But while this hedonistic effect of food in the brain is well known, new research reveals that calories - per se - can do exactly the same. The study, to be published on the 27th of March issue of the journal Neuron, reveals that not only can calories induce dopamine release independently of food palatability, but also, that this is done through activation of a brain area that also responds to sweet taste.
By showing that our eating behaviour is directly affected by the nutrients in food, the study reveals a powerful new factor behind overeating and obesity that needs to be considered when developing anti-obesity strategies. Interestingly the research might also help to explain why recent studies seem to reveal – contrary to what expected - a link between sweet non-caloric drinks and weight increase.
Weight increase, and eventually obesity, results from ingesting more calories than those spent. Although the body possesses homeostatic control mechanisms, which make us hungry when in need of nutrients, and satiated when we had enough, we all know how the pleasure of food can easily override this and result in overeating.
The nucleus accumbens (NAcc) of the ventral striatum and the orbitofrontal cortex (OFC) are two of several brain reward pleasure centres (areas that when stimulated lead to feelings of pleasure) known to respond to food. Both are activated by oral recognition of sweet tastes and in response produce dopamine - a neurotransmitter capable of provoking such strong feelings of pleasure and happiness that has been nicknamed ‘the courier of addiction’ for its role in heroin and cocaine dependence. In the same way, dopamine can lead to overeating when we like the food. These brain reward mechanisms probably developed to ensure the consumption of high-energy food in a time when they were still scarce, but in modern societies they are an important contributor to the present obesity epidemic and, as such, need to be better understood.
An important question related to this issue was the suspected existence - in addition to the oral-sensory food recognition - of signals in the digestive track, after food ingestion, capable to affect eating behaviour probably through the brain. It was to investigate this question that Albino J Oliveira-Maia, Ivan E. Araújo, Miguel A.L. Nicolelis, Sidney A. Simon and colleagues at Duke University in Durham, North Carolina, USA decided to study the behaviour and brain activity of normal and sweet-blind. Sweet-blind mice, as the name indicates, are incapable of orally detect sweet tastes as result of lacking TRPM5, a protein of the taste cells, which is essential for sweet and bitter recognition.
The researchers’ idea was to compare the mice feeding preferences, as well as their Nacc and OFC dopamine production and neural activity, when fed with either sweet-tasting high caloric sucrose, or sucralose - a non-caloric sucrose-derived sweetener – looking for evidences of food recognition mechanisms occurring post-ingestion (so after food has left the mouth).
And in fact, when sweet-blind mice were given two feeding bottles, one with water and one with sucrose, and after an initial period of no preferences, the animals – despite being incapable of orally recognising sucrose’s sweet taste - showed a clear preference for the bottle with this solution revealing the existence of an alternative mechanism of food recognition. Blood glucose levels – which are directly associated to sugar metabolism – were measured, during and after sucrose feeding, and found to be high and very similar to normal mice confirming that sweet-blind mice were in fact recognising and using sucrose.
When the experiment was repeated with water and sucralose – which, although having no calories, is, nevertheless, equally sweet –, the same mice, however, showed no preference between the two bottles. This was an unexpected and surprisingly suggested that it was the caloric content/nutrients of sucrose, and not its sweet taste, that was been recognised by sweet-blind mice in the first experiment.
Normal mice, able to recognise the sweetness of both sucrose and sucralose, preferred, as expected, these solutions to water in all experiments.
Next, Oliveira-Maia, Araújo and colleagues looked into NAcc and OFC responses to sucrose and sucralose feeding and here the dissimilarities between the two strains were elucidating. First, while in normal mice NAcc released dopamine after both sucrose and sucralose feedings, in sweet-blind mice NAcc only responded to sucrose. Additionally, in these modified mice, only the NAcc area became activated when the mice were fed with sucrose, while in normal mice both NAcc and OFC show neural activity after feeding with sucrose or sucralose.
These differences revealed that although the two brain zones recognise and respond to food sweet flavours, only NAac is capable of responding to calories. Supporting the idea that calories response depended on post-ingestive signals, in sweet-blind mice NAcc activation in response to sucrose only happened 10 minutes after its ingestion.
As Oliveira-Maia- a Portuguese researcher and one of the main authors of the paper explains: “these results are both novel and unexpected, in that they go against the current view that oral sensory reward and palatability are the primary driving forces behind overeating and obesity.”
In fact, and for the first time it is shown how food nutrients – per se (independently of food taste) - are sufficient to change eating behaviour. Not only that but Oliveira-Maia, Araújo and colleagues’ work reveals that both sweet and caloric recognition trigger a common brain area- NAcc. Both results contribute to a better understanding of the biological triggers of overeating and, as such, can contribute to better anti-obesity strategies but also raise interesting new questions.
For example, could these “dual” signals to a common brain area explain recent claims that non-caloric sweet drinks - such as diet coke – can contribute to weight increase? It is known that animals can learn to associate events – like the Pavlov’s dog did – and respond accordingly. In nature sweetness is usually a reliable indicator of high-caloric food and this information is probably used for homeostatic body weight regulation. So could low-calories sweet drinks or even sweeteners - by constantly sending to the brain a message that contradicts the usual “sweet taste - high caloric content” relationship - affect these homeostatic mechanisms, which, no doubt rely on being able to correctly identify the nutrients of different food? This could be no doubt an interesting topic for new research.
Obesity and overweight are major risk factors to a number of illnesses, including diabetes, heart disease and an alarming number of cancers. And if obesity was once a problem of developed countries, now it knows no frontiers, especially in urban settings. According to the World Health Organization in 2005 there was already 1.6 billion adults and 20 million children overweight, while other 400 million adults were obese and the prediction is that in 2015 2.3 billion of us will be overweight and more than 700 millions obese.
While much research has focused on genetically-determined neural and hormonal mechanisms behind obesity, environmental factors - such as the increasing consumption of high caloric fast foods - are believed to be the major reason behind the recent epidemic. And now, Oliveira-Maia, Araujo and colleagues’ results reveal that calories, per se, can trigger a mechanism known to be behind addiction, further highlighting the urgency to address, in the fight against obesity, not only our eating habits but also the politics of fast-food chains. In fact, Oliveira-Maia, Araujo and colleagues’ results have probably much to do with why it is so difficult to resist those Big Macs despite their absurd size.
Catarina Amorim | alfa
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