But the virus hadn’t wrecked Dowd’s lungs. In fact, she had only mild pneumonia. Instead, SARS-CoV-2 had ruptured her heart.
A lot of the early part of the article rehashes basics, like how viruses replicate. If you have basic knowledge of that sort, you can kind of skim until the mid point, where we find the above factoid.
I have been reading less about the virus of late, but this fits with everything I know. It causes blood clots. Ventilators aren't really fixing it. The lack of oxygen is probably more about what it does to the blood (than what it does to the lungs).
Later in the article, it talks about impacts on the feet suspected to be a side effect. Feet issues are commonly associated with blood/circulation issues. This is why diabetes can lead to feet being amputated.
The blood issues are well established and this has been known for some time. I'm somewhat aghast to see this article talking like we don't already know that detail.
This is the feature article in a special series of articles on combating the virus. As such it's presenting a summary of what we know about it so far, and references a lot of sources, some going back several months. Given that context I think that's exactly what I'd expect it to do.
Not everyone has done as much research as you, and the public perception and debate is still awash with "just a bad flu" disinformation, so its really important a clearer and more accurate picture is put out as widely as possible.
> If you have basic knowledge of that sort, you can kind of skim until the mid point, where we find the above factoid.
Well maybe you skimmed a little too much, because the article clearly talks about the negative effects of an overactive immune system response being characteristic in some patients, and there was plenty of evidence of that in some people's wrecked lungs. Part of the therapy is to guide and even suppress the complex immune system response to keep people's bodies from destroying themselves.
Your comment didn't mention any of that and might be read by some as a "move along, nothing to see here." I think this is definitely not the case and people would be better served to read the article itself instead of your comment dismissing it and instructing them to skip over the section about immune system response.
Nasim Taleb had a good point on the most recent EconTalk [0] about covid: We kinda know what the morality rate is, but we have no idea what the morbidity of covid looks like.
All the co-morbidities are essentially unknown and are likely to stay that way for a while. These side effects take time to suss out; more than the nine months we've had with covid.
With the unknown and potentially unbounded risks we are staring at, Taleb says that over-reaction is the best strategy. He and Russ Roberts go on to talk about the basic issues with statistics in these cases, a good trip back to the first week of any stats course that everyone promptly ignores.
Has been speculated on since as early as March (that I've seen) with more evidence in support since then that this strain of human coronavirus is behaving like that.
Explains the majority of symptoms. Low pulse ox, feet, brain, lung, kidney, etc etc.
> Ventilators aren't really fixing it. The lack of oxygen is probably more about what it does to the blood (than what it does to the lungs).
That's not right. It causes cytokine storms just like any other major repiratory virus. Ventilators do help, lots of people survive on them. They are a critically important piece of the treatment puzzle.
I don't think statements like that are very helpful. It's on the spectrum toward conspiracy nonsense.
> I'm somewhat aghast to see this article talking like we don't already know that detail.
It's not a scientific study, it's a review piece for general readers.
Yes, COVID-19 is a bad one but it’s just another virus at the end of the day. I feel they act as we rediscovering everything about viruses for sensationalism.
Blood clots might be caused by a change in angiogenesis that appears to be correlated with COVID-19. I found this autopsy analysis by an MD to be very enlightening:
I'd previously read that COVID-19 might be a cardiovascular disease, which would account for the blood clots and heart stuff.
From the OC:
Marcus plans to also start collecting data from wearable devices, including Fitbits and Zio patches, which wirelessly monitor heart rhythms. “There may be large numbers of people who are suffering from cardiovascular effects of COVID-19 in the absence of other symptoms,” Marcus says. “I’m worried we’re missing those cases.”
I have no idea what it means to regard COVID-19 in cardiovascular vs respiratory terms. I'm just repeating what I think I've read. I really don't understand this stuff.
If I get Covid19, my plan is to take aspirin wile at home. If I need to go the Emergency Room, then I'll leave it to the doctors to decide what I should get, but before I need urgent care, I'll use aspirin.
Yup. For example, there's a well-established effect where influenza causes heart attacks and strokes, big enough that the severity of the influenza season has a noticable effect on heart attack deaths. This is, naturally, taken into account when calculating the number of influenza deaths. The differencce is that instead of this being spun as proof that influenza is more deadly than people think, since Covid the press has been spinning it as proof it's leas deadly and that the official flu stats are overstating the number of deaths. For instance, this article - which was quite popular on HN - outright claimed that widespread flu deaths didn't exist because doctors didn't see people dying because of the flu and the CDC was misleading the public by claiming otherwise: https://blogs.scientificamerican.com/observations/comparing-...
