Coronavirus

[FreshPrince]

I guess Munro is right about tipping those cashiers:

The Un-Heroic Reality of Being an ‘Essential’ Restaurant Worker

"Before COVID, about half the restaurant’s takeout business typically came from the third-party delivery apps Caviar and Postmates. During quarantine, it’s grown to 80 percent. Since the customer tips the driver, not the restaurant, cashiers don’t make any money on those orders. As such, they are my lowest priority, and drivers end up with long wait times. They crowd the space around the counter, limiting the possibility of social distancing and creating additional stress. They hover and pester, and I snap back at them. Two newly deemed essential workers face off over whose time is more valuable."

 

[TheTalkingMule]

It's only 9.9% in Boston, the 2nd hardest hit city in the US behind the greater NYC metro area.

That was nearly a month ago, and two weeks before that it was assumed to be 1-2%.

Same trend as Swine Flu. Early assumption of 1% quickly turned to 10%, which turned to a final analysis of "15-21% or more". Since cv19 is far easier to spread, my bet is we see 20-45% infection/exposure identified by late summer or fall in most dense areas.

 

[SageBrush]

Try turning this statement around to understand some of us HCQ defenders. There's such a rabid dislike of the orange-haired POTUS who promoted HCQ that the drug was crucified before it had a fair trial. I could care less who supports it. If it works, I want it to have a fair chance of proving itself. If serious studies show it doesn't work, it's time to move on. Let's give this treatment a fair shake, though.

You are not a physician, so let me try and give you a tiny clue:

Any physician that tries to start an RCT today along the lines of the study that terminated early due to excess mortality in the HCQ arm will be censured by the ethics and research committees that approves studies.

Your personal opinion that the failed RCT was marred by politics is worth exactly squat.

 

[bkp_duke]

Try turning this statement around to understand some of us HCQ defenders. There's such a rabid dislike of the orange-haired POTUS who promoted HCQ that the drug was crucified before it had a fair trial. I could care less who supports it. If it works, I want it to have a fair chance of proving itself. If serious studies show it doesn't work, it's time to move on. Let's give this treatment a fair shake, though.

For the record (people that have followed me long term know this) - I voted for Trump, and as a physician I think his take on COVID-19 is bat-$hit crazy. It's not based on evidence, it's based on feelings and emotions, and that is not science.

The data for HCQ has NEVER been there. Nor has it for the combination of it with anything else (Zinc, Azithromycin, etc.).

Go back about 2 months in this thread and I really lay out the red flags on the early "studies" for HCQ and the bias in them and what they were lacking.

While FINISHED randomized control trials are not out, we do have enough preliminary data to support the conclusion that HCQ just doesn't work - both to treat COVID-19, and to prevent infection in the first place. The way RCTs work is that if there is definitive evidence that something makes a difference, that shows up pretty quickly (i.e. you don't need a lot of samples to see a big difference) and you actually stop the trial early because you have enough data to make a definitive statement that is backed by the statistics. The longer a RCT goes on and the more data it collects, the more you are starting to look for TINY variations (i.e. you need a lot more samples to power the statistics to see a 1% difference then a 10 or 50% difference).

If we see anything from HCQ, it's going to be small. And it won't get used for preventative medicine. I was listening to a physician podcast yesterday from Mt. Sinai in NY about their experience. They would not come down on one side or the other for sick patients on if this worked, but they were ADAMANT about not giving it to ambulatory patients as a preventative. They had seen increased mortality in that circumstance.

 

[Nuclear Fusion]

Study of the possible conversion of COVID-19 patients to ME / CFS | Open Medicine Foundation
ME / CFS - Myalgic Encephalomyelitis / Chronic Fatigue Syndrome

In a significant percentage of patients, serious viral infection preceded their development of ME / CFS. In this current COVID-19 pandemic, it seems likely that COVID-19 may also be a trigger, and that many people will develop ME / CFS. It is thought that up to 11% of patients who had severe infections from Epstein-Barr virus (EBV), Q fever (Coxiella burnetii), or Ross river virus (RRV), and others, develop ME / CFS. Other studies following SARS and MERS suggest an even higher proportion (50%) develop ME / CFS or Fibromyalgia.

