Peripheral neuropathy 5.6 a1c


50 something with peripheral neuropathy and 5.6 a1c; been taking amitriptyline for almost a decade but I’m getting more and more “HOT” foot (feet).

MD completely clueless.

Thanks in advance.

I was part of a group of newly-diagnosed type 1 diabetics subjected to a test of nervous system health after I having had excessive urine and excessive thirst for about two days before being put on insulin. I as well as all the others had measurable slowing of nerve conduction velocities, a sign of nervous system damage. Given the very little hyperglycemia we had suffered by the time of the test, my assumption was that something else about diabetes was causing this, and sure enough, recent research shows that autoimmunity and genetics play a role in producing diabetic neuropathy.

There are other causes for neuropathy besides diabetes. Nancy50

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Howdy! I was just diagnosed with mixed neuropathy in my legs and feet, and I’ve never had an A1c over 7.5 and my A1c has been between 4.6 and 5.2% since three months post-diagnosis. The neurologist told me that “it just happens like this sometimes, and we don’t know why. Keep doing what you’re doing, and don’t start drinking alcohol.”

Was news to me that alcohol could exacerbate or accelerate neuropathy, but my neurologist was pretty adamant about it. No big deal for me, since I don’t drink anyways.

There is a lot of evidence of the role that genes inherited along with the genes that predispose patients to develop type 1 diabetes in the first place also play a significant role in causing diabetic neuropathy, thus accounting for the disconnect between blood sugar levels and neuropathy. One example among the many studies on this topic is cited below:

BMC Med Genet. 2001;2:4. Epub 2001 Mar 28.

Polymorphisms in the Mn-SOD and EC-SOD genes and their relationship to diabetic neuropathy in type 1 diabetes mellitus.

Chistyakov DA, et al.


Oxidative stress, resulting in a marked increase in the level of oxygen free radicals (OFR), has been implicated in the etiology of diabetic neuropathy (DN). Antioxidant enzymes may protect against the rapid onset and progression of DN, by reducing the excess of OFR and peroxide. Mutations and polymorphisms in the genes encoding such enzymes may therefore result in predisposition to DN. We investigated the role of genes encoding two antioxidant enzymes, mitochondrial (Mn-SOD) and extracellular (EC-SOD) superoxide dismutase, in DN pathogenesis in a Russian population. We studied Ala(-9)Val and Ile58Thr polymorphisms of the Mn-SOD gene and Arg213Gly dimorphism of the EC-SOD gene in type 1 diabetic patients with (n = 82) and without DN (n = 84).


We developed and used a new polymerase chain reaction (PCR) assays for rapid detection of polymorphisms. These assays involved the use of mismatch PCR primers to create restriction sites in the amplified product only in presence of the polymorphic base. The PCR product was than digested with BshTI, Eco32I or Eco52I to detect Ala(-9)Val, Ile58Thr or Arg213Gly polymorphic site respectively. The frequencies of the Ala allele (50.6% vs. 68.5%, p < 0.002) and the Ala/Ala genotype (17.1% vs. 39.3%, p < 0.005) of the Mn-SOD gene were significantly lower in DN patients than in diabetic subjects without DN. In contrast, the Val allele (49.4% vs. 31.5%, p < 0.002) and the Val/Val genotype (15.9% vs. 2.4%, p < 0.01) were significantly more frequent in the DN patients than in the control group.


Ala(-9)Val substitution in the Mn-SOD gene was associated with DN in a Russian population

With all this talk about the role of genes and oxidative stress in causing complications you may wonder why your endocrinologist just prattles on about blood sugar control as the only issue. Granted, you can’t safely change your genetic profile, at least given the current state of genetic engineering, but you can do something to reduce oxidative stress, which many supplements diminish, so why shouldn’t that be part of the standard course of treatment?