Dr. Pastore is a practitioner, consultant and researcher in biomedicine and human nutrition. In all his efforts he strives to develop novel methods using an amalgam of biomedical and clinical informatics data, encompassing biological observations to solve or assist in resolving a problem.

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COVID-19 is not just a problem for the elderly population - young and healthy individuals can also end up hospitalized, or even on a ventilator, depending on their genetics.

There are reports of marathon runners under the age of 50 almost dying from COVID-19. I personally am aware of a case of a woman in her early 20s on a ventilator from COVID-19 complications. What is the reason why healthy people in addition to the elderly can succumb to COVID-19?

The term “cytokine storm” encompasses a multi-factorial hyperinflammation associated with increased expression of different cytokines including but not limited to interleukins (IL), chemokines, granulocyte colony-stimulating stimulating factors (G-CSF), and tumor necrosis factor-1a (TNF).

Cytokines are small proteins secreted by cells that have a major impact on the normal communication system between cells. Cytokines is a blanket term. There are many different cytokines, including named after the cells that secrete them such as monokines, the type of cytokines released by a type of white blood cell called monocytes.

I am aware of at least 14 different cytokines that have been reported to be significantly elevated in COVID-19 patients. This number will vary and change. Regardless, it is concerning.
According to recent published studies the body of available evidence suggests that a subgroup of patients with severe COVID-19 might have a cytokine storm syndrome. The culmination of this “storm” is a massive immune system response that actually ends up negatively impacting normal pulmonary function, in some cases leading to death.


Different cell types such as B cells (which create antibodies to help our immune system remember enemies and threats), T cells, macrophages, eosinophils and basophils work in concert, communicating with each other using the language of cytokines. 

For example, the phagocytes macrophages will use specific cytokines to create specific responses by B and T cells, and so on. This broad communication network uses many “dialects” of the language of cytokines. Meaning, many different cytokines are stimulated resulting in a chronic, always on alert immune system response.

Immunologically, the lungs are highly dependent on a vigilant immune system and inflammatory response because of their constant exposure to a wide variety of infectious agents, particulates and gases as per the process of respiration. In classic immunology we learn that as part of homeostasis living in a modern world the lungs mount a protective service by deploying cytokines that regulate host defense mechanisms.

One could say cytokines play a crucial role in immune homeostasis in the lungs. There is a law to cytokines in the lungs. First, they need to categorize friend from foe. Second, cytokines help the immune system ignore or attack. Third, cytokines must act as a conductor of a fine orchestra, and govern or regulate the symphony of that decision - to activate an all out immune attack, or calm the immune response, considering tolerance instead, and cease the attack once the battle is being won.

In cases of COVID-19 cytokines in the lungs react in an all-out war, first against the coronavirus that is behind the COVID-19 symptomatology and secondly against healthy lung tissue due to an exaggerated immune response. This infection is linked to cells in the lungs committing suicide (a process known as apoptosis) as part of the defense mechanism to prevent the spread of this virus. 

Additionally, there is solid evidence of a pro-inflammatory response that leads to capillary leakage and the stimulation of lymphocytes, neutrophils and macrophages that secrete cytokines targeting the vascular endothelial cells in the lungs, reducing the ability to breathe. That’s just one pathway in a highly complex process that can lead to the urgent need for a ventilator.

Clinical studies on treatments to address the cytokine storm include drugs such as Fingolimod, which is a sphingosine 1-phosphate receptor modulator. It is in a class of drugs used as immunomodulators. Other medications that directly address the cytokine storm include the anti-inflammatory medications sarilumab, anakinra, emapalumab and tocilizumab. 

These medications offer a calming influence on the immune system. Combining immunomodulators and or anti-inflammatory medications with antiviral medications and other palliative care methodologies are logical treatment paths to taming the storm and granting recovery.

I cover such research in my article titled An Overview of Treatment Research for COVID-19.

You can find my podcast covering some key aspects of COVID-19 here - 

https://drrobertpastore.com/podcasts/058-coronavirus-covid19

What is the reason why healthy people in addition to the elderly can succumb to COVID-19? One key reason is cytokine storm. The culmination of this “storm” is a massive immune system response that actually ends up negatively impacting normal pulmonary function, in some cases leading to death.  


