AP Psychology/Spencer
New pERSPECTOVES ON mENTAL iLLNESS
SUNDAY BOOK REVIEW
‘Infectious Madness,’ by Harriet A. Washington
ByMEGHAN O’ROURKE DEC. 31, 2015
One hundred and sixty odd years ago, Ignaz Semmelweis realized that physicians who didn’t wash their hands were carrying tiny germs from bedside to bedside and causing the childbed fever that killed many women. After doctors began washing their hands, fewer women died. The series of realizations in the 19th century that germs — bacteria and viruses — caused diseases like cholera and tuberculosis and influenza ushered in modern medicine. Mortality rates declined; children lived longer. Germ theory had a dramatic clarity to it. It pushed medicine away from holistic conceptions of illness as imbalance toward conceptions of illness as a specific entity. You get the germ, you fall sick, you take antibiotics or fight it off (or die). Ironically, though, the tidiness of this relationship helped obscure cases where germs may have less direct but still devastating effects — a complex reality we are now beginning to understand better.
Indeed, a handful of researchers are wondering whether mental illnesses are really caused by our immune system’s response to powerful microbial infections. As Harriet A. Washington reports in her new book, “Infectious Madness: The Surprising Science of How We ‘Catch’ Mental Illness,” some researchers in the field believe microbes may be responsible not only for clear-cut diseases like typhoid and tuberculosis, but also for mental illnesses such as anorexia, obsessive-compulsive disorder and schizophrenia — but in a less tidy manner. As she reports, research has found that 10 to 20 percent of mental illnesses, including autism, are partly caused by pathogens.
This new science, she excitedly claims, means we are on the verge of “a paradigm shift that replaces psychosocial factors with biological ones as the cause of mental illness.” (Washington is given to enthusiasm for her subject: If these infections can so far be said to cause only 10 to 20 percent of mental illnesses, is the shift as clear-cut as she says it is?)
To introduce us to this new paradigm, Washington, who won a National Book Critics Circle Award for her 2007 book “Medical Apartheid: The Dark History of Medical Experimentation on Black Americans From Colonial Times to the Present,” weaves together profiles, medical history and recent research, including that of Susan Swedo at the National Institutes of Health and E. Fuller Torrey at the Stanley Medical Research Institute. She delves into the history of medical advances and Freudianism to explain why the idea of an infectious origin of schizophrenia seems so strange to us. Along the way, she lays out the research showing that infections may shape us in utero and in our youth by triggering immune reactions our naïve immune system isn’t properly equipped to manage. (This can lead to out-of-control inflammation or autoimmune responses, in which the immune system attacks the body’s own tissue.)
While the work reported on in “Infectious Madness” seems powerful and indeed paradigm-shifting, Washington often fails to tease apart the complexities and nuances of the complicated science she is outlining, limiting herself to a rather reductive point of view. At one point, for example, she details the idea some researchers have that pathogenic infections help shape societies and major historical events, because evolution has selected for us to distrust the infected. It’s here that she is on thinnest ice — failing to take seriously the role of other factors like economics, cultural pressures and local history.
There are of course cases where we have long accepted that mental illness is caused by infection, as with paresis (in late-stage syphilis) and rabies. But Washington is trying to show that a host of other disorders are caused by it too. Among the most persuasive data she summarizes is evidence that obsessive-compulsive disorder, for example, can be triggered by strep throat practically overnight in a percentage of susceptible children. Take the story of Seth, who, until he had several bouts of sore throat, was “a quiet 10-year-old whose small rebellions rarely went beyond balking at bedtime.” One night after his illness, he refused to eat dinner and told his mother that his food might be poisoned. She woke to find he had been washing his hands raw in the sink — he had used nearly an entire bar of soap. An emergency room pediatrician diagnosed obsessive-compulsive disorder. As it happened, Susan Swedo at N.I.H. was Seth’s pediatrician. Swedo believes that strep throat can trigger O.C.D., Tourette’s and anorexia in the genetically predisposed by way of a condition she calls Pandas, or pediatric autoimmune neuropsychiatric disorders. In other words, the infection triggers an outsize immune response whose consequences manifest as, say, O.C.D. In one study, Swedo’s team studied a group of children whose “symptoms had been preceded by strep throat or similar infection.” They found that these children tended to have an antigen — a molecule that causes the body to make immune responses to it — making them vulnerable to rheumatic fever. In another study, when they gave immune-modulating interventions to 18 kids with O.C.D., 16 of the children, including Seth, improved.
