The psycho-metabolic consequences of sleep loss in people
H:son-Holmdahlsalen, Akademiska sjukhuset, ing 100, Uppsala 2023-02-03 kl 13:00
Night work is vital for maintaining our 24/7 society; however, in the long run, it may have adverse health consequences like obesity and Alzheimer’s disease. By performing one of the most extensive experimental in-laboratory studies to date, I sought to investigate how sleep deprivation impacts important features like how a person responds to others and how well a person can sustain attention and wakefulness during simulated night work. To this end, in Paper I, I used eye tracking to show that young adults were less visually attentive to faces after sleep deprivation, irrespective of the displayed emotion. Additionally, participants rated faces as less trustworthy and attractive after the nocturnal vigil. In conclusion, the observed effects suggest that night work may impact emotional regulation. Whether the change in face processing increases the odds of negative affect and social withdrawal remains unclear.
Using the same cohort in Paper II, I found that women and people with obesity struggled more with overnight wakefulness (measured by questionnaires, vigilance, and electroencephalography) than men and people with normal weight, respectively. Strikingly, these groups also exhibited increased blood levels of brain health biomarkers following total sleep loss. These results indicate that a person’s biological sex and weight status may moderate to which extent night work adversely affects brain health and occupational performance.
Sleep deprivation drives the development of obesity. However, whether similar mechanisms accounting for this weight-promoting effect of sleep loss apply to people who already have obesity is not well researched. Additionally, most experimental studies focused on the effects of acute sleep loss on the energy balance in men. With these gaps in mind, using the above-described cohort, Paper III focused on three prominent endocrine regulators of energy balance, namely leptin, known to promote satiety, and the hunger-promoting hormones ghrelin and adiponectin. Overall, I observed that lower blood leptin concentrations followed one night of total sleep deprivation while those of ghrelin and adiponectin increased. In addition, post-hoc analyses suggested some sex- and weight-specific differences in the hormonal response to sleep loss. For example, leptin dropped to a greater extent in women. These sex- and weight-specific differences must be replicated in larger studies.
While acute sleep loss may predispose humans to gain weight, what we eat can influence our sleep. At age 70, 970 participants from the Uppsala Longitudinal Study of Adult Men (ULSAM) filled out a seven-day food diary and questionnaires surveying for possible sleep problems. Thus, in Paper IV, I investigated whether healthy dietary habits were associated with lower odds of suffering from subjective sleep disturbances. Contrary to my hypothesis, neither the Mediterranean diet nor the Healthy Diet Indicator (based on WHO recommendations) was associated with sleep outcomes. Thus, more controlled interventional studies are needed to systematically evaluate how dietary habits may influence sleep in older men.