Wednesday 25 February 2009

Aspartame and Audrey
Molecule of the Month, February 2009








To begin my story, I need to introduce you to Audrey my mother in law to be. A force to reckoned with at the best of times, Audrey is never less of a menace than when she broaches the subject of aspartame. 'Don't drink that,' she once cried, as I innocently lifted a bottle of my favourite carbonated beverage (lilt, mon) to my lips during the first year I was dating my newly betrothed. Smacking the plastic from my grasp, she launched into a tirade of abuse about how aspartame could give me a whole host of ailments. As I imagine most people would, I avoided drinking anything fizzy and pineapplely for a few days: or at least until I really fancied another can. Of course, I didn't forget Audrey's words of warning, but simply chose to ignore them on the grounds that I'm 22, in perfect health and refuse to accept that anything might ever change that.

I’m not one for drinking lots of Coke as a rule. I think this is based on the ‘experiment’ we conducted with Mrs. Webb when I was in class 3 at primary school. We immersed a tooth (these were in ready supply, us being at that age where you endlessly concoct barmy schemes for dislodging baby teeth involving loops of string around door handles) in a test tube of Pepsi for a week. Believe it or not, the tooth was a shell of its former self after this treatment, although on reflection perhaps this test might have over estimated the typical amount of time Pepsi spends in the mouth.

Even so, I do indulge in a cheeky Coke every so often and although what I might be doing to my teeth doesn’t really enter my mind, I do find myself wondering if Audrey had a point about Aspartame.

Aspartame (the structure of the molecule is shown above) is a synthetic sweetener, often found in diet soft drinks as a replacement for sugar. Aspartame is about 180 times sweeter than sucrose (i.e. the sugar monomer which you get in Tate and Lyle bags). This is great for dieters as soft drink companies can use 180 times less aspartame than sucrose, which means a lot less carbohydrate mass in the drink and so fewer calories.
The compound in question was discovered by Jim Schaletter in 1965. He made it accidentally whilst trying to prepare a dipepetide (that is two amino acids joined together) which was at the time thought to be a promising drug candidate for the treatment of gastric ulcers. He accidentally licked his finger after working with the compound and to his (pressumable) amazement it was as sweet as a biscuit!

Schaletter, man of sagely intelligence that he was, decided to scrape the contents of his round bottomed flask into his coffee the following morning, to make sure it really was the compound, and not some disregarded doughnut remnant from his after dinner indulgences of the previous night, which had caused the aforementioned sweetness. Typically a chemist who tempts fate in such a way might expect a short trip to a long stay in hospital as his wages, but Schalatter - the lucky so and so - on realising his coffee was sweetened to perfection, started a chain of events which led to his company making billions of dollars a year: You will now find aspartame in a huge range of products: diet and regular soft drinks, confectionary, cereals and even yoghurts.

So why are people concerned? It is well known that Aspartame breaks down to aspartic acid, phenyl alanine and methanol when ingested. Potentially this could be worrying, because:

1. When exposed to biological conditions methanol can be converted to formaldehyde (the stuff you see dead things floating in at a school science laboratory) which is a known carcinogen.

2. Phenylalanine and aspartic acid are both neurotransmitters which up- regulate the firing of the neurons in your brain. They are part of a complex metabolic system and can be converted into other neurotransmitters such as dopamine and adrenaline. The theory runs that ingesting extra phenylalanine will mess up the delicate neurotransmitter balance and could have unpredictable effects on your mood. Potentially, since phenylalanine is an up-regulator, if you have an awful lot of it you could go a bit haywire.

3. In a recent study, aspartame itself has been shown to be an intercalator of DNA (1), which means it jams itself snugly into the gaps in the DNA double helix. This causes problems when the DNA has to be 'unzipped' for copying when the cell replicates. We understand enough about DNA replication and its connections with cancer to know for certain that this is in theory bad news – but scientists don’t know how this particular intercalation might affect us at the moment.

The points above are facts, however the arguments for aspartame being safe say that the amount of these substances which actually reach a site in the body where they can do any harm is very, very small. In any case it is also true that we eat and drink foods containing far higher concentrations of these substances on a daily basis. For example an average glass of milk provides 6 times more phenylalanine and 13 times more aspartic acid than the equivalent amount of aspartame sweetend beverage (2).

In public, the debate about aspartame still rumbles softly. Indeed, ‘safer’ alternatives such as sucralase (marketed as splenda) have been developed to combat these public fears, whether they are realistic or not.

In fact, all the scientific evidence is against any issues with the safety of aspartame. Repeated toxicological studies on various animals and human subpopulations (infants, the elderly and diabetics for example) have failed to find any ill effects caused by the sweetener (2). Millions of people consume products with aspartame in everyday and it does not appear to do them any harm at all.

To finish with, and in the interest of preserving my engagement, I'd just like to add here that I may have embelished some of incidents in which I cite Audrey's involvement for comic effect. In fact she is a lovely woman and I can only remember her knocking a drink from my hand once, and this was in an aspartame-unrelated situation. Honest.


References

(1) G. A. Karikas et al., Clin. Biochem., 1998, 31, 405 – 407.
(2) H. H. Butchko et al., Regulatory Toxicology and Pharmacology, 2002, 35, 1 - 92.