inflammatory bowel disease Archives - Amazing Health Advances

Could Our Next Superfood Be Colostrum From Cows?

AHA Publisher — Mon, 03 Oct 2022 07:00:22 +0000

Brian Blum via Israel21c – Here’s a riddle: What can strengthen the immune system, balance digestion and aid in brain and bone development? The answer is something most of us take for granted: breastmilk. More specifically, the colostrum “first milk” produced by the mammary glands in the first few days postpartum. Biomedical engineer Maya Ashkenazi-Otmazgin was thinking about the magical qualities of breastmilk when she had a baby four years ago. “There’s this one substance that contains all the important molecules necessary for our biological system to grow and evolve,” she tells ISRAEL21c. “Because of this milk, we are here, alive and kicking.” She wondered if the health benefits of breastmilk and colostrum could be harnessed to create a superfood that would be available to everyone – adults, athletes, the elderly… even pets. But Ashkenazi-Otmazgin didn’t envision asking mothers in the first few days of nursing to donate their colostrum. There was another source, whose proteins are 95% biosimilar to human breastmilk and is available in such abundance that 5 billion liters of it are thrown away every year around the world. Bovine colostrum. Modern dairy farms only allow a newborn calf to ingest the colostrum from its mother for a day or two before transitioning the calf to a set diet. But the mother cow produces colostrum for up to five days. That means a lot of colostrum is going to waste – some 25 to 35 liters per cow – and dairy producers can’t put it in the regular milk for both regulatory and taste reasons. “I wondered why we were not understanding the proteins inside breastmilk and trying to find bioequivalents in other sources,” Ashkenazi-Otmazgin says. After all, “breastmilk is the ‘gold standard’ for nutrients and grownups are being deprived of one of life’s greatest resources.” Functional Milk Protein In 2018, Ashkenazi-Otmazgin teamed up with Dr. Ariel Orbach and Eli Lerner. They raised $3.2 million in seed funding to start Maolac (M.A.O. are her initials, combined with “lac” for lactose), dedicated to introducing “human functional milk proteins into new segments,” Ashkenazi-Otmazgin, now the company’s CEO, says. Maolac uses the colostrum from days two to five. That ensures the calf isn’t being shortchanged for the benefit of human yogurt lovers. The Maolac team started by mapping out some 1,500 bioactive proteins in human breastmilk and then identifying the overlap with bovine colostrum. It turns out there are over 400 homologue proteins – that is, proteins containing genes similar in structure and evolutionary origin to genes in another species. “We created a smart algorithm that uses bioinformatic tools and proteomics to understand the combinations of several proteins for different indications,” Ashkenazi-Otmazgin says. “We were then able to find the same in bovine colostrum.” Improving Nature’s Recipe Maolac tranforms the bovine colostrum into a white powder that can be added to various foods – ice cream will be among Maolac’s first products – but Ashkenazi-Otmazgin stresses that it can be added to cooked foods such as pasta without losing functionality. The additive has no discernible taste, so it won’t ruin the flavor of your fettuccini al colostrum. “We found a way to take nature’s recipe and bring it into the 21st century,” Ashkenazi-Otmazgin says. Maolac’s business proposition is solidly win-win. If, in the past, farmers had to pay to dispose of biological waste like colostrum, Maolac flips that model and pays the farmers to take it off their hands. Food manufacturers can expect to pay around $500 per kilogram, similar to other protein supplements in the market, although Ashkenazi-Otmazgin says it takes less colostrum powder to achieve the same benefits, making the final price cheaper. Maolac’s first target audience is athletes, a $65 billion market. Because colostrum has anti-inflammatory properties, Ashkenazi-Otmazgin says consuming a food or beverage with “Maolac inside” should reduce muscle strain and improve recovery time. The same formula may also help improve mobility in the elderly. Moving beyond athletes, Ashkenazi-Otmazgin hopes Maoloc’s products will help with overall intestinal issues including IBD (inflammatory bowel disease) and leaky gut syndrome. IBD-related treatments are a $20 billion market, Ashkenazi-Otmazgin notes. “For IBD, our product is very effective even in very small doses of just a few hundred milligrams a day,” Ashkenazi-Otmazgin says. “That makes it easy to put in an energy bar or a beverage. If we can reduce cases of inflammation in the gut, we can allow someone to return to a normal routine. You would be able to go to a restaurant and not be afraid of what could happen. It wouldn’t influence your love life. And all this is happening by helping your body through its own immune mechanism to do the healing process. It’s not done in a synthetic way.” Ashkenazi-Otmazgin contrasts the Maolac approach to probiotics, where “you’re bringing to your own microbiome things from the outside. We support the natural healing process of the digestive system.” New Sources of Protein If Maolac’s timeframe holds, the first products should hit the market in the second half of 2023. Maolac was initially supported by the Strauss Group’s The Kitchen food-tech accelerator; the company now has its own offices in Tirat HaCarmel, south of Haifa. The total amount raised by the 12-person company is just over $4 million. The latest funding round, led by OurCrowd and The Kitchen, will go to building a small-scale pilot production facility. OurCrowd CEO Jon Medved calls “the idea of transforming the first, nutrient-rich milk of cows that have just given birth into a source for human protein a stroke of pure genius.” In a world “desperately searching for new sustainable sources of protein,” he adds, “the company is a perfect example of the circular economy in action” as it turns a waste product into a valuable item. Maoloc currently has a ready-to-go product and the company is in discussions with potential customers and third-party manufacturers, Ashkenazi-Otmazgin says. Plant-Based Product Planned Bovine colostrum is not the end of the Maolac story. “We can use our proteomics discovery platform to create new ingredients from plants – from fungi and algae,” Ashkenazi-Otmazgin says, although proteins created this way will have only 60% to 80% biosimilarity, compared with 95% for bovine colostrum. Nevertheless, “We wanted a solution for vegans. We need to respect everyone,” she says. “In the end, we will have a portfolio of products to sell to food companies, cosmetics companies, supplement companies. They will implement the ingredients in the finished product while we will do all the regulatory work and the clinical studies to prove the effectiveness and safety of each product,” Ashkenazi-Otmazgin says. For more information, click here To read the original article click here.

