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Journal of Clinical Endocrinology & Metabolism , doi:10.1210/jc.2007-0722
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The Journal of Clinical Endocrinology & Metabolism Vol. 92, No. 8 3155-3157
Copyright © 2007 by The Endocrine Society

BRIEF REPORT

Reduced Sun Exposure Does Not Explain the Inverse Association of 25-Hydroxyvitamin D with Percent Body Fat in Older Adults

Susan S. Harris and Bess Dawson-Hughes

Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts 02111

Address all correspondence to: Susan Harris, D.Sc., Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston, Massachusetts 02111. E-mail: susan.harris{at}tufts.edu.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Context: Greater adiposity is associated with lower blood levels of 25-hydroxyvitamin D [25(OH)D]. The extent to which this results from reduced sun exposure among heavier individuals is unknown.

Objectives: This analysis was conducted to determine whether sun exposure habits differ according to percent body fat (%FAT) in older adults and to what extent they explain the inverse association of adiposity with 25(OH)D in that population.

Design: We performed a cross-sectional analysis of baseline data from a randomized trial of calcium and vitamin D supplementation to prevent bone loss.

Setting: The study was performed at the Metabolic Research Unit at the Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts University.

Participants: A total of 381 generally healthy male and female volunteers age 65 and older participated in the study. Exclusion criteria included vitamin D and calcium supplement use, and medical conditions and medications known to affect bone metabolism.

Intervention: There were no interventions. Measurements for this analysis were made before participants received trial supplements.

Main Outcome Measures: Plasma 25(OH)D, an indicator of vitamin D status, was measured.

Results: Sunscreen use, hours spent outside per week, and percent of skin exposed did not differ across quartiles of %FAT (P > 0.43). 25(OH)D decreased across %FAT quartiles (P < 0.05) and was about 20% lower in the highest compared with the lowest quartile of %FAT after adjustments for age, sex, season, and vitamin D intake. Further adjustment for sun exposure habits had little effect on estimates of 25(OH)D.

Conclusions: In older adults, sun exposure habits do not vary according to adiposity and do not appear to explain lower 25(OH)D concentrations with increasing adiposity.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
GREATER ADIPOSITY IS associated with lower blood levels of vitamin D (1) and its liver metabolite, 25-hydroxyvitamin D [25(OH)D] (2, 3, 4, 5). Several potential explanations for this have been proposed and examined to varying degrees (1, 3, 6, 7). The most likely explanations, and they are not mutually exclusive, are that: 1) fat tissue may limit bioavailability of vitamin D by reducing its entry into the circulation (1, 6); and 2) fatter individuals receive less sun exposure because they spend less time outside and/or expose less skin when they do go out. This analysis was conducted to examine the latter possibility.


   Subjects and Methods
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 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
The subjects were participants in the baseline visit of a 3-yr trial of calcium and vitamin D supplementation to reduce bone loss in men and women aged 65 yr and older (8). Use of vitamin D or calcium supplements was an exclusion for the study, and no subjects were taking vitamin D or calcium supplements, including multivitamins, at the time the measurements for the present analysis were made. Other exclusion criteria included medical conditions and medications known to affect bone metabolism. The study was approved by the Investigational Review Board at Tufts University, and written informed consent was obtained from all participants. Of the 445 subjects enrolled in the supplement trial, five were excluded from the present analysis due to missing measurements of 25(OH)D, percent body fat (%FAT), or sun exposure. There were 15 excluded due to non-Caucasian race because of prior evidence that the association of adiposity with 25(OH)D differs by race (9), and 44 were excluded because they had traveled south of latitude 35° N in the month preceding the study visit.

All measurements used in this analysis were made at the baseline visit of the supplement trial. Sun exposure habits over the 3-month period preceding the study visit were assessed by questionnaire. Separate questions addressed the number of hours per week the subjects usually spent outside during the period (not including time spent in vehicles), the amount of skin that was usually exposed (e.g. face only, face and hands, etc.), and whether they wore sunscreen during any of the time they spent outside. Season of sun exposure was designated according to the middle month of each subject’s 3-month sun exposure recall period as November through April, when sun exposure is too weak to stimulate vitamin D production (10, 11), or May through October. Dietary vitamin D intake was estimated with a short food frequency questionnaire developed in this laboratory (11). Heights and weights were measured with a stadiometer and digital scale, respectively. Body fat was measured by dual-energy x-ray absorptiometry with a DPX-L scanner (Lunar Radiation, Madison, WI). %FAT was calculated from body fat weight and total weight, and divided into quartiles. Plasma 25(OH)D and 1,25 dihydroxyvitamin D [1,25(OH)2D] were measured by competitive protein binding methods having interassay coefficients of variation of 7.3% and 7.7%, respectively (12, 13).

