what factors cause schizophrenia?

Question

is schizophrenia inborn/genetic, is it environmental, does diet play a part, or are there other factors? is it a combination of several stressors? i won't ask if it is a figment of the sufferer's imagination though, as i used to think that till i came down with it, thinking work would cure me, and it didn't! schizophrenia is so real it's unreal, believe me, and it's generally scarier for the sufferer than the people witnessing the sufferer's distress.

i ask these questions in the hope of promoting understanding, and tackling the stigma attached to schizophrenia.

love and peace, swot xxx

Answer 1

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 and environmental stressors can act in combination to cause schizophrenia12.

The extent to which these factors influence the likelihood of being diagnosed with schizophrenia is debated widely, and currently, controversial. Schizophrenia is likely to be a disorder of complex inheritance (analogous to diabetes or high blood pressure). Thus, it is likely that several genes interact to generate risk for schizophrenia75. This, combined with disagreements over which research methods are best, or how data from genetic research should be interpreted, has led to differing estimates over genetic contribution.

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Genetic
There is substantial evidence that schizophrenia has a heritable component (some estimates are as high as 80%). However, current research suggests that environmental factors play a significant role in the expression of any genetic disposition towards schizophrenia (i.e. if one has the genes that increase risk, this will not automatically result in schizophrenia later in life). A recent review of the genetic evidence has suggested a 28% chance of one identical twin developing schizophrenia if the other already has it9 (see twin studies). However, the estimates of heritability of schizophrenia from twin studies varies a great deal, with some notable studies10 11 showing rates as low as 11.0%–13.8% among monozygotic twins, and 1.8%–4.1% among dizygotic twins.

A recent review of linkage studies listed seven genes as likely to be involved in the inheritance of schizophrenia or the risk of developing the disease.12 Evidence comes from research suggesting multiple chromosomal regions are transmitted to people who are later diagnosed as having schizophrenia. Genetic association studies have suggested some strong candidate genes which may contribute to risk for developing schizophrenia.75 The strongest evidence points towards genes called COMT (involved in encoding the dopamine catabolic enzyme catechol-O-methyl transferase,13) dysbindin (DTNBP1) and neuregulin-1 (NRG1).

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Environmental
There is considerable evidence indicating that stressful life events cause or trigger schizophrenia.15 Childhood experiences of abuse or trauma have also been implicated as risk factors for a diagnosis of schizophrenia later in life.16 17 18

There is also consistent evidence that negative attitudes towards individuals with (or with a risk of developing) schizophrenia can have a significant adverse impact. In particular, critical comments, hostility, and intrusive or controlling attitudes (termed 'high expressed emotion' by researchers) from family members have been found to correlate with a higher risk of relapse in schizophrenia across cultures.70 It is not clear whether such attitudes play a causal role in the onset of schizophrenia. The research has focused on family members but also appears to relate to professional staff in regular contact with clients.71 While initial work addressed schizophrenia, these attitudes have also been found to play a significant role in other mental health problems.66 This approach does not blame 'bad parenting' or staffing, but addresses the attitudes, behaviors and interactions of all parties.

Factors such as poverty and discrimination also appear to be involved in increasing the risk of schizophrenia or schizophrenia relapse, perhaps due to the high levels of stress they engender. Racism in society, including in diagnostic practices, and/or the stress of living in a different culture, may explain why minority communities have shown higher rates of schizophrenia than members of the same ethnic groups resident in their home country. The "social drift hypothesis" suggests that the functional problems related to schizophrenia, or the stigma and prejudice attached to them, can result in more limited employment and financial opportunities, so that the causal pathway goes from mental health problems to poverty, rather than, or in addition to, the other direction.

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 for.19 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 schizophrenia.20

One curious finding is that people diagnosed with schizophrenia are more likely to have been born in winter or spring21 (at least in the northern hemisphere). However, the effect is not large and it is still not clear why this may occur.

