Recently by Mark Sisson: The Definitive Guide to Sugar
BITE ME, ADA
We all know by now that type 2 diabetes is an epidemic. We’re seeing words like crisis and runaway all over the news and in the journals. Heart disease rates have been cut in half since the staggering margarine days of the 1980s, but diabetes has swiftly risen to fill that gaping void and meet the challenge of Completely Unnecessary Disease Epidemic.
Here’s my ultra-simple explanation of the entire insulin/blood sugar/type 2 diabetes mess. Big Agra could really care less about you. That’s just business. The pharmaceutical industry is not in it for the love of life. If that were the case, drugs would be much cheaper. The FDA has to think about public health, but it also has to think about treading carefully on the toes of corporate interests, because that’s how it works when you’re the biggest economy in the world.
Print this explanation out, stick it on your fridge, email it to your aunt. And put down the pasta.
When you eat food, the body digests the macronutrients: carbohydrates, proteins — actually many different amino acids — and fats. (Anything it can’t digest, like alcohol or fiber or toxins, either passes right on through or, if it makes it into the bloodstream, gets filtered by your liver, a beast of an organ if there ever was one.) We measure these macronutrients in grams and calories, but your body operates in terms of fuel. If you eat more fuel than your body needs — which most people do — the body is forced to store this excess. This ability to store excess fuel was an evolutionary imperative in a world that was in a state of constant u201Cfeast or famineu201D 50,000 years ago. In terms of Primal Health and our DNA blueprint, humans became very efficient fuel storage specialists and were able to survive the rigors of a hostile environment and pass those very same genes down to you and me. Thanks a lot, Grok!
Bear in mind that every type of carbohydrate you eat is eventually converted to a simple form of sugar known as glucose, either directly in the gut or after a brief visit to the liver. The truth is, all the bread, pasta, cereal, potatoes, rice (stop me when you’ve had enough), fruit, dessert, candy, and sodas you eat and drink eventually wind up as glucose. While glucose is a fuel, it is actually quite toxic in excess amounts unless it is being burned inside your cells, so the body has evolved an elegant way of getting it out of the bloodstream quickly and storing it in those cells.
It does this by having the liver and the muscles store some of the excess glucose as glycogen. That’s the muscle fuel that aerobic exercise requires. Specialized beta cells in your pancreas sense the abundance of glucose in the bloodstream after a meal and secrete insulin, a peptide hormone whose job it is to allow glucose (and fats and amino acids) to gain access to the interior of muscle and liver cells.
But here’s the catch: once those cells are full, as they are almost all the time with inactive people, the rest of the glucose is converted to fat. Saturated fat.
Insulin was one of the first hormones to evolve in living things. Virtually all animals secrete insulin as a means of storing excess nutrients. It makes perfect sense that in a world where food was often scarce or non-existent for long periods of time, our bodies would become so incredibly efficient. How ironic, though, that it’s not fat that gets stored as fat — it’s sugar. And that’s where insulin insensitivity and this whole type 2 diabetes issue get confusing for most people, including your very own government.
If we go back 10,000 or more years, we find that our ancestors had very little access to sugar — or any carbohydrates for that matter. There was some fruit here and there, a few berries, roots and shoots, but most of their carbohydrate fuel was locked inside a very fibrous matrix. In fact, some paleo-anthropologists suggest that our ancestors consumed, on average, only about 80 grams of carbohydrate a day. Compare that to the 350-600 grams a day in the typical American diet today. The rest of their diet consisted of varying degrees of fat and protein. And as fibrous (and therefore complex) as those limited carbohydrate foods were, their effect on raising insulin was minimal. In fact, there was so little carbohydrate/glucose in our ancestor’s diet that we evolved four ways of making extra glucose ourselves and only one way of getting rid of the excess we consume!
Today when we eat too many carbohydrates, the pancreas pumps out insulin exactly as the DNA blueprint tell it to (hooray pancreas!), but if the liver and muscle cells are already filled with glycogen, those cells start to become resistant to the call of insulin. The insulin u201Creceptor sitesu201D on the surface of those cells start to decrease in number as well as in efficiency. The term is called u201Cdown regulation.u201D Since the glucose can’t get into the muscle or liver cells, it remains in the bloodstream. Now the pancreas senses there’s still too much toxic glucose in the blood, so it frantically pumps out even more insulin, which causes the insulin receptors on the surface of those cells to become even more resistant, because excess insulin is also toxic! Eventually, the insulin helps the glucose finds it way into your fat cells, where it is stored as fat. Again — because it bears repeating — it’s not fat that gets stored in your fat cells — it’s sugar.
Over time, as we continue to eat high carbohydrate diets and exercise less, the degree of insulin insensitivity increases. Unless we take dramatic steps to reduce carbohydrate intake and increase exercise, we develop several problems that only get worse over time — and the drugs don’t fix it.
Ready for this? Let’s go:
1) The levels of blood glucose stay higher longer because the glucose can’t make it into the muscle cells. This toxic glucose is like sludge in the bloodstream clogging arteries, binding with proteins to form harmful AGEs (advanced glycated end-products) and causing systemic inflammation. Some of this excess glucose contributes to a rise in triglycerides, increasing risk for heart disease.