COVID-19 and Cytokine Storms

Review of Dr. Pastore’s qualifications 

PhD Biomedical informatics, nanomedicine and clinical informatics from Rutgers University, School of Health Professions

Expertise is understanding biomedical sciences, human genetics & RNA mechanisms, disease processes & systems, nanomedicine, drug discovery

Graduate degree in Human Nutrition, Certified Nutrition Specialist

All of the information today is backed by science 

What is the coronavirus, what is COVID-19 and how does this compare to SARS 

Coronavirus - simply type of virus, under microscope has pointed structure looks like it wears a crown

Been exposed to coronavirus for a long time - cold, mild upper respiratory tract infection where bodies fight back - no cure

“Novel” coronavirus = newly identified coronavirus type, no resistance against it

Severe acute respiratory syndrome, caused by a novel coronavirus at the time

Jumped from animal kingdom to humans, which is what is believed to have happened with the new 2019 coronavirus

The upper respiratory infection some people develop after contracting the novel 2019 coronavirus (hence the name COVID-19)


You can be exposed to the coronavirus, be a carrier of the coronavirus, potentially exhibiting zero symptoms ever, transmit the virus to someone else and they can develop COVID-19 symptoms 

Coronavirus is spreading faster than SARS in 2003 [8:00]

Less severe of an illness in the majority of those infected when compared to SARS

Those with strong immune systems may only ever feel incredibly mild cold/flu symptoms or nothing at all, yet are giving the coronavirus to others with weaker immune systems [9:40]

There are some individuals who do not feel sick, infect others, and then  develop COVID-19 symptoms

What makes the coronavirus so dangerous? 

Spreading faster than any other virus in history

Those that have passed away from COVID-19 experienced a “cytokine storm” [11:30]

Mutli-factorial hyper-inflammatory process

Over-stimulates the immune system factors, causing the lungs to shut down the normal process of breathing

Genetic polymorphism (genetic expression) in gene 

 can allow COVID-19 to get deeper into the lungs, greater chance of developing cytokine storm requiring hospitalization & ventilation [13:25]

As of April 9, 2020, 25% of people walk around asymptomatic (constantly changing) [17:00]

People need to behave like they have the infection

Less-known or more rare symptoms of the coronavirus beyond cough/fever/chills/aches 

3% of carriers present with pink-eye, can be the only symptom

Diarrhea & other gastrointestinal/digestive complaints can be your only symptoms, don’t assume it’s a stomach bug or bad food

Sudden confusion - potentially caused by reduced blood-oxygen levels

Dry “barking” cough, fever, chills, body aches, headache, shortness of breath, congestion

Virus is RNA strands that fool your own cells into reproducing the virus (making your body “photocopy” the virus to take over more of your body) and then bust out of cells & take over nearby healthy cells

Replication of virus + immune system response causes the common symptoms

Immediately notify your physician if these symptoms arise, get immediate medical help if you have trouble breathing or pale/bluish skin [24:30]

2-14 days from time of exposure, if at all

Some reports of people being sick/developing symptoms beyond that

Learning more about how long virus can survive.

can live 3 days on stainless steel, 24 hours on package delivered to your door [26:25]

Those with pre-existing conditions like diabetes, heart disease, lung diseases

Immuno-compromised individuals - HIV, autoimmune diseases, undiagnosed or newly diagnosed celiac disease patients that are sIgA deficient

Some feel fine after 3 days, some passing away - why?

