Pathophysiology and Pathogenesis of Type 2 Diabetes

Author Sidebar: When I was in the hospital (and after I came out of the coma), I remember the doctors and nurses telling me that I had Type 2 diabetes. They said I had a very severe blood sugar problem because my blood sugar was over 1300.

And, because my blood sugar was so high, I was given insulin to bring my blood sugar back down. 

At the time, this all made sense to me. So, I concluded (at that time) that once my blood sugar returned to normal, everything would be okay. 

But, instead, I was told that once my blood sugar returned to normal, everything would not be okay because I would still be diabetic. 

Needless to say, this was confusing and disheartening. But, I quickly realized that "high blood sugar" was not the real problem! -- it was a symptom of the problem. And, the real problem of having Type 2 diabetes was more than just a blood sugar problem. 

Type 2 diabetes is the most common form of diabetes, with more than 90% of diabetics being Type 2; and, 5% to 10% being Type 1. 

Type 2 diabetes mellitus is a heterogeneous disorder with varying prevalence among different ethnic groups.

In the United States the populations most affected are Native Americans, particularly in the desert Southwest, Hispanic-Americans, African-Americans, and Asian-Americans.

However, Caucasian-Americans are also affected, but not at the same disproportionate percentage levels.

Type 2 Diabetes Impacts ALL groups and cultures!

The pathophysiology of Type 2 diabetes mellitus is characterized by peripheral insulin resistance (insulin insensitivity), cell damage, glucose transport (GLUT4) dysfunction, impaired regulation of hepatic glucose production, excess toxicity, excess oxidation, vicious cycles of biochemical/hormonal imbalances, and later on: beta (ß) cell dysfunction, eventually leading to possible ß-cell failure.

Type 2 Diabetes Is More than a Blood Sugar Problem!

What is Type 2 Diabetes? It's a Beast of a Disease!

Type 2 diabetes is a complex metabolic disease that (silently) destroys your body one organ at a time.

Another way to look at this disease (as depicted in the following diagram), is to picture a hungry, ferocious (invisible) beast attached to you at the hip.

This beast quietly drains your body of its energy because your cells are unable to absorb glucose and produce energy. This beast gets stronger when you rely on diabetic drugs, eat unhealthy foods, don't exercise and live a very stressful life.

Type 2 Diabetes is a Beast That Destroys Your Organs One at a Time

As the beast gets stronger, it causes damage to your blood vessels, affecting your eyes, kidneys, feet, heart and brain. In addition, as the beast gets stronger, you get weaker. In fact, your immune system gets weaker exposing you to other diseases as well as preventing cuts, bruises and sores from healing properly.

However, when you start eating healthy foods, exercising and reducing the stress in your life, the beast gets weaker! And, as the beast gets weaker, you get stronger! And, as you get stronger, your body no longer requires the diabetic drugs. This, in turn, also weakens the beast, which enables you to reverse your diabetes, stop the diabetic complications and beat your diabetes naturally.

Cells with Damaged "Doors"

From a medical perspective, Type 2 diabetes is a complex metabolic disease of biochemical and hormonal imbalances that is characterized by high insulin levels and high blood glucose levels, along with chronic inflammation, excess oxidation, excess protein glycation and excess toxicity.

Insulin resistance and cellular inflammation reinforce each other via a positive feedback loop, causing more cell damage and preventing your body's cells from effectively using the insulin produced by the pancreas.

As depicted in the diagram (below), the insulin receptors ("doors") on the surface of each cell are damaged (inflamed), ignoring the presence of insulin in your blood and refusing to allow glucose from your blood to enter your cells and be transported throughout the cell via the glucose transporters  [1a].

Consequently, the glucose stays in the bloodstream, causing your blood glucose level to rise [1b].

As a result, the cells can't produce energy or burn fat [2] because they don't have enough glucose.

In addition, the cells are unable to remove toxins and waste [3]; and, over time, the cells may become further damaged and lose the ability to communicate with each other [4].

Type 2 Diabetes at the Cellular Level

The primary events are believed to be an initial insensitivity of insulin resulting in peripheral insulin resistance; and, later on, relative insulin deficiency.

The key message here is that the major cellular dysfunction that occurs in Type 2 diabetes is not associated with the pancreatic ß cells (as in Type 1 diabetes).

The major cellular dysfunction is associated with the damaged (glycated) red blood cells and the muscle, liver, and fat cells!

However, over a period of many years, major cellular dysfunction can occur with the beta cells, especially if the diabetes goes untreated and no changes are made to diet and lifestyle.

Author' Sidebar: During my medical workshops with doctors, nurses, and other healthcare professionals, they were shocked to discover that ß cell dysfunction is NOT the primary issue with Type 2 diabetics -- especially when I show them the data from thousands of Type 2 diabetics.

In fact, I was one of those Type 2 diabetics who was put on a drug protocol of 4 insulin shots a day because the doctors believed I was either a Type 1 diabetic, or a Type 2 diabetic with ß cell dysfunction and pancreatitis.

But, because of my biochemistry background I knew enough to ask for specific blood/urine/hormone tests that verified that I wasn't Type 1 and didn't have beta cell dysfunction, i.e. insulin serum test, c-peptide, urine ketone test, hemoglobin A1C, glutamic acid decarboxylase (GAD) antibody tests, islet cell antibody (ICA) tests, insulin antibody tests, GTT.

