Recent research suggests that low vitamin D may be associated with cardiovascular disease (CVD).
We prospectively evaluated the association of dietary plus supplemental vitamin D intake and serum 25(OH) vitamin D with CVD incidence in the Osteoporotic Fractures in Men (MrOS) Study. Vitamin D intake was measured using a food frequency questionnaire and self-reported supplemental intake in 3094 men (mean age 76.4 years). From a subset of this population, we measured 25(OH) vitamin D in 813 men. Median 25(OH) vitamin D was 25.3 ng/mL. During a median follow-up of 4.4 years, there were 472 CVD cases, including 371 from coronary heart disease (CHD) and 101 from cerebrovascular attack (CVA). In the 25(OH) vitamin D sub-cohort, there were 140 cases of CVD including 115 from CHD and 25 from CVA. We used a Cox proportional hazards regression to calculate hazard ratios (HR) for CVD by vitamin D quartile. After adjusting for age, season, and standard CVD risk factors, the lowest quartile of 25(OH) vitamin D (HR, 1.18; 95% CI, 0.69-2.03) and vitamin D intake (HR, 0.76; 95% CI, 0.56-1.04) were not significantly associated with CVD incidence, compared to the highest vitamin D quartiles. When 25(OH) vitamin D was further analyzed by sufficiency (≥30 ng/mL), insufficiency (≥15-29.9 ng/mL), and deficiency (<15 ng/mL), vitamin D deficiency was not significantly associated with CVD incidence compared to sufficiency (HR 1.34; 95% CI 0.65-2.77).
Vitamin D intake and serum 25(OH) vitamin D were not associated with CVD risk.
[Show abstract][Hide abstract] ABSTRACT: A poor vitamin D status, i.e. low serum levels of 25-hydroxyvitamin D [25(OH)D], is common in the general population. This finding is of concern not only because of the classic vitamin D effects on musculoskeletal outcomes, but also because expression of the vitamin D receptor (VDR) and vitamin D metabolizing enzymes in the heart and blood vessels suggests a role of vitamin D in the cardiovascular system. VDR-knockout mice suffer from cardiovascular disease (CVD), and various experimental studies suggest cardiovascular protection by vitamin D, including antiatherosclerotic, anti-inflammatory and direct cardio-protective actions, beneficial effects on classic cardiovascular risk factors as well as suppression of parathyroid hormone (PTH) levels. In epidemiological studies, low levels of 25(OH)D are associated with increased risk of CVD and mortality. Data from randomized controlled trials (RCTs) are sparse and have partially, but not consistently, shown some beneficial effects of vitamin D supplementation on cardiovascular risk factors (e.g. arterial hypertension). We have insufficient data on vitamin D effects on cardiovascular events, but meta-analyses of RCTs indicate that vitamin D may modestly reduce all-cause mortality. Despite accumulating data suggesting that a sufficient vitamin D status may protect against CVD, we still must wait for results of large-scale RCTs before raising general recommendations for vitamin D in the prevention and treatment of CVD. In current clinical practice, the overall risks and costs of vitamin D supplementation should be weighed against the potential adverse consequences of untreated vitamin D deficiency.
[Show abstract][Hide abstract] ABSTRACT: Alcohol is widely consumed across the world. It is consumed in both social and cultural settings. Until recently, two types of alcohol consumption were recognized: heavy chronic alcohol consumption or light consumption. Today, there is a new pattern of consumption among teenagers and young adults namely: binge drinking. Heavy alcohol consumption is detrimental to many organs and tissues, including bones, and is known to induce secondary osteoporosis. Some studies, however, have reported benefits from light alcohol consumption on bone parameters. To date, little is known regarding the effects of binge drinking on bone health. Here, we review the effects of three different means of alcohol consumption: light, heavy, and binge drinking. We also review the detailed literature on the different mechanisms by which alcohol intake may decrease bone mass and strength. The effects of alcohol on bone are thought to be both direct and indirect. The decrease in bone mass and strength following alcohol consumption is mainly due to a bone remodeling imbalance, with a predominant decrease in bone formation. Recent studies, however, have reported new mechanisms by which alcohol may act on bone remodeling, including osteocyte apoptosis, oxidative stress, and Wnt signalling pathway modulation. The roles of reduced total fat mass, increased lipid content in bone marrow, and a hypoleptinemia are also discussed.
Osteoporosis International 09/2011; 23(1):1-16. DOI:10.1007/s00198-011-1787-7 · 4.17 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Recent studies suggest an association between vitamin D activity and cardiometabolic risk.
We investigated vitamin D status and its association with subclinical atherosclerosis in a population-based cohort study, the Korean Longitudinal Study on Health and Aging (KLoSHA).
Participants were 439 men and 561 women aged 65 yr or older who were recruited by random stratified sampling for KLoSHA.
Anthropometric and biochemical parameters, the concentration of 25-hydroxyvitamin D (25-OHD), and intact PTH were measured.
We evaluated the coronary artery calcium score and stenosis using multidetector-row cardiac computed tomography, the intima-media thickness using carotid sonography, pulse wave velocity, and the ankle-brachial index.
Among the participants, 49.8, 44.2, and 6.0% had 25-OHD deficiency (<15 ng/ml), insufficiency (15-29.9 ng/ml), and adequacy (≥30 ng/ml), respectively. The frequency of coronary artery stenosis (>50%) differed between 25-OHD categories: 18.5, 12.9, and 1.9% in the 25-OHD-deficient, -insufficient, and -adequate groups, respectively (P < 0.05). After adjusting for cardiometabolic risks and intact PTH concentration, multivariate regression analysis showed that participants with a low 25-OHD concentration had a higher risk of significant coronary artery stenosis; the odds ratios were 2.08 for 25-OHD concentration of 15-29.9 ng/ml vs. at least 30 ng/ml and 3.12 for 25-OHD concentration below 15 ng/ml vs. at least 30 ng/ml (both P < 0.05).
The association between 25-OHD inadequacy and subclinical atherosclerosis underscores the clinical implications of vitamin D status. An intervention strategy to increase vitamin D level through vitamin D-fortified diet and adequate sun exposure may mitigate the consequences of vitamin D deficiency.
The Journal of Clinical Endocrinology and Metabolism 01/2012; 97(1):169-78. DOI:10.1210/jc.2011-1580 · 6.21 Impact Factor
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