After COVID-19 patients recover from the acute phase of their disease, they may be at significant risk for a prolonged period of a post-viral fatigue, which may last six months or more before returning to their previously normal state. However, for some patients, their fatigue may fail to resolve or become even more profound over these initial six months and continue indefinitely, converting to ME / CFS. A detailed genomic, metabolic and proteomic analysis over time will likely provide tremendous insights to understand how to identify those pathways that can be useful to predict, diagnose or treat ME / CFS.

The world is intensely focussed on COVID-19 at the moment. The likely conversion of thousands of patients to a disease that causes life-long suffering provides an unprecedented opportunity for the world to finally pay appropriate attention to ME / CFS.

 

[bkp_duke]

Study of the possible conversion of COVID-19 patients to ME / CFS | Open Medicine Foundation

What is ME / CFS?

Personal pet peeve on articles that do not define the abbreviations.

 

[scottf200]

What is ME / CFS?
Personal pet peeve on articles that do not define the abbreviations.

What is ME/CFS? | Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) | CDC

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a disabling and complex illness.
People with ME/CFS are often not able to do their usual activities. At times, ME/CFS may confine them to bed. People with ME/CFS have overwhelming fatigue that is not improved by rest. ME/CFS may get worse after any activity, whether it’s physical or mental. This symptom is known as post-exertional malaise (PEM). Other symptoms can include problems with sleep, thinking and concentrating, pain, and dizziness. People with ME/CFS may not look ill. However, ...

 

[OPRCE]

For the record (people that have followed me long term know this) - I voted for Trump, and as a physician I think his take on COVID-19 is bat-$hit crazy. It's not based on evidence, it's based on feelings and emotions, and that is not science.

The data for HCQ has NEVER been there. Nor has it for the combination of it with anything else (Zinc, Azithromycin, etc.).

Go back about 2 months in this thread and I really lay out the red flags on the early "studies" for HCQ and the bias in them and what they were lacking.

While FINISHED randomized control trials are not out, we do have enough preliminary data to support the conclusion that HCQ just doesn't work - both to treat COVID-19, and to prevent infection in the first place. The way RCTs work is that if there is definitive evidence that something makes a difference, that shows up pretty quickly (i.e. you don't need a lot of samples to see a big difference) and you actually stop the trial early because you have enough data to make a definitive statement that is backed by the statistics. The longer a RCT goes on and the more data it collects, the more you are starting to look for TINY variations (i.e. you need a lot more samples to power the statistics to see a 1% difference then a 10 or 50% difference).

If we see anything from HCQ, it's going to be small. And it won't get used for preventative medicine. I was listening to a physician podcast yesterday from Mt. Sinai in NY about their experience. They would not come down on one side or the other for sick patients on if this worked, but they were ADAMANT about not giving it to ambulatory patients as a preventative. They had seen increased mortality in that circumstance.

What do you think of this preprint re. retrospective NYC Hospital Study posted May 08, 2020?

They claim it shows 1st in vivo evidence that adding Zinc Sulphate to HCQ + Azithromycin significantly improves outcomes for COVID19 patient (decreasing the need for ventilation, admission to the ICU, and mortality or transfer to hospice for patients who were never admitted to the ICU):
Hydroxychloroquine and azithromycin plus zinc vs hydroxychloroquine and azithromycin alone: outcomes in hospitalized COVID-19 patients

 

[dfwatt]

Study of the possible conversion of COVID-19 patients to ME / CFS | Open Medicine Foundation
ME / CFS - Myalgic Encephalomyelitis / Chronic Fatigue Syndrome

This is actually one of my significant concerns in terms of possible long-term effects from covid-19 infection. When I was a staff member at our Alzheimer Disease Clinic I used to see a lot of patients with chronic fatigue syndrome status post viral infection, and we now know that chronic viral infection may be a pathway indeed an underappreciated pathway into Alzheimer disease. Severe chronic viral infections segue in a still mysterious fashion into chronic fatigue syndrome in a highly variable percentage of the time anywhere from a few percent to up to 40 to 50% with some of that variability hinged to the type of virus but also some of it hinged to the severity of the initial infection and how symptomatic people were.

