Table 2.

Effects of lifestyle interventions on plasma concentrations of HDL cholesterol and triglycerides

Intervention	▵ HDL-C	Mechanism	▵ triglycerides	Mechanism
Smoking cessation123	↑ 5–10%	↑ LCAT and cholesterol efflux; ↓CETP	No significant change reported	–
Weight loss124	↓ during active weight loss	↑ LCAT, LPL, cholesterol efflux	↓ by 0.015 mmol/L per kg weight loss	↑ VLDL clearance
	↑ after weight stabilization by 0.009 mmol/L per kg weight lost	↓ catabolism of HDL, apo A-I		↓ hepatic VLDL secretion
Exercise125–131
Aerobic	↑ 5–10% (moderate to high intensity)	↑ pre-β HDL, cholesterol efflux, LPL	↓ 10–20% (moderate to high intensity)	↓ hepatic VLDL-TG secretion;
		↑ in HDL size	↓ ∼30% in VLDL-TG	Beneficial adaptations in muscle fibre area, capillary density, glycogen synthase, and GLTU4 protein expression in T2DM or impaired glucose tolerance
Resistance	No significant change reported	Improved HDL functionality	↓ ∼ 5%
Alcohol132–134	↑ 5–10% (1–3 drinks/day)	↑ ABCA1, apo A-I	Variable response, ↑↑ in obese subjects	↑ synthesis of VLDL–TG with excess intake
		↓ CETP	↑↑ with excess intake
Dietary factors135–140
n-3-PUFAs, n-6-PUFAs, MUFAs	0 to ↑ 5%	Improves ratio of LDL-C/HDL-C	↓ 10–15%	↑ TG-rich lipoprotein clearance via pathways mediated by apo CIII and apo E
		Improves HDL anti-inflammatory activity		↓ VLDL apo B secretion
Omni-Heart	↑ by <5%		↓ 56% (increased protein)
			↓ 33% (increased USFA)

ABCA1, ATP-binding cassette transporter; apo, apolipoprotein; CETP, cholesteryl ester transfer protein; GLUT4, glucose transporter type 4; HDL, high-density lipoprotein; LCAT, lecithin:cholesterol acyltransferase; LDL, low-density lipoprotein; LPL, lipoprotein lipase; MUFA, monounsaturated fatty acids; PUFA, polyunsaturated fatty acids; TG, triglycerides; T2DM, type 2 diabetes mellitus; USFA, unsaturated fatty acids; VLDL, very low-density lipoprotein.