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Celiac.com 09/25/2023 - Professor Jeffrey Hubbell and a team of researchers at the University of Chicago's Pritzker School of Molecular Engineering has developed a novel type of vaccine known as an "inverse vaccine." This innovative vaccine has shown promise in laboratory settings for the treatment of autoimmune diseases such as multiple sclerosis, type 1 diabetes, and Crohn's disease. Importantly, it achieves this without suppressing the entire immune system, as is often the case with current treatments. Could such treatment work for celiac disease? How the Inverse Vaccine Works Traditional vaccines are designed to train the immune system to recognize and attack harmful viruses or bacteria. In contrast, the inverse vaccine takes a different approach. It aims to erase the immune system's memory of a specific molecule. This concept is particularly useful in autoimmune diseases, where the immune system mistakenly attacks the body's healthy tissues. The development of the inverse vaccine is based on the liver's natural mechanism of marking molecules from broken-down cells with signals that instruct the immune system not to attack them. Researchers combined an antigen (a molecule targeted by the immune system in autoimmune diseases) with a molecule resembling a fragment of an aged cell. This mimicry tricks the liver into recognizing the antigen as a friend rather than a foe, effectively stopping the autoimmune reaction. The research team successfully demonstrated the effectiveness of this inverse vaccine in halting autoimmune reactions in a disease model resembling multiple sclerosis. In multiple sclerosis, the immune system attacks myelin, the protective coating around nerves, leading to symptoms such as weakness, numbness, vision loss, and mobility problems. By linking myelin proteins to the molecule recognized by the liver, the researchers were able to prevent the immune system from attacking myelin. This allowed nerves to function properly again, ultimately reversing the disease's symptoms in animal subjects. Importantly, the inverse vaccine approach could have significant advantages over current treatments for autoimmune diseases. Many existing treatments involve broadly suppressing the entire immune system, which can lead to various side effects and increase the risk of infections. In contrast, the inverse vaccine offers a more targeted and specific way to modulate the immune response, potentially minimizing side effects. While further research is needed, initial phase I safety trials have already been conducted in humans with celiac disease, and are underway in multiple sclerosis. These trials are sponsored by the pharmaceutical company Anokion SA, which also contributed to the research. The development of clinically approved inverse vaccines is an exciting prospect, as they could provide more effective and precise treatments for autoimmune diseases, improving the quality of life for patients. Read more at the Pritzker School of Molecular Engineering

Celiac.com 10/20/2020 - Doctors diagnosing children for type 1 diabetes are increasingly finding other autoimmune conditions that can complicate the outlook for these patients. A team of researchers recently set out to study rates of comorbid autoimmune diseases, including celiac disease, and type 1 diabetes mellitus (T1D) in children. Rates of type 1 diabetes mellitus (T1D) in children are on the rise, but it's unclear what relationship, if any, this might have with other coexistent autoimmune conditions, since diabetes onset is not well understood. The team wanted to assess the incidence of T1D, and the rates of coexistent autoimmune illnesses, from the onset of diabetes mellitus in children over a nine year study period. In their retrospective study, the team calculated incidence rate for T1D as the total number of all newly diagnosed cases per 100,000 population in people between 0 and 18 years of age. The team studied 264 boys and 229 girls between 0 and 18 years old with newly diagnosed with T1D in one of the Polish centers from 2010–2018. They determined diagnoses for related autoimmune illnesses from initial data recorded when patients first received diagnosis for T1D. The team found that the standardized incidence rate of T1D in children rose 170% over the 9-year study period, while the incidence rate ratio rose 4% per year. As rates of T1D have risen rapidly in all children of all ages in recent years, so, too have rates of the autoimmune diseases that frequently accompany these conditions. Having an additional autoimmunity disorder is a serious burden for patients with new-onset T1D. Stay tuned for more information on the challenges faced by children with more than one auto-immune disease. Read more in Front Endocrinol (Lausanne). 2020; 11: 476. Reference: Głowińska-Olszewska B, Szabłowski M, Panas P, et al. Increasing co-occurance of additional autoimmune disorders at diabetes type 1 onset among children and adolescents diagnosed in years 2010-2018—single-center study. Front Endocrinol. Published online August 6, 2020. doi:10.3389/fendo.2020.00476. The research team included Barbara Głowińska-Olszewska, Maciej Szabłowski, Patrycja Panas, Karolina Żoła̧dek, Milena Jamiołkowska-Sztabkowska, Anna Justyna Milewska, Anna Kadłubiska, Agnieszka Polkowska, Włodzimierz Łuczyński, and Artur Bossowski. They are variously affiliated with the Department of Pediatrics, Endocrinology, Diabetology With Cardiology Division, Medical University of Bialystok, Białystok, Poland; the Department of Pediatrics, Rheumatology, Immunology and Metabolic Bone Diseases, Medical University of Bialystok, Białystok, Poland; the Department of Statistics and Medical Informatics, Medical University of Bialystok, Białystok, Poland; and the Department of Medical Simulations, Medical University of Bialystok, Białystok, Poland.