Unfortunately, most Type 2 diabetics don't know this, and are led to take diabetic drugs that don't really help in the long run. If I had not recognized this discrepancy I would still be diabetic today and I would be taking even more insulin.

The key cells that are affected when Type 2 diabetes initially develops (due to hyperglycemia and hyperinsulinemia) include the red blood cells; and, the muscle, fat, and liver cells.

These cells are designed to take glucose (sugar) out of the blood, pull it into the cells and change it into energy.

What Happens in a Non-diabetic's Body

But, before we look at Type 2 diabetes at the cellular level, let's take a look at how these cells function in a non-diabetic's body or how they used to perform before you became diabetic.

When you eat food, the carbohydrates are metabolized and broken down into glucose, which causes your blood glucose level to rise. This rise in blood glucose triggers the pancreas to secrete insulin. 

Then, the insulin (acting like a "key") activates the insulin receptors ("doors") on the surface of your cells to open up and signal the GLUT4 glucose transporters to come get the glucose.

So, the GLUT4 glucose transporters move to the outer edge of the cell and pull the glucose into the cell, which lowers the blood glucose level in your bloodstream.

Once inside the cell, the glucose is transported to the mitochondria (energy factories) where it is converted to energy (fuel) or adenosine triphosphate (ATP). Then, the cell uses that ATP to perform its primary functions.

What Happens in a Diabetic's Body

However, in a diabetic's body, the insulin doesn't activate the insulin receptors ("doors") -- in other words, the cells lose their sensitivity to insulin (a condition known as insulin resistance).

So, the insulin receptors don't signal the GLUT4 glucose transporters to come get the glucose.

As a result, the GLUT4 glucose transporters do NOT move to the outer edge and do NOT pull the glucose into the cell.

And, because the glucose is not pulled into the cell, it remains in the bloodstream, causing your blood glucose level to rise. And, this rise in blood glucose, again, triggers the pancreas to secret even more insulin creating a vicious cycle that can lead to hyperglycemia and hyper-insulinemia.

And, because the glucose is not transported to the mitochondria (energy factories), the cell is unable to produce energy (fuel) or adenosine triphosphate (ATP). As a result, the cell is unable to perform its primary functions effectively.

And, without energy, as a diabetic you may begin to feel tired. In addition, the excess glucose that is building up in your bloodstream is converted to fat (triglycerides), which can lead to unwanted weight gain and obesity.

Over time, the cells in the liver also become insulin resistant and respond by making too much blood glucose, which contributes to higher blood glucose levels — a condition known as hyperglycemia.

Red blood cells are damaged due to the high glucose levels, as glucose molecules are attached to the exterior part of the red blood cells, forming a crystalline (coarse) crust -- this is known as glycation (which creates AGEs or advanced glycation end products). These coarse red blood cells cause damage throughout the circulatory system, damaging arteries and capillaries.

This damage is repaired by the cholesterol produced by the liver, leading to arterial plaque formation -- all triggered by an inflammatory response. These coarse red blood cells cause greater damage in dense capillary areas such as the hands and feet, and fragile capillaries such as those that feed the kidneys and eyes.

You must break this cycle in order to stop the progression and damage being caused by your diabetes.

Cycle of Type 2 Diabetes

All of this leads to a continual vicious cycle of high blood glucose and insulin levels that further fuel the diabetes as it spreads its damage from cell to cell and throughout the body.

This damage eventually leads to diabetic complications, including blindness, kidney failure, amputation, heart attack and stroke. Other health issues include high blood pressure, high cholesterol, high inflammation markers, periodontal disease, and erectile dysfunction.

Key Point!: Given the cellular dysfunction of the muscle cells, fat cells, and the liver cells, you can see that diabetic drugs are not going to help defeat or reverse your diabetes. Why?

Because the majority of diabetic drugs are designed either to make the pancreas secrete more insulin or prevent the liver from releasing stored glycogen. The drugs do nothing to address the insulin resistance of the muscle and fat cells, or the inflammatory damage caused by the coarse (glycated) red blood cells.

You don't have to be a scientist to figure out that you need to reduce the insulin resistance (by increasing the insulin sensitivity of the cells) and reduce the cellular inflammation -- by reducing blood glucose levels and insulin levels.

Note: Some of the following information was extracted from PubMed and several other medical databases and clinical studies that addressed pathogenesis, beta cell dysfunction, and insulin resistance at the cellular level. This information is for medical professionals and others who are interested in the science behind Type 2 diabetes and insulin resistance.

For non-medical professionals, the key message here is that insulin resistance and beta cell dysfunction can be prevented and even reversed with a superior nutritional protocol, consistent exercise, and other lifestyle changes.

Looking at the pathophysiology of Type 2 diabetes at the cellular level will give you an insight into the disease so that you will see that Type 2 diabetes is a lot more than just a blood sugar problem.

The pathophysiology of Type 2 diabetes involves several biological processes that are harmful and damaging to your cells and tissues.

