COVID-19 Experimental Vaccine Fact Sheet & Risk Factors

Update – February 20, 2021

Dr. Nally has had hundreds of patients ask about the Experimental COVID-19 mRNA vaccines and whether they should consider taking one of them.

Here is a little education that comes directly from the available research we have regarding these vaccines, the CDC and the most recent literature available on this experimental vaccination.  Official package safety data does not currently exist and some vaccine manufactures have not released some of their safety data as of the writing of this update. 

Both the Pfizer/BioNTech and the Moderna Experimental COVID-19 vaccines consist of a snippet of genetic code directing production of the coronavirus’ spike protein, delivered in a tiny fat bubble called a lipid nanoparticle. Some researchers suspect the immune system’s response to that delivery vehicle is causing the short-term side effects.

The Centers for Disease Control and Prevention (CDC) has issued an update on those who should not receive the Experimental mRNA COVID-19 vaccines. Recommendations cover:

• Patients who have had a severe allergic reaction to a COVID-19 vaccine.
• Patients who have had an immediate non-severe allergic reaction to a COVID-19 vaccine.
• Patients who have had an allergic reaction to polyethylene glycol (PEG) or polysorbate.
• Patients who have had an allergic reaction to other types of vaccines or an injectable therapy.
• Patients who have had allergies not related to vaccines (food like shell fish, nuts, etc).

Common Side Effects that can and will occur with both versions of the vaccine (lower side effect profile in Pfizer/BioNtech version):

• Fever up to 104 F (40 C) for 24 hours in 2-4% of participants.
• Severe fatigue in 4%- 9.7% of participants
• Muscle pain in 8.9%
• Joint pain in 5.2%
• Headache in 2%-4.5%.

That’s a higher rate of severe reactions than people may be accustomed to. This is a higher likelihood of reaction than is ordinarily seen with most flu vaccines, even the high-dose versions of the flu vaccine. In fact, the likelihood of a severe problem if you get a COVID-19 infection is about 0.5%. Where the likelihood of side effects from the vaccine is 1-10%.

With those odds, you be the judge.

Pregnancy/Breast Feeding:

Until the placenta anti-body question brought up on December 1, 2020, by Pfizer’s former head respiratory researcher is answered, I would never let a woman of childbearing age take this medication.  

The syncytiotrophoblast is the outermost layer of the placenta, the part that is pressed against the uterus. It’s a layer of cells that have fused together, forming a wall. This wall of cells keeps mom and baby working in harmony and not killing each other. There’s no other structure like this anywhere else in the body.

There is significant potential for this vaccine to cause “spike protein antibodies” to the syncytiotrophoblasts (like anit-Syncytin-1 antibodies) leading to lifelong infertility. 

On December 1, 2020, the ex-Pfizer head of respiratory research Dr. Michael Yeadon and the lung specialist and former head of the public health department Dr. Wolfgang Wodarg filed an application with the European Medicine Agency responsible for European approval, for the immediate suspension of all SARS CoV-2 vaccine studies, in particular the BioNtech/Pfizer study on BNT162b.  One of the biggest reasons they cited was the possibility of lifelong infertility as described below:

“Several vaccine candidates are expected to induce the formation of humoral antibodies against spike proteins of SARS-CoV-2 Syncytin-1 which is derived from human endogenous retroviruses (HERV) and is responsible for development of placenta in mammals including humans and is therefore and essential prerequisite for a successful pregnancy.  This is also found in homologous form in the spike proteins of SARS viruses.  There is no indication whether antibodies against spike proteins of SARS viruses would also act like anti-Syncytin-1 antibodies.  However if this were to be the case this would also prevent the formation of a placenta which would result in vaccinated women essentially becoming infertile. To our knowledge Pfizer/BioNtech has not released any samples of written materials provided to patients so it is unclear what, if any, information regarding potential fertility-specific risks caused by antibodies is included.”

Because of this it could be 1-2 years before a noticeable number of cases of post-vaccination infertility could be observed. 

In spite of this information, and to the behest of hundreds of practicing physicians,  our government has persisted with the following recommendations

Directly from the CDC website: “Observational data demonstrate that, while the chances for these severe health effects are low, pregnant people with COVID-19 have an increased risk of severe illness, including illness that results in ICU admission, mechanical ventilation, and death compared with non-pregnant women of reproductive age. Additionally, pregnant people with COVID-19 might be at increased risk of adverse pregnancy outcomes, such as preterm birth, compared with pregnant women without COVID-19.”

“Based on how mRNA vaccines work, experts believe they are unlikely to pose a specific risk for people who are pregnant. However, the actual risks of mRNA vaccines to the pregnant person and her fetus are unknown because these vaccines have not been studied in pregnant women.”

“There are no data on the safety of COVID-19 vaccines in lactating women or on the effects of mRNA vaccines on the breastfed infant or on milk production/excretion. mRNA vaccines are not thought to be a risk to the breastfeeding infant. People who are breastfeeding and are part of a group recommended to receive a COVID-19 vaccine, such as healthcare personnel, may choose to be vaccinated.”

For those outside of the United States, the UK government’s safety instructions recommend that “no pregnancy or breast feeding should be planned within two months of each COVID-19 vaccine dose.”

Antibody-Dependent Enhancement (ADE):

A well-documented and serious side effect of vaccines is known as pathogenic priming or antibody dependent or immune enhancement. It is difficult to prove, with doctors and scientists and the public tend to initially deny its existence by saying a person has “a worse virus.” One way we learn that ADE is a real effect is by comparing vaccinated and
unvaccinated populations. If entire populations are immediately vaccinated with these experimental vaccines, the true incidence of ADE will never be known, as many cases will just be falsely described as a “new strain” or “more severe strain.”
Although most readers have never heard of it, antibody-dependent-enhancement is so well known, it even has its own Wikipedia page: https://en.wikipedia.org/wiki/Antibodydependent_enhancement. Note that coronaviruses are commonly implicated.

