An analysis of more than 17 million people in England — the largest study of its kind, according to its authors — has pinpointed a bevy of factors that can raise a person’s chances of dying from COVID-19, the disease caused by the coronavirus.

The paper, published Wednesday in Nature, echoes reports from other countries that identify older people, men, racial and ethnic minorities, and those with underlying health conditions among the more vulnerable populations.

“This highlights a lot of what we already know about COVID-19,” said Uchechi Mitchell, a public health expert at the University of Illinois at Chicago who was not involved in the study. “But a lot of science is about repetition. The size of the study alone is a strength, and there is a need to continue documenting disparities.”

Once an ecosystem is disturbed, restoring it can be difficult. And when the disturbed ecosystem is a patient’s microbiome, restoring the patient to health can be even more difficult. Just one ecosystem element that proliferates or diminishes beyond bounds may throw multiple elements into disarray, creating a dysbiosis that resists simple remedies.

Because a patient’s microbiome consists of interacting elements—including elements that extend beyond the microbiome itself—these elements cannot be seen in isolation. Rather, they are dynamic parts of a systemic whole. Touch any one of them, and the effects of doing so may ripple outward in unpredictable ways—unless the elements and their interactions are thoroughly understood.

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“We are covered by, and protected by, and interacted with by vast microbial ecosystems,” says Julius Goepp, MD, founder of Scaled Microbiomics. Everywhere the body comes into contact with the outside environment, you’ll find a thriving community of microbes. This includes places that are obviously “external”—like skin and hair (including the skin and hair of underarms and nostrils)—as well as places that we consider to be “internal,” like the gastrointestinal tract.

“The surface of our gut is continuous with the outside world,” Goepp points out. The miracle of our gut, he continues, is that it can transport “two pounds of very nasty material [while keeping] it one cell layer away from our precious, sterile, inside tissue.”

But one cell layer can prove precarious protection, especially if that microbial ecosystem gets out of balance. The gut’s microbial ecosystem, Goepp suggests, is like the Amazon rainforest ecosystem in that it is resilient, but only to a point. When subjected to stressors such as prolonged exposure to antibiotics, a diet high in certain additives and low in fiber, and environmental pollution, the microbial ecosystem can be tipped far enough out of balance that a new normal becomes established. This is called dysbiosis, and it’s increasingly linked with a number of noncommunicable diseases, such as diabetes, neurodegenerative diseases, and cancer.

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Elderly people are more prone to infectious diseases as the function of their immune system continuously declines with progression of age. This becomes especially apparent during seasonal influenza outbreaks or the occurrence of other viral diseases such as COVID-19. As the efficacy of vaccination in the elderly is strongly reduced, this age group is particularly vulnerable to such infectious pathogens and often shows the highest mortality rate. In addition to the age-related immune decline aged individuals are commonly affected by frailty that negatively impacts quality-of-life. Even though the average life-expectancy for humans continuous to rise, living longer is often associated with age-related health issues.

Important role of belly fat in aging processes identified

Researchers from the Department for BioMedical Reserarch (DBMR) and the Institute of Pathology at the University of Bern as well as the University Hospital Bern (Inselspital) have set out to identify new approaches to improve health-span in a fast-growing aging population. For many years scientists speculated that chronic low-grade inflammation accelerates aging processes and the development of age-related disorders. An international team of researchers under Bernese guidance has now demonstrated that visceral adipose tissue, known as belly fat, crucially contributes to the development of chronic low-grade inflammation. Scientist around Dr. Mario Noti, formerly at the Institute of Pathology of the University of Bern and Dr. Alexander Eggel from the Department for BioMedical Research (DBMR) of the Universität of Bern reported that certain immune cells in the belly fat play and an essential role in regulating chronic low-grade inflammation and downstream aging processes.