This is interesting data. I want to see Vitamin D status included in a large population study like this because I've been following two smaller studies covering about a thousand cases total that shows Vitamin D deficiency has a risk ratio of 10 to 20 (more even than being age 80+ in the above study). The studies:
Table 1 in each of those papers show Vitamin D status vs Outcomes. The correlation between Vitamin D status, where Normal is >30 ng/ml (or 75 nmol/L), and death rates is stark.
From [1] (which had n=780 cases) here is the punchline: "98.9% of Vitamin D deficient cases died while only 1.1% of them were active cases. 87.8% of Vitamin D insufficient cases died while only 12.2% of them were active cases. Only 4.1% of cases with normal Vitamin D levels died while 95.9% of them were active cases."
From [2] (which had n=212 cases) here is the punchline: "Of the 212 (100.0%) cases of Covid-2019, 49 (23.1%) were identified mild, 59 (27.8%) were ordinary, 56 (26.4%) were severe, and 48 (22.6%) were critical (Table 1). Mean serum 25(OH)D level was 23.8 ng/ml. Serum 25(OH)D level of cases with mild outcome was 31.2 ng/ml, 27.4 ng/ml for ordinary, 21.2 ng/ml for severe, and 17.1 ng/ml for critical."
Note: the classification for outcomes was "(1) mild – mild clinical features without pneumonia diagnosis, (2) ordinary – confirmed pneumonia in chest computer tomography with fever and other respiratory symptoms, (3) severe – hypoxia (at most 93% oxygen saturation) and respiratory distress or abnormal blood gas analysis results (PaCO2 >50 mm Hg or PaO2 < 0 mm Hg), and (4) critical – respiratory failure requiring intensive case monitoring."
I want to see a dozen more studies like [1] and [2] to see if this holds up to replication with larger populations.
In case you weren't aware, controlled trials have shown that vitamin d supplementation protects against respiratory disease [1]. This is evidence that the association you highlight is more than a spurious correlation.
NHS may say 'no evidence' - but it seems likely what they mean is that nobody has done a vitamin D-coronavirus trial. So it isn't that there is no evidence but rather the evidence is not overwhelming.
"No evidence" makes it sound like there is actually no evidence. There is evidence - it just got linked in the two comments that make up the root of this thread.
If it's true that Vitamin D is such a large factor in reducing the lethality of respiratory disease -- perhaps it's better to loosen lockdown rules to ensure the wider population can get more sun before they inevitably catch the virus.
It may explain why heavily indoors NYC had so many lethal cases, even as most infected were already keeping themselves indoors.
If the extra time out from loosening was all spent out in the sunshine, maybe it might just balance out the increase in cases, but there’s no way that’s what would happen. To make a significant difference requires an extra several hours a day out in sunshine. Better to just advise people to take supplements.
Sunnier countries can still have large vitamin D deficient populations. I read a study regarding the correlation between mental illness and vitamin D deficiency a few years ago, and Italian patients were still often very deficient. If people don't go out in the sun enough, or wear too much sun cream, it doesn't matter how sunny it is.
That's misleading because Europe is on the western edge of the Eurasian landmass, meaning it gets the benefit of warm air heated up over the ocean. By the time the air gets to the eastern edge of a landmass it's a lot colder, which is why London has a milder average temperature than NY and Vladivostok, despite being almost 10° further north than both.
Yes, but vitamin D production relates to direct sunlight ... I think the angle of the sun and amount of atmosphere it has to go through affects UV amounts so a warmer European country does have less direct sun therefor more potential for vitamin D deficiency ...
TBH I am not super solid on every one of these details.
That's a good point, but this paper seems to indicate that the amount of sunlight required over the summer in order to build enough vitamin D to last over winter isn't much for white Caucasians in the UK - nine minutes each day at lunchtime between March and September, assuming shorts and t-shirts are worn during the summer:
Vitamin D deficiency can still occur in sunny countries. To get the adequate amount of Sun from Vitamin D takes a day out in the sun entirely as opposed to basic supplementation.
A friend of mine had cancer and they had him taking D3 immediately.
also I was out shopping recently and they seemed to sell many varieties of D3, but I didn't see any other D vitamins offered for sale. Is D deficiency really D3 deficiency? or have the other D vitamins sold out?
