The Totally Civil Covid Thread. (Closing 31/05)

Quote from Mark U

Yeah those rapid antigen tests are too often false negatives.

Funny that you mention B12 and Iron. My wife went to the store three days ago to get some for me. Why? Friday night, my restless leg syndrome was off the charts, actually preventing me from getting a good night sleep. Saturday morning, my sickness began. The wife did some digging and found that B12 and Iron might help with restless leg. So now I'm taking a pill that has iron, B12 and folate.

I should mention that I supplement daily with Vitamin D3, about 3000 IU (summertime), but for about 10 days before I got sick I had run out of pills! (Coincidence?) So when my wife went out to get the Iron and B12, she also got the D3 for me, which she also read might help with restless leg. Of course I also supplement with magnesium biglycinate, vitamin C and A, zinc and NAC hehe. Also, I started taking Quercetin and melatonin when my symptoms started.

PS For anyone wondering what restless leg syndrome is, it's a persistent, achy, unpleasant crawly sensation in the legs, mostly lower legs. I've had this since I was a kid but only a few years ago I learned it was a 'thing' and had a name! People marvel that they seldom see me walking, I'm almost always running at various speeds. This is because running gives me some relief from the restless leg. Walking doesn't.

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For that restless leg, I heard that infared treatment shows great promise and I myself would try a tens machine for electrical stimulation and vibration

Vitamin D: A Role Also in Long COVID-19?

https://www.researchgate.net/publication/359941110_Vitamin_D_A_Role_Also_in_Long_COVID-19

Coronavirus disease 2019 (COVID-19) has quickly become a global pandemic. Reports from different parts of the world indicate that a significant proportion of people who have recovered from COVID-19 are suffering from various health problems collectively referred to as “long COVID-19”. Common symptoms include fatigue, shortness of breath, cough, joint pain, chest pain, muscle aches, headaches, and so on. Vitamin D is an immunomodulatory hormone with proven efficacy against various upper respiratory tract infections. Vitamin D can inhibit hyperinflammatory reactions and accelerate the healing process in the affected areas, especially in lung tissue. Moreover, vitamin D deficiency has been associated with the severity and mortality of COVID-19 cases, with a high prevalence of hypovitaminosis D found in patients with COVID-19 and acute respiratory failure. Thus, there are promising reasons to promote research into the effects of vitamin D supplementation in COVID-19 patients. However, no studies to date have found that vitamin D affects post-COVID-19 symptoms or biomarkers. Based on this scenario, this review aims to provide an up-to-date overview of the potential role of vitamin D in long COVID-19 and of the current literature on this topic.

Since we are being so totally civil here:

BBC Radio 4 - Death by Conspiracy?, 1. A Magical Town

What happened to Gary Matthews?

www.bbc.co.uk

Gary Matthews was into conspiracy theories - until he caught Covid and died. What role did falsehoods play in his death? BBC disinformation reporter Marianna Spring investigates.

South African Clinical Scientist Questions Ethics & Objectivity of COVID-19 ‘Experts” & their Dismissal of Ivermectin

South African Clinical Scientist Questions Ethics & Objectivity of COVID-19 ‘Experts” & their Dismissal of Ivermectin

Professor Colleen Aldous, a health care scientist at the University of KwaZulu-Natali, recently went on the record via South African media bringing…

www.trialsitenews.com

Professor Colleen Aldous, a health care scientist at the University of KwaZulu-Natali, recently went on the record via South African media bringing light to the current “mindless repetition” espoused by “experts” declaring “insufficient evidence” in regards to ivermectin’s efficacy as a COVID-19 regimen. Have these so-called experts delved into all of the literature on the topic? Did they know that there are 31 mechanisms of action papers, 22 in vivo studies, and 30 safety studies published in peer-reviewed journals? According to Aldous, most experts probably are reading what the Wall Street Journal headlines have to say about the topic of ivermectin and COVID-19, but perhaps not the deeper science.

