Celiac.com 02/02/2026 - Celiac disease is a lifelong immune condition in which eating gluten damages the small intestine. While genetics play an important role, genes alone do not explain why some people develop the disease while others with similar genetic backgrounds do not. Researchers have long suspected that early environmental factors, especially those affecting the developing immune system, may influence whether celiac disease emerges later in life.

One of the most important influences on the immune system during infancy is the community of bacteria living in the gut. These bacteria help train the immune system to recognize what is harmless and what is dangerous. Antibiotics, while often life-saving, can strongly disrupt these bacteria. This large population-based study explored whether antibiotic exposure during the first year of life is linked to a higher risk of developing celiac disease autoimmunity in childhood.

What the Researchers Studied

The researchers examined health records from a nationwide health care system that serves millions of people. They focused on children born over a long time span, from the mid-1990s through the early 2020s. By using this large and detailed database, the researchers were able to follow children from birth through childhood and observe both medication use and later immune-related outcomes.

The main question was simple but important: were children who received antibiotics during their first year of life more likely to develop celiac disease autoimmunity than children who did not? To answer this, the researchers looked not only at whether antibiotics were used, but also at how early they were given, how many times they were prescribed, and whether certain groups of children appeared more vulnerable.

How Antibiotic Exposure and Celiac Autoimmunity Were Defined

Antibiotic exposure was measured carefully. The researchers tracked the type of antibiotics prescribed, the age at which the first antibiotic was given, and the total number of prescriptions during the first year of life. This allowed them to look for patterns, such as whether repeated courses carried more risk than a single short treatment.

Celiac disease autoimmunity was defined using blood tests that detect immune reactions against the body’s own tissues related to gluten sensitivity. Children were considered to have celiac disease autoimmunity only if they had two separate positive test results. This strict definition reduced the chance that temporary or false-positive results would influence the findings.

The analysis also took into account factors that could affect health outcomes, including sex, ethnic background, and socioeconomic position. This helped ensure that the observed associations were not simply due to differences in access to care or social conditions.

Who Was Included in the Study

The study analyzed records from more than one million children, making it one of the largest investigations of this topic to date. Slightly more than half of the children received at least one antibiotic prescription during their first year of life, showing how common antibiotic use is in infancy.

Celiac disease autoimmunity was diagnosed in a relatively small percentage of the total group, but the large sample size made it possible to detect meaningful differences between exposed and unexposed children. On average, children were diagnosed with celiac disease autoimmunity in early school age, several years after their antibiotic exposure in infancy.

Main Findings: Antibiotics and Increased Risk

The study found a clear association between antibiotic use during the first year of life and an increased risk of developing celiac disease autoimmunity later in childhood. Children who received antibiotics in infancy were more likely to show signs of immune activity related to celiac disease than those who did not.

Timing also appeared to matter. Children who were exposed to antibiotics at a younger age had a higher risk than those whose first exposure occurred later in infancy. This suggests that the earliest months of life may be a particularly sensitive period for immune system development.

Perhaps most striking was the dose-related pattern. The risk of celiac disease autoimmunity increased as the number of antibiotic prescriptions increased. Children who received only a few courses had a modest increase in risk, while those who received many prescriptions during their first year of life had a much higher likelihood of developing immune markers associated with celiac disease.

Differences Between Groups

The researchers also found that the association between antibiotics and celiac disease autoimmunity was not the same for all children. The link appeared stronger in girls than in boys. Children from lower socioeconomic backgrounds also showed a stronger association between antibiotic exposure and later immune changes.

These differences suggest that biological factors, social conditions, or differences in early-life exposures may interact with antibiotics to influence immune development. While the study did not determine why these differences exist, it highlights the need for more personalized approaches to understanding risk.

Possible Explanations for the Findings

One likely explanation involves the gut microbiome. Antibiotics can reduce beneficial bacteria and alter the balance of microbes in the intestine. In infancy, when the immune system is still learning tolerance, this disruption may interfere with normal immune training.

Another possibility is that frequent infections, which often lead to antibiotic prescriptions, may themselves play a role in immune activation. However, the dose-related pattern and the timing of exposure suggest that antibiotics themselves may contribute independently to risk, beyond the infections they are used to treat.

What the Study Does Not Prove

It is important to understand that this study shows an association, not direct cause and effect. Antibiotics do not automatically lead to celiac disease, and many children who receive antibiotics in infancy never develop immune problems. Antibiotics remain essential and life-saving medications when used appropriately.

The study also did not examine specific types of infections or detailed dietary factors that might influence celiac disease development. These areas require further research.

Why This Study Matters for People with Celiac Disease

For individuals and families affected by celiac disease, this study adds important insight into how early-life factors may shape disease risk long before symptoms appear. It supports the growing idea that the roots of celiac disease may begin in infancy, during critical windows of immune development.

The findings do not suggest avoiding antibiotics when they are medically necessary. Instead, they emphasize the importance of thoughtful and appropriate use, especially in very young children. Reducing unnecessary antibiotic prescriptions may help protect the developing immune system while still allowing effective treatment of serious infections.

For families with a known genetic risk for celiac disease, this research may encourage discussions with health care providers about balancing the benefits and risks of antibiotic use. In the long term, studies like this may guide strategies aimed at prevention, earlier monitoring, or microbiome-supporting interventions.

Conclusion

This large population-based study found that antibiotic exposure during the first year of life is linked to a higher risk of developing celiac disease autoimmunity, particularly with earlier exposure and repeated prescriptions. The results highlight infancy as a critical period for immune development and reinforce the idea that environmental factors can influence lifelong health.

For people with celiac disease and those at risk, the study underscores the importance of early-life health decisions and opens the door to future research on prevention and immune resilience. While antibiotics remain a vital medical tool, using them wisely may help reduce unintended long-term immune consequences.

Read more at: journals.lww.com

Watch the video version of this article:

Watch the super short video version of this article:

Celiac.com 01/27/2026 - This study set out to answer a long-standing question in celiac disease research: where and how the immune system first becomes activated against gluten and the body’s own enzyme, transglutaminase. People with celiac disease produce antibodies against transglutaminase, even though it is a normal human protein. Scientists have known for years that this autoimmune response somehow depends on gluten, but the exact location and sequence of events that link gluten exposure to autoimmunity have remained unclear. This research uses a carefully designed mouse model to show that key immune interactions may begin directly within specialized immune structures in the gut wall called Peyer’s patches.

