Familiar symptoms of diabetic neuropathy include burning pain and numbness typically in the feet. The behavior of animals can be used as a model to substantiate the extent of neuropathy and its response to treatment. However, the aetiology of these disturbances is still unknown, although metabolic factors such as hyperglycemia or neurotransmitter alterations may be involved. The abnormalities seen the nerves of diabetic patients seem to be related to fluctuations in a cellular enzyme known as PKC or Protein Kinase C. In the complex scheme of energy creation in the cell, a chemical known as ATP is broken down and contributes a hi energy phosphate molecule, Protein Kinase C, is an enzyme responsible for this reaction.
This entire process, removing a phosphate molecule and transferring it to a protein, is called phosphorylation. The goal of this reaction is to either switch on or deactivate various metabolic pathways. There are many diverse forms of PKC, the one that appears most relevant to our discussion of diabetic neuropathy, appears to the PKC isoform Beta. Available research suggests that PKC~Beta appears to be the over-active form of PKC in diabetic patients. Another line of evidence supports the involvement of PKC in diabetic neuropathy. Drugs that block this enzyme ameliorate diabetic complications. Nerves contain both calcium and sodium channels that are accountable for their function. It appears that PKC, interacts with these channels and this interaction is at least partially responsible for the symptoms of pain and numbness in diabetic patients. Additional research suggests that PKC activation brings forth hyperexcitability in specific nerve fibers related to pain, the so called C-fibers. Activation and hyperactivity of pain carrying (C-fibers) is believed to develop many of the painful symptoms in patents with neuropathy. A number of studies protein kinase inhibitors and their effects on both nerve function and the signs and symptoms of neuropathy are appearing the scientific literature.
Interestingly, chemicals that block PKC, have the ability to reduce the volatility in damaged nerves in animals suffering from experimentally induced neuropathy. Blocking the CPK enzyme produces little or no effect on the function of normal nerves from control animals. This property, the normalizing of nerve function, occurred in a dose-dependent manner. That means the higher the dose of the PKC inhibitor, the more normalization of nerve function occurred. This and similar experiments, seem to indicate that the PKC enzyme plays an vital role in the development of the intense nerve pain of neuropathy and that agents that can block this enzyme can tone down or modulate the over-excited nerves that carry pain signals in neuropathy patients.
To further support the link between CPK and the nerve complications in diabetes, other experiments demonstrated that drugs that enhance the action of PKC actually will produce or aggravate the nerve abnormalities associated with diabetes. Thus the current experimental data implies that PKC activation will aggravate and PKC inhibition will ameliorate the abnormal nerve activity found in diabetes. Special nerve tests known as nerve conduction studies, also confirm the contention that PKC is related to nerve function and neuropathy. These nerve conduction study tests show that activation of PKC leads to enduring enhancement of electrical activity in a part of the spinal cord called the dorsal horn. The dorsal horn functions to carry sensation, including pain from the body to the brain. From all this data, one could conjecture that activation of PKC in diabetic nerves explains at least in part, the development irritating neuropathy. Currently there are a number of drugs under development that are designed to block or decrease the activity of the PKC enzyme and lighten neuropathic pain. The practitioner of Integrative Neurology might suggest naturally occurring PKC inhibitors as alternatives to drugs. Let's take a look at some natural substances that may serve as efficacious PKC enzyme inhibitors.
At this point in our discussion, I must issue a disclaimer: The information I am about to present to you is not intended to replace the recommendation given by a licensed healthcare provider. Natural therapies are usually safe, but you may be allergic or otherwise intolerant of them.
Furthermore they can and do interact with other natural and prescription medications. Always consult your doctor before adding or changing your treatment plan. So only use this information in conjunction with a licensed healthcare practitioner. Gingko Biloba: Gingko is one of the most widely used herbs. It is often taken to help with memory problems and to increase circulation. One of the therapeutic properties of Gingko may be related to its ability to suppress the activation of PKC enzymes. Which at least in theory, suggests it might be useful for patients suffering from neuropathy. EGb 761 is a Gingko derivative, that appears to block the PKC enzyme. This quality may in part explain Gingko's purported ability to protect nerves and neurons. Another study supported these findings, the authors conclude that the Gingko derivative, EGb 761 protects the nerves and brain via PKC inactivation. Taken together, these results support the hypothesis that dietary intake of natural substances that may inhibit the activation of PKC, may be beneficial in normal aging of the brain. Vitamin E: This vitamin has a long historical use in the prevention of heart disease and atherosclerosis. The mechanism of action of vitamin E may be related to its ability to antagonize the activation of the PKC enzyme.
Further, studies show that high doses of vitamin E were able to decrease the level of PKC induced by diabetes or prolonged high blood sugar. Thus animal and clinical studies have shown that high doses of vitamin E treatment can apparently reverse some of the complications seen in association with diabetes and high blood sugar. The apparent health benefits of vitamin E in diabetes are related to its ability to suppress PKC activation. So in diabetic patients, without contraindications or known sensitivity to Gingko and Vitamin E, the addition of these two nutrients to their standard diabetic management program may reduce, slow or even reverse some of the complications of high blood sugar including neuropathy.
Always consult your doctor before adding or changing your diabetes management program.
Dr. Kukurin is a Diplomat with the American Chiropractic Academy of Neurology (DACAN). To attain this prestigious status he attended a three year post-graduate program in neurology. Dr. Kukurin has also received post-graduate education from a number of leading medical schools including Harvard, Johns Hopkins, the Mayo Clinic, UNICO and the Russian People's Friendship University in Moscow.
Some of the treatment techniques he developed have been published in peer reviewed medical journals and are indexed in the National Library of Medicine. The results patients have obtained using his treatment approaches have appeared on FOX and ABC affiliate newscasts. He has been practicing as a chiropractic neurologist for over 20 years. He sees patients in offices located both in Litchfield Park Chiropractic and Pittsburgh Chiropractic
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