Is There a Role for Vitamins in the Management of Alcohol Use Disorder?

November 1, 2024

Clinical Questions Uncategorized 6 min read

By Chloe Fong

Peer Reviewed

The correlation between vitamin deficiency and alcohol use disorder (AUD) has been well documented in the literature, with a study from 1963 finding that 70% of patients admitted to the hospital for suspicion of alcohol intoxication had low folate (vitamin B9) levels.1 While more recent numbers on vitamin deficiency in AUD may be less jarring, with one study finding an 11% prevalence of folate deficiency,2 AUD continues to be associated with vitamin dysregulation. For instance, Gibson and colleagues found that a two-week controlled increase in alcohol consumption led to a significant decrease in folate (p<0.03) and vitamin B12 (p<0.001) levels.3 Laufer and colleagues found that alcohol use correlated with a 5% decrease in B12 levels (p=0.03),4 and Van der Gaag and colleagues found that alcohol consumption was linked to a 8-9% rise in homocysteine levels, a compound controlled by vitamin B stores.5 This association between AUD and vitamin deficiency suggests a role for vitamin supplementation in AUD management.

However, recommendations regarding supplementation in AUD are limited. Guidelines published in 2020 by the New York State Department of Health AIDS Institute make no mention of vitamin supplementation,6 while 2017 international guidelines on AUD treatment remark, “Vitamin deficiencies are common in patients with heavy alcohol intake. Supplementation is recommended, especially of B vitamins, including thiamine, to prevent the development of Wernicke-Korsakoff syndrome.”7 This begs the question, how should providers approach vitamin supplementation when it comes to AUD management?

One particularly feared complication related to AUD is thiamine deficiency with progression to Wernicke’s encephalopathy (WE). However, guidance on thiamine supplementation in the management of AUD and WE is sparse and conflicting. In their systematic review of AUD treatment guidelines, Pruckner and colleagues found that, while most guidelines mentioned thiamine supplementation, recommendations varied considerably, with some guidelines neglecting to suggest dosages and routes altogether.8 Accordingly, in their multicenter study on WE management, Novo-Veleiro and colleagues found wide variability in thiamine dosages and routes across different centers.9 Some of this ambiguity may be related to sparse evidence on the efficacy of thiamine supplementation in WE management. Ambrose and colleagues looked at 107 patients undergoing alcohol detoxification and divided them into treatment groups receiving anywhere from 2 mg to 200 mg intramuscular thiamine per day. Participants then performed a delayed alternation task, and researchers found that higher dose treatment correlated with superior performance on this test.10 Conversely, Dingwall et al. looked at WE prevention in asymptomatic at-risk patients with AUD, as well as WE management in symptomatic patients with AUD. Participants were divided into groups receiving varying thiamine dosages and were then asked to perform four different cognitive tasks. Researchers found no significant differences between thiamine dosage and neurological symptoms, as well as no significant differences between thiamine dosages and cognitive task performance, aside from a marginally significant difference between 300 mg and 100 mg thiamine treatment groups and performance on a story memory recall task in asymptomatic at-risk patients with AUD.11 Thus, the lack of standardized thiamine treatment recommendations in addition to limited evidence on thiamine efficacy leave a gray area when it comes to thiamine supplementation in AUD management.

Folic acid deficiency is also commonly associated with AUD. While the prevalence of folate deficiency in the US has declined following folic acid fortification of cereal-grain products in 1998,12,13 studies have found that alcohol use impairs folate absorption, suggesting that even with sufficient dietary intake, ineffective folate absorption may still influence functional folate status.14 However, guidance on folate acid supplementation in AUD management is lacking. One commonly cited suggestion is folate 0.4-1.0 mg daily; however, this recommendation comes without sufficient data to support these numbers.15 Despite limited guidance on dosage recommendations, Santhosh-Kumar and colleagues report that, among patients admitted for AUD rehabilitation, patients with initially sufficient folate levels did not accumulate additional folate following folate supplementation; accumulation was only significant in patients with initial folate levels in the lowermost quartile of study participants (p=0.002).16 Thus, concern for supraphysiologic folate accumulation need not dissuade folate administration.

AUD is associated with deficiencies beyond vitamin B, and several other vitamins have been identified as having potential therapeutic benefit in AUD management. In their study of 30 patients with alcoholic liver disease, Kolasani and colleagues found that vitamin E supplementation in addition to standard treatment led to a significant improvement in liver function markers compared to standard treatment alone.17 Conversely, Mezey and colleagues found improvements only in serum hyaluronic acid and not in other markers of liver function following vitamin E supplement in alcoholic hepatitis.18

One study found vitamin C deficiency to be as high as 96% in patients with alcohol-related illness, with significant improvement in vitamin C levels following a 5 day intravenous course of vitamin C (mean increase 108.32 +/- 34.98 nmol/108 WBC (p<0.001).19 Chen and colleagues found that pretreatment with vitamin C prior to alcohol consumption led to significant enhancements in blood ethanol clearance compared to no pretreatment (p<0.05),20 while Susick and Zannoni found that pretreatment with vitamin C prior to ethanol consumption not only significantly increased ethanol blood clearance (p<0.02), but also led to significantly less ethanol-induced impairment in motor coordination (p<0.03) and color discrimination (p<0.001) tasks.21

Thus, vitamin status does appear to have prognostic implications. However, varying recommendations across different management guidelines make vitamin supplementation a difficult task for providers. While prompt identification and treatment of vitamin deficiencies remains an integral part of AUD management, more research is needed on the benefits of vitamin supplementation in patients with AUD.

Chloe Fong is a Class of 2026 medical student at NYU Grossman School of Medicine

Reviewed by  Michael Tanner, MD, Executive Editor, Clinical Correlations

Image courtesy of Wikimedia Commons, source:  https://commons.wikimedia.org/wiki/File:Pill_Organizer_With_Vitamins_And_Medicines.jpg

References

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