Alpha lipoic acid acetyl l carnitine benefits

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Try out PMC Labs and tell us what you think. Learn More. Mitochondria produce reactive oxygen species that may contribute to vascular dysfunction. Alpha-lipoic acid and acetyl-L-carnitine reduce oxidative stress and improve mitochondrial function. Active treatment increased brachial artery diameter by 2.

Thus, mitochondrial dysfunction may contribute to the regulation of blood pressure and vascular tone. In addition to serving as the site of oxidative phosphorylation, it is now clear that mitochondria regulate many cellular functions, in part, by producing reactive oxygen species that al the adaptive response to environmental stress and injury. On the basis of these observations, we hypothesized that an intervention deed to improve mitochondrial function would have beneficial vascular effects in patients with cardiovascular disease.

We enrolled consecutive patients receiving care at Boston Alpha lipoic acid acetyl l carnitine benefits Center for stable coronary artery disease who were age 55 years or older. The presence of coronary disease was confirmed by coronary angiography, history of myocardial infarction, 17 or an imaging stress test demonstrating myocardial ischemia.

Exclusion criteria included supplementation with alpha lipoic acid, acetyl-L-carnitine, vitamin E, or vitamin C. Since alpha-lipoic acid has the potential to increase insulin sensitivity, 18 we excluded patients with a history of symptomatic hypoglycemia. Finally, we excluded patients if their physicians made a change in their anti-hypertensive regimen during the month prior to the study or during the study.

All subjects provided informed consent and the Boston Medical Center Institutional Review Board approved the protocol. Eligible patients were enrolled into a double blind, placebo-controlled crossover study that evaluated vascular function and blood pressure before and at the end of two eight-week treatment periods. Subjects were instructed to take one tablet twice daily. Study medications were packaged and dispensed in a blinded manner by the Research Drug Service of Boston Medical Center.

Prior to each of the four visits, subjects were asked to withhold vasoactive medications nitrates, calcium channel blockers, angiotensin converting enzyme inhibitors, other vasodilators, and beta-adrenergic blockers for 24 hours and to fast and refrain from smoking if applicable overnight. A blood sample was collected by venipuncture. Patients lay supine in bed in a darkened room for 10 minutes.

We then used an automatic physiological monitor Dynamap to measure pulse and blood pressure in the left arm and recorded the average of three measurements made two minutes apart. We then used vascular ultrasound to assess endothelium-dependent flow-mediated dilation and reactive hyperemia of the brachial artery in the right arm using established methodology. Reactive hyperemia was induced by five-minute occlusion of arterial flow with a narrow gauge blood pressure cuff positioned on the upper arm. Doppler als were recorded immediately after cuff release and two-dimensional images were recorded from 55 to 65 seconds following cuff release.

After a ten-minute rest period, we recorded two-dimensional images of the brachial artery before and three minutes after administering sublingual nitroglycerin 0. Five minutes after nitroglycerin administration, we repeated the blood pressure measurement before allowing subjects to get out of bed. We did not administer nitroglycerin to subjects with a history of migraine headaches or with adverse effects to nitroglycerin in the past. We measured brachial artery diameter using commercially available software Brachial Analyzer, Medical Imaging Applications, Inc.

Flow-mediated dilation was expressed as percentage change from baseline and as actual change in millimeters. Serum lipids and glucose levels were measured in the Boston Medical Center Clinical laboratory and low-density lipoprotein cholesterol levels were calculated using the Friedewald formula. We compared the clinical characteristics of the subjects randomized to placebo first and active treatment first using the unpaired t-test and the chi square test for continuous and categorical variables, respectively.

We used repeated measures analysis of variance ANOVA to examine the effect of treatment on brachial artery diameter, brachial artery flow-mediated dilation, nitroglycerin-mediated dilation, extent of reactive hyperemia, systolic and diastolic blood pressure, lipoprotein levels, glucose levels, and total serum carnitine levels. This analysis considered the effects of visit baseline vs. When the overall ANOVA was ificant, we performed post hoc pair-wise comparisons to compare mean values at baseline and during treatment.

The study was powered to detect a difference in flow-mediated dilation of 1. All analyses were completed using SPSS At total of 41 eligible subjects were entered into the study. Two subjects withdrew because of adverse reactions one with a pruritic rash and one with nausea. Three subjects were withdrawn because they had ificant changes in medical status while taking placebo one developed coronary restenosis, one developed unstable angina, and one suffered gastro-intestinal bleeding. Thus, 36 subjects were included in the study; their clinical characteristics according to treatment order are presented in Table 1.

