1st Drafts

Red heads and fair skin, Vit-D, ACE-II and of course COVID-19


Here are some articles placed here in response to Michelle Nyland.


"I have a question, why is “Caucasian with red hair and light complexion” specifically called out, specifically? Is there evidence of a trend?"



When we provided results from our questionnaire two years ago, results for race looked like this.


Results from November 2020 - Q6 - Race


Overall, not a huge number of respondents at that time, overwhelmingly 'White or Caucasian' (89%) and those few with 'red hair and fair skin' were less than 5%.


Why had they even been included among the usual choices for race/ ethnicity?


At the time of creating this questionnaire, topics of interest included:


  • characteristics of the COVID-19 illness (of course!), but also
  • findings potentially related to race
  • findings potentially related to use of vitamins/ supplements
  • especially Vitamin D as importantly related to COVID-19
  • findings potentially related to the ACE-II receptor and other components of the renin-angiotensin-aldosterone system usually thought of primarily related to blood pressure control.


So as subjects for further exploration had through the questionnaire, come to mind,

certain choices were made and the 'red hair/ fair skin' choice included.


During the two years since, most of the above list were confirmed as important with respect to COVID-19 and its clinical presentation.


So the reasoning behind it then was that since Vitamin D has a link to COVID-19 diagnosis and treatment, and since red heads with fair skin make more Vitamin D precursor in their skin than BAME populations (for comparison) and since the entry of the SARS-CoV-2 virus is related to ACE-II which is also found in the skin, ...


... would their be a hint about this in the results of the survey?  Meaning, a proportion of respondents with red hair/ fair skin would be typical of the population (2% to 4% depending on location, of course more dense among the Scots), or not. For the 6 respondents above, supplementation with Vitamin-D and measurement of blood levels was variable. Some took more, some not.


All that to mean that no striking discoveries emerged from this component of our study two years ago. But that's OK.


Would "red heads" create enough Vitamin-D due to their fair skin creating more precursor, and through that have added protection against COVID-19? 


We certainly did not answer that question two years ago! But it did encourage us to be thinking at a cellular level where the problem (and solution) linked to COVID-19 is certainly still going on.


But the 'red hair/ fair skin' topic remains quite interesting. 


Here is a little bibliography from the experts that provides a nice background.


Michael F. Hollick of Boston is certainly a key name to remember when it comes to everything about Vitamin D, and including characteristics of its creation (or its precursor)  in the skin in response to UV-B light. We'll leave the topic of melanoma and other skin cancers in those with the fair skin/ red hair genetics aside for some other venue.


Vita-D and melanin during COVID-19


Red Hair__ A Mutation, A Royal Trait, and Sometimes a Curse (Sheikh 2009)


Vitamin D and Health Evolution Biologic Functions_


The Vitamin D Epidemic and its Health Consequences (Michael F Hollick)


The evolution of human skin pigmentation involved the interactions of genetic, environmental, and cultural variables


Deciphering the Potential of Pre and Pro-Vitamin D of
Mushrooms against Mpro and PLpro Proteases of COVID-19


Effects of Angiotensin II Receptor Signaling during Skin Wound Healing


Association of Vitamin D Status with SARS-CoV-2 Infection or COVID-19 Severity__ A Systematic Review and Meta-analysis


A computational model for previtamin D3 production in skin


Is the shielding effect of cholecalciferol in SARS CoV-2 infection 
dependable? An evidence based unraveling


Aging Decreases the Capacity of Human Skin to Produce Vitamin D3



So the answer to Michelle's question is that all of these components contribute to 

our understanding of why some people catch COVID-19, and some don't, and some several times, and some get sicker than others, and in some it will last much longer (see this article for that recent update to Duration of Illness in our own study).


Certainly who one is (and the genes one carries) contributes to the COVID-19 experience and how it might manifest in each of us: red heads, BAMES, old folks and all the rest! One should not just think of this as "premorbid conditions" but try to get beyond that to a deeper level.


Thanks for the question Michelle !


When I was in Medical School and afterwards a Surgical Resident, I had the pleasure of working with Dr. Alex Breslow. He was a Pathologist best known for his system of analysis of melanomas and their prognosis based on depth of penetration into the skin. I even had the privilege of having him become one of my patients.


Anyway, Doctor Breslow was a wonderful man. Always quite busy of course as head of the Path department and Researcher.


But never too busy for a question.

