On Fri, 16 May 2008 12:09:15 -0600, Tiger_Lily <me[at]privacy.net> wrote:

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Agreed, also beware that the ALA may knock down your BG some, so it
can have a double whammy in improving the neuropathy per se and also
improving the BG. I use the non-time release kind and have found it
not only knocks out my overenthusiastic liver but leaves me prone to
getting down to near-hypo levels.

jay wrote:
- quote -

i don't know the details, i didn't write the article, nor do the
research for it

i DO KNOW 6 or 7 diabetics who no longer have the tingling/burning/socks
under the toes feelings that they used to have

good bg control is imperative as well....

--
kate
type 1 since 1987
www.diabetic-talk.org
http://www.diabetes-support.org.uk/n...diagnosed.html

jay wrote:
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In our collective clinical experience, no supplement(s) can overcome
the deleterious effect that PIACs from VAT (black fat) has on the
fragile efferent fibers of sensory neurons thereby causing the
peripheral neuropathy.

Be hungry... be healthy... be hungrier... be healthier...

Prayerfully in the awesome name of LORD Jesus Christ,

Andrew <> <
--
http://groups.google.com/group/sci.m...918679e6b3d6f?

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Thanks. They recommends a cocktail of slow-released Lipoic Acid, EPO
and Vitamin C. Is the reason why EPO helps neuropathy well
established? Is the below related?

Choice of oils for essential fat supplements can enhance production of
abnormal metabolites in fat oxidation disorders.

Patients with mitochondrial long-chain fat oxidation deficiencies are
usually treated with diets containing reduced fat and increased
carbohydrate, at times via gastrostomy feeding. To ensure adequate
intake of essential fatty acids, supplements are provided to their
diets using commercially available oils. These oils contain large
quantities of non-essential fats that are preferentially oxidized and
produce disease-specific metabolites (acyl-CoA intermediates) due to
the genetic defect. This study describes the concentrations of these
intermediates as reflected by acylcarnitines as well as the %
contribution from each of four fatty acids: palmitate, oleate,
linoleate, and alpha-linolenate when incubated with fibroblasts from
patients with VLCAD, LCHAD, and trifunctional protein (TFP)
deficiencies. Palmitate and oleate produce the majority of disease-
specific acylcarnitines with these defective cell lines (79-94%)
whereas linoleate and linolenate produced less (6-21%). On average,
the amount of acylcarnitines decreased with increasing unsaturation
(C18:1> C18:2> C18:3:34%> 11%> 3%, respectively. This relationship may
reflect the "gatekeeper" role of carnitine palmitoyltransferase I (CPT
I). A diet comparison between Canola and a combination of Flax/Walnut
oils revealed that the latter, containing the least amount of non-
essential fats, reduced blood acylcarnitine levels by 33-36%. The
etiology of the severe peripheral neuropathy of TFP deficiency may
result from the unique metabolite, 3-keto-acyl-CoA, after conversion
to a methylketone via spontaneous decarboxylation. Essential fatty
acid supplementation with oils should consider these findings to
decrease production of disease-specific acyl-CoA intermediates. PMID:
17825594

jay wrote:
- quote -

take a look at this article......... it includes the studies done as well
http://www.diabetic-talk.org/dpn.htm

--
kate
type 1 since 1987
www.diabetic-talk.org
http://www.diabetes-support.org.uk/n...diagnosed.html

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Below abstract says, in general LA more effective, but EPO/GLA better
for ileum related neuropathy. Is there any commonly available food
with GLA?

The effectiveness of treatments of diabetic autonomic neuropathy is
not the same in autonomic nerves supplying different organs.

The aim of the study was to investigate antioxidant (alpha-lipoic acid
[LA]) and gamma-linolenic acid treatments in the prevention of changes
in autonomic nerves induced in streptozotocin-diabetic rats. Autonomic
nerves supplying the heart, penis, and gut were examined using
immunohistochemical and biochemical techniques. LA and gamma-linolenic
acid (present in evening primrose oil [EPO]) were administered as
dietary supplements ( approximately 80 and 200 mg. kg(-1). day(-1),
respectively). LA treatment prevented the diabetes-induced decrease of
norepinephrine (NA) in the heart and of type I nitric oxide synthase
(NOS-I) expression in erectile tissue of the penis but failed to
prevent diabetes-induced changes in NA-, vasoactive intestinal
polypeptide-, or calcitonin gene-related peptide-containing nerves
supplying the ileum. LA partially prevented and EPO totally prevented
the increase in NOS-I activity induced by diabetes in the ileum. EPO
treatment failed to prevent any other diabetes-induced changes in the
heart, penis, or ileum. These results demonstrate that, whereas LA
treatment is more effective than EPO in preventing diabetes-induced
changes in autonomic nerves, the effectiveness of LA treatment varies
with the target organ studied. Diabetes-induced changes in nerves
supplying the ileum are more resistant to treatment than those of the
heart and penis.
PMID: 12502507

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Thanks.

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Inhibition of development of peripheral neuropathy in streptozotocin-
induced diabetic rats with N-acetylcysteine.

N-acetylcysteine (NAC) is a precursor of glutathione (GSH) synthesis,
a free radical scavenger and an inhibitor of tumour necrosis factor
alpha (TNF). Because these functions might be beneficial in diabetic
complications, in this study we examined whether NAC inhibits
peripheral neuropathy. Motor nerve conduction velocity (MNCV) was
significantly decreased in streptozotocin-induced-diabetic Wistar rats
compared to control rats. Oral administration of NAC reduced the
decline of MNCV in diabetic rats. Structural analysis of the sural
nerve disclosed significant reduction of fibres undergoing myelin
wrinkling and inhibition of myelinated fibre atrophy in NAC-treated
diabetic rats. NAC treatment had no effect on blood glucose levels or
on the nerve glucose, sorbitol and cAMP contents, whereas it corrected
the decreased GSH levels in erythrocytes, the increased lipid peroxide
levels in plasma and the increased lipopolysaccharide-induced TNF
activity in sera of diabetic rats. Thus, NAC inhibited the development
of functional and structural abnormalities of the peripheral nerve in
streptozotocin-induced diabetic rats. PMID: 8721770

"jay" <jaym1212[at]hotmail.com> wrote in message
news:739091c9-61a5-4257-844a-cbc2e72bd0e6[at]r66g2000hsg.googlegroups.com...
- quote -

I don't know what NAC is. But Evening Primrose Oil is not on your list.
That's the biggie. I think...

On Thu, 15 May 2008 09:46:29 -0700 (PDT), jay <jaym1212[at]hotmail.com>
wrote:

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I can get you an incredible deal on the Statue of Liberty, 25% off the
cheapest price you can find from anyone else.

What supplements provide relief from polyneuropathy? Would the
following be the most important? Already doing paleo-type diet,
moderate exercise and multi-vitamins.

Benfotiamine
Vitamin B6 (P-5-P)
R-Lipoic Acid
NAC
Acetyl-L-Carnitine