Celiac.com 05/10/2021 - A top physician in Turkey recently warned that rates of autoimmune diseases like Type 1 diabetes and celiac will likely rise in the wake of the coronavirus pandemic. Autoimmune diseases, including thyroid issues, happen when the body attacks its own tissues. The coronavirus causes the body's immune system to produce “attacking” antibodies. Because "[v]iruses serve as a mechanism that pull the trigger for autoimmune diseases,” an increase in rates of autoimmune diseases was unavoidable after a year of pandemic," says Professor Tufan Tükek, head of the Faculty of Medicine at Istanbul University. Lingering COVID-19 symptoms Impede Autoimmune Disease Management Ongoing coronavirus symptoms have been a problem for numerous recovered patients, and can impair the management of autoimmune diseases. For example, in diabetes patients, studies show that the symptoms influence blood sugar levels, and impede its management by causing fatigue and memory issues. In March 2020, Istanbul University became one of the first institutions in the country to establish an observation center for recovered coronavirus patients. Since then, they have monitored nearly 4,000 patients. Professor Tükek says that, in the early days of the pandemic, diarrhea was the main "long COVID-19" symptom, and then, after a second COVID-19 wave last summer, their team began seeing more memory issues and hair loss. Lately, Tükek said, they are seeing more cases of blood clots. COVID-19 Symptoms Can Linger for Months Dr. Huzeyfe Arıcı, a physician working at the observation center, said that COVID-19 symptoms can linger for up to eight weeks, in many cases. “We have patients suffering from back pain that long, something that cannot be cured by painkillers. We also see an increasing number of cases with memory lapses,” he stressed. With COVID-19 survivors numbering in the millions, it is an open question as to how many will be affected by lingering symptoms, for how long, and what can be done to help them. The idea that coronavirus could increase rates of diabetes, celiac or other autoimmune conditions is bit alarming. Quantifying and describing the problems and then creating a way to address them is crucial. Look for more information as other observation centers share their observations on COVID-19 survivors. Read more in Dailysabah.com

Celiac.com 05/14/2020 - We know a lot more than ever about celiac disease, but researchers still don't have very much good information about environmental risk factors in genetically susceptible populations. For example, does environmental exposure to organic pollutants increase the risk of celiac disease? Researchers have documented endocrine disruption caused by ongoing exposure to persistent organic pollutants. That, along with the interplay between the endocrine and immune systems, has led them to question whether POPs may be contribute to celiac disease. A team of researchers recently set out to shed some light on the connection between persistent organic pollutants and celiac disease. The research team included Abigail Gaylorda; Leonardo Trasande; Kurunthachalam Kannan; Kristen M.Thomas; Sunmi Leef; Mengling Liu; and Jeremiah Levine. For their single-site pilot study, they enrolled 88 patients from NYU Langone's Hassenfeld Children's Hospital outpatient clinic. Thirty of these patients were ultimately diagnosed with celiac disease via standard blood screens, and duodenal biopsy. Controlling for sex, race, age, BMI, and genetic susceptibility score, they found that odds of developing celiac disease are higher in both male and female patients with higher serum p,p’-dichlorodiphenyldichloroethylene (DDE), in female patients with perfluorooctane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA), and males with 2,2',4,4',5,5'-hexabromodiphenyl ether (BDE153). This is the first study to report on celiac disease with persistent organic pollutant exposure in children. These findings raise further questions of how environmental chemicals may affect autoimmunity in genetically susceptible individuals. The idea that exposure to organic pollutants might contribute to the development of inflammatory autoimmune conditions seems entirely reasonable, and the results from this study provide good evidence to support that idea. Stay tuned for more on this and related stories. Do you think pesticide exposure might have played a role in your celiac disease, or that of a loved one? Share your story in our comments section. Read more in Environmental Research The researchers are variously affiliated with the Department of Population Health, New York University School of Medicine, New York, NY, USA; the Department of Pediatrics, New York University School of Medicine, USA; the Department of Environmental Medicine, New York University School of Medicine, New York, NY, USA; the NYU Wagner School of Public Service, New York, NY, USA; NYU College of Global Public Health, New York, NY, USA; the NYU Medical Center, New York State Department of Health, Albany, NY, USA; the Department of Pathology, New York University School of Medicine, New York, NY, USA; and the Division of Pediatric Gastroenterology, New York University School of Medicine, New York, NY, USA.

