Introduction
The biopsychosocial model that underpins our understanding of disorders of gut-brain interaction (DGBI) has childhood trauma as a predisposing factor for adult symptoms1. The model is supported by empirical data linking childhood emotional, physical and sexual abuse to the severity of adult gastrointestinal (GI) symptoms2. However the mechanisms by which childhood trauma affects GI symptom burden later in life are poorly understood. Given the strong association between a number of adverse psychological traits and elevated GI symptom burden, one theory is that childhood adverse experiences (ACEs) induce a widespread negative attitude which might manifest as high levels of neuroticism and anxiety, among other possible traits3,4, leading to increased allostatic load and amplified perception of bodily sensations5. However whether this is actually what happens remains unknown.
Aims & Methods
We aimed to empirically evaluate the hypotheses that:
1. Traits that are negative at high levels, neuroticism, anxiety and depression provide indirect positive paths between ACEs and adult GI symptom burden
2. A trait that may buffer the effect of ACEs, higher dispositional mindfulness, provides a risk-protective path between ACEs and adult GI symptom burden
In contrast to many previous studies, we used a validated measure of ACEs6 as well as considering individual traumatic events. GI symptom burden was measured via the gastrointestinal symptom rating scale (GSRS)7 and other psychological traits through validated measures. Our primary hypotheses were tested via path models.
Results
A sample of n=241 community individuals was recruited, of whom n=10 reported a physician diagnosis of an organic GI condition and were excluded. Of the remaining sample, 38% (n=88) met Rome IV criteria for irritable bowel syndrome and/or functional dyspepsia and 76% were female. The sample was generally young adults with mean age 19 years (SD=2, min=18, max=36).
GSRS scores correlated positively with overall ACEs score (r=0.16, p=0.02), neuroticism (r=0.35, p<0.001), anxiety (r=0.38, p<0.001), depression (r=0.27, p<0.001), but negatively with dispositional mindfulness (r=-0.39, p<0.001). Conversely, ACEs scores correlated positively with neuroticism (r=0.34, p<0.001), anxiety (r=0.23, p<0.001), depression (r=0.22, p=0.001), but negatively with dispositional mindfulness (r=-0.32, p<0.001).
Of the individual paths between ACEs and GSRS taken separately, the strongest was for mindfulness which explained 74%, followed by neuroticism which explained 70% of the association between ACEs and GSRS. In a model (Figure 1) where all psychological traits are considered jointly, 98% of the association between ACEs and GSRS, 98% is accounted for by indirect paths via psychological traits. Of these paths, the strongest are via mindfulness (44%) and anxiety (23%).
Conclusion
This study provides empirical support for the hypothesis that adverse childhood experiences are associated with later adult GI symptom burden via upregulation of adverse psychological traits and downregulation of positive traits (mindfulness). These findings offer opportunity for early intervention with the buffering effects of positive traits and support previous findings that mindfulness can act as a buffer to negative traits, such as neuroticism8.
References
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