Summary: In this post I point out that the characteristics of covid waves don’t match that of a disease where every infected person goes on to infect others.
While I am no Dr or epidemiologist... I have worked with many pests and diseases in agriculture... I suspect your under playing the importance of transient environmental factors on a healthy person vulnerability.... ie most disasters in crops or pastures occur when infection coincides with one or two other factors ie cold week, windy conditions.. crops down in that window are very vulnerable but those sown a week later and coincided with warmer weather resist any disease or pests..
The highly seasonal pattern of influenza in the higher latitudes shows that...
In Au this year we had a remarkable cold May.... everyone felt it and by Early June colds abounded.. conditions warmed cover winter and cases dropped.. these were not Covid just normal virus..
point being that seasonal changes that put short term stress on the vulnerable start a wave but warmer sunnier condition only 10 days can make a big difference...
so while the “spreader” maybe a factor I suspect it’s vulnerabilities that really drives waves and short term changes in environment play a big role in outcomes..
I believe this to be one of the most insightful comments I have read on the pandemic. Showing this is by far and away a Vitamin D deficiency driven disease.
There was ample evidence two years ago of the role of vitamin D in protecting against upper respiratory tract infections for the government to have issued everyone with vitamin D supplements.
But they didn't, and thousands died.
I note that it is now six months since the ending of the Coronavit trial. Come on, Prof Adrian Martineau, where are the results.
The most valuable advice I received on Vitamin D has been a protocol or vitamin stack in particular the co-factors that enable it to work. By the time any serious RCT provides results the world will have moved on.
https://virologyj.biomedcentral.com/articles/10.1186/1743-422X-5-29 - "On the epidemiology of influenza" - is a paper I have been trying to finish over the last few weeks. They seem to propose (perhaps projecting my own thoughts into theirs) that there is a gradual decay of adaptive immunity day by day and a seasonal/Vitamin D based fluctuation in innate immunity. Additionally, the virus is ubiquitous but held in check by innate immunity even when cases stop. When population-wide innate immunity drops, fuel is abundant for an explosion of symptomatic / isolatable cases. When the explosion happens, the population-wide adaptive immunity decay that took place since the last wave is reversed. The cycle begins again. Some years do not feature enough Vit D deficiency to prompt a wave, implying potentially bigger peak next year.
This "two factor" model is what accords with my intuition. It allows for the possibility of widespread "marginal spread" - people whose innate immunity is on the boundary of suppressing the virus, but can both shed and be impacted by nearby marginal shedders to be put over the boundary of infection. Put twenty marginal spreaders in a room - or even let them interact with each other via discrete meetings on the same day - and you have a "superspreader." If the room had 100 people then of course you can find one who is coincidentally clinical/isolatable on the day of the event (given that the wave is already ongoing) and misattribute an essentially critical-mass-based event to direct spread.
Sequencing to establish chains of transmission is probably subject to the human tendency to distort reality to fit assumption. As happened in the Marin elementary school outbreak study where the teacher "patient 0" was never even sequenced.
My small contribution to the fight .... https://jeremypoynton.substack.com/ ... "Postcards to Johnson"
While I am no Dr or epidemiologist... I have worked with many pests and diseases in agriculture... I suspect your under playing the importance of transient environmental factors on a healthy person vulnerability.... ie most disasters in crops or pastures occur when infection coincides with one or two other factors ie cold week, windy conditions.. crops down in that window are very vulnerable but those sown a week later and coincided with warmer weather resist any disease or pests..
The highly seasonal pattern of influenza in the higher latitudes shows that...
In Au this year we had a remarkable cold May.... everyone felt it and by Early June colds abounded.. conditions warmed cover winter and cases dropped.. these were not Covid just normal virus..
point being that seasonal changes that put short term stress on the vulnerable start a wave but warmer sunnier condition only 10 days can make a big difference...
so while the “spreader” maybe a factor I suspect it’s vulnerabilities that really drives waves and short term changes in environment play a big role in outcomes..
I believe this to be one of the most insightful comments I have read on the pandemic. Showing this is by far and away a Vitamin D deficiency driven disease.
There was ample evidence two years ago of the role of vitamin D in protecting against upper respiratory tract infections for the government to have issued everyone with vitamin D supplements.
But they didn't, and thousands died.
I note that it is now six months since the ending of the Coronavit trial. Come on, Prof Adrian Martineau, where are the results.
The most valuable advice I received on Vitamin D has been a protocol or vitamin stack in particular the co-factors that enable it to work. By the time any serious RCT provides results the world will have moved on.
I like many things about your explanation of low secondary attack rates vs high perceived R0.
But at the same time, how come the initial spread is often so rapid? Like Omicron doubled every two days in the beginning. Why?
Could the spread be entirely NOT through the usual suspect (droplets) but through something else?
https://virologyj.biomedcentral.com/articles/10.1186/1743-422X-5-29 - "On the epidemiology of influenza" - is a paper I have been trying to finish over the last few weeks. They seem to propose (perhaps projecting my own thoughts into theirs) that there is a gradual decay of adaptive immunity day by day and a seasonal/Vitamin D based fluctuation in innate immunity. Additionally, the virus is ubiquitous but held in check by innate immunity even when cases stop. When population-wide innate immunity drops, fuel is abundant for an explosion of symptomatic / isolatable cases. When the explosion happens, the population-wide adaptive immunity decay that took place since the last wave is reversed. The cycle begins again. Some years do not feature enough Vit D deficiency to prompt a wave, implying potentially bigger peak next year.
This "two factor" model is what accords with my intuition. It allows for the possibility of widespread "marginal spread" - people whose innate immunity is on the boundary of suppressing the virus, but can both shed and be impacted by nearby marginal shedders to be put over the boundary of infection. Put twenty marginal spreaders in a room - or even let them interact with each other via discrete meetings on the same day - and you have a "superspreader." If the room had 100 people then of course you can find one who is coincidentally clinical/isolatable on the day of the event (given that the wave is already ongoing) and misattribute an essentially critical-mass-based event to direct spread.
Sequencing to establish chains of transmission is probably subject to the human tendency to distort reality to fit assumption. As happened in the Marin elementary school outbreak study where the teacher "patient 0" was never even sequenced.