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Pandemic cats following social distancing

Who ever said that every post had to do with statistical modeling, causal inference or social science?

(Above photo sent in by Zad.)


  1. Dzhaughn says:

    No face masks? Love the hat. Seems to be a sort of heirarchical modeling to me.

  2. Rahul says:

    …I want to know who did the nasopharyngeal swabs on that Bronx zoo tiger that apparently has Covid now!

  3. They have carefully positioned themselves 1.5 cat meters apart.

  4. Dalton says:

    A topical quote for you, both for the times and the usual subject matter of this blog:

    Peter Navarro on his disagreement with Anthony Fauci on the evidence for therapeutic use of hydroxychloroquine for COVID-19. “My qualifications, in terms of looking at the science, is that I’m a social scientist. I have a Ph.D. And I understand how to read statistical studies, whether it’s in medicine, the law, economics or whatever.”

    • Andrew says:


      I can’t imagine that Navarro can be saying that being a Ph.D. social scientist gives him expertise or qualifications on reading statistical studies; after all, Brain Wansink, Susan Fiske, Satoshi Kanazawa, etc etc. are Ph.D. social scientists too, and we wouldn’t even trust them to evaluate claims within their own subfields, let alone more generally.

      Perhaps Navarro is making a reverse statement: that just as he, Navarro, can have a Ph.D. and be wrong, similarly others with Ph.D.’s and M.D.’s can be wrong too. That is, Navarro’s point is that, if qualifications are what you’re after, there are a million people with doctorates in relevant fields, so we can’t think that just because someone has the degree, it means that we can take them seriously.

      I do share with Novarro an annoyance with a traditional deference to M.D.’s. For example, the linked news article says, “Although Navarro has no medical experience, he went on to assert that ‘doctors disagree about things all the time,’ and forcefully defended his credentials as sufficient for him to weigh in on the scientific deliberation over the drug.” But I don’t know how relevant it is that he “has no medical experience.” Dr. Oz has lots of medical experience, and where does it get him? Doctors do lots of great things, but it’s not at all clear to me that medical school and medical practice gives people any special ability to evaluate medical studies.

      • Nick Adams says:

        Is it still April 1st over there?
        Fauci makes a measured statement and Navarro whines like a baby.
        Maybe there is a reason people are deferential to MDs.

        • Andrew says:


          I guess I’m saying that Navarro’s argument is self-reinforcing. To the extent that Navarro comes off as foolish or corrupt, this just reinforces his implicit point that you shouldn’t automatically take someone seriously, even if he happens to have an advanced degree in a relevant field.

      • jrkrideau says:

        Who do you trust more, an epidemiologist,with a Ph.D,(not Fauci) or Peter Navarro who “has published peer-reviewed economics research on energy policy, charity, deregulation and the economics of trash collection”.

        From what I have read of medical schools, they probably do not teach how to evaluate medical studies the way a good research grad course does but Fauci seems to have spent a lot of his professional life in relevant research posts. He probably has learned something from 40 or 50 years on the job working with top-notch researchers. If nothing else he may have learned to listen to his experts and not some political appointee with no qualifications

        • Dalton says:

          For what it’s worth, “In a 2019 analysis of Google Scholar citations, Dr. Fauci ranked as the 41st most highly cited researcher of all time. According to the Web of Science, he ranked 8th out of more than 2.2 million authors in the field of immunology by total citation count between 1980 and January 2019.​”

          The prestige fallacy trap not-withstanding, I’d say that Dr. Fauci not only learned something working with top-notch researchers, he is a top-notch researcher, probably on one of the toppiest notches.

      • Jonathan (another one) says:

        Wait a sec… Being a social scientist doesn’t inoculate him from being wrong, but surely it gives him the tools to be right. He might have no ability to use these tools, but he is being criticized for not being a medical professional. That’s not a relevant criticism. Here’s the right way to proceed. Let him put his analysis out… if it sucks, it isn’t because he isn’t a doctor. If it doesn’t suck, it isn’t because it isn’t an RCT.

        • Andrew says:


          I agree 100% that it’s inappropriate for people to criticize Navarro for not being a medical professional. As you say, being a medical professional isn’t really much of a qualification at all for evaluating statistical evidence and medicine.