Sometimes, and rather sheepishly, a student would see Breslow's coat tails flying by and would risk a ... "Doctor Breslow... excuse me but ..." as introduction to a student's question.


Breslow would always wheel around and shout: "Yes?! Please!!" as if to say, thank you for stopping me to ask your question. If his obvious enthusiasm hadn't quickly scared off the student, he would get an answer to his question right then and there. Always.


So I'll close here and in memory of Doctor Breslow, say to Michelle: "Yes! Please!!"


And Thank you for asking.



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Updates on Duration of Illness

Here's a spot to place these data as they come in.


Goal? To update the Duration of Illness information collected back in August, September, thru November of 2020.


Haven't yet devoted 3 minutes to answering this survey's 8 questions? 

If you have "long-term" COVID-19 shame on you!


Here's the link (was already posted below), and share it with those who should be the respondents.


You know who they are. :


55 respondents so far is not bad. But we're shooting for millions! (Just like the virus did).



Data from Nov



As of 14 November, 2020 (55 respondents ) 

(but last responses came in on October 20, 2022, so we'd like to see more to give an update that's up to date).


55 Total Responses - ALL




Subgroups :


Still sick ...



40 - Illness Still Present




Almost Better ...


11 - Illness Resolving





No Longer Sick with "long-term" COVID-19...



4 - Illness No Longer Present




Other results from the survey on SurveyMonkey (8 questions) will be presented in a follow-up article once the number of responses has increased a bit.

I'll save interpretations and comments on the above until then.


If you haven't yet responded to this 8 question, 3 minutes to respond little survey, here is a link that will take you to it. Of course, only those who have or had a presentation suggesting "long-term" COVID-19 need apply.


And just FYI as you respond to this survey: "...respondents can change their answers on any survey page until they complete the survey." (After that, it is what it is).


Respondents above include individuals who responded to our first questionnaire from 

August to mostly November of 2020, and more recently on one of the Facebook Groups. 

Very nice to stay in contact with those from 2 years ago and be supportive as we can be from a distance. Also interesting to witness that their estimate of the day their illness began, varied little if at all from 2020 to today. (That's the value seen each time in the bottom right corner above).


If nothing else, the above duration numbers might serve to generate a bit more empathy

from the Medical Community for those with this "just too long now" illness, and drive towards deeper research in pursuit of the goal. Perhaps a bit more open-minded thinking about all of this as well ...


"The goal ... what's that ?"


To relieve suffering and heal the sick where possible. 


I thought it always was the goal.

But perhaps, 42 years and 3 months after I started to practice Medicine and Surgery, I'm now a little off the mark.




Well, still a disturbingly high number or percentage of people who are still sick after a long time.



Big Picture?


Well overall, including those that are getting better or over it, 73% of these respondents with "long-term" COVID-19 have an illness that's still present, and present on average  for 25.8 months.


Those figures emerged from the responses that were last given October 20, 2022.

So we'd still like to see some more responses.


Such data are a very clear call for help to sustain and support all those who have "long-term" COVID-19 and are still struggling with it.


And here below, the last update ...


67 Total Responses - ALL respondents




'nuff said.


But do come back from time to time.






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Updated data for Duration of Illness in "long-term" COVID-19.




First of all, for those who have responded this day (Oct. 10, 2022) to yesterday's outreach on Facebook in the Endurance Athletes Group, a huge "Thank You" !


As the (old) song used to say: "... Tell your Ma, Tell your Pa, our Love's Gonna Grow." (Bob Dylan).


So do spread the news. Either to others in your posts on FB or by personal contact as you see fit.


I'll be posting updates on these data as often as possible. Use it as you like, while underscoring when you do that these results are quite "young." I haven't yet tortured them statistically to augment their potential value. That will be coming down the road once the response is a bit more robust.


Here are the results from the incoming data in less than 24 hours after I made the following request.


Update Duration 1 thru 6


So get with it! Find more responders who understand what we're doing here together.


Again, and as I copied here from my Facebook Post:


"In screening potential subjects for inclusion in an ongoing study of “long-term” COVID-19, duration of illness (not surprisingly) is one such variable.