Aldous recently opined in South Africa’s BizNews; a media open to more than just the absolute universal narrative espoused by organized medicine in the major economies. The South African academic argues that while numerous randomized controlled trials involving ivermectin and COVID-19 have, in fact, been completed, most colleagues still point out that there is “still no evidence to support claims that it is a miracle cure and say more studies must be carried out to prove its clinical benefits in the treatment of COVID-19.”

Agreeing that ivermectin nor any other drug is a miracle cure for COVID-19, she nonetheless points to considerable evidence for efficacy and safety as a treatment. What's missing, according to the “experts”? One single large randomized controlled trial. That’s it. Just one study would close the gap from insufficient to sufficient, writes the author.

But what about 24 published relatively small randomized controlled trials? Nope. Aldous reminds the reader that critics will simply point out that they are probably of poor quality. Well, how about meta-analyses showing efficacy? While Aldous believes there to be compelling evidence, mainstream critics simply label it as “rubbish-in-and rubbish out.”

What’s ethically responsible?

The South African health scientist writes that no one should forget the ethics associated with medical research. For example, the Nuremberg Code (point no. 5): “No experiment should be conducted where there is any prior reason to believe that death or disabling injury will occur.”

According to Aldous, the 25 randomized controlled ivermectin studies now published show at least some evidence as to the decrease in mortality involving ivermectin. Professor Aldous argues that these cannot be ignored out of ethical and moral principles.

It’s better to consider broadening and diversifying whom people entrust with their healthcare and by extension their lives. She points out:

“This battle will not be won by trials or insults or banning or dismissiveness. People will again start looking out for themselves. It’s time we realized we have put our trust in too small a group, all with a common goal to protect their ivory tower values at the potentially enormous cost of human life.”

Lead Research/Investigator

Colleen Aldous is a doctorate, professor, and healthcare scientist at UKZN’s medical school, where she runs the doctoral academy at the College of Health Sciences. She has published over 130 peer-reviewed articles in rated journals

Double-blind, Randomized Clinical trials (DB-RCTs) Have Miserably Failed in COVID-19 – and Became No Longer the Gold Standard Type of Clinical Study

Double-blind, Randomized Clinical trials (DB-RCTs) Have Miserably Failed in COVID-19 – and Became No Longer the Gold Standard Type of Clinical Study

Double-blind, placebo-controlled, randomized clinical trials (DB-RCT) represent the most respected type of study in medical and clinical science. The only…

www.trialsitenews.com

Double-blind, placebo-controlled, randomized clinical trials (DB-RCT) represent the most respected type of study in medical and clinical science. The only types of studies that can have stronger evidence are actually reviews: systematic reviews and meta-analyses, which are statistical analysis of systematic reviews.

Why are DB-RCTs considered the most powerful type of study? Some key points: 1. The effect of placebo (improvement due to a belief that the intervention is bringing the improvement – irrespective of the actions of the intervention itself) is nullified because patients are blind; 2. Medical doctors who take care of patients are also blind, so they do not force or postpone actions, such as hospital discharges, avoidance of intubation or inclusion of additional drugs, based on the fact that their patients are taking the drug (or intervention) or not – it is natural for medical doctors to act differently according to the drugs patients are taking, so keeping blind avoid differences in terms of management between groups; 3. Randomization avoids purposely and inconscient biased or even grouped allocation according to whether it is drug or placebo, leading to naturally similar groups, in particular in larger trials; and 4. All other variables are controlled and equal between groups, so the sole variable that will drive outcomes is the intervention proposed in the DB-RCT.

Great. So we must believe in DB-RCTs blindly, as a religion.

No. Not at all.

And DB-RCTs have miserably failed in COVID-19, and consequently lost credibility (for any serious scientist or scientific community).

Why?

Because a DB-RCT is only a truly great study if the intervention proposed respects the disease pathophysiology, disease course, and is implemented following the expected mechanisms of action that have been hypothesized to bring the benefits for the disease to be studied.

Hence, we must understand the disease pathophysiology, mechanisms of pathogenicity and disease course in order to design an appropriate DB-RCT.