          But I disagree that being a social scientist gives Navarro “the tools to be right.” Being a social scientist could give him the tools to be right; alternatively, it could be giving him the tools to be overconfidence, in the manner of Kanazawa, Fiske, Tol, etc.

          • Jonathan (another one) says:

            I wasn’t in Navarro’s class at Harvard (or in any class at Harvard for that matter) and it is true that social scientists can be overconfident, particularly Harvard social scientists. But I don’t think anyone is *taught* to be overconfident, at least not directly. I must have missed the overconfidence classes at Yale, but I sure took a lot of statistic analysis classes, much of it with “anecdotal” data.

            • Andrew says:


              I think a lot of social scientists are taught in graduate school to be overconfident. They are taught to produce research in the style of existing published and celebrated articles, they’re taught to find statistically significant differences and label them as discoveries and to find non-statistically-significant differences and label them as null effects. Maybe some of the people we discuss on the blog figure out how to be overconfident all on their own, but I think a lot of them are trained to be that way.

              • Jonathan (another one) says:

                You may be right about that. But there is another grad school tradition of running down every lead and being extraordinarily cautious to guard your reputation. It is the personality that takes these two traditions and generates either caution or overconfidence. I take your point about NHST generating *any* confidence. That’s a training mistake. But this isn’t about NHST… the clinicians use it too!

                All that said, the claim that data is uninterpretable unless it comes from a clinical trial (a clinical trial which will, by the way, invariably use NHST to draw conclusions, alas) is just an error. If you believed it, then none of the epidemiological modeling work would be valid either!

              • Andrew says:


                Overconfidence may be a state of mind or a personality trait. But in grad school, these people learn the tools that allow them to be overconfident in an effective way that can get them publications etc. Kanazawa, Tol, etc. without graduate training would just be ranters. The methods training allows them to do the cargo-cult science thing effectively.

                To get back to the earlier discussion: getting a Ph.D. in social science is fine—I’ve been training social science Ph.D. students for a long time—but if you want to count that training as providing “the tools to be right” about quantitative research claims, then you should also count it as providing the tools to be overconfident.

              • jim says:

                “I think a lot of social scientists are taught in graduate school to be overconfident. “

                Even undergraduate school. A recent comment on another thread discussed the delicacy of the social science undergraduate ego and outlined a solution to this purported problem that, in my opinion, is virtually certain to produce students with low competence and high confidence.

            • I think teaching overconfidence is implicit, it happens in methods courses where they say essentially “here are the steps to follow to analyze whatever data you might have collected, and if you can get p less than 0.05 and tell a plausible post-hoc story you can be relatively sure you’re correct because the probability you’re wrong is 0.05”

              and then people go off confident that they know how to do research…. over-confident because they’re 100% wrong.

        • jim says:

          Great discussion.

          Education and the degrees that come with it *can* give a person the tools to be highly competent, but it’s no guarantee.

          However, when it comes to a given issue, the issue needs to be decided on the merits of the proposed actions, not the degree or background or experience of the people who proposed those actions.

          • > However, when it comes to a given issue, the issue needs to be decided on the merits of the proposed actions, not the degree or background or experience of the people who proposed those actions

            And this is where the fact that there are more high school dropouts in the US than there are people with a Masters degree runs headlong into every public discussion… (note: I haven’t verified that claim, it was a thing I read recently in the news)

            The fact seems to be, a huge fraction of the US doesn’t know enough to make heads or tails of the evidence on something like hydroxychloroquine, even if they had access to that evidence. So the US is one big shitshow of “my expert says this” and “but my expert says that neener neener”.

            • jim says:

              “The fact seems to be, a huge fraction of the US doesn’t know enough to make heads or tails of the evidence on something like hydroxychloroquine “

              Maybe. But a lot of people knew enough to be wearing masks when Cass Sunstein said there was nothing to worry about. OTOH, people in Iran killed themselves ingesting poison they thought would protect them from the virus. Probably people with Master’s degrees wouldn’t have done that. So I guess when you don’t know the answer, it’s hard to say what it might be.

