The growth of recovery capital in clients of recovery residences in Florida, USA: a quantitative pilot study of changes in REC-CAP profile scores.

BACKGROUND: There is a growing evidence base around predictors of retention and completion in a range of recovery residence models, particularly Oxford Houses and Sober Living Houses, and recovery housing is recognized as a clearly evidenced area of recovery intervention. The aim of the study was to quantitatively assess recovery capital in a sample of recovery residence clients. METHOD: The study used a repeated measures self-completion of a standardized recovery capital instrument (REC-CAP) for clients retained across various houses within one Level 2 recovery residence provider whose program was based on a 12-step approach. While 823 clients participated in the baseline assessment, a sample of 267 clients was achieved for six-month follow-up interview, based on those retained in the residence. A logistic regression model examined factors associated with retention and a repeated measures marginal mixed model evaluated the factors associated with changes in recovery capital between the baseline and the follow-up assessment. RESULTS: Members of the group that remained in recovery residences were more likely to be older with a record of high participation in recovery groups, with greater drop-out among younger residents, female residents and those with an identified housing need. For those retained to follow-up, greater recovery capital growth was associated with employment, higher levels of social support and more recovery group involvement, as well as age and a higher quality of life. The need for family support was shown to reduce levels of recovery capital. However, those younger people who were retained reported better recovery capital growth during the initial six months of residence. CONCLUSION: The key conclusion is that while recovery capital generally increases during a stay in a recovery residence, it does not do so consistently across the sample population. This has implications for how pathways to recovery group engagement are supported for women and young people and how social support (encompassing housing, employment and family issues) is provided to those populations during periods of residence. This suggests the potential need for training and guidance for house managers working with these groups.

Neuroprotective effects of erythropoietin on acute metabolic and pathological changes in experimentally induced neurotrauma.

OBJECT: Head trauma is a dynamic process characterized by a cascade of metabolic and molecular events. Erythropoietin (EPO) has been shown to have neuroprotective effects in animal models of traumatic brain injury (TBI). Acute in vivo mechanisms and pathological changes associated with EPO following TBI are unknown. In this study the authors compare acute metabolic and pathological changes following TBI with and without systemically administered EPO. METHODS: Right frontal lobe microdialysis cannulae and right parietal lobe percussion hubs were inserted into 16 Sprague-Dawley rats. After a 4- to 5-day recovery, TBI was induced via a DragonFly fluid-percussion device at 2.5-2.8 atm. Rats were randomized into 2 groups, which received 5000 U/kg EPO or normal saline intraperitoneally 30 minutes after TBI. Microdialysis samples for glucose, lactate, pyruvate, and glutamate were obtained every 25 minutes for 10 hours. Rats were killed, their brains processed for light microscopy, and sections stained with H & E. RESULTS: Erythropoietin administered 30 minutes after TBI directly affects acute brain metabolism. Brains treated with EPO maintain higher levels of glucose 4-10 hours after TBI (p<0.01), lower levels of lactate 6-10 hours after TBI (p<0.01), and lower levels of pyruvate 7.5-10 hours after TBI (p<0.01) compared with saline-treated controls. Erythropoietin maintains aerobic metabolism after TBI. Systemic EPO administration reduces acute TBI-induced lesion volume (p<0.05). CONCLUSIONS: Following TBI, neuron use initially increases, with subsequent depletion of extracellular glucose, resulting in increased levels of extracellular lactate and pyruvate. This energy requirement can result in cell death due to increased metabolic demands. These data suggest that the neuroprotective effect of EPO may be partially due to improved energy metabolism in the acute phase in this rat model of TBI.