These harmful processes go far beyond the usual insulin resistance, hyperglycemia, and hyperinsulinemia and include:

  • Hyperglycemia/Hypoglycemia
  • Insulin Resistance
  • Hyperinsulinemia
  • Hypercholesterolemia/Hypertriglyceridemia
  • Increase in Cortisol
  • Impacts to the Liver and Kidneys
  • Cellular Inflammation
  • Advanced Glycation End Products (AGEs)
  • Increase in Oxidation (Oxidative Stress)
  • Increase in Toxicity (Toxic Load)

Because these harmful biological processes feed upon each other, over a period of years, this causes Type 2 diabetes to continue to progress. And, as Type 2 diabetes continues to progress, this leads to cell and tissue damage throughout the body.

Key Point #1: This is why Type 2 diabetes is known as a progressive disease. And, since the diabetic drugs do nothing to stop this progression, it makes sense that the health of all Type 2 diabetics will continue to worsen over the years.

Key Point #2: About 5% to 10% of Type 2 diabetics are not overweight or obese. This is due to the fact that Type 2 diabetes is fueled by other harmful biological processes that can catabolize the body and prevent weight gain, e.g. cellular inflammation, oxidative stress, excess toxicity. 

Key Point #3: Most diabetes wellness programs focus strictly on controlling your blood sugar and fail to address these other harmful biological processes. Why is this important? Because if you only focus on blood sugar, your diabetes will still continue to progress at the cellular level, causing damage to your cells and tissues.

In addition, if you hit "the wall" and are unable to lower your blood sugar any further or if you can't consistently stabilize your blood sugar, it is probably due to one or more of these biological processes.

Note: For more details about these harmfulbiological processes and how to fight them, refer to our biological processes web page.

Insulin Resistance

The consistent presence of high blood glucose levels causes damage to the cells. These damaged cells begin to ignore insulin, which triggers the pancreas to produce even more insulin.

This leads to a condition known as insulin resistance. Insulin resistance is one of the initial triggers to the pathogenesis of Type 2 diabetes.

Insulin resistance is a condition in which multiple cells and tissues in the human body become resistant to the effects of insulin. Simply stated, insulin resistance occurs when cells and tissues ignore insulin and don't allow glucose to enter the cells and tissues.

A high carb diet (of processed foods and processed sugars) and/or a high protein/fat diet of conventional animal and dairy foods and processed fats (causing lipid overload in the liver) in combination with a sedentary lifestyle help to fuel insulin resistance and inflammation.

In insulin resistance, muscle, fat, and liver cells do not respond properly to insulin and thus cannot easily absorb glucose from the bloodstream. As a result, the body needs higher levels of insulin to help push the glucose into your cells.

The beta cells in the pancreas try to keep up with this increased demand for insulin by producing more insulin. As long as the beta cells are able to produce enough insulin to overcome the insulin resistance, blood glucose levels stay in the healthy range.

However, over time, the beta cells eventually are unable to keep up with the body's increased need for insulin. So, without enough insulin, excess glucose builds up in the bloodstream. As blood glucose levels escalate, this leads to hyperglycemia.

Because of insulin resistance and hyperglycemia, the pancreas is forced to secrete increasing amounts of insulin, resulting in a condition known as hyperinsulinemia.

And, hyperinsulinemia can lead to an increased activity and growth of fat cells, which further  fuels inflammation.

And, inflammation (along with glycation) causes cell damage, which increases oxidation, which is due to the increased production of free radicals.

Insulin Resistance: Cell Level

Insulin resistance, if uninterrupted can become a major factor in other disease pathologies such as heart disease, hypertension, obesity, and hyperlipidemia.

Insulin resistance creates high levels of insulin which leads to the release of the hormone, cortisol, from the adrenal glands.

Cortisol is the stress hormone that is involved in the fight-or-flight response when we're faced with what we believe is a life-threatening situation.

Cortisol triggers the release of high energy fatty acids into the blood stream, so that our body will have the necessary energy to respond to a life-threatening situation such as being chased by a bear in the woods. 

These systematic responses are normal in situations of high stress. After the life-threatening situation is over, cortisol would lower and return to its normal level. But, because we are leading stressful lives through worries and fears with very little physical activity and very poor eating habits, this leads to sustained high levels of cortisol, blood glucose and insulin.

Excessive levels of cortisol leads to excessive levels of fatty acids in our blood stream. These excessive levels can cause an over reaction of our immune system, and attack our own tissues. This, in turn, triggers an inflammatory response.

When these excessive fatty acids oxidize, this leads to a build up of fatty streaks and plaque formation in the artery walls along with calcification. This is why cardiovascular disease and hardening of the arteries is a major result of this metabolic syndrome.

Consequently, when the cells aren’t converting blood glucose for energy, it’s converted to fat for storage. Fat cells are responsible for hormone synthesis and storage of toxins.

Our environment is full of toxins from chemicals, detergents, pollution, drugs, food additives, pesticides, etc. When our fat cells get too big, they leak these toxins back into the blood stream. These toxins also inhibit the insulin function of the cells and stimulate inflammation.

Over the years, these conditions can lead to an increase in belly fat, also known as visceral fat, which surrounds our organs. Visceral fat is critical for keeping viruses, bacteria and other foreign bodies out of our vital organs.

Because visceral fat has the highest amount of cortisol receptors, this leads to a high level release of fatty acids around these organs. 

