Peters et al.1 explore the relationship between gluten ingestion and mental state in individuals with noncoeliac gluten sensitivity (NCGS). Following a randomised, placebo‐controlled, double‐blind, cross‐over, dietary re‐challenge study, the authors conclude that gluten may induce feelings of depression and that ‘feeling better’ on a gluten‐free diet (GFD) may be a consequence of psychological, rather than intestinal, well‐being.

Previous studies on food hypersensitivities have shown subjective health complaints, in particular the triad of irritable bowel, fatigue and musculoskeletal pains, to be commonly reported.2, 3 Anxiety and depression are also frequent findings, although it appears that these are associations rather than being implicated in the causation.4 It has been noted that treatment of the underlying disease process can lead to alleviation of anxiety and neuroticism.5

This may also be the case in NCGS subjects who exhibit low levels of somatisation while on a GFD,6 with Peters et al. subsequently demonstrating blinded gluten exposure to induce a state of depression.1 These findings are similar to that seen in coeliac disease where depression is commonly reported,7 and a GFD in symptomatic individuals leads to an improvement in perception of health and psychological well‐being.8

How does the current study tie in with the literature? Despite there being ongoing debate as to whether gluten is working alone or alongside other wheat components in inducing gastro‐intestinal symptoms,9, 10 the work by Peters et al. supports the existence of NCGS, albeit in the form of an extra‐intestinal manifestation. However, the study is limited by its small sample size and short duration of gluten challenge.

In addition, the psychological instrument used for assessment covered only four parameters; depression, anxiety, anger and curiosity. Future studies will benefit from evaluating a wider range of psychological co‐morbidities, plus validated questionnaires to specifically assess well‐being and quality of life. Furthermore, other commonly reported extra‐intestinal manifestations in NCGS such as joint pains, rash, headaches, numbness and confusion have yet to be explored.11

Finally, the mechanism by which gluten is inducing these changes is not yet apparent; the investigators did not find an alteration in salivary cortisol levels but speculate that gluten may induce depression as a consequence of alterations in brain serotonin, gluten exorphins or changes in gut microbiota. Other plausible hypothesis is whether it is targeted organ reactions to gluten, similar to that seen in gluten ataxia.12 Alternatively, the constellation of local and systemic symptoms reported may be a consequence of grumbling low‐grade gut inflammation, and changes in intestinal permeability, similar to that seen in post‐infectious irritable bowel syndrome.13, 14

Nevertheless, this certainly opens a gateway for further research and Peters et al. are to be congratulated for providing insight into this complex yet evolving clinical entity. Whether NCGS is a disease of the mind or gut is food for thought, but it is no longer a condition to be dismissed as functional and perceived as belonging to a ‘no‐man's land’.15