-Caveat Lector-
Pet Theory
Do Cats Cause Schizophrenia?
by Stephen Mihm
http://www.linguafranca.com/print/0012/cover_pet.html
"I THINK CATS ARE GREAT," says E. Fuller Torrey. His office decor would
seem to confirm this statement: A cat poster hangs on one wall; a cat
calendar sits on his desk; and a framed picture of a friend's cat leans
against the windowsill. He even admits to having a "cat library" at
home.
But Torrey's interest in felines is a bit different from that of your
typical cat lover. That's because Torrey, a psychiatry professor at the
Uniformed Services University of Health Science and the enfant terrible
of mental health research, believes that Felis domestica may carry
infectious diseases that could cause schizophrenia and bipolar disorder.
"My wife thinks I'm going to be assassinated by cat owners," says Torrey
with a sigh. "In fact, I like cats. Unfortunately, if we are correct
that they transmit infections..." Here his voice trails off, and he
pensively fingers his closely cropped beard.
Torrey often speaks in a self-deprecating manner of his "delusional"
notions, but he's dead serious about the cat connection. He thinks
"typhoid tabbies" are passing along Toxoplasma gondii, a parasite that
causes brain lesions and, if Torrey is right, schizophrenia.
Torrey first made the argument nearly thirty years ago. "It was
considered psychotic," he admits. But since then, his ideas, though
still outside the mainstream, have attracted converts, most notably the
Johns Hopkins virologist Robert Yolken, with whom he now collaborates.
Together, they're trying to prove that toxoplasmosis is but one of
several infectious diseases that cause most cases of schizophrenia and
bipolar disorder. It helps their case that previous explanations—bad
mothering, bad genes—have proven deficient to varying degrees. But
Torrey and Yolken have also uncovered some hard evidence to support
their claims, and they are about to put their theory to the test with
clinical trials of drugs that are new to the psychopharmacological
arsenal: antibiotics and antivirals similar to those used by AIDS
patients. If the duo finds that such drugs alter the course of
schizophrenia, Yolken observes, their results "would represent a major
advance in the treatment of this devastating disease as well as in
understanding its basic etiology."
"SCHIZOPHRENIA is a cruel disease," Torrey has written, with
considerable understatement. Although it affects only 1 percent of the
population, schizophrenia is among the most debilitating forms of mental
illness. Trapped in a world of private delusions, a schizophrenic might
cling, for example, to the belief that he is Jesus Christ, or that the
government has implanted a monitoring device in his mouth during a
routine dental procedure. Visual and auditory hallucinations can range
from the terrifying to the merely strange: gigantic spiders, voices that
insult or instruct. Some schizophrenics withdraw, becoming mute or
catatonic; others remain communicative but incoherent, jumping from one
topic to another without logical connections.
With little or no warning, schizophrenia usually manifests itself in
patients between the ages of sixteen and thirty. From then on, the
illness waxes and wanes, with symptoms generally becoming less severe as
the patient ages. Psychotherapy is of little help to schizophrenics, but
medication and constant medical care enable over 50 percent to make a
full recovery. Still, relapses are common, and many patients spend their
lives in halfway houses and institutions. Approximately 40 percent of
schizophrenics don't get the help they need and end up on the streets or
in prisons—or committing suicide.
There has never been a consensus on schizophrenia's etiology or cause.
Many nineteenth-century psychiatrists thought it was a biological
disorder; some speculated that it might have an infectious origin. As
far back as 1845, the French neurologist Jean E. Esquirol wrote that
"mental alienation is epidemic." He added: "It is certain that there are
years when...insanity seems suddenly to extend to a great number of
individuals." In 1874, the American Journal of Insanity published a
lengthy brief titled "On the Germ-Theory of Disease." By the early
twentieth century, doctors like Eugen Bleuler had suggested that "the
connection of [schizophrenia] to infectious process equally needs
further study." An outbreak of psychoses after the 1918 influenza
epidemic and the discovery that syphilis could cause dementia lent
further credence to such theories. In 1922, the psychiatrist Karl
Menninger hypothesized that schizophrenia was "in most instances" the
by-product of viral encephalitis.
Menninger later became a prominent Freudian psychoanalyst, following a
career trajectory that mirrored a larger movement in American psychiatry
away from biological explanations of mental illness. By the 1950s,
Freudian thought had solidified its grip on the American psychiatric
profession. That also happened to be the time when Torrey first began
thinking of a career in psychiatry.
