Aspartame Is Marketed as a Safer Sugar Swap But New Research Shows Long Term Low Doses May Strain the Brain and Heart

A year-long experiment raises new doubts about the safety limits of one of the most popular artificial sweeteners.

Aspartame, one of the most widely used artificial sweeteners, promises a way to enjoy sugariness without sugar, pleasure without the metabolic cost. Found in diet drinks, sugar-free snacks, and even medicines, it has become a daily habit for millions of people trying to cut calories. 

However, despite decades of research, one question has remained surprisingly difficult to answer: what happens when the body is repeatedly exposed to aspartame at realistic doses over long periods of time? 

A new year-long study suggests that the answer may be more unsettling than previously thought, showing that aspartame can cause lasting changes in brain energy use and heart function even at doses well below current safety limits.

Testing long-term, low-dose aspartame exposure

Many earlier studies examined extremely high doses of aspartame or lasted only weeks, making them poor reflections of real-life consumption. Regulators such as the FDA and WHO have relied heavily on this short-term data when concluding that aspartame is safe below the acceptable daily intake.

To address this gap, the team designed a year-long experiment using mice and deliberately chose a low dose. The animals received an amount equivalent to seven milligrams of aspartame per kilogram of body weight in humans—roughly one-sixth of the maximum daily limit allowed by international health agencies. 

“This dose is well below the maximum dose recommended by the World Health Organization, the EMA (European Medicines Agency), and the FDA (Food and Drug Administration), which is 50 mg/kg (22.7 mg/lb) per day,” the study authors said.

Eighteen mice were given aspartame intermittently (three days every two weeks), while 14 mice were kept as untreated controls.

To understand how the sweetener affected the brain, researchers used FDG-PET scans, which measure how much glucose different brain regions consume. Glucose is the brain’s primary fuel, so changes in its use can reveal stress long before visible damage appears. 

After just two months, the brains of aspartame-exposed mice showed a sharp increase in glucose uptake, about twice that of untreated animals. This suggested the brain was working harder than usual. However, the pattern did not hold. 

Unusual changes in heart and brain activity

By six months, glucose use began to drop, and by ten months it had fallen to roughly half the level seen in control mice. Instead of adapting, the brain appeared to move from an early state of overactivity to long-term energy suppression, a pattern commonly linked to metabolic dysfunction.

Chemical analysis of brain tissue reinforced this picture. Early in the experiment, levels of N-acetylaspartate, a marker of healthy neuronal metabolism, rose by about 13 percent. However, this improvement faded. 

By eight months, lactate levels in the brain had increased by around 2.5 times, signaling that cells were struggling to process energy efficiently. This imbalance likely disrupts the cooperation between neurons and astrocytes, the support cells that convert glucose into lactate for neurons to use. 

When lactate builds up instead of being efficiently consumed, neurons enter a stressed state that reduces their performance. In practical terms, this can weaken attention, learning capacity, and mental endurance. Behavioral tests reflected these biological changes. 

For instance, in the Barnes maze, which measures spatial learning and memory, aspartame-treated mice moved more slowly, explored less, and took almost twice as long to locate the escape hole during training. By eight months, performance deteriorated further, with some mice unable to complete the task at all. 

The heart showed its own signs of strain. Imaging revealed mild cardiac hypertrophy, a thickening of the heart muscle that made pumping less efficient. Although the structure of the heart appeared mostly intact, each heartbeat delivered less blood, reducing oxygen supply to organs, including the brain.

“Aspartame does indeed reduce fat deposits (by 20%) in mice, but it does so at the cost of mild cardiac hypertrophy and decreased cognitive performance. Also, to our knowledge, this is the first report to show that aspartame can provoke structural and functional changes in the heart,” the study authors wrote.

Time to rethink safety limits 

The study suggests that long-term consumption of aspartame, even at doses considered safe by current standards, can alter how the brain and heart manage energy, at least in mice. These effects unfolded slowly, which may explain why other experiments may miss meaningful risks that only appear after months of exposure.

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Although animal results do not automatically apply to humans, the findings still strengthen the case for long-term human studies that track brain metabolism, heart performance, and cognitive function over years rather than weeks.

The researchers also argue that existing intake limits should be re-examined and that chronic exposure deserves far closer scrutiny. For consumers, the study does not offer a final verdict, but it does challenge the assumption that low dose automatically means low risk. 

The study is published in the journal Biomedicine & Pharmacotherapy.