Our findings reveal objective sleep disturbances to be a key factor in the expression IBS symptoms. Abdominal pain and distress were perturbed by disordered sleep the preceding night, while bowel pattern and accessory IBS symptoms seem less affected by sleep quality. Sleep quality similarly was associated with general and IBS-specific HRQOL. We found the influences of sleep disturbances to extend beyond the gut, with relationships observed between sleep disruption and somatic pain (i.e. back pain, headache, neck pain), depression, and anxiety (generalised and visceral-specific). To our knowledge, this is the first study to prospectively assess the broad influence of sleep disturbances on the symptoms and function of the IBS patient using both objective and subjective measures.
Sleep disorders are very common, with symptoms affecting as many as 70 million Americans.[8,35] One in three individuals reporting sleep disturbances meet clinical criteria for IBS. As many as 74% of IBS patients characterise themselves as 'poor sleepers'; polysomnography has shown that IBS patients experience shallow, nonrestorative sleep. In our study, we found that IBS patients had similar sleep latency patterns and sleep duration as healthy controls, but had poorer sleep quality, with greater numbers of awakenings during sleep. Intuitively, it might be presumed that the poor sleep quality among IBS sufferers results from nighttime GI symptoms, preventing the onset of restorative sleep cycles, or leading to arousal from sleep. However, our data did not suggest either to be the case: IBS patients infrequently (less than 5% of the time) identified their GI symptoms to be a factor leading to sleep disruption. Longitudinal studies suggest that self-reported daytime IBS symptoms do not predict sleep quality the subsequent night. Observational evidence suggests that circadian disturbances instead may have a causative role in GI symptoms. Nojkov et al. found that nurses working rotating shifts had a significantly higher prevalence of IBS diagnoses and greater abdominal pain compared to their peers working fixed schedules. Similar data among medical residents revealed a 30% increased likelihood of an IBS diagnosis for every additional hour of on-call sleep deprivation. In the clinical laboratory, Schey and colleagues were able to induce visceral hypersensitivity in GERD patients following sleep deprivation. Collectively, these studies offer supportive evidence of a causal relationship of disturbed sleep augmenting visceral hypersensitivity in IBS.
In this study, we observe that disturbed sleep, particularly waking episodes after sleep onset, strongly correlated with worse abdominal pain the following day in IBS patients. In addition, sleep quality predicted IBS patient reports of GI symptom Bother, Severity, and number of symptomatic days. However, we did not find sleep to be a significant factor in bowel pattern or accessory IBS symptoms (e.g. bloating, mucus and urgency). These findings align with a previous exploratory study by Buchanan et al. which found that measured sleep quality did not predict following-day reports of nonpain GI symptoms. Sleep disturbances also were associated with a variety of non-GI pain complaints, including headache, back pain and neck pain in our IBS participants.
Sleep disturbances are known to have profound physiologic consequences, including increases in pro-inflammatory cytokines and cortisol levels, while at the same time diminishing parasympathetic tone. Such physiologic effects are particularly relevant to inflammatory bowel conditions, such as Crohn's disease, where patients exhibit poorer sleep quality. Downstream enhancements in nociception across a variety of noxious stimuli (e.g. heat, pressure) following sleep deprivation have been demonstrated in both animal models and healthy subjects. Disruptions in sleep also affect somatic pain syndromes such as fibromyalgia, where sleep complaints and abnormal sleep physiology commonly is detected. These physiologic and clinical observations suggest that a generalised hyperalgesia may result from sleep disturbances, perhaps as a result of central sensitisation of spinal sensory neurons or more proximal sensory neurocircuitry. Awakenings during sleep, as were observed prominently among our IBS group, are known to be detrimental to pain-inhibitory function. In IBS, several other factors have been demonstrated as relevant to visceral hypersensitivity, including alterations in neurotransmitters (e.g. serotonin), intestinal permeability, microinflammation and the bacterial milieu. The IBS patient population thus might be particularly susceptible to the untoward effect of sleep on sensitivity as a 'second hit,' further exacerbating these gut-based derangements.
A multitude of correlational studies highlight the relationship of poor sleep and mood disturbances.[15,48] From a physiologic view, sleep deprivation results in a diminished capacity to regulate emotional reactivity, leading to enhanced susceptibility to depression and/or anxiety. This relationship bears mention as psychological comorbidities, including depression, anxiety and somatisation all are common to IBS and are associated with more severe GI symptoms in affected individuals;[50,51] moreover, mood and sensory function have shared representation in the emotional-arousal and cognitive modulation brain neurocircuitry. Although it was not the intent of this study to decipher the complex interplay of these factors, we found statistical evidence that the negative effects of sleep on abdominal pain may be partially explained by the influence of disturbed sleep on mood, particularly depression and bowel-centric anxiety.
Simple self-report instruments, such as the Pittsburgh Sleep Quality Index, which correlated well with actigraphic sleep measures in our study and demonstrated significant associations with reports of GI and non-GI pain symptoms. When detected, sleep disturbances may serve as a critical therapeutic target in the management of IBS, and could be easily measured using such questionnaires in the clinic setting. Previous work has suggested that a common treatment for insomnia, melatonin, may be helpful in decreasing IBS symptoms,[52–54] the value of other insomnia therapies in IBS remain uninvestigated. Nevertheless, various treatment options, in particular nonpharmacologic approaches such as cognitive behavioural therapy, exercise and meditation have shown promise in improving sleep hygiene and symptoms in patients with other chronic pain conditions.
Strengths of this study included the prospective assessment of sleep quality using both objective (actigraphic) and validated self-report measures in a clinically defined IBS population, and the implementation of psychiatric measures deemed potentially relevant in understanding the relationship of sleep and IBS. In studying a real-world referral IBS population, efforts were not undertaken to exclude patients on TCAs; importantly, we did not observe any differences in the key findings of the study when excluding these cases. We acknowledge this tertiary IBS population to be more severely symptomatic and burdened with greater psychological comorbidity than community-based IBS populations; while limiting somewhat our ability to generalise these findings, we feel that the pervasiveness of disordered sleep in the general population compels a broad interest in these observations. Lifestyle factors potentially relevant to sleep, such as caffeine and alcohol intake and physical activity also were examined; these activities did not appear to conspicuously affect our sleep results, and were reported by the minority of participants. Although patients endorsing sleep diagnoses, such as obstructive sleep apnoea, were excluded from the study, we acknowledge that without formal polysomnographic studies it is possible that patients harbouring undiagnosed sleep conditions could have been included in the study.
In summary, our findings suggest that sleep disturbances lead to greater abdominal and somatic pain reporting in IBS patients. Mood symptoms and health-related quality of life also are negatively impacted by poor sleep quality in this population. Although additional work is required to elucidate the physiologic basis for these findings, the clinical detection of sleep issues using self-report measures may identify IBS patients who might benefit from targeted sleep interventions.
Aliment Pharmacol Ther. 2016;44(3):246-258. © 2016 Blackwell Publishing