Other variables besides mean illness duration used for initial screening include: delay of diagnosis, total symptom number during illness, physical symptom number, number of emotional symptoms, and the ratio of the two
to mention some others.
Initial results developed for such comparisons go back to 2020, and as already presented in detail at (have a look).
At that time, (Nov. 2020), the illness duration in months (from when illness began to when a subject with ongoing symptoms answered the questionnaire) was 6.575±1.743 months for females, 6.473±1.587 months for males. 54% of respondents became ill after 22 March, 2020, but often very close to that date. Other result findings from then, are available at the above site.
Clearly, (as we all now know), many individuals with “long-term” COVID-19 have a duration of illness quite different (and longer) than that initially discovered mean of about 6.5 months.
That earlier number is mostly of historic importance at this time. It should not be applied to categorize, compare, include or exclude those presenting with PASC or ‘long COVID’ today from further study. But duration of illness remains a most useful and essential parameter for further study.
So this is a request to members of this group to help with an update.
Responses will be tabulated and presented here as well as at, the site that summarizes our current intervention here in Belgium.
This doesn’t require an extensive questionnaire nor any personally identifying data.
If you know the exact date when your illness began, send that, and the date of your response to this request (or the date when your illness ended), to ‘’ If you don’t have an exact date but know the month and year, use that. The mid-month date of the 15th will be used in such cases. Values supplied will be used to generate a new and current estimate for duration of illness. While many large studies are currently underway and others have already published such information, estimates still present a wide range for duration of illness. So I’ve come back to this group as I did 2 years ago since so many responded at that time. Thanks in advance to those who can respond again now. For any questions, use the same email address or place questions here."
Again, if you have some data to input, send it by email to ''.
You could leave a comment here below, but that may be a little complicated since the host's format is in French. Not a problem? Then place it here below.
- Date when your illness began.
- If you have the month but not the day date, Month and Year. (we'll use Day 15 of the month)
- Is it over for you? If it is, Great ! Then include the date when you think this finished.
- It's not over yet? (Very Sorry! Prayers for a recovery soon ... ) Then we'll use your response date as the end date for duration (so far).

Be Well Soon !

Fire those off to 

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Thanks for visiting!

To translate this page, select your

language from the dropdown menu below:

Blood Tests to Be performed, and why.


One could select many tests, in pursuit of the many symptoms found in those experiencing the "long-term" variant of COVID-19. These clinical findings and their prevalence have been effectively summarized in this meta-analysis article. The list is similar to the symptomatic findings presented last year on our site, These symptoms that emerged from our previous questionnaire have been summarized on this page.


The selected analytes will focus on those that may prove most useful in evaluating this study's intervention using light.



  C - Reactive protein (CRP)  



The following summary is found at this link:


Aspects of CRP with a potentially important link to our study have been highlighted.



"C-reactive protein (CRP) was discovered by Tillett and Francis in 1930. The name CRP arose because it was first identified as a substance in the serum of patients with acute inflammation that reacted with the "c" carbohydrate antibody of the capsule of pneumococcus.

CRP is a pentameric protein synthesized by the liver, whose level rises in response to inflammation. CRP is an acute-phase reactant protein that is primarily induced by the IL-6 action on the gene responsible for transcription of CRP during the acute phase of an inflammatory/infectious process. There is some question of whether dysregulation of the role of CRP in the clearance of apoptotic cells and cellular debris plays a role in the pathogenesis of systemic lupus erythematosus (SLE), but this has not been definitively demonstrated. It has been demonstrated to have some protective properties in animal studies on lung tissue in alveolitis by reducing neutrophil-mediated damage to the alveoli and protein leakage into the lung.

CRP has both proinflammatory and anti-inflammatory properties. It plays a role in the recognition and clearance of foreign pathogens and damaged cells by binding to the phosphocholine, phospholipids, histone, chromatin, and fibronectin. It can activate the classic complement pathway and also activates phagocytic cells via Fc receptors to expedite the removal of cellular debris and damaged or apoptotic cells and foreign pathogens. This can become pathologic, however, when it is activated by autoantibodies displaying the phosphocholine arm in auto-immune processes, such as idiopathic thrombocytopenic purpura (ITP). It can also worsen tissue damage in certain cases by activation of the complement system and thus inflammatory cytokines.

As compared to the erythrocyte sedimentation rate, which is an indirect test for inflammation, the levels of CRP rise and fall rapidly with the onset and removal of the inflammatory stimulus respectively. Persistently elevated CRP levels can be seen in chronic inflammatory conditions such as chronic infections or inflammatory arthritides such as rheumatoid arthritis.

