What are “virosydes”?
Any topical antiseptic potent enough to disassemble a virion particle or interfere with cellular operations of the virus within an infected cell will almost certainly do severe harm to the body as well. The notion that you can just wash out the infection with a swig of some kind of antiseptic is nonsensical and the naive belief in this has resulted in hundreds or perhaps thousands of deaths in Iran.
Stranger
Well, as noted, reality is sometimes weird.
The bee-czar owns what he will.
ISTM that the major thing that has not been established is the role of confounding factors. Correlation does not equal causation, even assuming the data is solid. For example, smokers who are still smoking may be genetically predisposed to exceptionally robust respiratory systems. Every ex-smoker I know (yes, I realize this discussion is about current smokers, not ex-smokers, but hear me out) has been diagnosed with a respiratory disease. My sister-in-law was diagnosed with lung cancer after long-term smoking, which was deemed inoperable and she was given just a limited time to live. She survived due to dogged persistence and a lot of internet research that revealed a very new robotic surgery that most doctors didn’t even know about. Smoking is deadly shit. If there is some miracle ingredient in nicotine that deters the virus without worse side effects, then yes, we need to know about it, but I have serious doubts.
I doubt smoking results in a major improvement to immunity and far fewer cases. But it wouldn’t be unheard of - smokers can have a lower incidence of certain bowel diseases. Perhaps their lungs are already so damaged and chronically inflamed that they don’t unleash a cytokine storm. Even so, lung reserve can be a lot worse in smokers. And while smoking is not a great habit - and smokers should be encouraged to reduce or cut out consumption - it is true some smokers live long lives in good health.
Still, if I don’t see an adequately powered study, than to me smoking causes harm and worse outcomes.
This particular article is available from Pubmed Central, which is administered by NIH and is free to all:
ETA: granted, there’s not actually that much more to this particular article than the abstract.
A huge study out of the UK (n = 17,400,000) is out today, again showing that current smoking status (but not former smoking status) is associated with less severe outcomes from COVID-19:
Page 15: the apparent slight protective effective which disappeared when controlled for ethnicity. Former smokers did worse.
I smoked tobacco frugally in my youth and quit 45 years ago. The many medics who’ve inspected me recently say my lungs are clear. Have I any greater or lesser risk or resistance re: SARS-CoV-2?
Well, if nicotine levels in the blood interfered with viral uptake, as was hypothesized in one of the links upthread, than ex smokers with some moderate lung damage might be at more risk than never smokers or even newer smokers. Lots of ifs, I know, but interesting.
And here we have life imitating art,
If you look at page 6 where they show the actual numbers, it didn’t quite “disappear”. They say (emphasis added) “We also explored confounding by ethnicity, which was not adjusted in the primary model: among those with complete ethnicity, the current smoking HR adjusted for all variables except ethnicity was similar to in the full study population (0.88, 0.78-1.01) but this moved towards the null on adjustment for ethnicity (HR 0.94, 0.82-1.07).” So it looks to me like the protective effect was reduced by half rather than disappearing entirely. (Though it could be that enough of the CI is above 1.0 that they are can consider it disappearing.)
On the flip side, they also write “the change in HR appeared to be largely driven by adjustment for chronic respiratory disease (HR 0.93, 0.83-1.04 after adjustment) and deprivation (HR 0.98, 0.88-1.10 after adjustment)”. I don’t understand the logic of testing for the effect of smoking by adjusting for chronic respiratory disease, since CRD is itself frequently caused by smoking. That seems a lot like testing for the health effects of smoking after factoring out lung cancer etc. Unless their intention was to measure the effect of current smoking vs the effect of long term smoking on the body.
In any event, based on this it would appear that smoking is not a huge deal either way.
Another note: since this study looked at death only, it remains possible that smokers are less likely to be infected but if infected more likely to die. It seems likely, in fact, because if overall death rates are roughly comparable, then if you assume the latter, then the former would have to also be true for the numbers to even out.
Yes. 0.94 with that error bar becomes below significance and based on that, at least discounting for chronic respiratory disease (which I agree with odd), current smoking is not a huge deal either way. Damage from it in the past is.
Also of course much “remains possible”. It remains possible that current smokers are more likely to get infected and more likely to die more suddenly at home, both of COVID-19 and/or of a triggered heart attack or stroke and not be included in COVID-19 numbers at all. Honestly I’d suspect that but I have no evidence to support it. Yet.
Looks like smoking isn’t helpful.
That study doesn’t say what you think it says. All it says is that of the factors identified for increasing the risk in younger adults compared to other young adults, the most common one is smoking. Not an outcomes study.
Meanwhile there is this new huge study. See extended table 2. Controlling for confounders if anything slightly less risk for current smokers. I don’t buy that it lowers risk but surprisingly any increase is too small to see.
Never mind. It’s just the same study above now published.
It’s not at all definitive. I’m not sure I even believe 1 in 3 to 1 in 6 young people “are vulnerable” for severe cases. That isn’t what I’ve seen. But I’m certainly prepared to believe smoking is unhelpful. Better studies will not show, I would wager, a protective effect of smoking as was once hypothesized by a few.
Which I always understood was the reason that smokers were more susceptible to respiratory illness (as well as much more susceptible to dust damage). Which raises the question:
If normal cilia are not measurably effective in reducing COVID-19 infection, what does that say about COVID-19 modes of transmission?
Your body breathes in a lot of garbage. The nose, sinuses, nasopharynx and trachea catch a lot of debris. Viruses are much smaller, but it might not be fair to say the cilia do nothing.
Not sure but I don’t think this post-hoc analysis, factoring out controlling for the “confounder” of chronic respiratory disease, was in the preprint:
I am prepared to believe that smoking is unhelpful. This data though seems to show that there is no significant impact either way, despite what we’d reasonably expect. The most common “risk factor” for young adults is not much of a risk factor.
Interesting development:
Two of the paper’s authors had financial links to tobacco companies. When submitting the article to the journal, both stated “no potential conflicts of interest”.