Abstract

Previous research studies had suggested that low serum calcidiol could lead to the onset of chronic inflammatory conditions (CIC). This study used the dataset of National Health and Nutrition Examination Survey (NHANES) 2005-2006 to investigate whether serum calcidiol can predict CIC. The linear correlation between serum calcidiol and body mass index (BMI) was explored for therapeutic purposes. A point prevalence of serum calcidiol deficiency was 84.0% in each CIC group. People of African origin were eleven times more likely to suffer from vitamin-D deficiency (crude ORc=10.57[7.98-13.99]). Linear regression elicited strong negative correlation between calcidiol and C-reactive protein (CRP) after adjustment (R2=0.33; r=-0.57; p<0.001). Logistic regression showed non-significant association between calcidiol and CIC after adjustment ORa=1.16[0.93-1.44], 1.03[0.81-1.31] and 0.76[0.55-1.05] for asthma, arthritis and malignancy, respectively. Linear regression study showed a strong linear negative correlation between calcidiol and (BMI) after adjustment R2=0.27; r=-0.52; p<0.001. Although serum calcidiol is not an ideal predictor of CIC; however, we cannot completely rule out an association due to the complexity related to the presence of confounding, intermediate, and regulatory factors. Additional findings may suggest the potential for tailoring vitamin-D supplementation to individual’s weight. Key words: Calcidiol, NHANES 2005-2006, chronic inflammatory conditions, C-reactive protein, body max index.

Highlights

  • Vitamin-D is a steroid hormone and belongs to the family of fat-soluble vitamins

  • After its production in the hepatocyte, the fat-soluble calcidiol is carried by a binding protein through the blood stream to the kidneys, where the second hydroxylation occurs under 1-α-hydroxylase enzyme (Hewison et al, 2000); which is mainly regulated by serum levels of parathyroid hormone (PTH) and calcium

  • While calcidiol and body mass index (BMI) follow normal distribution; C-reactive protein (CRP) is skewed in the right, logarithmic transformation of CRP is required for appropriate use of linear regression analysis

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Summary

Introduction

Vitamin-D is a steroid hormone and belongs to the family of fat-soluble vitamins. Reports from many research studies had shown that both low sunlight exposure and poor dietary intake of vitamin-D, may substantially alter serum levels of calcidiol known as 25hydroxyvitamin-D, in humans (Vitamin D Fact Sheet for Health Professionals, 2011; Reinhold V, 1999; Institute of Medicine, 2010).When defining calcidiol deficiency as being less than 20 ng/ml in serum, approximately 42% of the US population is affected (Forrest and Stuhldreher, 2011). The interaction between sunlight and skin cholesterol referred to as 7-dehydrocholesterol, leads to the formation of the pro-vitamin-D, known as cholecalciferol This endogenous production constitutes the major natural source of vitamin-D in humans, the name “sunshine vitamin”. After its production in the hepatocyte, the fat-soluble calcidiol is carried by a binding protein through the blood stream to the kidneys, where the second hydroxylation occurs under 1-α-hydroxylase enzyme (Hewison et al, 2000); which is mainly regulated by serum levels of parathyroid hormone (PTH) and calcium. This ultimate chemical reaction converts 25hydroxyvitamin-D into 1-25-dihydroxyvitamin-D, known as calcitriol. The 24-hydroxylase enzyme (Anderson et al, 2003) alters both molecules calcidiol and calcitriol to their forms of elimination in the bile (24-25dihydroxyvitamin-D) and urine (1-24-25-trihydroxyvitaminD)

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