Low-Dose Oral Minoxidil for Androgenetic Alopecia Is Not Associated with Significant Changes in Alcohol Consumption: A Retrospective Study of 21,971 Patients

Abstract

Introduction

Oral minoxidil, used off-label for androgenetic alopecia, has been linked to alcohol hangover symptoms. We examined changes in alcohol consumption before and after low-dose oral minoxidil (LDOM) initiation.

Methods

Using Epic’s Cosmos database (2010–2024), we analyzed alcohol consumption 6 months pre- and post-minoxidil in patients with recorded data. A two-sample z test compared average daily alcohol intake.

Results

Among 21,971 patients, demographics and minoxidil dosing were similar between groups. Average alcohol consumption was unchanged pre- versus post-LDOM (0.264 vs. 0.260 drinks/day, p = 0.72).

Conclusion

LDOM does not significantly affect alcohol consumption, suggesting minimal impact on hangover symptoms. Prospective studies are needed, but patients can be reassured about the low likelihood of symptom exacerbation.

Introduction

Oral minoxidil, initially developed as an antihypertensive agent, has gained popularity as an off-label treatment for androgenetic alopecia (AGA) [1]. An observational study reported an association between alcohol hangover (veisalgia) symptoms and low-dose oral minoxidil (LDOM) treatment in 10 AGA patients [2]. The authors recommended that physicians advise patients to refrain from taking their LDOM dose on days they anticipate excessive alcohol consumption. Supporting their hypothesis, per an online drug interaction checker, minoxidil and alcohol may have additive effects in lowering blood pressure [3], which may exacerbate hangover symptoms including headache and dizziness. This association is noteworthy as it suggests a potential interaction between minoxidil and alcohol that could negatively affect patient quality of life and medication adherence. Therefore, we sought to examine changes in patient alcohol consumption before and after starting oral minoxidil as a surrogate for assessing alcohol hangover.

Methods

Patients prescribed oral minoxidil 2010–2024 regardless of dose or indication were identified from Epic’s Cosmos, a database including over 257 million de-identified patient records. Patients without information on alcohol drinking habits were excluded. Average daily alcohol consumption values based on self-reported data were queried 0–6 months before and after minoxidil prescription. Alcohol consumption data presented in drinks/week were converted to drinks/day. A two-sample unequal variance z test was conducted to compare average daily alcohol consumption between time periods with significance set at p < 0.05.

Results

A total of 9,084 and 12,887 patients were included for the pre- and post-minoxidil analyses, respectively, with similar demographics between groups for legal sex (47.8% vs. 49.0% female, respectively, p = 0.212), mean age (57 ± 16.6 vs. 57 ± 16.4 years, respectively, p = 1.00), and race (p = 0.328) (Table 1). The majority of minoxidil prescriptions were low dose (≤5 mg daily) in both cohorts (84.3% vs. 84.2%, respectively, p = 0.766). Average number of alcoholic drinks was similar in the pre- and post-minoxidil groups (0.264/day vs. 0.260/day, respectively, z = 0.358, p = 0.72) (Table 2).

Table 1.

Demographics of patients before and after initiating LDOM

	Before minoxidil	After minoxidil	Two-sided p value
Patients, n	9,084	12,887
Age, mean±SD, years	57±16.6	57±16.4	1.00
Legal sex, f (n)
Female	0.478 (4,344)	0.490 (6,321)	0.212
Race/ethnicity, f (n)
White	0.719 (6,531)	0.726 (9,352)	0.351
Black	0.200 (1,814)	0.195 (2,519)	0.730
Asian	0.041 (372)	0.038 (492)	0.835
Hispanic	0.049 (445)	0.051 (655)	0.891

Mean age and the proportion of the pre- and post-minoxidil cohorts per demographic category were compared using z test. An additional Pearson’s chi-squared test of race was used to verify independence between the pre- and post-minoxidil cohorts.

f, frequency; n, number; SD, standard deviation.

Table 2.

