Vitamin D Intake and Status Are Associated with Lower Prevalence of Metabolic Syndrome in U.S. Adults: National Health and Nutrition Examination Surveys 2003

Abstract

Background:

Previous reports have shown that metabolic syndrome and some metabolic syndrome components are associated with serum 25-hydroxyvitamin D [25(OH)D].

Methods:

Using the National Health and Nutrition Examination Surveys (NHANES), 2003–2006, we evaluated the associations of vitamin D intake (n=3543) and vitamin D status [25(OH)D; n=3529], with the prevalence of metabolic syndrome and its components in adults 20 years and older. Exclusion criteria included nonfasted subjects, those pregnant and/or lactating, and, for intake analyses, those with unreliable 24-h recall records. Subjects were separately classified into quartiles of vitamin D intake (both including and excluding supplements) and serum 25(OH)D. Logistic regression was used to determine odds ratios (OR) for metabolic syndrome after adjusting for multiple confounders.

Results:

Those in the highest quartile of serum 25(OH)D had 60% lower odds for metabolic syndrome as compared to those in the lowest quartile [OR=0.40; 95% confidence interval (CI) 0.27, 0.59]. Elevated waist circumference (OR=0.57; 95% CI 0.39, 0.84), low high-density lipoprotein cholesterol (HDL-C) (OR=0.54; 95% CI 0.39, 0.75), and high homeostasis model assessment of insulin resistance (HOMA-IR) (OR=0.40; 95% CI 0.29, 0.55) were the main components associated with serum 25(OH)D. Compared with the lowest vitamin D intake quartile (excluding supplements), those in the highest intake quartile had 28% lower odds for metabolic syndrome (OR=0.72; 95% CI 0.58, 0.90). No components of metabolic syndrome were significantly associated with dietary intake of vitamin D with supplements included or excluded.

Conclusions:

We conclude that higher 25(OH)D, and, to a lesser degree, greater dietary vitamin D intake, are associated with reduced prevalence of metabolic syndrome.

Introduction

S everal recent cross-sectional and prospective studies have reported increased prevalence or incidence of cardiometabolic disease with low vitamin D status, as assessed by circulating serum levels of 25-hydroxyvitamin D [25(OH)D].^1
–3 For example, 25(OH)D <37.4 nmol/L was associated with a marked increase in incident cardiovascular events [hazard ratio (HR) 1.62, 95% confidence interval (CI) 1.11, 2.36] in the Framingham Offspring Study,³ and an increased risk for myocardial infarction in the U.S. Health Professionals Study compared to those at a level of 25(OH)D, defined as ≥74.9 nmol/L.⁴

Low vitamin D status has also been associated with metabolic syndrome and its components in children, adults, and morbidly obese men and women.^5

–8 A recent systematic review of the literature and meta-analysis of 28 cross-sectional studies found 51% lower odds for metabolic syndrome and 33 and 55% lower odds for cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM) comparing the highest to the lowest serum vitamin D levels.⁹ The aim of the present investigation was to assess the relationships between 25(OH)D status, dietary vitamin D intake from foods, and total vitamin D intake including supplements with metabolic syndrome and its components in a large, nationally representative survey of U.S. adults.

Methods

Between 2003 and 2006, a representative sample of the noninstitutionalized civilian U.S. population, selected using a multistage stratified sample design, participated in the National Health and Nutrition Examination Surveys (NHANES 2003–2004 and NHANES 2005–2006). Survey participants were interviewed and invited for a clinical examination, as described elsewhere.¹⁰ Metabolic syndrome was defined according to the National Cholesterol Education Program (NCEP) criteria.¹¹ Detailed descriptions of the anthropometric, blood pressure, and laboratory procedures for each of the metabolic syndrome components have been reported elsewhere.¹² Although not part of the definition for metabolic syndrome, relationships with non-high-density lipoprotein cholesterol (non-HDL-C) and the homeostasis model assessment of insulin resistance (HOMA-IR) were also evaluated. Non-HDL-C was calculated as the difference between total cholesterol and HDL-C and ≥160 mg/dL was selected as the cutoff for elevated non-HDL-C.¹³ HOMA-IR was calculated using the following formula: fasting serum insulin (μU/mL)×fasting plasma glucose (mg/dL)/405.¹⁴ A cutoff of ≥2.5 for HOMA-IR was used to define insulin resistance, consistent with previously published reports.^15,16

Concentrations of 25(OH)D were measured in a single blood sample using radioimmunoassay and were adjusted due to assay drift.^17,18 Dietary data were obtained from a single 24-h recall in What We Eat in America, the dietary interview component of the NHANES 2003–2006¹⁹ and were analyzed using the U.S. Department of Agriculture (USDA) Food and Nutrient Database for Dietary Studies (FNDDS), versions 2.0 and 3.0 for NHANES 2003–2004 and NHANES 2005–2006, respectively. Supplement use was obtained via a questionnaire that assessed supplement practices over the previous 30-day period. Detailed descriptions of the dietary recalls and data collection are available in the NHANES Dietary Interviewer's Training Manual.²⁰

Statistical analyses were conducted with SUDAAN release 9.0 (Research Triangle Institute, Research Triangle Park, NC). The analyses for 25(OH)D included three models with adjustment for the following: model 1, age; model 2, age, sex, race or ethnicity, education, smoking status, serum cotinine, C-reactive protein, alcohol use, physical activity, sum of total fruit and vegetable Healthy Eating Index scores, daily intake of vitamin D from dietary supplements; and model 3 (metabolic syndrome components only), adjusted for all variables in model 2 plus other components of the metabolic syndrome. The dietary vitamin D analyses included the following: model 1, adjusted for daily energy intake (kcal), sex, age, race, or ethnicity; model 2, adjusted for daily energy intake (kcal), sex, age, race or ethnicity, income (% of poverty level), physical activity, TV/computer use, smoking; and model 3, adjusted for all variables in model 2 plus daily vitamin D intake from dietary supplements.

