Abstract
Pacific populations, including those in Micronesia such as Kiribati, suffer a high burden of metabolic disease. While there have been extensive studies of metabolic diseases, including Type 2 Diabetes Mellitus (T2DM), gout, and others, undertaken globally, Pacific peoples, including I-Kiribati (The Indigenous people of Kiribati), are under-represented. In particular, very few studies exploring the genetics contributing to disease risk in Micronesian populations, such as I-Kiribati, have been undertaken. This thesis focuses on exploring metabolic disease in I-Kiribati living in Aotearoa, New Zealand (NZ), using a range of different approaches – both quantitative and qualitative. I aimed to: 1. Develop and apply a culturally appropriate research strategy to investigate the current metabolic health status of I-Kiribati in NZ; 2. Test for the association of known genomic markers associated with metabolic disease in other Pacific populations in NZ I Kiribati ; 3. Investigate the shared genetic ancestry between I-Kiribati and the broader Pacific, which may have implications for our understanding of metabolic disease, and 4. Undertake a preliminary investigation of the lived experiences of I-Kiribati living with metabolic disease. This research metaphorically followed the steps of making a Kiribati cultural string, Te Kora, by combining Western and I-Kiribati cultural aspects into my research steps to investigate metabolic health, which were all guided by an elder, Kiribati community members and a cultural advisor, to ensure that my research steps were culturally appropriate. A cohort of 174 I-Kiribati was recruited throughout New Zealand. My research confirmed that metabolic disease is a health burden for the NZ I-Kiribati community, in particular, gout and T2DM. A pattern of early onset T2DM was detected, and there was a consistent trend of non-compliance with prescribed medications for those suffering from gout. A number of common genetic variants associated with disease risk in other populations were also found to contribute risk in I-Kiribati, including variants in CREBRF, APOC1, TCFL2 and GCKR. However, not all genetic risk variants previously detected among other Pacific populations were significantly associated with metabolic disease among I-Kiribati. This was likely related to the small sample size of this study but may also be a result of genetic ancestry differences between Polynesians and Micronesians. I-Kiribati have higher genetic affinities to Central/Eastern Micronesians than Western Micronesians and Polynesians.
My qualitative interviews into the lived experiences of I-Kiribati suffering from metabolic diseases revealed that those suffering disease faced social stigma, and the diseases significantly negatively impacted their lives. If we want to see positive health outcomes for I-Kiribati, there must be earlier intervention and an increase in community education through workshops or meetings/maroro conducted by I-Kiribati health care workers in collaboration with health agencies to raise awareness on the signs, symptoms and the importance of taking medications to alleviate metabolic symptoms. Genomically-informed treatments for metabolic disease should consider the genetic variation that exists within Pacific populations; in doing so, this will allow the development of efficient and appropriate precision medicine to Pacific communities, rather than applying a “one-size fits all” approach.