How Does a High-Fat Diet Trigger Prostate Cancer Spread?

Fat-heavy diets — particularly fried foods common in the Western diet — were known to increase prostate cancer risk, but the underlying mechanisms were unclear. Nature Geneticspublished new research explaining how fats, together with genetic factors, facilitate cancer cell spread. Findings illuminate the complex interaction between genes and dietary fats promoting prostate cancer spread.

The results are compelling reasons for lifestyle changes and open the way for treatments targeting cellular lipid/fat pathways.

What Is the Western Diet?

It is defined as eating mainly processed foods such as unsaturated fats, red meats, carbohydrates and junk food, with little fresh produce, whole grains, seafood or poultry. It is associated with hypertension, cardiovascular disease, high cholesterol, diabetes, obesity and certain cancers.

Prostate Cancer and the Western Diet

It is widely accepted that Western eating may promote progression. Direct evidence for a strong association between its commonly used fats and prostate cancer has nevertheless been lacking.

One study showed men eating a Western diet had 2,5 times the prostate cancer mortality risk of those eating diets rich in fruit, vegetables and whole grains.

Genes and Diet – Could an Obesity Drug Treat Cancer?

This study investigated genetic reasons why fats common in Western diets trigger spread, finding additional evidence.

Scientists knew an important role was played by PTEN in prostate cancer formation, because it is a tumor suppressor geneand animal studies showed its absence when cancer spread. Earlier research suggested losing it alone was insufficient to trigger metastasis .

Researchers analyzed tumor genomic data to identify another cooperating gene causing metastasis with PTEN, finding another tumor suppressor, PML, in prostate tumors that had not yet metastasized. Both suppressors were absent in approximately 20% of spreading tumors.

Another important finding in analyzing these metastatic tumors was that the cells contained abnormally high quantities of fat .

Thinking that stopping fat storage might prevent metastasis or even treat metastatic cancer, researchers gave mice on normal, low-fat or plant-based diets an obesity drug called fatostatin . Surprisingly, it blocked lipogenesis (fat production), with tumor regression and no metastasis.

This study points to a nongenetic, environmental factor in prostate cancer spread. It also suggests two treatment ideas: low-fat diets for patients with metastatic tumors, and fat-blocking drugs such as fatostatin. These claims require clinical studies for confirmation.