| 1. |
- Aroniadis, O. C., et al.
(author)
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A Perspective on Brain-Gut Communication: The American Gastroenterology Association and American Psychosomatic Society Joint Symposium on Brain-Gut Interactions and the Intestinal Microenvironment
- 2017
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In: Psychosomatic Medicine. - : Ovid Technologies (Wolters Kluwer Health). - 0033-3174 .- 1534-7796. ; 79:8, s. 847-856
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Journal article (peer-reviewed)abstract
- Background: Alterations in brain-gut communication and the intestinal microenvironment have been implicated in a variety of medical and neuropsychiatric diseases. Three central areas require basic and clinical research: (1) how the intestinal microenvironment interacts with the host immune system, central nervous system, and enteric nervous system; (2) the role of the intestinal microenvironment in the pathogenesis of medical and neuropsychiatric disease; and (3) the effects of diet, prebiotics, probiotics, and fecal microbiota transplantation on the intestinal microenvironment and the treatment of disease. Methods: This review article is based on a symposium convened by the American Gastroenterology Association and the American Psychosomatic Society to foster interest in the role of the intestinal microenvironment in brain-gut communication and pathogenesis of neuropsychiatric and biopsychosocial disorders. The aims were to define the state of the art of the current scientific knowledge base and to identify guidelines and future directions for new research in this area. Results: This review provides a characterization of the intestinal microbial composition and function. We also provide evidence for the interactions between the intestinal microbiome, the host, and the environment. The role of the intestinal microbiome in medical and neuropsychiatric diseases is reviewed as well as the treatment effects of manipulation of the intestinal microbiome. Conclusions: Based on this review, opportunities and challenges for conducting research in the field are described, leading to potential avenues for future research.
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| 2. |
- Bodin, Fernando, 1991, et al.
(author)
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The Association of Cigarette Smoking With High-Frequency Heart Rate Variability: An Ecological Momentary Assessment Study
- 2017
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In: Psychosomatic Medicine. - : Ovid Technologies (Wolters Kluwer Health). - 0033-3174 .- 1534-7796. ; 79:9, s. 1045-1050
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Journal article (peer-reviewed)abstract
- Objective Evidence from both laboratory and observational studies suggests that acute and chronic smoking leads to reduced high-frequency heart rate variability (HF-HRV), a measure of cardiac vagal regulation. We used ecological momentary assessment (EMA) to study the effect of smoking on concurrent HF-HRV in a trial measuring the effects of hostility reduction and compared 24-hour HF-HRV in smokers and nonsmokers. Method Ambulatory electrocardiogram data were collected before randomization from 149 healthy individuals with high hostility levels (20-45 years, body mass index 32 kg/m(2)) and paired with concurrent EMA ratings of smoking and physical position during waking hours. A multilevel mixed model was estimated associating ln(HF-HRV) from smoking status (between-person factor) and person-centered momentary smoking (within-person factor, treated as a random effect), adjusting for momentary physical position, medication use, and consumption of alcohol and caffeine. Results Thirty-five smokers and 114 nonsmokers provided both EMA and HF-HRV data. Within smokers, ln HF-HRV was reduced by 0.31 millisecond(2) (p = .04) when participants reported having recently smoked cigarettes, compared with when they had not. The 24-hour HF-HRV was significantly lower in smokers (M [SD] = 5.24 [0.14] milliseconds(2)) than nonsmokers (5.63 0.07 milliseconds(2), p = .01). Conclusions In healthy smokers with high hostility levels used as their own controls during daily living, smoking acutely reduced HF-HRV. HF-HRV was also reduced in smokers as compared with nonsmokers. Although limited by a small sample of individuals with high hostility levels, these findings nonetheless provide additional evidence that cardiac vagal regulation is lowered by cigarette smoking, which may be one of the numerous pathophysiological effects of smoking.
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| 3. |
- de Clercq, N. C., et al.