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New Study Shows Bidirectional Link Between Inflammatory Bowel Disease and Depression

AHA Publisher — Fri, 03 Jun 2022 07:00:12 +0000

University of Southern California (USC) Health Sciences via Newswise – Inflammatory bowel disease (IBD) is a chronic condition involving inflammation of the digestive tract, affecting some 1.6 million Americans. Depression affects more than 16 million Americans. A new study from Keck Medicine of USC shows that patients diagnosed with IBD were nine times as likely to develop depression than the general population. In addition, their siblings who did not suffer from IBD were almost two times as likely to develop depression. Conversely, patients with depression were two times as likely to develop IBD, and their siblings without depression were more than one and a half times as likely to develop IBD. “This research reveals a clinical overlap between both conditions, and is the first study to investigate the two-way association between IBD and depression in siblings,” said Bing Zhang, MD, a gastroenterologist with Keck Medicine and co-lead author of the study. Zhang and his fellow researchers analyzed the data of more than 20 million people from Taiwan’s National Health Insurance Research Database, which contains comprehensive medical information on more than 99% of Taiwanese residents. For 11 years, they tracked patients with either IBD or depression and their siblings without either condition, comparing onset of depression or IBD with a control group of people without either condition, but with similar age, sex and socioeconomic status. Zhang hypothesizes that many factors may contribute to the bidirectional nature of the disorders, including environmental stressors, the gut microbiome (consisting of bacteria, fungi and viruses) and genetics. “The finding that people with IBD are more prone to depression makes sense because IBD causes constant gastrointestinal symptoms that can be very disruptive to a patient’s life,” he said. “And the elevated depression risk among siblings of IBD patients may reflect caregiver fatigue if the siblings have a role in caring for the patient.” What surprised researchers was that patients with depression were prone to IBD. Zhang speculates that this discovery may have to do with what is known as the gut-brain axis, a scientifically established connection between the gastrointestinal system and the central nervous system, which consists of the spinal cord and the brain. For example, he said, inflammation of the brain, which plays a role in depression, may be linked to the inflammation of the gastrointestinal tract, a hallmark of IBD. The researchers are not sure why siblings of patients with depression are more likely to be diagnosed with IBD. Zhang surmises that there may be a shared genetic susceptibility for either disease that presents differently in family members. Zhang hopes that the study findings will encourage health care professionals to take both family history and the relationship between gastrointestinal and mood disorders into consideration when evaluating or treating patients with either IBD or depression. Through more research and better understanding of the gut-brain axis, he envisions leveraging the newfound connection between the conditions to improve the prevention, diagnosis and treatment of IBD and mental disorders. The study was supported by grants from the Taipei Veterans General Hospital and the Ministry of Science and Technology, Taiwan. To read the original article click here.

