Allergies and Me: 02. Around 1983

I graduated from Kumamoto University in 1983 and joined the Department of Otorhinolaryngology at the university. As the department was actively engaged in allergy research, I conducted studies on allergies using laboratory animals—such as mice—during my residency. Allergy research was flourishing nationwide at the time, and I recall that this was a global trend as well. In Kumamoto, that period marked the beginning of a rise in the number of people developing Japanese cedar pollinosis. Furthermore, allergies were believed to be hereditary; it was thought that once the PCR method—introduced in 1985—became widespread and the entire human genome was mapped, the specific genes responsible for allergies would be identified. However, I also found myself wondering: if allergies are hereditary, why was the number of people suffering from cedar pollinosis increasing?

At that time, the only available treatments for allergic rhinitis were antihistamines (which had short-lasting effects and caused drowsiness), steroids, and steroid or anti-allergic nasal sprays; immunotherapy—then known as desensitization therapy—was also widely practiced. Subsequently, improved medications offering longer-lasting effects and reduced drowsiness appeared, yet there were still no drugs effective against nasal congestion.

There is a class of anti-allergic drugs known as leukotriene receptor antagonists. Leukotrienes are a type of chemical mediator, and they share the same precursor substance as prostaglandins. In 1982, the scientists who discovered and conducted research on prostaglandins were awarded the Nobel Prize. I believe that research related to these chemical mediators was the focal point of allergy studies during that era. I was invited to join the field of allergy research myself, but at the time, I lacked interest in the subject and did not pursue a career in that area of ​​research.