Subsequently, more oxidation occurs and this causes a large immune response, sending out white blood cells to destroy the invaders. This causes the body to be in a constant state of inflammation which can lead to the attack of all types of tissues in the body.

This, in turn, can lead to various disease pathologies such as allergies, chronic fatigue, high blood pressure, high cholesterol, heart disease, diabetes, and autoimmune disease, just to name a few.

The Liver

With the increase in insulin resistance, the liver in type 2 diabetes is programmed to both overproduce and under-utilize glucose.

First, the elevated free fatty acid levels play a role in the increased release of glucose from the liver. 

Later, after insulin resistance develops, the liver cells become insulin-resistant feeding into this metabolic syndrome and Type 2 diabetes pathogenesis.

As previously mentioned, high glucose levels leads to damaged insulin receptors and dysfunctional glucose transporters (GLUT4) , insulin resistance and an increase in fatty acids, which leads to an increase in visceral or belly fat.

And, this leads to an increase in oxidative stress and glycation, causing the (glycated) red blood cells to cause damage to the inner walls of the arteries.

This, in turn, triggers an immune response of cellular inflammation in order to release repair agents and chemicals to repair the damage to the arterial walls, which leads to an increase in inflammation.

Normally, inflammation is the first stage of cellular repair, but, in this scenario, the inflammation is ongoing and leads to cell and tissue damage.

Cellular Inflammation Flow Chart

The increase in glucose levels in the blood causes the glucose molecules to attach (glycate) to the hemoglobin molecule contained in the red blood cells.

Glucose attached to red blood cells are called advanced glycation end products or AGEs for short. These AGEs have very coarse edges, which cause damage to our arteries and capillaries as they circulate throughout our circulatory system. 

The damage to the arteries triggers the release of cholesterol from the liver to try to repair the damage (repair mode). But, instead of repairing the damage, it creates more plaque formation.

Fragile capillaries can also be damaged by these coarse red blood cells. Capillaries are the small blood vessels in our bodies that feed our kidneys, eyes (retina), and feet. This, in turn, can lead to kidney failure, blindness and lower leg/foot amputation.

In addition, poor flow of blood caused by damaged capillaries can result in bruises and sores that don't heal and infections that cause even more damage.

If you imagine what your body will go through due to the inflammation and damage caused by these coarse red blood cells, you will be able to understand why diabetic patients experience so many terminal problems.

The following diagram depicts a glycated red blood cell. Looking at this picture, you can see how this can cause damage inside your body.

Glycated Red Blood Cell

Advanced glycation end products (AGEs) form at a constant but slow rate in the normal body, starting in early embryonic development, and accumulate with time. However, their formation is markedly accelerated in diabetes because of the increased availability of glucose.

Note: The amount of glucose attached to the hemoglobin molecule increases if the levels of glucose in your blood are high [Ref: Hemoglobin A1C test].

So, once a red blood cell becomes damaged from the glycation, how can the body repair the cell? You may recall from basic cell biology that cells contain the "code" or "instructions" within their nucleus and DNA to divide or repair themselves.

But, red blood cells do not contain a nucleus, so they can't divide orrepair themselves. For more details, read the section below titled "Red Blood Cells Lifecycle" -- it explains why you can't reverse or cure your diabetes in 30 days or less, despite some of the claims being made by people on the Internet.

Note: For more details about insulin resistance, glycation, inflammation and oxidation, refer to the Insulin Resistance, Inflammation, Oxidation and Glycation web page.

Candida Problems

If you have diabetes, chances are good you will also have problems with a bacteria known as candida. Why? Because every living human has candida in his or her system.

Usually the "friendly bacteria" keep the non-friendly candida at bay, but certain factors such as high glucose levels can allow the candida to flourish.

Foods that can trigger candida include sugar, flour, alcohol, corn, potatoes, pasta, rice, bread and other processed foods that contain sugar or flour. Coincidentally, these foods are known as the author's 5 "Dead" Foods ...

By eliminating these "dead" foods, most people can get rid of their candida. Ironically, these are the same foods that diabetics need to avoid to better control their blood glucose levels. Focus on periodic detox and eating more organic yogurt, fermented foods and raw vegetables, especially those that inhibit the growth of candida, e.g. broccoli, cabbage, raw garlic, onions, turnips, kale.

For most people, it appears that they transition from being non-diabetic to being diabetic in one step. But, actually, it happens in stages.

The progression and development of Type 2 diabetes at the macro level consists of seven major stages:

  1. Hyperglycemia: This develops if glucose levels continue to rise primarily due to poor eating habits of consuming excess sugar and fats from overly-processed foods. 
  2. Insulin Resistance: Develops due to high blood glucose levels sustained over a period of years. Usually leads to weight gain. Note: This is the first stage that can be measured by your doctor with the fasting insulin blood test. 
  3. Hyperinsulinemia: This develops due to insulin resistance when there is no intervention over a period of years, causing excessive high levels of insulin being produced by the pancreas to try to meet the demands of high blood glucose levels. Note: Inflammation, Oxidation, and Glycation processes escalate and create vicious cycles that feed upon each other. This leads to cell and tissue damage; and, a further increase in insulin resistance and hyperinsulinemia.
  4. Impaired Fasting Glucose (IFT)/Pre-diabetes: Develops when there is a consistent fasting blood glucose level of 100-125 mg/dL. Inflammation, oxidation and glycation continue. 
  5. Impaired Glucose Tolerance (IGT): is a pre-diabetic state of hyperglycemia that is associated with insulin resistance and increased risk of cardiovascular pathology. Impaired glucose tolerance occurs when a patient has a raised glucose level of 140-199 mg/dL after 2 hours. This is usually accompanied with other health issues, e.g. obesity, high blood pressure, high cholesterol. Although some people may lose weight, studies show that more than 92% of the population will gain weight and become obese in the presence of continued insulin resistance, inflammation, hyperglycemia and hyperinsulinemia. From 10 to 15 percent of adults in the United States have impaired glucose tolerance or impaired fasting glucose. 
  6. Full-blown Type 2 diabetes: If the above dysfunctions continue, this can lead to Metabolic Syndrome X or consistent fasting blood glucose levels of 126 mg/dL and above. In most cases, patients are shocked when their doctor tells them that they are now diabetic.  
  7. Diabetic Complications: As Type 2 diabetes progresses with more insulin resistance, glycation, oxidation, toxicity and inflammation, this leads to cell/tissue degradation, blood vessel damage and biological dysfunction.  This leads to other health problems such as Dyslipidemia (elevation of plasma cholesterol, triglycerides (TGs), or a low HDL cholesterol level); Hypercholesterolemia ( high cholesterol, a form of hyperlipidemia, high blood lipids, and hyperlipoproteinemia (elevated levels of lipoproteins in the blood); and, 

    Hypertriglyceridemia (elevated triglyceride levels). This is often caused or exacerbated by uncontrolled diabetes mellitus, obesity, and sedentary habits

    All or a combination of these types of problems leads to atherosclerosis, cardiovascular diseases, macrovascular and microvascular health problems and diseases and eventually organ/system failure, e.g. high blood pressure, retinopathy, neuropathy, nephropathy, obesity, sexual dysfunction, gum disease, heart disease, heart attack, stroke, etc.     

The 7 Stages of How Type 2 Diabetes Develops

Type 2 Diabetes Pathogenesis

These stages are not distinctly separate as they tend to overlap and run simultaneously as Type 2 diabetes continues to progress over the years. And, these stages will continue unless there is some kind of intervention, e.g. diet and lifestyle changes.

Key Point: Unfortunately, most doctors do not measure your fasting insulin, which is the first measurable sign that prediabetes and full-blown diabetes are on the horizon. Therefore, because rising blood glucose levels lag behind rising insulin levels, it is possible to have high insulin levels with blood glucose levels still in the normal range.

We suspect that doctors ignore the fasting insulin blood test or don't put much value in it because there is no drug that they can prescribe that will lower your fasting insulin level (insulin resistance). But, once your blood glucose reaches 126 or higher, they can prescribe a drug to lower your blood glucose.

More specifically, if the initial stages of Type 2 diabetes pathogenesis (e.g. hyperglycemia, insulin resistance and pre-diabetes) are not interrupted, this will lead to full-blown diabetes more than 77% of the time!

You may be wondering: Why is it so important to understand how Type 2 diabetes develops?

Answer: By understanding how Type 2 diabetes develops and progresses over time, it made it easier to figure out how to stop the progression of the disease and then, reverse its progression and complications.

In addition, by understanding how Type 2 diabetes changes the biochemistry of a person's body from a non-diabetic state to a diabetic state, it made it easier to figure out how to reverse that person's diabetes by changing their biochemistry back from a diabetic state to a non-diabetic state -- as depicted in the diagram below.

6 Stages of Reversing Diabetes

Key Point: Taking diabetic medication does not interrupt these stages from occurring! The medication may lower the blood glucose level, but, the underlying biological mechanisms of insulin resistance, inflammation, oxidation and glycation are still occurring. 

Note: For healthcare professionals who want to know more about the pathology and pathogenesis of Type 2 diabetes and impact of nutritional science, refer to the DTD Science of Diabetes ebook.

Diabetes Affects Multiple Organs and Tissues!

Diabetes (both Type 1 and Type 2) affects many different types of cells, organs and tissues.

The primary system that is initially affected is the cardiovascular system. But, since there are no nerve cells in your arteries, you do not feel any pain as the diabetes causes damage to your arteries and other blood vessels.

As depicted in the following flow diagram, the damage caused by diabetes affects many types of cells: red blood, white blood, fat, liver, kidney, skin, epithelial, nerve, brain (neuron), etc.


And, these damaged cells eventually leads to problems with your eyes (blindness), kidneys (protein leaking in your urine, kidney failure), feet (ulcers, amputation), heart (atherosclerosis, high blood pressure), brain (stroke, Alzheimer's), etc.

However, as depicted in the following diagram, diabetes affects almost every system, organ and tissue in your body! Why is that? Because every organ and tissue in your body uses your blood vessels to receive nutrients and remove waste. And, since diabetes causes damage to your blood vessels, this can lead to nutrient starvation and damage to almost any organ/tissue.


Gut-Brain Axis (GBA) and Thyroid Effects on Blood glucose Regulation

Blood glucose regulation is very complex and can be affected by other organs such as the thyroid, gut, brain, etc.