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Antibiotic use Associated with Inflammatory Bowel Disease in Older Adults

AHA Publisher — Fri, 20 May 2022 07:00:54 +0000

American Gastroenterological Association (AGA) via Newswise – The more antibiotics prescribed to patients 60 and older, the more likely they were to develop inflammatory bowel disease, suggesting antibiotic use could explain some of the growth in Crohn’s disease and ulcerative colitis in older people, according to a review of 2.3 million patient records in a study selected for presentation at Digestive Disease Week® (DDW) 2022. “In older adults, we think that environmental factors are more important than genetics,” said Adam S. Faye, MD, MS, lead researcher on the study and assistant professor of medicine and population health at NYU Grossman School of Medicine. “When you look at younger patients with new diagnoses of Crohn’s disease and ulcerative colitis, there’s generally a strong family history. But that is not the case in older adults, so it’s really something in the environment that is triggering it.” Using Denmark’s national database, which includes nearly all medical records for residents, researchers reviewed prescribing records for people aged 60 and older who were newly diagnosed with inflammatory bowel disease from 2000 to 2018. The study looked at the number of courses of antibiotics prescribed, how recently they had been prescribed in relation to the diagnosis and specific classes of antibiotics used. The study found any antibiotic use was associated with higher rates of inflammatory bowel disease, and the risk went up substantially with each course. After one prescription, patients were 27 percent more likely than those with no antibiotic use to be diagnosed with inflammatory bowel disease. With two courses, the risk rose by 55 percent and with three courses it rose by 67 percent. With four courses, risk rose by 96 percent; and with five or more, seniors were more than 2.3 times, or 236 percent, more likely to receive a new inflammatory bowel disease diagnosis than those with no antibiotics in the previous five years. New diagnoses were highest when antibiotics were prescribed one to two years before, but the risk remained elevated for prescriptions in the period two to five years before diagnosis. The relationship was found for all types of antibiotics, except nitrofurantoin, which is commonly prescribed for urinary tract infections. Antibiotics usually prescribed for gastrointestinal infections were the most likely to be associated with a new inflammatory bowel disease diagnosis. Researchers omitted prescriptions less than a year before diagnosis to reduce the chance that prescriptions had been for symptoms of a yet-undiagnosed gastrointestinal disease. The study has implications for diagnosing older adults with new gastroenterological symptoms. Inflammatory bowel disease, which can easily be overlooked in this age group, should be considered, especially when there’s a history of antibiotic prescriptions, Dr. Faye said. The research also has ramifications for antibiotic stewardship. In addition to preventing the development of multi-drug resistant organisms, judicious antibiotic use is crucial to preventing inflammatory bowel disease. “Antibiotic stewardship is important; but avoiding antibiotics at all costs is not the right answer either,” Dr. Faye said. “If you’re not sure what you are treating, I would be cautious. If patients are coming in with clear infections, and they need antibiotics, they should not be withheld because of these findings.” The study was conducted in partnership with the Danish National Center of Excellence PREDICT Program. Authors did not report any conflicts of interest related to this study. To read the original article click here.

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Gut Inflammation? You Might Not Need That Colonoscopy

