“I guess diabetes is a bunch of family curses. That is how it started.
Like, my momma had it, father got it, and all of us just got a curse on us.
If it runs in your family, you will wind up getting it.”
Monique, age 48, South Carolina
Monique’s belief is understandable. Perhaps you share it. The experts have been telling us for decades that diabetes is in our genes. You may know from your own or friends’ experience that diabetes does, indeed, run in families.
But diabetes is not written in our genes. Just because your family had it doesn’t mean you have to get it. Just because they developed complications doesn’t mean you will. And just because they died from it doesn’t mean you have to. Yes, your genes can make you vulnerable, but you have the power to defeat them with the lifestyle you choose.
In his book, The Blood Sugar Solution, Dr. Mark Hyman writes, “In truth, diabetes is almost entirely induced by environmental and lifestyle factors. While there are some predisposing genes, these genes get turned on (or “expressed”) only under conditions of poor diet, sedentary lifestyle, stress, and exposure to environmental toxins.” So, if you change your life, he says, you can effectively turn those genes off.
This is important to understand, because if we believe our health is controlled by our genes, we might lose hope. What’s the sense in trying, if our genes control everything? But if, as science shows, diabetes is mainly caused by environment and lifestyle, then we can indeed do something about it. We can defeat Type 2 diabetes and enjoy a normal, healthy life.
Blaming genes isn’t exactly a lie, but it’s extremely misleading. The Pima Indians in southern Arizona have the highest rates of Type 2 in the world, well over 50%. So, their genes have been blamed. Tens of millions of dollars have been spent studying the Pima, looking for the cursed genes that make them sick, but without results.
Meanwhile, 100 miles away in Mexico’s Sonora state, another tribe of Pima live with essentially the same genes, but a more traditional diet and lifestyle. They have low rates of diabetes, about the same as their non-Pima neighbors.1 So, how could the Arizona Pimas’ genes be at fault?
The answer is genetics isn’t the reason the Arizona Pima have so much diabetes. Their Western diet of sugar and refined carbs is the real culprit.
An equally striking example occurs in Alaska. The native people there have sky-high rates of diabetes. Again, their genes are blamed. But across the Bering Straits in Siberia, their genetically similar cousins have a rate ten times lower.2 How could this be?
The Pima and the Alaska Natives’ genes evolved from a life of physical activity and a diet of gathered fruits and greens and hunted meat and fish. They were not prepared for the diet of processed foods and refined carbs, or for the sedentary lifestyle that was pushed on them after they were conquered. And they weren’t prepared for the terrible stress of being dominated by an outside culture.
Like the Natives, most people in modern society have been placed in food, stress, and limited activity environments that are radically different than our hunter-gatherer roots. Highly-refined foods, sugars, sedentary jobs, and chronic stress are not what our genes evolved to handle. As a result, Type 2 diabetes rates are soaring.
Some people are gifted with genes that can resist these things. A small percentage of people can sit around and eat sweets all day without getting diabetes, or even gaining weight. The genes that might contribute to diabetes are “switched off.” But for the rest of us, changing what we eat and how much we move will do more to protect us – and cure us – than any drugs or genetic engineering.
1. Mexico vs. Arizona Pima Indians, Indian Country Today Media Network, December 2010 http://indiancountrytodaymedianetwork.com/2010/12/01/mexicos-pima-indians-vs-arizonas-pima-indians-3258
2. Young T, C Shraer, E Shubnikoff, E Szathmary, Y Nikitin, Prevalence of Diagnosed Diabetes in Circumpolar Indigenous Populations, International Journal of Epidemiology, 1992, Volume 21, Issue 4 Pp. 730-736 http://ije.oxfordjournals.org/content/21/4/730.abstract