
Diabetic neuropathy is a decrease in nerve function typically affecting the lower limbs in people and animals with diabetes. The peripheral nerves become damaged as a result of metabolic changes (including oxidative stress) that accompany persistently elevated blood sugar levels. Many people with diabetes, whether Type I (juvenile) or Type II (adult-onset), will eventually come down with some form of diabetic neuropathy.
In addition to muscle weakness, depressed reflexes, and disturbances in gait or balance, the symptoms of diabetic neuropathy in humans typically include sensations of numbness, tingling, burning, or shooting pains. As the nerves continue to degenerate, sensation can become completely lost; as a result, minor injuries to the feet may go unnoticed, at least initially. At the same time, damage to the autonomic nervous system results in impaired circulation, so that wounds don’t heal properly. Thus, minor injuries can quickly escalate to major ones, greatly increasing the risk of gangrene. Once gangrene has set in, the conventional treatment is amputation—of the toes or even the entire foot.
Fortunately, there exists a number of nutritional therapies for diabetic neuropathy, of which one of the best is methyl B12. Effective treatment of diabetic neuropathy has reportedly been achieved with methyl B12 delivered intrathecally, i.e., injected directly into the spinal cord via lumbar puncture. 1 Don’t try this one at home, folks—obviously, it’s an experimental procedure done only in a hospital setting. However, according to another study, the same beneficial results can also be obtained with oral supplements of methyl B12 in sufficiently large doses. 2 There have been anecdotal reports of people getting relief from 1 to 3 tablets of Xobaline methylcobalamin per day. The use of methyl B12 can halt degeneration of peripheral nerves, improve or eliminate painful sensations, and in some cases even restore sensation to limbs which have previously gone completely numb.
The mechanism for these beneficial effects is not yet completely understood. It is known that serum B12 deficiency is not especially common in diabetic neuropathy 3, implying that the effectiveness of methyl B12 is not due to repletion of an underlying systemic vitamin B12 deficiency. Nevertheless, a marked tissue deficiency of methyl B12 only (and not of other forms of B12 occurring naturally in the body) has been reported in the sciatic nerves of diabetic patients compared to controls. 4 Thus, a clear rationale exists for supplementing with methyl B12 rather than with other forms of the vitamin, such as cyanocobalamin.
Perhaps even more significant for the treatment of diabetic neuropathy is the discovery that methyl B12 has neuroprotective effects. In certain neurological conditions—such as Alzheimer’s, Parkinson’s, amyotrophic lateral sclerosis, and AIDS-related dementia—nerve cells are thought to be exposed to excessive amounts of the neurotransmitter glutamate, resulting in neurotoxicity. 5 Recently high-dose methyl B12 has been shown to diminish glutamate-related neurotoxicity in animals 6, thus offering hope that neurodegenerative diseases can be effectively treated with methyl B12. Peripheral neuropathic pain is similarly associated with activation of glutamate receptors in the spinal cord. 7 Hence methyl B12 may be beneficial for all forms of peripheral neuropathy, including diabetic neuropathy, by regulating neural signaling in the spinal cord.
Diabetes afflicts animals as well as humans, so it’s not surprising that cats can also suffer from diabetic neuropathy. As in humans, diabetes in cats is caused either by inadequate production of insulin by the pancreas (Type 1 diabetes) or by impaired response of cells to insulin (Type 2 diabetes). Although diabetes can strike cats of any age, it typically occurs most often in older, fatter animals. Diabetic neuropathy in cats is characterized by symptoms such as progressive weakness in the hind legs and walking on the hocks (the back part of the legs) rather than on the toes. Cats so afflicted become incapable of climbing stairs or trees and lose the ability to jump to higher surfaces. Often they can’t take more than a few steps without the hind legs sliding out from under them. Cats with neuropathy also seem to tire quickly and tend to rest more often after taking short walks.
The staff at LifeLink has recently told me that many cat lovers are treating their diabetic pets with Xobaline, apparently with great success. 8 A single Xobaline tablet administered once per day appears sufficient to reverse most or all of the symptoms of feline diabetic neuropathy within a few weeks. Although Xobaline is intended as a sublingual supplement for humans, cats aren’t likely to tolerate any attempts at sublingual administration! Fortunately, Xobaline seems to work fine when given the same way as any other pill to these animals. Although we’re not in the veterinary business and cannot promote the use of Xobaline for veterinary purposes, we’re proud that Xobaline has been singled out as a useful supplement for cats (and their humans). 8
References
[1] Ide H, Fujiya S, Asanuma Y, Tsuji M et al. Clinical usefulness of intrathecal injection of methylcobalamin in patients with diabetic neuropathy. Clin Ther. 1987;9(2):183-92. [Abstract]
[2] Yaqub BA, Siddique A, Sulimani R. Effects of methylcobalamin on diabetic neuropathy. Clin Neurol Neurosurg. 1992;94(2):105-11. [Abstract]
[3] Khan MA, Wakefield GS, Pugh DW. Vitamin B12 deficiency and diabetic neuropathy. Lancet. 1969;2(7624):768-70.
[4] Tanaka N, Yamazaki Y, Sakato H, Maeno H et al. Relation of partial deficiency of cobalamins to occurrence of diabetic neuropathy. In: Gato Y et al., eds., Diabetic Neuropathy, Excerpta Medica International Congress Series 581. Amsterdam: Excerpta Medica; 1982:114-119.
[5] Hugon J, Vallat JM, Dumas M. Role of glutamate and excitotoxicity in neurologic diseases [in French]. Rev Neurol (Paris). 1996;152(4):239-48. [Abstract]
[6] Yamamoto Y, Shibata S, Hara C, Watanabe S. Methylcobalamin attenuates the hypoxia/hypoglycemia- or glutamate-induced reduction in hippocampal fiber spikes in vitro. Eur J Pharmacol. 1995;281(3):335-40. [Abstract]
[7] Kawamata M, Omote K. Involvement of increased excitatory amino acids and intracellular Ca2+ concentration in the spinal dorsal horn in an animal model of neuropathic pain. Pain. 1996;68(1):85-96. [Abstract]