Aspartame Toxicity. Not.

Aspartame is an artificial, non-saccharide, sweetener used as a sugar substitute in some foods and beverages usually so that they can be labelled as “lite” or “diet” products. In the European Union, it is coded as E951. Aspartame is a methyl ester of aspartic acid and phenylalanine, two natural components of proteins found in a wide range of foods. Aspartame was first sold under the brand name NutraSweet, was first synthesized in 1965 and its patent expired in 1992.

It has been a controversial product and the subject of countless internet hoaxes regarding its safety over the years. You can read about some of these on Snopes. I first wrote about such controversies for my Catalyst column on back in the late 1990s. There is no evidence that aspartame used at levels found in carbonated soft drinks and the like is harmful.

So, it was with interest that I read an email this morning from a correspondent highlight new research that proclaims that:

“aspartame water in rats for 6 months causes liver harm”

Well, I’m no apologist for the aspartame manufacturers, but I cannot abide BS chemistry. The paper in question discusses dosing rats in the laboratory with 500 mg or 1000 mg of aspartame in water every day for six months and shows various apparently detrimental effects on liver function in rats. Perhaps not surprising at that dose…1000 mg is the equivalent of an adult drinking 400 12oz cans of artificially sweetened drink every day for six months. Now, even the most ardent cola fan on a diet could not physically achieve that.

According to the Nutrasweet company, a standard 12oz can contains 180 mg of aspartame. Rats were dosed at 500 mg or 1000 mg per kg of body weight, which for an 80kg adult would mean having to ingest 40 or 80 grams of aspartame per day. That’s 222 or 444 aspartame-containing drinks every day.

The EHSO says that the Acceptable Daily Intake (ADI) for aspartame is 50 mg per kg of body weight. Studies show that even the most frequent consumers of aspartame-containing products get just 4-7 percent of that figure. Yet the Nair paper is dosing rats at 10 or 20 times the ADI, which is up to 300 times what people who use the most aspartame products ingest.

I am really not sure how can that represent a fair assessment of aspartame’s real effects on real people drinking or eating aspartame-products at realistic levels? When

I first wrote about the aspartame controversy, I pointed out that the compound is metabolised to its two component amino acids and a tiny amount of methanol. These common amino acids are ingested by most of us on a daily basis from our food. Methanol is present in very small amounts in some alcoholic drinks and is also a by-product of several metabolic processes, so we are regularly exposed to that compound too.

I asked Nair to take a look at my calculations and estimates on this and he corroborated what I said.

“The dose which we used in our study was a high dose (1000 mg/kg body weight),” he told Sciencebase. “Usually in toxicological research, the toxicity of a compound is analysed at the initial level with higher doses. We used the above dose to understand the exact toxicological mechanism.” He points out that there is no oxidative stress observed in the study. “The results denote alterations in liver enzymes and glutathione system,” he adds. “We support your argument that the dose is not an ADI. But people in developing countries are not particular in ADI. Epidemiological studies are required for the assessment of the effects of long-term consumption of aspartame in human subjects,” Nair told me.

There is pretty much no reason to be scared of aspartame at the levels found in “lite” food and drink. But, if one were really concerned about aspartame products there is a simple answer – just don’t use them. Nair adds despite the lack of definitive evidence that too great an intake may alter the body’s homeostasis. He adds that the team is currently studying low doses.

If only he had come up with some feasible mechanism beyond the experimental overdosing of rats I might have been inclined to agree. Even if someone is not particular about an ADI, that person would still have to drink several hundred cans of diet cola regardless to replicate the concentration used in his toxicological studies. Nair hinted that he thought at least part of the effect on the liver (the change in the glutathione system), “is probably due to methanol metabolites.” So, not aspartame per se, just methanol itself.

Anyway, forget so-called diet products. Eat, drink (plenty of water) and be merry and don’t forget to get a daily dose of fresh air and exercise if you can. That’s my personal “Ix” for health.

Abhilash, M., Paul, M., Varghese, M., & Nair, R. (2011). Effect of long term intake of aspartame on antioxidant defense status in liver Food and Chemical Toxicology DOI:10.1016/j.fct.2011.02.019

This article has been reproduced from Sciencebase Science News. Copyright David Bradley.

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About David Bradley Science Writer

David Bradley has worked in science communication for more than twenty years. After reading chemistry at university, he worked and travelled in the USA, did a stint in a QA/QC lab and then took on a role as a technical editor for the Royal Society of Chemistry. Then, following an extended trip to Australia, he returned and began contributing as a freelance to the likes of New Scientist and various trade magazines. He has been growing his portfolio and and has constructed the Sciencebase Science News and the Sciencetext technology website. He also runs the SciScoop Science Forum which is open to guest contributors on scientific topics.
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