NeuroFAST the Integrated Neurobiology of Food Intake, Addiction and Stress

Abstract

This special edition of OBESITY FACTS contains a series of review papers based around components and themes of the NeuroFAST research programme, which is funded by the European Union Seventh Framework programme (FP7-KBBE-2009-3; grant agreement 245009). The NeuroFAST project was constructed in response to the published call text entitled ‘Stress, Addiction and Eating Behaviour’, which reflected the common ground in terms of neurochemical pathways and brain regions between eating behaviour, including eating disorders, and addiction biology. The project was designed to ask the question ‘Does food addiction exist?’. The growing obesity epidemic is driven by over-consumption of calories, and evidence strongly implicates processes beyond homeostatic energy balance. Accordingly, addiction to food, or more frequently specific food items such as chocolate, is often touted in the popular press as a potential cause of over-consumption and weight gain. This possibility is also the subject of debate within the scientific literature where several lines of evidence substantiate similarities in mechanism, molecule, anatomy, and clinical and behavioural characteristics between over-eating and chemical addiction. For example, functional brain imaging studies in obese and addicted individuals have shown similar activation patterns when subjects are exposed to palatable food or drugs of abuse. However, the validity of the concept of food addiction has not been conclusively proven, and a more solid evidence base is required in this controversial area.The aim of this special issue is to produce a focussed collection of reviews that will be of interest to a range of specialties within the broader scientific community, and that will also aid the NeuroFAST consortium in the generation of targeted research briefs. These are intended to provide European public health policy makers and other stakeholders with digestible scientific information to support future decision making. The contributions to the special issue cover the rewarding properties of food, the molecular and neuroanatomical components involved in food reward and addiction, and how stressors are integrated into these processes. The collected papers, authored by NeuroFAST scientists, draw information from both pre-clinical and clinical studies to assess the current evidential status of food addiction and how this compares, firstly, to the medically recognised forms of addiction that categorise substance use disorders as specific conditions with distinct definitions and diagnostic features and, secondly, to emerging concepts of behavioural addiction. For example, the term food addiction is mainly used in the context of industrially refined, ‘highly palatable’, multi-component, foods, such as sweetened beverages or high-fat diets, rather than of single components, which are the basis of chemical addiction. Obesity is in essence the result of consumption of calories in excess of homeostatic requirements. Palatable food readily stimulates relative caloric over-consumption in both humans and laboratory animals, an outcome related to food reward and possibly to addiction-like processes. Pandit et al. [1] review the effects of a range of obesogenic diets on feeding behaviour, leptin resistance and hypothalamic neuropeptide systems, and how the properties of the diet influence these parameters. These interactions could be important in dietary reformulation to limit over-consumption and weight gain. Pandit et al. [1] argue that by understanding how and why the composition of the diet affects its reward value and addictive potential, it may be possible to develop novel foods that limit consumption and weight gain. The relationships between food properties and their sensory and physiological effects are discussed. The ability of different solid or liquid palatable diets or supplements to induce obesity and influence leptin signalling is discussed, before the authors proceed to consider effects on the brain reward circuitry. The neurobiological accompaniments to sucrose addiction are compared to those recorded from animals exposed to drugs of abuse, including the involvement of the endogenous opioid circuitry, which is dealt with in more detail by Noguieras et al. [2].Many of the neural structures involved in addictive behaviour are also involved in food reward. Opioids (including endorphins, enkephalins, dynorphins and endomorphins) play an important role in neural reward processes that lead to addictive behaviour, both homeostatic and hedonic feeding mechanisms involve opioid neuropeptide systems, and opioid antagonists inhibit consumption of both addictive drugs and palatable food. These relationships suggest the existence of a form of opioid-related addiction focussed on palatable foods. Nogueiras et al. [2] review the pharmacological and endogenous evidence of opioid receptor involvement in energy balance, including their interactions with the melanocortin, neuropeptide Y and or