Background: Why Transglutaminase and Gluten Are Linked

Celiac disease is unusual among autoimmune disorders because the target of the immune response is a normal enzyme that is present throughout the body. Transglutaminase modifies gluten proteins during digestion, and this chemical interaction appears to create a bridge between gluten and the immune system. Immune cells that recognize gluten provide help to other immune cells that specifically recognize transglutaminase. This cooperation leads to the production of antibodies against transglutaminase, which are a defining feature of celiac disease and are widely used for diagnosis.

Despite this understanding, researchers have struggled to explain where transglutaminase and gluten first meet in a way that triggers immunity. One possibility is that this interaction happens deep in the intestinal tissue after gluten has crossed the gut barrier. Another possibility is that the interaction begins much earlier, closer to the gut surface, within immune structures that actively sample material from the intestinal contents.

Purpose of the Study

The main goal of this study was to determine whether immune cells located in gut-associated lymphoid tissues can directly encounter complexes formed between transglutaminase and gluten. Specifically, the researchers wanted to test whether B cells that recognize transglutaminase can capture this enzyme from the gut lumen and, with help from gluten-reactive T cells, initiate the autoimmune response characteristic of celiac disease.

To address this, the researchers developed a specialized mouse model that reproduces essential features of human celiac disease, including genetic susceptibility and the presence of gluten-reactive immune cells.

How the Mouse Model Was Designed

The researchers used mice that were genetically engineered to express a human immune molecule strongly associated with celiac disease. These mice were given two specific types of immune cells: B cells that recognize transglutaminase and T cells that recognize gluten. This setup allowed the investigators to observe how these cells interact after gluten exposure.

The mice were then fed a specially designed protein that mimics the interaction between transglutaminase and gluten. This protein included parts that could be recognized by both B cells and T cells, ensuring that cooperation between these immune cells could occur. An immune-stimulating agent was included to encourage responses in the gut, allowing the researchers to closely track immune activation in intestinal tissues.

Development of a Celiac-Like Immune Response

After oral exposure, the mice developed immune responses that closely resembled those seen in people with celiac disease. Antibodies directed against transglutaminase appeared both in the bloodstream and in the gut. In the intestinal lining, immune cells that produce these antibodies were detected in locations similar to those seen in untreated human disease.

This confirmed that the model successfully reproduced key features of celiac autoimmunity, making it possible to study where and how the immune response begins.

The Role of Peyer’s Patches

A major focus of the study was Peyer’s patches, which are organized immune structures embedded in the wall of the small intestine. These structures are strategically positioned to sample material from the gut lumen and initiate immune responses when necessary.

The researchers found that transglutaminase-specific B cells became activated and expanded within Peyer’s patches after oral exposure to the model antigen. These B cells showed features of active immune participation, including characteristics associated with antibody refinement and long-term immune memory. At the same time, gluten-reactive T cells in the same locations showed signs of providing help to these B cells, consistent with cooperative immune activation.

Direct Sampling of Transglutaminase From the Gut Lumen

One of the most important experiments in the study tested whether B cells in Peyer’s patches can directly sample transglutaminase from inside the gut. To do this, the researchers introduced labeled transglutaminase into a section of the intestine that contained Peyer’s patches and then examined the tissue using high-resolution imaging.

They observed that B cells specific for transglutaminase captured the enzyme from the gut lumen. This uptake occurred in precise regions of Peyer’s patches that are known to specialize in antigen sampling. Importantly, this process was selective: only B cells that recognized transglutaminase took up the enzyme, while other immune cells did not.

This finding provides direct evidence that transglutaminase present in the gut lumen can be captured by immune cells without needing to first cross the intestinal barrier in a non-specific way.

A New Model for How Celiac Disease Begins

Based on these results, the researchers propose a model in which transglutaminase binds gluten in the gut lumen during digestion. These enzyme-protein complexes are then sampled by specialized B cells in Peyer’s patches. Once captured, the B cells present gluten fragments to gluten-reactive T cells, receiving help that drives the production of antibodies against transglutaminase.

This sequence of events offers a coherent explanation for how dietary gluten leads to a highly specific autoimmune response. It also suggests that the earliest steps of celiac disease may occur at the gut surface rather than deeper within intestinal tissue.

What the Study Does and Does Not Show

While the findings are compelling, the study does not directly demonstrate the uptake of naturally occurring transglutaminase-gluten complexes formed during normal digestion. Instead, it shows that transglutaminase itself can be sampled from the gut lumen by specific immune cells. The researchers also note that other immune cells may contribute to antigen presentation and that further work is needed to fully map all pathways involved.

Even so, the model provides a powerful experimental platform for studying early immune events that are difficult or impossible to observe directly in humans.

Why This Study Matters for People With Celiac Disease

For people with celiac disease, this research offers a clearer picture of how gluten exposure can rapidly lead to immune activation. It supports the idea that the disease may begin within the gut wall itself, without requiring a generalized breakdown of the intestinal barrier. This challenges older theories that focused on widespread gut leakiness as the primary trigger.

Understanding that immune activation may start with specific interactions in Peyer’s patches opens new possibilities for treatment. Therapies could be designed to block the formation or uptake of transglutaminase-gluten complexes, interfere with early B cell and T cell cooperation, or target transglutaminase activity in the gut lumen. Such approaches could one day complement a gluten-free diet or reduce the immune consequences of accidental gluten exposure.

In summary, this study provides strong evidence that the roots of celiac disease lie in carefully orchestrated immune sampling events within the gut wall. By identifying where and how the autoimmune response begins, it moves the field closer to more precise and potentially transformative therapies for people living with celiac disease.

Read more at: gastrojournal.org and medscape.com

Watch the video version of this article:

Watch the super short video version of this article:

Celiac.com 01/26/2026 - This study explored a rare cell type in the human small intestine called the microfold cell. Microfold cells sit in specialized areas of the gut that sample material from the intestinal contents and help train the immune system. For many years, most detailed knowledge about these cells came from mouse experiments. The researchers set out to build a strong human-based model so they could learn what human microfold cells do, how they form, and whether they might play a direct role in the immune reaction to gluten that drives celiac disease.

Why Microfold Cells Matter in the Gut

The small intestine has a difficult job: it must absorb nutrients efficiently while also detecting harmful microbes and other foreign substances. In certain immune-rich regions of the intestine, including structures called Peyer patches, the lining contains microfold cells that act like “sampling ports.” These cells help move material from the gut surface toward immune cells positioned underneath. Traditionally, microfold cells were thought to function mainly as transporters, handing off particles to professional immune cells that then decide whether to tolerate the material or mount an immune response.

However, celiac disease raises a key question: how does gluten, a food protein, become visible to immune cells in a way that leads to damaging inflammation in the small intestine? Understanding the earliest steps that bring gluten into contact with immune cells is central to understanding why celiac disease begins and how it might be prevented.

