The data indicates that there is both small and large fibre loss in alcohol-related neuropathy, neuropathy alcohol risk but that small fibre loss is generally predominant 3, 51, 53, 56, 59, 63, 86. Hypertriglyceridemia is an important risk factor for cardiovascular diseases. Moreover, elevated triglyceride levels can cause severe inflammation of the pancreas (i.e., pancreatitis). Heavy drinking (i.e., more than 140 grams of pure alcohol, or approximately 12 standard drinks, per day) can cause alcohol-induced hypertriglyceridemia in both diabetics and nondiabetics (Chait et al. 1972).
ALN Pathophysiology
While one may find relief from conventional treatment, the addictive nature or side effects of some medications makes it undesirable to use it for the long term. These treatments, in some cases, only suppress the symptoms but do not treat the underlying pathology. However, alternative therapies do not have side effect and tackle nutritional deficiencies and oxidative stress. Intensive research has been done on medications like alpha-lipoic acid, benfotiamine, acetyl-l-carnitine, and methylcobalamin. Other botanical or nutrient therapies include myo-inositol, vitamin E, topical capsaicin, and N-acetylcysteine.
- However, simultaneous use of erythropoietin and corticosteroids in studies without control groups complicates evaluating erythropoietin’s independent efficacy.
- In total, 585 papers did not meet the inclusion/exclusion criteria and were excluded.
- In a similar study, SSR was used to assess the number of reactive sweat glands (SGN), which turned out to be decreased in alcohol-dependent patients 164.
- Alcohol causes neuropathy via multifactorial processes, many of which are still under investigation.
- Based on these studies, it can be determined that there is a high rate of peripheral neuropathy amongst chronic alcohol abusers.
Treatment / Management
- Avoiding alcohol is the best way to treat these conditions and relieve symptoms.
- Toxic and nutritional optic neuropathy both present with symmetric and progressive bilateral vision loss, decreased color vision, central or cecocentral scotomas on formal visual field testing, and the absence of a relative afferent pupillary defect.
- The reason for better results in the benfotiamine alone group than in the Milgamma-N group, despite the fact that the benfotiamine dosage was equivalent, is not completely understood.
- This commonly presents with pain, paresthesias, and ataxia in the distal lower extremities.
- But according to the Centers for Disease Control and Prevention (CDC), drinking less or not at all may help you avoid neurological harm.
Affected nerves include the peripheral nerves, primarily located in the arms and legs, and the autonomic nerves, which help regulate our internal body functions. About 46% of chronic alcohol users will eventually develop this condition. Thirteen studies provided data from the biopsy of the sural nerve or the skin in patients with alcohol-related peripheral neuropathy. Alcohol-related peripheral neuropathy appears to be characterised by severe loss of myelinated fibres; and although profound small fibre loss can also be present, this appears to occur more variably 3, 51, 53, 59, 85.
Role of nutritional status other than thiamine deficiency
Heavy and chronic drinking is also often tied to nutritional deficiencies. what is alcoholism Someone who struggles with alcoholism may replace meals with alcohol, take in a lot of empty calories, and not maintain a healthy and balanced diet. Alcohol can also deplete the body of essential nutrients, and thiamine (vitamin B1) deficiency is common in people who battle alcoholism. Malnutrition due to alcoholism can contribute to nerve damage and alcoholic polyneuropathy as well.
Alcohol-Induced Neuropathy in Chronic Alcoholism: Causes, Pathophysiology, Diagnosis, and Treatment Options
If you are having difficulty avoiding alcohol, there are resources that can help you quit. While not specifically approved for the treatment of alcoholic neuropathy, antidepressant medications are often prescribed to help control the pain. Anti-seizure medications are sometimes prescribed as a way to manage pain. Alcoholic neuropathy is caused by nutritional deficiency, as well as toxins that build up in the body. Alcohol decreases the absorption of nutrients such as magnesium, selenium, and vitamins B1 and B2, causing significant deficits that affect many areas of the body, including the nerves. In general, it takes years for alcoholic neuropathy to develop, so a long-standing history of heavy alcohol use is typical.
When to Contact a Medical Professional
These individuals draw the majority of calories from calorie rich alcoholic beverages with low nutritive value. Chronic abuse of alcohol depletes the pool of liver proteins which are consumed for energy production and insufficient intake of proteins only worsens this imbalance. Resulting disturbances in protein and lipid metabolism lead to undernourishment which adversely influences other metabolic pathways, including those influencing the function of the nervous system. Alcoholic polyneuropathy is progressive and gets worse over time, as the damage to the nerves increases with continued alcohol abuse. The problems that alcoholic neuropathy causes with muscle weakness, balance, and coordination can make a person more at risk for falling down and getting injured. Not being able to tell when things are too hot because of the way the nerve damage interferes with the ability to sense temperature changes can make one more susceptible to burns.
What are risk factors for alcoholic neuropathy?
The US National Library of Medicine (NLM) warns that around 50 percent of long-term heavy drinkers will suffer from alcoholic neuropathy. Chronic alcohol consumption leads to malnutrition with dysfunctions in protein and lipid metabolism which affect the metabolic pathways and progression of ALN symptoms within the central and peripheral nervous systems 89. The direct toxic effects of alcohol and its metabolites (mainly acetaldehyde) are crucial in ALN etiology 64. It has been demonstrated that incubation of neural cells with advanced glycation end products of acetaldehyde (AA-AGE) induced dose-dependent degradation of neuronal cells while the addition of AA-AGE antibodies reduced neurotoxicity 51, 90. Other findings showed that decreased activity of aldehyde dehydrogenase leads to peripheral neuropathy 76, 91. Alcoholic neuropathy, also known as alcoholic peripheral neuropathy, refers to damage of the nerves due to chronic and excessive alcohol consumption.
