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COVID-19 Series: What Does the Future Hold?

What should we expect in the coming months and years with SARS-CoV-2? And what other pandemics might the future hold?

This episode features audio from How COVID-19 Ends: Vaccination, Mutations, and Herd Immunity and The COVID-19 Pandemic May Just Be a Dress Rehearsal. Visit the video pages for all sources and doctor’s notes related to this podcast.


What should we expect in the coming months and years with SARS-CoV-2?  Let’s look at the facts.

Will COVID-19 just go away naturally as warmer weather approaches? We shouldn’t count on it. Though the common cold coronaviruses follow a seasonal pattern like the flu, peaking every winter, there are other respiratory viral infections that peak in the spring or summer. In fact, MERS-CoV, the last deadly coronavirus to cause an epidemic, peaked in August, in the sweltering heat and blistering sun of the Arabian Peninsula.

The mechanisms underlying the seasonality of viral respiratory infections remain a subject of scientific debate. It’s likely a combination of factors involving the virus itself (for example, viral viability at different temperatures and humidity), host immunity (such as vitamin D status and the drying of our airways), and host behavior (like the crowding of susceptible individuals indoors). However, the near-universal susceptibility to novel pandemic viruses may supersede these seasonal factors. All the recent flu pandemics emerged in the spring or summer months, though secondary waves did tend to hit during the following winter. Even if the contagiousness of the COVID-19 virus drops this summer in the Northern Hemisphere due to warmer, wetter weather, it is not expected to make a large dent in the pandemic curve.

What would stop the pandemic is herd immunity: having a critical portion of the populace immune to the virus. An infection can only burn through a population if there are enough susceptible individuals for the viral sparks to jump from one person to the next. Immune individuals who can’t get or transmit the virus act as firebreaks to slow the spread, or like control rods in a nuclear reactor to break the chains of transmission. Ideally, this is accomplished through mass vaccination. Vaccines are a way to fight fire with fire: using the virus to fight the virus by generating the benefits of infection (immunity) without the risks (disease and death). Unfortunately, even though we are now developing vaccines at pandemic speed, it’s humbling to realize that the average vaccine takes over 10 years to create and has a 94% chance of failure. Without a vaccine, herd immunity is only achieved the hard way: through mass infection.

The proportion of the population that needs to acquire immunity to stop a pandemic can be roughly estimated from the basic reproduction number I talked about before: the number of people a single infected individual tends to go on to infect. The basic equation is: Pcrit = 1 – 1/R0, where Ris the basic reproduction number and Pcrit is what we’re looking for, the minimum proportion of a population needed to be vaccinated or have recovered with subsequent immunity to smother an outbreak within that population. So, if every COVID-19 case leads to two others becoming infected, then half of the population may need to be vaccinated or infected before the pandemic dies down. But, if each person on average infects four others, then one would need closer to three-quarters of the population to be immune to stop it. This is an overly simplistic model, but offers a ballpark approximation.

Based on Restimates for the COVID-19 virus from large outbreaks in affected countries, the minimum population immunity required ranges from about 30 percent (based on South Korea’s R0 estimate of 1.43) to more like 80 percent (based on an early R0 estimate from Spain that was closer to 5).

That’s why it’s so important to enact curve-flattening measures like social distancing to reduce the number of contacts and drive the basic reproduction number down as low as possible. You don’t want to have to wait until 80 percent of the population is infected.

Of course, this is all working under the assumption that people who recover from COVID-19 acquire immunity to reinfection. It works in rhesus monkeys. Scientists re-challenged two recovered monkeys with the COVID-19 virus and were unable to successfully re-infect them. We don’t yet have a definitive answer as to whether humans become immune after infection, but the fact that at least a small case series reported potential treatment benefit from “convalescent plasma,” the transfusion of blood products from a recovered patient, suggests the buildup of at least temporary immunity.

We have three lines of defense against viral reinfection: circulating antibodies that can neutralize the virus, memory B cells that can create new antibodies upon re-exposure (memory B cells are the reason people can remain immune from the chickenpox virus for 50 or more years, for example), and thirdly, memory T cells that can help hunt down virus-infected cells. The benefit of convalescent plasma derives from the antibodies, but a six-year follow-up study of patients recovered from SARS found that about 90 percent no longer had any detectable anti-SARS antibodies in their bloodstreams. But that’s okay, because their memory B cells could just make more, right? Unfortunately, not a single SARS-specific memory B cell was found in any of the former SARS patients. So, it’s definitely not something like chickenpox. Now, about 60 percent were able to mount a memory T cell response––though it’s not clear if that alone would be able to protect them from reinfection.

