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As clinicians involved in the care of patients with disorders of gut–brain interaction (DGBIs), we—and many colleagues—have the impression that social media are adversely shaping the nature, presentation, and ability to manage these disorders, especially at the severe end of the DGBI clinical spectrum. We turned to the research literature to see if these clinical impressions were corroborated but found it virtually nonexistent. Social media have rapidly become a ubiquitous, pervasive part of the lives of most people on the planet. Although they bring many benefits, they are also replete with health misinformation, reinforcement of abnormal sick‐role behavior, and undermining of the legitimacy of psychological care. We first set out four reasons for concern about social media and DGBIs, particularly severe DGBIs. These reasons stem from phenomena described in medical fields outside DGBIs, but there is no reason to think DGBIs should be exempt from such phenomena. We then present the results of a literature search, which yielded only eight disparate recent empirical studies. We review these studies, which, although not uninformative, reveal a field in its infancy. We set out implications, most urgently multidisciplinary research directly addressing the role of social media and evaluation of interventions to mitigate its ill effects. Gastroenterological clinicians involved in DGBI care and research need to collaborate with experts in social media research, which is a very rapidly evolving, specialized field. Although knowledge is at an early stage, there are implications for specialist practice, education and training, and DGBI service delivery. [ABSTRACT FROM AUTHOR]

Background: Patients with gastrointestinal disorders are prone to heightened awareness of dietary intake. When diet‐related thoughts or behaviors are excessive, they may lead to psychological distress, nutritional compromise, and impair medical treatment. Identification of disordered eating behavior and eating disorders is crucial for effective management, but data on their prevalence within this population remain scarce. We conducted a systematic review of the prevalence of disordered eating behavior and eating disorders in adults with gastrointestinal disorders. Methods: MEDLINE, PubMed, and PsycInfo databases were searched up to June 2021. Studies examining disordered eating in adult patients with a primary gastrointestinal diagnosis were included. Key Results: A total of 17 studies met the inclusion criteria for the review. The range of gastrointestinal disorders examined included disorders of gut‐brain interaction (DGBI), coeliac disease, and inflammatory bowel disease (IBD). The methods for examining disordered eating were highly variable. The prevalence of disordered eating ranged from 13–55%. The prevalence was higher in patients with disorders of gut‐brain interaction (DGBI) than in those with organic gastrointestinal disorders. Factors associated with disordered eating included female sex, younger age, gastrointestinal symptom severity, anxiety and depression, and lower quality of life. Conclusions & Inferences: Disordered eating is highly prevalent in adult patients with gastrointestinal illness, particularly those with DGBI. Understanding whether a patient's primary underlying diagnosis is that of an eating disorder or gastroenterological disorder remains a challenge for clinicians. There is an unmet need to identify at‐risk patients so that psychological intervention can be included in the therapeutic strategy. [ABSTRACT FROM AUTHOR]

Background: A diverse range of treatments are available for the treatment of functional gastrointestinal disorders (FGIDs). Individual treatments, including drug therapies, behavioral therapy ("biofeedback"), psychological therapies, and dietary therapies, have been well validated in controlled, randomized trials and real‐life case series. However, few studies have evaluated models of delivery of care for the whole population of referred patients with an FGID. This review evaluates models of specialist outpatient care for the management of FGIDs. Methods: A systematic review was performed of full‐text articles published until October 2018 in Pubmed/Medline and Embase. Studies were included if they evaluated a model of outpatient care in a specialist setting for the treatment of adult patients with an FGID and included patient‐reported outcomes comprising symptoms, quality of life, or psychological well‐being. Results: Few studies have evaluated the delivery of care for the whole population of referred patients with an FGID, and there was one randomized comparison of different models of care. Two studies that evaluated the outcome of gastroenterologist‐only clinics suggested poor long‐term results. Two non‐comparative case series reported the outcome of multidisciplinary care, including gastroenterologists and psychological therapists, suggesting improved patient quality of life and psychological well‐being. Conclusions: Despite the high prevalence and cost of treating FGIDs, and the availability of effective treatments, there are few data and limited randomized comparisons reporting the outcome of different types of specialist care. The few data available suggest that multidisciplinary care is superior to gastroenterologist‐only care, but this needs to be validated in prospective comparative studies. [ABSTRACT FROM AUTHOR]

