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Painful neuropathy is often the initial presentation of diabetes. This was the case for GJ. Three years ago he went to his primary physician with burning pain and numbness in his toes. GJ's blood sugar was high - the diagnosis of adult onset diabetes was made. Metformin (insulin sensitizer) therapy was initiated and GJ modified his diet. During the summer months GJ exercises on a regular basis; this keeps his fasting sugars in the 110-130 range and the foot burning to a minimum. During the winter, GJ exercises less; his sugars rise above 130 and with this he has more pain.

Blood flow to GJ's lower extremity is intact. His neurometer readings returned abnormal (See separate discussion of neurometer testing - a neurometer score of zero is normal and 12 reflects sensory nerve failure). GJ's baseline readings were in the 10-16 range, with a mean value of 12.5. GJ received 80 hours of MME over 8 days. GJ reports complete resolution of his foot pain, and a return of cutaneous sensation. In his words - "Doc, I'm 100% better". Objectively, GJ's neurometer readings improved, now with a mean value of 9.9. GJ received an additional 40 hours of MME. His mean neurometer score is now 9.4. On a 1 to 10 scale, his overall neuropathy pain level has fallen from a 4 at baseline to 0 post-MME.

For GJ, in 8 days MME resolved neuropathy symptoms that had been present for 3 years. For GJ, in 8 days MME reversed nerve dysfunction that had taken years to develop. How does this work? To understand how MME works we first must understand the causes of diabetic neuropathy.

First, what causes diabetic neuropathy? What is it about high blood sugar and the diabetic condition that leads to nerve failure. Let's break this down:

1. Glycation - Excess sugar, beyond that needed for energy metabolism, can bind irreversibly to proteins within the nerve cell and elsewhere in the body. This process is termed "glycation". The higher your sugar, and the more persistent the elevation, the greater is the potential for glycation. Red blood cells persist in our circulation for three months; after that they break down and are replaced by new red cells. %HbA1c, the percentage of red cell hemoglobin that is glycated by glucose, thus serves as a running 3-month average of your sugar values. Glycation damages peripheral nerves. The higher the sugar, the longer the sugar is high, the more nerve damage. This is why GJ's symptoms are worse over the winter months; his sugar is higher then, so ongoing nerve damage is greater.

2. EFA imbalance - In diabetics, the enzymes that convert dietary essential fatty acids into downstream fatty acids and prostaglandins are rendered dysfunctional. Nerve cell membranes are constructed primarily of fatty acids, and their metabolism is directed by fatty acid derived prostaglandins. If you can't make the right fatty acids, nerve cell membrane function will be defective. If you can't make the right prostaglandins, nerve cell metabolism will be off. Diabetics tend not to take in a healthy mix of EFAs in the first place, and even if they did, they'd have trouble converting them into the desired prostaglandin molecules. High dose EFA supplementation, at least in part, rectifies this situation, and has been shown in multiple studies to reduce the symptoms of diabetic neuropathy.

3. Sorbitol accumulation - Glucose can diffuse into and out of the cell. Sorbitol, an intracellular metabolite of glucose, cannot. A cell flooded with glucose is soon flooded with sorbitol particles. They can't leave the cell, so the cell must admit water molecules, to allow its osmotic pressure to match that of the surrounding extracellular fluid (the concentration of particles, molecules and other structures, within the cell must match that of the extracellular environment). The cell thus swells, taking up too much space, damaging adjacent cells and bodily structures. Sorbitol accumulation is felt to play a major role in diabetic neuropathy and cataract formation.

4. Microvascular insufficiency - You are familiar with the macrovascular complication of diabetes - "big vessel" blockage, leading to heart attack, stroke, and peripheral vascular disease. The small vessels, especially those serving the peripheral nerves, are also affected, choking off the flow of oxygen and nutrients to the peripheral nerves.

5. Nutritional deficiency - Diabetes "wastes" nutrients. When the sugar is high, some "spills" out into the urine, carrying with it valuable nutrients. As your body attempts to cope with its high sugar load, other nutrients are utilized at a rate far grater than Mother Nature ever planned on. The result is deficiency of key nutrients such as potassium, magnesium, and pertinent to this discussion, the B vitamins. B vitamins are crucial to peripheral nerve function and they are in short supply in diabetics.