As he tells it, the formative event for him came between his second and
third years at Princeton. His sister, who was due to start college that
fall, began hallucinating and yelling, "The British are coming!" The
diagnosis was acute schizophrenia. "My mother was told that it was
because my father had died," Torrey says with disgust. "I thought, 'This
is absurd—a lot of people's fathers die and they don't develop
schizophrenia.' There was this disconnect between what I was looking at
and what I was being told."
As Torrey wrapped up his degree at Princeton and went on to medical
school at McGill, he began seriously to contemplate a career in
psychiatry. After two years as a Peace Corps doctor in Ethiopia and a
year in the South Bronx helping to set up one of the area's first
neighborhood health centers, Torrey began a psychiatry residency in
Stamford, Connecticut. "It looked to me as if psychiatry was at least
twenty years behind the rest of medicine," he recalls. "It was more
likely to move and be exciting during my practicing lifetime."
That wasn't what attracted most people to the field in the 1960s. Says
Torrey, "Psychiatry was the thing you could do if you found yourself in
medical school and realized that you had made a terrible mistake—that
giving people rectal exams was pretty unsavory and not what you wanted
to do. You could still be paid to be a doctor and talk to people about
their problems." Those problems didn't include schizophrenia, Torrey
remembers: "To specialize in schizophrenia was about the lowest form of
psychiatric practice."
Torrey was undeterred. Not long after he went to work as a special
assistant to the director of the National Institute of Mental Health
(NIMH), he attracted controversy by publishing a bruising attack on
Freudian psychoanalysis. In The Death of Psychiatry (Chilton, 1974),
Torrey argued that psychiatry should either limit itself to the
treatment of patients with severe brain disorders—schizophrenia, bipolar
disorders—or abandon its medical pretensions altogether. In 1976, he
moved from NIMH to St. Elizabeth's Hospital in Washington, D.C., where
he achieved considerable renown as an advocate for the seriously
mentally ill. He also helped found the National Alliance for the
Mentally Ill, a nationwide patient advocacy group.
The turning point in Torrey's career came in 1983, when he published two
books: Surviving Schizophrenia, which soon became the authoritative text
for patients and families; and The Roots of Treason, a biography of Ezra
Pound based on research conducted at St. Elizabeth's. The second book,
which was nominated for an award by the National Book Critics Circle,
was inspired by rumors that Pound had sought refuge at St. Elizabeth's
after World War II to avoid standing trial for treason. When Torrey
researched the case, he discovered that a hospital administrator had
colluded to protect Pound by declaring him insane. It was a great piece
of detective work, but the book earned Torrey a demotion at St.
Elizabeth's. Disillusioned, he retired two years later and began
pursuing his unorthodox theories of schizophrenia. That meant getting
inside the brain of the schizophrenic—literally.
"THE BRAIN is in a very inconvenient place," says Torrey, guiding me up
the walkway to a boxy white building on the grounds of the Naval
Hospital in Bethesda, Maryland. "People just don't like you opening up
their heads and looking around while they're alive." This building, he
tells me, houses a solution to that problem. He opens a door and we
enter what looks and smells like the maintenance area of an indoor pool.
"The Navy has a dive chamber here," says Torrey, pointing to something
that looks like a beached bathysphere in the middle of a large
warehouse. "We're sharing space with them for now."
This is home to the Stanley Foundation Brain Bank and Neuropathology
Consortium's laboratories. Scattered throughout the building's corridors
and storerooms are some fifty-five freezers containing the brains of
about 385 people—schizophrenics, manic depressives, people with severe
depression, and so-called normal controls. The bank obtains the brains
with the assistance of designated medical examiners and the permission
of surviving family members. Each brain comes with a complete set of
medical records, family medical histories, and other clinical
information. The brains are then made available to mental illness
researchers worldwide, including Torrey and his colleagues. The whole
undertaking, along with a number of related projects, is funded by
Theodore and Vada Stanley, wealthy philanthropists who made their money
selling mail-order collectibles. (In one of his many roles, Torrey is
the executive director of the Stanley Foundation, an organization that
dispensed some twenty-one million dollars in research funds last year.)
As we wind our way down hallways packed with gigantic freezers, Torrey
stops to turn on the light in what looks like a storage closet. "Here
are the brains," he says, pointing to countless plastic pails stacked on
metal shelves. "We put half of each brain in formalin and half in the
freezers." Torrey turns out the lights. "Sometimes I take a brain to
show my students. They always enjoy that."