How the Researchers Studied Human Microfold Cells

To study human microfold cells directly, the team developed an intestinal organoid system. Organoids are miniature tissue structures grown in the laboratory from human cells that can mimic key features of real organs. Using carefully designed growth conditions, the researchers were able to coax intestinal cells into forming microfold cells and then follow the developmental steps that lead to that identity.

They mapped the path of differentiation by examining patterns of gene activity across the developing cells. This allowed them to reconstruct a “developmental trajectory,” meaning a step-by-step view of how a typical intestinal cell becomes a microfold cell under the influence of specific signals. They also tested how these microfold cells behave by placing them in contact with immune cells, including gluten-responsive T lymphocytes, in controlled co-culture experiments.

Key Finding One: Human Microfold Cells Act More Like Immune Cells Than Expected

A central discovery was that human microfold cells share striking similarities with dendritic cells. Dendritic cells are immune cells famous for capturing antigens and presenting them to T lymphocytes. Antigens are small pieces of proteins that the immune system uses to recognize what is foreign. The researchers found that human microfold cells do not simply move material across the intestinal lining. Instead, they appear to take on features associated with antigen presentation, a function usually reserved for specialized immune cells.

In practical terms, this suggests that microfold cells may participate directly in the process of showing dietary or microbial proteins to the immune system, rather than serving only as a delivery route to other immune cells.

Key Finding Two: Signals That Drive Microfold Cell Formation Overlap With Immune Pathways

The study also identified signals and regulatory factors that promote the formation of microfold cells in the human model. The investigators reported that microfold cell development was induced by specific immune-related signals and required particular transcription factors that guide cell identity. This matters because it supports the idea that microfold cells are positioned at the intersection of the intestinal lining and the immune system, and that their development is closely tied to immune signaling networks.

By defining these developmental requirements, the study provides a clearer blueprint for how microfold cells arise in humans, which can help researchers build improved models and test interventions that either increase or decrease microfold cell activity depending on the clinical goal.

Key Finding Three: Human Microfold Cells Can Process and Present Gluten to T Lymphocytes

The most celiac-relevant finding is that microfold cells with the human leukocyte antigen DQ2.5 genetic background were able to process gluten and present gluten-derived antigen to gluten-responsive T lymphocytes in organoid and immune-cell co-culture experiments. In celiac disease, this genetic background is strongly associated with susceptibility because it helps the immune system bind and display certain gluten fragments to T lymphocytes.

Showing that microfold cells can perform this antigen presentation step is important because it places these cells much closer to the start of the disease process than previously appreciated. Instead of gluten needing to pass through multiple handoffs before reaching the critical immune recognition step, microfold cells themselves may contribute directly to the moment when gluten becomes “visible” to the immune system in a disease-triggering form.

What This Could Mean for Understanding Celiac Disease

Celiac disease involves a misdirected immune response to gluten that damages the lining of the small intestine. Many people think of the disease as an interaction between gluten, genetics, and immune cells. This study adds a new and potentially crucial participant: a specialized epithelial cell that is part of the intestinal barrier itself.

If microfold cells can present gluten antigen to T lymphocytes, then they may act as an early gateway that helps initiate or amplify the immune cascade. This does not mean microfold cells are the only route by which gluten reaches the immune system, but it suggests that microfold cells could be one of the most efficient or influential routes in susceptible individuals.

This perspective could also help explain why certain intestinal regions rich in immune structures are hotspots for immune activation. If microfold cells in these areas are especially capable of antigen presentation, then they may help shape whether the immune system becomes tolerant of dietary proteins or shifts toward inflammation.

Limitations and Next Questions

Because much of the work was performed in laboratory-grown tissue models, it will be important to confirm how often and how strongly this microfold-cell antigen presentation occurs in living human intestines. Laboratory systems are powerful because they allow controlled experiments, but they cannot perfectly capture every feature of a person’s complex gut environment, including microbiome influences, inflammation states, and long-term immune conditioning.

Future research will likely focus on questions such as:

• How frequently microfold cells present gluten antigen in people with and without celiac disease.
• Whether microfold cells become more active or more abundant during early disease development.
• Whether blocking microfold cell antigen presentation can reduce gluten-driven immune activation.
• How microbes and intestinal inflammation alter microfold cell behavior and antigen presentation.

Why This Study Could Be Meaningful for People With Celiac Disease

For people living with celiac disease, the only current proven treatment is strict lifelong gluten avoidance, which can be difficult and socially limiting. This study is meaningful because it identifies a specific human gut cell type that may participate directly in the earliest step that connects gluten exposure to harmful immune activation.

If future research confirms that microfold cells are a key gateway for gluten antigen presentation in susceptible individuals, that could open new paths for prevention and treatment. For example, therapies might be developed to reduce gluten antigen presentation at the intestinal surface, to modify microfold cell development in high-risk individuals, or to interrupt the interaction between microfold cells and gluten-reactive T lymphocytes. Even if such approaches are years away, pinpointing where gluten first becomes an immune trigger in the human gut is a major step toward more targeted solutions beyond dietary restriction alone.

Read more at: nature.com

Watch the video version of this article:

Watch the super short video version of this article:

Celiac.com 07/16/2025 - Long before the word “gluten” became mainstream and entire grocery store aisles were devoted to gluten-free products, celiac disease was a medical mystery. For centuries, it went misunderstood and misdiagnosed, leaving patients to suffer with debilitating symptoms ranging from chronic diarrhea and weight loss to stunted growth and even death. Without a known cause, early treatments for what we now understand as celiac disease were often strange, misguided, or outright harmful.

Today, people with celiac disease or gluten sensitivity benefit from decades of medical research that culminated in the gluten-free diet—an effective, life-saving intervention. But getting to this point involved a long and bizarre journey through medical history. Let’s explore the unusual treatments that were once believed to cure or alleviate celiac disease, and what this evolution reveals about the importance of accurate diagnosis and dietary awareness.

Ancient Observations: Recognizing the Disease Before Gluten Had a Name

One of the earliest recorded descriptions of a celiac-like illness dates back to the second century, when the Greek physician Aretaeus of Cappadocia described a condition he called “koiliakos,” meaning “suffering in the bowels.” He observed patients with chronic digestive issues, malnutrition, and fatigue, and recommended a diet based on easily digestible foods—but had no idea what triggered the illness.

This vague guidance left patients at the mercy of trial and error. The word “celiac” itself is derived from the Greek koilia (abdomen), but no one at the time suspected that bread, the staple of the Mediterranean diet, was the hidden culprit.

