Tap (Draft) Beer and Monoamine Oxidase Inhibitor Dietary Restrictions

Kenneth I Shulman, MD, SM, FRCPC¹, Sandra AN Tailor, PharmD², Scott E Walker, MScPharm³, David M Gardner, BScPharm⁴

Objective: Traditional monoamine oxidase inhibitors (MAOIs) continue to play an important role in the management of a wide variety of clinical conditions. Accordingly, a practical and safe approach to MAOI dietary restrictions remains an essential component of patient management.

Method: In an effort to refine MAOI dietary recommendations, we report a case of hypertensive crisis following the consumption of a modest amount of tap beer.

Results: A well-documented case report involving tap (draft) beer consumed while on an MAOI supports an earlier study, which recommended that all tap beers be restricted on MAOI diets. The 2 cases were remarkably similar in terms of the offending substance, quantity consumed, and subsequent reaction.

Conclusions: As a result of recent tyramine analyses and 2 well-documented case reports, all tap (draft) beers should now be absolutely restricted on MAOI diets because they represent a very significant risk at modest levels of consumption.

(Can J Psychiatry 1997;42:310–312)

Key Words: monoamine oxidase inhibitors, tap beer, draft beer, hypertension, diet

Recent attempts to simplify MAOI diets have focused on the need to balance safety, compliance, and clinical benefit (1,2). As a result, dietary recommendations have taken an approach that emphasizes the “absolute restriction” of a small number of food items (2). Among alcoholic beverages, only tap beers were recommended for absolute restriction following the analysis of Tailor and others (3), who found that a number of draft beers have dangerously high tyramine levels. The study by Tailor and others (3) was stimulated by the case of a 27-year-old male who experienced a hypertensive crisis after consuming only 14 oz of Upper Canada Lager beer on tap. We now report a second case with very similar features.

Case Report

A 27-year-old white male with a history of bipolar disorder and migraine headache was treated with phenelzine sulfate for a major depressive episode in a psychiatric hospital. The dosage of phenelzine had been increased on the day prior to the episode from 75 mg/day to 90 mg/day. Other maintenance psychotropic drugs included carbamazepine 400 mg/day and clonazepam 2 mg/day.

While on a pass from hospital, he drank a single glass of Upper Canada Lager beer on tap. Earlier in the day, he had consumed some chocolate and coffee without any ill effects, as he had done on several previous occasions. Within 30 minutes of consuming the beer, he developed sudden onset of a severe occipital headache (qualitatively different from anything he had previously experienced), pressure behind his eyes, chest discomfort, lightheadedness, photophobia, nausea, and a stiff neck. He returned to the psychiatric hospital, where his blood pressure was recorded twice at 205/115 mmHg and 220/120 mmHg (posture not reported), his pulse was 86 beats per minute and regular, and his temperature registered 36.8 °C. He was immediately given 20 mg of nifedipine by the physician on call and sent to the emergency room of a general hospital. On arrival, his blood pressure was recorded as 140/100 mmHg and pulse 100 beats per minute and regular. In the emergency room, he was given intravenous phentolamine, which dramatically reduced his blood pressure to 80/60 mmHg. Subsequently, he experienced an episode of syncope upon standing and apparently struck his head when he fell down. A computed tomography scan showed a small intracerebral hemorrhage in the left frontal lobe, but it was felt that the hemorrhage was secondary to the head injury and was not typical of a hypertensive bleed. He was observed in the intensive care unit, where his blood pressure stabilized at 110/70 mmHg, and his pulse was recorded at 80 beats per minute and regular. He subsequently pursued an uneventful clinical course and was transferred back to the psychiatric hospital after 4 days.

Discussion

This is the second reported case to have produced a documented hypertensive crisis as a result of the consumption of a modest amount of tap beer. The 2 cases are remarkably similar. Both involve young, white men who consumed similar amounts of Upper Canada Lager beer on tap while taking moderately high doses of the MAOI phenelzine. Both cases occurred in Ontario, but in different cities. Onset of symptoms occurred acutely within 45 minutes of consumption, and the syndrome was characterized by severe occipital headache, chest pain, nausea, and neck stiffness. Hypertension was well documented in both cases, with systolic blood pressures of approximately 200 mmHg and diastolic blood pressures ranging from 110 to 120 mmHg at maximum. Fortunately, no permanent damage occurred in either case. In the case reported here, however, iatrogenic problems arose as a result of the hypertensive episode, namely the syncope and head injury.

In the earlier analysis by Tailor and others (3), of the 49 different tap beers analyzed, 4 were found to contain levels of tyramine greater than 27 mg/L, with the index beer having the highest level (113 mg/L). It is likely that an amount greater than 40 mg of tyramine was consumed in both reported cases. None of the bottled beers, including 9 dealcoholized beers, had dangerous tyramine levels on the assumptions that 8 mg of tyramine is the maximum allowable (4) and that 25 mg of tyramine represents a “dangerous” level (5). DaPrada and others (6) have reported very high levels of tyramine in one Irish beer and in 5 Czechoslovakian beers, although all were bottled beers (unpublished observation). In keeping with the principle of recommending “absolute restriction” of a small number of foodstuffs, Gardner and others (2) suggested an absolute restriction on all tap beers and allowed all bottled beers in moderation (maximum 12 fluid oz per day).

