The primary finding of this investigation is that adults with CP are at risk for insufficient and deficient serum vitamin D; however, vulnerability was not associated with the severity of motor impairment. It is well known that severely impaired individuals with CP experience significant feeding issues and are at greater risk for malnutrition, which are in-turn thought to be the primary drivers of musculoskeletal fragility and altered growth trajectories in this population. Interestingly, we found that individuals classified in the highest severity category (i.e., GMFCS V) had a similar serum vitamin D (25(OH)D) status (30.8 ng/mL) as individuals in the least impaired category (i.e., GMFCS I) (27.9 ng/mL). This does not imply that severity of motor impairment is unrelated to nutrition status, growth, and/or bone health in CP; however, it does highlight an independent factor that may pose an even greater risk for vitamin D insufficiency. The overall prevalence of vitamin D insufficiency or deficiency was approximately 56%, which is similar to the typically-developed adult population [21, 24]. Interestingly, unlike the general population , BMI was not associated with serum 25(OH)D in this study.
Rather, abdominal obesity was the strongest predictor for serum vitamin D in this heterogeneous sample of adults with CP, even after adjusting for age, sex, race, season, and level of motor function. Indeed, there is a well-established link between vitamin D deficiency, abdominal obesity and cardiometabolic risk [12, 26], and yet most studies do not account for at-risk populations with severe motor disabilities. Moreover, although several studies have identified a general increased prevalence of obesity among children with CP [27, 28], the influence of obesity on secondary health complications has yet to be studied through the lifespan. It is of course logical to presume that the primary neurological insult associated with CP is the underlying cause for impaired growth and risk for musculoskeletal deterioration, but it is also likely that excessive central adiposity may lead to exaggerated risk for a non-CP, comorbid sequela as children with CP transition into adulthood. The current findings clearly support the need for greater clinical attention to assessments of serum vitamin D status in all patients with CP. Particular attention should also be given to individuals with CP who are African American, as vitamin D was significantly lower as compared to Non-Hispanic white individuals.
Moreover, children and adults with CP have significantly diminished lean body mass  and greater intermuscular adipose tissue , which collectively highlights the implications of skeletal muscle deterioration. Thus, even normal BMIs in this population may disguise excess body fat (i.e., “obesity misclassification” ), and risk for cardiovascular and metabolic dysregulation. Based on standard BMI cutoffs, our data revealed that overweight and obesity are common in adults with CP; however, BMI was not associated with vitamin D status. This is congruent with our previous work , and that of others  which demonstrates that indicators of central adiposity are potentially more sensitive for detecting standard clinical markers of cardiometabolic risk (e.g. triglycerides, HDL-cholesterol, total cholesterol to HDL cholesterol ratio, LDL-cholesterol, HOMA-IR, etc..) in adults with CP. Collectively, these findings support our ongoing contention that adults with CP are at higher risk for normal weight obesity and cardiometabolic dysregulation , and that indicators of central adiposity are superior to BMI for risk stratification. This is not surprising considering the mounting evidence in support of this diagnostic paradigm shift, even among the general population , and thus clinicians should be aware of the appropriate gender- and race/ethnicity-specific recommended waist circumference thresholds for abdominal obesity [34, 35].
In the general population, recent data have also revealed a link between vitamin D and preservation of muscular strength . This may have significant implications for individuals with CP over the lifespan, as even children with CP have impaired recruitment of target musculature during voluntary activity, and an over-recruitment and co-activation of antagonist musculature . Premature sarcopenia and muscular weakness in CP are suggested to translate to acute functional deficit and disability . As a result, functional loss, especially of mobility, is a major issue in adults with CP. The minority of individuals that actually report preservation of mobility throughout adulthood accredit this to maintenance of strength, balance and overall fitness. It is therefore critical to gain a greater understanding of how treatment of such modifiable risk factors as vitamin D deficiency could impact long term preservation of functional capacity and activity participation.
An obvious limitation in this study is that we could not account for dietary intake of calcium or vitamin D. Thus, it is possible that more severely affected individuals were adhering to a stricter regimen of nutrient supplementation (as is commonly recommended with anticonvulsant therapies), which would explain the lack of differences across GMFCS levels. Future research should account for nutrient intake, as well as any medication that may interfere with calcium and vitamin D. Further, as with all cross-sectional investigations, a limitation of this study is the inability to disentangle the cause-effect relationship between predictors and outcomes. Perhaps just as importantly, with this design we were unable to examine numerous potential mediators that were not measured. For example, no measures of muscle strength were made, and thus although vitamin D status was not associated with GMFCS in this study, it is possible that vitamin D status may affect muscle strength differently among individuals with more severe mobility impairments. It is also plausible that vitamin D deficiency may lead to diminished vitamin D receptor (VDR) in type II muscle fiber (see recent review ), and thus have a direct influence on muscular weakness, or conversely, strength improvement, with supplementation .