19th Century Missteps: From Starvation to Strange Substitutes

By the 1800s, Western physicians had begun to define celiac disease as a specific type of malabsorption disorder, but treatments were still rooted in guesswork.

The "Banana Diet" and the Battle Against Carbohydrates

In the early 20th century, one popular (and bizarre) treatment was the "banana diet," introduced by American pediatrician Sidney Haas in the 1920s. Believing that carbohydrates were to blame for the symptoms, he prescribed a diet consisting almost entirely of bananas, milk, and meat. While it helped some children by coincidentally eliminating gluten-containing grains, the actual reason for improvement wasn’t understood at the time.

Other carb-restrictive regimens followed, including the potato-free, bread-free, and even sugar-free diets—none of which accurately targeted the root cause of celiac disease.

The Starvation Treatment

In some cases, doctors even prescribed a form of fasting or near-starvation, reasoning that reducing the workload on the digestive system might help it "reset." Tragically, these treatments could be more damaging than the disease itself, particularly for already-malnourished children. The irony? Bread was still commonly allowed during "light eating" phases, worsening symptoms without anyone realizing why.

The Breakthrough Years: World War II and the Accidental Discovery

The true turning point in celiac disease research came during World War II in the Netherlands. Due to wartime food shortages, bread became scarce and was replaced by alternative foods like potatoes. Dutch pediatrician Dr. Willem-Karel Dicke noticed that children suffering from celiac disease dramatically improved during the bread shortages—and relapsed when wheat was reintroduced after the war.

This serendipitous observation led to a groundbreaking revelation: it wasn’t carbohydrates in general, but a specific protein in wheat—gluten—that was the trigger. Dr. Dicke’s postwar studies cemented gluten as the key dietary cause of celiac disease, and finally gave doctors a clear path toward effective treatment.

Gluten-Free Before Gluten-Free Was Cool: The 1950s to 1980s

After gluten was identified as the cause of celiac symptoms, researchers worked to define which grains were harmful (wheat, barley, rye) and which were safe (rice, corn, later quinoa and buckwheat). The challenge, however, was that gluten was—and still is—ubiquitous in Western diets.

During the mid-20th century, “gluten-free” products were rare. Patients were often told to bake their own bread using rice flour or potato starch. There was no labeling system, and restaurants had no concept of gluten cross-contact. People with celiac disease had to become their own researchers, cooks, and advocates to manage their condition.

Still, it was a vast improvement over earlier eras. For the first time, patients could improve through a logical, evidence-based diet rather than surviving on bananas, broth, or starvation.

The Rise of the Gluten-Free Movement: 1990s to Present Day

The 1990s and early 2000s saw a surge in gluten-free awareness, due in part to better diagnostic tools (such as blood tests and intestinal biopsies) and increasing rates of diagnosis. The food industry responded by creating gluten-free products, although not always with the needs of people with celiac disease in mind.

As the gluten-free diet became trendy among celebrities and wellness influencers, it brought more options to grocery stores—but also created confusion. People with celiac disease had to distinguish between those avoiding gluten for general health reasons and those doing so out of medical necessity.

Today, while gluten-free eating is more accessible than ever, those with celiac disease must still be vigilant. Cross-contact remains a threat, and not all gluten-free labeled foods are safe unless they are certified. Still, compared to the “banana diet” and bread-based fasting of the past, the modern celiac patient has access to a wealth of tools and knowledge.

Lessons for People with Celiac Disease and Gluten Sensitivity

Looking back at the history of celiac disease treatments underscores a few key messages for those navigating gluten-free living today:

• Understanding Matters: Knowing what triggers symptoms—and why—empowers patients to make safer choices. Historical treatments failed largely due to lack of understanding.
• Beware of Trends: Not every “miracle” diet is safe or effective. From bananas to fasting, history shows the danger of unproven methods. Stick with science-backed treatments.
• Advocacy is Key: The progress made in celiac care has often been led by patients, caregivers, and researchers pushing for answers. Today’s patient community continues that tradition.
• We’ve Come a Long Way: Though managing celiac disease still requires effort, we’re fortunate to live in an era of diagnosis, understanding, and gluten-free accessibility. That wasn’t always the case.

Conclusion: From Misery to Empowerment

The journey from ancient descriptions of chronic digestive suffering to today’s medically validated gluten-free diet is a testament to the power of observation, perseverance, and science. While some past treatments for celiac disease were bizarre, dangerous, or completely misguided, each chapter of this history led closer to the truth.

For people with celiac disease or gluten sensitivity, the weird history of treatments is more than just a curiosity—it’s a reminder of how far medicine has come and why accurate diagnosis, informed eating, and continued research are so important. With greater awareness and continued innovation, the future of living gluten-free looks far brighter than its strange and painful past.

Watch the video version of this article:

Celiac.com 03/24/2025 - Celiac disease is an autoimmune condition triggered by gluten consumption in genetically predisposed individuals. While gluten exposure is a known factor in its development, other dietary components may influence risk. A study published in Gastroenterology, based on data from The Environmental Determinants of Diabetes in the Young (TEDDY) study, explores the relationship between dietary fiber intake during early childhood and the likelihood of developing celiac disease later in life.

Study Overview

The TEDDY study followed 6,520 children with genetic markers associated with celiac disease. These children were tracked over several years, with researchers analyzing their dietary habits and celiac disease outcomes. The primary focus was on fiber intake between six months and five years of age, assessing whether higher fiber consumption influenced the risk of developing the disease.

Key Findings

Higher Fiber Intake Linked to Lower Celiac Disease Risk

One of the most important findings of the study was that children who consumed more dietary fiber before the age of two had a lower risk of developing celiac disease later. This relationship remained significant even after adjusting for other dietary factors, including gluten intake.

Critical Time Window: First Two Years of Life

The study found that the protective effect of fiber was most pronounced when consumed during the first two years of life. After this period, fiber intake did not appear to have a significant impact on celiac disease risk. This suggests that early childhood is a crucial window for dietary interventions that might influence immune system development.

Possible Mechanisms

The researchers propose that fiber may influence gut microbiota composition, promoting beneficial bacteria that support gut health and immune function. A well-balanced gut microbiome may reduce inflammation and improve gut barrier integrity, potentially lowering the risk of autoimmune conditions like celiac disease.

Implications for Celiac Disease Prevention

These findings suggest that dietary fiber intake in infancy and early childhood could play a role in celiac disease prevention, especially for children with genetic susceptibility. Parents and healthcare providers may consider incorporating fiber-rich foods, such as fruits, vegetables, and whole grains (when gluten-free options are needed), into the diets of young children to support gut health.

