The human microbiome is overly exposed to antibiotics, due, not only to their medical use, but also to their utilization in farm animals and crops. Microbiome composition can be rapidly altered by exposure to antibiotics, with potential immediate effects on health, for instance through the selection of resistant opportunistic pathogens that can cause acute disease. Microbiome alterations induced by antibiotics can also indirectly affect health in the long-term. The mutualistic microbes in the human body interact with many physiological processes, and participate in the regulation of immune and metabolic homeostasis. Therefore, antibiotic exposure can alter many basic physiological equilibria, promoting long-term disease. In addition, excessive antibiotic use fosters bacterial resistance, and the overly exposed human microbiome has become a significant reservoir of resistance genes, contributing to the increasing difficulty in controlling bacterial infections. Here, the complex relationships between antibiotics and the human microbiome are reviewed, with focus on the intestinal microbiota, addressing (1) the effects of antibiotic use on the composition and function of the gut microbiota, (2) the impact of antibiotic-induced microbiota alterations on immunity, metabolism, and health, and (3) the role of the gut microbiota as a reservoir of antibiotic resistances.

/pdf/antibiotics-and-the-human-gut-microbiome-dysbioses-and-1ph182qns5.pdf

Antibiotics and the Human Gut Microbiome: Dysbioses and Accumulation of Resistances

Interest toward the human microbiome, particularly gut microbiome has flourished in recent decades owing to the rapidly advancing sequence-based screening and humanized gnotobiotic model in interrogating the dynamic operations of commensal microbiota. Although this field is still at a very preliminary stage, whereby the functional properties of the complex gut microbiome remain less understood, several promising findings have been documented and exhibit great potential toward revolutionizing disease etiology and medical treatments. In this review, the interactions between gut microbiota and the host have been focused on, to provide an overview of the role of gut microbiota and their unique metabolites in conferring host protection against invading pathogen, regulation of diverse host physiological functions including metabolism, development and homeostasis of immunity and the nervous system. We elaborate on how gut microbial imbalance (dysbiosis) may lead to dysfunction of host machineries, thereby contributing to pathogenesis and/or progression toward a broad spectrum of diseases. Some of the most notable diseases namely Clostridium difficile infection (infectious disease), inflammatory bowel disease (intestinal immune-mediated disease), celiac disease (multisystemic autoimmune disorder), obesity (metabolic disease), colorectal cancer, and autism spectrum disorder (neuropsychiatric disorder) have been discussed and delineated along with recent findings. Novel therapies derived from microbiome studies such as fecal microbiota transplantation, probiotic and prebiotics to target associated diseases have been reviewed to introduce the idea of how certain disease symptoms can be ameliorated through dysbiosis correction, thus revealing a new scientific approach toward disease treatment. Toward the end of this review, several research gaps and limitations have been described along with suggested future studies to overcome the current research lacunae. Despite the ongoing debate on whether gut microbiome plays a role in the above-mentioned diseases, we have in this review, gathered evidence showing a potentially far more complex link beyond the unidirectional cause-and-effect relationship between them.

