© 2012 Dr. Dale Peterson & drdalepeterson.com

Diabetes mellitus, often referred to as sugar diabetes, is one of the most common chronic diseases in the United States. According to the National Diabetes Fact Sheet, which was released in January 2011, nearly 19 million children and adults have a diagnosis of diabetes. It is estimated that 7 million more have the condition, but have not yet been diagnosed. It is believed that 79 million people in the United States are in a pre-diabetic state. 1.9 million new cases are identified each year.

The prevalence of diabetes rises with age. It afflicts 1 in 400 children and adolescents, but slightly more than 1 in 10 adults. Over a quarter of those aged 65 or older have diabetes.

Diabetes is commonly classified as “Type 1” or “Type 2.” Type 1 diabetes was called “juvenile onset” in the past because it was generally a condition that appeared in children and adolescents. Type 1 diabetes is characterized by an inability to manufacture adequate amounts of insulin. It is an autoimmune condition in which antibodies are destroying the islet cells of the pancreas, which are the body’s insulin factories. Type 1 diabetes cannot be managed without insulin.

From time to time I am approached by an enthusiastic marketer who assures me that if I simply convince insulin-dependent diabetics to purchase a particular nutritional support product they will no longer need to take insulin shots. He or she cites testimonials of “Type 1 diabetics” who have been able to discontinue the use of insulin after starting the marvelous product. I do not dispute the fact that some individuals have reported an ability to stop insulin, but they clearly did not have type 1 diabetes. Insulin had been prescribed to augment, not replace, that being produced by their own pancreas and when their condition improved they no longer required the additional insulin. There is no drug or nutritional supplement that will replace insulin in someone who is unable to manufacture it.

Type 2 diabetes is characterized not by an inability to manufacture insulin, but by an inability to use it effectively. Type 2 diabetics struggle with insulin resistance rather than a lack of insulin. Insulin levels in type 2 diabetes are often higher than normal as the body pours out more and more insulin in an attempt to overcome the resistance that is being encountered. Strategies to reduce insulin resistance are the most effective way to manage type 2 diabetes in its early stages.

Type 2 diabetes was once called “adult onset” or “late onset” because it tended to appear late in life and was considered a grandpa/grandma disease. Today, however, one out of every three children with newly diagnosed diabetes has type 2.

Classification is not as simple as it is popularly portrayed, however. Type 1 diabetics often develop insulin resistance over time. Likewise, many type 2 diabetics eventually lose the ability to keep up with the demand for insulin and require insulin injections to effectively control their condition. Failure to recognize that the two types of diabetes are not exclusive of each other can severely hamper efforts to effectively manage the disease. Management strategies must evolve over time as conditions change if diabetes is to be successfully controlled. Unfortunately, few physicians recognize this. As a result, they often fail to address insulin resistance or augment insulin appropriately.

I have known many insulin dependent diabetics who were able to reduce their insulin dosage and control fluctuations in their blood sugar more effectively when supports to overcome insulin resistance were added to their regimen. Conversely, I have seen a number of people with type 2 diabetes who were unable to bring their blood sugar into an acceptable range without the use of insulin.

Diabetes is generally regarded as a sugar control problem, but the challenge is much greater. Diabetes is first and foremost a disease of accelerated aging. This is why serious complications are common. Diabetic complications include retinopathy, nephropathy, neuropathy, and angiopathy. The suffix “opathy” means “disease.” Therefore the terms refer respectively to eye disease, kidney disease, nerve disease, and blood vessel disease.

Diabetic retinopathy is a disorder affecting the eyes. In its early stages miniature bulges, called microaneurysms, form on the tiny blood vessels in the back of the eye. As the condition progresses small vessels may close causing veins to swell. Nerve fibers in the retina, the surface upon which light is focused, also swell. In advanced situations new blood vessels begin to grow or leak into the jelly-like substance that fills the eye. The retina may detach from the back surface of the eye and scar tissue may form. Pressure in the eye may rise.

Early in the course of retinopathy vision is normal and no symptoms are present. As retinopathy progresses, spots called floaters may appear, vision may become blurred or fluctuate, night vision may deteriorate, dark or empty spaces may develop in the field of vision, and colors may become indistinct. Ultimately, blindness may occur. In fact, diabetic retinopathy is the leading cause of blindness in the United States for people between the ages of 20 and 74.

Diabetic nephropathy affects kidney function. The kidneys are designed to filter the blood as it passes through tiny blood vessels. If the blood vessels weaken or deteriorate, protein and other substances will begin to leak into the urine. As the condition deteriorates the filtering function of the kidney can fail leading to a need for dialysis. In 2008, the last year for which records are currently available, 202,290 individuals were receiving chronic (long-term) dialysis due to diabetic nephropathy, making it the leading reason for chronic dialysis in the United States.