Conclusion

This study provides new insights into the potential role of dietary fiber in reducing celiac disease risk among genetically at-risk children. While more research is needed to establish causality, the findings emphasize the importance of early nutrition in shaping long-term health outcomes. Future studies may further explore how specific types of fiber and gut microbiota interactions contribute to autoimmune disease prevention.

Read more at: gastrojournal.org

Watch the video version of this article:

Celiac.com 03/13/2025 - Proton pump inhibitors, commonly prescribed to reduce stomach acid, have become a staple treatment for conditions such as gastroesophageal reflux disease, peptic ulcers, and dyspepsia. However, the long-term effects of these medications are still being investigated, particularly in relation to their impact on the gut microbiome and immune response. A growing body of research suggests that prolonged use of proton pump inhibitors may contribute to the development of celiac disease, especially in individuals with a genetic predisposition. This review examines the relationship between proton pump inhibitor use and celiac disease, highlighting the need for further research into how these medications may influence disease progression.

Understanding Proton Pump Inhibitors and Their Effects

Proton pump inhibitors work by blocking the production of stomach acid, providing relief from acid-related digestive conditions. Since their introduction in the late 1980s, they have been widely used to manage esophageal and gastric disorders. While these medications are effective, they also alter the gut environment by reducing acid levels, which can impact the balance of bacteria in the digestive system. Changes in the gut microbiome have been linked to various gastrointestinal conditions, including celiac disease.

Genetic Risk Factors for Celiac Disease

Celiac disease is an autoimmune disorder triggered by the ingestion of gluten, leading to damage in the small intestine. The disease primarily affects individuals who carry specific genetic markers known as HLA-DQ2 and HLA-DQ8. While these genetic factors are necessary for developing celiac disease, they are not the sole cause. Environmental factors, including diet, infections, and medication use, may contribute to triggering the disease in genetically predisposed individuals.

How Proton Pump Inhibitors May Contribute to Celiac Disease Development

Recent studies have explored how proton pump inhibitors may play a role in initiating or accelerating celiac disease in those with genetic susceptibility. Because proton pump inhibitors significantly alter the stomach environment, they can disrupt the normal breakdown of proteins, including gluten. This could lead to an increased exposure of gluten peptides to the immune system, potentially triggering an inflammatory response in individuals with HLA-DQ2 or HLA-DQ8 genes. Additionally, proton pump inhibitors have been shown to affect gut bacteria, which are thought to play a role in immune regulation and intestinal health. Disruptions in the gut microbiome could further contribute to the inflammatory processes associated with celiac disease.

The Need for Personalized Medicine and Further Research

Although proton pump inhibitors are effective in managing acid-related disorders, their potential impact on celiac disease risk raises important questions about their long-term use. Individuals with genetic susceptibility to celiac disease may need to carefully evaluate the risks and benefits of prolonged proton pump inhibitor therapy. More research is needed to determine whether alternative treatments or modified use of these medications could reduce the risk of developing celiac disease.

Conclusion

The link between long-term proton pump inhibitor use and celiac disease is an emerging area of research that highlights the complex interplay between genetics, medication use, and gut health. For individuals with HLA-DQ2 or HLA-DQ8 genetic markers, extended use of these medications may pose a risk by altering the gut environment in ways that could contribute to the onset of celiac disease. This study underscores the importance of personalized medicine and the need for further investigation into safer treatment options for managing acid-related disorders without increasing the risk of autoimmune conditions like celiac disease.

Read more at: journals.lww.com

Watch the video version of this article:

Celiac.com 06/13/2024 - Clinically speaking, celiac disease is a chronic gluten-sensitive immune-mediated disorder that primarily affects the small intestinal mucosa. Celiac disease arises in individuals with the human leukocyte antigen (HLA) DQ2 and/or DQ8 alleles; after they consume gluten, such persons can experience a host of deleterious clinical symptoms, from the gastrointestinal to the neurologic.

Despite having been first identified in ancient Greece, much of what we know about celiac disease comes from the past few decades, when a dogged group of epidemiologists and researchers began tracing its millennia-old path around the globe. This presentation charts their hard work and how a once obscure but increasingly prevalent disease improbably birthed the biggest diet trend going. 

The Long Roots of Celiac Disease

Mankind's turn toward agricultural practices around 10,000 years ago provided the conditions upon which human civilization was built; it also represented a radical schism in terms of what we put in our bodies. From a hunter/gatherer diet of meat and foraged fruits and vegetables, our digestive systems suddenly had to contend with a new item on the menu: gluten. A storage protein that allows certain flowering plants to nourish their seeds, gluten is found in such grains as wheat, barley, and rye.

Although gluten-containing plants took several thousands of years to spread across the globe, from an evolutionary point of view, it occurred in the blink of an eye. This effect was compounded by the fact that the gluten content of available grain varieties has notably increased within the past 500 years, leading to theories that our immune systems were not given sufficient time to develop adaptive mechanisms to process the "new" substance.

Celiac Disease Earns a Name, and War Reveals its Triggers

The first-known description of celiac disease comes from nearly 2,000 years ago, via the Greek physician Aretaeus of Cappadocia. In discussing a patient with symptoms that included diarrhea and malabsorption, Aretaeus used the term "coeliac," from the Greek "koiliakos" or "abdominal."

A full description of celiac disease would not appear in the literature until the late 19th century, when the London-based physician Samuel Gee reported its appearance, primarily in young children aged 1-5 years who presented with chronic indigestion. Gee correctly understood celiac disease to be caused by food-related malabsorption, and recommended dietary intervention consisting of—unfortunately—toast.

The next major breakthrough would occur through a combination of serendipity and disaster. As World War II raged on, disruptions to the food supply ravaged the Netherlands, making wheat a rare commodity. The Dutch pediatrician Willem Karel Dicke observed a corresponding drop in mortality among children with celiac disease, thereby making the causative link that would jumpstart the gluten-free diet, the main therapeutic intervention to this day.

Searching for Celiac

As detailed in the book Gluten Freedom, by Alessio Fasano, MD, the global search for answers that followed Dicke's observation was launched from an erroneous assumption that this condition primarily affected children from Northern Europe. The underlying theory was that natural selection had eliminated the disease from regions where agriculture first appeared.

Beginning in the 1990s, pioneering epidemiologic work upended notions that celiac disease was not a global disease. By the end of the decade, celiac disease had been identified in countries extending from Italy to India, and has now been observed in nearly every corner of the world where gluten is consumed.

Yet even in the current day, the role that geographic region plays in celiac disease remains debated. A recent study even found the prevalence to be higher among those in northern latitudes of the United States than in their counterparts to the south. 