Analyses were limited to men and nonpregnant women ≥20 years of age and fasted ≥8 h. In addition, for the dietary assessments, those with unreliable dietary records as assessed by the USDA were excluded. On the basis of the final analytical sample, we created quartiles of concentrations of 25(OH)D and dietary intake of vitamin D (both with and without supplements) from their distributions determined using the sampling weights. To compare proportions across quartiles of both serum concentrations and dietary intake of vitamin D, a test for linear trend was employed. In addition, the associations between the metabolic syndrome and its components and related factors were examined by multiple logistic regression analysis. To account for the complex survey design, we used SUDAAN and the medical examination clinic sampling weights to produce weighted estimates and standard errors. Values in the text for continuous variables are reported as mean±standard error of the mean (SEM), unless otherwise specified.

Results

The characteristics of the study sample are shown in Table 1. A total of 3529 adults were included in the 25(OH)D analysis and 3543 in the dietary intake analyses. Quartile ranges for 25(OH)D (nmol/L) and dietary intake of vitamin D with and without supplements (μg/day) are shown in Tables 2 and 3. Median (minimum, maximum) values for each quartile were as follows—25(OH)D (nmol/L): Q1, 32.4 (7.5, 44.9), Q2, 49.9 (45.0, 59.9), Q3, 64.9 (60.0, 74.9), Q4, 84.9 (75.0, 215.0); dietary intake (μg/day): Q1, 0.64 (0, 1.22), Q2, 1.95 (1.23, 2.86), Q3, 4.03 (2.86, 5.67), Q4, 9.03 (5.67, 117.85); and dietary intake of food plus supplements (μg/day): Q1, 0.94 (0, 2.03), Q2, 3.64 (2.03, 5.56), Q3, 8.99 (5.56, 12.0), Q4, 16.22 (12.01, 118.52).

Table 1.

Study Sample Characteristics

	Full sample N=3543
	n (%)
Sex
Female	1705 (48.1)
Male	1838 (51.9)
Race
White	1889 (53.3)
Black/African American	725 (20.5)
Other	929 (26.2)
Ethnicity
Hispanic/Latino	787 (22.2)
Non-Hispanic/Latino	2614 (73.8)
Other	142 (4.0)
Poverty income ratio
0–1.00	547 (15.4)
1.01–1.85	773 (21.8)
1.86–3.50	946 (26.7)
>3.50	1106 (31.2)
Missing	171 (4.8)
Physical activity
None	1431 (40.4)
Light	639 (18.0)
Moderate	1108 (31.3)
Vigorous	365 (10.3)
TV/computer use (h/day)
<2	864 (24.4)
2–3	1486 (41.9)
4+	1193 (33.7)
Smoked cigarettes in past 5 days
Yes	765 (21.6)
No	2778 (78.4)
Vitamin D intake from dietary supplements
Yes	1319 (37.2)
No	2224 (62.8)

	Mean±SD
Energy intake (kcal/day)	2132±993
Body mass index (kg/m²)	28.8±6.8
Waist circumference (cm)	98.8±15.5
Systolic blood pressure (mmHg)	125.2±20.2
Diastolic blood pressure (mmHg)	68.9±13.8
Triglycerides (mg/dL)	144.9±126.0
Non-HDL-C (mg/dL)	143.8±42.7
LDL-C (mg/dL)	115.7±35.5
HDL-C (mg/dL)	54.2±16.1
Glucose (mg/dL)	105.3±32.1
HOMA-IR	3.05±3.81

SD, standard deviation; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; HOMA-IR, homeostasis model assessment of insulin resistance.

Table 2.

Adjusted Prevalence, Odds Ratios and 95% Confidence Intervals for Metabolic Syndrome, Metabolic Syndrome Components, and HOMA-IR by Quartiles of Serum Vitamin D Concentration Among 3529 U.S. Adults Aged ≥20 years, NHANES 2003–2004 and NHANES 2005–2006

