Received: by alpheratz.cpm.aca.mmu.ac.uk id SAA11779 (8.6.9/5.3[ref pg@gmsl.co.uk] for cpm.aca.mmu.ac.uk from fmb-majordomo@mmu.ac.uk); Sun, 29 Apr 2001 18:03:36 +0100 Subject: Fwd: A Host with Infectious Ideas Date: Sun, 29 Apr 2001 12:59:21 -0400 x-sender: wsmith1@camail2.harvard.edu x-mailer: Claris Emailer 2.0v3, Claritas Est Veritas From: "Wade T.Smith" <wade_smith@harvard.edu> To: "Memetics Discussion List" <memetics@mmu.ac.uk> Content-Type: text/plain; charset="iso-8859-1" Content-transfer-encoding: quoted-printable Message-ID: <20010429165921.AAA342@camailp.harvard.edu@[205.240.180.35]> Sender: fmb-majordomo@mmu.ac.uk Precedence: bulk Reply-To: memetics@mmu.ac.uk
A Host with Infectious Ideas
By Steve Mirsky
http://www.sciam.com/2001/0501issue/0501profile.html
Paul W. Ewald argues that most cancers, heart disease and other chronic
ills stem from infections. If correct, his theory will change the course
of medicine
AMHERST, MASS.‹Newton had a falling apple. Darwin mused on finches. Paul
W. Ewald's inspiration was diarrhea. "I wish I had something more
romantic," says the Amherst College evolutionary biologist. It gets
uglier: Ewald, then a graduate student studying bird behavior, was camped
near a Kansas garbage dump. As he waged a three-day battle against his
sea of troubles, he contemplated the interactions between a host‹himself,
in this case‹and a pathogen. "There's some organism in there," Ewald
remembers thinking during that 1977 experience, "and this diarrhea might
be my way of getting rid of the organism‹or it might be the organism's
way of manipulating my body" to maximize its chances of passage to the
next victim by, for example, contaminating the water supply. "If it's a
manipulation and you treat it, you're avoiding damage," he notes. "But if
it's a defense and you treat it, you sabotage the host."
Host-pathogen relationships have dominated Ewald's thoughts ever since,
leading to numerous articles, two books and, depending on whom you talk
to, the respect or scorn of scientists and physicians. The admiration
comes from those who think he was on to something really big in his
earlier publications, which he summed up in his 1994 book Evolution of
Infectious Disease. "I think that Paul Ewald has been a pioneer in using
evolutionary theory to attack hard questions in pathogenesis," comments
Stephen Morse, a virologist and epidemiologist at Columbia University.
"His work has, for the first time, shown a way to generate testable
hypotheses to study such questions as the evolution of virulence‹once
thought intractable‹and infectious causes of chronic diseases." Indeed,
the Atlantic Monthly referred to Ewald as "the Darwin of the microworld"
(to which Ewald responds, "No, Darwin is Darwin of the microworld, too").
Any antipathy is the result of his latest research, outlined in last
year's Plague Time. The 47-year-old Ewald argued in the book that
infection may play a role in cancer, atherosclerosis, Alzheimer's and
other chronic conditions ordinarily thought of as inevitable consequences
of genetics, lifestyle or aging. "Some of his recent work is
controversial," Morse states. "I'd personally prefer to reserve judgment
for now on those questions, at least until more data are in." Others are
less gracious. One prominent atherosclerosis researcher politely panned
Ewald in public but privately referred to his ideas using an eight-letter
word, the first half of which is "bull."
In an April 1993 Scientific American article, Ewald smashed the old, and
unfortunately still widely accepted, notion that parasites and their
hosts inevitably evolve toward a benign coexistence. The tendency toward
benignity is reserved for conditions passed directly from person to
person. Someone too sick to mingle with others would indeed be a dead end
for the most dangerous infections, but Ewald showed that infectious
agents that use intermediate vectors for transmission, such as malaria's
mosquitoes and cholera's contaminated water, are free to evolve toward
greater destructive power. After all, a mosquito is free to feed on the
sickest malaria victims and thus pass on the worst pathogens. Even more
provocative was Ewald's exegesis on our potential to drive the evolution
of pathogens through judicious public health measures. "The evolutionary
hypothesis says that if you can make it so that sick people cannot pass
on infections and that only healthy people can, you should favor the
evolution of more benign strains," he explains.
