A Resource Guide to Investing in Biotechnology
Directory - Encyclopedia - Stock Index - Pipeline Drugs 

Biotechnology Encyclopedia


Schizophrenia is a psychiatric diagnosis denoting a persistent, often chronic, mental illness variously affecting behavior, thinking, and emotion. The term schizophrenia comes from the Greek words (schizo, split or divide) and (phrenos, mind) and is best translated as "shattered mind". Schizophrenia is commonly confused with multiple personality disorder, a different diagnosis.


Schizophrenia is most commonly characterized by both 'positive symptoms' (those additional to normal experience and behaviour) and 'negative symptoms' (the lack or decline in normal experience or behaviour). Positive symptoms are grouped under the umbrella term psychosis and typically include delusions, hallucinations, and thought disorder. Negative symptoms may include inappropriate or lack of emotion, poverty of speech, and lack of motivation. Some models of schizophrenia include thought disorder and planning problems in a third grouping, the 'disorganization syndrome'. Additionally, neurocognitive deficits may be present. These take the form of reduction or impairment in basic psychological functions such as memory, attention, problem solving, executive function and social cognition. The onset is typically in late adolescence and early adulthood, with males tending to show symptoms earlier than females.

Psychiatrist Emil Kraepelin was first to make the distinction between what he called dementia praecox and other forms of madness. This classification was later renamed 'schizophrenia' by psychiatrist Eugen Bleuler in 1911 as it became clear Kraepelin's name was not an adequate description of the condition.

The diagnostic approach to schizophrenia has been opposed, most notably by the anti-psychiatry movement, who argue that classifying specific thoughts and behaviours as illness allows social control of people that society finds undesirable but who have committed no crime.

More recently, it has been argued that schizophrenia is just one end of a spectrum of experience and behaviour, and everybody in society may have some such experiences in their life. This is known as the 'continuum model of psychosis' or the 'dimensional approach' and is most notably argued for by psychologist Richard Bentall and psychiatrist Jim van Os.

Although no definite causes of schizophrenia have been identified, most researchers and clinicians currently believe that schizophrenia is primarily a disorder of the brain. It is thought that schizophrenia may result from a mixture of genetic disposition (genetic studies using various techniques have shown relatives of people with schizophrenia are more likely to show signs of schizophrenia themselves) and environmental stress (research suggests that stressful life events may precede a schizophrenic episode).

It is also thought that processes in early neurodevelopment are important, particularly those that occur during pregnancy. In adult life, particular importance has been placed upon the function (or malfunction) of dopamine in the mesolimbic pathway in the brain. This theory, known as the dopamine hypothesis of schizophrenia largely resulted from the accidental finding that a drug group which blocks dopamine function, known as the phenothiazines, reduced psychotic symptoms. These drugs have now been developed further and antipsychotic medication is commonly used as a first line treatment. However, this theory is now thought to be overly simplistic as a complete explanation.

Differences in brain structure have been found between people with schizophrenia and those without. However, these tend only to be reliable on the group level and, due to the significant variability between individuals, may not be reliably present in any particular individual.


Accounts that may relate to symptoms of schizophrenia date back as far as 2000 BC in the Book of Hearts, part of the ancient Ebers papyrus. However, a recent study1 into the ancient Greek and Roman literature showed that whilst the general population probably had an awareness of psychotic disorders, there was no recorded condition that would meet the modern diagnostic criteria for schizophrenia in these societies.

This nonspecific concept of madness has been around for many thousands of years and schizophrenia was only classified as a distinct mental disorder by Kraepelin in 1887. He was the first to make a distinction in the psychotic disorders between what he called dementia praecox (a term first used by psychiatrist Benedict A. Morel) and manic depression. Kraepelin believed that dementia praecox was primarily a disease of the brain2, and particularly a form of dementia. Kraepelin named the disorder 'dementia praecox' (early dementia) to distinguish it from other forms of dementia (such as Alzheimer's disease) which typically occur late in life. He used this term because his studies focused on young adults with dementia.22

The term schizophrenia is derived from the Greek words 'schizo' (split) and 'phrene' (mind) and was coined by Eugene Bleuler to refer to the lack of interaction between thought processes and perception. He was also the first to describe the symptoms as "positive" or "negative."22 Bleuler changed the name to schizophrenia as it was obvious that Krapelin's name was misleading. The word "praecox" implied precocious or early onset, hence premature dementia, as opposed to senile dementia from old age. Bleuler realized the illness was not a dementia (it did not always lead to mental deterioration) and could sometimes occur late as well as early in life and was therefore misnamed.