          • Jonathan (another one) says:

            I agree completely. When someone asks Navarro “why should we listen to you instead of Fauci” his answer ought to be “here is the data and here is what I have done with it. Criticize that all you like. If you aren’t comfortable criticizing the analysis, my degrees are entirely irrelevant.” His answer to the question was clearly not aimed at someone ready to look at the data, but at someone making a credentialing point… He might well be a terrible analysis of data, but the data and his analysis will demonstrate that, not his resume.

    • yyw says:

      Using credential to defend your argument or attack others is stupid. Similarly, one of my pet peeves is people using conflict of interest real or perceived to dismiss a study.

  5. Nick Adams says:

    No sensible person would choose to use observational data if RCT data was available. Epidemiological modelling is only used because an RCT is impossible. An RCT of chloroquine could be done in a week or two and I imagine that is happening now. 30 years perusing the medical literature has taught me that trying to use observational data to make clinical decisions is like chasing squirrels.

    • Andrew says:


      Good point. Still, even with experimental data, you’ll need some combination of theory and observational data to generalize to real-world populations and conditions.

    • Jonathan (another one) says:

      Because of people who might die in that “week or two?” Is an RCT superior? Sure. Are there circumstances where you shouldn’t wait for definitive RCT evidence? Yes. Is this one of them? Dunno… depends on the strength of the observational evidence.

    • BoseQC35 says:

      RCT for the efficacy signal.
      I’d hesitate to privilege safety, tolerability, compliance, adherence, and cost benefit information from an RCT over an obs study.
      In situations like this we need interlocking sources of evidence, not a hierarchy.

    • yyw says:

      If your objective is to determine the effectiveness, sure wait for a week or two. With thousands dying everyday and no known effective treatment, a physician shouldn’t wait unless the potential risk of side effect is unacceptable given the patient condition.

      I also don’t know if it is ethical to conduct a RCT for critically ill patients that could tolerate the drug. Are such RCTs being conducted or are they mostly conducted on patients with mild to moderate symptoms?

        • Anoneuoid says:

          Discussion of ER and critical care doctors (“this goes against every dogma”):

          – A lot of us associated this with HAPE syndrome (high-altitude pulmonary edema)

          – Looking at HAPE the mechanism is really hydrostatic pulmonary edema caused by hypoxemia

          – At high altitude, the pulmonary artery pressure increases because of alveolar hypoxia which leads to arterial vasoconstriction that is patchy and not homogenous

          – Comparing a HAPE chest x-ray to covid, it appears similar.

          -One of my attendings who actually suffered HAPE in Aspen said he was walking around, talking, with a heart rate of 130 and an O2 sat of 39%

          In my reading of available evidence, patients with COVID-19 PNA who get intubated have a mortality rate of anywhere from 50 – 90%. Many studies reporting in the 80% range. This is not a causation of intubation and mechanical ventilation but an association as most of these reports are observational and retrospective. In other words, maybe the patients were just so sick they were going to have a high mortality anyways. On the flip side this higher mortality may also be the fact that we are intubating patients early and using the ARDSnet protocol.

        • Thanks for these. I know a lot of people get frustrated with Anoneuoid but I think the gadfly approach is important to include in science. This lays out a mechanism that makes sense and at least needs to get tested and some trials directed at these sorts of treatments.

        • Here is at least some kind of investigation of the biochemistry of this through structural chemical interaction computations:

          which is interesting and a bit more useful than some random guy on who doesn’t cite any references at all.

          Anoneuoid: given the biochemical ideas expressed in these papers, what is your opinion on the vitamin C and other antioxidant approaches? Is it primarily keeping tissues from being damaged by peroxides produced by the free radical iron. Does that make sense still? It clearly isn’t going to help with replacing hemoglobin.

          Do you think that the smoking link you mentioned in the past could be caused by the fact that smoking damages oxygen transport ability and people’s bodies adapt to produce red blood cells at higher rates? That makes a lot more sense to me than the idea that somehow smoke in your lungs protects your lungs, a theory I find unlikely.

          • Anoneuoid says:

            Thanks for your interest Daniel. I started collecting my thoughts and it became a big summary of what is going on afaict.

            May as well dump it below:
            Clinical stuff

            Basically what happened is there were a bunch of large international RCTs done to determine a standard protocol for severe pneumonia and ARDS but the results don’t generalize to this illness (in fact it may be actively harmful, like increasing mortality from 0 to 60% harmful). It took awhile for people to notice because usually the ICU only sees patients after they have already progressed and the ER only sees the initial phases. So specialization was hiding the true picture of the disease.

