Total recorded<unk> onsumption per capita of individuals 15 years or older, in liters of pure alcohol.<unk> m is the main cause of<unk> . In 2020 the NIH quoted an estimate that in the United States 25% to 66% of chronic alcohol users experience some form of neuropathy. The rate of incidence of<unk>  involving sensory and motor polyneuropathy has been stated as from 10% to 50% of<unk> s depending on the subject selection and diagnostic criteria. If electrodiagnostic criteria are used,<unk>  may be found in up to 90% of individuals being assessed. The distribution and severity of the disease depends on regional dietary habits, individual drinking habits, as well as an individual's genetics. Large studies have been conducted and show that<unk>  severity and incidence correlates best with the total lifetime consumption of alcohol. Factors such as nutritional intake, age, or other medical conditions are correlate in lesser degrees. For unknown reasons,<unk>  has a high incidence in women. Certain<unk>  beverages can also contain congeners that may also be bioactive; therefore, the consumption of varying alcohol beverages may result in different health consequences. An individual's nutritional intake also plays a role in the development of this disease. Depending on the specific dietary habits, they may have a deficiency of one or more of the following: thiamine (vitamin B1), pyridoxine (vitamin B6), pantothenic acid and biotin, vitamin B12, folic acid, niacin (vitamin B3), and vitamin A. Acetaldehyde Conversion of ethanol to acetaldehyde. The toxic buildup of acetaldehyde may result in<unk> . It is also thought there is perhaps a genetic predisposition for some<unk> s that results in increased frequency of<unk>  in certain ethnic groups. During the body's processing of alcohol, ethanol is oxidized to acetaldehyde mainly by alcohol dehydrogenase; acetaldehyde is then oxidized to acetate mainly by aldehyde dehydrogenase (ALDH). ALDH2 is an isozyme of ALDH and ALDH2 has a polymorphism (ALDH2*2, Glu487Lys) that makes ADLH2 inactive; this allele is more prevalent among Southeast and East Asians and results in a failure to quickly metabolize acetaldehyde. The neurotoxicity resulting from the accumulation of acetaldehyde may play a role in the pathogenesis of<unk> .
Alcoholic polyneuropathy
Tropical neuropathy
Diabetic neuropathy
Critical illness polyneuropathy
Chronic inflammatory demyelinating polyneuropathy
Paraneoplastic cerebellar degeneration
Vasculitic neuropathy
Polyneuropathy