Some have the ACE2 polymorphism that better prevents the coronavirus from infecting the body

Pre-existing conditions, those with poor health

Body produces surfactant chemical that makes lungs sponge-like [31:05]

Genetic polymorphism that lowers surfactant production, makes lungs less sponge-like and makes breathing more challenging with COVID-19

Social distancing - use technology to virtually connect with others

REALLY wash your hands - scrub & sing “Happy Birthday” twice

Other types are NOT designed to kill novel/new viruses

Stay home as much as possible - 6 feet from others is not enough

Don’t touch your face before washing your hands

Study showed even trained, educated medical professionals touch their face 23 times per hour

Clean & disinfect all surfaces that could have been exposed (groceries, counter where you rested groceries, car surfaces)

Alcohol-based surface cleaners need to have at least 70% alcohol

Strip off & wash your clothing in hot water, warm shower with soap as soon possible

So far, we know virus can live on cloth for 3 days

How is COVID-19 treated? Current research shows….

No FDA/CDC/WHO approved medical treatment

Hospitals are practicing palliative care, symptom treatment

Ongoing experimental medical trials around the world (approx. 60 so far)

NYU hyperbaric oxygen therapy - putting COVID-19 patients in more oxygen-rich environment, previously used to treat lung damage

Repurposing FDA-approved drugs to treat COVID-19 [47:15]

Scientists are using drugs that have already been approved for other conditions and are currently being studied on effect to combat COVID-19 & slowing the spread within the body

Limits the virus spread so your own immune system can battle it

Believed to inhibit the action of RNA polymerase, intravenous delivery

Viral RNA-polymerase binder, intravenous delivery

Transmembrane protease, serine 2 inhibitor

Blocks penetration of coronavirus to get into cell

Dr. Pastore shares the science and latest research behind coronavirus, how it differs from COVID-19 and what makes it so dangerous. As he is actively treating those with the virus, he covers the lesser-known symptoms, the genetic polymorphisms (gene expression) that put some more at risk than others beyond age and pre-existing medical conditions, the current status of treatment for COVID-19 and what you can do to keep you and those around you safe. 

#058 - On the Coronavirus & COVID-19

Celiac disease is a serious autoimmune disease that is not receiving the attention it should by many medical professionals and even the National Institutes of Health. It can act as a clinical chameleon, eluding diagnosis, and this has resulted in the average time to diagnosis being ten years, which I refer to as the “decade to diagnosis.” Here are some startling facts.

Data suggests 83% of those with celiac disease are undiagnosed.

Prevalence in the general population is 1 out of 100 but increases to 1 out of 10 if there is a relative with the disease.

The incidence in the United States has doubled every 15 years since 1974.

There is a 2 to 4 times increased risk in coronary artery disease and small intestinal cancer for those with celiac disease over the general population.

There is an increase in all-cause mortality for those who are undiagnosed.

Currently, the ONLY accepted treatment is a strict life-long gluten free diet, but data is indicating inadvertent exposure to gluten from certain prescription medications, cross-contamination and the contamination of foods routinely thought of as being gluten free.

While those facts can be alarming, for me the true story goes back to the clinical aspects of the disease, the delay in diagnosis and how it presents to the medical professional in practice. Often symptoms are vague, outside of the gastrointestinal tract, and cause the physician or even specialist to either not consider celiac disease as a possibility, or an incomplete diagnostic panel is undertaken, which can result in misdiagnosis.

Deepening this story is the strong potential that the physician may not be fully aware of the nuances of celiac disease testing and result in continued patient suffering and the decade to diagnosis. McCormick and colleagues presented this potential issue at an American College of Gastroenterology conference and Assiri and colleagues and Zipser and colleagues discovered similar findings.

 For example, for many doctors an IgA tissue transglutaminase antibody analysis could be the first and only blood test used to determine risk in a patient. Yet, a selective IgA deficiency has a rate of occurrence 10 to 15 times more frequent in celiac disease patients than their non-celiac counterparts.

 With that in mind, if testing a single IgA based gluten test, it is wise for physicians to measure total serum IgA first, because that should dictate the correct testing course of action. An IgA deficiency renders the most popular initial blood test screening moot and physicians should consider other serology, measuring gliadin DGGL gliadin deaminated IgG antibodies.

There are some options for serology testing for the potential celiac disease and should be selected on unique requirements of the individual patient. These tests include tissue transglutaminase IgA and IgG, DGLDN gliadin deaminated antibodies IgG and IgA, endomysial antibodies IgA as well as celiac associated HLA-DQ alpha 1 and DQ beta 1 medium high-resolution DNA typing.

