Scientists have long debated whether artificial sweeteners influence insulin levels and cardiovascular risk. A recent study found that consuming aspartame, a popular artificial sweetener, sharply increased insulin secretion in mice and monkeys, a process driven by parasympathetic nervous system activation.

Researchers fed mice a diet containing 0.15% aspartame and measured changes in blood insulin levels. They also surgically severed the vagus nerve in some animals to assess whether parasympathetic activation was involved. To examine insulin’s role in atherosclerosis, they implanted slow-release insulin pumps in mice to mimic chronically elevated insulin levels. Finally, they tested aspartame’s effects in Cynomolgus monkeys, which are metabolically similar to humans.

They found that mice that consumed aspartame experienced a sharp increase in insulin secretion, an effect eliminated after severing the vagus nerve. Long-term aspartame consumption worsened atherosclerosis, and implanting insulin pumps had a similar effect. In monkeys, aspartame triggered an insulin spike comparable to the effects of sucrose. However, instead of raising blood sugar, it lowered it, potentially driving insulin resistance, inflammation, and increased risk of atherosclerosis. Further analysis revealed that aspartame-induced insulin secretion activated cell signaling pathways linked to arterial inflammation and plaque formation.

These findings suggest that aspartame consumption worsens cardiovascular risk by increasing insulin secretion, altering glucose metabolism, and promoting inflammation and plaque buildup in the arteries. Notably, the aspartame dose used in the experiment greatly exceeds what most humans consume. While the study provides insight into biological effects, its relevance to typical human intake is unclear due to the high exposure levels. Learn more about artificial sweeteners and other sugar substitutes in Aliquot #66: Sugar substitutes: Risks and benefits