            Now there is a bunch of institutional pushback preventing adoption of a new strategy, which basically amounts to treating the patient instead of religiously following the protocol. Eg in that interview Slidell mentions patients with very low spO2 (% hemoglobin bound to oxygen in the blood) who are clinically not in distress. This normally demands intubation and increasing pressure to push up the spO2, but if it’s a problem with the blood carrying O2 instead of with the lungs this is largely futile. Normally that dangerous treatment is only done because a patient like that is expected to die soon anyway, which doesn’t seem to be the case here.

            In the past, we haven’t seen patients who are talking in full sentences and not complaining of overt shortness of breath, with saturations in the high 70s. It’s just not something we typically see when we’re intubating some of these patients. That is to say, when we’re putting a breathing tube in, they tend to drop their saturations very quickly; we see saturations going down to 20 to 30. Typically, one would expect some kind of reflexive response from the heart rate, which is to say that usually we see tachycardia, and if patients go too low, then we see bradycardia. These are things that we just weren’t seeing. I’ve seen literally a saturation of zero on a monitor, which is not something we ever want and something we actively try to avoid. And yet we saw it, and many of my colleagues have similarly seen saturations of 10 and 20.


            To be honest, I’ve run into a great deal of resistance within my institution, which is not to say that anyone is trying to stymie the progress at all. These are the protocols that are in every major (and minor) hospital.


            We ran into an impasse where I could not morally, in a patient-doctor relationship, continue the current protocols which, again, are the protocols of the top hospitals in the country. I could not continue those. You can’t have one doctor just doing their own protocol. So I had to step down from my position in the ICU, and now I’m back in the ER where we are setting up slightly different ventilation strategies.


            perhaps all the studies on ARDS in the 2000s and 2010s, which were large, randomized, well-performed, well-funded studies, perhaps none of those patients in those studies had COVID-19 or something resembling it.


            For whatever reason, I trained in critical care and I was an ER doctor, and I think part of that allowed me to see it a little bit better. Because if you just received these patients in the ICU on breathing tubes, it’s very hard to see this physiology. I was running around the hospital from the ER to the floors to the ICU, and I saw them in all stages of this disease. When you see them in all those different stages, you’re able to see that something physiologically doesn’t make sense. So, in a way, I do feel that somehow my training and my position, being in New York City, allowed me to see this.


            In the editorial, Dr. Gattinoni and colleagues explained further that ventilator settings should be based on physiological findings – with different respiratory treatment based on disease phenotype rather than using standard protocols.

            ‘“This, of course, is a conceptual model, but based on the observations we have this far, I don’t know of any model which is better,” he said in an interview.

            Anecdotal evidence has increasingly demonstrated that this proposed physiological approach is associated with much lower mortality rates among COVID-19 patients, he said.

            While not willing to name the hospitals at this time, he said that one center in Europe has had a 0% mortality rate among COVID-19 patients in the ICU when using this approach, compared with a 60% mortality rate at a nearby hospital using a protocol-driven approach.


            We’ve learned that pretty much all the symptoms mimic high altitude sickness.

            Symptoms of COVID-19

            The most characteristic symptom of patients with COVID-19 is respiratory distress, and most of the patients admitted to the intensive care could not breathe spontaneously. Additionally, some patients with COVID-19 also showed neurologic signs, such as headache, nausea, and vomiting.


            Almost all the patients had bilateral lung ground glass opacity on computed tomography imaging. The initial symptoms included fever (98%), cough (76%), dyspnea (55%), myalgia or fatigue (44%), sputum production (28%), headache (8%), hemoptysis (5%), and diarrhea (3%). Only one patient did not present fever in the early stage of disease.


            Of them, 20 (33.9%) reported at least one taste or olfactory disorder and 11 (18.6%) both. Twelve patients (20.3%) presented the symptoms before the hospital admission, whereas 8 (13.5%) experienced the symptoms during the hospital stay. Taste alterations were more frequently (91%) before hospitalization, whereas after hospitalization taste and olfactory alteration appeared with equal frequency.


