Was World War I The "Real" Cause Of The Spanish Flu Pandemic?

[tankasnowgod]

Since seeing the news about the Corona Virus in Wuhan (sometimes being referred to as nCoV-2019, maybe due to the fact that people are realizing Corona Viruses have been around awhile) and the reaction to it, I wanted to dig a little deeper into the last real Pandemic. Well, I dug up a few journal articles, and noticed some interesting overlap with what I had suspected was a cause of the epidemic, World War I.

One thing that is striking is that the mortality rate overall was highest in the 20-40 year old age group. This is a bizzare feature of the Spanish Flu.

Observations on Mortality during the 1918 Influenza Pandemic | Oxford Academic

The average age of soldiers in WW1 was about 25 by the end of the war, it was about 30 in the first year. So, men aged 20-40 years old would have been the bulk of the fighters. They would have been in incredibly stressful situations, likely unique up to any war at that point in history, and probably faced harsher conditions on the field than future wars, due to improvements in supplies, food, transportation, and housing of those fighting in foreign conditions.

The mortality rate from Spain also illustrates this. It's basically a linear downward trend from 1900 to 1970, with a spike at 1918, and a less pronounced upward rounded curve from 1936-1943 (which overlaps quite a bit with WW2).

The 1918 “Spanish Flu” in Spain | Oxford Academic

Another thing this Article points out is that the Spanish Flu in Spain came in three different different periods. In the first in May 1918 lasting through the summer, the disease wasn't that serious. The death rate was low, at 0.65 per 1000. This period ended quickly.

The second period came in the Autumn and Winter 1918. This period lasted longer, and the mortality rate was much higher, up to 14 per 1000 in the depths of winter. The article blames this on the virus itself, but the higher rates were also likely influenced by the season (longer nights, colder temperatures).

The third period lasted from January 1919 to June 1919. It was much milder than the previous period, with mortality rates at 1.4 per 1000.

1918 “Spanish Flu” in Spain

Observations on Mortality during the 1918 Influenza Pandemic

 

[Inaut]

good post amigo

 

[dfspcc20]

I came to a similar conclusion re: polio. It seems to frequently pop up in war zones and places where there are a lot of refugees living in stressful conditions. I.e. Pakistan, Afghanistan, Syria, etc.

Tom Cowan had a different take, though, in his newsletter. I haven't read Firstenberg's book yet. I wonder if Wuhan has a 5G network running...

"For example, in Arthur Firstenberg’s brilliant book, “The Invisible Rainbow,” he traces the timing of each of the six major flu pandemics in the past 150 years to a dramatic change in the electrification of the earth. Whether it was the introduction of electrical power lines, radar, radio signals or other wireless devices, each pandemic occurred within six months of the introduction of one of these technologies. Furthermore, in many cases, the epidemiology of the outbreaks suggested that a contagious cause was impossible. For example, in 1918, the Spanish flu pandemic happened simultaneously world wide, spreading faster than any possible physical contact between these disparate people. In investigating the cause of this outbreak, the Boston Health Department tried to deliberately infect people by exposing them to the mucus or secretions from people who were suffering from the flu. They were unable to transmit the disease and concluded there was no contagious agent involved."

 

[tankasnowgod]

Tom Cowan had a different take, though, in his newsletter. I haven't read Firstenberg's book yet. I wonder if Wuhan has a 5G network running...

I don't know, but Wuhan's numbers don't come anywhere near the Spanish Flu, even in Spain (which was one of the milder hit countries, despite the name) in even the mildest period. The rate in the summer maxed out at 0.65 per 1000 (which is total pop, not diagnosed cases). Wuhan has a pop of 11.08 Million and the total deaths so far attributed to Corona Virus are 1300. That is a rate of 0.11 per 1000, an order of magnitude six times lower, and Wuhan is supposed to be the epicenter of this epidemic.

 

[tankasnowgod]

Another thing that is interesting about the articles.... both suggest the virus that caused the Spanish Flu was H1N1. This is the same thing as the "Swine Flu" that was being touted as a Pandemic in 2009. Even the Wikipedia article for H1N1 lists both- Influenza A virus subtype H1N1 - Wikipedia

The Spanish Flu in 1918 is estimated to have killed 20-50 Million people worldwide (notable that the margin of error in these estimates is 1.5 times the low end estimate.)

The Swine Flu in 2009 is estimated to have killed 18,138 people.

Even using the low end estimate for the Spanish Flu, the same virus (at least genetically) killed a tiny fraction of what it did in 2009 compared to 1918. It's an order of magnitude 1,000 times smaller.