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Neurobiological influences
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Early neurodevelopment
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 schizophrenia22. 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 found out about their husbands' death after pregnancy23, suggesting that even psychological trauma in the mother may have an effect. Furthermore, there is now significant evidence that prenatal exposure to infections increases the risk for developing schizophrenia later in life, providing additional evidence for a link between developmental pathology and risk of developing the condition.73

Some researchers have proposed that environmental influences during childhood also interact with neurobiological risk factors to influence the likelihood of developing schizophrenia later in life. The neurological development of children is considered sensitive to features of dysfunctional social settings, such as trauma, violence, lack of warmth in personal relationships and hostility. These have all been found to be risk factors for the later development of schizophrenia. It is thought that the effects of the childhood environment, favorable or unfavorable, interact with genetics and the processes of neurodevelopment, with long-term consequences for brain function. This is thought to influence the underlying vulnerability for psychosis later in life, particularly during the adult years.24


Data from a PET study25 suggests the less the frontal lobes activated (red) during a working memory task, the greater the increase in abnormal dopamine activity in the striatum (green), thought to be related to the neurocognitive deficits in schizophrenia.[edit]
Role of dopamine
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 because newer antipsychotic medication (called atypical antipsychotic medication) is equally effective as older medication (called typical antipsychotic 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 treatments.26

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Role of glutamate and the NMDA receptor
Interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in the development of schizophrenia. This theory has largely been suggested by abnormally low levels of glutamate receptors found in postmortem brains of people previously diagnosed with schizophrenia27 and the discovery that the glutamate blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition.59 The fact that reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function and that glutamate can affect dopamine function, all of which have been implicated in schizophrenia, have suggested the glutamate hypothesis of schizophrenia as an increasingly popular explanation.28 Further support of this theory has come from trials showing the efficacy of molecules, which are coagonists at the NMDA receptor complex, in reducing schizophrenic symptoms. The precursors D-serine, glycine, and D-cycloserine all enhance NMDA function through the glycine co-agonist site. Several placebo controlled trials have shown a reduction mainly in negative symptoms with high dose therapy.60 Currently type 1 glycine transporter inhibitors are in late-state preclinical for the treatment of schizophrenia. They increase glycine concentrations in the brain thus causing increased NMDA receptor activation and a reduction in symptoms.61

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Anatomy and physiology of the brain
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 with schizophrenia, for whom negative symptoms were most prominent29. However, this finding has not proved particularly reliable on the level of the individual person, with considerable variation between patients. A letter to the editor of the American Journal of Psychiatry links ventricular enlargement with exposure to antipsychotic drugs [1].

More recent studies have shown a large number of differences in brain structure between people with and without diagnoses of schizophrenia.30 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 imaging 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 lobes31. 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.

Electroencephalograph (EEG) recordings of persons with schizophrenia performing perception oriented tasks showed an absence of gamma band activity in the brain, indicating weak integration of critical neural networks in the brain.32 Those who experienced intense hallucinations, delusions and disorganized thinking showed the lowest frequency synchronization. None of the drugs taken by the persons scanned had moved neural synchrony back into the gamma frequency range. Gamma band and working memory alterations may be related to alterations in interneurons that produced the neurotransmitter GABA. Alterations in a subclass of GABAergic interneurons which produce the calcium binding protein parvalbumin have been shown to exist in the DLPFC in schizophrenia. 33

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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. Although rare, there are also instances of childhood onset schizophrenia and late-onset schizophrenia that occurs in the elderly.

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%34. 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 year per 100,000 population.

Schizophrenia is also a major cause of disability. In a recent 14-country study35, active psychosis was ranked the third most disabling condition after quadriplegia and dementia and before paraplegia and blindness.

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Treatment
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Medication and hospitalization
The first line pharmacological therapy for schizophrenia is usually the use of antipsychotic medication 72. The concept of 'curing' schizophrenia is controversial as there are no clear criteria for what might constitute a cure, although some criteria for the remission of symptoms have recently been suggested63. Therefore, antipsychotic drugs are only thought to provide symptomatic relief from the positive symptoms of psychosis. The newer atypical antipsychotic medications (such as clozapine, risperidone, olanzapine, quetiapine, ziprasidone and aripiprazole) are usually preferred over older typical antipsychotic medications (such as chlorpromazine and haloperidol) due to their favorable side-effect profile. Compared to the typical antipsychotics, the atypicals are associated with a lower incident rate of extra pyramidal side-effects (EPS) and tardive dyskinesia (TD) although they are more likely to induce weight gain and so increase risk for obesity-related diseases62. It is still unclear whether newer drugs reduce the chances of developing the rare but potentially life-threatening neuroleptic malignant syndrome (NMS). While the atypical antipsychotics are associated with less EPS and TD than the conventional antipsychotics, some of the agents in this class (especially olanzapine and clozapine) appear to be associated with metabolic side effects such as weight gain, hyperglycemia and hypertriglyceridemia that must be considered when choosing appropriate pharmacotherapy.

