Instruct: Given a question, retrieve relevant documents that answer the question.
Query: How many people have schizophrenia?
Schizophrenia affects around 0.3–0.7% of people at some point in their life,[1] or 21million people worldwide as of 2011 (about one of every 285).[2] By using precise methods in its diagnosis and a large, representative population, schizophrenia seems to occur with relative consistency over time during the last half-century.[3]
In alternative medicine, some practitioners believe that there are a vast number of physical causes of what ends up being diagnosed as schizophrenia.[186] While some of these explanations may stretch credulity, others (such as heavy metal poisoning and nutritional imbalances) have been supported at least somewhat by research.[68][187][188] However, it is not entirely clear how many (if any) patients initially diagnosed with schizophrenia these alternative explanations may account for.
People with severe mental illness, including schizophrenia, are at a significantly greater risk of being victims of both violent and non-violent crime. Schizophrenia has been associated with a higher rate of violent acts, but most appear to be related to associated substance abuse. Rates of homicide linked to psychosis are similar to those linked to substance misuse, and parallel the overall rate in a region. What role schizophrenia has on violence independent of drug misuse is controversial, but certain aspects of individual histories or mental states may be factors. About 11% of people in prison for homicide have schizophrenia and 21% have mood disorders. Another study found about 8-10% of people with schizophrenia had committed a violent act in the past year compared to 2% of the general population.
A 2003 study of over 50,000Swedish conscripts found that there was a small but significant protective effect of smoking cigarettes on the risk of developing schizophrenia later in life.[131] 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 a cohort study of Israeli conscripts found that healthy adolescent smokers were more likely to develop schizophrenia in the future than their nonsmoking peers.[132]
While there haven't been many studies linking environmental factors to schizophrenia-related epigenetics mechanisms at this point in the field, a few studies have shown interesting results.
Advanced paternal age is one of the risk factors for schizophrenia, according to recent research. This is through mutagenesis, which cause further spontaneous changes, or through genomic imprinting. As the parent ages, more and more errors may occur in the epigenetic process. There is also evidence of the association between the inhalation of benzene through the burning of wood and schizophrenic development. This might occur through epigenetic changes. Methamphetamine has also been linked to schizophrenia or similar psychotic symptoms. A recent study found that methamphetamine users had altered DNMT1 levels, similar to how patients with schizophrenia have shown abnormal levels of DNMT1 in GABAergic neurons.
Women who were pregnant during the Dutch famine of 1944, where many people were close to starvation (experiencing malnutrition) had a higher chance of having a child who would later develop schizophrenia.[45] 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 significantly more likely to develop schizophrenia when compared with mothers who found out about their husbands' death after pregnancy, suggesting that maternal stress may have an effect.[46]
Some people may develop symptoms of schizophrenia as a result of using cannabis or other street drugs such as cocaine and amphetamines. In persons who already have schizophrenia, using street drugs can make the symptoms worse. Drinking alcohol and smoking may also limit how effectively medicines treat the symptoms of schizophrenia. 
As amphetamines trigger the release of dopamine and excessive dopamine function is believed to be responsible for many symptoms of schizophrenia (known as the dopamine hypothesis of schizophrenia), amphetamines may worsen schizophrenia symptoms.[123] Methamphetamine, a potent neurotoxic amphetamine derivative, induces psychosis in a substantial minority of regular users which resembles paranoid schizophrenia. For most people, this psychosis fades away within a month of abstinence but for a minority the psychosis can become chronic. Individuals who develop a long lasting psychosis, despite abstinence from methamphetamine, more commonly have a family history of schizophrenia.[124]
"EastEnders" worked closely with experts from the National Schizophrenia Fellowship to make the plot as accurate as possible. Gary Hogman of the fellowship said "It was the largest ever schizophrenia awareness initiative, reaching an audience of 10 million people three times a week. People could watch Joe going through the motions. We showed things were not so bad and how you could get help. There is so much misinformation about schizophrenia with the media focusing on extreme cases. And Joe was a handsome young man, not a spotty loner. He showed that schizophrenia can happen to anyone and made it easier for people to talk about it."
Regarding posthumous diagnoses: only a few famous people are believed to have been affected by schizophrenia. Most of these listed have been diagnosed based on evidence in their own writings and contemporaneous accounts by those who knew them. Also, persons prior to the 20th century may have incomplete or speculative diagnoses of schizophrenia.
