Research report The effects of prefrontal cortex transcranial direct current stimulation (tDCS) on food craving and temporal discounting in women with frequent food cravings ☆ Maria Kekic *, Jessica McClelland, Iain Campbell, Steffen Nestler, Katya Rubia, Anthony S. David, Ulrike Schmidt Institute of Psychiatry, King’s College London, 16 De Crespigny Park, London SE5 8AF, UK ARTICLE INFO Article history: Received 11 December 2013 Received in revised form 4 March 2014 Accepted 9 March 2014 Available online 20 March 2014 Keywords: Transcranial direct current stimulation (tDCS) Brain stimulation Food cravings Obesity Eating disorders Temporal discounting (TD) ABSTRACT Bulimia nervosa, binge-eating disorder, and some forms of obesity are characterised by compulsive over- eating that is often precipitated by food craving. Transcranial direct current stimulation (tDCS) has been used to suppress food cravings, but there is insufficient evidence to support its application in clinical prac- tice. Furthermore, the potential moderating role of impulsivity has not been considered. This study used a randomised within-subjects crossover design to examine whether a 20-minute session of sham- controlled bilateral tDCS to the dorsolateral prefrontal cortex (anode right/cathode left) would tran- siently modify food cravings and temporal discounting (TD; a measure of choice impulsivity) in 17 healthy women with frequent food cravings. Whether the effects of tDCS on food craving were moderated by in- dividual differences in TD behaviour was also explored. Participants were exposed to food and a film of people eating, and food cravings and TD were assessed before and after active and sham stimulation. Craving for sweet but not savoury foods was reduced following real tDCS. Participants that exhibited more re- flective choice behaviour were more susceptible to the anti-craving effects of tDCS than those that dis- played more impulsive choice behaviour. No differences were seen in TD or food consumption after real versus sham tDCS. These findings support the efficacy of tDCS in temporarily lowering food cravings and identify the moderating role of TD behaviour. © 2014 Elsevier Ltd. All rights reserved. Introduction It has been proposed that certain foods – particularly those high in sugar – are addictive, and that obesity and eating disorders, such as bulimia nervosa (BN) and binge-eating disorder (BED), can be conceptualised as forms of addiction (Avena, Rada, & Hoebel, 2009). Food cravings (intense urges to consume particular foods) are thought to precipitate the compulsive overeating that characterises these con- ditions, and have been positively associated with binge-eating (Ng & Davis, 2013), daily calorie intake (Lafay et al., 2000), BMI (Franken & Muris, 2005), daytime sleep (Landis, Parker, & Dunbar, 2009), and dieting failure (Meule, Westenhöfer, & Kübler, 2011). There is also evidence that excessive craving for sweet foods is associated with drug and alcohol abuse (for a review see Pelchat, 2002). Extensive behavioural and neurobiological data indicate many commonalities between food craving and drug craving (for a review see Pelchat, 2009). For instance, both lead to foraging and inges- tion habits that persist and strengthen despite the threat of nega- tive health and social consequences (Volkow & Wise, 2005) and, furthermore, cravings can predict both relapse to drug taking in ab- stinent substance users (Rosenberg, 2009) and weight regain after bariatric surgery in obese patients (Odom et al., 2010). The neu- rotransmitter systems implicated in food craving overlap substan- tively with those involved in drug craving; for example, exposure to both food and drug craving-provoking stimuli is associated with increased levels of reward circuitry dopaminergic activation in the brain (Blum, Liu, Shriner, & Gold, 2011). Food craving and drug craving are also mediated by shared functional neuroanatomy. Several brain regions appear to be involved (for a review see Tang, Fellows, Small, & Dagher, 2012), but most data suggest that the left, right, or bilat- eral dorsolateral prefrontal cortex (DLPFC; an area in the prefron- tal cortex important for executive functioning) is activated in response to cues that induce both food (Gearhardt et al., 2011; Siep et al., 2009) and drug cravings (Bonson et al., 2002; Hayashi, Ko, Strafella, & Dagher, 2013; Maas et al., 1998). The level of cue- elicited prefrontal activation can predict prospective food intake ☆ Acknowledgements: Maria Kekic is supported by an Institute of Psychiatry (IOP) Excellence Studentship. Anthony David and Ulrike Schmidt receive salary support from the National Institute for Health Research (NIHR) Specialist Biomedical Re- search Centre for Mental Health at the South London and Maudsley NHS Founda- tion Trust and IOP, King’s College London. * Corresponding author. E-mail address: maria.kekic@kcl.ac.uk (M. Kekic). http://dx.doi.org/10.1016/j.appet.2014.03.010 0195-6663/© 2014 Elsevier Ltd. All rights reserved. Appetite 78C (2014) 55–62 Contents lists available at ScienceDirect Appetite journal homepage: www.elsevier.com/locate/appet