In one sentence:
We eat too many carbs.
Carbohydrates now supply 50-65% of our calories rather than the 20% our ancestors ate. Some of this is in the form of sugar, which is particularly damaging to metabolic pathways.
We do not need to compare ourselves to our caveman ancestors to see a shocking change in our carbohydrate intake - our great-grandparents also ate only a fraction of the carbohydrates that we consume today.
Our collective demand for sweet taste has driven science to create new, sweeter agricultural hybrids - fruits, vegetables, and grains - that are extremely carbohydrate-dense.
Ever-sweeter hybrids keep arriving on supermarket shelves because they “sell like hotcakes”. These new extra-high-carb foods cause a much more rapid and longer-lasting rise in blood sugar than anything our metabolisms evolved to process.
Our entire way of eating has become highly unnatural, yet it is so widespread and culturally accepted that to us it seems completely “normal”.
Most of us are unable to see the connection between what we are all eating and the sickness we see around us. We all know someone - family member, friend, coworker - who succumbs to one of these diseases, and in our grief we think “This shouldn’t have happened to them… they are so young!”.
But the diseases of modern civilization proceed silently within us, cell-by-cell, for decades until they seem to arrive suddenly out of the blue.
Our metabolisms have been trying to adapt and compensate for our unnatural diets for years. Dr. Jason Fung states that our metabolisms begin to go haywire 12-15 years before diabetes is diagnosed.1
We now eat a diet so high in carbohydrate that our metabolisms are not able to sustainably handle the blood sugar load and eventually become deranged trying to do so. Obesity, diabetes, cancer, heart disease and Alzheimer’s are all diseases of deranged metabolism.
When we eat carbs of any kind: sugar, fruit, processed and whole grains, root vegetables, legumes etc., our digestive system breaks them down primarily into one (or both) of two simple sugars, glucose and fructose.
Fructose is toxic, and is not used for energy. When ingested, it is escorted by insulin directly to the liver, where it is immediately converted into fat. It is not burned for energy directly. It does not cause a rise in blood sugar, and for this reason used to be considered a “healthy” alternative for diabetics. This mechanism of fructose-to-fat is why some people blame high fructose corn syrup for the obesity epidemic, but that is only a part of a fundamentally bigger metabolic problem.
Glucose in the blood stimulates the pancreas to secrete insulin, the hormone that shuttles glucose into our cells where it is burned for energy. Inside almost every cell of our body are tiny organelles called mitochondria, which are little metabolic power plants that use glucose and oxygen to generate energy and heat, to literally “power our lives”. (They are alternately capable of running on fat for fuel, but that is a later chapter in the story…)
Insulin also shuttles some of the glucose into liver and muscle cells, where it is converted to glycogen, a molecule that stores a small amount of glucose-energy for quick release later if needed. Glycogen is used to tide us over when we don’t have glucose in the bloodstream, such as between meals or when we’re exercising or sleeping. It acts like a short-term bank account for fuel.
As insulin successfully shuttles glucose out of the bloodstream and into the cells, the glucose level in the blood drops back down. This drop stimulates hunger hormones, which make us crave and eat more carbs to bring our blood sugar level back up. This creates another insulin surge that brings our blood sugar back down. Most of us are familiar with this sugar high/sugar crash cycle - it is what keeps us snacking between meals.
Since glucose is a relatively short-term fuel source, on a carb-based diet we need to replenish our energy (eat) frequently. We feel satisfied and full for a short time, perhaps even “high” if we ate sugar and experienced its associated dopamine rush, but the insulin spike and subsequent blood sugar crash causes us to enter into a cycle of eat and repeat that keeps insulin levels consistently high. This is a very important point.
Insulin does more than ferry glucose into cells for the mitochondria to burn for energy. Insulin is called the “master hormone” and carries out at least a dozen metabolic duties, three of which are of particular concern to those wanting to control their weight and avoid diabetes and heart disease. These three functions are:
So on a high-carb diet which keeps insulin levels chronically high, these three functions of insulin have us in a metabolic Catch-22: we become metabolically trapped into gaining weight.
