We conducted a systematic review and meta-analysis to compare the prevalence of small intestinal bacterial overgrowth (SIBO) in patients with irritable bowel syndrome (IBS) and controls.
Electronic ...databases were searched up to December 2018 for studies reporting SIBO prevalence in patients with IBS. Prevalence rates, odds ratios (ORs), and 95% confidence intervals (CIs) of SIBO in patients with IBS and controls were calculated.
We included 25 studies with 3,192 patients with IBS and 3,320 controls. SIBO prevalence in patients with IBS was significantly increased compared with controls (OR = 3.7, 95% CI 2.3-6.0). In studies using only healthy controls, the OR for SIBO in patients with IBS was 4.9 (95% CI 2.8-8.6). With breath testing, SIBO prevalence in patients with IBS was 35.5% (95% CI 33.6-37.4) vs 29.7% (95% CI 27.6-31.8) in controls. Culture-based studies yielded a SIBO prevalence of 13.9% (95% CI 11.5-16.4) in patients with IBS and 5.0% (95% CI 3.9-6.2) in controls with a cutoff value of 10 colony-forming units per milliliter vs 33.5% (95% CI 30.1-36.9) in patients with IBS and 8.2% (95% CI 6.8-9.6) in controls with a cutoff value of 10 colony-forming unit per milliliter, respectively. SIBO prevalence diagnosed by lactulose breath test is much greater in both patients with IBS (3.6-fold) and controls (7.6-fold) compared with glucose breath test. Similar difference is seen when lactulose breath test is compared with culture methods. OR for SIBO in patients with IBS-diarrhea compared with IBS-constipation was 1.86 (95% CI 1.83-2.8). Methane-positive breath tests were significantly more prevalent in IBS-constipation compared with IBS-diarrhea (OR = 2.3, 95% CI 1.2-4.2). In patients with IBS, proton pump inhibitor was not associated with SIBO (OR = 0.8, 95% CI 0.5-1.5, P = 0.55).
This systematic review and meta-analysis suggests a link between IBS and SIBO. However, the overall quality of the evidence is low. This is mainly due to substantial "clinical heterogeneity" due to lack of uniform selection criteria for cases and controls and limited sensitivity and specificity of the available diagnostic tests.
Background
According to Rome IV criteria, functional dyspepsia (FD) and irritable bowel syndrome (IBS) are distinct functional gastrointestinal disorders (FGID); however, overlap of these conditions ...is common in population-based studies, but clinical data are lacking.
Aims
To determine the overlap of FD and IBS in the clinical setting and define risk factors for the overlap of FD/IBS.
Methods
A total of 1127 consecutive gastroenterology outpatients of a tertiary center were recruited and symptoms assessed with a standardized validated questionnaire. Patients without evidence for structural or biochemical abnormalities as a cause of symptoms were then categorized based upon the symptom pattern as having FD, IBS or FD/IBS overlap. Additionally, this categorization was compared with the clinical diagnosis documented in the integrated electronic medical records system.
Results
A total of 120 patients had a clinical diagnosis of a FGID. Based upon standardized assessment with a questionnaire, 64% of patients had FD/IBS overlap as compared to 23% based upon the routine clinical documentation. In patients with severe IBS or FD symptoms (defined as symptoms affecting quality of life), the likelihood of FD/IBS overlap was substantially increased (OR = 3.1; 95%CI 1.9–5.0) and (OR = 9.0; 95%CI 3.5–22.7), respectively. Thus, symptom severity for IBS- or FD symptoms were significantly higher for patients with FD/IBS overlap as compared to patients with FD or IBS alone (
p
all < 0.01). Age, gender and IBS-subtype were not associated with overlap.
Conclusion
In the clinical setting, overlap of FD and IBS is the norm rather than the exception. FD/IBS overlap is associated with a more severe manifestation of a FGID.
Cancer is a leading cause of disease burden in Australia, particularly fatal burden, accounting for an estimated thirty percent of deaths. Many cancers develop because of exposure to lifestyle and ...environmental factors that are potentially modifiable. We aimed to quantify the proportions and numbers of cancer deaths and cases in Australia in 2013 attributable to 20 modifiable factors in eight broad groupings that are established causes of cancer, namely: tobacco smoke (smoking and second‐hand), dietary factors (low intake of fruit, non‐starchy vegetables and dietary fibre; and high intake of red and processed meat), overweight/obesity, alcohol, physical inactivity, solar ultraviolet radiation, infections (seven agents), and reproductive factors (lack of breastfeeding, menopausal hormone therapy use, combined oral contraceptive use). We estimated population attributable fractions (PAF) using standard formulae incorporating exposure prevalence and relative risk data. Of all cancer deaths in Australia in 2013, approximately 38% overall (males 41%, females 34%) could be attributed to the factors assessed; the corresponding PAF for cancer cases was 33% (males 34%, females 32%). Tobacco smoke was the leading cause of cancer deaths and cases, with PAFs of 23 and 13%, respectively, followed by dietary factors (5% deaths/5% cases), overweight/obesity (5%/4%) and infections (5%/3%). Cancer sites with the highest numbers of potentially preventable deaths/cases were lung (n = 6,776/9,272), colorectum (n = 1,974/7,380) and cutaneous melanoma (n = 1,390/7,918). We estimate that about 16,700 cancer deaths and 41,200 cancer cases could be prevented in Australia each year if people's exposures to 20 causal factors were aligned with levels recommended to minimise cancer risk.
