Why Optimization of the Resolution Response Is Critical For Your Health Outcome If You Become Infected with the Coronavirus
It is always a very dangerous situation when humans are exposed to a new virus. First, since the virus is new, there are no antibodies in your body to fight the virus. Second, there are no anti-viral drugs directed toward this new virus, and the ones we already have aren’t very good to begin with. Third, your best defense against such a new microbial invader is always your own immune system. With the new pandemic of the coronavirus upon us, let me explain each of these options in more detail.
First, a little background on this new coronavirus known as SARS-CoV-2 (to distinguish it from the more lethal SARS-CoV-1 that causes SARS). The disease caused by the SARS-CoV-2 infection is called Covid-19. There are many coronaviruses that infect humans with various degrees of mortality. The mortality associated with Covid-19 will probably end up being around 0.5% of those infected once all the asymptomatic infected individuals (about 80% of those actually infected) are eventually counted. An 0.5% eventual mortality rate estimate suggests the final mortality rate will be about 5 times the rate of the influenza virus (about 0.1%) based on the last flu season (1). However, other coronaviruses are more far more lethal than SARS-CoV-2. This includes the SARS-CoV-1 virus that causes SARS (with about a 10% mortality rate) or MER-CoV virus that causes MERS (with about a 35% mortality rate) (2). Both of these coronaviruses kill their hosts so quickly that there is little chance to infect others. This is why they were contained. Yet there are other coronaviruses including those that cause the common cold that causes virtually no mortality (3). The SARS-CoV-2 virus represents a pathological sweet spot to cause maximum damage since it has a low enough mortality rate not to quickly kill. But it can infect everyone since there are no antibodies to the SARS-CoV-2 virus in anyone except the few who have been infected.
It is always the first wave of infection of any new virus that is always the most lethal. The first wave of influenza killed between 25-50 million worldwide in 1918-1919 (4). Although there are vaccines for the influenza virus, they are not all that effective because the influenza virus changes from year to year. Furthermore, the mortality rates from the flu have dropped since 1918 because all new viruses tend to mutate to reduce their initial lethality so as not to kill their hosts needed for their replication. I expect future waves of Covid-19 will also become less lethal with time, but not anytime soon.
Immunity from any virus that infect humans only occurs when enough individuals in the general population have generated sufficient antibodies to the virus to prevent epidemic infections. This is called herd immunity. There are two potential ways to generate such antibodies. One is being infected by the virus. The other is being inoculated with an effective vaccine to generate antibodies to the virus.
Unfortunately, I feel it is unlikely that there will ever be an effective vaccine for the SARS-CoV-2 virus for the same reason there is no vaccine to the common cold. All the viruses associated with the common cold, and especially those of the coronavirus family mutate too rapidly to make an effective vaccine (5). So, in my opinion, waiting 18 months for a truly effective vaccine to prevent Covid-19 is like hoping to win the lottery.
What is the solution to build sufficient herd immunity if you can’t develop an effective vaccine? The answer is becoming infected by the SARS-CoV-2 virus. This is why quarantining may be initially successful in lowering the initial infection rate, but once the quarantine is over, the virus still has enough unprotected hosts available to begin another epidemic. This is because 80% of the people infected with the SARS-CoV-2 virus are asymptomatic. They remain carriers of the virus and can infect others once they are released from quarantine back into the general population. Two recent reports seem to indicate this potential (6,7). The result of such temporary quarantines will enable waves of infection to continue until herd immunity finally develops.
The percentage of the population that has effective antibodies in their blood depends on how infectious a virus is. For example, the measle virus is about five times more infectious than the SARS-CoV-2 virus (8). This means about 95% of the population has to have antibodies to the measle virus to prevent future epidemics. I estimate that since the SARS-CoV-2 virus is less infectious, you may need to only have about 66% of the population with antibodies to the virus to stop future Covid-19 epidemics. Currently, the percentage of the U.S. population with antibodies to the SARS-CoV-2 virus is virtually zero. Thus, without an effective vaccine (like we against measles), controlled exposure is the only way to generate necessary antibodies until about 2/3 of the U.S. population has been infected. This means about 200 million people will have to be infected. Using my estimated mortality rate of 0.5%, this would also suggest that about 1 million Americans may die from Covid-19 before herd immunity is finally obtained in the United States.
Modeling by leading epidemiologists at the Imperial College in the UK demonstrated that quarantining will “flatten the curve” of people requiring immediate intensive care thus preventing overloading of existing medical facilities (9, 10). Furthermore, it may even cut the overall mortality by about 50%, but in the process, it will also dramatically increase the time until herd immunity is achieved unless there is a magical 100% effective vaccine that appears quickly (again highly unlikely in my opinion). Of course, by extending the time of economic disruption with such rolling quarantines, the world economy will likely enter into a severe economic depression that may last for a decade or more, and cause far greater economic damage than the medical costs of the Covid-19.
Anti-viral drugs have a poor track record against viral infections. This is because the virus is so simple that it simply hijacks the more sophisticated metabolism of the cells of the infected host to make more copies of itself. The viral drugs that seem somewhat effective against AIDS do so because the replication of that virus requires very unique host enzymes that can be targeted by a drug (often with considerable side-effects). The relatively simple SARS-CoV-2 virus doesn’t require such specialized host cell metabolism for replication; therefore, it presents fewer potential drug targets once it enters into the cell. This is why attempts to use anti-viral drugs developed for HIV infection have not worked to treat those infected with SARS-CoV-2 (11). Since there is no drug that is effective against the common cold, I doubt any truly effective anti-viral drug will be easily developed for preventing Covid-19.