(author)
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Gut Microbiota and the Gut-Brain Axis: New Insights in the Pathophysiology of Metabolic Syndrome
- 2017
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In: Psychosomatic Medicine. - : Ovid Technologies (Wolters Kluwer Health). - 0033-3174 .- 1534-7796. ; 79:8, s. 874-879
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Journal article (peer-reviewed)abstract
- Objective: Emerging preclinical evidence has shown that the bidirectional signaling between the gastrointestinal (GI) tract and the brain, the so-called gut-brain axis, plays an important role in both host metabolism and behavior. In this review, we discuss the potential mechanisms of the brain-gut axis in relation to the pathophysiology of metabolic syndrome. Methods: A selective literature review was conducted to evaluate GI and brain interactions. Results: Evidence suggests reduced microbial diversity in obesity and metabolic dysregulation. However, findings of microbiota composition in obese individuals are inconsistent, and the investigation of causality between gut microbiota and energy homeostasis is complex because multiple variables contribute to the gut microbiota composition. The microbial metabolites short chain fatty acids are found to exert numerous physiologic effects, including energy homeostasis through the regulation of GI hormones such as cholecystokinin, glucagon-like peptide 1, peptide tyrosine-tyrosine, and leptin. Preclinical studies show that modifying rodents' microbiota through fecal transplantation results in alterations of these GI hormones and subsequently an altered metabolism and behavior. However, whether and to what extent preclinical findings translate to human metabolism is unclear. Conclusions: One of the major limitations and challenges in this field of research is interindividual variability of the microbiome. Future research needs to combine recent insights gained into tracking the dynamics of the microbiome as well as the metabolic responses. Furthermore, advanced mapping of the human microbiome is required to investigate the metabolic implications of the gut-brain axis to develop targeted interventions for obesity and metabolic syndrome.
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| 4. |
- Kask, Jan, et al.
(author)
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Mortality in Women With Anorexia Nervosa : The Role of Comorbid Psychiatric Disorders
- 2016
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In: Psychosomatic Medicine. - 0033-3174 .- 1534-7796. ; 78:8, s. 910-919
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Journal article (peer-reviewed)abstract
- Objective To investigate mortality in anorexia nervosa (AN) with a psychiatric comorbidity. Methods Using Swedish registers, data for 8069 female inpatients with AN were retrospectively collected for 1973-2010. Mortality patterns were assessed using standardized mortality ratios (SMRs), Cox regression-derived hazard ratios, and incidence rate ratios. A control cohort of 76,995 women was used. Results Patients with AN and a psychiatric comorbidity had higher mortality rates did than those without a comorbidity. The SMRs for patients with AN and a psychiatric comorbidity were 5.4 (95% confidence interval [CI] = 4.6-6.4) and 18.1 (95% CI = 15.2-21.3) for natural and unnatural causes of death, respectively. The SMRs for patients with AN without a comorbidity were 2.8 (95% CI = 2.3-3.5) and 3.1 (95% CI = 2.2-4.1) for natural and unnatural causes of death, respectively. The adjusted hazard ratios for mortality from natural or unnatural causes were 2.0 (95% CI = 1.5-2.7) and 5.7 (95% CI = 3.9-8.2), respectively. Incidence rate ratios comparing patients with AN and controls, both with psychiatric comorbidities, suggest a negative synergistic effect of comorbid AN and psychiatric disorder on mortality, which was greater for unnatural causes of death. Conclusions Mortality in patients with AN was greater in the presence of a psychiatric comorbidity, and even more pronounced for unnatural causes of death and suicides. Substance abuse, especially alcohol use disorder, increased mortality from natural causes of death. These findings highlight the need for early detection and treatment of psychiatric comorbidity in AN, to potentially improve long-term outcomes.
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| 5. |
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| 6. |
- Konttinen, Hanna, et al.
