Insulin Insufficiency: The Truth About Insulin and Glucagon on Low Carb

If you don't eat to your carbohydrate tolerance,
your insulin level can drop too low!
Here's the truth about insulin and glucagon

One of the largest misunderstandings circulating within the low-carb community is the mistaken idea that everyone who is overweight or obese has insulin resistance.

While many ketogenic dieters do have some type of metabolic problem or defect, diabetes and obesity are not always a result of insulinemia. Sometimes, the problem isn't that you secrete too much insulin in reaction to eating carbs.

Sometimes, the problem is that you don't secrete ENOUGH.

For those with insulin resistance, the problem can be easy to solve:

Just restrict carbs to your personal tolerance level and save carby treats for special occasions.

This increases insulin sensitivity and provides better blood glucose control for those with Type 2 diabetes or metabolic syndrome.

If you have insulin insufficiency, however, the problem is reversed, so in this post we're going to reveal the truth about insulin and glucagon that the low-carb community tends to ignore.

Stop Fearing Insulin! 

A fear of carbs and insulin is very common among ketogenic dieters, but insulin is vital to your survival. If you don’t produce enough insulin, you’ll die.

Insulin is a peptide hormone secreted by the beta cells inside the pancreas. A small amount is released about every 5 to 10 seconds, and then a larger quantity is secreted into the bloodstream after eating.

The larger spurts are divided 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. The body looks for patterns and adapts to the patterns you set up.

First phase insulin is released within a few minutes because it is triggered by a rise in blood sugar level. The amount of blood sugar has nothing to do with the height of insulin elevation. Insulin secretion is stimulated by the rise in blood glucose itself.

The second insulin phase is what the body quickly manufacturers and then releases into the bloodstream IF the blood glucose level hasn’t dropped below 100 mg/dl after about 30 minutes. This second phase insulin is what low carbers are talking about when referring to an insulin spike. Most try to avoid this second phase.

Higher blood glucose levels can actually be a result of the body mis-guessing how much insulin you are going to need to process the meal. It is not always a sign of insulin resistance.

If you ate more carbs than usual, the body won't be prepared for the incoming carbs and will have to manufacture what it needs to bring the blood sugar back down. This higher glucose level doesn't mean that you can't make enough insulin.

In this case, you can.

The purpose of both of these insulin phases is to keep blood glucose levels within a tight margin of safety.

What Does Insulin DO In the Bloodstream?

What insulin does in the bloodstream is attach itself to insulin receptors on the outside of your body's cells. This attachment, or joining, signals the cell that fuel is available for use.

What body cells cannot immediately use for energy is stored as glycogen in muscle tissue or the liver, or as triglyceride in fat cells – and it's stored in that order.

Carbohydrates do not immediately turn into body fat.

That's a myth. In fact, that potential outcome is actually quite rare.

What carbs do is replace your glycogen storage in muscles and liver. They are only turned into triglycerides and stored as body fat if your glycogen stores are full.

For carbs to be stored as body fat, your glycogen
stores have to already be full.
Overeating carbs is what drives fat storage.

Granted, people who are severely overweight or obese tend to overeat carbs. And it's overeating carbohydrates that drive fat storage, not insulin itself. But it's inaccurate to say that carbs are automatically stored as body fat. They aren't.

In fact, overeating fat is much more likely to make you fat than an occasional sweet potato or serving of rice.

Once glucose is used or stored, insulin degrades, which shuts down the glucose-availability signaling. This degrading of insulin takes about an hour in a normally functioning metabolism. At that point, the body uses either stored glycogen for fuel or fatty acids, 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 rather than body fat. Glucose is also glucagon’s first choice for fuel.

Role of Glucagon

Many low-carb dieters sing the praises of glucagon. However, it's not as keto-friendly as some of the keto influencers suggest.

When blood glucose falls to dangerous levels or when there is an excess of amino acids in the blood stream, 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 up to a safe level. Glucagon is a stress hormone and mobilizes resources to handle the stress.

It does that by attaching itself to glucagon receptors on the surface of liver cells, forcing the liver to convert its glycogen stores into glucose.

Whenever glucagon attaches to the glucagon receptors in the liver, glucose is immediately dumped into the bloodstream to handle the stress, regardless of how much glucose is already in the bloodstream.

Glucagon is an catabolic hormone. It does whatever it needs to do to get the body fuel. This freedom is what swings the metabolism to the low carber’s favor.

When glycogen is not available to be used, glucagon stimulates the liver and kidneys to begin the process of gluconeogenesis. While amino acids can be oxidized directly for fuel, it's not practical to burn muscle for more than a few days, so the body begins recycling some forms of degraded glucose.

Glucose can be taken from the glycerol molecule attached to triglyceride, but this only amounts to 10 percent of the fat molecule. The liver can also use pyruvate and non-essential amino acids like glutamine, and a few other things like worn-out protein structures.

Only as a last resort does the liver convert dietary protein into glucose. The process is slow and inefficient, so the body exhausts all other sources of glucose first.

To accomplish all of this, glucagon turns off glycolysis, which is good new for low carbers, but that's 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.

Ketones are a by-product of this triglyceride breakdown.

The Dance Between Insulin and Glucagon  

Insulin and glucagon work synergistically to keep the blood glucose level within a tight, narrow margin.

The fact that glucagon encourages fat mobilization is a protective life-saving defense mechanism. Both insulin and glucagon are 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 will be 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. The alpha cells 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: 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
• 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 is because the liver interprets a low insulin level to mean low blood sugar.

All of this can be particularly problematic if you’re under stress or eating a large amount of protein. This occurs because glucagon’s job is to raise blood sugar. It works in opposition to insulin, which lowers blood sugar.

My Own Experience 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.

This isn’t always the case, however, because many individuals are diagnosed with type 2 diabetes instead. Physicians rarely test for Type 1 or Type 1-1/2 in adults. 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, the doctor told me he couldn’t treat me.

Neither did any of the other gynecologists I saw over the years, even though I went into gestational diabetes 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 just enough insulin to take care of your own needs, when pregnant, you can’t make enough insulin to handle the glucose increase.

Once you deliver the baby, 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 and more common, even when you're not pregnant. This is exactly what I'm seeing in myself.

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 Diabetes run in my family. There are no cases of Type 2 that I'm aware of.

While some medical professionals are beginning to recognize the problem of not enough beta cells 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 Type 1-1/2 Diabetes because you have to test for each problematic gene individually. Currently, there are six known defects but scientists suspect there are 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, 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. However, many people with the problem prefer using insulin because pills that stimulate insulin release can often be too strong. It's easier to manage with injected insulin.

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 is 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 if you have insulin insufficiency or are insulin sensitive, rather than insulin resistant. 

What you can eat depends on your defect – which is why a low-carb diet works best when you personalize it to fit your own medical condition and carbohydrate tolerance.