COVID-19: Why it kills the elderly and what we should do about it
Most of us already recognize that 2020 is a year where everything changed. In just a few months, the COVID-19 pandemic has dramatically impacted the lives of billions of people, many of which will never be the same.
One of the most striking features of COVID-19 is its disproportionate impact on the elderly. Indeed, the first recognized outbreak in the U.S. killed 35 residents at the Life Care Center nursing home in Kirkland, Washington. This occurred in early March after the virus had spread silently in the local population for several weeks, but it was only upon exposure of this vulnerable group that the severity of COVID-19 began to be appreciated. Now only two months later, more than 80,000 Americans and nearly 300,000 people worldwide have succumbed to COVID-19, the majority of these deaths occurring in those over 65.
Several explanations have been put forth for why this virus preferentially targets the elderly. Older adults are more likely to have pre-existing conditions, which can increase lethality of COVID-19. The elderly tend to be frail and have lower resistance to stress. Our immune systems stop functioning properly as we age, providing an opportunity for the virus to gain a foothold the body can’t fight off. All of these are true. They also all miss the most important point.
The reason COVID-19 kills the elderly is because of aging — specifically, the biological mechanisms of aging, which drive each of these other factors.
Scientists agree on the existence of a biological process underlying the myriad declines in function we see among the elderly. Scientists also agree that it is possible to modify that process. The mechanisms of aging have even been formalized into several “hallmarks” which can be targeted to delay, or even reverse, aspects of biological aging. This has important implications for how we should approach diseases of aging, particularly in the context of COVID-19.
Consider as a simple thought experiment the impact of a treatment for immune aging that causes the immune system of a typical 70 year-old to function as it did when that person was 50. Current data suggest that risk of dying from COVID-19 increases approximately 10-fold for every 20 years of age. So, we could expect a 90 percent reduction in lethality from such an intervention. Suddenly, a global pandemic that has wrought generational economic and social devastation becomes a mild flu season.
Consider further that much of our current hope for a return to normalcy rests on the development of a COVID-19 vaccine. Assuming this is accomplished, it may provide effective immunity in younger people but will still not work well in the vulnerable older population. We should not fool ourselves into thinking that a COVID-19 vaccine will be a cure, unless we also find a way to boost immunity in the elderly, allowing them to develop an appropriate response to the vaccine.
As a biologist, these kinds of thought experiments are what keep me awake at night. Not because we don’t yet have the ability to target biological aging, but precisely because we do. Yet, we are failing to harness that knowledge to save lives.
Several candidate therapies exist, which could protect against multiple age-related diseases such as Alzheimer’s disease, heart disease and viral infections like influenza and coronavirus. Some have even been shown to improve immune function in the elderly. For example, two recent clinical trials found that just six weeks of treatment with one such therapy was able to boost response to a flu vaccine and simultaneously reduce the risk of respiratory infections in healthy people over 65. If extrapolated to the general population, the entire COVID-19 pandemic could have been avoided. Yet, the resources put toward development of such treatments lags far behind what appear to be largely futile efforts to cure age-related diseases.
Perhaps COVID-19 can provide a wakeup call. What should happen now is an immediate effort toward testing whether already established candidates can boost immunity in healthy older people in a large, randomized clinical trial. If this works as expected, it both reduces the risk of COVID-19 infection and also enhances the ability of a future COVID-19 vaccine to protect vulnerable individuals. Because the immune-boosting effect is not specific to COVID-19, we can also anticipate a similar reduction in influenza and other respiratory infections.
If the patients receiving the therapy are also protected against Alzheimer’s disease, heart disease, cancer and other age-related diseases, well, I guess that’s just a nice “side effect”.
Matt Kaeberlein is a fellow of the American Association for the Advancement of Science and a professor of pathology at the University of Washington School of Medicine, where he directs the Healthy Aging and Longevity Research Institute, the Biological Mechanisms of Healthy Aging Training Program and the NIH Nathan Shock Center of Excellence in the Basic Biology of Aging.
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