Sleep epigenetics is the field of how epigenetics (heritable characteristics that do not involve changes in DNA sequence) affects sleep.
Research in the field of epigenetics has time and time again proven the significance of various environmental experiences. Changes in sleep can cause critical changes to the epigenome, while changes to the epigenome can, in turn, have a crucial influence on experiences related to sleep. Early life experiences with stress can produce lifelong changes in the number of glucocorticoid receptors and impair sleep. Additionally, sleep deprivation alters individuals’ epigenome via changes to methylation, histones, and non-coding RNA. The development of sleep disorders such as insomnia, sleep apnea, and narcolepsy can be greatly impacted by epigenetic changes. Additionally, various methods have been discovered that can reverse, prevent, and treat sleep-related issues by causing epigenetic changes.
Stress
Exposure to stress, particularly during early life, has significant impacts on an individual's response to future experiences of stress. Research on epigenetic changes caused by differences in the amount of time rats were nurtured by their mother is one example of these significant impacts. When examining the epigenome of rat offspring, it is noted that alterations to the epigenome occur at the glucocorticoid receptor (GR) gene promoter in the hippocampus. This happens when the offspring experience a significant amount of licking and grooming from their mother at an early age. The offspring that experience a significant amount of licking and grooming develop differences in DNA methylation compared to the offspring that receive an insignificant amount of licking and grooming. The offspring that are inadequately nurtured by their mother become highly susceptible to stressful environments. These epigenetic differences can be seen as early as the first week of life and persist into adulthood. However, evidence shows that when offspring are cross-fostered to receive a good amount of licking and grooming, the epigenetic differences are reversed, supporting a causal relationship between the maternal effect and the epigenetic stress responses in offspring. This proposes that the offspring's epigenome can be altered and established through early life experiences.
The effect of stress on sleep can be predicted long before a baby is born. It is hypothesized that increasing cortisol levels in mothers reduces the amount of glucocorticoid receptors (GRs) in an infant's hippocampus, lowering the physiological role of the negative feedback loop on the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis is important for regulating the wake-sleep cycle but works with other factors that help modulate sleep as well. When the negative feedback loop is disrupted due to stress, the HPA axis in newborns becomes hyperactive and the amount of cortisol in circulation elevates. However, the hyperactivity of the HPA axis and the elevated levels of cortisol in the hippocampus can be reversed or lowered to normal levels after demethylation of the hippocampal GR promoter, further providing evidence of the involvement of epigenetic mechanisms in HPA axis modifications.
Glucocorticoids are a necessity for life. They play a large role in a majority of physiological functions involving metabolism, blood pressure, breathing, the immune system, and behavior. Either acute or chronic stress can alter the response of the HPA axis. However, the stage of life at which an individual is exposed to stress will determine the magnitude of the consequences they will face in the future. Early life exposure to stress during the critical period of childhood development can result in permanent changes to adult response systems.