What's new?
Cancer is the leading cause of death in Australia. Yet many of these deaths could be prevented if known causes were avoided. In this study, the authors estimated the number and fraction of cancer deaths and cancer cases in Australia attributable to modifiable factors. They found that 38% of all cancer deaths and 33% of cancer cases could be attributed to 20 factors. Tobacco smoke was the leading cause of cancer death, followed by dietary factors, overweight/obesity, infections and solar ultraviolet radiation.
Hepatocellular (HCC) and extrahepatic cancers have been associated with non-alcoholic fatty liver disease (NAFLD); however, the extent and nature of these relationships remain unclear. We aimed to ...estimate the absolute incidence rates of these cancers in adults with NAFLD with respect to key demographic and clinical factors.
We searched PubMed, Embase, Cochrane Library and Web of Science databases for studies reporting the incidence rates of any cancer in adults with NAFLD from inception to 31 August 2020. The main meta-analysis outcomes were pooled incidences of cancers in NAFLD using random-effects modelling. Subgroup analyses examined the effects of NAFLD disease stage.
In total, 64 studies were eligible for analysis of HCC and extrahepatic cancer incidence including 625,984 and 41,027 patients, respectively. The pooled HCC incidence rate was 1.25 per 1000 person-years (95% CI 1.01 to 1.49; I2 = 94.8%). In patients with NAFLD with advanced liver fibrosis or cirrhosis, the HCC incidence rate was 14.46 per 1000 person-years (95% CI 10.89 to 18.04; I2 = 91.3%). The pooled extrahepatic cancer incidence rate was 10.58 per 1000 person-years (95% CI 8.14 to 13.02; I2 = 97.1%). The most frequently occurring extrahepatic cancers were uterine, breast, prostate, colorectal, and lung. Extrahepatic cancer incidence rates were not higher in patients with NAFLD with advanced liver fibrosis or cirrhosis.
The rate of HCC development in patients with NAFLD who have progressed to advanced liver fibrosis or cirrhosis supports current HCC surveillance recommendations targeted for this group. Extrahepatic cancers are over eight-fold more frequent than HCC in NAFLD and not associated with liver fibrosis stage. As the global prevalence of NAFLD is approximately 25% and increasing, these findings support a focus on its prevention and the early detection of cancer in adults with NAFLD.
•HCC risk in NAFLD with advanced fibrosis/cirrhosis exceeds surveillance thresholds.•Extrahepatic cancers are over eight-fold more frequent than HCC in NAFLD.•Risk of extrahepatic cancers in NAFLD is not associated with liver fibrosis stage.
Abstract
Kendall, BJ, Siekirk, NJ, and Lai, Q. Effects of acute high-intensity interval training on information processing speed.
J Strength Cond Res
36(11): 3081–3086, 2022—This study investigated ...the effects of acute exercise on reaction time (RT), premotor time (i.e., central processing), and motor time (i.e., peripheral processing) using surface electromyography to fractionate RT. Fifty-eight young adults (27 men, 31 women) between the age of 18 and 40 years participated in 2 testing sessions. During visit one, subjects performed a simple RT task under regular (i.e., consistent timing) and irregular (i.e., variable timing) foreperiods. Subjects were then randomized to either an aerobic-only high-intensity interval training (HIIT) group (HIIT-A), an aerobic/resistance HIIT group (HIIT-AR), or a resting control group (CG). Both exercise groups performed a 20-minute, digital video disc-delivered HIIT exercise protocol. After exercise or rest, when controlling for cardiovascular fitness, no statistical differences were observed for the regular foreperiod conditions (
p
> 0.05). For the irregular foreperiod conditions, the HIIT-A group (M = 219.8,
SE
= 6.5) and the HIIT-AR group (M = 218.2,
SE
= 5.8) had significantly faster mean RTs than the CG (M = 248.1,
SE
= 8.1). In addition, the HIIT-A (M = 172.1,
SE
= 4.6) and HIIT-AR exercise groups (M = 171.3,
SE
= 4.8) had significantly faster mean PMTs than the CG (M = 189.7,
SE
= 5.7). These findings suggest that tasks dependent on central processing may benefit from an acute bout of exercise.
