In 1994 I was diagnosed with celiac disease, which led me to create Celiac.com in 1995. I created this site for a single purpose: To help as many people as possible with celiac disease get diagnosed so they can begin to live happy, healthy gluten-free lives. Celiac.com was the first site on the Internet dedicated solely to celiac disease, and since then it has become an invaluable resource to people worldwide who seek information about celiac disease and the gluten-free diet.
In 1998 I created The Gluten-Free Mall, Your Special Diet Superstore! which was also another Internet first—it was the first gluten-free food site to offer a shopping cart-style interface, and the ability for people to order gluten-free products manufactured by many different companies at a single Web site.
I am also co-author of the book Cereal Killers, and founder and publisher of Journal of Gluten Sensitivity.
Am J Med 2004;116:312-317.
Italian researchers have concluded that as many as 73% of patients with untreated celiac disease have at least one brain region that is hypoperfused (the blood vessels are damaged), although the condition is rare in the non-celiac and treated celiac disease populations. Dr. Giovanni Addolorato, from the Catholic University in Rome, and colleagues looked at 15 untreated and 15 treated (on gluten-free diets) celiac disease patients and compared them with 27 healthy controls. They found that 11 (73%) of the untreated celiac disease patients exhibited hypoperfusion in at least one cerebral region, when only one treated patient and no controls had the problem. Additionally they found that in 7 of the 26 brain regions that they looked at, blood flow was significantly lower in untreated patients than in controls, and no blood flow differences were detected between the treated group and the control group.
According to the researchers the cause of the vascular brain damage in celiac disease is unclear at this point, but it may be related to the increased intestinal blood flow, and/or endothelial inflammation caused by the autoimmune disease, perhaps involving antigliadin antibodies or unidentified neurotoxic antibodies.