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Schizophrenia (/ˌskɪtsɵˈfrɛniə/ or /ˌskɪtsɵˈfriːniə/) is a mental disorder characterized by a breakdown in thinking and poor emotional responses.[1] Common symptoms include delusions, such as paranoia; hearing voices or noises that are not there; disorganized thinking; a lack of emotion and a lack of motivation. Schizophrenia causes significant social and work problems. Symptoms begin typically in young adulthood and about 0.3–0.7% of people are affected during their lifetime.[2] Diagnosis is based on observed behavior and the person's reported experiences.
Genetics, early environment, psychological and social processes appear to be important contributory factors. Some recreational and prescription drugs appear to cause or worsen symptoms. The many possible combinations of symptoms have triggered debate about whether the diagnosis represents a single disorder or a number of separate syndromes. Despite the origin of the term from the Greek roots skhizein ("to split") and phrēn ("mind"), schizophrenia does not imply a "split personality", or "multiple personality disorder"—a condition with which it is often confused in public perception.[3] Rather, the term means a "splitting of mental functions", reflecting the presentation of the illness.[4

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Causes
Main article: Causes of schizophrenia
A combination of genetic and environmental factors play a role in the development of schizophrenia.[2][3] People with a family history of schizophrenia who have a transient psychosis have a 20–40% chance of being diagnosed one year later.[26]
Genetic
Estimates of heritability vary because of the difficulty in separating the effects of genetics and the environment;[27] averages of 0.80 have been given.[28] The greatest risk for developing schizophrenia is having a first-degree relative with the disease (risk is 6.5%); more than 40% of monozygotic twins of those with schizophrenia are also affected.[3] If one parent is affected the risk is about 13% and if both are affected the risk is nearly 50%.[28]
It is likely that many genes are involved, each of small effect and unknown transmission and expression.[3] Many possible candidates have been proposed, including specific copy number variations, NOTCH4, and histone protein loci.[29] A number of genome-wide associations such as zinc finger protein 804A have also been linked.[30] There appears to be overlap in the genetics of schizophrenia and bipolar disorder.[31] Evidence is emerging that the genetic architecture of schizophrenia involved both common and rare risk variation.[32]
Assuming a hereditary basis, one question from evolutionary psychology is why genes that increase the likelihood of psychosis evolved, assuming the condition would have been maladaptive from an evolutionary point of view. One idea is that genes are involved in the evolution of language and human nature, but to date such ideas remain little more than hypothetical in nature.[33][34]
Environment
Environmental factors associated with the development of schizophrenia include the living environment, drug use and prenatal stressors.[2] Parenting style seems to have no major effect, although people with supportive parents do better than those with critical or hostile parents.[3] Living in an urban environment during childhood or as an adult has consistently been found to increase the risk of schizophrenia by a factor of two,[2][3] even after taking into account drug use, ethnic group, and size of social group.[35] Other factors that play an important role include social isolation and immigration related to social adversity, racial discrimination, family dysfunction, unemployment, and poor housing conditions.[3][36]
Substance use
About half of those with schizophrenia use drugs or alcohol excessively.[37] Amphetamine, cocaine, and to a lesser extent alcohol, can result in psychosis that presents very similarly to schizophrenia.[3][38] Although it is not generally believed to be a cause of the illness, people with schizophrenia use nicotine at much greater rates than the general population.[39]
Alcohol abuse can occasionally cause the development of a chronic substance-induced psychotic disorder via a kindling mechanism.[40] Alcohol use is not associated with an earlier onset of psychosis.[41]
A significant proportion of schizophrenics use cannabis to help cope with its symptoms.[37] Cannabis can be a contributory factor in schizophrenia,[42][43][44] but cannot cause it alone;[44] its use is neither necessary nor sufficient for development of any form of psychosis.[44] Early exposure of the developing brain to cannabis increases the risk of schizophrenia,[42] although the size of the increased risk is difficult to quantify;[42][43] only a small proportion of early cannabis recreational users go on to develop any schizoaffective disorder in adult life,[43] and the increased risk may require the presence of certain genes within an individual[44] or may be related to preexisting psychopathology.[42] Higher dosage and greater frequency of use are indicators of increased risk of chronic psychoses.[43] Tetrahydrocannabinol (THC) and cannabidiol (CBD) produce opposing effects; CBD has antipsychotic and neuroprotective properties and counteracts negative effects of THC.[43]
Other drugs may be used only as coping mechanisms by individuals who have schizophrenia to deal with depression, anxiety, boredom, and loneliness.[37][45]
Developmental factors
Factors such as hypoxia and infection, or stress and malnutrition in the mother during fetal development, may result in a slight increase in the risk of schizophrenia later in life.[2] People diagnosed with schizophrenia are more likely to have been born in winter or spring (at least in the northern hemisphere), which may be a result of increased rates of viral exposures in utero.[3] The increased risk is about 5 to 8%.[46]
Mechanisms
Main article: Mechanisms of schizophrenia
A number of attempts have been made to explain the link between altered brain function and schizophrenia.[2] One of the most common is the dopamine hypothesis, which attributes psychosis to the mind's faulty interpretation of the misfiring of dopaminergic neurons.[2]
Psychological
Many psychological mechanisms have been implicated in the development and maintenance of schizophrenia. Cognitive biases have been identified in those with the diagnosis or those at risk, especially when under stress or in confusing situations.[47] Some cognitive features may reflect global neurocognitive deficits such as memory loss, while others may be related to particular issues and experiences.[48][49]
Despite a demonstrated appearance of blunted affect, recent findings indicate that many individuals diagnosed with schizophrenia are emotionally responsive, particularly to stressful or negative stimuli, and that such sensitivity may cause vulnerability to symptoms or to the disorder.[50][51] Some evidence suggests that the content of delusional beliefs and psychotic experiences can reflect emotional causes of the disorder, and that how a person interprets such experiences can influence symptomatology.[52][53][54] The use of "safety behaviors" to avoid imagined threats may contribute to the chronicity of delusions.[55] Further evidence for the role of psychological mechanisms comes from the effects of psychotherapies on symptoms of schizophrenia.[56]
Neurological

