CLOSE

Neuroscientists Explain How Deep Breathing May Calm the Mind

Yoga and meditation practitioners claim that breathing can calm the mind. Skeptics may think this is all in their heads. Well, it is. In the brainstem, to be precise.

Researchers have found a subgroup of about 175 neurons in the brainstem of mice that seem to monitor breathing rhythms and influence how calm or aroused the animal is, according to the study published today in Science.

These neurons are found in the breathing control center in the brainstem, surrounded by several thousand neurons that generate the breathing rhythm used by respiratory muscles.

The newly identified neurons, however, are not involved in generating breathing rhythms. Mice that lack these neurons are still able to breathe, but become exceptionally calm. When put in a new environment with a lot of exciting odors that normally incite the animals to explore, these mice take a laid-back approach and spend most of their time sitting and grooming.

The finding reveals one way that neurons behind a basic autonomous function such as breathing can communicate with areas governing higher-order mental states. It could explain why yogis and meditators can use slow, controlled breathing to achieve tranquil states, and why people in stressful situations or during panic attacks may benefit from taking deep breaths.

In other words, just like your mental state influences how you breathe, your breathing rhythm can also influence how you feel.

“We think this is a two-way connection,” Kevin Yackle, a researcher now at UC-San Francisco and the study’s co-author, tells mental_floss. “These neurons are monitoring the breathing activity and then relaying it back to the rest of the brain to indicate what the animal is doing. This breathing signal then influences the brain state of the animal.”

A SERENDIPITOUS FINDING

This was an unexpected finding for the researchers, Yackle says.

The study’s goal was to paint a more accurate picture of how each type of neuron contributes to breathing. Understanding the details of this machinery can have important medical implications, Yackle says. In cardiology, for example, our detailed understanding of how the cardiac rhythm is generated has led to the development of medications that can control heart muscle contractions. “But when you think about breathing, we don't have any ways for pharmacologically controlling it,” Yackle says. Such a pharmacological approach could help preterm infants, for example, whose neural circuits for breathing are not fully developed, leaving them in need of mechanical ventilation.

The team started out by looking at a cluster of neurons called the preBötzinger Complex, which controls breathing rhythms. It was discovered in 1991 by Jack Feldman, a professor of neurobiology at UCLA and the co-author of the current study. (The same team recently revealed the biological importance of sighing.) The goal was to identify the different subsets of neurons within this cluster and find what each type of neuron does to contribute to breathing.

The researchers landed on a small group of 175 neurons with a particular genetic profile that suggested a crucial role in generating the breathing rhythm. But killing these cells in the brainstem of mice proved that their guess was wrong. The mice continued to breathe normally.

“I was really disappointed,” Yackle recalls. “But we had put so much effort in the project by that point that I just continued looking at it, trying to find what was happening.”

However, Yackle soon noticed one subtle difference: The mice were breathing more slowly.

An illustration of the pathway (green) that directly connects breathing center to arousal center and rest of the brain. Image Credit: Kevin Yackle, Lindsay A. Shwarz, Kaewen Kam, Jordan M. Sorokin, John R. Huguenard, Jack L. Feldman Liqun Luo, and Mark Krasnow

 

A CLOSED LOOP

One way to explain a shift like that was to imagine that the breathing pattern was influenced by the mental state of the animals. The researchers found more evidence for this idea.

Usually, mice explore a new cage by sniffing all throughout it. If the idea about a connection between breathing and the rest of the brain is true, then these bursts of short deep breaths could reinforce the alert state of the exploring animals, creating a feedback loop. But if a key component in this chain is missing, the loop is broken. When the researchers tested this theory, as expected, the mice that lacked the subgroup of neurons appeared less aroused than their unaffected cagemates when put in stimulating environments. The animals’ brain waves patterns, measured by EEG, also suggested a calm mental state.

Tracing the neurons revealed that they connect to another part of the brainstem, locus coeruleus, which is known for its role in physiological responses to stress, as well as alertness and attention.

“We think that these neurons in the breathing center are relaying the breathing signal to the locus coeruleus, and by doing this they are basically sending a signal throughout many parts of the brain that then can cause change in arousal,” Yackle says.

The authors note that panic attacks triggered by respiratory symptoms are responsive to clonidine, a drug that "silences" the locus coeruleus. Deep breathing could play a similar role, quelling the arousal signals coming from this subgroup of respiratory neurons to the locus coeruleus.

"Although breathing is generally thought of as an autonomic behavior, higher-order brain functions can exert exquisite control over breathing," they write. "Our results show, conversely, that the breathing center has a direct and powerful influence on higher-order brain function."

It would be challenging to test this directly in humans. But indirect evidence from other studies suggests that breathing can influence brain states.

