While few people can remember the details of their first hit, everyone can identify with the rush of satisfaction, the tingling delight that starts on the tip of your tongue and then courses through your entire body.
It can lift you to the heights of happiness—but only fleetingly, causing you to seek a way of repeating the experience; desperately trying to silence your better judgement’s insistent whispers that, should you refrain, you would be better off in the long run. Still, the temptation is often much too strong to resist. Why can’t we seem to resist sugar’s allure? Are we high on sugar?
How harmful is sugar?
Of course, we will reject being labelled “addicts”, which we’d much rather use for people who give in when tempted with other white powders, which taste bitter, not sweet. These days, however, more and more voices, some coming from people with professional or scientific authority, are saying that sugar might be a drug. Let’s go over a few headlines from the Romanian national press and internet which speak for themselves: “Addiction— Sugar, drug for the brain”; “Sugar acts like a drug at brain level. What do nutritionists say about chocolate, bread and fruit?”; “What is the most dangerous drug? A health expert gives a totally unexpected answer.” (The expert in this case is Paul van der Velpen, director of the health service in Amsterdam; the answer to the question is: “It might seem exaggerated or far-fetched, still sugar is the most dangerous drug of our day, and it’s easy to obtain.”) Other headlines include, “Doctors’ warning: sugar is the most dangerous drug”; “Sugar: energy or drug? A story produced by ‘Romania, I love you’”; “Sugar is a drug causing addiction, obesity and other serious illness.”
The rhetoric of concern centred on sugar is not unique to the Romanian media. We can find similar headlines in the foreign media, like “Death by sugar” (New York Post) or “Sweet and vicious. Is sugar toxic?” (The New York Times). Prestigious journals such as the British Medical Journal echo these sentiments with headlines like, “Sugar is the new tobacco”, and serious researchers are rediscovering John Yudkin’s book from 1950, “Pure, white and deadly”. How does sugar kill us and what can we do to stop it?
Statistical records reveal that in 1998 Romanians consumed an average of 20 kilograms of sugar per person per year, almost half a kilogram of sugar each week. By 2008, the average sugar consumption had risen to around 30 kilograms per year for each Romanian. Measured again in 2014, the yearly average of sugar consumption in Romania was 25 kilograms.
Of course, most statistics should be taken with a pinch of salt, since they can be affected by errors: the methodology of data collection, the sources’ reliability, the definition of the variables used and so forth. For instance, it’s possible that not all the sugar sold in Romania (and reported in the statistics) would be destined for human consumption, which would reduce the annual averages. On the other hand, it’s not clear to what degree the statistics include the sugar consumed when eating foods containing sugar. A statistic based on data from Euromonitor (a multinational company specialised in market research) claims that the daily consumption of sugar per capita in Romania is around 31,5 grams, which equates to an approximate annual consumption of 11,5 kilograms. The statistics referred to earlier suggest that the Euromonitor figure is probably an under-estimation. A variety of internet pages in Romania declare numbers around 20-30 kilograms/year, sometimes even more, for the period 1980-2015. Of course, this depends on what we measure: just the pure sugar sold in bags or also the sugar in cakes, candy and soft drinks? What about the sugar added in ketchup, jams or breakfast cereal? Then, the definition of sugar is problematic in itself. Different people mean different things when they talk about “sugar”?
What is “sugar”?
When thinking of sugar most people think of the tiny white crystals usually sold in one kilogram bags labelled “Sugar”. From a chemical point of view, this substance is called “sucrose”. Others, when thinking about sugar, think of carbohydrates containing glucose or fructose. So “high-fructose corn syrup” (a sweetener rich in fructose formed by hydrolysing cornstarch), maple syrup, agave syrup (which contains a mixture of fructose and glucose), honey (which mostly contains fructose and glucose, but also small quantities of maltose and sucrose) can also be considered “sugar”. The degree to which some sugars are healthier or more dangerous than others is an interesting and controversial topic of debate which would exceed the space allotted for this article, so we will focus mainly on sucrose.
