Short Sleep and Sweet Dreams

It is not a stretch to claim that most of us think 6 to 7 hours of sleep is acceptable, or even a luxury. Yet, the recommended sleep duration for teenagers is 8 to 10 hours a night.

While this may point to a larger issue that is depriving us students of our sleep, it is interesting to note that most of us do know that sleep is important. We know of its benefits and feel the short-term harms that occur when we don’t have it. Yet, what is less often talked about are the long-term harms of sleep deprivation—the ones we don’t feel immediately after pulling an all-nighter.

Thus, this piece hopes to unpack long-term impacts of sleep deprivation, especially on glucose regulation and the risk of diabetes.

The Context of Glucose

When we eat, our organs along the digestive tract work together to break down complex food molecules into a variety of smaller molecules, which our body can then absorb to use in metabolic processes. Of those, glucose is of particular interest to us as it is an important substrate with which our body makes energy, through various processes that result in the complete oxidation of glucose and the production of ATP.

The level of glucose circulating in our body is thus of importance, as it indicates the amount of glucose available for our cells to use. This is often approximated as blood glucose levels, which are tightly regulated by various feedback mechanisms to prevent massive fluctuations in levels which could be harmful to our body.

Blood Glucose Levels during Normal Sleep Conditions

Sleep is thus a massive challenge to our body’s regulation of blood glucose levels. Sleep is a form of fasting — a relatively long period in which no food is consumed and no digestion occurs. Intuitively, this may suggest that sleep causes a decrease in blood glucose levels. However, our body is much smarter than intuition. Through various regulatory processes, different periods during sleep and different parts of the sleep cycle will have observable increases and decreases in blood glucose levels.

For one, since sleep results in a decrease in metabolism, there is a corresponding decrease in glucose utilisation. This causes an initial increase in blood glucose levels during the early part of sleep. However, towards the end of sleep, there is a noticeable peak in both blood glucose and insulin levels, which causes a return of blood glucose levels to the baseline as we wake up. Interestingly, this response happens regardless of the time of day that sleep occurs, indicating that this circadian regulation is independent of external time factors.

It is also possible to compare blood glucose levels at different stages of the sleep cycle. During non-REM sleep, there is a sharpest decrease in whole-brain glucose metabolism and a reduction in peripheral glucose utilisation, which thus leads to the sharpest increase in blood glucose levels. Blood glucose levels then gradually decrease during REM sleep, due to increased glucose utilization, and eventually return to baseline when the individual is awake.

Defining Sleep Deprivation

Various studies have been conducted on how sleep deprivation thus affects the kind of blood glucose regulation observed in normal conditions, and it is helpful to consider certain parameters often used. Among these, defining what sleep deprivation is and the types of sleep deprivation is useful here. While it is easy to describe it as any duration of sleep that is less than that recommended, sleep deprivation is often broken into Total Sleep Deprivation and Partial Sleep Deprivation, of which the former can be further divided into Short-Term and Long-Term.

Total Sleep Deprivation (TSD) refers to an extended period without any sleep at all, during which an individual remains awake beyond what is typical. Conversely, Partial Sleep Deprivation (PSD) is more applicable in daily life, as it refers to sleep which is less than what an individual’s body needs. Instead, due to shorter sleep durations or fragmented sleep, the individual experiences reduced sleep but is not continuously awake. Interestingly, it has been noted that there are differences in blood glucose levels and blood glucose levels depending on the duration of Partial Sleep Deprivation.

Impact of Sleep Deprivation on Blood Glucose Levels

Individuals undergoing TSD (TSD Individuals)

During the first half of sleep, TSD individuals showed lower increases in blood glucose levels than normal individuals. During the second half of sleep, TSD individuals showed a decrease in blood glucose levels that was about two times the initial nighttime increase, compared to normal individuals, whose decrease in blood glucose levels was similar to the initial nighttime increase.

In addition, for TSD individuals, higher blood glucose levels were observed in the mid-morning to late afternoon despite similar insulin levels, which also suggests a decrease in daytime insulin action.

