Psychiatric explanations of poor oral intake: A clinically focused review.

BACKGROUND: Poor oral intake (POI) among medical-surgical inpatients can cause malnutrition and delay recovery due to medical consequences and the need for more invasive nutritional support. Many psychiatric conditions can cause POI; however, the role that psychiatric conditions play in POI has received limited attention to date. OBJECTIVE: This review aggregates available information on POI due to psychiatric conditions and provides a framework for the clinical approach to these conditions in hospitalized adult patients. METHODS: We searched PubMed and EMBASE for reviews of POI due to psychiatric causes, but no relevant publications were identified. Diagnostic criteria for relevant conditions in the DSM-5-TR and Rome IV were reviewed, as were C-L psychiatry textbooks and relevant society websites. This review was further supplemented by a case conference at the authors' institution. RESULTS: We have divided results into five sections for clinical utility: (1) the need to rule out medical and psychotropic causes of POI; (2) unpleasant somatic experiences causing POI; (3) mood, psychotic, catatonic, and neurocognitive disorders that can present with POI; (4) eating and feeding disorders; and (5) personal and interpersonal explanations of POI. Within each section, we review how to identify and manage each condition, specifically considering effects of treatment on oral intake. CONCLUSIONS: The clinical management of POI varies based on cause. For instance, psychostimulants can cause POI due to inappetence; however, they can treat POI due to abulia by improving motivation. The fact that such a broad range of psychiatric conditions can cause POI calls for a systematic clinical approach that considers the categories of potential causes. We also identified a need for prospective studies focused on the management of POI due to psychiatric conditions, as the literature on this topic is limited to case reports, case series, and retrospective cohort studies.

Induction of a Timed Metabolic Collapse to Overcome Cancer Chemoresistance.

Cancer relapse begins when malignant cells pass through the extreme metabolic bottleneck of stress from chemotherapy and the byproducts of the massive cell death in the surrounding region. In acute myeloid leukemia, complete remissions are common, but few are cured. We tracked leukemia cells in vivo, defined the moment of maximal response following chemotherapy, captured persisting cells, and conducted unbiased metabolomics, revealing a metabolite profile distinct from the pre-chemo growth or post-chemo relapse phase. Persisting cells used glutamine in a distinctive manner, preferentially fueling pyrimidine and glutathione generation, but not the mitochondrial tricarboxylic acid cycle. Notably, malignant cell pyrimidine synthesis also required aspartate provided by specific bone marrow stromal cells. Blunting glutamine metabolism or pyrimidine synthesis selected against residual leukemia-initiating cells and improved survival in leukemia mouse models and patient-derived xenografts. We propose that timed cell-intrinsic or niche-focused metabolic disruption can exploit a transient vulnerability and induce metabolic collapse in cancer cells to overcome chemoresistance.