With the name 'schizophrenia' Bleuler intended the name to capture the separation of function between personality, thinking, memory, and perception, however it is commonly misunderstood to mean that affected persons have a 'split personality' (something akin to the character in Robert Louis Stevenson's The Strange Case of Dr. Jekyll and Mr. Hyde). Schizophrenia is commonly, although incorrectly, confused with multiple personality disorder (now called 'dissociative identity disorder'). Although people diagnosed with schizophrenia may 'hear voices' and may experience the voices as distinct personalities, schizophrenia does not involve a person changing between distinct multiple personalities. The confusion perhaps arises in part due to the meaning of Bleuler's term 'schizophrenia' (literally 'split mind'). Interestingly, the first known misuse of this word schizophrenia to mean 'split personality' (in the Jekyll and Hyde sense) was in an article by the poet T. S. Eliot in 19333.

In the first half of the twentieth century, schizophrenia was considered by many as a "hereditary defect", and people with schizophrenia became the target of the eugenics programs of many countries. Hundreds of thousands were forcibly sterilized, the majority in Germany, the United States, and various Scandinavian countries.

Diagnosis and presentation (signs and symptoms)

Like many mental illnesses, the diagnosis of schizophrenia is based upon the behaviour of the person being assessed. There is a List of diagnostic criteria which must be met for a person to be so diagnosed. These depend on both the presence and duration of certain signs and symptoms.

The most commonly-used criteria for diagnosing schizophrenia are from the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM) and the World Health Organisation's International Statistical Classification of Diseases and Related Health Problems (ICD). The most recent versions are ICD-10 ( and DSM-IV-TR (

Below is an abbreviated version of the diagnostic criteria from the DSM-IV-TR, the full version is available here ( (DSM cautionary statement)

To be diagnosed as having schizophrenia, a person must display:

  • A) Characteristic symptoms: Two or more of the following, each present for a significant portion of time during a one-month period (or less, if successfully treated)
    • delusions
    • hallucinations
    • disorganized speech (e.g., frequent derailment or incoherence). See thought disorder.
    • grossly disorganized or catatonic behavior
    • negative symptoms, i.e., affective flattening (lack or decline in emotional response), alogia (lack or decline in speech), or avolition (lack or decline in motivation).
Note: Only one Criterion A symptom is required if delusions are bizarre or hallucinations consist of hearing voices.
  • B) Social/occupational dysfunction: For a significant portion of the time since the onset of the disturbance, one or more major areas of functioning such as work, interpersonal relations, or self-care, are markedly below the level achieved prior to the onset.
  • C) Duration: Continuous signs of the disturbance persist for at least six months. This six-month period must include at least one month of symptoms (or less, if successfully treated) that meet Criterion A.

Historically, schizophrenia in the West was classified into simple, catatonic, hebephrenic, and paranoid. The DSM now contains five sub-classifications of schizophrenia. These are

  • catatonic type (where marked absences or peculiarities of movement are present),
  • disorganized type (where thought disorder and flat or inappropriate affect are present together),
  • paranoid type (where delusions and hallucinations are present but thought disorder, disorganized behaviour, and affective flattening is absent),
  • residual type (where positive symptoms are present at a low intensity only) and
  • undifferentiated type (psychotic symptoms are present but the criteria for paranoid, disorganized, or catatonic types has not been met).

Symptoms may also be described as 'positive symptoms' (those additional to normal experience and behaviour) and negative symptoms (the lack or decline in normal experience or behaviour). 'Positive symptoms' describe psychosis and typically include delusions, hallucinations and thought disorder. 'Negative symptoms' describe inappropriate or nonpresent emotion, poverty of speech, and lack of motivation. In three-factor models of schizophrenia, a third symptom grouping, the so called 'disorganisation syndrome' is also given. This considers thought disorder and related disorganized behaviour to be in a separate symptom cluster from delusions and hallucinations.