 The goal of any tests for celiac disease risk is to identify if a biopsy is required, which is the gold standard for celiac disease diagnosis in the United States.

In other cases, uncommon symptoms may actually be the dominant ones presenting in clinical practice. They were for me and contributed in my more than a decade to diagnosis. Referencing the aforementioned work by McCormick, Assiri, Zipser and their respective colleagues, not all health care practitioners may be aware of all the associated symptomatology. Take a look at an example of classic symptoms and non-classic symptoms and manifestations below.

Now look at an example of sIgA deficiency symptoms and imagine how this can present to a physician without experience in celiac disease diagnostics.

Incomplete or incorrect medical decision-making and my personal experience was the catalyst for my work in enhancing diagnostic knowledge and the understanding of the symptomatology, culminating in the creation, study and publication of a clinical decision-making expert system for celiac disease assessment.

Regarding treatment being a life-long gluten free diet, data collected by researchers from the pharmaceutical company Takeda and the Celiac Disease Foundation reported 74% of individuals with celiac disease claimed they were exposed to gluten within the past 30 days.

 If you really think about it that is not a shocking piece of information when gluten is omnipresent and cross contamination risk is so high. In 2010, Thompson and colleagues had twenty-two gluten free grains and seeds sent to a lab for gluten analysis.

 Seven of the products were contaminated with gluten.

 These products were considered gluten free by default because they are naturally gluten free and therefore were not labeled gluten free. Products studied included millet flour, millet grain, buckwheat, soy, brown rice, amaranth and flaxseed.

 These are gluten free foods by nature, but obviously gluten contamination occurred via processing.

 Strict gluten free labeling and testing is required to assure a product is gluten free.

Moreover, there are known current conditions and diseases that have been linked to celiac disease in multiple studies in peer-reviewed literature.

 Any of these diseases below should alert a physician to test for celiac disease risk.

It can take a village for a proper diagnosis to transpire. Celiac disease encompasses many different diseases, leaving signs to alert practitioners to start the diagnostic process. The Canadian Dental Association released a clinical diagnosis guide for dentists based on the oral manifestations of celiac disease, which include chronic dental carries, weak enamel and aphthous stomatitis, in an effort to screen patients for further testing.

 The American Journal of Clinical Dermatology published a guide for dermatologists to enhance the recognition of cutaneous manifestations of celiac disease, with dermatitis herpetiformis being the primary sign.

 Turco and colleagues noted an increase in anxiety and depression in children with celiac disease and functional intestinal disorders.

Due to the fact that celiac disease can present as a clinical chameleon, alter the microbiome, is implicated in other autoimmune diseases, and can present with signs and symptoms that will most likely be seen by many different specialists in health care, a focus on obtaining an accurate diagnosis is key. If all these specialists are up to date in their knowledge of the many ways celiac disease can present in clinical practice and linked together in a health care information system, and sharing data via an electronic health record, may create an environment for a more accurate and prompt diagnosis, and improved continuity of care.

Celiac disease is a serious autoimmune disease that is not receiving the  attention it should by many medical professionals and even the National Institutes of Health. It can act as a clinical chameleon, eluding diagnosis, and this has resulted in the average time to diagnosis being ten years, which I refer to as the “decade to diagnosis."

Celiac Disease: A Clinical Chameleon

In this episode, Dr. Pastore covers infertility in men and women could be caused by Celiac Disease. If you have the HLADQ2 or HLADQ8 Celiac gene but do not have Celiac disease, your child still could be born with or develop Celiac disease. If one of the biological parents are a gene carrier or are a diagnosed Celiac, a gluten-free diet should be followed during pregnancy

Dr. Robert Pastore, PhD, CNS

Dr. Pastore is a practitioner, consultant and researcher in biomedicine and human nutrition. In all his efforts he strives to develop novel methods using an amalgam of biomedical and clinical informatics data, encompassing biological observations to solve or assist in resolving a problem.

Dr. Pastore in the Press

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