Hypothesis: if you have any pre-existing lung conditions, you are more likely to quit smoking. In other words, if you're the sort with pre-existing conditions that make you more likely to be hospitalized if you get Covid-19, then you would be more likely to have quit smoking (or died before now if you didn't).
Still an interesting result, but not, needless to say, a reason to start smoking.
It's important to be careful here: the finding above is with symptomatic covid, not hospitalization. We don't know whether or not it makes you more likely to be hospitalized.
Right, or that there's some other confounding factor that leads smokers to be less likely to contract the disease or seek treatment. This kind of science (teasing data out of uncontrolled sampling) is really hard.
Same here, although I already suspected it based on the fact that Japan's death total is very low; smoking is more prevalent in Japan than most advanced economies, I believe.
Depends on what you mean as a "condition". In a medical record, smoking status is often stored as a top-level value tied directly to the patient, and also often coded into their condition list[0]. In the FHIR standard, a physician's observation of a patient's smoking history is usually represented with an observation resource, but often will be "upgraded" to a condition resource[1].
But, yeah, from a non-healthcare data standpoint, what a "condition" is really just depends on your definition.
I believe they raised and tried to address this confounding factor by determining whether or not one is a smoker based on a date prior to COVID-19 hitting. But I only skimmed it, so can’t be sure what they did.
This paper is terrible. There are errors in the abstract. It uses percentage of percentages to make results look important. It relies on self reporting when people are strongly encouraged to misreport. It excludes groups arbitrarily (no ICU patients, no one treated by certain departments). Its all about 1 hospital for a few weeks in one part of France.
Its like a test paper to teach people to spot errors and weaknesses in papers.
We don't have any data for China. None of their numbers are reliable, they make them up. This is one of the biggest issues in this pandemic: we don't know shit partly because China insist on lying...
Interesting support for your claims. Not saying they are wrong, but a classified US intelligence report doesn't really carry much weight either (link 1).
Link 2 is about the latest revision of the death toll in Wuhan. Now, you must think the current US death toll is totally accurate. Will you claim that the US makes things up when those figures are revised (which they will be) too?
Interesting, they hypothesize that nicotine is responsible:
> There are however, sufficient scientific data to suggest that smoking protection is likely to be mediated by nicotine. SARS-CoV2 is known to use the angiotensin converting enzyme 2 (ACE2) receptor for cell entry[14-16], and there is evidence that nicotine modulates ACE2 expression[17]which could in turn modulate the nicotinic acetyl choline receptor (manuscript submitted).
Nicotine (smoking) has been known to act as an immunomodulator and can act as a preventative for gastrointestinal inflammatory disease such as ulcerative colitis. This could be attenuating the inflammatory response and reducing symptoms for COVID-19 patients.
Perhaps the additives are keeping COVID-19 patients alive by supporting breathing in difficult circumstances? There are hundreds of additives so figuring out if any of them help would be difficult:
This might be a joke, but I'm "addicted" to nicotine gum (and don't otherwise smoke). I probably caught the virus early on, and it wasn't particularly bad for me (even compared to typical flu).
That's not even really a single data point, but I'm curious to see how this pans out.
> I probably caught the virus early on, and it wasn't particularly bad for me (even compared to typical flu).
Do you have reason to believe that, or were you sick in January/February and just kind of assume that was it, even though we were at the height of regular cold and flu season?
Just circumstantial. I was knocked down with something I self-diagnosed as "walking pneumonia", which turned out to be the thing a lot of these cases were diagnosed as before the virus was widely known. Several days after a flight. Main symptom was lots of coughing and some fever. Felt better after 7-10 days, but coughed frequently for several more weeks. Not really the aches of flu, nor any nasal/sinus symptoms--just totally wiped out.
Until we have antibody tests, no way to know. And I'm locked down hard--not assuming anything.
Its far to premature to even conclude that inhaled nicotine protects the lungs. This is just one study. Don't do anything stupid, like go develop a nicotine addiction, just because of one headline.
Obviously I would never think of suggesting that people start smoking tobacco. My comment was meant to discourage people from leaping to conclusions and getting addicted to nicotine lozenges when, as far as I know, there is little that suggests they'd be beneficial.
Not in medical field, but nicotine is generally biotoxic and used as a pesticide so i'm not at all surprised. Detriments to any symbiotic microorganisms aside, regularly spraying the lungs and other airways with a light coating of biotoxic film seems a good way to generally inhibit replication or damage any negative bioparticles, so long as the damage doesn't overwhelmingly interfere with the smoker's own biological functions and weaken the overall system ...
Being toxic to an insect or human doesn't mean it will have any effect on a virus.
IIRC the reason nicotine is poisonous to humans is because it binds to receptors involved in nerve function, which in turn are required to control muscles.
It would make sense if smoking (the oxidants from smoke) kills the virus.
However, once the infection actually progresses it is clear that smokers are worse off.
The nicotine explanation in the article discussion isn't actually studied, it is just pure speculation (which is fine, mine is as well). But there's no explanation why there's fewer smokers even though smokers have more ACE2 receptors. That's table stakes for having a hypothesis on this.