AHA Publisher — Thu, 03 Feb 2022 08:00:25 +0000

Naama Barak via Israel21c – Undergoing a colonoscopy is no picnic. It is invasive, frightening and likely the butt of all your friends’ jokes. But thanks to a new method developed in Israel, it may also become a thing of the past, at least for detecting inflammatory bowel diseases such as Crohn’s and ulcerative colitis. Researchers from the Weizmann Institute of Science and Sheba Medical Center in Israel have come up with a way to replace colonoscopy data with analysis of fecal samples. Their findings were published in the journal Gut. The study took off when researchers realized that cells shed from the gut lining of mice and expelled in the feces stay alive for several hours. This led to a method that could provide testing for inflammation that is less invasive, much cheaper than colonoscopy and at least as reliable. The researchers analyzed cells collected from the gut lining of 30 patients with inflammatory bowel disease during the course of colonoscopy and compared them with those taken from fecal samples or biopsies of 30 healthy people who had undergone colonoscopies as part of routine cancer screening. Using RNA sequencing and other advanced methods, they determined which cell types were present in each of the samples and found that the fecal samples contained four immune-related cell types associated with inflammation. They then ran algorithms to identify distinct expression patterns, or RNA signatures, of the cells in each sample. These signatures helped reveal the exact proportion of each immune-related cell type in the gut lining and enabled the scientists to determine whether a person had an active case of intestinal inflammation. The fecal samples proved to be more reliable than the biopsies. “A biopsy can miss inflammation because it provides a snapshot of the narrow spot from which it was removed, whereas a fecal sample contains cells shed from the entire lining of the gut,” explains Weizmann Prof. Shalev Itzkovitz. “Moreover, a fecal sample can sometimes be more revealing than the examination of the lining during colonoscopy, which is done by eye, because certain forms of inflammation produce no visible signs.” To read the original article click here.

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Engineered Yeast Probiotic Developed to Treat Inflammatory Bowel Disease

AHA Publisher — Mon, 19 Jul 2021 07:00:56 +0000

Brigham and Women’s Hospital via EurekAlert – The world of microbes living in the human gut can have far-reaching effects on human health. Multiple diseases, including inflammatory bowel disease (IBD), are tied to the balance of these microbes, suggesting that restoring the right balance could help treat disease. Many probiotics — living yeasts or bacteria — that are currently on the market have been optimized through evolution in the context of a healthy gut. However, in order to treat complex diseases such as IBD, a probiotic would need to serve many functions, including an ability to turn off inflammation, reverse damage and restore the gut microbiome. Given all of these needs, researchers from Brigham and Women’s Hospital have developed a “designer” probiotic — a thoughtfully engineered yeast that can induce multiple effects for treating IBD. Preclinical results from their work are published in Nature Medicine. “We’ve taken yeast — the very yeast that’s used to make beer — and we’ve given it the ability to sense inflammation and secrete an anti-inflammatory molecule,” said corresponding author Francisco Quintana, PhD, an investigator in the Ann Romney Center for Neurologic Diseases at the Brigham. “We call this new platform ‘Y-bots’ (yeast robots) and see the potential here for developing therapeutics that can treat diseases of the gut tissue and more.” Previous research from the Quintana lab has helped illuminate the connection between the gut and diseases that affect the brain, suggesting potential applications for engineering probiotics beyond IBD. Quintana and colleagues developed their probiotic using Saccharomyces cerevisiae, a species of yeast used in winemaking, baking and brewing. Using the gene editing technology CRISPR/Cas9, the researchers introduced genetic elements that could sense inflammation and respond to it by secreting an enzyme that can degrade a key molecule involved in inflammation. The engineered yeast can secrete different levels of enzyme, depending upon how much of the inflammatory signal is present at a location in the gut. This means that the probiotic can have a highly localized response to inflammation. In mice, the engineered yeast successfully suppressed intestinal inflammation, reduced fibrosis and restored a balanced gut microbiome. To bring this new therapeutic platform to bear on IBD and other diseases in humans, Quintana and colleagues will need to conduct safety studies. They also plan to further refine and test the engineered yeast to see if they can speed up tissue repair. Beyond IBD, the team plans to investigate the use of engineered probiotics for treating a common side effect of cancer immunotherapy, colitis. “We want to use the tools of synthetic biology to engineer what can be found in nature,” said Quintana. “By engineering probiotics, our goal is to create more personalized, localized and highly controlled medications for treating diseases of the gut and beyond.” To read the original article click here.