For example, sleep researchers have shown that in sleeping people, a change in breathing pattern sometimes precedes periods of brain activity that resemble an alert or wakeful state.

nextArticle.image_alt|e
iStock
arrow
science
Why Is Your First Instinct After Hurting Your Finger to Put It in Your Mouth?
iStock
iStock

If you close your fingers in a car door or slam your funny bone into a wall, you might find your first reaction is to suck on your fingers or rub your elbow. Not only is this an instinctive self-soothing behavior, it's a pretty effective technique for temporarily calming pain signals to the brain.

But how and why does it work? To understand, you need to know about the dominant theory of how pain is communicated in the body.

In the 17th century, French scientist and philosopher René Descartes proposed that there were specific pain receptors in the body that "rang a bell in the brain" when a stimulus interacted with the body, Lorne Mendell, a professor of neurobiology and behavior at Stony Brook University in New York, tells Mental Floss. However, no study has effectively been able to identify receptors anywhere in the body that only respond to painful stimuli.

"You can activate certain nerve fibers that can lead to pain, but under other circumstances, they don't," Mendell says. In other words, the same nerve fibers that carry pain signals also carry other sensations.

In 1965, two researchers at MIT, Patrick Wall and Ronald Melzack, proposed what they called the gate control theory of pain, which, for the most part, holds up to this day. Mendell, whose research focuses on the neurobiology of pain and who worked with both men on their pain studies, explains that their research showed that feeling pain is more about a balance of stimuli on the different types of nerve fibers.

"The idea was that certain fibers that increased the input were ones that opened the gate, and the ones that reduced the input closed the gate," Mendell says. "So you have this idea of a gate control sitting across the entrance of the spinal cord, and that could either be open and produce pain, or the gate could be shut and reduce pain."

The gate control theory was fleshed out in 1996 when neurophysiologist Edward Perl discovered that cells contain nociceptors, which are neurons that signal the presence of tissue-damaging stimuli or the existence of tissue damage.

Of the two main types of nerve fibers—large and small—the large fibers carry non-nociceptive information (no pain), while small fibers transmit nociceptive information (pain).

Mendell explains that in studies where electric stimulation is applied to nerves, as the current is raised, the first fibers to be stimulated are the largest ones. As the intensity of the stimulus increases, smaller and smaller fibers get recruited in. "When you do this in a patient at low intensity, the patient will recognize the stimulus, but it will not be painful," he says. "But when you increase the intensity of the stimulus, eventually you reach threshold where suddenly the patient will say, 'This is painful.'"

Thus, "the idea was that shutting the gate was something that the large fibers produced, and opening the gate was something that the small fibers produced."

Now back to your pain. When you suck on a jammed finger or rub a banged shin, you're stimulating the large fibers with "counter irritation," Mendell says. The effect is "a decrease in the message, or the magnitude of the barrage of signals being driven across the incoming fiber activation. You basically shut the gate. That is what reduces pain."

This concept has created "a big industry" around treating pain with mild electrical stimulation, Mendell says, with the goal of stimulating those large fibers in the hopes they will shut the gate on the pain signals from the small fibers.

While counter irritation may not help dull the pain of serious injury, it may come in handy the next time you experience a bad bruise or a stubbed toe.

nextArticle.image_alt|e
Jamie McCarthy/Getty Images for Bill & Melinda Gates Foundation
arrow
Medicine
Bill Gates is Spending $100 Million to Find a Cure for Alzheimer's
Jamie McCarthy/Getty Images for Bill & Melinda Gates Foundation
Jamie McCarthy/Getty Images for Bill & Melinda Gates Foundation

Not everyone who's blessed with a long life will remember it. Individuals who live into their mid-80s have a nearly 50 percent chance of developing Alzheimer's, and scientists still haven't discovered any groundbreaking treatments for the neurodegenerative disease [PDF]. To pave the way for a cure, Microsoft co-founder and philanthropist Bill Gates has announced that he's donating $100 million to dementia research, according to Newsweek.

On his blog, Gates explained that Alzheimer's disease places a financial burden on both families and healthcare systems alike. "This is something that governments all over the world need to be thinking about," he wrote, "including in low- and middle-income countries where life expectancies are catching up to the global average and the number of people with dementia is on the rise."

Gates's interest in Alzheimer's is both pragmatic and personal. "This is something I know a lot about, because men in my family have suffered from Alzheimer’s," he said. "I know how awful it is to watch people you love struggle as the disease robs them of their mental capacity, and there is nothing you can do about it. It feels a lot like you're experiencing a gradual death of the person that you knew."

Experts still haven't figured out quite what causes Alzheimer's, how it progresses, and why certain people are more prone to it than others. Gates believes that important breakthroughs will occur if scientists can understand the condition's etiology (or cause), create better drugs, develop techniques for early detection and diagnosis, and make it easier for patients to enroll in clinical trials, he said.

Gates plans to donate $50 million to the Dementia Discovery Fund, a venture capital fund that supports Alzheimer's research and treatment developments. The rest will go to research startups, Reuters reports.

[h/t Newsweek]

SECTIONS

arrow
LIVE SMARTER
More from mental floss studios