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Chronic viral infections in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).
Rasa, S, Nora-Krukle, Z, Henning, N, Eliassen, E, Shikova, E, Harrer, T, Scheibenbogen, C, Murovska, M, Prusty, BK
Journal of translational medicine. 2018;16(1):268
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The causes of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) are currently unknown, however viruses have been implicated. The absence of well-designed studies has hindered the understanding of this disease and the aim of this review was to discuss the literature regarding viruses and ME/CFS. Several viruses were discussed including the herpes virus, which is responsible for illnesses such as chicken pox and cold sores. This virus has not always been associated with the onset of ME/CFS, however it may be in certain individuals. The enteroviruses, which are responsible for illnesses such as hand, foot and mouth and polio, were also reviewed and it was concluded that it is unlikely that these have a role in ME/CFS. Several other viruses were also discussed. The authors then went on to describe how these viruses can affect human cells, potentially causing ME/CFS. It was concluded that the data available is controversial and only certain individuals may be affected, better studies are required. This study could be used by healthcare professionals to identify individuals at risk of ME/CFS following viral infection and understanding how ME/CFS may develop.
Abstract
BACKGROUND AND MAIN TEXT Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex and controversial clinical condition without having established causative factors. Increasing numbers of cases during past decade have created awareness among patients as well as healthcare professionals. Chronic viral infection as a cause of ME/CFS has long been debated. However, lack of large studies involving well-designed patient groups and validated experimental set ups have hindered our knowledge about this disease. Moreover, recent developments regarding molecular mechanism of pathogenesis of various infectious agents cast doubts over validity of several of the past studies. CONCLUSIONS This review aims to compile all the studies done so far to investigate various viral agents that could be associated with ME/CFS. Furthermore, we suggest strategies to better design future studies on the role of viral infections in ME/CFS.
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Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty.
Ferrucci, L, Fabbri, E
Nature reviews. Cardiology. 2018;15(9):505-522
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Inflammageing is a term used to describe elevated blood inflammatory markers that leads to frailty and increases an individual’s risk for heart disease, kidney disease and other physical and mental illnesses. Whether inflammageing is causal in heart disease is still uncertain. This large review of 310 papers aimed to understand the causes and role of inflammageing in heart disease and other illnesses associated with ageing. Causes of inflammageing were discussed and mechanisms are not fully understood. Genetic susceptibility, obesity, gut microbiota, gut permeability, when cells can no longer divide, and chronic infections were all implicated. The role of inflammageing in heart disease was a focus and the authors deduced that it was likely to be both causal and a result of heart disease. However, the administration of anti-inflammatories in heart disease has not always proved a successful treatment. Possible causes of inflammageing are likely to be linked and cumulative and although inflammation may cause age related diseases, its role in protecting the body means that its benefits outweigh its consequences. It was concluded that controlling inflammageing may prevent heart disease and other diseases associated with ageing. This study could be used by healthcare professionals to help understand what inflammageing is and its role in age related diseases.
Abstract
Most older individuals develop inflammageing, a condition characterized by elevated levels of blood inflammatory markers that carries high susceptibility to chronic morbidity, disability, frailty, and premature death. Potential mechanisms of inflammageing include genetic susceptibility, central obesity, increased gut permeability, changes to microbiota composition, cellular senescence, NLRP3 inflammasome activation, oxidative stress caused by dysfunctional mitochondria, immune cell dysregulation, and chronic infections. Inflammageing is a risk factor for cardiovascular diseases (CVDs), and clinical trials suggest that this association is causal. Inflammageing is also a risk factor for chronic kidney disease, diabetes mellitus, cancer, depression, dementia, and sarcopenia, but whether modulating inflammation beneficially affects the clinical course of non-CVD health problems is controversial. This uncertainty is an important issue to address because older patients with CVD are often affected by multimorbidity and frailty - which affect clinical manifestations, prognosis, and response to treatment - and are associated with inflammation by mechanisms similar to those in CVD. The hypothesis that inflammation affects CVD, multimorbidity, and frailty by inhibiting growth factors, increasing catabolism, and interfering with homeostatic signalling is supported by mechanistic studies but requires confirmation in humans. Whether early modulation of inflammageing prevents or delays the onset of cardiovascular frailty should be tested in clinical trials.
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Synbiotics modulate gut microbiota and reduce enteritis and ventilator-associated pneumonia in patients with sepsis: a randomized controlled trial.
