"Food addiction" has become a focus of interest for researchers attempting to explain certain processes and/or behaviors that may contribute to the development of obesity. Although the scientific discussion on "food addiction" is in its nascent stage, it has potentially important implications for treatment and prevention strategies. As such, it is important to critically reflect on the appropriateness of the term "food addiction", which combines the concepts of "substance-based" and behavioral addiction. The currently available evidence for a substance-based food addiction is poor, partly because systematic clinical and translational studies are still at an early stage. We do however view both animal and existing human data as consistent with the existence of addictive eating behavior. Accordingly, we stress that similar to other behaviors eating can become an addiction in thus predisposed individuals under specific environmental circumstances. Here, we introduce current diagnostic and neurobiological concepts of substance-related and non-substance-related addictive disorders, and highlight the similarities and dissimilarities between addiction and overeating. We conclude that "food addiction" is a misnomer because of the ambiguous connotation of a substance-related phenomenon. We instead propose the term "eating addiction" to underscore the behavioral addiction to eating; future research should attempt to define the diagnostic criteria for an eating addiction, for which DSM-5 now offers an umbrella via the introduction on Non-Substance-Related Disorders within the category Substance-Related and Addictive Disorders.

The maximum rate of sustained energy intake (SusEI) may limit reproductive effort and other aspects of animal performance. We have previously suggested that lactating mice are not limited centrally by the alimentary tract or peripherally by the mammary glands, but that the limits to SusEI are imposed by the capacity of the animal to dissipate body heat generated as a by-product of processing food and producing milk. To explore the nature of the limits to SusEI, we bred MF1 laboratory mice at 21°C and then dorsally shaved lactating females to reduce their external insulation and thereby elevate their capacity to dissipate body heat. These mice increased their food intake by 12.0% and assimilated on average 30.9 kJ day^–1 more energy than unshaved animals. With nearly identical mean litter sizes (11.4 pups for shaved and 11.3 pups for unshaved mice), shaved mothers exported 15.2% (22.0 kJ day^–1) more energy as milk than control individuals. The elevated milk production of shaved mice enabled them to wean litters that were 15.4% (12.2 g) heavier than offspring produced by unshaved mice. Our results argue against central, peripheral or extrinsic limits to SusEI at peak lactation and provide strong support for the heat dissipation limit hypothesis. More generally, we see many situations where heat dissipation may be a previously unrecognised factor constraining the evolution of endothermic animals – for example, the latitudinal and altitudinal trends in clutch and litter sizes and the migration patterns of birds.

Siberian hamsters display photoperiodically regulated annual cycles in body weight, appetite, and reproduction. Previous studies have revealed a profound up-regulation of type 3 deiodinase (DIO3) mRNA in the ventral ependyma of the hypothalamus associated with hypophagia and weight loss in short-day photoperiods. DIO3 reduces the local availability of T(3), so the aim of this study was to test the hypothesis that decreased hypothalamic T(3) availability underlies the short-day-induced catabolic state. The experimental approach was to determine whether a local increase in T(3) in the hypothalamus of hamsters exposed to short days could reverse the behavioral and physiological changes induced by this photoperiod. In study 1, microimplants releasing T(3) were placed bilaterally into the hypothalamus. This treatment rapidly induced a long-day phenotype including increased appetite and body weight within 3 wk of treatment and increased fat mass and testis size by the end of the 10-wk study period. In study 2, hypothalamic T(3) implants were placed into hamsters carrying abdominal radiotelemetry implants. Again body weight increased significantly, and the occurrence of winter torpor bouts was dramatically decreased to less than one bout per week, whereas sham-implanted hamsters entered torpor up to six times a week. Our findings demonstrate that increased central T(3) induces a long-day metabolic phenotype, but in neither study was the molt cycle affected, so we infer that we had not disrupted the initial detection of photoperiod. We conclude that hypothalamic thyroid hormone availability plays a key role in seasonal regulation of appetite, body weight, and torpor.

Male C57BL/6 mice fed ad libitum on control diet but allowed access to a palatable high fat diet (HFD) for 2 h a day during the mid-dark phase rapidly adapt their feeding behaviour and can consume nearly 80% of their daily caloric intake during this 2 h-scheduled feed. We assessed food intake microstructure and meal pattern, and locomotor activity and rearing as markers of food anticipatory activity (FAA). Schedule fed mice reduced their caloric intake from control diet during the first hours of the dark phase but not during the 3-h period immediately preceding the scheduled feed. Large meal/binge-like eating behaviour during the 2-h scheduled feed was characterised by increases in both meal number and meal size. Rearing was increased during the 2-h period running up to scheduled feeding while locomotor activity started to increase 1 h before, indicating that schedule-fed mice display FAA. Meal number and physical activity changes were sustained when HFD was withheld during the anticipated scheduled feeding period, and mice immediately binged when HFD was represented after a week of this “withdrawal” period. These findings provide important context to our previous studies suggesting that energy balance systems in the hypothalamus are not responsible for driving these large, binge-type meals. Evidence of FAA in HFD dark phase schedule-fed mice implicates anticipatory processes in binge eating that do not involve immediately preceding hypophagia or regulatory homeostatic signalling.

A substantial proportion of noncommunicable disease originates in habitual overconsumption of calories, which can lead to weight gain and obesity and attendant comorbidities. At the other end of the spectrum, the consequences of undernutrition in early life and at different stages of adult life can also have major impact on wellbeing and quality of life. To help address some of these issues, greater understanding is required of interactions with food and contemporary diets throughout the life course and at a number of different levels: physiological, metabolic, psychological, and emotional. Here we review the current literature on the effects of dietary manipulation on anxiety-like behaviour. This evidence, assembled from study of preclinical models of diet challenge from gestation to adult life, supports a role for diet in the important connections between psychology, physiology, and behaviour. Analogous processes in the human population in our current obesogenic environment are likely to contribute to individual and societal challenges in this area.