Why do we crave the explosive gustatory taste of sugar? Neural short circuits, sensory pleasures and environmental factors, such as sleep deprivation, amplify our desire for sugar. But new research suggests that some of us – much more than others – might also be genetically suited to wanting this sweet nourishment.
An international group analyzed the genes of over 6,500 Danish citizens who participated in a large study on heart disease. They found that those who owned one of two particular variants of the FGF21 gene were 20 percent more likely to prefer and look for sugary substances.
“This study gives us an idea of the molecular basis of the preference for sweet taste, which I think is a fundamental factor: why on a biological level are we greedy for sweets?” Asks Matthew Gillum, researcher in the field of Novo Nordisk metabolism Foundation Center for Basic Metabolic Research of the University of Copenhagen and co-author of the study, whose results have appeared recently on “Cell Metabolism”.
FGF21 provides instructions for the synthesis of a hormone with the same name that is associated with the regulation of food intake in rodents and non-human primates. However, this new work indicates that FGF21 can modulate certain appetites even in humans and that the liver – the organ that secretes the hormone FGF21 and controls insulin resistance – can play a more important role in the management of snacking than considered so far, because it produces this hormone and communicates with the brain.
To investigate a possible link between FGF21 and food preferences, the researchers examined thousands of reports on dietary preferences of volunteers, in addition to their cholesterol and blood sugar values. The group also analyzed the FGF21 genes of the participants, and found that subjects who reported having a strong propensity to sugar and consumed more had a greater chance of possessing one of two specific variants of FGF21.
The same alleles – gene variants – of FGF21 were also associated with an increase in the consumption of other problematic substances: the researchers also found a weaker link between these gene variants and a greater aptitude for cigarette smoking and alcohol consumption.
The article does not specify exactly which neural path could be at work to explain these enticing relationships.
But an area of the brain calledatanucleus accumbens is considered to be the epicenter of the mechanisms of reward, desire and addiction – and it is possible that the desire for sugar and these other substances can converge in this region, says David Ludwig, Boston Children’s Hospital professor , specializing in nutrition and obesity, not involved in the new study.
However, since the article published in “Cell Metabolism” is observational, the relationship between FGF21 and gluttony for sweets “far from being definitive, is generating a series of hypotheses”, emphasizes Ludwig. He believes it is impossible to know whether individuals with or without these gene variants may differ for other important traits.
Although nutrition experts had already identified other internal factors that help control our food cravings, some elements mediating this process and transmitting signals about sucrose satiety remained mysterious.
Gillum now believes that FGF21, like leptin – another hormone that regulates appetite – can suppress the neural response to rewards, as regards both their research and their achievement.
“We are still investigating why the liver would have developed such mechanisms, but we hypothesize it could be to limit excessive sugar consumption, or to prevent its deleterious effects or to promote diversification of the diet,” says Gillum.
There are many unanswered questions in this article, such as why people who have these gene variants and who consume more sugar tend to have lower body mass indexes (BMI) than those who do not, which is a surprising result, considering the well-established relationship between a higher sugar intake and obesity.
“Studying if there is a certain genetic component that determines human preferences in terms of food flavor can help us to understand which populations may be particularly at risk”, emphasizes Ludwig.
Furthermore, Gillum hopes to undertake further genetic studies on the effect of these variations on body weight and type 2 diabetes, among other issues.
“We have seen that mice lacking FGF21 consume substantially twice as much sucrose than those who possess it,” he says. “We want to study subjects who are completely free of FGF21 and answer the question: will they be super-sweet for alcohol or sugar?”
(The original of this article was published in Scientific American on May 2, 2017)