"It is possible that geographic and environmental differences, particularly feeding habits, may dictate the final onset and clinical presentation of celiac disease that may account for this apparent difference as reported by this study," said Dr Fasano, the W. Allan Walker Chair of Pediatric Gastroenterology and Nutrition Professor of Pediatrics at Harvard Medical School. 

The North American Puzzle

As epidemiologic researchers planted the flag of  across the globe, one region proved surprisingly impervious to their efforts. Despite having all the conditions necessary for it to occur, including an abundance of gluten-based products, celiac disease was considered exceptionally rare in North America in the early 1990s.

Dr Fasano and his colleagues set out to solve the puzzle of just why this was. At the risk of what Dr Fasano describes in his book as "professional suicide," they procured 2000 blood samples from the American Red Cross and tested them for autoantibodies to celiac disease. The investment paid off, with their findings moving the disease from the status of "rare" to one with a prevalence then believed to be closer to 1 in 250. Several years later, a greatly expanded epidemiologic study from this team indicated that the prevalence of celiac disease was as high as 1 in 133, in line with figures from Europe at that time.

With their efforts, a missing piece of the map fell into place, and celiac disease's status as a global disease was secured. 

Looking for Answers

Because celiac disease can present subclinically, with limited or even no intestinal symptoms, it can be difficult to pin down. Confounding earlier notions of the disease, celiac disease now presents more often without malabsorptive symptoms or malnutrition, and affects both underweight patients and overweight patients at approximately the same rate.

What was also once thought to be a disease diagnosed mainly among pediatric patients is now seen at a much higher rate of 9 to 1 in adults between the fourth and sixth decades of life.

Yet young patients with celiac disease still present specific concerns, with evidence suggesting that they experience psychiatric conditions at approximately 1.5 times the rate of the general population.

"This probably represents a paradigm of the gut/brain axis, with two-way crosstalk between these two organs," said Dr Fasano. "Pediatric patients who present with symptoms that include anxiety, depression, attention-deficit/hyperactivity disorder, or even autism deserve special attention, particularly in monitoring these symptoms after implementation of a gluten-free diet."

Celiac Disease Rates Continue to Rise

The conditions required for celiac disease to manifest itself are ever-thriving, supported by an increasing dietary reliance on gluten-based foods. Furthermore, the transition from hunter/gatherer society to mass-produced agriculture is not solely a vestige of history, but continues to this day among indigenous tribes, such as those of the Coast Salish First Nations population of western Canada.

Further exposure to gluten is expected in fast-growing economies such as China, where the Western diets that are currently in vogue are expected to lead to an uptick in celiac disease.

How High Can Celiac Rates Go?

If the celiac disease research community's past half-century was primarily spent getting their colleagues to accept that this was a disease with a global footprint, the coming years will probably be spent determining its full impact. It is estimated that as many as 7 out of 8 people with celiac disease have not been diagnosed.

If true, this would represent a notable unrepresented cohort for a disease that has already seen its prevalence rate surge since the 1950s.

"Previous studies from our group and others suggest a doubling of celiac disease prevalence every 15 years," said Dr Fasano. "When a long-enough surveillance of time has been performed, similar data have been reported in Europe. Indeed, no signs of a celiac disease plateau have been reported in Europe, despite good awareness around the disease and the fairly widespread adoption of the gluten-free diet as an effective medical treatment for celiac disease."

Celiac Disease Triggers a Dietary Trend

As the prevalence in the general population, and the profile of celiac disease within the medical community began to rise, so too did a strange, and probably related, phenomenon: the popularity of the gluten-free diet among the general public. Like all dietary trends before it, the origins are hard to source, although the factor that accelerated it is certainly not.

"The gluten-free diet has been indisputably fueled by its adoption by high-profile people, particularly actresses, actors, and sports champions," said Dr Fasano.

The 2015 book The Gluten Lie noted that this is not the first time that celiac disease may have birthed a dietary craze. In the 1920s, doctors in the United States recommended that their patients with celiac disease subsist on bananas and milk, thinking that special enzymes were responsible for their marked improvement. A decade later, this diet had skipped out of the clinic and into the mainstream as a fashionable means for taking off the pounds.

Gluten-Free Dietary Burden Shrinks as Options Expand

A study published in 2005 that was based on interviews with patients with celiac disease reported that their lives were substantially influenced by feelings of shame, isolation, and fear, given their limited ability to find foods that they could safely consume.

In the intervening years, the improbable rise of gluten-free diets has rendered this study a relic of the past. With upward of 5% of the population thought to now be following gluten-free diets, supermarkets and restaurants are suddenly awash in offerings for those with celiac disease, wheat allergies, or non-celiac gluten sensitivity. However, the majority of people driving this trend have no medical necessity for adopting a gluten-free diet, a fact that may carry its own health risks.

What's Next for Celiac Disease?

We may be in the grip of a gluten-free diet boom, but according to Dr Fasano, there has not been a trickle-down effect when it comes to funding for celiac research. "Funding was almost nonexistent 15 years ago, and it remains extremely low to date," he said. "Nevertheless, the interest of the research community into celiac disease as a model of autoimmunity has indisputably increased." He added that researchers are now looking at , and in particular its key genetic component (HLA DQ2/DQ8) and environmental trigger (gluten), as a means for understanding other chronic inflammatory diseases. Dr Fasano and his colleagues are currently conducting the prospective Celiac Disease Genomic Environmental Microbiome and Metabolomic Study. 

Time will tell what its findings may add to our understanding of this ever-evolving disease that's been many thousands of years in the making. 

Read more at: medscape.com

Celiac.com 10/30/2023 - A recent study has shed light on the intriguing link between zonulin, a protein responsible for regulating the permeability of the intestines, and the risk of celiac disease in children. Not only does this research suggest that zonulin could be a potential biomarker for identifying preclinical celiac disease, but it also reveals a fascinating connection between antibiotic use and the likelihood of developing celiac disease.

This study's findings, presented at the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN) 2023 Annual Meeting, indicate that elevated levels of zonulin in infants and toddlers are associated with a higher chance of being diagnosed with celiac disease.

Led by Dr. Maureen Leonard, Clinical Director of the Center for Celiac Research & Treatment at MassGeneral Hospital for Children, the research team uncovered a significant correlation between antibiotic courses and increased zonulin levels. This intriguing connection implies that multiple courses of antibiotics might elevate the risk of celiac disease in children who are already predisposed to it.

In an interview with HCPLive at the NASPGHAN 2023 conference, Dr. Leonard discussed the study's significance and how it contributes to our understanding of the triggers behind celiac disease.