Shimizu, K, Yamada, T, Ogura, H, Mohri, T, Kiguchi, T, Fujimi, S, Asahara, T, Yamada, T, Ojima, M, Ikeda, M, et al
Critical care (London, England). 2018;22(1):239
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The gut microbiota is disrupted in critically ill patients. Synbiotics are combinations of probiotics and prebiotics (nondigestible food ingredients that selectively stimulate the growth and/or activity of specific beneficial bacteria in the colon). The aim of this single-blind study was to evaluate whether synbiotics maintain the microbiota and reduce infectious complications in mechanically ventilated patients with sepsis. 72 such patients were randomly assigned to either receiving a synbiotic within three days of admission or not receiving a synbiotic. The synbiotic contained Lactobacillus casei strain Shirota, Bifidobacterium breve strain Yakult and galactooligosaccharides. Patients receiving the synbiotic had an increase in total bacteria, in particular Bifidobateria, Lactobacilli and Atopobium species, as well as higher organic acids (the fermentation products of bacteria) than the no-synbiotic group. There were significantly less infectious complications in the synbiotic group, including less enteritis (an inflammation of the small intestine) and less ventilation associated pneumonia. There were no differences in bacteraemia (the presence of bacteria in the bloodstream) or mortality between the two groups.
Abstract
BACKGROUND Commensal microbiota deteriorate in critically ill patients. The preventive effects of probiotic/synbiotic therapy on microbiota and septic complications have not been thoroughly clarified in patients with sepsis. The objective of this study was to evaluate whether synbiotics have effects on gut microbiota and reduce complications in mechanically ventilated patients with sepsis. METHODS Sepsis patients who were mechanically ventilated in the intensive care unit (ICU) were included in this randomized controlled study. Patients receiving daily synbiotics (Bifidobacterium breve strain Yakult, Lactobacillus casei strain Shirota, and galactooligosaccharides) initiated within 3 days after admission (the Synbiotics group) were compared with patients who did not receive synbiotics (the No-Synbiotics group). The primary outcome was infectious complications including enteritis, ventilator-associated pneumonia (VAP), and bacteremia within 4 weeks from admission. The secondary outcomes included mortality within 4 weeks, fecal bacterial counts, and organic acid concentration. Enteritis was defined as the acute onset of continuous liquid stools for more than 12 h. RESULTS Seventy-two patients completed this trial; 35 patients received synbiotics and 37 patients did not receive synbiotics. The incidence of enteritis was significantly lower in the Synbiotics than the No-Synbiotics group (6.3% vs. 27.0%; p < 0.05). The incidence of VAP was also significantly lower in the Synbiotics than the No-Synbiotics group (14.3% vs. 48.6%; p < 0.05). The incidence of bacteremia and mortality did not differ significantly between the two groups. In the analysis of fecal bacteria, the number of Bifidobacterium and Lactobacillus in the Synbiotics group was significantly higher than that in the No-Synbiotics group. In the analysis of fecal organic acids, total organic acid concentration, especially the amounts of acetate, were significantly greater in the Synbiotics group than in the No-Synbiotics group at the first week (p < 0.05). CONCLUSIONS Prophylactic synbiotics could modulate the gut microbiota and environment and may have preventive effects on the incidence of enteritis and VAP in patients with sepsis. TRIAL REGISTRATION UMIN, R000007633 . Registered on 29 September 2011.
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Longitudinal Study of the Psoriasis-Associated Skin Microbiome during Therapy with Ustekinumab in a Randomized Phase 3b Clinical Trial.
Loesche, MA, Farahi, K, Capone, K, Fakharzadeh, S, Blauvelt, A, Duffin, KC, DePrimo, SE, Muñoz-Elías, EJ, Brodmerkel, C, Dasgupta, B, et al
The Journal of investigative dermatology. 2018;138(9):1973-1981
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Chronic plaque psoriasis is an immune-mediated disease of the skin and joints. A growing appreciation of the role of the innate immune system in psoriasis pathogenesis stems from the prominent role of inflammatory cytokines and cells associated with innate immunity in the disease and associations observed between psoriasis and genetic variations involved in innate immunity. The aim of this study was to assess changes of the skin microbiome in the setting of a longitudinal phase 3b study of patients receiving up to 2 years of ustekinumab therapy. Results show that prior to treatment, there were minor, body-site specific differences in microbial diversity and composition when comparing lesional with non-lesional skin. Microbial heterogeneity was greater in lesional skin than non-lesional skin. During ustekinumab treatment, the composition of microbiota diverged further between lesional and non-lesional skin across body sites. The divergence observed between lesional and non-lesional skin during ustekinumab treatment varied by body site. Authors conclude that their findings may help inform future study design and it may also have medically relevant implications for diagnostics and therapeutics involving the skin microbiome.