Frequency of daily alcoholic drink average before and after minoxidil

Daily drink average	Before minoxidil (n = 9,084)	After minoxidil (n = 12,887)
0, f (n)	0.29 (2,640)	0.29 (3,756)
>0 and <1, f (n)	0.55 (5,021)	0.56 (7,156)
≥1 and <2, f (n)	0.10 (947)	0.10 (1,301)
≥2 and <3, f (n)	0.03 (294)	0.03 (424)
≥3 and <4, f (n)	0.01 (76)	0.01 (99)
≥4, f (n)	0.01 (106)	0.01 (151)

A two-sample unequal variance z test between the cohorts showed z = 0.358 and p = 0.72.

f, frequency; n, number.

Discussion

We found that oral minoxidil treatment was not associated with changes in alcohol consumption, suggesting that minoxidil does not exacerbate alcohol hangover symptoms or that any exacerbation is mild. Additive hypotensive effects of both minoxidil and alcohol, and evidence of increased expression of sulfotransferase 1A1 in rats exposed to minoxidil and alcohol versus minoxidil and water [4], have been proposed as mechanisms for exacerbation of alcohol hangover symptoms [2]. Other suggested mechanisms for veisalgia symptom exacerbation include minoxidil and alcohol interacting in the same metabolic pathways and skin metabolism of alcohol into acetaldehyde [5], but there is little basis for these hypotheses.

In addition, minoxidil may cause fluid retention and increased heart rate and cardiac output [6]. Fluid retention could potentially exacerbate hangover symptoms by contributing to swelling and discomfort, which might worsen headache and nausea symptoms. Increased heart rate and cardiac output could also compound the hypotensive effects of alcohol, leading to more pronounced symptoms, including dizziness and lightheadedness.

Our study suggests that these proposed interactions between minoxidil and alcohol metabolism do not occur or are clinically insignificant. Hangover symptoms including headache, nausea, and light sensitivity are subjective and may vary widely between individuals, complicating the assessment of their severity and the determination of potential interactions between minoxidil and alcohol consumption.

Limitations include retrospective and ecologic data sampling design, potential inconsistencies in variable coding, and reliance on aggregate data reported by Epic Cosmos, which uses interval scales, lowering the precision of summary statistics. Data on alcohol consumption were self-reported, and patient adherence to minoxidil was not measured. While demographics were similar between cohorts, we did not control for potential confounding factors, including diet and physical activity, which could have varying effects on hangover symptoms. Changes in alcohol consumption may not accurately reflect changes in hangover symptoms, as the severity of hangover symptoms may increase without corresponding changes in drinking behavior.

In conclusion, our study shows that oral minoxidil administration does not change alcohol consumption, which might suggest minimal to no exacerbated alcohol hangover effects. Prospective studies that directly measure hangover presence and severity are needed to corroborate these findings. In the meantime, dermatologists may inform AGA patients treated with LDOM who consume alcohol that while exacerbation of hangover symptoms is possible, it is unlikely.

Acknowledgments

Data used in this study came from Epic Cosmos, a dataset created in collaboration with a community of Epic health systems representing more than 257 million patient records from over 1,548 hospitals and 34,600 clinics from all 50 states and Lebanon.

Statement of Ethics

Written informed consent was not obtained from any adults participating in this study. This retrospective study is exempt from informed consent. The data reviewed are a secondary analysis of existing data, do not involve intervention or interaction with human subjects, and are de-identified per the de-identification standard defined in Section §164.514(a) of the HIPAA Privacy Rule. The process by which the data are de-identified is attested to through a formal determination by a qualified expert as defined in Section §164.514(b)(1) of the HIPAA Privacy Rule. This formal determination by a qualified expert refreshed on December 2020.

Conflict of Interest Statement

The authors have no conflicts of interest to declare.

Funding Sources

This study was not supported by any sponsor or funder.

Author Contributions

Conceptualization and methodology: M.M.O. and S.R.L.; data curation and formal analysis: Z.N.; investigation: M.M.O. and Z.N.; supervision: S.R.L.; writing – original draft: M.M.O.; writing – review and editing: Z.N. and S.R.L.

Funding Statement

This study was not supported by any sponsor or funder.

Data Availability Statement

The data that support the findings of this study are not publicly available due to their containing information that could compromise the privacy of research participants but are available from the corresponding author S.R.L. or the data sharing committee dataprivacy@med.cornell.edu upon reasonable request.