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Understanding Gut Inflammation May Hold Clues to Mitigating Parkinson’s Onset

AHA Publisher — Mon, 14 Jun 2021 07:00:31 +0000

Van Andel Research Institute via EurekAlert – GRAND RAPIDS, Mich. (JUNE 8, 2021) — Chronic inflammation in the gut may propel processes in the body that give rise to Parkinson’s disease, according to a study by scientists at Van Andel Institute and Roche. The study, published in Free Neuropathology, is the latest in a growing list that links the gut and the immune system to Parkinson’s. The researchers’ findings in an experimental mouse model of gut inflammation track with several large-scale epidemiological studies that show an association between Parkinson’s and inflammatory bowel diseases, such as ulcerative colitis and Crohn’s disease. Epidemiological evidence from other groups indicates the risk of developing Parkinson’s fades in certain people whose inflammatory bowel disease is treated with anti-TNF, a standard-of-care anti-inflammatory therapy, which suggests that reducing gut inflammation may have promise for mitigating Parkinson’s onset. “There is increasing evidence that changes in the gut can affect a variety of neurological and psychiatric brain disorders,” said Patrik Brundin, M.D., Ph.D., VAI deputy chief scientific officer and co-corresponding author of the study. “Parkinson’s is a complex disease with a wide range of factors that work in concert to spark its onset and progression. We need to understand the gut’s likely influence on Parkinson’s development better. This study provides novel insights, and this new knowledge can facilitate the development of improved treatment approaches.” In their disease models, the team found that chronic gut inflammation triggers a protein called alpha-synuclein to clump together in walls of the colon, as well as in local immune cells called macrophages. A similar process may play out in the colons of some people — such as those with inflammatory bowel diseases — thereby increasing their risk to develop Parkinson’s as shown in studies by other groups. Similarly, in the brains of people with Parkinson’s, “sticky” alpha-synuclein aggregates also develop. For reasons that still are unclear, these aggregates can clog the molecular machinery that keep neurons alive. The resulting loss of some of these critical cells — and the chemical messenger they produce called dopamine — causes Parkinson’s hallmark movement-related symptoms, such as freezing and loss of voluntary movement. The additional wide-spread development of alpha-synuclein aggregates throughout the brain also may be associated with the disease’s non-motor symptoms and may fuel its progression, which cannot be slowed or stopped with existing treatments. The study also revealed that chronic inflammation in the gut early in life can exacerbate alpha-synuclein clumping throughout the brain in older mice. While it isn’t clear exactly how this happens, the team has two theories: first, they suggest inflammatory chemicals may travel from the gut to the brain via the bloodstream, triggering a runaway inflammatory immune response that leads to protein aggregation. Another idea is that alpha-synuclein aggregates may travel to the brain via the vagus nerve, one of the longest nerves in the body and a “superhighway” between the gut and the brain. Once there, the proteins may then execute their toxic activity in the brain. “We now know that systems throughout the body contribute to Parkinson’s,” said Emmanuel Quansah, Ph.D., a postdoctoral fellow in Brundin’s lab and a key contributor and co-author of the study. “It was striking to see protein aggregation pathology in the brain that mirrored pathology in the colon brought on by inflammation. A particularly intriguing observation was the loss dopamine-producing nerve cells — which play a major role in Parkinson’s onset — in our models that had gut inflammation a year-and-a-half earlier.” Notably, the team also found that modulating immune activation in the colitis mouse model by genetic or therapeutic means tuned the level of alpha-synuclein clumps in the colon up or down. “Our results in mice, together with the genetic and epidemiological data by others in humans, make a strong case for further exploring systemic immune pathways for future therapies and biomarkers for Parkinson’s,” said Markus Britschgi, Ph.D., Senior Principal Scientist and Section Head in the Neuroscience and Rare Diseases Research Department at the Roche Innovation Center Basel and co-corresponding author of the study. Authors include first author Stefan Grathwohl, Ph.D. (previously a Roche postdoctoral fellow), Nazia Maroof, Ph.D. (previously a Roche postdoctoral fellow), Liz Spycher, Krisztina Oroszlan-Szovik, M.S., Helga Remy, Markus Haenggi M.S., and Marc Stawiski of Roche Pharma Research and Early Development, Neuroscience and Rare Diseases Discovery and Translational Area, Roche Innovation Center Basel; Jennifer A. Steiner, Ph.D., Zachary Madaj, M.S., and Martha L. Escobar Galvis, Ph.D., of VAI; Fethallah Benmansour, Ph.D., of Roche Pharma Research and Early Development, pREDi, Roche Innovation Center Basel; Gonzalo Duran-Pacheco, Ph.D., Juliane Siebourg-Polster, Ph.D., Matthias Selhausen, Pierre Maliver, EVCP, Arel Su, DVM, and Annika Herrmann, DECVP, of Roche Pharma Research and Early Development, Pharmaceutical Sciences, Roche Innovation Center Basel; Andreas Wolfert and Thomas Emrich, Ph.D., of Roche Pharma Research and Early Development, Pharmaceutical Sciences, Roche Innovation Center Munich; and Christoph Mueller, Ph.D., of Institute of Pathology, University of Bern. To read the original article click here.

