Copper-carrying proteins disarm oxygen radicals and power electron transport. Humans with copper deficiency have increased cholesterol levels, clot formation, oxidative tissue damage, and heart disease. Cardiac tissue biopsies of heart attack victims show a great reduction in copper levels.

In mice with stress-induced heart disease, the team now shows, increased heart size and decreased heart function can both be restored to normal levels by a small increase in the daily intake of copper, even when the stress stimulus is maintained. But without the copper supplement, stressed mice suffer heart failure after two months.

The authors show that mice receiving dietary copper supplements have increased activity of a transcription factor called HIF-1, leading to increased production of the vascular endothelial growth factor (VEGF) protein, which promotes angiogenesis. Blocking VEGF activity inhibits the ability of copper to reverse heart enlargement and dysfunction. It is not clear, however, how angiogenesis helps decrease muscle mass or how copper gets pushed out of the heart during stress.

The human equivalent of the beneficial dose of copper used in this study is 3.0 mg/day. The current recommended daily intake for humans, however, is only 0.9 mg/day. Increasing copper intake may be a cheap way to reduce mortality associated with heart disease.