Statins May Help Prevent Certain Forms of Cancer

Demehri’s research rests on two major claims: there is a mechanism that leads to cancer-causing chronic inflammation, and that pitavastatin suppresses this mechanism.

In the study, the team identified a specific immune system signaling pathway that is linked to chronic inflammation, known as Toll-like receptor (TLR)3/4-TBK1-IRF3.

In a healthy individual, one of the functions of this pathway is to induce the production of a protein known as interleukin 33 (IL-33), which is part of the body’s immune system response. IL-33 signals the body to produce other immune system cells when an injury or infection occurs.

However, overproduction of IL-33 can lead to chronic inflammation, which is when an immune-system response continues to linger in the body beyond when it is needed, which leads to a host of negative health outcomes.

By suppressing this pathway, researchers knew they could shut down a major driver of chronic inflammation.

They subsequently began testing a battery of FDA-approved drugs in both mouse and in-vitro models to see if anything would work. Out of all the drugs tested, pitavastatin was identified as having an inhibiting effect on the signaling pathway.

“What we found is a very potent inhibitor of this pathway. So, if you’re looking at cancer in the context of chronic inflammation, where this pathway is really active, then blocking this pathway is the main benefit,” said Demehri.

To confirm their findings, the researchers also included an observational study as part of their findings. There they looked at pancreatic cancer outcomes among patients who were prescribed pitavastatin versus a control group who were not.

Patients who took pitavastatin had significantly decreased risk of both chronic pancreatitis and pancreatic cancer risk.

“Statins do reduce inflammation. Some of this is related to their cholesterol-reducing effects. If you’re reducing the amount of cholesterol burden someone has…you’ll reduce inflammation. But statins also do appear to reduce inflammation in some ways independently from their cholesterol-lowering effects,” Matthew Feinstein, MD, Associate Professor of Cardiology at the Northwestern University Feinberg School of Medicine, told Healthline. Feinstein wasn’t affiliated with the research.

Feinstein is a specialist in the field of inflammation and heart disease who recently published an editorial on statins and inflammation.

He told Healthline that there has been a lot of interest in the anti-inflammatory effects of statins, especially as they pertain to cancer, but that it has been hard to draw hard conclusions.

“In the big picture there’s been a lot of noise regarding statins, whether they’re helpful or harmful in the setting of cancers…There may be some benefit for certain cancer subsets, but that is still far from proven at scale in humans,” he said.

Observational studies have found significantly lower rates of breast cancer among statin users. Other research has posited that statins could cut the risk of aggressive prostate cancer.

However, none of these associations have been rigorously determined in clinical trials. The mechanism through which statins affect cancer outcomes isn’t clear either. In Demehri’s research it is apparently due to its anti-inflammatory effects, but this may not be the case for other forms of cancer.

Feinstein is cautiously optimistic about the research, but cautions that it is still very early to know if the promise of statins in cancer prevention will be borne out.

“I think the general inflammation-reducing properties are reasonably well supported systemically. But there are tons of questions on the actual chemo prevention arm of this,” he said.

Researchers believe that statins could play a role in preventing certain forms of cancer associated with chronic inflammation.

Statins are widely-used cholesterol-lowering medications that have documented anti-inflammatory properties.

Despite the promising findings, the research is still very early and needs to undergo trials in humans to be validated.