Diet and physical activity in childhood cancer survivors: a review of the literature.

Treatment advances have led to a growing population of childhood cancer survivors. Many are at risk for developing treatment-related late effects. Diet and physical activity may affect levels of health risk. A number of papers have examined these behaviors in childhood cancer survivors. The purpose of this study was to provide a review and summary of the published studies in the areas of diet, physical activity, and related interventions among childhood cancer survivors. A systematic search was conducted for studies published prior to October 2009. Descriptive and intervention studies that included survivors of childhood cancers and a measurement of diet and/or physical activity were reviewed. Twenty-six manuscripts met criteria: ten addressed diet; 20 addressed physical activity, and six included intervention studies. Results suggest that childhood cancer survivors engage in health-promoting activities at rates comparable to the general population. Behavioral interventions have mostly targeted physical activity. Results, overall, are not encouraging, due primarily to difficulties recruiting and retaining participants. Although more rigorous studies are needed, recommendations for health-promoting behaviors should be a regular topic of discussion between health care providers and their childhood cancer survivor patients.

Design and recruitment of the Chicago Healthy Living Study: a study of health behaviors in a diverse cohort of adult childhood cancer survivors.

BACKGROUND: Adult childhood cancer survivors are at higher risk for developing late medical effects related to their cancer treatments. Health-promoting behaviors may reduce the risk of some late effects and the severity of others. This article describes the design and recruitment of the Chicago Healthy Living Study (CHLS), an on-going study designed to examine the health behaviors and body mass index of minority adult childhood cancer survivors compared with nonminority survivors and noncancer controls. METHODS: Survivors are identified by the hospital cancer registries at 5 treating institutions in the Chicago area; then, a multilevel recruitment plan will be implemented with the objective of enrolling 450 adult survivors of childhood cancer (150 in each racial/ethnic group). Simultaneously, 375 adult African-American, Hispanic, and non-Hispanic white noncancer controls (125 in each racial/ethnic group) living in the Chicago area will be recruited by using listed, targeted digit dialing. All participants will complete a 2-hour interview of questionnaires related to diet, physical activity, smoking, and associated mediators. Height and weight also will be measured. CONCLUSIONS: The CHLS will provide important information on the health behaviors of adult minority childhood cancer survivors that can be used to inform the development of interventions to improve modifiable risks.

Chronic 3,4-dihydroxyphenylalanine treatment induces dyskinesia in aphakia mice, a novel genetic model of Parkinson's disease.

L-DOPA-induced dyskinesia (LID) is one of the main limitations of long term L-DOPA use in Parkinson's disease (PD) patients. We show that chronic L-DOPA treatment induces novel dyskinetic behaviors in aphakia mouse with selective nigrostriatal deficit mimicking PD. The stereotypical abnormal involuntary movements were induced by dopamine receptor agonists and attenuated by antidyskinetic agents. The development of LID was accompanied by preprodynorphin and preproenkephalin expression changes in the denervated dorsal striatum. Increased FosB-expression was also noted in the dorsal striatum. In addition, FosB expression was noted in the pedunculopontine nucleus and the zona incerta, structures previously not examined in the setting of LID. The aphakia mouse is a novel genetic model with behavioral and biochemical characteristics consistent with those of PD dyskinesia and provides a more consistent, convenient, and physiologic model than toxic lesion models to study the mechanism of LID and to test therapeutic approaches for LID.