There are numerous causes of an elevated C-reactive protein. These include acute and chronic conditions, and these can be infectious or non-infectious in etiology. However, markedly elevated levels of CRP are most often associated with an infectious cause (an example of pathogen-associated molecular pattern recognition). Trauma can also cause elevations in CRP (alarmin response). More modest elevations tend to be associated with a broader spectrum of etiologies, ranging from sleep disturbances to periodontal disease."


Another reference for CRP, including normal and abnormal levels seen.


Pertinent to CRP findings in those with COVID-19, one can find many references. The following selected reference serves well:


C-reactive protein and clinical outcomes in patients with COVID-19






  Lactate Dehydrogenase (LDH)  


A detailed summary from a biochemical perspective is found here.


Though not very specific, elevated LDH levels are taken as a sign of tissue damage or disease.

Normally, it is part of the process of converting sugars into energy.


Strenuous exercise will also increase LDH.


Normal levels of LDH in the blood can vary depending on the lab, but usually range between 140 units per liter (U/L) to 280 U/L for adults and tend to be higher for children and teens. In cerebrospinal fluid, normal levels are: 70 U/L or lower for newborns. 40 U/L or lower for adults.


In the setting of COVID-19, increased LDH levels have been reported to signal clinical deterioration in several studies. Here is one such study.





  Inorganic Phosphate (Pi)  


Our analysis of results from our questionnaire of COVID-19 sufferers last October 2020, included a review of the probable importance of Inorganic Phosphate (Pi) for this population.

Rather than repeating those topics here, a link to the related page on our site will be of practical use. It can be viewed at this link: Inorganic Phosphate - A Syndromic Approach: Respiratory Alkalosis and Hypophosphatemia.


The above information once reviewed, should leave one with a clear sense of why Inorganic Phosphate (Pi) has been selected for inclusion in the objective data obtained through labwork of samples from enrollees in our protocol. Hypophosphatemia-induced Cardiomyopathy is a topic that should also be of more than passing interest, especially for endurance athletes participating in the present work. The topic of virally-acquired myocarditis (heart muscle inflammation) appears with increasing frequency.


This is an appropriate place to mention that while we are committed to the importance of inorganic phosphate to energy generation at a cellular level, we feel that the energetics problem suffered by most with "long-term" COVID-19 occurs upstream to incorporation of phospate. Part of the electron transport chain has been hijacked by the virus and left broken or damaged after the virus is no longer present. As explained elsewhere, that component is the principle target of the present study's intervention using specific wavelengths of light.


Supplementing low phosphate levels when present, may not be fully effective as long as key electron transport chain components remain damaged. Normal levels of cellular energetics may not be obtained, or only very slowly over prolonged periods, if this is not first addressed.





  Haptoglobin (Hp)  


Red blood cells contain hemoglobin (Hb) as the iron-containing oxygen carrier. 

When red cells become old (senescent) and eventually break down, hemoglobin fragments are released into the circulation. These have a toxic effect. 


Haptoglobin (Hp) binds this free hemoglobin, reducing its toxic oxidative effects.

The usual rate of chronic destruction of red cells normally, does not overpower the ability of usual haptoglobin levels in dealing with demand. So Hp levels remain normal. 


Red cells can also break down in various disease states, apart from the normal breakdown seen with aging cells. One can summarize these as hemolytic anemias reflected in diminished red cell mass.


During hyper-hemolytic conditions or with chronic hemolysis, Hp is depleted and Hb readily distributes to tissues where it might be exposed to oxidative conditions. In such conditions, heme can be released from ferric Hb. The free heme can then accelerate tissue damage by promoting peroxidative reactions and activation of inflammatory cascades.


So usually, as hemolytic breakdown increases, haptoglobin levels will drop because it is being used up in the process of controlling increases in free hemoglobin in the plasma.


Here is a useful review of these interactions of haptoglobin (Hp).


In pursuing evidence for hemoglobin damage due to COVID-19, this has also been studied in this illness as presented here.






  Complement C3   


C3 is the central component of the complement activation system, a vital component of the immune response system. It can be activated through 3 different pathways, converting inactive proteins into functional fragments. This complex response system is well summarized in this resource. It represents an innate immune response tool which responds to platelet activation and/ or contact with antibody molecules.


Local inflammation, thrombosis and tissue damage also result from activation of the complement system. Therefore its relation to COVID-19 cases and the present study, since it behaves as an overactive complement-mediated disease.


