From the Guidelines
Alcoholics develop thiamine deficiency primarily because alcohol directly interferes with thiamine absorption, metabolism, and storage in the body, as evidenced by the most recent guideline 1. Chronic alcohol consumption damages the lining of the gastrointestinal tract, reducing the intestine's ability to absorb thiamine from food. Additionally, alcohol inhibits the enzymes needed to convert thiamine into its active form (thiamine pyrophosphate), which is essential for carbohydrate metabolism and proper brain function. Many alcoholics also have poor dietary habits, often substituting alcohol calories for nutritious food, further reducing their thiamine intake. The liver, which stores thiamine, becomes damaged through chronic alcohol use, decreasing the body's ability to maintain adequate thiamine reserves. This deficiency can lead to serious neurological conditions like Wernicke-Korsakoff syndrome, characterized by confusion, memory problems, and coordination difficulties. Some key points to consider in the management of thiamine deficiency in alcoholics include:
- Reduced gastrointestinal absorption due to disease or surgery, increased gastrointestinal or renal losses, and obesity pre-bariatric surgery and post-surgery are all risk factors for thiamine deficiency 1.
- IV thiamine 250 mg is required to manage encephalopathy in patients with chronic alcohol ingestion due to poor absorption 1.
- Thiamine supplementation is used routinely in clinical practice to prevent Wernicke's encephalopathy and Korsakoff psychosis, as supported by guidelines 2. Treatment typically involves immediate thiamine supplementation, with a recommended dose of 250 mg IV to manage encephalopathy 1, along with addressing the underlying alcohol use disorder through comprehensive rehabilitation approaches. It is essential to prioritize thiamine supplementation in individuals with alcohol use disorder to prevent serious neurological conditions and improve overall morbidity, mortality, and quality of life. The clinical strategy will depend on the situation, and prevention of encephalopathy with thiamine is supported by guidelines 1.
From the FDA Drug Label
CLINICAL PHARMACOLOGY: ... If intake is insufficient, tissues become depleted of their vitamin content. ... Body depletion of vitamin B 1 can occur after approximately three weeks of total absence of thiamine in the diet. Individuals with alcohol use disorder (AUD) may develop thiamine (Vitamin B1) deficiency due to insufficient intake of thiamine.
- The exact mechanism of thiamine deficiency in AUD is not directly stated in the label.
- However, it can be inferred that inadequate diet may contribute to thiamine deficiency, as the label states that body depletion of vitamin B1 can occur after approximately three weeks of total absence of thiamine in the diet 3.
From the Research
Causes of Thiamine Deficiency in Individuals with Alcohol Use Disorder (AUD)
- Inadequate dietary intake of thiamine 4, 5, 6
- Impaired absorption of thiamine from the gastrointestinal tract due to ethanol consumption 4, 6
- Impaired thiamine utilization in the cells 5
- Reduced thiamine phosphorylation to thiamine pyrophosphate (TPP) in the brain 4
- Increased urinary excretion of thiamine 7
Mechanisms of Thiamine Deficiency
- Ethanol inhibits the active component of thiamine transport in the intestine, impeding the cellular exit of thiamine across the basolateral or serosal membrane 6
- Ethanol reduces the rate of intestinal absorption and the net transmural flux of thiamine 6
- Impairment of thiamine movement out of the enterocyte correlates with a fall in the activity of Na-K ATPase 6
- Ethanol increases the fluidity of enterocyte brush border and basolateral membranes, potentially contributing to the impairment of thiamine transport 6
Consequences of Thiamine Deficiency
- Wernicke-Korsakoff syndrome 4, 5
- Peripheral neuropathy 7, 8
- Congestive heart failure 7
- Gastrointestinal beriberi 7
- Intensive care unit complications, such as heart failure, delirium, critical care neuropathy, gastrointestinal dysfunction, and unexplained lactic acidosis 7
- Permanent neurological deficits or fatal outcomes if left untreated or diagnosed late 8