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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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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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Disruption of the Gut Ecosystem by Antibiotics.
Yoon, MY, Yoon, SS
Yonsei medical journal. 2018;59(1):4-12
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The gut microbiome is a complex ecosystem of different micro-organisms, such as bacteria, viruses and fungi, living in the human intestines. It’s involved in numerous functions, such as extracting energy and nutrition from food, protecting against disease-causing microorganisms, and supporting the immune system of the host, and therefore affecting human health and disease. This paper is a review of studies on the effects of antibiotics on the gut microbiota. It outlines how different types of antibiotics can alter the intestinal environment and the composition of the microbes, resulting in various physiological changes that can trigger disease. Relevant mechanisms, such as inflammatory response and the use of intestinal nutrients by infectious bacteria are discussed. Finally, it discusses faecal microbiota transplantation (FMT) and probiotics as treatment approaches, aimed at restoring a disturbed intestinal environment.
Abstract
The intestinal microbiota is a complex ecosystem consisting of various microorganisms that expands human genetic repertoire and therefore affects human health and disease. The metabolic processes and signal transduction pathways of the host and intestinal microorganisms are intimately linked, and abnormal progression of each process leads to changes in the intestinal environment. Alterations in microbial communities lead to changes in functional structures based on the metabolites produced in the gut, and these environmental changes result in various bacterial infections and chronic enteric inflammatory diseases. Here, we illustrate how antibiotics are associated with an increased risk of antibiotic-associated diseases by driving intestinal environment changes that favor the proliferation and virulence of pathogens. Understanding the pathogenesis caused by antibiotics would be a crucial key to the treatment of antibiotic-associated diseases by mitigating changes in the intestinal environment and restoring it to its original state.
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Gut Microbiota-Immune System Crosstalk and Pancreatic Disorders.
Pagliari, D, Saviano, A, Newton, EE, Serricchio, ML, Dal Lago, AA, Gasbarrini, A, Cianci, R
Mediators of inflammation. 2018;2018:7946431
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Gut microbiota homeostasis plays a central role in modulating the mucosal immune system. Increasing research has shown a correlation between an imbalanced gut microbiota, called dysbiosis, and various pancreatic disorders. The aim of this review was to analyse current data linking the gut microbiome and several pancreatic disorders. The current evidence demonstrates gut dysbiosis is correlated with the duration and prognosis of pancreatic disorders. While this may lead to early detection of several pancreatic disorders, it remains unclear whether dysbiosis is a cause or effect of pancreatic disorders. Based on these results, the authors conclude future studies are required to better understand the crosstalk between gut microbiota and the immune system to improve diagnostic and treatment strategies for pancreatic disorders.
Abstract
Gut microbiota is key to the development and modulation of the mucosal immune system. It plays a central role in several physiological functions, in the modulation of inflammatory signaling and in the protection against infections. In healthy states, there is a perfect balance between commensal and pathogens, and microbiota and the immune system interact to maintain gut homeostasis. The alteration of such balance, called dysbiosis, determines an intestinal bacterial overgrowth which leads to the disruption of the intestinal barrier with systemic translocation of pathogens. The pancreas does not possess its own microbiota, and it is believed that inflammatory and neoplastic processes affecting the gland may be linked to intestinal dysbiosis. Increasing research evidence testifies a correlation between intestinal dysbiosis and various pancreatic disorders, but it remains unclear whether dysbiosis is the cause or an effect. The analysis of specific alterations in the microbiome profile may permit to develop novel tools for the early detection of several pancreatic disorders, utilizing samples, such as blood, saliva, and stools. Future studies will have to elucidate the mechanisms by which gut microbiota is modulated and how it tunes the immune system, in order to be able to develop innovative treatment strategies for pancreatic disorders.
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Factors Affecting Gastrointestinal Microbiome Development in Neonates.