Atypical and typical antipsychotics are generally thought to be equivalent for the treatment of the positive symptoms of schizophrenia. It has been suggested by some researchers that the atypicals have some beneficial effects on negative symptoms and cognitive deficits associated with schizophrenia, although the clinical significance of these effects has yet to be established. However, recent reviews have suggested that typical antipsychotics, when dosed conservatively, may have similar effects to atypicals.36 The atypical antipsychotics are much more costly as they are still within patent, whereas the older drugs are available in inexpensive generic forms. Aripiprazole is a drug from a new class of antipsychotic drugs (variously named 'dopamine system stabilizers' or 'partial dopamine agonists'37) that recently been developed and is now widely licensed to treat schizophrenia.

The efficacy of schizophrenia treatment is often assessed by using standardized assessment methods, one of the most common being the positive and negative syndrome scale (PANSS).68

Hospitalization 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 people to be treated against their will. However, in many countries such legislation does not exist, or does not have the power to enforce involuntary hospitalization or treatment.

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Therapy and community support
Psychotherapy or other forms of talk therapy may be offered, with cognitive behavioral 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. Although the results of early trials with cognitive behavioral therapy (CBT) were inconclusive38, more recent reviews suggest that CBT can be an effective treatment for the psychotic symptoms of schizophrenia39.

A relatively new approach has been the use of cognitive remediation therapy, a technique aimed at remediating the neurocognitive deficits sometimes present in schizophrenia. Based on techniques of neuropsychological rehabilitation, early evidence has shown it to be cognitively effective, with some improvements related to measurable changes in brain activation as measured by fMRI.40

Electroconvulsive therapy (also known as ECT or 'electroshock therapy') may be used in countries where it is legal. It is not considered a first line treatment but may be prescribed in cases where other treatments have failed. Psychosurgery has now become a rare procedure and is not a recommended treatment for schizophrenia.

Other support services may also be available, such as drop-in centers, 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 destigmatize 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 with schizophrenia in non-Western countries may actually be much better41 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.

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Dietary supplements
Omega-3 fatty acids (found naturally in foods such as oily fish, flax seeds, hemp seeds, walnuts and canola oil) have recently been studied as a treatment for schizophrenia. Although the number of research trials has been limited, the majority of randomized controlled trials have found omega-3 supplements to be effective when used as a dietary supplement.64

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Prognosis
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.

One retrospective study has 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 ill.42 A more recent study using stricter recovery criteria (i.e. concurrent remission of positive and negative symptoms and specific instances of adequate social / vocational functioning) reported a recovery rate of 13.7%.43

The exact definition of what constitutes a recovery has not been widely defined, however, although criteria have recently been suggested to define a remission in symptoms.63 Therefore, this makes it difficult to give an exact estimate as recovery and remission rates are not always comparable across studies.

The World Health Organization conducted two long-term follow-up studies involving more than 2,000 people suffering from schizophrenia in different countries, and discovered these patients have much better long-term outcomes in poor countries (India, Colombia and Nigeria) than in rich countries (USA, UK, Ireland, Denmark, Czechoslovakia, Japan, and Soviet Union),44 despite the fact antipsychotic medication is typically not widely available in poorer countries.

Prognosis also depends on some other factors. Females tend to show recovery rates higher than males, and acute and sudden onset of schizophrenia is associated with higher rates of recovery, while gradual onset is associated with lower rates. Most studies done on this subject, however, are correlational in nature, and a clear cause-and- relationship is difficult to establish. Pre-morbid functioning and positive prognosis also seem to be correlated.

In a study of over 168,000 Swedish citizens undergoing psychiatric treatment, schizophrenia was associated with an average life expectancy of approximately 80-85% of that of the general population. Women with a diagnosis of schizophrenia were found to have a slightly better life expectancy than that of men, and as a whole, a diagnosis of schizophrenia was associated with a better life expectancy than substance abuse, personality disorder, heart attack and stroke.45

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 lifetime.46 Another study suggested that 10% of persons with schizophrenia die by suicide.47

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Schizophrenia and drug use
The relationship between schizophrenia and drug use is complex, meaning that a clear causal connection between drug use and schizophrenia has been difficult to tease apart. There is strong evidence that using certain drugs can trigger either the onset or relapse of schizophrenia in some people. It may also be the case, however, that people with schizophrenia use drugs to overcome negative feelings associated with both the commonly prescribed antipsychotic medication and the condition itself, where negative emotion, paranoia and anhedonia are all considered to be core features.

