Friday, June 02nd, 2023

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New science proves that merely BREATHING fights off respiratory viruses – now we know why they push masks

New science proves that merely BREATHING fights off respiratory viruses – now we know why they push masks

(Natural News) For the past two years, the world was told that wearing a face covering would stop the spread of the Wuhan coronavirus (Covid-19) and keep everyone “safe.” The truth, though, is that masks interfere with breathing, which a new Harvard University study found is one of the ways that the human body wards off infections.

The natural exchange of carbon dioxide (CO2) waste for fresh oxygen in the lungs, also known as respiration, is a powerful antiviral activity that masks directly interfere with, putting the body at risk.

Inside your lungs are tiny sacs that exchange CO2 for oxygen. With every breath you take, these alveoli facilitate the transaction of CO2, which your body exhales, for oxygen, which your body inhales. This process oxygenates your blood and boosts immune function.

A mask, however, traps CO2 inside the lungs while blocking oxygen intake. This creates a chemical imbalance inside the body, leaving it prone to infection and disease (Related: More than 400 studies prove that masks provide no benefits and are harmful.)

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The “authorities” told everyone that masks would end the plandemic, but this latest science suggests that masks more than likely made it worse. How many people ended up getting sick and dying because of the mask mandates, we wonder?

Who knew that proper breathing is a natural anti-viral?

Published in the journal Nature Communications, the Harvard study utilized a “lung chip” to mimic the mechanical forces of breathing to tests “dead” influenza bugs.

Researchers evaluated how breathing impacts the uptake of these bugs, to which they discovered that respiration is basically an anti-viral activity that the body engages in automatically.

“This research demonstrates the importance of breathing motions for human lung function, including immune responses to infection, and shows that our Human Alveolus Chip can be used to model these responses in the deep portions of the lung, where infections are often more severe and lead to hospitalization and death,” said co-author Dr. Haiqing Bai from Harvard’s Wyss Institute.

The simple act of breathing also exercises the lungs, stretching and relaxing them with every inhale and exhale. This natural motion influences both the development and vital function of the lungs, which naturally combats infection.

Two parallel microfluidic channels were lined with different types of living human cells, recreating the interface between human air sacs and their blood-transporting capillaries. The upper channel was given alveolar lung cells while the lower channel was given lung blood vessel cells.

The channel lined with alveolar cells was then pumped with air while the blood vessel channel was provided with a flowing culture medium containing nutrients that are normally delivered by the blood.

The research team then separated the two channels using a porous membrane that allowed molecules to flow between them before pumping H3N2 influenza into them. Upon doing this, they noticed several hallmarks of infection, including the breakdown of junctions between cells, a 25 percent increase in cell death, an increase in levels of multiple inflammatory cytokines, and the initiation of cellular repair programs.

The blood vessel cells of infected chips also expressed much higher levels of immune cells, though there was 50 percent less viral mRNA observed in the alveolar channels of chips exposed to natural breathing motions, as well as a massive reduction in inflammatory cytokine levels.

A follow-up genetic analysis revealed that the mechanical strain activated molecular pathways associated with immune defense and multiple antiviral genes. When the cyclical stretching stopped, however, mimicking no more breathing, these activations reversed.

“This was our most unexpected finding – that mechanical stresses alone can generate an innate immune response in the lung,” said fellow co-author Prof. Longlong Si.

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