Some 'presumed' causes of Schizophrenia and/or Psychosis

During the course of my wanderings over the past few years I have come across a number of presumed causes of schizophrenia and/or psychosis. I thought it would be informative to compile a list of all presumed causes.

Should you be aware of a "cause" that's not yet been included, do feel free to chime in. If possible, I suggest you link to an article that backs the claim of the cause.

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Music of the Hour:

Cause: Cat Poop

Pet Theory: Do Cats Cause Schizophrenia?

"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."

[...]

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."

[...]

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."

Read the full article here: Pet Theory - Do Cats Cause Schizophrenia

Cause: Milk

Got Schizophrenia?

University of Florida researchers reported in the March 1999 issue of the journal Autism findings from two novel animal studies indicating autism and schizophrenia may be linked to an individual's inability to properly break down a protein found in milk.

The digestive problem might actually lead to the disorders' symptoms, whose basis has long been debated, said UF physiologist Dr. J. Robert Cade. Further research is needed before scientists have a definitive answer. When not broken down, the milk protein produces exorphins, morphine-like compounds that are then taken up by areas of the brain known to be involved in autism and schizophrenia, where they cause cells to dysfunction.

The animal findings suggest an intestinal flaw, such as a malfunctioning enzyme, is to blame, says Cade, whose team also is putting the theory to the test in humans. Preliminary findings from that study - which showed 95 percent of 81 autistic and schizophrenic children studied had 100 times the normal levels of the milk protein in their blood and urine - have been presented at two international meetings in the past year but have not yet been published.

When these children were put on a milk-free diet, at least eight out of 10 no longer had symptoms of autism or schizophrenia, says Cade, a professor of medicine and physiology at UF's College of Medicine and inventor of the Gatorade sports drink. His research team includes research scientist Dr. Zhongjie Sun and research associate R. Malcolm Privette.

"We now have proof positive that these proteins are getting into the blood and proof positive they're getting into areas of the brain involved with the symptoms of autism and schizophrenia," Cade said.

Read the full article here: Milk, Autism &amp; Schizophrenia

Cause: Demon Possession:

Can people be possessed by evil spirits?

Channel 4 seems to think so, and next week plans to broadcast "as live" the exorcism of a young man who says he is possessed by evil.

Scientists intend to monitor the man's brain with electrodes to see whether the procedure has any measurable effect.

Even within the Church of England, the idea of possession raises eyebrows. "The number of metaphysical assumptions it makes is quite incredible. It means there are such things as non-human evil spirits that can take possession of a human being and require to be told to go somewhere else by a greater power," says Canon Michael Perry, who holds a doctorate in deliverance and edits the Christian Parapsychologist.

"Some Christians believe it happens frequently - they see demons under every rug and will perform exorcisms at the drop of a hat. My view is possession is very rare."

Look back over case histories of supposed possessions and it's often easy to identify a real psychiatric condition, says Christopher French, who heads the anomalistic psychology research unit at Goldsmith's College in London.

"Epilepsy, Tourette's syndrome and some forms of schizophrenia have all been labelled as possessions in the past," he adds.

Read the full article here: <a href=http://www.guardian.co.uk/life/thisweek/story/0,12977,1415683,00.html>The Guardian</a>

Cause: Trauma

The psychiatric establishment is about to experience an earthquake that will shake its intellectual foundations. When it has absorbed the juddering contents of the latest edition of one of its leading journals, Acta Psychiatrica Scandinavica, it will have to rethink many of its most cherished assumptions. Not since the publication of RD Laing's book Sanity, Madness and the Family, in 1964, has there been such a significant challenge to their contention that genes are the main cause of schizophrenia and that drugs should be the automatic treatment of choice.

