Should I Take Aspirin to Prevent Heart Disease?

Everyone knows that aspirin protects against heart disease, right?

Well, it turns out that aspirin may only protect some people from heart disease, and for others, it can actually slightly increase the risk of heart disease.  It all seems to depend on a variant of the COMT gene.

Catechol-O-methyltransferase (COMT) is the gene that codes for an enzyme that breaks down dopamine, epinephrine, and norepinephrine, as well as other substances.  There are many studies on the common genetic polymorphisms of the COMT gene, and most of the studies focus on the neurological aspects of the enzyme.

study published in the Journal of the American Heart Association looked at the effect of a common COMT polymorphism on cardiovascular disease.  The study also looked at the combined effect of the variant along with either aspirin or vitamin E and cardiovascular disease.

The study 23,000 women and analyzed the incidences of cardiovascular disease over a 10 year period.  It looked at the COMT Val158Met polymorphism, rs4680, where Val is the same as the G allele and Met is the same as the A allele. Those with homozygous Val/Val variant (G/G) have approximately a 4 times faster rate of dopamine metabolism as those with the Met/Met variant (A/A).[ref]

The findings of the cardiovascular disease study show that women with the Val/Val (G/G) variant are naturally at a lower risk of cardiovascular disease than those with the Met/Met (A/A) allele.

The study also showed that taking aspirin (100mg every other day) or Vitamin E (600 IU alpha-tocopherol every other day) significantly reduced the risk of cardiovascular disease for those with the Met/Met (A/A) allele.  The opposite was true for women with the Val/Val (G/G); they actually had a higher risk of cardiovascular disease with aspirin supplementation and no protection from Vitamin E.

Check your genetic data for rs4680 (23andMe v4, v5, AncestryDNA):

  • G/G:  naturally at a slightly lower risk of heart disease; aspirin supplementation increased the risk for heart disease[ref]
  • A/G: in the middle for heart disease risk, no significant effect on heart disease from aspirin
  • A/A: generally higher risk for heart disease; both aspirin and vitamin E significantly decreased the risk for heart disease


The benefits of aspirin for heart disease are due, at least in part, to its ability to thin the blood.  A genetic variant in the ITGB3 gene impacts aspirins ability to thin the blood.  The gene codes for a protein called Human Platelet Antigen-1 that is involved in how platelets form clots.

Carriers of the rs5918 variant (known also as P1A1/A2) have been shown in studies to be at a greater risk of heart attacks. Studies also show that people carrying the P1A2 variant are more resistant to the anticoagulant effects of aspirin.[ref] Note that some studies show no increase in the risk of cardiovascular disease, so other diet or lifestyle factors may be at play here.[ref]

Check your genetic data for rs5918 (23andMe v4, v5; AncestryDNA):

  • C/C: increased risk of heart disease, may not benefit from aspirin for heart attack prevention [ref][ref][ref]
  • C/T: somewhat increased risk of heart disease, may not benefit as much from aspirin for heart attack prevention [ref][ref][ref]
  • T/T: normal



Talk with your doctor about this one, especially if you are already on aspirin therapy.

Try looking for an inexpensive aspirin without a lot of extra ingredients.

While the study used only alpha-tocopherol as the Vitamin E supplement, many recommend using a natural, mixed tocopherol if supplementing with Vitamin E.


Author Information:   Debbie Moon
Debbie Moon is the founder of Genetic Lifehacks. She holds a Master of Science in Biological Sciences from Clemson University. Debbie is a science communicator who is passionate about explaining evidence-based health information. Her goal with Genetic Lifehacks is to bridge the gap between scientific research and the lay person's ability to utilize that information. To contact Debbie, visit the contact page.

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