Instruct: Given a question, retrieve relevant documents that can help answer the question.
Query: Does schizophrenia run in families?
Evidence suggests that genetic vulnerability with environmental factors can act in combination resulting in the development of schizophrenia.[8] Although schizophrenia is very strongly heritable, there is also some evidence that all cases are not caused by heredity. Many people who appear to carry "schizophrenia genes" may not become schizophrenic.[9] Recent research suggests that genetic vulnerability to schizophrenia is multifactorial, caused by interactions of several genes.[10]
The glutamate hypothesis of schizophrenia models the subset of pathologic mechanisms linked to glutamatergic signaling. The hypothesis was initially based on a set of clinical, neuropathological, and, later, genetic findings pointing at a hypofunction of glutamatergic signaling via NMDA receptors. While thought to be more proximal to the root causes of schizophrenia, it does not negate the dopamine hypothesis, and the two may be ultimately brought together by circuit-based models. The development of the hypothesis allowed for the integration of the GABAergic and oscillatory abnormalities into the converging disease model and made it possible to discover the causes of some disruptions.
Ketamine and PCP were observed to produce significant similarities to schizophrenia. Ketamine produces more similar symptoms (hallucinations, withdrawal) without observed permanent effects (other than ketamine tolerance). Both arylcyclohexamines have some(uM) affinity to D2 and as triple reuptake inhibitors. PCP is representative symptomatically, but does appear to cause brain structure changes seen in schizophrenia. Although unconfirmed, Dizocilpine discovered by a team at Merck seems to model both the positive and negative effects in a manner very similar to schizophreniform disorders.
Both bipolar disorder and schizophrenia appear to result from gene–environment interaction. Evidence from numerous family and twin studies indicates a shared genetic etiology between schizophrenia and bipolar disorder. Geoffroy, Etain, and Houenou note that the largest family study available found a combined heritability for bipolar disorder and schizophrenia of approximately 60%, with environmental factors accounting for the remainder. Genetic contributions to schizoaffective disorder appear to be entirely shared with those contributing to schizophrenia and mania.
Lyman C. Wynne (1923–2007) was an American psychiatrist and psychologist with a special interest in schizophrenia. His early research helped lay the foundation for family-based therapies, influencing others such as R. D. Laing. He made a number of discoveries about the interaction of genetics and the environment in the development of schizophrenia, working with adopted twins. He published numerous articles and co-edited "The Nature of Schizophrenia" (1978), received the Frieda Fromm-Reichmann Award for schizophrenia research from the American Academy of Psychoanalysis in 1965, the Meritorious Service Medal from the U.S. Public Health Service in 1966, and received two awards from the American Family Therapy Academy, one in 1981 and another in 1989.
Meehl’s dominant schizogene theory had a substantial influence on subsequent research efforts. His theorizing increased interest in longitudinal study of individuals at risk for psychosis and family members of people with schizophrenia who may be carrying the schizogene. Meehl’s descriptions of schizophrenia as largely a neurological phenomenon and schizotypy as a genetically-based risk factor for schizophrenia have been supported. However, researchers have not uncovered strong evidence for a single schizogene, and instead believe the genetic risk for schizophrenia is better explained by polygenic combinations of common variants and rare genetic mutations.
The dopamine hypothesis of schizophrenia or the dopamine hypothesis of psychosis is a model that attributes symptoms of schizophrenia (like psychoses) to a disturbed and hyperactive dopaminergic signal transduction. The model draws evidence from the observation that a large number of antipsychotics have dopamine-receptor antagonistic effects. The theory, however, does not posit dopamine overabundance as a complete explanation for schizophrenia. Rather, the overactivation of D2 receptors, specifically, is one effect of the global chemical synaptic dysregulation observed in this disorder.
Family studies on schizophrenia were reviewed. That the disorder runs in families did not suggest it was genetically inherited, since cultural transmission occurs from parents to children. Twin and adoption studies were presented as the standard methods to disentangle contributions from genes and the environment. Gottesman used a computer-based method for calculating the odds of becoming schizophrenic based on the many causes. The book examines the problems caused by schizophrenia for relatives of patients and for society at large, larger-scale ones exemplified by the eugenics policies of states such as Nazi Germany. Two final chapters cover molecular biology and neuroanatomy briefly. Newer methods of behavioral genetics being researched at the time of publication, such as linkage analysis which used the likelihood of neighboring genes being inherited together, were not covered.
Schizophrenia is a chronic psychiatric illness characterized by excessive dopamine activity in the mesolimbic tract and insufficient dopamine activity in the mesocortical tract leading to symptoms of psychosis along with poor cognition in socialization. Under the Diagnostic and Statistical Manual of Mental Disorders, people with schizophrenia have a combination of positive, negative and psychomotor symptoms. These cognitive disturbances involve rare beliefs and/or thoughts of a distorted reality that creates an abnormal pattern of functioning for the patient. The cause of schizophrenia has a substantial genetic component involving many genes. While the heritability of schizophrenia has been found to be around 80%, only about 60% of sufferers report a positive family history of the disorder, and ultimately the cause is thought to be a combination of genetic and environmental factors. It is believed that the experience of stressful life events is an environmental factor that can trigger the onset of schizophrenia in individuals who already are at risk from genetics and age. The level of self-awareness among patients with schizophrenia is a heavily studied topic.
