Peripheral Neuropathy in Diabetics; what steps can we take to avoid it?
You might already be aware that of the many deteriorative conditions related to diabetes; ‘peripheral neuropathy’ is perhaps the most common, with an estimated 60-70% of diabetics reportedly experiencing symptoms. ‘Neuropathy’ describes damage, whether moderate or severe, to the peripheral nervous system (the ‘external’ portion of the nervous system, situated beyond the brain and spinal cord), which transmits information directly from the brain and spinal cord to the rest of the body.
Our nervous system acts very similarly to an electrical cable; with the nerve’s ‘impulse’ adopting the role of the electrical wire itself, and the ‘myelin sheath’ (the ‘skin’ of the nerve), mimicking the insulation surrounding the wire. If the wire becomes damaged, then the nerve signal will not travel efficiently along the wire, nor will it transmit the intended messages as instantaneously. This delay results inevitably in the ‘classic’ symptoms of neuropathy; namely; tingling, numbness, ‘burning’ and pain.
A causative link has been drawn between neuropathy and deficiencies of long-chain polyunsaturated fatty acids within the body. Indeed, insulin itself plays a pivotal role in the metabolism of EFAs (essential fatty acids), by alerting the genes necessary for enzyme-conversion to begin the process of converting short-chain fatty acids into a bio-available (i.e. usable by the body) long-chain fatty acid.
Where insulin is absent, or enzyme-activity impeded, the enzymes needed to create specific fatty acids cannot be produced and a deficiency results. Of the myelin layer which protects our vulnerable nerves, an estimated 75 % is composed exclusively of EFA’s (these are termed ‘essential’ because the body cannot generate them independently, but must instead source them externally from the diet). Depletion of this fatty, insulatory layer, leads to severe nerve damage (Neuropathy).
Nutrition, as all Diabetics are painfully aware, is central to the manufacture of insulin and for creating the right ‘biological environment’ to encourage enzyme conversions to take place. By boosting or supplementing our dietary levels of long-chain fatty acids we can essentially sidestep the risk that the enzyme-mediated conversions will fail to progress past the initial hurdle.
Fatty acid supplementation nourishes the myelin sheath, and prevents further degeneration of inter-cellular communication; it reduces the risk of developing Neuropathy, and actually reinvigorates nerve endings to overcome numbness and the likelihood of eventual tissue loss. However, EPA, a specific omega-3 fatty acid found in fish oil that appears to have significant beneficial effects on diabetic neuropathy and serum lipids as well as other diabetic complications such as nephropathy (kidney damage) and macroangiopathy (damage to the blood vessels). EPA plays a role in the compaction, stabilization, and maintenance of myelin sheaths by regulating the production of proteolipid protein or PLP. PLP is literally the ‘glue’ that hold in place the sheets of protective fats that cover the nerve axon. Loss of PLP is associated with many conditions that have nerve damage including Multiple sclerosis, Alzheimer’s disease and Huntington chorea.
OmegaForce is a patented formulation of omega-3 and 6 long-chain fatty acids with a multitude of health-enhancing properties, including anti-inflammatory and pain-relieving actions. For more information on the relationship between EPA deficiency and the pathogenesis of Diabetic Neuropathy, please go to www.igennus.com