Diabetic neuropathy is a condition in which nerves are damaged and unable to carry messages effectively. Neuropathy usually begins with numbness in the hands or feet. This is the reason it is important that people with diabetes check their feet daily for signs of injury. A blister that would cause pain under normal circumstances may be asymptomatic when neuropathy is present. Over time numbness may give way to tingling and then to severe, often disabling, pain.

Diabetic angiopathy, disease of blood vessels, contributes to retinopathy and nephropathy, but its effects go much further. Two thirds of people with diabetes have high blood pressure. Diabetics are 2 to 4 times more likely to experience a stroke or heart attack. Diabetic angiopathy is the leading cause of non-traumatic amputation of a leg in the United States. A major reason is that while diabetics and non-diabetics alike are prone to hardening and narrowing of large blood vessels, diabetics also develop narrowing of small blood vessels, a condition that is more difficult to detect and treat. Narrowing in main arteries can be addressed by placement of a stent or by doing a bypass graft, but nothing can be done to counter the effects of small vessel disease.

Medical management of diabetes is almost exclusively directed toward control of blood sugar levels. While this is important, sugar control alone has not proven effective in preventing the devastating complications of the disease. If we wish to significantly reduce the incidence of retinopathy, nephropathy, neuropathy, and angiopathy we must look beyond blood sugar levels and begin addressing the underlying causes of the accelerated aging seen in people with diabetes.

A number of theories on why aging occurs have emerged over the past several decades. Three of them are of particular interest in diabetes. They are the free radical theory of aging, the inflammatory theory of aging, and the cross-linking or glycosylation theory of aging.

Free radicals are usually, but not always, oxygen-based molecules. In the environment they cause metals to rust, window treatments to fade, tires to dry rot, and car finishes to oxidize. In the body they damage cell membranes, DNA, and cause oxidation of LDL cholesterol. The free radical theory of aging suggests that the cumulative damage done in the body by these unbalanced molecules over time explains in part why aging occurs.

Superoxide is called the “master oxygen radical” because it leads to the production of many other free radicals. Superoxide is formed when a free electron attaches itself to an oxygen molecule. Studies have found that superoxide production increases as blood sugar levels rise. This overproduction of superoxide places diabetics at greater risk of free radical damage than those without the disease. Free radical (oxidative) damage is one of the factors leading to loss of nerve function. Oxidative stress also damages and inflames the lining of blood vessels predisposing to the deposition of plaque within arterial walls. Overproduction of superoxide plays a major role in the accelerated appearance of large blood vessel disease in diabetes.

The overproduction of superoxide and the oxidants derived from it create inflammation in the tissues of people with diabetes. As a result, diabetics are exposed to a greater amount of chronic (ongoing) inflammation than those without the disease. The inflammatory theory of aging states that chronic inflammation is responsible for many of the tissue changes associated with the aging process.

The cross-linking or glycosylation theory of aging suggests that aging is caused by the stiffening of proteins as they interact with sugar in the presence of oxygen. The rate or extent of cross-linking is related to the level of sugar in the blood and tissues of the body. One of the tests used to monitor diabetes is called hemoglobin A1C or glycosylated hemoglobin. It is a measure of how rapidly cross-linking (glycosylation) is taking place in the hemoglobin molecule of red blood cells. Since the rate of glycosylation is strongly related to the amount of sugar present, the level of glycosylated hemoglobin can be used to determine the average blood sugar level over time. The average life expectancy of a red blood cell is 120 days, so a glycosylated hemoglobin tests gives an indication of what the blood sugar has been over a period of approximately three months.

Glycosylation produces what are referred to as advanced glycation end products, appropriately designated by the acronym AGEs. Diabetics have been found to have 2 – 3 times the usual number of AGEs. Cross-linking can damage the lining of blood vessels, accelerate the development of cataracts in the lens of the eye, and adversely affect the ability of nerves to carry signals to the brain. Cross-linking provides a good explanation for the appearance of small blood vessel disease in diabetes, and it provides further insight into the development of retinopathy and nephropathy.

Clearly, slowing free radical damage, inflammation, and cross-linking should greatly reduce the risk of developing the complications commonly associated with diabetes. Fortunately, it is possible to successfully address all three of the factors responsible for the accelerated aging seen in diabetes.

Diet, activity, and nutritional supplementation must all be addressed if diabetes is going to be managed successfully and complications are to be avoided. Medications may or may not be necessary depending upon the type and severity of the condition.

The diet should be anti-inflammatory in nature. This can be accomplished by restricting the protein content to one-third of the meal. The other two-thirds should consist of colorful fruits and vegetables sprinkled with a dash of oil. This is the approach popularized by Dr. Barry Sears in his book The Zone.

I recommend that additional precautions be taken. Avoid foods that would be unpalatable without reheating if being eaten as left overs. An example would be fried chicken. Nearly everyone would peel away the skin and congealed fat before slicing up the lean meat for use in a sandwich or salad. The message is if you wouldn’t eat it at room temperature don’t eat it hot and juicy either. This rule gets the potentially harmful saturated animal fat out of the diet.

