It’s not always obvious which of the multitude of species of bacteria riding around in us should be classified as germs and attacked, and which are essential workers that should be nurtured.

One that’s particularly hard to classify is H. pylori, which was the subject of the 2005 Nobel Prize for the discovery that it causes peptic ulcers. But more recent studies have connected it with benefits, including lowering the risk of esophageal cancer. In a paper published in Science Advances, researchers in Sweden described how the bacteria can inhibit the formation of amyloid deposits, which are found in the brains of individuals with Alzheimer’s and Parkinson's disease.

Scientists are just beginning to understand the microbes that have been with us for millennia — the so-called microbiome, which is being drastically depleted as an unintended consequence of antibiotic use, dietary changes, and other aspects of modern life.

Until the start of the 20th century, we all carried H. pylori. Now, it’s headed for global extinction. But before it disappears, it’s worth understanding what it does and why we all once carried it.

While many doctors are happy to say good riddance to H. pylori — which also has been associated with stomach cancer — scientists are discovering more positive benefits, including a few studies that have shown it might also lower the risk of asthma and allergies and help protect against obesity and Type 2 diabetes. As I’ve written previously, this stomach bug is a feature of our biology, not just a problem that needs to be eliminated.

These newest findings on its effects related to amyloid deposits identified a protein called CagA — secreted by most strains of human H. pylori — as the key component. That doesn’t necessarily mean CagA protects us against Alzheimer’s; scientists don’t know whether amyloid deposits are a cause of the disease, a symptom, or an attempt by the body to slow its progression.

Still, researchers continue to study the protein, which may lead to new strategies for preventing the disease. The findings also add to a growing understanding of the connection between the microbiome and the risk of developing Alzheimer’s and other neurodegenerative diseases.

They also serve as a warning: we don’t know enough about the unintended consequences of eradicating H. pylori. Genetic comparisons suggest that the bacteria have been residing in the human stomach for at least 60,000 years, and likely much longer.

Biologist Martin Blaser of Rutgers University has been one of the most vocal advocates for understanding the pros and cons of H. pylori, which he describes in his 2014 book, Missing Microbes: How the Overuse of Antibiotics is Fueling Our Modern Plagues. He said every mammal has some stomach bacteria — a relative of our H. pylori.

He was particularly excited by the findings on CagA. It was his work that initially identified the protein and showed that the only so-called CagA-positive strains were more closely connected to all health risks and benefits, including ulcers and stomach cancers, as well as a decreased risk of asthma and esophageal cancer. He later collaborated on a study that suggested a connection between the CagA-positive strains and decreased risk of stroke. “The protein is a double-edged sword,” he said.

Biologist Gefei Chen of Uppsala University in Sweden, one of the amyloid study researchers, said the CagA protein prevents other bacteria from forming communities called biofilms. This ability gives H. pylori an edge over competitors by preventing would-be rivals from forming the biofilms they would need to colonize the stomach. The effect on our health may be either beneficial, detrimental, or a combination of both.

The biofilms are held together with a scaffolding that is similar to the deposits found in the brains of Alzheimer’s patients. Chen said he wanted to see if the protein from the bacteria could also affect amyloid deposits in the brain. He and his colleagues created deposits in the lab and exposed them to CagA. “It works so well, it's so efficient ... that's a big surprise for us.”

He’s currently using gene editing to modify H. pylori to determine whether it can be altered to control its function in the body. CagA could also be used to break up bacterial biofilms, which, like walled cities for bacteria, can prevent antibiotics from reaching infections. Harmful biofilms can also coat medical devices, such as catheters, and they form the stubborn plaque on our teeth.

Blaser said H. pylori is quickly disappearing — even without our help. He anticipates there may come a time when we’ll attempt to regain it. Perhaps it will be an edited version that highlights the benefits of the bacteria without its downsides.

It was an oversimplification to consider that microbes are all either good or bad. Our microbes are evolving in ways that help them to survive and reproduce, which may benefit or harm us depending on our stage of life and other environmental factors. They might be good in one part of the body and one stage of life, but bad in another part at another stage. It’s not in their evolutionary interest to kill us, their hosts.

Perhaps someday doctors will be able to tip the balance toward the bacteria’s benefits — with probiotics, perhaps, or even with gene editing. However, our microbial diversity is half of what it was in pre-industrial societies, and it is declining rapidly. Scientists must act quickly to understand what these bugs do while we still have them.

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This column reflects the personal views of the author and does not necessarily reflect the opinion of the editorial board or Bloomberg LP and its owners.

F.D. Flam is a Bloomberg Opinion columnist covering science. She is host of the “Follow the Science” podcast.

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