It is worth noting that many of the positive or psychotic symptoms may occur in a variety of disorders and not only in schizophrenia. The psychiatrist Kurt Schneider tried to list the particular forms of psychotic symptoms which he thought were particularly useful in distinguishing between schizophrenia and other disorders which could produce psychosis. These are called first rank symptoms or Schneiderian first rank symptoms and include delusions of being controlled by an external force, the belief that thoughts are being inserted or withdrawn from your conscious mind, the belief that your thoughts are being broadcast to other people and hearing hallucinated voices which comment on your thoughts or actions, or may have a conversation with other hallucinated voices. As with other diagnostic methods, the reliability of 'first rank symptoms' has been questioned4, although they remain in use as diagnostic criteria in many countries.

Diagnostic issues and controversies

It has been argued that the diagnostic approach to schizophrenia is flawed, as it relies on an assumption of a clear dividing line between what is considered to be mental illness (fulfilling the diagnostic criteria) and mental health (not fulfilling the criteria). Recently it has been argued, notably by psychiatrist Jim van Os and psychologist Richard Bentall, that this makes little sense, as studies have shown that psychotic symptoms are present in many people who never become 'ill' in the sense of feeling distressed, becoming disabled in some way or needing medical assistance6.

Of particular concern is that the decision as to whether a symptom is present is a subjective decision by the person making the diagnosis or relies on an incoherent definition (for example, see the entries on delusions and thought disorder for a discussion of this issue). More recently, it has been argued that psychotic symptoms are not a good basis for making a diagnosis of schizophrenia as "psychosis is the 'fever' of mental illness — a serious but nonspecific indicator".5

Perhaps because of these factors, studies examining the diagnosis of schizophrenia have typically shown relatively low, or inconsistent levels of diagnostic reliability. Most famously, David Rosenhan's 1972 study, published as On being sane in insane places, demonstrated that the diagnosis of schizophrenia was (at least at the time) often subjective and unreliable. More recent studies have found agreement between any two psychiatrists when diagnosing schizophrenia tends to reach about 65% at best33. This, and the results of earlier studies of diagnostic reliability (which typically reported even lower levels of agreement) have led some critics to argue that the diagnosis of schizophrenia should be abandoned34.

Proponents have argued for a new approach that would use the presence of specific neurocognitive deficits to make a diagnosis. These often accompany schizophrenia and take the form of a reduction or impairment in basic psychological functions such as memory, attention, executive function and problem solving. It is these sorts of difficulties, rather than the psychotic symptoms (which can in many cases be controlled by antipsychotic medication), which seem to be the cause of most disability in schizophrenia. However, this argument is relatively new and it is unlikely that the method of diagnosing schizophrenia will change radically in the near future.

The diagnostic approach to schizophrenia has also been opposed by the anti-psychiatry movement, who argue that classifying specific thoughts and behaviours as an illness allows social control of people that society finds undesirable but who have committed no crime. They argue that this is a way of unjustly classifying a social problem as a medical one to allow the forcible detention and treatment of people displaying these behaviours, which is something which can be done under mental health legislation in most western countries.

An example of this can be seen in the former Soviet Union, where an additional sub-classification of sluggishly progressing schizophrenia was created. Particularly in the RSFSR (Russian Soviet Federated Socialist Republic) this diagnosis was used for the purpose of silencing political dissidents or forcing them to recant their ideas by the use of forcible confinement and treatment. In 2000 similar concerns about the abuse of psychiatry to unjustly silence and detain members of the Falun Gong movement by the Chinese government led the American Psychiatric Association's Committee on the Abuse of Psychiatry and Psychiatrists to pass a resolution to urge the World Psychiatric Association to investigate the situation in China.

Western psychiatric medicine tends to favour a definition of symptoms that depends on form rather than content (an innovation first argued for by psychiatrists Karl Jaspers and Kurt Schneider). Therefore, you should be able to believe anything, however unusual or socially unacceptable, without being diagnosed delusional, unless your belief is judged to be held in a particular way. In principle, this would stop people being forcibly detained or treated simply for what they believe. However, the distinction between form and content is not easy, or always possible, to make in practice (see delusion). This had led to accusations by anti-psychiatry, surrealist and mental health system survivor groups that psychiatric abuses exist to some extent in the West as well.


While the reliability of the schizophrenia diagnosis introduces difficulties in measuring the relative effect of genes and environment (for example, symptoms overlap to some extent with severe bipolar disorder or major depression), there is evidence to suggest that genetic vulnerability modified by environmental stressors can act in combination to cause schizophrenia.