In COVID-19 patients Complement C3 has been identified as a unique risk factor for disease severity.


In COVID-19, complement inhibition is being pursued as a way of reducing tissue damage.






  Interleukin 6 (IL-6)  


Interleukin-6 is one of several, (here numbered 1 to 23), proteins or glycoproteins.


Their name arose from the observation that they function in communication between (inter) white blood cells (leukocytes).


They are a vital part of the machine that is the ever-vigilant human immune system.


One can find that a tremendous amount of research has been done to define the widespread role of the 17 to 20 different human interleukins in normal immune functioning. They can also malfunction at times, leading to auto-immune diseases in which cells produce substances that attack human cells when no such attack is indicated. In this specific domain, and others relating to chronic diseases such as psoriasis, much remains unknown about interleukin-6 (IL-6) activities. Nevertheless, a great deal is known about specific structure-function relationships of this molecule.


IL-6 is also known as B-cell stimulatory factor 2 or BSF-2, and interferon beta-2, and has had other names as well, usually based in discovery of specific functions. It is a cytokine (the word means ‘cell mover’), involved in many biological functions such as driving the differentiation of B cells into cells that secrete immunoglobulins (antibodies). It also drives nerve cell differentiation and activates certain hepatocyte functions in the liver. The gene for IL-6 is located at chromosome 7p21 in humans.


IL-6 can be produced by several different cell types including fibroblasts, B cells, macrophages, and endothelial cells lining blood vessels. It stimulates several types of leukocytes (White Blood Cells). It stimulates liver cells to rapidly produce Acute Phase Proteins.


IL-6 directs B-cells (a type of white blood cell) to differentiate into plasma cells that produce antibodies.


In driving such events normally, one might find levels of IL-6 in the blood plasma of 0 to 30 pg (picograms) par mL. Measured levels in serum are normally 1-5 pg/mL. Levels rise rapidly in response to infection. Strenuous physical/ muscular activity also increases IL-6 levels. Increased levels of IL-6 influence the levels of reactive oxygen species in muscle. Overexpression of IL-6 can lead to oxidative stress in muscle tissues.


IL-6 signaling is involved in several aspects of cardiovascular biology and related illnesses such as obesity, insulin resistance and atherosclerosis.


IL-6 plays a central role in host defense through immune and hematopoetic (blood cell forming) activities that make it critical to the induction of the ‘acute phase response’ when the organism is under attack. It is at the foundation of inflammation as a defense mechanism.


Adding to its complex roles, IL-6 often displays hormone-like properties affecting metabolism through the neuroendocrine system with effects on lipid metabolism, iron transport and insulin resistance.


It drives immune homeostasis and health, responding during infection, but also is found participating in autoimmunity, cancer and chronic diseases. Rheumatoid arthritis and other joint diseases are involved with IL-6. These diseases are almost never seen in IL-6 deficient laboratory animals. In moving from an acute to chronic disease, IL-6 actions change the inflammatory infiltrate from polymorphonuclear leukocytes (PMNs) to monocytes and macrophages. This also brings the acute phase of inflammation under control, avoiding tissue damage.


IL-6 levels are elevated in complicated cases of COVID-19, and associated with adverse clinical outcomes.


Of particular interest to the present study, IL-6 mediates certain mitochondrial activities. Increased IL-6 increases mitochondrial reactive oxygen species (ROS) production. This is mediated via opening of the mitochondrial transition pore (mPTP). These effects are also seen in aging and obesity. IL-6 has a protective effect on astrocyte mitochondria in a septic condition, reducing damage, maintaining mitochondrial DNA, and mitochondrial biogenesis and viability.


IL-6 has been suggested as a mediator of the neuropsychiatric symptoms of “long-term” COVID-19.


The present study’s intervention with specific wavelengths of light should be usefully paired to identification of changes, if any, in levels of IL-6 at specific points as defined in the protocol.





  Procalcitonin (proCT)  



We first measured serum and urine calcitonin in patients with acute inflammation (large burns) in 1982. That study confirmed elevated levels and suggested the possibility of a pulmonary origin due to inhalational injury. 


The same samples, carefully preserved, were subsequently used in 1992 to measure procalcitonin levels which were also found to be elevated. And in a follow-up study at a mean of 8.2 years after their initial injuries, some still had chronically elevated calcitonin and procalcitonin values, taken as evidence of late pulmonary sequelae.