Celiac.com 03/31/2020 - There are over one-hundred different autoimmune diseases. One thing they have in common is that they are driven by the body's own cells; by rare and elusive immune cells that target the body's own healthy organs and tissues, instead of harmful foreign bacteria and viruses. Researchers call such cells 'rogue cells." For the first time, a team led by researchers at the Garvan Institute of Medical Research have used patient samples to document the existence of specific cells that cause autoimmune disease. They also figured out the mechanism that allows cells to 'go rogue' by evading checkpoints that normally stop immune cells from targeting the body's own tissues. "We have developed a technique that allows us to look directly at the cells that cause autoimmune disease—it's as though we're looking through a new microscope lens for the first time, learning more about autoimmune disease than was ever possible before," says Professor Chris Goodnow, co-senior author of the paper, and Executive Director of the Garvan Institute and Director of the UNSW Sydney Cellular Genomics Futures Institute. Potential for New Diagnosis and Treatments In addition to revealing the root cause of an autoimmune disease, the research findings offer huge potential for future treatments to target the cause of all autoimmune diseases. "Current treatments for autoimmune disease address only the symptoms, but not the cause. To make more targeted treatments that address disease development and progression, we first need to understand the cause...Identifying these rogue immune cells is a significant step forward for how we study autoimmune disease—and crucially the first step to finding ways to eliminate them from the body entirely," says Professor Goodnow. "In our study, we uncovered specific mutations that mark early stages of autoimmune disease. If we can diagnose a patient at these stages, it may be possible to combine our knowledge of these mutations with new targeted treatments for lymphoma to intervene in disease progression or to track how well a patient is responding to treatments," says Dr. Reed. The researchers are now planning follow-up studies to investigate mutations of autoimmune cells in a range of other diseases, including lupus, celiac disease and type 1 diabetes. The team's findings, published in the journal Cell today, are part of the visionary Hope Research program, could lead to major advances in the diagnosis and treatment of autoimmune disease. Read more in MedicalExpressNews.com

Celiac.com 10/23/2019 - One approach to celiac disease that's been getting attention lately is the effort to develop ways to prevent the adverse immune reaction that is triggered by gluten that leads to gut damage in untreated celiacs. Several companies have tried that approach, including the promising, but now failed drug NexVax2. The idea is to train the immune system to become tolerant of gluten, kind of like the way allergists train the immune system to tolerate pollen, and thus, reduce or even eliminate allergic reactions. Data from a recent trial of new medical technology provides encouraging evidence that it is possible for people with celiac disease to achieve an immune tolerance to gluten, effectively reversing the autoimmune disease. The technology is a biodegradable nanoparticle containing gluten that teaches the immune system the antigen (allergen) is safe. The nanoparticle, called COUR nanoparticle, CNP-101, conceals the allergen in an innocuous cell covering, and convinces the immune system not to attack it. Celiac patients treated with CNP-101 were able to eat gluten with a substantial reduction in inflammation. The phase 2 results indicate that the treatment protects patients’ small intestine from gluten exposure, and point the way toward treatments that could allow celiac patients safely consume gluten in their diet. In addition to potentially reversing celiac disease, the technology, which uses a nanoparticle containing the antigen triggering the allergy or autoimmune disease, has the potential to treat myriad diseases and allergies, including multiple sclerosis, type 1 diabetes, peanut allergy, asthma, among others. The research team will present their findings on Oct. 22nd at the European Gastroenterology Week conference in Barcelona, Spain. The technology was devised in the lab of Stephen Miller, the Judy Gugenheim Research Professor of Microbiology and Immunology at Northwestern University Feinberg School of Medicine, who has refined it over decades. In addition to providing the first proof that the technology works in patients, the study shows that "we can encapsulate myelin into the nanoparticle to induce tolerance to that substance in multiple sclerosis models, or put a protein from pancreatic beta cells to induce tolerance to insulin in type 1 diabetes models,” said Miller. The technology works by causing the immune system to see the allergen-loaded nanoparticle as innocuous debris, and to disregard it. Once ignored, the