In practical terms, what must be addressed in a design, and consequently, what can lead to failure of DB-RCTs?

This is a short list of a vast array of factors that can mislead results of DB-RCTs:

Treatment duration – too-short of a treatment can lead to rebound or lack of improvement in the analyses of the longer-term outcomes

Treatment timing – too-early can be harmful instead of helpful; too late can do nothing

Lack of combined therapies (interestingly, this was particularly common for unpatented drugs in the case of COVID-19) for diseases known to have complex pathophysiology, such as viruses including HIV, hepatitis B and C, and SARS-CoV-2 – DB-RCTs performed with a single drug only will hardly achieve great effect size (could this be a strategy to annihilate therapeutic options – one-by-one – to fit into a ‘script’?)

Insufficient dose – The minimal effective concentration may vary according to the disease for which the intervention or drug is proposed

Inappropriate population – Too low-risk population or too-high risk population for a certain intervention

It seems that after two years of COVID-19, we still have not fully understood the disease.

To make things worse, outcomes matter. And some of them have always mattered and are considered as important surrogate markers of efficacy. However, for unknown reasons, previous assumptions in infectious disease were cancelled for COVID-19, such as considering viral load as a predictor of disease severity. This used to be and is still the case for the vast majority of the other viral infections.

Strangely, from an ethical perspective, until we find data on more important and direct outcomes, such as COVID-19 mortality rate, we were supposed to use what we could have in hand in terms of evaluation for prediction of efficacy. Hence, reduction of viral load should have been considered as a relevant outcome.

Interestingly, for SARS-CoV-2 vaccines, COVID-19 mortality rate and chances of dying from COVID-19 were not required – exactly because we could not wait for more solid data.

So, why did we act in the opposite direction when it came to treatments?

As an additional sign that we are not looking at patients, we pretended that viral load could not predict long-COVID, which is entirely wrong. I mean, under uncertainties, if we had focused on patients, instead of spreadsheets alone, we would have realized that viral load could have been used as a predictor of long COVID, a relevant outcome that brought burden to the planet.

Yes, where is long COVID as an outcome for DB-RCT in terms of treatments for COVID-19? Mortality is by far the most important outcome. However, is not dying enough for everyone? How many DB-RCTs have been designed also focusing on prolonged COVID, everlasting COVID, long COVID or post-COVID?

The trial on Paxlovid that led to its approval for COVID-19 is a great example of pitfalls on RCT for COVID-19:

A 5-day treatment regimen was already known to be insufficient, according to the duration of the viral replication in COVID-19. Importantly, we demonstrated, with a different molecule (proxalutamide – pruxelutamide), that shorter courses could lead to relapse, and due to our sensible analysis, we were able to correct and increase the treatment duration to seven days right in the beginning of the trials. We published a paper over a year ago informing that treatment duration was critical – and too-short treatment courses could be even worse for patients. We shared via social media. And we know almost everyone reads., but they ignored.

Subjects enrolled after 03 days of symptoms were excluded. They realized that timing matters. Interestingly, the median time to start treatment in trials with ivermectin was five to six days – and, oppositely to what happened with Paxlovid, in these trials subjects enrolled with more than 03 days of disease were not excluded.

Paxlovid is a combination between two antiviral agents. They knew the importance of the synergistic effects between different molecules for a disease with multiple targets as COVID-19. Why this has not been considered for unpatented drugs, like ivermectin and nitazoxanide, is unknown.

The vast majority of the studies gave ivermectin too little, too late. At times not too little, but still too late.

Serious scientists can never conclude that ivermectin does not work. Serious scientists would rather say: if ivermectin is administered not so early in COVID-19, or more than 04 days of disease, it tends to be insufficiently effective or ineffective.

Interestingly, even observing a trend of efficacy (I am not presuming that ivermectin is effective here), serious scientists must have proposed combined therapies aiming higher efficacy through synergistic actions between groups for further DB-RCTs. Have you seen any organization, authority, or ‘mainstream’ medical society recommending this?

