Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Monday, February 27, 2017

Increase in noncalcified plaque associated with testosterone treatment in older men

Well your doctor has a lot of studying to do. 

Testosterone Improves Woman’s Brain Functions

FDA Concludes Testosterone Use May Increase Risk of Cardiovascular Events


FDA warns about blood clot risk with testosterone products


Testosterone increases neurotoxicity of glutamate in vitro and ischemia-reperfusion injury in an animal model


Thinking with your gonads: testosterone and cognition


Effect of testosterone on functional recovery in a castrate male rat stroke model


Lower Testosterone Levels Predict Incident Stroke and Transient Ischemic Attack in Older Men


Could androgens maintain specific domains of mental health in aging men by preserving hippocampal neurogenesis?


 The latest here:

Increase in noncalcified plaque associated with testosterone treatment in older men

Testosterone treatment in older men was linked to a significantly greater increase in coronary artery noncalcified plaque volume, according to a new study in JAMA.
“Although testosterone replacement is increasingly being used clinically, the [CV] benefits and risk of testosterone administration to older men with age-related decline in testosterone levels remain uncertain,” Matthew J. Budoff, MD, professor of medicine at David Geffen School of Medicine at UCLA and program director and director of cardiac CT at Harbor-UCLA Medical Center, and colleagues wrote. “Several observational studies show an inverse association between serum testosterone concentration and adverse [CV] outcomes, the metabolic syndrome, diabetes, and mortality, independent of traditional [CV] risk factors.”
In a double blind, placebo-controlled trial, Budoff and colleagues analyzed 170 men aged 65 years or older with an average of two serum testosterone levels lower than 275 ng/dL and symptoms suggestive of hypogonadism. Participants were enrolled between June 2010 and June 2014 and were randomly assigned testosterone gel (n = 82) or placebo gel (n = 88) for 12 months.
Matt Budoff
Matthew J. Budoff
Of those enrolled, data were available for 138 participants (73 receiving intervention, 65 receiving placebo; mean age, 71 years; 81% white). At baseline, 50.7% participants (n = 70) had a coronary artery calcification (CAC) score higher than 300 Agatston units.
The primary outcome was noncalcified plaque volume and was determined by coronary CTA.
From baseline to 12 months, participants in the testosterone arm had a significantly greater increase in noncalcified plaque volume (from median value 204 mm3 to 232 mm3) compared with placebo (from median value 317 mm3 to 325 mm3) with an estimated difference of 41 mm3 (95% CI, 14-67; P = .003).
The median total plaque volume increased in the testosterone group from 272 mm3 to 318 mm3, compared with 499 mm3 to 541 mm3 for placebo (estimated difference, 47 mm3; 95% CI, 13-80; P = .006). The median CAC score decreased in in the testosterone group (from 255 to 244 Agatston units) and increased in the placebo group (from 494 to 503 Agatston units) from baseline to 12 months (estimated difference, –27 Agatston units; 95% CI, –80 to 26 Agatston units), according to the researchers.
No one in either group had a major adverse CV event.
“The increase in coronary artery noncalcified and total plaque volumes in men treated with testosterone is concerning because any limitation of the vascular lumen could be considered deleterious,” Budoff and colleagues wrote. “The clinical significance of these increases could depend on the differential effects of testosterone on the individual components of noncalcified plaque.”
The researchers concluded that larger studies are needed to understand the clinical implications. – by Cassie Homer

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