It is well known that in the long run, eating fatty foods is bad for you and can increase your risk of having a stroke or heart attack, but as per a new study, a high-fat diet may actually be beneficial to your health and help to reduce heart attack damage.

W. Keith Jones of Loyola University Chicago Stritch School of Medicine said that the study improves the understanding of the relationship between diet and health, adding learning about how fat, in the short run, protects against heart attacks could help in the development of better therapies

The study, which is not a license to eat a lot of cheeseburgers and ice cream, may provide new insight into the “obesity paradox”: Obesity is a major risk factor for heart disease, but once a heart attack or heart failure does occur, moderately obese patients tend to live longer.

In the study, mice were given a high-fat diet (60 percent of calories from animal fat) before experiencing heart attacks. Mice that consumed a high-fat diet for either one day, one week or two weeks before the heart attack experienced about half as much heart damage as mice that ate a control diet. The benefit was greatest among mice that ate a high-fat diet for one week before the heart attack.

But in mice that ate a high-fat diet for six weeks, the protective effect disappeared. Further research is needed to understand why this is so; the reason may be due to the bad effects of a persistent high-fat diet, said Jones.

Proteins damaged by the heart attack are removed from heart cells as if they were garbage, thus increasing the chances the cells will survive. Acutely, a high-fat diet increases levels of a molecule in the blood that activates protective pathways in heart muscle. This increases the readiness of the “garbage trucks,” which means that the cell becomes resistant to damage when the heart attack occurs as a result, more heart muscle survives.

First author Lauren Haar added that the study opens a new perspective on the acute effects of a high-fat diet and future work will determine whether these effects are linked to the obesity paradox and whether studying the mechanism can identify therapeutic targets for cardioprotection.

The study appears in the American Journal of Physiology – Heart and Circulatory Physiology.