As long as we maintain high levels of insulin by eating a high-carb diet, overall caloric reduction (dieting) or caloric expenditure (exercise) will have little effect on weight loss. All calories are not the same, because they do not have the same metabolic pathways or cause the same effects. Only carbohydrates spark high insulin levels, and it’s the elevated insulin levels that tell the body, in these three different ways, to create and maintain fat stores. High insulin is subsequent to ingesting carbs, not fat or protein, so unless we cut carb consumption specifically and reduce the levels of insulin in the blood, we will be very challenged in losing weight.
Once we are metabolically trapped in this way, being overweight is not our most serious problem, however.
Chronically high insulin levels cause the cells of the body to start to become resistant to insulin’s effects, a condition known as insulin resistance. Insulin works on the cell membrane like a lock and key: insulin is the key that unlocks the door to the cell so that it can ferry glucose in. There are two ways of interpreting what is happening in insulin resistance.
The old paradigm of insulin resistance says that insulin resistance represents a failure of the lock and key, wherein the lock has become “sticky” and insulin cannot easily ferry the glucose in. This is the standard paradigm accepted and practiced by the American Medical Association and the followed by the American Diabetes Association.
But the latest research points to a new way of understanding the mechanisms involved in insulin resistance and is giving us new hope for ways to reverse it.
The new paradigm of insulin resistance says that the cell has become overstuffed with glucose, creating sort of an osmotic “backpressure”, requiring more and more insulin to push the same amount of glucose into the cells2. There is nothing wrong with the lock and key - the door is open but the cell is too stuffed to let more glucose in. The situation is analogous to those guys at the train stations in Japan whose job it is to shove, literally shove, passengers into overfilled trains. They are called train pushers, and you can see them in action on YouTube if you Google “Train Pushers at Work”. Picture the train as the cell, glucose as the passengers, and insulin as the train pushers.
Under this new paradigm, when the cells are already overstuffed insulin becomes unable to clear the glucose out of the bloodstream any more. At this point even fasting blood sugars start to rise. And since blood levels of glucose remain high, the pancreas secretes even more insulin to try to clear the chronically elevated blood sugar.
This difference between the old and new ways of understanding insulin resistance and the diabetes that follows may seem like mere technical details, but they call for profoundly different treatment protocols and have very different outcomes, which we will see in a moment.
With all this excess glucose circulating in the blood, which even high levels of insulin are unable to clear, the liver now takes on the job. The liver tries to “dispose of” excess blood glucose by bundling it with fat to create triglycerides, which circulate in the blood and cause the body to store this extra energy in the fat cells (think beer belly, love handles, arm flab and pear hips). Once deposited, unless insulin levels drop to baseline and remain there for more than 13 hours at a time, this fat will not be burned for fuel.
If the liver cannot clear all the triglycerated fat it is producing from fructose and excess glucose quickly enough, the fat will begin to accumulate in pockets within the liver itself, producing a condition known as fatty liver disease. According to Jason Fung, MD1, the progression is this: chronically high insulin causes fatty liver, fatty liver creates insulin resistance, and insulin resistance in turn leads to Type 2 diabetes.
As insulin resistance proceeds to the point where blood glucose remains chronically high, we develop full-blown Type 2 Diabetes*. The overworked pancreas tries its best to produce enough insulin to shove the glucose into the cells, but eventually it becomes overwhelmed by the unnatural glucose load and the resistance of the cells to admit more glucose. It may partially or completely give up "burn out" as it becomes unable to produce enough insulin to clear glucose out of the bloodstream.
*There are two types of diabetes, which are fundamentally different. This paper only addresses Type 2.
