Summary: Aspartame, a sweetener found in diet foods and beverages, has been linked to an increased risk of developing anxiety behaviors in a new mouse study. The effects of aspartame exposure extended for up to two generations.
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Researchers at Florida State University College of Medicine have linked aspartame, an artificial sweetener found in nearly 5,000 diet foods and beverages, with anxiety-like behavior in mice.
In addition to producing anxiety in the mice that consumed aspartame, the effects extended up to two generations of males exposed to the sweetener.
The study is published in the Proceedings of the National Academy of Sciences.
“What this study shows is that we need to look back at environmental factors, because what we see today is not just what’s happening today, but what happened two generations ago and maybe even longer,” said co-author Pradeep Bhide. , the Jim and Betty Ann Rodgers Eminent Scholar Chair in Developmental Neuroscience in the Department of Biomedical Sciences.
The study arose, in part, because of previous research by the Bhide Laboratory on the transgenerational effects of nicotine in mice. The research showed temporary, or epigenetic, changes in the sperm of mice. Unlike genetic changes (mutations), epigenetic changes are reversible and do not modify the DNA sequence; however, they can change the way the body reads a DNA sequence.
“We were working on the effects of nicotine in the same type of model,” Bhide said. “The father smokes. What happened to the children?
The US Food and Drug Administration (FDA) approved aspartame as a sweetener in 1981. Today, nearly 5,000 metric tons are produced each year. When consumed, aspartame is converted to aspartic acid, phenylalanine, and methanol, all of which can have potent effects on the central nervous system.
Led by PhD candidate Sara Jones, the study involved giving mice drinking water containing aspartame at about 15% of the FDA-approved maximum daily human intake. The dose, equivalent to six to eight 8-ounce cans of diet soda per day for humans, continued for 12 weeks in a study spanning four years.
Pronounced anxiety-like behavior in mice was observed through a variety of maze tests in multiple generations offspring of aspartame-exposed males.
“It was such a strong anxiety-like trait that I don’t think any of us anticipated that we would see it,” Jones said. “It was completely unexpected. Usually you see subtle changes.”
When given diazepam, a drug used to treat anxiety disorder in humans, mice of all generations stopped displaying anxiety-like behavior.
The researchers are planning a further publication of this study focused on how aspartame affected memory. Future research will identify the molecular mechanisms that influence the transmission of the effect of aspartame between generations.
Other coauthors were Department of Biomedical Sciences faculty members Deirdre McCarthy, Cynthia Vied, and Gregg Stanwood, and FSU Department of Psychology Professor Chris Schatschneider.
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original research: Open access.
“Transgenerational transmission of aspartame-induced anxiety and changes in glutamate-GABA signaling and gene expression in the amygdala” by Sara K. Jones et al. PNAS
Summary
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Transgenerational transmission of aspartame-induced anxiety and changes in glutamate-GABA signaling and gene expression in the amygdala
We report the effects of aspartame on anxiety-like behavior, neurotransmitter signaling, and gene expression in the amygdala, a brain region associated with the regulation of anxiety and fear responses. C57BL/6 mice consumed drinking water containing 0.015% or 0.03% aspartame, a dose equivalent to 8-15% of the FDA recommended maximum daily intake in humans, or plain drinking water.
Robust anxiety-like behavior (assessed by open field test and elevated zero maze) was observed in male and female mice consuming aspartame-containing water.
Diazepam, a GABA-A receptor allosteric modulator, alleviated anxiety-like behavior. RNA sequencing of the amygdala followed by KEGG biological pathway analysis of differentially expressed genes showed significantly enriched glutamatergic and GABAergic synapse pathways.
Quantitative PCR showed upregulation of mRNA for the 2D subunit of the NMDA glutamate receptor (grimace2d) and metabotropic receptor 4 (grm4) and downregulation of GABA-A receptor-associated protein (gabarap) mRNA. Thus, taken together, our diazepam and gene expression data show that aspartame consumption shifted the excitation-inhibition balance in the amygdala toward excitation.
Even more surprising, anxiety-like behavior, their response to diazepam, and changes in amygdala gene expression were passed on to male and female offspring in two generations descending from the aspartame-exposed males.
Extrapolation of the results to humans suggests that consumption of aspartame at doses below the FDA’s recommended maximum daily intake may produce neurobehavioral changes in aspartame users and their offspring.
Therefore, the human population at risk of potential mental health effects of aspartame may be greater than current expectations, which only include people who consume aspartame.
