Deans' stroke musings: Warfarin use and fracture risk: an evidence-based mechanistic insight

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 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:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. 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.

Tuesday, October 14, 2014

Warfarin use and fracture risk: an evidence-based mechanistic insight

Something for your doctor to maybe warn you about.
http://link.springer.com/article/10.1007/s00198-014-2912-1

This is an excerpt from the content

Dear Editor,

There is a long-standing debate on the association between use of warfarin, prescribed to millions of people to decrease their risk of clotting, and fracture risk [1]. In a large population-based cohort in the UK, Misra and colleagues [2] found that warfarin use was not linked to an increase in fracture risk. Here, we would like to present an evidence-based, reasonable insight into the mechanisms by which this drug affects bone strength.

Osteocalcin, the most abundant non-collagenous protein in bone, is incorporated into bone through vitamin K-dependent γ-carboxylation. Warfarin, a vitamin K antagonist, decreases osteocalcin content in bone and impairs bone material hardness in rats [3], which is consistent with data in mice that osteocalcin deficiency causes a decrease in bone tissue hardness [4]. Consistently, in older patients undergoing chronic therapy with oral vitamin K antagonists [5], undercarboxylated osteocalcin levels in blood were inversely related to cortical ul ...