A fascinating read, seems to explain some complicated science in terms goofs like me can understand.
harvardmagazine.com/2019/05...
Excerpts:
. . . tests seeking to clarify what effect the same anti-inflammatory drug, canakinumab, might have on illnesses seemingly unrelated to cardiovascular disease: arthritis, gout, and cancer.
. . . canakinumab, an orphan drug that blocks a specific pro-inflammatory pathway called IL-1beta.
THE 2017 clinical trial, called CANTOS (Canakinumab Anti-Inflammatory Thrombosis Outcomes Study), is the result of a long-term collaboration between Paul Ridker and Peter Libby, who suspected as long ago as the 1980s that inflammation played a role in cardiovascular disease. Ridker, an epidemiologist who is Braunwald professor of medicine, came to this conclusion through studies of cardiac patients. He is the physician-scientist who first demonstrated that a molecule called C-reactive protein (CRP), easily measured by a simple and now ubiquitous blood test, could be used like a thermometer to take the temperature of a patient’s inflammation. Elevated CRP, he discovered years ago, predicts future cardiovascular events, including heart attacks. Although nobody knows what it does biologically, this marker is downstream from IL-1beta, and thus provides a reliable yardstick of that pro-inflammatory pathway’s level of activation.
. . . another possibility that doesn’t include any risk of immunosuppression: resolving inflammation through a recently discovered class of molecules called specialized pro-resolving mediators.
In work published as this magazine went to press, Serhan and colleagues showed that aspirin stimulates the production of a distinct type of SPM that fights cancer tumors in mice, and another SPM that inhibits cancer tumor formation in the first place.
Because these compounds have not yet been synthesized as pharmaceuticals, maintaining healthy levels of SPMs is best supported by foods rich in the essential fatty acids EPA, DHA, and arachidonic acid.
“To treat excessive inflammation, whether it is chronic or the result of an acute tissue injury, we don’t want to block the inflammatory response. We want to stimulate the resolution pathways.”
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