“Junk food may be addictive in the same way as heroin or cocaine,” The Independent reported. It said researchers have found that a high-calorie diet of fatty, sugary food leads to compulsive overeating in rats and causes changes to the brain similar to those in humans who are addicted to the drugs.
The study behind this news report is a well-conducted laboratory study in rats. The researchers found that rats with extended access to a high-fat, high-sugar diet had changes in the area of the brain associated with reward and developed compulsive eating habits.
This research furthers our understanding of the brain’s complex responses to food, which can lead to overeating, and paves the way for further research. It is not clear how relevant these findings are to obesity and overeating in humans as the psychological and neurological basis of reward is likely to be different between rats and humans. Further research would be needed to establish this.
Where did the story come from?
The research was carried out by Dr Paul M Johnson and Paul J Kenny from the Scripps Research Institute in Florida. The study was funded by a Bank of America Fellowship, the Landenberger Foundation and a grant from the US National Institutes of Health. The research paper was published in the peer-reviewed medical journal Nature Neuroscience.
The Daily Telegraph’s report is somewhat misleading as it suggests that a human brain was involved, but all newspapers make it clear that this study was conducted in rats.
What kind of research was this?
This was a laboratory study conducted in rats. The researchers investigated the effects of restricted or extended access to food on the reward system in the brain, i.e. how diet affects the brain’s sense that it has been rewarded by the food that has been eaten. They also investigated the effects on the brain of over-consumption of palatable food to see whether this had any link with compulsive eating.
What did the research involve?
The researchers prepared a group of rats for the experiment by inserting stimulating electrodes into the “pleasure centre” of their brains. This procedure rewards rats with a pleasure sensation when the electrode is stimulated. For a 10–14 day “training period”, the rats were given the ability to stimulate the electrode themselves. To gauge the rats’ “baseline reward threshold”, the researchers set the level of stimulation delivered by the electrodes at varying intensities to establish the minimum level of intensity needed for the rats to be encouraged to self-stimulate. This threshold would later be compared to the reward levels following experimental dietary conditions.
The rats were allocated to three different dietary groups, which were given different levels of access to a “cafeteria-style” diet (bacon, sausage, cheesecake, pound cake, frosting and chocolate). All the rats also had free access to standard laboratory food (chow). The first group had no access to the cafeteria diet, the second group had access for one hour a day (restricted access) and the third group had access for 18 to 23 hours (extended access) for a total of 40 days. The rats’ reward thresholds, weight gain and intake of calories were recorded throughout.
A forced abstinence period followed, in which the cafeteria diet was withdrawn and rats had unlimited access to standard chow.
Further experiments investigated the effects of this diet on brain structure and particularly on dopamine D2 receptors, chemicals in the brain that play an important role in the reward system. Previous research has shown that reduced levels of these chemicals “predispose individuals to substance dependence disorders”.
The researchers wanted to test their theory that problems in the dopamine system might contribute to the compulsive-like eating that developed in rats given extended access to the cafeteria diet. They also investigated whether the rats that had extended access to the cafeteria diet would eat this food even when “punished” (with foot shocks).
What were the basic results?
As expected, weight increased in the rats with extended access to the cafeteria food compared to the chow-only rats and rats with restricted access. At the same time, the reward thresholds in the extended-access rats rose over time, meaning that the rats on unlimited cafeteria food needed more stimulation to register the same level of pleasure as rats on healthier diets.
The researchers say the cafeteria-style diet had the same effect as that seen in studies of rats with extended access to intravenous cocaine or heroin self-administration. Calorie intake was higher in the rats with extended access to the cafeteria food and even those with restricted access developed binge-like eating behaviour, where they took in 66% of their daily calories from this food during their hour of access. During abstinence, there was a reduction in calorie intake and body weight, although the raised reward thresholds (compared to the other groups) remained for at least two weeks.
The researchers found that the heavier the rats were, the lower their levels of dopamine D2 receptors in a region of the brain called the striatum, which in humans is associated with addiction. They also found that rats with extended access to the high-fat diet did not respond to light cues to eat, nor did their intake reduce when they were essentially being punished for eating (foot shocks).
How did the researchers interpret the results?
The researchers concluded that extended, but not restricted, access to a high-fat diet “induces addiction-like reward deficits, overeating and loss of homeostatic energy balance (the balance between energy intake and energy expenditure)”.
They say that over-stimulation of the brain’s reward systems through consumption of this diet leads to compulsive-like eating. This response in obese rats is probably because of problems in the dopamine systems. The research supports previous work and indicates that “obesity and drug addiction may arise from similar neuroadaptive responses in brain reward circuits”.
This laboratory study has furthered our understanding of the complex responses to reward from food intake in rats. The researchers have demonstrated that rats given unrestricted access to a high-fat diet develop responses to it that are similar to those seen in rats addicted to cocaine and heroin. How applicable these findings are to humans and human health is unclear at present. Rats and humans are likely to have different neurological and psychological components of reward.
The lead researcher, Dr Paul Kenny, says that the study “presents the most thorough and compelling evidence that drug addiction and obesity are based on the same underlying neurobiological mechanisms”. The Daily Telegraph quotes Dr Kenny as saying that the research supports what obese patients have been saying for years: that, like addiction to other substances, junk food bingeing is extremely difficult to stop.
Given the prevalence of obesity in the UK and the serious diseases that are linked to it, any research that furthers the understanding of overeating will be welcomed. More research is needed before these findings will inform prevention or treatment strategies for obesity in humans.
Links to the headlines
Junk food could be addictive ‘like heroin’. The Independent, March 29 2010
Junk food as addictive as ‘heroin and smoking’. The Daily Telegraph, March 29 2010
Junkie food. Daily Mirror, March 29 2010
Links to the science
Paul M Johnson & Paul J Kenny. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience 2010 (advance online publication)