We enter the room where most of his staff work. Torrey is in his
element, clapping pathologists on the shoulder, joking with them,
seemingly oblivious (unlike me) to the business at hand: carving up
brains with what looks disturbingly like the meat slicer used at the
local deli. The staff are equally upbeat, even when describing the
downside of the work. "It can be a little depressing at times," admits
Dr. Maree Webster, who runs the bank. "Many of the brains are from
suicides, that sort of thing. It's really tragic."
The Brain Bank is the culmination of Torrey's dream to study
schizophrenia from the inside out. He hopes that the collection will
ultimately lead researchers to the cause of the disease. As for himself,
he's hoping that one day he and his colleagues will find their
hypothetical virus, though, as Webster admits, "it's a little like
trying to find a needle in a haystack. The brain is a big place."
And viruses are pretty small.
TORREY DATES his obsession with infectious disease to the early 1970s.
"I was becoming aware of proven cases of viral encephalitis that had
been diagnosed as cases of schizophrenia or cases of manic depressive
illness," he recalls. Torrey discovered some of the cases in the work of
Menninger and others near the turn of the century. It was also during
the 1970s that the future Nobel Prize winner Daniel Carleton Gajdusek
published some of his first research on so-called slow viruses—pathogens
that lie quiescent for twenty or thirty years before emerging as
full-blown infections.
Intrigued, Torrey met with Gajdusek. In conversation, the elder
scientist mentioned a trip he had made to the highlands of Papua New
Guinea to catalog neurological disorders. He told Torrey that he had
never found a cut-and-dried case of schizophrenia there, despite the
fact that the disease is supposed to afflict about 1 percent of the
world's population. Torrey himself made several trips and confirmed as
much. "But on the coast," he recounts, "where there had been missions
and contact with outsiders for a hundred years, you found occasional
cases." To Torrey, that raised the tantalizing possibility that some
kind of infectious agent was at work.
Torrey's theory started to look even more plausible when he began to
collaborate with Robert Yolken, who now runs the Stanley Division of
Developmental Neurovirology, based at the Johns Hopkins Children's
Center. Yolken, a summa cum laude graduate of Harvard who stayed on for
a medical degree, is a study in contrasts with Torrey. Whereas Torrey
spins stories and lingers on words for effect, Yolken speaks without
affect at an extraordinarily rapid rate, as though his tongue can barely
keep pace with his brain. Pictures of ski vacations with his family and
Torrey are taped to the shelves above his computer.
When the two scientists began working together in the 1980s, genetic
explanations had usurped traditional psychoanalytic theories about the
cause of schizophrenia. The new biological paradigm held that it was
only a matter of time before some hypothetical "schizophrenia gene"
would be identified, solving the mystery. But Torrey and Yolken remained
skeptical. There were some things that genetics couldn't explain. For
starters, several studies had shown that children born in urban areas
were more likely to develop schizophrenia than those born in rural
regions. Household crowding, too, had been demonstrated to be a risk
factor. And both urban living and household crowding increase exposure
to infectious agents.
Schizophrenia also appeared to correlate with birthdays. More than 250
epidemiological studies, including some of Torrey's own, have
demonstrated that both schizophrenic and manic depressive patients are
between 5 and 15 percent more likely to have been born in the winter or
spring months. Part of that statistical bump, in Torrey's opinion, could
be attributed to the increased rate of viral infection in the colder
months. "The seasonality data make the geneticists very uncomfortable,"
says Torrey.
Paul Ewald, a professor of biology at Amherst College and a specialist
in infectious diseases, is a bit more blunt. "With schizophrenia, you
have seasonal correlations, which is a telltale sign of infectious
agents. There are not that many things that can explain that
association," he says. "Unless you believe in astrology."
Ewald is little known in mental health circles, but his theories have
already earned him considerable attention among infectious disease
specialists. He and his collaborator, Gregory Cochran, believe that many
diseases—heart disease, various forms of cancer, multiple sclerosis,
cerebral palsy, most major psychiatric diseases—are often caused by
infectious agents. Their reasoning is simple: Any gene that adversely
affects an individual's ability to reproduce and care for offspring will
ultimately fall victim to natural selection. Therefore, severe common
diseases—those having an incidence higher than one in a thousand—can't
be chalked up simply to bad genes. Some kind of environmental factor,
either infectious or noninfectious, must play a role as well.