	Quartiles of 25(OH)D (nmol/L) ^a
	1 (7.5–44.9)	2 (45.0–59.9)	3 (60.0–74.9)	4 (75.0–215.0)	P for trend
Metabolic syndrome^b
Model 1^c
Prevalence	41.9±1.7	37.1±2.7	35.1±2.9	24.4±2.4
OR (95% CI)	1.00	0.80 (0.60, 1.07)	0.73 (0.53, 1.01)	0.42 (0.30, 0.58)	<0.001
Model 2^d
Prevalence	42.5±2.2	36.5±2.4	34.6±2.7	24.9±2.4
OR (95% CI)	1.00	0.75 (0.54, 1.03)	0.69 (0.49, 0.96)	0.40 (0.27, 0.59)	<0.001
Model 3^e
Prevalence	42.5±2.2	36.5±2.4	34.6±2.7	24.9±2.4
OR (95% CI)	1.00	0.75 (0.54, 1.03)	0.69 (0.49, 0.96)	0.40 (0.27, 0.59)	<0.001
Abdominal obesity^f
Model 1^c
Prevalence	63.5±1.8	54.8±3.0	51.4±2.6	43.3±2.6
OR (95% CI)	1.00	0.69 (0.50, 0.94)	0.59 (0.45, 0.78)	0.42 (0.32, 0.56)	<0.001
Model 2^d
Prevalence	62.4±2.3	54.5±2.5	51.9±2.5	44.7±2.5
OR (95% CI)	1.00	0.69 (0.49, 0.97)	0.62 (0.46, 0.83)	0.45 (0.32, 0.63)	<0.001
Model 3^e
Prevalence	59.3±2.2	53.0±2.5	52.4±2.1	48.6±2.4
OR (95% CI)	1.00	0.71 (0.50, 1.0)	0.69 (0.49, 0.96)	0.57 (0.39, 0.84)	0.023
Hypertriglyceridemia^g
Model 1^c
Prevalence	33.0±1.7	35.0±1.7	34.2±2.2	24.4±2.2
OR (95% CI)	1.00	1.10 (0.90, 1.34)	1.06 (0.81, 1.38)	0.65 (0.51, 0.84)	<0.001
Model 2^d
Prevalence	36.2±1.9	34.2±1.6	32.8±2.2	23.3±2.2
OR (95% CI)	1.00	0.91 (0.74, 1.13)	0.86 (0.65, 1.14)	0.53 (0.38, 0.73)	<0.001
Model 3^e
Prevalence	31.9±1.6	33.6±1.5	33.9±1.9	27.1±2.5
OR (95% CI)	1.00	1.11 (0.89, 1.38)	1.12 (0.82, 1.54)	0.76 (0.52, 1.10)	0.023
Low HDL-C^h
Model 1^c
Prevalence	32.3±1.5	28.0±1.7	23.5±1.8	15.4±1.5
OR (95% CI)	1.00	0.82 (0.67, 0.98)	0.64 (0.51, 0.81)	0.38 (0.30, 0.49)	<0.001
Model 2^d
Prevalence	32.3±1.7	27.6±1.7	23.6±1.6	15.8±1.4
OR (95% CI)	1.00	0.80 (0.63, 1.02)	0.65 (0.50, 0.83)	0.39 (0.29, 0.51)	<0.001
Model 3^e
Prevalence	29.8±1.6	26.3±1.8	23.3±1.7	19.6±1.7
OR (95% CI)	1.00	0.86 (0.66, 1.13)	0.72 (0.54, 0.95)	0.54 (0.39, 0.75)	0.001
High blood pressureⁱ
Model 1^c
Prevalence	47.7±1.4	40.3±1.8	39.6±2.0	35.5±2.6
OR (95% CI)	1.00	0.68 (0.53, 0.88)	0.66 (0.52, 0.84)	0.53 (0.38, 0.74)	<0.001
Model 2^d
Prevalence	46.4±1.8	40.6±1.7	39.8±1.8	36.3±2.6
OR (95% CI)	1.00	0.73 (0.55, 0.98)	0.71 (0.54, 0.93)	0.57 (0.39, 0.84)	0.012
Model 3^e
Prevalence	44.1±1.7	39.5±1.5	39.0±1.7	38.3±2.3
OR (95% CI)	1.00	0.77 (0.58, 1.01)	0.74 (0.55, 1.00)	0.71 (0.49, 1.02)	0.125
Hyperglycemia^j
Model 1^c
Prevalence	43.3±2.0	42.0±2.4	39.1±2.7	32.9±2.5
OR (95% CI)	1.00	0.94 (0.74, 1.20)	0.83 (0.63, 1.09)	0.61 (0.49, 0.76)	<0.001
Model 2^d
Prevalence	42.7±2.3	41.1±2.3	39.1±2.6	34.6±2.3
OR (95% CI)	1.00	0.93 (0.72, 1.19)	0.84 (0.63, 1.13)	0.66 (0.51, 0.86)	0.005
Model 3^e
Prevalence	39.6±2.3	40.6±1.8	39.5±2.3	36.5±2.0
OR (95% CI)	1.00	1.04 (0.82, 1.33)	0.99 (0.72, 1.35)	0.82 (0.64, 1.06)	0.100
High HOMA-IR^k
Model 1^c
Prevalence	53.2±2.3	43.5±2.8	34.5±2.2	23.2±2.1
OR (95% CI)	1.00	0.67 (0.52, 0.87)	0.46 (0.35, 0.59)	0.26 (0.20, 0.35)	<0.001
Model 2^d
Prevalence	51.5±2.5	42.2±2.4	34.7±2.2	26.1±1.8
OR (95% CI)	1.00	0.67 (0.53, 0.85)	0.48 (0.36, 0.65)	0.30 (0.22, 0.41)	<0.001
Model 3^e
Prevalence	46.0±2.0	41.8±1.7	35.2±1.6	31.8±1.8
OR (95% CI)	1.00	0.80 (0.64, 1.0)	0.54 (0.40, 0.73)	0.40 (0.29, 0.55)	<0.001

Data represent % (standard error of the mean).