A recent review listed seven genes as likely to be involved in the inheritance of schizophrenia or the risk of developing schizophrenia26. Evidence comes from research (such as linkage studies) suggesting multiple chromosomal regions are transmitted to people who are later diagnosed as having schizophrenia. Some family association studies have demonstrated a relationship to a gene known as COMT that is involved in encoding the dopamine catabolic enzyme catechol-O-methyl transferase27. This is particularly interesting because of the known link between dopamine function, psychosis, and schizophrenia.

While highly heritable (some estimates are as high as 70%), schizophrenia is a disorder of complex inheritance (analogous to diabetes or high blood pressure). Thus, several genes interact to generate risk for schizophrenia. Genetic evidence for the role of the environment comes from the observation that identical twins do not universally develop schizophrenia. A recent review of the genetic evidence has suggested a 28% chance of one identical twin developing schizophrenia if the other already has it7.

A study conducted about schizophrenia in twins, carried out for persons in the Finnish Twin Cohort, involving 16,649 like-sexed twin pairs, found a concordance rate for schizophrenia of only 11.0% among monozygotic twins, and only 1.8% among dizygotic twins 37.

There is also considerable evidence indicating that stress may trigger episodes of schizophrenia. For example, emotionally turbulent families8 and stressful life events9 have been shown to be risk factors for relapses or triggers for episodes of schizophrenia. Other factors such as poverty and discrimination may also be involved. This may explain why minority communities have much higher rates of schizophrenia than when members of the same ethnic groups are resident in their home country.

One particularly stable and replicable finding has been the association between living in an urban environment and risk of developing schizophrenia, even after factors such as drug use, ethnic group and size of social group have been controlled for29. A recent study of 4.4 million men and women in Sweden found a 68–77% increased risk of psychosis for people living in the most urbanized environments, a significant proportion of which is likely to be accounted for by schizophrenia30.

One curious finding is that people diagnosed with schizophrenia are more likely to have been born in winter or spring32 (at least in the northern hemisphere). However, the effect is not large and it is still not clear why this may occur.

It is also thought that processes in early neurodevelopment are important, particularly during pregnancy. For example, women who were pregnant during the Dutch famine of 1944, where many people were close to starvation, had a higher chance of having a child who would later develop schizophrenia10. Similarly, studies of Finnish mothers who were pregnant when they found out that their husbands had been killed during the Winter War of 1939–1940 have shown that their children were much more likely to develop schizophrenia when compared with mothers who were found out about their husbands' death before or after pregnancy11, suggesting that even psychological trauma in the mother may have an effect.

In adult life, particular importance has been placed upon the function (or malfunction) of dopamine in the mesolimbic pathway in the brain. This theory, known as the dopamine hypothesis of schizophrenia largely resulted from the accidental finding that a drug group which blocks dopamine function, known as the phenothiazines, reduced psychotic symptoms. These drugs have now been developed further and antipsychotic medication is commonly used as a first line treatment.

However, this theory is now thought to be overly simplistic as a complete explanation. Partly as newer antipsychotic medication (called atypical antipsychotic medication) is equally effective as older medication, but also affects serotonin function and may have slightly less of a dopamine blocking effect. Psychiatrist David Healy has also argued that pharmaceutical companies have promoted certain oversimplified biological theories of mental illness to promote their own sales of biological treatments12.

Much recent research has focused on differences in structure or function in certain brain areas in people diagnosed with schizophrenia.

Early evidence for differences in the neural structure came from the discovery of ventricular enlargement in people diagnosed as schizophrenic, for whom negative symptoms were most prominent35. However, this finding has not proved particularly reliable on the level of the individual person, with considerable variation between patients.

More recent studies have shown a large number of differences in brain structure between people with and without diagnoses of schizophrenia36. However, as with earlier studies, many of these differences are only reliably detected when comparing groups of people, and are unlikely to predict any differences in brain structure of an individual person with schizophrenia.

Studies using neuropsychological tests and brain scanning technologies such as fMRI and PET to examine functional differences in brain activity have shown that differences seem to most commonly occur in the frontal lobes, hippocampus, and temporal lobes13. These differences are heavily linked to the neurocognitive deficits which often occur with schizophrenia, particularly in areas of memory, attention, problem solving, executive function and social cognition.

Incidence and prevalence

Schizophrenia is typically diagnosed in late adolescence or early adulthood. It is found approximately equally in men and women, though the onset tends to be later in women, who also tend to have a better course and outcome.