Chong, CYL, Bloomfield, FH, O'Sullivan, JM
Nutrients. 2018;10(3)
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This narrative review looks at factors affecting the development of the gastrointestinal (GI) microbiome, before, during and after birth. Animal studies suggest that composition and activity of the microbiome affects the structural and functional development of the GI tract. Although evidence is still limited, it is now believed that microbial colonisation starts in utero (before birth). Mode of birth, vaginal versus caesarean section (CS), appears to play an important role in the development of the gut microbiome and can lead to long-term metabolic and immunological consequences, including a higher risk for a number of conditions in those born by CS. Likewise, breast-feeding versus formula-feeding can affect the microbiome composition. These differences are attributed to both bacteria being transferred directly through breast milk and prebiotic factors in breast milk. Maternal and infant perinatal (during birth) exposure to antibiotics has been linked to an increased risk of several conditions, including asthma, obesity, inflammatory bowel disease and other allergic and inflammatory conditions in children. Other factors that appear to affect the development of the microbiome in infants include maternal lifestyle (e.g. rural versus urban), maternal diet, and environment, in particular, staying in a Neonatal Intensive Care Unit. A limitation the authors point out in comparing study results is that different techniques, both culture based and non-culture based, are used for determining the bacterial microflora.
Abstract
The gut microbiome is established in the newborn period and is recognised to interact with the host to influence metabolism. Different environmental factors that are encountered during this critical period may influence the gut microbial composition, potentially impacting upon later disease risk, such as asthma, metabolic disorder, and inflammatory bowel disease. The sterility dogma of the foetus in utero is challenged by studies that identified bacteria, bacterial DNA, or bacterial products in meconium, amniotic fluid, and the placenta; indicating the initiation of maternal-to-offspring microbial colonisation in utero. This narrative review aims to provide a better understanding of factors that affect the development of the gastrointestinal (GI) microbiome during prenatal, perinatal to postnatal life, and their reciprocal relationship with GI tract development in neonates.
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Relationship between intestinal microbiota and ulcerative colitis: Mechanisms and clinical application of probiotics and fecal microbiota transplantation.
Shen, ZH, Zhu, CX, Quan, YS, Yang, ZY, Wu, S, Luo, WW, Tan, B, Wang, XY
World journal of gastroenterology. 2018;24(1):5-14
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Ulcerative colitis (UC) is an inflammatory bowel disease that affects the large intestine. This review study looks at the evidence for intestinal bacteria (the gut microbiome) in triggering the disease and in treatment. It is not clear what causes UC, however it is believed to be an imbalance in the gut bacterial profile (a larger and/or smaller number of certain bacteria in comparison to normal) and the intestinal immune system, which leads to heightened inflammation. Therefore, intestinal dysbiosis (when the gut bacteria get out of balance) is thought to be part of the disease triggering mechanism. A meta-analysis of probiotic therapy in the treatment of active UC concluded that probiotics significantly increased the rate of disease remission, with the probiotic VSL#3 showing the most significant improvement. However, results of probiotics for UC treatment have not been consistent and more, larger randomised controlled trials are needed to clarify their role. Faecal microbiota transplantation also shows promise as a treatment in UC, however only limited evidence exists and efficacy is inconsistent.
Abstract
Ulcerative colitis (UC) is an inflammatory disease that mainly affects the colon and rectum. It is believed that genetic factors, host immune system disorders, intestinal microbiota dysbiosis, and environmental factors contribute to the pathogenesis of UC. However, studies on the role of intestinal microbiota in the pathogenesis of UC have been inconclusive. Studies have shown that probiotics improve intestinal mucosa barrier function and immune system function and promote secretion of anti-inflammatory factors, thereby inhibiting the growth of harmful bacteria in the intestine. Fecal microbiota transplantation (FMT) can reduce bowel permeability and thus the severity of disease by increasing the production of short-chain fatty acids, especially butyrate, which help maintain the integrity of the epithelial barrier. FMT can also restore immune dysbiosis by inhibiting Th1 differentiation, activity of T cells, leukocyte adhesion, and production of inflammatory factors. Probiotics and FMT are being increasingly used to treat UC, but their use is controversial because of uncertain efficacy. Here, we briefly review the role of intestinal microbiota in the pathogenesis and treatment of UC.
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Gut microbiota, cognitive frailty and dementia in older individuals: a systematic review.