Metabolic syndrome is diagnosed based on the presence of any three of the following criteria: abdominal obesity, elevated triglycerides, low HDL-C, elevated blood pressure, and/or elevated glucose (each of which is specifically defined in the footnotes below).

Model 1: Adjusted for age.

Model 2: Adjusted for age, sex, race or ethnicity, education, smoking status, serum cotinine, C-reactive protein, alcohol use, physical activity, sum of total fruit and vegetable Healthy Eating Index scores, daily intake of vitamin D from dietary supplements.

Model 3: Adjusted for all variables in model 2 plus other components of the metabolic syndrome; HOMA-IR models using the same variables as for hyperglycemia.

Abdominal obesity: waist circumference >102 cm for men and >88 cm for women.

Hypertriglyceridemia: ≥150 mg/dL.

Low HDL-C: <40 mg/dL in men, <50 mg/dL in women.

High blood pressure: systolic blood pressure ≥130 mmHg, diastolic blood pressure ≥85 mmHg, or currently taking antihypertensive medication.

Hyperglycemia: ≥100 mg/dL, currently using insulin, or currently taking oral hypoglycemic medication.

High HOMA-IR: ≥2.5, currently using insulin, or currently taking oral hypoglycemic medication.

HOMA-IR, homeostasis model assessment of insulin resistance; NHANES, National Health and Nutrition Examination Survey; 25(OH)D, 25-hydroxyvitamin D; OR, odds ratio; CI, confidence interval; HDL-C, high-density lipoprotein cholesterol.

Table 3.

Adjusted Prevalence, Odds Ratios, and 95% Confidence Intervals for Metabolic Syndrome, Metabolic Syndrome Components, and HOMA-IR by Quartiles of Dietary Intake of Vitamin D (Excluding Supplements) Among 3543 U.S. Adults Aged ≥20 years, NHANES 2003–2004 and NHANES 2005–2006

	Quartiles of vitamin D intake (μg/day)
	1 (0.0–1.22)	2 (1.23–2.86)	3 (2.87–5.67)	4 (5.68–117.85)	P for trend
Metabolic syndrome^a
Model 1^b
Prevalence	37.9±2.0	36.0±2.2	33.3±1.9	31.6±1.5
OR (95% CI)	1.00	0.91 (0.70, 1.19)	0.80 (0.63, 1.03)	0.73 (0.59, 0.90)	0.015
Model 2^c
Prevalence	37.8±1.9	35.7±2.3	33.8±1.9	31.5±1.4
OR (95% CI)	1.00	0.90 (0.68, 1.18)	0.82 (0.64, 1.05)	0.72 (0.58, 0.90)	0.016
Abdominal obesity^f
Model 1^b
Prevalence	55.5±1.7	54.4±2.2	50.8±2.4	52.7±2.3
OR (95% CI)	1.00	0.95 (0.74, 1.21)	0.81 (0.66, 1.00)	0.88 (0.69, 1.12)	0.228
Model 2^c
Prevalence	55.5±1.7	54.0±2.3	51.2±2.5	52.6±2.1
OR (95% CI)	1.00	0.93 (0.73, 1.19)	0.82 (0.65, 1.03)	0.88 (0.68, 1.12)	0.333
Hypertriglyceridemia^g
Model 1^d
Prevalence	34.3±1.9	30.8±1.6	30.4±1.9	31.2±1.4
OR (95% CI)	1.00	0.82 (0.64, 1.05)	0.81 (0.62, 1.05)	0.84 (0.66, 1.08)	0.298
Model 2^e
Prevalence	34.0±1.9	30.9±1.6	30.5±1.8	31.1±1.3
OR (95% CI)	1.00	0.84 (0.65,1.07)	0.82 (0.63, 1.08)	0.85 (0.66, 1.10)	0.410
Low HDL-C^h
Model 1^d
Prevalence	26.9±1.5	22.7±1.6	26.1±2.0	24.0±2.0
OR (95% CI)	1.00	0.79 (0.62, 1.01)	0.96 (0.72, 1.29)	0.84 (0.60, 1.19)	0.164
Model 2^e
Prevalence	26.6±1.5	22.7±1.6	26.3±2.0	24.1±2.1
OR (95% CI)	1.00	0.80 (0.63, 1.02)	0.99 (0.74, 1.33)	0.86 (0.61, 1.23)	0.189
High blood pressureⁱ
Model 1^d
Prevalence	42.1±1.7	42.9±1.9	39.0±1.8	38.4±1.7
OR (95% CI)	1.00	1.03 (0.75, 1.41)	0.83 (0.64, 1.07)	0.78 (0.58, 1.05)	0.055
Model 2^e
Prevalence	42.0±1.6	42.9±1.9	39.2±1.8	38.3±1.7
OR (95% CI)	1.00	1.03 (0.75, 1.41)	0.84 (0.65, 1.08)	0.78 (0.58, 1.05)	0.070
Hyperglycemia^j
Model 1^d
Prevalence	39.7±1.8	41.4±2.5	36.4±1.9	40.5±2.0
OR (95% CI)	1.00	1.07 (0.85, 1.36)	0.82 (0.64, 1.05)	1.01 (0.80, 1.27)	0.214
Model 2^e
Prevalence	39.5±1.8	41.1±2.4	36.6±1.9	40.5±2.0
OR (95% CI)	1.00	1.08 (0.85, 1.36)	0.83 (0.65, 1.06)	1.01 (0.80, 1.27)	0.239
High HOMA-IR^k
Model 1^b
Prevalence	37.2±2.3	39.9±1.9	39.7±1.7	39.0±2.0
OR (95% CI)	1.00	1.19 (0.84, 1.68)	1.18 (0.81, 1.72)	1.13 (0.81, 1.56)	0.769
Model 2^c
Prevalence	37.0±2.4	39.9±1.8	40.0±1.8	39.0±1.9
OR (95% CI)	1.00	1.21 (0.85, 1.72)	1.23 (0.83, 1.83)	1.14 (0.82, 1.59)	0.705