/pdf/the-human-gut-microbiome-a-potential-controller-of-wellness-4iblq6fqqr.pdf

The human gut microbiome - A potential controller of wellness and disease

Excess body weight, as defined by the body mass index (BMI), has been associated with several diseases and includes subjects who are overweight (BMI≥25–29.9 kg/m2) or obese (BMI≥30 kg/m2). Overweight and obesity constitute the fifth leading risk for overall mortality, accounting for at least 2.8 million adult deaths each year. In addition around 11% of colorectal cancer (CRC) cases have been attributed to overweight and obesity in Europe. Epidemiological data suggest that obesity is associated with a 30–70% increased risk of colon cancer in men, whereas the association is less consistent in women. Similar trends exist for colorectal adenoma, although the risk appears lower. Visceral fat, or abdominal obesity, seems to be of greater concern than subcutaneous fat obesity, and any 1 kg/m2 increase in BMI confers additional risk (HR 1.03). Obesity might be associated with worse cancer outcomes, such as recurrence of the primary cancer or mortality. Several factors, including reduced sensitivity to antiangiogenic-therapeutic regimens, might explain these differences. Except for wound infection, obesity has no significant impact on surgical procedures. The underlying mechanisms linking obesity to CRC are still a matter of debate, but metabolic syndrome, insulin resistance and modifications in levels of adipocytokines seem to be of great importance. Other biological factors such as the gut microbita or bile acids are emerging. Many questions still remain unanswered: should preventive strategies specifically target obese patients? Is the risk of cancer great enough to propose prophylactic bariatric surgery in certain patients with obesity?

https://gut.bmj.com/content/gutjnl/62/6/933.full.pdf

Obesity and colorectal cancer

BACKGROUND & AIMS
A cascade of precursor lesions (eg, atrophic gastritis, intestinal metaplasia, and dysplasia) precedes most gastric adenocarcinomas. Quantification of gastric cancer risk in patients with premalignant gastric lesions is unclear, however. Consequently, endoscopic surveillance is controversial, especially in Western populations.


METHODS
To analyze current surveillance practice and gastric cancer risk in patients with premalignant gastric lesions, all patients with a first diagnosis between 1991 and 2004 were identified in the Dutch nationwide histopathology registry (PALGA); follow-up data were evaluated until December 2005.


RESULTS
In total, 22,365 (24%) patients were diagnosed with atrophic gastritis, 61,707 (67%) with intestinal metaplasia, 7616 (8%) with mild-to-moderate dysplasia, and 562 (0.6%) with severe dysplasia. Patients with a diagnosis of atrophic gastritis, intestinal metaplasia, or mild-to-moderate dysplasia received re-evaluation in 26%, 28%, and 38% of cases, respectively, compared with 61% after a diagnosis of severe dysplasia (P < .001). The annual incidence of gastric cancer was 0.1% for patients with atrophic gastritis, 0.25% for intestinal metaplasia, 0.6% for mild-to-moderate dysplasia, and 6% for severe dysplasia within 5 years after diagnosis. Risk factors for gastric cancer development were increasing severity of premalignant gastric lesions at initial diagnosis (eg, severe dysplasia, hazard ratio 40.14, 95% confidence interval 32.2-50.1), increased age (eg, 75-84 years, hazard ratio 3.75, 95% confidence interval 2.8-5.1), and male gender (hazard ratio 1.50, 95% CI 1.3-1.7).


CONCLUSIONS
Patients with premalignant gastric lesions are at considerable risk of gastric cancer. As current surveillance of these patients is inconsistent with their cancer risk, development of guidelines is indicated.

Gastric cancer risk in patients with premalignant gastric lesions

This review summarizes studies on the epidemiology and public health implications of Helicobacter pylori published in peer-reviewed journals from April 2010 through March 2011. Prevalence rates vary widely between different geographical regions and ethnic groups. An interesting study from the USA identified the degree of African ancestry as an independent predictor of H. pylori infection. Two studies have demonstrated early childhood as the period of transmission of infection and identified an infected sibling as an important risk factor. An oral–oral route of spread has been substantiated with several studies showing the presence of H. pylori in the oral cavity. Studies have shown the presence of H. pylori in drinking water and the role of poor living conditions and sanitation in H. pylori infection, supporting an oral–fecal route of spread. Screening for H. pylori as a gastric cancer pre-screening strategy has been described in Japan, and the importance of H. pylori eradication as a gastric cancer–prevention strategy has now been further emphasized in Japanese guidelines. Two studies have shown a decrease in the burden of dyspepsia and peptic ulcer disease with H. pylori eradication.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1523-5378.2011.00874.x