Abstract
Plaque psoriasis, a chronic inflammatory disease primarily affecting the skin, is thought to have a multifactorial etiology, including innate immune system dysregulation, environmental triggers, and genetic susceptibility. We sought to further understand the role of skin microbiota in psoriasis pathogenesis, as well as their response to therapy. We systematically analyzed dynamic microbiota colonizing psoriasis lesions and adjacent nonlesional skin in 114 patients prior to and during ustekinumab treatment in a phase 3b clinical trial. By sequencing the bacterial 16S ribosomal RNA gene from skin swab samples obtained at six anatomical sites, we identified minor, site-specific differences in microbial diversity and composition between pretreatment lesional and nonlesional skin. During therapy, microbial communities within lesional and nonlesional skin diverged, and body-site dispersion increased, reflecting microbial skin site-specificity. Microbiota demonstrated greater pretreatment heterogeneity in psoriatic lesions than in nonlesional skin, and variance increased as treatment progressed. Microbiota colonizing recurrent lesions did not overlap with pretreatment lesional microbiota, suggesting colonization patterns varied between initial and recurrent psoriatic lesions. While plaque psoriasis does not appear to be associated with specific microbes and/or microbial diversity, this large dataset provides insight into microbial variation associated with (i) disease in different body locations, (ii) initial versus recurrent lesions, and (iii) anti-IL12/23 therapy.
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Long-term outcome of patients with steroid-refractory acute severe UC treated with ciclosporin or infliximab.
Laharie, D, Bourreille, A, Branche, J, Allez, M, Bouhnik, Y, Filippi, J, Zerbib, F, Savoye, G, Vuitton, L, Moreau, J, et al
Gut. 2018;67(2):237-243
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Intravenous steroids are the first-line therapy for ulcerative colitis (UC) patients who are hospitalised during a severe UC flare-up. In the 40% of patients who don’t respond to steroids, the drugs ciclosporin and infliximab have been found to be efficient in preventing surgery to remove part or all of the colon, but there is a lack of data on the long-term outcomes of using these medications in UC patients. The aim of this study was to assess long-term outcome of patients included in a randomised trial comparing ciclosporin and infliximab. Between 2007 and 2010, 115 patients with UC that did not respond to steroids were randomised to receive ciclosporin or infliximab in association with azathioprine. Patients were followed to January 2015 or death. After a median follow-up of 5.4 years, colectomy-free survival rates at 1 and 5 years were, respectively, 70.9% and 61.5% in patients who received ciclosporin and 69.1% and 65.1% in those who received infliximab. Long-term colectomy-free survival was independent from initial treatment. However, a higher proportion of patients initially treated with ciclosporin needed a new treatment compared with those who received infliximab first. The researchers concluded that these results further confirm a similar efficacy and good safety profiles of both drugs.
Abstract
OBJECTIVE Ciclosporin and infliximab have demonstrated short-term similar efficacy as second-line therapies in patients with acute severe UC (ASUC) refractory to intravenous steroids. The aim of this study was to assess long-term outcome of patients included in a randomised trial comparing ciclosporin and infliximab. DESIGN Between 2007 and 2010, 115 patients with steroid-refractory ASUC were randomised in 29 European centres to receive ciclosporin or infliximab in association with azathioprine. Patients were followed until death or last news up to January 2015. Colectomy-free survival rates at 1 and 5 years and changes in therapy were estimated through Kaplan-Meier method and compared between initial treatment groups through log-rank test. RESULTS After a median follow-up of 5.4 years, colectomy-free survival rates (95% CI) at 1 and 5 years were, respectively, 70.9% (59.2% to 82.6%) and 61.5% (48.7% to 74.2%) in patients who received ciclosporin and 69.1% (56.9% to 81.3%) and 65.1% (52.4% to 77.8%) in those who received infliximab (p=0.97). Cumulative incidence of first infliximab use at 1 and 5 years in patients initially treated with ciclosporin was, respectively, 45.7% (32.6% to 57.9%) and 57.1% (43.0% to 69.0%). Only four patients from the infliximab group were subsequently switched to ciclosporin. Three patients died during the follow-up, none directly related to UC or its treatment. CONCLUSIONS In this cohort of patients with steroid-refractory ASUC initially treated by ciclosporin or infliximab, long-term colectomy-free survival was independent from initial treatment. These long-term results further confirm a similar efficacy and good safety profiles of both drugs and do not favour one drug over the other. TRIAL REGISTRATION NUMBER EudraCT: 2006-005299-42; ClinicalTrials.gouv number: NCT00542152; post-results.
