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Diabetic Peripheral Neuropathy
Neuropathy is disease of the nerves. In a diabetic, it takes two forms: Autonomic Neuropathy and Peripheral Neuropathy.
The autonomic nervous system is the one that operates in the background, controlling things like breathing, heartbeat, stomach emptying, etc.
The most common diabetes-related autonomic neuropathy is gastroparesis, or delayed/irregular stomach emptying. Many longtime Type-1s can tell you how this can make insulin bolus dosing a nightmare. Other symptoms are aberrations in sweating, postural hypotension, bladder control, abnormal febrile responses, impotence, diarrhea, nausea, and on and on.
You can do a simple test for autonomic neuropathy simply by taking your pulse. This is called the R-R Interval. Take your pulse and note the (hopefully) regular beat when inhaling. Your pulse will normally slow when exhaling. If it doesn't, it may be an indication of autonomic neuropathy which should be checked with your doc.
One of the first complications noted by many diabetics is a tingling, pain, or loss of sensation in the toes and feet. This is often a symptom of Diabetic Peripheral Neuropathy or DPN.
Not every ache, pain, or numb feeling is DPN. It should not be confused with numbness on one side only, as it most often presents bilaterally (on both sides of the body) and tends to start in areas farthest from the heart, i.e., in the toes, feet and fingers. If you have one-sided symptoms, it is more likely a pinched nerve, sprained or strained muscle, tendon or ligament, carpal tunnel or something else completely unassociated with diabetes. It could also be a symptom of a blocked blood vessel, which is a potentially life threatening condition. Only your doctor can diagnose the cause, so it is wise to seek medical attention as soon as possible. You might have to visit a neurologist for specialized tests described below.
Causes of DPN
The current theory seems to be that there are two potential causes DPN. They are Advanced Glycation Endproducts [AGE] and what is being called "Oxidative Stress."
Glycation is the attachment of glucose. AGEs are the result of the glycation of proteins, a particular problem in diabetics due to our hyperglycemia. Like the glycation of hemoglobin (measured as HbA1c) or the glycation of albumin (measured as fructosamine), other proteins can become glycated. One course of study centers around the glycation of lipoproteins, like HDL, LDL, and triglycerides. It is thought that this glycation makes the proteins sticky, causing aggregation in the blood vessels, and hence the formation of plaque in the arteries, and the subsequent increased cardiac risk. Since it is believed that a major contributor to this process is free radicals, the use of antioxidants is being studied to scavenge the free radicals.
Oxidative Stress is thought to be part of the process related to diabetic neuropathy and retinopathy. Again, the free radicals apparently cause damage to the vessels and nerves. There is still much research to be done, and we do not have all the answers yet, but even the most pessimistic should agree that this line of research has potential.
Symptoms of DPN
Most diabetics who are experiencing DPN have shooting pains, burning pains, hyper-sensitivity, or numbness in their toes and feet. Untreated, this can eventually spread up the legs and also cause similar symptoms in the fingers and hands. Some report that they feel like they are wearing socks when they aren't, or that they feel a non-existent fold or crease in the socks they are wearing.
Testing for DPN
Common tests for DPN can be carried out in your doctor's office using two simple tools: monofilament, and a tuning fork. Monofilament is a short piece of common fishing line. By using a specific length of a specific diameter of monofilament, your doctor will touch the skin of your toes and feet and ask you when you feel the touch. Similarly, the doctor will strike the tuning fork to start it vibrating and hold it to your foot, asking you to report when you can no longer feel the vibration. Depending on your doctor's interpretation of these tests, you may be referred to a neurologist for additional testing.
A neurologist will probably want to do two somewhat more complex tests, called NCV and EMG. Nerve conduction velocity (NCV) tests the speed of conduction of impulses through a nerve. The nerve is stimulated, usually with patch-like electrodes on the skin (similar to those used for ECG) over the nerves at various locations. One electrode stimulates the nerve with a very mild electrical impulse. The resulting electrical activity is recorded by the other electrodes. The distance between electrodes and the time it takes for electrical impulses to travel between electrodes are used to calculate the nerve conduction velocity.