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Western Diet Impairs the Gut Immune System, Could Increase Risk of Inflammatory Bowel Disease

AHA Publisher — Fri, 21 May 2021 07:00:34 +0000

Washington University in St. Louis via News-Medical – Eating a Western diet impairs the immune system in the gut in ways that could increase risk of infection and inflammatory bowel disease, according to a study from researchers at Washington University School of Medicine in St. Louis and Cleveland Clinic. The study, in mice and people, showed that a diet high in sugar and fat causes damage to Paneth cells, immune cells in the gut that help keep inflammation in check. When Paneth cells aren’t functioning properly, the gut immune system is excessively prone to inflammation, putting people at risk of inflammatory bowel disease and undermining effective control of disease-causing microbes. The findings, published May 18 in Cell Host & Microbe, open up new approaches to regulating gut immunity by restoring normal Paneth cell function. “Inflammatory bowel disease has historically been a problem primarily in Western countries such as the U.S., but it’s becoming more common globally as more and more people adopt Western lifestyles. Our research showed that long-term consumption of a Western-style diet high in fat and sugar impairs the function of immune cells in the gut in ways that could promote inflammatory bowel disease or increase the risk of intestinal infections.” Ta-Chiang Liu, MD, PhD, Stydy Lead Author and Associate Professor of Pathology & Immunology, Washington University Paneth cell impairment is a key feature of inflammatory bowel disease. For example, people with Crohn’s disease, a kind of inflammatory bowel disease characterized by abdominal pain, diarrhea, anemia and fatigue, often have Paneth cells that have stopped working. Liu and senior author Thaddeus Stappenbeck, MD, PhD, chair of the Department of Inflammation and Immunity at Cleveland Clinic, set out to find the cause of Paneth cell dysfunction in people. They analyzed a database containing demographic and clinical data on 400 people, including an assessment of each person’s Paneth cells. The researchers found that high body mass index (BMI) was associated with Paneth cells that looked abnormal and unhealthy under a microscope. The higher a person’s BMI, the worse his or her Paneth cells looked. The association held for healthy adults and people with Crohn’s disease. To better understand this connection, the researchers studied two strains of mice that are genetically predisposed to obesity. Such mice chronically overeat because they carry mutations that prevent them from feeling full even when fed a regular diet. To the researchers’ surprise, the obese mice had Paneth cells that looked normal. In people, obesity is frequently the result of eating a diet rich in fat and sugar. So the scientists fed normal mice a diet in which 40% of the calories came from fat or sugar, similar to the typical Western diet. After two months on this chow, the mice had become obese and their Paneth cells looked decidedly abnormal. “Obesity wasn’t the problem per se,” Liu said. “Eating too much of a healthy diet didn’t affect the Paneth cells. It was the high-fat, high-sugar diet that was the problem.” The Paneth cells returned to normal when the mice were put back on a healthy mouse diet for four weeks. Whether people who habitually eat a Western diet can improve their gut immunity by changing their diet remains to be seen, Liu said. “This was a short-term experiment, just eight weeks,” Liu said. “In people, obesity doesn’t occur overnight or even in eight weeks. People have a suboptimal lifestyle for 20, 30 years before they become obese. It’s possible that if you have Western diet for so long, you cross a point of no return and your Paneth cells don’t recover even if you change your diet. We’d need to do more research before we can say whether this process is reversible in people.” Further experiments showed that a molecule known as deoxycholic acid, a secondary bile acid formed as a byproduct of the metabolism of gut bacteria, forms the link between a Western diet and Paneth cell dysfunction. The bile acid increases the activity of two immune molecules -; farnesoid X receptor and type 1 interferon -; that inhibit Paneth cell function. Liu and colleagues now are investigating whether fat or sugar plays the primary role in impairing Paneth cells. They also have begun studying ways to restore normal Paneth cell function and improve gut immunity by targeting the bile acid or the two immune molecules. To read the original article click here.

