Natural Diabetic Nerve Pain Treatment Book
The health-care cost of problems related to the diabetic foot, the most common cause of hospitalization in patients with diabetes, is estimated to be more than 1 billion annually (73). In 2003, the total annual cost of diabetic peripheral neuropathy and its complications were estimated to be between 4.6 and 13.7 billion (74). In large cohort studies, prevalence rates for neuropathy have ranged from 7.5 percent at time of diagnosis of diabetes, to 50 percent 25 years after initial diagnosis (75). It is present in more than 80 percent of diabetic patients with foot lesions (73). Poor glycemic control is associated with an increased risk for neuropathy and amputation (76). In one study, a HbA1c 13.4 was associated with 2.2 relative risk of amputation (76). In another study, a 50 mg dl increase in the mean random glucose was associated with a 1.6 OR for amputation (76). Diabetic peripheral neuropathy predisposes to foot ulceration and lower-extremity amputation (74). The presence of...
Because thiamin deficiency can reduce pain tolerance, supplemental thiamin may ease chronic pain. Thiamin may be effective in peripheral neuropathy,5 particularly in inflammatory nerve disorders (such as trigeminal neuralgia). It may also be effective in diabetic neuropathy.
In addition to peripheral neuropathy, common signs in wet beriberi include oedema, tachycardia, wide pulse pressure, cardiomegaly and congestive heart failure. Patients with wet beriberi respond dramatically to intramuscular doses of 25mg for 7-14 days, followed by oral doses of 10mg three times a day until the patient fully recovers (Tanphaichitr, 1999). A peripheral neuropathy, dry beriberi is characterised by a symmetric impairment of sensory, motor and reflex functions affecting the distal segments of the limbs more severely than the proximal ones (Thurnham, 2000). Dry beriberi can be more resistant to treatment. Disappearance of impaired sensation occurs between 7 and 120 days, and recovery of motor weakness within 60 days of the start of treatment (Tanphaichtir, 1999).
Gamma linolenic acid (GLA) and omega-3 fatty acids have been shown to partially correct this membrane defect and improve insulin receptor function. We already know that GLA levels are low in diabetics, and recent studies indicate that supplementation is helpful for relieving peripheral neuropathy. GLA-rich primrose oil has shown promise in relieving diabetic neuropathy. Ounce for ounce, borage oil contains more GLA than primrose, and is less expensive, but studies have shown that it is not as effective as primrose for relieving diabetic neuropathy.
One study of twenty-one type II diabetics given 900 mg of vitamin E for six months found a significant improvement in the nerve conduction velocity test (NCV), which evaluates damage or disease in peripheral nerves. Histological evidence of nerve fiber regrowth was also seen in a large number of the patients. Those given a placebo did not improve.408 Alpha-lipoic acid is also one of the most useful supplements in treating and preventing peripheral neuropathy associated with diabetes.410 Several studies have shown that it can improve electrical conduction in affected nerves and dramatically improve symptoms. The degree of improvement depends on the length of time the problem has existed. The sooner the supplement is begun, the better the results.
While there's nothing wrong with taking a daily multivitamin, megadoses aren't a good idea because their long-term safety remains in question. Over the years, various supplements have been recommended for an assortment of ailments. B-vitamins, for instance, were used to treat diabetic neuropathy, but their beneficial role was never proven and they're not recommended as a therapeutic option. Although chromium piccolinate was reported to have a good effect on blood-sugar control, it was never conclusively demonstrated. One antioxidant, alphalipoic acid, is a prescription drug in Germany that has been used to treat diabetic neuropathy. Although studies are underway in the United States, results will not be available for years.
Sorbitol can be further metabolized to fructose (B) if there is excess fructose, this reaction may be reversed. Excess fructose also inhibits the conversion of sorbitol made from glucose to fructose, resulting in an accumulation of sorbitol. Aldol reductase and sorbitol dehydro-genase are present in all tissues, catalyzing the conversion from sorbitol to fructose and the reverse (C). In the Schwann cells of the peripheral nervous system, in the papillae of the kidneys, and in the epithelia of the eyes' lenses, there is intense aldol reductase activity. Aldol reductases are also common in the pancreatic islets of Langerhans here, release of sorbitol is part of the signaling mechanism for insulin secretion.