With his colleagues, guest editor John Read (whose name I shall use as a generic term for this body of evidence), a leading New Zealand psychologist, slays these sacred biological cows. The fact that some two-thirds of people diagnosed as schizophrenic have suffered physical or sexual abuse is shown to be a major, if not the major, cause of the illness. Proving the connection between the symptoms of post-traumatic stress disorder and schizophrenia, Read shows that many schizophrenic symptoms are directly caused by trauma.

The cornerstone of Read's tectonic plate-shifting evidence is the 40 studies that reveal childhood or adulthood sexual or physical abuse in the history of the majority of psychiatric patients (see, also, Read's book, Models of Madness). A review of 13 studies of schizophrenics found rates varying from 51% at the lowest to 97% at the highest.

Read the full article here: The Guardian

Cause: Lack of Sunlight/Vitamin D

Studies have indicated that children who born during certain times of the year (winter and early spring) have a higher than normal incidence of schizophrenia.

According to an article in the New Scientist magazine, research suggests people who develop schizophrenia in Europe and North America are more likely to be born in the winter and early spring (February and March in the Northern Hemisphere) In other words, the subjects who were born during these months had a slightly higher than average rate of schizophrenia, while subjects born in August and September had a slightly lower than average rate. There seems to be about a 10% difference in risk of schizophrenia between the high (Winter and Spring) and low risk months of birth.

One possible reason for the association between winter/spring births and schizophrenia may be related to sunlight exposure. A lack of sunlight (for example, during the shorter days of winter) can lead to vitamin D deficiency, which scientists believe could alter the development of a child's brain in the mother's womb and after birth.

Read the full article here: Low Sunlight Exposure/Vitamin D deficiency is associated with higher risk of schizophrenia

Cause: Marijuana

Reefer Madness:
A pair of articles in the Canadian Journal of Psychiatry has resurrected the "reefer madness" argument about marijuana and its links to mental illness.

Cannabis use can trigger schizophrenia in people already vulnerable to the mental illness -- and this fact should shape marijuana policy, argue two psychiatric epidemiologists in this month's journal.

The link between marijuana use and schizophrenia is generally accepted in the psychiatric community. The problem is that the vulnerable population -- mostly teenagers -- generally isn't eager to absorb the message.

Australian epidemiologists Louisa Degenhardt and Wayne Hall reviewed eight international studies of teens and young adults that examined the link between marijuana use and schizophrenia. They concluded using marijuana can precipitate schizophrenia in users who have a personal or family history of schizophrenia.

[b]Read the full article here: Journal articles link marijuana to schizophrenia

Cause: Niacin Deficiency

... We decided to tackle the most important single problem, schizophrenia. Half of our mental hospital beds were occupied by these patients, and one quarter of all hospital beds in Canada were these patients. But there were very few tangible leads. Psychoanalysis was sweeping into North American psychiatry, and the biological psychiatrists were facing imminent defeat in their views about the nature of this disease.

Dr. Osmond and Dr. J. Smythies had discovered that the mescaline experience resembled the schizophrenic experience, and he and Smythies postulated that there might be a substance in the body with the properties of mescaline and related to adrenalin. Dr. Osmond and I developed this idea, which became known as the adrenochrome hypothesis of schizophrenia.

[...]

Arising from this research are the following discoveries: (1) That adrenochrome is an hallucinogen, (2) that it could be made in the body. It is now known to be present and easily measured. (3) That megadoses of vitamin B-3 and ascorbic acid were therapeutic for schizophrenia. This was one of the roots of orthomolecular psychiatry and medicine as it is known today. (4) That niacin lowers cholesterol levels. This vitamin is now one of the world's standard materials for doing so. It also extends life and does not increase deaths from violent acts as some of the other compounds which lower cholesterol do. (5) The HOD (Hoffer-Osmond Diagnostic) and EWI tests for assisting in the diagnosis of schizophrenia. This is an excellent test, hardly known to the profession.

Read the full article: About Abram Hoffer M.D.

