Insomnia is the most common sleep condition in the world, with half of adults globally reporting occasional episodes. Chronic insomnia, though far less prevalent, affects as many as 10 to 15 percent of the adult population.
Though these sleep problems are extremely common, the neurobiological mechanisms behind insomnia are not entirely understood. Research suggests that emotional stressors do play an outsized role in contributing to sleep problems, and it is well documented that mood and anxiety disorders are common comorbidities with insomnia. This seems like common sense. Emotional arousal, whether due to a state of anxiety or because of intrusive thoughts, makes it difficult to relax, thereby inhibiting one’s ability to either initiate sleep or get back to sleep after waking.
This line of reasoning suggests that researchers may come to better understand insomnia by examining the mechanisms underlying how our body responds to stress.
The Limbic System
The parts of the brain that are responsible for processing and responding to stress are collectively known as the limbic system. All animals possess some iteration of a limbic system, and it allows them to quickly respond to perceived threats. When a threat is identified, the limbic system jumps into action to prepare our bodies to either escape the threat or combat it. This reaction is known as the fight-or-flight response.
The fight-or-flight response is crucial for survival because it gives animals, including humans, a surge in neurotransmitters, which gives them a better chance to escape or fight back against predators. Anyone who has been startled and felt their heart began to race knows how powerful this response can be. However, the same system is activated for humans living in more modern settings even if the reason for the sudden spike in neurotransmitters is less than dire. Consequently, an approaching deadline or a potentially awkward future meeting may trigger the same biophysiological mechanism, even though these kinds of situations do not pose a significant threat to our existence.
The Anatomy of the Limbic System
The limbic system has two primary components, the amygdala and the hippocampus. The amygdala responds to stimuli by producing emotional responses, particularly feelings of fear or aggression, as well as positive emotions when the body senses arousing or pleasant stimuli. The hippocampus is responsible for the creation and consolidation of memory.
The limbic system also communicates with several other parts of the brain. In particular, the hypothalamus plays a major role in the limbic system, even though it also performs many other functions. The hypothalamus can be thought of as the body’s control center because it regulates much of the autonomic nervous system (ANS), which is responsible for controlling vital bodily functions that we do not have to think about. Some of these functions include breathing, blood pressure, body temperature, and heart rate, to name a few.
Activation of the Limbic System
When we perceive a danger, the amygdala sends distress signals to the hypothalamus, which in turn sends chemical messages to the adrenal glands to release epinephrine (or adrenaline) into the bloodstream. This boost in adrenaline activates a division of the ANS known as the sympathetic nervous system (SNS), which activates the physiological changes in the body that will ultimately help us fight off a threat or flee to safety. For example, as adrenaline courses through the body, it dilates airways in our lungs to bring more oxygen into the body, it causes our heart rates to increase to push more oxygen-rich blood to our muscles, and it releases enzymes that cause fat that has been stored in our bodies to be converted into glucose, which then gives us more energy. Even our eyesight and hearing get keener.
If the threat is not resolved immediately, the body can maintain this state of hyperawareness by activating what is known as the hypothalamic-pituitary-adrenal axis (HPA axis). This cascade of hormonal responses begins when the hypothalamus releases corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP), which tells the pituitary gland to release adrenocorticotropic hormone (ACTH). ACTH orders the adrenal glands to produce cortisol, which keeps the body in a state of alertness. For this reason, cortisol is often referred to as the “stress hormone.”
Once the threat has passed, another division of the autonomic nervous system, the parasympathetic nervous system (PNS), takes over and returns our bodies to a state of repose. The PNS is not only responsible for easing our bodies out of a state of heightened alertness; it also regulates sexual activity, salivation, digestion, urination, and defecation. Broadly speaking, the SNS involves fight-or-flight, the PNS involves feed and breed.
The Role of the Hippocampus in the Limbic System
Most memories are not merely collections of perceptions. They also include the way we felt at the time a memory was created because the amygdala and the hippocampus act in concert to encode memories with emotion. On the one hand, this conditions us to repeatedly participate in activities that are tied to positive emotions. On the other, it conditions us to avoid activities that are tied to negative emotions and allows us to be better prepared for a fight-or-flight scenario.
If we find ourselves in a dangerous situation and escape, we may become conditioned to avoid not only the situation itself, but activities or stimuli associated with that situation. Such a fear is not based on instinct, but rather on memory. As an extreme example, if one almost drowns in the ocean at a young age, this may create a fear not only of the ocean, but of any body of water.
While this interplay between emotion and memory may lead to various phobias that can be disruptive to one’s normal life, the connection is integral to survival. Without it, we would not be able to remember potential threats or dangerous activities. Such a person would be both fearless and most likely not long for this world.
The Limbic System and Sleep
The good news is that many of us no longer live in a world where we need to be constantly vigilant about predators or other potential dangers, but we are still hardwired to be ready to spring into action should a threat arise. Additionally, many of us have a difficult time shutting off the figurative “on switch” in our minds, which means that our stress levels remain high even when we are trying to lull ourselves to sleep.
This is a relatively normal, if unfortunate, occurrence. In most cases, once the cause of the stress is resolved, individuals can resume normal sleeping patterns. For those with insomnia, however, the stressor appears to be the lack of sleep, and the desire for sleep becomes a stressor in itself. In other words, the fixation on getting sleep leads to feelings of stress over not falling asleep, which begins a vicious loop. According to a model first proposed by Kales et al. in 1976, patients can develop a conditioned fear of not being able to sleep, which puts them in a state of hyperarousal when they attempt to fall asleep. This makes their inability to sleep a self-fulfilling prophecy.
Supplemental research has corroborated this model. A German study published in the journal Sleep in 2014 observed that patients with insomnia responded to insomnia-related stimuli with increased amygdala activity that is associated with negative emotions. Once again, this indicates that the fear of insomnia, which may be aroused by stimuli patients associate with insomnia, can be at the root of insomnia itself.
For clinicians, the authors of the study suggest that treatment options should include strategies that address the negative emotions associated with insomnia and sleep. This would include offering relaxation training (breathing techniques, meditation, guided imagery, etc.), as well as cognitive-behavioral treatment (CBT) in more difficult cases.
Ultimately, the objective may not be to merely to treat the patient’s insomnia, but to also treat the patient’s fear of insomnia and to resolve any negative emotions associated with sleep.
Dr. Ahmad reports no conflict of interest. He is not a speaker, advisor, or consultant and has no financial or commercial relationship with any biopharmaceutical entity whose product/device may have been mentioned in this article.
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