OBJECTIVE-Hypovitaminosis D and reduced IGF-1 are associated, individually, with metabolic syndrome. Physiological interactions between vitamin D and IGF-1 are reported; this is the first study to investigate their combined associations with metabolic syndrome prevalence.
RESEARCH DESIGN AND METHODS-Data on 25-hydroxyvitamin D (25(OH)D), IGF-1, and metabolic syndrome abnormalities (abdominal obesity; raised A1C, blood pressure, and triglycerides; and low HDL cholesterol) were collected from 6,810 British white subjects in the 1958 cohort, surveyed during 2002-2004 (age 45 years).
RESULTS-IGF-1 concentrations increased with 25(OH)D up toϳ75-85 nmol/l but not thereafter. Both 25(OH)D and IGF-1 were inversely associated with metabolic syndrome. There was an interaction between 25(OH)D and IGF-1 (P ϭ 0.025) on metabolic syndrome prevalence: IGF-1 was not significantly associated with metabolic syndrome among those with the lowest levels of 25(OH)D (P Ͼ 0.09), whereas higher 25(OH)D was associated with metabolic syndrome at all IGF-1 concentrations (P Յ 0.006). Metabolic syndrome prevalence was lowest for participants with the highest concentrations of both 25(OH)D and IGF-1 (odds ratio for highest vs. lowest third of both 0.26 [95% CI 0.17-0.40], P Ͻ 0.0001; adjusted for sex, month, hour, inactivity, alcohol consumption, smoking, and social class). 25(OH)D was associated with the prevalence of high A1C, blood pressure, and triglycerides after adjustment for IGF-1, obesity, and social and lifestyle variations (P Յ 0.004 for all comparisons). (1,2); however, for both factors, lower concentrations have been associated with disturbed glucose metabolism (3-8), high blood pressure (9 -11), adverse lipid profiles (2,12,13), and cardiovascular disease (8,14,15) independently of body mass. The evidence for associations between vitamin D and IGF-1 axes with metabolic risk includes prospective studies, clinical trials, and dose-related effects, suggesting that associations may prove to be causal. Mechanisms by which vitamin D and IGF-1 axes may lead to human disease are, however, not fully understood, and despite evidence for physiological interaction between these risk factors (16 -18), little is known about their joint effects, and we can find no previous studies investigating their combined associations with metabolic syndrome.
CONCLUSIONS-SerumVitamin D is a hormone precursor, which before exerting its metabolic effects undergoes two successive hydroxylations.