Cause: Stress

Stress may cause highly activated mythic images to erupt from the psyche's deepest levels in the form of turbulent visionary experience. Depending on whether the interactions between the individual and the immediate surroundings lean toward affirmation or invalidation, comprehension of these visions can turn the visionary experience into a step in growth or into a disorder, as an acute psychosis. Based on his clinical and scholarly investigations, John Weir Perry has found and formulated a mental syndrome which, though customarily regarded as acute psychosis, is in actuality a more natural effort of the psyche to mend its imbalances. If the upset is received in the spirit of empathy and understanding, and allowed to run its course, an acute episode can be found to reveal a self-organizing process that has self-healing potential.

Source: <a href=http://www.sunypress.edu/details.asp?id=53985</a>Trials of the Visionary Mind</a>

Cause: Caffeine

Nearly 80% of the world's population uses caffeine, and 25% of the population is diagnosed with a mental disorder. Clinical studies indicate that there may be significant overlap between those figures, and that many people diagnosed as mentally ill are in fact merely suffering from caffeine poisoning. Caffeine also exacerbates the symptoms of patients suffering from organic, non-caffeine-induced mental illness.

As a small, lipid-soluble molecule (like alcohol, nicotine, and certain antidepressants), caffeine is one of the few substances capable of penetrating the blood-brain barrier, which is critical to maintaining cerebral homeostasis. Once it has penetrated this barrier, it is capable of affecting its victims' thoughts and behavior, sometimes to an alarming degree.

Because self-awareness is one of the first casualties of a toxic brain, caffeinism victims may not even suspect they are ill or (if they do) that caffeine is at the root of their symptoms.

It is the purpose of this site to alert the public to the dangers of caffeine intake, and to urge the medical community to eliminate caffeine from patients’ diets before diagnosing them with psychiatric disorders including anxiety, ADD/ADHD, mania, depression, personality disorder and schizophrenia.

Read more here: The Caffeine Web

Cause: Dopamine Dysfunction

Many studies have investigated the possible role of brain neurotransmitters in the development of schizophrenia. Most of these studies have focused on the neurotransmitter called dopamine. The "dopamine theory of schizophrenia" states that schizophrenia is caused by an overactive dopamine system in the brain. There is strong evidence that supports the dopamine theory, but there are also some data that do not support it:

Evidence FOR the Dopamine Theory of Schizophrenia:<blockquote>[*] Drugs that block dopamine reduce schizophrenic symptoms. [*] Drugs that block dopamine have side effects similar to Parkinson's disease. Parkinson's disease is caused by a lack of dopamine in a parts of the brain called the basal ganglia. [*] The best drugs to treat schizophrenia resemble dopamine and completely block dopamine receptors. [*] High doses of amphetamines cause schizophrenic-like symptoms in a disorder called "amphetamine psychosis." Amphetamine psychosis is a model for schizophrenia because drugs that block amphetamine psychosis also reduce schizophrenic symptoms. Amphetamines also make the symptoms of schizophrenia worse. [*] Children at risk for schizophrenia may have brain wave patterns similar to adults with schizophrenia. These abnormal brain wave patterns in children can be reduced by drugs that block dopamine receptors.</blockquote>

Evidence AGAINST the Dopamine Theory of Schizophrenia:<blockquote>[*] Amphetamines do more than increase dopamine levels. They also alter other neurotransmitter levels. [*] Drugs that block dopamine receptors act on receptors quickly. However, these drugs sometimes take many days to change the behavior of people with schizophrenia. [*] The effects of dopamine blockers may be indirect. These drugs may influence other systems that have more impact on the schizophrenic symptoms. [*] New drugs for schizophrenia, for example, clozapine, block receptors for both serotonin and dopamine.</blockquote>

Read more here: Schizophrenia

Cause: Neuroleptics

Mad in America

In 1998 ... the University of Pennsylvania did an MRI study in which they studied people placed on neuroleptics. They found that indeed the brains of those people so treated started showing changes in brain volumes. So you start seeing a shrinkage of the frontal lobes and an enlargement of the basal ganglia.

