This past weekend we celebrated Ukrainian Christmas, which is something I grew up with on my Dad’s side of the family. The meal includes 12 meatless dishes that have significance in the history of the Ukrainian people. The meal has multiple courses and imparts a rich, comforting feeling for me and my family. It starts with Kuktya, a cold wheat berry soup, then a hot beet soup known as borscht. The main course is filled with fish and wheat dishes. Ukrainians identify strongly with an abundance of wheat. It is a spiritual symbol as well as one of sustenance. So in this meal there are a LOT of refined carbohydrates in the form of white wheat flour. I watch my intake of white flour because of my family history of type 2 diabetes. I choose whole grains as often as I can, make sourdough bread and limit my portion of white flour based foods.
Family history can play a major role in our risk for diseases such as diabetes, heart disease and cancer. Understanding your family history can be a strong motivator for habits and behaviors that can reduce your risk. My Dad saw his father lose his leg to diabetes and be confined to a wheel chair for the last three years of his life. The fear of this fate inspired him to make resistance exercise a part of his day while watching his intake of simple carbohydrates and sugar to maintain a healthy weight through adulthood. And so far it's worked! He still loves his crackers but he was able to mobilize one of his greatest fears into an action plan that has kept him active and healthy well into his 70s.
Understanding our roots is a powerful way to connect our own experience with the knowledge of our ancestors to inspire us to be a better version of ourselves. I see nutrigenomics testing as a connector as well. By learning about the genes that influence how our body uses different energy sources, metabolizes nutrients and weaknesses in our metabolism we can target specific interventions and lower the risk of negative outcomes.
Genes are inherited from our parents. We get one copy of the “allele” from our mother and one from our father. So just because one parent has a condition, does not mean you will inherit it. The combination of alleles you inherit will inform your risk. For example, The TCF7L2 can predict the odds of developing type 2 diabetes. In studies it has been shown to demonstrate an increased risk of 30%–50% for each allele inherited. I have two G alleles for the TCF7L2 gene. Fortunately, this is not the risk variant “T”. I got one G from my mother and one from my father. It is not that simple though (shocker!). There are up to 70 genes that have been shown to influence type 2 diabetes risk. Each gene codes for one of the many components of a well tuned insulin response. In the nutrigenomics report, I look for not only the TCF7L2 gene but also the CLOCK gene, GLUT2, FTO, ADIPOQ, IRS1, ADCY5, TRPM6 and SLC30A3. All of these have key nutrition interventions that can be targeted to optimize blood sugar control. Such as increasing magnesium rich foods in the diet to compensate for an elevated risk of low levels in people with the T allele of the TRPM6 gene. A low magnesium level has been associated with metabolic syndrome and type 2 diabetes development. Increasing magnesium intake has been shown to reduce diabetes risk and complications in susceptible people. So if you have the T allele like I do, you can benefit from eating more magnesium rich foods like nuts, beans and whole grains.
Genetics is a complicated field, and although the science of nutrigenomics starts back over 30 years, we are just beginning to be able to use it reliably to improve outcomes in personalized medicine. If it all looks like alphabet soup to you, that’s ok. The benefits of genetic counseling are cutting through the complexities and serving digestible insights along with actionable strategies.
It can be hard to decide where to put your effort when it comes to reducing disease risk. Nutrigenomic testing can help identify where you’ll get the most benefit. When I read your report, I’m bringing together your personal food story and the key optimizations you can make so your persistence can have the biggest impact.
Even though I don’t have the risk variant for the TCF7L2 gene, I do have it for the TPM6 and SLC30A3. I prioritize magnesium and zinc rich foods. Want to know more about what your genetic history would tell you to eat? Schedule a free Discovery Call to get started. You can listen to my introduction to Nutrigenomics and Personalized Nutrition here.
Enjoy this beautiful, flavonoid rich soup. Add white kidney beans for a magnesium and protein boost!
Borscht
Adapted from More Cooking Favorites by St. Andrew’s Ukrainian Orthodox Ladies’ Auxiliary
I make quick work out of the root vegetable chopping by putting it all through the shredder in my food processor. This was the way my Baba made it (although using a box grater) but you can dice the beets, carrots and potatoes with a knife too.
Ingredients
1 cup of fresh brown mushrooms
1 large onion, chopped
1 clove garlic, crushed
3 tbsp olive oil
2 cups of beets, shredded
1 cup carrots, shredded
1 small red or yellow potato, shredded
1 cup celery, diced
¼ cup parsley, chopped
3 cups purple cabbage, shredded
2 tbsp tomato paste
Lemon juice or vinegar
Salt and pepper
8-10 cups water
1 cup canned white beans, rinsed and drained (optional)
Directions
Over low medium heat in a stockpot, saute onion and celery in oil until transparent.
Add mushrooms and sweat until they lose half of their volume, then stir in tomato paste for 1-2 minutes. Remove the mixture from the pot and set aside.
To pot add beets, carrots, potato and parsley, then cover with water and cook until barely tender.
Add cabbage and cook for an additional 5 minutes. Add back onion mixture and beans, if using.
Add salt, pepper and lemon juice/vinegar to taste. Bring to boil and serve.
References
Berna, G. Nutrients. Nutrigenetics and Nutrigenomics Insights into Diabetes Etiopathogenesis. 2014 Nov 21;6(11):5338–5369
Lyssenko V. Mechanisms by which common variants in the TCF7L2 gene increase the risk of type 2 diabetes. J. Clin. Investig. 2007;117:2155–2163.
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