Objectives This study aimed to test whether a specific serotonin transporter (5HTT) gene polymorphism interacting with life stress increased the risk of depression in patients with epilepsy. Methods The Tasmanian Epilepsy Register Mood Study (TERMS) used a cross-sectional study design of a community sample of patients with epilepsy previously recruited into the Tasmanian Epilepsy Register. It employed a mailed self-complete questionnaire and saliva DNA collection. Depression was assessed using the Center for Epidemiologic Studies Depression Scale. Environmental measures were selected to cover recent stressful events, epilepsy-related stress, current social support, and early life stress. Results Of 820 eligible participants, 553 (67%) participants completed the study. Experience of at least one stressful life event was very common, with a significant association between depression and the stressful life events (F = 26.2, df = 3, p < 0.001). There was no association between serotonin transporter genotype and level of depressive symptoms reported (F = 0.421, df = 2, p = 0.7). There was no evidence of any adverse life experiences interacting with serotonin transporter genotype to moderate the risk of depression. Significance The failure to demonstrate a main effect of genotype on depression or a gene × environment interaction differs from several studies of patients with other chronic diseases. However, it is consistent with larger general population studies. [ABSTRACT FROM AUTHOR]

A single non-anaesthetic dose of ketamine, a non-competitive NMDA receptor (NMDAR) antagonist with hallucinogenic properties, induces cognitive impairment and psychosis, and aggravates schizophrenia symptoms in patients. In conscious rats an equivalent dose of ketamine induces key features of animal models of acute psychosis, including hyperlocomotor activity, deficits in prepulse inhibition and gating of auditory evoked potentials, and concomitantly increases the power of ongoing spontaneously occurring gamma (30-80 Hz) oscillations in the neocortex. This study investigated whether NMDAR antagonist-induced aberrant gamma oscillations could be modulated by acute treatment with typical and atypical antipsychotic drugs. Extradural electrodes were surgically implanted into the skull of adult male Wistar rats. After recovery, rats were subcutaneously administered either clozapine (1-5 mg/kg, n = 7), halo-peridol (0.05-0.25 mg/kg; n = 8), LY379268 (a preclinical agonist at mGluR2/3 receptors: 0.3-3 mg/kg; M = 5) or the appropriate vehicles, and 30 min later received ketamine (5 mg/kg s.c.). Quantitative measures of EEG gamma power and locomotor activity were assessed throughout the experiment. All three drugs significantly reduced the power of baseline EEG gamma oscillations by 30-50 %, an effect most prominent after LY379268, and all inhibited ketamine-induced hyperlocomotor activity. However, only pretreatment with LY379268 attenuated trough-to-peak ketamine-induced gamma hyperactivity. These results demonstrate that typical and atypical antipsychotic drugs acutely reduce cortical gamma oscillations, an effect that may be related to their clinical efficacy. [ABSTRACT FROM AUTHOR]