As a vegan, I learned that there's D2 (comes from plants) and D3 (comes from animals), and they are the same as far as I know. Not sure about using them for treatments.
There are a number of other studies on this. From what little I've read, if the effect is real,it seems the it is relatively weak, but still worth doing.
[2] is pretty scary. As a 30 year old I know that my chance of death is low, but I’d like to avoid a “severe” or “critical” case. There are a large number of unpleasant states between “fine” and “dead” that I’d like to not experience. A 50/50 chance of it being no big deal are worse odds than I’d prefer.
[1] is sending me back out onto the patio this weekend for tanning.
I agree, we need better evidence on all the vitamin D claims. Comparing rich white people in the suburbs who have lots of open land to get sun and use for exercise versus poorer darker skinned people in dense inner city apartments who spend most of their time inside introduces numerous confound factors that will be highly correlated with vitamin D.
> I agree, we need better evidence on all the vitamin D claims.
Not really. We should be blasting "get your Vitamin D supplements" from the rooftops, because maybe that's a significant factor in COVID-19 and it's safe and people should get them anyway. There's no downside.
If in a few years it then turns out that Vitamin D had nothing to do with it, it doesn't matter. If it turns out that Vitamin D really was a big factor, we'll be sorry for being hesitant with a safe and cheap intervention.
You are right that vitamin D is relatively safe compared to other potential treatments that were bandied about like hydroxychloroquine. But while there are fewer health risks from taking it, there are still the same behavioral issues that were present with hydroxychloroquine. The first is causing a run on vitamin D that prevents other people from acquiring if for their proven treatments. However the main issue that I think we want to prevent is luring people into a false sense of security that causes them to decrease the proven preventive measures. We don't need large groups of people gathering on beaches because they think the sun will be a miracle cure and they don't have to worry about getting sick. So if you want to personally start taking it without changing your behavior, be my guest. But any advice to take it needs to be clear that the evidence it helps is still very suspect at this point.
> The first is causing a run on vitamin D that prevents other people from acquiring if for their proven treatments.
Vitamin D is an easily manufactured supplement, it's not medicine that some people absolutely have to take every day.
Also, we're heading into summer and the sun is still rising every day.
> However the main issue that I think we want to prevent is luring people into a false sense of security that causes them to decrease the proven preventive measures.
We've had the same discussion about masks, so I think that one's settled.
> We don't need large groups of people gathering on beaches because they think the sun will be a miracle cure and they don't have to worry about getting sick.
If you don't want people gathering on the beaches, prohibit it. Having said that, the risk of infection outdoors is generally considered to be quite low.
> So if you want to personally start taking it without changing your behavior, be my guest. But any advice to take it needs to be clear that the evidence it helps is still very suspect at this point.
The evidence that Vitamin D supplementation works is there and it has already been recommended for everyone with low serum levels, well before COVID-19.
The problem is that people often aren't even aware that their serum levels are low, so that is highly prevalent - especially in the elderly and people with darker skin.
Hand sanitizer is also easy to manufacture and I haven't seen it in a local store for over 10 weeks. The ease to manufacture is just one of the steps to getting it on the shelves. Also getting vitamin D from the sun isn't an option for some people, especially those with darker skin.
The difference between masks and vitamin D is that one is proven to work and one might work. If vitamin D doesn't help as much as people here are claiming, there is a real downside if people are behaving as if it works. That applies to my arbitrary example of beach gatherings as well as other behavior the government has no hope of preventing.
Once again, this doesn't necessarily mean that vitamin D doesn't help. We just need better data. The early indication was that hydroxychloroquine helped too and we all know how that turned out.
What does "proven to work" mean with regard to masks? A lot of the measures put in place are unproven but thought to be reasonable.
Hand washing and social distancing appear to be the most important. That means soap and 6+ feet for at least the next 2 years. That is definitely doable. I don't see masks as a long-term strategy.
> The preponderance of evidence indicates that mask wearing reduces the transmissibility per contact by reducing transmission of infected droplets in both laboratory and clinical contexts. [1]
When the primary vector of spread is through water droplets expelled while talking, coughing, or sneezing, I would think the importance of reducing the travel distance of those droplets would be self evident.