Analyses were conducted with SPSS version 14.0 (SPSS, Inc., Chicago, IL). P values < 0.05 were considered to indicate statistical significance. Analysis of covariance was used to compute regression coefficients (ß), and adjusted means and SEMs of sun exposure and 25(OH)D values across quartiles of %FAT. Potential interactions among predictor variables were examined in preliminary analyses, and none was identified.


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
The mean age of the 381 subjects (173 men and 208 women) was 71 ± 5 yr (SD), and mean vitamin D intake was 4.6 ± 2.6 µg/d (185 ± 105 IU/d). Mean %FAT was 34 ± 9 and, as expected, was lower in men (28 ± 6) than women (39 ± 7; P < 0.001). There was a significant inverse correlation of %FAT with vitamin D intake (r = 0.15; P = 0.003), but not with age (r = –0.09; P = 0.077).

Predictors of sun exposure habits

Only 16% of subjects (10% of men, 21% of women) reported that they had used any sunscreen when they were outside, and %FAT did not differ by sunscreen use in the group as a whole (P = 0.771) or in the subjects measured in either season (P > 0.800).

We examined sex, age, season, and %FAT as predictors of hours per week spent outside. The results were similar whether %FAT was included as a continuous variable or categorized into quartiles. When all four potential predictors were considered simultaneously in analysis of covariance models, sex was a significant predictor (mean ± SEM hours per week was 21 ± 1 for men vs. 15 ± 1 for women; P < 0.001), and season was a significant predictor (Table 1Go; P < 0.001), but age and %FAT were not. Mean hours per week spent outside are shown by quartiles of %FAT in Table 1Go. Subset analyses indicated that, although hours per week spent outside were higher in May through October than November through April, they did not differ across %FAT quartiles in either season.


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  		TABLE 1. Mean ± SEM sun exposure habits by quartiles of %FAT

 
We conducted similar analyses of age, sex, season, and %FAT as predictors of the amount of skin that was typically exposed. The percent of skin that was exposed was higher in May through October than November through April (P < 0.001) but did not differ across %FAT quartiles (Table 1Go).

25(OH)D, %FAT, and sun exposure

25(OH)D decreased significantly across quartiles of %FAT before and after adjustment for sex, age, season, and vitamin D intake (Table 2Go). After adjustment for sex, age, season, and vitamin D intake, hours per week spent outside (ß = 0.138; P = 0.017) and percent of skin exposed (ß = 0.151; P = 0.001), but not sunscreen use (P = 0.095), were significantly and positively associated with 25(OH)D. However, adjustment for these variables had little effect on estimates of 25(OH)D across the %FAT quartiles (Table 2Go). In contrast to 25(OH)D, 1,25(OH)2D did not differ across %FAT quartiles (P = 0.654). The means ± SEM for 1,25(OH)2D from the lowest to the highest %FAT quartiles were: 34.2 ± 0.9, 35.3 ± 0.9, 35.7 ± 0.9, and 35.3 ± 0.9.


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  		TABLE 2. Mean ± SEM 25(OH)D (ng/ml)1 by quartiles of %FAT

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
In this group of older men and women, those in the highest %FAT quartile (more than ~40% fat) had 20% lower 25(OH)D concentrations than those in the lowest quartile (less than ~28% fat) after adjustment for potential confounders, including sex, age, season, and vitamin D intake. Further adjustment for sun exposure habits had little effect on the estimates, indicating that differences in sun exposure do not explain the inverse association of 25(OH)D with adiposity in older people. Evidence from this and prior studies suggests that two other potential explanations are also unlikely. First, it does not appear that adiposity influences the skin synthesis of previtamin D3 or its conversion to vitamin D3 (6). Second, it has been proposed that elevated 1,25(OH)2D in obesity may reduce 25(OH)D via negative feedback on its hepatic production (7). However, this mechanism does not explain the inverse association of 25(OH)D with adiposity in this study or that of Parikh et al. (3), neither of which observed an increase in 1,25(OH)2D with increasing adiposity. If differences in sun exposure can be excluded, the most likely explanation for the association seems to be that vitamin D is sequestered in fat tissue, reducing its entry into the circulation (1, 6). This explanation is consistent with the fact that adiposity is inversely associated with increases in vitamin D3 after skin irradiation (6), and increases in vitamin D (6) and 25(OH)D after treatment with vitamin D supplements (14). It is also supported by the observation that directly measured adipose tissue is more strongly inversely associated with 25(OH)D than are other anthropometric measures that reflect body size as well as adiposity (4). There is some evidence that sc fat stores may influence blood levels of 25(OH)D more than visceral fat stores do (4), but further studies are needed to characterize the specific mechanisms by which adipose tissue of varying types contributes to reduced 25(OH)D concentrations in overweight and obese individuals.