The lifetime prevalence of schizophrenia is commonly given at 1%; however, a recent review of studies from around the world estimated it to be 0.55%14. The same study also found that prevalence may vary greatly from country to country, despite the received wisdom that schizophrenia occurs at the same rate throughout the world. It is worth noting however, that this may be in part due to differences in the way schizophrenia is diagnosed. The incidence of schizophrenia was given as a range of between 7.5 and 16.3 cases per 100,000 of the population.

Schizophrenia is also a major cause of disability. In a recent 14-country study15, active psychosis was ranked the third most disabling condition after quadriplegia and dementia and before paraplegia and blindness.


The first line treatment for schizophrenia is usually the use of antipsychotic medication. The newer atypical antipsychotic medication (such as olanzapine, risperidone and clozapine) is preferred over older typical antipsychotic medication (such as chlorpromazine and haloperidol), as the atypicals have different side effect profiles, including less frequent development of extrapyramidal side-effects. However, it is still unclear whether newer drugs reduce the chances of developing the rare but potentially life-threatening neuroleptic malignant syndrome.

Atypical antipsychotics have been claimed to have additional beneficial effects on negative as well as positive symptoms. However, the newer drugs are much more costly as they are still within patent, whereas the older drugs are available in inexpensive generic forms. Aripiprazole a drug from a new class of antipsychotic drugs (variously named 'dopamine system stabilizers' or 'partial dopamine agonists') has recently been developed and early research suggests that it may be a safe and effective treatment for schizophrenia16.

Hospitalisation may occur with severe episodes. This can be voluntary or (if mental health legislation allows it) involuntary (called civil or involuntary commitment). Mental health legislation may also allow a person to be treated against their will. However, in many countries such legislation does not exist, or does not have the power to enforce involuntary hospitalisation or treatment.

Psychotherapy or other forms of talk therapy may be offered, with cognitive behavioural therapy being the most frequently used. This may focus on the direct reduction of the symptoms, or on related aspects, such as issues of self-esteem, social functioning, and insight. There have been some promising results with cognitive behavioural therapy, but the balance of current evidence is inconclusive17.

Other support services may also be available such as drop-in centres, visits from members of a 'community mental health team' and patient-led support groups. In recent years the importance of service-user led recovery based movements has grown substantially throughout Europe and America. Groups such as the Hearing Voices Network and more recently, the Paranoia Network, have developed a self-help approach that aims to provide support and assistance outside of the traditional medical model adopted by mainstream psychiatry. By avoiding framing personal experience in terms of criteria for mental illness or mental health, they aim to destigmatise the experience and encourage individual responsibility and a positive self-image.

In many non-Western societies, schizophrenia may be treated with more informal, community-led methods. A particularly sobering thought for Western psychiatry is that the outcome for people diagnosed as schizophrenic in non-Western countries may actually be much better18 than for people in the West. The reasons for this recently discovered fact are still far from clear, although cross-cultural studies are being conducted to find out why. One important factor may be that many non-Western societies (including intact Native American cultures) are collectivist societies, in that they emphasize working together for the good of other society members. This is in contrast to many Western societies, which can be highly individualistic. Collectivist societies tend to stress the importance of the connectedness of extended family, providing a useful support mechanism for the stress that mental illness plays on both the ill and others around them.


Prognosis for any particular individual affected by schizophrenia is particularly hard to judge as treatment and access to treatment is continually changing as new methods become available and medical recommendations change.

However, retrospective studies have shown that about a third of people make a full recovery, about a third show improvement but not a full recovery, and a third remain ill19.

There is an extremely high suicide rate associated with schizophrenia. A recent study showed that 30% of patients diagnosed with this condition had attempted suicide at least once during their lifetime20. Another study suggested that 10% of persons with schizophrenia die by suicide21.

Schizophrenia and drug use

Schizophrenia can sometimes be triggered by heavy use of stimulant or hallucinogenic drugs, although some claim that a predisposition towards developing schizophrenia is needed for this to occur. There is also some evidence suggesting that people suffering schizophrenia but responding to treatment can have relapse as a result of subsequent drug use.

Drugs such as methamphetamine, ketamine, PCP and LSD have been used to mimic schizophrenia for research purposes, although this has now fallen out of favour with the scientific research community, as the differences between the drug induced states and the typical presentation of schizophrenia have become clear.

Hallucinogenic drugs were also briefly tested as possible treatments for schizophrenia by psychiatrists such as Humphry Osmond and Abram Hoffer in the 1950s. Ironically, it was mainly for this experimental treatment of schizophrenia that LSD administration was legal, briefly before its use as a recreational drug led to its criminalization.