Schizophrenia, says Ewald, must be one of these diseases, because it
seriously diminishes a person's reproductive fitness. At the same time,
neither he nor Torrey and Yolken suggest that genetic factors are
irrelevant. After all, there's plenty of evidence that genes play a role
in schizophrenia. One measure of that is the monozygotic twin test,
which yields the percentage of identical twins who both develop a
particular disease. A concordance rate of 100 percent is evidence of a
purely genetic disease, one that is little influenced by environmental
factors like infection, nutrition, or toxins. Huntington's disease, for
example, has a concordance rate of 100 percent. Similarly, Down's
syndrome has a concordance rate of 95 percent; autism, 82 percent. By
contrast, a viral infection like polio has a concordance rate of only 36
percent among identical twins—thus, genetics plays some role, but most
of the blame lies with the polio virus. What about schizophrenia?
According to Torrey's (controversial) calculations, the concordance rate
averages approximately 28 percent. With a rate that low, says Ewald, "we
have to look elsewhere."
For Torrey, Ewald, and others, that means looking for some kind of
infectious agent that may exploit a genetic weakness when invading a
host. This interplay of genetics and infectious disease is complex and
has a lot to do with whether a faulty gene permits the virus, bacterium,
or parasite in question to lock onto cells. As Yolken explains it, these
"genetic determinants" are different from those involved in typical
"genetic" diseases like Huntington's in that a person's genetic
susceptibility doesn't surface unless he or she comes into contact with
a particular environmental factor. In theory, that's why one identical
twin and not the other will come down with schizophrenia: Only one is
exposed to the "schizovirus."
Torrey says that these theories aren't news to most people in the
medical profession, particularly those working with infectious diseases.
"Psychiatrists," he notes in an exasperated tone, "are the only ones
that are surprised by this."
TORRY IS talking about cats again. "I've given talks on the cat stuff
and people's response is almost universal: 'I'm not surprised—I've known
my cat is schizophrenic for years!'" He chuckles. "One talk I gave at a
department of psychiatry, a fellow came up to me and said, 'I don't want
you to repeat this, but the former chairman of our department of
psychiatry was convinced that his cat was hallucinating, so he gave him
liquid Thorazine and it really seemed to help.'" Torrey looks at me and
smiles. "People find cats strange, so they don't find this idea so odd."
Yolken, who owns two cats, is less critical of our feline friends, but
he agrees that there may be a connection. "Cat feces are the biggest
source of toxoplasma infections in the United States," he says,
preparing to guide me through a PowerPoint presentation at his desk.
Toxoplasma, Yolken informs me, is one of the more adaptable parasites,
able to set up shop in any number of mammals. Although most humans can
battle, or even carry, toxoplasma without ill effects, the parasite
poses a special danger to people with compromised immune systems. It is
also hazardous to pregnant mothers and their fetuses, causing serious
brain lesions and retardation in infants when contracted during the
first trimester of pregnancy. That's why doctors now forbid expectant
mothers to clean litter boxes. Torrey and Yolken speculate that a
toxoplasma infection contracted during pregnancy or infancy could lie
dormant in some patients' central nervous system, only to be reactivated
when the host's immune system is compromised by a secondary infection in
late adolescence.
Cats, meanwhile, don't seem to suffer toxoplasma's ill effects. They
pick up the parasite from eating infected rodents, typically rats or
mice. In the rodents themselves, the parasite produces brain lesions and
a host of rather odd behaviors. Infected rats, for example, lose their
instinctive fear of cat urine, making them more likely to be caught and
eaten by feline predators. As Ewald explains, "The parasite gets to the
next host in its life cycle by messing up the rodents' minds." Once in
the cat, the parasites infect the lining of the small intestine,
reproduce asexually, and encase themselves in a sturdy membrane. These
oocysts, or spores, are then shed in the cat's feces. The cycle begins
anew when human beings and other mammals become infected from handling
the feces or, in some cases, breathing and swallowing the airborne
spores.
Torrey first postulated that toxoplasmosis might cause schizophrenia in
the 1970s, when he read several articles attributing an outbreak of
multiple sclerosis in the Faeroe Islands to the introduction of dogs
there during World War II. Could indoor pets like cats, which had become
widely popular only in the nineteenth century, also be reservoirs of
infectious agents? Torrey, who had recently completed a book manuscript
arguing that in the late nineteenth century schizophrenia and bipolar
disorder went from being rare diseases to relatively common ones, became
convinced that cats were central to that story. "The cat craze began
with the cat shows in the late nineteenth century," he explains. "And
when I went back and looked at what we know about cats as pets, it
corresponded almost perfectly to what we know about the rise of
psychosis."
