Diabetes is More Than Just Controlling Blood Sugar

The growth in our understanding of why people develop Diabetes Mellitus Type 2 (DMT2) is greatly out-pacing our present treatment strategy.

In the early 1900s, the primary fear about getting DMT2 was from the very elevated levels of blood sugar (glucose in the 400-700 mg/dl range) that would trigger a deadly condition called diabetic ketoacidosis.  Diabetic ketoacidosis differs from mild ketoacidosis, which occurs from restricting carbohydrates in the diet.

In 1921 insulin was discovered, and the fatal complication of diabetic ketoacidosis was now, in many cases, avoided. Now instead of dying from a diabetic coma, patients were living longer, and their more common cause of death from DMT2 was the consequence of chronically elevated blood sugar within the bloodstream. 

Atherosclerosis in DMT2 occurs when the blood sugar (glucose greatly than 137 or a HgbA1c level greater than 6.4%) is not enough to trigger the deadly ketoacidosis. Still, it is enough to act as a toxic irritant to the surface of the blood vessels.  The chronic toxic nature of this concentration in diabetes of blood sugar damages the inner lining of the blood vessels and leads to blindness, kidney failure, amputations, and premature death.

In the more modern era, the development of additional blood sugar-lowering medications has given diabetics the ability to maintain their blood sugar HgbA1C levels at less than 6.4%. Keeping one’s blood sugar in this range greatly reduces the toxic complications of blindness, numbness in the feet, kidney failure, and amputations and greatly increases survival.

Diabetes and Cytokines

Today our understanding of DMT2 has grown even further.  There is overwhelming evidence that DMT2 is fueled by a chronic elevation of inflammation chemicals released by white blood cells.  Known as pro-inflammatory cytokines, these chemicals circulate throughout the bloodstream and can trigger a wide array of genetic disorders, including DMT2.

These proinflammatory cytokines not only turn on the gene(s) that trigger DMT2, but they also influence the level of abnormal blood sugar elevation.  The higher the levels of inflammatory cytokines in someone with a gene for DMT2, the higher their blood sugar level.  And conversely, the lower the cytokine levels, the lower their blood sugar.

These inflammatory cytokines also activate other genes leading to the development of cancer, hypertension, and  Alzheimer’s dementia. It can cause direct damage to the tissues throughout the body, which leads to sensory neuropathy (numbness in the feet), osteoarthritis, heart disease, osteoporosis, and, most dangerously, damage to the autonomic nervous system. 

Is managing blood sugar enough to control diabetes?

Unfortunately, the present goal of diabetes management of reducing blood sugars without also focusing on the elevated cytokine levels has led to continued high rates of sudden death, cancer, and Alzheimer’s in patients whose blood sugar levels are “under control.”

Insulin, metformin, and the ever-growing number of prescription medications that lower blood sugar does little to nothing to lower inflammation.  The toxic effects of inflammatory cytokines continue to damage the body and activate other dangerous genes continues unabated.

The persistent elevation of inflammation is why patients with controlled diabetes have a much higher incidence of cancer, strokes, and heart attacks than people without a diagnosis of DMT2.

Furthermore, the single most common cause of death in individuals with DMT2 is due to direct inflammatory damage of the autonomic nervous system, a condition known as diabetic autonomic neuropathy or cardiac autonomic neuropathy (CAN). 

Cardiac autonomic neuropathy is a profoundly weakened state of the parasympathetic branch of the autonomic nervous system and results in the instability of heart rate control.  Diabetics have other autonomic issues from parasympathetic dysfunction, such as bloating, heartburn, constipation, widely fluctuating blood pressure, and gastroparesis.

In fact, the autonomic nervous system of a diabetic prematurely ages because of inflammation and often has the functional capacity of someone approximately 20 years older than a person the same age without diabetes.  The autonomic function is critical to maintaining good health and a prolonged lifespan because a healthy autonomic nervous system is required for your brain to properly control your heart.

Patients die from sudden cardiac death due to cardiac autonomic neuropathy because their heart rates will suddenly jump to 300 beats per minute, so they cannot maintain any blood pressure at this point. Then they die of cardiovascular system collapse.  In 2016, the SAVOR-TIMI 53 Trial determined that approximately 1/3 of deaths in persons with DMT2 were caused by sudden cardiac death.

There are no symptoms or warning signs as cardiac autonomic neuropathy silently develops.  It can be easily detected with a physician’s common electrocardiogram (ECG or EKG) through a measurement known as heart rate variability (HRV).  If it is detected, death can easily be prevented by reversing the underlying inflammation or blocking the arrhythmia with medication. Still, unfortunately, most modern ECG machines do not provide physicians with that simple information.

How the Nemechek Protocol® Can Help

The Nemechek Protocol® was developed with this condition in mind, and CAN be the reason why I became interested in testing and treating the autonomic nervous system.  Cardiac autonomic neuropathy can easily be detected by assessing the autonomic nervous system with a simple 17-minute test known as spectral analysis. 

Once detected, my patients are started on The Nemechek Protocol®, and their cardiac autonomic neuropathy (CAN) is often reversed in 3 to 5 months.  During that time, patients are temporarily placed on a medication that greatly reduces the risk of sudden cardiac death from occurring while the protocol allows the autonomic nervous system to recover.

Over the last few decades, we have witnessed DMT2 occurring in younger and younger individuals.  This is because the abnormal elevation of chronic inflammatory cytokines begins at younger and younger ages as well.

If you have diabetes, there are several things you can do to prevent yourself from dying from CAN and sudden cardiac death.

First, ask your physician to refer you to a cardiologist capable of determining whether cardiac autonomic neuropathy exists.  Second, study and learn everything you can about chronic metabolic inflammation and how it affects your health. And finally, start developing a program to lower your inflammatory cytokines. 

The Nemechek Protocol® is a great place to start.  Supplementing your diet with omega 3’s (fish oil), omega 9’s (extra virgin olive oil) and reducing your intake of calories, carbohydrates, and advanced glycation end products (AGE’s are abnormal molecules formed when food is cooked quickly and at high temperatures) all have an additive effect on lower inflammation and helping your autonomic nervous system to recover.

With time you will be able to detect the reduction of inflammation in your blood work.  Look for reductions in your fasting blood sugar, HgbA1c level, and triglycerides.  Reductions in those numbers are all indications that your inflammation is declining.  Additional tests, such as the highly sensitive C-reactive protein (hs-CRP), will also decline once your inflammation is lowered.

The Nemechek Protocol® also encompasses the use of transcutaneous Vagus nerve stimulation to get substantial recovery of autonomic function.  This is a type of electric neuromodulation to the Vagus nerve, completely controlling inflammation throughout the body.

Diabetes management is no longer just about taking pills to keep blood sugar levels low because diabetes is never under control in a high inflammation environment.  Diabetes management must include a focus on inflammation control by the combined benefit of calorie reduction, carbohydrate reduction, AGE reduction, and improvement of autonomic nervous system health to prevent death from sudden cardiac death.