Alcoholic Neuropathy: Causes, Symptoms, & Treatments

Nerve damage typically affects the axons, which are the projections that send electrical signals from one nerve to another. It also impacts the myelin, which is the fatty coating that protects the nerves. Heidi Moawad is a neurologist and expert in the field of brain health and neurological disorders. If liver damage is evident, appropriate consultation with a transplantation service is recommended. However, neuropathy is generally an exclusion criterion for transplantation. People who struggle with alcoholism Substance abuse should try to eat a healthy and balanced diet, even if they don’t feel hungry.

Effects of Alcohol Consumption in the Fed State

Alcohol consumption can exacerbate the diabetes-related lipid abnormalities, because numerous studies have shown that heavy drinking can alter lipid levels even in nondiabetics. In people with either type 1 or type 2 diabetes, single episodes of alcohol consumption (i.e., acute alcohol consumption) generally do not lead to clinically significant changes in blood sugar levels. In fact, some studies have indicated that isolated episodes of drinking with a meal may have a beneficial effect by slightly lowering blood sugar levels that tend to rise too high in diabetics (Swade and Emanuele 1997). This potentially beneficial effect was observed in both men and women, regardless of age. The alcohol amounts administered in those studies were usually between 0.5 g/kg (gram per kilogram body weight) and 1 g/kg, leading to blood alcohol levels (BALs) between approximately 0.03 and 0.1 percent2 (McDonald 1980). Those doses are equivalent to approximately 2.5 to 5 standard drinks.3 Interestingly, studies of acute alcohol exposure in nondiabetic people have yielded quite variable results, noting decreases, increases, or no changes in glucose levels.

Review Date 4/29/2023

• One of the other important issues in alcoholic individuals is the source of their calorie intake.
• As axons break down, the nerve fibers become less dense and cannot function properly.
• Constant pain in the hands or feet is one of the most bothersome aspects of alcoholic neuropathy.
• Besides blood chemistry test and complete blood count (CBC), esophagogastroduodenoscopy is needed when a patient vomits and has nausea for an unknown reason; X-rays of the gastrointestinal tract can also be performed.
• Deficiency of vitamins other than thiamine may also contribute to clinical features of alcoholic neuropathy.

Later, the results have been supported by Victor and Adams (1961)—among 12 patients with ALN, neuropathic symptoms were alleviated just after thiamine supplementation, even though the alcohol consumption was previously completely reduced 149. Koike et al. (2003) compared clinical and histological differences between ALN with and without thiamine deficiency 65. Also, the results of the group of 32 patients with non-alcoholic thiamine deficiency neuropathy were considered.

Peripheral Neuropathy

Acetaldehyde dehydrogenase is a mitochondrial enzyme which undergoes a single amino acid substitution (mutation) in about 50% of the Asian population in a way similar to the genetic changes in sickle cell anaemia 21. Thus, in alcoholics with the mutated dehydrogenase enzyme, acetaldehyde concentrations may reach values about 20 times higher than in individuals without the mutation. A certain amount of acetaldehyde is not metabolized by the usual pathways (Figure 2) and binds irreversibly to proteins which results in the creation of cytotoxic proteins which adversely affect the function of nervous system cells.

Enhancing Healthcare Team Outcomes

It is important to supplement the diet with vitamins, including thiamine and folic acid. Symptoms can include numbness in hands and feet, digestive issues, and loss of balance due to loss of nerve function. Especially if you have been drinking heavily for many years, coping with alcohol use disorder is not easy. But with the https://ecosoberhouse.com/ proper resources to help, you are better set up for success with sobriety. Several treatment options and interventions can help a person recover from alcohol dependence.

Role of caspases in alcoholic neuropathy

The exact mechanism behind alcoholic neuropathy is not well understood, but several explanations have been proposed. Some other studies have indicated that chronic alcohol intake can decrease the nociceptive threshold with increased oxidative-nitrosative stress and release of pro-inflammatory cytokines coupled with activation of protein kinase C (Figure 1) 10, 16. Therefore, alcoholic neuropathy may occur by a combination of the direct toxic effects of ethanol or its metabolites and nutritional deficiencies, including thiamine deficiency. The precise mechanisms responsible for toxicity on the peripheral alcoholism neuropathy nervous system, however, have not yet been clarified.