            Symptoms of high altitude sickness

            AMS is commonly seen in healthy individuals who ascend too rapidly to high altitude. 1 Symptoms of AMS are characterized by headache, nausea, vomiting, anorexia, lack of energy, and disturbed sleep.
            Subjects with known chronic disease that could cause them to be more susceptible to altitude illness 3 were excluded from participating in the study. These conditions included a cardiac history of congestive heart failure or myocardial infarction within the previous 2 years; pulmonary history for recurrent pneumonia or pulmonary fibrosis; obesity; hematologic disorders such as thalassemia, sickle cell disease/trait, or anemia; renal disease; and neurologic diseases, such as stroke or aneurysm.


            HAPE was misdiagnosed for centuries, as evidenced by frequent reports of young, vigorous men suddenly dying of “pneumonia” within days of arriving at high altitude.
            Early symptoms of HAPE include a subtle nonproductive cough, dyspnoea on exertion and reduced exercise performance. As HAPE progresses, cough worsens and the subject may have a debilitating degree of dyspnoea, even at rest. Orthopnea may occur. Gurgling in the chest and pink frothy sputum indicate advanced cases. The clinical features are cyanosis, tachypnoea, tachycardia and elevated body temperature generally not exceeding 38.5°C. Rales are discrete initially and located over the middle lung fields. Imaging of the thorax reveals patchy opacities with inconsistent predominance of location, but often infiltrates are seen in the region of the right middle lobe
            Subclinical HAPE probably occurs and causes no or minimal symptoms which can be ignored or attributed to other factors. The true incidence is unknown, but two recent studies have suggested that upwards of 50% of persons may have subclinical fluid accumulation in the lungs, consistent with occult edema which resolves spontaneously even though subjects remain at high altitude

            During normobaric hypoxia olfactory sensitivity and intensity estimates were significantly reduced.


            To begin with, in severe cases, both COVID-19 and HAPE exhibit a decreased ratio of arterial oxygen partial pressure to fractional inspired oxygen (Pao2:FiO2 ratio) with concomitant hypoxia and tachypnea [4,5]. There also appears to be a tendency for low carbon dioxide levels in COVID-19 as the median partial pressure of carbon dioxide (PaCO2) level was 34 mmHg (inter-quartile range: 30-38; normal range: 35-48) in a recent JAMA article describing 138 hospitalized cases [6]. Initial exposure to hypoxia at high altitude leads to an immediate increase in ventilation that blows off large quantities of carbon dioxide, producing hypocapnia as well [7]. Furthermore, blood gases of non-acclimatized mountaineers with severe illness were accompanied by a significant decrease in arterial oxygen due to an increase in alveolar- arterial oxygen difference, although herein arterial PaCO2 did not change significantly [8]. In short, hypoxia and hypocapnia are seen in both conditions, but there is more.

            Radiologic findings of ground-glass opacities are present in up to 86% of patients with COVID- 19 with 76% having bilateral distribution and 33% peripheral [9]. Notably, lung cavitations, discrete pulmonary nodules, pleural effusions, and lymphadenopathy were absent [10]. In addition to this, patchy infiltrates are present [11]. Patients with HAPE also exhibit patchy infiltrates throughout the pulmonary fields, often in an asymmetric pattern and CT findings reveal increased lung markings and ground glass-like changes as well [12-14]. It has been shown that widespread ground-glass opacities are most commonly a manifestation of hydrostatic pulmonary edema and this is a central point to consider going forward [15].


            Cigarettes as an aid to climbing Report, November 21 1922

            Captain GJ Finch, who took part in the Mount Everest expedition, speaking at a meeting of the Royal Geographical Society, London, last evening on the equipment for high climbing, testified to the comfort of cigarette smoking at very high altitude. He said that he and two other members of the expedition camped at 25,000ft for over 26 hours and all that time they used no oxygen.

            About half an hour after arrival he noticed in a very marked fashion that unless he kept his mind on the question of breathing, making it a voluntary process instead of an involuntary one, he suffered from lack of air. He had 30 cigarettes with him, and as a measure of desperation he lit one. After deeply inhaling the smoke he and his companions found they could take their mind off the question of breathing altogether … The effect of a cigarette lasted at least three hours, and when the supply of cigarettes was exhausted they had recourse to oxygen, which enabled them to have their first sleep at this great altitude.


