Serum 25-Hydroxy Vitamin D and Insulin Resistance, Metabolic Syndrome, and Glucose Intolerance Among Arab Americans

The methods have been described in detail elsewhere (5,–7). Briefly, we studied 542 randomly selected Arab Americans 20–75 years of age. Demographic, anthropometric, and behavioral characteristics were measured. To examine food preferences, we calculated the ratio of Arab meals to total meals consumed in 1 week; a higher ratio indicates consumption of more Middle Eastern foods (diet rich in meat, yogurt, grains, and vegetables, and low in food fortified with vitamin D such as milk and breakfast cereals). Subjects performed strenuous physical activity if they engaged in exercise for ≥20 min that made them breathe hard and sweat ≥3 times per week. Those engaging in strenuous activity <3 times weekly performed moderate physical activity and all others were considered inactive. Smoking status was self-reported and verified by serum cotinine (Siemens Healthcare Diagnostics, Deerfield, IL). Acculturation was assessed with a validated four-item survey.

Fasting glucose, insulin, lipids, and A1C were measured and glucose tolerance assessed with 75-g oral glucose tolerance tests. IR was defined as homeostasis model assessment of insulin resistance ≥3.8 (8). Subjects meeting the revised National Cholesterol Education Program Adult Treatment Panel III criteria were defined as having MS (9). Glucose intolerance was defined as impaired fasting glucose, impaired glucose tolerance, or diabetes (10).

Serum 25-OH-D samples were coded, centrifuged, and stored at −70°C. In 2009, serum 25-OH-D was measured using the ¹²⁵I Radioimmunoassay kit (DiaSorin, Stillwater, MN) and quality control materials provided by the manufacturer. The inter-assay coefficients of variation are 7.3% at 13.7 ng/ml and 9.6% at 53.4 ng/ml. 25-OH-D status was classified as: deficiency, <5 ng/ml; insufficiency, 5 to <20 ng/ml; hypovitaminosis D, 20 to <40 ng/ml; sufficiency, 40 to <100 ng/ml; and toxicity, ≥100 ng/ml (11).

All analyses were performed separately by sex. Data are expressed as means ± SD or percentage. Continuous or categorical data were analyzed utilizing ANOVA or χ² tests. 25-OH-D levels were described by demographic, anthropometric, behavioral characteristics and by measures of disease status. Spearman correlation coefficients were calculated to examine the association between 25-OH-D levels and measures of disease status. Analyses were performed using SAS, version 9.1 (SAS Institute, Cary, NC).

The mean age of the subjects was 38 ± 13 years and 39% were men. The mean BMI was 28.4 ± 5.5 kg/m². Subjects consumed mostly traditional Middle Eastern foods. The majority of the subjects were inactive or only moderately physically active (52%). One-third reported smoking cigarettes. Acculturation was low. IR was present in 46%, MS in 33%, and glucose intolerance in 42% of subjects.

Vitamin D insufficiency was present in 75% and hypovitaminosis D in 24%; only four subjects had 25-OH-D levels in the normal range. Serum 25-OH-D levels were lower in women (14.1 ± 7.1) than men (18.1 ± 6.4) (P < 0.0001). Only two subjects reported taking vitamin D supplements.

Vitamin D levels as a function of glucose tolerance status and other factors is shown in Table 1. In men, 25-OH-D levels were lower in those with glucose intolerance than in those who were normoglycemic (P = 0.005). No such difference was found in women. 25-OH-D levels also varied by season (P < 0.0001) and by level of cotinine (P = 0.04) in men. Men with IR, hypertriglyceridemia, and glucose intolerance had lower serum 25-OH-D levels than men who were insulin sensitive (P = 0.01), had triglycerides <150 mg/dl (P = 0.0016), and fasting plasma glucose <100 mg/dl (P = 0.023). Decreased 25-OH-D levels were present in women with MS compared with those without MS (P = 0.0086). Women with low HDL levels had low 25-OH-D levels compared with those with HDL levels ≥50 mg/dl (P = 0.0016).

In men, serum 25-OH-D was negatively correlated with homeostasis model assessment of insulin resistance (r = −0.19; P = 0.0043), triglycerides (r = −0.18; P = 0.0069), fasting plasma glucose (r = −0.15; P = 0.027), and A1C (r = −0.14; P = 0.038). In women, 25-OH-D was positively correlated with HDL (r = 0.19; P = 0.0008).

This study provides population-based estimates of vitamin D status among Arab American and reports associations between 25-OH-D levels and IR, MS, and glucose intolerance. Our findings are similar to those reported from a convenience sample of 87 Arab American women and a representative sample of 6,228 people in the United States (12–13) in whom vitamin D levels were not adequate. 25-OH-D levels have been inversely associated with diabetes in non-Hispanic whites and Mexican Americans, but not in non-Hispanic blacks despite their high prevalence of diabetes and inadequate vitamin D levels (14–15). Our findings in Arab American males are similar to those reported in Hispanic whites and Mexican Americans.

There are several potential limitations to our study. First, factors influencing skin synthesis of vitamin D such as traditional Islamic dress, ultraviolet exposure, and sunscreen utilization and dietary consumption of vitamin D were not assessed. Second, the cross-sectional design of our study limited our ability to examine causal relationships between levels of 25-OH-D and IR, MS, and glucose intolerance.

In summary, the prevalence of inadequate vitamin D levels is high among Arab American men and women. Very few subjects reported taking supplements. In men, lower 25-OH-D levels were associated with IR, components of MS, and glucose intolerance. In women, lower 25-OH-D was associated with lower HDL cholesterol levels. Greater public awareness and interventions to encourage vitamin D consumption are needed in the Arab American community.

This study was funded by the American Diabetes Association and through a Clinical and Translational Science Award from the Michigan Institute for Clinical & Health Research by Grant UL1RR024986 from the National Institutes of Health. Statistical support was provided by the Biostatistics and Economic Modeling Core, and laboratory analysis was conducted by the Chemistry Laboratory Core of the Michigan Diabetes Research and Training Center funded by Grant DK020572 from the National Institute of Diabetes and Digestive and Kidney Diseases.

No potential conflicts of interest relevant to this article were reported.