Higher blood glucose levels are likely due in part to the absence of slow-wave sleep and thus decreased growth hormone secretion. While slow-wave sleep is normally associated with cerebral restoration and recovery, as well as sleep maintenance and consolidation, it also leads to peaks of growth hormone secretion. The absence of slow-wave sleep hence decreases overall growth hormone levels. This impacts not only growth and muscle development, but also tissue regeneration and repair — all of which are normally glucose-heavy processes that decrease blood glucose levels.

However, the exact mechanism by which decreased daytime insulin action arises remains not well explored.

Individuals undergoing PSD (PSD Individuals)

Laboratory studies found that short-term PSD individuals experience a decreased rate of glucose clearance, which refers to the rate at which glucose is absorbed from the blood by tissues and cells around the body. This decrease was similar to that in older adults with impaired glucose tolerance. Moreover, short-term PSD individuals have a decreased acute insulin response to glucose, similar to those with ageing and gestational diabetes. This is particularly concerning, especially since acute insulin response to glucose is a common marker used for detecting diabetes. In addition, short-term PSD Individuals display decreased glucose effectiveness, which refers to the ability of glucose to mediate its disposal. The discrepancy between their glucose effectiveness and that of normal individuals was found to be similar to the difference between groups of patients with type-2 diabetes and healthy white men. Lastly, it was found that short-term PSD individuals have a higher glucose response to breakfast despite similar insulin secretion, which could suggest and be diagnosed as impaired glucose tolerance. These changes in short-term PSD individuals are remarkably similar to those seen in those with type-2 diabetes, which is concerning.

To explain these changes in glucose regulation, one of the key mechanisms proposed involves the hypothalamic-pituitary axis, which is often associated with regulating our stress response, among others. Under normal conditions, glucose tolerance and insulin sensitivity improve during the later part of the night, thus reflecting a delayed effect of low cortisol levels during the evening and early part of the night.

However, due to short-term PSD, there are disturbances in the secretion of various hormones like growth hormones and cortisol, which could interfere with normal glucose regulation. For example, extended and elevated nighttime growth hormone levels caused by PSD can induce a rapid decrease in muscular glucose uptake, thus leading to an increase in blood glucose levels. In addition, PSD-induced increased evening cortisol levels could also reduce insulin sensitivity the following morning, thus also increasing blood glucose levels.

Interestingly, long-term PSD individuals display similar glucose clearance rates as healthy individuals. However, studies have found that they do this through increased insulin secretion, which aims to compensate for the changes in glucose regulation that short-term   PSD individuals experience. Thus, while long-term PSD individuals may not display the same changes in glucose regulation, their increased insulin secretion could lead to lower insulin sensitivity, which may encourage insulin resistance in the future.

Conclusion

While we should take sleep-based studies with a pinch of salt, since sleep is a complicated process with many variables which are difficult to identify and control, the evidence seems to overwhelmingly suggest that any form of sleep deprivation will cause a change in the way our body regulates glucose. It is these changes which are concerning — as risk factors or precursors to type-2 diabetes, they may increase the likelihood of us getting diabetes sometime down the road.

With this, let’s try to correct our broken sleeping patterns, and seek sweet dreams tonight :D

References:

1. About sleep. (2024, May 15). Sleep. https://www.cdc.gov/sleep/about/index.html

2. Knutson, K. L. (2007). Impact of sleep and sleep loss on glucose homeostasis and appetite regulation. Sleep Medicine Clinics, 2(2), 187–197. https://doi.org/10.1016/j.jsmc.2007.03.004

3. Lam, N. (2024, October 30). 8 years ago, Singapore declared war on diabetes. Is it winning? CNA. https://www.channelnewsasia.com/today/big-read/eight-years-war-diabetes-winning-4698451#:~:text=According%20to%20the%20latest%20available,8.5%20per%20cent%20in%202022.

Media:

1.  https://www.vecteezy.com/vector-art/20840307-good-sleep-and-sweet-dreams-concept-small-kid-with-smile-on-face-lying-in-bed-on-moon-sleeping-having-sweet-dreams-with-falling-hanging-stars-from-sky-vector-illustration