ADE is especially tricky because it is a delayed reaction. Initially all seems well. The person seems to have a great immune response but then becomes deadly when the person is exposed to the virus in the wild. It is well known that you must do animal testing first to try
to rule out ADE.

Strong vaccine advocates, Dr. Offit and Dr. Hotez, who initially implied ADE was a possibility before the release of the vaccine, have since changed their position on the vaccine. They have openly stated  in recent interviews that because no ADE was seen in phase III clinical trials, and because ADE hasn’t been seen in those receiving convalescent plasma treatment for severe cases, ADE is unlikely.  

However, ADE takes up to 12 months to be seen whether it comes from a vaccine or from infusion of convalescent plasma.  Two to three different types of ADE have been theorized in association with coronaviruses, and ADE is often misdiagnosed.  Only time will tell with this vaccine, released emergently without completion of phase IV clinical trials. 

Antibody Dependent Enhancement (ADE), is when anti-COVID antibodies, created by a vaccine, instead of protecting the person, cause a more severe or lethal disease when the person is later exposed to SARS-CoV-2 in the wild. The vaccine amplifies the infection rather than preventing damage. It may only be seen after months or years of use in
populations around the world. This paradoxical reaction has been seen in other vaccines and animal trials. One well-documented example is with the Dengue fever vaccine, which resulted in avoidable deaths. It happened with the RSV vaccine and with the COVID SARS-1 vaccine (which is 78% similar to COVID-19).

The Phase III trials from Pfizer, Moderna and AstraZeneca provide little insight into ADE, also called vaccine associated hypersensitivity (VAH). Not only is the sample size of vaccinated participants who developed COVID-19 very small, but, based on the information publicly available, it is unknown which strains of SARS-CoV-2 afflicted the participants in the trials.

This ADE response is so concerning that many scientists already agree the risk is much too high to release these experimental vaccines to the public at large. On December 1, 2020, Dr. Michael Yeadon and Dr. Wolfgang Wodarg ADE was included in the application with the European Medicine Agency responsible for approving drugs in the European Union, for the immediate suspension of all SARS CoV 2 vaccine studies, in particular the BioNtech/Pfizer study on BNT162b.
Another reason they cited was the formation of so-called “non-neutralizing antibodies” can lead to an exaggerated immune reaction, especially when the test person is confronted with the real, “wild” virus after vaccination. This so-called antibody-dependent amplification, ADE, has long been known from experiments with corona vaccines in cats, for example. In the course of these studies all cats that initially tolerated the vaccination well died after catching the wild virus.

Other Known Problems:

COVID-19 Experimental Vaccines should be expected to have similar problems as other vaccines, including neurologic disorders and possible racial disparities in vaccine responsiveness. Known complications of vaccines include neurological diseases such as transverse myelitis, multiple sclerosis, and Guillain-Barre.

As a note, autism was previously thought to have been associated with components found in some vaccines (like thimerosal or mercury), however, this assertion made in a retracted 1998 study has been disproven in 10 follow up studies that included over 1.2 million children. 

In 1976 the government attempted a mass vaccination of the population with a newly created Swine Flu vaccine. The vaccination program was aborted after about 450 people came down with Guillain-Barre.

The extremely limited experimental COVID-19 vaccine data already has revealed two transverse myelitis cases.

Sources:

• https://www.cdc.gov/…/recommendations/pregnancy.html);
• https://www.gov.uk/government/publications/regulatory-approval-of-pfizer-biontech-vaccine-for-covid-19/information-for-healthcare-professionals-on-pfizerbiontech-covid-19-vaccine)
• https://2020news.de/en/dr-wodarg-and-dr-yeadon-request-a-stop-of-all-corona-vaccination-studiesand-call-for-co-signing-the-petition/?fbclid=IwAR3yoj0SCIK8WaaS0-w1vIoig4qNYydTxT3aK01NJDwHut3jWpygtnnbNY)
• https://2020news.de/wpcontent/uploads/2020/12/Wodarg_Yeadon_EMA_Petition_Pfizer_Trial_FINAL_01DEC2020_EN_unsi gned_with_Exhibits.pdf)
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7642463/
• https://www.nature.com/scitable/topicpage/host-response-to-the-dengue-virus-22402106/
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7642463/
• https://www.nature.com/articles/d41586-020-02706-6
• https://pubmed.ncbi.nlm.nih.gov/24814559/ 

Vaccines and Herd Immunity

Update – July 10, 2020

In order to fully understand the current “pandemic” coronavirus (COVID-19) infection, it is essential that one understands some basics about the immune system.  Second, we will look at how a poor understanding of the immune system has duped many about how the body actually responds to this virus.

Normal functions of the immune system include defense against infections and detection and destruction of malignant or abnormal cells. As our immune system ages and these capabilities decline, there is increased susceptibility to infections and cancer and an increased incidence of autoimmune disorders. The study of age-related changes in immune function is a relatively new area of investigation, which is limited by incomplete understanding of the complexities of immune mechanisms in general.  These age related changes make it clear why COVID-19 is mild in some and severe in others.

The coronavirus tends to be more problematic in those over age 55.  In fact, 87% of all deaths in Arizona due to COVID-19 are in those over age 55.  The clinical presentation of infections in older patients may be different from that in younger patients. Older adults with severe infections tend to have fewer symptoms, and fever is absent or blunted in 20 to 30% of those over age 55 years old. This suggests a decreased ability to mount inflammatory cytokine responses (small proteins used as signaling molecules between cell) in the face of infection. Signs of infection in older adults can be nonspecific and include falls, delirium (confusion), anorexia (loss of appetite), or generalized weakness (Norman DC, Clin Infect Dis. 2000;31(1):148).

