Research suggests you can recover from some or all of the nerve damage caused by alcohol-related neuropathy. Abstaining from alcohol can help restore your nutritional health, improve your symptoms, and prevent further nerve damage. Individuals with alcoholic neuropathy can make a partial or full recovery, depending on the extent and duration of their alcohol consumption. A person should speak with a doctor about their individual outlook.
As a result, there’s no exact amount of alcohol that brings on this disorder. However, individuals shouldn’t use this as an excuse to continue drinking. When a specific cause is unknown, people alcoholic neuropathy stories will use that as an excuse to continue addictive behavior. Department of Health and Human Services’ Dietary Guidelines for alcohol consumption (one drink a day for women and two for men) doesn’t carry nearly any risk for developing this disease.
Deficiency of vitamins other than thiamine may also contribute to clinical features of alcoholic neuropathy. Chronic alcoholism can alter the intake, absorption and utilization of various nutrients (nicotinic acid, vitamin B2, vitamin B6, vitamin B12, folate or vitamin E). Thus, these vitamin deficiencies were not considered to be major causal factors of neuropathy 26. Like many other types of diseases, neuropathy from alcohol abuse doesn’t progress in all individuals the exact same way. Some people may end up drinking excessively their entire lives without developing this disorder. Others can see symptoms within several years of heavy alcohol abuse.
The most important thing you can do to treat alcohol-related neuropathy is to stop consuming alcohol. People who drink heavily on a regular basis and have one or more of the following symptoms should contact a doctor. Doctors will help you mitigate the damage, while a physician may prescribe various supplements that will replenish your system.
Apart from above function, over-activation of epsilon form of protein kinase C (PKCε) is known to be involved in mediating neuropathic pain, such as pain induced by cancer chemotherapy (vincristine) 56 and diabetes 57. PKC and protein kinase A (PKA) are both known to be important in nociceptor function 57–59. There are several studies suggesting the involvement of protein kinases in alcoholic neuropathy. Dina et al. 16 maintained rats on a diet to simulate chronic alcohol consumption in humans and found mechanical hyperalgesia by the fourth week which was maximal at 10 weeks. Thermal hyperalgesia and mechanical allodynia were also present with decreased mechanical threshold of C-fibres.
Females can be more susceptible than males to many of the negative consequences of alcohol use, such as nerve damage, as they may begin to see effects from a lower amount of alcohol consumption. This may be due to body weight and other biological differences. A diet poor in nutrients or avoiding eating can make nutritional deficiencies worse. Nerve damage caused by alcoholic neuropathy causes the muscles to not receive the signals from nerves properly. This causes the muscles to become weakened and unable to function properly.
In 47 of these patients sural nerve biopsy was performed, with discrimination in terms of their thiamine status 3. The ethanol consumption of these patients was more than 100 g day–1 for more than 10 years. These patients were divided into two groups based on thiamine status. The subgroup without thiamine deficiency consisted of 36 patients, while the subgroup with thiamine deficiency consisted of 28 patients. In addition, 32 patients with nonalcoholic thiamine deficiency neuropathy were also evaluated for comparison. The subgroup without thiamine deficiency, considered to be a pure form of alcoholic neuropathy, uniformly showed slowly progressive, sensory dominant symptoms.