Fourteen RCTs (n=1,235), of which two (n=57) were crossover trials, were included.
Cholesterol and triglycerides.
There was no significant difference between ALA and placebo for change in total cholesterol (WMD -0.01 mmol/L, 95% CI: -0.08, 0.06), based on 11 studies with significant heterogeneity (P<0.05). There was a statistically significant but clinically unimportant decrease in HDL cholesterol with ALA supplementation (WMD -0.01 mmol/L, 95% CI: -0.02, 0.00), based on 10 studies with no evidence of heterogeneity. There were no significant differences observed for LDL or VLDL cholesterol or for triglycerides.
Body weight and BP.
There was no significant difference between ALA and placebo for change in BMI (WMD -0.04 kg/m2, 95% CI: -0.11, 0.03; 3 studies) or weight (WMD -0.18 kg, 95% CI: -0.72, 0.36; 3 studies). There were also no differences for systolic BP (WMD -0.72 mmHg, 95% CI: -2.01, 0.58; 3 studies) or diastolic BP (WMD -0.17 mmHg, 95% CI: -0.82, 0.48; 3 studies). There was no evidence of heterogeneity for any of these outcomes.
Glucose and fibrinogen.
There was a significant reduction in fasting plasma glucose after ALA supplementation (WMD -0.20 mmol/L, 95% CI: -0.30, -0.10; 2 studies). There was also a significant reduction in fibrinogen (WMD -0.17 micromol/L, 95% CI: -0.30, -0.04; 3 studies). There was no evidence of heterogeneity for either outcome.
Emerging cardiovascular risk markers.
One study reported changes in plasma markers. Vascular cell adhesion molecule 1 was the only marker that was significantly different between treatments.
Other analyses.
Subgroup analyses by placebo type or ALA dose did not show any significant differences (results not presented). Funnel plots suggested no evidence of publication bias (plots not presented).