We shouldn't be telling people to overdose on Vitamin D, obviously. I dread the day that Donald Trump mentions "Vitamin D", but then again even a massive overdose of Vitamin D isn't going to be life-threatening.
The generally safe amount is 4000 IU daily, which should get almost everybody to healthy levels. However, if your doctor finds that you have low levels, he may prescribe far higher amounts for a while.
Then do not overdose. Tell people to take 1000IE per day, not more. This will have no negative impact on the health or economy, but if we are lucky, it will help reduce the impact of COVID-19.
Shutting down the economy is clearly dangerous, yet enough people do not seem to have a problem with that.
Vitamin D pills is just a quick fix. Moderate exercise and fresh air would probably save more lives. Healthy vitamin levels are good, but its many little things which affects health.
Another critical question: Why hasn't this been properly researched, yet? There were indications before, that Vitamin D insufficiency increases risk of respiratory diseases.
That, or perhaps a lack of sun exposure is linked to having preexisting conditions. Diabetics, COPD, asthmatics, etc as a group probably tend to spend less time outside.
There's nothing particular that is required in the diet to synthesize Vitamin D3 from the sun.
Without sun exposure, you'd have to be eating several pounds of fatty fish every day to get to "healthy" levels from diet alone. You need a supplement.
Keep in mind, non-severe Vitamin D deficiency doesn't cause any significant evolutionary pressure, so migrating humans just rolled with it - to this day.
> I want to see Vitamin D status included in a large population study like this
Although vitamin D is not mentioned in this study, it does show that black people have a hazard ratio of about 2 compared to whites. In the UK black people would be more vitamin D deficient than white people.
Now that I think about it, isn't the potential for vitamin D deficiency the reason there are white people in the first place?
> Now that I think about it, isn't the potential for vitamin D deficiency the reason there are white people in the first place?
Yes. Pale skin has better vitamin D production in low light, while black skin avoids skin damage even in extreme sunlight. Skin color is just evolution finding the right trade-off for the local climate.
From NHS advice on vitamin D referenced in my previous comment
“Some people will not get enough vitamin D from sunlight because they have very little or no sunshine exposure.”
..
“ If you have dark skin – for example you have an African, African-Caribbean or south Asian background – you may also not get enough vitamin D from sunlight.”
> Unsurprisingly there's no direct clinical evidence.
"We searched for trials and didn't find any"
Unsurprisingly, there haven't been any (completed) trials on this particular combination of novel disease and possible prevention/treatment yet.
I'm concerned that people conflate "no evidence for efficacy" with "it doesn't work" instead of "we don't know if it works". You always start out with "no evidence".
There are studies that put serum Vitamin D levels against COVID-19 outcomes and they show a highly significant correlation. That's not "causal evidence", but it should put you on alert, you shouldn't be waiting for 2021 for possible Vitamin-D trials to complete.
As the authors of that review are saying, you should be supplementing anyway, whether there is a causal relationship or not.
I don't see why, since vitamin D is not patentable. If you spend the money on research others can make money from it making you lose out. Same reason why herbs are not researched even though they've been used for medicinal purposes for thousands of years: you can't patent a plant.
I think that's a poor summary of the paper, here's the rest of the abstract:
"There is some evidence that daily vitamin D3 supplementation over weeks to months may prevent other acute respiratory infections, particularly in people with low or very low vitamin D status. This evidence has limitations, including heterogeneity in study populations, interventions, and definitions of respiratory infections that include upper and lower respiratory tract involvement."
"The current advice is that the whole population of the UK should take vitamin D supplements to prevent vitamin D deficiency. This advice applies irrespective of any possible link with respiratory infection."
However, evidence of absence is unlikely to be found as the vast majority of researchers tend not to bother publishing papers with negative results. So if an idea seems like it should have been researched already, but no research papers are to be found, it may very well be because the evidence of absence simply hasn't been shared.
I wonder how many papers give a negative result because p was found to be .049 or so. I'm recalling that thread here a while back debating whether the statistical critical value is too high.
"98.9% of Vitamin D deficient cases died while only 1.1% of them were active cases. 87.8% of Vitamin D insufficient cases died while only 12.2% of them were active cases. Only 4.1% of cases with normal Vitamin D levels died while 95.9% of them were active cases."
