Biome

Long-term survival of lung transplant recipients (LTRs) is limited by the occurrence of bronchiolitis obliterans syndrome (BOS). Recent evidence suggests a role for microbiome alterations in the occurrence of BOS, although the precise mechanisms are unclear. In this study we evaluated the relationship between the airway microbiome and distinct subsets of immunoregulatory myeloid-derived suppressor cells (MDSCs) in LTRs.

Do Antibiotics Cause Celiac Disease? Some researchers say yes they can. Especially in those with genetic susceptibility to gluten sensitivity. Antibiotics cause a yeast overgrowth, and emerging research shows that yeast - AKA candida, can create a protein that mimics gluten, causing an intestinal reaction leading to the development of celiac disease. To connect with Dr. Osborne visit: Facebook: https://www.facebook.com/DoctorPeterO... Pinterest: https://www.pinterest.com/docosborne/ Instagram: https://www.instagram.com/drosborne Twitter: https://twitter.com/glutenology *These statements have not been evaluated by the Food and Drug Administration. This video is not intended to diagnose, treat, cure or prevent any disease. It is strictly intended for educational purposes only. Additionally, this information is not intended to replace the advice of your physician. Dr. Osborne is not a medical doctor. He does not treat or diagnose disease. He offers nutritional support to people seeking an alternative from traditional medicine. Dr. Osborne is licensed with the Pastoral Medical Association.

Researchers have made the first direct demonstration that fecal donor microbes remained in recipients for months or years after a transplant to treat the diarrhea and colitis caused by recurrent Clostridium difficile infections -- a serious and stubborn cause of diarrhea after an antibiotic treatment for some other illness.

Healthy digestion within a resilient, repair-enabled microbiome is essential for 21st century survival. The human microbiome will be explained in functional and practical terms. Issues such as leaky gut, SIBO and IBS will be explored.Those who are proactive about their health, particularly about what they eat and drink, think and do can achieve a healthy microbiome. Eating and drinking what can be digested, assimilated and eliminated without immune burden provides a context for this presentation.

What effect do artificial sweeteners such as sucralose (Splenda), saccharin (Sweet & Low), aspartame (Nutrasweet) and acesulfame K (Sweet One) have on our gut bacteria? Subscribe to NutritionFacts.org’s free newsletter to receive our B12 infographic that covers the latest research takeaways and Dr. Greger’s updated recommendations: https://nutritionfacts.org/subscribe/ Can’t get enough of artificial sweeteners? Check out • Diet Soda and Preterm Birth (http://nutritionfacts.org/video/diet-soda-and-preterm-birth/) • Aspartame Induced Fibromyalgia (http://nutritionfacts.org/video/aspartame-induced-fibromyalgia/) • Aspartame and the Brain (http://nutritionfacts.org/video/Aspartame-and-the-Brain) Even for nontoxic low calorie sweeteners like erythritol (Erythritol May Be a Sweet Antioxidant http://nutritionfacts.org/video/erythritol-may-be-a-sweet-antioxidant/), there are some caveats. See: • How Diet Soda Can Make Us Gain Weight (http://nutritionfacts.org/video/how-diet-soda-could-make-us-gain-weight/) • Neurobiology of Artificial Sweeteners (http://nutritionfacts.org/video/neurobiology-of-artificial-sweeteners/) • Unsweetening the Diet (http://nutritionfacts.org/video/unsweetening-the-diet/) Who cares if our gut flora gets disrupted? Wait until you see how important the little puppies are: • Microbiome: The Inside Story (http://nutritionfacts.org/video/microbiome-the-inside-story) • Prebiotics: Tending Our Inner Garden (http://nutritionfacts.org/video/prebiotics-tending-our-inner-garden) • What’s Your Gut Microbiome Enterotype? (http://nutritionfacts.org/video/whats-your-gut-microbiome-enterotype) • How to Change Your Enterotype (http://nutritionfacts.org/video/how-to-change-your-enterotype) • Paleopoo: What We Can Learn from Fossilized Feces (http://nutritionfacts.org/video/paleopoo-what-we-can-learn-from-fossilized-feces) Have a question for Dr. Greger about this video? Leave it in the comment section at http://nutritionfacts.org/video/effect-of-sucralose-splenda-on-the-microbiome and he'll try to answer it! Image Credit: Dave Crosby via Flickr. https://NutritionFacts.org • Subscribe: https://nutritionfacts.org/subscribe • Donate: https://nutritionfacts.org/donate • Podcast : https://nutritionfacts.org/audio • Facebook: www.facebook.com/NutritionFacts.org • Twitter: www.twitter.com/nutrition_facts • Instagram: www.instagram.com/nutrition_facts_org • Books (including the NEW How Not to Diet Cookbook): https://nutritionfacts.org/books • Shop: https://drgreger.org

OMICS: A Journal of Integrative Biology

Abstract. Multiple environmental factors induce dysbiosis in the gut microbiome and cause a variety of human diseases. Previously, we have first demonstrated th

How can we lower our risk of dementia, dissolve brain fog, and maximize our mental capacity?

