A recent published article by the National Institute of Health indicates that metabolic correction of the biochemical derangements and diabetic peripheral neuropathy is an emerging treatment strategy for which the peer-reviewed clinical evidence is growing and showing increase in results and safety.
This recent article was published in the Current Clinical Pharmacology Journal in November 2011 and was reviewed and published by the National Institute of Health in its NIH Public Access: Author Manuscript: Metabolic Correction in the Management of Diabetic Peripheral Neuropathy: Improving Clinical Results beyond Symptom Control.
The article states the current clinical management guidelines of diabetic peripheral neuropathy are based on blood sugar control and symptomatic pain relief but does not completely prevent the progression of disease. Complications of diabetic peripheral neuropathy as it continues its normal course produces increasing pain and discomfort, loss of sensation, ulcers, infections, amputations and even death
In the US alone, it has been estimated that there are more than 5 million patients suffering from diabetic peripheral neuropathy and the total annual cost of treating this disease and its complications is over 10,000 million dollars.
The causes of diabetic peripheral neuropathy is thought to be a multi-faceted metabolic process that increasingly deteriorates tissues. High blood sugar, increase sorbitol and protein kinase C, elevated homocysteine reduced nitric oxide and excessive reactive oxygen species damage endothelium tissues and produce a change that increases vascular resistance and reduces blood flow to the nerves. This means that it irritates and damages the lining of the blood vessels resulting in reduced flow of blood, therefore oxygen to the nerves, particularly in the peripheral areas like the hands and feet. The health of the blood vessels is compromised by numerous factors such as glycosylation, hyperlipidemias, hypertension, excessive platelet activity, smoking, reduced nitric oxide and excessive degeneration of reactive oxygen species.
An interesting finding in this report indicates anyone with elevated homocysteine increases the risk of developing peripheral vascular disease. In patients The author goes on to state that there is a growing number of articles documenting an increase in blood homocysteine levels and the risk of developing diabetic peripheral neuropathy in patients that are taking metformin (Glucophage). Long-term use of metformin is associated with poor absorption of vitamin B12, an elevated fasting homocysteine and methylmalonic acid which may have bad effects on peripheral nerves in patients with type 2 diabetes. The author goes on to state that metformin increases total serum homocysteine in non-diabetic male patients with coronary heart disease, and adding metformin to insulin therapy which resulted in increased and homocysteine levels within 12 weeks. It appears of this report there could be a relationship between the development of diabetic peripheral neuropathy and metformin usage.
The author states that there is an enzyme called methylene–tetrahydrofolate reductase that any human beings is encoded by the MTHFR gene. Studies indicate that there is a polymorphism (abnormal expression) of this gene in anywhere from 10% to 37% of the population, that interferes with the body’s ability to convert certainly be vitamins which can result in low level of active folate. Which can lead to increase endothelial damage, resulting in reduced blood flow and exacerbating diabetic peripheral neuropathy.
Studies have shown that metformin therapy for more than 6 months in patients with this dysfunctional MTHFR polymorphism could be considered a pharmacogenetics cause for exacerbation of diabetic peripheral neuropathy.
The author states that taken altogether these report suggests a potential clinical association between MTHFR genotypes and the metformin- treated patient’s risk of worsening diabetic peripheral neuropathy.
The author points out that the goal of the treatment guidelines for diabetic peripheral neuropathy management is to relieve pain and improve quality of life. With proper use of medications suggested in the guidelines, many patients do not achieve more than a 30-50% pain reduction. The limitations of the recommendations of this guidelines are that it does not recommend any therapy that potentially changes the underlying pathology and natural history of disease process or contribute to improve the metabolic deficiencies related to the neuropathy.
What this means is, if the patient has lost sensation, it will not come back and the pain will return soon after the medication is discontinued. In addition, pain relief medications are often accompanied with adverse effects that include dizziness, drowsiness, gastrointestinal distress, constipation, headaches, dry mouth and sexual dysfunction.