Wait, only 13.3% (1.1 + 12.2) of all the active cases in total were vitamin D insufficient or worse? I thought the majority of people had insufficient vitamin D.
This data doesn't fully make sense to me. How come that so few people with a vitamin D insufficiency were active cases? I get that most of them died. But I don't get that so few, less than 15 percent, got to become an active case.
Edit: ah, it's an Indonesian study. Nevermind, I wouldn't know the numbers from there.
Since aging reduces vitamin D production in skin, we have that vitamin D level is correlated with age that is correlated with worse response to COVID-19.
Aging reduces vitamin D production in skin. There is a decrease in the concentration of 7-dehydrocholesterol in the epidermis in old compared with young individuals and a reduced response to UV light, resulting in a 50% decrease in the formation of previtamin D3
Is there any data showing which patients took D supplements (or daily multivitamin) vs having naturally normal/high levels? Medical people, does the answer matter?
I am curious, what does it take to innovate in vitamin level testing space? Being able to know vitamin level in your body at any given day just like you can measure your heart rate. Not via mailing in blood sample, but something simpler. is it too far fetched to think that we can have something like a watch to be able to measure our vitamin levels regularly?
I'd picture something like a finger-prick blood sampler akin to a glucose meter.
Might not be something I'd do every day forever, but I could see doing daily samples for a week to get a feel for aboroption, then occasionally to check how my supplements and sun exposure are working.
If you could build a thing that can measure several different parameters depending on which test strips you load into it, I'd buy a pack of vitamin D strips, a pack of vitamin B, a pack of testosterone, and pack that looks for markers of inflammation. Heck yeah. My doctor would eat that data right up.
I've been thinking about vitamin D all last week after listening to Dr. Rhona patrick on joe rogan podcast( dont' hate).
I haven't found and answer to this, if Vitamin D is such big factor then why aren't vitamin D deficient populations in the subcontinent ( india/pakistan ..) being hit hard.
I'm a little bit hesitant about vitamin deficiency. this sounds like orthomolecular medicine and I wouldn't trust that. I'm especially hesitant if that vitamin is fat-soluble because it can accumulate in your body fat and eventually be poisonous.
It seems like a lot of people are interpreting this data as causal. I've already had people tell me they were surprised to learn that smoking protects against Covid!
Here's a fantastic explanation of why you should not let your brain tell you that you're learning about things that cause Covid complications and death:
It's not unthinkable - in the case of Keytruda (a checkpoint inhibitor for lung cancer), it works way better for smokers than for non-smokers, for understood reasons.
You're much more likely to have lung cancer if you smoke than if you don't -- but once you DO have lung cancer, a history of smoking makes keytruda more likely to work.
The thread is good, but a possible link with nicotine has been observed before. This might just be the unlikely case where smoking does indirectly confer some health benefit.
In this specific case, going outside would help reduce exposure to aerosolized saliva.
Imagine people at a bar. The smokers would stand outside in the cold, smoking, while the non-smokers inside are warmer but at higher risk of catching an infection.
it might work like a mask if you always inhale through a filter and an inferno.
It might even purify your second-hand smoke.
but yes, you have a very real point. I remember reading about some drug that seemed to give people heart attacks, but it actually cured what it was supposed to and heart attacks were the next statistically likely thing to get you.
That's pretty speculative given the amount of extra time a smoker might spend outside - combined with another speculative idea that small amounts of sun exposure has a meaningful impact on outcomes.
Seems more likely that nicotine itself might have a direct interaction, or that there is no benefit at all, and it's all just noise in the data.
Notably, this research is being publicized by Ben Goldacre of Bad Science (among other accomplishments). Goldacre also gets last author on the non-alphabetized list of authors on the preprint, suggesting his primary involvement.
Yes he is an Epidemiologist by profession and I think it is his team that came up with the way to access medical data. I tried to get it in the title but it seems to have been edited out.
The title / headline is overstating it a little. The sample only contains 5,683 people who died of the virus. The 17M is the sample of hospital patients in general. I don't know if this is on purpose, but it makes the study sound artificially more significant. Every study could claim the "17M" figure by this practice.
As far as I understand it, they are comparing the statistics of the 5,683 sample to the 17M in order to determine whether anything stands out. If Covid-19 deaths had no associated factors, then we shouldn't see much of a difference between the two.