There is now increasing evidence that cannabis use can be a contributing trigger to developing schizophrenia. The most recent studies suggest that cannabis is neither a sufficient nor necessary factor in developing schizophrenia, but that cannabis may significantly increase the risk of developing schizophrenia and may be, among others, a significant causal factor31.

It has been noted that the majority of people with schizophrenia (estimated between between 75% and 90%) smoke tobacco. However, people diagnosed with schizophrenia have a much lower than average chance of getting and dying from lung cancer. While the reason for this is unknown, it may be because of a genetic resistance to the cancer, a side-effect of drugs being taken, or a statistical effect of increased likelihood of dying from causes other than lung cancer22. It is argued that the increased level of smoking in schizophrenia may be due to a desire to self-medicate with nicotine. A recent study of over 50,000 Swedish conscripts found that there was a small but significant protective effect of smoking cigarettes on the risk of developing schizophrenia later in life.28 Whilst the authors of the study stressed that the risks of smoking far outweigh these minor benefits, this study provides further evidence for the 'self-medication' theory of smoking in schizophrenia and may gives clues as to how schizophrenia might develop at the molecular level.

Alternative approaches to schizophrenia

An approach broadly known as the anti-psychiatry movement, notably most active in the 1960s has opposed the orthodox medical view of schizophrenia as an illness.

Psychiatrist Thomas Szasz has argued that psychiatric patients are not ill but are just individuals with unconventional thoughts and behaviour that make society uncomfortable. He argues that society seeks to unjustly control such individuals by classifying their behaviour as an illness and forcibly treating them as a method of social control. An important but subtle point is that Szasz has never denied the existence of the phenomena that mainstream psychiatry classifies as an illness (such as delusions, hallucinations or mood changes) but simply does not believe that they are a form of illness.

Similarly, psychiatrist R. D. Laing has argued that the symptoms of what we call mental illness are just reasonable (although perhaps not always obviously comprehensible) reactions to impossible demands that society and particularly family life puts on some individuals. Laing was revolutionary in valuing the content of psychotic experience as worthy of interpretation, rather than considering it simply as a secondary but essentially meaningless marker of underlying psychological or neurological distress.

It is worth noting that neither Szasz nor Laing ever considered themselves to be 'anti-psychiatry' in the sense of being against psychiatric treatment, but simply believed that it should be conducted between consenting adults, rather than imposed upon anyone against their will.

In the 1976 book The Origin of Consciousness in the Breakdown of the Bicameral Mind, psychologist Julian Jaynes proposed that until the beginning of historic times, schizophrenia or a similar condition was the normal state of human consciousness. This would take the form of a "bicameral mind" where a normal state of low affect, suitable for routine activities, would be interrupted in moments of crisis by "mysterious voices" giving instructions, which early people characterized as interventions from the gods. This theory was briefly controversial. Continuing research has failed to either further confirm or refute the thesis.

Psychiatrist Tim Crow has argued that schizophrenia may be the evolutionary price we pay for a left brain hemisphere specialisation for language25. Since psychosis is associated with greater levels of right brain hemisphere activation and a reduction in the usual left brain hemisphere dominance, our language abilities may have evolved at the cost of causing schizophrenia when this system breaks down.

Researchers into shamanism have speculated that in some cultures schizophrenia or related conditions may predispose an individual to becoming a shaman24. Certainly the experience of having access to multiple realities is not uncommon in schizophrenia, and is a core experience in many shamanic traditions. Equally, the shaman may have the skill to bring on and direct some of the altered states of consciousness psychiatrists label as illness. (See anti-psychiatry.)

Alternative medicine tends to hold the view that schizophrenia is primarily caused by imbalances in the body's reserves and absorption of dietary minerals, vitamins, fats, and/or the presence of excessive levels of toxic heavy metals. The body's adverse reactions to gluten are also strongly implicated in some alternative theories (see gluten-free, casein-free diet).

