Insulin Insufficiency and a Low Carb Diet


One of the largest misunderstandings circulating within the low carb community is the mistaken idea that everyone on a low carb diet has insulin resistance. While most of us have some type of metabolic problem or defect, it isn’t always from insulinemia. Sometimes, the problem is not too much insulin; sometimes, it’s actually not enough.

For those with insulin resistance, the problem can be easy to solve: Just restrict carbs to your personal level of tolerance and save carby treats for special occasions. That results in increased sensitivity to insulin and better blood glucose control. If you have insulin insufficiency, however, the problem is more complex.

Role of Insulin

A fear of carbs and insulin is common among low carb dieters, but insulin is vital to survival. If you don’t produce enough insulin, you’ll die. Insulin is a peptide hormone secreted by the beta cells inside the pancreas. It’s released about every 5 to 10 seconds at a very small level, and then in larger quantities after eating. These larger spurts divide into two separate phases.

The first phase is what the body has had a chance to store since dealing with your previous meal or snack. The amount of insulin secreted depends upon how many carbohydrates you ate at your prior meal or snack. It has nothing to do with what you are currently eating. Consistent snacking or eating an inconsistent number of carbohydrates at each meal or snack can seriously affect the amount of insulin you release to handle a meal. First phase insulin is released within a few minutes because it’s triggered by a rise in blood sugar level. This has nothing to do with the height of elevation. It is stimulated by the rise itself.

The second phase is what the body manufacturers and then releases if the blood glucose level hasn’t dropped below 100 mg/dl after about 30 minutes. The purpose of both phases is to keep blood glucose levels within a tight margin of safety. What insulin does is attach itself to insulin receptors on the outside of body cells. That signals the cell that fuel is available. What those body cells cannot immediately use for energy is stored in muscle tissue, the liver or fat cells – in that order. Carbohydrates do not immediately turn into fat. They go to replace your glycogen storage. Carbohydrates are only turned into triglycerides and stored as body fat if your glycogen storage is full.

Once glucose is used or stored, insulin degrades, which shuts down the signaling. This takes about an hour in a normal metabolism. At that point, the body uses either stored glycogen or fatty acids for fuel depending on the body’s needs. Fatty acids take longer to mobilize than glycogen does, so quick bursts of energy such as aerobic exercise use glycogen. That is also glucagon’s first choice for fuel: glucose.

Role of Glucagon

When blood glucose falls to dangerous levels or when there is an excess of amino acids in the blood, the alpha cells within the pancreas secrete glucagon. Like all stress hormones, the role of glucagon is to mobilize energy sources, so that blood glucose can be brought back to a safe level. Glucagon is a stress hormone and mobilizes resources to handle the stressor. It does that by attaching itself to glucagon receptors on the surface of liver cells and then forcing the liver to convert its glycogen stores into glucose. This glucose is immediately dumped into the bloodstream to handle the stress.

Glucagon is an anti-anabolic hormone. It does whatever it needs to do to get the body fuel. That is what swings the metabolism to the low carber’s favor. When glycogen is not available, glucagon stimulates the liver and kidneys to begin the process of gluconeogenesis where amino acids are turned into glucose. To do that, it turns off glycolysis, but only because glucose is not presently available. Glucagon regulates glucose production through lipolysis. It encourages the liver to use fatty acids to fuel the process of gluconeogenesis, so it can save what little glucose there is for the brain and central nervous system.

If ample amino acids are available, the liver will use them to create glucose. About 58 percent of the protein you eat can be used for this purpose, provided you’re eating more than you need for daily tissue and cell repair. The body can also use the glycerin backbone attached to triglycerides, but since that amounts to only 10 percent of the fat molecule, it can’t mobilize enough fat to get the amount of glucose the body needs. When amino acids are not easily available, the body goes into a catabolic state and breaks down muscle tissue instead.

The Dance Between Insulin and Glucagon  

Insulin and glucagon work synergistically to keep the blood glucose level within a narrow margin. The fact that glucagon encourages fat mobilization is a protective device. That makes both hormones essential for health. In a normal situation, glucagon comes into play when insulin levels are low, but that isn’t always the case. When glucagon is triggered due to excess amino acids in the blood, both insulin and glucagon are active and high at the same time. It is not true that when insulin is high, glucagon is always low. Nor do all body cells have insulin receptors. Uptake of glucose by the liver, brain and kidneys occur independently without the help of insulin.

