A recent study published in Sleep Medicine Reviews summarized the inter-relationship between diet, glucose metabolism, and sleep.
Study: The interrelationship between sleep, diet, and glucose metabolism. Image Credit: OleksandraNaumenko/Shutterstock.com
The prevalence of obesity continues to increase in the United States. Several environmental factors influence individuals’ relations with their food environments, which interact with physiologic/genetic risk factors and influence obesity risk.
Environmental factors and food insecurity are known determinants of poor sleep outcomes, insufficient sleep, and sleep disorders. In the present study, the authors posit sleep as an intrinsic behavior that might influence the risk of obesity and chronic diseases.
Effects of dietary patterns on sleep quality
One study evaluated the relationship of a plant-based diet with inflammation and sleep in overweight/obese females aged 28-48. The study showed that an unhealthy plant-based diet was linked to inflammation and poor sleep quality and suggested that healthy diets provide antioxidants that might improve sleep quality.
Another study revealed that female workers in Japan with higher vegetable consumption had good sleep quality, whereas those with a higher intake of confectionaries had poor quality. Furthermore, higher Mediterranean diet adherence has been linked to better sleep quality, lower sleep onset latency (SOL), less daytime dysfunction, and fewer sleep disturbances in college students.
A study specifically focusing on food intake in the evening and its association with sleep found that fat intake, sleep efficiency, and rapid-eye movement (REM) sleep were negatively associated. In females, increased fat intake was associated with longer REM sleep latency and lower sleep efficiency.
Macronutrients and sleep quality
Few studies have assessed the effects of very-high carbohydrate diets on sleep. One study noted that consuming a high-carbohydrate/low-fat (HC/LF) diet resulted in more REM sleep and less slow-wave sleep (SWS).
Another study evaluated the effects of late-day carbohydrate intake on sleep and found that participants had less SWS following an HC/LF dinner than after a low-carbohydrate/high-fat (LC/HF) dinner.
Others have studied the effect of moderate carbohydrate consumption on sleep. In a study involving middle-aged obese/overweight adults, the diet providing 55% energy from carbohydrates and 20% from protein was reported to have the best sleep outcomes, with no differences between higher and lower carbohydrate diets.
Effects of glucose metabolism on sleep
Reduced systemic glucose utilization has been reported during sleep, driven by lower brain activity and brain glucose metabolism compared to the awake state. One study found decreased interstitial fluid glucose levels during REM sleep in individuals with normal glucose tolerance, suggesting that this decline might be a risk factor for nighttime hypoglycemia.
A group of researchers examined the effect of late-evening meals on glycemic excursions in type 2 diabetes (T2D) patients. The incremental glucose area under the curve (AUC) was higher at night, with a greater peak when dinner was consumed at 9 PM than at 6 PM.
Besides, the average amplitude of glycemic excursion was more likely to be higher with 9 PM dinners than with 6 PM dinners.
High glycemic response to evening meals and compensatory hyperinsulinemia might plausibly lead to mild reactive hypoglycemia. Hypoglycemic events could cause awakenings and compromise sleep efficiency. Previously, the current study’s authors suggested that a high glycemic index (GI) diet might elevate insomnia risk through peripheral glucose excursions at night.
This might implicate sleep regulatory molecules and systems sensitive to glucose sensing in the periphery. Orexin is associated with sleep-wake cycle regulation and metabolic function. Orexin neurons excite brain nuclei with a critical role in wakefulness and can also sense nutritional status through peripheral signals, such as ghrelin, glucose, and leptin.
It has been reported that physiologic glucose levels enhance the excitability of hypothalamic melanin-concentrating hormone (MCH) neurons in a dose-dependent manner, which, conversely, exerts opposite effects on that of orexin neurons.
Therefore, the glucose-sensing orexin neurons could represent a mechanism for nighttime awakening triggered by acute hypoglycemic events through orexin neuron excitation and MCH silencing.
Intriguingly, orexin neurons exhibit different behavior when other energy-producing molecules exist. Specifically, they only respond to changes in glucose levels when other energy molecules are present in low concentrations. Glucose/lactate concentrations are elevated in T2D and insulin resistance.
While increased glucose typically would cause orexin antagonism and promote sleep, elevated lactate concentrations that precede insulin resistance may perturb peripheral glucose sensing.
Improving insulin resistance/sensitivity could alter serum orexin levels. In a sample of T2D patients on anti-hyperglycemic therapy, a negative correlation between insulin resistance and orexin has been reported, but three-month treatment improved insulin sensitivity, elevating orexin levels.
Although sleep was not evaluated, interventions for improving insulin resistance may normalize orexin availability, translating into better homeostatic sleep regulation.
In summary, the available evidence from the literature corroborates the relationship between sleep and the risk of T2D and obesity. Dietary changes, such as low GI foods in the evenings and focus on the dietary carbohydrate-to-protein ratio, may benefit sleep outcomes.
Future studies should mechanistically determine the role of orexin systems in glycemic excursions and their effects on sleep quality.