Transcranial Magnetic Stimulation and the Urge to Eat: A Comment on Lowe, Vincent, and Hall (2017)
Different therapeutic approaches have been used to ameliorate craving in obesity and eating disorders including pharmacological and psychotherapeutic strategies, but these have had limited efficacy. Repeated transcranial magnetic stimulation (rTMS) is a neuromodulation technique with growing evidence to treat a myriad of conditions, including food craving.
We provide meta-analytic results on the efficacy of rTMS to reduce food craving in studies conducted thus far. Medline and Embase databases were reviewed as were controlled trials by contacting specialists in the field and searching “clinicaltrials.gov” for additional trials. Eligible articles had to 1) be written in English, Spanish, or Portuguese (all retrieved articles were written in English); 2) be randomized, controlled trials; and 3) provide data in the article or upon request for the main outcomes: mean (SD) values and response and remission rates. Studies excluded were case reports, series of cases, non–controlled trials, and trials assessing other conditions than the use of rTMS for food craving. Hedges' g was used as the measure of effect size, which is appropriate for studies of small sample sizes. The pooled effect size was weighted by the inverse variance method and measured using the random effects model. Heterogeneity was assessed using the Q statistic and I2 index. We further used funnel plots to test for the presence of publication bias.
A total of 5 studies were included in the final analysis (n = 169) (3–7). This sample is significantly larger than the previous meta-analysis adding two recently published studies, which represents 125% augmentation. Food craving was assessed in patients with either a visual analog scale or a food craving questionnaire. Table 1 describes the study populations and design. All studies evaluated similar rTMS protocols as also shown in Table 1. We did not find rTMS to be superior to sham stimulation in reducing food craving (Hedges' g = −0.23; 95% CI = −0.52 to 0.07; p = .852). Quality analysis underscores low heterogeneity among studies (I2 = 0.0%; p = .852). We also found low publication bias; in fact all studies were within the funnel plot limits.
It has been suggested that food and drug cravings share neurobiological processes (8). Both food and drugs activate brain circuitry involved in reward, motivation, and decision-making (9). Functional neuroimaging studies have revealed decreased basal metabolism in the prefrontal cortex and striatum, as well as dopaminergic alterations and increased activation of reward regions of the bran in people with obesity in response to food cues (10).
The dorsolateral prefrontal cortex (DLPFC) has been related to executive functions that support cognitive control of food intake. Overall, the underlying hypothesis is that enhancing DLPFC activity may alter the reward-cognition balance toward facilitation of cognitive control and possibly suppression of reward-related mechanisms that drive food craving and overeating (11). Two possible mechanisms through which stimulation may decrease craving levels have been proposed by Addolorato et al. (12). First, interconnections of the DLPFC with the ventral tegmental area may increase dopamine excretion from the ventral tegmental area to the ventral striatum, an area that plays a major role in reward processing.