However, we are seeing differences, for example with diabetes.
Yes that's true, but the 17M figure isn't the interesting / groundbreaking thing. At least it shouldn't be made out to be as if that's the significant thing.
17M just provides the baseline of "normal". Tons more data isn't needed to get that right. 170M wouldn't make a difference. I bet 1.7M wouldn't make a big difference either.
What we really need to know right now is how the Covid deaths behave. All that this offers is the 5,683 sample, but the title inflates it to emphasize the 17M. We need the 5,683 sample to be merged with other samples to reach 56,830, etc. That is the significant thing.
The 17M is the data set from detailed primary care records linked to 5,683 of the deaths recorded in English hospitals in the time period. The data could be improved by linking to more primary care records - but the population of England is 56 million so they already captured almost a third.
Sadly there will be more data as there are more deaths, and this team will be able to pull more analytics out. However 5,683 is a big enough sample size to find some interesting information on hazard rates.
For the team doing the analysis, plugging data analytics into 17 million primary care records is definitely a significant achievement. Medical records are intended for use by doctors and letting researchers into them has confidentiality issues. The process they followed was covered in the paper and seemed thorough.
You misunderstand. The only reason the study has enough power to make statements about the relative risk of, say, obesity independently of age, sex, and ethnicity is because there are 17 million patients to use as "controls".
I think one of the key takeaways is in the abstract:
> People from Asian and black groups are at markedly increased risk of in-hospital death from COVID-19, and contrary to some prior speculation is only partially attributable to pre-existing clinical risk factors or deprivation
Could be dietary related too, or factors relating to multiple generations of families cohabiting. That said, these are prevalent in the sunny parts of Asia too, which doesn’t appear to be suffering so much, so my suspicion would be Vit-D related.
Source?
I've never got that impression as an English person. I consider it to be non-specific.
However, if you're in a place like Southall or Bradford then the "Asian" people around you are indeed more likely to be south Asian.
Because obviously people with darker skins produce less vitamin D naturally and are more vitamin D deficient and all indications are that vitamin D deficiency is a big factor in Covid19 morality.
Women have a more "advanced" immune system, since many of the genes involved in the immune system are located on the X chromosome. The downside of this is that women are also more at risk of auto-immune disease.
There was a post on HN a few days ago about a study that found low testosterone levels were correlated with worse Covid-19 outcomes. I think vitamin D is technically a hormone (or maybe is hormone-like?) so I wonder if it’s absorbed differently by men than women. Or maybe low testosterone is just a side effect of a vitamin D deficiency in men.
It could also be low levels of sex hormones in general - having neither estrogen nor testosterone in your body causes osteoporosis, for example. Excess testosterone is metabolized into estrogen, as well.
But the endocrine system is ferociously complex - maybe endocrine abnormalities are a proxy for obesity, or an underlying thyroid issue etc.
According to [0], vitamin D deficiency is associated with higher free testosterone in men and lower estradiol in women. Higher testosterone is associated with cardiovascular problems, which are a big COVID risk factor.
But that doesn't jib well with the study you find, so I dunno what to make of it.
I think that low testosterone levels is correlated with being older which is correlated with worse Covid-19 outcomes, so age is the important factor here.
I was surprised to hear that figure! I did my own research and it appears to be correct (in fact, it's greater than 2x in recent years). However, that ratio ignores vehicle miles driven. Once you account for that, the comparative ratio is slightly lower:
> The number of driver fatal crash involvements per 100 million miles driven in 2017 was 62 percent higher for males (2.1 per 100 million miles traveled) than for females (1.3 per 100 million miles traveled). Rates were substantially higher for males than for females ages 16-29, but were only slightly higher for ages 30 and older. The gender difference was largest among drivers ages 20-29.
So in some sense the real figure is 1.62x for men as women per mile driven, although (1) men driving more miles is still a real thing and as a result more men die, and (2) I don't know to what extent super-distance drivers (like commercial truck drivers, who skew heavily male) are putting their finger on the scale.
If you ignore teenagers, that difference comes out to 1.59x; and leaving out persons <30, 1.46x. Still much higher than 1.0.