nanoparticle and its hidden antigen get eaten by a macrophage, kind of a garbageman that rids the body of cellular debris and pathogens. “The vacuum-cleaner cell presents the allergen or antigen to the immune system in a way that says, ‘No worries, this belongs here,'” Miller said. “The immune system then shuts down its attack on the allergen, and the immune system is reset to normal.” In the celiac trial, Miller's team loaded the nanoparticle with gliadin, the protein in gluten that triggers the adverse reaction in people with celiac disease. After a week of treatment, the patients consumed gluten for two weeks. Untreated celiac patients who ate gluten showed clear immune responses to gliadin and related damage to the small intestine. Meanwhile, celiac patients treated with CNP-101 showed 90% less immune-related inflammation than untreated patients. By preventing the inflammatory response, CNP-101 showed the ability to protect the gut from gluten-related damage. Most autoimmune diseases are currently treated with immune suppressants, which lessen symptoms, but degrade the immune response and carry the potential for toxic side-effects. CNP-101 does not work by suppressing the immune system, but by preventing the inflammatory response, and thus reversing the course of the autoimmune disease. Celiac disease a perfect target for the nanoparticle induced immune tolerance approach, because the triggers are well documented, and the disease has no other treatment than a gluten-free diet. CNP-101 has been granted Fast Track status by the U.S. Food and Drug Administration, and brought to patients in collaboration with Takeda Pharmaceuticals, which has acquired an exclusive global license to develop and commercialize this treatment for celiac disease. In addition to celiac disease, COUR is looking to develop treatments for peanut allergy and multiple sclerosis, and to expand their offerings to other autoimmune conditions, said John J. Puisis, president and chief executive officer of COUR. Read more in sciencedaily.com

Celiac.com 09/04/2019 - Class II human leukocyte antigen (HLA) allele combinations exert strong genetic control over susceptibility to numerous autoimmune diseases. Researchers know that these genes are the most significant risk factors for Type 1 diabetes and celiac disease, but they still know very little about how HLA influences the makeup of the human gut microbiome, which could be an environmental factor for disease susceptibility. A team of researchers recently compared the gut microbiomes of kids with high genetic risk for Type 1 diabetes against those of kids with low genetic risk. Their results show that the two groups have very different gut microbiomes. The research team included Jordan T. Russell, Luiz F. W. Roesch, Malin Ördberg, Jorma Ilonen, Mark A. Atkinson, Desmond A. Schatz, Eric W. Triplett and Johnny Ludvigsson. Using data from a study of All Babies in Southeast Sweden, the team found that genetic risk for the development of Type 1 diabetes autoimmunity is associated with clear changes in the gut microbiome, with both core microbiome and beta diversity differing according to HLA risk group and genotype. Interestingly, protective HLA haplotypes are connected with bacterial genera Intestinibacter and Romboutsia. These results show that general population cohorts can help researchers spot potential environmental triggers or protective factors for autoimmune diseases that can otherwise remain obscured by strong genetic influence. Certain bacterial species were totally absent in children with high genetic risk, but present in children with low or no risk. "[T]his could mean that certain species [of gut bacteria] have protective effects and may be useful in future treatment to prevent autoimmune diseases. It may be that certain species cannot survive in individuals with high genetic risk”, says Johnny Ludvigsson, senior professor in the Department of Clinical and Experimental Medicine, Linköping University, and senior consultant at HRH Crown Princess Victoria Children’s Hospital, Linköping University Hospital. Read more in Nature Communications volume 10, Article number: 3621 (2019) The researchers in this study are variously affiliated with the Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences University of Florida, Gainesville, FL, USA; the Biological Sciences, Universidade Federal do Pampa, São Gabriel, Brazil; the Crown Princess Victoria Children’s Hospital, Region Östergötland, Division of Pediatrics, Linköping University, Linköping, Sweden; the Immunogenetics Laboratory, Institute of Biomedicine, University of Turku, and Clinical Microbiology, Turku University Hospital, Turku, Finland; the Department of Pathology, University of Florida Diabetes Institute, Gainesville, FL, USA; the Department of Pediatrics, College of Medicine, University of Florida, Gainesville, FL, USA; and the Department of Microbiology and Cell Science, Institute of Food and Agricultural Sciences University of Florida, Gainesville, FL, USA.

