Aspartame is one of the dietary sweeteners that can replace sugar to reduce calorie intake and lower blood sugar levels; it is about 200 times sweeter than sugar but contains no calories. Aspartame was one of the first substances of this type, and is approved for a daily intake of 40 mg per kg of body weight for humans. This equates to approximately 250 mg per litre in soft drinks sweetened with aspartame. There are now two derivatives or variants of aspartame, as well as 16 other substances and two plant-based sugar substitutes.
Aspartame has been studied extensively in animal trials and to a lesser extent in patients. Aspartame is broken down in the gut into phenylalanine, which is an amino acid similar to L-dopa. Studies have therefore investigated whether aspartame might interact with or conflict with L-dopa and impair the drug’s effectiveness. A study was conducted for this purpose and concluded that doses of up to 600 mg did not cause any problems, but that problems could occur at an intake of 1200 mg – however, as no products contain such quantities, it was concluded that there is no reasonable risk of problems arising. The other 18 sugar substitutes share these properties and have no theoretical potential to affect the efficacy of L-dopa.
Aspartame has also been tested in animal models of Parkinson’s disease (32 studies). Given the similarities between a breakdown product of aspartame and L-dopa, some studies have shown that, for example, the toxin MPTP has a slightly greater damaging effect when administered with aspartame. There are no studies on patients with Parkinson’s disease and any possible links or different disease progression.
Animal models are not the same as Parkinson’s disease, and it is therefore not possible to directly apply conclusions from animal experiments to patients.
My assessment is that there is no evidence to suggest that aspartame has anything to do with the disease process in (human) Parkinson’s disease, and that the use of approved and reasonable doses of aspartame does not affect the therapeutic effects of treatments for Parkinson’s symptoms.
/Håkan Widner