The condition was called celiac disease, and a young doctor by the name of Sidney Haas revolutionized its treatment with the introduction of his “banana diet.” Dr. Haas noticed that a diet, based almost entirely in consumption of bananas, enlivened his young patients and ultimately resolved their gastrointestinal complaints. He published his finding in a medical journal in 1924 entitled “The Value of the Banana in the Treatment of Celiac Disease,” stating that bananas were the “cure” for celiac disease.
Though gluten was later established as the causative agent of disease, and bananas disproven as the cure, Dr. Haas and his so-called “banana babies” made history for celiac disease. Soon the “celiac world,” as we know it, will experience another historic and frame-shift-altering landmark in our conceptualization of how we identify, predict and prevent celiac disease. Like Dr. Haas and his “banana babies,” this landmark will also stem from evidence collected from our youngest researchers – infants – and will come in the form of our CDGEMM babies.
Now we’re uncovering hidden GEMMs to help us...
Our microbiome – the trillions of microbes that naturally reside in our intestines - has recently emerged as an important agent of maintaining the balance between health and disease. These intestinal, or gut, microbes help us to break down or digest foods and even create important vitamins that our bodies need. Recent scientific evidence also suggests that these gut microbes and our immune system develop hand-in-hand, reciprocally influencing one another. Much of the development of our microbiome takes place during the early stages of life. When a person reaches 3 years of age, the microbial communities within the gut stabilize and reflect what researchers now recognize as an “adult-like” pattern. Despite this stabilization, food and medications can cause subtle alternations to our microbiome at any age, including “who” of our gut bacteria are there and how many of them.
We are hopeful that the secret to understanding why certain individuals develop celiac disease will stem from an in-depth look at the microbial communities and patterns present in the gut. Thus, while a major aim of the study is to further validate the early microbial signature of celiac disease, another important component of the study involves children who, based on their genetic make-up, will never develop CD. Prediction of who will develop CD will only prove valuable if we understand how to intervene and ultimately prevent the clinical onset of disease. Thus, the study also aims to identify a specific microbial signature, in children lacking the necessary predisposing genes, that is “protective” against developing CD. If such a signature is identified, it may be possible to administer therapeutic agents to at-risk children in the future to mold their “celiac-bound” microbiome into one that is “celiac-protective.”
We are hopeful that the future standard of care for celiac disease will involve screening for the “pre-celiac” microbial signatures and administering treatments to help children achieve a healthier distribution of microbes. The newly introduced microbes would alter the host intestines, re-colonizing the gut in a fashion that is incompatible with the development of celiac disease. Through use of stool samples collected from CDGEMM participants, our research team aims to apply these principles to the identification and ultimate prevention of celiac disease, paving the way for the future of personalized prevention of celiac disease.