The consumption of dietary supplements and cold therapies containing high concentrations of zinc is now being called into question, following research that suggests it may worsen Clostridium difficile infection.

Two studies - one in mice and the other in human subjects - offer the first definitive evidence that exercise alone can change the composition of microbes in the gut. The studies were designed to isolate ...

At first glance, fecal microbiota transplantation (FMT) appears to be a far-fetched procedure devised as a slapstick plot for a sit-com series. However, this innovative technique may revolutionize the future of medical treatments for a host of maladies including autoimmune and allergic diseases as well as autism spectrum disorder.

The future of probiotics is here

The intestinal microbial communities play critical roles in various aspects of body function of the host. Prebiotics, such as dietary fiber, can affect health of the host by altering the composition of intestinal microbiota. Although brown seaweed Laminaria japonica is rich in dietary fiber, studies on its prebiotic potential are quite rare. In this study, basal diet (control), basal diet supplemented with dried L. japonica (DLJ), heat-treated dried L. japonica (HLJ), or heated dried L. japonica with added fructooligosaccharide (FHLJ) was fed to rats for 16 weeks. Serum concentrations of IgG, triglyceride, and cholesterol were measured. In addition, the intestinal microbiota composition was analyzed by high-throughput sequencing of 16S rRNA gene. As compared to the control group, DLJ, HLJ, and FHLJ groups showed significantly higher serum IgG concentration, but had lower weight gain and serum triglyceride concentration. Moreover, DLJ, HLJ, and FHLJ groups showed lower Fimicutes to Bacteroidetes ratio when compared with the control group. As compared with the control group, obesity-associated bacterial genera (Allobaculum, Turicibacter, Coprobacillus, Mollicute, and Oscilibacter), and the genera with pathogenic potentials (Mollicute, Bacteroides, Clostridium, Escherichia, and Prevotella) decreased while leanness-associated genera (Alistipes, Bacteroides, and Prevotella), and lactic acid bacterial genera (Subdoligranulum, Streptococcus, Lactobacillus, Enterococcus, and Bifid...

Abundant clinical, epidemiological, imaging, genetic, molecular, and pathophysiological data together indicate that there occur an unusual inflammatory reaction and a disruption of the innate-immune signaling system in Alzheimer’s disease (AD) brain. Despite many years of intense study, the origin and molecular mechanics of these AD-relevant pathogenic signals are still not well understood. Here, we provide evidence that an intensely pro-inflammatory bacterial lipopolysaccharide (LPS), part of a complex mixture of pro-inflammatory neurotoxins arising from abundant Gram-negative bacilli of the human gastrointestinal (GI) tract, are abundant in AD-affected brain neocortex and hippocampus. For the first time, we provide evidence that LPS immunohistochemical signals appear to aggregate in clumps in the parenchyma in control brains, and in AD, about 75% of anti-LPS signals were clustered around the periphery of DAPI-stained nuclei. As LPS is an abundant secretory product of Gram-negative bacilli resident in the human GI-tract, these observations suggest (i) that a major source of pro-inflammatory signals in AD brain may originate from internally derived noxious exudates of the GI-tract microbiome; (ii) that due to aging, vascular deficits or degenerative disease these neurotoxic molecules may “leak” into the systemic circulation, cerebral vasculature, and on into the brain; and (iii) that this internal source of microbiome-derived neurotoxins may play a particularly strong role...

The gut microbiome is an important modulator of host gene expression, impacting important functions such as the innate immune response. Recent evidence suggests that the inter-domain communication between the gut microbiome and host may in part occur via microRNAs (small, non-coding RNA molecules) which are often differentially expressed in the presence of bacteria and can even be released and taken up by bacteria. The role of microRNAs in microbiome–host communication in intestinal diseases is not fully understood, particularly in diseases impacted by exposure to environmental toxicants. Here, we review the present knowledge in the areas of microbiome and microRNA expression-based communication, microbiome and intestinal disease relationships, and microRNA expression responses to intestinal diseases. We also examine potential links between host microRNA–microbiota communication and exposure to environmental toxicants by reviewing connections between (i) toxicants and microRNA expression, (ii) toxicants and gut diseases, and (iii) toxicants and the gut microbiome. Future multidisciplinary research in this area is needed to uncover these interactions with the potential to impact how gut-microbiome associated diseases [e.g., inflammatory bowel disease (IBD) and many others] are managed.