(author)
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Socioeconomic Position and Antidepressant Use as Predictors of Coronary Heart Disease Mortality : A Population-Based Registry Study of 362,271 Finns
- 2016
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In: Psychosomatic Medicine. - 0033-3174 .- 1534-7796. ; 78:2, s. 144-152
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Journal article (peer-reviewed)abstract
- Objective: The interplay between depression and socioeconomic position (SEP) in predicting cardiovascular outcomes has rarely been examined. We investigated whether SEP modified the effect of antidepressant use on coronary heart disease (CHD) mortality.Methods: The data consisted of an 11% random sample of the Finnish population aged 40 to 79 years at the end of 1999 with an oversample of 80% of those who died in 2000 to 2007. Participants free of CHD at baseline (n = 362,271) were followed up for CHD mortality in 2000 to 2007. SEP was assessed via registry-based information on education, occupational position, and income. Antidepressant use served as a proxy for depression and was derived from registry data on prescription medication purchases in the 5-year period preceding baseline. Age- and sex-adjusted Cox regression models with sampling weights were used.Results: Individuals with antidepressant purchases in any year 1995 to 1999 had a higher risk of CHD deaths (hazard ratio [HR] = 1.68, 95% confidence interval [CI] = 1.62-1.75) than did those without purchases. Basic level of education (HR = 2.09, 95% CI = 2.01-2.17), blue-collar occupations (HR = 1.70, 95% CI = 1.65-1.75), and the lowest income tertile (HR = 2.79, 95% CI = 2.69-2.91) were related to increased relative risks for CHD mortality. No significant (p < .05) interactions emerged between the SEP indicators and antidepressant purchases indicating that the effect of antidepressant use on the relative risk for CHD was similar across varying levels of SEP.Conclusions: Our study demonstrates that in a country with tax-funded universal health care services, low SEP does not exacerbate the adverse effects of depressionas measured by antidepressant treatmenton cardiovascular health.
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| 7. |
- McCaffery, Jeanne M., et al.
(author)
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Replication of the Association of BDNF and MC4R Variants With Dietary Intake in the Diabetes Prevention Program
- 2017
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In: Psychosomatic Medicine. - : Lippincott Williams & Wilkins. - 0033-3174 .- 1534-7796. ; 79:2, s. 224-233
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Journal article (peer-reviewed)abstract
- Objective: Genomewide association studies (GWAS) have identified consistent associations with obesity, with a number of studies implicating eating behavior as a primary mechanism. Few studies have replicated genetic associations with dietary intake. This study evaluates the association between obesity susceptibility loci and dietary intake. Methods: Data were obtained as part of the Diabetes Prevention Program (DPP), a clinical trial of diabetes prevention in persons at high risk of diabetes. The association of 31 genomewide association studies identified obesity risk alleles with dietary intake, measured through a food frequency questionnaire, was investigated in 3,180 participants from DPP at baseline. Results: The minor allele at BDNF, identified as protective against obesity, was associated with lower total caloric intake (beta = -106.06, SE = 33.13; p = .0014) at experimentwide statistical significance (p = .0016), whereas association of MC4R rs571312 with higher caloric intake reached nominal significance (beta = 61.32, SE = 26.24; p = .0194). Among non-Hispanic white participants, the association of BDNF rs2030323 with total caloric intake was stronger (beta = -151.99, SE = 30.09; p < .0001), and association of FTO rs1421085 with higher caloric intake (beta = 56.72, SE = 20.69; p = .0061) and percentage fat intake (beta = 0.37, SE = 0.08; p =. 0418) was also observed. Conclusions: These results demonstrate with the strength of independent replication that BDNF rs2030323 is associated with 100 to 150 greater total caloric intake per allele, with additional contributions of MC4R and, in non-Hispanic white individuals, FTO. As it has been argued that an additional 100 kcal/d could account for the trends in weight gain, prevention focusing on genetic profiles with high dietary intake may help to quell adverse obesity trends.
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| 8. |
- Ronaldson, Amy, et al.
(author)
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Optimism and recovery after acute coronary syndrome : a clinical cohort study.
- 2015
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In: Psychosomatic Medicine. - 0033-3174 .- 1534-7796. ; 77:3, s. 311-8
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Journal article (peer-reviewed)abstract
- OBJECTIVE: Optimism is associated with reduced cardiovascular mortality, but its impact on recovery after acute coronary syndrome (ACS) is poorly understood. We hypothesized that greater optimism would lead to more effective physical and emotional adaptation after ACS and would buffer the impact of persistent depressive symptoms on clinical outcomes.METHODS: This prospective observational clinical study took place in an urban general hospital and involved 369 patients admitted with a documented ACS. Optimism was assessed with a standardized questionnaire. The main outcomes were physical health status, depressive symptoms, smoking, physical activity, and fruit and vegetable consumption measured 12 months after ACS, and composite major adverse cardiac events (cardiovascular death, readmission with reinfarction or unstable angina, and coronary artery bypass graft surgery) assessed over an average of 45.7 months.RESULTS: We found that optimism predicted better physical health status 12 months after ACS independently of baseline physical health, age, sex, ethnicity, social deprivation, and clinical risk factors (B = 0.65, 95% confidence interval [CI] = 0.10-1.20). Greater optimism also predicted reduced risk of depressive symptoms (odds ratio = 0.82, 95% CI = 0.74-0.90), more smoking cessation, and more fruit and vegetable consumption at 12 months. Persistent depressive symptoms 12 months after ACS predicted major adverse cardiac events over subsequent years (odds ratio = 2.56, 95% CI = 1.16-5.67), but only among individuals low in optimism (optimism × depression interaction; p = .014).CONCLUSIONS: Optimism predicts better physical and emotional health after ACS. Measuring optimism may help identify individuals at risk. Pessimistic outlooks can be modified, potentially leading to improved recovery after major cardiac events.