>> is only partially attributable to pre-existing clinical risk factors or deprivation
I'd expect more it is attributable to less access to premium healthcare (remember, in the UK everyone gets healthcare, but not everyone gets privately-sponsored add-on healthcare)
UK privately-sponsored healthcare specialises in things that you cannot get free from the National Health Service or things where the wait time is long - for example knee surgery.
People don’t use private healthcare for emergencies or intensive care.
For example the prime minister was in intensive care in April - in an NHS hospital.
Reading the full paper, the population surveyed was people registered for at least one year with General Practice doctors using SystmOne software. That covers 40% of the English population.
It is probably safe to assume that almost everyone in England is registered with a GP. There is variance in the GP use of the specific SystmOne software - the paper mentions on page 13 that only 17% of London GP practices use it.
The quirk of the UK system is that private insurance companies have no legal or moral obligation to cover anything as you will always be able to fall back to the NHS. So getting cover than includes preexisting conditions or severe long term illness (e.g. MS) is very expensive and rarely negotiated by employers except in firms who can afford to do it.
Same in countries with public healthcare in the EU; when you have an emergency, you end up in public healthcare (which, in the countries I have lived in, is excellent), when you have a knee or hip operation, you benefit from private if you have it.
It would be surprising if in any EU country private clinics dealt with covid19 unless you're maybe super rich with personal doctors around you all the time.
Not that private healthcare providers are actually providing resources to the NHS so its possible that you could end up in a private hospital even though you don't have private health insurance.
Currently private hospitals in England were requisitioned to cope with surge demand for NHS patients. They're going to reopen to private patients soonish.
Early in the outbreak I remember seeing some research that indicated people of Asian descent (East Asian) are genetically predisposed to more severe cases of this coronavirus, something to do with higher expression of the ACE-2 receptor.
> People from Asian and black groups are at markedly increased risk of in-hospital death from COVID-19, and contrary to some prior speculation this is only partially attributable to pre-existing clinical risk factors or deprivation;
I noted that. However, "partially attributable" doesn't suggest to me one way or the other whether or not they corrected for that impact in figure 3. Or maybe I'm misreading the sentence.
The UK BAME population is largely located in a couple of Large more densely populated cities. Whereas the country as a whole is around 87% white, London has areas with < 50% white people, for example Newham/Straford is 70% non white[1].
Surely the geographical relationship between dense cities and their inhabitants demographics is more than enough to explain it.
> The overall cumulative incidence of COVID-19 hospital death at 80 days from the study start date was <0.01% in those aged 18-39 years, rising to 0.35% and 0.17% in men and women respectively aged ≥80 years, with a trend by age.
How do those rates compare to the seasonal flu in the UK?
It is not very useful to compare them with flu because people are much more likely to have flu than to have covid. These rates seem very small but remember that the study started in the beginning of february, when there were likely only a handful if any covid carriers in the uk.
If you could preselect a group of people that you know had covid and measure their death rate, the numbers are likely to be much higher. This study did not do this. This is probably because this would require that all patients are tested for covid as they visit their doctor and this was obviously not happening.
Also flu deaths have been greatly exaggerated. Which explains how with a supposed 50k flu deaths in a year in the USA, it has never inundated hospitals like this.
85k coronavirus deaths haven't inundated hospitals in the US either, except in the absolute epicenter in NYC, and even then not to the point originally feared. It's very easy to imagine 50k flu deaths geographically spread evenly not overwhelming US hospitals, especially given that they'd be spread over something like 3x the current coronavirus epidemic timespan. I'm very skeptical of the sudden "oh those flu deaths aren't real" narrative.
The last bad hit on the hospitals was in 2017-2018
"Through the USISS mandatory scheme, a total of 3,454 ICU/HDU admissions of confirmed influenza were reported across the UK from week 40 2017 to week 15 2018, including 372 deaths, based on combined data from England, Scotland and Northern Ireland."
The death rate from anybody admitted to ICU from flu seems to be about 10%.
Admission rates for flu during that bad season was 0.22 per 100k
From what little data there is on Covid-19 it looks like that admission rates to ICU are about 0.30 per 100k, with a wide range (0.20 to 0.40). We won't know the average until it is over.
About 30% die (and again the range is anything up to 50%).
The UK data for Covid-19 in any depth is incomplete.