Ewald suggests an experiment that could never be ethically done: "Select
two countries, one with bad water and one with clean water, and introduce
cholera into both." Theory holds that water in which microbes can thrive
serves as a vector that lets dangerous virulence continue or worsen. On
the other hand, treated water would kill cholera strains relying on
diarrhea for transport; only mild strains would survive because their
hosts would be healthy enough to transmit the pathogen directly to other
people. "Essentially, that's what happened in 1991," Ewald says,
referring to a cholera outbreak in Peru that spread through Latin
America. He and his students analyzed cholera from Peru and Guatemala,
which has unsafe water, and from Chile, whose water is trustworthy. They
found that over the 1990s Chile's cholera did indeed become less
virulent, whereas highly toxic strains persisted in the other countries.
This concept should motivate public health officials to do things they
should already be doing anyway, such as providing safe water and
mosquito-proof housing. Although these ideas have yet to permeate medical
school curricula fully, they seem beyond reproach theoretically. When
Ewald wanders into the fields of chronic disease, however, he steps into
some eight-letter castigation. Given evolutionary principles and the
available evidence, he argues in Plague Time, infectious agents should be
considered as at least part of the etiology of apparently noninfectious
conditions. Of course, the connection between Helicobactor pylori and
peptic ulcers is now taken for granted, although medical texts of 20
years ago were mute on the subject. Associations between infections and
some cancers‹hepatitis virus with liver cancer, papillomavirus with
cervical cancer‹have become accepted in only the past few decades. Ewald
thinks that more cancers, perhaps the majority, as well as numerous other
common, widespread and ancient chronic diseases, will eventually become
linked with various infections: for atherosclerosis and Alzheimer's
disease, he points to studies showing associations with Chlamydia
pneumoniae. He even holds that schizophrenia may be related to infection
with the protozoan Toxoplasma gondii.
"People have put much more emphasis on genetic causation and
noninfectious environmental causation," Ewald says. "And when they find
evidence that those kinds of causation are occurring, then they make this
fundamental error in science: throwing out a hypothesis [infection] just
because you have evidence that other hypotheses are probably at least
partly right." Disease instead may result from a subtle interplay between
a gene's product and an infectious agent.
Arguably, natural selection should have gotten rid of most of the solely
genetic diseases long ago. (Genetic conditions such as sickle-cell
disease get an evolutionary pass, however: one copy of the gene protects
against disease‹malaria, in the case of sickle cell‹so the potentially
destructive gene will survive in a population.) The standard argument is
that genes that cause illness after the prime reproductive years don't
get selected against. Ewald counters by arguing that the elderly‹and he
believes that there were always people who would be considered old by
today's standards, even at times when life was supposed to be "nasty,
brutish and short"‹ were important sources of information and caregiving,
and evolution does indeed try to keep them around.
To find possible infectious relationships to seemingly noninfectious
diseases, Ewald suggests the creation of a program akin to that used to
monitor adverse reactions to vaccines: what he calls the Effects of
Antimicrobials Reporting System, or EARS. Physicians worldwide may be
sitting on a gold mine of data, in the form of anecdotes about remissions
that accompany antibiotic treatment for a concurrent condition. "If you
accumulate the shared experiences, real cause and effect should pop out,"
he says. "Then we'd know if this was something we should do a controlled
study on."
Ewald believes that the associations between chronic diseases and
infections will be slowly accepted, perhaps in a few decades. Should his
viewpoint prevail some distant day, he may repeat the words his physicist
father once spoke. The elder Ewald, recovering from a heart attack when
Paul's 1993 article appeared in this, his favorite publication, said,
"Well, this was worth living for."
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