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| 9. |
- Sundin, Johanna, et al.
(author)
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Understanding the Gut Microbiota in Inflammatory and Functional Gastrointestinal Diseases
- 2017
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In: Psychosomatic Medicine. - : Lippincott Williams & Wilkins. - 0033-3174 .- 1534-7796. ; 79:8, s. 857-867
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Research review (peer-reviewed)abstract
- Objective: During the last decade, experimental and observational studies have shown that patients with inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) may have an altered intestinal microbial composition compared with healthy individuals. However, no uniform microbial signature has as yet been detected for either IBD or IBS. This review summarizes the current knowledge of microbial dysbiosis and its potential relationship to the pathophysiology in IBD and IBS. Methods: A selective review was conducted to summarize the current knowledge of gut microbiota in the pathophysiology of IBD and IBS. Results: Experimental and observational studies provide good evidence for intestinal microbial dysbiosis in subgroups of IBD and IBS. Still, no uniform disease pattern has been detected. This is most likely due to the heterogeneous nature of IBD and IBS, in combination with the effects of intrinsic and extrinsic factors. Such intrinsic factors include genetics, the gastrointestinal environment, and the host immune system, whereas extrinsic factors include early life diet, breastfeeding, and method of infant delivery. Conclusions: Recent and ongoing work to define microbial dysbiosis in IBD and IBS shows promise, but future well-designed studies with well-characterized study individuals are needed. It is likely that the microbial dysbiosis in IBD and IBS is dependent on the natural disease course of IBD and symptom pattern in IBS. Therefore, assessment of the entire microbiota along the gastrointestinal tract, in relationship to confounding factors, symptom fluctuations, and other pathophysiological factors, is needed for further understanding of the etiology of these common diseases.
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| 10. |
- Sundin, Johanna, et al.
(author)
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Understanding the Gut Microbiota in Inflammatory and Functional Gastrointestinal Diseases
- 2017
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In: Psychosomatic Medicine. - : Ovid Technologies (Wolters Kluwer Health). - 0033-3174 .- 1534-7796. ; 79:8, s. 857-867
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Journal article (peer-reviewed)abstract
- Objective: During the last decade, experimental and observational studies have shown that patients with inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) may have an altered intestinal microbial composition compared with healthy individuals. However, no uniform microbial signature has as yet been detected for either IBD or IBS. This review summarizes the current knowledge of microbial dysbiosis and its potential relationship to the pathophysiology in IBD and IBS. Methods: A selective review was conducted to summarize the current knowledge of gut microbiota in the pathophysiology of IBD and IBS. Results: Experimental and observational studies provide good evidence for intestinal microbial dysbiosis in subgroups of IBD and IBS. Still, no uniform disease pattern has been detected. This is most likely due to the heterogeneous nature of IBD and IBS, in combination with the effects of intrinsic and extrinsic factors. Such intrinsic factors include genetics, the gastrointestinal environment, and the host immune system, whereas extrinsic factors include early life diet, breastfeeding, and method of infant delivery. Conclusions: Recent and ongoing work to define microbial dysbiosis in IBD and IBS shows promise, but future well-designed studies with well-characterized study individuals are needed. It is likely that the microbial dysbiosis in IBD and IBS is dependent on the natural disease course of IBD and symptom pattern in IBS. Therefore, assessment of the entire microbiota along the gastrointestinal tract, in relationship to confounding factors, symptom fluctuations, and other pathophysiological factors, is needed for further understanding of the etiology of these common diseases.
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