Alcoholic Neuropathy Symptoms

Ketoacidosis typically occurs in patients with type 1 diabetes who completely lack insulin. In rare cases, however, the condition also may affect people with type 2 diabetes. In those people, insulin levels are diminished, because the fasting has considerably lowered their blood sugar levels, thereby depriving the pancreas of its stimulus to produce and secrete insulin. Ketoacidosis, which occurs primarily in diabetics, is a condition characterized by excessive levels of certain acids called ketone bodies (e.g., acetone, acetoacetate, and β-hydroxybutyrate) in the blood.

• Nerve damage from chronic alcohol consumption can develop over several years.
• Diabetic eye disease (i.e., retinopathy) is another troublesome tissue complication of diabetes and one of the leading causes of blindness in the United States today.
• Ethanol and its toxic degradation metabolites affect neuronal metabolism including the metabolic pathways of nucleus, lysosomes, peroxisomes, endoplasmatic reticulum and cytoplasm 21.
• If you notice you are developing signs of alcoholic neuropathy (such as numbness after drinking alcohol), in addition to seeing a physician, try to stay away from alcohol altogether.
• This article provides an overview of alcoholic neuropathy, including symptoms, causes, and diagnosis.
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Hypoglycemia can have serious, even life-threatening, consequences, because adequate blood sugar levels are needed to ensure brain functioning. Primarily, it was assumed that the progression of ALN symptoms is due to malnutrition and micronutrient deficiency (mainly B1 hypovitaminosis) 82, 83. Indeed, these factors contribute to the progression of ALN symptoms; however, they do not constitute direct factors that manifest in ALN development 84.

Can alcohol cause pain in your feet?

• An essential risk factor regarding the etiology of ALN is the amount of alcohol consumed throughout the years since alcohol displays direct toxicity on nerve fibers 55.
• Activation of spinal cord microglia, mGlu5 spinal cord receptors, and hypothalamic-pituitary-adrenal axis appear to be implicated in this process 92,93,94,95,96,97.
• The evidence points toward alcohol-related peripheral neuropathy being a form of toxic neuropathy, rather than nutritional neuropathy.
• Alcohol abuse treatment might lead to a resolution of neuropathic pain and alleviation of its symptoms.

Activation of spinal cord microglia, mGlu5 spinal cord receptors, and hypothalamic-pituitary-adrenal axis also seem to be implicated in the pathophysiology of this alcoholic neuropathy. The goal of treatment is to impede further damage to the peripheral nerves while also restoring their normal physiology. Ammendola and colleagues conducted a study to assess differences between men and women in the development of alcoholic neuropathy. 26 This study used the sural sensory nerve action potential (SNAP) amplitude (ie, nerve conduction study) as the variable measure to detect significant neuropathy in a population of males and females with chronic alcoholism. Although the study provided control for nutritional deficiencies, the female group with chronic alcoholism had a significantly lower sural SNAP amplitude compared with the male group with similar total lifetime dose of ethanol consumption (TLDEC). This study suggested that females may demonstrate increased sensitivity to the toxic effects of alcohol on peripheral nerves.

In fact, insulin-resistant people have higher than normal insulin levels (i.e., are hyperinsulinemic1). Ultimately, insulin secretion declines even further, to levels below those seen in nondiabetics (although generally still higher than those seen in type 1 diabetics). At that point, when a deficit in insulin secretion is combined with a state of insulin resistance, the person develops type 2 diabetes. Thus, whereas type 1 diabetes is characterized by a complete lack of insulin production, type 2 is characterized by reduced insulin production plus insulin resistance. The reasons underlying defective insulin secretion and insulin resistance, which are still under investigation, are complex and beyond the scope of this article (for a review, see DeFronzo 1997).