The vast majority, if not virtually all DB-RCTs with repurposed drugs that have been published in highly prestigious journals are fatally wrong. Paradoxically, other DB-RCTs with much better quality in terms of drug treatment timing, dosing, duration, targeted population, appropriate outcomes measured – but maybe not belonging to friends of the editor, of the Big Pharma or of Big Universities – have been systematically rejected without sufficiently plausible arguments. Coincidently, these DB-RCTs that have been rejected were positive for repurposed drugs.

What has happened?

Is it because we ‘unlearned’ science and got blind to what truly makes actual valid DB-RCTs? Or is there something else we still need to know?

Public Health Leadership Becomes More Reckless: Choices Prolong the Pandemic & Pad Pfizer’s Pockets

Public Health Leadership Becomes More Reckless: Choices Prolong the Pandemic & Pad Pfizer’s Pockets

Are games being played on the COVID-19 vaccine front with a Fall booster forthcoming? After much deliberation on June 28th, the Food and Drug Administration…

www.trialsitenews.com

Are games being played on the COVID-19 vaccine front with a Fall booster forthcoming? After much deliberation on June 28th, the Food and Drug Administration (FDA) essentially instructed the vaccine manufacturers to include BA.4/5 (which are identical to each other) in their Fall vaccine candidates.

Below is the link to Pfizer's Phase 2 clinical trial that was just posted on July 25th. Notice that they do not include a candidate with BA.5 at all. They include two bivalent candidates. The first is Wuhan/BA.1 and the second is Wuhan/BA.2. It's possibly a mistake to include Wuhan since it may reinforce immune imprinting (aka: Original Antigenic Sin). It's an even bigger mistake to then also not use the currently dominant BA.5 which differs markedly from other Omicron subvariants. Two of the amino acid mutations that it codes for are highly correlated with antibody immune evasion.

Below is Pfizer's in vivo data of their Wu/BA.1 (left), BA.5 only (center), and Wuhan/BA.5 (right). Notice how much higher the NABs are for the monovalent BA.5. This slide came from Pfizer's presentation to the FDA Vaccine and Related Biological Products Advisory Committee (VRBPAC) in June, covered by TrialSite and is what led to the FDA's memorandum to include BA.5.

So, according to Pfizer's clinical trial, not only is the obviously best option (center) off the table, but so is the second-best option (right). We'll either get the left option or another one that's almost the same as the left option.

As a result of this unfortunate direction, the output will be a vaccine that will be a fraction as efficacious as it should and could be. However, if you just take it twice as often, it will still provide excellent protection, according to the manufacturers. Of course, when the protection quickly wanes, they'll move the goalposts and state it still provides excellent protection against severe illness and death.

Pfizer snuck in a change to the Fall vaccines last week, however. They are NOT going to include the BA.5 like the FDA instructed them to do. Their clinical trial was registered last week, as TrialSite reported. However, it only includes two candidates, and neither include BA.5 as directed by the FDA. The first is BA.1/Wuhan, and the second is BA.2/Wuhan. The first will yield a negligible improvement over the current vaccine. The second will be an improvement, but their in vivo data already demonstrates the best approach points to the monovalent BA.5. Long story short, the American public will be shortchanged yet again and pay a heavy price both in extra doses of vaccines needed, more treatments needed and the cost of more serious illness. The American public will be faced with only marginally effective vaccines, limited therapeutics, and dangerous reinfections. Of course, the taxpayer is on the hook for much of the pandemic costs via the privatization of pandemic profits via the heavy socialization of clinical development, production, and commercialization costs.

