This thesis explores the impact of type 2 diabetes among Indian and Pakistani migrants. Indians and Pakistanis living in the UK have a high incidence of type 2 diabetes and associated complications. Research is needed in order to understand factors that make it difficult to adhere to lifestyle advice about diet, exercise and medication. Drawing on data collected during a sixteen-month ethnographic investigation, this thesis explores Indians’ and Pakistanis’ perceptions of diabetes. The research revealed that Indians and Pakistanis related the onset of diabetes to processes of migration and settling in the UK as well as to stress and depression. In particular, holding on to negative thoughts and worries, were perceived by respondents as directly affecting the body by causing stress, depression and eventually illness. Struggles over diabetes control were also perceived as to cause distress. Specifically, respondents struggled to adhere to a healthy diet regime, since food, especially taste, played a crucial role in forming, reinforcing and demarcating social relations and in ensuring cultural continuity. In addition, respondents struggled to ‘adhere’ to their prescriptions of diabetes medications due to the uncomfortable side effects that they experienced, particularly in the stomach. Respondents, however, counteracted side effects by turning to alternative medications which were perceived to facilitate flow within the circulatory and digestive system. Thus, in spite of the difficulties that Indians and Pakistanis experienced in following biomedical recommendations for diabetes control, they still actively engaged in searching and using different treatments available to them in order to control the disease.

Long-term memories turn labile with reactivation and undergo a re-stabilization process, termed reconsolidation, involving molecular changes that allow updating of an existing memory trace. Such molecular changes may involve the activation of kinases and expression of proteins related to the increase of synaptic plasticity and memory formation. A kinase reported to have a role in a variety of memory tasks is the extracellular signal-regulated kinase 1/2 (ERK1/2). The downstream activation of ERK targets other regulatory enzymes, transcription factors and cytoskeletal proteins, which allow structural changes in the neuron due to protein synthesis up-regulation. Among the proteins up-regulated by ERK activity is the activity-regulated cytoskeleton-associated protein (ARC), an immediate early gene related to synaptic plasticity. The phase-dependent roles of ERK and ARC have not been examined as part of the molecular mechanisms triggered after a learning experience. In this study I used conditioned taste aversion (CTA) as the learning paradigm and investigated the expression of pERK and ARC in brain regions critical for taste information processing such as the insular cortex and the amygdala. A differential pattern of protein expression was observed in the insular cortex (IC) two hours after taste memory acquisition: pERK activity increased in the aversively conditioned group while ARC increased in the group that received only the novel taste. The central amygdala (CeA) showed a significant increase in pERK, but not ARC activity after CTA training. Immunoblotting experiments performed after memory retrieval in the appetitive group show that pERK continues to signal aversive taste to the IC with ARC exhibiting heightened expression an hour later. An increase in ARC expression 30 minutes after reactivation of the aversive taste was seen in the basolateral amygdala and the CeA exhibited a similar increase at 60 and 90 minutes. Local infusion of ARC antisense oligonucleotides within the IC interfered with the consolidation of safe taste memories, but not with their acquisition. Trace update experiments showed that ARC influences the memory switch from aversive to safe, but not the reverse. Our results indicate that ARC plays a critical role in consolidation and updating of safe taste memories, and the ARC signaling could possibly elicit ERK activation.