"Clinicians, too, were seeing surprising numbers of COVID-19 patients develop heart problems – muscle weakness, inflammation, arrhythmias, even heart attacks. “We’re not used to respiratory viruses having such dire consequences on the heart in such apparently high numbers,” says cardiologist Gregory Marcus, MD. Many patients whose hearts acted up also had failing lungs. But others had no other symptoms or, like Dowd, only mild ones."
Every other source online says that you can’t get Covid from eating, but this one says your stomach cells are particularly susceptible.
> Gut specialists are finding that 20% to 40% of people with the disease experience diarrhea, nausea, or vomiting before other symptoms, says gastroenterologist Michael Kattah, MD, PhD, a UCSF assistant professor. If you swallow virus particles, he says, there’s a good chance they will infect cells lining your stomach, small intestine, or colon. As in the lungs and heart, these cells are studded with vulnerable ACE2 portals.
In that case, is the info about not getting it from eating as thoughtless and parroting as saying masks don’t work, or is this article fake news? It makes a huge life changing difference to know for high risk people
1. Does the virus remain infectious in food? In particular, does hot or reheated food affect it?
2. The digestive process produces more acid. Will that kill the virus?
3. Will the virus even touch the wall of the stomach? It may be in food after chewing, rather than directly on the stomach wall
There are some reasons to think that swallowing virus replicating in your throat is different than having some inside a chewed up piece of food surrounded by saliva.
We don’t know of course, and someone super high risk should perhaps avoid takeout salads. But as of yet we haven’t had any case cluster reports where a superspreader cook spread the virus to their colleagues + customers via food. No country has reported a single instance of a traced infection via takeout.
This doesn’t mean it’s impossible, as contact tracing is not perfect. But the lack of any evidence so far is suggestive.
Interesting explanation for why children rarely get sick or transmit this disease:
> Fattahi’s team has found evidence suggesting that male sex hormones such as testosterone may increase the number of ACE2 receptors that cells produce, which could help explain why SARS-CoV-2 seems to wreak greater havoc on men than on women and why kids rarely get sick.
This is only true for Children under 10. Children over 10 transmit contract and transmit at similar rates. Considering 11 is when puberty kicks in for many kids, this appears to support Fattahi's findings.
The article based on studies by UCSF is a good read for many who are not understanding the basics of what is happening. I would suggest giving this out to friends and family who have concocted their own version of science and are refusing to wear a mask.
If a lot of the damage is often caused by an overreacting immune system, why isn't this disease harder on younger people who presumably have stronger immune systems? Kind of like the Spanish flu?
This doesn't add up for me and this article doesn't dwell on that either.
There is still no proof for this but some scientists suggest people over 80 years old came in contact with a similar virus when they were young and now their immune system is overreacting (like when the second sting of a wasp can be much worst that the first).
In the Netherlands they found out by coincidence that some people who have a broken TLR7 gene don't fight the virus so the virus hits them very hard.
The issue with young people and the Spanish flu wasn’t “they have stronger immune systems so they cytokine storm harder and die in greater rates”, it was that there was an earlier endemic flu like 40 years before and basically everyone over like ~40 had been exposed to it and they had immunity, and anyone under that age had not been exposed so they lacked immunity.
I've seen the idea of cross-reactivity and T-cell immunity being passed around.
I think the idea is that younger, healthier people with better immune systems are able to prevent the virus from replicating as much, whereas sluggish immune systems and bodies that are highly inflamed like overweight ppl, diabetics, etc. (high leptin, also related to il-6) get overwhelmed.
T-cell immunity/cross-reactivity meaning that most people have the ability to fight the virus from exposure to other coronaviruses.
I think a major component of the death toll from the pandemic is basically a consequence of obesity. I'm suspicious that govt interventions, planning, etc make that much difference when the US is an order of magnitude more obese than Japan, for example.
Always interesting to learn more about the virus and that there is a lot of knowledge about handling ventilators. But even so, the numbers from New York say that 80% of people over 80 years do not make it once they are on the ventilator.
I do hope that more attention will be focused on telling that this virus is both causing respiratory issues and heart issues.
The leading comorbidities data from New York says it very clearly.
I will get beat up for bringing this up, but I think that these facilities are operating in bubbles / silos. The reason I believe this, is that for months everything discussed in the article has also been discussed by an ER doctor in Riverside, CA that makes Youtube videos in his down time. [1] He is just reading the research available on nih.gov and a few other sites. What would it take to get all of the medical research groups to start collaborating on a common platform? Is the issue that they do not have a platform to share findings, theories, tests, or is everyone depending on the scientific review process and waiting for peer reviewed papers? Should we set up a forum for all the medical groups to share findings, theories, debate theories, etc?