To convert Quartiles of vitamin D intake to International Units/day, multiply μg/day by 40.

Model 1: Adjusted for daily energy intake (kcal), sex, age, race or ethnicity.

Model 2: Adjusted energy intake (kcal), sex, age, race or ethnicity, income (% of poverty level), physical activity, TV/computer use, smoking.

Model 1: Adjusted for daily energy intake (kcal), sex, age, race or ethnicity, body mass index (kg/m²).

Model 2: Adjusted for daily energy intake (kcal), sex, age, race or ethnicity, body mass index (kg/m²), income (% of poverty level), physical activity, TV/computer use, smoking.

Abdominal obesity: waist circumference >102 cm for men and >88 cm for women.

Hypertriglyceridemia: ≥150 mg/dL.

Low HDL-C: <40 mg/dL in men, <50 mg/dL in women.

High blood pressure: systolic blood pressure ≥130 mmHg, diastolic blood pressure ≥85 mmHg, or currently taking antihypertensive medication.

Hyperglycemia: ≥100 mg/dL, currently using insulin, or currently taking oral hypoglycemic medication.

High HOMA-IR: ≥2.5, currently using insulin, or currently taking oral hypoglycemic medication.

HOMA-IR, homeostasis model assessment of insulin resistance; NHANES, National Health and Nutrition Examination Survey; OR, odds ratio; CI, confidence interval; HDL-C, high-density lipoprotein cholesterol.

After adjustment for multiple confounders, the prevalence of metabolic syndrome was inversely associated with 25(OH)D (P<0.001; Table 2). Among the individual components for metabolic syndrome, abdominal obesity (P=0.014), low HDL-C (P=0.001), and high HOMA-IR (P=0.001) decreased progressively from the first to fourth quartiles of 25(OH)D (Table 2). Greater dietary intake of vitamin D was associated with a lower prevalence of metabolic syndrome (P=0.016; Table 3) but was not significantly associated with any of the individual metabolic syndrome components. There was no association between total dietary intake of vitamin D (diet+supplements) and metabolic syndrome prevalence (Table 4). Non-HDL-C was not associated with 25(OH)D, total dietary intake of vitamin D (diet+supplements), or dietary intake of vitamin D from food (data not shown).

Table 4.

Adjusted Prevalence, Odds Ratios, and 95% Confidence Intervals for Metabolic Syndrome, Metabolic Syndrome Components, and HOMA-IR by Quartiles of Dietary Intake of Vitamin D (Food+Supplements) Among 3543 U.S. Adults ≥20 Years, NHANES 2003–2004 and NHANES 2005–2006