Functional magnetic resonance imaging (fMRI) and other brain imaging technologies allow for the study of differences in brain activity in people diagnosed with schizophrenia. The image shows two levels of the brain, with areas that were more active in healthy controls than in schizophrenia patients shown in orange, during an fMRI study of working memory.
Schizophrenia is associated with subtle differences in brain structures, found in 40 to 50% of cases, and in brain chemistry during acute psychotic states.[2] 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 lobes.[57] Reductions in brain volume, smaller than those found in Alzheimer's disease, have been reported in areas of the frontal cortex and temporal lobes. It is uncertain whether these volumetric changes are progressive or preexist prior to the onset of the disease.[25] These differences have been linked to the neurocognitive deficits often associated with schizophrenia.[58] Because neural circuits are altered, it has alternatively been suggested that schizophrenia should be thought of as a collection of neurodevelopmental disorders.[59]
Particular attention has been paid to the function of dopamine in the mesolimbic pathway of the brain. This focus largely resulted from the accidental finding that phenothiazine drugs, which block dopamine function, could reduce psychotic symptoms. It is also supported by the fact that amphetamines, which trigger the release of dopamine, may exacerbate the psychotic symptoms in schizophrenia.[60] The influential dopamine hypothesis of schizophrenia proposed that excessive activation of D2 receptors was the cause of (the positive symptoms of) schizophrenia. Although postulated for about 20 years based on the D2 blockade effect common to all antipsychotics, it was not until the mid-1990s that PET and SPET imaging studies provided supporting evidence. The dopamine hypothesis is now thought to be simplistic, partly because newer antipsychotic medication (atypical antipsychotic medication) can be just as effective as older medication (typical antipsychotic medication), but also affects serotonin function and may have slightly less of a dopamine blocking effect.[61]
Interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in schizophrenia, largely because of the abnormally low levels of glutamate receptors found in the postmortem brains of those diagnosed with schizophrenia,[62] and the discovery that glutamate-blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition.[63] Reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function, and glutamate can affect dopamine function, both of which have been implicated in schizophrenia, have suggested an important mediating (and possibly causal) role of glutamate pathways in the condition.[64] But positive symptoms fail to respond to glutamatergic medication.[65]

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An increasing number of scientific studies conducted in recent years have found a significant relationship between marijuana use and schizophrenia, with the use of marijuana found to about double an individual's risk of developing the illness. But does marijuana use actually cause schizophrenia? Scientific studies have yet to establish a causal relationship, leaving this a question open for debate.

What do we know?

Studies have found connections between THC (marijuana's primary psychoactive ingredient) and brain abnormalities that lead to symptoms seen in schizophrenia, suggesting that marijuana use could possibly trigger or exacerbate the illness. Other studies have consistently found that young people who regularly use marijuana increase their risk of developing schizophrenia and experience an earlier onset of the illness than they general population.

What do we think?

Many experts believe that marijuana use has the potential to trigger schizophrenia in people who already have a genetic vulnerability to the disease. There is not a lot of evidence to suggest that people with no predisposition to schizophrenia will develop the illness due to cannabis use (although it should be pointed out that it isn't always possible for people who are vulnerable to schizophrenia to be aware of that fact).

The Bottom Line

Marijuana is the most widely used drug among schizophrenics, but it isn't clear whether people begin using marijuana as a way to cope with schizophrenia symptoms, or develop schizophrenia symptoms as a result of marijuana use. The only thing that can be said for sure is that some relationship exists. So if you're looking to decrease your chances of developing schizophrenia, avoiding marijuana couldn't hurt.

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