Classification of feeding and eating disorders: review of evidence and proposals for ICD-11

Current classification of eating disorders is failing to classify most clinical presentations; ignores continuities between child, adolescent and adult manifestations; and requires frequent changes of diagnosis to accommodate the natural course of these disorders. The classification is divorced from clinical practice, and investigators of clinical trials have felt compelled to introduce unsystematic modifications. Classification of feeding and eating disorders in ICD-11 requires substantial changes to remediate the shortcomings. We review evidence on the developmental and cross-cultural differences and continuities, course and distinctive features of feeding and eating disorders. We make the following recommendations: a) feeding and eating disorders should be merged into a single grouping with categories applicable across age groups; b) the category of anorexia nervosa should be broadened through dropping the requirement for amenorrhoea, extending the weight criterion to any significant underweight, and extending the cognitive criterion to include developmentally and culturally relevant presentations; c) a severity qualifier "with dangerously low body weight" should distinguish the severe cases of anorexia nervosa that carry the riskiest prognosis; d) bulimia nervosa should be extended to include subjective binge eating; e) binge eating disorder should be included as a specific category defined by subjective or objective binge eating in the absence of regular compensatory behaviour; f) combined eating disorder should classify subjects who sequentially or concurrently fulfil criteria for both anorexia and bulimia nervosa; g) avoidant/restrictive food intake disorder should classify restricted food intake in children or adults that is not accompanied by body weight and shape related psychopathology; h) a uniform minimum duration criterion of four weeks should apply.     

SREBP1 is required for the induction by glucose of pancreatic beta-cell genes involved in glucose sensing

Previous studies have reported both positive and negative effects of culture of islets at high glucose concentrations on regulated insulin secretion. Here, we have reexamined this question in mouse islets and determined the role of changes in lipid synthesis in the effects of glucose. Glucose-stimulated insulin secretion (GSIS) and gene expression were examined in islets from C57BL/6 mice or littermates deleted for sterol-regulatory element binding protein-1 (SREBP1) after 4 days of culture at high glucose concentrations. Culture of control islets at 30 versus 8 mmol/l glucose led to enhanced secretion at both basal (3 mmol/l) and stimulatory (17 mmol/l) glucose concentrations and to enhanced triacylglycerol accumulation. These changes were associated with increases in the expression of genes involved in glucose sensing (glucose transporter 2, glucokinase, sulfonylurea receptor 1, inwardly rectifying K(+) channel 6.2), differentiation (pancreatic duodenal homeobox 1), and lipogenesis (Srebp1, fatty acid synthase, acetyl-coenzyme A carboxylase 1, stearoyl-coenzyme A desaturase 1). When cultured at either 8 or 30 mmol/l glucose, SREBP1-deficient (SREBP1(-/-)) islets displayed reduced GSIS and triacylglycerol content compared with normal islets. Correspondingly, glucose induction of the above genes in control islets was no longer observed in SREBP1(-/-) mouse islets. We conclude that enhanced lipid synthesis mediated by SREBP1c-dependent genes is required for the adaptive changes in islet gene expression and insulin secretion at high glucose concentrations.     

Cardiac conduction disorders in six infants with "near-miss" sudden infant deaths.

Cardiac conduction disorders caused sudden serious illnesses in six infants that might have been fatal if diagnosis and treatment had been delayed. These cases provide circumstantial evidence to support a link between cardiac conduction disorders and some sudden infant deaths. A further potential long-term effect of these disorders is illustrated in one child in whom psychomotor retardation seemed to develop after an episode of cerebral hypoxia that was probably by an arrhythmia associated with the Wolff-Parkinson-White syndrome. Cardiac conduction disorders may be detected by routine neonatal ECG screening, and it may therefore be appropriate to start prophylactic antiarrhythmic treatment in certain children before clinical signs develop.     

