Poor sleep is strongly linked to increased risk for type 2 diabetes. The two problems—which have been referred to as twin epidemics—present serious public health risks in the United States and worldwide. Sleep problems are also linked to risk for obesity, a primary risk factor for diabetes, and to metabolic syndrome, a condition that often precedes diabetes.
Research has indicated that sleep deprivation disrupts glucose metabolism, the process by which the body regulates blood sugar and processes that sugar into energy. Disruptions to healthy glucose functioning include decreases to insulin sensitivity and glucose tolerance, both of which contribute to elevated, unhealthful levels of blood sugar that eventually can lead to diabetes.
We have a great deal of evidence that establishes this connection between sleep and diabetes. But we don’t yet understand well the mechanics behind this connection. A new study points to a possible pathway by which insufficient sleep influences the development of diabetes. Recent research has found that sleep deprivation in mice leads to altered cell function in the pancreas, an organ that plays an important role in regulating blood sugar. Endocrine cells in the pancreas produce hormones—including the hormone insulin—that help process and regulate glucose. What’s more, researchers found that age played a significant factor. They discovered older mice experienced more significantly the negative cellular effects of sleep deprivation compared to younger mice, whose systems were able to cope more effectively with the cellular stress that resulted from lack of sleep.
Researchers at the University of Pennsylvania’s Perelman School of Medicine examined the effects of sleep deprivation on cell function and cellular stress in mice. They focused attention on the cells within the pancreas, as well as looking at changes in glucose metabolism. The study also investigated age as a factor in the relationship between cell function and glucose metabolism. Researchers submitted two groups of mice—young and old—to periods of both acute and chronic sleep deprivation, and studied the response of cells in the pancreas, including the endocrine cells that are involved in regulating blood sugar. In particular, researchers were looking for changes in a process known as the unfolded protein response. This is a protective response of the body to cellular stress that helps maintain healthy cell function. Changes to the activity level of the unfolded protein response are more likely to occur with age, and are linked to a number of serious and chronic diseases related to aging, including Alzheimer’s Disease and Parkinson’s, as well as to type 2 diabetes.
Researchers found that after being deprived of sleep, both younger and older mice experienced both cellular stress and increases to blood glucose levels. Younger mice, however, demonstrated signs that their bodies were able to cope with these alterations more effectively than older mice:
- After periods of sleep deprivation, the degree of cellular stress was significantly higher in older mice than in younger mice.
- Older mice showed increased levels of a protein that is indicative of cell death after being deprived of sleep. The younger mice did not.
- Sleep deprivation appeared to magnify the impairment of the body’s reaction to cell stress in older mice, weakening a protective response that is already challenged by age.
- While all the mice experienced negative changes to glucose metabolism after sleep deprivation, the younger mice appeared to weather these changes better than older mice. The younger mice showed significantly better control of their blood glucose than older mice. After acute sleep deprivation, older mice became hyperglycemic and experienced changes to insulin levels.
These results suggest that sleep deprivation may result in alterations to cell function that disrupt normal glucose metabolism, raising the risk of diabetes. These results also strongly indicate that age may make us increasingly ill-prepared to cope with these challenges. Older bodies are less adept at protecting cells from dysfunction, and lack of sleep appears to diminish this ability even further. This latest research builds upon an earlier investigation that showed sleep deprivation diminished the effectiveness of the unfolded protein response—that protective response to cell stress—in older mice. With these latest results, we’re beginning to see how this consequence of insufficient sleep has an impact on specific functions within the body.
The relationship between sleep and diabetes is complicated and multi-faceted, and there are other pathways by which sleep problems increase risk for the disease, including the significant effects of poor sleep on weight. But this research may present a significant development in our understanding of at least one way that sleep deprivation can influence the development of diabetes, and how this risk becomes more serious we age. It is also a striking and important view inside how deeply sleep can impact our bodies, placing us under physiological stress in ways that are potentially damaging to our health—especially as we grow older.
Michael J. Breus, PhD
The Sleep Doctor™