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Summary Objectives Although monitoring is considered a key component of effective behaviour change, the development of apps has allowed consumers to constantly evaluate their own diet, with little examination of what this might mean for eating behaviour. The aim of this study was to investigate whether self‐monitoring of diet using the app MyFitnessPal or daily self‐weighing increases the reported occurrence of eating disorders in adults with overweight/obesity following a weight loss programme. Methods Two hundred fifty adults with body mass index ≥ 27 kg/m2 received diet and exercise advice and were randomized to one of four monitoring strategies (daily self‐weighing, MyFitnessPal, brief monthly consults or self‐monitoring hunger) or control for 12 months. The Eating Disorder Examination Questionnaire 6.0 was used to assess eating disorder symptoms and behaviours for the previous 28 d at 0 and 12 months. Results There were no significant differences in the global Eating Disorder Examination Questionnaire score or the subscales between those in the four monitoring groups and the control at 12 months (all p ≥ 0.164), nor were there differences in binge eating, self‐induced vomiting, laxative misuse or excessive exercise at 12 months (p ≥ 0.202). The overall prevalence of one or more episodes of binge eating was 53.6% at baseline and 50.6% at 12 months, with no change over time (p = 0.662). Conclusions There was no evidence that self‐monitoring, including using diet apps like MyFitnessPal or daily self‐weighing, increases the reported occurrence of eating disorder behaviours in adults with overweight/obesity who are trying to lose weight.

Complement component 1 Q subcomponent-binding protein (C1QBP; also known as p32) is a multi-compartmental protein whose precise function remains unknown. It is an evolutionary conserved multifunctional protein localized primarily in the mitochondrial matrix and has roles in inflammation and infection processes, mitochondrial ribosome biogenesis, and regulation of apoptosis and nuclear transcription. It has an N-terminal mitochondrial targeting peptide that is proteolytically processed after import into the mitochondrial matrix, where it forms a homotrimeric complex organized in a doughnut-shaped structure. Although C1QBP has been reported to exert pleiotropic effects on many cellular processes, we report here four individuals from unrelated families where biallelic mutations in C1QBP cause a defect in mitochondrial energy metabolism. Infants presented with cardiomyopathy accompanied by multisystemic involvement (liver, kidney, and brain), and children and adults presented with myopathy and progressive external ophthalmoplegia. Multiple mitochondrial respiratory-chain defects, associated with the accumulation of multiple deletions of mitochondrial DNA in the later-onset myopathic cases, were identified in all affected individuals. Steady-state C1QBP levels were decreased in all individuals' samples, leading to combined respiratory-chain enzyme deficiency of complexes I, III, and IV. C1qbp -/- mouse embryonic fibroblasts (MEFs) resembled the human disease phenotype by showing multiple defects in oxidative phosphorylation (OXPHOS). Complementation with wild-type, but not mutagenized, C1qbp restored OXPHOS protein levels and mitochondrial enzyme activities in C1qbp -/- MEFs. C1QBP deficiency represents an important mitochondrial disorder associated with a clinical spectrum ranging from infantile lactic acidosis to childhood (cardio)myopathy and late-onset progressive external ophthalmoplegia.