Adult onset diabetes is not genetic and is curable. Many in the medical profession would disagree with both. Quantitative Medicine clinical practice has cured adult onset diabetes consistently and repeatedly.
This the third post in an in depth series which examines the cause of Adult Onset Diabetes, or, as it is also called, Type II Diabetes. We’ll abbreviate it AODM.
How Does AODM Start?
As chronic diseases go, AODM is something of a con game. The victim, as it were, is lured in with sugar and starch. Then hormones and cellular metabolism change and make him dependent on it—in effect locking him in. It becomes difficult to roll this back.
The mechanism that powers this trap is called insulin resistance, and the trap itself works like this:
Fat in the form of triglycerides circulates in the blood, packaged in lipoprotein particles: chylomicrons and VLDL particles. Any hungry cell can snatch a triglyceride molecule from the passing particle parade. This is the “fuel” we are evolved to use, and the fuel we run most efficiently on.
Glucose is different. All carbohydrate food that is digested is converted to glucose, and enters the bloodstream as such, but muscle and fat cells don’t grab passing glucose particles unless there is also some insulin in the blood as well. The insulin acts as a glucose command center. If the insulin level is up, grab that passing glucose. If not, ignore it. Other glucose eating cells, like neurons, don’t do this little dance with the insulin. Neurons will grab what they need.
This insulin switch is an odd complication. Why not just let the muscle and fat cells grab the glucose if they want to?
Probably the body is doing this so that the brain won’t starve. The brain cells won’t eat most circulating fat. Actually, they probably would if they could, but blood that is available to the brain has to cross a fine mesh filter called the blood-brain barrier.
And it’s really fine. Even though fat molecules are pretty small, the most common ones in our diet can’t get across this barrier. Short-chain fats like butyric acid, ‘butter fat,’ do cross the blood-brain barrier as do other short-chain fats. These fats are important to brain health; but as these fats are usually not found in our ‘modern’ diet they are outside the scope of this article. Bacteria and viruses are far too large. Glucose, though, is a very tiny molecule and makes it across. So the brain runs on glucose. The brain has top priority. Therefore, the other cells, muscle and fat, are not going to be allowed to hog the glucose. Hence the insulin on-off switch.
However, after a meal that includes a lot of starch or sugar, there’s a surplus. So all the cells get to use glucose, and up goes the insulin. It circulates, attaches to cell receptors (little chemical detector gadgets stuck on the surface of every cell), and effectively rings a dinner bell. The cells then activate transporters (little cellular gadgets which stick through the cells wall and move material in and out of the cell) that can pull in the glucose. But the insulin does a bit more than just start a glucose feeding frenzy. It also signals the cells to stop eating fat. If circulating glucose is high, a storage molecule called glycogen, which is found in the liver and muscle (but not in the fat cells) is topped up. Once these are full, the rest of the glucose is converted to fat and stored in the fat cells. The body clearly does not want high levels of circulating glucose. High levels foul up cellular function.
At least this is how it is supposed to all work: eat sugar or starch and the body produces enough insulin to rapidly clear it back down to the background level—80 mg/dl or so.
The Topsy-Turvy World of Insulin Resistance
Suppose glucose levels stay high? We aren’t “designed,” as it were, to run on glucose. Our hunter-gatherer ancestors normally got little. Our body treats excess glucose like a windfall and tends to store it, but it really doesn’t handle excess amounts very well. (Fat is a different story: The body deals quite efficiently with excess fat.)
Suppose the cells refuse to take up any more glucose. The glucose is high, insulin is high, but the cells turn up their noses. Then we are stuck at these high levels of glucose and insulin. This cellular refusal to take in the glucose is at the core of insulin resistance. The cell is “resisting” the insulin’s orders to use the glucose. This insulin resistance trap is sometimes called Syndrome-X.
Now why would cells refuse glucose? This isn’t fully known, but we can speculate. Possible reason #1 we already mentioned: they’re full. This could certainly apply to muscle cells. They maintain little local glycogen storage depots to store excess glucose, but once these are full, they’ve got no place for more glucose. But fat cells don’t get full so easily. They stretch and expand to make room for more. Possible reason #2: The cells have aged. They just don’t respond to insulin like they used to. Possible reason #3: Fat cells appear to have their limits too. Once a fat cell is reaching its limits, it gets inflamed and won’t store more.
This does make some sense. High insulin is an attempt at force-feeding the cells, but they just aren’t going for it. Actually, the body’s ability to produce insulin tends to become impaired in a high glucose environment as well, further adding to the problem. High glucose tends to kill insulin producing Beta Cells. Carried to the extreme, this can result in Type 1 diabetes on top of the Type 2 version.
Why Does Insulin Shut Down Fat Metabolism?
There may be several reasons, but one is that high insulin and glucose are significantly more dangerous than high fat. So insulin-glucose clearance gets a priority.
On a more anthropological level, let’s take it as a given that, metabolically speaking, we handle food the same way as our hunter-gatherer ancestors. What did these guys eat? Animals they could hunt and foods they could gather. Animals year round, vegetables for a greater portion of the year, and fruit in the summer.
Food shortages were a way of life for many hunter-gatherers. Those living in the north would also have to contend with ice-age winters. So when that summertime fruit was available, why not store it all as fat for the impending ice-age winter? That’s what bears do. That’s what we did and still do. We don’t hibernate, but we have a lot of the skill set. So high insulin? Store everything.
The Effects of High Glucose and High Insulin
A consequence of chronically high glucose is high triglycerides—circulating fat. It might seem odd that levels of fat would be high in conditions of glucose overload, but there are two reasons for this. First, as mentioned, high insulin shuts down fat metabolism, so circulating fat naturally piles up, and second, the liver makes more fat particles.
Why would the liver do that? The liver makes those fat particles from the circulating glucose. So it seems that the liver is also participating in the effort to reduce glucose levels. The body can safely tolerate a much broader range of circulating of fat. Triglyceride levels from 20 to 500 would not cause any immediate problems, whereas glucose at either of those extremes would be quite dangerous.
These high circulating triglyceride (fat) levels led the medical profession on a multi-decade wild goose chase. Somewhere in the 70’s it was concluded the saturated fat must be the cause of AODM. So most AODM diets since that time recommend cutting fat, but not glucose. This has been a health fiasco without peer. In the next post, we will discuss the cure. It’s easy, logical, sensible, provable, and always works. Stay tuned.
Adult Onset Diabetes – Part 1 – Introduction
Adult Onset Diabetes – Part 2 – Diagnosis and Impact
Adult Onset Diabetes – Part 3 – The Cause
Adult Onset Diabetes – Part 4 – The Cure
Adult Onset Diabetes – Part 5 – Strange “Standard” Practice
Adult Onset Diabetes – Part 6 – Case Study 1
Adult Onset Diabetes – Part 7 – Case Study 2
Adult Onset Diabetes – Part 8 – Summary