            AMS, according to the Lake Louise score, was significantly lower in smokers; the value was 14.9%, 95% CI (6.8 to 23.0%) in smokers and 29.4%, 95% CI (23.5 to 35.3%) in non-smokers with an adjusted OR of 0.54, 95% CI (0.31 to 0.97) independent of gender, age and maximum altitude reached.
            Probably because of its influence on the blood’s oxygen transport as well as through its effects on vasoconstriction, smoking is a protective factor for the onset of AMS.


            Vitamin C

            given the biochemical ideas expressed in these papers, what is your opinion on the vitamin C and other antioxidant approaches? Is it primarily keeping tissues from being damaged by peroxides produced by the free radical iron. Does that make sense still? It clearly isn’t going to help with replacing hemoglobin.

            The main thing it does is limits oxidative damage, which is common to every disease process. That’s why it gets made fun of as “magic”. I think they need to measure vitamin c levels and determine if there is a deficiency (as a general rule there will be if they are very sick, exceptions are, eg, if the kidney isn’t excreting anything) then give enough to correct that deficiency.

            But, if we assume there is something going on with hemoglobin/iron:

            Methemoglobinemia is a disorder characterized by the presence of a higher than normal level of methemoglobin (metHb, i.e. ferric [Fe3+] rather than ferrous [Fe2+] hemoglobin) in the blood. It is caused as a result of administrating oxidizing agents with the associated oxygen–hemoglobin dissociation curve therefore shifted to the left. Methemoglobinemia can be congenital, but its acquired form is more often (1). The acquired form might be seen after consumption of some foods and additives, and exposure to certain chemicals and drugs. Although local anaesthetics which are widely used in hospitalized and outpatients are usually safe for use, sometimes can cause life threatening methemoglobinemia (2). Prilocaine is one of the most frequently used anaesthetics in children, rarely causing methemoglobinemia (3, 4). Here, we present a case of a methemoglobinemia treated with ascorbic acid successfully to emphasize the use of ascorbic acid as an alternative method especially in regions where glucose-6-phosphate dehydrogenase (G6PD) deficiency is more frequent.


            However, at high concentrations in the presence of iron ascorbate can also cause a net production of hydroxyl radicals:

            Ascorbate-mediated killing of C. albicans depends on oxygenation and metabolism, involves iron-catalyzed generation of hydroxyl radicals via Fenton reaction and depletion of intracellular NADH.
            The Fenton reaction and the coupled Haber–Weiss reaction together comprise the following steps: (Equation 1) ferrous ion reacts with oxygen to produce superoxide (Equation 2), which in turn generates H2O2 via dismutation (Equation 3), H2O2 then reacts with ferrous ion to form HO. (Equation 4) ascorbate can reduce Fe3+ back to Fe2+ to allow the cycle to continue


            That could theoretically be a very bad side-effect, but so far the reports out of china do not reflect that:

            Dr. Mao stated that his group treated ~50 cases of moderate to severe cases of Covid-19 infection with high dose IVC. The IVC dosing was around 10,000 mg – 20,000 mg a day for 7-10 days, with 10,000 mg for moderate cases and 20,000 for more severe cases by the pulmonary status (mostly the oxygenation index) and the coagulation status. All patients who received IVC improved and there was no mortality. Compared to the average of 30-day hospital stay for all Covid-19 patients, those patients who received high dose IVC had a hospital stay that‘s about 3-5 days shorter than the overall patients. Dr. Mao discussed one severe case in particular who was deteriorating rapidly. He gave a bolus of 50,000 mg Vit C IV over a period of 4 hours. They watched the patient’s pulmonary (oxygenation index) status stabilizing and improving in real-time. There were no side effects reported to all the cases treated with high dose IVC.


            There are 3 lessons that we learned about this Covid-19 infection, Dr. Wang said:
            1. Early and large dose IVC is quite helpful in helping Covid-19 patients. The data is still being finalized and the formal papers will gradually be published.
            2. Covid-19 patients appear to have a high rate of hyper-coagulability. Among the severe cases, ~40% severe cases showed hyper-coagulability, whereas the number among the mild to moderate cases was 15-20%. Heparin was used among those with coagulation issues.


