Brief Exposure to Junk Food Affects Appetite and Memory

A study published this week by Stevenson and colleagues provides the first direct evidence that consuming a high-fat/high-sugar "Western diet"—for as little as one week—impairs normal brain function in humans. Specifically, junk food seems to affect our ability to regulate appetite and thereby consumption, so that eating junk food makes it genuinely harder to resist eating more of the same.

In animals, extensive previous research has suggested that a high-fat/high-sugar Western diet selectively impairs the kind of memory that is dependent on the hippocampus. It has long been known that the hippocampus is involved in certain kinds of memory, particularly for spatial information and memory for one-off events, but also the regulation of appetite.

Stevenson and colleagues' study aimed to find out whether brief exposure to a Western diet affected memory and appetite in young, slim, healthy people in a similar way to that expected from animal studies.

One hundred and ten participants who generally ate a healthy diet were assigned to either a Western-style (WS) diet group and consumed a WS-diet for one week, or a control group who retained their usual diet over the same period. All participants were given a laboratory breakfast on day one and day 8 of a toasted sandwich and a milkshake. For the WS group, this lab breakfast was high in saturated fat and added sugar, whereas, for the control group, it was low in fat and sugar.

In addition, the WS group was instructed to eat two Belgian waffles for breakfast or dessert on four days between days 2-7, and eat a main meal from a fast-food restaurant on the other two days, otherwise keeping their diet close to normal. The control group was instructed to eat as normal on days 2-7.

Participants were given tests of hippocampal function and appetite before and after breakfast on day one (the first day of any diet changes) and on day eight after any dietary intervention had occurred.

The key findings were as follows:

Just one week of exposure to the WS diet led to a reduction in the ability to control appetite. Participants were tested for how much they liked a given food (say, Cheerios or waffles), and how much they wanted that food, both before and after breakfast. When sated, participants would be expected to be less likely to want food, even if they like it. However, the study found that for participants exposed to one week of WS food, the "want" response to junk foods remained stronger after eating than for those on a healthy diet.

The participants on the WS diet also showed poorer performance than those on the healthy diet on the Hopkins verbal learning test (HVLT), which is known to be dependent on the hippocampus. Performance on the HVLT was strongly correlated with the reduction in appetitive control, suggesting that the effects on appetite depended on the hippocampus.

The other key finding was that the WS diet-triggered impairments on appetite control and hippocampally-dependent learning were reversed three weeks after returning to a healthy diet.

The current study thus extends the previous findings of Attuquayefio and colleagues (2016) that had also found a reduced ability to suppress wanting when sated in habitual WS diet consumers by suggesting that impairments may be a direct and rapidly-acting effect of the consumption of high-fat/high-sugar food.

These findings thus go some way to making sense of the paradox that the consumption of high-calorie food tends to lead people to consume more, even when they have previously maintained a healthy weight and diet. Understanding that such "excess hunger" is an effect that can be reversed by improving diet (at least after brief periods of a poor diet) can give succor to those attempting to wean themselves off junk food.

More generally, this study reveals measurable hippocampal impairments after even brief exposure to poor diet. Scientists believe that a high-fat/high-sugar diet causes inflammatory (and other) processes that lead to a reduction of BDNF—a hormone that supports synaptic changes and neurogenesis in the hippocampus.

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In recent years, there has been increasing interest in the idea that a well-functioning hippocampus is crucial for the maintenance of mental health and recovery from conditions such as depression and anxiety (see Cocks et al., 2016, special issue of Neural Plasticity). Thus, Stevenson and colleague's study provides some of the clearest evidence to date that improving our diet if it is poor may directly benefit our mental health through its effect on hippocampal function.