See also

Famous people affected by schizophrenia

Recommended reading

External links


1 Evans, K., McGrath, J., & Milns, R. (2003) ( Searching for schizophrenia in ancient Greek and Roman literature: a systematic review. Acta Psychiatrica Scandanavica, 107(5), 323–330.
2 Kraepelin, E. (1907) Text book of psychiatry (7th ed) (trans. A.R. Diefendorf). London: Macmillan.
3Turner, T. (1999) 'Schizophrenia'. In G.E. Berrios and R. Porter (eds) A History of Clinical Psychiatry. London: Athlone Press. ISBN 0485242117
4Bertelsen, A. (2002) ( Schizophrenia and Related Disorders: Experience with Current Diagnostic Systems. Psychopathology, 35, 89–93.
5Tsuang, M. T., Stone, W. S., & Faraone, S. V. (2000) ( Toward reformulating the diagnosis of schizophrenia. American Journal of Psychiatry, 157(7), 1041–1050.
6Verdoux, H., & van Os, J. (2002) ( Psychotic symptoms in non-clinical populations and the continuum of psychosis. Schizophr Res, 54(1–2), 59–65.
7Torrey, E.F., Bowler, A.E., Taylor, E.H. & Gottesman, I.I (1994) Schizophrenia and manic depressive disorder. New York: Basic books. ISBN 0465072852
8Bebbington, P., Kuipers, L. (1994) ( The predictive utility of expressed emotion in schizophrenia: an aggregate analysis. Psychological Medicine, 24 (3),707–18.
9Day R, Nielsen JA, Korten A, Ernberg G, Dube KC, Gebhart J, Jablensky A, Leon C, Marsella A, Olatawura M et al (1987) ( Stressful life events preceding the acute onset of schizophrenia: a cross-national study from the World Health Organization. Culture, Medicine and Psychiatry, 11 (2), 123–205
10Susser E, Neugebauer R, Hoek HW, Brown AS, Lin S, Labovitz D, Gorman JM (1996) ( Schizophrenia after prenatal famine. Further evidence. Archives of General Psychiatry, 53(1), 25–31.
11Huttunen MO, Niskanen P. (1978) ( Prenatal loss of father and psychiatric disorders. Archives of General Psychiatry, 35(4), 429–31.
12Healy, D. (2002) The Creation of Psychopharmacology. Cambridge, MA: Harvard University Press. ISBN 0674006194
13Green, M.F. (2001) Schizophrenia Revealed: From Neurons to Social Interactions. New York: W.W. Norton. ISBN 0393703347
14Goldner EM, Hsu L, Waraich P, Somers JM (2002) ( Prevalence and incidence studies of schizophrenic disorders: a systematic review of the literature. Canadian Journal of Psychiatry, 47(9), 833–43.
15άstόn TB, Rehm J, Chatterji S, Saxena S, Trotter R, Room R, Bickenbach J, and the WHO/NIH Joint Project CAR Study Group (1999) ( Multiple-informant ranking of the disabling effects of different health conditions in 14 countries. Lancet (, 354(9173), 111–115.
16Potkin SG, Saha AR, Kujawa MJ, Carson WH, Ali M, Stock E, Stringfellow J, Ingenito G, Marder SR (2003) ( Aripiprazole, an Antipsychotic With a Novel Mechanism of Action, and Risperidone vs Placebo in Patients With Schizophrenia and Schizoaffective Disorder. Archives of General Psychiatry, 60(7), 681–90.
17Cormac I, Jones C, Campbell C. (2002) ( Cognitive behaviour therapy for schizophrenia. Cochrane Database of Systematic Reviews, (1), CD000524.
18Kulhara P. (1994) ( Outcome of schizophrenia: some transcultural observations with particular reference to developing countries. European Archives of Psychiatry and Clinical Neuroscience, 244(5), 227–35.
19Harding CM, Brooks GW, Ashikaga T, Strauss JS, Breier A. (1987) ( The Vermont longitudinal study of persons with severe mental illness, II: Long-term outcome of subjects who retrospectively met DSM-III criteria for schizophrenia. American Journal of Psychiatry, 144(6), 727–35.
20Radomsky ED, Haas GL, Mann JJ, Sweeney JA (1999) ( Suicidal behavior in patients with schizophrenia and other psychotic disorders. American Journal of Psychiatry, 156(10), 1590–5.
21Caldwell CB, Gottesman II. (1990) ( Schizophrenics kill themselves too: a review of risk factors for suicide. Schizophrenia Bulletin, 16(4), 571–89.
