What Six Months of Soup Can Teach Me
Part 3 – How Genetics and Lifestyle Interact, Good or Bad
The big question for all of us to address is how much of our health and disease outcomes will be determined by genetics and how much will be determined by lifestyle, particularly diet. If you accept that genetics is largely responsible, you will be absolved of most responsibility for the outcome. Your only hope is medical breakthroughs if you drew poor genetic cards.
If you accept that lifestyle is primarily determinant, it puts the control of your health fate squarely on you. To my thinking, this is the best case scenario. What science has shown us since the completion of the analysis of the entire human genome in 2000, the reality is that our health fate is a mixture of both genetics and lifestyle.
There are approximately 23,000 genes in each of us that our responsible for the design of the proteins, enzymes and other things that form are makeup and function. Each gene can have many little variations called single nucleotide polymorphisms, or SNPs, with “many” being defined as 40-60. Some 3.5 million SNPs have been identified in the human genome so we all have thousands of them.
If a polymorphism of a gene that makes an important enzyme in carbohydrate and sugar management exists, the resulting enzyme will function more weakly than normal rendering that person less carbohydrate and sugar tolerant. Another way of saying that is that they will get in metabolic trouble more quickly eating a higher carb/sugar diet.
The reason I choose this example is that this pattern seems to exist in about 75-80% of the U.S. population including me. My dominant genetic pattern comes from my mother’s side of the family, Irish transplants from the earlier 1900’s. Diabetes and heart disease were the norm in the preceding two generations I knew. A favorite uncle died of a second heart attack before the age of 40.
So what difference would this Irish/Western European genetic background have to do with carbohydrate tolerance? It seems when our ancestors left Africa way back, they came to a fork in the road. They must have listened to one of my favorite philosophers, Yogi Berra who was quoted saying, “if you come to a fork in the road, take it!” My group turned left up into Europe, while others went to the middle east and beyond.
Two dominant gene patterns naturally occurred in these populations with implications about carbohydrate tolerance. Those in the middle eastern group who genetically were favored to handle larger amounts of carbohydrate tended to be much healthier, while those who had the less able carbohydrate genetic pattern struggled. One of the early victims of metabolic stress is fertility so each population became fairly uniform in genetic pattern suited to the food supply of the area.
My tribe was Paleo-type diet suited. Migrate us again to the U.S and put our genetic pattern into a 55% carbohydrate, refined sugar and high grain dietary environment and metabolic chaos has ensued.
Fortunately, those who have genetic mediated difficulty in managing carbs/sugars problems can largely be prevented with parts of two different strategies. The first is keep yourself in a dietary environment that does not stress your metabolic weaknesses. This is the lower carbohydrate (<40% of energy), very low sugar eating pattern. Carbs should also come only from whole, complex carbohydrates and are dominantly from vegetables rather than grains. Grains have a glycemic load (they raise blood sugar and sugar management stress) 8-10 times higher than the same grams of carbs from vegetables.
The second part to managing genetic weaknesses is a targeted nutrient program.
The diagram shows an important enzyme reaction in converting a breakdown product of sugar, pyruvate, to acetyl CoA which becomes energy.
The conversion of pyruvate to energy is begun by the enzyme, pyruvate dehydrogenase, When the gene responsible makes a copy of the enzyme, it is inactive. It is activated by “cofactor” which in this case is vitamin B1 or thiamine. Those with a gene pattern that causes them to make a weak version of the enzyme can increase its activity by adding higher amounts of co-factor or vitamin B1.
The best approach to our genetic weaknesses is to consume a diet that is compatible with our strengths and places little stress on the weaknesses as well as supplementing extra nutrients known to increase weak enzyme activities.
But how can one tell what their pattern is? There are a few ways. First is family history, although that is not foolproof. A lot of processed carbohydrate products didn’t exist when grandma was a kid, sugar wasn’t added to everything, nor was processed grain a staple as it is now. She could have had a subtler carbohydrate intolerance that her diet didn’t not exploit, but ours will.
The second is “wait and see” which many are doing. If we end up at 55 years old with diabetes and 2 or 3 other related diseases, it tells us more about our intolerances. I don’t think this “wish I had known sooner” approach is the right way to go for me.
The third approach is that different tests such as blood chemistry profiles show the stress of an imbalance between genetic mediated metabolic ability and our diet. This allows the pre-empting of the potential bad outcome before it has done the damage. I will talk about how to do that in the next post.
So what does all of this have to do with modified fasting and the chicken soup? Everything! If the body is saying we have a metabolic mismatch between fuel and the ability to manage it, modified fasting periodically helps perform a “system restore”. I do it every so often to keep my computer healthy, why not for my health?