One could, unfortunately, come to the conclusion that the pandemic is now being extended for profits. Pfizer makes $530/Paxlovid per treatment course. We know they would love to cash in on the alarmingly high rate of rebound cases, too, with a second course of treatment (a la Fauci). They only make about $15 per vaccine dose in the US. Therefore, a marginally effective vaccine that requires frequent boosters (i.e., every 6 months) and still requires a high % of infected cases to seek out their antiviral treatment of Paxlovid yields maximum profits. The question we have: at what cost as measured in monetary, illness, and deaths? Based on the data presented, changing the vaccine to BA.5 monovalent would mean far less would become reinfected, wouldn't need a booster for at least another year, slow the mutation rate of the virus, and very few breakthroughs infections would need Paxlovid. Perhaps now we can start to understand the rationale for not following the FDA’s direction and bypassing the BA.5 booster option.

Another motive is political: note that this pivot links to the big news the White House announced last week where the booster vaccines would be available in September instead of the Oct/Nov timeline that the manufacturers said was needed. Could it be that in order for the manufacturers to meet the White House's tighter timeline, they had to go with the bivalent formulas that they already had further developed and gathered pre-clinical data from?

Of course, this isn't mentioned because the White House wants to come across as saving the day by making the vaccines available faster, but the reduction in efficacy is going to be massive and certainly not worth the stepped-up delivery. We should note that Pfizer outlined an expedited regulatory process that would cut the current 8-month vaccine update time down to 3 months during their VRBPAC presentation. The FDA said they were working on an expedited approval process way back in early 2021. Obviously, they haven't done anything on that front, and the American public is suffering the consequences of an outdated vaccine being used to battle a highly mutated escape variant. Now when they are finally going to update the vaccines, which is long overdue—especially considering one of the main selling points of using mRNA was the associated agility and flexibility—now they opt for two extinct variants to include in the update, brilliant

A central role for amyloid fibrin microclots in long COVID/PASC: origins and therapeutic implications

Post-acute sequelae of COVID (PASC), usually referred to as ‘Long COVID’ (a phenotype of COVID-19), is a relatively frequent consequence of SARS-CoV-2 infection, in which symptoms such as breathlessness, fatigue, ‘brain fog’, tissue damage, inflammation, and coagulopathies (dysfunctions of the blood coagulation system) persist long after the initial infection. It bears similarities to other post-viral syndromes, and to myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Many regulatory health bodies still do not recognize this syndrome as a separate disease entity, and refer to it under the broad terminology of ‘COVID’, although its demographics are quite different from those of acute COVID-19. A few years ago, we discovered that fibrinogen in blood can clot into an anomalous ‘amyloid’ form of fibrin that (like other β-rich amyloids and prions) is relatively resistant to proteolysis (fibrinolysis). The result, as is strongly manifested in platelet-poor plasma (PPP) of individuals with Long COVID, is extensive fibrin amyloid microclots that can persist, can entrap other proteins, and that may lead to the production of various autoantibodies. These microclots are more-or-less easily measured in PPP with the stain thioflavin T and a simple fluorescence microscope. Although the symptoms of Long COVID are multifarious, we here argue that the ability of these fibrin amyloid microclots (fibrinaloids) to block up capillaries, and thus to limit the passage of red blood cells and hence O2 exchange, can actually underpin the majority of these symptoms. Consistent with this, in a preliminary report, it has been shown that suitable and closely monitored ‘triple’ anticoagulant therapy that leads to the removal of the microclots also removes the other symptoms. Fibrin amyloid microclots represent a novel and potentially important target for both the understanding and treatment of Long COVID and related disorders.

Emerging Role of Vitamin D and its Associated Molecules in Pathways Related to Pathogenesis of Thrombosis

Emerging Role of Vitamin D and its Associated Molecules in Pathways Related to Pathogenesis of Thrombosis

