COPD Foundation Announces ‘JW Walsh Fund to Cure COPD’
The memorial fund was created as a way to honor Walsh’s commitment to the foundation and to find a cure for chronic obstructive pulmonary disease (COPD) after he, his mother, his sister, and his twin brother were afflicted by this lung condition.
John Walsh had an impact in the design and execution of research studies, in how the industry views the patient’s voice, and even changed the way patients are integrated into medical education.
The COPD Foundation is committed to continuing Walsh’s passion to engage, educate, and empower patients.
Walsh’s memory received the rare honor of an obituary published in The New York Times.
John Waldo Walsh IV was born on Feb. 4, 1949, in Arlington, Massachusetts. He majored in political science at Norwich University in Northfield, Vermont, and left right after to become a staff assistant for the U.S. Senate. He also joined the Army Special Forces Reserve and served as an Army Ranger.
“As an advocate, as a friend, and as a visionary he was simply indefatigable,” Craig Kephart, CEO of the COPD Foundation, said in a press release. “I can think of no better way to honor him and this fund will carry on his legacy.”
Walsh was known to be an “impatient patient” in the sense that he had an unstoppable drive to change things for COPD patients. In 2004, he founded the COPD Foundation and the programs developed under his supervision were far-reaching and patient-centered.
“John’s real legacy is the spark he created in all of us. He led us by example,” said Grace Anne Dorney Koppel, president of the COPD Foundation.
All donations in his memory should be made to the JW Walsh Fund, at his family’s request. The fund will be administered by the COPD Foundation.
Walsh also had alpha-1 antitrypsin (AAT) deficiency, a genetic disorder in which the body does not make enough of a protein that protects the lungs and liver from damage. In rare cases, AAT can cause COPD.
AAT is a protein produced in the liver that protects the lungs, but the disorder changes its shape and the protein cannot leave the liver cells to reach the lungs. Without this protein, white blood cells can damage the lungs and people become at higher risk for emphysema. People with asthma may also develop COPD if they have this genetic condition.