Furthermore, anti-viral drugs only work after the virus has entered the cell. This is why antibodies generated by infection or being exposed to an effective vaccine are far more effective than any therapeutic potential of any anti-viral drug. This is because the antibodies bind the virus before it can enter the cell. Once the antibody binds to the virus, the virus-antibody complex is targeted for elimination by the immune system. But without an effective vaccine, you can only obtain those antibodies by prior infection. Even then, you hope the immunity lasts a lifetime. For some viral infections like measles that is the case. For other viral infections like the flu, the time span of the immunity is much less thereby requiring new vaccine infections on a yearly basis. For the common cold, any immunity generated by the viral infection lasts only a short period of time before you can come down with another cold.
Optimizing Your Resolution Response
It is the third approach that has the greatest potential benefit for fighting the SARS-CoV-2 virus in the absence of establishing a long-term herd immunity to the virus. It is also your most sophisticated defense against any virus. This third approach is optimizing your internal Resolution Response™ as described in my book, The Resolution Zone (12). Any viral infection will cause an initial inflammatory response. It is the body’s internal Resolution Response that reduces the initial virus-induced inflammatory damage, then resolves the virus-induced inflammation, and finally repairs the damaged tissue caused by virus-induced inflammation. The Resolution Response coordinates both the innate and the adaptive immune systems to bring about healing.
The primary target organ of the SARS-CoV-2 virus is the lungs. The unresolved inflammation in the lung generated by the virus causes Acute Respiratory Distress Syndrome (ARDS) that requires hospitalization in about 20% of those infected. In the most severe cases, this will also require a ventilator for the patient to survive. The early data from China indicates even in those who survive the ARDS caused by the virus may have extensive continuing lung damage that could take many years to heal (13). The likely cause of such residual lung damage is due to fibrosis or scar tissue formation. ARDS and lung fibrosis are both a consequence of a blocked Resolution Response. The more optimal your internal Resolution Response, the less damage to the lung (and other organs) will be caused by the SARS-CoV-2 infection.
There is no drug to optimize your internal Resolution Response, but it may be optimized through strong dietary control. In particular, using a highly defined Pro-Resolution Nutrition system as I have described in detail in my newest book, The Resolution Zone, is the necessary dietary intermediate step to orchestrate your immune response to the inflammation created by any injury including viral infections (12).
Pro-Resolution Nutrition requires no breakthroughs in biotechnology or government funding effort yet it could be at the forefront of managing Covid-19 through its ability to alter diet-induced hormones and gene expression. If you are already following Pro-Resolution Nutrition, I believe you are more likely to be protected against infection of the lungs because you are increasing the effectiveness of the mucus barrier that lines the lungs to prevent access of the virus to the lung tissue. Following Pro-Resolution Nutrition also improves the tightness of the epithelial layer that lines the lung tissue further reducing the entry of the virus into the lungs. Of course, both of these events take some time to build up.
If the virus does penetrate into the lungs, then optimizing your internal Resolution Response can help bring into action the necessary hormonal and genetic expression changes to minimize inflammation, repair and regenerate the damaged tissue, and help protect against scarring.
If you are infected by the SARS-CoV-2 virus following Pro-Resolution Nutrition, in my opinion, might be the difference between mild to severe symptoms. How do you know your internal Resolution Response is optimal? The answer comes from the blood tests that define the Zone (12). If you are in the Zone as determined by those simple blood markers, then you have done everything possible to optimize your internal Resolution Response that will allow you to control and minimize damage caused by infection with the SARS-CoV-2 virus.
Ultimately, herd immunity to the SARS-CoV-2 virus will develop. However, that only means that future epidemics (as opposed to the current pandemic) will be less likely. However, individual cases will still occur. You can be prepared for those situations by maintaining yourself in the Zone by a consistent lifetime application of the dietary principles of Pro-Resolution Nutrition. All it requires is treating your diet as if it were a drug to be taken at the right time and the right dose.
- The SARS-Cov-2 virus that causes Covid-19 is here to stay like the common cold and the flu.
- Your best defense against Covid-19 is an optimal Resolution Response.
- You can maintain your Resolution Response by following a Pro-Resolution Nutrition program.
- Ng O-H and Tan Y-J. “Understanding bat SARS-like coronaviruses for the preparation of future coronavirus outbreaks.” Human Vaccines Immunotherapeutics 13: 1860189 (2017)
- Makela MJet al. “Viruses and bacteria in the etiology of the common cold.” J Clin Microbiol 36: 539-542 (1998)
- Su S et al. “Epidemiology, genetic recombination, and pathogenesis of coronaviruses.” Trends Microbiol. 24:490502((2016)
- Rothe C et al. “Transmission of 2019-nCOV infection from an asymptomatic contact in Germany.” NewEngl J Med 382: 970-971 (2020)
- Bai Y et al. “Presumed asymptomatic carrier transmission of COVID-19.” JAMA 10.1001/jama.2020.2565. (2020)
- Hamblin J. “You’re likely to get the coronavirus.” The Atlantic. February 24, 2020. https://www.theatlantic.com/health/archive/2020/02/covid-vaccine/607000/
- Kristoff N. “The best-case outcome for the coronavirus, and the worst.” New York Times. March 20, 2020. https://www.nytimes.com/2020/03/20/opinion/sunday/coronavirus-outcomes.html
- Cao B et al. “A trial of Lopinavir-Ritonavir in adults hospitalized with severe COVID-19.” NewEnglJ Med doi: 10.1056/NEJMoa2001282 (2020)
- Sears B. The Resolution Zone. Zone Press. Palm City, FL (2019)
- Hosseiny M et al. “Radiology perspective of coronavirus disease 2019 (COVID-19): Lessons from severe acute respiratory syndrome and Middle East respiratory syndrome.” Am J Roentgenol 214: 1-5 (2020)
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