The hypothesized cause of high tyramine levels in tap beer is the contamination of the lines from the keg to the tap with bacteria capable of converting tyrosine to tyramine. Although this hypothesis was not supported by visible bacterial growth, it does not preclude the possibility that the bacterial growth and tyramine production occurred earlier and resulted in death of the contaminating bacteria by the time the assays were performed (4).

We report this second case of hypertensive crisis associated with tap beer in order to highlight the need for restriction of all tap beers on MAOI diets. It is important to note that both cases came to our attention because some practitioners were aware of our interest in this issue. One can only speculate that a significant number of similar episodes have gone unreported elsewhere. An overview of MAOI dietary issues and recommendations is discussed fully by Gardner and others (2), and readers are referred to this review for further information. Gardner and others (2) note that most alcoholic beverages consumed in moderation are considered safe, including the once-dreaded Chianti wine, which became inextricably associated with MAOI diets. Moreover, the common headaches that many people experience with consumption of red wines must be differentiated from a true hypertensive crisis.

While most tap beers (45 of 49 tested) are also in the safe range, the extraordinarily high levels reported in a few brands (3), as well as these 2 well-documented case reports, support the argument that tap beer presents a significant risk with MAOIs. Since traditional “irreversible” MAOIs continue to play a role in a wide variety of clinical conditions (7), the issue of appropriate, practical, and safe dietary recommendations remains an important clinical consideration. The restriction of tap beers should now be a vital component of all MAOI diets.

Acknowledgement

We thank Dr G Hasey for providing us with the clinical details of the case reported.

References

1. Shulman KI, Walker SE, MacKenzie S, Knowles S. Dietary restriction, tyramine and the use of monoamine oxidase inhibitors. J Clin Psychopharmacol 1989;9:397–402.

2. Gardner DM, Shulman KI, Walker SE, Tailor SAN. The making of a user friendly MAOI diet. J Clin Psychiatry 1996;7:99–104.

3. Tailor SAN, Shulman KI, Walker SE, Moss J, Gardner D. Hypertensive episode associated with phenelzine and tap beer—a re-analysis of the role of pressor amines in beer. J Clin Psychopharmacol 1994;14:5–14.

4. Bieck PR, Antonin K. Oral tyramine pressor test and the safety of monoamine oxidase inhibitor drugs: comparison of brofaromine and tranylcypromine in healthy subjects. J Clin Psychopharmacol 1988;8:237–45.

5. Blackwell B, Mabbitt LA. Tyramine in cheese related to hypertensive crises after monoamine oxidase inhibition. Lancet 1965;1:938–40.

6. DaPrada M, Zurcher G, Wuthrich I, Haefely WE. On tyramine, food, beverages and the reversible MAO inhibitor moclobemide. J Neural Transm Suppl 1988;26:31–56.

7. Kennedy S. Clinical advances in monoamine oxidase inhibitor therapies. Washington (DC): American Psychiatric Press; 1994.

Résumé

Objectif : Les inhibiteurs de la monoamine-oxydase (IMAO) classiques jouent encore un rôle important dans le traitement d’un vaste éventail de pathologies cliniques.  Ainsi, une approche pratique et sûre à l’égard des restrictions alimentaires relatives aux IMAO demeure une composante essentielle du traitement.

Méthode : Dans le cadre d’un effort visant à améliorer les recommandations alimentaires relatives aux IMAO, nous signalons un cas de crise d’hypertension après la consommation d’une faible quantité de bière pression.

Résultats : Un exposé de cas bien documenté au sujet de la consommation d’une bière pression pendant un traitement aux IMAO corrobore une étude antérieure, qui recommandait d’interdire la consommation de toute bière pression dans les régimes alimentaires des patients traités aux IMAO.  Les 2 cas présentaient des similitudes frappantes quant à la substance en cause, la quantité consommée et la réaction ultérieure.

Conclusions : Par suite de récentes analyses de la tyramine et des 2 exposés de cas bien documentés, toutes les bières pression devraient maintenant faire l’objet d’interdiction absolue dans les régimes alimentaires de patients traités aux IMAO parce qu’elles constituent un risque très important à de faibles niveaux de consommation.

Manuscript received August 1996, revised October 1996.

¹Professor, Department of Psychiatry, University of Toronto; Psychiatrist-in-Chief, Sunnybrook Health Science Centre, Toronto, Ontario.

²Clinical Co-ordinator/Infectious Disease, Department of Pharmacy, Sunnybrook Health Science Centre, Toronto, Ontario.

³Co-ordinator Quality Control, Department of Pharmacy, Sunnybrook Health Science Centre; Associate Professor, University of Toronto, Toronto, Ontario.

⁴Pharmacist, Department of Psychiatry, Sunnybrook Health Science Centre, Toronto, Ontario.

Address for correspondence: Dr KI Shulman, Department of Psychiatry, 2075 Bayview Avenue, Toronto, ON M4N 3M5

Can J Psychiatry, Vol 42, April 1997