The latest issue of Discover
magazine (June 2010) has an interesting article that examines some contemporary research on schizophrenia that
offers a radical departure from traditional assumptions of what schizophrenia is, where it comes from and how it ought to be treated. I found it
incredibly interesting and somewhat shocking in its implications, so I thought I'd research a little and share.
E. Fuller Torrey, Executive Director of the Stanley Medical Research Institute, is a world-renowned research psychiatrist, specializing in
schizophrenia (a specialty spawned by the schizophrenia of his sister which began noticeably manifesting in 1937). Torrey has studied psychiatry for
over forty years. Almost right away, Torrey began noticing things amongst schizophrenics and the research available at the time that veered from the
status quo that, much like today, considers schizophrenia a mental disorder, likely with a genetic component; though it is important to emphasize that
it seems the field is much more open to the possibility of schizophrenia, typically, requiring a genetic predisposition and the negative influence of
specific environmental factors.
For example, schizophrenics have specific, physical symptoms that imply the characteristics of issues not
typically restricted, necessarily, to
many mental maladies. They have inflamed white blood cells, enlarged brain ventricles, decreased brain tissue, etc. Their blood also contains
lymphocytes that mirror the infection-fighting agents present in the blood of patients stricken with mononucleosis. Furthermore, many of these
symptoms, and specifically inflammation and loss of brain tissue, correspondingly increase as the schizophrenia in the individual grows in severity.
Based on these observations, Torrey began to develop a hypothesis that schizophrenia was not a psychological disorder, but an infectious brain
So Torrey began to explore schizophrenia with a different strategy - rather than examining personal backgrounds for emotional trauma and utilizing
analysis to compile records that would, hopefully, reveal common, collective patterns in individual lives, he rejected Freudian approaches and
psychoanalysis, all together. He has also suggested that the accepted genetic component of schizophrenia is significantly overemphasized. [Note that
the rule, rather than the exception, is that amongst twins, it is almost always the case that only one develops schizophrenia.] Torrey began
investigating schizophrenia as an infectious disease; next, he started to search for the agent of infection.
Torrey found from other researchers that schizophrenics possess antibodies within their bloodstream for toxoplasma, as well as the Epstein-Barr virus
which causes mononucleosis ("mono" or "the kissing disease" - a type of herpes which has affected 90% of all people) and cytomegalovirus (also a
type of herpes whose antibodies are found in 40% of the world population). Toxoplasma is a parasitic protozoa, spread by house cats, that is
generally relatively malign, but can be fatal to developing fetuses. Also, the Epstein-Barr virus does not only cause these "minor" conditions. It
is also implicated as the causative agent for a wide range of much more serious conditions like lymphoma, lupus, HIV-related central nervous system
lymphomas and multiple sclerosis. But, as mentioned, possessing the antibodies for conditions sparked by Epstein-Barr is hardly unusual in the
Possession of these agents necessitate prior exposure; however, the actual infectious agent, itself, was never found in the patients, implying a
long-ago condition. It may be important to note here that schizophrenia almost always develops in the 20s and early 30s. People that develop
schizophrenia in childhood or middle or old age are exceedingly rare.
Robert Yolken, Distinguished Professor of Neurobiology at Johns Hopkins University, has studied the role of retroviruses in schizophrenics and has
suggested that the HERV-W retrovirus group play a significant role in the development of schizophrenia, whether as the cause or as a symptom.
Retroviruses are viruses that "hijack" the DNA-producing capacities of cells in order to perpetually reproduce themselves, from their own RNA,
within the genome of the host ... and continue to infect additional cells (HIV, the virus that causes AIDS, is, of course, a retrovirus). MSRV is a a
specific retrovirus within the HERV-W group that is linked with multiple sclerosis.
Some retroviruses spread to other hosts while their host is still alive; else they die when the host dies. Endogenous retroviruses, though, rather
than "infecting" their host, become intwined within the genetic code of the host and pass themselves on just as any other genetic material is passed
on, perpetuating themselves for thousands, perhaps millions of years. I believe the human genome contains retroviruses that were accumulated before
humans ever existed, or mammals, for that matter.
HERV-W is an endogenous retrovirus group.
As for cutting to the chase and focusing on any direct relationship between schizophrenia and multiple sclerosis, Yolken notes that the two disorders
are distinct and possess very different pathological characteristics. However, on the other hand, there are profound similarities between them, as
well, including age of onset of symptoms, time of the year that victims are born (this seems rather insignificant, but it can be critical when you
consider, for example, that diseases can be caused by other conditions that are specifically caused by temporal conditions like cold weather or the
diseases that flourish in cold weather - possibly because of suppressed immune systems) and even the geographical location of victims. Note that a
common given for schizophrenia is that victims are far more often than not, born in winter and early spring.
While our report doesn't explain why the retrovirus becomes active in the first place, it presents clues as to what may happen when it does become
Our ultimate hope is that we can interfere with the retrovirus by preventing it from becoming active. If we can do that, it may give doctors another
method of treating schizophrenia.