The benefits of corn oil keep rolling in. In a new study by Stephen Freedland's group at Duke, feeding mice a diet rich in butter and lard didn't promote the growth of transplanted human prostate cancer cells any more than a low-fat diet (1).
Why do we care? Because other studies, including one from the same investigators, show that corn oil and other industrial seed oils strongly promote prostate cancer cell growth and increase mortality in similar models (2, 3).
From the discussion section:
I do have one gripe with the study. They refer to the diet as "saturated fat based". That's inaccurate terminology. I see it constantly in the diet-health literature. If it were coconut oil, then maybe I could excuse it, because coconut fat is 93% saturated. But this diet was made of lard and butter, the combination of which is probably about half saturated. The term "animal fat" or "low-omega-6 fat" would have been more accurate. At least they listed the diet composition. Many studies don't even bother, leaving it to the reader to decide what they mean by "saturated fat".
* The average American eats 7-8% omega-6 by calories. This means it will be difficult to see a relationship between omega-6 intake and cancer (or heart disease, or most things) in observational studies in the US or other industrial nations, because we virtually all eat more than 4% of calories as omega-6. Until the 20th century, omega-6 intake was below 4%, and usually closer to 2%, in most traditional societies. That's where it remains in contemporary traditional societies unaffected by industrial food habits, such as Kitava. Our current omega-6 intake is outside the evolutionary norm.
Why do we care? Because other studies, including one from the same investigators, show that corn oil and other industrial seed oils strongly promote prostate cancer cell growth and increase mortality in similar models (2, 3).
From the discussion section:
Current results combined with our prior results suggest that lowering the fat content of a primarily saturated fat diet offers little survival benefit in an intact or castrated LAPC-4 xenograft model. In contrast to the findings when omega-6 fats are used, these results raise the possibility that fat type may be as important as fat amount or perhaps even more important.The authors seem somewhat surprised and pained by the result. Kudos for publishing it. However, there's nothing to be surprised about. There's a large body of evidence implicating excess omega-6 fat in a number of cancer models. Reducing omega-6 to below 4% of calories has a dramatic effect on cancer incidence and progression*. In fact, there have even been several experiments showing that butter and other animal fats promote cancer growth to a lesser degree than margarine and omega-6-rich seed oils. I discussed that here.
I do have one gripe with the study. They refer to the diet as "saturated fat based". That's inaccurate terminology. I see it constantly in the diet-health literature. If it were coconut oil, then maybe I could excuse it, because coconut fat is 93% saturated. But this diet was made of lard and butter, the combination of which is probably about half saturated. The term "animal fat" or "low-omega-6 fat" would have been more accurate. At least they listed the diet composition. Many studies don't even bother, leaving it to the reader to decide what they mean by "saturated fat".
* The average American eats 7-8% omega-6 by calories. This means it will be difficult to see a relationship between omega-6 intake and cancer (or heart disease, or most things) in observational studies in the US or other industrial nations, because we virtually all eat more than 4% of calories as omega-6. Until the 20th century, omega-6 intake was below 4%, and usually closer to 2%, in most traditional societies. That's where it remains in contemporary traditional societies unaffected by industrial food habits, such as Kitava. Our current omega-6 intake is outside the evolutionary norm.
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