Celiac disease is an autoimmune disorder triggered by the consumption of gluten, a protein found in wheat, rye, and barley. It affects approximately 1% of the population and can lead to various health problems if left untreated. One of the mysteries surrounding celiac disease is that while about 40% of the population carries the genetic markers that make them susceptible to the condition, only 2-3% of these individuals actually develop the disease. This leaves scientists searching for other factors that contribute to its onset.

Antibiotic Courses in Young Children Boost Zonulin Levels

Dr. Leonard's research reveals an exciting piece of the puzzle. The study suggests that zonulin, the protein responsible for controlling intestinal permeability, plays a crucial role. Increased levels of zonulin were found to be linked to a higher risk of celiac disease diagnosis in infants and toddlers. Moreover, the more antibiotic courses these young children were exposed to, the greater the increase in zonulin levels.

However, Dr. Leonard emphasizes that antibiotics are essential and sometimes life-saving medications. The key is to use them judiciously, especially in children at risk of developing celiac disease. This research underscores the importance of cautious antibiotic use in pediatric patients who may already have genetic factors predisposing them to celiac disease.

High Zonulin Levels May Trigger Celiac Disease

While this study is a significant step forward in our understanding of celiac disease, further research is needed to uncover all the triggers behind this complex condition. The connection between zonulin, antibiotics, and celiac disease risk adds a new dimension to the ongoing quest to solve the celiac disease puzzle and improve our ability to diagnose and treat this autoimmune disorder in children.

Zonulin's role as a potential biomarker for celiac disease, and its connection to antibiotics offer promising avenues for future research, and may ultimately contribute to better management of celiac disease risk in children.

Learn more at the Conference|North American Society For Pediatric Gastroenterology, Hepatology & Nutrition

Celiac.com 05/09/2022 - Data from gene expression, lipidomic and growth impairment indicate that celiac disease begins long before the body starts to have an immune response to gluten. The influence of gluten intake in the first years of life as a potential risk factor for celiac disease is currently debated among researchers. 

A team of researchers recently set out to estimate the risk of developing celiac disease based on the amount of gluten intake and the serum inflammatory profile in genetically predisposed infants. The research team included Auricchio Renata, Calabrese Ilaria, Galatola Martina, Cielo Donatella, Carbone Fortunata, Mancuso Marianna, Matarese Giuseppe, Troncone Riccardo, Auricchio Salvatore & Greco Luigi 

They are variously affiliated with the Department of Translational Medical Science, University Federico II, Via S. Pansini 5, 80131, Naples, Italy; the European Laboratory for Food Induced Diseases, University Federico II, Via S. Pansini 5, 80131, Naples, Italy; the Department of Clinical Medicine and Surgery, University Federico II, Naples, Italy; the Laboratory of Immunology, Institute for Experimental Endocrinology and Oncology, National Research Council (IEOS-CNR), Naples, Italy; the Neuroimmunology Unit, IRCCS Fondazione Santa Lucia, Rome, Italy; and the the Department of Molecular Medicine and Medical Biotechnology, University Federico II, Naples, Italy.

The team evaluated an Italian cohort of children at risk for celiac disease, and enrolled twenty-seven children who developed celiac disease, along with fifty-six control subjects, matched by sex and age. The team also conducted a dietary interview at 9, 12, 18, 24 and 36 month intervals. They assessed serum levels of cytokines INFγ, IL1β, IL2, IL4, IL6, IL10 IL12p70, IL17, and TNFα, at four and thirty-six months. 

They found that infants who went on to develop celiac disease by six years of age showed increased serum cytokine levels at four months of age before gluten introduction. Elevated cytokines included INFγ, IL1β, IL2, IL6, IL10, IL12p70 and TNFα.

Children who later developed celiac disease consumed substantially more gluten in their second year of life than the controls.  For those children, gluten intake in the second year of life was strongly correlated with serum cytokines INFγ, IL2, IL4, IL12p70, IL17 at thirty-six months. 

The dietary pattern of infants who developed celiac disease was marked by high consumption of biscuits and fruit juices and low intake of milk products, legumes, vegetables and fruits, which may invite questions about pre-celiac gut microbiota health in these subjects.

The researchers found that genetically predisposed infants who developed celiac disease showed a unique serum cytokine profile at 4 months before gluten consumption. In these children, gluten intake was strongly correlated with an inflammatory profile in serum cytokines at thirty-six months.

This is one of the first studies to demonstrate such a clear relationship between cytokine profiles and infant gluten intake in advance of the development of celiac disease. Further study could help to develop preventative screening that 

Read more in Scientific Reports volume 12, Article number: 5396 (2022)
 

Celiac.com 08/02/2021 - Researchers currently know very little about the causative molecular pathways underlying the development of celiac disease. A team of researchers recently set out to discover new aspects of celiac disease formation and development. To uncover new aspects of disease development, their team used microarrays to measure changes in gene expression of duodenal biopsies.

The team used cDNA microarrays representing 19,200 genes to compare gene expression profiles of duodenal biopsies from 15 celiac disease patients with Marsh III villous atrophy, along with seven control subjects with normal biopsies (Marsh 0). They also looked at the specific effect of gluten by comparing the expression profiles of Marsh III lesions of seven patients exposed to gluten with four patients on a gluten free diet.

The lesions of Marsh III celiacs versus Marsh 0 control subjects showed that expression levels of 109 genes differed substantially between the two groups.

Many of these genes play roles in proliferation and differentiation pathways, and could be important for proper gut villi development. Changes in these pathways could result in the classic hyperplasia and villous atrophy seen in celiac disease. 

The team's comparison patients on a gluten-free diet with those exposed to gluten showed another 120 differentially expressed genes, which could strengthen their observation of increased cell proliferation in the presence of gluten.

The team's findings indicate the role of new candidate genes in the development of celiac disease. Based on their results, they hypothesize that villous atrophy in celiac disease patients arises when cells fail to differentiate properly. 

The new candidate genes are involved in pathways not previously implicated in celiac disease development and they may be strong targets for new celiac treatments and therapies. These findings could open new doors for better understanding celiac disease, and lead to new approaches to the study, diagnosis, and treatment of this chronic inflammatory condition.

Read more in Gut. 2004 Jul; 53(7): 944–951.

