The hypothesis that sugar is addictive will not withstand scientific verification. Professor David Benton, of Swansea University in Great Britain, has examined all the current hypotheses and the assumptions derived from them. He evaluated 160 studies and found no confirmation at all. Thus, alleged sugar addiction is relegated to the realms of nutritional myth.

The hypothesis that sugar can also produce physical dependence in humans had its origins in experiments on rats. Researchers had not fed these rats for twelve hours and subsequently offered them unlimited amounts of laboratory food and, optionally, a sugar solution. After one month, the animals showed signs of addiction. They ingested large amounts of sugar when first offered food, and this was classified as a “feeding frenzy”. Special medications, which trigger withdrawal symptoms in drug addicts, also had a similar effect on the animals. The scientists concluded from this that these observations of the animals also allowed similar conclusions for humans, at least for the overweight and for patients with a so-called binge eating disorder (an eating disorder with periodic bouts of ravenous hunger). (1)

Professor David Benton wanted to find this out for certain and reassessed a great number of studies in order to find out whether the hypotheses and the assumptions derived from them were supported by research findings on humans. (2,3) His conclusion: “None of the hypotheses based on the animal model in respect of an addiction to sugar is confirmed for humans.”

Inter alia, the scientific review unearthed the following:

Drug abuse and all “natural gratifications” lead to the release of dopamine in the brain, although the reaction patterns differ.

Measurements in the animals had shown that the messenger substance, dopamine, is released in the brain after the intake of sugar, which is also the case after drug use. Professor Benton demonstrates that not only after the consumption of something flavourful, such as sugar, but a release of dopamine can also be measured as a result of all “natural gratifications” - among these are classed such pleasant experiences as listening to music, the anticipation of a benefit, seeing a friendly or attractive face, being in love. Moreover, there are substantial differences between the brain’s reaction pattern for drugs and that for “natural gratifications”. The measurement of a release of the messenger substance alone is insufficient, therefore, to substantiate the similarities.

Many foodstuffs can trigger a strong craving - not just sweet foodstuffs. Let us suppose that there were a physical dependence on sugar. As with drugs, there would have to be a strong craving for sugar. Studies show, however, that many foodstuffs trigger cravings in humans - not just sweet foodstuffs, but also savoury foodstuffs such as hamburger, sausage and fried chicken.

After abstinence – e.g. after dieting – attacks of ravenous hunger occur less often, which, according to the addiction hypothesis, would have to be quite the opposite.

Typical of drug addiction is that after periods of abstinence there is a severe craving and, hence, often relapse.

According to the addiction hypothesis, therefore, attacks of ravenous hunger would have to be reinforced after a period of dieting where food has been foregone. Several of the studies reviewed by Professor Benton, however, show the exact opposite: attacks of ravenous hunger decrease markedly after a period of dieting. And it appears that a severe craving for foodstuffs is more associated with boredom, feelings of anxiety and alienation than with not having eaten a foodstuff for longer period of time.

A diet with a high proportion of energy derived from sugar is not associated with excess weight.

If an addiction to sugar were a determining factor for body weight, there would have to be a link between sugar intake and being overweight. Many studies also show the opposite here: a diet with a high proportion of energy derived from sugar is associated with low body weight.

After a period of dieting, patients with a binge eating disorder experience fewer feeding frenzies instead of more and medications, which provoke withdrawal symptoms in drug addicts, have no affect. As well, in patients suffering from a binge eating disorder, none of the hypotheses that assume an association with an addiction to sugar is confirmed: after a period of dieting, feeding frenzies also decrease in these individuals instead of increasing.

Even taking specific medications, which induce withdrawal symptoms in drug addicts, have no sequellae for patients with this eating disorder, i.e. there are no withdrawal symptoms in the form of feeding frenzies.

Based on his review, Professor David Benton urges caution against transferring results from the animal model to humans and against making hasty conclusions. Animal experiments were only able to be used to develop hypotheses, which, however, must be validated in each individual case by reference to insights from studies on humans.

References

(1)  Avena N. M., Rada P., Hoebel B. G. (2008): Evidence for sugar
addiction: Behavioral and neurochemical effects of intermittent,
excessive sugar intake. Neurosc Biobehav Rev 32: 20-39

(2)  Benton, D. (2010): The plausibility of sugar addiction and its
role in obesity and eating disorders. Clinical Nutrition 29: 288-303

(3)  Benton D. (2010): Macht Zucker süchtig? Keine der vom Tiermodell
abgeleiteten Hypothesen lässt sich für den Menschen bestätigen. In:
Moderne Ernährung heute. Wissenschaftlicher Pressedienst 3/2010,
Matissek R. (Hrsg.), Lebensmittelchemisches Institut (LCI) des
Bundesverbandes der Deutschen Süßwarenindustrie, Köln URL:
http://www.suessefacts.de/wissenschaft/wpd_moderne_ernaehrung/

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