Also deeply intriguing, if less fully convincing, is Washington’s account of research being done on schizophrenia. E. Fuller Torrey, a psychiatrist, has been frustrated by the lack of answers about schizophrenia ever since his sister was given a diagnosis of the disease while he was a pre-med student at Princeton. At the time — in the Freudian heyday — doctors still believed that poor mothering caused schizophrenia, and they suggested “dysfunctional” family relationships as a cause. Torrey didn’t buy that. He came across facts that complicate the view of schizophrenia as purely psychological or just genetic. There is an element of seasonality to schizophrenia: Schizophrenics are about 5 to 8 percent more likely to be born in winter and early spring — not a huge upward tick, but one that is consistent across multiple studies in different countries. Schizophrenics also have elevated white blood cell counts, suggesting they may be fighting an infection, and they have gait disturbances, suggesting some change in their brains.
Torrey also noticed reports that schizophrenia rates rose in the United States the same year cat ownership became popular, a fact that has led researchers to look into Toxoplasma gondii, a parasite that cats transmit to humans. It’s not harmful to everyone — though it appears to make those who harbor it more sexually aggressive — but a pregnant woman can pass it to her child in the womb, where it causes damage. Washington quotes from a study in the American Journal of Psychiatry that found that “children of mothers who contracted T. gondii while pregnant did suffer higher rates of schizophrenia than other children.” Another doctor, Hervé Perron, has identified a virus, HERV-W, that he believes is involved in schizophrenia; it turns out that “49 percent — nearly half — of people with schizophrenia harbor HERV-W, while only 4 percent of people without schizophrenia do,” Washington informs us. One theory is that viruses like the flu or infections like toxoplasmosis cause the body to “release” HERV-W viruses, overwhelming the immune system and causing inflammation in some people.
While Washington’s interest in her material is enticing, she overstates her case and the evidence. In the later chapters, she digresses into conversion disorders, gun violence and ethnic conflict in South Sudan, reporting on research that high rates of infection correspond to increased levels of war and ethnic violence, which, as she puts it, “explains why some societies are more bellicose than others.” The result is a scattered and at times disappointingly limited exploration of the issues at hand. It’s interesting to think about the fact that anorexia may be triggered by a virus, but a girl’s desire to be thin is certainly also culturally and socially influenced. At many points “Infectious Madness,” in neglecting to take a nuanced view, undermines the reader’s confidence in the author’s ability to make discerning assessments. For example, Washington talks about neurasthenia as evidence that the flu causes mental symptoms, but neglects to mention how broad a diagnosis of neurasthenia once was, dependent on erroneous ideas about how the nervous system functioned.
In her zeal to persuade us, Washington fails to unpack some of the obvious questions raised by the research she reports on. If she is correct, 51 percent of people with schizophrenia don’t have HERV-W. Is their schizophrenia triggered by another constellation of viruses? Or by a different mechanism altogether? Are we even defining “schizophrenia” correctly, as a single disease, or is it in fact a range of responses to different kinds of inflammation in the brain? Is some schizophrenia psychosocial in origin? What combination of genetics, environment and infection might we be talking about here? And if the abnormal response of schizophrenics to illness is itself abnormal, how do we conceptualize infection, pathology and health? What ethical and pragmatic implications are there at work?
