ABSTRACT
INTRODUCTION: American Indian/Alaska Native (AI/AN) pregnant people face barriers to health and healthcare that put them at risk of pregnancy complications. Rates of severe maternal morbidity (SMM) among Indigenous pregnant people are estimated to be twice that of non-Hispanic White (NHW) pregnant people. METHODS: Race-corrected Oregon Hospital Discharge and Washington Comprehensive Hospital Abstract Reporting System data were combined to create a joint dataset of births between 2012 and 2016. The analytic sample was composed of 12,535 AI/AN records and 313,046 NHW records. A multilevel logistic regression was used to assess the relationship between community-level, individual and pregnancy risk factors on SMM for AI/AN pregnant people. RESULTS: At the community level, AI/AN pregnant people were more likely than NHW to live in mostly or completely rural counties with low median household income and high uninsured rates. They were more likely to use Medicaid, be in a high-risk age category, and have diabetes or obesity. During pregnancy, AI/AN pregnant people were more likely to have insufficient prenatal care (PNC), gestational diabetes, and pre-eclampsia. In the multilevel model, county accounted for 6% of model variance. Hypertension pre-eclampsia, and county rurality were significant predictors of SMM among AI/AN pregnant people. High-risk age, insufficient PNC and a low county insured rate were near-significant at p < 0.10. DISCUSSION: Community-level factors are significant contributors to SMM risk for AI/AN pregnant people in addition to hypertension and pre-eclampsia. These findings demonstrate the need for targeted support in pregnancy to AI/AN pregnant people, particularly those who live in rural and underserved communities.
What is already known on this subject? American Indian and Alaska Native pregnant people face higher rates of severe maternal morbidity and mortality, and the risk is exacerbated for rural Indigenous pregnant people.What this study adds? This publication uses a multilevel model to assess the contribution of community-level factors in severe maternal morbidity risk for American Indian and Alaska Native pregnant people. This analysis highlights the important role that rurality, prenatal care adequacy and access to insurance play in maternal morbidity risk and discusses how those risks are disproportionately felt by American Indian and Alaska Native pregnant people in the Pacific Northwest.
Subject(s)
American Indian or Alaska Native , Pregnancy Complications , Residence Characteristics , Social Determinants of Health , Female , Humans , Pregnancy , Alaska Natives/statistics & numerical data , American Indian or Alaska Native/statistics & numerical data , Hypertension/epidemiology , Hypertension/ethnology , Indians, North American/statistics & numerical data , Logistic Models , Pre-Eclampsia/epidemiology , Pre-Eclampsia/ethnology , Washington , Social Determinants of Health/ethnology , Social Determinants of Health/statistics & numerical data , Residence Characteristics/statistics & numerical data , Pregnancy Complications/epidemiology , Pregnancy Complications/ethnology , Pregnancy Complications/etiology , Pregnancy Complications/therapy , Rural Population/statistics & numerical data , Northwestern United States/epidemiology , Medically Underserved Area , Medically Uninsured/ethnology , Medically Uninsured/statistics & numerical dataABSTRACT
Synaptic pathology and mitochondrial oxidative damage are early events in Alzheimer's disease (AD) progression. Loss of synapses and synaptic damage are the best correlates of cognitive deficits found in AD patients. Recent research on amyloid beta (Aß) and mitochondria in AD revealed that Aß accumulates in synapses and synaptic mitochondria, leading to abnormal mitochondrial dynamics and synaptic degeneration in AD neurons. Further, recent studies using live-cell imaging and primary neurons from amyloid beta precursor protein (AßPP) transgenic mice revealed reduced mitochondrial mass, defective axonal transport of mitochondria and synaptic degeneration, indicating that Aß is responsible for mitochondrial and synaptic deficiencies. Tremendous progress has been made in studying antioxidant approaches in mouse models of AD and clinical trials of AD patients. This article highlights the recent developments made in Aß-induced abnormal mitochondrial dynamics, defective mitochondrial biogenesis, impaired axonal transport and synaptic deficiencies in AD. This article also focuses on mitochondrial approaches in treating AD, and also discusses latest research on mitochondria-targeted antioxidants in AD. This article is part of a Special Issue entitled: Antioxidants and Antioxidant Treatment in Disease.