Chronic fatigue syndrome has been dismissed by a lot of Physicians but it's finally getting traction and recognition as a real syndrome even if we don't understand it very well. It could be some kind of neuroendocrine shift orchestrated by our immune systems possibly reflecting some kind of chronic over activation of the system, but we still lack a definitive understanding of mechanism. I wonder if it reflects epigenetic change but again I'm just guessing here. In any case it's really part and parcel of the long-term negative effects of severe viral infection and it's part of why you really don't want to mess with this kind of virus and if possible instead get immunity the easy way through a vaccination.

 

[TheTalkingMule]

My assumed exposure in early March was 100% followed by fibromyalgia-like symptoms. Moderate for about 2 weeks then mild for another month. I can only describe it as being very similar to shingles.

If I weren't so sedentary and eating so poorly during lockdown, I would have been back to 100% by maybe 2nd week of April.

I guess novel viruses can really trigger a lot of ancillary syndromes lying dormant. Makes sense.

 

[bkp_duke]

What do you think of this preprint re. retrospective NYC Hospital Study posted May 08, 2020?

They claim it shows 1st in vivo evidence that adding Zinc Sulphate to HCQ + Azithromycin significantly improves outcomes for COVID19 patient (decreasing the need for ventilation, admission to the ICU, and mortality or transfer to hospice for patients who were never admitted to the ICU):
Hydroxychloroquine and azithromycin plus zinc vs hydroxychloroquine and azithromycin alone: outcomes in hospitalized COVID-19 patients

The most important paragraph of the paper is this one:

The addition of zinc sulfate did not impact the length of hospitalization, duration of ventilation, or ICU duration. In univariate analyses, zinc sulfate increased the frequency of patients being discharged home, and decreased the need for ventilation, admission to the ICU, and mortality or transfer to hospice for patients who were never admitted to the ICU. After adjusting for the time at which zinc sulfate was added to our protocol, an increased frequency of being discharged home (OR 1.53, 95% CI 1.12-2.09) reduction in mortality or transfer to hospice remained significant (OR 0.449, 95% CI 0.271-0.744).


Basically, they had to do some regression analyses to see if they could find any variable between the groups that showed a possible statistical significance. With massaging of the data, and removing the sickest of patients (those that went to the ICU) they showed a possible improvement in patients with less acute symptoms.

The researchers conclusions are sound, which basically states that "there might be something here, but we need to do a lot more studies and control for other variables to tease this out." They, appropriately, DO NOT make a treatment recommendation based upon their findings.

This study has several limitations. First, this was an observational retrospective analysis that could be impacted by confounding variables. This is well demonstrated by the analyses adjusting for the difference in timing between the patients who did not receive zinc and those who did. In addition, we only looked at patients taking hydroxychloroquine and azithromycin. We do not know whether the observed added benefit of zinc sulfate to hydroxychloroquine and azithromycin on mortality would have been seen in patients who took zinc sulfate alone or in combination with just one of those medications. We also do not have data on the time at which the patients included in the study initiated therapy with hydroxychloroquine, azithromycin, and zinc. Those drugs would have been started at the same time as a combination therapy, but the point in clinical disease at which patients received those medications could have differed between our two groups. Finally, the cohorts were identified based on medications ordered rather than confirmed administration, which may bias findings towards favoring equipoise between the two groups. In light of these limitations, this study should not be used to guide clinical practice. Rather, our observations support the initiation of future randomized clinical trials investigating zinc sulfate against COVID-19.

 

[OPRCE]

The most important paragraph of the paper is this one:

The addition of zinc sulfate did not impact the length of hospitalization, duration of ventilation, or ICU duration. In univariate analyses, zinc sulfate increased the frequency of patients being discharged home, and decreased the need for ventilation, admission to the ICU, and mortality or transfer to hospice for patients who were never admitted to the ICU. After adjusting for the time at which zinc sulfate was added to our protocol, an increased frequency of being discharged home (OR 1.53, 95% CI 1.12-2.09) reduction in mortality or transfer to hospice remained significant (OR 0.449, 95% CI 0.271-0.744).


Basically, they had to do some regression analyses to see if they could find any variable between the groups that showed a possible statistical significance. With massaging of the data, and removing the sickest of patients (those that went to the ICU) they showed a possible improvement in patients with less acute symptoms.