   Footnotes
 
This study was supported by a grant (AG10353) from the National Institutes of Health and by a contract (58-1950-7-707) with the Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts University. This article does not necessarily reflect the views or policies of the United States Department of Agriculture, nor does mention of trade names, commercial products, or organizations imply endorsement by the United States government.

Disclosure Statement: The authors have nothing to disclose.

First Published Online May 29, 2007

Abbreviations: 1,25(OH)2D, 1,25 Dihydroxyvitamin D; 25(OH)D, 25-hydroxyvitamin D; %FAT, percent body fat.

Received April 4, 2007.

Accepted May 17, 2007.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

  1. Liel Y, Ulmer E, Shary J, Hollis BW, Bell NH 1988 Low circulating vitamin D in obesity. Calcif Tissue Int 43:199–201[Medline]
  2. Hypponen E, Power C 2006 Vitamin D status and glucose homeostasis in the 1958 British birth cohort: the role of obesity. Diabetes Care 29:2244–2246[Abstract/Free Full Text]
  3. Parikh SJ, Edelman M, Uwaifo GI, Freedman RJ, Semega-Janneh M, Reynolds J, Yanovski JA 2004 The relationship between obesity and serum 1,25-dihydroxy vitamin D concentrations in healthy adults. J Clin Endocrinol Metab 89:1196–1199[Abstract/Free Full Text]
  4. Snijder MB, van Dam RM, Visser M, Deeg DJ, Dekker JM, Bouter LM, Seidell JC, Lips P 2005 Adiposity in relation to vitamin D status and parathyroid hormone levels: a population-based study in older men and women. J Clin Endocrinol Metab 90:4119–4123[Abstract/Free Full Text]
  5. Rizzoli R, Eisman JA, Norquist J, Ljunggren O, Krishnarajah G, Lim SK, Chandler J 2006 Risk factors for vitamin D inadequacy among women with osteoporosis: an international epidemiological study. Int J Clin Pract 60:1013–1019[CrossRef][Medline]
  6. Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF 2000 Decreased bioavailability of vitamin D in obesity. Am J Clin Nutr 72:690–693[Abstract/Free Full Text]
  7. Bell NH, Epstein S, Greene A, Shary J, Oexmann MJ, Shaw S 1985 Evidence for alteration of the vitamin D-endocrine system in obese subjects. J Clin Invest 76:370–373[Medline]
  8. Dawson-Hughes B, Harris SS, Krall EA, Dallal GE 1997 Effect of calcium and vitamin D supplementation on bone density in men and women 65 years of age or older. N Engl J Med 337:670–676[Abstract/Free Full Text]
  9. Looker AC 2005 Body fat and vitamin D status in black versus white women. J Clin Endocrinol Metab 90:635–640[Abstract/Free Full Text]
  10. Webb AR, Kline L, Holick MF 1988 Influence of season and latitude on the cutaneous synthesis of vitamin D3: exposure to winter sunlight in Boston and Edmonton will not promote vitamin D3 synthesis in human skin. J Clin Endocrinol Metab 67:373–378[Abstract/Free Full Text]
  11. Krall EA, Sahyoun N, Tannenbaum S, Dallal GE, Dawson-Hughes B 1989 Effect of vitamin D intake on seasonal variations in parathyroid hormone secretion in postmenopausal women. N Engl J Med 321:1777–1783[Abstract]
  12. Preece MA, O’Riordan JL, Lawson DE, Kodicek E 1974 A competitive protein-binding assay for 25-hydroxycholecalciferol and 25-hydroxyergocalciferol in serum. Clin Chim Acta 54:235–242[CrossRef][Medline]
  13. Reinhardt TA, Horst RL, Orf JW, Hollis BW 1984 A microassay for 1,25-dihydroxyvitamin D not requiring high performance liquid chromatography: application to clinical studies. J Clin Endocrinol Metab 58:91–98[Abstract/Free Full Text]
  14. Barger-Lux MJ, Heaney RP, Dowell S, Chen TC, Holick MF 1998 Vitamin D and its major metabolites: serum levels after graded oral dosing in healthy men. Osteoporos Int 8:222–230[CrossRef][Medline]



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