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Ill sleep exacerbates pain. Maybe scientists have figured out why



Sleep deprivation can interfere with the body’s endocannabinoid system’s regular operations.

Sleep is impeded by pain, and pain is exacerbated by sleep deprivation. It’s a vicious cycle where one ailment feeds the other. The numerous comorbid disorders of sleep insufficiency, such as stress, exhaustion, anxiety, depression, and a weakened immune system, may then get worse as a result. The one-third of adult Americans who report having a sleep disturbance or not getting enough sleep are probably familiar with this issue.

Regretfully, medical practitioners are unaware of the fundamental processes that keep this cycle going. The immune system, the pineal gland, and portions of the central nervous system that are not connected to the brain are just a few of the systems in the body that are involved in both circadian rhythm and pain perception. The issue is a medical enigma, a convoluted “whodunit?” in which nobody jumps out as the primary suspect.

However, a recent study headed by experts at the Massachusetts General Research Institute may have found a crucial hint in the thalamus, more precisely in the region known as the “thalamic reticular nucleus.” It is a relay center that uses a network of nerve fibers to transmit information to the outermost layers of the brain. It is essential to the sleep-wake cycle, attentional regulation, and the processing of sensory data, including pain.

For these reasons, the researchers postulated that it could aid in our comprehension of how sleep disruption affects sensitivity to pain. And their research offers hope for a potential solution that could one day lessen or possibly end the cycle.

More than just relaxation for beauty

In order to measure how quickly the mice would leave the pen, the researchers would pinch the mice or heat up a particular area of the floor. They discovered that the mice who had not had enough sleep were considerably more sensitive to these irritants and quickly withdrew. These findings corroborated human self-reports that indicated increased sensitivity and greater pain scores were caused by sleep disruption.

Subsequently, the metabolites within the thalamic reticular nucleus of the mice’s brains were examined by the researchers. Mice lacking sleep had reduced NADA levels in their bodies.

NADA is a member of the neurotransmitter family that stimulates the body’s endocannabinoid system receptors. Research on this cell-signaling system is still in its infancy, having only been identified in 1988. However, the research indicates that the system is involved in numerous physiological processes, including immune response, metabolism, sleep, and pain management. These are the most significant physiological processes for our objectives.

The thalamic reticular nucleus’s cannabinoid receptors were less active in the absence of NADA, and this may have had an impact on how pain was perceived. In order to test this, the scientists used a microinjection of NADA into the mice’s brains. The mice who got this injection experienced a restoration to normal pain sensitivity. This finding implies that the reduction of pain sensitivity during sleep deprivation is dependent on both the synthesis of NADA and the activation of cannabinoid receptors.

Shiqian Shen, co-senior author of the study and clinical director of Massachusetts General Hospital’s Tele Pain Program, said, “We provide a mechanism as to how sleep disruption leads to exaggerated pain, suggesting that harnessing the endocannabinoid system might break the vicious cycle between pain and sleep loss.”

Enough NADA

Obviously, human outcomes from mouse research are not always comparable. They merely make suggestions and point to potential areas of further research that could be useful. Nevertheless, the scientists point out that their findings are a part of an expanding corpus of knowledge about the endocannabinoid system.

The article cites a number of pharmacological investigations that demonstrate the dual effects of NADA on pain signal transmission and inhibition in the nervous system. They also mention the connection between endocannabinoids, such as NADA, and a number of neurological conditions, including epilepsy, Parkinson’s disease, and Alzheimer’s.

The findings of this study imply that further investigation into the physiological functions of NADA, which the researchers note is presently mainly absent, may pave the way for novel therapeutic approaches that could aid in the treatment of many neurological illnesses as well as the pain-sleep cycle.


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