Why do some experts consider sugar a drug?
When they float the idea in the public space that sugar is a drug, various experts do not use it just as a figure of speech, but in the literal sense of the term. The classification of this much-loved ingredient as a drug is based on a series of observations following certain experiments conducted on animals, which are similar to the ones observed in the case of traditional drugs. Research labs have conducted experiments which show that lab animals (usually mice or white rats) come to eat sweet food in excess when it is provided to them intermittently. In one study, the animals were restricted from accessing food for 12 hours each day and then, a sugar formula (with a similar concentration to that of commercial soft drinks) is offered to them with their normal rodent food. After a few days, animals start consuming a larger quantity of sugar. After the animals have been exposed to this kind of treatment for 28 days, the animals’ access to food is restricted for 36 hours. Human beings would not find this a very pleasant experience! The researchers noticed a higher degree of anxiety in the animals who had received sugar in the previous four weeks, in comparison with the animals who had been given free access to rodent food and who were also deprived of food for 36 hours. Researchers measured the level of sugar in the blood of the animals and did not notice any difference between the two groups, confirming that the state of anxiety was not the expression of a glycaemic deficit. Furthermore, the animals who consumed sugar showed a high degree of extracellular acetylcholine (one of the main chemical messengers through which neurons communicate with each other) and a low level of dopamine (often described in popular language as one of the happy hormones). Such observations are similar to those found in lab animals who had been administered opioids, such as morphine, and then had been cut off from receiving the opioid.
In another experiment in which animals could choose between food which was chocolate flavoured and rich in sugar, and typical, cereal-based rodent food, the rodents preferred the former (and consumed over 90% of their total calories from this source). Three days of access to sugar proved enough for the rats to start excessively consuming sugar, even when they were already full (hyperphagia), consuming, however, a bit of the regular food, while waiting for or anticipating the sugar-rich food (anticipatory hypophagy). The administration of an opioidergic antagonist (nalmefene, a drug with an opposite action to opioids) reduced the excessive consuming of sugar-rich food—a finding consistent with what is already known about the involvement of opioid receptors in regulating the consumption of substances for hedonistic purposes and not in order to satisfy nutritional needs. The females which received a bottle of plain water and one with sugar formula daily, consumed large quantities of sugar, estimated at approximately 65 grams per kilo. When the two bottles were removed briefly to be refilled, as soon as they were put back the females licked the sugar bottle for a few minutes, although the bottle had been missing just for a short period of time. When, in the second week, the sugar was removed, an obvious aggressiveness was noticed, manifested by gentle biting (gripping with the mouth, without pressure) of the pen or the researcher’s hand.
In other experiments, administering glucose in large quantities (in just 10 days the rats were consuming double the quantity of glucose as compared to the first day) was associated with sensitisation of the dopamine and mu receptors. The observation is consistent with a previous experiment where, in the case of rats fed for a longer period with bakery products, the naloxone administration led to symptoms typical for the abstinence syndrome observed when the administration of opioids was stopped (the same type of symptoms as if the animals were drugged). Naloxone is an antagonist of opioid receptors, used in diagnosing acute overdoses of opioids, because it antagonises the opioids’ action and leads to quick elimination of respiratory depression and the altered consciousness state. For people who have the same symptoms generated by other causes this has no effect.
It is also known that opioids alter the preference for tasty foods. People who are addicted to opioids have an accentuated preference for sweets and carbohydrate-rich foods (a preference which is diminished by antagonists such as naloxone). Butorphanol, a drug with effects similar to morphine, has induced hyperphagia manifestations in animals who had been deprived of food in the past. This was, however, not the case for animals who hadn’t been food deprived.
Unanimity? Not really.
