Vitamin D and spinal cord injury

Introduction

Based on data collected from the National Health and Nutrition Examination Survey (NHANES), the prevalence of vitamin D deficiency (< 50 nmol/L) in the United States is estimated to be 39.9% ( ). Historically, vitamin D is known for its role in supporting bone health and preventing osteoporosis ( ; ). However, vitamin D is also important for various functions in the body including immunity, cell growth, and neuromuscular function ( ). The discovery of vitamin D receptors in skeletal muscle tissue has led to an increase in research examining vitamin D and its potential effects on exercise performance. Active individuals with spinal cord injury (SCI) have been suggested to be at an increased risk for vitamin D insufficiency and deficiency due to low dietary intake of foods high in vitamin D ( ), anticonvulsant medications which interfere with vitamin D metabolism ( ), and lifestyle factors such as reduced exposure to sunlight ( ; ). Thus, a sufficient vitamin D (> 75 nmol/L) status is dependent on diet, location of residence, skin pigmentation, time spent outdoors and whether an individual wears sunscreen or sun protective clothing ( ; ). Research has suggested that dietary intake for both micronutrients and macronutrients are insufficient in the para-athlete population ( ).

Vitamin D recommendations: Intake, sources, and status

Vitamin D, also referred to as calciferol, is a fat-soluble vitamin that acts like a prohormone. Vitamin D can be obtained from sun exposure, supplements, and foods like fatty fish, beef liver, eggs, mushrooms, and fortified foods (see Table 1 ), which are the main source of dietary vitamin D in American diets ( ).

While there are several forms (vitamers) of vitamin D, two major forms include cholecalciferol (D ₃ ) and ergosterol (D ₂ ). Ergosterol is added to foods to fortification purposes (i.e., cereal), and it naturally present in fungi like mushrooms. Vitamin D ₃ is synthesized in the skin as well as consumed in the diet through animal sources ( ). When exposed to ultraviolet B (UVB) radiation, 7-dehydrocholesterol (7-DHC) is converted into previtamin D ₃ , and later converted vitamin D ( ) ( Fig. 1 ).

This type of synthesis is influenced by variables like skin exposure, season, and location of residence. There are seasonal variations in vitamin D synthesis for individuals greater than 35 to 37 degrees N latitude during the winter due to the unavailability of UVB radiation during winter months in these locations. Excessive pollution and cloud cover are also variables that can impact the ability to synthesize vitamin D through UVB radiation ( ). Other variables that affect the ability to synthesize vitamin D via sunlight are sunscreen and clothing choice. Recent research suggests that sunscreen use may not play a large role in low 25(OH)D status when using moderate sun protection factor (SPF). Currently, research has not examined the use of high SPF sunscreens and the effect they may have on 25(OH)D concentrations ( ). Protective clothing as well as increased indoor activity does decrease skin exposure to the sun which may negatively impact 25(OH)D status. Individuals that have dark pigmented skin are at higher risk for vitamin D deficiency as well since darker skin pigmentation requires more sun exposure to absorb the same amount of UVB radiation as someone with lighter skin pigmentation ( ). Fig. 2 displays risk factors for low 25(OH)D status.

Whether synthesized in the skin or ingested through foods and supplements, vitamin D is hydroxylated by the liver into the major circulating form of vitamin D, 25(OH)D, which is the form of vitamin D measured to assess vitamin D status ( ). 25(OH)D is further hydroxylated in the kidneys to form 1,25(OH) ₂ D Vitamin D, which is the biologically active form of vitamin D, performing many functions in the body related to its interactions with vitamin D receptors (VDR) ( ). Vitamin D that has been synthesized by the sun stays in circulation two to three times longer than vitamin D that is taken in supplement form. This is because vitamin D taken in supplement form is partially bound to lipoproteins which is cleared from the system before being absorbed ( ). Since vitamin D is a fat-soluble vitamin, there is research showing an inverse relationship between adiposity and low vitamin D status, which puts those who are obese at greater risk for vitamin D deficiency ( ; ).

The recommended intakes of vitamin D from the Institutes of Medicine (IOM) and Endocrine Society are noted in Table 2 . The IOM guidelines are created from a population model aiming to prevent vitamin D deficiency in most of the population ( ). IOM notes that most of the population intakes enough vitamin D to reach “sufficient” serum 25(OH)D levels (20 ng/mL) ( ). Guidelines from the Endocrine Society recommend higher intakes of vitamin D, as it is based from a medical model that incorporates the wide array of vitamin D functions, and suggests 30 ng/mL 25(OH)D levels are beneficial, and that there is a higher upper limit than IOM suggests ( ).

25(OH)D status can be measured in either nanograms (ng/mL) or in nanomoles (nmol/L). The World Health Organization and Endocrine Society considers a vitamin D deficiency as < 50 nmol/L (< 20 ng/ml), insufficiency as 50 to 75 nmol/L (25–30 ng/mL) and a sufficient status would be > 75 nmol/L (> 30 ng/mL) ( ). The best indicator of vitamin D status is a serum concentration of 25(OH)D according to the National Institute of Health due to its 15-day half-life ( ). 1,25(OH) ₂ D concentration, on the other hand, is not a good indicator of vitamin D status since concentrations are constantly changing related to metabolic processes ( ).

Function and physiology

Vitamin D plays an important role in many different functions of the body, including immunity, bone health, muscle and neuromuscular function, hormone synthesis, cell development, and gene expression. Vitamin D has also been linked to a reduction in cancer risk, autoimmune disorders, and chronic disease ( ).