The researchers conclusions are sound, which basically states that "there might be something here, but we need to do a lot more studies and control for other variables to tease this out." They, appropriately, DO NOT make a treatment recommendation based upon their findings.

This study has several limitations. First, this was an observational retrospective analysis that could be impacted by confounding variables. This is well demonstrated by the analyses adjusting for the difference in timing between the patients who did not receive zinc and those who did. In addition, we only looked at patients taking hydroxychloroquine and azithromycin. We do not know whether the observed added benefit of zinc sulfate to hydroxychloroquine and azithromycin on mortality would have been seen in patients who took zinc sulfate alone or in combination with just one of those medications. We also do not have data on the time at which the patients included in the study initiated therapy with hydroxychloroquine, azithromycin, and zinc. Those drugs would have been started at the same time as a combination therapy, but the point in clinical disease at which patients received those medications could have differed between our two groups. Finally, the cohorts were identified based on medications ordered rather than confirmed administration, which may bias findings towards favoring equipoise between the two groups. In light of these limitations, this study should not be used to guide clinical practice. Rather, our observations support the initiation of future randomized clinical trials investigating zinc sulfate against COVID-19.

Cheers for that!

The paragraph immediately preceding your last quote is also interesting:

The main finding of this study is that after adjusting for the timing of zinc therapy, we found that the addition of zinc sulfate to hydroxychloroquine and azithromycin was found to associate with a decrease in mortality or transition to hospice among patients who did not require ICU level of care, but this association was not significant in patients who were treated in the ICU. This result may be reflective of the proposed mechanism of action of zinc sulfate in COVID-19. Zinc has been shown to reduce SARS-CoV RNA dependent RNA polymerase activity in vitro [13]. As such, zinc may have a role in preventing the virus from progressing to severe disease, but once the aberrant production of systemic immune mediators is initiated, known as the cytokine storm, the addition of zinc may no longer be effective [17]. Our findings suggest a potential therapeutic synergistic mechanism of zinc sulfate with hydroxychloroquine, if used early on in presentation with COVID-19. However, our findings do not suggest a prophylactic benefit of zinc sulfate in the absence of a zinc ionophore, despite interest in this therapy for prevention. A prophylactic strategy of zinc sulfate should be evaluated to help answer this question.

i.e. the study suggests that the earlier zinc + HCQ combo is applied, the better the outcome. Of course this remains to be confirmed in a RCT, but I believe such studies are now underway, e.g. this one (open-label for unexplained reason):

A Randomized Study Evaluating the Safety and Efficacy of Hydroxychloroquine and Zinc in Combination With Either Azithromycin or Doxycycline for the Treatment of COVID-19 in the Outpatient Setting
Hydroxychloroquine and Zinc With Either Azithromycin or Doxycycline for Treatment of COVID-19 in Outpatient Setting - Full Text View - ClinicalTrials.gov

[results expected by EoY 2020]

 

[bkp_duke]

Cheers for that!

The paragraph immediately preceding your last quote is also interesting:



i.e. the study suggests that the earlier zinc + HCQ combo is applied, the better the outcome. Of course this remains to be confirmed in a RCT, but I believe such studies are now underway, e.g. this one (open-label for unexplained reason):

A Randomized Study Evaluating the Safety and Efficacy of Hydroxychloroquine and Zinc in Combination With Either Azithromycin or Doxycycline for the Treatment of COVID-19 in the Outpatient Setting
Hydroxychloroquine and Zinc With Either Azithromycin or Doxycycline for Treatment of COVID-19 in Outpatient Setting - Full Text View - ClinicalTrials.gov

[results expected by EoY 2020]

Yes, if (and that's a BIG IF) HCQ (+/- anything) is going to have an effect, it will be seen in the more moderate patients and those treated earlier.

But I'm going to state this very clearly:
All data we have to date is that HCQ is inferior to Remdesivir. Currently, that is "standard of care" (i.e. the gold standard) for COVID-19 treatment.

 

[OPRCE]

Yes, if (and that's a BIG IF) HCQ (+/- anything) is going to have an effect, it will be seen in the more moderate patients and those treated earlier.

