Astaxanthin, a natural antioxidant, lowers cholesterol and markers of cardiovascular risk in individuals with prediabetes and dyslipidaemia

Abstract

Aim: To determine the effects of astaxanthin treatment on lipids, cardiovascular disease (CVD) markers, glucose tolerance, insulin action and inflammation in individuals with prediabetes and dyslipidaemia.

Materials and methods: Adult participants with dyslipidaemia and prediabetes (n = 34) underwent baseline blood draw, an oral glucose tolerance test and a one-step hyperinsulinaemic-euglycaemic clamp. They were then randomized (n = 22 treated, 12 placebo) to receive astaxanthin 12 mg daily or placebo for 24 weeks. Baseline studies were repeated after 12 and 24 weeks of therapy.

Results: After 24 weeks, astaxanthin treatment significantly decreased low-density lipoprotein (-0.33 ± 0.11 mM) and total cholesterol (-0.30 ± 0.14 mM) (both P < .05). Astaxanthin also reduced levels of the CVD risk markers fibrinogen (-473 ± 210 ng/mL), L-selectin (-0.08 ± 0.03 ng/mL) and fetuin-A (-10.3 ± 3.6 ng/mL) (all P < .05). While the effects of astaxanthin treatment did not reach statistical significance, there were trends toward improvements in the primary outcome measure, insulin-stimulated, whole-body glucose disposal (+0.52 ± 0.37 mg/m² /min, P = .078), as well as fasting [insulin] (-5.6 ± 8.4 pM, P = .097) and HOMA2-IR (-0.31 ± 0.16, P = .060), suggesting improved insulin action. No consistent significant differences from baseline were observed for any of these outcomes in the placebo group. Astaxanthin was safe and well tolerated with no clinically significant adverse events.

Conclusions: Although the primary endpoint did not meet the prespecified significance level, these data suggest that astaxanthin is a safe over-the-counter supplement that improves lipid profiles and markers of CVD risk in individuals with prediabetes and dyslipidaemia.

Keywords: antidiabetic drug; cardiovascular disease; clinical trial; dyslipidaemia; type 2 diabetes.

Figure 1.

Safety Measures. A. Vital signs. Open bars – baseline, green bars – 12 weeks evaluation, blue bars – 24 weeks. B. Safety laboratory values. Visit #1 – baseline, visit #2 – randomization, visit #3 - 6 weeks, visit #4 – 12 weeks evaluation, visit #5 - 18 weeks, visit #6 – 24 weeks evaluation, visit #7 – follow-up Results are Ave + SEM *p<0.05 vs visit #1 eGFR reported as value <60 or >60

Figure 2.

Treatment effects on fasting lipid levels. Open bars – baseline, green bars – 12 weeks evaluation, blue bars – 24 weeks evaluation. Results are Ave + SEM. * p<0.05 vs paired baseline value † p<0.01 vs paired baseline value

Figure 3.

Treatment effects on selected circulating markers for CVD. Open bars – baseline, green bars – 12 weeks evaluation, blue bars – 24 weeks evaluation. Results are Ave + SEM. * p<0.05 vs paired baseline value †p<0.01 vs paired baseline value

Figure 4.

Treatment effects on measures of glycemic control, insulin secretion, insulin action and substrate oxidation. A. Fasting values: HbA1c, glucose, insulin, c-peptide. B. Fasting-derived indices of insulin action and secretion: HOMA-IR, HOMA-%B, liver insulin sensitivity index, adipose tissue insulin sensitivity index. C. OGTT-derived indices of insulin action and secretion: AUC_glucose, AUC_insulin, AUC_c-peptide, 2 hr [glucose], early-phase insulin release (InsAUC₃₀/GluAUC₃₀), Matsuda index. D. Clamp-derived values: insulin-stimulated glucose disposal rate, suppression of FFA levels. E. Indirect calorimetry-derived substrate oxidation: resting energy expenditure, respiratory quotient, metabolic flexibility. For panels A-D: Open bars – baseline, green bars – 12 weeks evaluation, blue bars – 24 weeks. For panel E: open bars – fasting state, orange bars – clamp state. * p<0.05 vs paired baseline value † p<0.01 vs paired fasting state value #p< 0.05 vs paired V2 value