I'm surprised to read the stuff about asymptomatic cases. I thought the current thinking was that asymptomatic people are really pre-symptomatic, because of the incubation period. In other words, truly asymptomatic cases are rare. Am I wrong about that?
This is potentially concerning, but it's worth playing devil's advocate. What are the confounders? Most people have been more sedentary than usual this year. What impact does that have on circulation?
I read a lot on this topic, and while I don’t disagree some people are dealing with serious long term effects, your assessment is wildly overblown and offered without qualification. I’m aware of cases that are dealing with serious short to medium term effects. There’s no doubt this is real, but the likelihood of their occurrence is a topic of research. Furthermore, the 1+ year outcomes have not been measured in any meaningful way. Conjecture is not evidence.
I just came back from hiking vacation with my wife who had COVID-19 in April. It looks like she will have to get back in queue and wait for the next turn.
You've somehow summed up a long and elaborate article containing a multitude of stories and detailing multiple seemingly detached symptoms into a "tl;dr we're fucked". Seriously, how did you manage to do that?
It's only been an hour, and insightful comments take more time to type out than ignorant speculation. Have some faith that this community isn't just another Reddit.
> If we did a mass testing campaign on 300 million Americans right now, I think the rate of asymptomatic infection would be somewhere between 50% and 80% of cases
Wow that’s incredible. 200 million Americans could have the virus.
That's not what it says. It says if you tested everyone, out of those who tested positive, 50-80% would be asymptomatic, not 50-80% of the whole population.
[+] [-] DoreenMichele|5 years ago|reply
A lot of the early part of the article rehashes basics, like how viruses replicate. If you have basic knowledge of that sort, you can kind of skim until the mid point, where we find the above factoid.
I have been reading less about the virus of late, but this fits with everything I know. It causes blood clots. Ventilators aren't really fixing it. The lack of oxygen is probably more about what it does to the blood (than what it does to the lungs).
Later in the article, it talks about impacts on the feet suspected to be a side effect. Feet issues are commonly associated with blood/circulation issues. This is why diabetes can lead to feet being amputated.
The blood issues are well established and this has been known for some time. I'm somewhat aghast to see this article talking like we don't already know that detail.
[+] [-] simonh|5 years ago|reply
Not everyone has done as much research as you, and the public perception and debate is still awash with "just a bad flu" disinformation, so its really important a clearer and more accurate picture is put out as widely as possible.
[+] [-] coldtea|5 years ago|reply
It's an article, not a news story or a scientific paper. So it's neither about breaking news nor innovative research results.
So, they don't presume what the public knows at any substantial level (heck, many still don't know/believe the virus is not real).
I, on the other hand, am more aghast for the use of the word aghast for such a trivial matter :-)
[+] [-] titzer|5 years ago|reply
Well maybe you skimmed a little too much, because the article clearly talks about the negative effects of an overactive immune system response being characteristic in some patients, and there was plenty of evidence of that in some people's wrecked lungs. Part of the therapy is to guide and even suppress the complex immune system response to keep people's bodies from destroying themselves.
Your comment didn't mention any of that and might be read by some as a "move along, nothing to see here." I think this is definitely not the case and people would be better served to read the article itself instead of your comment dismissing it and instructing them to skip over the section about immune system response.
[+] [-] Balgair|5 years ago|reply
All the co-morbidities are essentially unknown and are likely to stay that way for a while. These side effects take time to suss out; more than the nine months we've had with covid.
With the unknown and potentially unbounded risks we are staring at, Taleb says that over-reaction is the best strategy. He and Russ Roberts go on to talk about the basic issues with statistics in these cases, a good trip back to the first week of any stats course that everyone promptly ignores.
[0] https://www.econtalk.org/nassim-nicholas-taleb-on-the-pandem...
[+] [-] jfoster|5 years ago|reply
[+] [-] huffmsa|5 years ago|reply
Has been speculated on since as early as March (that I've seen) with more evidence in support since then that this strain of human coronavirus is behaving like that.
Explains the majority of symptoms. Low pulse ox, feet, brain, lung, kidney, etc etc.
[+] [-] newacct583|5 years ago|reply
That's not right. It causes cytokine storms just like any other major repiratory virus. Ventilators do help, lots of people survive on them. They are a critically important piece of the treatment puzzle.
I don't think statements like that are very helpful. It's on the spectrum toward conspiracy nonsense.
> I'm somewhat aghast to see this article talking like we don't already know that detail.
It's not a scientific study, it's a review piece for general readers.
