The Relationship Between Stress & Insomnia
Sleep is a biological process that involves communication between multiple body systems, and its relationship with stress plays an important role. The hypothalamic-pituitary-adrenal (HPA) axis and sleep interact in multiple ways to maintain alertness as well as the body’s physiological response to stress. Dysfunction and, in particular, hyper-reactivity within the HPA axis can often be the cause of sleep disruptions as the role of hormones such as cortisol and corticotrophin-releasing hormone (CRH) are both involved in circadian-dependent wake rhythms and modulation of the stress response.
The prevalence of both stress and insomnia in the United States is high, with between 10 to 30 percent of adults struggling with chronic insomnia and 44 percent reporting an increase in psychological stress over the past five years.1,2 Stress tends to acutely worsen sleep, and cortisol is a key hormone secreted during the stress response. In insomnia, cortisol release increases particularly in the evening and at the start of the sleep period, and in chronic insomnia the activity of both limbs of the stress system (i.e., the HPA axis and sympathetic system) positively relate to the degree of an individual’s objective sleep disturbance.3 Therefore, supporting adaptivity to stress and reducing HPA overactivation can play an important role in promoting healthy levels of restorative sleep.
What is Restorative Sleep?
Non-restorative sleep (NRS) affects 10 percent of people worldwide, leading to poor sleep quality as well as physical and cognitive fatigue.4 Restorative sleep consists of more than just what occurs over a few hours at night. Instead, it involves the completion of all stages of sleep alongside the physiological changes that occur within the course of a day that allow the brain and various body systems to repair, heal, and grow. There are four sleep stages identified by the American Academy of Sleep Medicine grouped by their classification as “non-REM” (NREM) and “REM,” and each night is comprised of several alternating cycles.
These stages are defined primarily by electroencephalographic criteria where the frequency spectrum of the electroencephalogram (EEG) is shifted toward lower values during deeper sleep, and the waking state is characterized by higher frequencies. The fluctuation from NREM and REM is considered part of a circadian rhythm, which is the sleep/wake cycle completed within 24 hours. Each sleep stage is important, with slow-wave sleep considered to be the deepest stage of sleep and which is most difficult to awaken from.5
(delta or slow-wave sleep, SWS)
|Stage REM (rapid eye movement sleep)||
Sleep and the HPA Axis
Dysfunction of the HPA axis may play a causative role in insomnia, as there is a known association between CRH, cortisol and their effects on sleep EEG. Increases in EEG frequency tend to negatively impact sleep, causing lighter sleep and wakefulness, and CRH appears to be an important factor in increasing sleep EEG.6 Under normal conditions, CRH is released in a circadian-dependent, pulsatile fashion from the hypothalamus. Accordingly, cortisol secretion is lowest around midnight and begins to rise approximately 2-3 hours after sleep onset and continually thereafter into the early waking hours. Cortisol levels are highest in the morning, and as the day continues there is a gradual decline and leveling-off as the cycle repeats again. Sleep initiation (and slow wave sleep in particular) occurs concurrently with low HPA axis activation, and cycles of REM sleep tend to begin as cortisol levels begin to fall.7 Moreover, nocturnal awakenings are associated with pulsatile releases of cortisol.8
The Role of Adaptogens
Interventions aimed at normalizing HPA axis dysfunction may be considered beneficial for treating underlying physiological disturbances in many cases of stress and insomnia. Herbal treatments aimed at decreasing nocturnal HPA axis hyperactivity (namely CRH and cortisol) may play an important role when utilized throughout the day and in the evening to subsequently support slow wave and restorative sleep throughout the night. These plants are collectively referred to as adaptogens, and though each plant will have its own unique traits, their overall therapeutic effects are achieved in large part through adaptation and alteration of the HPA axis and cortisol activity.
Adaptogenic herbs such as Ashwagandha (Withania somnifera) and Schisandra (Schisandra chinensis) are both key examples known for their anxiolytic, sedating, and cortisol-modulating effects. 9-12 An animal study showed that lignans from Schisandra significantly improved sleep quality, increased sleep time, shortened sleep latency, and prolonged sleep duration.13 In one study with Ashwagandha, the root extract given over 10 weeks was found to improve sleep quality and sleep onset latency in patients with insomnia.14 In another, Ashwagandha was specifically evaluated for its ability to improve overall sleep quality in subjects diagnosed with non-restorative sleep, and over six weeks, those who received treatment reported a 72 percent increase in sleep quality (compared with 29 percent in the placebo group).15