The second test is called Electromyography (EMG). For an EMG, a needle electrode is inserted through the skin into the muscle. The electrical activity detected by this electrode is displayed on an oscilloscope, and may be heard through a speaker.
After placement of the electrodes, you may be asked to contract the muscle (for example, by flexing your foot). The presence, size, and shape of the wave form produced on the oscilloscope provide information about the ability of the muscle to respond when the nerves are stimulated.
Treatment of DPN
The first, best, and most important step in treating DPN is to reestablish normal blood sugars.
In addition, your doctor has pharmaceutical tools, such as small doses of tri-cyclic antidepressants like amitriptyline, or the more potent anti-seizure meds like Tegetrol (carbamazepine), Dilantin (phenytoin), and Neurontin (gabapentin). These will mask the symptoms, but do nothing to address the underlying pathology.
Another approach attempts to treat the underlying causes of DPN, i.e., Advanced Glycation Endproducts and Oxidative Stress through the use of antioxidants, specifically Alpha Lipoic Acid, which is also known as Thioctic Acid, and Gamma Linolenic Acid. Probably the most leading-edge work is being done in Germany, and has been reported in the DEKAN Study (see footnote below).
The DPN Cocktail
The following is a recommendation for treatment of DPN by use of anti-oxidants, and is based on the research of Stan Angilley. It has been used successfully by many diabetics to reduce or even eliminate DPN. Before starting on this regimen, you should discuss it with your doctor, as you may have other medical issues which would contraindicate its use. It is likely that your doctor will have heard little or nothing about this approach, so we have provided citations to applicable literature below.
The DPN cocktail has three components:
Alpha Lipoic Acid (ALA), Gamma Linolenic Acid (GLA) as contained in Evening Primrose Oil (EPO), and
Vitamin C. These components are
available from many sources, including pharmacies, health food stores, and
over the internet. The ALA component is somewhat expensive, so we will provide
some internet sources that many have used successfully. We have no profit
motive here, and suggest that you research sources to find your best buy. The
unique properties of the components make this cocktail synergistic, in other
words, the parts work together to reinforce and replenish each other.
Gamma-linolenic acid (GLA) is an n-6 (omega-6) polyunsaturated fatty acid commonly contained in Evening Primrose Oil (EPO) and Borage Oil (BO). EPO typically contains more GLA than BO. Depending on the method of extraction from the plants, EPO can contain varying amounts of GLA. Buy a brand of EPO that contains at least 10% GLA. For example, choose a 1300mg EPO tablet that contains at least 130mg of GLA.
The last component is Vitamin C. There is nothing special required in selecting a specific form of Vitamin C, so you can choose generic, Rosehips, or Ester C.
The components of the cocktail are:
Starting off, take one cocktail morning and night. After you get relief from the neuropathy feelings, you should be able to reduce this to a maintenance dose of once a day. Most report improvements in DPN after about 3 months of use. Some report stomach upset from the cocktail, so taking it with a meal may help. No other serious adverse reactions have been reported.
Again, we have no vested interest in where you get the components. Here are several internet sources should you have difficulty in obtaining them from your local pharmacy or health food store. Prices change, so research your best buy.
Citations to Literature for Your Skeptical Doctor
Alpha-Lipoic Acid Improves Symptomatic Diabetic Polyneuropathy
Diabetes Care 2006;29:2365-2370.
Alpha-lipoic acid (ALA) given orally improves symptoms in patients with diabetic polyneuropathy, according to a report in the November issue of Diabetes Care.
A recent meta-analysis showed that daily intravenous treatment with ALA could reduce pain, paresthesia, and numbness in diabetic patients, the authors explain, but little work has been done to investigate the use of oral ALA.
Dr. Dan Ziegler from Heinrich Heine University, Duesseldorf, Germany and colleagues compared three doses of oral ALA to placebo in 166 patients with symptomatic diabetic polyneuropathy.
Mean total symptom scores and stabbing/lancinating and burning pain subscores were significantly reduced after 5 weeks in all active treatment arms compared with the placebo arm, the authors report.
