NeuroTalk Support Groups - Diabetic Neuropathy:

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Diabetic Neuropathy:

I am starting this thread to put up links to information about this common trigger for peripheral neuropathy.

Anyone who wants to ask questions or contribute experience and/or more links is welcome:

This is a link to a paper on impaired glucose tolerance, which may precede type II diabetes by many years:

http://www.citeulike.org/user/wrs1/article/6499468

Quote:

Idiopathic neuropathy, prediabetes and the metabolic syndrome.
by: A. Gordon Smith, J. Robinson Singleton
Journal of the neurological sciences, Vol. 242, No. 1-2. (15 March 2006), pp. 9-14. doi:10.1016/j.jns.2005.11.020 Key: citeulike:6499468

View FullText article

DOI, Pubmed, Hubmed, Pubget

Abstract

Peripheral neuropathy is a common problem encountered by neurologists and primary care physicians. While there are many causes for peripheral neuropathy, none can be identified in a large percentage of patients ("idiopathic neuropathy"). Despite its high prevalence, idiopathic neuropathy is poorly studied and understood. There is evolving evidence that impaired glucose tolerance (prediabetes) is associated with idiopathic neuropathy. Preliminary data from a multicenter study of diet and exercise in prediabetes (the Impaired Glucose Tolerance Neuropathy Study) suggests a diet and exercise counseling regimen based on the Diabetes Prevention Program results in improved metabolic measures and small fiber function. Prediabetes is part of the Metabolic Syndrome, which also includes hypertension, hyperlipidemia and obesity. Individual aspects of the Metabolic Syndrome influence risk and progression of diabetic neuropathy and may play a causative role in neuropathy both for those with prediabetes, and those with otherwise idiopathic neuropathy. Thus, a multifactorial treatment approach to individual components of Metabolic Syndrome may slow prediabetic neuropathy progression or result in improvement.

And I just found this article while searching something else the other day:

http://www.ncbi.nlm.nih.gov/pubmed/21205116
new information as of 2011:

Quote:

Diabetes Obes Metab. 2011 Mar;13(3):243-50. doi: 10.1111/j.1463-1326.2010.01344.x.
Chronic treatment with D-chiro-inositol prevents autonomic and somatic neuropathy in STZ-induced diabetic mice.
Farias VX, Macêdo FH, Oquendo MB, Tomé AR, Báo SN, Cintra DO, Santos CF, Albuquerque AA, Heimark DB, Larner J, Fonteles MC, Leal-Cardoso JH, Nascimento NR.
Source

Department of Physiology and Pharmacology, Superior Institute of Biomedical Sciences, Fortaleza, Ceará, Brazil.
Abstract
AIM:

D-chiro-inositol (DCI) has been shown to prevent and reverse endothelial dysfunction in diabetic rats and rabbits. The present study evaluates the preventive effect of DCI on experimental diabetic neuropathy (DN).
METHODS:

Streptozotocin-induced (STZ) diabetic mice were treated by oral gavage for 60 days with DCI (20 mg/kg/12 h) or saline (NaCl 0.9%; 0.1 ml/10 g/12 h; Diab) and compared with euglycaemic groups treated with saline (0.1 ml/10 g/12 h; Eugly). We compared the response of the isolated sciatic nerve, corpora cavernosa or vas deferens to electrical stimulation.
RESULTS:

The electrically evoked compound action potential of the sciatic nerve was greatly blunted by diabetes. The peak-to-peak amplitude (PPA) was decreased from 3.24 ± 0.7 to 0.9 ± 0.2 mV (p < 0.05), the conduction velocity (CV) of the first component was reduced from 46.78 ± 4.5 to 26.69 ± 3.8 ms (p < 0.05) and chronaxy was increased from 60.43 ± 1.9 to 69.67 ± 1.4 ms (p < 0.05). These parameters were improved in nerves from DCI-treated mice (p < 0.05). PPA in the DCI group was 5.79 ± 0.8 mV (vs. 0.9 ± 0.2 mV-Diab; p < 0.05) and CV was 45.91 ± 3.6 ms (vs. 26.69 ± 3.8 ms-Diab; p < 0.05). Maximal relaxation of the corpus cavernosum evoked by electrical stimulation (2-64 Hz) in the Diab group was 36.4 ± 3.8% compared to 65.4 ± 2.8% in Eugly and 59.3 ± 5.5% in the DCI group (p < 0.05). Maximal contraction obtained in the vas deferens was 38.0 ± 9.2% in Eugly and 11.5 ± 2.6% in Diab (decrease of 69.7%; p < 0.05), compared to 25.2 ± 2.3% in the DCI group (p < 0.05 vs. diabetic). Electron microscopy of the sciatic nerves showed prevention of neuronal damage.
CONCLUSIONS:

DCI has a neuroprotective action in both autonomic and somatic nerves in STZ-induced DN.

© 2011 Blackwell Publishing Ltd.

PMID:
21205116
[PubMed - indexed for MEDLINE]

d-chiro inositol is related to myoinositol which is also called inositol. It has been suggested that diabetics use inositol because it is lost in the urine in people with diabetes. The d-chiro form is just an isomer and is over the counter. It is currently used by the PCOS community to help reverse infertility in women with PCOS. (poly cystic ovary syndrome).
I took it for a year..hoping it would help my A1C and it did not.
A therapeutic dose of d-chiro inositol costs about $60 a month.
This is a reputable brand:
http://www.chiralbalance.com/
I also see that Swanson's has it now, but the dose they offer is very low only...30mg. The chiral balance is 300mg/cap.

I'll be adding to this thread with time. And I repeat -- others who have questions or information to share are welcome.

Why magnesium is important:

Magnesium is very important for people with diabetic neuropathy.

http://ods.od.nih.gov/factsheets/magnesium

Quote:

Early signs of magnesium deficiency include loss of appetite, nausea, vomiting, fatigue, and weakness. As magnesium deficiency worsens, numbness, tingling, muscle contractions and cramps, seizures (sudden changes in behaviors caused by excessive electrical activity in the brain), personality changes, abnormal heart rhythms, and coronary spasms can occur [1,3-4]. Severe magnesium deficiency can result in low levels of calcium in the blood (hypocalcemia). Magnesium deficiency is also associated with low levels of potassium in the blood (hypokalemia) [1,19-20].....

Individuals with poorly-controlled diabetes may benefit from magnesium supplements because of increased magnesium loss in urine associated with hyperglycemia [21].

This link is very important to understand magnesium and also to
help patients choose an effective method (either food or quality supplements) to normalize their magnesium levels. I have linked to this NIH website many times.

Here is my magnesium thread on NeuroTalk:
http://neurotalk.psychcentral.com/thread1138.html

Benfotiamine for peripheral neuropathy

Befotiamine is a synthetic form of thiamine that has shown to be very beneficial for peripheral neuropathy. There has been a lot of research on this supplement. Many promising studies out of Germany and Japan. I frequently recommend it for my patients. It is available in a cream and capsule form.
Hope this helps.

Quote:

Originally Posted by Matt DC (Post 811229)

Thanks for the reminder, Matt. I have a thread on the subform about Benfotiamine already.
I started this thread for Diabetic Neuropathy, because it should really have its own title. This will aid people coming in from Google searches too.

here is what I have so far, and when I make the benfotiamine post here I will link to it, and perhaps find even new papers on it:
http://neurotalk.psychcentral.com/post653193-4.html

--I should also reprise my postings of articles about neuropathy in people with impaired glucose tolerance but not yet diagnosable with frank diabetes, as too many are told even by physicians that they can't get diabetic neuropathy unless they've had diabetes for years. This is not true, and often neuropathic symptoms are the presenting complaint in those with glucose tolerance issues:

Even blood sugar readings that would not be considered in the range of frank diabetes, but would just be considered "impaired glucose tolerance", such as those in the range of around 100-125, have been associated with peripheral neuropathy, particularly those of the small fibers, which tends to be burning, lancating, and electrical in symptoms, and not necessarily the stereotypical "numb". There's been a lot of research coming out about this in the last few years; I keep a list of papers and studies on this that includes:

http://intl.neurology.org/cgi/content/abstract/60/1/108

http://www3.interscience.wiley.com/c...TRY=1&SRETRY=0

http://www.ncbi.nlm.nih.gov/entrez/q..._uids=16448668

http://www3.interscience.wiley.com/c...07929/ABSTRACT

http://www.ncbi.nlm.nih.gov/entrez/q...d_AbstractPlus

There are a lot more, but you get the idea.

Here is a good link to Dr. Sahelian's website.

http://www.raysahelian.com/diabeticneuropathy.html

He has collected some research on the common supplements often suggested for PNers that are diabetic.

I think the link is worth reading.

I have a supplement thread here on the subforum as well.
Benfotiamine

acetyl carnitine so far.

http://neurotalk.psychcentral.com/thread121683.html

I'll be doing lipoic acid soon....that will be the next post.

Depletion of Taurine in Experimental Diabetic Neuropathy: Implications for Nerve Metabolic, Vascular, and Functional Deficits

http://www.sciencedirect.com/science...14488600975915

Taurine and Inositol are often recommended for diabetics.

Inositol is lost in the urine of diabetics like magnesium.

Statins now linked to type II diabetes:

http://old.news.yahoo.com/s/ap/20120...thbeat_statins

This is one other study showing some statins actually lead to insulin resistance:

Quote:

Atherosclerosis. 2011 Mar;215(1):1-8. Epub 2010 Nov 2.
Differential metabolic effects of distinct statins.
Koh KK, Sakuma I, Quon MJ.
Source

Vascular Medicine and Atherosclerosis Unit, Cardiology, Gachon University, Gil Medical Center, 1198 Kuwol-dong, Namdong-gu, Incheon 405-760, Republic of Korea. kwangk@gilhospital.com
Abstract

Reciprocal relationships between endothelial dysfunction and insulin resistance suggest that therapies improving endothelial dysfunction will simultaneously improve insulin sensitivity and other metabolic parameters. However, previous studies with some statins either did not alter insulin sensitivity or promoted insulin resistance despite significant improvements in endothelial dysfunction and decreases in circulating pro-inflammatory markers. This may be due to pleiotropic or off-target effects of some statins to cause insulin resistance by diverse mechanisms unrelated to endothelial dysfunction. Indeed, there is evidence of other differential metabolic actions of distinct statins including effects on hydroxymethylglutaryl-CoA reductase inhibition, isoprotenoid synthesis, calcium release, glucose transport, insulin secretion, and/or insulin resistance. Pravastatin increases expression of adiponectin mRNA, enhances adiponectin secretion, increases plasma levels of adiponectin, and enhances insulin sensitivity in mice and humans. Clinical studies including large scale randomized controlled trials demonstrate potential differences between individual statins, with pravastatin promoting risk reduction for new onset of diabetes. Conversely, other statins including atorvastatin, rosuvastatin, and simvastatin all promote significant increase in this risk. Given the frequent concordance of metabolic diseases including diabetes, obesity, and metabolic syndrome with cardiovascular diseases associated with hyperlipidemia, it is important to understand the potential metabolic risks and benefits of therapies with distinct statins. In this review, we discuss these differential effects of statins on metabolic homeostasis and insulin sensitivity.

Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.

PMID:
21130454
[PubMed - indexed for MEDLINE]

This is only one example of the emerging data on statins and insulin resistance. More are out there like the Yahoo article, and I think once the patents on Lipitor and Crestor expire, we will see many more negative studies.

Magnesium reduces pain in diabetic neuropathy:

Thanks to bent98 for finding this article:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3002451/