6. Oxidative stress - The impaired metabolism that characterizes the diabetic condition leads to excessive free radical formation. You are likely familiar with free radical oxidation as a key player in heart disease. Free radicals also damage peripheral nerves and the microvasculature that serves them.

Now that we've discussed the pathophysiology of diabetic neuropathy, let's talk about its treatments, conventional and nutritional..

1. Universal recommendation - Keep the sugar down. All physicians agree that keeping your sugar values down will improve your current symptoms and decrease the rate at which you progress to irreversible (well, we always thought that diabetic nerve failure was irreversible) nerve failure.

2. Nutritional recommendations - You won't see this on TV adds, but nutritional supplementation can have a dramatic affect on the course and symptomatic status of the patient with diabetic neuropathy. Study after study confirms this. If EFA deficiency is a problem, than supplement with EFAs. If free radical stress is a problem, then take Lipoic acid (fat and water soluble antioxidant that readily enters peripheral nerves). If B vitamin deficiency is a problem, then increase your B vitamin intake. This is a no brainer for us. Our nutritional recommendations for the patient with diabetic neuropathy are outlined in a separate section below.

3. Pharmacologic recommendations - There are no drugs that neutralize or reverse the metabolic abnormalities that underlie diabetic neuropathy. Sure, there are drugs that help lower your blood glucose values, and we are big advocates of the insulin sensitizers, Metformin and drugs of the Thiazolidinedione class, but drugs don't decrease oxidative stress, drugs don't provide you with B vitamins, and no drug company is ever going to make a man-made fatty acid that works better than the fatty acids that Mother Nature created for us. Rather, drug therapy for diabetic peripheral neuropathy consists of man-made chemicals that numb your nerves. The underlying condition is not affected. Your neuropathy does not improve, but your symptoms do. Drugs that are otherwise used for seizure control or an antidepressants will reduce your symptoms. They slow conduction in the pain sensory nerves, so you feel less pain. Drugs for diabetic neuropathy convert you from "painful" neuropathy to "totally numb" neuropathy. That can be a blessing for the patients who can't sleep at night due to intractable pain, but the underlying problem is not affected.

4. Bipolar magnetic insoles - This is not MME and actually shares little physiology with MME, but if you wear bipolar magnetic insoles 24 hours a day your painful symptoms may certainly improve. In a randomized, blinded study, subjects with painful diabetic neuropathy wore either active or placebo magnetic insoles over the 1st or 2nd month of the study, and then all subjects wore active insoles for an additional two months. The insoles were worn 24 hours a day. Pain levels fell in a statistically significant fashion, but non-invasive measures of nerve function did not change. Symptoms recurred after insole therapy was discontinued. The researchers felt that bipolar magnetic insole therapy worked by slowing transmission of the nerve fibers (unmyelinated type C fibers if you want to get technical) that carried the "pain message" from your feet to your brain. Think of this as a sort of "magnetic numbing". Numbing the nerve fibers with a magnetic field is probably safer than numbing them with a man-made prescription drug, but nerve function does not improve, the nerves are not healed, and pain returns if you stop wearing the insoles.

5. Magnetic Molecular Energizer (MME) - I can't tell you exactly how MME reduces symptoms and improves neurometer readings in patients with painful diabetic neuropathy. To do this I would need to treat a bunch of you, do extensive chemical tests, then remove your nerves and look at them under a microscope - any volunteers? What I can do is share with you my ideas, based on what I see in patients and from the scientific literature that I have read regarding the effects of magnetic fields on our biology. I think that we are restoring function and repairing the still viable peripheral nerve cells, and also replacing the irreversibly damaged ones with new nerve cells. Let me explain:

A. Improved blood supply - Obviously we are not providing to the patient B vitamins or essential fatty acids by applying MME, but we may be speeding their delivery to the cells in question by improving their blood supply. Static magnetic fields dilated blood vessel and increase blood flow to the cells exposed to the field. This is fact, demonstrated in both US and European studies. Better blood supply means better nutrient delivery, and more oxygen, needed by the nerves to generate energy.

