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Hospital Form To Make Sure You Aren't Given Aspartame As A Patient - Print This Out, Please

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Phenytoin is a key in managing epilepsy. When convulsions are associated with or aggravated by aspartame products (Chapter III), the patient confronts several dilemmas. First, the dose of phenytoin is likely to be increased, possibly to the point of toxicity (see Case III-35). Second, other anti-epilepsy drugs may be added, thereby increasing the potential for side effects. Third, the continuation of these drugs in high doses could result in "rebound" toxicity after stopping aspartame.

The apparent potentiation of valproic acid (Depakene; Depacote), another antiepileptic drugs, was personally reported to the author by a 51-year-old man who drank considerable diet cola daily. When his physician increased the dose, he became comatose and required hospitalization.

Representative Case Report

Case IX-I-3

A 28-year-old man suffered seizures after a head injury while serving in the Marines. As a civilian, his convulsions unexpectedly increased despite multiple anti-epileptic medications, causing him to lose his job.

The patient's mother noted that he "acted like he was intoxicated." She expressed concern over his large consumption of aspartame sodas. Shortly after discontinuing them, he had to be taken to an emergency room for phenytoin intoxication - presumably representing the rebound phenomenon.

C. Antidepressant Drugs

Aspartame may interfere with the action of important drugs used to treat depression, particularly imipramine (a tricyclic antidepressant). Others have made similar observations.


Walton (1986) described a 54-year-old woman with recurrent major depression who had been well controlled on a maintenance dose of 150 mg imipramine at bedtime. She subsequently experienced marked behavioral changes, manic behavior characterized by inappropriate euphoria and flighty ideas, and a grand mal seizure. It was then learned that she had been drinking considerable aspartame-sweetened iced tea for several weeks prior to the seizure. All evidence of manic activity subsided within four days after stopping aspartame and the addition of lithium. Her depression recurred, however, two months later. Imipramine was resumed at the previous dosage with no recurrence of severe depression or mania over the ensuing 13 months.


The monoamine oxidase inhibitors (MAOIs), another group of antidepressant drugs, can have additional adverse effects when aspartame is consumed. These include phenelzine (Nardil), isocarboxazide (Marplan), and tranylcypromine (Parnate).

It is pertinent that hypertensive crisis have occurred in patients so treated after they consumed foods and beverages containing tyramine and tryptophan. This response probably represents vasospasm caused by amino acid-derived sympathomimetic substances such as norepinephrine and tyramine (Chapters IX-C and XXIII).

The serotonin-elevating action of fluoxetine (Prozac) for treating depression could be counteracted by aspartame. It can block tryptophan entry to the brain, thereby inhibiting synthesis of serotonin (Chapter VII).

A Minnesota physician called to inquire about a possible interaction between Prozac and aspartame. He had suffered depression for which Prozac was prescribed, but without much benefit until he avoided aspartame. At what point, the drug proved helpful.

D. Propranolol (Inderal)
The occurrence or aggravation of benign ("essential") tremor by aspartame was described in Chapter VI-J. This condition usually can be controlled with small or modest doses of propranolol. Several patients and correspondents stressed that their tremor intensified after consuming aspartame - even with increased dosage of propranolol - and improved when they avoided when they avoided such products.


E. Thyroid Replacement Therapy

The increased susceptibility of hypothyroid to aspartame (Chapter IX-E) has been repeatedly emphasized. Conversely, there may be interference with the activity of thyroid replacement therapy.

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