The Neurons Brain Circuit That Causes Insomina Linked To Stress And The Immune System

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Your Immune System Can Be Weakened From Insomnia Caused By Chronic Stress

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It is a well known fact that psychosocial or environmental stress can negatively affect the body’s immune function.

Insomnia is also commonly associated with stress.

But the question now is, do these two stress-induced conditions share the same neural circuitry?

A new study, conducted by neuroscientists from Stanford University, at Cold Spring Harbor Laboratory (CSHL) have identified the circuit in the brain that is responsible for sleepless nights in times of stress—and it turns out that, that circuit does more than make count sheep.

Their study with mice, ties the same neuronal connections that trigger insomnia to stress-induced changes in the immune system, which weaken the body’s defenses against a host of threats.

In mice, they found that signals from the hormone-releasing brain cells have a strong effect on the insomnia-inducing neurons.

Interfering with that connection enabled mice to sleep peacefully even after being exposed to a stressful situation, whereas artificial simulation of the stress-sensitive cells instantly roused slumbering animals.

The study, reported on September 9, 2020, in the journal Science Advances, connects and explains two familiar problems, says CSHL Assistant Professor Jeremy Borniger.

“This sort of stress-induced insomnia is well known among anybody that’s tried to get to sleep with a looming deadline or something the next day,” he says.

“And in the clinical world, it’s been known for a long time that chronically stressed patients typically do worse on a variety of different treatments and across a variety of different diseases.”

“It seems like it’s a pretty sensitive switch, in that even very weak stimulation of the circuit can drive insomnia,” says Borniger.

Like many aspects of the body’s stress response, these effects are thought to be driven by the stress hormone cortisol.

Working in the Stanford lab of Luis de Lecea, where Borniger completed a postdoctoral fellowship prior to joining CSHL, the research team found a direct connection between stress-sensitive neurons in the brain that trigger cortisol’s release and nearby neurons that promote insomnia.

The same connection, they found, also has a potent effect on the immune system. Stress significantly disrupts the abundance of certain immune cells in the blood, as well signaling pathways inside them, and the team was able to recreate these changes simply by stimulating the same neurons that link stress to insomnia.

Understanding this circuitry opens the door to a deeper understanding of the consequences of stress, not just in healthy individuals but also in persons with certain types of disease.

Borniger says understanding how stress triggers both insomnia and immunosuppression helps researchers look to novel treatments for a number of autoimmune diseases.

Interfering with this brain circuit could offer new ways to treat disease. And, of course, new ways to potentially reduce the negative effects of stress on our sleep.

He continues: “I’m really interested in how we can manipulate distinct circuits in the brain to control not just the immune system at baseline, but in disease states like inflammatory bowel disease or in cancer or in psoriasis–things that are associated with systemic inflammation.”

“Because if we can understand and manipulate the immune system using the natural circuitry in the body rather than using a drug that hits certain targets within the system, I think that would be much more effective in the long run, because it just co-opts the natural circuits in the body.”

Very interesting and informative!

What do you think about these new discoveries, especially pertaining to the chronic stressors in your daily life, and your immune system? You must give serious considerations to these matters, as a matter of top priority in putting yourself in the best position to combat the Coronavirus.

The new study was published in the journal Science Advances.