Are your cavities caused by genetics?

Friends accuse me of thinking that everything is genetic, and, well, there is some truth to that accusation!  To be honest, though, there are a lot of things that have genetic connections that really surprise me.

I had always assumed that my cavities were due to bad dental hygiene or bad dietary choices. That is what the hygienist always said. It turns out, genetics plays a big role in whether or not someone gets cavities. As always, though, genetics combines with lifestyle and habits when it comes to the final outcome.

Dental Caries

I like the term dental caries better than ‘cavity’ –  sounds fancier and less like a big hole in the tooth. No matter how you refer to it, a cavity consists of a damaged area of the tooth enamel that turns into a hole full of decay.

Everyone knows that sugar causes cavities. The party line from dentists is that sugar feeds the bacteria on your teeth, which then produce acid that eats away at the enamel.

So all you need is some sugar, bacteria, and failure to brush for two minutes, twice a day.

But wait…

There are a lot of people who eat sugar, don’t brush well, and don’t have a mouth full of cavities. What is going on?

It is estimated by researchers that the ‘heritability’ or genetic component of dental caries is about 50%.[ref]

There are two ways that researchers can dig into how genes impact a disease or trait.

  • They can start with an idea of which gene should be involved and then check to see if genetic variants in the gene change the risk of the disease/trait.
  • Researchers can take genetic data from a large population and combine it with data on who has a particular disease/trait to see which genetic variants are related to the disease risk.

This second way – looking at large populations and searching the whole genome – has given us some interesting insights into the formation of dental caries.

Genetics research on cavities shows us…

The genetic variants associated with an increased risk of cavities fall into two categories:

  • genes that affect the oral microbiome
  • genes that affect the formation of tooth enamel.

Some genetic research points to how the oral microbiome interacts with foods. For example, a research study found that kids who carry a GALK2 variant along with Streptococcus mutans, a bacteria that increases the risk of cavities, are at a much greater risk of cavities.[ref]

The GALK2 gene codes for an enzyme that phosphorylates galactose at high concentrations. The genetic variant causes low concentrations of GALK2, and thus higher amounts of galactose are available in the mouth for the S. mutans to munch on. Galactose is a simple sugar that is found in higher amounts in dairy products. So perhaps the combo of dairy intake, S. mutans bacteria, and low galactose causes cavities for some of us.

Genetic variants in the DEFB1 gene link the oral microbiome to an increased risk of cavities, and the IL32 gene variants show that your immune system’s response to bacteria is also important in balancing your oral microbiome.


Genetic Variants Linked to Cavities

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DEFB1 gene: codes for an oral antimicrobial peptide

Check your genetic data for rs11362 (23andMe v4; AncestryDNA):

  • C/C: increased risk of cavities[ref]
  • C/T: normal risk of cavities
  • T/T: typical

Members: Your genotype for rs11362 is .

Check your genetic data for rs1799946 (23andMe v4; AncestryDNA):

  • T/T: increased risk of cavities[ref]
  • C/T: normal risk of cavities
  • C/C: typical

Members: Your genotype for rs1799946 is .

 

IL32 gene: codes for an immune system response to bacteria

Check your genetic data for rs4786370 (23andMe v4, v5; AncestryDNA):

  • CC: much more likely to carry the bacteria that causes cavities (S. mutans)[ref]
  • C/T: more likely to carry the bacteria that causes cavities
  • T/T: typical

Members: Your genotype for rs4786370 is .

 

GALK2 gene: galactose metabolizing enzyme, galactose is a sugar found in dairy

Check your genetic data for rs11635005 (23andMe v4; AncestryDNA):

  • T/T: carrying S. mutans bacteria doesn’t increase the risk of cavities
  • C/T: carrying S. mutans bacteria doesn’t increase the risk of cavities
  • C/C: Carrying S. mutans significantly increases the risk of cavities, lower GALK2 enzyme activity[ref]

Members: Your genotype for rs11635005 is .

 

AMELX gene: codes for amelogenin which is involved in the formation of tooth enamel

Check your genetic data for rs946252 (23andMe v4):

  • T/T: increased risk of cavities[ref]
  • C/T: increased risk of cavities
  • C/C: typical

Members: Your genotype for rs946252 is .

 

AQP6 gene: aquaporin 6, important in the generation of saliva and tears

Check your genetic data for rs1996315 (23andMe v4; AncestryDNA):

  • G/G: typical
  • A/G: decreased risk of cavities
  • A/A: decreased risk of cavities[ref]

Members: Your genotype for rs1996315 is .

 

WNT10A gene: important in the prenatal development of many tissues, including teeth

Check your genetic data for rs121908120 (AncestryDNA only):

  • T/T: typical
  • A/T: fewer decayed teeth
  • A/A: fewer decayed teeth[ref]

Members: Your genotype for rs121908120 is .

 

C5orf66 gene: long, non-coding RNA which regulates the expression of other genes, including Ring1[ref]

Check your genetic data for rs1122171 (23andMe v4 only):

  • T/T: an average of 2.4 more cavities[ref]
  • C/T: an average of 1.2 more cavities
  • C/C: typical number of cavities

Members: Your genotype for rs1122171 is .


Lifehacks:

Below are natural ways to kill the bacteria that cause cavities (S. mutans) as well as research-backed methods of remineralizing teeth.

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About the Author:
Debbie Moon is the founder of Genetic Lifehacks. Fascinated by the connections between genes, diet, and health, her goal is to help you understand how to apply genetics to your diet and lifestyle decisions. Debbie has a BS in engineering and also an MSc in biological sciences from Clemson University. Debbie combines an engineering mindset with a biological systems approach to help you understand how genetic differences impact your optimal health.