Attraction of Culex pipiens to uropygial gland secretions does not explain feeding preference for American robins

Culex pipiens, the endemic mosquito vector of West Nile virus in eastern North America, is responsible for maintenance of the virus in avian reservoir hosts, the most important of which appears to be the American robin. One reason for the greater involvement of robins is believed to be the feeding preference of Cx. pipiens, however, the basis of this preference is not understood. We tested the hypothesis that the species‐specific chemical profile of avian uropygial gland secretions are used by Cx. pipiens as cues to locate birds and, therefore, may contribute to the observed feeding preferences. We used gas chromatography‐mass spectrometry to identify the semi‐volatile components of the uropygial gland secretions of American robins and two other common reservoir host species, the house sparrow and European starling. We found that the chemical composition of the robin secretions was different from those of the sparrows and starlings. Through behavioral choice trials conducted in a dual‐port olfactometer, we also found that Cx. pipiens did not prefer the secretions of robins over the other two species. Surprisingly, however, we found that Cx pipiens were more often attracted to live starlings over robins and to the secretions of starlings over those of robins.     

Remembering the good and the bad: memory-based mediation of the food–safety trade-off in dynamic landscapes

Predator–prey interactions are central to fitness as animals simultaneously avoid death and consume resources to ensure growth and reproduction. Along with direct effects, predators can also exert strong non-consumptive effects. For example, prey shift habitat use in the presence of predators, a potentially learned behavior. The impact of cognition on movement and predator interactions is largely unexplored despite evidence of learned responses to predation threat. We explore how learning and spatial memory influence predator–prey dynamics by introducing predators into a memory-driven movement modeling framework. To model various aspects of risk, we vary predator behavior: their persistence and spatial correlation with the prey’s resources. Memory outperforms simpler movement processes most in patchy environments with more predictable predators that are more easily avoided once learned. In these cases, memory aids foragers in managing the food–safety trade-off. For example, particular parameterizations of the predation memory reduce encounters while maintaining consumption. We found that non-consumptive effects are highest in landscapes of concentrated, patchy resources. These effects are intensified when predators are highly correlated with the forager’s resources. Smooth landscapes provide more opportunities for foragers to simultaneously consume resources and avoid predators. Predators are able to effectively guard all resources in very patchy landscapes. These non-consumptive effects are also seen with the shift away from the best quality habitat compared to foraging in a predator-free environment.     

Effects of a partially purified factor from chick embryos on macromolecular synthesis of embryonic pancreatic epithelia

Essentially normal development of early embryonic pancreatic epithelium occurs only in the presence of mesenchymal tissues (Golosow and Grobstein, 1962), or a particulate fraction (MF) obtained from extracts of chicken embryos (Rutter et al., 1964). We have shown that this fraction also stimulates the incorporation of thymidine-³H into DNA. This stimulatory activity was detected in particulate fractions from homogenates of several mesodermal tissues from rat and chick embryos, as well as in fibroblasts cultured from these tissues, but not in embryonic epithelial tissues. This activity may thus be related to the mesodermal tissue requirement for pancreatic development. MF was solubilized and partially purified from homogenates of chick embryos. It is stable to collagenase, hyaluronidase, and neuraminidase. Activity is lost by heating and by treatment with trypsin. It is presumed, therefore, that the factor is associated with a protein that is not collagen.The effects of the MF upon macromolecular synthesis were tested in pancreatic tissues from 12-day rat embryos. When isolated epithelia were cultured in the absence of mesoderm or MF, the rate of thymidine-³H incorporation into DNA decreased to low levels. The specific activities of DNA polymerase and deoxycytidylate deaminase in epithelial extracts also declined. In contrast, the rate of thymidine-³H incorporation into DNA increased 5- to 8-fold over the initial rates in epithelia cultured with MF. Concurrently DNA polymerase activity in tissue extracts increased by 2- to 3-fold; deoxycytidylate deaminase activity declined slightly.MF also affected RNA and protein synthesis. The rate of leucine-³H incorporation into protein and uridine-¹⁴C incorporation into RNA in isolated pancreatic epithelia was comparable to that of intact rudiments. Cultures in the presence of MF increased these rates severalfold after 20 hr. These results suggest that MF, and by implication, mesoderm, may supply a growth factor for epithelial tissue and thus serves a permissive rather than a determining role in the differentiation process in pancreatic development.