Increased rates of smoking among people with schizophrenia have a number of serious impacts, including increased rates of mortality, increased risk of cardiovascular disease, reduced treatment effectiveness, and greater financial hardship. Studies have also shown that in a male population, having a schizophrenia spectrum disorder puts a patient at risk of excess tobacco use. As a result, researchers believe it is important for mental health professionals to combat smoking among people with schizophrenia.
Many people with childhood schizophrenia are initially misdiagnosed as having pervasive developmental disorders (autism spectrum disorder, for example).
"Early onset schizophrenia" (EOS) is not childhood schizophrenia, because this term is used to identify adolescence patients who develop first episode of psychosis before the age of 18. Childhood schizophrenia manifests before the age of 13, so its correct names are "childhood-onset schizophrenia" (COS) and "very early-onset schizophrenia" (VEOS).
Despite a demonstrated appearance of blunted affect, recent findings indicate that many people 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. 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. The use of "safety behaviors" (acts such as gestures or the use of words in specific contexts) to avoid or neutralize imagined threats may actually contribute to the chronicity of delusions. Further evidence for the role of psychological mechanisms comes from the effects of psychotherapies on symptoms of schizophrenia.
The epigenetics of schizophrenia is the study of how the inherited epigenetic changes is regulated and modified by the environment and external factors, and how these changes shape and influence the onset and development of, and vulnerability to, schizophrenia. Epigenetics also studies how these genetic modifications can be passed on to future generations. Schizophrenia is a debilitating and often misunderstood disorder that affects up to 1% of the world's population. While schizophrenia is a well-studied disorder, epigenetics offers a new avenue for research, understanding, and treatment.
In many non-Western societies, schizophrenia may only be treated with more informal, community-led methods. Multiple international surveys by the World Health Organization over several decades have indicated that the outcome for people diagnosed with schizophrenia in non-Western countries is on average better there than for people in the West. Many clinicians and researchers hypothesize that this difference is due to relative levels of social connectedness and acceptance, although further cross-cultural studies are seeking to clarify the findings.
Schizophrenia is a major cause of disability. Approximately three quarters of people with schizophrenia have ongoing disability with relapses. Still some people do recover completely and additional numbers function well in society.
People with paranoid schizophrenia are often more articulate or "normal" seeming than other people with schizophrenia, such as disorganized schizophrenia (hebephrenia)-afflicted individuals. The diagnosis of paranoid schizophrenia is given based on the presence of bizarre delusions or hallucinations that defy the natural laws of basic logical thought processes, or thought disorders and withdrawal due to these thoughts and delusions. The paranoid subset of schizophrenia tends to have a better prognosis than other subtypes (disorganized and simple–type in particular), as the intellect and personality are relatively preserved, thus enabling a greater degree of cognitive and interpersonal functioning.
People with schizophrenia may have a high rate of irritable bowel syndrome, but they often do not mention it unless specifically asked. Psychogenic polydipsia, or excessive fluid intake in the absence of physiological reasons to drink, is relatively common in people with schizophrenia.
Schizophrenia is often described in terms of positive and negative (or deficit) symptoms. "Positive symptoms" are those that most people do not normally experience, but are present in people with schizophrenia. They can include delusions, disordered thoughts and speech, and tactile, auditory, visual, olfactory and gustatory hallucinations, typically regarded as manifestations of psychosis. Hallucinations are also typically related to the content of the delusional theme. Positive symptoms generally respond well to medication.
The Maudsley–Bethlem study also hypothesized that schizophrenia was caused by a mixture of many small traits working together. These endophenotypes could be used for diagnosis. Endophenotypes have been interpreted as a link between genes and the final behavior, acted on by the environment and chance elements, with biochemical and epigenetic influences changing the genome but not being passed on to children. Molecular-biological studies in genetics have referred to endophenotypes to explain genetic causes of psychopathology. The researchers also examined how schizoids, those with mild, schizophrenia-like personality disorders, were linked to schizophrenics. Gottesman and Shields extended the term to classes of mild psychological disorders in twins and relatives of schizophrenics. The researchers had hypothesized that schizoida in a twin was how a schizophrenia carrier gene, one in a non-schizophrenic still passing on a genetic risk, expressed itself. The twin study did not confirm this.
The grey matter in the cerebral cortex of the brain shrinks over time in people with schizophrenia; the question of whether antipsychotic medication exacerbates or causes this has been controversial. A 2015 meta-analysis found that there is a positive correlation between the cumulative amount of first generation antipsychotics taken by people with schizophrenia and the amount of grey matter loss, and a negative correlation with the cumulative amount of second-generation antipsychotics taken.