B. Reduced free radical stress - Magnetic fields have been shown to decrease the production of free radicals. These electron sharks damage peripheral nerves just as they oxidize LDL cholesterol and damage the vascular wall.

C. Increased energy generation - The driving force underlying all useful chemical reactions in the cell is its concentration of ATP, the cellular energy packets derived from the burning of dietary sugar and fat. Healthy cell are loaded with ATP. Sick cells are low in ATP. That is why they are sick; without ATP they can't function well, nor can they repair themselves. It has been demonstrated that magnetic fields increase ATP production and increases the activity of the enzyme systems that utilize ATP to repair cell structures and power cell activity. More power to you!

OK - so blood supply improves, potentially damaging free radicals are squelched, and the cell can make more ATP. Thus sick peripheral nerve cells should function better. Pain should lessen and nerve function should improve. But what if the nerve cells are irreversibly damaged. Could MME "bring them back to life"? The answer is no, but it's not necessary to bring dead cells back to life - not if you can generate replacement cells.

D. Stem cell proliferation - Within our organs there is a small population of in situ stem cells. These serve as a source of replacement cells. We used to believe that you were born with all the brain cells or heart cells that you were going to get, and that if these cells died they could not be replaced. Remember from high school - they told us that drinking a beer would kill one million brain cells and that they would never grow back. This isn't correct. The brain contains stem cells that can proliferate and migrate to replace cells lost due to disease states, toxins, or trauma. They lied to us. This is a good thing, because none of us paid much attention to this admonition and drank beer and our brains turned out just fine (if we consumed beer in moderation, that is). Stem cells in the heart activate when the heart is damaged. Stem cells in the liver turn on readily when the liver is damaged (you can lose 90% of you liver and the stem cells of the remaining 10% can regenerate a normally functioning liver). We know that magnetic fields increase stem cell activity in the brain (well worked out in animal studies). We think that MME stimulates the proliferation of stem cells within the peripheral nerves of patients with diabetic neuropathy. We'll prove the physiology some day. Right now our goal is to prove that it works. The first step is to carry out a randomized, double blind study of MME vs. sham MME in the treatment of painful diabetic neuropathy. This study is in the works. The patients reported on in this section received open therapy. They knew and I knew that they were getting active MME. Thus there could be a placebo effect. Just because they improved subjectively and demonstrated an improvement in nerve function doesn't mean that other patients will get better and improve their neurometer scores. We have to prove the point. We have work to do and intend to do it.

BR has been under my care for over a decade, but he's had heart disease for over two decades, and he's been a diabetic even longer. Bypass surgery was carried out in 1990, but now BR has a pattern of recurrent coronary disease not amenable to stent placement or further surgery. BR was one of my earlier EECP patients in '98. An integrated program of nutritional and pharmacologic therapies has been continued, and he hasn't set foot in the hospital for a cardiac problem since.

However, BR's feet do hurt, and up until now I didn't have anything to offer him. BR sees an internist and an endocrinologist. He watches his diet, takes insulin at least twice a day, and exercises on a regular basis. His HbA1c level has been at 7 or below since 1998, but a burning sensation in his feet on the basis of diabetic neuropathy has remained a problem. BR's baseline neurometer score was 11.3. BR received 86 hours of MME over 7 days. BR rates his pain as 60% improved, and his mean neurometer score fell to 8.9. BR received an additional 40 hours of MME. His mean neurometer score is now down to 8.6. On a 10 point scale, his overall neuropathy pain level, 5 pre-treatment, is now down to a 1. 1.

I've always enjoyed being able to help patients with recurrent or inoperable coronary disease with EECP. Helping them resolve their neuropathy symptoms with MME should be a lot of fun as well.

WT's feet weren't keeping up with his arteries, nor with the rest of his body for that matter - so we treated his diabetic neuropathy with MME. In early '01, WT's primary problem was intermittent claudication, effort related calf discomfort on the basis of impaired lower extremity blood flow (angina of the legs). Surgery was recommended and eventually carried out, but WT's 1/01 pre-operative Persantine Cardiolite study (chemical stress test) returned abnormal. Coronary angiography revealed a long, 80% narrowing in WT's diffusely diseased Right Coronary Artery, 50 and 60% narrowings in the major branch vessels of the Circumflex and Left Anterior Descending, respectively, and a non-flow restrictive, 40% Left Main narrowing. The RCA narrowing was not felt to be amenable to angioplasty or stent placement. Anti-ischemic medical therapy (lowers HR and BP to decrease the heart's requirement for oxygenated blood) was given and WT got through his lower extremity vascular reconstructive surgery intact.