An essential role for C22 6n-3 in brain and retinal PL was described by Neuringer and Connor, who demonstrated C18 3n-3 deficiency in rhesus monkeys fed during gestation diets with safflower oil (n-6 n-3 ratio of 255 1) as the sole source of fat (133). Their offspring reared on the same diet developed abnormal electroretinograms compared with those of the control group of offspring fed soybean oil (n-6 n-3 ratio of 7). Decreased concentrations of C18 3n-3 and long-chain n-3 PUFA in plasma PL were observed in offspring who showed loss of visual activity. Learning capacity, as tested in a spatial-reversal learning task, was not affected, possibly because of the observed compensatory increase of n-6 PUFA, particularly C22 5n-6, in PL. Retinal n-3 PUFA deficiency was reversed at the ages of 10 and 24 months by feeding a fish oil diet rich in C20 5n-3 and C22 6n-3 (133). Although such extremely high n-6 n-3 ratios rarely occur in human nutrition because of the wide availability of n-3 PUFA...
Characterized by extreme voluntary weight loss due to self-starvation or binge eating followed by purging, AN occurs in 0.5-3 of the female population 3, 4 . Clinical signs and symptoms of AN include an emaciated appearance, prepubertal features, lethargy, lanugo, alopecia, acrocyanosis, hypothermia, swollen joints, pitting edema, and bradycardia and hypotension. Biochemical evaluation often shows fluid and electrolyte disturbances and hypercarotenemia as well as endocrine and hematologic abnormalities such as hypothyroidism and anemia, respectively. Several cardiovascular irregularities develop along with a host of gastrointestinal complications, particularly in those with the binge eating-purging type of AN. Osteoporosis and skeletal fractures are common in persons with AN. Some may experience peripheral neuropathy and seizures. Mortality is as high as 22 in women with long-term AN 5 .
Clinical signs of deficiency are inflammation of the tongue, lesions of the lips and corners of the mouth however, these symptoms are also seen in riboflavin deficiency. Peripheral neuropathy is found in thiamin as well as in pyridoxine deficiency. Finally, microcytic hypochromic (sideroblastic) anaemia associated with pyridoxine deficiency is caused by impaired synthesis of haem (Thurnham, 2000).
Long-term use of very high doses of vitamin B6 ( 1000mg day) may cause a peripheral nerve condition characterized by numbness and tingling in the hands and feet. This is thought to occur when the liver's capacity to convert vitamin B6 to PLP is exceeded. For this reason, when very high doses are used in therapy, supplements of PLP may be preferred to vitamin B6, as PLP may be associated with less toxicity. Doses of vitamin B6 not exceeding
Thiamin located in the nerve cell membrane is important for the transmission of nerve impulses in the brain and peripheral nerves.2 Thiamin also plays an important role in the metabolism of several brain neurotransmitters (including ace-tylcholine and serotonin).
Thiamin functions as the coenzyme thiamin pyrophosphate (TPP) in the metabolism of carbohydrate and in conduction of nerve impulses. Thiamin deficiency causes beri-beri, which is frequently seen in parts of the world where polished (white) rice or unenriched white flour are predominantly eaten. There are three basic expressions of beriberi childhood, wet, and dry. Childhood beriberi stunts growth in infants and children. Wet beriberi is the classic form, with swelling due to fluid retention (edema) in the lower limbs that spreads to the upper body, affecting the heart and leading to heart failure. Dry beriberi affects peripheral nerves, initially causing tingling or burning sensations in the lower limbs and progressing to nerve degeneration, muscle wasting, and weight loss. Thiamine-deficiency disease in North America commonly occurs in people with heavy alcohol consumption and is called Wernicke-Korsakoff syndrome. It is caused by poor food intake and by decreased absorption and...
Other characteristic features seen with B12 deficiency include paresthe-sia in the limbs, inability to maintain balance when walking, weakness and excessive fatigue, loss of vibration and position sense, and a range of psychiatric disorders including disorientation, depression, mood disturbances, irritability, memory loss, and dementia. The lesions result from the patchy and progressive demyelination in peripheral nerves, the spinal cord, and the brain. Vitamin B12 deficiency is fairly common in the elderly and is associated with impairment in cognitive function or the exacerbation of coexisting dementia in the geriatric population.117
Peripheral Neuropathy Natural Treatment Options
This guide will help millions of people understand this condition so that they can take control of their lives and make informed decisions. The ebook covers information on a vast number of different types of neuropathy. In addition, it will be a useful resource for their families, caregivers, and health care providers.