Diabetes—a condition of marked glucose dysregulation—is a major cause of death globally. The World Health Organization estimates that over 420 million people are suffering from the condition, which carries a direct societal cost of $760 billion each year. These preventable mortality and financial costs are projected to increase markedly over the next decade(1).
Evidence demonstrated that one causal factor impairing blood glucose equilibrium is insufficient sleep(2).
Both acute and chronic partial sleep restriction, including non-rapid eye movement (NREM) slow-wave sleep, impair glucose tolerance and insulin sensitivity. Conversely,
sleep extension enhances glucose metabolism.
It is currently not clear what the mechanism is in which sleep optimally governs next-day glucose homeostasis in humans. Recent evidence suggests a candidate pathway in which hippocampal sharp-wave ripples – which are temporally coupled with NREM slow oscillations and sleep spindles(3) – were associated with precise regulation of peripheral blood glucose through activation of the hypothalamus.
These findings lead to a recent study that investigated both the extent and quality of coupled NREM slow oscillations spindle events in humans would predict optimal next-day regulation of peripheral blood glucose levels(4).
In culmination, these findings support NREM sleep-oscillation brain-body framework of glucose homeostasis in humans in which there is a strong association between prior slow oscillation spindle coupling and next day glucose homeostasis.
The above NREM sleep-oscillation framework of brain-to-body glucose homeostasis can be considered across at least two different timescales, which may not be mutually exclusive.
The first involves a longer (i.e., hours), feedforward association, such that NREM slow oscillation-spindle coupling predicts superior next-day glucose homeostasis. The second involves a short-term feedback loop (i.e., seconds to minutes) between hippocampal sharp wave ripple activity and concurrent changes in circulating glucose during sleep. Both processes, either independently or interactively may help in generalized glycemic homeostasis.
Importantly, these two pathways offer disease insights into the brain (sleep)-body (glucose) mechanisms that help explain the well-characterized associations between short and disrupted sleep, hyperglycemia, and type-II diabetes(2).
Findings from this research indicate that the association with blood glucose homeostasis appears to be most prudently explained by a link between NREM sleep oscillations and a select alteration in insulin sensitivity rather than regulating pancreatic beta cell function or insulin synthesis/secretion.
One possible mechanism explaining the recognized link between
deficient sleep and impaired blood glucose control is an alteration of autonomic sympathovagal balance resulting in a biased state of sympathetic activity over parasympathetic activity, which may chronically lead to insulin resistance and metabolic dysfunction.
This research demonstrates that slow oscillation-spindle coupling is not only a sensitive glycemic index, such coupling offers the highest predictive sensitivity of next-day glucose homeostasis. This predictive relationship with glucose status exceeded that of all other sleep measures assessed, including total sleep amount,
sleep efficiency, NREM slow-wave sleep, as well as sleep apnea severity.
These results establish the measure of slow oscillation-spindle coupling as an additional, independent contributing feature of sleep, one that offers insights into potential disease pathways associated with diabetes.
These findings suggest a sleeping-brain—glycemic-body framework of insulin-associated glucose homeostasis in humans, and further re-emphasize the importance of sleep in the clinical management of hyperglycemia and diabetes.
Type 2 diabetes is a serious disease characterized by elevated blood sugar (glucose) levels. Over time high blood sugar levels can damage the body’s tissues and organs, leading to numerous health problems and a shortened lifespan so it's important that you provide your body the foundation to utilize glucose optimally.
ADALOAD is a potent combination of ingredients shown in evidence-based research to reduce blood sugar levels in individuals with high blood glucose.
It helps your cells utilize glucose and move it to your liver, muscles, and fat and your body retain nutrients by blocking their conversion to glucose that ends up in your bloodstream.
References:
1. Williams R, Karuranga S, Malanda B, et al: Global and regional estimates and projections of diabetes-related health expenditure: Results from the International Diabetes Federation Diabetes Atlas, 9th edition. Diabetes Res Clin Pract 162:108072, 2020
2. Briançon-Marjollet A, Weiszenstein M, Henri M, et al: The impact of sleep disorders on glucose metabolism: endocrine and molecular mechanisms. Diabetol Metab Syndr 7:25, 2015
3. Oyanedel CN, Durán E, Niethard N, et al: Temporal associations between sleep slow oscillations, spindles and ripples. Eur J Neurosci 52:4762-4778, 2020
4. Vallat R, Shah VD, Walker MP: Coordinated human sleeping brainwaves map peripheral body glucose homeostasis. Cell Rep Med 4:101100, 2023