Eager to test the theory, he and Yolken conducted a study in the early
1990s wherein parents of schizophrenics and nonschizophrenics were asked
whether they owned a cat during pregnancy or when their offspring were
young. That study revealed a higher incidence of cat ownership among the
parents of children who developed schizophrenia (51 percent) versus
those who did not (38 percent). A second study, much larger in scope,
looked into nineteen different factors, including cat ownership, dog
ownership, complications during pregnancy, breast feeding, and urban
versus rural residence. Only five of the variables proved statistically
significant, cat ownership among them (52 percent of those who developed
schizophrenia had lived with cats versus 42 percent of the
nonschizophrenics). Dog ownership, by contrast, was marginally more
common among nonschizophrenics (78 percent) than among schizophrenics
(73 percent).
Such epidemiological data are further supported by a recent study by
Yolken and Stephen Buka of the Harvard School of Public Health. The two
stumbled onto medical records and blood samples taken from some
fifty-five thousand pregnant women taken between 1959 and 1966 as part
of a study on the causes of cerebral palsy. Buka tracked down about
twenty-five hundred families from Providence, Rhode Island, who took
part in the study. Among these families, twenty-seven children had
exhibited psychoses. Buka matched these with some fifty-four controls of
the same age, sex, race, and month and year of birth. Yolken then
subjected the blood samples of both groups to a battery of tests for
different antibodies. The mothers of the children who later developed
psychoses were approximately 4.5 times more likely to have antibodies to
toxoplasmosis than the mothers of the healthy controls.
"It's been known for a long time that toxo can get into the brain," says
Yolken. But can it cause schizophrenia? One bit of evidence, he says,
comes from the AIDS epidemic. "It turns out," he explains, "that about
30 percent of the adult population is toxo-positive"—that is, has
antibodies to toxoplasmosis—"and that if you suppress our immune systems
enough, we'll get toxoplasmosis. Most HIV patients who are toxo-positive
will eventually show signs of toxoplasmosis." Today many such patients
get medication to prevent this, but a decade ago, Yolken recalls, "we
saw massive toxo." He thinks it was probably there all along,
hibernating in the brain. So far, his and Torrey's attempts to find
evidence of toxoplasma in the brains of schizophrenics have failed. "The
brain is a big place," says Yolken with a sigh. "And it doesn't take
much toxo to start an infection."
Of the other diseases that Yolken tried to correlate with
schizophrenia—rubella, influenza, cytomegalovirus, chlamydia, and herpes
simplex 2 (HSV-2)—only herpes was significant. Tests showed that mothers
of schizophrenic children were 5.8 times more likely to have antibodies
to HSV-2 than mothers of the healthy controls.
How might a herpes infection contracted in the womb lead to mental
illness years later? As Yolken sees it, the age when most schizophrenics
first develop symptoms suggests exposure to some sort of "infectious
agent which has a higher rate of transmission in late adolescence and
early adulthood." Yolken hypothesizes that the herpes virus remains
quiescent in the brain until adolescence, when it is triggered by the
Epstein-Barr virus that causes mononucleosis, also known as the kissing
disease. Another theory holds that it is reactivated by another version
of itself picked up in sexual contact. How such an infection translates
into schizophrenia is still a matter of considerable speculation. Yolken
is wary of saying that herpes causes schizophrenia. "These represent
complex disorders," he says.
Adding to the complexity, Yolken thinks that other kinds of viruses also
play a role in severe mental disorders. He and Torrey have just
completed a study in which more than 17 percent of patients who recently
manifested schizophrenia had antibodies to the multiple sclerosis
retrovirus. Equally interesting to Yolken is evidence that in nearly 30
percent of recent-onset schizophrenics, endogenous retroviruses had made
copies of themselves. In both cases, the rate for the controls was zero
percent.