Type 1 diabetes is caused by damage to the pancreas, which reduces or eliminates its ability to produce insulin. With no insulin to shuttle glucose into cells, blood sugar levels are uncontrolled and have devastating effects on nerves and other tissues throughout the body. Damage to the pancreas usually occurs through autoimmune disease, in which the body’s immune system attacks cells of its own body because of their similarity to foreign proteins. In Type 1 diabetes there is not enough insulin. Type 1 diabetes is a completely different disease than Type 2, which is a disease caused by too much insulin. This article does not apply to Type 1 diabetes. (End footnote)
The cascade of metabolic derangements discussed above is diagnosed as Type 2 diabetes when our fasting blood sugar is consistently over 126 mg/dL.
“A fasting blood sugar level less than 100 mg/dL (5.6 mmol/L) is normal. A fasting blood sugar level from 100 to 125 mg/dL (5.6 to 6.9 mmol/L) is considered prediabetes. If it's 126 mg/dL (7 mmol/L) or higher on two separate tests, you have diabetes.” (Mayo Clinic)
(“Normal” as defined by the Mayo Clinic is actually quite high. In populations not exposed to high-carb diets or with normal metabolic function, normal fasting blood sugar levels are 75-83.)
In Type 2 diabetes, high glucose in the blood as well as in all the overstuffed cells of the body, causes serious inflammatory damage to all of our tissues, organs, and especially, to nerves and blood vessels.
Many people with diabetes go blind, have gangrenous feet or legs amputated, or die of heart attacks or kidney failure, all because of how toxic sustained high levels of glucose and insulin are to cells.
It takes about 10-15 years of this carb-driven hyper-insulin cycle for diabetes to creep up on us, developing slowly and silently as we continue to eat the high-carb, low-fat diet that the “experts” keep telling us is good for us, and that everyone around us eats.
Under the old paradigm diabetes is managed by giving diabetics higher and higher doses of insulin (or other blood-sugar lowering drugs) to help force the glucose through the “sticky locks”, lowering the glucose in the blood. This paradigm is the standard one currently taught in medical schools and still held by the American Diabetes Association. This paradigm doesn’t address the high glucose levels inside the cells or the perils of chronic high circulating insulin. It focuses on reducing blood sugar, but does nothing to address our metabolic derangement. (Other drugs have been developed to lower blood sugar through other pathways, but none of them address the core of the problem either.)
For instance, the ADA still recommends that diabetics eat about 50 grams of carbohydrate per meal and then “cover it” by taking enough insulin to shove it into the cells. As diabetes progresses, it takes higher and higher levels of insulin to try to lower blood sugar. Since they are using the wrong understanding of what’s happening, people invariably get worse rather than better.
“If you eat 2,000 calories a day, you should consume about 250 grams of complex carbohydrates per day. A good starting place for people with diabetes is to have roughly 45 to 60 grams of carbs per meal and 15 to 30 grams for snacks.” (ADA website)
The old paradigm of insulin resistance is caught in a bind because of its deeply-entrenched but false belief that fat is the root of heart disease and so must be avoided at all cost, especially since they know that diabetics are at much higher risk of heart disease.
The new paradigm addresses the core issue: why our blood sugars got so high in the first place. It recognizes that we’ve been consuming carbs at a much higher level than our bodies evolved to handle, and offers us a way of eating that over time can reverse insulin resistance and repair the metabolic derangement. If we stop eating carbs, our blood sugars will eventually normalize. Since it can take 10-15 years of eating too many carbs for our metabolisms to get so out of whack that we develop diabetes, it takes time for our metabolic derangements to reverse and heal after we stop eating a high-carb diet.
Once diabetes is full-blown, eliminating carbs may not be sufficient to manage the disease entirely, but stopping carbs and replacing the missing calories with fat is part of the plan for healing. A very low-carb, high-fat diet is called a ketogenic diet, and is proving itself to be very effective in treating diabetes, and even more effective in preventing it in the first place.
1) The Diabetes Code by Jason Fung, MD
2) Jason Fung, MD Low Carb Breckenridge 2017.