Objective Weight‐biased attitudes and views held by health care professionals can have a negative impact on the patient‐provider relationship and the provision of care, but studies have found mixed results about the extent and nature of bias, which warrants a review of the evidence. Methods A systematic review and random‐effects meta‐analysis were conducted by including studies up to January 12, 2021. Results A total of 41 studies met inclusion criteria, with 17 studies providing sufficient data to be meta‐analyzed. A moderate pooled effect (standardized mean difference = 0.66; 95% CI: 0.37‐0.96) showed that health care professionals demonstrate implicit weight bias. Health care professionals also report explicit weight bias on the Fat Phobia Scale, Antifat Attitudes Scale, and Attitudes Towards Obese Persons Scale. Findings show that medical doctors, nurses, dietitians, psychologists, physiotherapists, occupational therapists, speech pathologists, podiatrists, and exercise physiologists hold implicit and/or explicit weight‐biased attitudes toward people with obesity. A total of 27 different outcomes were used to measure weight bias, and the overall quality of evidence was rated as very low. Conclusions Future research needs to adopt more robust research methods to improve the assessment of weight bias and to inform future interventions to address weight bias among health care professionals.

Studies in non-neuronal cells show that c-Jun N-terminal kinases (JNK) play a key role in apoptotic celldeath. In some neurons JNK is also thought to initiate cell death by the activation of c-Jun. JNK inhibition has been achieved pharmacologically by inhibiting upstream kinases, but there has been no direct demonstration that inhibition of JNK can prevent neuronal death. We have therefore examined whether the JNK binding domain (JBD) of JNK-interacting protein-1 (JIP-1, a scaffold protein and specific inhibitor of JNK) can inhibit c-Jun phosphorylation and support the survival of sympathetic neurons deprived of NGF. We show that expression of the JBD in >80% of neurons was sufficient to prevent the phosphorylation of c-Jun and its nuclear accumulation as well as abrogate neuronal cell death induced by NGF deprivation. JBD expression also preserved the capacity of mitochondria to reduce MTT. Interestingly, although the PTB domain of JIP was reported to interact with rhoGEF, expression of the JBD domain was sufficient to localize the protein to the membrane cortex and growth cones. Hence, JNK activation is a key event in apoptotic death induced by NGF withdrawal, where its point of action lies upstream of mitochondrial dysfunction.

Neurocognitive abilities have frequently been claimed to be involved in the aetiology of psychopathology. Neurocognitive deficits have been reported across many disorders, and theoretical perspectives associate these deficits to the onset and maintenance of the symptomology. Recently, the heterogeneity of symptoms, and comorbidity of disorders, have motivated the development of structural models of psychopathology. Structural models indicate that factors such as internalising, externalising, thought disorder and the p-factor account for a wide variety of symptomology. It is unclear how neurocognitive abilities are best examined within these structures to advance our understanding of psychopathology. In this paper, we use Caspi et al.’s seminal writings as a framework to describe how neurocognitive abilities have been previously associated with categorical disorders and recently associated, and claimed to drive, the factors of psychopathology. We discuss the implications of the p-factor as a substantive construct or statistical artefact, and how this impacts the exploration of neurocognitive abilities and psychopathology. Further, we provide the case for alternative structural approaches, describe an innovative hypothesis of neurocognitive functioning, the multidimensional hypothesis, and explain how this may further our understanding of the heterogeneity of neurocognitive performance and psychopathology at the individual level. Finally, we provide a road forward for the future examination of neurocognitive abilities in psychopathology.

Neurocognitive deficits have been consistently associated with a wide range of psychopathology and are proposed to not only be a consequence of the development of psychopathology but also directly involved in its aetiology. However, there is no clear understanding of what neurocognitive processes are particularly important to mental health. In this paper, we explored the association between neurocognitive abilities and the factors derived from structural models of psychopathology. Four hundred participants from a representative community sample completed measures of symptomology and substance use, as well as 8 neurocognitive tasks. We found a correlated-factors model, with internalising and externalising as the higher-order factors, and a single-factor model with only the p-factor, to be good fits for the data. Tasks that measured the speed of processing were significantly associated with internalising, externalising, and the p-factor, and accounted for significant amounts of unique variance in the factors after accounting for the common variance of the other tasks. Tasks that measured working memory, shifting, and inhibition were not significantly associated with psychopathology factors. Our findings suggest that neurocognitive abilities may not be differentially associated with psychopathology factors, but that speed of processing is a common correlate of the factors. We emphasise the importance of examining neurocognitive abilities and psychopathology on the individual level.