Epidemiology of Helicobacter Pylori Infection and Public Health Implications

https://www.gastrojournal.org/article/S0016-5085(10)01237-0/pdf

Abdominal Visceral Adipose Tissue Volume Is Associated With Increased Risk of Erosive Esophagitis in Men and Women

Recently, some studies have shown that diabetes mellitus and metabolic syndrome increase the risk of colorectal neoplasms. Although the mechanism is not known, those have been proposed to contribute to this phenomenon, including insulin resistance, oxidative stress, and adipokine production. The objective of this study was to assess the association between metabolic risk factors and colorectal neoplasm. Study participants visited the National Cancer Center, Korea, for screening (2007–2009). A total of 1,771 diagnosed adenoma patients and 4,667 polyp-free controls were included. The association between risk factors and colorectal neoplasm was evaluated using logistic regression models. High waist circumference, blood pressure, and serum triglyceride levels were associated with an increased risk of colorectal adenoma. Metabolic syndrome (MS) was associated with an increased risk of adenoma (OR = 1.44, 95 % CI = 1.23–1.70). The association between MS and colorectal adenoma was observed regardless of advanced/low-risk adenoma, and multiplicity. MS affected right colon adenomas (OR = 1.50, 95 % CI = 1.22–1.85), left colon adenomas (OR = 1.36, 95 % CI = 1.05–1.76), and adenomas in multiple anatomical locations (OR = 1.59, 95 % CI = 1.19–2.12), but was not associated with rectum. Central obesity, triglyceride level, and MS are risk factors for colorectal adenoma including advanced adenoma and multiplicity.

Association of colorectal adenoma with components of metabolic syndrome

Abdominal Visceral Adipose Tissue Predicts Risk of Colorectal Adenoma in Both Sexes

Effect of Helicobacter pylori Infection and Its Eradication on Reflux Esophagitis and Reflux Symptoms

Background

We aimed to examine the relationship of current Helicobacter pylori infection with lipid profile and cardiovascular disease and its eradication effect.



Methods

Healthy subjects, who underwent routine checkup between October 2003 and December 2007, were followed up until June 2009. Helicobacter pylori and lipid profiles were measured both baseline and follow-up. Multiple logistic regression models for odds ratios (ORs) and 95% confidence intervals (CIs) were used to estimate the effects of H. pylori infection and its eradication, on lipids and cardiovascular disease.



Results

Current infection with H. pylori with 50.5% (6759/13383) at baseline increased low-density lipoprotein (LDL) and decreased high-density lipoprotein (HDL) than H. pylori-negative group. Successful eradication of H. pylori decreased the risk of high LDL compared with the persistent infection (OR 0.76, 95% CI 0.59–96), which was comparable to that of the persistent negative group (OR 0.82, 95% CI 0.70–0.97), and decreased the risk of low HDL (OR 0.68, 95% CI 0.49–0.96). Current infection of H. pylori increased the risk of cardiovascular disease (OR 3.27, 95% CI 1.31–8.14) at baseline, but its eradication failed to decrease the risk at a 2-year follow-up. However, persistent negative infection decreased the risk (OR 0.57, 95% CI 0.35–0.94) comparing to persistent positive infection at follow-up.



Conclusions

Current infection with H. pylori had a positive association with high LDL, low HDL, and cardiovascular disease. Successful H. pylori eradication decreased the risk of high LDL and low HDL, but did not reduce the risk of cardiovascular disease.

Kum Hei Ryu

Papers

Abdominal Visceral Adipose Tissue Volume Is Associated With Increased Risk of Erosive Esophagitis in Men and Women

Association of colorectal adenoma with components of metabolic syndrome

Abdominal Visceral Adipose Tissue Predicts Risk of Colorectal Adenoma in Both Sexes

Effect of Helicobacter pylori Infection and Its Eradication on Reflux Esophagitis and Reflux Symptoms

Effects of Helicobacter pylori infection and its eradication on lipid profiles and cardiovascular diseases.