WT began reading about nutritional approaches to cardiovascular disease and put himself on an extensive, well thought out regimen. His 4/02 follow-up Persantine study, while still abnormal, showed an interval improvement. WT's symptoms, however, did not resolve, and when we met in early '03 WT was experiencing 14 episodes of angina every week, requiring the same number of NTG tabs. WT had a number of atherosclerotic risk factors (see table) which we addressed as best we could.

Lipid Abnormality	+ N. sanguineum serology	Inflammation - CRP 18.3 mg/L	Low Testosterone level
Adult onset Diabetes	RBC Cadmium & Lead	Low Thyroid status	Prior Mercury Fillings
Hypertension	Long-standing Smoking	Viscous Blood - Fibrinogen 552 mg/dl

WT underwent 35 hours of EECP, and began Nanobiotic therapy; with these measures angina frequency fell from 14 to 1 episode per week. WT was later switched from Nanobiotic therapy to DeToxMax plus, which provides oral EDTA and Phosphatidylcholine, and Lumbrokinase (an oral clot dissolving agent) was added to his program. With these measures WT's angina has all but resolved, and we demonstrated plaque regression in WT's carotid arteries (see chart below).

The chart depicts the velocity of blood flow within WT's right and left carotid arteries, in systole (following cardiac contraction), and in diastole (cardiac relaxation). When an artery is narrowed, the volume of blood ejected by the heart will flow more rapidly through the vessel. (What happens to the velocity of water flow when you partially obstruct the end

of a garden hose with your thumb?) The tighter the narrowing, the greater will be the velocity. Following carotid artery reconstructive surgery, the flow velocity will decrease; if the artery plugs up again, the velocity of blood flow will rise. If a medical therapy decreases the velocity of blood flow within a carotid artery, that medical therapy has opened up the artery, to a degree commensurate with the recorded drop in blood flow velocity. The 2nd set of data points, designated as "Base", correspond to WT's carotid velocities before beginning DeToxMax and Lumbrokinase, and the 3rd set of data points to his carotid velocities after 5 months of treatment. You can see from the data that WT had been worsening, as the baseline velocities were greater than the velocities recorded just 4 months earlier. Treatment with DeToxMax and Lumbrokinase turned the situation around, with a reduction in velocity readings within 5 months, corresponding to an improvement in blood flow within the left, and particularly in the right, carotid arteries. We expect that the same phenomena was occurring within every artery in WT's body, as with this approach we are treating the entire circulation of the patient, not an isolated narrowing as when we carry out an angioplasty, stent, or surgical procedure.

This is all well and good. Well actually this is fantastic, but WT's feet continued to hurt. The problem was not vascular insufficiency; that had improved with surgery and our anti-atherosclerotic measures. The problem was diabetic neuropathy, pain and numbness over both feet due to sensory nerve damage from diabetes (glycation, free radical stress, sorbitol accumulation, and disordered prostaglandin metabolism within the nerve cells are the mechanisms by which diabetes damages nerve cells). WT was numb over both feet, such that if he stepped on a tack, he might not feel it. His feet burned constantly; a 5 mg Duragesic patch (slow release of narcotic) and oral Vicodin (rapid release narcotic) were required to control WT's pain to the point where he could function at a reasonable level.

So how do we address this problem, this problem of diabetic neuropathy? First we do all in our power to lower the patient's sugar values, and WT was receiving insulin and Glucophage, an oral insulin sensitizer. A number of nutritional agents, along with Testosterone replacement therapy, were on board, all aiming to optimize sugar control. WT was also receiving Lipoic Acid 3-600 mg/day and Gamma Linolenic Acid, 3 gelcaps daily, aiming specifically at his neuropathic symptoms (please see our general diabetes and diabetic neuropathy recommendations in the next section), but WT was still hurting. WT was still hurting, despite our best nutritional and pharmacological efforts. When MME became available in Toledo, WT decided to give MME a try.