Celiac.com 06/20/2019 (originally published 07/12/2010) - Autoimmune diseases taken together are the third leading cause of death in the US. The list of autoimmune diseases is long and varied—M.S., type 1 diabetes, lupus, Hashimoto’s thyroiditis, rheumatoid arthritis, Sjogren’s, and fibromyalgia to name just a few. But the autoimmune disease celiac, unlike all the others, has a unique feature—it’s the only autoimmune disease where the exact trigger is known. Gluten is the trigger for celiac disease and when that trigger is removed the body stops destroying its own small intestine. Why is this profound? Two reasons: There is no other autoimmune disease where the exact trigger is known. Gluten and the damage it causes to the small intestine may very well be the root cause of other autoimmune diseases! We have appreciated the interesting phenomenon where people “develop” gluten intolerance at different ages. It used to be perplexing because it was assumed that if the problem was genetically driven, as soon as the body received its first gluten “insult” damage should begin to occur. When patients stated that they felt perfectly fine until a certain age, it was thought that the damage had probably begun far earlier but the patient had just not noticed. What we have come to realize is that a genetic propensity plus the presence of gluten in the diet are only two of the three necessary constituents of the puzzle—the third is damage to the small intestine. A completely healthy, intact small intestine seems to be quite able to defend itself against gluten. But once damage has occurred, the gut becomes “leaky” and not only can digestive complaints result but symptoms arise in other body systems. There has been proof for many years that the intestine is not the only tissue targeted by the immune reaction to gluten. The prime example of this is a disease called dermatitis herpetiformis where the gluten sensitivity manifests primarily in skin, with only mild or no intestinal involvement. Now, more recent research reveals that perhaps a vast number of autoimmune diseases may also involve an immune response to dietary gluten as well as its consequent autoimmune reaction to tissue transglutaminase. This may be the main immunologic cause. [Note: Although we typically think of tissue transglutaminase as an enzyme in the gut, it is, in fact, an enzyme found throughout the body. This is perhaps another reason why gluten has such far-reaching effects in other systems of the body.] The substance that dictates the permeability between the barrier cells that line the small intestine is called zonulin. Increased zonulin causes the intestine to become leaky, thereby allowing substances to leave the intestine that normally shouldn’t. Research has shown that in patients with celiac disease, gliadin activates zonulin signaling, leading to increased intestinal permeability. But how does this extend to other autoimmune diseases? Dr. Alessio Fasano performed a brilliant study on rats that were genetically predisposed to develop type 1 diabetes. The premise was that if the gut was not affected negatively by zonulin and remained intact and healthy, then perhaps the auto-antibodies made against specific cells of the pancreas that create diabetes would be prevented from leaving the gut and thereby stopped from causing damage to the pancreas. Sure enough 2/3 of these rats who were highly predisposed to develop diabetes did not! This study was the first time that an autoimmune disease was prevented by blocking intestinal permeability. It further puts a new face on the entire concept of how and why autoimmune disease develops. We’ve always thought that the genetic predisposition was an overriding characteristic of autoimmune diseases that overshadowed any effort to sublimate it. This study opens a new field of investigation into the relationship between the health of the intestine and the basis of many diseases. Imagine if the “unknown trigger” of autoimmune disease turns out to be gluten and its effect of creating a leaky gut! It is for this reason that I am so passionate about early diagnosis of gluten intolerance. Whether it be celiac disease or gluten sensitivity, the effect that gluten imposes on the integrity of the small intestine has far-reaching implications. I see it clinically in my patients on a daily basis, but the above research puts a point on it that we must consider seriously. A study from Italy showed that the longer gluten sensitive people eat gluten, the more likely they are to develop autoimmune diseases. They found that in childhood celiacs, the prevalence of autoimmune disease rose from a baseline of 5% at age 2 to almost 35% by age 20. Imagine if screening of all children for gluten intolerance resulted in reductions of future autoimmune