	Quartiles of vitamin D intake (μg/day)
	1 (0–2.03)	2 (2.03–5.55)	3 (5.56–12.00)	4 (12.01–118.52)	P for trend
Metabolic syndrome^a
Model 1^b
Prevalence	37.5±1.8	36.7±1.8	31.7±2.0	32.9±2.4
OR (95% CI)	1.00	0.97 (0.78, 1.19)	0.75 (0.57, 0.99)	0.80 (0.60, 1.06)	0.119
Model 2^c
Prevalence	36.8±1.8	36.2±1.7	32.2±2.1	33.6±2.3
OR (95% CI)	1.00	0.97 (0.78, 1.21)	0.78 (0.59, 1.04)	0.84 (0.64, 1.12)	0.280
Model 3^d
Prevalence	36.7±2.1	36.1±1.7	32.2±2.0	33.7±2.4
OR (95% CI)	1.00	0.97 (0.77, 1.22)	0.79 (0.59, 1.06)	0.85 (0.60, 1.21)	0.337
Abdominal obesity^h
Model 1^b
Prevalence	56.8±1.3	53.9±1.9	49.9±2.2	52.9±2.5
OR (95% CI)	1.00	0.88 (0.72, 1.07)	0.74 (0.60, 0.91)	0.84 (0.66, 1.08)	0.014
Model 2^c
Prevalence	56.5±1.3	53.6±1.9	50.2±2.2	53.2±2.5
OR (95% CI)	1.00	0.88 (0.72, 1.07)	0.76 (0.61, 0.94)	0.86 (0.66, 1.12)	0.042
Model 3^d
Prevalence	53.6±2.0	51.9±1.9	51.6±2.2	56.3±2.8
OR (95% CI)	1.00	0.92 (0.75, 1.14)	0.91 (0.69, 1.20)	1.12 (0.77, 1.63)	0.392
Hypertriglyceridemiaⁱ
Model 1^e
Prevalence	30.6±2.0	30.6±1.9	32.5±2.2	32.9±1.7
OR (95% CI)	1.00	0.99 (0.76, 1.29)	1.09 (0.79, 1.51)	1.10 (0.85, 1.43)	0.830
Model 2^f
Prevalence	29.9±2.0	30.3±1.9	32.7±2.2	33.6±1.7
OR (95% CI)	1.00	1.01 (0.76, 1.34)	1.14 (0.83, 1.57)	1.19 (0.92, 1.54)	0.478
Model 3^g
Prevalence	31.3±2.3	31.1±2.0	32.1±2.2	32.1±2.0
OR (95% CI)	1.00	0.99 (0.74, 1.32)	1.03 (0.72, 1.48)	1.02 (0.71, 1.47)	0.994
Low-HDL-C^j
Model 1^e
Prevalence	26.8±1.7	28.0±1.9	23.9±1.9	21.1±2.0
OR (95% CI)	1.00	1.06 (0.85, 1.32)	0.85 (0.60, 1.19)	0.70 (0.52, 0.95)	0.032
Model 2^f
Prevalence	26.0±1.6	27.5±1.8	24.2±1.8	22.0±2.1
OR (95% CI)	1.00	1.09 (0.87, 1.36)	0.90 (0.65, 1.25)	0.77 (0.58, 1.03)	0.096
Model 3^g
Prevalence	25.9±1.8	27.4±1.7	24.3±2.0	22.2±2.7
OR (95% CI)	1.00	1.09 (0.87, 1.38)	0.91 (0.62, 1.35)	0.79 (0.51, 1.21)	0.343
High blood pressure^k
Model 1^e
Prevalence	41.2±1.2	40.4±1.8	41.7±1.8	39.1±2.0
OR (95% CI)	1.00	0.95 (0.75, 1.21)	1.02 (0.81, 1.28)	0.88 (0.66, 1.16)	0.748
Model 2^f
Prevalence	41.0±1.2	40.3±1.8	41.7±1.8	39.3±2.1
OR (95% CI)	1.00	0.95 (0.75, 1.21)	1.03 (0.81, 1.30)	0.89 (0.65, 1.22)	0.811
Model 3^g
Prevalence	41.8±1.6	40.7±1.9	41.4±1.7	38.5±2.2
OR (95% CI)	1.00	0.93 (0.73, 1.19)	0.96 (0.75, 1.23)	0.81 (0.55, 1.19)	0.710
Hyperglycemia^l
Model^e
Prevalence	39.8±2.1	39.9±2.4	39.0±2.3	39.4±2.1
OR (95% CI)	1.00	0.99 (0.75, 1.30)	0.95 (0.74, 1.20)	0.96 (0.72, 1.29)	0.968
Model 2^f
Prevalence	39.4±2.2	39.7±2.4	39.2±2.4	39.7±2.1
OR (95% CI)	1.00	0.99 (0.75, 1.31)	0.97 (0.75, 1.25)	1.00 (0.74, 1.35)	0.995
Model 3^g
Prevalence	39.2±2.2	39.5±2.4	39.3±2.4	39.9±2.2
OR (95% CI)	1.00	0.99 (0.75, 1.31)	0.98 (0.76, 1.26)	1.01 (0.73, 1.41)	0.996
High HOMA-IR^m
Model^e
Prevalence	37.9±2.4	42.5±2.1	38.5±1.9	37.0±2.0
OR (95% CI)	1.00	1.33 (0.91, 1.96)	1.07 (0.71, 1.61)	0.98 (0.71, 1.35)	0.241
Model 2^f
Prevalence	37.5±2.3	42.2±2.1	38.7±1.9	37.5±1.9
OR (95% CI)	1.00	1.36 (0.92, 2.01)	1.11 (0.73, 1.69)	1.04 (0.76, 1.43)	0.333
Model 3^g
Prevalence	37.0±2.2	41.9±2.1	38.9±1.9	38.0±2.3
OR (95% CI)	1.00	1.37 (0.94, 2.00)	1.14 (0.78, 1.67)	1.08 (0.76, 1.54)	0.404

To convert Quartiles of vitamin D intake to International Units/day, multiply μg/day by 40.

Model 1: Adjusted for daily energy intake (kcal), sex, age, race or ethnicity.

Model 2: Adjusted for daily energy intake (kcal), sex, age, race or ethnicity, income (% of poverty level), physical activity, TV/computer use, smoking.

Model 3: Adjusted for all variables in model 2 plus daily vitamin D intake from dietary supplements.

Model 1: Adjusted for daily energy intake (kcal), body mass index (kg/m²), sex, age, race or ethnicity.

Model 2: Adjusted for daily energy intake (kcal), body mass index (kg/m²), sex, age, race or ethnicity, income (% poverty level), physical activity, TV/computer use, smoking.

Model 3: Adjusted for daily energy intake (kcal), body mass index (kg/m²), sex, age, race or ethnicity, income (% poverty level), physical activity, TV/computer use, smoking, daily vitamin D intake from dietary supplements.

Abdominal obesity: waist circumference >102 cm for men and >88 cm for women.

Hypertriglyceridemia: ≥150 mg/dL.

Low HDL-C: <40 mg/dL in men, <50 mg/dL in women.

High blood pressure: systolic blood pressure ≥130 mmHg, diastolic blood pressure ≥85 mmHg, or currently taking antihypertensive medication.

