Marketing Scoops: Research Discovered Something Unsettling About Sleeping Pills

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You’ve probably heard of your body’s lymphatic system, but what about the glymphatic system? As the authors of a 2022 paper in Nature Reviews Drug Discovery phrased it, it’s “a fluid clearance pathway in the central nervous system” in other words, something that clears out old fluids and replaces them with fresh versions on a regular basis. However, a recent study published in the journal Cell shows evidence that sleeping pills can interfere with this system……Continue reading…..

By: Tobias Carroll

Source: InsideHook

Critics:

A publication by L. Xie and colleagues in 2013 explored the efficiency of the glymphatic system during slow wave sleep and provided the first direct evidence that the clearance of interstitial waste products increases during the resting state. Using a combination of diffusion iontophoresis techniques pioneered by Nicholson and colleagues, in vivo 2-photon imaging, and electroencephalography to confirm the wake and sleep states.

Xia and Nedergaard demonstrated that the changes in efficiency of CSF–ISF exchange between the awake and sleeping brain were caused by expansion and contraction of the extracellular space, which increased by ~60% in the sleeping brain to promote clearance of interstitial wastes such as amyloid beta. On the basis of these findings, they hypothesized that the restorative properties of sleep may be linked to increased glymphatic clearance of metabolic waste products produced by neural activity in the awake brain.

Pathologically, neurodegenerative diseases such as amyotrophic lateral sclerosis, Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease are all characterized by the progressive loss of neurons, cognitive decline, motor impairments, and sensory loss. Collectively these diseases fall within a broad category referred to as proteinopathies due to the common assemblage of misfolded or aggregated intracellular or extracellular proteins.

According to the prevailing amyloid hypothesis of Alzheimer’s disease, the aggregation of amyloid-beta (a peptide normally produced in and cleared from the healthy young brain) into extracellular plaques drives the neuronal loss and brain atrophy that is the hallmark of Alzheimer’s dementia. Although the full extent of the involvement of the glymphatic system in Alzheimer’s disease and other neurodegenerative disorders remains unclear, researchers have demonstrated through experiments with genetically modified mice that the proper function of the glymphatic clearance system was necessary to remove soluble amyloid-beta from the brain interstitium.

In mice that lack the AQP4 gene, amyloid-beta clearance is reduced by approximately 55 percent. The glymphatic system also may be impaired after acute brain injuries such as ischemic stroke, intracranial hemorrhage, or subarachnoid hemorrhage. In 2014, a group of researchers from the French Institute of Health and Medical Research (INSERM) demonstrated by MRI that the glymphatic system was impaired after subarachnoid hemorrhage, because of the presence of coagulated blood in the paravascular spaces.

Injection of tissue plasminogen activator (a fibrinolytic drug) in the CSF improved glymphatic functioning. In a parallel study, they also demonstrated that the glymphatic system was impaired after ischemic stroke in the ischemic hemisphere, although the pathophysiological basis of this phenomenon remains unclear. Notably, recanalization of the occluded artery also reestablished the glymphatic flow.

Familial natural short sleep is a rare, genetic, typically inherited trait where an individual sleeps for fewer hours than average without suffering from daytime sleepiness or other consequences of sleep deprivation. This process is entirely natural in this kind of individual, and it is caused by certain genetic mutations. A person with this trait is known as a “natural short sleeper”. This condition is not to be confused with intentional sleep deprivation, which leaves symptoms such as irritability or temporarily impaired cognitive abilities in people who are predisposed to sleep a normal amount of time but not in people with FNSS.

This sleep type is not considered to be a genetic disorder nor are there any known harmful effects to overall health associated with it; therefore it is considered to be a genetic, benign trait. The genes DEC2, ADRB1, NPSR1 and GRM1 are implicated in enabling short sleep. The quality of sleep may be evaluated from an objective and a subjective point of view. Objective sleep quality refers to how difficult it is for a person to fall asleep and remain in a sleeping state, and how many times they wake up during a single night.

Poor sleep quality disrupts the cycle of transition between the different stages of sleep. Subjective sleep quality in turn refers to a sense of being rested and regenerated after awaking from sleep. A study by A. Harvey et al. (2002) found that insomniacs were more demanding in their evaluations of sleep quality than individuals who had no sleep problems. Homeostatic sleep propensity (the need for sleep as a function of the amount of time elapsed since the last adequate sleep episode) must be balanced against the circadian element for satisfactory sleep.

Along with corresponding messages from the circadian clock, this tells the body it needs to sleep. The timing is correct when the following two circadian markers occur after the middle of the sleep episode and before awakening: maximum concentration of the hormone melatonin, and minimum core body. Human sleep-needs vary by age and amongst individuals; sleep is considered to be adequate when there is no daytime sleepiness or dysfunction.

Moreover, self-reported sleep duration is only moderately correlated with actual sleep time as measured by actigraphy, and those affected with sleep state misperception may typically report having slept only four hours despite having slept a full eight hours. Researchers have found that sleeping 6–7 hours each night correlates with longevity and cardiac health in humans, though many underlying factors may be involved in the causality behind this relationship.

Sleep difficulties are furthermore associated with psychiatric disorders such as depression, alcoholism, and bipolar disorder. Up to 90 percent of adults with depression are found to have sleep difficulties. Dysregulation detected by EEG includes disturbances in sleep continuity, decreased delta sleep and altered REM patterns with regard to latency, distribution across the night and density of eye movements. Sleep duration can also vary according to season. Up to 90% of people report longer sleep duration in winter, which may lead to more pronounced seasonal affective disorder.

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