Tuesday, February 14, 2017

Association of exhaled carbon monoxide with stroke incidence and subclinical vascular brain injury

You'll have to ask your doctor about all these benefits vs. this negative article.

Carbon Monoxide Releasing Molecule-A1 (CORM-A1) Improves Neurogenesis: Increase of Neuronal Differentiation Yield by Preventing Cell Death

Carbon monoxide may actually protect the brain from damage after subarachnoid hemorrhage

Deadly carbon monoxide prevents miscarriage

we found that inhaled low dose carbon monoxide was anti-inflammatory. It reduced the amount of cell death (apoptosis), and increased levels of the anti-apoptotic molecule BAG-1, in the placenta and additionally increased the level of vascular endothelial growth factor (VEGF), which is associated with angiogenesis and blood vessel repair." 

 

 


The negative article here:

Association of exhaled carbon monoxide with stroke incidence and subclinical vascular brain injury

Stroke, 02/12/2016
The authors related exhaled carbon monoxide (CO) to magnetic resonance imaging measures of subclinical cerebrovascular disease cross–sectionally and to incident stroke/transient ischemic attack prospectively in the Framingham Offspring study. In this large, community–based sample of individuals without clinical stroke/transient ischemic attack at baseline, higher exhaled CO was associated with a greater burden of subclinical cerebrovascular disease cross–sectionally and with increased risk of stroke/transient ischemic attack prospectively. Further investigation is necessary to explore the biological mechanisms linking elevated CO with stroke.

Methods

  • The authors measured exhaled CO in 3313 participants (age 59±10 years; 53% women), and brain magnetic resonance imaging was available in 1982 individuals (age 58±10 years; 54% women).
  • Participants were analyzed according to tertiles of exhaled CO concentration.

Results

  • In age- and sex-adjusted models, the highest tertile of exhaled CO was associated with lower total cerebral brain volumes, higher white-matter hyperintensity volumes, and greater prevalence of silent cerebral infarcts (P<0.05 for all).
  • The results for total cerebral brain volume and white-matter hyperintensity volume were consistent after removing smokers from the sample, and the association with white-matter hyperintensity volume persisted after multivariable adjustment (P=0.04).
  • In prospective analyses (mean follow-up 12.9 years), higher exhaled CO was associated with 67% (second tertile) and 97% (top tertile) increased incidence of stroke/transient ischemic attack relative to the first tertile that served as referent (P<0.01 for both).
  • These results were consistent in nonsmokers and were partially attenuated upon adjustment for vascular risk factors.
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