Immune System & Aging

All immune cells originate from stem cells in the bone marrow, and there is a general decline in the total bone marrow cellular tissue as we age (Geiger H, Rudolph KL. Trends Immunol. 2009;30(7):360). Production of pro-B cells is significantly decreased with aging, resulting in a smaller number of B cells leaving the bone marrow, while T cell precursors seem to be less affected (Cancro MP, Hao Y, Scholz JL, Riley RL, Frasca D, Dunn-Walters DK, Blomberg BB., Trends Immunol. 2009;30(7):313. e-pub 2009 Jun 18). 

The immune system is divided into innate and adaptive immunity. The innate immunity refers to immune responses that are present from birth and not learned, not adapted, and not refined as a result of exposure to micro-organisms/antigens. In contrast, adaptive immunity, which consists of the responses of T and B lymphocytes, is generated and then refined over the lifetime of a person as a result of repeated exposure to antigens from bacteria, viruses or fungi. Aging affects both innate and adaptive immunity, although innate immune mechanisms are better preserved overall (Weiskopf D, Weinberger B, Grubeck-Loebenstein B, Transpl Int. 2009; 22(11):1041).

Innate Immunity

The innate immune system consists of epithelial barriers (skin, gastrointestinal and respiratory protective lining), macrophages, neutrophils, natural killer (NK) cells, natural killer T (NKT) cells, dendritic cells (DCs), and complement proteins. Additional normal defenses include production of mucus in the proper quantity and viscosity, local antimicrobial proteins, and normal sweeping function ciliary cells.

Though some innate immune mechanisms are decreased in the adult over 55 years old, other mechanisms appear to be more active.. The result of these changes is a propensity to develop chronic inflammation. The result of aging of the innate immune system may be most accurately characterized as a state of immune dysregulation characterized by low-grade, chronic inflammatory changes  (Shaw AC, Joshi S, Greenwood H, Panda A, Lord JM, Curr Opin Immunol. 2010;22(4):507).  This is why many of my patients feel that the “Golden Years” are full of lead.

Adaptive Immunity

 Adaptive immunity consists of the functioning of two types of white blood cells: T and B lymphocytes.  T and B lymphocytes mediate control cellular and humoral immune responses, respectively.

Cellular Immune Response and the T Cells

There are several key changes that occur to T cells during aging.

Thymus – The thymus gland is most active early in life, reaches maximum size within the first year of life, and then undergoes a steady decline with age. By age 7, the part of the thymus and it’s activity decrease to less than 10 percent of the total thymic space. The functional thymic cortex and medulla are progressively replaced by fatty tissue. These changes become almost complete some time between the ages of 40 to 50 (Flores KG, Li J, Sempowski GD, Haynes BF, Hale LP. J Clin Invest. 1999;104(8):1031).  As a result, the number of T cells exiting the thymus is significantly decreased and gets progressively lower between the age groups of 40 to 54, 55 to 69, and 70 to 90 (Naylor K, Li G, Vallejo AN, Lee WW, Koetz K, Bryl E, Witkowski J, Fulbright J, Weyand CM, Goronzy JJ. J Immunol. 2005; 174(11):7446).

T Cells Change Over Time – T cell receptors become less divers after age 65.  The production of new T cells is dramatically reduced in the very old. T cell populations are largely composed of persistent long-lived lymphocytes. Age-related defects in the signaling pathways of CD4 T cells have been identified due to changes in T cell receptors (Li G, Yu M, Lee WW, Tsang M, Krishnan E, Weyand CM, Goronzy JJ. Nat Med., 2012 Sep;18(10):1518-24. e-pub 2012 Sep 30).

T Cell Numbers Decrease – There is a decrease in the numbers of (helper) CD4 T cells, an increase in CD8 T cells, and a decrease in CD28 with aging. Reduction in CD28 results in an impaired ability of T cells to proliferate and secrete IL-2, an essential cytokine in promoting growth of T cells (Kaltoft K, Exp Clin Immunogenet., 1998;15(2):84).  Because (helper) CD4 T cells are important in stimulating B cells, the ability of T cells to help B cells grow, expand and produce antibodies diminishes with aging (Haynes L, Maue AC., Curr Opin Immunol, 2009;21(4):414. E-pub 2009 Jun 6).

Decreased Cytokine Signaling – T cells respond specifically to cytokines like IL-2, IL-6, TNF-alpha. With aging over 50 years, production and signaling of these cytokines diminishes and has been found to be directly correlated with degree of frailty in older adults (Marcos-Pérez D, et al., Front Immunol. 2018;9:1056. Epub 2018 May 16).

Humoral Immunity

B Cells – B cells produce their own surface membrane immunoglobulin and differentiate into plasma cells, which then make immunoglobulin for the blood or secretions. These immunoglobulins are the mediators of humoral immunity. B cells respond to antigen exposure (protein markers or flags on the surface of bacteria or viruses) by producing antibodies, which then bind to antigens to fight concurrent infections or prevent future infections.  B cells produce primarily the immunoglobulin IgM. Upon stimulation with and antigen, B cells switch to the production of IgG, IgA, or IgE. The ability of B cells to respond to antigens and produce antibodies is their main job.

The numbers of B cells precursor in the bone marrow (pre-B cells), as well as peripheral B cells, decrease with age.  Immunoglobulin levels (IgM), on the other hand, do not change with aging, and may actually increase (Frasca D, Landin AM, Lechner SC, Ryan JG, Schwartz R, Riley RL, Blomberg BB. J Immunol. 2008;180(8):5283). However, quantities of specific antibodies (ie, those generated by encounters with antigens through infection or vaccination) decline with age (Lazuardi L, Jenewein B, Wolf AM, Pfister G, Tzankov A, Grubeck-Loebenstein B, Immunology. 2005;114(1):37).