Avoid foods made with refined sugars, flours, and grains. Also stay away from items filled with additives and preservatives. If you have difficulty pronouncing the ingredients on a label put the product back on the shelf rather than into your body. Include good fats such as olive oil, flax oil, and coconut oil. Include high fiber foods such as legumes, crucifers, artichoke, fruits and vegetables with skin, nuts, berries, and whole grains.

Get your body moving for at least 30 minutes daily. Time spent is more important than the pace at which the activity is performed. Move at a pace at which you can last for 30 minutes without stopping, talk out loud while you are doing the activity, and at which you don’t feel stiff and sore the next day. Perform strength training exercises once or twice weekly.

Protecting against free radical (oxidative) damage begins with taking a comprehensive nutritional supplement that is rich in the many nutrients required to support the body’s antioxidant defense system. It should contain all vitamins, all minerals, and all essential amino acids. It may contain other supports as well. I personally use a product called Lifetime that provides over 120 nutrients.

Oligomeric proanthocyanidins (OPCs) are super antioxidants that are extracted from sources such as grape skins and grape seeds. They are highly effective in reducing oxidative damage in the body. They provide the additional benefit of strengthening small blood vessels such as those in the back of the eye, an action that can significantly lower the risk of developing retinopathy.

Alpha lipoic acid is a substance that has strong antioxidant properties. It has been shown to be of benefit in slowing the progression or even reversing diabetic neuropathy. An appropriate amount appears to be 600 mg daily.

There is no good test to monitor free radical damage, but a blood test called high sensitivity C-reactive protein (HS-CRP) is an indicator of inflammation. It is widely available as it is recognized as a risk factor for heart disease. Inflammation can be controlled by supplementing omega-3 fatty acids, which are needed to manufacture anti-inflammatory substances. The two most effective fatty acids are EPA and DHA. A minimum of 1000 mg. of combined EPA and DHA should be taken daily. Fish oils are the riches sources of EPA and DHA. It is important to check the specific fatty acid content on the label of oil supplements. I have seen products containing as little as 150 mg. of EPA/DHA per 1000 mg. capsule and others containing 500 mg. per 1000 mg. capsule. If the HS-CRP remains elevated the amount of fatty acids may be increased or other supports may be added.

Some vegetarian sources of omega-3 oils are flax, borage, and evening primrose. Flax oil is the most economical of these. It is important to note that the effective amount is two or more tablespoons daily. Each tablespoon is equivalent to 14 capsules of oil. Taking one or two flax oil capsules daily is an exercise in futility, since the effective amount would be at least 28 capsules daily.

I have recently seen krill oil and calamarine (squid) oil promoted as alternatives to fish oil. The major factor emphasized by advocates of krill oil is the presence of an antioxidant in addition to omega-3 fatty acids. Unfortunately, krill oil is relatively low in omega-3 making it difficult to obtain the recommended daily amounts through this source. Proponents downplay the low omega 3 levels by saying that they are better utilized, but I know of no scientific evidence to support this.

Calamarine oil is promoted as having a higher ratio of DHA to EPA and as being a sustainable source of omega-3 oils. It is currently significantly higher in price than traditional fish oil, but it may prove to be a good alternative if prices become more comparable.

Enzymes can be used to reduce inflammation. If pancreatic enzymes are taken during or shortly after a meal they go to work digesting food in the stomach. If they are taken at least an hour before or two hours after eating they are absorbed and travel throughout the body clearing areas of debris or inflammation. Some other supports that can reduce inflammation include curcumin (turmeric), capsaicin (cayenne), glucosamine, and irvingia (West African wild mango).

One of the most exciting advances in the management of diabetes in recent years has been the discovery that certain vitamins and amino acids are capable of blocking or slowing the cross-linking process. The primary support in preventing cross-linking and its effects is benfotiamine, which is a fat-soluble form of vitamin B1. Vitamin B1, or thiamine, is ineffective in preventing cross-linking, perhaps because it is water-soluble and washes out of the body very quickly. Benfotiamine, however, has been shown to block all three mechanisms by which cross-linking occurs. Benfotiamine prevents the formation of advanced glycation end products and has been shown to not only delay the onset and progression of retinopathy, nephropathy, and neuropathy, but actually reverse some of the damage that is already present. It is not as easy to demonstrate, but the development of small blood vessel disease should also be prevented or slowed since cross-linking is believed to be the primary mechanism responsible. The effective amount of benfotiamine appears to be 300 mg. daily. The amino acids L-carnitine and L-carnosine are also showing promise in preventing cross-linking in diabetes. The effective amount of each is believed to be 1000 mg. daily.

It is important to view diabetes as a condition of accelerated aging. Addressing the processes that cause aging can significantly slow the development of and reduce the severity of its many devastating complications.

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