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Researchers Link “Genetic Signatures” of Bacteria in the Human Gut to Multiple Diseases

AHA Publisher — Thu, 20 May 2021 07:00:24 +0000

Harvard Medical School via News-Medical – We are truly never alone, not even within our own bodies. Human beings play host to trillions of bacteria, fungi, viruses, and other microorganisms that make up the human microbiome. In recent years, the mix of these resident bacteria, and the presence of specific bacterial species, has been linked to conditions ranging from obesity to multiple sclerosis. Now, going a step farther, researchers at Harvard Medical School and Joslin Diabetes Center have gone beyond microbial species. Analyzing the genetic makeup of bacteria in the human gut, the team has successfully linked groups of bacterial genes, or “genetic signatures,” to multiple diseases. The work brings scientists closer to developing tests that could predict disease risk or identify disease presence based on a sampling of the genetic makeup of a person’s microbiome. The findings, to be published May 18 in Nature Communications, link sets of bacterial genes to the presence of coronary artery disease, cirrhosis of the liver, inflammatory bowel disease, colon cancer, and type 2 diabetes. The analysis indicates that three of these conditions–coronary artery disease, inflammatory bowel disease, and liver cirrhosis–share many of the same bacterial genes. In other words, people whose guts harbor these bacterial genes seem more likely to have one or more of these three conditions. The work represents a significant advance in the current understanding of the relationship between microbes residing in the human gut and specific diseases, the team said. If confirmed through further research, the results could inform the design of tools that could gauge a person’s risk for a range of conditions based on analysis of a single fecal sample, they added. “This opens a window for the development of tests using cross-disease, gene-based indicators of patient health. We’ve identified genetic markers that we think could eventually lead to tests, or just one test, to identify associations with a number of medical conditions.” (Braden Tierney, Study First Author and Graduate Student, Biological and Biomedical Sciences Program, Harvard Medical School) The researchers caution that their study was not designed to elucidate exactly how and why these microbial genes may be linked to different diseases. Thus far, they said, it remains unclear whether these bacteria are involved in disease development or are mere bystanders in this process. The goal of the study was to determine whether groups of genes could reliably indicate the presence of different diseases. These newly identified microbial genetic signatures, however, could be studied further to determine what role, if any, the organisms play in disease development. “Our study underscores the value of data science to tease out complex interplay between microbes and humans,” said study senior author Chirag Patel, associate professor of biomedical informatics in the Blavatnik Institute at HMS. The researchers started out by collecting microbiome data from 13 groups of patients totaling more than 2,500 samples. Next, they analyzed the data to pinpoint linkages between seven diseases and millions of microbial species, microbial metabolic pathways, and microbial genes. By trying out a variety of modeling approaches–computing a total of 67 million different statistical models–they were able to observe what microbiome features consistently emerged as the strongest disease-associated candidates. Of all the various microbial characteristics–species, pathways, and genes–microbial genes had the greatest predictive power. In other words, the researchers said, groups of bacterial genes, or genetic signatures, rather than merely the presence of certain bacterial families, were linked most closely to the presence of a given condition. Some of the main observations included: Clusters of bacterial genes, or genetic signatures, rather than individual bacterial genes, appear implicated in various types of human disease. Coronary artery disease, inflammatory bowel disease, and liver cirrhosis have similar gut microbiome genetic signatures. Type 2 diabetes, by contrast, has a microbiome signature unlike any other phenotype tested. The analysis did not find a consistent link between the presence of the bacterial species Solobacterium moorei and colon cancer–an association previously reported in numerous studies. However, the researchers did identify particular genes from a S. moorei subspecies associated with colorectal cancer. This finding indicates that gene-level analysis can yield biomarkers of disease with greater precision and more specificity compared with current approaches. Patel said this result underscores the notion that it is not merely the presence of a given bacterial family that may portend risk, but rather the strains and gene signatures of the microbes that matter. The ability to identify interconnections with such precision will be critical for designing tests that can measure risk reliably, he added. Thus, in this specific example, a test intended to measure colon-cancer risk by merely detecting the presence of S. moorei in the gut may not be as reliable as a more refined test that measures bacterial genes to detect the presence of specific strains of S. moorei that are associated with colon cancer. Two conditions–ear inflammation and benign soft-tissue tumors called adenomas–showed weak associations with the gut microbiome, suggesting that microorganisms residing in the human gut are not likely to play a role in the development of these conditions, nor are they likely to be reliable indicators that these conditions are present. In a previous study, the HMS team used massive amounts of publicly available DNA-sequencing data from human oral and gut microbiomes to estimate the size of the universe of microbial genes in the human body. The analysis revealed that there may be more genes in the collective human microbiome than stars in the observable universe. Given the sheer number of microbial genes that reside within the human body, the new findings represent a major step forward in understanding the complexity of the interplay between human diseases and the human microbiome, the researchers said. “The ultimate goal of computational science is to generate hypotheses from a huge swath of data,” said Tierney. “Our work shows that this can be done and opens up so many new avenues for research and inquiry that we are only limited by the time, people, and resources needed to run those tests.” To read the original article click here.