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Dietary Cholesterol and the Lack of Evidence in Cardiovascular Disease.
Soliman, GA
Nutrients. 2018;10(6)
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For years, dietary cholesterol was implicated in increasing blood cholesterol levels, therefore contributing to the development of cardiovascular disease (CVD). While it is known that saturated fatty acids and trans-fatty acids increase CVD risk, the evidence of dietary cholesterol increasing this risk remains inconclusive. This review summarises the current evidence regarding dietary cholesterol, blood cholesterol, saturated fatty acids and the risk of CVD. This review found that the current literature does not support the notion that dietary cholesterol increases the risk of heart disease in healthy individuals. The fact that dietary cholesterol is common in foods that are high in saturated fats may have contributed to the hypothesis that dietary cholesterol increases the risk of CVD. Based on these results, the author suggests individuals incorporate nutrient-dense, calorie controlled, balanced meals in eating patterns.
Abstract
Cardiovascular disease (CVD) is the leading cause of death in the United States. For years, dietary cholesterol was implicated in increasing blood cholesterol levels leading to the elevated risk of CVD. To date, extensive research did not show evidence to support a role of dietary cholesterol in the development of CVD. As a result, the 2015⁻2020 Dietary Guidelines for Americans removed the recommendations of restricting dietary cholesterol to 300 mg/day. This review summarizes the current literature regarding dietary cholesterol intake and CVD. It is worth noting that most foods that are rich in cholesterol are also high in saturated fatty acids and thus may increase the risk of CVD due to the saturated fatty acid content. The exceptions are eggs and shrimp. Considering that eggs are affordable and nutrient-dense food items, containing high-quality protein with minimal saturated fatty acids (1.56 gm/egg) and are rich in several micronutrients including vitamins and minerals, it would be worthwhile to include eggs in moderation as a part of a healthy eating pattern. This recommendation is particularly relevant when individual’s intakes of nutrients are suboptimal, or with limited income and food access, and to help ensure dietary intake of sufficient nutrients in growing children and older adults.
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Association between plasma fatty acids and inflammatory markers in patients with and without insulin resistance and in secondary prevention of cardiovascular disease, a cross-sectional study.
Bersch-Ferreira, ÂC, Sampaio, GR, Gehringer, MO, Torres, EAFDS, Ross-Fernandes, MB, da Silva, JT, Torreglosa, CR, Kovacs, C, Alves, R, Magnoni, CD, et al
Nutrition journal. 2018;17(1):26
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It is known that people with cardiovascular disease (CVD) have increased inflammation and raised levels of circulating inflammatory molecules. The presence of insulin resistance is thought to increase these levels, as are certain fatty acids coming from dietary fats. The aims of this cross-sectional study were to compare the levels of inflammatory biomarkers in patients with CVD with and without insulin resistance, and to evaluate the possible link between the blood levels of fatty acids and inflammatory biomarkers among these patients. The authors concluded that the CVD patients with insulin resistance had a higher concentration of some inflammatory molecules in the blood than those without insulin resistance. They also observed that saturated fatty acids were linked to higher levels of inflammatory molecules in the blood, while unsaturated fatty acids correlated with lower levels.