But I'm going to state this very clearly:
All data we have to date is that HCQ is inferior to Remdesivir. Currently, that is "standard of care" (i.e. the gold standard) for COVID-19 treatment.

Sure but HCQ + Zinc are cheap as chips generics, thus much more widely available worldwide. I think in e.g. India, Turkey or Brazil, Remdesivir must be fairly scarce and/or prohibitively expensive.

I believe in the former 2 countries, at least, HCQ is very much part of the treatment strategy, whether with zinc or not, am unsure on that part.

 

[KenC]

Indeed and this is the topic of a large study initiated in Germany. If you look at the incidence maps there you can see immediately that former East Germany is much less affected than the West. The suspicion is that areas where TBC inoculation was compulsory produce this effect. That particular inoculation has a broad effect on the immune system. I have so far not found a quotable paper on the particular topic, but the press notice was attributed to a

CRC Hannover scientist where this is being investigated. In this context note also the difference between Portugal and Spain

Yes, Germany's data is very intriguing. I took a screenshot a month ago:

And yes, the Portugal-Spain differences are very interesting. Hopefully, all the research being done will give us some answers. Would be nice if BCG, a widely-used vaccine could help until a Covid vaccine is ready.

 

[FreshPrince]

Couple of examples in support of not trusting COVID-19 numbers coming out of Florida:

https://www.miamiherald.com/news/coronavirus/article242773056.html

"The state official managing Florida’s public “dashboard” of COVID-19 data says that her office has been removed from the project — and questioned the Department of Health’s commitment to “accessibility and transparency.”

“They are making a lot of changes,” she added. “I would advise being diligent in your respective uses of this data.”

What’s in the censored Florida Medical Examiners database of COVID-19 deaths?

"since at least April 20, the Florida Department of Health has blocked the Medical Examiners Commission from releasing their own detailed spreadsheet of the COVID-19 dead. On Wednesday, the state released the medical examiners’ spreadsheet but redacted the narratives and cause of death entries."

 

[dfwatt]

Yes, if (and that's a BIG IF) HCQ (+/- anything) is going to have an effect, it will be seen in the more moderate patients and those treated earlier.

But I'm going to state this very clearly:
All data we have to date is that HCQ is inferior to Remdesivir. Currently, that is "standard of care" (i.e. the gold standard) for COVID-19 treatment.

Plus, it's entirely possible that all of the possible 'signal' related to zinc plus HCQ (either in terms of potentially moderating risk of infection or severity vector) is actually coming from the zinc (well documented to disrupt viral hijacking of ribosomes if it can get intracellularly) plus any passable ionophore (including perhaps such non-toxic ones as several polyphenols). So whatever protection there might be, if there is any, may have little to do with HCQ per se. Obviously, a lot of ifs in all that! But what else is new when you are chasing down the unknown.

 

[Papafox]

For the record (people that have followed me long term know this) - I voted for Trump, and as a physician I think his take on COVID-19 is bat-$hit crazy. It's not based on evidence, it's based on feelings and emotions, and that is not science.

The data for HCQ has NEVER been there. Nor has it for the combination of it with anything else (Zinc, Azithromycin, etc.).

Go back about 2 months in this thread and I really lay out the red flags on the early "studies" for HCQ and the bias in them and what they were lacking.

While FINISHED randomized control trials are not out, we do have enough preliminary data to support the conclusion that HCQ just doesn't work - both to treat COVID-19, and to prevent infection in the first place. The way RCTs work is that if there is definitive evidence that something makes a difference, that shows up pretty quickly (i.e. you don't need a lot of samples to see a big difference) and you actually stop the trial early because you have enough data to make a definitive statement that is backed by the statistics. The longer a RCT goes on and the more data it collects, the more you are starting to look for TINY variations (i.e. you need a lot more samples to power the statistics to see a 1% difference then a 10 or 50% difference).

If we see anything from HCQ, it's going to be small. And it won't get used for preventative medicine. I was listening to a physician podcast yesterday from Mt. Sinai in NY about their experience. They would not come down on one side or the other for sick patients on if this worked, but they were ADAMANT about not giving it to ambulatory patients as a preventative. They had seen increased mortality in that circumstance.