Vitamin D, besides having an essential role in calcium and bone metabolism, also acts as a mediator of many non-calcemic effects through modulations of several…

www.ncbi.nlm.nih.gov

Abstract

Vitamin D, besides having an essential role in calcium and bone metabolism, also acts as a mediator of many non-calcemic effects through modulations of several biological responses. Vitamin D exists in its two major forms, vitamin D2, or commonly known as ergocalciferol, and vitamin D3, or commonly known as cholecalciferol. Both of these forms bind to vitamin D-binding protein to get transported to all vital target organs, where it serves as a natural ligand to vitamin D receptors for enabling their biological actions. Clinical reports corroborating vitamin D deficiency with an increase in thrombotic episodes implicate the role of vitamin D and its associated molecule in the regulation of thrombosis-related pathways. Thrombosis is the formation and propagation of a blood clot, known as thrombus. It can occur either in the arterial or the venous system resulting in many severe complications, including myocardial infarction, stroke, ischemia, and venous thromboembolism. Vitamin D, directly or indirectly, controls the expression of several genes responsible for the regulation of cellular proliferation, differentiation, apoptosis, and angiogenesis. All of these are the processes of potential relevance to thrombotic disorders. This review, thus, discussed the effects of vitamin D on pathways involved in thrombosis, such as hemostatic process, inflammatory pathway, and endothelial cell activation, with a focus on the molecular mechanisms associated with them.

Relationship between Lymphocyte Subpopulations and Vitamin D Levels in COVID-19 Pneumonia Patients

Relationship between Lymphocyte Subpopulations and Vitamin D Levels in COVID-19 Pneumonia Patients - PubMed

This preliminary study confirms the high prevalence of vitamin D deficiency in patients with COVID-19 pneumonia and that vitamin D deficiency is associated…

pubmed.ncbi.nlm.nih.gov

Abstract

Background: Some studies have shown that patients who are hospitalized with severe COVID-19 also have low levels of vitamin D. It is known that vitamin D can reduce the risk of infections and down regulate the immune/inflammatory reaction.

Objectives: To investigate the association between vitamin D status and lymphocyte subpopulations in hospitalized pneumonia COVID-19 patients.

Methods: In 33 positive severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) patients with radiologic evidence of interstitial pneumonia and in 16 healthy control subjects matched for age, sex, and seasonality lymphocyte subpopulations and vitamin D levels were evaluated.

Results: The majority of patients with COVID-19 pneumonia (70.8%) presented vitamin D deficiency. The percentages of neutrophils presented a negative correlation (r = -0.74; P < 0.001), whereas the percentages of lymphocytes presented a positive correlation (r = 0.43; P < 0.01) with 25(OH)D. Moreover, vitamin D levels were positively correlated with CD3+ (r = 0.37, P < 0.05), CD4+ (r = 0.41, P < 0.05), CD8+ (r = 0.32, P < 0.07), and CD19+ (r = 0.38, P < 0.05).

Conclusions: This preliminary study confirms the high prevalence of vitamin D deficiency in patients with COVID-19 pneumonia and that vitamin D deficiency is associated with a reduction of lymphocyte subsets and altered T-lymphocyte activation. This finding may contribute to clarify the mechanisms by which vitamin D influences the course and outcome of COVID-19 pneumonia.

Vitamin D3 Suppresses Class II Invariant Chain Peptide Expression on Activated B-Lymphocytes: A Plausible Mechanism for Downregulation of Acute Inflammatory Conditions

Vitamin D3 Suppresses Class II Invariant Chain Peptide Expression on Activated B-Lymphocytes: A Plausible Mechanism for Downregulation of Acute Inflammatory Conditions

Class II invariant chain peptide (CLIP) expression has been demonstrated to play a pivotal role in the regulation of B cell function after nonspecific…

www.ncbi.nlm.nih.gov

Genome-wide association study reveals class I MHC–restricted T cell–associated molecule gene (CRTAM) variants interact with vitamin D levels to affect asthma exacerbations

Genome-wide association study reveals class I MHC–restricted T cell–associated molecule gene (CRTAM) variants interact with vitamin D levels to affect asthma exacerbations

It has recently been shown that vitamin D deficiency can increase asthma development and severity and that variations in vitamin D receptor genes are …

www.sciencedirect.com

Background

It has recently been shown that vitamin D deficiency can increase asthma development and severity and that variations in vitamin D receptor genes are associated with asthma susceptibility.

Objective

We sought to find genetic factors that might interact with vitamin D levels to affect the risk of asthma exacerbation.