Diabetes affects your brain, which affects your gut. Diabetes also affects your gut, which affects your brain. And, the impact to the brain and gut also affect your emotions!

These negative effects occur because of the gut-brain axis, which is a biochemical, neural connection between the gut and the brain.

As depicted in the following gut-brain diagram, it's a complex, vicious cycle that is partially due to the connection between the gut and the brain, along with connections to the immune system, blood glucose regulation and inflammation.

In addition, food affects your brain and gut; and, your brain and gut affect your food choices! Refer to our blood glucose regulation web page for more information about the gut-brain axis.

Gut-Brain Axis GBA

To further complicate matters, in certain scenarios ( as depicted in the following diagram), the thyroid can also be involved in these complex interactions and affect blood glucose regulation.

Thyroid Autoimmune Connection

Note: For more details, refer to the Thyroid & Autoimmune Diseases web page.


Red Blood Cells Lifecycle | Why You Can't Reverse Type 2 Diabetes in 30 Days or Less

There are 20-30 trillion red blood cells in your body, each with a lifecycle of about 120 days. That's a very important number to remember.

FYI: Red blood cells don't have a nucleus so they don't have the built-in code and instructions that tell a cell how to repair or duplicate itself. So, red blood cells die off and are swept away (in the liver and spleen) and eaten by the macrophages.

If you are diabetic with a high blood glucose level and/or a high hemoglobin A1C, this means that you have too much glucose in your blood and too many red blood cells (at least 1.5 trillion) with too much glucose attached (glycated) to the the protein portion of the red blood cell called hemoglobin.

The bone marrow creates about a billion new red blood cells every hour that are not glycated -- until they enter your bloodstream and begin to circulate throughout your body. 

As these damaged (glycated) red blood cells circulate, their "sharp" edges cause damage to the walls of your arteries. This leads to cellular inflammation and an increase in oxidation (free radicals) that cause further damage to your arteries and other tissues, starting with the kidneys and eyes. Why? Because the small delicate blood vessels that feed into the eyes (retina) and the kidneys (nephrons and glomeruli) become damaged.

So, you may be asking: How can the body repair the damaged red blood cells if these cells don't have a nucleus? 

Believe it or not, you can repair the damage by first reducing the amount of glucose in your bloodstream.

You can accomplish this by changing to a plant-based diet and exercising every day so that you reduce the amount of glucose in your bloodstream. Then, there will be less glucose in your blood, causing your fasting blood glucose level to decrease.

In addition, less and less new red blood cells will become glycated or damaged because there is less glucose in the bloodstream. As the older red blood cells reach 120 days, they die off and are replaced by the new (unglycated) red blood cells from your red bone marrow. This, in turn, eventually causes your hemoglobin A1C to decrease.

But, this process takes a lot more than 30 days! -- especially since the lifecycle of your red blood cells is 120 days!

So, you see, given the lifecycle of a red blood cell, it is almost impossible to reverse your diabetes in 30 days. So, when you come across a diabetes program that promises you that they can reverse your diabetes in 30 days (or less), then, run the other way! -- you'll know that they are lying to you.

Sidebar: Now, just to be clear -- that doesn't mean that you won't notice your blood glucose level starting to come down in less than 120 days. If you're following an effective diabetes program (like ours :-)), you will definitely notice your blood glucose level starting to come down, usually within the first 7 to 10 days.

But, that doesn't mean that you've reversed your diabetes during those first 7 to 10 days! -- you have to stick with the program a lot longer than that to reap the long-term benefits.

Of course, the overall process explained here is a lot more complex than this, but, hopefully, this simpler explanation has been helpful.

FYI: Here is a diagram that shows the lifecycle of a red blood cell and how red blood cells become damaged from the diabetes. 

Red Blood Cells Life Cycle -- Death to Diabetes

More About Red Blood Cells

Blood is a specialized body fluid that is comprised of four main components:

  • Plasma
  • Red blood cells
  • White blood cells
  • Platelets

The blood that runs through the veins, arteries, and capillaries is known as whole blood, a mixture of about 55 percent plasma and 45 percent blood cells. About 7 to 8 percent of your total body weight is blood. An average-sized man has about 12 pints of blood in his body, and an average-sized woman has about 9 pints.


The liquid component of blood is called plasma, a mixture of water, sugar, fat, protein, and salts.

Plasma is made up of 90% water, 7-8% soluble proteins (albumin), 1% carbon dioxide, and 1% elements in transit. One percent of the plasma is salt, which helps with the pH of the blood. The largest group of solutes in plasma contains three important proteins: albumins, globulins, and clotting proteins.

The main job of the plasma is to transport blood cells throughout your body along with nutrients, waste products, antibodies, clotting proteins, chemical messengers such as hormones, and proteins that help maintain the body's fluid balance.

Red Blood Cells

Red blood cells are also called erythrocytes or RBCs.

Known for their bright red color, red cells are the most abundant cell in the blood, accounting for about 40-45 percent of its volume. The shape of a red blood cell is a biconcave disk with a flattened center - in other words, both faces of the disc have shallow bowl-like indentations (a red blood cell looks like a donut).

Production of red blood cells is called erythropoiesis, which is controlled by erythropoietin, a hormone produced primarily by the kidneys.