Hyperglycemia: ≥100 mg/dL, currently using insulin, or currently taking oral hypoglycemic medication.

High HOMA-IR: ≥2.5, currently using insulin, or currently taking oral hypoglycemic medication.

Discussion

In this nationally representative cross-sectional sample of U.S. adults, we observed an inverse association between both 25(OH)D and dietary vitamin D intake (excluding supplements) and metabolic syndrome. When examining the specific components of metabolic syndrome, lower 25(OH)D concentrations were associated most strongly with abdominal obesity and low-HDL-C. The prevalence of high HOMA-IR was also strongly associated with lower 25(OH)D. Those in the highest dietary vitamin D intake quartile excluding supplements had a lower odds for metabolic syndrome compared to the lowest vitamin D intake quartile. However, individual components of metabolic syndrome and HOMA-IR were not significantly associated with dietary intake of vitamin D in fully adjusted models.

The present results are consistent with those from previous clinical investigations^9,21 and surveys^4,5,22,23 showing that low vitamin D status is inversely associated with metabolic syndrome. For example, Ford et al.²² reported an odds ratio (OR) of 0.46 (95% CI 0.32, 0.67; P<0.001) for metabolic syndrome in the highest quintile of 25(OH)D (≥96.3 nmol/L) versus the lowest quintile (≤48.4 nmol/L) using NHANES III (1988–1994) data. This is similar to the OR of 0.40 (95% CI 0.27, 0.59; P<0.001) for the highest quartile of vitamin D status in the present study (≥75.0 nmol/L) with more recent NHANES data (2003–2004 and 2005–2006). Reis et al.²³ also showed a strong inverse association (OR 0.27, 95% CI 0.15, 0.46) in a cross-sectional analysis of 1654 men and women comparing the highest quintile of 25(OH)D (≥78.6 nmol/L) to the lowest (<36.9 nmol/L). It is interesting to note that in these analyses, the greatest reduction in the prevalence for metabolic syndrome was noted for circulating 25(OH)D levels >75.0 nmol/L, which exceeds recent population-based recommendations of >50 nmol/L for maintaining optimal bone health in the United States.²⁴

In a previous cross-sectional study, we showed that in a group of healthy men and women, the majority of whom had 25(OH)D levels >75.0 nmol/L, there was an inverse association between metabolic syndrome and circulating 25(OH)D levels comparing the top (≥114.8 nmol/L) to the bottom tertile (≤84.9 nmol/L).⁶ While this study was small (n=257), it suggests that the association between metabolic syndrome and vitamin D status may persist over a wide range of circulating 25(OH)D levels. In the present study, the upper limit for the first quartile of 25(OH)D levels was 44.9 nmol/L and the lower limit for the fourth quartile was 75.0 nmol/L, which suggests that the current recommended level of ≥50 nmol/L may be suboptimal if reduced vitamin D status proves to be causally related to metabolic syndrome. If results from future studies suggest a causal inference is justified, it may be important to consider the risk of developing metabolic syndrome when establishing optimal 25(OH)D recommendations. However, it should be noted that 25(OH)D levels >100 nmol/L have been associated with increased total mortality and cancer risk in community-based cohort studies.^25,26

The present investigation also confirmed prior results indicating that abdominal obesity and low HDL-C were the components of metabolic syndrome most strongly inversely associated with 25(OH)D.^6,27 Previously, we reported that each 25 nmol/L increase in 25(OH)D was associated with a 0.11 mmol/L increase in HDL-C on the basis of data from a cross-sectional study of 257 men and women.⁶ Similarly, Liu et al.²⁷ reported that each 25 nmol/L increase in 25(OH)D was associated with a 0.10 mmol/L increase in plasma HDL-C after adjusting for multiple factors including age, sex, waist circumference, and triglycerides. The relationship between vitamin D status and HDL-C is of considerable potential importance given that each 0.026 mmol/L increment in HDL-C is associated with a 2%–4% reduction in coronary heart disease risk.^28,29 However, in a previous investigation, we evaluated changes in HDL-C concentration following an 8-week supplementation period with 30 μg/day vitamin D and noted no changes in HDL-C or other lipid outcomes.⁶ Other studies have also failed to show increases in HDL-C following exposure to whole-body irradiation using ultraviolet A and B radiation³⁰ or vitamin D supplementation up to 1000 μg vitamin D per week for 1 year.³¹ Future studies are warranted to further elucidate the influence of altering circulating levels of 25(OH)D on HDL-C concentration.

Previous studies have reported below-normal circulating 25(OH)D levels in obese individuals,^22,32,33 which align with the present results showing an inverse association between vitamin D status and abdominal adiposity. It has been proposed that individuals with obesity may have decreased sun exposure secondary to reduced outdoor activity; however, differences in sun exposure alone do not appear to account for the difference in vitamin D status between lean and obese individuals.^32,33 It has also been suggested that vitamin D is sequestered in adipose tissue, thereby decreasing the circulating concentration of 25(OH)D.^34,35 Other possible explanations for this relationship include reduced 25(OH)D synthesis in the liver relative to lean individuals and an increase in total body clearance of vitamin D secondary to obesity-related inflammation.³³ It is also possible that differences in vitamin D-binding protein differ according to adiposity, although data at present are conflicting regarding this association.^36,37