Abstract
BACKGROUND Proinflammatory biomarkers levels are increased among patients with cardiovascular disease, and it is known that both the presence of insulin resistance and diet may influence those levels. However, these associations are not well studied among patients with established cardiovascular disease. Our objective is to compare inflammatory biomarker levels among cardiovascular disease secondary prevention patients with and without insulin resistance, and to evaluate if there is any association between plasma fatty acid levels and inflammatory biomarker levels among them. METHODS In this cross-sectional sub-study from the BALANCE Program Trial, we collected data from 359 patients with established cardiovascular disease. Plasma fatty acids and inflammatory biomarkers (interleukin (IL)-1β, IL-6, IL-8, IL-10, IL-12, high sensitive C-reactive protein (hs-CRP), adiponectin, and tumor necrosis factor (TNF)-alpha) were measured. Biomarkers and plasma fatty acid levels of subjects across insulin resistant and not insulin resistant groups were compared, and general linear models were used to examine the association between plasma fatty acids and inflammatory biomarkers. RESULTS Subjects with insulin resistance had a higher concentration of hs-CRP (p = 0.002) and IL-6 (p = 0.002) than subjects without insulin resistance. Among subjects without insulin resistance there was a positive association between stearic fatty acid and IL-6 (p = 0.032), and a negative association between alpha-linolenic fatty acid and pro-inflammatory biomarkers (p < 0.05). Among those with insulin resistance there was a positive association between monounsaturated fatty acids and arachidonic fatty acid and adiponectin (p < 0.05), and a negative association between monounsaturated and polyunsaturated fatty acids and pro-inflammatory biomarkers (p < 0.05), as well as a negative association between polyunsaturated fatty acids and adiponectin (p < 0.05). Our study has not found any association between hs-CRP and plasma fatty acids. CONCLUSIONS Subjects in secondary prevention for cardiovascular disease with insulin resistance have a higher concentration of hs-CRP and IL-6 than individuals without insulin resistance, and these inflammatory biomarkers are positively associated with saturated fatty acids and negatively associated with unsaturated fatty acids.
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Antidepressant utilisation and incidence of weight gain during 10 years' follow-up: population based cohort study.
Gafoor, R, Booth, HP, Gulliford, MC
BMJ (Clinical research ed.). 2018;361:k1951
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Obesity is an increasing concern worldwide and the USA and UK have some of the highest rates of obesity in the world. Anti-depressant medications are also increasing prescribed, and there is an established association between obesity and depression. These medications may also contribute to weight gain, although the mechanisms for this are not clearly understood. This large UK-population based cohort study aimed to evaluate the long term association between anti-depressant prescriptions and body weight, using data from the UK Clinical Practice Research Datalink from 2004-2014. Weight gain of >=5% was measured. The number of incidences of >=5% weight gain was significantly higher for patients prescribed an anti-depressant than those who were not, after adjusting for confounding factors such as age, smoking status, social status, comorbidity and co-prescribing. This was particularly so during the 2nd and 3rd year of treatment, when there was a 46% higher risk of >=5% weight gain compared to the general population. It was also found that some anti-depressants contributed to higher weight gain than others. Whilst the associations may not be causal, the potential for weight gain should be considered when anti-depressant medications are indicated.
Abstract
OBJECTIVE To evaluate the long term association between antidepressant prescribing and body weight. DESIGN Population based cohort study. SETTING General practices contributing to the UK Clinical Practice Research Datalink, 2004-14. PARTICIPANTS 136 762 men and 157 957 women with three or more records for body mass index (BMI). MAIN OUTCOME MEASURES The main outcomes were antidepressant prescribing, incidence of ≥5% increase in body weight, and transition to overweight or obesity. Adjusted rate ratios were estimated from a Poisson model adjusting for age, sex, depression recording, comorbidity, coprescribing of antiepileptics or antipsychotics, deprivation, smoking, and advice on diet. RESULTS In the year of study entry, 17 803 (13.0%) men and 35 307 (22.4%) women with a mean age of 51.5 years (SD 16.6 years) were prescribed antidepressants. During 1 836 452 person years of follow-up, the incidence of new episodes of ≥5 weight gain in participants not prescribed antidepressants was 8.1 per 100 person years and in participants prescribed antidepressants was 11.2 per 100 person years (adjusted rate ratio 1.21, 95% confidence interval 1.19 to 1.22, P<0.001). The risk of weight gain remained increased during at least six years of follow-up. In the second year of treatment the number of participants treated with antidepressants for one year for one additional episode of ≥5% weight gain was 27 (95% confidence interval 25 to 29). In people who were initially of normal weight, the adjusted rate ratio for transition to overweight or obesity was 1.29 (1.25 to 1.34); in people who were initially overweight, the adjusted rate ratio for transition to obesity was 1.29 (1.25 to 1.33). Associations may not be causal, and residual confounding might contribute to overestimation of associations. CONCLUSION Widespread utilisation of antidepressants may be contributing to long term increased risk of weight gain at population level. The potential for weight gain should be considered when antidepressant treatment is indicated.
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Is waist-to-height ratio the best predictive indicator of hypertension incidence? A cohort study.
