The thesis also seems so crude. I would never approve it at my university. There is an established gut-brain 2-way connection that regulates mood and gut-microbes. These would be state like fluctuations, although someone with dysbiosis could be stuck in particular states for long periods. However "emotional traits" is by definition not state-like and suggests enduring and innate.
There are also hormone/cortisol feedback systems in the regulation of immunity and emotion - especially stress response. There is some literature on chronic stress, changes in Hypothalamic–pituitary–adrenal axis and onset of IBD - for some but certainly not all IBD patients.
There is also well documented gene alleles and gene-sequence-snips that correlate with IBD. Hundreds of them. Plausibly some of these variations could also correlate with physiological development and neurotransmitter availability that might shape emotion and personality over time. Possibly even influence the development of more innate temperament. But then any study trying to use emotion as a causal precursor to changes in immunity would be making a 3rd variable problem because both the temperament and the immunity would be not directly related, but in fact each related to underlying genetics.
In short, the theoretical framework is complex, and there are several existing literatures to consider, such that your clumsy question about
the association of emotional traits and IBD is poor-science. It carries the risk of leading patients to blame themselves (i.e., their emotions) for their disease, and should not pass an institutional review board for human subject research.
Finally there is a rich literature on the emotional state and well being of those with chronic and long term illness (especially cancer patients). This literature suggests that it is difficult to use cross-sectional studies assessing emotion/personality after diagnosis and treatment with prior emotion/personality. The measurement instruments are seldom invariant across diagnosis, and truth cannot be separated from bias.
It would be one thing to look for "associations" and discuss findings in this rich theoretical framework existing across several literatures. But you assert you want to examine "predisposing" - which cannot be done with your study, and is poorly connected to the existing scientific literature, and has potential harm to subjects. I think you need to be come a better scientist before working with human populations.
Post Edited (DBwithUC) : 3/22/2018 9:07:38 AM (GMT-6)