![]() ![]() We used data from two clinical trials to illustrate that relaxing the 1:1 WTP/WTA assumption has an impact on the CEACs. Depending on this ratio, the area within the southwest quadrant of the cost-effectiveness plane in which any bootstrap cost-effect pairs will be considered to be cost effective will be smaller, resulting in a lower CEAC. The discrepancy between WTP and WTA for health changes can be expressed as a ratio: the accept/reject ratio (which can vary between 1 and infinity). Previous empirical evidence has shown that the relationship between WTP and WTA is not 1:1. The objective of this paper is to explore the impact that differences between WTP and WTA health changes have on CEACs. Construction of the curves relies on the assumption that the willingness to pay (WTP) for health gain is identical to the willingness to accept (WTA) health loss. Severens, Johan L Brunenberg, Daniëlle E M Fenwick, Elisabeth A L O'Brien, Bernie Joore, Manuela AĬost-effectiveness acceptability curves (CEACs) are a method used to present uncertainty surrounding incremental cost-effectiveness ratios (ICERs). It is argued that the CEAC is still a useful tool in describing and quantifying uncertainty around the ICER, especially in combination with other tools such as plots on the CE plane and value-of-information analysis.Ĭost-effectiveness acceptability curves and a reluctance to lose. ![]() Many of the perceived limitations can be attributed to the practice of interpreting the CEAC as a decision rule while it was not developed as such. Additionally, this paper reviews the advantages and limitations of the CEAC. In this paper, first the construction and interpretation of the CEAC is explained, both in the context of modelling studies and in the context of cost-effectiveness (CE) studies alongside clinical trials. Since the introduction of the cost-effectiveness acceptability curve (CEAC) in 1994, its use as a method to describe uncertainty around incremental cost-effectiveness ratios (ICERs) has steadily increased. Finally, we discuss the possibility of exploiting the greater accessibility of the gut relative to the brain in identifying targets to treat compulsive behavior disorders.Cost-effectiveness acceptability curves revisited. We posit a potential mechanism whereby gut barrier dysfunction-associated type 2 inflammation may drive compulsive behavior through histamine regulation of dopamine neurotransmission. Next, we discuss potential connections between gut barrier dysfunction, type 2 inflammation, and compulsive behavior. We examine connections between compulsive behavior and type 2 inflammation in Tourette syndrome, obsessive–compulsive disorder, autism, addiction, and post-traumatic stress disorder. ![]() Here, we discuss a potential link between gut barrier dysfunction and compulsive behavior that is mediated through “type 2” rather than “type 1” inflammation. Much less attention has been directed to potential connections between gut microbiota and compulsive behavior. To date, much of the focus of gut-brain axis research has been on gut microbiota regulation of anxiety and stress-related behaviors.
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