ALA treatment had no measurable effect on paresthesia and numbness, the results indicate.
Symptoms improved significantly as early as 1 week with the highest ALA dose (1800 mg daily) and within 2 weeks with the other doses (600 mg and 1200 mg daily), the researchers note, and there were no significant differences among the three ALA groups for changes in mean total symptom score at any time point.
The findings were similar when Neurology Symptoms and Change Score was used instead of mean total symptom score, the report indicates.
Nausea, vomiting, and vertigo were more common with ALA treatment than with placebo treatment, the investigators say.
"Whether the observed favorable short-term effect of ALA on neuropathic symptoms and deficits can be translated into slowing the progression of diabetic polyneuropathy in the long term is unknown," the authors write. "However, our finding that neuropathic deficits such as impaired sensory function were improved is encouraging, because these are major risk factors in the development of neuropathic foot ulcers."
"In the absence of a dose response and because the higher doses resulted in increased rates of gastrointestinal side effects, 600 mg once daily seems to be the most appropriate oral dose," the researchers add.
of treatment with the antioxidant alpha-lipoic acid on cardiac autonomic
neuropathy in NIDDM patients. A 4-month randomized controlled multicenter
trial (DEKAN Study). Deutsche Kardiale Autonome Neuropathie.
Mayo Clinic in Rochester
Monday, April 07, 2003
Antioxidant Alpha Lipoic Acid (ALA) Significantly Improves Symptoms of Diabetic Neuropathy
ROCHESTER, Minn. -- A collaborative study between Mayo Clinic and a medical center in Russia found that alpha lipoic acid (ALA) significantly and rapidly reduces the frequency and severity of symptoms of the most common kind of diabetic neuropathy. Symptoms decreased include burning and sharply cutting pain, prickling sensations and numbness.
The findings appear in the March 2003 issue of Diabetes Care, http://care.diabetesjournals.org/.
1997 Sep;46 Suppl 2:S62-6
Ziegler D, Gries FA Diabetes
Research Institute at the Heinrich Heine University,
treatment has been shown to prevent nerve dysfunction in
J Neural Transm 1998;105(8-9):1005-15
Loske C, Neumann A, Cunningham AM, Nichol
K, Schinzel R, Riederer P,
Oxidative stress, caused by
enhanced free radical synthesis, may play an important role in contributing to
the pathogenesis of diabetic neuropathy.[19,20,30]
In the limited clinical trials published so
far, ALA administration has yielded small but significant improvements
87.Nagamatsu M, Nickander
KK, Schmelzer JD, et al:
is focusing more and more on oxidative stress
Early in the disease, the main unsaturated
lipid aldehydes accumulating
4.Fathallah L, et al. Accumulation of
4-Hydroxyalkenals is an early
of cellular reducing equivalent homeostasis by alpha-lipoic acid. Mechanisms
and implications for diabetes
and ischemic injury. (Roy S; Biochem Pharmacol, 1997 Feb 7)
The effect of alpha-lipoic acid on the
neurovascular reflex arc in patients with diabetic neuropathy assessed by
Alpha-lipoic acid: antioxidant potency
against lipid peroxidation of neural tissues in vitro and implications for
Effects of alpha-lipoic acid on
neurovascular function in diabetic rats: interaction with essential fatty
acids. (Cameron NE; Diabetologia, 1998 Apr)
Stimulation by alpha-lipoic acid of glucose
transport activity in
Differential effects of lipoic acid
stereoisomers on glucose metabolism
alpha-Lipoic acid: a
metabolic antioxidant which regulates NF-kappa B
changes in lens antioxidant status, glucose utilization
Alpha-lipoic acid reduces
expression of vascular cell adhesion
glycation end product-induced activation of NF-kappaB is
and treatment with the antioxidant alpha-lipoic acid
acid: effect on glucose uptake, sorbitol pathway, and
alpha-Lipoic acid decreases
oxidative stress even in diabetic patients
Advanced glycation end product-induced
activation of NF-kappaB is
and treatment with the antioxidant alpha-lipoic acid on endothelial and
neurogenic responses of corpus cavernosum in rats.
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