So you’re experiencing neuropathy, but do you know how you got to this point? Many cases of neuropathy are actually considered idiopathic, so the cause is unknown, but just as many cases are caused by diabetes. The rest of the cases, also called acquired neuropathy, are caused by any of the following:
- Trauma or pressure on nerves. This could be caused by anything from a cast or crutch to repetitive motion like typing on a keyboard. We all need to be careful with this now that everyone is becoming tech savvy.
- Nutritional problems or a lack of vitamins, so make sure you get your dose of vitamin B!
- Alcoholism and a poor diet.
- Autoimmune diseases. For example: lupus, rheumatoid arthritis, and Guillain-Barre syndrome
- Tumors, which press up against nerves in many cases.
- Other diseases and infections, such as kidney disease, liver disease, Lyme disease, HIV/AIDS, or hypothyroidism
- Inherited disorders, also known as hereditary neuropathies.
- Poison exposure from toxins like heavy metals, and certain medications and cancer treatments.
Your case of neuropathy is more than likely leaving you in pain, but there are treatments available to help treat or reduce these pains, such as Neurvasia, a scientifically formulated medical food which enhances the physiological function of the neurovascular system.
So far so good.
! That is why we pay attention to the quality of the medications.
Prevention of cardiac autonomic neuropathy in dogs with Benfotiamine.
In Gries FA, Federlin K.
Benfotiamin in the Therapy of Polyneuropathy.
New York: Georg Thieme Verlag, 1998; 45-9.
Experimentally-induced diabetes of the dog leads to disturbances in the autonomous neurological function of the heart after approximately 3 months of continuously- observed diabetes. As signs of autonomic cardiac neuropathy, the heart rate variability and Valsalva ratio clearly fell in the untreated diabetic animals. Oral benfotiamine, administered from the sixth day after diabetes-induction, prevented or at least delayed these changes. According to the results, treatment with fat-soluble benfotiamine can play an important role in the therapy and prevention of cardiac autonomic neuropathy, apart from any effect on diabetic metabolic
Effectiveness of different benfotiamine dosage regimens in the treatment of painful diabetic neuropathy.
Arzneimittelforschung 1999 Mar; 49(3): 220-4.
Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P.
I am very pleased with my first order from the price to the check out to the shipment. ? Sixty-three percent, 74%, and 82% of the patients on 25 mg, 50 mg and 100 mg of our medications, respectively, reported an improvement in their health.
The therapeutic effectiveness of a benfotiamine (CAS 22457-89-2)-vitamin B combination (Milgamma-N), administered in high (4 x 2 capsules/day, = 320 mg benfotiamine/day) and medium doses (3 x 1 capsules/day), was compared to a monotherapy with benfotiamine (Benfogamma) (3 x 1 tablets/day, = 150 mg benfotiamine/day) in diabetic patients suffering from painful peripheral diabetic neuropathy (DNP). In a 6-week open clinical trial, 36 patients (aged 40 to 70 yrs) having acceptable metabolic control (HbA1c < 8.0%) were randomly assigned to three groups, each of them comprising 12 participants. Neuropathy was assessed by five parameters: the pain sensation (evaluated by a modified analogue visual scale), the vibration sensation (measured with a tuning fork using the Riedel-Seyfert method) and the current perception threshold (CPT) onthe peroneal nerve at 3 frequencies: 5, 250 and 2000 Hz). Parameters were registered at the beginning of the study and at the end of the 3rd and 6th week of therapy. An overall beneficial therapeutic effect on the neuropathy status was observed in all three groups during the study, and a significant improvement in most of the parameters studied appeared already at the 3rd week of therapy (p < 0.01). The greatest change occurred in the group of patients receiving the high dose of benfotiamine (p < 0.01 and 0.05, resp., compared to the other groups). Metabolic control did not change over the study. It is concluded that benfotiamine is most effective in large doses, although even in smaller daily dosages, either in combination or in monotherapy, it is effective.
Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy.
I use this for my health after doctor told me to do it. I am very surprised with the result. . Canadian drugs are only shipped from our affiliated Canadian dispensary.
Nat Med 2003 Mar; 9(3): 294-9.
Hammes HP, Du X, Edelstein D, Taguchi T, Matsumura T, Ju Q, Lin J, Bierhaus A, Nawroth P, Hannak D, Neumaier M, Bergfeld R, Giardino I, Brownlee M.
Three of the major biochemical pathways implicated in the pathogenesis of hyperglycemia induced vascular damage (the hexosamine pathway, the advanced glycation end product (AGE) formation pathway and the diacylglycerol (DAG)-protein kinase C (PKC) pathway) are activated by increased availability of the glycolytic metabolites glyceraldehyde-3-phosphate and fructose-6-phosphate. We have discovered that the lipid-soluble thiamine derivative benfotiamine can inhibit these three pathways, as well as hyperglycemia-associated NF-kappaB activation, by activating the pentose phosphate pathway enzyme transketolase, which converts glyceraldehyde-3-phosphate and fructose-6-phosphate into pentose-5-phosphates and other sugars. In retinas of diabetic animals, benfotiamine treatment inhibited these three pathways and NF-kappaB activation by activating transketolase, and also prevented experimental diabetic retinopathy. The ability of benfotiamine to inhibit three major pathways simultaneously might be clinically useful in preventing the development and progression of diabetic complications.