Micronutrient Supplementation and Ergogenesis — Vitamins
Luke Bucci in Nutrients as Ergogenic Aids for Sports and Exercise, 2020
Pantethine (the disulfide of pantetheine) consists of pantothenate bound to cysteamine and is a direct precursor of coenzyme A. Coenzyme A levels in perfused rat livers after pantethine administration were significantly elevated compared to control or pantothenate perfusion.238 Pantethine administration has been shown to have antiarrhythmic actions on rodent and canine hearts, with increases in intracellular ATP hypothesized to account for these actions.239–241 Pantethine supplementation significantly reduces elevated blood lipids and increases HDL cholesterol and apolipoprotein A in human subjects,242–245 with a postulated mechanism of accelerated coenzyme A synthesis. Oral pantetheine administration (1 g/d) increased peak serum pantothenate levels tenfold.246 Possible effects of increased pantothenate levels arising from pantetheine administration on athletes have not been reported, however. Since large doses of thiamine and pantothenate appeared to have ergogenic properties (see Table 2),206,228,230 studies using congeners of these two vitamins to explore potential ergogenic effects are indicated.
The Role of Nutrition and Nutritional Supplements in the Treatment of Dyslipidemia
Stephen T. Sinatra, Mark C. Houston in Nutritional and Integrative Strategies in Cardiovascular Medicine, 2015
Pantethine is the disulfide derivative of pantothenic acid and is metabolized to cystamine-SH, which is the active form in treating dyslipidemia.5,113–117 Over 28 clinical trials have shown consistent and significant improvement in serum lipids. TC is decreased 15%, LDL by 20%, APO-B by 27.6%, and TG by 36.5% over 4–9 months. HDL and APO-A1 are increased 8%. 5,113–118 The effects on lipids are slow with peak effects at 4 months but may take up to 6–9 months.5,113–118 In addition, pantethine reduces lipid peroxidation of LDL, decreases lipid deposition, intimal thickening and fatty streak formation in the aorta and coronary arteries.5,113–117 Pantethine inhibits cholesterol synthesis and accelerates FA metabolism in the mitochondria by inhibiting hepatic acetyl-CoA carboxylase, increases CoA in the cytoplasm, which stimulates the oxidation of acetate at the expense of FA and cholesterol synthesis, and increases the Krebs cycle activity.5,113–117 In addition, cholesterol esterase activity increases and HMG-CoA reductase activity is decreased.5,113–117 There is 50% inhibition of FA synthesis and 80% inhibition of cholesterol synthesis.5 Its lipid effects are additive to statins, niacin, and fibrates. The recommended effective dose is 300 mg three times per day or 450 mg twice per day with or without food.5,113–118
Thiamin
Judy A. Driskell, Ira Wolinsky in Sports Nutrition, 2005
In a similar study from the same group, Webster86 investigated the effects of derivatives of thiamin (allithiamin) and pantothenic acid (pantethine) on 2,000m time trial performance in trained cyclists (VO2max=61.8 ± 2.1 ml O2/kg/min; n=6). The subjects supplemented with the intervention compound (1 g of allithiamin and 1.8 g of a pantethine–pantothenic acid compound) or a placebo for 7 days. A randomized double-blind crossover design was used so that each subject served as his or her own control. On the testing days, the cyclists performed a steady-state 50 km ride at 60% of their VO2max followed by the 2,000m time trial. Performance times were not different (p=0.58) between the treatment ride (170.7 ± 10.2 s) or the placebo ride (178 ± 8.4 s). However, even though the rides were not statistically different, the 8-second difference between groups might be of athletic importance. The results from these two studies seem to indicate that supplementation with thiamin derivatives does not enhance glycolytic-dependent exercise in trained or untrained men.
Efficacy and safety of coenzyme A versus fenofibrate in patients with hyperlipidemia: a multicenter, double-blind, double-mimic, randomized clinical trial
Published in Current Medical Research and Opinion, 2020
Ya-Qin Chen, Shui-ping Zhao, Hui-Jun Ye
Statin therapy has long been the cornerstone of cardiovascular disease (CVD) prevention for reducing levels of atherogenic LDL-C12. However, the residual risk in statin treated patients remains significant, despite reaching LDL-C goals. Increasing studies focus on atherogenic dyslipidemia, which includes increased TG, prevalence of smaller and denser LDL particles and low HDL-C13,14. Based on current knowledge, nutraceuticals might exert significant lipid-lowering, and their use has several advantages – they have natural origins and are mainly extracted from natural products, they are mostly safe and very well tolerated and their use is supported by the findings from randomized controlled trials and meta-analyses; finally, the lipid-lowering effect of most nutraceuticals is multimechanistic, which makes them potential candidates for improving the effects of current lipid-lowering drugs when used in combination15,16. CoA is a naturally occurring physiological compound which is proved to be effective in accelerating the clearance of TG from plasma17. Our previous data shows that oral CoA 400 U/d effectively lowered serum TG in hypertriglyceridemic patients9. In our more recent study, the lipid lowering effect of CoA is better than that of pantethine which is a commonly used lipid lowering agent in China and Japan10. In line with these results, the present study supported the TG lowering effect of both fenofibrate and CoA although the extent of lipid lowering effect is relatively weaker in CoA group. Moreover, we demonstrate TC and non-HDL-C are slightly lowered and HDL-C is mildly increased in patients treated with CoA. However, CoA is less effective than fenofibrate in HDL-C modifying. While definitive support for therapeutic options targeting atherogenic dyslipidemia to reduce residual cardiovascular risk remains awaited, the newly developed oral CoA may be an additional agent as an adjunct to improving diet and other non-pharmacological treatments (e.g. exercise, weight reduction) for the treatment.