 

[Steven Bussinger]

Rene Dubos, in Mirage of Health (1959, pg 70):

"Cataclysmic epidemics have continued to occur here and there during the past century. Most of them have been rather limited in area, exhibiting great killing power only in populations newly exposed to particular species of microbe or placed under conditions of great physiological misery. That epidemics can still strike far and wide was proved during 1918 and 1919 when several consecutive waves of influenza killed some 20 million persons -- far more than had died as a direct result of the preceding five years of unrestricted global warfare."​

His thesis was that populations become more resistant over time due to an elimination of the more susceptible organisms, but I liked that he still made allowances for the role of stressful existence. Connecting a stressful existence to disease susceptibility is much less interesting to study than emergent disease resistance through culling, though.

One could formulate a pithy rejoinder to the pithy "what doesn't kill me makes me stronger":

"If the event doesn't kill you now... maybe the stress will later."

 

[Steven Bussinger]

For example, in 1918, the Spanish flu pandemic happened simultaneously world wide, spreading faster than any possible physical contact between these disparate people. In investigating the cause of this outbreak, the Boston Health Department tried to deliberately infect people by exposing them to the mucus or secretions from people who were suffering from the flu. They were unable to transmit the disease and concluded there was no contagious agent involved."

Today, the general assumption is that it's healthier to be a European than an American, but for two thirds of the 20th century, the reverse was probably true.

 

[methylenewhite]

WW1 is non direct cause for sure. Living in wartime is stress, living in country directly involved in a war is more stressful. Stress=glycolysis. Glycolysis=much severe viral infection.

 

[member10327]

also if your not a soldier you were definitely protein deficient because all the meat was being sent to the front lines, the rations for the general public was a couple pounds per month for entire families

 

[JudiBlueHen]

Wasn't WWI the introduction of chemical warfare? What did this do to survivor's immune systems?

 

[Lyla]

I wonder if Wuhan has a 5G network running...

Wuhan is one of the first big cities in mainland China to have 5g network, along with the beijing, Shanghai and Hangzhou, all of which are among the most hit cities in the mainland.

 

[Kunstruct]

Wasn't WWI the introduction of chemical warfare? What did this do to survivor's immune systems?

Yes it was.
Soldiers even received either opiates or cocaine on a smaller scale in the better armies as not all armies in the entire war in all countries were well equipped.
People keep talking about mustard gas, but more simple substances like chlorine were used to cause issues for the enemy.
Look at the amount of tons of Chroline used for the purpose of being a weapon. Not to mention once someone retreated they were going to "poison" everything while retreating, more or less.
Again not all armies had these capabilities, people mostly think of French and German when they think about WW1 but many other countries fought with much less resources and technologies and of course many could not use any chemical warfare.

 

[schultz]

I read a very interesting paper on this recently. They had various theories. Obviously the prominent theory (aside from the ludicrous "healthy people die because of superior immune system and 'cytokine storm' theory") is that peoples immune systems were low because of the war, but that doesn't mean that other things couldn't add to that.

I think this was the article, which took me a long time to re-find because apparently there are a million articles on the spanish flu.

Back to the Future: Lessons Learned From the 1918 Influenza Pandemic

I think everybody should read it because the 1919 flu is often used by the mainstream to prove how a pandemic can occur and how certain types of flu can specifically target young, healthy people (supposedly). But it's not that simple. For one thing, it's difficult to study because it was 100 years ago and back then we didn't have the same technology. The article explains how it has been investigated, which is fascinating to me.

I'm going to just paste parts that I found interesting:

"Alternatively, it is tempting to speculate that military camps, with their high population density, close proximity to livestock, high mobility, and large number of people with pre-existing lung conditions (due to exposure to toxic gasses in the trenches) served as the perfect breeding ground for the emergence of this catastrophic pandemic"

"An individual's age played a major role in determining one's risk of death during the 1918 influenza pandemic. Typically, when the mortality rates of seasonal influenza are graphed against the age of the population, a “U” shaped curve is produced, as the highest mortality occurs in the very young and old (Johnson, 2006). In contrast, pandemic outbreaks (to various degrees) are characterized by a shift in case-fatality toward younger age groups (Simonsen et al., 1998; Olson et al., 2005; Ahmed et al., 2007; Georgantopoulos et al., 2009). This was particularly pronounced during 1918 pandemic when young adults (15–30 years) displayed such usually high mortality rate that a “W” shaped mortality curve was produced (Olson et al., 2005; Ahmed et al., 2007; Shanks and Brundage, 2012). The underlying mechanisms driving this mortality shift are not fully understood but are likely to be associated with the host's immune status."

"However, it is important to note that all experimental 1918 influenza virus studies to date have been performed in immunologically-naïve animals. This is not necessarily indicative of the human situation in 1918, as influenza viruses caused epidemics and pandemics prior to 1918 (Dowdle, 1999; Johnson, 2006; Morens and Fauci, 2007; Morens et al., 2009; Valleron et al., 2010). It can therefore be assumed that a large proportion of the human population in 1918, with the possible exception of isolated countries/communities, would have encountered at least one previous influenza virus infection, resulting in pre-existing humoral and cellular immunity. It remains unclear whether such pre-existing immunity would cross-react with the 1918 H1N1 virus, and if so, whether it would enhance or dampen any dysregulated pro-inflammatory response in young adults."

