LDL is an issue. However, research on the drug has been discontinued after it was discovered to cause rapid cancer development in several organs in rats.