So now we're seeing morphological changes in the brain. And here's the clincher: They found that those volume changes in the brain were associated with a worsening of the target symptoms. So the puzzle now all comes together, doesn't it? It fits with the World Health Organization's study. It tells you why people are becoming chronic -- because you're giving them an agent that causes an abnormality in brain function, that causes changes in the brain that lend themselves to greater psychosis.

Read the full article here: Interview: Robert Whitaker

Cause: Lack of Polyunsaturated fatty acid

BACKGROUND: Limited evidence gives support to an hypothesis suggesting that the symptoms of schizophrenia may result from altered neuronal membrane structure and metabolism. The latter are dependent on blood plasma levels of certain essential fatty acids (EFAs) and their metabolites. Several studies have shown those with schizophrenia often have low levels of the particular EFAs necessary for normal nerve cell membrane metabolism.

OBJECTIVES: To review the effects of supplementing standard antipsychotic treatment with polyunsaturated fatty acids, whether essential (EFAs) or non-essential, for those with schizophrenia and, in recent updates to also evaluate the effects of EFA's as a sole antipsychotic treatment. To evaluate the relative efficacy of different types of fatty acid supplementation.

[...]

MAIN RESULTS: Four relatively small trials (total n=204) showed low levels of loss to follow up and adverse effects for those taking essential fatty acids. Early results from a few trials suggest a positive effect of eicosapentaenoic acid (EPA) over placebo for scale-derived mental state outcomes. The data, however, is limited making these results difficult to analyse and interpret with confidence. A single small study (n=30) investigated the value of using EPA as sole treatment for people hospitalised for relapse. Results suggest that EPA may help one third of people avoid instigation of standard antipsychotic drugs for 12 weeks (RR 0.6, CI 0.4-0.91). There were no clear effects of primrose oil (omega-6) EFA supplementation.

REVIEWER'S CONCLUSIONS: All data are preliminary, but results look encouraging for fish oil. EPA does not seem harmful, may be acceptable to people with schizophrenia and have moderately positive effect. A further trial is soon to be reported from the USA and more are underway or planned in the South Africa and Norway. Considering that EPA may be an acceptable intervention, large, long simple studies reporting clincially meaningful data should be anticipated.

Source: Polyunsaturated fatty acid (fish or evening primrose oil) for schizophrenia.

Cause: Genetics

Heredity and the Genetics of Schizophrenia

... schizophrenia definitely has a very significant genetic component. Those who have a third degree relative with schizophrenia are twice as likely to develop schizophrenia as those in the general population. Those with a second degree relative have a several-fold higher incidence of schizophrenia than the general population, and first degree relatives have an incidence of schizophrenia an order of magnitude higher than the general populace.

It is of much interest, though, that the correlation of schizophrenia between identical twins, who have identical genomes, is less than one-half. This indicates that schizophrenia is NOT entirely a genetic disease.

The current belief is that there are a number of genes that contribute to susceptibility or pathology of schizophrenia, but none exhibit full responsibility for the disease. It is believed that schizophrenia is much like cancer, which is caused by a number of genetic and environmental factors.

Read the full article here: Heredity and the Genetics of Schizophrenia

Cause: Social Environment

A familial vulnerability to schizophrenia is agreed even though the exact genes involved seem elusive. But despite epidemiological evidence showing different rates of schizophrenia in sociocultural groups that would be considered genetically similar, the causal role of the environment is still hotly contested. Many service users, social scientists and clinicians are convinced that social factors cause schizophrenia and, therefore, that behavioural or environmental change might offer a more tangible route to prevention than gene manipulation. However, a comparison of the monies given to research into the genetics and the social aetiology of schizophrenia would suggest that funders of research are not convinced. For instance, the Medical Research Council, Wellcome Trust and UK Department of Health have launched Biobank, billed as the largest ever study of nature and nurture. The aim is to investigate complex interactions between genes, lifestyle and the environment. Half a million people between the ages of 45 and 69 will be asked to take part. Unfortunately, the generally earlier onset of schizophrenia will mean that it will be difficult to research in this illness. Would we have benefited from a Biobank for 16- to 25-year-olds?

