MORE THAN TWICE AS MUCH FAT

In the study, several groups of rats were given food with the same number of calories. One group's grub had normal fat content, with 17 percent of the calories coming from fat. The other group got high-fat diets, with around 43 percent of the calories coming from fat, mostly omega-6 fats derived from corn oil. A third group was given a normal diet with estrogen supplements, as earlier research had shown that fatty diets raised estrogen levels during pregnancy, and the researchers wanted to see if higher estrogen levels were somehow to blame.


Some offspring of these rats were then allowed to mate, either with rats whose parents had normal diets or those that also got exposed to high-fat diets in the womb.

Their granddaughter rats' mammary tissue was investigated after the researchers treated them with a carcinogen to help the tumors grow.

What the researchers found was intriguing. When both parents had been exposed to high-fat diets in the womb, about 80 percent of their granddaughters developed mammary cancer, compared with controls, of which only 50 percent got the cancer. For rats with only one parent exposed in utero to the junk diet, about 69 percent came down with the disease.

As for estrogen, although daughters of rats given estrogen while pregnant had a higher risk of mammary cancers, their own female offspring did not, suggesting there could be two different cancer pathways at work, de Assis said.

There were structural differences in the mammary tissue, too, as offspring of rats in the high-fat diet group had more terminal end buds, an undifferentiated structure where de Assis suspects the tumors arise.

The researchers aren't sure why the risk persists across generations in the high-fat groups, but de Assis said they believe it has to do with epigenetic changes -- changes in the helper substances that turn genes on and off, triggered by the diet. Culprits could be methylation, or the adding of a methyl group to DNA code, modification of histone proteins, or even changes to microRNAs, which are RNA snippets that switch on and off RNA strands.

But the real reason awaits further research, as de Assis and her team are currently studying the mechanisms involved. When they've learned more, they hope to publish the paper in a peer-reviewed journal.

Perhaps the burning question is: Will the findings apply to humans? de Assis noted that epigenetic effects of diet have been shown in human studies, and that people on average eat diets with a fat content not too far below the one studied in the presentation, in the 25 to 30 percent range. But she refused to speculate.

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