Everyone knows sugar-rich, fatty foods are unhealthy, but we keep eating them. The diet industry is booming, but so are waistlines. In the UK, 1 out of 5 adults is obese; in the US, the figure is 1 of every 3 adults. Why don’t we eat better? Are we just too weak-willed? Maybe not. The picture emerging from recent research into the neurobiology of eating tells a different story, in which our evolutionary history and changing environment have created a dangerous new relationship with our food.

We like the taste of sugars and oils because they’re rich in energy. Foods with a high concentration of them are a valuable energy source, so our ancestors evolved a preference for them. It’s not just a question of taste, though. Rich foods also trigger the release of dopamine, a neurotransmitter involved in our brain’s reward system, which makes us seek them out. It makes sense — after all, rich foods get you more energy for the same amount of effort, which is great when you’re out foraging. The catch, though, is that the whole system — and its controls — evolved in an environment where these kinds of foods where uncommon. Nowadays, energy-packed foods full of sugars and fats are cheap and ubiquitous, a change that’s played havoc with our reward system.

In a 2005 paper entitled “How Can Drug Addiction Help Us Understand Obesity?”, Nora Volkow and Roy Wise summarized a raft of data showing that food and addictive drugs activate the same reward circuitry. In both cases, consistent over-stimulation of the circuit weakens its response, creating the need for a stronger stimulus and leading to the compulsive behaviour we call addiction. The duo argued that drug addiction provides a useful framework for understanding how we eat, writing: “Although each condition has its own interface with brain mechanisms of motivation, the motivational mechanisms themselves largely overlap. […] The guidelines for prevention and treatment of the two disorders are remarkably similar, and some of the same pharmacological interventions that are promising for the control of drug intake are also promising for controlling the intake of food.”

More recently, research by Paul Johnson and Paul Kenny showed that rats fed a so-called “cafeteria diet” (bacon, sausage, cheesecake, and chocolate) showed changes similar to those seen in rats addicted to drugs. Like drugs, the rich diet increased the rats’ reward threshold, making it harder for them to get satisfied. The higher threshold was a result of the rats having fewer dopamine receptors, which is also the case in humans addicted to drugs. Since there are fewer receptors, more dopamine is needed to activate the reward signal, which takes more stimulus — food or drugs. Scientists have also discovered that obese humans tend to have a lower density of dopamine receptors.

Rats fed a cafeteria diet didn’t just show neurological changes; they also kept eating even when exposed to a light that they had been trained to associate with an electric shock. Rats addicted to cocaine also ignored risks to get their reward, while those fed only ordinary chow gave up their food in order to avoid the light. To me, one of the most striking findings was how long it took the reward circuitry to recover when the rats were taken off the cafeteria diet. The reward system recovers in about 48 hours in rats coming off a cocaine addiction, but it took at least two weeks to get back to normal after over-eating.

It’s important to realize that the effect of rich foods on the reward circuit isn’t because of their taste. Mice prefer sugar over the artificial sweetener sucralose even though sucralose is 600 times sweeter. In fact, mutant mice which can’t taste sweet food still like sugar better. This is because sugar, unlike sucralose, activates the dopamine pathway in the reward circuit, which acts together with the taste to create a preference — or an addiction. Last year, a team of scientists identified the neurons that release dopamine in response to sugar. They genetically engineered mice in which these neurons could be activated with a pulse of laser light, and then showed that activating them while the mice ate sucralose made them prefer the artificial sweetener. By contrast, mice engineered to lack these neurons altogether showed no preference between sugar and sucralose.

So what does all this mean? Basically, our reward system evolved to encourage us to seek out rich foods, but it’s getting short-circuited by the overabundance in our environment these days. It’s the same short-circuit that happens in drugs users, and it leads to the same outcome — addiction (in this case, to fatty, sugar-rich foods).

This post strays a bit from the usual purview of Inspiring Science, but I feel like it’s worth writing about and discussing. Many people may not have heard about this research, which is something we can fix together. Hopefully that will help change the conversation about obesity and diet, and the relationship we have with food. I’ll forego my usual flowery ending and instead close with a quote from the Volkow & Wise paper: “Few fields seem to offer as much potential for cross-fertilization as the fields of addiction and obesity research.”

References
Volkow ND, & Wise RA (2005). How can drug addiction help us understand obesity? Nature neuroscience, 8 (5), 555-60 PMID: 15856062
Johnson PM, & Kenny PJ (2010). Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature neuroscience, 13 (5), 635-41 PMID: 20348917
Domingos AI, Sordillo A, Dietrich MO, Liu ZW, Tellez LA, Vaynshteyn J, Ferreira JG, Ekstrand MI, Horvath TL, de Araujo IE, & Friedman JM (2013). Hypothalamic melanin concentrating hormone neurons communicate the nutrient value of sugar. eLife, 2 PMID: 24381247
García-Cáceres C, & Tschöp MH (2014). The emerging neurobiology of calorie addiction. eLife, 3 PMID: 24399459