| |
Chronic Supplementation With a Mitochondrial Antioxidant (MitoQ) Improves Vascular Function in Healthy Older Adults
|
| |
| |
Editorial coming in next email.
Download the PDF here
"Overall, although future studies are needed to elucidate responsible mechanisms, our findings provide the first evidence for chronic MitoQ supplementation lowering aortic stiffness in late MA/O adults with age-related aortic stiffening. These data have important implications for reducing the risk of CVD and numerous other age-related disorders linked with elevated aortic stiffness.”
Perspectives
Here, we demonstrate for the first time that supplementation with the mitochondria-targeted antioxidant MitoQ is safe and well tolerated in late MA/O adults, improves vascular endothelial function (likely by suppressing excess mtROS), reduces aortic stiffness in MA/O adults with elevated initial levels, and decreases oxidized LDL, a circulating marker of oxidative stress. Collectively, these findings establish the experimental basis for conducting a larger scale clinical trial in older adults or clinical populations, particularly those associated with endothelial dysfunction and elevated aortic stiffness. In the broadest terms, our results provide initial support for the idea that MitoQ, and potentially other mitochondria-targeted antioxidants, may be an effective treatment for improving vascular function and possibly decreasing the risk of CVD and other clinical disorders of aging, including cognitive dysfunction and chronic kidney disease.
Novel antioxidant makes old blood vessels seem young again
https://scienmag.com/novel-antioxidant-makes-old-blood-vessels-seem-young-again/
Older adults who take a novel antioxidant that specifically targets cellular powerhouses, or mitochondria, see age-related vascular changes reverse by the equivalent of 15 to 20 years within six weeks, according to new University of Colorado Boulder research.
The study, published this week in the American Heart Association journal Hypertension, adds to a growing body of evidence suggesting pharmaceutical-grade nutritional supplements, or nutraceuticals, could play an important role in preventing heart disease-the nation's No. 1 killer. It also resurrects the notion that oral antioxidants, which have been broadly dismissed as ineffective in recent years, could reap measurable health benefits if properly targeted, the authors say.
"This is the first clinical trial to assess the impact of a mitochondrial-specific antioxidant on vascular function in humans," said lead author Matthew Rossman, a postdoctoral researcher in the department of integrative physiology. "It suggests that therapies like this may hold real promise for reducing the risk of age-related cardiovascular disease."
For the study, Rossman and senior author Doug Seals, director of the Integrative Physiology of Aging Laboratory, recruited 20 healthy men and women age 60 to 79 from the Boulder area.
Half took 20 milligrams per day of a supplement called MitoQ, made by chemically altering the naturally-occurring antioxidant Coenzyme Q10 to make it cling to mitochondria inside cells.
The other half took a placebo.
After six weeks, researchers assessed how well the lining of blood vessels, or the endothelium, functioned, by measuring how much subjects' arteries dilated with increased blood flow.
Then, after a two-week "wash out" period of taking nothing, the two groups switched, with the placebo group taking the supplement, and vice versa. The tests were repeated.
The researchers found that when taking the supplement, dilation of subjects' arteries improved by 42 percent, making their blood vessels, at least by that measure, look like those of someone 15 to 20 years younger. An improvement of that magnitude, if sustained, is associated with about a 13 percent reduction in heart disease, Rossman said. The study also showed that the improvement in dilation was due to a reduction in oxidative stress.
In participants who, under placebo conditions, had stiffer arteries, supplementation was associated with reduced stiffness.
Blood vessels grow stiff with age largely as a result of oxidative stress, the excess production of metabolic byproducts called free radicals which can damage the endothelium and impair its function. During youth, bodies produce enough antioxidants to quench those free radicals. But with age, the balance tips, as mitochondria and other cellular processes produce excess free radicals and the body's antioxidant defenses can't keep up, Rossman said.
Oral antioxidant supplements like vitamin C and vitamin E fell out of favor after studies showed them to be ineffective.
"This study breathes new life into the discredited theory that supplementing the diet with antioxidants can improve health," said Seals. "It suggests that targeting a specific source-mitochondria-may be a better way to reduce oxidative stress and improve cardiovascular health with aging."
###
The study was funded by the National Institutes of Health. MitoQ Limited provided supplements and some financial support.
This summer, Rossman and Seals plan to launch a three-month follow-up study to confirm the findings in a larger number of subjects and look more closely at the impact the compound has on mitochondria.
The same lab published another study recently, showing that a compound called nicotinamide riboside may also be able to reverse vascular aging in healthy subjects.
"Exercise and eating a healthy diet are the most well-established approaches for maintaining cardiovascular health," said Seals. "But at the public health level, not enough people are willing to do that. We're looking for complementary, evidence-based options to prevent age-related changes that drive disease. These supplements may be among them.”
--------------------------------------------
Chronic Supplementation With a Mitochondrial Antioxidant (MitoQ) Improves Vascular Function in Healthy Older Adults
Matthew J. Rossman, Jessica R. Santos-Parker, Chelsea A.C. Steward, Nina Z. Bispham, Lauren M. Cuevas, Hannah L. Rosenberg, Kayla A. Woodward, Michel Chonchol, Rachel A. Gioscia-Ryan, Michael P. Murphy, Douglas R. Seals
Originally published April 16, 2018
See pdfs attached
Abstract
Excess reactive oxygen species production by mitochondria is a key mechanism of age-related vascular dysfunction. Our laboratory has shown that supplementation with the mitochondrial-targeted antioxidant MitoQ improves vascular endothelial function by reducing mitochondrial reactive oxygen species and ameliorates arterial stiffening in old mice, but the effects in humans are unknown. Here, we sought to translate our preclinical findings to humans and determine the safety and efficacy of MitoQ. Twenty healthy older adults (60-79 years) with impaired endothelial function (brachial artery flow-mediated dilation <6%) underwent 6 weeks of oral supplementation with MitoQ (20 mg/d) or placebo in a randomized, placebo-controlled, double-blind, crossover design study. MitoQ was well tolerated, and plasma MitoQ was higher after the treatment versus placebo period (P<0.05). Brachial artery flow-mediated dilation was 42% higher after MitoQ versus placebo (P<0.05); the improvement was associated with amelioration of mitochondrial reactive oxygen species-related suppression of endothelial function (assessed as the increase in flow-mediated dilation with acute, supratherapeutic MitoQ [160 mg] administration; n=9; P<0.05). Aortic stiffness (carotid-femoral pulse wave velocity) was lower after MitoQ versus placebo (P<0.05) in participants with elevated baseline levels (carotid-femoral pulse wave velocity >7.60 m/s; n=11). Plasma oxidized LDL (low-density lipoprotein), a marker of oxidative stress, also was lower after MitoQ versus placebo (P<0.05). Participant characteristics, endothelium-independent dilation (sublingual nitroglycerin), and circulating markers of inflammation were not different (all P>0.1). These findings in humans extend earlier preclinical observations and suggest that MitoQ and other therapeutic strategies targeting mitochondrial reactive oxygen species may hold promise for treating age-related vascular dysfunction.
se.
|
|
| |
| |
|
|
|