Ticinesi, A, Tana, C, Nouvenne, A, Prati, B, Lauretani, F, Meschi, T
Clinical interventions in aging. 2018;13:1497-1511
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Cognitive frailty is defined as the existence of both physical frailty and mild cognitive impairment, in the absence of a diagnosis of Alzheimer’s Disease or other form of dementia. As such, is considered to be the main pre-condition to developing dementia. Some recent studies have suggested an association between frailty and the gut microbiota, although little data exists on the links between the microbiome and cognitive health. This systematic review aimed to summarise the links made in the science between the gut microbiome and cognitive impairment and the effects of pre and pro-biotics on cognitive decline. 47 papers were identified (31 on animals and 16 on humans). Whilst a number of animal studies supported the link between cognitive impairment and the gut microbiota, there was a substantial lack of human data, preventing the researchers from formulating any clinical recommendations at this stage. Further research in human subjects is required to further our knowledge on the links between the gut microbiome and various forms of cognitive decline and dementia.
Abstract
Cognitive frailty, defined as the coexistence of mild cognitive impairment symptoms and physical frailty phenotype in older persons, is increasingly considered the main geriatric condition predisposing to dementia. Recent studies have demonstrated that gut microbiota may be involved in frailty physiopathology by promoting chronic inflammation and anabolic resistance. The contribution of gut microbiota to the development of cognitive impairment and dementia is less defined, even though the concept of "gut-brain axis" has been well demonstrated for other neuropsychiatric disorders. The aim of this systematic review was to summarize the current state-of-the-art literature on the gut microbiota alterations associated with cognitive frailty, mild cognitive impairment and dementia and elucidate the effects of pre- or probiotic administration on cognitive symptom modulation in animal models of aging and human beings. We identified 47 papers with original data (31 from animal studies and 16 from human studies) suitable for inclusion according to our aims. We concluded that several observational and intervention studies performed in animal models of dementia (mainly Alzheimer's disease) support the concept of a gut-brain regulation of cognitive symptoms. Modulation of vagal activity and bacterial synthesis of substances active on host neural metabolism, inflammation and amyloid deposition are the main mechanisms involved in this physiopathologic link. Conversely, there is a substantial lack of human data, both from observational and intervention studies, preventing to formulate any clinical recommendation on this topic. Gut microbiota modulation of cognitive function represents, however, a promising area of research for identifying novel preventive and treatment strategies against dementia.
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Probiotic monotherapy and Helicobacter pylori eradication: A systematic review with pooled-data analysis.
Losurdo, G, Cubisino, R, Barone, M, Principi, M, Leandro, G, Ierardi, E, Di Leo, A
World journal of gastroenterology. 2018;24(1):139-149
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Helicobacter pylori (H-pylori) is a parasite that resides in the human stomach and is associated with the development of stomach ulcers, amongst other conditions. Conventional treatment relies on a combination of antibiotics and stomach acid suppressants, however failure rates for standard treatments have been rising and alternatives are required. Probiotics (live bacteria that provide health benefits to their host) have been used alongside antibiotic treatment for H-pylori in some cases to reduce medication side effects. This systematic review of 11 studies including 517 H-pylori infected patients, aimed to assess the effects of probiotic therapy alone on H-pylori status. The study found that the eradication rate of H-pylori with a variety of probiotic strains was 12-16%, compared to a 0% success rate in the placebo groups. Clinically, this rate is low, however the authors conclude that probiotics may have a role to play in a multi-therapy approach for the eradication of H-pylori.