Subsequent to those early studies, procalcitonin became a frequently measured marker for pulmonary, and more generally, septic involvement with infection. Endotoxin and the importance of procalcitonin are presented here. The evolution of procalcitonin as a marker and mediator of sepsis is reviewed here.


Pertinent to the present study, does procalcitonin measurement have a role in managing those with COVID-19? Are abnormal levels found and how should these be interpreted?


Serum levels of proCT are elevated in COVID-19 and are proportional to the severity of the disease (duration of mechanical ventilation for example) and overall mortality rates as well.


In caring for those with more severe forms of this viral disease, as with other illnesses in which critical care unit admission and stay is required, secondary bacterial infections are relatively common (up to 50% of patients in some series). Faced with this fact, physicians often order antibiotics on admission or shortly thereafter. ProCt levels have been used effectively to reduce antibiotic use (or misuse) in patients who do not have secondary bacterial infections. This "stewardship" role of proCT has been well described. At times proCT is paired with CRP measurements with the same goal of optimizing antibiotic therapy decisions.


The application of proCT measurements is not always conducted in a systematic or consistent manner, which has also been presented. It's appropriate role is still being defined.


A video has even been published to clarify how proCT levels can be usefully applied to antibiotic management.


While an important function, associating proCT uniquely as a guide to antibiotic therapy may in fact limit its utility. Our first study of calcitonin in burn patients more than 30 years ago presented strikingly high values that were rather surprising at the time. These pointed towards neuroendocrine functions and anatomic origins in pulmonary tissues that continue to be expanded on today. Here is one example, a "Functional Exploration of the Pulmonary NeuroEndocrine Body (NEB).


So the results from studying this substance once again in the present study population of "long-term" COVID-19 enrollees are likely to be quite instructive. This, especially given the controlled comparisons that the study protocol offers.



  Prolactin (PRL)  


Prolactin (PRL) is normally produced by the posterior part of the pituitary gland, and in both women and men. Gender differences are important since levels rise in women during and after pregnancy in support of breast feeding, as the name suggests. 


Normal levels might be as follows:

Males: 2 - 18 nanograms/ mL (ng/mL)

Nonpregnant females: 2 - 29 ng/ mL

Pregnant females: 10 - 209 ng/ mL


Abnormal levels arise in several clinical situations that will not be fully presented here.

Pertinent to COVID-19 and its "long-term" variant, autoimmune diseases occur more often in females than males, paralleling this distribution in the viral illness of interest. Also of interest, prolactin can be produced in extra-pituitary locations including adipose tissue, brain and immune cells.

Breast tenderness or discharge when not pregnant, headaches and vision problems may prompt head scans looking for a benign pituitary tumor called a prolactinoma.

Prolactin plays an active role in the development of Peripartum Cardiomyopathy where an abnormal cytokine profile is found associated with left ventricular dysfunction and slow recovery.


Prolactin has both hormonal and cytokine effects, again a topic of mutual interest for our protocol. Hormonally it relates most often to motherhood and its lactogenic effect. But prolatin has more than 300 known different efects. As an immune modulator, its effects are widely distrubuted through receptors found on monocytes, lymphocytes, macrophages, natural killer cells, granulocytes and thymic epithelial cells. Binding of prolactin to its receptor activates signaling pathways that influence cell proliferation, differentiation into other cells, secretion and cell survival for those cells in the above family. It stimulates B- and T-cells directly. The immune-neuroendocrine network is quite prolactin linked, and quite associated with auto immune diseases as the above reference presents.


Enhancement of PRL levels can lead to an increase in survival in many critical conditions, this too with a gender advantage for women.


There are many endocrine changes associated with the SARS-CoV-2 illness, including increased prolactin levels. This is not surprising since any form of stress, including infections, will increase prolactin levels. Prolactin modulates immune and inflammatory responses.


In those with COVID-19, prolactin can be increased using dopaminergic drugs and even drugs commonly presecribed for nausea such as domperidone/ metaclopromide. "... at least seven little-understood salient observations in coronavirus patients can apparently be explained by considering the role of enhanced PRL."


Mechanisms of COVID-19 progression and etiology of symptoms that persist focus more on brain effects than pulmonary effects and are pertinent to our inclusion of prolactin (PRL) in our present protocol focusing on those with the "long-term" variant of COVID-19.






  Antibody to SARS-CoV-2 (Ab)  











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