How Genetic Testing Changed The Way That I Eat

Recently I took my first nutritional genetics test through Nutrigenomix in Canada. I’d been toying with the idea of getting tested for a while, but finally bit the bullet after I taking a 5-week course on nutritional genetics through Monash University in Melbourne. Here’s what I learned about myself and how it’s changed the way that I eat.  

My first encounter with nutritional genetics was in 2012 at the International Congress of Dietetics in Sydney. Back then only a handful of researchers and super-sleuth dietitians knew what nutritional genetics was. I remember listening to a lecture given by Sylvia Escott-Stump, former President of the Nutrition and Dietetics Academy, and thinking to myself ‘This is cool.’.

Since then there has been tons of progress in the field but nutritional genetics still remains relatively new in nutrition practice. It’s a hot topic of conversation amongst dietitians in other countries (like Australia and Canada) however there’s less chatter about it in the US. Yes, it's complicated but there's a growing body of evidence to suggest that nutritional genetic testing provides valuable insight. 

Now, onto the juicy stuff. What did I learn from getting tested?

 

The Test

Firstly, a little background on the test I took. Nutrigenomix looks at 45 genes via saliva sample. I took the sports version which means that some of the genes analysed are specifically related to nutrition for sports performance. I chose Nutrigenomix because it’s developed by some of the leading researchers in nutritional genetics.  

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My Results

Nutrigenomix gives you a bucket load of information back. Some nutrition-gene relationships are stronger and more substantiated than others, but the most interesting findings for me were:

 

Vitamin D.

I have written about being low in Vitamin D before but I don’t have the genetic variants that predispose me to reduced vitamin D binding capacity or activation, so there’s no need for me to go bonkers on my vitamin D dose when my levels return to normal.

 

Vitamin B12. 

I have a genetic variant that affects vitamin B12 absorption and transport, and has been linked with lower circulating levels of vitamin B12. This means that going vegetarian is probably not the best choice for me and if I ever choose to go exclusively plant-based I will need to supplement vitamin B12 and/or be vigilant about consuming B12-fortified foods. Vitamin B12 is only found naturally in animal-derived foods.

 

Folate.

Folate metabolism is partly controlled by a gene called MTHFR. I have variants of this gene which mean that I don’t convert folate into its active form as readily as others. In other words, I need to include more folate-rich foods in my diet to achieve adequacy.  Folate is important for cell division, and DNA replication, and not getting enough of it can have fairly serious consequences, particularly early-on in pregnancy. My MTHFR genotype has also been linked with cardiovascular disease, psychiatric disease, and cancer risk when folate intake is low however the findings are inconsistent [1]. There’s definitely more to come on this one. For now, lots of leafy greens for me!

 

Caffeine. 

I am genetically pre-dispositioned to be a slow caffeine metabolizer. That means that above roughly 200mg of caffeine per day (2-3 espresso shots, or 2 cups of coffee), my risk of high blood pressure, and heart attack goes up. Furthermore, I am less likely to see the endurance performance benefits of caffeine than a fast metabolizer. Does that mean I am cutting out coffee? Absolutely not. However, I will be switching to decaf after my morning cappuccino.

 

Gluten sensitivity.

No surprises here. According to the Nutrigenomix algorithm which looks at 6 different genes involved in gluten intolerance my risk is ‘medium’. About 20% of people have a ‘medium’ risk profile, and another 10% are considered high risk. This explains why gluten and I often have a tenuous relationship.

 

Sodium. 

This one caught me by surprise. I am pretty liberal with the salt shaker, and have seldom noticed ill-effects. However, I have a variant of the ACE gene that makes me more likely to experience blood pressure changes with excess sodium intake.  

 

Caveats

Before you run off and spit into a tube like I did, there are a few things to keep in mind about nutritional genetic testing: 

 

It’s not a standalone tool for evaluating the best dietary approaches for someone.

It’s just one piece of the total nutrition picture. Diet history, weight changes, medical history, social context, other lab results, medications, etc are still important factors for determining the right eating pattern for you. 

 

It provides insight into genetic predisposition, not gene expression.

Just because you have the genes for gluten-sensitivity doesn’t mean that you currently react to gluten and just haven’t noticed it, or you are definitely going to wind up gluten-sensitive in the future. Nutritional genetic testing indicates that you are at higher risk for certain nutrition-related conditions, and some nutrition-gene relationships are stronger than others. 

 

Some risks can be mitigated with a well-rounded, nutrient-dense diet. 

Sure, I may metabolize folate and vitamin B12 less efficiently than others but that doesn’t mean that I need to supplement. In many cases--especially if there’s no evidence of deficiency--adequacy can still be achieved with wholesome, nutrient dense foods.

 

Final Thoughts...

After going through the nutritional genetic testing process I find myself wanting to try more biometric services. I've never thought of myself as a 'biohacker' but it’s been really interesting to learn more about what I am made of! While I haven’t made any dramatic changes to my diet since I got my results back, I feel increasingly empowered to eat meat and seafood for B12, keep an eye on my folate intake, limit gluten, and switch to decaf coffee after my morning caffeine hit. Over the course of a lifetime, those little changes can be really meaningful!


References: 

[1] Homocysteine and MTHFR Mutations. Moll S, Varga EA. Circulation. 2015 Jul 7;132(1):e6-9. doi: 10.1161/CIRCULATIONAHA.114.013311. Review. No abstract available.