The research team included Diosdado, M C Wapenaar, L Franke, K J Duran, M J Goerres, M Hadithi, J B A Crusius, J W R Meijer, D J Duggan, C J J Mulder, F C P Holstege, and C Wijmenga. They are variously affiliated with the Complex Genetics Group, Department of Biomedical Genetics, University Medical Centre, Utrecht, the Netherlands; the Complex Genetics Group, and Genomics Laboratory, Department of Biomedical Genetics, University Medical Centre, Utrecht, the Netherlands; the Department of Gastroenterology and Hepatology, Rijnstate Hospital, Arnhem, the Netherlands; the Department of Gastroenterology, Free University Medical Centre, Amsterdam, the Netherlands; the Laboratory of Gastrointestinal Immunogenetics, Free University Medical Centre, Amsterdam, the Netherlands; the Department of Pathology, Rijnstate Hospital, Arnhem, the Netherlands; the National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, MD, USA; and the Genomics Laboratory, Department of Physiological Chemistry, University Medical Centre, Utrecht, the Netherlands.

Celiac.com 07/26/2021 - Cases of chronic inflammatory autoimmune conditions, such as celiac disease are rising at a rate that concerns many researchers. 

To better understand the etiology and pathogenesis of celiac disease, especially the role of environmental stimuli, and gut microbiota in connection with the immune system, a team of researchers recently conducted a study, in which they did both cross-sectional and longitudinal analysis of gut microbiota, functional pathways, and metabolites, starting from 18 months before celiac disease onset in 10 infants who developed celiac, compared with 10 infants who did not. 

The research team included Maureen M. Leonard, Francesco Valitutti, Hiren Karathia, Meritxell Pujolassos, Victoria Kenyon, Brian Fanelli, Jacopo Troisi, Poorani Subramanian, Stephanie Camhi, Angelo Colucci, Gloria Serena, Salvatore Cucchiara, Chiara Maria Trovato, Basilio Malamisura, Ruggiero Francavilla, Luca Elli, Nur A. Hasan, Ali R. Zomorrodi, Rita Colwell, Alessio Fasano, and The celiac disease-GEMM Team.

Cross-sectional analysis at celiac onset showed altered levels of six microbial strains and several metabolites between cases and control subjects, but no change in microbial species or pathway levels. 

Meanwhile, longitudinal analysis showed increased levels of several microbial species/strains/pathways/metabolites before celiac onset. These had previously been linked to autoimmune and inflammatory conditions, such as Dialister invisus, Parabacteroides sp., Lachnospiraceae, tryptophan metabolism, and metabolites serine and threonine. Others, found in reduced levels before celiac onset, are known to have anti-inflammatory effects, such as Streptococcus thermophilus, Faecalibacterium prausnitzii, and Clostridium clostridioforme. 

They also found previously unreported microbes/pathways/metabolites, including Porphyromonas sp., high mannose–type N-glycan biosynthesis, and serine, that point to celiac-specific biomarkers. 

The team found clear changes in the gut microbiota, functional pathways, and molecular biochemistry before the start of celiac disease. This finding indicates that this information could be used to improve celiac disease prediction. 

The researchers hope that by identifying the early warning signs of celiac disease, they may be able to eventually provide preventive interventions to reestablish tolerance and prevent autoimmune disfunction.

Read more in PNAS July 20, 2021 118 (29) e2020322118

The researchers are variously affiliated with the Division of Pediatric Gastroenterology and Nutrition, MassGeneral Hospital for Children, Harvard Medical School, Boston, MA; the Mucosal Immunology and Biology Research Center, MassGeneral Hospital for Children, Harvard Medical School, Boston, MA; the Celiac Research Program, Harvard Medical School, Boston, MA; the European Biomedical Research Institute of Salerno, Salerno, Italy; the Pediatric Unit, Maternal and Child Health Department, Azienda Ospedaliera Universitaria San Giovanni di Dio e Ruggi d’Aragona, 84125 Salerno, Italy; the Cosmos ID Inc., Rockville, MD; the Theoreo srl, University of Salerno, Salerno, Italy; the Department of Medicine, Surgery and Dentistry, Scuola Medica Salernitana, University of Salerno, Salerno, Italy; the Pediatric Gastroenterology, Sapienza University of Rome, Rome, Italy; the Pediatric Unit, Maternal and Child Health Department, Azienda Ospedaliera Universitaria San Giovanni di Dio e Ruggi d’Aragona, Salerno, Italy; the Pediatric Gastroenterology, University of Bari, Bari, Italy;
lCenter for Prevention and Diagnosis of Celiac Disease, Fondazione Department and University Hospital (IRCCS) Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy; and the Center for Bioinformatics and Computational Biology, University of Maryland, College Park, MD.

Celiac.com 11/30/2020 - Despite some good data on childhood antibiotic exposure, researchers still don't know much about the possible connections between antibiotic exposure in the first two years of life, and the risk of childhood immunological, metabolic, and neurobehavioral health conditions. A team of researchers recently set out to see what they could learn about potential connections between antibiotic exposure in the first two years of life, and the risk of childhood immunological, metabolic, and neurobehavioral health conditions.

The research team included Zaira Aversa, MD, PhD; Elizabeth J. Atkinson, MS; Marissa J. Schafer, PhD; Regan N. Theiler, MD, PhD; Walter A. Rocca, MD; Martin J. Blaser, MD, and Nathan K. LeBrasseur, PhD. They are variously affiliated with the Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN; the Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, MN; the Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN; the Department of Obstetrics and Gynecology, Mayo Clinic, Rochester, MN; the Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, MN; and the Department of Neurology, Mayo Clinic, Rochester, MN; and the Center for Advanced Biotechnology and Medicine, Rutgers University, Piscataway, NJ.

For their population-based study, the team used the Rochester Epidemiology Project medical records-linkage system to look at data from all children born in Olmsted County, Minnesota, between January 1, 2003, and December 31, 2011. They used the Rochester Epidemiology Project infrastructure to note demographic characteristics, antibiotic prescriptions, and diagnostic codes through June 30, 2017. They analyzed time-to-event to determine the influence of antibiotic exposure on the risk of numerous health problems.

This study included 14,572 children, just over half of whom were boys. About 70% of the children had received at least 1 antibiotic prescription during the first 2 years of life. The team found that early antibiotic exposure was tied to an increased risk of childhood-onset asthma, allergic rhinitis, atopic dermatitis, celiac disease, overweight, obesity, and attention deficit hyperactivity disorder. The number, type, and timing of antibiotic exposure all influenced the connections. 

Moreover, children exposed to antibiotics had a higher odds of developing multiple conditions, especially if they had received multiple prescriptions. The team's data points out strong associations between early life antibiotic exposure and several childhood health disorders. 

The team calls for additional research to create practical guidelines for maximizing the benefits and minimizing the risk of antibiotics exposure in children.

Read more at the Mayo Clinic Proceedings