Red blood cells start as immature cells with a nucleus in the bone marrow. They then undergo a process known as enucleation in which their nucleus is removed. Enucleation occurs roughly when the cell has reached maturity. So, after approximately seven days of maturation, the red blood cells are released into the bloodstream.

Because red blood cells have no nucleus, they can easily change shape, helping them fit through the various blood vessels in your body. However, while the lack of a nucleus makes a red blood cell more flexible, it also limits the life of the cell as it travels through the smallest blood vessels, damaging the cell's membranes and depleting its energy supplies. The red blood cell survives on average about 120 days.

The absence of a nucleus is an adaptation of the red blood cell for its role. It allows the red blood cell to contain more hemoglobin and, therefore, carry more oxygen molecules. It also allows the cell to have its distinctive bi-concave shape which aids diffusion. This shape would not be possible if the cell had a nucleus in the way.

The main component of a red blood cell (RBC) is hemoglobin protein, of which there are about 250 million per cell. The word hemoglobin comes from "hemo" meaning blood and "globin" meaning protein.

Hemoglobin helps to carry oxygen from the lungs to the rest of the body and then returns carbon dioxide from the body to the lungs so it can be exhaled.

Blood appears red because of the large number of red blood cells, which get their color from the interaction of hemoglobin, iron and oxygen. The percentage of whole blood volume that is made up of red blood cells is called the hematocrit and is a common measure of red blood cell levels.

Another interesting point about red blood cells: Red blood cells cannot be repaired like other cells because red blood cells don't contain a nucleus. Consequently, red blood cells have to be replaced. 

The absence of a nucleus is an adaptation of the red blood cell for its role. It allows the red blood cell to contain more hemoglobin and, therefore, carry more oxygen molecules. It also allows the cell to have its distinctive bi-concave shape which aids diffusion.

Because of the lack of nuclei and organelles, mature red blood cells do not contain DNA and cannot synthesize any RNA, and consequently cannot divide and repair themselves. 

White Blood Cells

White blood cells are also called leukocytes or WBCs, e.g.macrophages, neutrophils, T cells, B cells, etc.

White blood cells protect the body from infection and help to repair the body. They are much fewer in number than red blood cells, accounting for about 1 percent of your blood.

The major types of white blood cells are Basophils, Eosinophils, Neutrophils, Monocytes, B-cell lymphocytes and T-cell lymphocytes.

Basophils store and synthesize histamine which is important in allergic reactions. They enter the tissues and become "mast cells" which help blood flow to injured tissues by the release of histamine. Eosinophils are chemotoxic and kill parasites.

Neutrophils are the most common type of white blood cell, which is the "immediate response" cell and accounts for 55 to 70 percent of the total white blood cell count. Neutrophils fight bacteria and viruses by phagocytosis which mean they engulf pathogens that may cause infection. The life span of a Neutrophil is only about 12-48 hours, so your bone marrow must constantly make new neutrophils to maintain protection against infection.

Monocytes are the biggest of the white blood cells and are responsible for rallying the cells to defend the body. Monocytes carry out phagocytosis and are also called macrophages.

Lymphocytes help with our immune response. There are two types of Lymphocytes: the B cell and T cell. 

T cells help regulate the function of other immune cells and directly attack various infected cells and tumors.

B cells produce antibodies, which are proteins that specifically find and mark pathogens (bacteria, viruses) for destruction. 

Note: For more details about white blood cells, refer to our immune system or autoimmune disease web pages.


Platelets are also called thrombocytes.

Unlike red and white blood cells, platelets are not actually cells but rather small fragments of cells without a nucleus. Platelets help the blood clotting process (or coagulation) by gathering at the site of an injury, sticking to the lining of the injured blood vessel, and forming a platform on which blood coagulation can occur.

This results in the formation of a fibrin clot, which covers the wound and prevents blood from leaking out. Fibrin also forms the initial scaffolding upon which new tissue forms, thus promoting healing.

Less than 1% of whole blood consists of platelets. They result from fragmentation of large cells called Megakaryocytes - which are cells derived from stem cells in the bone marrow.

Platelets are produced at a rate of 200 billion per day. Their production is regulated by the hormone called Thrombopoietin. The circulating life of a platelet is 8–10 days. The sticky surface of the platelets allow them to accumulate at the site of broken blood vessels to form a clot. This aids in the process of hemostasis ("blood stopping").

Platelets secrete factors that increase local platelet aggregation (e.g. Thromboxane A), enhance vasoconstriction (e.g. serotonin), and promote blood coagulation (e.g. thromboplastin).

A higher than normal number of platelets can cause unnecessary clotting, which can lead to strokes and heart attacks; however, thanks to advances made in antiplatelet therapies, there are treatments available to help prevent these potentially fatal events. Conversely, lower than normal counts can lead to extensive bleeding.

Understanding diabetes (your enemy) is very important if you want to defeat your enemy. You don't have to be an expert, but, you should, at least, understand the basics.

Key Point: A clear understanding of the biochemical and hormonal processes that fuel Type 2 diabetes provides insight into how diabetes is damaging your body and will help you better understand the changes you need to make in order to control your diabetes and achieve tighter blood glucose control, insulin control and utilization, and blood glucose stability.