I was joking the other day that it would be funny if the reason that Covid19 was less sever in Asian countries was not the high rate of mask usage but the high rate of smoking!
It's an interesting data discrepancy - fewer smokers in covid-19 infected individuals - but it doesn't tell us much. The survival bias is a problem. They took the smoking status of alive patients, not in the ICU. The results could indicate the opposite effect. Smokers tend to be in the ICU or die at an accelerated rate so are under-represented. That said, one would expect counter-acting effects in such a situation that would make the counter-intuitive result of fewer smokers meaning it's worse for smokers less likely, e.g. greater diagnosis rate in smokers due to increased severity, higher rates of infection in smokers, etc.
I don't think any conclusions can be drawn from this study. It does suggest that there is value in investigating the impacts of smoking on Covid-19.
There is a story from the Golden Age of Science Fiction called Pandemic by JF Bone. It postulates a global virus the cure for which in the end turns out to be smoking tobacco.
And the improbably beautiful nurse marries the curmudgeon who is her boss.
I find it fascinating how willing people are to accept the vital importance of chemicals not directly related to covid 19 or coronaviruses. People were very willing to swallow Chloroquine as a "cure" or treatment, but that is (was?) used for treating malaria (not a virus). Now tobacco smoke is preventative? And that must be because of nicotine. Not one of 1000s of other chemicals in the same smoke? And forget that other research found smoking increased the density of the proteins covid 19 binds to to enter cells (another small study with unverified results I think).
Jesus people, the solution to this problem will not be as simple as antimalarials or taking up Cuban cigars. Stop grasping at straws like they are lifeboats!
This has nothing to do with "accept the vital importance of chemicals" and everything to do with the fact that we record smoker status when patients enter hospitals and HOLY COW, LOOK, A TREND IN THE DATA.
> Now tobacco smoke is preventative?
Maybe! If you just casually ignore data, you will miss opportunities for important discovery.
> And that must be because of nicotine. Not one of 1000s of other chemicals in the same smoke?
That's called a _hypothesis_. Hypotheses are somewhat important for research.
Now you're in trouble. You named a hypothesis but the experiment doesn't test that hypothesis does it? No one checked whether any or all of these people actually smoked. Weirdly they let them report different levels of smoking but don't include that data
And no one thought to ask about vaping (where there are far fewer chemicals and you would have a stronger case to pin point nicotine). Plus they included Chinese data which is mostly made up. And they excluded random arbitrarily groups (no ICU patients, maybe all the smokers went straight there?).
A good experiment is one where you learn something. You prove or disprove your hypothesis.
This paper doesn't mean anything. Like you say, the answer to the question si "maybe". Maybe nicotine helps, maybe it doesn't. Maybe literally any chemical helps, maybe it doesn't. Great, thanks for wasting everyone time...
> You named a hypothesis but the experiment doesn't test that hypothesis does it?
This paper doesn't claim to be an experiment to test that hypothesis. That's all you.
This paper claims to be a data record highlighting an interesting trend for future experimentation.
The hypothesis for cause is in the DISCUSSION section at the end and references things that we already know about interactions between nicotine, ACE2, and sars-cov-2.
Call it what you like, experiment or report, hypothesis (your word) or trend (I think this the wrong term but I can't think of abetter one...).
As it is, they have found nothing because they did such a bad job of looking. Leaving aside that apparently 601% of patients were men (now there is a concerning trend), they haven't tested nicotine or smokers because their methods don't differentiate the Corona cases involving those factors from ones that don't.
Nicotine could kill every user and this study wouldn't find that, nicotine could make its users immortal and this study wouldn't notice. That's what makes it bad: they found nothing because they did a bad job of looking.
This is a badly dressed up version of "my aunt smoked and she lived to be 97 so it can't be all bad".
That's maybe because someone who has a "strong enough health" to tolerate smoking, builds some resistance in the short term. That's in the long term that smoking is really deadly though
That kind of study would also find out that people doing daily physical exercise would be much less affected by Covid, etc..
The study is done with a Covid positive population.
They didn’t study if people who smoked where less likely to get Covid. The study goal, as I understand it, was to theorize the idea that smoking serves as some sort of protection leading to less severe symptoms.
Otherwise the study wouldn’t make sense. The study must have clearly accounted for ratios in the smoking general population against the sample population. That’s the only way it makes sense.
I’m curious what makes you think that smokers isolated earlier than anyone else. I don’t think being a smoker makes you more self-aware of your own health. If anything is quite the contrary.
digs aside, this is highly culturally dependent - before smoking was quasi-taboo in the west, smokers were often more social and smoking was a 'good' way to meet people - just join the local smoking circle outside. Same is likely still true in less smoking hostile countries.
Very few habits are hand to mouth in the way smoking does. Smokers will touch their hands to their mouths hundreds of times a day...without a thought as to where that hand has been.
Still an interesting result, but not, needless to say, a reason to start smoking.