Authors: Panagiota Kaisari, Colin T Dourish, Pia Rotshtein, Suzanne Higgs
Introduction: It is unclear whether core symptoms of attention deficit hyperactivity disorder (ADHD) relate to specific types of disordered eating and little is known about the mediating mechanisms. We investigated associations between core symptoms of ADHD and binge/disinhibited eating and restrictive eating behavior and assessed whether negative mood and/or deficits in awareness and reliance on internal hunger/satiety cues mediate these relationships.
Methods: In two independent studies, we used a dimensional approach to study ADHD and disordered eating. In Study 1, a community-based sample of 237 adults (72.6% female, 18–60 years [M = 26.8, SE = 0.6]) completed an online questionnaire, assessing eating attitudes/behaviors, negative mood, awareness, and reliance on internal hunger/satiety cues and ADHD symptomatology. In Study 2, 142 students (80.3% female, 18–32 years [M = 19.3, SE = 0.1]) were recruited to complete the same questionnaires and complete tasks assessing interoceptive sensitivity and impulsivity in the laboratory.
Results: In each study, core symptoms of ADHD correlated positively with both binge/disinhibited and restrictive eating and negative mood mediated the relationships. Deficits in awareness and reliance on internal hunger/satiety signals also mediated the association between inattentive symptoms of ADHD and disordered eating, especially binge/disinhibited eating. The results from both studies demonstrated that inattentive symptoms of ADHD were also directly related to binge/disinhibited eating behavior, while accounting for the indirect pathways of association via negative mood and awareness and reliance on internal hunger/satiety signals.
Conclusion: This research provides evidence that core symptoms of ADHD are associated with both binge/disinhibited eating and restrictive eating behavior. Further investigation of the role of inattentive symptoms of ADHD in disordered eating may be helpful in developing novel treatments for both ADHD and binge eating.
Spetter MS, Feld GB, Thienel M, Preissl H, Hege MA, Hallschmid M.
Sci Rep. 2018 Feb 9;8(1):2736. doi: 10.1038/s41598-018-20963-4.
Abstract: The hypothalamic neurohormone oxytocin decreases food intake via largely unexplored mechanisms. We investigated the central nervous mediation of oxytocin’s hypophagic effect in comparison to its impact on the processing of generalized rewards. Fifteen fasted normal-weight, young men received intranasal oxytocin (24 IU) or placebo before functional magnetic resonance imaging (fMRI) measurements of brain activity during exposure to food stimuli and a monetary incentive delay task (MID). Subsequently, ad-libitum breakfast intake was assessed. Oxytocin compared to placebo increased activity in the ventromedial prefrontal cortex, supplementary motor area, anterior cingulate, and ventrolateral prefrontal cortices in response to high- vs. low-calorie food images in the fasted state, and reduced calorie intake by 12%. During anticipation of monetary rewards, oxytocin compared to placebo augmented striatal, orbitofrontal and insular activity without altering MID performance. We conclude that during the anticipation of generalized rewards, oxytocin stimulates dopaminergic reward-processing circuits. In contrast, oxytocin restrains food intake by enhancing the activity of brain regions that exert cognitive control, while concomitantly increasing the activity of structures that process food reward value. This pattern points towards a specific role of oxytocin in the regulation of eating behaviour in humans that might be of relevance for potential clinical applications.
This month we have the honour to welcome Dr Helen Ruddock into our reserach group. Helen has a background in psychology focusing on addiction-like eating. Her work at the EBRG will focus on research that examines the mechanisms which underlie the social facilitation of eating (i.e. the tendency for people to eat more in social situations). This is a 3-year ESRC-funded project in collaboration with Professor Jeff Brunstrom from the University of Bristol and Associate Professor Lenny Vartanian from the University of New South Wales, Australia.
New review out in Current Obesity Reports
by Suzanne Higgs & Maartje Spetter
PURPOSE OF REVIEW: The present review organises the recent literature on the role of memory in eating behaviours and provides an overview of the current evidence relating to the associations between memory and weight gain.
RECENT FINDINGS: Research over the last few years has highlighted working memory as an important cognitive process that underpins many aspects of appetite control. Recent work on episodic memory and appetite has replicated work showing that manipulating memory for recent eating affects later consumption and extended this work to examine associations between individual differences in memory and eating behaviours. Poorer episodic memory ability is related to a reduced sensitivity to internal states of hunger and satiety and a tendency towards uncontrolled eating. There is also recent evidence to suggest that working memory and episodic memory impairments are related to weight gain and high BMI. Working memory and episodic memory are core cognitive processes that are critical for food-related decision-making, and disruption to these processes contributes to problems with appetite control and weight gain, which suggests that weight loss programmes might be improved by the addition of cognitive training.
This week Jinyu Liu has succesfully passed her PhD viva! We here at the EBRG are very proud of Dr Liu’s wonderful achievement and very happy for the new doctor! !Well done! Her thesis focuses on social influences on adults’ eating behaviour. When you want to know more see Dr Liu’s great 3 min-thesis presentation!
Angela Meadows successfully passed her PhD viva at the University of Birmingham! We congratulate Dr Meadows on this great achievement! The EBRG is very happy and proud for/of the new doctor and her accomplishments! Well done!
We are looking for a new Reserach Fellow to join our EBRG team!!!
The research fellow will work on a project that aims to conducting the first systematic examination of the mechanisms that underlie social facilitation of eating and assess whether these effects are compensated over time. Findings from the studies will enhance understanding external drivers of overconsumption and provide novel data on how overeating in social context may be avoided.
See http://www.jobs.ac.uk/job/BFV781/research-fellow/ for more details
For more information please contact Suzanne Higgs; email@example.com
This week Panagiota Kaisari succefully passed her PhD viva at the University of Birmingham. We congratulate Dr Kaisari on this great achievement! Her thesis titled ‘Neurocognitive processes in disordered eating‘; here Dr Kaisari aimed to better understand the specific cognitive and neural mechanisms that may serve as risk factors to the development of disordered eating behaviour. Her work provided novel and theoretical insights into the role of attention in guiding eating behaviour. We as the ERGB are very proud of the fresh doctor and her accomplishment. !Well done!
New paper in by Thomas, J. M., Dourish, C. T., Tomlinson, J., Hassan-Smith, Z., Hansen, P. C., & Higgs, S.
The present study examined the effects of the 5-HT2C receptor agonist meta-chlorophenylpiperazine (mCPP) on food consumption, eating microstructure and blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) responses to food pictures in healthy female volunteers. Methods: In a double-blind, placebo-controlled, crossover design, participants were randomized immediately after screening to receive oral mCPP (30mg) in a single morning dose, or placebo, in a counterbalanced order. Test foods were served from a Universal Eating Monitor (UEM) that measured eating rate and fMRI BOLD signals to the sight of food and non-food images were recorded. Results: mCPP decreased rated appetite and intake of a palatable snack eaten in the absence of hunger but had no significant effect on the consumption of a pasta lunch (although pasta eating rate was reduced). mCPP also decreased BOLD fMRI responses to the sight of food pictures in areas of reward-associated circuitry. A post hoc analysis identified individual variability in the response to mCPP (exploratory responder-non-responder analysis). Some participants did not reduce their cookie intake after treatment with mCPP and this lack of response was associated with enhanced ratings of cookie pleasantness and enhanced baseline BOLD responses to food images in key reward and appetite circuitry. CONCLUSIONS: These results suggest that 5-HT2C receptor activation in humans inhibits food reward-related responding and that further investigation of stratification of responding to mCPP and other 5-HT2C receptor agonists is warranted.