Antibody production from vaccination is also noted to be lower in those over age 55.  This is why booster vaccinations are required (Weinberger B, et al, Front Immunol. 2018;9:1035. Epub 2018 May 15).

Memory B & T Cells – The generation of long-lasting protective immune memory is one of the most unique and important characteristics of the adaptive immune system. Memory is essential for individual defense from infections to which you have previously been exposed. As the thymic output declines, individuals rely more on re-expansion of experienced memory cells for defense against infections.

Memory responses from immunoglobulins to previous infections appear to be relatively well-preserved as we get older, compared with new responses of B and T cells. Data suggest that memory B and T cells, once elicited by antigen during youth, are quite resilient to the impact of age (Stacy S, et al, Mech Ageing Dev, 2002;123(8):975;  Kovaiou RD, et al, Int Immunol, 2005;17(10):1359. Epub 2005 Sep 1).

An example of this  was seen during the 2009 H1N1 influenza pandemic, in which older adults were better protected from H1N1 infection than middle-aged adults, probably because of the persistence of memory lymphocytes producing antibodies generated in response to an H1N1 virus that circulated prior to 1957 (Hancock K, Veguilla V, Lu X, Zhong W, Butler EN, Sun H, Liu F, Dong L, DeVos JR, Gargiullo PM, Brammer TL, Cox NJ, Tumpey TM, Katz JM. N Engl J Med. 2009;361(20):1945). The antibody avidity for 2009 H1 was higher in older adults than in middle-aged adults (Monsalvo AC, Batalle JP, Lopez MF, Krause JC, et al. Nat Med. 2011;17(2):195. E-pub 2010 Dec 5).

Ketogenic Diets Improve T Cell Function

T Cells were found to function more efficiently on fatty acid oxidation, instead of glucose metabolism.  Ketogenic diets have been found to have a protective effect on preservation of T cell immune responses  (Goldberg EL, et al, Sci Immunol Nov 2019 4(41): eaav2026).  The ketogenic diet was found to expand the presence of T cells and improve the inflammatory changes common with aging and diminished immune function (Goldberg EL, Shchukina I, Asher JL, et al. Nat Metab 2020: 2, 50–61).

COVID-19 and the Immune System

Information about the coronavirus has dramatically changed in the last six months since it was discovered.  Initially, it was suspected that humoral related antibodies were essential to mount an effective attack against COVID-19.  This is why the focus has been directed at screening for active infection, quarantine and measurement of antibodies.

What we now know is that most individuals with asymptomatic or mild symptoms generate a highly functional T cell response.  In fact, 50% of  those who have been exposed to coronavirus formed a T cell (cellular immunity) response without activation of B cell response (humoral immunity) and had no antibody formation  (Li X, Geng M, Peng Y, Meng L, Lu S. J Pharm Anal. Apr 2020; 10(2): 102-108).

A large Swedish study demonstrated that twice as many exposed family members and healthy individuals who donated blood during the pandemic of COVID-19 generated memory T cell responses (cellular immunity) versus those generating antibody responses (humoral immunity). This imply’s that the seroprevaleance (presence of antibodies like IgG & IgM found on B-cells) as an indicator has grossly underestimated the extent of population level immunity against SARS-CoV-2 (COVID-19). And none of these patients with this type of immune response have experience further episodes of COVID-19 to date (Sekine T, Perez-Potti A, Rivera-Ballesteros O, et al. bioRxiv (Biology) Jun 2020; e-pub:  174888).

What this all means is that 50% of people get exposed and form immunity with T cells, instead of B cells an may never even know they’ve had the virus.

Increased Susceptibility to COVID-19

As you can see above, age over 55 places one at greater risk for severe COVID-19 infection and complications.  This is due to the effect age has on the immune system.

Three additional maladies (hypertension, diabetes, elevated cholesterol & coronary artery disease) are also significant risk factors for severe COVID-19 infections.  These are also are the four most common medical problems that I see in my clinic, and they affect 85% of the people in my practice.  All four are caused and driven by hyperinsulinemia.

Hyperinsulinemia is defined as an elevated insulin production (2-30 times normal) when ingesting any form of carbohydrate or starch.  It starts 15-20 years before the onset of diabetes and is the cause of hypoglycemia, elevated fasting blood sugar, pre-diabetes, metabolic syndrome, chronic kidney disease, idiopathic neuropathy, hypertension and coronary artery disease.

Elevated insulin, even small elevations, puts a load on the immune system.  The higher your insulin response to starches or sugars, the more likely you are to have hypertension, diabetes and heart disease.  We found that those with elevated insulin levels and those over 45 years old with stressed immune systems are the most susceptible to severe COVID-19 infection.

We know that just four or more hours of elevated blood sugar and insulin increases the cytokine IL-6 significantly.  This has a suppressive effect on T cell immunity.  The body raises insulin chronically to protect itself from the damage caused by chronic elevation in blood sugar.  Chronic elevated blood sugars can lead to severe inflammation and clotting disorders.  The body attempts to raise insulin to protect angainst these issues, however, the chronic elevation in insulin leads to chronic elevation in the cytokines IL-2, IL-6, TNF-alpha, PAI-1, NF-kB, ROS and eventually IL-33.

Should We Be Waiting For A Vaccine?

As a preface to this section, please be aware that I am a very strong proponent of safe and effective vaccine use.  Because the RNA vaccines are so new, long-term efficacy, safety and adverse reaction studies are essential before these vaccines can be recommended across the board.  It takes at least 4-5 years to 1) bring a vaccine to market and 2) complete adequate safety studies.

