Bryan Johnson Was Diagnosed With Autoimmune Gastritis, a Disease in Which the Immune System Attacks the Stomach

Bryan Johnson Was Diagnosed With Autoimmune Gastritis, a Disease in Which the Immune System Attacks the Stomach

On July 15, Andrew Steele, author of a book on aging, reviewed Johnson's public medical history. His ferritin, a marker of the body's iron stores, had remained low for eleven years. A new medical team linked this finding to his autoimmune thyroid disease, examined his intestines and stomach, and confirmed autoimmune gastritis through biopsies.

In his account, Johnson describes how his low ferritin was attributed to his plant-based diet, exercise, sauna use, and oxygen treatments. He tried iron-rich foods and supplements, but his iron stores did not recover. His hemoglobin remained normal, so he did not have anemia.

“People continued to explain the low ferritin without correcting it,” Johnson wrote about the preceding years.

The new diagnostic workup began after Johnson changed doctors. At age 48, he underwent his first colonoscopy. The US preventive recommendation advises this screening for people at average risk starting at age 45. The colonoscopy ruled out occult blood loss from the intestines. His doctors then considered his longstanding autoimmune thyroid disease together with his persistent iron deficiency, tested for antibodies against stomach cells, and collected five biopsies.

The biopsies showed autoimmune gastritis. In this disease, the immune system damages the stomach lining that produces acid and supports iron absorption. At an early stage, the disease may cause no visible abnormalities during an examination. The American Gastroenterological Association specifically recommends considering atrophic gastritis in patients with unexplained iron deficiency and confirming the diagnosis through histology, which examines tissue under a microscope.

In his analysis, Steele places two facts from Johnson's account side by side: the Immortals Care protocol, which costs one million dollars per year, and the years during which clinicians explained his low ferritin without investigating its cause. Sensors collect numbers. A diagnostic hypothesis connects those numbers to a cause and a test.

On June 30, Steele compared personal protocols with a 45–70 million dollar trial of metformin. A project of that kind seeks a general answer to whether an inexpensive intervention works in humans. Johnson's case adds a clinical sequence to this calculation: first identify the cause of the disease, then test the treatment.

Johnson now wants to move beyond observation. His plan begins with monitoring and supportive care, then progresses to interventions targeting immune signals and regulatory T-cells, which normally restrain immune attacks. In the longer term, he is considering CAR/CAAR-T, a strategy involving modified T-cells designed to target the immune cells that attack a specific tissue. He also discusses AI-designed antibodies and synthetic proteins. Johnson describes these stages as experimental because some of the approaches still need to be developed specifically for autoimmune gastritis.

If one patient improves after receiving a complex combination of interventions, the contribution of each intervention remains unknown. The natural course of the disease and the role of standard supportive care also remain unknown. A trial with a comparable group of patients can distinguish an effective method from a favorable coincidence.