Objective Methods Results Significance Many people with epilepsy experience comorbid anxiety and depression, and antidepressants remain a primary treatment for this. Emerging evidence suggests that these agents may modulate epileptogenesis to influence disease severity. Here, we assessed how treatment with the selective serotonin reuptake inhibitor (SSRI) antidepressant fluoxetine impacts epileptogenic, behavioral, and pathological sequelae following status epilepticus.Male Wistar rats received kainic acid to induce status epilepticus (SE) or vehicle (sham). Animals then received either fluoxetine (10 mg/kg/day) or vehicle for 8 weeks via subcutaneous osmotic pump. Video‐electroencephalography was recorded continuously until behavioral testing at day 56, including assessments of anxiety‐ and depression‐like behavior and spatial cognition. Postmortem immunocytochemistry studies examined mossy fiber sprouting.Fluoxetine treatment significantly accelerated epileptogenesis following SE, reducing the average period to the first spontaneous seizure (from 32 days [vehicle] to 6 days [fluoxetine], p < .01). Also, fluoxetine exposure magnified the severity of the resultant epilepsy, increasing seizure frequency compared to vehicle (p < .01). Exposure to fluoxetine was associated with improved anxiety‐ and depression‐like behaviors but significantly worsened cognition. Mossy fiber sprouting was more pronounced in fluoxetine‐treated rats compared to vehicle (p < .0001).Our studies demonstrate that, using a model exhibiting spontaneous seizures, epileptogenesis is accelerated and magnified by fluoxetine, an effect that may be related to more severe pathological neuroplasticity. The differential influence of fluoxetine on behavior indicates that different circuitry and mechanisms are responsible for these comorbidities. These findings suggest that caution should be exercised when prescribing SSRI antidepressants to people at risk of developing epilepsy. [ABSTRACT FROM AUTHOR]

A single non-anaesthetic dose of ketamine, a non-competitive NMDA receptor (NMDAR) antagonist with hallucinogenic properties, induces cognitive impairment and psychosis, and aggravates schizophrenia symptoms in patients. In conscious rats an equivalent dose of ketamine induces key features of animal models of acute psychosis, including hyperlocomotor activity, deficits in prepulse inhibition and gating of auditory evoked potentials, and concomitantly increases the power of ongoing spontaneously occurring gamma (30-80 Hz) oscillations in the neocortex. This study investigated whether NMDAR antagonist-induced aberrant gamma oscillations could be modulated by acute treatment with typical and atypical antipsychotic drugs. Extradural electrodes were surgically implanted into the skull of adult male Wistar rats. After recovery, rats were subcutaneously administered either clozapine (1-5 mg/kg, n=7), haloperidol (0.05-0.25 mg/kg; n=8), LY379268 (a preclinical agonist at mGluR2/3 receptors: 0.3-3 mg/kg; n=5) or the appropriate vehicles, and 30 min later received ketamine (5 mg/kg s.c.). Quantitative measures of EEG gamma power and locomotor activity were assessed throughout the experiment. All three drugs significantly reduced the power of baseline EEG gamma oscillations by 30-50%, an effect most prominent after LY379268, and all inhibited ketamine-induced hyperlocomotor activity. However, only pretreatment with LY379268 attenuated trough-to-peak ketamine-induced gamma hyperactivity. These results demonstrate that typical and atypical antipsychotic drugs acutely reduce cortical gamma oscillations, an effect that may be related to their clinical efficacy.

The pathogenesis of mesial temporal lobe epilepsy (MTLE), the most prevalent form of refractory focal epilepsy in adults, is thought to begin in early life, even though seizures may not commence until adolescence or adulthood. Amongst the range of early life factors implicated in MTLE causation (febrile seizures, traumatic brain injury, etc.), stress may be one important contributor. Early life stress is an a priori agent deserving study because of the large amount of neuroscientific data showing enduring effects on structure and function in hippocampus and amygdala, the key structures involved in MTLE. An emerging body of evidence directly tests hypotheses concerning early life stress and limbic epilepsy: early life stressors, such as maternal separation, have been shown to aggravate epileptogenesis in both status epilepticus and kindling models of limbic epilepsy. In addition to elucidating its influence on limbic epileptogenesis itself, the study of early life stress has the potential to shed light on the psychiatric disorder that accompanies MTLE. For many years, psychiatric comorbidity was viewed as an effect of epilepsy, mediated psychologically and/or neurobiologically. An alternative - or complementary - perspective is that of shared causation. Early life stress, implicated in the pathogenesis of several psychiatric disorders, may be one such causal factor. This paper aims to critically review the body of experimental evidence linking early life stress and epilepsy; to discuss the direct studies examining early life stress effects in current models of limbic seizures/epilepsy; and to suggest priorities for future research.