Major Finding: Vitamin D deficiency was associated with a 3.3-fold increased likelihood of CAC being present at 3 years after adjusting statistically for age, gender, and hours of exposure to daylight.
Data Source: 374 type 1 diabetes patients with a mean age of 40 years in the CACTI study.
Disclosures: The CACTI study was funded by the National Institutes of Health. Dr. Rewers declared having no relevant financial interests.
KEYSTONE, COLO. – Vitamin D deficiency strongly predicted rapid progression of coronary artery calcification in adults with type 1 diabetes in a large, prospective study.
The association between low vitamin D and progression of coronary artery calcification was independent of the standard coronary artery disease risk factors. This suggests vitamin D may be related to early coronary atherosclerosis through a novel pathway, Dr. Marian Rewers observed at the conference, sponsored by the University of Colorado and the Children's Diabetes Foundation at Denver.
The findings came from the prospective CACTI (Coronary Artery Calcification in Type 1 Diabetes) study. This portion of CACTI included 374 type 1 diabetes patients with a mean age of 40 years. More than half were women. Coronary artery calcification (CAC) was measured by electron-beam CT at baseline and 3- and 6-year follow-up. Serum 25-hydroxyvitamin D was measured at the 3-year mark.
One-quarter of the subjects had insufficient vitamin D – a serum level of 20–30 ng/mL. Another 10% were vitamin D deficient. Deficiency was associated with a 3.3-fold increased likelihood of CAC at 3 years after adjustment for age, gender, and hours of exposure to daylight. Patients with vitamin D insufficiency had an adjusted significant 1.8-fold increased risk, said Dr. Rewers, principal investigator for CACTI.
Among subjects who were free of CAC at the 3 years, vitamin D deficiency predicted development of CAC between years 3 and 6 of follow-up. A novel finding in CACTI was that vitamin D deficiency at 3 years was a significant predictor of developing CAC during the next 3 years only in the subgroup with the vitamin D receptor M1T CC genotype. Vitamin D deficiency in patients with the CC genotype was associated with a 6.5-fold increased likelihood of CAC, compared with that of subjects with a normal vitamin D level.
In contrast, vitamin D deficient patients with the CT or TT genotypes weren't at significantly increased risk, noted Dr. Rewers, professor of pediatrics and preventive medicine, and clinical director of the Barbara Davis Center for Childhood Diabetes at the university.
CAC is a well-established marker of arterial plaque burden and a strong predictor of future coronary events. The CACTI findings suggest vitamin D may be involved in the early stages of CAC.
Audience members asked Dr. Rewers and other speakers how much vitamin D they're taking.
“Every time I come home from a medical meeting I take more vitamin D,” quipped Dr. David M. Kendall, chief scientific and medical officer for the American Diabetes Association and a diabetologist at the University of Minnesota, Minneapolis. He was referring to evidence suggesting benefits ranging from cardioprotection to anticancer and antidementia effects and beyond.
Like Dr. Kendall, Dr. Matthew C. Riddle now takes 2,000 mg of vitamin D daily.
“We don't know the answer as to the 'right' amount. But the risk vs. benefit is appealing. There are some real potential benefits,” said Dr. Riddle, professor of medicine at Oregon Health & Science University, Portland.
Vitamin D may be related to early coronary atherosclerosis through a novel pathway.
Source DR. REWERS