[+] [-] hartator|5 years ago|reply
[+] [-] danesparza|5 years ago|reply
https://youtu.be/1HTionnTT9I
[+] [-] specialist|5 years ago|reply
From the OC:
Marcus plans to also start collecting data from wearable devices, including Fitbits and Zio patches, which wirelessly monitor heart rhythms. “There may be large numbers of people who are suffering from cardiovascular effects of COVID-19 in the absence of other symptoms,” Marcus says. “I’m worried we’re missing those cases.”
I have no idea what it means to regard COVID-19 in cardiovascular vs respiratory terms. I'm just repeating what I think I've read. I really don't understand this stuff.
[+] [-] credit_guy|5 years ago|reply
[+] [-] twic|5 years ago|reply
[+] [-] makomk|5 years ago|reply
[+] [-] WhompingWindows|5 years ago|reply
"Clinicians, too, were seeing surprising numbers of COVID-19 patients develop heart problems – muscle weakness, inflammation, arrhythmias, even heart attacks. “We’re not used to respiratory viruses having such dire consequences on the heart in such apparently high numbers,” says cardiologist Gregory Marcus, MD. Many patients whose hearts acted up also had failing lungs. But others had no other symptoms or, like Dowd, only mild ones."
[+] [-] thedrbrian|5 years ago|reply
[+] [-] CraigJPerry|5 years ago|reply
[+] [-] gentleman11|5 years ago|reply
> Gut specialists are finding that 20% to 40% of people with the disease experience diarrhea, nausea, or vomiting before other symptoms, says gastroenterologist Michael Kattah, MD, PhD, a UCSF assistant professor. If you swallow virus particles, he says, there’s a good chance they will infect cells lining your stomach, small intestine, or colon. As in the lungs and heart, these cells are studded with vulnerable ACE2 portals.
In that case, is the info about not getting it from eating as thoughtless and parroting as saying masks don’t work, or is this article fake news? It makes a huge life changing difference to know for high risk people
[+] [-] graeme|5 years ago|reply
1. Does the virus remain infectious in food? In particular, does hot or reheated food affect it?
2. The digestive process produces more acid. Will that kill the virus?
3. Will the virus even touch the wall of the stomach? It may be in food after chewing, rather than directly on the stomach wall
There are some reasons to think that swallowing virus replicating in your throat is different than having some inside a chewed up piece of food surrounded by saliva.
We don’t know of course, and someone super high risk should perhaps avoid takeout salads. But as of yet we haven’t had any case cluster reports where a superspreader cook spread the virus to their colleagues + customers via food. No country has reported a single instance of a traced infection via takeout.
This doesn’t mean it’s impossible, as contact tracing is not perfect. But the lack of any evidence so far is suggestive.
[+] [-] tomohawk|5 years ago|reply
> Fattahi’s team has found evidence suggesting that male sex hormones such as testosterone may increase the number of ACE2 receptors that cells produce, which could help explain why SARS-CoV-2 seems to wreak greater havoc on men than on women and why kids rarely get sick.
[+] [-] zspade|5 years ago|reply
(https://www.nytimes.com/2020/07/18/health/coronavirus-childr...)
[+] [-] g3houdini|5 years ago|reply
[+] [-] stanski|5 years ago|reply
[+] [-] thdrdt|5 years ago|reply
In the Netherlands they found out by coincidence that some people who have a broken TLR7 gene don't fight the virus so the virus hits them very hard.
So there may be multiple reasons.
[+] [-] 0xB31B1B|5 years ago|reply
[+] [-] gnusty_gnurc|5 years ago|reply
I think the idea is that younger, healthier people with better immune systems are able to prevent the virus from replicating as much, whereas sluggish immune systems and bodies that are highly inflamed like overweight ppl, diabetics, etc. (high leptin, also related to il-6) get overwhelmed.
T-cell immunity/cross-reactivity meaning that most people have the ability to fight the virus from exposure to other coronaviruses.
I think a major component of the death toll from the pandemic is basically a consequence of obesity. I'm suspicious that govt interventions, planning, etc make that much difference when the US is an order of magnitude more obese than Japan, for example.
[+] [-] roaur|5 years ago|reply
[+] [-] sharken|5 years ago|reply
Source: https://www.google.dk/amp/s/www.washingtonpost.com/health/el...
I do hope that more attention will be focused on telling that this virus is both causing respiratory issues and heart issues. The leading comorbidities data from New York says it very clearly.
Source: https://www.the-hospitalist.org/hospitalist/article/220457/c...
[+] [-] LinuxBender|5 years ago|reply
[1] - https://www.youtube.com/user/MEDCRAMvideos/videos
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[+] [-] hellofunk|5 years ago|reply
Wow that’s incredible. 200 million Americans could have the virus.
[+] [-] cataflam|5 years ago|reply
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[+] [-] IAmGraydon|5 years ago|reply