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Indulging in a junk food binge can have lasting effects on your brain, even after you return to your usual eating habits. A recent study found that five days of overeating high-calorie, nutrient-poor foods temporarily boosted brain insulin sensitivity but caused a drop in responsiveness once participants switched back to a healthier diet.

Researchers assigned 29 healthy-weight men, ages 19 to 27, to one of two groups: One followed a junk food diet for five days, while the other stuck to their regular eating habits. They measured participants' brain insulin activity through imaging techniques and insulin administration before and after the binge.

At the peak of the junk food binge, researchers observed heightened insulin activity in key brain regions. However, just one week after returning to their usual diet, participants who had overindulged experienced lower brain insulin sensitivity, particularly in areas associated with memory and food-related reward, such as the hippocampus and fusiform gyrus. Interestingly, while the junk food group showed increased liver fat, there were no noticeable changes in weight or peripheral insulin sensitivity.

These findings suggest that the effects of overeating go beyond immediate metabolic changes, potentially contributing to cognitive decline and influencing eating behaviors over time. They also underscore how even a brief junk food binge can disrupt insulin function in the brain, impairing areas critical to memory and decision-making. Behavioral strategies like mindfulness can help curb overeating. Learn more in this clip featuring Dr. Ashley Mason.

Many people with prediabetes never receive structured treatment, even though early intervention offers the best chance of reversing high blood sugar. While lifestyle changes are the primary recommendation, they are challenging to implement and often ineffective. A recent study found that a broccoli sprout extract rich in sulforaphane modestly lowered fasting blood sugar in some people with prediabetes.

Researchers conducted a 12-week, randomized, double-blind, placebo-controlled trial involving 74 participants with prediabetes who had not previously taken medication for the condition. Participants took a daily dose of broccoli sprout extract or a placebo, and researchers measured changes in their fasting blood sugar. They also analyzed gut microbial composition and genetic markers to explore potential differences in response.

Overall, the extract slightly reduced fasting blood sugar levels (3.6 milligrams per deciliter, mg/dL) compared to the placebo but did not meet the predefined target for effectiveness. However, a subgroup of participants with mild obesity, lower insulin resistance, and reduced insulin secretion saw a greater reduction in blood sugar—about 7.2 mg/dL. These participants also had a distinct gut microbiota composition, including a higher abundance of bacterial genes linked to sulforaphane activation.

Sulforaphane forms when glucoraphanin, found in broccoli sprouts, interacts with the enzyme myrosinase. Myrosinase activates when the plant cells are damaged, such as during chewing or processing. In the absence of myrosinase, some people’s gut microbes produce similar enzymes, helping convert more glucoraphanin into sulforaphane. This variation in gut bacteria may explain why some people respond more strongly to sulforaphane-rich foods or supplements.

These findings suggest that gut microbes and individual metabolic traits may influence the effectiveness of nutritional interventions for prediabetes. One in three people in the U.S. has prediabetes. Learn more in this clip featuring Dr. Michael Snyder.

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