In the context in which the media and specialist journals have made a trend of referring to sugar as a drug, with arguments like the ones presented above, there are still unconverted scientists, who remain sceptical to such labelling of sugar. These admit that sugar (sucrose) can trigger addictive behaviours, but believe these must be understood within a particular context. For instance, animal studies have shown that addictive reactions are manifestations to the sweet taste and not the caloric content (these manifestations being similar for administering saccharine, which is sweet but has no caloric intake). Also, the preference for sugar is manifested in rats and in studies designed for interventions at the level of the animal’s body, so that, once the sugar goes into the animal’s mouth it can be eliminated out of the body, not reaching the stomach and, therefore, not penetrating the vascular bed (except for a very small amount). This suggests that we are dealing with the effect of the sweet taste rather than the “drug” effect.
Secondly, these addictive behaviours obtained with sugar are only based on a diet consisting of intermittent access to sugar. However, similar behaviours are not observed in animals which are given free access to sugar. Generally, for these kinds of experiments, only animals who prefer sugar formulas in the early stages are selected. Therefore, it is admitted that a combination between the sweet taste and intermittent access to sugar may trigger a state similar to drug addiction, and the respective animals have a more intense response to drugs that have never been administered to them, like amphetamine and alcohol. But just how relevant is this effect to regular sugar consumption?
To quote certain researchers, “it is important to emphasise that these behaviours similar to addiction are observed only in diets with intermittent access but not in those with ad libitum access” to sugar.
In this context, “intermittent access” means that animals are offered sugar for a certain period, for example, for 12 hours, and then this access is limited for another 12 hours and so on.
Moreover, other aspects contradict the existence of the “drug” effects of sugar. For instance, rodents which are given access to sugar for a long period are affected by the negative consequences of consuming sugar, like adding a substance which induces nausea. In such situations, animals refuse to continue consuming sugar. On the other hand, in the case of cocaine or heroin, animals keep consuming these drugs despite the negative consequences. As far as the limited data we have from humans goes, it is difficult to make a distinction between natural consumption of sweet foods and a pathological state of addiction. In the studies carried out so far, it has been proven that the consumption of energy-dense foods which are nutrient-poor, such as candy and fast-food, is correlated with a score used for diagnosing “food addiction” and with the body mass index. The total consumption of carbohydrates and sugar from different foods, including that from breakfast cereal and fruits, hasn’t been significantly associated with this score.
Drug or food?
The sceptical camp underline the idea that “sugar is no more obesogenic than any other tasty, energy-rich food,” A fact which many of sugar’s critics take into consideration. Nutritional experts are not suggesting the complete banning of sugar, but rather to limiting it to levels which are compatible with a healthy life.
Besides, authors who believe in labelling sugar and highly processed foods as “addictive” admit to the fact that numerous studies which have examined sugar’s causal role in diabetes or obesity, did not establish a clear and unique causal relationship and that it is rather the energy excess (that is within food, irrespective of it being sweets, fats or even proteins) which leads to excessive body weight, obesity and type II diabetes: “Neither the consumption of sugar per se, nor the consumption of a sole nutrient can uniquely cause these morbid conditions. (…) Once the analysis for the total energy intake is adjusted, many published studies haven’t actually shown a relationship between sugar consumption and body weight.”
The risks of consuming too much sugar
According to a meta-analysis based on around 60 studies, when sugar is replaced with other nutrients with a similar energy content, “no adjustment in body weight occurs”. However, one should not ignore the fact that there is convincing observational proof that soft drinks (which contain sugar), consumed on a frequent basis, are associated with a 25% higher risk of diabetes, compared to the risk profile of people consuming such drinks just once a month or less. On the other hand, critics of the “drug” label applied to sugar rather wish to avoid stigmatising sugar. They do admit, however, that it is “indisputable that sugars, as a dense part, caloric-wise, of our diets, contributes to obesity. It is also indisputable that reducing sugar (together with reducing other energy-dense foods) should be part of any weight loss diet. We must be very careful not to conclude that this is the only harmful nutrient”.
In other words, whether sugar is or isn’t a drug might be besides the point, since opinions seem to converge on the need to reduce sugar consumption irrespective of what we label it.