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NEW Study: Vitamin D Helps to Improve Gut Function and Your Immune Response

AHA Publisher — Wed, 11 Nov 2020 08:00:41 +0000

Joy Jensen via NaturalHealth365 – Inflammatory bowel disease (IBD) is a phrase used to describe a group of conditions, including ulcerative colitis and Crohn’s disease, all of which involve chronic inflammation throughout the gastrointestinal tract. According to the U.S. Centers for Disease Control and Prevention (CDC), more than three million adults have been diagnosed with the disease, and it’s becoming increasingly common. But, the big question is: what does science tell us about how vitamin D can improve this condition? Well, previous studies have found that vitamin D deficiency is common among individuals with IBD, and lower levels of this vitamin correlate with a more complicated course of the disease and higher disease activity. In a new study, researchers took a closer look at why a vitamin D deficiency seems to play a part in these diseases and how the vitamin regulates immune response in the gut. The connection between vitamin D deficiencies and IBD patients This new study, published in Autoimmunity Reviews, was built on evidence collected in the past that has shown the protective role vitamin D plays on gut health, which is why a deficiency is linked to poor outcomes and greater disease activity. Not only did researchers review the evidence and confirm that vitamin D deficiencies are higher among patients who have IBD, but they also found out more about how this vitamin works in the gut. Experts believe that leaky gut, which is an insufficient intestinal barrier, is central to how IBD develops. In addition, research has shown that vitamin D seems to work on the cellular level to help increase the integrity of that barrier, reducing problems with leaky gut. It also promotes the interplay between the gut’s microbiome, intestinal epithelial cells, and immune cells, helping to regulate the immune response of the intestines. Although researchers caution that there’s still work to do to further reveal how vitamin D works in the gut, it once again highlights the serious complications that may occur in individuals with a vitamin D deficiency. Scientifically CLEAR: There are serious consequences to this hormone deficiency Beyond its role in the gut, studies also show that vitamin D deficiency comes with additional serious consequences. Being deficient in this important vitamin, particularly if you have blood levels under 30 ng/ml, increases your risk of premature death from any cause. To be clear: Premature death from respiratory disease, heart disease, fracture, and cancers have all been linked to having chronically low vitamin D levels. While that may sounds scary, it’s easy to take control of your vitamin D levels to reduce your risk of chronic disease and premature death. Start by getting 20 minutes daily of direct sunlight so the body is able to create its own. Naturally, if you live in more northern climates … direct sunlight – that’s strong enough to produce a positive result – may not be realistic. The fact is: it’s more difficult to produce this hormone (naturally from sun exposure) during the wintertime or if you live in an area that just doesn’t get as much sunshine, on a regular basis throughout the year. This is where D3 supplementation can help to solve the problem. Just keep in mind, you’ll need to ensure it’s taken with fat-containing foods for the best absorption since it’s a fat-soluble vitamin. And, finally (for best results), you may want to consider taking all the cofactors that enhance absorption such as, zinc, boron and (of course) vitamin K2. Ultimately, if you’re deficient and concerned, it’s a good idea to consult with an experienced (integrative) physician before making any significant changes to your diet or supplement routine. Bottom line: It’s good to know what your vitamin D levels are … so, get a simple blood test and make it a health priority to maintain blood levels of about 50 – 80 ng/ml to protect your health. Sources for this article include: ScienceDirect.com, NIH.gov, NaturalHealth365.com To read the original article click here. For more articles from NaturalHealth365 click here.

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