Endogenous retroviruses, admits Yolken, "are not well known in the
scientific community." They are viruses that are incorporated into the
human genome. In other words, he explains, at some point in evolutionary
history, "progenitors of humans or primates got infected with a
retrovirus, and the retrovirus got into the genome and stayed in the
genome." As a consequence, foreign bits of genetic material are
scattered through the human genome. "In most cases, they don't seem to
do very much," Yolken says reassuringly. But it seems that in some cases
they can be activated by other viruses. Then the little stowaways begin
to make copies of themselves, perhaps wreaking havoc on adjacent genes
and, Yolken conjectures, triggering schizophrenia.
If schizophrenia is caused by a virus, can it be cured? "What we don't
know is whether the infection is reversible," says Yolken. "If the
damage is done in childhood, then treating patients as adults may not
work." Still, he and Torrey are going to try: They are administering
acyclovir, an antiviral drug better known for its efficacy against
herpes infections, to groups of schizophrenic patients. They're
encouraged by several previous studies, including one of their own,
which have shown that antipsychotic drugs like Thorazine, Haldol, and
clozapine inhibit viral replication. Torrey and Yolken hypothesize that
the drugs' efficacy may have something to do with their antiviral
properties. In a subsequent trial, they will administer antibiotics
customarily used to treat toxoplasmosis.
ALTHOUGH Torrey and Yolken's theory that an infectious disease causes
schizophrenia has gained some acceptance, or at least respect, it is
still far from the prevailing view. Torrey in particular has many
critics, even among colleagues with whom he has collaborated.
Take Irving Gottesman, a professor of psychology and clinical pediatrics
at the University of Virginia and a major proponent of genetic
explanations of schizophrenia. The two men maintain a friendly
relationship despite their differences. "The thing that keeps us
together," explains Gottesman, "is that we have common enemies: the
Freudians, the sociologists, the cultural anthropologists"—anyone, in
other words, who wants to ascribe schizophrenia to nonbiological causes.
They frequently co-author articles attacking what they perceive to be
misallocations of mental health research funds. But when it comes to
explaining schizophrenia, they part ways.
Gottesman casts doubt on Torrey's data for the rate of concordance for
schizophrenia among identical twins. "He's always trying to lower the
rates," claims Gottesman. "I'm just doing it the way geneticists have
always done." Gottesman's statistical method, known among geneticists as
probandwise concordance, samples admissions to a particular hospital. If
one member of an identical-twin pair shows up with schizophrenia and the
other member shows up at a different hospital with schizophrenia, too,
then the twin pair counts as one concordant pair. But if one twin shows
up at the hospital and the other twin shows up at the same hospital,
each twin counts as a concordant pair, thus yielding two pairs instead
of one. This method produces a concordance rate that's close to 50
percent. "Geneticists use probandwise to avoid errors when comparing
rates with the general population rate," explains Gottesman.
"I call it a system of double counting," says Torrey of Gottesman's
method. "I don't know of any other people outside of psychiatry who use
the probandwise concordance rate." Paul Ewald agrees. In an e-mail, he
notes that "proband concordance is vulnerable to overestimates on the
basis of selection biases.... I trust Torrey's figures for
schizophrenia," he writes. "They don't incorporate this bias."
Nonetheless, Gottesman is certain that genes play a bigger role than
Torrey and his colleagues admit. In fact, Gottesman has helped formulate
a multiple-gene theory of schizophrenia, which holds that the disorder
arises from a complex set of interactions between many different genes.
He's also interested in what he calls epigenetics, the study of
environmental factors—drugs and other toxins, for example—that control
or trigger gene events.
"Viruses could be epigenetic contributors, too," concedes Gottesman. But
he will accompany Torrey only so far down that road. Back in 1994, when
Gottesman and Torrey published the findings of a landmark study of twins
and schizophrenia, they offered their differing interpretations of the
results not as a traditional conclusion but in the form of a fictional
conversation among three experts. Gottesman, who spoke for the
geneticists under the pseudonym Dr. Mendel M. Malgene, urged Torrey, who
assumed the nom de plume Dr. Dena S. Daverus, not to dismiss or diminish
the complex interplay of different genes. He also pointed out that the
brain scans they had conducted in the course of their study revealed
broad, scattered types of changes in the structure of schizophrenic
brains. Infectious diseases like rabies or polio, by contrast, afflict
very specific types of cells or regions of the brain. And anyhow, says
Gottesman today, "If schizophrenia is caused by an infectious disease,
why is it that psychiatric nurses and psychiatrists don't have higher
rates?" He pauses. "Why don't spouses of schizophrenics have higher
rates of the disease?"