Is there evidence that social factors cause schizophrenia and, if there is, does it negate or complement the theory that schizophrenia is a genetic illness? We asked Professor Jim van Os from Maastricht University, one of Europe's top social psychiatry researchers, and Professor Peter McGuffin, a psychiatrist and geneticist who heads the Social, Genetic and Developmental Psychiatry Research Centre at the Institute of Psychiatry, London, to debate the question: Can the social environment cause schizophrenia?

Read the full article here: Can the social environment cause schizophrenia?

Cause: Shamanic Calling

Shamanism is humanity's oldest religion and healing art, dating back to the Paleolithic era. Originally, the word shaman referred specifically to healers of the Tungus people of Siberia. In recent times, that name has been given to healers in many traditional cultures around the globe who use consciousness altering techniques in their healing work.

Historically, shamanism has been confused with schizophrenia by anthropologists because shamans often speak of altered state experiences in the spirit world as if they were "real" experiences. While the shaman and the person in a psychotic episode both have unusual access to spiritual and altered state experiences, shamans are trained to work in the spirit world, while the psychotic person is simply lost in it.

But in many traditional cultures, psychotic episodes have served as an initiatory illness that calls a person into shamanism. Mircea Eliade writes:<blockquote>The future shaman sometimes takes the risk of being mistaken for a "madman". . .but his "madness" fulfills a mystic function; it reveals certain aspects of reality to him that are inaccessible to other mortals, and it is only after having experienced and entered into these hidden dimensions of reality that the "madman" becomes a shaman. (Mircea Eliade. Myths, Dreams, and Mysteries. New York: Harper and Row, 1960. Page 80-81)</blockquote>
As the person accepts the calling and becomes a shaman, their illness usually disappears. The "self-cure of a psychosis" is so typical of the shaman that some anthropologists have argued that anyone without this experience should be described only as a healer. The concept of the "wounded healer" addresses the necessity of the shaman-to-be entering into extreme personal crisis in preparation of his/her role in the community as a healer (Halifax, Joan. Shamanic Voices. New York: Dutton, 1979).

Read the full article here: Shamanic Crisis

Cause: Attempt at Self-Healing

Over half a century ago in Küsnacht, Switzerland, the psychiatrist Carl Gustav Jung came to feel that psychological health is a dynamic, on-going process of personal development into greater maturity and spiritual awareness. This process – which he called individuation – is, he said, nourished by a continuous flow of symbolic insights transmitted from the unconscious Self to the conscious Ego, in a variety of ways including dreams, insight, and flashes of intuition. Should this inner communication flow get blocked for any reason, one may find oneself increasingly frustrated, for the simple reason that one has lost touch with the built-in guiding system of one's deeper Self.

In Jung's view, if such a blockage persists in time, one becomes alienated – in the sense that one may no longer be able to use the considerable resources of one's innate common sense to adapt effectively to one's social environment. Alienation, of course, also happens on a collective level within the family, society, and civilisation, in which case the context one may have trouble adapting to includes not only the social, but the ecological environment as well. Whether individual or collective, a chronic blockage of the psyche's inner communications process may lead beyond a mere sense of ennui, and eventually jeopardise the ability to be responsible for one's health and survival.