In the present study, the associations of dietary intake of vitamin D with metabolic syndrome, its components, and HOMA-IR were less robust than the association for 25(OH)D (60% versus 30% reduced odds for metabolic syndrome for the highest quartile of vitamin D status and dietary intake, respectively). However, vitamin D intake in the highest quartile was 5.68–118 μg/day, with the median intake only 9 μg/day. We have previously shown that supplementation of 30 μg/day for 8 weeks was not sufficient to increase 25(OH)D concentrations to greater than or equal to 75.0 nmol/L in the majority of an overweight and obese sample.⁶ Therefore, it is possible that other factors, such as the delivery form or the availability of vitamin D-binding proteins, influenced the aforementioned results. Polymorphisms in vitamin D-binding proteins may also explain differences in the strengths of associations between vitamin D status and intake with metabolic syndrome and its components.³⁶ Confounding by sun exposure or the cross-sectional design of this investigation may have also influenced these results. Data on sun exposure or latitude as a proxy for sun exposure were not available in the NHANES datasets.

The strong inverse association of 25(OH)D quartile with the prevalence of high HOMA-IR indicates that low vitamin D status is related to insulin resistance. Although the strength of this relationship was somewhat attenuated by adjustment for waist circumference and other components of the metabolic syndrome, the association remained highly significant. Whether this represents cause and effect, and, if so, whether low vitamin D status is the cause or effect is uncertain. Studies on vitamin D supplementation suggest that insulin sensitivity is unaffected at doses up to 4,000 IU/day for 12 weeks,^38,39 and the authors are unaware of any trials that have evaluated the influence of insulin-sensitizing agents on vitamin D status. Additional research is needed to further clarify this issue.

That we did not identify an association between total dietary intake of vitamin D, including supplements, and metabolic syndrome is intriguing. One of the principal sources of dietary vitamin D is fortified dairy foods.²⁴ Previous observational and intervention studies have suggested an inverse association between consumption of dairy foods and components of metabolic syndrome, specifically blood pressure and abdominal adiposity.^40
–42 Authors of a review of the observational evidence concluded that the odds for metabolic syndrome were 0.71 (95% CI, 0.57, 0.89) for the highest dairy intake (3–4 servings/day) versus the lowest intake (0.9–1.7 servings/day).⁴³ It is possible that the combination of nutrients in dairy foods, rather than a single nutrient, influence the expression of metabolic syndrome risk factors. Additionally, the food matrix in which vitamin D is delivered may have an effect on absorption and regulation of 25(OH)D, and subsequently other vitamin D metabolites. It is also possible that the method of assessment of dietary supplement intake (questionnaire about habits over the last 30 days) does not adequately represent actual intake over longer periods. The combination of these factors may explain, at least in part, the absence of significant relationships between use of vitamin D supplements with metabolic syndrome and its components. Future studies should continue to track the association between certain foods containing vitamin D and 25(OH)D levels and assess the impact of other tools used to measure dietary supplement intake.

This investigation had several strengths and limitations. The dataset employed was from a nationally representative sample that included greater representation from minority groups than some prior surveys, which may enhance generalizability. However, because the data are cross-sectional, the causative nature of associations cannot be determined. Also, seasonal variations and regional differences in sun exposure could not be controlled for because such data are not available in the NHANES datasets. Abdominal obesity was assessed by waist circumference, which does not distinguish between adipose and lean tissue or between subcutaneous adipose tissue and visceral adipose tissue. In addition, vitamin D was measured only at one time point for each participant; therefore, it is possible that seasonal variation may have affected circulating vitamin D levels. Another limitation is the possible underreporting of food intake, which might result in underestimation of vitamin D consumption, especially by some overweight and obese individuals.⁴⁴

In summary, serum 25(OH)D level was inversely associated with the prevalence of metabolic syndrome, abdominal obesity, and low HDL-C concentration. Dietary intake of vitamin D was inversely associated with metabolic syndrome prevalence; however, total vitamin D intake, which included supplemental vitamin D, was not associated with odds for metabolic syndrome or its components. These results suggest that clinical trials are warranted to assess the impact of increasing vitamin D intake from foods on the metabolic cardiovascular risk factor profile.

Footnotes

Acknowledgments

These analyses were funded by Dairy Research Institute, Inc.

Author Disclosure Statement

V.L.F., M.R.R., and K.M.P. designed the research; V.L.F., D.R.K., K.C.M., and T.M.R. analyzed and interpreted the data; K.C.M. and T.M.R wrote the manuscript; and K.C.M. had primary responsibility for the final content. All authors read and approved the final manuscript.

K.C. Maki and T.M. Rains are employees of Biofortis Clinical Research, which has received research grant support from Dairy Research Institute, Inc. V.L. Fulgoni and D.R. Keast are employees of Nutrition Impact, LLC, and Food & Nutrition Database Research, Inc., respectively, and also received research grant support from Dairy Research Institute, Inc. K.M. Park and M.R. Rubin are employees of Dairy Research Institute, Inc.

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Vitamin D Intake and Status Are Associated with Lower Prevalence of Metabolic Syndrome in U.S. Adults: National Health and Nutrition Examination Surveys 2003–2006

Abstract

Background:

Methods:

Results:

Conclusions:

Introduction

Methods

Results

Discussion

Footnotes

Acknowledgments

Author Disclosure Statement

References