Fucoidan is a functional food that possesses various biological activities. This study aims to determine the effects of fucoidan from Undaria pinnatif…

Antibiotic treatment, as an important therapeutic intervention, can cause damage to the host microbiome and the intestinal mucosal barrier. In order to find a way to alleviate the side effects of antibiotics, the present study investigated the effects of fucoidan (ANP) isolated from Ascophyllum nodosum on gu

Background The human oral microbiome is formed early in development. Its composition is influenced by environmental factors including diet, substance use, oral health, and overall health and disease. The influence of human genes on the composition and stability of the oral microbiome is still poorly understood. We studied both environmental and genetic characteristics on the oral microbiome in a large twin sample as well as in a large cohort of unrelated individuals. We identify several significantly heritable features of the oral microbiome. The heritability persists in twins even when their cohabitation changes. The heritability of these traits correlates with the cumulative genetic contributions of over half a million single nucleotide sequence variants measured in a different population of unrelated individuals. Comparison of same-sex and opposite sex cotwins showed no significant differences. We show that two new loci on chromosomes 7 and 12 are associated with the most heritable traits. Results An analysis of 752 twin pairs from the Colorado Twin Registry, shows that the beta-diversity of monozygotic twins is significantly lower than for dizygotic or unrelated individuals. This is independent of cohabitation status. Intraclass correlation coefficients of nearly all taxa examined were higher for MZ than DZ twin pairs. A comparison of individuals sampled over 2-7 years confirmed previous reports that the oral microbiome remains relatively more stable in individuals over that time than to unrelated people. Twin modeling shows that a number of microbiome phenotypes were more than 50% heritable consistent with the hypothesis that human genes influence microbial populations. To identify loci that could influence microbiome phenotypes, we carried out an unbiased GWAS analysis which identified one locus on chromosome 7 near the gene IMMPL2 that reached genome-wide significance after correcting for multiple testing. Another locus on chromosome 12 near the non-coding RNA gene INHBA-AS1 achieved genome-wide significance when analyzed using KGG4 that sums SNP significance across coding genes. Discussion Using multiple methods, we have demonstrated that some aspects of the human oral microbiome are heritable and that with a relatively small sample we were able to identify two previously unidentified loci that may be involved.

Certain types of bacteria in the gut can leverage the immune system to decrease the severity of stroke, according to new research. This finding can help mitigate stroke -- which is the second leading cause of death worldwide.

Antibiotic resistant urinary tract infections are increasingly common, leaving many looking for natural alternatives. Grapefruit seed extract may be an effective treatment that is safe, affordable and easily accessible

Spinal cord injury alters the type of bacteria living in the gut and that these changes can exacerbate the extent of neurological damage and impair recovery of function, new research suggests. The study demonstrates that counteracting these changes with probiotics could aid patients’ recovery from spinal cord injuries.

Children and teenagers who are obese have different microorganisms living in the digestive tract than their lean counterparts, according to a new study.

Background Microorganisms in the human intestine (i.e. the gut microbiome) have an increasingly recognized impact on human health, including brain functioning. Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder associated with abnormalities in dopamine neurotransmission and deficits in reward processing and its underlying neuro-circuitry including the ventral striatum. The microbiome might contribute to ADHD etiology via the gut-brain axis. In this pilot study, we investigated potential differences in the microbiome between ADHD cases and undiagnosed controls, as well as its relation to neural reward processing. Methods We used 16S rRNA marker gene sequencing (16S) to identify bacterial taxa and their predicted gene functions in 19 ADHD and 77 control participants. Using functional magnetic resonance imaging (fMRI), we interrogated the effect of observed microbiome differences in neural reward responses in a subset of 28 participants, independent of diagnosis. Results For the first time, we describe gut microbial makeup of adolescents and adults diagnosed with ADHD. We found that the relative abundance of several bacterial taxa differed between cases and controls, albeit marginally significant. A nominal increase in the Bifidobacterium genus was observed in ADHD cases. In a hypothesis-driven approach, we found that the observed increase was linked to significantly enhanced 16S-based predicted bacterial gene functionality encoding cyclohexadienyl dehydratase in cases relative to controls. This enzyme is involved in the synthesis of phenylalanine, a precursor of dopamine. Increased relative abundance of this functionality was significantly associated with decreased ventral striatal fMRI responses during reward anticipation, independent of ADHD diagnosis and age. Conclusions Our results show increases in gut microbiome predicted function of dopamine precursor synthesis between ADHD cases and controls. This increase in microbiome function relates to decreased neural responses to reward anticipation. Decreased neural reward anticipation constitutes one of the hallmarks of ADHD.

Background: Since the description of the normal human gut microbiome in healthy individuals using broad-range polymerase chain reaction, there has been great advancement in the techniques used to conduct microbiome research and applications of this research across health, gastrointestinal diseases, and nongastrointestinal diseases. Summary and Key