Three Years In--Changing Plan Features in the U.S. Health Insurance Marketplace

Background: A central objective of recent U.S. healthcare policy reform, most notably the Affordable Care Act\u27s (ACA) Health Insurance Marketplace, has been to increase access to stable, affordable health insurance. However, changing market dynamics (rising premiums, changes in issuer participation and plan availability) raise significant concerns about the marketplaces\u27 ability to provide a stable source of healthcare for Americans that rely on them. By looking at the effect of instability on changes in the consumer choice set, we can analyze potential incentives to switch plans among price-sensitive enrollees, which can then be used to inform policy going forward. Methods: Data on health plan features for non-tobacco users in 2512 counties in 34 states participating in federally-facilitated exchanges from 2014 to 2016 was obtained from the Centers for Medicaid & Medicare Services. We examined how changes in individual plan features, including premiums, deductibles, issuers, and plan types, impact consumers who had purchased the lowest-cost silver or bronze plan in their county the previous year. We calculated the cost of staying in the same plan versus switching to another plan the following year, and analyzed how costs vary across geographic regions. Results: In most counties in 2015 and 2016 (53.7 and 68.2%, respectively), the lowest-cost silver plan from the previous year was still available, but was no longer the cheapest plan. In these counties, consumers who switched to the new lowest-cost plan would pay less in monthly premiums on average, by $51.48 and$55.01, respectively, compared to staying in the same plan. Despite potential premium savings from switching, however, the majority would still pay higher average premiums compared to the previous year, and most would face higher deductibles and an increased probability of having to change provider networks. Conclusion: While the ACA has shown promise in expanding healthcare access, continued changes in the availability and affordability of health plans are likely to result in churning and switching among enrollees, which may have negative ramifications for their health going forward. Future healthcare policy reform should aim to stabilize marketplace dynamics in order to encourage greater care continuity and limit churning

Three years in – changing plan features in the U.S. health insurance marketplace

Abstract Background A central objective of recent U.S. healthcare policy reform, most notably the Affordable Care Act’s (ACA) Health Insurance Marketplace, has been to increase access to stable, affordable health insurance. However, changing market dynamics (rising premiums, changes in issuer participation and plan availability) raise significant concerns about the marketplaces’ ability to provide a stable source of healthcare for Americans that rely on them. By looking at the effect of instability on changes in the consumer choice set, we can analyze potential incentives to switch plans among price-sensitive enrollees, which can then be used to inform policy going forward. Methods Data on health plan features for non-tobacco users in 2512 counties in 34 states participating in federally-facilitated exchanges from 2014 to 2016 was obtained from the Centers for Medicaid & Medicare Services. We examined how changes in individual plan features, including premiums, deductibles, issuers, and plan types, impact consumers who had purchased the lowest-cost silver or bronze plan in their county the previous year. We calculated the cost of staying in the same plan versus switching to another plan the following year, and analyzed how costs vary across geographic regions. Results In most counties in 2015 and 2016 (53.7 and 68.2%, respectively), the lowest-cost silver plan from the previous year was still available, but was no longer the cheapest plan. In these counties, consumers who switched to the new lowest-cost plan would pay less in monthly premiums on average, by $51.48 and$55.01, respectively, compared to staying in the same plan. Despite potential premium savings from switching, however, the majority would still pay higher average premiums compared to the previous year, and most would face higher deductibles and an increased probability of having to change provider networks. Conclusion While the ACA has shown promise in expanding healthcare access, continued changes in the availability and affordability of health plans are likely to result in churning and switching among enrollees, which may have negative ramifications for their health going forward. Future healthcare policy reform should aim to stabilize marketplace dynamics in order to encourage greater care continuity and limit churning.https://deepblue.lib.umich.edu/bitstream/2027.42/144501/1/12913_2018_Article_3198.pd

Decreasing physical and verbal aggression in a brain injured nursing home resident

Following a traumatic brain injury, patients often suffer a series of psychological and psychiatric sequalae. This study presents the case of Mr. K, a 52-year-old brain-injured nursing home resident who exhibited problematic physical aggression and verbal abuse toward staff and residents. His problem behaviors were intertwined with an ethical issue involving a heterosexual relationship with another resident who also was brain injured. Following a functional assessment of antecedents and consequences, a differential reinforcement of other behavior (DRO) schedule was implemented. Specifically, the resident was rewarded with short-term and long-term reinforcers following periods of time during which behaviors other than the target behavior were emitted. Although the behavior plan was successful, it resulted in a more noticeable decrease in physically aggressive behaviors than verbally abusive behaviors. Implications include increasing awareness of use of behavior plans in nursing homes and of ethical and behavioral issues associated with sexuality among nursing home residents