Let’s start by looking at the effectiveness of current RNA viral vaccines. The most common RNA vaccine currently in use is the influenza vaccine, quadravalent (four flu strains) and high dose (five flu strains) versions.  Over the last 20 years, the percentage of seniors getting flu shots increased sharply from 15% to 65%. It stands to reason that flu deaths among the elderly should have taken a dramatic dip due to increased flu vaccination each year.

Instead, as you can see above, influenza deaths among the elderly continued to climb. It was hard to believe, so researchers at the National Institutes of Health set out to do a study adjusting for all kinds of factors that could be masking the true benefits of the shots. But no matter how they crunched the numbers, they got the same disappointing result: flu shots had not reduced deaths among the elderly.

It’s not what health officials hoped to find.  I was shocked when I read these studies.  Two studies, here and here, demonstrate that yearly flu vaccine for those over age 65 does nothing to decrease influenza related death. These studies funded by the government in 2005 and 2006 were suppressed and I never heard about them. Yet the CDC still emphasizes to the elderly, “Get your flu shot.”

One reason these vaccines are ineffective is that viruses like influenza and corona-viruses are highly antigenic.  That means that there are hundreds of strains and the virus is changing rapidly.  Influenza has over 600 strains.  Our current high dose vaccine only covers five of these strains.

SARs-CoV-2 (COVID-19) is known to have over 160 strains. “There are too many rapid mutations to neatly trace a COVID-19 family tree.” Said Peter Forster, geneticist at the University of Cambridge.  “We used a mathematical network algorithm to visualize all the plausible trees simultaneously.” (Proceedings of the National Academy of Sciences, 2020).  Dr. Forster’s research identifies 160 genomes within the hundreds of additional variants of the three central COVID-19 strain variants.

A second reason, as stated above, is that 50% of people who are exposed to COVID-19 mount a T cell immune response without ever forming antibodies through B cell immunity.  And, the antibodies that do form only give 3-4 months of protective effect.

Another other very fascinating concern found when making RNA virus vaccines is the potential to increase susceptibility to other viruses.  In a Department of Defense study, looking at 6000 military personal vaccinated in the 2017-2018 season, those who got the influenza vaccine demonstrated an increases susceptibility to corona-viruses by 36%. Those who were vaccinated with the flu vaccine had additional increased susceptibility to non-influenza viruses by 15%, and increased susceptibility to human metapneumovirus by 59%.

A second influenza study demonstrated an increased risk of para-influenza virus in adults (increased by 4.6% of vaccinated adults and only 2.6% of un-vaccinated adults.)  Though the researchers dismissed it as calculation error, the p value reflects that the vaccine played some roll (P=0.04) in the increased susceptibility.

Herd Immunity?

As with any other infection, there are two ways to achieve herd immunity: A large proportion of the population either gets infected or gets a protective vaccine. Based on early estimates of this virus’s infectiousness, we will likely need at least 70% of the population to be immune to have herd protection.

If the Penn State study is correct, the up to 50% of the U.S. population may have already been exposed as of the first week in March 2020, and by today, we may already be at Herd Immunity levels.  This may be why we are now seeing continued drop in death rates across the country, despite increase infection counts (due to increased testing frequency).

Should we push for a vaccine?  Do the math on a vaccine that covers only four out of 600+ strains like the quadravalent influenza vaccine.  For a vaccine to create “herd immunity,” currently being touted across the airwaves as the way to return to normal, it would require the average human to be vaccinated every year for 100 years, and would take 200-400 years to create any semblance of herd immunity.  And, that’s after 4-5 years studying the safety of a vaccine in large populations.

Influenza and HPV, the two most widely used RNA vaccines, still have a number of post-market adverse reactions including: Guillain-Barré syndrome (GBS), convulsions, febrile convulsions, myelitis (including encephalomyelitis and transverse myelitis), facial palsy (Bell’s palsy), optic neuritis/neuropathy, brachial neuritis, syncope (shortly after vaccination), dizziness, and paresthesia (tingling of the extremities) (Package-Insert—Gardasil.pdf; Package-Insert—Fluzone High Dose.pdf).  Though these adverse events occur more rarely, it is essential you and I understand the risks of these newer RNA vaccines.  Because it is an RNA virus, any coronavirus vaccine will come with similar risks.

What Can You & I Do?

First, our focus should be continued protection of our elderly and immune-compromised.  Our focus should be placed on improving the immune systems of those at risk through diet, hand washing & quarantine of the ill.  The evidence does not support quarantine of the healthy.  Evidence does not support general public mask wearing.  And there is no evidence that continued business closure is beneficial.

• Reduce your risk of hyperinsulinemia.  Follow a carbohydrate restricted diet, exercise, control blood sugar, blood pressure, cholesterol and limit risk factors that suppress your immune system. Quit smoking, vaping, etc.
• For my patients with insulin resistant/hyperinsulinemia, I recommend Berberine 500mg twice daily with meals. (Talk to your doctor before you add any supplements or medications.)
• Use over-the-counter Zinc 10-30mg once daily – this has been shown to improve T cell control of viral replication.
• Use over-the-counter Melatonin 5-10mg nightly – this helps in sleep recovery and strengthening the T and B cell immune response.
• If you have been diagnosed with COVID-19, using Vitamin B3 (Niacin) has been show to be protective on the lungs.  Niacin is found in meat, fish and eggs (there’s reason for that ketogenic diet, again!)
• Ensure your loved ones, especially the elderly and immune suppressed, understand the truth about their risk of infection.
• Make a list of the things this pandemic has taught you. What can you do to better protect yourself in the future?
  1. We live in a society with a limited supply chain.
  2. We have become excessively dependent upon foreign business and supply
  3. We have become dependent upon “just-in-time” and over-night delivery systems
  4. We have a number of local and Federal deficiencies in our health care system
  5. How important to your health, personal liberty and constitutional rights is defense of the borders?
  6. How has freedom of speech, freedom of religion and freedom of assembly affected your family and your physical, emotional or spiritual health?