Gastro-oesophageal reflux disease (GERD) has heterogeneous aetiology primarily attributable to its symptom-based definitions. GERD genome-wide association studies (GWASs) have shown strong genetic ...overlaps with established risk factors such as obesity and depression. We hypothesised that the shared genetic architecture between GERD and these risk factors can be leveraged to (1) identify new GERD and Barrett's oesophagus (BE) risk loci and (2) explore potentially heterogeneous pathways leading to GERD and oesophageal complications.
We applied multitrait GWAS models combining GERD (78 707 cases; 288 734 controls) and genetically correlated traits including education attainment, depression and body mass index. We also used multitrait analysis to identify BE risk loci. Top hits were replicated in 23andMe (462 753 GERD cases, 24 099 BE cases, 1 484 025 controls). We additionally dissected the GERD loci into obesity-driven and depression-driven subgroups. These subgroups were investigated to determine how they relate to tissue-specific gene expression and to risk of serious oesophageal disease (BE and/or oesophageal adenocarcinoma, EA).
We identified 88 loci associated with GERD, with 59 replicating in 23andMe after multiple testing corrections. Our BE analysis identified seven novel loci. Additionally we showed that only the obesity-driven GERD loci (but not the depression-driven loci) were associated with genes enriched in oesophageal tissues and successfully predicted BE/EA.
Our multitrait model identified many novel risk loci for GERD and BE. We present strong evidence for a genetic underpinning of disease heterogeneity in GERD and show that GERD loci associated with depressive symptoms are not strong predictors of BE/EA relative to obesity-driven GERD loci.
Abstract
Symptoms related with gastro-esophageal reflux disease (GERD) were previously shown to be linked with increased risk for the 2019 coronavirus disease (COVID-19). We aim to interrogate the ...possibility of a shared genetic basis between GERD and COVID-19 outcomes. Using published GWAS data for GERD (78 707 cases; 288 734 controls) and COVID-19 susceptibility (up to 32 494 cases; 1.5 million controls), we examined the genetic relationship between GERD and three COVID-19 outcomes: risk of developing severe COVID-19, COVID-19 hospitalization and overall COVID-19 risk. We estimated the genetic correlation between GERD and COVID-19 outcomes followed by Mendelian randomization (MR) analyses to assess genetic causality. Conditional analyses were conducted to examine whether known COVID-19 risk factors (obesity, smoking, type-II diabetes, coronary artery disease) can explain the relationship between GERD and COVID-19. We found small to moderate genetic correlations between GERD and COVID-19 outcomes (rg between 0.06 and 0.24). MR analyses revealed a OR of 1.15 (95% CI: 0.96–1.39) for severe COVID-19; 1.16 (1.01–1.34) for risk of COVID-19 hospitalization; 1.05 (0.97–1.13) for overall risk of COVID-19 per doubling of odds in developing GERD. The genetic correlation/associations between GERD and COVID-19 showed mild attenuation towards the null when obesity and smoking was adjusted for. Susceptibility for GERD and risk of COVID-19 hospitalization were genetically correlated, with MR findings supporting a potential causal role between the two. The genetic association between GERD and COVID-19 was partially attenuated when obesity is accounted for, consistent with obesity being a major risk factor for both diseases.
Background
Certain dietary constituents may provoke symptoms of functional dyspepsia (FD); however, there is an absence of dietary trials testing specific dietary interventions. Empirically derived ...dietary strategies and the low FODMAP diet are frequently used in practice. This study aimed to compare the effectiveness of low FODMAP dietary advice with standard dietary advice for reducing epigastric and overall gastrointestinal symptoms in individuals with FD.
Methods
Data were collected from 59 consecutive eligible individuals with FD attending an initial and review outpatient dietetic consultation at Princess Alexandra Hospital. Of these, 40 received low FODMAP advice and 19 received standard dietary advice. As part of usual care, the Structured Assessment of Gastrointestinal Symptom Scale (SAGIS) was used to assess epigastric (maximum score = 28) and overall gastrointestinal symptoms (maximum score = 88). Dietary adherence data were collected, and change in symptom score and proportion of responders (defined as a ≥30% reduction in score) for epigastric and total symptoms was calculated.
Key Results
Most individuals (48/59, 81%) had FD and coexisting irritable bowel syndrome. There was a greater reduction in epigastric score in those receiving low FODMAP dietary advice compared with those receiving standard advice (est. marginal mean 95% CI: −3.6 −4.9, −2.2 vs. −0.9 −2.9, 1.1, p = 0.032) and total symptom score (−9.4 −12.4, −6.4 vs. −3.3 −7.7, 1.1 p = 0.026). A greater proportion receiving low FODMAP dietary advice were responders versus those receiving standard advice (50% vs. 16%, p = 0.012). Dietary adherence did not differ between groups (p = 0.497).
Conclusions & Inferences
The low FODMAP diet appears more effective for improving epigastric symptoms in people with FD compared with standard advice. A randomized controlled trial is required to substantiate these findings.
Low FODMAP dietary advice leads to greater epigastric symptom improvement compared with standard dietary advice in an observational study of individuals with functional dyspepsia.
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