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My wife, Judith, and I left Brisbane after my second year of residency in 1964, bound for England where I experienced the National Health System firsthand while I got my membership of Royal College of Physicians London in 1967. In 1968, we took "the road less travelled by" to Iowa where I did a fellowship in gastroenterology and was introduced to academic medicine.
In 1970, we returned to Australia where I became a research and NHMRC fellow at the A.W. Morrow Gastroenterology Department, Royal Prince Alfred Hospital, and a lecturer at University of Sydney. While there, I got my MD degree (University of Queensland) in 1971 and my membership of the Royal Australian College of Physicians, MRCP 1975 (FRACP 1978).
In 1975, we returned to America and I accepted an associate professorship of medicine at the University of Missouri and the Harry S. Truman Memorial Veteran's Hospital. It was here that I did significant clinical medical research using the newly developed flexible optical gastroscope. We demonstrated by gastroscope that aspirin was a major cause of gastric mucosal damage and peptic ulcers in human volunteers and patients. These studies added to the significant work other Australian gastroenterologists had done on the role of aspirin in causing peptic ulceration and gastrointestinal bleeding, but their work had always been denied by the aspirin/big pharma lobby.
Morton Grossman, chairman & professor of physiology at UCLA — then the most prominent gastric physiologist in the US and world — told me that my work proved to him that gastric damage was indeed a local effect of aspirin and not a systemic effect (as it was in rats). In my MD thesis I showed the mechanism by which aspirin damages gastric mucosa. The stomach is able to digest a big steak with its acid secretion; the gastric mucosa is protected. However, if one ingests aspirin – acetyl salicylic acid – before eating said steak, the gastric mucosa loses its protective barrier and starts to digest itself. My research observed this process with the gastroscope: within an hour after administering two aspirin tablets, we saw visible bleeding in the gastric lining. Over a few hours these developed into erosions - visible breaks in the stomach lining, In patients taking aspirin over longer periods these erosions eventually formed into deeper lesions- aka a peptic ulcer. Our research further showed that if one neutralized the acid in acetyl salicylic acid by giving the aspirin as Alka Seltzer, no gastric damage occurred. Similarly, if we gave the aspirin as an enteric coated aspirin so it is not absorbed in the stomach, little gastric damage occurred. We demonstrated that chronic peptic ulcers in patients who continued taking aspirin daily were healed by drugs inhibiting gastric acid secretion.
When I was in medical school, peptic ulcer was a very common chronic disease; sometimes the only cure was a drastic one - devastating gastric surgery. There were two basic causes of peptic ulcers: the first, a bacterium called Helicobacter pylori, was discovered to cause peptic ulceration mainly in the duodenum just beyond the stomach. The second, where my research was focused, was aspirin, which caused more ulcers in the stomach itself. As a result of my research and that of other GI scientists including Australian Nobel Prize winner Barry Marshall, these two causes were eliminated and so too was chronic peptic ulceration. Few have the satisfaction of seeing the disease they researched eliminated in their lifetime but I had that privilege.
In 1980, I became a professor of medicine at the University of California. We settled in Orange County, a climate and style of living that reminded us of Australia and raised our family of four children and eight grandchildren. Having achieved my major goals in academic medicine, I retired in the first decade of this century and substituted my goal of publishing 100 original manuscripts to bike riding 100km when I turn 100 years of age.