Author + information
- Received August 16, 2013
- Revision received October 25, 2013
- Accepted October 25, 2013
- Published online January 1, 2014.
- Adela Hruby, PhD, MPH∗,
- Christopher J. O'Donnell, MD, MPH†,‡,§,
- Paul F. Jacques, ScD∗,
- James B. Meigs, MD, MPH§,‖,
- Udo Hoffmann, MD, MPH§,¶ and
- Nicola M. McKeown, PhD∗∗ ()
- ∗Nutritional Epidemiology Program, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts
- †National Heart, Lung, and Blood Institute (NHLBI) Division of Intramural Research, and NHLBI's Framingham Heart Study, Framingham, Massachusetts
- ‡Cardiovascular Division, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts
- §Harvard Medical School, Boston, Massachusetts
- ‖General Medicine Division, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts
- ¶Massachusetts General Hospital Cardiac MR PET CT Program and the Department of Radiology, Massachusetts General Hospital, Boston, Massachusetts
- ↵∗Reprint requests and correspondence:
Dr. Nicola M. McKeown, Nutritional Epidemiology Program, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, 9th Floor, Boston, Massachusetts 02111.
Objectives The aim of this study was to examine whether magnesium intake is associated with coronary artery calcification (CAC) and abdominal aortic calcification (AAC).
Background Animal and cell studies suggest that magnesium may prevent calcification within atherosclerotic plaques underlying cardiovascular disease. Little is known about the association of magnesium intake and atherosclerotic calcification in humans.
Methods We examined cross-sectional associations of self-reported total (dietary and supplemental) magnesium intake estimated by food frequency questionnaire with CAC and AAC in participants of the Framingham Heart Study who were free of cardiovascular disease and underwent Multi-Detector Computed Tomography (MDCT) of the heart and abdomen (n = 2,695; age: 53 ± 11 years), using multivariate-adjusted Tobit regression. CAC and AAC were quantified using modified Agatston scores (AS). Models were adjusted for age, sex, body mass index, smoking status, systolic blood pressure, fasting insulin, total-to-high-density lipoprotein cholesterol ratio, use of hormone replacement therapy (women only), menopausal status (women only), treatment for hyperlipidemia, hypertension, cardiovascular disease prevention, or diabetes, as well as self-reported intake of calcium, vitamins D and K, saturated fat, fiber, alcohol, and energy. Secondary analyses included logistic regressions of CAC and AAC outcomes as cut-points (AS >0 and AS ≥90th percentile for age and sex), as well as sex-stratified analyses.
Results In fully adjusted models, a 50-mg/day increment in self-reported total magnesium intake was associated with 22% lower CAC (p < 0.001) and 12% lower AAC (p = 0.07). Consistent with these observations, the odds of having any CAC were 58% lower (p trend: <0.001) and any AAC were 34% lower (p trend: 0.01), in those with the highest compared to those with the lowest magnesium intake. Stronger inverse associations were observed in women than in men.
Conclusions In community-dwelling participants free of cardiovascular disease, self-reported magnesium intake was inversely associated with arterial calcification, which may play a contributing role in magnesium's protective associations in stroke and fatal coronary heart disease.
- abdominal aortic calcification
- computed tomography
- coronary artery calcification
- Framingham Heart Study
At the time of writing, Dr. Hruby was supported by an American Heart Association Predoctoral Fellowship. This work was also supported by the National Heart, Lung, and Blood Institute's Framingham Heart Study (contract no. N01-HC-25195) and the United States Department of Agriculture (USDA agreement no. 58-1950-0-014). Dr. Jacques has been a member of the Bay State Milling Nutrition Science Advisory Council and of the Dannon Yogurt Advisory Board. Dr. Meigs is supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) (K24 DK080140). All authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received August 16, 2013.
- Revision received October 25, 2013.
- Accepted October 25, 2013.
- American College of Cardiology Foundation