What really took Jung's colleagues by surprise, however, was his declaration that the so-called acute schizophrenic break phenomenon is actually no disease, but rather a natural (and temporary!) healing process – which automatically activates itself in response to the underlying blockage which I have just described. Jung maintained that the spontaneous onset of the visionary state of consciousness is nature's self-organising way for the alienated psyche to become whole again. In his view, when the Ego has become cut off from the rest of the psyche to a point of real distress, the Self "comes to the rescue" through a temporary, but complete overpowering of the conscious personality by means of a vivid upwelling of hallucinatory voices and visions from the deeper levels of the unconscious. The conscious Ego, that is, falls apart and comes back together again, renewed. If one understands the essentially life-affirming nature of the visions which occurs during this metamorphosis, appreciates their symbolic relevance to the problems at hand, and integrates their deeper meaning, the result is a healing of the alienated condition which prevailed before the onset of the so-called illness itself – and a rebirth of the personality as a more integrated, invigorated whole.

Read the full article here: The Inner Apocalypse

Cause: Cultural Memes & Mutations

1. Liane Gabora's (1998) target article is a systematic attempt to draw together knowledge from different fields to answer the question of the origin of culture, offering some important suggestions. Several elements in Gabora's article draw upon the most recent discoveries in neuroscience. I will now dwell on one particular point which has especially significant implications.

2. According to Gabora, the origin of culture may be defined as "the bootstrapping of a system by which information patterns self-replicate, (leading to) the selective proliferation of some variants of these self-replicating patterns over others." In this context the term "meme" is used to refer to a unit of cultural information as represented in the brain.

3. It is evident that each meme must coincide with the set of neurons which expresses it. In Gabora's paper, the mind is described as a structure used to filter the flow of memes (i.e. of organized neuronal discharges) on the basis of internal and external cues able to activate these specific sets of neurons.

4. Gabora refers to "myths" about the origin of human culture (Donald, 1991), which hypothesize that "in the beginning" there existed a totally "episodic" mind, i.e. one able to manage only memories linked to immediate stimuli (not only environmental, but also bodily: hunger, thirst, etc.).

5. From this chaos of episodic (and therefore ephemeral) events was born a mind organized in such a manner as to allow it to evoke informational units (memes) even in the absence of external stimuli, it was able to have abstract thoughts, and therefore make associations on a second level (between actual stimuli and representations of stimuli; then between these and representations of the associations themselves, or even between these other stimuli or representations of stimuli, whether past or present).

6. The birth of this "memetic" mind is attributed to a genetic mutation, and it is hard to imagine that it could have arisen in any other way. Such a mutation would have modified the threshold of filtering of the association between information units. As a consequence, memes which would otherwise be filtered out of the operational memory (consciousness?) gain access to this sector of the mind, bringing into operation other memes in a cycle which can lead to creative (i.e. innovative) associations, but also to severe behavioural problems.

7. Gabora refers to neurobiological models of schizophrenia to illustrate the consequences of her hypothesis. Many hypotheses about schizophrenia indeed suggest that a deficit in the systems involved in information-processing could contribute to the symptomatology of the disorder (McGhie & Chapman, 1961; Hansefus & Magaro, 1976; Braff & Geyer, 1990; Cornblatt & Kellp, 1994). Such a deficit could be expressed in a severe behavioural disorder, but it could also favour creative associations between information units (Hansefus & Magaro, 1976; Preti & Miotto, 1997). Many studies have explored the propensity toward innovation and originality in people suffering from psychoses (Arieti, 1974; Preti & Miotto, 1997). This psychosis-linked creative ability is evident in the arts and in language, but is also seen in the sciences and even in extremely abstract disciplines such as mathematics (Hayes, 1998).

Read the full article here: Creativity, Genetics and Mental Illness

Cause: Double-Bind Theory & The Family

Bateson et al. (1956) proposed that schizophrenic symptoms are an expression of social interactions in which the individual is repeatedly exposed to conflicting injunctions, without having the opportunity to adequately respond to those injunctions, or to ignore them (i.e., to escape the field). For example, if a mother tells her son that she loves him, while at the same time turning her head away in disgust, the child receives two conflicting messages about their relationship on different communicative levels, one of affection on the verbal level, and one of animosity on the nonverbal level. It is argued that the child's ability to respond to the mother is incapacitated by such contradictions across communicative levels, because one message invalidates the other. Because of the child's vital dependence on the mother, Bateson et al. argue that the child is also not able to comment on the fact that a contradiction has occurred, i.e., the child is unable to metacommunicate (Bateson et al., 1956).