Rezende, AC, Souza, LG, Jardim, TV, Perillo, NB, Araújo, YCL, de Souza, SG, Sousa, ALL, Moreira, HG, de Souza, WKSB, do Rosário Gondim Peixoto, M, et al
BMC public health. 2018;18(1):281
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A variety of methods of measuring body fat are used as tools to predict the risk of developing certain lifestyle-related diseases such as high blood pressure. It is not yet clear which of these methods is the most accurate. The aim of this study was to evaluate and compare the effectiveness of using different measures of body fat to predict high blood pressure. The study was performed in Brazil. Adult volunteers with normal blood pressure were assessed for body fat using waist-to-height ratio (WHtR), body mass index (BMI) and waist circumference (WC), and then followed-up 13 years later to find out whether they had developed high blood pressure. 44% of the participants developed high blood pressure during the study period. BMI, WC and WHtR were all associated with the risk of high blood pressure and had similar accuracy in predicting the disease. However, the associations were only significant for women. The cut-off points for predicting high blood pressure agreed with current recommendations, except for the WC in men. The results suggest that both overall obesity (BMI) and central obesity (WC and WHtR) indicators can be used in this population to evaluate the risk of developing high blood pressure.
Abstract
BACKGROUND The best anthropometric indicator to verify the association between obesity and hypertension (HTN) has not been established. We conducted this study to evaluate and compare the discriminatory power of waist-to-height ratio (WHtR) in relation to body mass index (BMI) and waist circumference (WC) in predicting HTN after 13 years of follow-up. METHODS This study was an observational prospective cohort study performed in the city of Firminópolis, in Brazilian's midwest. The cohort baseline (phase 1) was initiated in 2002 with the evaluation of a representative sample of the normotensive population (≥ 18 years of age). The incidence of HTN was evaluated as the outcome (phase 2). Sociodemographic, dietary and lifestyle variables were used to adjust proportional hazards models and evaluate risk of HTN according to anthropometric indices. The areas under the receiver operating characteristic (ROC) curves were used to compare the predictive capacity of these indices. The best HTN predictor cut-offs were obtained based on sensitivity and specificity. RESULTS A total of 471 patients with a mean age of 38.9 ± 12.3 years were included in phase 1. The mean follow-up was 13.2 years, and 207 subjects developed HTN. BMI, WC and WHtR were associated with risk of HTN incidence and had similar power in predicting the disease. However, the associations were only significant for women. The cut-off points with a better HTN predictive capacity were in agreement with current recommendations, except for the WC in men. CONCLUSIONS The results suggest that both overall obesity (BMI) and central obesity (WC and WHtR) anthropometric indicators can be used in this population to evaluate the risk of developing hypertension.
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Gut microbiota associations with common diseases and prescription medications in a population-based cohort.
Jackson, MA, Verdi, S, Maxan, ME, Shin, CM, Zierer, J, Bowyer, RCE, Martin, T, Williams, FMK, Menni, C, Bell, JT, et al
Nature communications. 2018;9(1):2655
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The human gut microbiome has been associated with many health and disease states. Our knowledge is growing in relation to the abundance of particular bacteria and certain diseases, as well as the effects of certain medications on the profile of the gut microbiome. This population based cohort study using the UKTwins data set aimed to assess the associations between 38 common diseases and 51 prescription medications with the gut microbiome. 17 diseases had significant associations with at least one microbiota marker, including Type 2 diabetes, constipation, IBS, IBD, Coeliac Disease, food allergy, urinary incontinence, acne and osteoarthritis. Reduced microbiota diversity was found to be the most significant factor for disease states, having exclusively negative effects. Few associations were found for anxiety, respiratory diseases and hypercholesterolaemia. Significant associations were observed between 19 medications and the gut microbiome, including PPIs, antibiotics, paracetamol, opioids, SSRIs, and inhaled anticholinergics. The authors conclude that a complex mixture of disease and medication-specific effects are responsible for the observed microbiota associations.
Abstract
The human gut microbiome has been associated with many health factors but variability between studies limits exploration of effects between them. Gut microbiota profiles are available for >2700 members of the deeply phenotyped TwinsUK cohort, providing a uniform platform for such comparisons. Here, we present gut microbiota association analyses for 38 common diseases and 51 medications within the cohort. We describe several novel associations, highlight associations common across multiple diseases, and determine which diseases and medications have the greatest association with the gut microbiota. These results provide a reference for future studies of the gut microbiome and its role in human health.