Schizophrenia disorders in children are rare. Boys are twice as likely to be diagnosed with childhood schizophrenia. There is often an disproportionately large number of males with childhood schizophrenia, because the age of onset of the disorder is earlier in males than females by about 5 years. People have been and still are reluctant to diagnose schizophrenia early on, primarily due to the stigma attached to it.
Some evidence links T. gondii to schizophrenia.[148] Two 2012 meta-analyses found the rates of antibodies to T. gondii in people with schizophrenia was 2.7 times higher than controls.[151][152] T. gondii antibody positivity was therefore considered an intermediate risk factor in relation to other known risk factors.[151] Cautions noted include that the antibody tests do not detect toxoplasmosis directly, most people with schizophrenia do not have antibodies for toxoplasmosis, and publication bias might exist.[152] The majority of these studies tested people already diagnosed with schizophrenia for T. gondii antibodies, associations between T. gondii and schizophrenia have been found prior to the onset of schizophrenia symptoms.[124] Studies attempting to explain the sex differences in schizophrenia onset have suggested it can be accounted for by a second peak of T. gondii infection incidence occurring from ages 25–30 observed in females only.[153] Although a mechanism supporting the association between schizophrenia and T. gondii infection is unclear, studies have attempted to discern a molecular mechanism to explain the correlation.[153] Antipsychotic drugs used in schizophrenia appear to inhibit the replication of T. gondii tachyzoites in cell culture.[124] Provided there is in fact a causal link between T. gondii and schizophrenia, studies have yet to determine why some individuals with latent toxoplasmosis develop schizophrenia while others do not, however, some plausible explanations include differing genetic susceptibility, parasite strain differences, and differences in the route of the acquired T. gondii infection.[154]
A study of the volume of the gray and white matter in the anterior cingulate gyrus in people with schizophrenia and their healthy first and second degree relatives revealed no significant difference in the volume of the white matter in the people with schizophrenia and their healthy relatives. Nonetheless a significant difference in the volume of gray matter was detected, people with schizophrenia had smaller volume of gray matter than their second degree relatives, but not relative to their first degree relatives. Both the person with schizophrenia and their first degree healthy relatives have smaller gray matter volume than the second degree healthy relatives. It appears that genes are responsible for the decreased volume of gray matter in people with schizophrenia.
Fujiwara et al. (2007) did an experiment in which they correlated the size of anterior cingulate gyrus in people with schizophrenia with their functioning on social cognition, psychopathology and emotions with control group. The smaller the size of anterior cingulate gyrus, the lower was the level of social functioning and the higher was the psychopathology in the people with schizophrenia. The anterior cingulate gyrus was found to be bilaterally smaller in people with schizophrenia as compared with control group. No difference in IQ tests and basic visuoperceptual ability with facial stimuli was found between people with schizophrenia and the control.
Besides biological effects, smoking has a profound social impact on people with schizophrenia. One major impact is financial, as people with schizophrenia have been found to spend a disproportionate amount of their income on cigarettes. A study of people with schizophrenia on public assistance found that they spent a median amount of $142 per month on cigarettes out of a median monthly public assistance income of $596, or about 27.36%. Some argue that this results in further social impacts as people with schizophrenia are then unable to spend money on entertainment and social events that would promote well-being, or may even be unable to afford housing or nutrition.
A large interest in sensory gating research is directed at improving deficits among people diagnosed with Schizophrenia. People with schizophrenia often have deficits in gating the neuronal response of the P50 wave. Since people with schizophrenia can often have an overload of attended stimuli, the P50 wave may serve a critical role in illuminating sensory gating at a neurological level. 
Increased smoking among people with schizophrenia has a number of impacts on this population. One well-documented consequence is the increase in premature death among people with schizophrenia. Life expectancy among people with schizophrenia is generally 80-85% that of the general population, which results from both unnatural causes such as suicide but also natural causes such as cardiovascular disease, to which smoking is an important contributor. People with schizophrenia have a higher incidence of smoking diseases, with heart disease deaths 30% more likely and respiratory disease deaths 60% more likely. 2/3 of people with schizophrenia die from coronary heart disease, versus less than 1/2 of the general population. Ten-year coronary heart disease risk is significantly elevated in people with schizophrenia, as well as diabetes and hypertension.