Reducing mental health disparities through transformative learning: a social change model with refugees and students.

Distribution of power and resources greatly impacts the mental health of individuals and communities. Thus, to reduce mental health disparities, it is imperative to address these social determinants of mental health through social change. Engaging in social change efforts requires people to critically engage with present conditions on personal, local, national, and global levels and to develop knowledge, capacity, and experience with envisioning and creating more equitable conditions. This critical engagement can be fostered through a process of transformative learning. In this article, we examine the Refugee Well-being Project (RWP), a program that aims to improve the mental health of refugees in the United States. From 2007 to 2009, participants in the RWP in New Mexico were refugees from the Great Lakes region of Africa. The RWP paired undergraduate students with refugees to engage in mutual learning and advocacy. Data from in-depth qualitative interviews with 72 refugees and 53 undergraduate students suggest that participation in the RWP constituted a transformative learning experience through which refugees and students came to new understandings of the relationship between social inequities and well-being. For many, this provided an impetus to work toward change at multiple levels.

Reducing refugee mental health disparities: a community-based intervention to address postmigration stressors with African adults.

Refugees resettled in the United States have disproportionately high rates of psychological distress. Research has demonstrated the roles of postmigration stressors, including lack of meaningful social roles, poverty, unemployment, lack of environmental mastery, discrimination, limited English proficiency, and social isolation. We report a multimethod, within-group longitudinal pilot study involving the adaptation for African refugees of a community-based advocacy and learning intervention to address postmigration stressors. We found the intervention to be feasible, acceptable, and appropriate for African refugees. Growth trajectory analysis revealed significant decreases in participants' psychological distress and increases in quality of life, and also provided preliminary evidence of intervention mechanisms of change through the detection of mediating relationships whereby increased quality of life was mediated by increases in enculturation, English proficiency, and social support. Qualitative data helped to support and explain the quantitative data. Results demonstrate the importance of addressing the sociopolitical context of resettlement to promote the mental health of refugees and suggest a culturally appropriate, and replicable model for doing so.

Fetal alcohol exposure alters GAP-43 phosphorylation and protein kinase C responses to contextual fear conditioning in the hippocampus of adult rat offspring.

BACKGROUND: The growth- and plasticity-associated protein GAP-43 plays a significant role in the establishment and remodeling of neuronal connections. We have previously shown that GAP-43 levels, protein kinase C (PKC) activity, and GAP-43 phosphorylation increase during contextual fear conditioning and that fetal alcohol exposure (FAE) decreases PKC activity and GAP-43 phosphorylation in the hippocampus of adult offspring. Drawing on these observations, we hypothesized that FAE manifests its cognitive impairment by disrupting PKC activation and membrane translocation, thereby decreasing GAP-43 phosphorylation and function. METHODS: Three groups of pregnant rat dams (FAE and two control diet groups) were placed on different diet regimens. Offspring from each of these groups were placed into each of four test groups, a contextual fear conditioned (CFC) group, a naïve unhandled group, and two nonlearning stress control groups. Hippocampi were dissected, homogenized, and used to prepare a cytosolic and a membrane fraction. These fractions were probed for total GAP-43, PKC-phosphorylated GAP-43, and several PKC subtypes. PKC activity also was measured in total homogenates. RESULTS: Compared with both control diet groups, FAE animals showed a deficit in the activation of PKC in the hippocampus at 24 hr but not at 1.5 hr after CFC. Likewise, we found that the amount of GAP-43 and its phosphorylation were decreased 24 hr after CFC in FAE rats but not at early times after training. Analysis of the translocation of various PKC isoforms revealed that FAE animals had decreased levels of membrane-bound PKC beta2 and PKC epsilon 24 hr after CFC. CONCLUSIONS: Considering the role of PKC activation and GAP-43 phosphorylation in synaptic plasticity, our results suggest that deficient translocation of PKC beta2 and PKC epsilon in the hippocampus may mediate the electrophysiological and behavioral deficits observed in fetal alcohol exposed animals.