Insulin (part 2): The clue is in the liver
We have discussed the nine general functions of insulin in the human body, listed in order of what it affects first as its concentration increases. The organs—the pancreas, liver, fat, and muscles—are all interconnected via this hormone.
Without insulin, there is no signal for the pancreas to stop making its glucose-friendly counter-hormone, glucagon. Without insulin, the liver will produce glucose nonstop. Without insulin, fat cells will be depleted of energy, and no one can build up muscle mass. Essentially, without insulin, anabolism (building up) becomes catabolism (breaking down). Beyond the functions listed in the previous article, insulin’s action continues on to affect the blood vessels, bone, skin, the immune system, and the brain.
As essential as insulin is, Goldilocks's rule always prevails in the human body. While too little insulin means life is not possible, too much of it will work against life itself. This is why I believe life, health, and everything observable in nature carry God's signature of balance—a principle I observe constantly in medicine. Some health enthusiasts demonise insulin so much that they forget we need its signal and its spikes to maintain our body’s delicate needs. I understand that many people have seen how too much insulin causes disease, but that does not justify vilifying the hormone in its entirety.
This leads us directly into the next part of this discussion: What happens when there is too much insulin?
If you look at the steps in order, the first thing you notice is that the liver will have a lot of stored glucose because it hasn't had the chance to use it up. Next, the fat cells will enlarge to the point of saturation; it becomes impossible for them to take up more cholesterol, leaving the excess in the bloodstream. When this is left unchecked for too long, and your doctor eventually reviews your lipid profile, you will be lucky if they don't fall off their chair. Unfortunately, you won't achieve that muscular or "beefy" appearance as easily as you have allowed your fat cells to grow; although insulin stimulates muscle growth, the muscle fibers need a special mechanical signaling to complete this process. In the modern day, we call this resistance training.
In other words, long before your sugar starts to look suspicious on a fasting blood test, there are very good ways to evaluate your insulin status if your practitioner has a proper understanding of insulin, both in health and in disease. That is a big 'IF', of course, as in my 14 years as a doctor, I have yet to personally meet one who does. If you think hard about it, the liver and/or cholesterol will let the secret out early on about insulin resistance in most people. The honest truth is that I have not seen a single person with insulin resistance without these early signs. The problem is that, on top of the fact that no one pays attention to this, both our health practitioners and the public—even when they look for these early signs—are only going to end up being falsely reassured by the values they are scrutinising, as they often lie well within the lab ranges.
When there is chronic insulin signaling, the liver accumulates glycogen without having the chance to clear it out from time to time. Too much glycogen can cause some breakdown in the liver cells, a principle we learned from studying Glycogen Storage Disease. Since the liver contains Alanine Transaminase (ALT), which is present only in insignificant amounts in other parts of the body, the serum (blood) ALT enzyme will increase when there is liver breakdown. The problem in insulin overload is compounded by the fact that the liver adipocytes (fat cells) become too fat and overfilled, causing fatty liver. This is a major stress on the liver, causing the hepatocytes (liver cells) to disintegrate.
If you wait for the diagnosis of fatty liver, however, you might as well wait for the chickens to have teeth in some cases. I have met many diabetics who were never told they had fatty liver until they saw me. Conversely, most patients with fatty liver don't know they have an insulin issue, as their blood sugar is (still) 'perfect'. With the right understanding of insulin, there is no more confusion between the two, as both are manifestations of insulin resistance. These manifestations are dictated by how badly broken this mechanism is, its chronicity, concurrent assault, circadian rhythm, toxic load, exposure to sunlight, and many other individual variations. I have seen patients with insulin resistance, without the typical blood sugar rise, who have chronic, debilitating liver pain from their enlarged fatty liver pushing on the Glisson’s capsule—pain so severe they wished they had diabetes instead. The bad news is we don't get to choose how insulin resistance will manifest. The good news is we have a choice to stop it from happening. The even better news is that it is almost always reversible.