Deans' stroke musings

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Wednesday, October 12, 2016

Calcium Intake From Diet and Supplements and the Risk of Coronary Artery Calcification and its Progression Among Older Adults: 10‐Year Follow‐up of the Multi‐Ethnic Study of Atherosclerosis (MESA)

Read the conclusion a couple of times to understand it properly, that way you can educate your doctor.
http://jaha.ahajournals.org/content/5/10/e003815.full
  1. Erin D. Michos, MD, MHS, FACC, FAHA (edonnell@jhmi.edu)*,8
+ Author Affiliations
  1. 1Department of Nutrition, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, NC
  2. 2Department of Epidemiology, University of Washington, Seattle, WA
  3. 3Department of Epidemiology and Biostatistics, Indiana University, Bloomington, IN
  4. 4Division of Public Health Sciences, Wake Forest School of Medicine, Winston Salem, NC
  5. 5Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA
  6. 6Patient‐Centered Outcomes Research Institute, Washington, DC
  7. 7Division of Cardiology, Los Angeles Biomedical Research Institute at Harbor‐UCLA Medical Center, Torrance, CA
  8. 8Division of Cardiology, Johns Hopkins University, Baltimore, MD
  1. *Correspondence to:
    Erin D. Michos, MD, MHS, FACC, FAHA, Division of Cardiology, Ciccarone Center for the Prevention of Heart Disease, Johns Hopkins University School of Medicine, Blalock 524‐B, 600 N Wolfe St, Baltimore, MD 21287. E‐mail: edonnell@jhmi.edu
  • Received May 31, 2016.
  • Accepted August 16, 2016.
This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

Abstract

Background Recent randomized data suggest that calcium supplements may be associated with increased risk of cardiovascular disease (CVD) events. Using a longitudinal cohort study, we assessed the association between calcium intake, from both foods and supplements, and atherosclerosis, as measured by coronary artery calcification (CAC).
Methods and Results We studied 5448 adults free of clinically diagnosed CVD (52% female; aged 45–84 years) from the Multi‐Ethnic Study of Atherosclerosis. Baseline total calcium intake was assessed from diet (using a food frequency questionnaire) and calcium supplements (by a medication inventory) and categorized into quintiles. Baseline CAC was measured by computed tomography, and CAC measurements were repeated in 2742 participants ≈10 years later. At baseline, mean calcium intakes across quintiles were 313.3, 540.3, 783.0, 1168.9, and 2157.4 mg/day. Women had higher calcium intakes than men. After adjustment for potential confounders, among 1567 participants without baseline CAC, the relative risk (RR) of developing incident CAC over 10 years, by quintile 1 to 5 of calcium intake, were 1 (reference), 0.95 (0.79–1.14), 1.02 (0.85–1.23), 0.86 (0.69–1.05), and 0.73 (0.57–0.93). After accounting for total calcium intake, calcium supplement use was associated with increased risk for incident CAC (RR=1.22 [1.07–1.39]). No relation was found between baseline calcium intake and 10‐year changes in log‐transformed CAC among those participants with baseline CAC >0.
Conclusions High total calcium intake was associated with a decreased risk of incident atherosclerosis over long‐term follow‐up, particularly if achieved without supplement use. However, calcium supplement use may increase the risk for incident CAC.

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