The symptomatology of schizophrenia, it is argued, reflects the accommodation of the individual to a prolonged exposure to such interactions. Once 'victims' have learned to perceive their universe in terms of contradictory environmental input, the inability to respond effectively to stimuli from the environment is no longer contingent on the extent to which stimuli from the environment are contradictory in specific interactive sequences. Instead, the individual will generally experience any input from the environment as conflicting information without being able to discriminate between different communicative levels. In the long run, this inability manifests itself as typically schizophrenic symptoms such as flattened affect, delusions and hallucinations, and incoherent thinking and speaking (Bateson et al., 1956).

It is further stipulated by Bateson et al. (1956) that double bind interactions have a pathogenic effect only if they occur in a context where the accurate discrimination of messages is of vital importance for the participants, and in a relational context which is characterized by intense levels of involvement between the participants. The interaction between parents and children within the nuclear family is a typical example of such a relational context.

Read the full article here: Schizophrenia and the Family: Double Bind Theory Revisited

Cause: Brain Trauma

... Malaspina and her colleagues zeroed in on some 600 individuals who had at least two first-degree relatives with schizophrenia, that is, they were persons who were presumably at genetic risk of schizophrenia. In fact, some of the study subjects had schizophrenia themselves. Data about these subjects had been collected as part of the National Institute of Mental Health Genetics Initiative for Schizophrenia and Bipolar Disorders—a cooperative project involving six university sites. Malaspina and her team then used the data that had been collected to see whether they could find any link between brain injury and schizophrenia. They could, they report.

For example, when they compared the rates of brain injury for subjects who had been diagnosed with schizophrenia with those who had not, they found a threefold increase in head-injury rates among those with schizophrenia.

One might ask, of course, whether the link between head injury and schizophrenia was due to schizophrenia’s causing head injury, not the other way around. Malaspina and her colleagues do not believe, however, that this was the case.

One reason, she explained to Psychiatric News, is that whereas the analysis included head injuries both before and after schizophrenia, "if you restricted it to head injuries before illness, you saw the same thing. Head injury before illness increased the risk."

Another reason Malaspina and her coworkers believe that head injury is a risk factor for schizophrenia is that they not only analyzed data from the approximately 600 subjects who were part of the schizophrenia pedigree group, but also compared those data with data from some 1,300 persons who had at least two first-degree relatives with bipolar disorder and who were thus presumably at genetic risk for that disorder. When the researchers compared the rate of brain injury in the schizophrenia pedigree with that in the bipolar group, they found that the rate was significantly higher in the former. In the researchers’ view, this finding implies that a genetic predisposition to schizophrenia may also be capable of predisposing a person to head injury.

But how might a genetic predisposition to schizophrenia open a person to risk of head injury? Malaspina and her team offered a possible explanation: "Schizophrenia genes may increase exposure to head trauma, with head trauma further increasing the risk for schizophrenia."

And how might schizophrenia genes increase exposure to head trauma? Malaspina and her colleagues proffer a possible explanation here as well: Schizophrenia genes could code for difficulty paying attention, and inattention in turn could open a person to accidents and head injury. Indeed, difficulty paying attention has long been noted as one of the symptoms of schizophrenia. In fact, it may be not only a vulnerability factor for schizophrenia, but also one of the earliest indicators of the disease ...

Read the full article here: <a href=http://pn.psychiatryonline.org/cgi/content/full/36/7/37</a>Head Injury May Tip Schizophrenia Scales</a>