Nevertheless, Washington’s broader point that the body really does shape the mind is an important one. However much our health care system may excel at acute care and detailed surgeries, it’s not great at dealing with vague illnesses it does not yet understand. In particular, medicine seems particularly blind to its own limitations when it comes to its conception of the mind-body relationship. Medicine continues to put faith in a “reductionist anachronism of mind/body dualism,” Washington writes, quoting from the website of the DSM-IV, despite the recent triumph of realizing that depression is a physical disease. The more we learn about the brain and the immune system, the more the duality between psychiatry and “functional” or “organic” medical issues begins to look anachronistic. We need a new framework for understanding disease that is more complex. After all, we’ve realized that autoimmune diseases also stem from a complex interplay of genetics, environment and viruses that “pull the trigger.” In this new framework, it seems likely, we will come to understand there are multiple pathways to many diseases. Doing the research to understand more is crucial. But as Washington notes, this kind of research is often rejected because it involves radical new ways of conceptualizing disease. As it happens, the reflexive rejection of new paradigms of thought in medicine is termed the Semmelweis Reflex, because so many doctors initially rejected Semmelweis’s insights, leading to the unnecessary loss of many lives.
INFECTIOUS MADNESS
The Surprising Science of How We “Catch” Mental Illness
By Harriet A. Washington
292 pp. Little, Brown & Company. $28.
Meghan O’Rourke is writing a book about poorly understood chronic illnesses, including autoimmune disease and chronic fatigue syndrome.
Catching Madness
Can we catch OCD, anorexia, or schizophrenia the way we can the flu?
By Harriet Washington, published on November 3, 2015 - last reviewed on June 10, 2016
Cats have been viral on the internet for years. The fractured grammar of LOLcats "I can has cheezburger?" is as ubiquitous as the animal itself. As far as domesticated animals go, cats are an oddly appropriate meme because they carry viruses that the world is only now fully recognizing.
E. Fuller Torrey, a psychiatrist with the Stanley Medical Research Institute, has been studying the connection between cats, parasites, and mental illness. According to Torrey, a known parasite that can lead to madness is carried by the common household cat. In his book,The Invisible Plague, he reveals that around 1808,schizophreniawas swiftly transformed from a rare to a relatively common disease. That same year, as cat ownership became popular in the United States, as well as in other parts of the world, U.S. schizophrenia rates rose sharply.
This is no coincidence, Torrey contends. Cats transmit the one-celled parasiteToxoplasma gondiithat causes the disease toxoplasmosis. It is already implicated in prenatal brain damage, abnormal head size, deafness, seizures, cerebral palsy, retinal damage, and mental retardation. Torrey and others think it does more: They argue thatT. gondiiinfection causes schizophrenia.
Illustration by John Gall
Researchers are unmasking the microbial roots of myriad illnesses; maladies as seemingly trivial as a sore throat can breedanorexia, Tourette's,obsessive-compulsive disorder, or schizophrenia. Researchers estimate that infectious organisms cause from 10 percent to 75 percent of serious mental disorders. Bacteria, viruses, fungi, and other infectious agents are responsible for many of the illnesses that we have long ascribed togenetics.
As forT. gondii, Torrey and colleagues suspect that it causes subtle changes to an infected fetus that could lead to schizophrenia 20 years later. In 2008, Torrey andRobert Yolken of Johns Hopkins published a study indicating that the peak age for becoming infected byT. gondii,between 18 and 35, coincides with the peak age for the first signs of schizophrenia. They also noted that in areas where felines are rare the prevalence rates of both toxoplasmosis and schizophrenia are low. By 2005, studies reported in journals like theAmerican Journal of Psychiatryfound that children of mothers who contractedT. gondiiwhile pregnant had higher rates of schizophrenia in adulthood than did other children. But Torrey also found that, in fact, the most strongly positive schizophrenia correlations were not withT. gondiiinfections acquired in the womb, but with those that struck children andteenagers.
Torrey and Yolken argue that sandboxes are a possible culprit. "A likely mechanism for exposure toT. gondiiinchildhoodis playing in the dirt of sandboxes contaminated withT. gondiioocysts," they write, explaining that each uncovered public sandbox studied is used as a litterbox by four to 24 cats. The cats shedT. gondiieggs and cysts that find their way onto the hands of children. The sandboxes provide convenient sites for research showing how urban areas where cats have a high rate of infection become areas where children's later schizophrenia rates are similarly elevated.