A paradox that rewrote the playbook
In the 1970s, Danish physicians Jørn Dyerberg and Hans Olaf Bang traveled to Greenland to investigate an epidemiologic puzzle: middle-aged Greenland Inuit were suffering far fewer heart attacks than Danes of similar age and sex. On paper, that shouldn’t have been true. Their traditional diet was rich in fat and cholesterol and short on fruit, vegetables, and fiber—the opposite of the prevailing “heart-healthy” advice of the day. Something wasn’t adding up.
When standard risk factors didn’t explain the difference
The first pass looked familiar: measure cholesterol profiles and triglycerides. Those numbers, however, didn’t diverge enough between Inuit and Danes to solve the mystery. The real signal appeared when the researchers analyzed plasma fatty acids. Inuit living traditionally in Greenland carried strikingly higher levels of the long-chain omega-3s—EPA and DHA—than Inuit who had moved to Denmark and adopted a Danish diet. EPA was roughly seven times higher and DHA about four times higher in the Greenland group. That biochemical imprint begged two questions: where were these fats coming from, and what were they doing?
From the sea to the bloodstream
Diet diaries supplied the source. Coastal Inuit were eating seal, fish, and whale regularly, pushing daily intakes of EPA to roughly two to two-and-a-half grams and DHA to about two grams—on the order of four to five grams of EPA+DHA per day. Danes, by contrast, were consuming well under one gram combined. The diet–blood connection was clear: eat marine foods, raise circulating EPA and DHA. But the protective mechanism was still speculative.
The platelet clue: why EPA calms clots
Attention turned to platelets, the tiny blood cells that plug cuts—and, when over-activated, can form clots inside coronary arteries. At the time, heart attacks were understood largely as the endpoint of a plaque rupture followed by platelet-driven thrombosis. Biochemistry offered a neat twist: arachidonic acid (AA), an omega-6 fatty acid, is converted in platelets to thromboxane A₂, a potent pro-aggregator. EPA, nearly identical in structure but with one extra double bond, yields thromboxane A₃, which is far less aggregatory. In other words, more EPA and less AA shifts the chemical balance away from clotting.
In classic lab experiments, Dyerberg and Bang suspended platelets in solution and tracked how quickly the cloudy mixture cleared as the cells clumped. Adding AA ramped up aggregation; adding EPA did not. When they triggered aggregation with ADP, AA amplified the response, while EPA blunted it. Parallel pathways in the vessel wall—prostacyclin “series” made from AA versus EPA—pointed in the same direction: the EPA-derived mediators were less pro-thrombotic overall. The implication was elegant and practical. Enrich platelet membranes with EPA, and you make spontaneous, artery-plugging clots less likely.
A hypothesis goes public—and holds up
In 1978, the team distilled these insights into a Lancet paper proposing that marine-derived EPA reduces the risk of thrombosis and atherosclerosis by modulating platelet biology. The idea fit the Greenland observations and, over the ensuing decades, won support from basic science, clinical physiology, and outcomes studies. Other mechanisms have since joined the story—anti-inflammatory signaling, stabilization of cardiac electrophysiology, improved endothelial function—but the “platelet pivot” was the spark that lit a vast research program.
The legacy of the Greenland clue
Those first expeditions helped launch one of nutrition science’s most productive chapters. Today, omega-3 fatty acids are among the most intensely studied nutrients, with a literature base rivaling that of marquee cardiovascular drugs. It all traces back to a paradox on Arctic shores—and to the careful work that connected a seafood-rich diet to blood chemistry, platelet behavior, and, ultimately, protection for the heart.