Diabetic neuropathy typically requires 75-150 hours of MME. Our plan was for WT to undergo 100-150 hours of MME to his feet - an initial 100 hours, and then an additional 50 hours, depending upon his response. Tactile function improved with 50 hours, such that WT could feel light touch on the bottom of his feet, but his burning neuropathic foot pain had increased, as had WT's requirement for pain meds. WT wasn't distressed by this, and neither was I, as we both understood that for the nerves to "hurt", to mediate the signal of pain, that they first must be able to function - the increase in WT's perception of pain was actually a good sign, a sign that his sensory nerves, damaged from long-standing diabetes, were regenerating. Four weeks later, without further MME, WT's pain level was less, as was his pain med requirement - first the nerves regenerate, then they heal. WT just completed 50 additional hours of MME; we hope that his improvement will continue.

Disclaimer - The following recommendations are based on the studies presented by Dr. Roberts in his nutritional medicine lecture series. While these therapies are safe, low in cost, supported by published literature, and in general quite effective, they should not be interpreted as specific medical advice. Working with your physician is important. Your sugar levels will fall, sometimes markedly, when these nutritional interventions are added to your current dietary and drug program, and you and your doctor must be ready to decrease the dose of your medications. Copies of the slides, the talk bibliography, and the tape of the talks are available to you and your physician. When reviewing the following general recommendations, please note that bid means twice a day, tid refers to three times a day, and qid to four times a day dosing.

1. Exercise, the more the better, in a form enjoyable to you, at an intensity level appropriate to your overall health. If you have concerns, ask your doctor.

2. Dietary Modification - Always tailored to an individual’s health status, but several general principles apply:

A. 25% carbohydrate, 45% protein, & 30% fat. Low glycemic index, higher fiber carbohydrates are emphasized and sweets and simple carbohydrates avoided. Fats should be primarily unsaturated. Liberal intake of vegetables and low glycemic fruits is encouraged. Balancing carbohydrate and protein portions at each meal provides additional benefits (Enter The Zone by Dr. Barry Sears).

B. Markedly overweight diabetics may benefit from more stringent carbohydrate restriction, especially when weight loss is an important goal (Protein Power by Drs. Eades & Dr. Adkins Diet Revolution by Dr. Roberts Adkins).

C. Patients with active coronary disease and angina may do better with primary emphasis on fat restriction, to < 15% of calories. Lean protein, vegetables, and low glycemic index carbohydrate sources are emphasized (Pritikin or Ornish diets). After coronary problems have been stabilized, then consideration can be given to shifting to a more carbohydrate restrictive program.

3. Weight Control: Through diet and exercise, lose the weight that made you diabetic in the first place. Insulin sensitivity improves early in the process; a little weight loss can make a big difference.

4. Dietary Fiber: 25 gms/day of dietary fiber is recommended. If that isn’t practical, fiber supplementation can be carried out as:

5. Iron Overload: Excess iron promotes free radical oxidation, compromises insulin sensitivity, and increases coronary risk. If your ferritin level (measures stored iron) is elevated, lower your iron stores to normal by periodically donating blood to the Red Cross or through a series of Desferoxamine injections.

6. Nutritional supplementation (click Diabetes References for the citations in the medical literature)

B. Vitamin E (preferably Unique E or a preparation containing mixed tocopherols) 800 IU and vitamin C 1000 mg extra

I. Nicotinamide 500 mg tid - preserves pancreatic function

M. Potassium - patients on diuretics should aim for a level in the mid-normal range

N. Testosterone - In men, Testosterone replacement therapy (preferable utilizing implanted pellets) improves insulin sensitivity and glucose control. Te Testosterone has a favorable effect on many cardiovascular risk factors and has a direct beneficial effect in angina, claudication, and CHF.

AMRI of NW Ohio provides MME treatment under the guidelines of an Investigational Review Board, consistent with FDA regulations.

Please note that MME treatment is considered to be experimental by the FDA. Although many patients have improved, no guarantee of success is implied.