Obesity, of course, is a major factor. It's hard to pull apart Type II Diabetes and breathing disorders from it, too, so a realistic assessment of disorders that would be mitigated if the patient lost weight might show it as the absolute major contributor.
Judging from the chart at p. 11 age is really the dominant factor. Moving the "hazard ratio" from 0.25 (<50) to 10+ (>80). Completely dwarfing other factors such as sex, obesity, and various health problems (that the study has categorised).
Interesting that being an ex-smoker increases the risk, but being a current smoker decreases it. Seems like there is some short term benefit to smoking that outweighs its long term negative health effects.
Take it with a shovel of salt, but I've read the following speculative claim: Nicotine docks to a kind of receptor that is also used by COVID-19, thereby denying opportunity to the Virus. But at the same time, habitual smokers tend to develop a higher density of these receptors. That would make smokers less susceptible while they can smoke regularly, but more susceptible upon smoking cessation.
As someone who relatively freshly started smoking 1.5 years ago, I find it insidious. After stopping for a day or two, I actually feel better as tension goes away and I sleep a lot. Shortly, however, I start randomly getting sneezes, runny nose, and slight ill-like feeling in my head.
Part of what makes me start again is the desire to avoid spooking others with those flu-like symptoms in the middle of an epidemic, since I live in a densely populated area.
I don’t have a clear idea of what mechanism is at work here, my hypothesis is that the withdrawal somehow suppresses my immune system.
Unfortunately, as far as I can tell, nicotine patches aren’t as good (or useful at all) at reducing the respiratory symptoms in short term. I suppose it’s not purely nicotine withdrawal that’s causing this.
This is a real effect. Smoking paralyses the cilia; about 4–6 days after cessation, the cilia become active again and start to bring up mucus from the lungs.
The good news is that these symptoms are temporary.
Public health communications on the benefits of cessation don’t usually mention this. I wonder if that’s a mistake. I would have thought it puts a lot of people off quitting, and maybe if they knew what was happening it would be easier to deal with.
This is definitely useful to know. I reckon some smokers suffering from this upon withdrawal would suspect immunosuppression, and choose to continue.
When I have a week or so apart from the crowds, I’ll see how long it takes to push through those symptoms.
(I thought if withdrawal causes immune system suppression, this effect could explain the apparent COVID statistic correlation mentioned by 0-_-0 in parent comment, but from your information it’s unlikely to.)
I think the leading hypothesis is that nicotine may have a protective effect against COVID-19, which is strong enough to more than counteract the negative influence of the lung damage caused by smoking.
(This would explain why former smokers are worse off, since they have residual lung damage but no protective nicotine.)
Of course this is all quite hypothetical, and may turn out to be wrong, but I gather it’s biochemically plausible.
Maybe people who are ex-smokers have had serious lung issues, quit smoking, and are more susceptible. While people smoking have not yet progressed to that stage.
Could it be a measurement error or that smokers who would’ve died because of covid already did die of something else or get a different condition before, essentially making it survivor bias?
I was wondering about that too. After some research it seems to be something like poverty. I.e., being deprived of decent living conditions, education opportunities employment opportunities, etc.
A hazard rate can be thought of as a patient's one day probability of mortality. A hazard ratio is a ratio of two hazard rates, so 1.25 would mean that people in one group were dying at a 1.25x rate relative to a comparison group.
I'd quibble slightly with the interpretation of the Hazard Ratio (or rate) here and say that it's more like "the instantaneous relative risk (or probability, if you like) of the event of interest [in this case mortality but not necessarily] between those with confirmed coronavirus and those without it, given that both groups have survived until time t and holding [set of covariates of interest, e.g. race, age, etc] constant."
Don't mean to sound like a pedant here even though it totally reads that way. I figured with enough epidemiology in the news these days, people may see a lot of "Hazard ratios" or "Cox regression" or "survival analysis" and be at risk of some confusion. I work with these concepts and I get tripped up myself sometimes.
Indices of Multiple Deprivation use a bunch of factors to measure how much it sucks to live somewhere. Other people are saying "poverty" but that's only part of the problem.
For example suppose you are very poor but you live where I grew up in Metroland. Lack of money sucks pretty badly, but in Metroland other deprivation factors are mostly low.