Consider the following poem in all of this:

Don’t be afraid to go outside and be a human being again.  And, pass the bacon.

May 13th, 2020 Update

So, now that we have the evidence regarding risk and infectivity, wearing a cloth mask that only decreases your likelyhood of infection by 1-20% isn’t really that helpful.

See the analogy:

Since Arizona has hit 100 degree temperatures our death count has dropped significantly.  Temperature is one of many factors that plays a role, but it does play a role.

April 24, 2020 Update

A recent paper written by Qasim Bukhari and Yusuf Jameel, both from the Massachusetts Institute of Technology, analyzed global cases of the disease caused by the virus, COVID-19.  They found that 90% of the infections occurred in areas that are between 37.4 and 62.6 degrees Fahrenheit (3 to 17 degrees Celsius), and in areas with an absolute humidity of 4 to 9 grams per cubic meter (g/m3).  Absolute humidity is defined by how much moisture is in the air, regardless of temperature.

Arizona just hit temperatures of 90 degrees Fahrenheit this week, the last week in April. This means, if the research is correct, there should be a notable decline in the transmission and number of infections in hot and/or humid areas of the country like the south and south west regions.

(https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3556998)

April 17, 2020 Update

Cases of coronavirus (COVID-19) in Arizona appear to have peaked.  Data from the Arizona Department of Health shown below.  Our state appears to be on a decline in regards to the number of cases overall. 

Also, reassuring, the numbers of deaths in Arizona from this virus appears to have peaked at the end of March.  Self-quarantine behaviors appear to have been effective in reducing exposures and deaths over the last two weeks.   I would anticipate with this good news, our Governor will issue return to work recommendations shortly.

April 6, 2020 Update

As of this morning, COVID-19 has doubled it’s numbers in Arizona in the last 6 days.  This is consistent around the world currently.  Current numbers place Arizona at: 

How Do I Know If I Should Get Checked?

Many people are asking me, “when should I get checked out?”  How should I know if this is worth going in to the doctors office to get checked out.  How do you know if you have COVID-19 or another common viral infection that arises during this time of year?  Use the table below to compare your symptoms. 

If you live in Arizona, the current recommendations and precautions are as follows:

• Effective close of business Friday, March 20, all restaurants in Arizona counties with confirmed COVID-19 cases are required to provide dine-out options only.
• Effective close of business Friday, March 20, all bars, movie theaters, and gyms in counties with confirmed COVID-19 cases are required to close.
• Halt all elective surgeries in the state of Arizona.
• If someone in your family has tested positive for COVID-19, keep the entire household at home and contact your medical provider.
• Expiration dates on Arizona driver licenses are delayed.
• State-wide closures of Arizona schools through Friday, April 10, 2020.
  • When school resumes, school administrators should develop and implement precautions to ensure schools are a safe learning environment, including social distancing measures, regular intervals for administrators to wash and sanitize their hands, and guidance on how to properly and frequently sanitize equipment and common surfaces.
• Recommendations to cancel or postpone mass gatherings of 10 or more people.
• Recommend telework and other alternatives when available.

There is a statistical projection tool just developed that I find very important.  It was created by a team of data scientists, engineers, and designers in partnership with epidemiologists, public health officials, and political leaders to help understand how the COVID-19 pandemic will affect their region. 

You can check it out here.

April 1st, 2020 COVID-19 Update

Note: Currently, there are no established antiviral therapies for COVID-19 infection.  A number of agents are being investigated based on in-vitro, “off-label” or extrapolated evidence.  Use of these medications and/or enrollment in a clinical trials with the risks and benefits must be discussed individually with the patient or the patient’s proxy.   

Antiviral or supportive therapies currently being studied include remdesivir, a novel nucleotide analogue, chloroquine, hydroxychloroquine, and tocilizumab, an interleukin-6 inhibitor. A registry of international clinical trials can be found on the WHO website and at clinicaltrials.gov.

“Doc, I Know I Had It!”

For all of you who are convinced you had COVID-19 in January or February, I highly doubt it.  I’ve been doing viral cultures on people since February.  These are the other common viral infections that act like COVID-19 and the flu (influenza A & B).  These often start with a sore throat, runny nose and chest congestion.  They ALL can cause identical symptoms of fever, fatigue, body aches, and could cause a dry cough:

• Parainfluenza Virus
• Coxsackie Virus
• Epstein-Barr Virus
• Herpes simplex Virus
• Adenovirus
• Echovirus
• Cytomegalovirus
• Measles Virus
• Varicella-Zoster Virus
• Human Immunodeficiency Virus (HIV)
• Dengue Virus

All of these can have prolonged symptoms for 2-8 weeks. Thankfully,  all of the patients who have been in my office, up to this point, had one of the above illnesses, not COVID-19.

What About Immunity?

One of the big questions that I get asked by my patients, by my family, especially my wife, is that of immunity after exposure.  What do we know?

Antibodies to the virus are induced in those who have become infected. Preliminary evidence suggests that some of these antibodies are protective, but this remains to be definitively established. Moreover, it is unknown whether all infected patients mount a protective immune response and how long any protective effect will last.

Data on protective immunity following COVID-19 are emerging but still in very early stages.  One study derived monoclonal antibodies from healing patients’ B-cells that targeted the receptor-binding domain of the spike protein and had neutralizing activity in a pseudovirus model[1]. 

Another study reported that rhesus macaques infected with SARS-CoV-2 did not develop reinfection following recovery and rechallenge [2].  However, neither of these studies has been published in a peer reviewed journal, and further confirmation of these findings is needed.