Unlike HIV, which keeps parts of itself hidden to evade the immune system and establish a long, latent infection, the COVID-19 virus appears to take more of a smash-and-grab approach. It brazenly displays its array of spike proteins in a presumed attempt to better bind to its victim but counts on jumping ship before immunity develops by quickly being coughed onto a new host. This bodes well for both the post-recovery acquisition of immunity and the prospects of vaccine development. A trait the COVID-19 virus does share with HIV, however, is its rapid mutation rate.

One reason RNA viruses, like HIV and coronaviruses and all flu viruses, represent a higher pandemic threat than those that use DNA as their genetic material is that viral RNA replication can be sloppy. Every copying cycle can result in multitudes of mutants, most of which probably aren’t even viable. But the flipside of this intrinsic inefficiency is that rare mutants may arise from this diverse population of variants that come exploding out of each infected cell that are either better adapted to the current host or tailored toward new ones.

The high mutation rate of coronaviruses may help explain their proclivity to jump across species barriers in the first place. But the question we face now is: what this new virus will do next. The genetic sequences of viral copies recovered from COVID-19 patients around the world have already diverged as much as 15 percent as different strains spread around the globe. Here’s how rapidly the various COVID-19 strains have splayed out across the world in just a few short months.

In the SARS epidemic, certain early mutants went on to dominate, which led to the supposition that genetic adaptation to humans was helping to drive the outbreak. But that remains to be substantiated. Though continued mutation of the COVID-19 virus doesn’t yet offer insight into the direction of its evolution, we cannot rule out the possibility that the virus could transform to become even more transmissible or dangerous in the near future. 

In our final story – we consider a scary scenario: the COVID-19 pandemic may be just a dress rehearsal. There may be an even deadlier pandemic threat waiting in the wings…of chickens.

Even with some suppression strategies in place, millions around the world are expected to die in the COVID-19 pandemic. In the United States, a “best guess” estimate presented to the American Hospital Association was about a half a million American deaths. With sufficient social distancing, that may be reduced to around 100,000. Even at a half million, though, it still—unbelievably, could be much, much worse.

With thousands already dead and millions projected to perish, billions in lockdown, and trillions lost as markets tumble, COVID-19 is still only shaping up to be a Category 2 or 3 pandemic. This is from the CDC’s pandemic planning guidelines. The Pandemic Severity Index is fashioned after the Hurricane Severity Index to define the destructive capacity of a storm. Well, this is the CDC’s attempt at classifying the destructive capacity of a pandemic. It is based on case fatality ratio, also known as the case fatality rate, the percentage of those who fall ill who eventually succumb to the infection. In the 1918 flu pandemic, about one in three fell ill and, of those, about 2 percent died. That made the 1918 pandemic a Category 5, analogous to a “super typhoon” with sustained winds exceeding 150 miles per hour. The rate of those dying from COVID-19 infection is much lower. If you include those who tested positive that were asymptomatic, it’s looking like around the mortality of the last two flu pandemics, or a bad seasonal flu season. If you’re talking about true cases, people who actually get sick, we’re talking closer to the 0.5% cut-off between a category 2 and category 3 pandemic, meaning about 1 in 200 cases dying.

As you can see, the 2 percent case fatality like the 1918 pandemic is just where Category 5 starts. COVID-19 shows that SARS-like coronaviruses can escape our grasp and spark a full-blown pandemic. SARS was rapidly stamped out by fever-monitoring travelers, but by the time it was all over, there were about 800 deaths out of 8,000 cases. That’s a case fatality ratio of 10 percent. Thank heavens we’re dealing with a pandemic from the SARS-CoV-2 and not the original SARS coronavirus. Even more lethal, MERS killed more like 850 out of 2,500, which is a 34 percent case fatality rate. A one in three chance of dying if you come down with it.

Since 2002 with SARS and then 2012 with MERS, we learned that coronaviruses could become deadly. They’re not just the common cold viruses we thought they were. Now, with COVID-19, we realize this family of viruses can also explode unfettered onto the global stage. So, coronaviruses have already shown us they can do both. It’s not hard to imagine a combination of transmissibility and lethality that makes the next coronavirus pandemic worse by an order of magnitude or more.

But there’s an even greater cautionary tale to be told, which is the primary subject of my new book. We’ve long known about the pandemic potential of the flu virus, but the deadliest it ever appeared to get was the 2 percent fatality of the 1918 influenza. Now, 2 percent was enough to kill up to a hundred million people, making it the single deadliest event in human history—but an even greater threat may be waiting in the wings… of a chicken. In 1997, a flu virus was discovered in chickens that would forever change our understanding of how bad pandemics could get. So far, it’s remained a disease of poultry not people, but of the hundreds of rare individuals it has infected, more than half have died. A flu virus with a case fatality rate exceeding 50%. What if a virus like that were to mutate to acquire easy human transmissibility? The last time a bird flu virus jumped directly to humans and caused a pandemic it triggered the deadliest plague in human history. What if instead of a 2 percent death rate, it was more like… a flip of a coin?