"In contrast to young adults, older adults (aged 30–60 years) fared significantly better during the 1918 pandemic (Luk et al., 2001). This observation is likely to reflect the beneficial effects of pre-existing humoral immunity. It is theorized that an H1 and/or N1 influenza virus circulated in the human population prior to 1889, when it was replaced by a H3 influenza virus that caused the so-called “Russian” influenza pandemic (1889–1892) (Ahmed et al., 2007). Accordingly, individuals born before 1889 (i.e., those 30 years or older during the 1918 pandemic) would have had cross-protective antibodies, while people born after 1889 would have been immunological naïve to the 1918 H1N1 pandemic virus (Dowdle, 1999; Ahmed et al., 2007)."

Interestingly, unlike the majority of elderly populations worldwide, elderly populations in remote settings, including Indigenous Australians, Alaskan Natives, and Latin Americans, experienced high mortality during the 1918 pandemic. This most likely reflects the fact that these remote populations were not exposed to the previously circulating influenza viruses that conferred cross-protection (Ahmed et al., 2007).

"Conclusive evidence that protective influenza virus-specific antibody responses are indeed long-lived came from the 2009 influenza pandemic. Here, elderly people who were exposed to the 1918 influenza virus (or its immediate descendant), 60–90 years prior to the pandemic of 2009, were protected from infection and severe disease, as they maintained the antibody response that cross-reacted with the 2009 pandemic strain (Yu et al., 2008; Hancock et al., 2009; Ikonen et al., 2010; Reed and Katz, 2010)."

Host nutritional status has long been recognized as an important factor in the outcome of a variety of different infectious diseases (Cohen, 2000). In India in 1918, the effects of malnutrition and famine on influenza severity were particularly pronounced. The 1918 influenza pandemic hit India during a widespread drought, which affected the viability of many important food crops (Mills, 1986). Consequently, many Northern-Western, Western and Central Indian provinces experienced a famine during 1918 (Mills, 1986). It was these provinces which also experienced the highest 1918 influenza mortality rates (Mills, 1986).

"For example, data from a Swiss sanatorium during the 1918 pandemic suggested that the risk of influenza death was higher among tuberculosis (TB) patients than non-TB controls (Oei and Nishiura, 2012). Similarly, individuals with TB were 2.2 times more likely to contract the 1918 influenza virus than non-TB individuals living in the same household (Noymer and Garenne, 2000; Noymer, 2011). A synergistic relationship between M. tuberculosis and influenza viruses has also been supported by experimental studies (Redford et al., 2014). The predominance of TB amongst young adults in 1918 may have contributed to the striking “W shaped” mortality curve associated with the 1918 influenza pandemic (Oei and Nishiura, 2012)."

"In addition to individuals with bacterial co-infections, mortality during the 1918 influenza pandemic was considerably higher amongst malaria-infected individuals (Langford and Storey, 1992; Afkhami, 2003; Shanks, 2015). Although the underlying mechanism is not fully understood, a malaria-induced procoagulant state could play a role in increasing inflammation and subsequent clinical outcome (Shanks, 2015)."

It is estimated that if a pandemic influenza virus were to re-appear today, with a similar virulence and attack-rate as the 1918 influenza virus, mortality could rise to 21–147 million (Murray et al., 2006; Madhav, 2013). However, the high morbidity and mortality rates associated with the 1918 influenza pandemic resulted from a complex interplay between factors intrinsic to the 1918 virus itself, the host's immune response and the social context in which the pandemic struck. It is thus unlikely that this exact combination of factors would repeat itself in the future.

 

[RealNeat]

How are they certain the first case in the US was actually the novel celeb COVID19?

Understanding how they are testing is a crucial step in understanding how much is bs.

Coronavirus Disease 2019 (COVID-19)

 

[tankasnowgod]

One other thing I realized, that maybe drove the worst period of Spanish Flu....... Armistice Day was November 11th, 1918. Right near the peak of deaths for many countries. If there was some sort of bug (or several) to spread around the world, returning soldiers might be the perfect vehicle at that time period to do it.

The younger pop remained more susceptible to illness in the following years, too.

"Two interesting observations were apparent from examination of the 1918 age-specific excess P&I mortality data. First, the height of the excess P&I mortality peak among young adults in 1918 declined in 1919 and 1920 but remained relatively higher than the excess P&I mortality among very young individuals. The decline in the peak of the excess rates suggests that most of the susceptible young adults were infected in 1918, during the first wave of the pandemic. The susceptible population, however, was probably not completely exhausted, because excess mortality among young adults still occurred in 1919 and 1920, although to a lesser extent.

 

[JamesGatz]