You've probably never heard of it, but this hormone is essential for your metabolic health
There is a new way to understand type 2 diabetes. This new perspective — this new paradigm — is built on a ground-breaking discovery in human metabolism. This is new science that explains how the nutrient energy you get from food can be stored between meals in a healthy way or in a dangerous way.
Will the food you eat strengthen you, or will it damage your organs and compromise your well-being?
Your body is like a factory: It takes in raw materials and turns them into usable products. And just like a factory, there is a network of pipes and conveyor belts to move the stuff around. These are veins, arteries, ducts, and nerves. Hormones are like messengers — delivering instructions around the building (your body.)
When your stomach digests the food you eat, most of the nutrient energy it produces is absorbed into the bloodstream as glucose, which is a type of sugar.
Digestion triggers three distinct signals:
- The first is a feeding signal from the stomach to the brain, which then tells the liver to increase nitric oxide levels.
- The second is a feeding signal from the stomach to the liver, which responds by increasing glutathione levels.
- The third signal, coming from the pancreas, is a pulse of insulin that travels directly to your liver through a blood vessel known as the portal vein.
When the liver receives all three signals, it releases the hormone “hepatalin” into your bloodstream. This ground-breaking discovery: isolating and quantifying hepatalin action, was only completed a few years ago.
Your bloodstream carries glucose molecules to various tissues in the body. At the same time, hepatalin is released from the liver and carried throughout the body. Hepatalin activates receptors that trigger glucose absorption in muscle, the heart, and the kidneys.
In a healthy body, hepatalin’s effect on muscle, the heart, and kidneys accounts for two-thirds of glucose absorption immediately after a meal. This means that most of the glucose is not being stored as body fat. This is perfect partitioning of the nutrients.
But if any of the three signals (insulin, glutathione, or nitric oxide) are reduced or removed, hepatalin production will decrease or completely stop. This slows the absorption of glucose by the muscles, the heart, and the kidneys. This leaves too much glucose in the bloodstream.
At this point, the well-balanced process is thrown off-kilter. The pancreas detects the heightened levels of glucose and releases pulse after pulse of insulin. Insulin stimulates glucose uptake and storage of nutrient energy as fat throughout the body. At the same time, the liver steps in to absorb and store some of the glucose as chains of glycogen.
When the liver has absorbed as much excess glucose as it can, it converts the rest to triglycerides, which are secreted as very low-density lipoprotein into the bloodstream. All remaining nutrient energy from a meal now circulates in the bloodstream as either glucose or triglycerides and will be absorbed primarily by fat cells and stored as unhealthy body fat. This acute process takes place after every meal you eat.
If your hepatalin levels are low for days or weeks, early indicators of poor health will rise including post-meal insulin levels, triglycerides, bad cholesterol, heart dysfunction, and blood pressure. If your hepatalin levels remain low for months, muscle mass decreases, while elevated insulin levels will cause a dangerous build-up of fat in your vital organs and on your body. If hepatalin levels are low for years, the amount of insulin needed to compensate causes a condition known as hyperinsulinemia and what has been called insulin resistance.
This dangerous trajectory of pathologies is called the “absence of meal-induced insulin sensitization syndrome” or AMISS. It is a more complete expression of what is sometimes called metabolic syndrome or syndrome X.
Through the lens of AMISS, we see a predictable progression of illness caused by decreasing levels of hepatalin and it begins with changes in insulin levels and triglycerides after eating, followed by an increase in cholesterol, heart dysfunction, a loss of muscle mass, and an increase in body fat, all occurring before elevated fasting glucose — the usual indicator of prediabetes — can even be detected. After this point, pancreatic exhaustion leads to type 2 diabetes.
Like the discovery of insulin 100 years ago, the discovery of hepatalin changes the way we detect and treat diabetes.
A synthetic version of the hepatalin hormone is currently in development as a long-term therapeutic treatment of type 2 diabetes.
Hepatalin marks the next paradigm change in healthcare. It’s a new way to help put an end to the type 2 diabetes epidemic. This will allow millions of people to recover their well-being, and live longer and healthier lives.