As shown, the majority of subjects were men with a high prevalence of risk factors for coronary artery disease. Subjects in the placebo-first and active treatment-first groups had similar clinical characteristics. As shown, there was a strong trend for an effect of treatment on total carnitine levels, but no other ificant effects on these blood markers. For analysis of vascular function, we excluded one additional subject because of technically inadequate ultrasound images.

There were no effects of treatment on baseline flow or vasodilator function. As shown in Table 4there was no statistically ificant effect on systolic blood pressure on active treatment. As shown in Table 4the subgroups of subjects with systolic blood pressure above the median and subjects with the metabolic syndrome had ificant decreases in systolic blood pressure after active treatment.

There was no effect in the subgroup of older subjects data not shown. There was no relation between change in carnitine level and change in blood pressure in the group as a whole or in the subgroups with higher blood pressure or the metabolic syndrome data not shown. These findings suggest the possibility that these mitochondria-directed antioxidants reduce basal arterial tone, particularly in two clinically relevant subgroups.

In contrast, we observed no effect of treatment on the dilator responses to increased flow, nitroglycerin, or ischemia reactive hyperemia. Our study differs from several human studies that examined the effects of lipoic acid or carnitine on endothelial function. For example, Heitzer and colleagues observed an acute improvement in endothelium-dependent dilation of forearm microvessels following an intra-arterial infusion of lipoic acid final concentration 0.

The mechanisms ing for the increased brachial artery diameter and suggestive anti-hypertensive effects of alpha-lipoic acid and acetyl-L-carnitine in our study remain undefined. We observed no effect of treatment on serum lipids, glucose, and insulin, which might have influenced endothelial function or arterial diameter.

Experimental studies indicate that alpha-lipoic acid and acetyl-L-carnitine play important and potentially synergistic roles in normal mitochondrial function, and that reduced levels of these compounds are associated with increased mitochondrial oxidant production. It is important to point out, however, that these systemic markers may not accurately reflect events in the vascular wall. Despite the effects on blood pressure and basal diameter, it is notable that we only observed a trend for increased total serum carnitine following treatment.

It is known that acetyl-L-carnitine and alpha-lipoic acid are rapidly metabolized in human subjects with plasma half lives of 4. Similarly, the lack of effect of treatment on urine F2 isoprostanes does not rule out an effect of active treatment on oxidative stress at the tissue level. This syndrome of insulin resistance is associated with hypertension; improvement of insulin sensitivity could have an anti-hypertensive effect. Consistent with our findings, several experimental studies suggest a blood pressure-lowering effect in models of diabetes mellitus or insulin resistance.

Our study has a of limitations. First, we observed a ificant effect on baseline arterial diameter in all subjects, but the observed effects on blood pressure were ificant only in subgroup analyses. These findings are difficult to reconcile, but could reflect a preferential effect on basal conduit artery tone. Further studies will be required to confirm these findings and elucidate the responsible mechanisms. Secondly, arterial tissue was not available for mechanistic analysis in this human study, so it remains speculative whether our findings actually reflect improved mitochondrial function and reduced oxidative stress.

Third, we studied the combination of alpha-lipoic acid because these compounds may act synergistically, 32 but it remains unknown whether either compound given alone would have had a similar effect. Finally, our observations about blood pressure were based on subgroup analyses, and as such, could reflect chance findings. Balancing these limitations is the double blind, prospective, crossover de of our study. Our are consistent with prior experimental work, and the reduction in initial blood pressure, blood pressure after nitroglycerin, and the observed increase in brachial artery diameter all support an effect of active treatment on arterial Alpha lipoic acid acetyl l carnitine benefits and blood pressure.

The findings of the present study could have clinical implications. Hypertension remains the most prevalent form of cardiovascular disease, and there is a growing need for new and well-tolerated therapeutic approaches. However, our appear to be consistent with the possibility that mitochondrial Alpha lipoic acid acetyl l carnitine benefits contributes to the pathogenesis of hypertension, particularly in the setting of insulin resistance, and that therapy deed to restore mitochondrial function might prove useful for patient management.

Juvenon, Inc. Jiankang Liu measured carnitine levels. Conflict of Interest Statement: Tory Hagen is a founder of Juvenon, Inc, a company that markets the compound used in this trial. The authors have no other conflicts of interest to declare. National Center for Biotechnology InformationU. J Clin Hypertens Greenwich. Author manuscript; available in PMC Aug Craig J.

Alpha lipoic acid acetyl l carnitine benefits

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