The rate of substance use is known to be particularly high in this group. In a recent study, 60% of people with schizophrenia were found to use substances and 37% would be diagnosable with a substance use disorder.74

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Hallucinogens
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 because of subsequent drug use. Some widely known cases where hallucinogens have been suspected of precipitating schizophrenia are Pink Floyd founder-member Syd Barrett and Beach Boys songwriter Brian Wilson.

Drugs such as methamphetamine, ketamine, PCP and LSD have been used to mimic schizophrenia for research purposes, although this has now fallen out of favor 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. 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.

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Cannabis
There is increasing evidence that cannabis use can contribute to the onset of schizophrenia. Some 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 other things, a significant causal factor. Nevertheless, some previous research in this area has been criticised as it has often not been clear whether cannabis use is a cause or effect of schizophrenia. To address this issue, a recent review of studies from which a causal contribution to schizophrenia can be assessed has suggested that cannabis doubles the risk of developing schizophrenia on the individual level, and may be responsible for up to 8% of cases in the population.48

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Tobacco
It has been noted that the majority of people with schizophrenia (estimated between 75% and 90%) smoke tobacco. However, people diagnosed with schizophrenia have a much lower than average chance of developing 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 cancer49.

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.50 While 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 give clues as to how schizophrenia might develop at the molecular level. Furthermore, many people with schizophrenia have smoked tobacco products long before they are diagnosed with the illness, and some groups advocate that the chemicals in tobacco have actually contributed to the onset of the illness and have no benefit of any kind.

It is of interest that cigarette smoking affects the liver's function such that the antipsychotic drugs used to treat schizophrenia are broken down in the blood stream more quickly. This means that smokers with schizophrenia need slightly higher doses of antipsychotic drugs in order for them to be effective than do their non-smoking counterparts.

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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 argues that psychiatric patients are not ill but are just individuals with unconventional thoughts and behavior that make society uncomfortable. He argues that society unjustly seeks to control such individuals by classifying their behavior as an illness and forcibly treating them as a method of social control. It is worth noting that Szasz has never considered himself to be "anti-psychiatry" in the sense of being against psychiatric treatment, but simply believes that it should be conducted between consenting adults, rather than imposed upon anyone against their will. Szasz co-founded the anti-psychiatry group Citizens' Commission on Human Rights with the Church of Scientology, who are well-noted for their anti-psychiatric stance.

Similarly, psychiatrists R. D. Laing, Silvano Arieti, Theodore Lidz and to a certain degree Colin Ross have argued that the symptoms of what is normally called mental illness are comprehensible reactions to impossible demands that society and particularly family life places on some sensitive individuals. Laing, Arieti and Lidz were 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. Laing's work, co-authored with Aaron Esterson, Sanity, Madness and the Family (1964) described eleven case studies of people diagnosed with schizophrenia and argued that the content of their actions and statements was meaningful and logical in the context of their family and life situations. Arieti's Interpretation of Schizophrenia won the 1975 scientific National Book Award in the United States.

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 specialization for language.56 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 shaman57. 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.) Speculations regarding primary and important religious figures as having schizophrenia abound. Some commentators have endorsed the idea that major religious figures experienced psychosis, heard voices and displayed delusions of grandeur.

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).

One theory put forward by psychiatrists E. Fuller Torrey and R.H. Yolken is that the parasite Toxoplasma gondii leads to some, if not many, cases of schizophrenia.58

An additional approach is suggested by the work of Richard Bandler who argues that "The usual difference between someone who hallucinates and someone who visualizes normally, is that the person who hallucinates doesn't know he's doing it or doesn't have any choice about it." (Time for a Change, p107). He suggests that because visualization is a sophisticated mental capability, schizophrenia is a skill, albeit an involuntary and dysfunctional one that is being used but not controlled. He therefore suggests that a significant route to treating schizophrenia might be to teach the missing skill - how to distinguish created reality from consensus external reality, to reduce its maladaptive impact, and ultimately how to exercise appropriate control over the vizualization or auditory process. Hypnotic approaches have been explored by the physician Milton H. Erickson as a means of facilitating this.