DHODH modulates transcriptional elongation in the neural crest and melanoma

Melanoma is a tumour of transformed melanocytes, which are originally derived from the embryonic neural crest. It is unknown to what extent the programs that regulate neural crest development interact with mutations in the BRAF oncogene, which is the most commonly mutated gene in human melanoma1. We have used zebrafish embryos to identify the initiating transcriptional events that occur on activation of human BRAF(V600E) (which encodes an amino acid substitution mutant of BRAF) in the neural crest lineage. Zebrafish embryos that are transgenic for mitfa:BRAF(V600E) and lack p53 (also known as tp53) have a gene signature that is enriched for markers of multipotent neural crest cells, and neural crest progenitors from these embryos fail to terminally differentiate. To determine whether these early transcriptional events are important for melanoma pathogenesis, we performed a chemical genetic screen to identify small-molecule suppressors of the neural crest lineage, which were then tested for their effects on melanoma. One class of compound, inhibitors of dihydroorotate dehydrogenase (DHODH), for example leflunomide, led to an almost complete abrogation of neural crest development in zebrafish and to a reduction in the self-renewal of mammalian neural crest stem cells. Leflunomide exerts these effects by inhibiting the transcriptional elongation of genes that are required for neural crest development and melanoma growth. When used alone or in combination with a specific inhibitor of the BRAF(V600E) oncogene, DHODH inhibition led to a marked decrease in melanoma growth both in vitro and in mouse xenograft studies. Taken together, these studies highlight developmental pathways in neural crest cells that have a direct bearing on melanoma formation

Surface Feature-Guided Mapping of Cerebral Metabolic Changes in Cognitively Normal and Mildly Impaired Elderly

Purpose: The aim of this study was to investigate the longitudinal positron emission tomography (PET) metabolic changes in the elderly. Procedures: Nineteen nondemented subjects (mean Mini-Mental Status Examination 29.4±0.7 SD) underwent two detailed neuropsychological evaluations and resting 2-deoxy-2-[F-18]fluoro-D-glucose (FDG)-PET scan (interval 21.7±3.7 months), baseline structural 3T magnetic resonance (MR) imaging, and apolipoprotein E4 genotyping. Cortical PET metabolic changes were analyzed in 3-D using the cortical pattern matching technique. Results: Baseline vs. follow-up whole-group comparison revealed significant metabolic decline bilaterally in the posterior temporal, parietal, and occipital lobes and the left lateral frontal cortex. The declining group demonstrated 10–15 % decline in bilateral posterior cingulate/precuneus, posterior temporal, parietal, and occipital cortices. The cognitively stable group showed 2.5–5% similarly distributed decline. ApoE4-positive individuals underwent 5–15 % metabolic decline in the posterior association cortices. Conclusions: Using 3-D surface-based MR-guided FDG-PET mapping, significant metaboli

New genetic loci link adipose and insulin biology to body fat distribution.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe

Fine-mapping analysis including over 254,000 East Asian and European descendants identifies 136 putative colorectal cancer susceptibility genes

Genome-wide association studies (GWAS) have identified more than 200 common genetic variants independently associated with colorectal cancer (CRC) risk, but the causal variants and target genes are mostly unknown. We sought to fine-map all known CRC risk loci using GWAS data from 100,204 cases and 154,587 controls of East Asian and European ancestry. Our stepwise conditional analyses revealed 238 independent association signals of CRC risk, each with a set of credible causal variants (CCVs), of which 28 signals had a single CCV. Our cis-eQTL/mQTL and colocalization analyses using colorectal tissue-specific transcriptome and methylome data separately from 1299 and 321 individuals, along with functional genomic investigation, uncovered 136 putative CRC susceptibility genes, including 56 genes not previously reported. Analyses of single-cell RNA-seq data from colorectal tissues revealed 17 putative CRC susceptibility genes with distinct expression patterns in specific cell types. Analyses of whole exome sequencing data provided additional support for several target genes identified in this study as CRC susceptibility genes. Enrichment analyses of the 136 genes uncover pathways not previously linked to CRC risk. Our study substantially expanded association signals for CRC and provided additional insight into the biological mechanisms underlying CRC development