            I include the second point just because it also seems to indicate a blood disorder. But if we were going to see a harmful systemic pro-oxidant effect due I’d think it would have happened in the severely ill patient who was determining rapidly. It’s also possible that the peroxyl radical generation is more localized and deactivates the virus… Or maybe all the iron released (assuming it is) is bound to ferritin which is reportedly increased in these patients:

            Univariate analysis showed that comorbidity, age >50, lymphocyte counts <1500 /μL and serum ferritin >400 ng/mL at presentation were predictive of progression to severe diseases.



            Do you think that the smoking link you mentioned in the past could be caused by the fact that smoking damages oxygen transport ability and people’s bodies adapt to produce red blood cells at higher rates? That makes a lot more sense to me than the idea that somehow smoke in your lungs protects your lungs, a theory I find unlikely.

            See the above quotes about smoking and high altitude illness. For some reason it seems to help there as well, possibly even having an acute effect in addition to whatever long term effect according to that Captain GJ Finch. Of course, once again, there has been a general refusal by the medical community to figure out what is going on.

            One interesting thing I found is that patients with COPD have a lower O2 saturation than usual:

            In patients with COPD, hypoxic pulmonary vasoconstriction is the most efficient way to alter the Va/Q ratios to improve gas exchange. This physiological mechanism is counteracted by oxygen therapy and accounts for the largest increase of oxygen-induced hypercapnia. A titrated oxygen therapy to achieve saturations of 88% to 92% is recommended in patients with an acute exacerbation of COPD to avoid hypoxemia and reduce the risk of oxygen-induced hypercapnia.


            Same with asthmatics:

            Pulse oximetry values of <90% are less commonly associated with problems, although CO 2 retention and a low partial pressure of oxygen value may be missed.
            Patients who are hypoxemic should receive enough supplemental oxygen to target saturation of 93–95% in adults (94 –98% in children)


            And also in smokers once you correct for higher carbon monoxide levels:

            According to these data, the determination of oxyhaemo- globin saturation by pulse oximetry overestimates the real value of HbO in smokers to a greater or lesser extent, depending on the rate of HbCO. Therefore, we think that the use of pulse oximetry in those studies in which the ‘true’ value of HbO, is required is questionable.


            So perhaps there is already some adaptation they have to deal with these lower oxygen levels that is also protective against this illness (characterized by low spO2 levels). But I don’t see why that is any more plausible than a remodeling of the respiratory tract (via altering ACE2 expression, or otherwise). Usually when somthing has such a huge effect it is via multiple mechanisms, so I would guess it is both.

            Here is a recent meta-analysis on smoking and COVID-19 btw:

            In fact, the consistently low prevalence of current smoking among Chinese patients with COVID-19 was further supported by the recent data recently released from the US CDC.28 From a total of 7162 patients in the US, only 1.3% were current smokers. low smoking prevalence was also observed among hospitalized non-ICU (2.1%) and ICU cases (1.1%), while the population smoking prevalence in the US is 13.8%. These observations raise a possible hypothesis that nicotine might reduce the risk for severe COVID-19. Hospitalization for COVID-19 will inevitably result in abrupt withdrawal of nicotine and its beneficial effect linked to this hypothesis in smokers or users of other nicotine products. This could, at least partly, explain the association between smoking and COVID-19 severity among hospitalized patients.27 Nicotine has been found to prevent acute lung injury in an animal ARDS model and has immunomodulatory effects.29,30 There is also evidence for an interaction between nicotine and the renin-angiotensin-aldosterone axis, although such interactions remain unclear.2-5 In any case, the observations of a consistently low prevalence of smoking among COVID-19 cases in China and the US, together with the potential mechanisms through which nicotine interacts with the inflammatory process and the renin-angiotensin-aldosterone axis involved in the development of COVID-19, warrant an urgent investigation of the clinical effects of pharmaceutical nicotine on COVID-19 susceptibility, progression and severity.


            They miss that the same thing was true for the first SARS, a bunch of papers are not included, and that there are no missing smokers for influenza or heart disease, etc. And they say that even if smoking helped with COVID-19 the risks of other diseases would outweigh it (interesting we don’t shut down the world economy over these other diseases). But it is pretty good.

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