I get asked a lot of questions. One of the hardest ones to answer is what question I get asked the most often. Although I can’t say that I keep exact stats, my feeling is that queries about artificial sweeteners, particularly aspartame, top the list. Sometimes the question is about the value of sweeteners in the battle against the bulge, but far more often the focus is on safety. “Which is the safest artificial sweetener?” “Which is the least carcinogenic sweetener?” Such questions attest to a mistrust of regulatory agencies and a belief that substances known to be hazardous are allowed on the market.
Well, yes, hazardous substances are allowed on the market. But this doesn’t mean the population is at risk. “Hazard” is not the same as “risk.” A hazard exists when a substance or activity has an innate ability to cause an adverse effect. Risk is the chance that a hazardous substance or activity will actually cause harm. Risk therefore depends on the magnitude of the hazard and the extent of exposure to it. A grizzly bear is a hazard. It can certainly cause harm. Should you encounter one in the wild, you would be in a pretty risky situation. But in a zoo, the risk is almost nil. A brown bear is also a hazard. But you would much rather encounter this fellow in the wild than a grizzly. In other words, risk is a function both of inherent hazard and of exposure.
Any application to introduce an artificial sweetener to the marketplace has to be accompanied by piles of studies describing its hazard and attesting to its low risk. Yes, low, not zero risk. Absolute safety can never be guaranteed. “Industry must prove that a substance is safe before marketing it,” is the appealing battle cry many non-government organizations use to rally the troops, but it is unrealistic. Every action, every substance, has a degree of risk associated with it. But while chasing an elusive zero risk is naïve, it is reasonable to expect compelling evidence of low risk. I believe that for artificial sweeteners this evidence exists.
Let’s begin with hazard. Sweeteners would rate very low. One way of getting a grip on hazard is through a comparison of LD-50 values. This is an accepted, though not particularly palatable, measure of toxicity and is arrived at by determining the dose required to kill 50% of a rodent population. It is usually expressed in terms of mg/kg of body weight, meaning that the smaller the number, the more toxic or hazardous the substance. LD-50 for artificial sweeteners is in the ballpark of 10,000 mg/kg. Salt is more toxic at 3000 mg/kg. Aspirin weighs in at 1500 mg/kg and acetaminophen at 500 mg/kg. Obviously, sweeteners are not particularly hazardous. But risk is a measure both of hazard and exposure, so we have to take a look at consumption. Since a diet drink contains about 130 mg of aspartame, an average human would have to consume about 5400 cans to approach a lethal dose, and that would have to be done without visiting the bathroom.
Of course, even the most vocal enemies of aspartame don’t suggest that gulping a glass of diet soda is lethal. It is the long term consequences they scream about, often with vigilante-like fervour. They claim aspartame causes cancer, multiple sclerosis and various other problems that they collectively refer to as “aspartame disease.” They trot out questionable rodent studies, and passionate, but ambiguous anecdotal accounts as they mumble about industry cover-ups and government incompetence. While side effects, mostly headaches, along with a few idiosyncratic reactions, have been documented, the majority of claims do not stand up to scientific scrutiny.
The most popular target of the anti-aspartame crusaders is methanol, one of the products of aspartame metabolism. Indeed, methanol is released when aspartame is broken down in the body, and methanol can produce some nasty effects including visual disturbances. It is also true that methanol is further metabolized into formaldehyde, a recognized carcinogen. But numbers matter! A banana or a glass of tomato juice contains far more methanol, naturally occurring, than that produced from a serving of a diet beverage. The methanol argument is just not plausible.
It would, however, be unscientific to dismiss the anti-aspartame allegations based on lack of plausibility. It is the lack of epidemiological evidence of harm, despite vast world-wide exposure, that skewers the claims. Numerous studies comparing cancer patients with healthy controls have failed to find any link to artificial sweeteners. No study, however, will ever derail the anti-aspartame arguments, for the simple reason that they are based more on emotion than on science, and are often formulated to support various hidden agendas.
If the value of sweeteners is to be questioned, it is on grounds of efficacy. Do they really reduce overall calorie intake? Perhaps not. Some recent functional magnetic resonance (fMRI) imaging studies have shown that sugar-sweetened drinks activate different parts of the brain than artificially sweetened beverages. Sugar activates “reward” areas more significantly, triggering a satiation response, while artificial sweeteners activate only the areas that register pleasant tastes. The implication is that reward will be sought by consuming something calorific later.
The possibility that the brain can somehow subconsciously detect calories while food is still in the mouth is backed up by a study of stationary bikers who were asked to either rinse their mouths either with a solution of glucose or one of saccharin, without swallowing. Amazingly, the glucose solution improved performance, somehow suggesting to the cyclists’ brains that more calories were on their way. So, what does this all mean? That there may be more to the appeal of sugary foods than just sweetness. A craving for sweetness may actually be a craving for calories, and since artificial sweeteners deliver the sweetness but not the calories, they leave the consumer looking for a calorie fix. That, not safety, may turn out to be the bitter side of artificial sweeteners.