Abstract
AIM: To define probiotic monotherapy effect on Helicobacter pylori (H. pylori) status by performing a systematic review. METHODS Methods of analysis and inclusion criteria were based on PRISMA recommendations. Relevant publications were identified by searching PubMed, MEDLINE, Science Direct, and EMBASE. The end-point was to estimate eradication rate and urea breath test delta value before and after probiotic monotherapy across all studies and, overall, with a pooled data analysis. Adverse events of probiotic therapy were evaluated. The data were expressed as proportions/percentages, and 95%CIs were calculated. For continuous variables, we evaluated the weighted mean difference. Odd ratios (ORs) were calculated according to the Peto method for the comparison of eradication rates between probiotics and placebo. RESULTS Eleven studies were selected. Probiotics eradicated H. pylori in 50 out of 403 cases. The mean weighted eradication rate was 14% (95%CI: 2%-25%, P = 0.02). Lactobacilli eradicated the bacterium in 30 out of 235 patients, with a mean weighted rate of 16% (95%CI: 1%-31%). Saccharomyces boulardii achieved eradication in 6 out of 63 patients, with a pooled eradication rate of 12% (95%CI: 0%-29%). Multistrain combinations were effective in 14 out of 105 patients, with a pooled eradication rate of 14% (95%CI: 0%-43%). In the comparison of probiotics vs placebo, we found an OR of 7.91 in favor of probiotics (95%CI: 2.97-21.05, P < 0.001). Probiotics induced a mean reduction in delta values higher than placebo (8.61% with a 95%CI: 5.88-11.34, vs 0.19% for placebo, P < 0.001). Finally, no significant difference in adverse events was found between probiotics and placebo (OR = 1, 95%CI: 0.06-18.08). CONCLUSION Probiotics alone show a minimal effect on H. pylori clearance, thus suggesting a likely direct role.
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Potential of Mushroom Compounds as Immunomodulators in Cancer Immunotherapy: A Review.
Ayeka, PA
Evidence-based complementary and alternative medicine : eCAM. 2018;2018:7271509
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Edible mushrooms strengthen the immune system and are considered biological response modifiers (BRMs). This article reviews the research behind the use of mushroom compounds in cancer therapy. Beta-glucans from the cell walls of mushrooms are the major polysaccharide fraction that is responsible for immune modulating effects, through a number of mechanisms which are explored in this review article. Other important components include other polysaccharides, polysaccharide-protein complexes, agaritine, ergosterol, selenium, polyphenols, and terpenoids. Anti-cancer effects are mediated by stimulating lymphocytes, NK cells, and macrophages (all three specific immune cells), enhancing production of cytokines (immune messengers), inhibiting proliferation of cancer cells, promoting apoptosis (programmed cell death), and blocking angiogenesis (the development of blood vessels that feed the tumour), in addition to being cytotoxic to cancer cells. Medicinal mushrooms from which these compounds are derived and which have been researched for the treatment of various cancers include Ganoderma lucidum, G. tsugae, Schizophyllum commune, Sparassis crispa, Pleurotus tuberregium, P. rhinoceros, Trametes robiniophila Murill, Coriolus versicolor, Lentinus edodes, Grifola frondosa, and Flammulina velutipes, among others. Cancers in which benefits from medicinal mushrooms have been reported include breast, colorectal, cervical, skin, liver, ovarian, bladder, prostate, gastric, skin, lung, leukaemia, and stomach cancers.
Abstract
Since time immemorial, plants and their compounds have been used in the treatment and management of various ailments. Currently, most of conventional drugs used for treatment of diseases are either directly or indirectly obtained from plant sources. The fungal group of plants is of significance, which not only provides food directly to man but also has been source of important drugs. For instance, commonly used antibiotics are derived from fungi. Fungi have also been utilized in the food industry, baking, and alcohol production. Apart from the economic importance of the microfungi, macrofungi have been utilized directly as food, which is usually got from their fruiting bodies, commonly known as mushrooms. Due to their richness in proteins, minerals, and other nutrients, mushrooms have also been associated with boosting the immune system. This makes mushrooms an important food source, especially for vegetarians and immunosuppressed individuals including the HIV/AIDS persons. In complementary and alternative medicines (CAMs), mushrooms are increasingly being accepted for treatment of various diseases. Mushrooms have been shown to have the ability to stimulate the immune system, modulate humoral and cellular immunity, and potentiate antimutagenic and antitumorigenic activity, as well as rejuvenating the immune system weakened by radiotherapy and chemotherapy in cancer treatment. This potential of mushrooms, therefore, qualifies them as candidates for immunomodulation and immunotherapy in cancer and other diseases' treatment. However, a critical review on mushroom's immune modulating potential in cancer has not been sufficiently addressed. This review puts forward insights into the immune activities of mushroom associated with anticancer activities.