Methods

We conducted a genome-wide study of gene–vitamin D interaction on asthma exacerbations using population-based and family-based approaches on 403 subjects and trios from the Childhood Asthma Management Program. Twenty-three polymorphisms with significant interactions were studied in a replication analysis in 584 children from a Costa Rican cohort.

Results

We identified 3 common variants in the class I MHC–restricted T cell–associated molecule gene (CRTAM) that were associated with an increased rate of asthma exacerbations based on the presence of a low circulating vitamin D level. These results were replicated in a second independent population (unadjusted combined interaction, P = .00028-.00097; combined odds ratio, 3.28-5.38). One variant, rs2272094, is a nonsynonymous coding polymorphism of CRTAM. Functional studies on cell lines confirmed the interaction of vitamin D and rs2272094 on CRTAM expression. CRTAM is highly expressed in activated human CD8+ and natural killer T cells, both of which have been implicated in asthmatic patients.

Conclusion

The findings highlight an important gene-environment interaction that elucidates the role of vitamin D and CD8+ and natural killer T cells in asthma exacerbation in a genome-wide gene-environment interaction study that has been replicated in an independent population. The results suggest the potential importance of maintaining adequate vitamin D levels in subsets of high-risk asthmatic patients.

A subgroup of lupus patients with nephritis, innate T cell activation and low vitamin D is identified by the enhancement of circulating MHC class I-related chain A

They told you whats in the vaccines?

One in 8 patients seen to have long covid symptoms', says study

Covid symptoms: 'One in 8 patients seen to have long covid symptoms', says study - The Economic Times

According to the study, of adults who have had Covid-19, 21.4% experienced at least one new or severely increased symptom three to five months post-infection compared to before infection. This was against 8.7% of uninfected people in the same time period, suggesting that one in eight Covid-19 patients (12.7%) in general population experience long-term symptoms due to Covid-19.

Symptomatic Bradycardia Manifesting as Acute Hypothyroidism Following COVID-19 Infection: A Case Report

Symptomatic Bradycardia Manifesting as Acute Hypothyroidism Following COVID-19 Infection: A Case Report

The role of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus and associated autoimmune phenomenon behind pathology development has been a…

www.cureus.com

Abstract

The role of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus and associated autoimmune phenomenon behind pathology development has been a scientific mystery since the onset of the pandemic in 2020. Early on, scientific studies showed coronavirus disease 2019 (COVID-19) being linked to many pathological consequences including blood clots, neurocognitive dysfunction, and cardiomyopathy. We present a case of acute hypothyroidism in an 88-year-old female with no previous history of thyroid dysfunction or disease. The eventual workup revealed a thyroid-stimulating hormone (TSH) of greater than 100,000 milli-international units per liter (mlU/L) and a thyroxine (free T4) level of less than 0.10 nanograms per deciliter (ng/dl). At the time of presentation, she was found to have a positive COVID-19 test despite being vaccinated. She was started on a levothyroxine injection, which led to eventual symptom resolution. Our aim of this case report is to highlight the possibility of her acute hypothyroidism being triggered by the onset of COVID-19.

Association between vitamin D deficiency and hypothyroidism: results from the National Health and Nutrition Examination Survey (NHANES) 2007–2012

https://bmcendocrdisord.biomed…%20in%20the%20long%2Dterm.

Abstract

Purpose

Many smaller studies have previously shown a significant association between thyroid autoantibody induced hypothyroidism and lower serum vitamin D levels. However, these finding have not been confirmed by large-scale studies. In this study, we evaluated the relationship between hypothyroidism and vitamin D levels using a large population-based data.

Methods

For this study, we used National Health and Nutrition Examination Survey (NHANES) during the years 2007–2012. We categorized participants into three clinically relevant categories based on vitamin D levels: optimal, intermediate and deficient. Participants were also split into hypothyroid and hyperthyroid. Weighted multivariable logistic regression analyses were used to calculate the odds of being hypothyroid based on vitamin D status.