diseases! I am currently working on a program with my patients who are gluten intolerant to restore their small intestines to the healthiest possible condition. This is important from the obvious viewpoint that optimal digestion and absorption is critical to good health. But it is also vital from the perspective of understanding and managing zonulin and its long-term effects on health. I would recommend that you take the following steps to ensure that you are doing everything you can to restore your small intestine to optimal functioning. Have a comprehensive stool analysis performed to ensure that no pathogenic organisms (bacteria, amoeba, parasites, etc) are present. Such a test should also measure the effect of your body’s enzymes to see how effectively your food is being broken down and absorbed. It should also assess the health of your intestinal bacteria or probiotics. Eliminate dairy foods from your diet. There is considerable evidence to suggest that consuming milk from other mammals is not conducive to good health, especially in our digestive tracts. The inflammation that dairy can cause could well be contributing to a leaky gut, despite the elimination of gluten. Once you have taken the above steps, see how you’re feeling. Some patients require supplements such as glutamine, quercitin, reduced glutathione, N-acetylcysteine, omega 3 fatty acids, and vitamins A, E, B and zinc to help the intestinal lining heal fully. Once the above have been done, have a lab test performed for leaky gut. It’s called a lactulose/mannitol test and will show whether large molecules are crossing the intestinal barrier. This is a non-invasive, non-drug test. Just to reiterate: encourage parents you know to have their children evaluated for gluten intolerance. The more we can affect an early diagnosis, the healthier our future generations will be. Last but not least, show your doctor this data. There is still too much ignorance in our profession about gluten and its broad reaching negative effects. I hope you find this information helpful. Many of the steps mentioned above are best administered with the help of a clinician so let me know if I can assist you to find someone in your area who can help. References: Scandinavian Journal of Gastroenterology. 2006 Apr;41(4):408-19. Annals N Y Academy Science. 2009 May;1165:195-205. “Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms.” Clinical Gastroenterology & Hepatology. 2005 Apr;3(4):335-41. “Permeability, zonulin production, and enteropathy in dermatitis herpetiformis.” Gut. 2003 Feb;52(2):218-23. “Early effects of gliadin on enterocyte intracellular signalling involved in intestinal barrier function.”

Celiac.com 04/25/2018 - A team of Yale University researchers discovered that bacteria in the small intestine can travel to other organs and trigger an autoimmune response. In this case, they looked at Enterococcus gallinarum, which can travel beyond the gut to the spleen, lymph nodes, and liver. The research could be helpful for treating type 1 diabetes, lupus, and celiac disease. In autoimmune diseases, such as type 1 diabetes, lupus, and celiac disease, the body’s immune system mistakenly attacks healthy cells and tissues. Autoimmune disease affects nearly 24 million people in the United States. In their study, a team of Yale University researchers discovered that bacteria in the small intestine can travel to other organs and trigger an autoimmune response. In this case, they looked at Enterococcus gallinarum, which can travel beyond the gut to the spleen, lymph nodes, and liver. They found that E. gallinarum triggered an autoimmune response in the mice when it traveled beyond the gut. They also found that the response can be countered by using antibiotics or vaccines to suppress the autoimmune reaction and prevent the bacterium from growing. The researchers were able to duplicate this mechanism using cultured human liver cells, and they also found the bacteria E. gallinarum in the livers of people with autoimmune disease. The team found that administering an antibiotic or vaccine to target E. gallinarum suppressed the autoimmune reaction in the mice and prevented the bacterium from growing. "When we blocked the pathway leading to inflammation," says senior study author Martin Kriegel, "we could reverse the effect of this bug on autoimmunity." Team research team plans to further investigate the biological mechanisms that are associated with E. gallinarum, along with the potential implications for systemic lupus and autoimmune liver disease. This study indicates that gut bacteria may be the key to treating chronic autoimmune conditions such as systemic lupus and autoimmune liver disease. Numerous autoimmune conditions have been linked to gut bacteria. Read the full study in Science.