The Insidious Effects of Lost Sleep

Question: Does sleep play a role in glucose metabolism and the development of type 2 diabetes?

Answer: Before I answer this question directly, I think it is important to note that Americans' sleep habits have changed significantly over the last century. The National Sleep Foundation's annual surveys of Americans' sleep habits indicate that Americans are sleeping less and less.¹ Even though the average requirement for sleep is likely 8–9 hours, many Americans average <7 hours, with some getting 5–6 hours most of the time.² Thus, sleep deprivation is endemic in our society.

With this as the backdrop, an increasing body of epidemiological and experimental data suggests that sleep deprivation hurts our overall health and functioning, and specifically may affect the development of diseases such as diabetes.

Epidemiological studies—largely conducted in men—have shown fairly consistently that those who regularly sleep ≤5 hours, or >8 hours, are at some increased risk for developing type 2 diabetes.^3,4 There is also evidence that individuals with type 2 diabetes who report poor quality sleep or short sleep duration have increased glycated hemoglobin (A1C) levels.⁵

Experimental studies also support this phenomenon and reveal some possible mechanisms for the relationship. Sleep loss in normal volunteers appears to significantly affect the hypothalamic pituitary system, as well as the autonomic nervous system, both of which in turn affect metabolism and, specifically, insulin resistance.⁶

Sleep curtailment alters the pattern of growth hormone secretion, reduces concentrations of thyroid stimulating hormone, and increases evening cortisol levels, all of which can be mechanisms for an increase in insulin resistance. Other characteristics of sleep deprivation are increased sympathetic activity and less parasympathetic activity, which also affect glucose metabolism and the release of insulin.

Yet more experimental data shed light on sleep deprivation's impact on hormones related to appetite and satiety. Sleep restriction appears related to reductions in the appetite suppressant leptin and elevations in the appetite stimulant ghrelin. As a result, people low on sleep tend to experience increased hunger and appetite, especially for foods with high carbohydrate content.⁷ Sleep loss, therefore, seems to alter the ability of leptin and ghrelin to accurately signal caloric need, and could lead to excessive caloric intake when food is freely available. Thus, sleep loss could drive individuals toward obesity, cardiometabolic risk, and sleep apnea.

Lastly, an increasing body of data indicates that obstructive sleep apnea is an independent risk factor for type 2 diabetes. Further, it appears that apnea may also be modulated through autonomic dysfunction and metabolic and endocrine changes that affect insulin resistance.⁸

I strongly recommend that individuals diagnosed with type 2 diabetes be screened for obstructive sleep apnea syndrome, especially if they are overweight. Similarly, physicians should be alert to the possibility of impaired glucose tolerance or insulin resistance in patients who have obstructive sleep apnea, particularly if those patients are overweight. ▪