Regarding schizophrenia as a waking dreamer syndrome, Jie Zhang hypothesizes that the hallucinations of schizophrenia are caused by the activation of the continual-activation mechanism during waking, a mechanism that induces dreaming while asleep, due to the malfunction of the continual-activation thresholds in the conscious part of brain

Answer 2

I believe schizophrenia causes ioslation. Isolation may cause some neurotic behavior, but rarely, if at all, schizophrenia.

Answer 3

This Site Might Help You.

RE:
what factors cause schizophrenia?
is schizophrenia inborn/genetic, is it environmental, does diet play a part, or are there other factors? is it a combination of several stressors? i won't ask if it is a figment of the sufferer's imagination though, as i used to think that till i came down with it, thinking work would...

Answer 4

I am sorry to hear about your diagnosis. Schizophrenia can be an absolutely devastating disease. Genetics are a factor, however there is usually a trigger that causes it to manifest. A friend of mine in jr high and high school had an extremely stressful family breakdown, and that (I believe) caused his illness to "awaken". Most people I have been privileged to meet with Schizophrenia have been extremely intelligent. I don't know if there is a connection. I do not believe diet has much if anything to do with it. When you really break it down, Schizophrenia is a break down of the connections to different parts of the brain. What is real and imaginery can become indistiguishable. For example, if I decided I wanted to go to the kitchen, my mind might go over all the reasons why and why not during the decision making process. In a Schizophrenic person, those thought patterns may manifest as external voices. Sometimes, the lines between the real world and the dream world blur, causing visual disturbances. Or an imaginery friend from your childhood may suddenly appear to come to life.
I sincerely hope that you can find a course of treatment that will allow you to live a somewhat normal life. Best of luck and God bless.

Answer 5

Looking for the great things about salmon but you don't feel at ease cooking fish? Try canned salmon as a simple and affordable alternative.

Answer 6

There are genetic factors, as well as factors of what they call 'behaviour learning' (=learning to use schizophrenic behaviour when growing up with schizophrenic parents for instance). But none of them is usually enough to cause the illness to develop if the social and sentimental environment doesn't play its role too. More specifically, in most cases of schizophrenic males we find a symbiotic mother and an apathetic father in the family environment.

Answer 7

Doctor's probably say it's a chemical imbalance in the brain, but if you look at it from a spiritual point of view, in the bible and in real life, people who are possessed have similar symptoms to schizophrenia.

Answer 8

Always have vegetables on hands. Saute a big bag regarding frozen mixed vegetables in coconut oil and garlic. Add some red pepper as well as turmeric for additional flavor and also separate into portion-sized containers for that fridge.

Answer 9

Give your protein extra low-calorie flavor with the addition of a salsa or chutney rather then a gooey cream sauce.

Answer 10

hi swot,

i have a great homepage for you (that is was not too hard to find, actually):

http://www.schizophrenia.com/hypo.php

here you find loads of info about the causes. and if you go to the starting page (schizophrenia.com) you find all the other infos also.

quote:
"Although the exact cause of schizophrenia remains unknown, experts do agree that schizophrenia develops as a result of interplay between biological predisposition (for example, inheriting certain genes) and the kind of environment you are exposed to. These lines of research are beginning to converge: brain development disruption is likely the result of genetic and/or environmental stressors early in development (during pregnancy or early childhood), leading to subtle alterations in the brain that make a person susceptible to developing schizophrenia. Environmental factors later in life (during early childhood and adolescence) can either damage the brain further and thereby increase the risk of schizophrenia, or lessen the expression of genetic or neurodevelopmental defects and decrease the risk of schizophrenia."

Answer 11

well my brother has scizophrenia and its formed from deppression and a unborn child can get it while in the mothers stomach if the mother is depressed and related problems..
there is no cure but there is treatment..and its medication. alot of ppl have come out of this phase,,and the most important things are u have to take yo medications at a daily basis and u cant all the sudden be off medication which will cause a relapse.. and another thing is u have to be active and buzy..such az work..in my brothers case wen ever he goes to work he behaves much better,