Posted September 4, 2012: by Bill Sardi
Comment: Postmenopausaal women don’t have cholesterol/heart disease, they have calcium/heart disease. As their bones wither with the loss of estrogen, calcium is lost from bone and deposited in arteries.
The largest increase in cardiovascular risk is immediately following the onset of menopause. Measuring cholesterol, C-reactive protein, insulin resistance, amounted to measuring incorrect markers of disease, not disease itself. Women’s arteries stiffen due to calcifications. Calcium represents ~50% of arterial plaque, cholesterol about 3-20%. This is why supplemental calcium also increases the risk for mortal heart attacks.
You have to ask yourself, if doctor’s don’t know this, why are they treating your mother? Vitamin D is an anti-calcifying agent, not an anti-cholesterol agent. It appears this study was intentionally designed to fail.
Bill Sardi, Knowledge of Health, Inc.
The Journal of Clinical Endocrinology & MetabolismAugust 3, 2012 jc.2012-2126
Address all correspondence and requests for reprints to: Helen M. Macdonald, Ph.D., Health Sciences Building, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, United Kingdom. E-mail: firstname.lastname@example.org.
Context: Observational studies show an association between low vitamin D status assessed by circulating 25-hydroxyvitamin D and cardiovascular events and mortality. Data from randomized controlled trials are limited.
Objective: The aim of this study was to test whether daily doses of vitamin D3 at 400 or 1000 IU/d for 1 yr affected conventional markers of cardiovascular disease (CVD) risk.
Design: We conducted a parallel-group, double-blind, placebo-controlled randomized controlled trial. Randomization was computer generated. Participants and study investigators were blinded to intervention groupings throughout the trial.
Setting: The study was conducted at the Clinical Research Facility, University of Aberdeen, United Kingdom.
Participants: A total of 305 healthy postmenopausal women aged 60–70 yr were recruited for the study.
Intervention: Each woman received a daily capsule of 400 or 1000 IU vitamin D3 or placebo randomly allocated.
Main Outcome Measures: Primary outcomes were serum lipid profile [total, high-density lipoprotein, and low-density lipoprotein cholesterol; triglycerides; and apolipoproteins A-1 and B100], insulin resistance (homeostatic model assessment), inflammatory biomarkers (high-sensitivity C-reactive protein, IL-6, soluble intracellular adhesion molecule-1), and blood pressure.
Results: A total of 265 (87%) participants completed all study visits. Small differences between groups for serum apolipoprotein B100 change [repeated measures ANOVA, P = 0.04; mean (SD), −1.0 (10.0) mg/dl (400 IU); −1.0 (10.0) mg/dl (1000 IU); and +0.02 (10.0) mg/dl (placebo)] were not considered clinically significant. Other systemic markers for CVD risk remained unchanged. There was significant seasonal variation in systolic and diastolic blood pressure independent of vitamin D dose (P < 0.001, linear mixed model). Mean (SD) reduction in systolic blood pressure from winter to summer was −6.6 (10.8) mm Hg.
Conclusions: Improving vitamin D status through dietary supplementation is unlikely to reduce CVD risk factors. Confounding of seasonality should be recognized and addressed in future studies of vitamin D.