By understanding these processes, you'll be able to make a better, more informed decision about what diabetes program or book will be best for you. You'll also be able to recognize if it's a scam designed to take your money and run.

In addition, by understanding these processes, you can try the Death to Diabetes Wellness Program (before you buy the book) to make sure that it will work for you.

And, if you're into engineering, then, you'll have an understanding of how the Death to Diabetes Wellness Program used "reverse engineering" as one of the many engineering methodologies to better define how to first control the disease; then, stop the progression of the disease, and, finally, reverse the progression of the disease.

Summary and Conclusion

Studies have led to a new way of looking at visceral fat. It now actually appears to be a very active endocrine organ. A disturbance in this endocrine function helps to contribute to the metabolic syndrome of insulin resistance, inflammation and glycation; and, the development of Type 2 diabetes.

However, the good news is that the majority of Type 2 diabetes cases can be treated with a superior plant-based nutritional program and without the need for toxic drugs -- as long as you don't wait too long and allow too much damage to occur to the organs, tissues, and cells.

If you want to reverse your diabetes and prevent the complications, then, get one of the following books from the ex-diabetic engineer and author:

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  2. Grundy SM, Brewer Jr HB, Cleeman JI, Smith Jr SC, Lenfant C. Definition of Metabolic Syndrome. Report of the National Heart, Lung, and Blood Institute/American Heart Association Conference on Scientific Issues Related to Definition. Circulation 2004;109:433-438.
  3. Williams RH, Foster DW, Kronenberg HM, Larsen PR, Wilson J Md. Williams Textbook of Endocrinology, 10th ed. W B Saunders; Copyright [c] January 2003 Elsevier.
  4. Baron AD. Insulin resistance and vascular function. J Diabet Complications. 2002;16:92-102.
  5. Wheatcroft SB, Williams I L, Shah AM, Kearney MT. Pathophysiological implications of insulin resistance on vascular endothelial function. Diabetic Med. 2003;20:255-268.
  6. Unger RH. The Physiology of Cellular Liporegulation. Annu Rev Physiol 2003;65:333-347.
  7. Unger RH. Lipotoxic Diseases. Annu Rev Med. 2002;53:319-336.
  8. Angulo P. Nonalcoholic fatty Liver Disease. N Engl J Med. 2002;346:1221-1231.
  9. Garg A. Acquired and Inherited Lipodystrophies N Engl J Med. 2004;350:1220-1234.
  10. Rea R, Donnelly R. Resistin: an adipocyte-derived hormone. Has it a role in diabetes and obesity? Diabetes Obes Metab. 2004;6:163-170.
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  12. Ukkola O, Santaniemi M. Adiponectin: a link between excess adiposity and associated comorbidities? J Mol Med. 2002;80(11):696-702.
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  15. Hoppener JWM, Nieuwenhuis MG, Vroom TM, Ahren B, Lips CJM. Role of islet amyloid in type 2 diabetes mellitus: consequences or cause? Mol Cell Endocrinol. 2002;197:205-212.
  16. Hull RL, Westermark G, Westermark P, Kahn SE. Islet Amyloid: a critical entity in the pathogenesis of type 2 diabetes. J Clin Endocrinol Metab. 2004;89(8):3629-3643.
  17. Boden G. Effects of free fatty acids (FFA) on glucose metabolism: significance for insulin resistance and type 2 diabetes. Exp Clin Endocrinol Diabetes. 2003;111(3):121-124.
  18. Boden G, Chen X. Effects of fat on glucose uptake and utilization in patients with non-insulin-dependent diabetes. J Clin Invest. 1995;96(3):1261-1268.
  19. Eriksson J, Franssila-Kallunki A, Ekstrand AV, Saloranta C, Widen E, Schalin C, et al. Early metabolic defects in persons at increased risk for non-insulin-dependent diabetes mellitus. N Engl J Med 1989; 321 : 337-43.
  20. DeFronzo RA, Bonadonna RC, Ferrannini E. Pathogenesis of NIDDM. A balanced overview. Diabetes Care 1992;15 : 318-68.
  21. Kelley DE, He J, Menshikova EV, Ritov VB. Dysfunction of mitochondria in human skeletal muscle in type 2 diabetes. Diabetes 2002; 51 : 2944-50.
  22. Sreekumar R, Halvatsiotis P, Schimke JC, Nair KS. Gene expression profile in skeletal muscle of type 2 diabetes and the effect of insulin treatment. Diabetes 2002; 51: 1913-20.
  23. Mootha VK, Lindgren CM, Eriksson K-F, Subramanian A, Sihag S, Lehar J, et al. PGC-1a-responsive genes involved in oxidative phosphorylation are coordinately downregulated in human diabetes. Nat Genet 2003; 34 :267-73.
  24. Stump CS, Short KR, Bigelow ML, Schimke JC, Nair KS. Effect of insulin on human skeletal muscle mitochondrial ATP production, protein synthesis, and mRNA transcripts. Proc Natl Acad Sci USA 2003; 100 : 7996-8001.
  25. Ritov VB, Menshikova EV, He J, Ferrell RE, Goodpaster BH, Kelley DE. Deficiency of subsarcolemmal mitochondria in obesity and type 2 diabetes. Diabetes 2005; 54 : 8-14.

Understanding Pathology Helped the Author!

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