Purpose of Review Diet, physical activity, and sleep are three major modifiable lifestyle factors. This selective review examines the evidence for strong and reliable associations between these three lifestyle factors and risk of dementia and cognitive decline, in an effort to assist clinicians with providing more informed answers to the common questions they face from patients. Recent Findings Certain aspects of nutrition can decrease risk for dementia. Physical activity has also been associated with delayed or slower age-related cognitive decline. In addition, emerging evidence links sleep dysfunction and dementia, with amyloid deposition being a possible mediator. Summary Data from further clinical trials are needed before more definitive conclusions can be drawn regarding the efficacy of these lifestyle interventions for lowering the risk of incident dementia and cognitive decline. Nevertheless, it is reasonable to make recommendations to our patients to adopt certain dietary changes and to engage in regular physical activity to improve cardiovascular risk factors for dementia. It is also reasonable to include questions on sleep during cognitive evaluations of the elderly, given the common co-occurrence of sleep dysfunction and cognitive impairment in the elderly population.

Objective: Studies have detected differences in various measures of bone health between individuals with autism spectrum disorder (ASD) and their peers. However, these measures do not amount to direct clinical evidence of increased orthopedic pathology in this population. Some of the most compelling evidence to this effect comes from case reports of nutritional rickets in children with ASD. We report on 1 such case that, to our knowledge, is the first report of nutritional rickets in ASD necessitating corrective surgery. Methods: Case report, review of relevant literature, and implications for further research. Results: An 11-year-old girl with ASD was admitted for postoperative medical comanagement after successful repair of bilateral genu valgum (knock knees). On admission, the patient's mother reported that the patient was a “picky eater.” No cause had been determined preoperatively, although the deformity had developed at 10 years of age, thereby qualifying as pathologic. The medical team considered rickets because of the patient's limited diet. Subsequent laboratory work demonstrated hypocalcemia, vitamin D deficiency, and secondary hyperparathyroidism. The patient was diagnosed with nutritional rickets due to inadequate vitamin D intake, a consequence of severe food selectivity associated with ASD. Conclusion: This case exemplifies the extreme orthopedic and metabolic complications that can result from food selectivity in children with ASD, pointing to the need for further research into the prevalence and causes of orthopedic pathology and nutritional rickets in this population. The case also underscores the need for evidence-based guidelines to prevent orthopedic pathology in children with ASD.

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