The "good" cholesterol — reverse cholesterol transport. Often inversely correlated with cardiovascular risk, but not the strongest signal.
HDL (high-density lipoprotein) carries cholesterol from peripheral tissues back to the liver for excretion or reuse — a process called reverse cholesterol transport. HDL has historically been called "good cholesterol" because higher levels associate with lower cardiovascular risk.
The relationship is more nuanced than originally thought. Pharmacologically RAISING HDL hasn't reliably reduced CV events in trials (CETP inhibitor trials famously failed). The protective effect appears to require functional HDL — not just elevated levels.
HDL is influenced by: aerobic exercise (one of the strongest non-pharma raisers), alcohol intake (modestly raises), genetics (large individual variance), body fat (visceral fat lowers), insulin resistance (lowers), smoking (lowers), saturated fat (modestly raises), low-carb diets (modestly raise), and pharmacologic agents — niacin raises modestly; statins modestly raise; GLP-1 agonists modestly raise.
Don't chase HDL aggressively in isolation. Focus on ApoB and the Triglycerides/HDL ratio (>3 = atherogenic dyslipidemia signal). On GLP-1s, expect modest HDL improvements alongside primary triglyceride and ApoB shifts. Very low HDL (<35) warrants attention — usually correctable with exercise + body composition work.
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Start tracking →Informational only — not medical advice. Reference ranges vary by lab and individual context. Work with a licensed provider to interpret your specific results.