The core finding from the new research study, from the University of Cambridge, is that statins may reduce cancer risk through mechanisms separate to cholesterol. Specifically, it has been found that statins reduce levels of low-density lipoprotein (LDL) cholesterol, the so-termed ‘bad’ cholesterol. This occurs by inhibiting an enzyme named HMG-CoA-reductase (HMGCR), the rate-controlling enzyme of the mevalonate pathway, responsible for cholesterol and other isoprenoid biosynthesis.
Earlier clinical trials have provided strong evidence that statins can reduce the risk of heart attacks together with other cardiovascular diseases. Until now, evidence for the potential effect of statins to reduce the risk of cancer, has been less apparent. The researchers set out to explore the extent that lipids including cholesterol play a role in the development of cancer, and whether anti-cholesterol drugs can mitigate the effects.
To examine the potential effects, the researchers collected genetic associations with the risk of overall and 22 site-specific cancers. These data were drawn for 367,703 individuals vontained in the U.K. Biobank (a national and international health resource). In total, 75,037 individuals had some form ofa cancer event.
The findings reveal that variants in the HMGCR gene region, which represent proxies for statin treatment, were associated with overall cancer risk. This finding indicates that statins may be able to lower overall cancer risk. This inference will be subject to additional research.
The research was originally posted on the preprint server medRxiv. Following peer review, the paper has been published in the journal eLife. The research is titled “Predicting the effect of statins on cancer risk using genetic variants: a Mendelian randomization study in UK Biobank.”