The COVID-19 pandemic is devastating, but food is still being restocked in our grocery stores. The internet may be slow, but it’s still up. The lights are still on and safe drinking water is still flowing from the tap. If the predictions are correct and “only” about 100,000 Americans die, that’s less than 1 in 3,000. In the pandemic of 1918, in which 2% of the cases succumbed, 1 in 150 Americans died. Imagine if it were ten times as bad as 2% with 1 in 15 dying. Or twenty-five times as bad, killing 1 in 6 of us.

The good news is: there is something we can do about it. Just as eliminating the exotic animal trade and live animal markets may go a long way towards preventing the next coronavirus pandemic, reforming the way we raise domestic animals for food may help forestall the next killer flu.

We got off easy in the last pandemic. Swine flu only triggered a Category 1 pandemic in 2009, but it showed a new origin point for pandemic viruses: pork production. It was like “epidemiological blowback” from our globalizing these intensive confinement methods.

The unprecedented emergence of H5N1 and the 10 other new bird flu viruses infecting humans around the world… has been blamed on industrial poultry production. When we overcrowd tens of thousands of animals in these cramped filthy football-field sized sheds to lie beak-to-beak atop their own waste, it’s just a breeding ground for disease. The sheer numbers of animals, the overcrowding, the stress crippling their immune systems, the ammonia from the decomposing waste burning their lungs, the lack of fresh air, and the lack of sunlight. Put all these factors together and what you have is really kind of a Perfect Storm environment for the emergence and spread of these so-called “superstrains” of influenza.

That’s why the United Nations has urged that governments, local authorities, and international agencies need to take a greatly increased role in combating the role of what they call factory farming, which, combined with these live animal markets, provide ideal conditions for the flu virus to spread and mutate into a more dangerous form. These so-called CAFOs, Concentrated Animal Feeding Operations, have vastly altered the evolution of the influenza virus.

The H5N1 virus started out like all bird flu viruses as harmless waterborne intestinal infections of waterfowl, but only gained airborne transmission and the ramping up of extreme virulence within massive intensive poultry production. Perhaps only a change in conditions as great as 10-million bird mega-farms could account for the dramatic series of mutations sufficient to create such a monster.

There also seems to be an acceleration of human influenza problems over the last few decades, involving an increasing number of species, and, according to the Food and Agriculture Organization of the United Nations, this is also expected to largely relate to the intensification of the poultry (and possibly pig) production. Big Ag may be brewing up Big Flu. For the underlying science, the evolutionary biological mechanisms, allow me to refer you to the invited review I wrote for Critical Reviews in Microbiology where I lay out all the evidence. It’s free; no paywall. Just go to bit.ly/flureview.

Currently the CDC considers the bird flu virus H7N9 to be our gravest threat, the virus with the highest pandemic emergence risk and the highest potential impact. An estimate was published as to what an H7N9 pandemic might look like in the United States and they concluded: millions of Americans dead.

So far, H7N9 has killed about 600 of the first 1,500 people it infected. That’s around 40%. Two in five people. Thankfully, neither H5N1 nor H7N9 have acquired the capacity for easy human-to-human transmission. But given that both H5 and H7 viruses have displayed the propensity to infect humans, there is heightened concern that they may evolve the ability to transmit between people and initiate a pandemic.

They’re still out there, still mutating. H7N9 may just be within three mutations away from effectively transmitting between people. Pandemics are always a matter of not if, but when. And a pandemic with more than a few percent mortality wouldn’t just threaten financial markets, but civilization itself as we know it.

How can we stop the emergence of pandemic viruses in the first place? If there is one concept to draw from my work on preventing and reversing chronic diseases, it’s that—whenever possible—treat the cause.

What does the poultry industry have to say for itself? The executive editor of Poultry magazine put it this way: “The prospect of a virulent flu to which we have absolutely no resistance is frightening. However, to me, the threat is much greater to the poultry industry. I’m not as worried about the U.S. human population dying from bird flu as I am that there will be no chicken to eat.”

Others are more self-reflective. Drawing on his 37 years of experience witnessing the failings in the factory farming model in terms of spreading disease, one industry insider concluded his trade publication article, “Poultry Reality Check Needed,” with these prophetic words: “Now is the time to decide. We can go on with business as usual, hoping for the best as we charge headlong toward lower costs. Or, we can begin making the prudent moves needed to restore a balance between economics and long-range avian health. We can pay now or we can pay later. But it should be known and it must be said, one way or another, we will pay.”

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