Treatment should be directed at underlying causes.
The author suggested that the therapeutic objectives should not be just to improve symptoms, but to normalize or optimize all factors involved in nerve and vascular to prevent diabetic peripheral neuropathy progression or even development.
The American Diabetic Association recommends that treatment should be directed at underlying causes, even when effective symptomatic treatments are available to prevent further manifestations of diabetic peripheral neuropathy and autonomic neuropathy.
Dietary minerals are the chemical elements required by living organism’s present in common organic molecules. There are 17 required minerals to support self-structure and function in human health processes. The proper intake of micronutrients for each person varies according to age, genetic constitution, diseases and exposure to stress or toxins. These metabolic processes can be seen as links in a chain where every element must be addressed, in order for the body to perform at peak efficiency. Any breakdown in this link will compromise the entire system. A significant fraction of the American population appears not to obtain even the Recommended Daily Allowance (RDA) of some critical nutrients from their food. This deficiency produces recognized deficiency diseases. The author goes on to state that supplementation with specific nutrients has been estimated to be cost effective in preventing disease
He states further that food along may not provide sufficient micronutrients for preventing deficiencies and a large portion of older adults do not consume sufficient amounts of many nutrients and approximately half of this population use no supplementation. The author states further that many carriers of 50 human genetic diseases, that are due to defective enzymes, can be remedied or improved by the administration of high doses of vitamins with the corresponding needed coenzyme which raises the level of function and at least may partially restore the needed enzymatic activity.
Acetyl L Carnitine:
Acetyl L carotene is an amino acid derivative that the body manufactures by synthesizing from other amino acids. It promotes peripheral nerve regeneration and has been shown to have pain relieving effects in patients with HIV–related or chemotherapeutic origin peripheral neuropathy.
Alpha Lipoic Acid:
This substance is also known as theoctic acid, a naturally occurring compound that can potentially regenerate other antioxidants such as vitamin C, vitamin E and glutathione. This compound is considered a potential therapeutic alternative for chronic diseases associated with oxidative stress. It may increase glutathione, an important endogenous antioxidant. Studies indicate that 600-1800 mg a day may be beneficial in the treatment of diabetic peripheral neuropathy.
This is a form of thiamine (vitamin B1) developed in Japan in the late 1950s to treat alcoholic neuropathy, sciatica and other painful nerve conditions. A study assessed patients with diabetic peripheral neuropathy that were treated with a combination of this compound and vitamin B6 and they manifested significant improvement in pain and other symptoms.
Active B Vitamins:
Water soluble B–complex vitamins, L-methylfolate, Methylobalamin, pyrodoxal–5–phosphate are key active cofactors in many metabolic reactions. There are certain conditions for which there is an increased need for these nutrients. Certain genetic defects that were discussed earlier render the interactive forms of these vitamins less effective and therefore increase the susceptibility to develop certain conditions. If an individual has genetic defects mentioned earlier, then standard forms of the vitamins may not be effective.
The author summarizes the metabolic correction of the biomechanical derangement in diabetic peripheral neuropathy patient is an emergent treatment strategy for which the peer-reviewed clinical evidence is growing and showing increased effectiveness and safety. This strategy can achieve pain relief, improvement of sensation and quality of life. Metabolic correction is extremely safe and goes beyond symptom control to also provide improvement in circulation, sensation and restoration of nerve function and fiber density. He reiterates that based on the available data it would be expected that metabolic correction can either slow or stop the disease progression, and even reverse the damage of disease in some cases.
So what does this mean?
If you have diabetic peripheral neuropathy, there is more you can do other than just medicate and try to control your blood sugar.
You need to find a healthcare provider that can provide you with the proper information, testing and metabolic treatment strategies that may slow, stop or reverse your terrible, life-changing condition.
I would like to thank the National Institute of Health, The Journal of Current Clinical Pharmacology for the information contained in this article.
G Phillip Paulk DC
Paulk Chiropractic Stockbridge LLC