Aspartame, also called L-aspartate-L-phenylalanine methyl ester, is an artificial sweetener used extensively in the food industry to replace sugar. The growth in demand for diet drinks initially fuelled increased consumption of aspartame amongst humans. However, more recently it has become common to add aspartame to non-diet product alongside sugar, as well as to hide its presence in foods by use of other names and re-branding. This evidence suggests that aspartame is being abused as a food additive amongst the food industry, with complicit governments aiding this lack of transparency. Concerns over the safety of aspartame continue to grow as it becomes clear that the food industry is obfuscating the dangers of the sweetener. Some studies have reported an association between aspartame consumption and cancer (here), and human experiments showering associations with cancer risk are supported by clinical trials in animals. Studies also suggest that aspartame alters neurological function, with specific effects on the serotonin pathways of the brain.
The question of whether aspartame alters brain chemistry is interesting for a number of reasons. Firstly, most of the studies to date have been performed on rats. The reason for this is that the level of biochemical detail that can be obtained from experimentation on animals exceeds that which can be obtained from humans due to the ability to sacrifice the animals. However, rats are not human and so extrapolation of results to humans is controversial. Secondly, it has become apparent that there are now so many anecdotal medical reports of aspartame neurotoxicity, that the scientific community can no longer ignore the public and pretend that aspartame is without major effects, at least in sensitive individuals. In fact, a growing body of evidence supports the contention that high doses of aspartame can reduce the normal rise in brain tryptophan levels that accompany a meal. This phenomenon is known to results from competition between large neutral amino acids for entry to brain tissue, one of which is the phenylalanine moiety of aspartame.
Serotonin synthesis is increased significantly following a high carbohydrate meal because the associated insulin release causes the branched chain amino acids to enter skeletal muscle cells. This removes competition for the large neutral amino acid (LNAA) transporter, and as a result tryptophan gains a competitive advantage for entry to the brain. Because tryptophan hydroxylase, the rate limiting step in serotonin synthesis, is only half saturated in the fasting state, increased brain tryptophan can significantly increase serotonin synthesis. Potentially, aspartame alters brain chemistry because during digestion phenylalanine is released and then absorbed, and this raises plasma levels of phenylalanine significantly. Circulating phenylalanine is able to lower the rate of tryptophan entry to the brain because it can compete for transport across the blood brain barrier via the LNAA transporter. By reducing the rate of tryptophan transport into the brain, phenylalanine can significantly lower brain levels of serotonin.
The contention that aspartame alters brain chemistry therefore pivots on the attenuation of the postabsorptive carbohydrate rise in serotonin synthesis by the phenylalanine moiety of aspartame. To date much of the work in relation to this has been performed on rats, but results from such studies support the hypothesis that serotonin brain levels are inhibited in the post-absorptive state with administration of aspartame. For example, in one study1, researchers measured the changes to the tryptophan hydroxylation rate following ingestion of a high carbohydrate meal at different concentrations of aspartame. Ingestion of the carbohydrate meal alone caused a significant increase in the rate of tryptophan hydroxylation, but addition of 530 mg per kg body weight aspartame caused a significant decrease in the hydroxylation rate. However the effect of aspartame in this experiment only occurred at this supraphysiological dose of aspartame, with lower doses of aspartame having no effect on the rate of tryptophan hydroxylation.
Therefore aspartame alters brain chemistry, but may only do this at very high doses. Whether these brain altering effects are present at lower more physiological doses is more controversial. However, some evidence, albeit from rat studies again, does suggest that at lower doses, aspartame alters brain chemistry detrimentally. For example, the neurochemistry researcher Richard Wurtman wrote to the New England Journal of Medicine reporting data from a rat study in which he administered a dose of aspartame that would be achievable in an eight year old child2. This dose caused a doubling of phenylalanine concentrations in the brains of rats, an effect that was increased a further 100 % with concomitant administration of a carbohydrate meal. Certainly the increasing anecdotal reports appearing in the medical literature reporting strange neurological symptoms with aspartame ingestion support the contention that aspartame alters brain chemistry. The reluctance of researchers to risk their grant money and perform proper trials may however be proof enough to some people.
RdB
