BUY AMERICAN FEVER NOW!


View American Fever's OFFICIAL VIDEO BOOK TRAILER!

Join American Fever's FACEBOOK PAGE!

TWITTER: @PeterChristHall

 

This website contains the entire novel—linked and illustrated—along with information on influenza and bird flu, an art gallery & opportunities to buy personal protection gear and cultural merchandise (including books, movies, and music cited by American Fever's blogger).
 

Search

 

Explore American Fever:
Powered by Squarespace
Thursday
Sep032009

Day 83-6: Hope-Simpson Sheds Light on Flu

A retired Scottish doctor has emailed from Buenos Aires, Argentina, to tell me that answers to my questions about flu transmission have been staring me in the face for months. “You need to go back and look into who discovered the role Vitamin D plays in influenza. Follow your own links!”

That’s all he said.

So I’ve spent days compiling information about the thoughts of a deceased English doctor named R. Edgar Hope-Simpson (1908-2003), who spent his final decades challenging and rethinking everything that was known about influenza. A true debunker!

HOPE-SIMPSON'S BELOVED CIRENCESTER, SHORTLY BEFORE HE DIED IN 2003 (Chris Jefferies)

Not that anyone paid much heed. Hope-Simpson’s research was published before the digital age. His papers and his book are out of print. I’ve stumbled on the Gene Clark of viral research, a once-famous man whose greatest work is ignored.

Devoted readers will recall my Round One post about Vitamin D, wherein I noted that flu epidemics correspond to seasonal declines in exposure to sunlight. I failed to digest a Scott McPherson blog entry about Hope-Simpson’s work way back in 2007. Apart from abstract summaries of Hope-Simpson papers once presented in Britain’s Journal Of Hygiene (now Epidemiology & Infection, which has published more recent research on it, too), Hope-Simpson’s work is best accessed via the Vitamin D Council’s excellent and intriguing summation of the actual papers.

R. Edgar Hope-Simpson was a country doctor who riveted the medical world by proving on his own in 1965 that childhood chickenpox virus reactivates in adults as the painful condition called shingles. The British establishment was charmed and impressed that a general practitioner could conceive, research, and demonstrate something important that had eluded research labs and universities. (It brought Nobel prizes to others who followed his work, though a shingles vaccine that hit the market in 2006 isn’t selling because it costs too much.)

Hope-Simpson could have spoken at banquets for the rest of his life, the establishment’s pet exception to the rule that proper research is conducted in well-heeled institutions.

So Who Does Spread Influenza?

He was just getting started on another virus he suspected lurked in seemingly healthy people, as he had shown chickenpox does. While maintaining his practice, Hope-Simpson spent the rest of his life arguing that seasonal flu isn’t spread by sick people!

That’s no misprint: The good doctor surmised that seasonal influenza is activated by an unidentified force that circulates among people whose paths don’t need to cross during flu season. People who are not only symptomless—but entirely well. (Hinting at the mystery is a New York Times story on the peculiarities of swine flu transmission in a Pennsylvania community.)

Like all great thinkers, Hope-Simpson started with good questions.

What makes influenza roar into our lives every year, only to depart abruptly with so many promising subjects yet to be infected? The Black Death didn’t do that. The measles don’t. Disease normally spreads as fast and as far as it can until it runs out of carriers or creatures to infect.

What brings influenza back so regularly? How does it explode across continents and oceans faster—when you consider the necessary incubation period—than jets can carry it? And how did it do this before the Wright Brothers?

Why is the second wave of a pandemic supposed to be worse than the first? How does a disease come to kill more people after it’s made a run through the populace? Shouldn’t people become immune to it?

For that matter, what makes change such a constant feature of all influenza A strains? Why do they inevitably mutate—evolve away from our control—so that health authorities have to guess which varieties to fight against in each new vaccine?

Hope-Simpson began by noting that his hometown in Southwest England came down with epidemic influenza at the same time every year as Prague. (They share the same latitude.) He pored over ancient church registers showing that influenza spread just as quickly back when Britain’s roads were impassible.

He further observed that tropical flu breaks out in the rainy season, when the inhabitants' sun exposure plummets. This was confirmed in a study published by others the year Hope-Simpson died.

‘Solar Radiation’—Vitamin D

He also detected patterns involving sunspots, which reduce the quality of rays that reach us. He surmised that a drop in solar radiation levels triggered seasonal flu in Europe’s dark months and in tropical rainy seasons. Vitamin D’s immunological properties weren’t known yet.

Essentially, Hope-Simpson concluded that epidemics spring up as Vitamin D levels plunge in the population, activating symptomless carriers who caught flu the previous year and then repressed it with natural antibodies.

He also said the flu vanishes broadly every year because carriers stop being infectious after six to eight weeks.

Since many people are known to spread influenza without showing symptoms, Hope-Simpson’s claim isn’t as radical as it seems. Until you consider that he also asserted that active influenza sufferers do not transmit seasonal virus as much.

His studies of communities in Wales and England showed that in most families, only one member catches flu in a given season. He opined that this individual becomes the vector that spreads flu to his or her uninfected kin during the next epidemic—not the schoolchildren we customarily blame for transmitting flu.

Seasonal flu hides quietly, evolving inside the previous year’s victims and mutating to trick its way past their immune systems. Then it competes with other active flu strains to infect potential hosts. They all play hopscotch in us, among us, competing to replicate. Each year’s flu victims select the viral variety against which they have the least immunity; the winner becomes the new season’s hit strain. That’s why the medical establishment must gamble on which strains to batch into each annual vaccine.

It’s not clear if carriers can spread seasonal flu in July—or if they simply harbor it in an inactive form until their Vitamin D levels drop low enough to let the virus circulate. So I won’t be selling masks on the beach.

Next: What this means for pandemic flu….

« Day 80-2: Along Comes Evelyn | Main | Day 87-9: We’re All Animals on This Leaky Ark »