When beta cells become defective or die, the alpha cells within the pancreas become accustomed to lower levels of beta cells or non-functioning beta cells and lose their ability to sense the level of glucose in the bloodstream appropriately. This confuses both the alpha cells and the liver. Without an adequate amount of appropriately functioning beta cells, insulin secretion will not be enough to clear the bloodstream of excess glucose. Alpha cells won’t know when to secrete glucagon and when not to. The result is a tendency to over secrete glucagon rather than under secrete it, which leads to elevated glucose levels and eventually an insulin deficient diabetes.

Insulin Insufficiency’s Effect on a Low Carb Diet

The fewer beta cells you have, the less insulin you can manufacture and secrete. Since elevated blood glucose levels do not inhibit glucagon, the longer glucagon remains elevated the more glucose the liver pumps into the bloodstream. This can result in dangerously high and toxic levels of glucose in the blood, which can then cause insulin resistance to the lower amount of insulin you do have.

A low carb diet causes insulin levels to fall quickly. Generally, insulin production slows down within a few days. If you have insulin resistance and insulinemia, a lower insulin level is a good thing. A low carb diet can bring your insulin down to normal output levels and correct insulin resistance. If you have insulin insufficiency due to a hereditary defect or severely reduced number of beta cells, a low carb diet can cause your glucose levels to skyrocket. If those levels continue, they will cause mild insulin resistance and weight gain rather than fat loss.

Since glucagon can be released by alpha cells when insulin levels are low, insulin defects do not prevent glucagon secretion. But with epinephrine (adrenaline), arginine, alanine, acetylcholine and cholecystokinin also stimulating glucagon production, the liver can get confused and keep dumping glucose into the bloodstream – even when your glucose level is high. This can be particularly problematic if you’re eating a large amount of protein. That’s because glucagon’s job is to raise blood sugar. It works in opposition to insulin, which lowers blood sugar.

My Own Problems With Insulin Insufficiency

Typically, insulin insufficiency surfaces as a young adult. It’s more likely to be diagnosed correctly if you’re a woman because it will surface as gestational diabetes with your first child. That isn’t always the case, however, because many individuals are diagnosed with type 2 diabetes instead. Plus, most physicians are not trained to recognize insulin insufficiency.

I had gestational diabetes starting with my first child but since my blood sugar dropped to a pre-diabetes level after the baby was born, my doctor told me he couldn’t treat me. Neither did any of my other gynecologists when the same thing occurred with each child. Nothing was known about insulin insufficiency back then – only that it existed.

Pregnancy places a large amount of stress on the body, so glucagon mobilizes resources to help provide the fuel the baby needs to grow. While you might have had just enough insulin to take care of your previous needs, when pregnant, you can’t make enough insulin to handle the glucose increase. Once you deliver, glucose levels return to normal because glucagon is no longer being triggered. Physicians see this corrective measure and believe everything is fine – even though it’s not. As the years of insulin insufficiency continue, elevated glucose levels become more common even when you're not pregnant.

Insulin insufficiency is responsible for about 5 percent of all cases of diabetes. Since it’s hereditary, it’s unusual to have the problem without a strong family tendency towards diabetes. Both type 1 and type 1-1/2 runs in my family. While some medical professionals are beginning to recognize the problem and have labeled it type 1-1/2, there are many subdivisions depending on the specific genetic defect.

It is very expensive to test for because you have to test for each problematic gene. Currently, there are six known defects but scientists suspect more. Unlike other hereditary issues, it only takes one gene from a single parent to cause insulin deficiency. If you have a parent with this problem, you have a 50 percent chance of having it yourself. In those who inherit one defective gene from each parent, their diabetes is more likely to be pretty severe.

The good news is that insulin deficiency doesn’t always require injected insulin. Many times, it can be treated through diet, or pills and diet, alone. Insulin deficiency doesn’t always mean you have to go to using insulin, although many people with the problem prefer that method because pills that stimulate insulin release can often be too strong.

When you have insulin deficiency, it is vital to find the correct amount of carbohydrates that will keep your blood sugars as close to normal as possible. That will probably be a higher number than found on a standard low carb diet because you have to keep your insulin level from falling too low. If you don’t, the elevated glucose that results from the release of glucagon can cause serious diabetic complications such as neuropathy even before you are diagnosed with diabetes.

This is why it’s extremely important not to project your own experiences with a low carb diet onto others. A no carb or very low carb diet can make metabolic issues worse rather than better. So far, my own experience has found that 20 to 40 carbs per meal is necessary to keep my glucose levels normal. For someone else, that might be much too high. The specific foods I eat also makes a difference. It just depends upon your own type of defect – which is why a low carb diet works best when you personalize it to fit your own medical condition.

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