I recently uploaded a post on how to reverse type 2 diabetes (T2D) (here). It’s a dietary solution (ketogenic diet) to a dietary problem. Some call it a cure because medication can usually be stopped. If you think of diabetes as ‘glucose intolerance’, then the answer is don’t eat glucose. That’s it. Glucose and starchy carbohydrates (which are also glucose) are non-essential nutrients (contrary to conventional thinking). If you have diabetes or are pre-diabetic, details on how to go about this are in the link.
In the post, I claimed that insulin resistance (IR) was the primary cause of T2D (not obesity, as is frequently claimed by health authorities). However, the question I didn’t address properly was – what causes the IR? I didn’t elaborate on that point because the answer was not clear to me at the time.
Recently, I became aware of an explanation that I find enlightening and compelling: IR is the normal way a cell regulates glucose – IR is not a dysfunction, disorder or disease. Instead, IR is the way a cell protects itself from glucose overload – IR is a cell’s solution to a problem posed by our dietary choices.
Our staple carbohydrates (wheat, maize, rice, potato), and the products made from them (bread, pasta, chips), are essentially starch. Starch is a molecule built almost entirely of glucose molecules that are linked together. There can be hundreds of thousands (up to millions) of glucose molecules linked together to form a single molecule of starch. When we eat starchy carbohydrates, our digestive system breaks these links, meaning we now have a digestive system full of glucose. We don’t notice that carbohydrates are glucose when we eat them, because the molecules of starch are too large to activate the sweet-receptors on the tongue. But the reality is that as far as the body is concerned, and without us realising it, every time we eat starchy carbohydrates we are eating a heap of glucose.
A high-carbohydrate diet is thus a high-glucose diet. Following current dietary guidelines (45-65% of our daily calories from carbohydrates) means that the body is inundated daily by glucose. Then, factor in food that is naturally sweet and high in sugars (fruits, especially juiced, agave nectar or honey) as well as sugar added to carbohydrate-based manufactured products (biscuits, cakes) and everything else (ice-cream, chocolate, yoghurt, soft drinks).
What are the body’s options for all this glucose?
If there wasn’t so much of it everything would be fine. The pancreas would be triggered to release insulin, which then binds to insulin receptors on cells everywhere in the body that allows glucose to enter the cells and be burned as fuel. In parallel, insulin receptors in the liver trigger the liver to convert excess glucose to triglycerides (fats) that are then transported to adipose tissue and stored (this is why starchy carbohydrates are fattening). Some glucose is stored in liver and muscle as glycogen. As blood glucose levels fall back to baseline, the pancreas stops releasing insulin and everything settles down again.
When everything functions properly, blood glucose is maintained at almost negligible levels – the equivalent of about 1 teaspoon of sugar in the entire blood-pool (which is about 5 kgs). That is an incredibly low concentration (about 0.1%) and it is maintained tightly. If the fasting-level was just 2 teaspoons, then you could be diagnosed with T2D. To put this into some perspective, the average Australian consumes something like 30 teaspoons of sugar a day. This figure does not even include glucose from starchy carbohydrates, it is just natural and added sugars.
The reason for getting glucose out of the blood circulation so firmly (even desperately) and keeping it low, is that the glucose molecule is damaging to us. Glucose results in a process called glycation, which randomly damages proteins and fatty acids. Indeed, glycation is considered as damaging as oxidation.
Burning the glucose for energy gets rid of it (the byproducts are carbon dioxide and water). However, a cell has use for only so much glucose. If glucose enters the cell and is not burned for energy, then it can be just as damaging for the contents of the cell as it is when it’s in the circulation (e.g. it gets fermented into lactate and lactate levels rise in the cell). Insulin doesn’t know about that, it just keeps putting glucose into cells. Any cell will do (muscle, liver, heart, kidney, eye, etc). Insulin also up-regulates the conversion of glucose into fat in the liver, resulting in non-alcoholic fatty liver and increased fat stores in the body leading to obesity. Obesity will usually be apparent before blood glucose has risen enough for a diagnosis of T2D to be made. This leads to the erroneous conclusion that obesity causes T2D.
Diabetes causes widespread damage because every cell in the body is under attack by insulin and glucose. It might be cells in the eye (causing blindness), kidney (requiring dialysis), peripheral vasculature and tissue (amputation), or heart and arteries (the usual cause of death). Excess glucose fuels cancer. Even the brain doesn’t get off – Alzehimer’s disease may be a form of IR.
These are serious consequences, so it should not come as a surprise if cells had a defence mechanism against excess glucose. This is a different way of looking at IR – the cell resists insulin’s attempt to overfill it with glucose. It could do this by modifying its insulin receptors to be less responsive to insulin and making it harder for glucose to get in. From the outside, we see this as IR (because blood-glucose is elevated). However, it’s different when seen from inside the cell – the cell has mounted a defence against insulin/glucose. It just depends on one’s perspective.
Presumably, such a mechanism would be a short-term fix. Our evolutionary biology would be expecting dietary glucose to drop at some point, letting things go back to normal – the cell can safely take in glucose again. Hence, IR is reversible. However, we never give up the glucose onslaught. We’re encouraged to make carbohydrates (especially starchy ones) our principle macronutrient. Over the longer-term, cells lose the battle. Administering insulin in T2D may hasten this if cells are resisting insulin for their survival.
We can now see why a ketogenic diet works for T2D – minimise glucose from carbohydrates (including sugar) and the system settles down. The body doesn’t miss dietary glucose because it can burn ketones for fuel. Cells become sensitive to insulin again. The diabetes goes away and stays away, as long as glucose in the diet is kept low. Medicines are no longer necessary because there are no longer any symptoms to treat. Weight normalises.
So, the answer to the question I posed at the beginning is this: IR is a reversible physiological response to a diet that is abnormally and persistently high in glucose.
That’s what a ketogenic diet addresses, and why it matters for diabetes. Diabetes is a dietary problem with a dietary solution. Spread the word.
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Note: The content of this post is intended to be educational and informative. It should not be taken as medical advice.
C J Nolan et al. Insulin Resistance as a Physiological Defense Against Metabolic Stress: Implications for the Management of Subsets of Type 2 Diabetes. Diabetes (2015) 64:673–686 | Link dx.doi.org/10.2337/db14-0694
H Taegtmeyer et al. Comment. Diabetes (2015) 64:e37 | Link: dx.doi.org/10.2337/db15-0655
C J Nolan et al. Response to Comments. Diabetes (2015) 64:e38–e39 | Link:: dx.doi.org/10.2337/dbi15-0002
There is a more approachable (and expansive) explanation by Jason Fung here.