The Numbers

As of Wednesday evening, April 1, 2020, there are almost 215,200 cases of COVID-19 in the United states, and there have been 5,110 deaths.  This is now over twice as many cases seen in Italy at 110,574 infections.  Yet, Italy has had 13,155 deaths.   There are multiple factors that relate to these differences that I have discussed in my recent videos here, here & here. 

As of this evening, there are 1413 cases of COVID-19 and 29 deaths related to this viral infection in Arizona. 

This week, the white house recommended social distancing precautions to be extended to April 30th, 2020.  And, Arizona tightened up it’s recommendations on shelter-in-place recommendations.   

References:

1. Ju B, Zhang q, Ge Z, et al. Potent human neutralizing antibodies elicited by SARS-CoV-2 infection. https://www.biorxiv.org/content/10.1101/2020.03.21.990770v2  
2. Bao L, Deng W, Gao H, et al. Reinfection could not occur in SARS-CoV-2-infected rhesus macaques. https://www.biorxiv.org/content/10.1101/2020.03.13.990226v1.full.pdf

March 26th, 2020 Update

Recent study published in JAMA this week about the first 21 critically ill patients in Washington State reveal that the average age of these patients was 70 years old.   Many of these patient came from a nearby skilled nursing facility where exposure had occurred. 

Similar to those in China and Italy, the most common presenting symptoms were shortness of breath (76%), fever (52%), and cough (48%).  The average onset of symptoms prior to requiring hospitalization was 3.5 days. And 17% of those were admitted to the ICU within 24 hours of hospital admission.  

Of this group who was admitted, there has been a 67% mortality rate. 

95% of those requiring admission had pneumonia or bilateral pneumonia (86%).  This is consistent with other studies listed on this page below. 

This article supports the need to limit exposures to those who are older, have pre-existing heart and lung conditions and reside in nursing care facilities. 

Recent review of the literature reveals a stark difference in those that died from the 1918 influenza pandemic when social distancing was put into place in St Louis, versus Philadelphia.

 The first cases of influenza among civilians in Philadelphia were reported on September 17, 1918, but authorities downplayed their significance and allowed large public gatherings, notably a city-wide parade on September 28, 1918, to continue.  School closures, bans on public gatherings, and other social distancing interventions were not implemented until October 3, when disease spread had already begun to overwhelm local medical and public health resources.

In contrast, the first cases of the flu among civilians in St. Louis were reported on October 5, and authorities moved rapidly to introduce a broad series of measures designed to promote social distancing, implementing these on October 7.  The difference in response times between the two cities (~ 14 days, when measured from the first reported cases) represents approximately three to five doubling times for an influenza epidemic. The costs of this delay appear to have been significant.  By the time Philadelphia responded, it faced an epidemic considerably larger than the epidemic St. Louis faced.

Philadelphia ultimately experienced a pneumonia and influenza (P&I) death rate of 257/100,000 and a cumulative excess P&I death rate (CEPID) during the period September 8 – December 28, 1918 (the study period) of  a total 719/100,000 deaths.   

St. Louis, on the other hand, experienced a peak P&I death rate, while social distancing orders were in place, of 31/100,000 and had a CEPID during the study period of 347/100,000.

This is a stark difference.  It should be noted that after the social distancing orders were removed, there was a surge in deaths between November 30 – December 21st in St. Louis.  We can learn from this and be prepared for it in the coming months. 

March 21, 2020 Update

As Europe’s governments ramp up isolation restrictions to curb the coronavirus and the severe secondary pneumonia that occurs in most of those with severe infection, authorities in Rome on Friday announced 5,986 new cases and a record 627 new deaths.  This raises the totals to 47,021 infections and 4,032 fatalities in Italy. 

Spain had a huge surge in fatalities reporting 233 deaths yesterday, bringing their totals to 1326. Germany saw a surge yesterday as well with 1804 new cases in 24 hours. 

As of this morning, it appear that Italy and France have stopped public reporting of coronavirus (COVID-19) infections and deaths.  There comes a point where counting and public reporting are no longer helpful.  However, as of this afternoon, Italy reported 793 new deaths and 53,578 total cases.

The physicians and healthcare worker in Italy call it a “catastrophic apocalypse like no other ever seen.”  Their message to us is “get ready.”  

However, on the bright side of this, there is evidence that two simple medications that have been around for over 20 years may be effective in treatment of COVID-19.

Four  studies recently published reveal that treatment for COVID-19 with Chloroquine or hydroxychloroquine (Plaquinil), combined with azithromycin for 6 days is highly curative (1, 2, 3, 4). I discuss this in my YouTube video below. 

Chloroquine and hydroxychloroqine are commonly used for the treatment of malaria, rheumatoid arthritis and other connective tissue diseases.  Azithromycin is an antibiotic with some viral suppression properties.  Per President Trump’s announcement yesterday, the FDA is looking at approving these drugs individually for treatment of COVID-19. 