JOINING Dr. Daverus and Dr. Malgene in the fictional schizophrenia
debate was Dr. A. Dominic D'Velupmoni, modeled after Daniel Weinberger,
who in real life represents what has since become the dominant school of
thought about the disease. Weinberger, who is chief of the Clinical
Brain Disorders Branch Intramural Research Program at the National
Institute of Mental Health, is one of the most articulate spokesmen for
what is known as the neurodevelopmental hypothesis. Writes Weinberger,
"It has recently become de rigueur to refer to schizophrenia as a
neurodevelopmental disorder in which the primary cerebral insult or
pathological process occurs during brain development long before the
illness is clinically manifest." In other words, as Weinberger explains
it to me, something "disrupts the normal programs of brain development."
That could be a faulty gene or an obstetric complication. Or something
else: Like Gottesman, Weinberger is willing to consider that viruses
might play a role. "Genetics can't explain it all," he says. "There have
to be environmental factors, too, and viruses may be one of those." But
though he describes Torrey's viral theory as "very provocative, very
interesting," Weinberger argues that "it's been supported by very little
credible scientific data."
The neurodevelopmental theory "is not a theory about a specific cause;
it's a theory about timing," counters Torrey. "We have fashions in
schizophrenia research, and the neurodevelopmental theory is very
fashionable right now." As he sees it, Weinberger needs to explain what
exactly causes the schizophrenic brain to develop in the way it does.
Attributing some of that process to obstetric complications or
malnutrition during pregnancy, as some proponents of the
neurodevelopmental hypothesis do, doesn't add up. Areas of the world
that have the worst prenatal care, diet, and rates of obstetric
complications do not have higher rates of schizophrenia; if anything,
Torrey points out, the incidence of schizophrenia may be lower in such
places.
Neurodevelopmental thinking nonetheless remains at the center of current
psychiatric accounts of schizophrenia. And though Torrey and Yolken's
views currently sit on the margins, Ewald does not think they will
remain there. "Infectious causation has been seriously underestimated
from the 1800s onward," he notes. "Many people who suggested infectious
causes of diseases were dismissed but later proven right." Take gastric
ulcers. Only in the last decade did researchers prove that Helicobacter
pylori bacteria, not stress and hot food, cause most ulcers—even though
evidence for this had been accumulating for over a century. With a
disease as complex and mysterious as schizophrenia, Ewald admonishes,
researchers need to be careful not to reject infectious disease
hypotheses out of hand.
To be sure, the field is less divided today than it was when Torrey
began his training some thirty years ago. Almost everyone in psychiatry
now accepts the biological model of mental illness. No surprise, then,
that Torrey, Yolken, Gottesman, and Weinberger all admit that their
theories may well be compatible. At the same time, none shows much
willingness to dilute a life's worth of research with such compromise.
"The best theory of all would be one that integrates all of them without
preconceptions," says Gottesman. "But," he says sadly, "who's going to
do that?"
Stephen Mihm is the producer of The New York Times Magazine on the Web
and a doctoral candidate in history at New York University. He lives in
New York City with his three cats, all of whom declined to be
interviewed for this story.
<A HREF="http://www.ctrl.org/">www.ctrl.org</A>
DECLARATION & DISCLAIMER
==========
CTRL is a discussion & informational exchange list. Proselytizing propagandic
screeds are unwelcomed. Substance—not soap-boxing—please! These are
sordid matters and 'conspiracy theory'—with its many half-truths, mis-
directions and outright frauds—is used politically by different groups with
major and minor effects spread throughout the spectrum of time and thought.
That being said, CTRLgives no endorsement to the validity of posts, and
always suggests to readers; be wary of what you read. CTRL gives no
credence to Holocaust denial and nazi's need not apply.
Let us please be civil and as always, Caveat Lector.
========================================================================
Archives Available at:
http://peach.ease.lsoft.com/archives/ctrl.html
<A HREF="http://peach.ease.lsoft.com/archives/ctrl.html">Archives of
[EMAIL PROTECTED]</A>
http:[EMAIL PROTECTED]/
<A HREF="http:[EMAIL PROTECTED]/">ctrl</A>
========================================================================
To subscribe to Conspiracy Theory Research List[CTRL] send email:
SUBSCRIBE CTRL [to:] [EMAIL PROTECTED]
To UNsubscribe to Conspiracy Theory Research List[CTRL] send email:
SIGNOFF CTRL [to:] [EMAIL PROTECTED]
Om