There are jobs in Metroland. The schools are pretty good. There's a hospital, and a nearby doctor with a friendly manner (remember Britain has universal healthcare, but universal does not mean universally excellent). You can't afford private rent here, but local government can find you somewhere to live, and not in six months but maybe six days.
The local crime isn't too bad. Vandals, maybe the odd burglary you suspect a neighbour is on the game (prostitution), but you don't fear for your life. The surrounding space is nice, there's a play park, rolling hills, fresh air if you like that sort of thing.
So in Metroland even the poor aren't very deprived.
In contrast, in some deprived Northern cities in particular, even the middle class suffer pretty badly, and will strive to get out.
It’s an interesting counter factual to imagine how differently the media would be covering the situation if the genders were reversed and women had about twice the chance of dying from COVID-19..
Obligatory, "Fucking Twitter thread" complaint. I dread reading
- Bullet point
- After bullet point
- In the form of a tweet per bullet point
- Trying to skip the bullshit
- And find the conclusion
(I'll stop now) ...and having the anxiety to be disappointed that I'll read so much bullshit and end up with nothing. Yes, in the end he links to the abstract which has the (unfortunately harder to parse) meat, but also yes, the Twitter thread disappoints, because he ends up tooting his own horn that they were the first, "this [study is] extremely important" and how he needs a sandwich... and seemingly that's where the thread ends? (TBH, thank god for that).
Given "AI's" inability to understand time and temporal relations, and given the incredible amount of hidden dynamics and game theory in economics, just going to go ahead and facepalm
It’s not surprising that historically plague-ridden Europeans would be less susceptible to a new blight then other ethnicities. Disease resistance has been selected for.
Cystic fibrosis is a predominantly Caucasian genetic disorder because one copy of the gene helps protect against certain historical plagues in Europe without being too debilitating. But two copies kill you gruesomely at a young age. And it kills you primarily by making you more prone to infection.
Kind of like how Sickle Cell works. It helps protect against malaria, but two copies of the gene are bad news.
In western countries at least, an obvious confounded for those of asian or black ethnic descent is _poverty_ and thus access to healthcare, malnutrition, sleep deprivation, poor education and everything else that goes with poverty.
The two regions often responded very dissimilarly. nKyle Harper'sbThe Fate of Rome looks at this in depth.
TL:DR; civilisation's patterns (cities, trade, travel) co-evolve diseases. Populations tend to evolve resistance to local endemic disease, but are susceptible to novel agents, including foreign infections. Rome infected China and vice versa.
This is interesting data. I want to see Vitamin D status included in a large population study like this because I've been following two smaller studies covering about a thousand cases total that shows Vitamin D deficiency has a risk ratio of 10 to 20 (more even than being age 80+ in the above study). The studies:
[1] https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3585561
[2] https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3571484
Table 1 in each of those papers show Vitamin D status vs Outcomes. The correlation between Vitamin D status, where Normal is >30 ng/ml (or 75 nmol/L), and death rates is stark.
From [1] (which had n=780 cases) here is the punchline: "98.9% of Vitamin D deficient cases died while only 1.1% of them were active cases. 87.8% of Vitamin D insufficient cases died while only 12.2% of them were active cases. Only 4.1% of cases with normal Vitamin D levels died while 95.9% of them were active cases."
From [2] (which had n=212 cases) here is the punchline: "Of the 212 (100.0%) cases of Covid-2019, 49 (23.1%) were identified mild, 59 (27.8%) were ordinary, 56 (26.4%) were severe, and 48 (22.6%) were critical (Table 1). Mean serum 25(OH)D level was 23.8 ng/ml. Serum 25(OH)D level of cases with mild outcome was 31.2 ng/ml, 27.4 ng/ml for ordinary, 21.2 ng/ml for severe, and 17.1 ng/ml for critical."
Note: the classification for outcomes was "(1) mild – mild clinical features without pneumonia diagnosis, (2) ordinary – confirmed pneumonia in chest computer tomography with fever and other respiratory symptoms, (3) severe – hypoxia (at most 93% oxygen saturation) and respiratory distress or abnormal blood gas analysis results (PaCO2 >50 mm Hg or PaO2 < 0 mm Hg), and (4) critical – respiratory failure requiring intensive case monitoring."
I want to see a dozen more studies like [1] and [2] to see if this holds up to replication with larger populations.