I've been watching the results from HCQ usage carefully and there's mixed results. When HCQ or Chloroquine was given in combination with zinc and Azithromycin, and given early enough to prevent the battle in the lungs, then most data I've seen so far suggests it is reasonably effective. For example consider this recent finding by NYU's Grossman School of Medicine researchers that the drug combo led to 44% fewer deaths than in patients compared to those not on the combo. I find such results intriguing, not overwhelmingly conclusive, but intriguing. We really do need a controlled study in which the preferred use of HCQ is tested, and that includes being given in combination with zinc and azithromycin and being given to patients who are in at risk groups but given soon after detection of the virus so that the viral counts can be pulled down within a half dozen days so that ICU, ventilators, and the battle in the lungs can largely be prevented.

That's my wish: do a study of Hydroxychloroquine in the usage that makes the most sense (in combo and given relatively early in disease progression). Until that test is done this drug combo should not be eliminated as a possible treatment. You as a man of science should really be hoping the test is done as well so that we can either agree that HCQ has value as a treatment when done correctly or we can dismiss this treatment candidate and move on. What's been done in the past is certainly NOT conclusive.

 

[bkp_duke]

I've been watching the results from HCQ usage carefully and there's mixed results. When HCQ or Chloroquine was given in combination with zinc and Azithromycin, and given early enough to prevent the battle in the lungs, then most data I've seen so far suggests it is reasonably effective. For example consider this recent finding by NYU's Grossman School of Medicine researchers that the drug combo led to 44% fewer deaths than in patients compared to those not on the combo. I find such results intriguing, not overwhelmingly conclusive, but intriguing. We really do need a controlled study in which the preferred use of HCQ is tested, and that includes being given in combination with zinc and azithromycin and being given to patients who are in at risk groups but given soon after detection of the virus so that the viral counts can be pulled down within a half dozen days so that ICU, ventilators, and the battle in the lungs can largely be prevented.

That's my wish: do a study of Hydroxychloroquine in the usage that makes the most sense (in combo and given relatively early in disease progression). Until that test is done this drug combo should not be eliminated as a possible treatment. You as a man of science should really be hoping the test is done as well so that we can either agree that HCQ has value as a treatment when done correctly or we can dismiss this treatment candidate and move on. What's been done in the past is certainly NOT conclusive.

Yeah - mixed results = not so good.

You want a CLEAR CUT improvement. Not something where you have to "hope" and "wish" and do all kinds of advanced statistics to see the result.


We are now over two months into the HCQ story, with tens of thousands upon tens of thousands of people having taken it for COVID-19. If it were that effective, we would know by now.

Everyone now is just looking for these tiny, marginal effects. When you get that small, you then have to start having serious conversations about the benefits outweighing the side effects.

Basically, everyone still looking at HCQ is splitting hairs and is too emotionally attached to this medication.

 

[omgwtfbyobbq]

This is actually one of my significant concerns in terms of possible long-term effects from covid-19 infection. When I was a staff member at our Alzheimer Disease Clinic I used to see a lot of patients with chronic fatigue syndrome status post viral infection, and we now know that chronic viral infection may be a pathway indeed an underappreciated pathway into Alzheimer disease. Severe chronic viral infections segue in a still mysterious fashion into chronic fatigue syndrome in a highly variable percentage of the time anywhere from a few percent to up to 40 to 50% with some of that variability hinged to the type of virus but also some of it hinged to the severity of the initial infection and how symptomatic people were.

Chronic fatigue syndrome has been dismissed by a lot of Physicians but it's finally getting traction and recognition as a real syndrome even if we don't understand it very well. It could be some kind of neuroendocrine shift orchestrated by our immune systems possibly reflecting some kind of chronic over activation of the system, but we still lack a definitive understanding of mechanism. I wonder if it reflects epigenetic change but again I'm just guessing here. In any case it's really part and parcel of the long-term negative effects of severe viral infection and it's part of why you really don't want to mess with this kind of virus and if possible instead get immunity the easy way through a vaccination.

My guess is that CFS is a mixture of autoimmune dysfunction like you said, neurotransmitter disorders, and one or more other things, depending on the person/specifics..