References: 

1. Yao X, Ye F, Zang M, et al., In Vitro Antiviral Activity and Projection of Optimized Dosing Design of Hydroxycholoroquine for the treatment of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), Clin Infect Dis. 2020 Mar 9,   pii: ciaa237. doi: 10.1093/cid/ciaa237. [Epub ahead of print].
2. Devaux CA, Rolain JM, Colson P, Raoult D., New insights on the antiviral effects of chloroquine against coronavirus: what to expect for COVID-19?, Int J Antimicrob Agents. 2020 Mar 11:  105938. doi: 10.1016/j.ijantimicag.2020.105938. [Epub ahead of print].
3. Wang M, Cao R, Zhang L, Yang X, Liu J, Xu M, et al. Remdesivir and chloroquine effectively inhibit the recently emerged novel coronavirus (2019-nCoV) in vitro. Cell Res. 2020. https://doi.org/10.1038/s41422-020- 0282-0 [Epub ahead of print].   https://www.nature.com/articles/s41422-020-0282-0
4.  Gautret et al. (2020) Hydroxychloroquine and azithromycin as a treatment of  COVID‐19: results of an open‐label non‐randomized clinical trial. International Journal of  Antimicrobial Agents – In Press 17 March 2020 – DOI : 10.1016/j.ijantimicag.2020.105949 .   https://www.mediterranee-infection.com/wp-content/uploads/2020/03/Hydroxychloroquine_final_DOI_IJAA.pdf

The One Difference in Survivors of COVID-19

I’ve taken a tremendous interest in the recent deaths caused by the  corona-virus infection.   The reason for my interest is high C-reactive protein (CRP) and high interleukin-6 (IL-6) levels in patients with this illness.   Recent data, literally hot off the press, demonstrates that those with the greatest risk of death had the highest CRP and IL-6.

I have a large population of metabolic syndrome, hyperinsulinemia and diabetic patients in my practice. About 85% of my practice has hyperinsulinemia.  They over produce insulin between 2-30 times normal in response to any form of ingested carbohydrate (simple and complex sugars, fruit, pasta, cereal, oatmeal, etc.) High insulin causes elevated CRP and IL-6

Why is this a problem?

A very interesting fact was published four days ago in The Lancet. They published a study looking at 191 patients in two hospital centers in China.  The authors found that the highest rates of death occurred in those with current hypertension, diabetes and/or coronary artery disease (heart disease or atherosclerosis of the arteries).  This virus traditionally causes a simple common cold.  Seeing this data in this particular viral strain dramatically changed my perspective on this virus.

These three maladies (hypertension, diabetes & coronary artery disease) are the three most common medical problems that I seen in my clinic, and they affect 85% of my practice population.  All three are caused and driven by hyperinsulinemia.  The higher your insulin response to starches or sugars, the more likely you are to have hypertension, diabetes and heart disease.

Insulin Raises Cytokine Levels

This elevated insulin in response to any starch or sugar, hyperinsulinemia, causes a rise in C-Reactive Protein (CRP) and Interleukin-6 (IL-6).  These two cytokines are responsible for mediating the inflammatory response to illness, injury and stress in the body.   These two hormones are ALWAYS chronically elevated in patients with hypertension (elevated blood pressure), pre-diabetes, diabetes, coronary heart disease and obesity.

C-Reactive Protein

CRP is a reactive protein produced by the liver in response to inflammation.  It is an “acute phase reactant” signaling the body’s immune system to respond to stress, inflammation or infection.  The presence of insulin directly raises CPR.  In my clinical experience, CRP normalizes within about three days of insulin returning to a normal level.

Interleukin-6

IL-6 is a cytokine.  It stimulates increased body temperature, regulates fevers and stimulates immune cells to function when infection or inflammation occur.   This dual acting hormone is produced by a number of cells, but predominantly by the adipocytes (fat cells), and has a negative feedback on the livers ability to sense the presence of insulin.  Elevated insulin levels over time cause increased size of fat cells.  This causes abnormally high levels of IL-6 production from the adipocytes and decreases the signal of insulin on the liver – leading to insulin resistance, pre-diabetes and diabetes.   Elevation of IL-6 often persists until the fat cells shrink back down to a non-obese size.  IL-6 can also stimulate elevated CRP as well.

Risk of Death

Patients with elevated IL-6 and CRP were at much greater risk of mortality when exposed to COVID-19.  Those that died, all of them, from this viral infection had IL-6 and CRP levels twice as high as those who recovered from the illness. That is profound.

Temporal changes in laboratory markers from illness onset in patients hospitalized with COVID-19.

What does this mean?

What does this mean to you and me?  It means that those with elevated IL-6 are more likely to experience a severe complication if exposed to this virus.  That means that 85% of my practice is at higher risk of mortality.  That’s what got my attention.  Hopefully, it gets your attention.

What can you and I do?

What can be done about it?  Follow a ketogenic lifestyle.  Studies published in November, 2019, reveal that a ketogenic lifestyle has an enhancing effect on immunity by suppressing viral replication and barrier effect through γδ T cells in the lung. 

This dietary approach is, also, the only one that I have seen clinically lowering CRP and IL-6 when using it long term.  Ketosis may be the perfect prevention.  Over the last 16 years of using ketogenic lifestyles, I have seen this pattern improve thousands of times.  The presence of ketones immediately suppresses the production of IL-6 and improves the stimulus for CPR production at the liver.  Cutting out carbohydrates lowers insulin back to a normal baseline within 3-7 days for most people.  CRP returns to normal within three days of fixing your diet.  And, IL-6 begins to decline immediately.  In my obese patients, it can take 18-24 months for IL-6 to return back to normal.

Additional Measures

Don’t stress.  The overly hyped fear mongering produced in the media in the last two weeks raises your stress level.  Turn off the T.V. and stop listening to the 24 hour news cycles.  Over the next couple of weeks, while the risk of viral exposure is the highest, the following precautions are essential:

1. Follow good hand washing practices
2. Limit exposure to those who may be carrying this illness through social distancing
3. Get good sleep (six or more hours of restful sleep)
4. Use a complete pharmaceutical grade vitamin
5. Spend 20-30 minutes outside
6. Do something physicalfor 20-30 minutes 5-6 days per week

Taiwan and Hong Kong have instituted strict quarantines and you can see their effect in the graph below.

Above all, enjoy some bacon.  Seriously.

You can’t eat bacon?  Have a nice rib eye.  Either way, based on the data above, your ketogenic lifestyle is the very best thing you can do to avoid serious infections, including COVID-19.

I talk about this an much more here on my YouTube video: