Endurance Enhancers, High-Fat Diet, Associated With Higher Risk of Pancreatic Cancer

A recent study suggests that high-fat diets and a synthetic material found in unregulated performance enhancers activated a cell nuclear receptor which contributes to the progression of pancreatic cancer.

The study, published in the prestigious peer-reviewed paper Nature Communication  was led by Imad Shureiqi, MD, professor of internal medicine at the University of Michigan Medical School. According to the study, pancreatic ductal adenocarcinoma is a severe form of cancer that is rising in prevalence. Many cases are caused by pre-cancerous lesions, or pancreatic intraepithelial neoplasia and it’s estimated that 55 to 80 percent of adults over aged 40 have these low-grade pancreatic lesions. To get a better understanding of how these lesions are caused, researchers in the study decided to take a closer look at the transcriptional receptor peroxisome proliferator activated receptor-delta (PPARδ)

“We became interested in studying the effects of PPARδ on pancreatic carcinogenesis because our prior observations showed that PPARδ strongly promoted other gastrointestinal cancers. But there’s very limited information about PPARδ’s role in pancreatic cancer’s development,” Shureiqi said in a statement.

According to the study, activation of PPARδ has been associated with certain ligands. These ligands are both natural and synthetic. For instance, the fatty acids included in high-fat diets are natural ligands of PPARδ. Synthetic forms of ligands are found in a substance named cardarine (GW501516) that can be found in certain exercise supplements. According to the study, while pharmaceutical companies stopped using cardarine in their products after studies showed correlations between the substance and cancer development, unregulated Internet outlets continue to use cardarine in their performance enhancing products and claim that it helps build muscle and burn fat.

Using mice, scientists tested the effects of PPARδ on pre-cancerous pancreatic lesions and found that PPARδ, both natural and synthetic, increased the risk of the lesions. In addition, they found that even low-grade lesions can lead to a higher risk of pancreatic cancer in mice. These results indicate that over-consumption of PPARδ could contribute to the development of pancreatic cancer.

“This new information should alert individuals to the potential serious health risks from using synthetic PPARδ agonists,” Shureiqi said. “We're trying to spread the message that using those substances is not a good idea. It might enhance muscle endurance, but it also enhances cancer’s ability to use energy and grow.”