22"Conditions in Occupational Therapy: effect on occupational performance." ed. Ruth A. Hansen and Ben Atchison (Baltimore: Lippincott Williams & Williams, 2000), 54–74. ISBN 0-683-30417-8
23Psychiatrie. 8. Aufl., Bd. 1: Allgemeine Psychiatrie; Bd. 11: Klinische Psychiatrie, 1. Teil. Barth, Leipzig 1909. Bd. 111, 1913; Bd. IV, 1915. (Translation of section on the disease from the German)
24Polimeni J, Reiss JP. (2002) ( How shamanism and group selection may reveal the origins of schizophrenia. Medical Hypothesis, 58(3), 244–8.
25Crow, T. J. (1997) ( Schizophrenia as failure of hemispheric dominance for language. Trends in Neuroscience, 20(8), 339–343.
26Harrison PJ, Owen MJ. (2003) ( Genes for schizophrenia? Recent findings and their pathophysiological implications. Lancet (, 361(9355), 417–9.
27Shifman S, Bronstein M, Sternfeld M, Pisante-Shalom A, Lev-Lehman E, Weizman A, Reznik I, Spivak B, Grisaru N, Karp L, Schiffer R, Kotler M, Strous RD, Swartz-Vanetik M, Knobler HY, Shinar E, Beckmann JS, Yakir B, Risch N, Zak NB, Darvasi A (2002) ( A highly significant association between a COMT haplotype and schizophrenia. American Journal of Human Genetics, 71(6), 1296–302.
28Zammit S, Allebeck P, Dalman C, Lundberg I, Hemmingsson T, Lewis (2003) ( Investigating the association between cigarette smoking and schizophrenia in a cohort study. American Journal of Psychiatry, 160 (12), 2216–21.
29Van Os J. (2004) ( Does the urban environment cause psychosis? British Journal of Psychiatry, 184 (4), 287–288.
30Sundquist K, Frank G, Sundquist J. (2004) ( Urbanisation and incidence of psychosis and depression: Follow-up study of 4.4 million women and men in Sweden. British Journal of Psychiatry, 184 (4), 293–298.
31Arseneault L, Cannon M, Witton J, Murray RM. (2004) ( Causal association between cannabis and psychosis: examination of the evidence. British Journal of Psychiatry, 184, 110–7.
32Davies G, Welham J, Chant D, Torrey EF, McGrath J. (2003) ( A systematic review and meta-analysis of Northern Hemisphere season of birth studies in schizophrenia. Schizophrenia Bulletin, 29 (3), 587–93.
33McGorry PD, Mihalopoulos C, Henry L, Dakis J, Jackson HJ, Flaum M, Harrigan S, McKenzie D, Kulkarni J, Karoly R. (1995) ( Spurious precision: procedural validity of diagnostic assessment in psychotic disorders. American Journal of Psychiatry, 152 (2), 220–3.
34Read, J. (2004) Does 'schizophrenia' exist ? Reliability and validity. In J. Read, L.R. Mosher, R.P. Bentall (eds) Models of Madness: Psychological, Social and Biological Approaches to Schizophrenia. ISBN 1583919066
35Johnstone EC, Crow TJ, Frith CD, Husband J, Kreel L. (1976) ( Cerebral ventricular size and cognitive impairment in chronic schizophrenia. Lancet, 30;2 (7992), 924-6.
36Flashman LA, Green MF (2004) ( Review of cognition and brain structure in schizophrenia: profiles, longitudinal course, and effects of treatment. Psychiatric Clinics of North America, 27 (1), 1-18, vii.
37Koskenvuo M, Langinvainio H, Kaprio J, Lonnqvist J, Tienari P.(1984) ( Psychiatric hospitalization in twins. Acta Genet Med Gemellol (Roma), 33(2),321-32.

Biotech100 Index
· What are the Requirements to be listed in the Biotech100 Index?
 Biotech100 list of companies
· Pipeline drugs for the Biotech100

Clinical Trials
· What is a Clinical Trial?
·Phase I ,-- Phase II, -- PhaseIII
·What is Randomized Control?
 What is a Double Blind Experiment?
·What is the role of the FDA?

Investing in Stocks
· Small Cap Stocks
· Stocks and Bonds
· Biotech100 Index

Sponsored Links

Careers and Employment
· Biotechnology and Pharmaceutical
· What are the Fastest Growing Careers?

Key Biotech Terms


All text is available under the terms of the GNU Free Documentation License (see Copyrights for details). Disclaimers. Wikipedia is powered by MediaWiki, an open source wiki engine..

Copyright © 2005 BIOTECH100.COM. All rights reserved.