Results

A total of 7943 participants were included in this study, of which 614 (7.7%) were having hypothyroidism. Nearly 25.6% of hypothyroid patients had vitamin D deficiency, compared to 20.6% among normal controls. Adjusted logistic regression analyses showed that the odds of developing hypothyroidism were significantly higher among patients with intermediate (adjusted odds ratio [aOR], 1.7, 95% CI: 1.5–1.8) and deficient levels of vitamin D (aOR, 1.6, 95% CI: 1.4–1.9).

Conclusion

Low vitamin D levels are associated with autoimmune hypothyroidism. Healthcare initiatives such as mass vitamin D deficiency screening among at-risk population could significantly decrease the risk for hypothyroidism in the long-term.

Torsade de Pointes with severe vitamin D deficiency, an unusual presentation of a common problem

Torsade de Pointes with severe vitamin D deficiency, an unusual presentation of a common problem

Torsade de Pointes (TdP) is a rare cardiac arrhythmia that is associated with prolonged QTc interval. Hypocalcemia is a common cause of prolonged QTc. Although…

www.ncbi.nlm.nih.gov

<Learning objective: Severe vitamin D deficiency is common especially in elderly patients. The diagnosis and treatment of this disorder are simple, but the consequences of severe depletion of vitamin D storage can lead to deep electrolyte abnormalities and life-threatening arrhythmia such as Torsade de Pointes. A simple screening test is effective in preventing a dreadful outcome.>

Quote from Fm1

three to five months post-infection

Everybody has a new medical symptom every 3-5 months... This has nothing to do with "long" Covid. Vaccination is much more likely ... and well documented.

This is why such studies should only be made by professionals with a degree in psychiatry that are able to understand the categorization of "soft facts"...

I would say that most cases are long mask or long "lock-down"...

Quote from Wyttenbach

Everybody has a new medical symptom every 3-5 months... This has nothing to do with "long" Covid. Vaccination is much more likely ... and well documented.

This is why such studies should only should be made by professionals with a degree in psychiatry that are able to understand the categorization of "soft facts"...

I would say that most cases are long mask or long "lock-down"...

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more to the point the study shows 1 in 8 around 12% of the population, whereas early reports were in the 1 in 3 or 30% suffered from long COVID. Brings it into better perspective. Covid severity as well as long COVID and Covid kick back from remdesivir and Paxcrap are a result of vitamin d deficency leading to low B1,B3,B12 and iron.

Quote from Seatrout

They told you whats in the vaccines?

Right here:

https://www.fda.gov/media/151707/download

Federal law says they must tell everyone who gets any vaccine what is in it. For the last 116 years, all food and drugs have included a full set of ingredients. See the pure food and drug act of 1906. Drugs must also include a full list of known warnings, precautions and adverse reactions.

Quote from Fm1

Double-blind, Randomized Clinical trials (DB-RCTs) Have Miserably Failed in COVID-19 – and Became No Longer the Gold Standard Type of Clinical Study

Since this is reported in TrialSiteNews we can apply the Boolean NOT function. The very opposite must be true. Randomized clinical trials are better than ever. That is a reasonable, because big data computer tracking of events patient outcomes are far more detailed and up-to-date than they were in the past. Also because COVID vaccine tests were by far the largest in history. They were larger with more patients than some drugs are for the entire life of the drug, including post-test inoculations. Plus, subsequent post-test COVID vaccine data collected from patients worldwide is irrefutable proof that the randomized clinical studies were accurate. The mRNA vaccines are by far the safest vaccines ever deployed. They have not killed anyone in the U.S., and probably only one or two people elsewhere in the world.

Those are facts. What you read in TrialSiteNews are lies from Lunatic Death Cult Fanatics. Read that stuff, follow their advice, and you may kill yourself or spend the rest of your life on oxygen, or unable to taste food, climb stairs or have sex. Your choice: you can have real science and effective modern medicine, or you can play Russian Roulette and kill yourself or destroy you life for no reason.