Publications

CONTEXT

A single measurement of 25-hydroxyvitamin D (25 [OH] D) may not accurately reflect long-term vitamin D status. Little is known about change in 25(OH)D levels over time, particularly among blacks.

OBJECTIVE

The objective of the study was to determine the longitudinal changes in 25(OH)D levels among Atherosclerosis Risk in Communities (ARIC) study participants.

DESIGN

This was a longitudinal study.

SETTING

The study was conducted in the general community.

PARTICIPANTS

A total of 9890 white and 3222 black participants at visit 2 (1990-1992), 888 whites and 876 blacks at visit 3 (1993-1994), and 472 blacks at the brain visit (2004-2006) participated in the study.

MAIN OUTCOME MEASURE

The 25(OH)D levels were measured, and regression models were used to assess the associations between clinical factors and longitudinal changes in 25(OH)D.

RESULTS

Vitamin D deficiency (<50 nmol/L [<20 ng/mL]) was seen in 23% and 25% of whites at visits 2 and 3, and in 61%, 70%, and 47% of blacks at visits 2, 3, and the brain visit, respectively. The 25(OH)D levels were correlated between visits 2 and 3 (3 y interval) among whites (r = 0.73) and blacks (r = 0.66). Among blacks, the correlation between visit 2 and the brain visit (14 y interval) was 0.33. Overall, increases in 25(OH)D levels over time was associated with male gender, use of vitamin D supplements, greater physical activity, and higher high-density lipoprotein-cholesterol (P < .001). Decreases in 25(OH)D levels over time were associated with current smoking, higher body mass index, higher education, diabetes, and hypertension (all P < .05).

CONCLUSIONS

Among US blacks and whites, 25(OH)D levels remained relatively stable over time. Certain modifiable lifestyle factors were associated with change in 25(OH)D levels over time.

BACKGROUND

Alcohol use may accelerate HIV disease progression, but the plausible biological mechanisms have not been clearly elucidated.

METHODS

HIV-positive persons who were not on antiretroviral therapy (ART) completed the baseline assessment for a longitudinal study examining the association of alcohol use with HIV disease markers. Oversampling drinkers, baseline samples were tested for markers of monocyte activation (soluble CD14 [sCD14]), inflammation (interleukin-6 [IL-6]-6), and coagulation (d-dimer). We defined "unhealthy alcohol use" as testing positive using the Alcohol Use Disorders Identification Test-Consumption (≥3 for women and ≥4 for men) in the past 3 months or testing positive using a biomarker of heavy drinking, phosphatidylethanol (≥50 ng/ml). Multiple linear regression was used to examine the associations of unhealthy alcohol use with sCD14, log10 IL-6, and d-dimer.

RESULTS

Compared to those who were abstinent from alcohol, unhealthy drinkers had significantly higher sCD14 levels (mean = 1,676 vs. 1,387 ng/ml; mean difference [95% confidence interval (CI)] = 289 [83, 495], p < 0.01). In analyses adjusted for demographic factors, current cigarette smoking, and HIV disease markers, unhealthy drinkers continued to display significantly higher sCD14 levels compared to those who were abstinent from alcohol (adjusted mean = 1,670 vs. 1,406 ng/ml; adjusted mean difference [95% CI] = 264 [47, 480], p = 0.02). Unhealthy alcohol use was not significantly associated with IL-6 or d-dimer levels.

CONCLUSIONS

Unhealthy alcohol use was independently associated with a marker of monocyte activation (i.e., higher sCD14) that predicts mortality in treated HIV infection. Longitudinal research should examine whether unhealthy alcohol use predicts changes in sCD14 prior to and following ART initiation.