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Teenage snacking may leave lasting damage on the brain, according to a new study.
Researchers observed that adolescent rats fed on a junk food diet had lower levels of key neurotransmitters associated with memory than their snackless counterparts. More concerningly, these memory deficits appeared to last into adulthood, after the rodents had been switched to a healthier diet.
The researchers say the findings could have worrying implications for human teens growing up on Western diets of ultra-processed foods.
Their results were published in Brain, Behavior, and Immunity.
Total ratcall
Intrigued by the known link between poor diet and Alzheimer’s disease, the researchers from the University of Southern California (USC) set out to test how junk food may affect memory earlier in life.
They fed one group of adolescent rats a high-fat, high-sugar chow diet (made from Reese’s pieces, Ruffles potato chips and other junk food) and gave them high-fructose corn syrup and water to drink (which, together, served as a soda drink substitute). Another group of “teenage” rats were fed “healthy, standard chow” and water.
All rats were routinely placed in a shifting environment to test their memory. If the rats sniffed a newly placed object, this was taken as recognition of its altered surroundings and, in turn, memory of the objects’ prior positions.
To begin with, there were no differences between the sniffing behaviors of either rat groups. Once the “unhealthy” rats had their diets switched to the healthier chow, however, they explored the recently moved objects less, although this divergence wasn’t deemed significant.
Fecal samples were also taken to study the rodents’ gut microbiomes, and – once the rats were euthanized – brain slices were taken to study their levels of acetylcholine, a neurotransmitter involved in memory processing.
Judging from fecal samples, the “Western diet” did reduce the biodiversity of the rats’ gut microbiomes. However, this deficit was reversed once the rats were put on the healthy chow diet.
What wasn’t undone was the reduction in acetylcholine, which stubbornly remained at lower levels in the rats initially fed unhealthy chow. This finding, say the researchers, hints that the rats’ poor diet during their teenage years may have caused long-term damage to their memory.
“Acetylcholine signaling is a mechanism to help them encode and remember those events, analogous to ‘episodic memory’ in humans that allows us to remember events from our past,” said Dr. Anna Hayes, a post-doctoral fellow at USC and lead author of the paper. “That signal appears to not be happening in the animals that grew up eating the fatty, sugary diet.”
What mechanism could be underpinning such a food-to-brain effect? Given that the rats’ gut microbiomes rebounded after their dietary shift, Hayes ruled out gut bacteria. Instead, she and her colleagues posit that a gastrointestinal-originating vagus nerve signaling pathway could be involved.
The team stress that, whether in rats or humans, adolescence is a sensitive period for the brain when important changes occur.
“I don’t know how to say this without sounding like Cassandra and doom and gloom,” said Scott Kanoski, a professor of biological sciences at the USC Dornsife College of Letters, Arts and Sciences, “but, unfortunately, some things that may be more easily reversible during adulthood are less reversible when they are occurring during childhood.”
Fortunately, “less reversible” isn’t the same as irreversible, as the research team did manage to restore the affected rats’ memory recall with two drugs that bind to acetylcholine receptors, Carbachol and PNU-282987.
Hayes and Kanoski say more studies will be needed to further test this potential for memory restoration, as well as studies to investigate whether a junk food–memory damage relationship is present in humans.
This article is a rework of a press release issued by the University of Southern California. Material has been edited for length and content.
Reference: Hayes AMR, Lauer LT, Kao AE, et al. Western diet consumption impairs memory function via dysregulated hippocampus acetylcholine signaling. Brain Behav Immun. 2024;118:408–422. doi: 10.1016/j.bbi.2024.03.015