Novel antioxidant [MitoQ] makes old blood vessels seem young again

Andy

Retired committee member
Older adults who take a novel antioxidant that specifically targets cellular powerhouses, or mitochondria, see aging of their blood vessels reverse by the equivalent of 15 to 20 years within six weeks, according to new CU 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 diseasethe 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.
https://www.colorado.edu/today/2018/04/19/novel-antioxidant-makes-old-blood-vessels-seem-young-again
 
Annoyingly only 20 test subjects but interesting ...not sure whether there is a tangible link to how this translates into better health rather than a general association with improvements to stiffening of arteries in old age. Be interesting to know whether there is a difference taking the horrendously expensive MitoQ once per day vs a larger dose of the supposedly inferior (but cheaper) ubiquinol several times a day?

The Montoya study though discounts this as an effective treatment I seem to recall....(my recall is pretty poor so forgive me if this is misremembered) but I seem to remember that this used weak methodology?

I wish we could have something more definitive like 200 test subjects double blinded with a detailed objective set of measures over 3-6 months.
 
...not sure whether there is a tangible link to how this translates into better health rather than a general association with improvements to stiffening of arteries in old age
According to the article,
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.
(My bold).
 
Something I meant to add to my original post.

It also makes me wonder whether this is a good or a bad thing for us. From memory, there is some evidence for endothelial dysfunction in ME patients, if this improved the range of function (dilation and contraction) then great, if it simply helps to dilate blood vessels then not so great.
 
It also makes me wonder whether this is a good or a bad thing for us. From memory, there is some evidence for endothelial dysfunction in ME patients,
According to the study done by D Newton and colleagues, as summarised by ME research,
Flow-mediated dilatation was significantly lower in the 30 CDC-defined patients than in the 27 age and gender-matched control subjects (median of 5.99 versus 9.24%, respectively, p<0.001). Importantly, after glyceryl trinitrate was given to patients and controls, there was no significant difference between the groups, demonstrating that the impaired flow-mediated dilatation was most likely to be due to endothelial dysfunction and not to some other cause (such as damaged smooth muscle). As regards the small vessels, ME/CFS patients had a significantly lower blood flow response in forearm skin than did control subjects (peak flow 38.33 versus 69.80 arbitrary units, respectively, p=0.002). ME/CFS patients also had significantly higher levels of serum hs-CRP and triglycerides, and lower levels of HDL cholesterol in blood samples – all indicative of increased oxidative stress and cardiovascular risk.

The importance of this investigation was that it was the first ever to measure and demonstrate vascular endothelial dysfunction directly in ME/CFS patients. Since the experiments measured the response of the vascular endothelium to a “shear stress” (i.e., the stopping and starting of blood flow), the reduced vascular responses support the hypothesis that some functions of the endothelium are damaged in ME/CFS patients, both in large vessels and in the small-vessel microcirculation. The authors of the scientific paper say that their findings “build on previous work reporting indirect markers of endothelial dysfunction, such as increased oxidative stress, inflammation and arterial stiffness”, and that these results taken together with previous evidence “point to an increased cardiovascular risk in ME/CFS patients”.
I don't know much about this, but it sounds as if MitoQ's effects - increased flow mediated dilation, reduced arterial stiffness, reduced oxidative stress - could be potentially helpful for us.

(The Newton paper is currently available via http://sci-hub.hk, doi.org/10.1016/j.ijcard.2011.10.030)
 
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