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The leading risk factor of death among males between the ages of 15 and 59 is alcohol, showing how much of a problem drinking in excess has become. 
This is the consequence of the following: 
The sheer amount of alcohol consumed determines the level of toxicity. If the levels of alcohol consumption have become chronic, this may result in alcoholic neuropathy. This is a condition characterised by nerve damage from long-term alcohol abuse. 
The mechanisms behind alcoholic neuropathy are rarely understood due to its pathobiology, despite several explanations.
These suggestions have included (all due to alcohol consumption):
Alcohol neuropathy has been found to be more prevalent in women compared to men, with greater severity and more rapid onset. 
Despite the unknown formation of alcohol neuropathy, all people that suffer from this condition have peripheral nerve damage.
Peripheral nerves have important motor and sensory functions, such as bowel and bladder control, walking, sex, limb movement, and speech.
The thiamine deficiency seen in most alcoholics appears to be a leading cause of alcohol neuropathy. Alcohol reduces the body’s ability to be able to absorb thiamine, causing malabsorption.
Furthermore, patients who consume an excessive amount of alcohol tend to lack general nutrition and vitamins.
This has led experts to believe alcohol neuropathy occurs through a combination of:
The exact and precise amount of alcohol that causes alcoholic neuropathy is challenging to estimate, as everyone’s alcohol tolerance and reactions are different. The duration of alcohol use, amount consumed per sitting, and period of use all influence the development of this condition.
One study has suggested that if you consume over 100grams of alcohol per day over the course of many years, it is likely to lead to alcohol-related neuropathy.
10ml or 8grams of alcohol is equivalent to one unit of alcohol, the amount that an adult is able to process in one hour. It has been considered safe for people to drink 2 – 3 units a day, or around 21 units a week (not all in one sitting). 
Alcoholic neuropathy is not life-threatening, in reference to morbidity. However, this condition can decrease the quality of life as it impacts movement and forms of sensation.
One of the noticeable symptoms of alcohol neuropathy is hyperalgesia and allodynia. Hyperalgesia is an abnormally heightened sensitivity to pain.
Allodynia is a condition that is characterised by a feeling of pain to a stimulus that normally does not cause any discomfort.
The other symptoms of alcoholic neuropathy are:
Symptoms develop slowly, appearing over months and years. The abnormalities in sensory and motor functions lead to painful and uncomfortable symptoms that may be incapacitating. 
Once you begin to see any signs of alcohol neuropathy, get in touch with a doctor or any medical professional in order to get diagnosed. This involves being honest about your alcohol consumption and daily life, including diet and other aspects of living.
The tests that may identify alcoholic neuropathy include:
The largest treatment for alcoholic neuropathy will include the decision to stop drinking alcohol. Treatment will primarily focus on alcohol abuse, such as rehabilitation (inpatient and outpatient) and therapy at a professional clinic.
Outside of alcohol use, doctors will focus on the characteristics and symptoms of alcoholic neuropathy. Management of this condition is critical as nerve damage can be completely debilitating.
Treatment plans may include:
Usually, nerve damage is permanent and will only get worse if the drinking continues. If caught early, however, doctors and medical professionals are able to minimise nerve damage and chronic pain leading to disability.
Alcohol neuropathy is a form of nerve damage caused by a combination of:
This health condition has a variety of treatment options, but the severity of the condition is dependent on alcohol intake and lifestyle.
 World Health Organization . Global status report on alcohol and health. WHO Press; Geneva, Switzerland: 2011.
 Zaridze D, Brennan P, Boreham J, Boroda A, Karpov R, Lazarev A, et al. Alcohol and cause-specific mortality in Russia: a retrospective case-control study of 48,557 adult deaths. Lancet. 2009;373:2201–2214.
 Zakhari S. Overview: how is alcohol metabolized by the body? Alcohol Res Health. 2006;29:245–254.
 Chopra K, Tiwari V. Alcoholic neuropathy: possible mechanisms and future treatment possibilities. Br J Clin Pharmacol. 2012 Mar;73(3):348-62. doi: 10.1111/j.1365-2125.2011.04111.x. PMID: 21988193; PMCID: PMC3370340.
 Ammendola A, Gemini D, Iannaccone S, Argenzio F, Ciccone G, Ammendola E, Serio L, Ugolini G, Bravaccio F. Gender and peripheral neuropathy in chronic alcoholism: a clinical-electroneurographic study. Alcohol Alcohol. 2000;35:368–71.
 Koike H, Sobue G. Alcoholic neuropathy. Curr Opin Neurol. 2006;19:481–6.
Although many individuals may consider alcohol not to be a drug, it is in fact one of the most dangerous and commonly consumed substances. Predominantly made up of the chemical …