Schizophrenia has no definite cause; however, certain risk factors such as family history seem to correlate. There is no known cure, but childhood schizophrenia is controllable with the help of behavioral therapies and medications.
Concerns have been raised that long-term therapy with stimulants for ADHD might cause paranoia, schizophrenia and behavioral sensitization.[125] Family history of mental illness does not predict the incidence of stimulant toxicosis in ADHD children. High rates of childhood stimulant use have been noted in patients with a diagnosis of schizophrenia and bipolar disorder independent of ADHD. Individuals with a diagnosis of bipolar or schizophrenia who were prescribed stimulants during childhood typically have a significantly earlier onset of the psychotic disorder and suffer a more severe clinical course of psychotic disorder. It has been suggested that this small subgroup of children who develop schizophrenia due to stimulant use during childhood have a genetic vulnerability to developing psychosis.[126] In addition, amphetamines are known to cause a stimulant psychosis in otherwise healthy individuals that superficially resembles schizophrenia, and may be misdiagnosed as such by some healthcare professionals.
The chance of developing schizophrenia has been found to increase with the number of adverse social factors (e.g. indicators of socioeconomic disadvantage or social exclusion) present in childhood.[138][139] Stressful life events generally precede the onset of schizophrenia.[140] A personal or recent family history of migration is a considerable risk factor for schizophrenia, which has been linked to psychosocial adversity, social defeat from being an outsider, racial discrimination, family dysfunction, unemployment, and poor housing conditions.[114][141] Unemployment and early separation from parents are some important factors which are responsible for the higher rates of schizophrenia among British African Caribbean populations, in comparison to native African Caribbean populations. This is an example which shows that social disadvantage plays an equally major hand in the onset of schizophrenia as genetics.[142]
Randye Kaye's first book, "Ben Behind His Voices: One Family's Journey from the Chaos of Schizophrenia to Hope," was published by Rowman and Littlefield on August 16, 2011. Represented by Claire Gerus, and currently available on Amazon and in bookstores and libraries (hardcover, e-reader and audiobook versions), it is a memoir of her experiences with the onset, development and recovery of her son Ben's schizophrenia. Ben, who developed schizophrenia in his late teens and was hospitalized multiple times, now has proper treatment. Kaye claims her goal with the memoir is to help other families with resources and reduce the stigma of schizophrenia. She frequently speaks to medical providers, legislators, and families on the experiences of mental illnesses. Kaye recently spoke at the American Psychiatric Association, NAMI National Convention, and at Bridgeport Hospital.
Family Therapy or Education, which addresses the whole family system of an individual with a diagnosis of schizophrenia, may be beneficial, at least if the duration of intervention is longer-term. A 2010 Cochrane review concluded that many of the clinical trials that studied the effectiveness of family interventions were poorly designed, and may over estimate the effectiveness of the therapy. High-quality randomized controlled trials in this area are required. Aside from therapy, the impact of schizophrenia on families and the burden on careers has been recognized, with the increasing availability of self-help books on the subject. There is also some evidence for benefits from social skills training, although there have also been significant negative findings. Some studies have explored the possible benefits of music therapy and other creative therapies.
Experiments on mice have provided evidence that several stressors can act together to increase the risk of schizophrenia. In particular, the combination of a maternal infection during pregnancy followed by heightened stress at the onset of sexual maturity markedly increases the probability that a mouse develops symptoms of schizophrenia, whereas the occurrence of one of these factors without the other does not.[161]
Gottesman researched and published on the abuse of genetic research in Nazi Germany, and provided expert testimony in a Chinese human rights case involving schizophrenia in the family. His scholarly books on schizophrenia also highlighted the human costs of the disorder. In "Schizophrenia Genesis: The Origins of Madness", he provided chapters in which patients describe their experiences of the disease, and those of their families. Gottesman emphasized that genetics influences patients' behavior in concert with the family, social, economic, and cultural contexts. Gottesman also highlighted random events as an important "third element" determining behavior and what unfolds as apparent destiny. In his writings, he reflected that the interaction between these elements is known only at the level of probabilities, and not as fixed and precise quantities.
The implication of genetics in psychiatric illnesses is not unique to schizophrenia, though the heritability of schizophrenia has been calculated as high as 80%. The continued research of the family following the discovery of the translocation yielded statistical analysis of the probability of observing the simultaneous occurrence, or co-inheritance, of psychological afflictions and the translocation. This concept was measured quantitatively using the LOD, or logarithm of the odds value. The higher the LOD value, the stronger the correlation between the presence of the translocation and given disease(s) is thought to be. The LOD for the chromosome 1 translocation and identification of schizophrenia alone in the Scottish family was found to be 3.6. The LOD value of the translocation and a broader number of diagnoses (including schizophrenia, schizoaffective disorder, bipolar affective disorder, and recurrent major depression) was found to be 7.1.
A combination of genetic and environmental factors play a role in the development of schizophrenia. People with a family history of schizophrenia who have a transient psychosis have a 20–40% chance of being diagnosed one year later.
Much interest in dysbindin has arisen through pedigree-based family-association studies of families with a history of schizophrenia, where a strong association was found between expression of a particular dysbindin allele and a clinical expression of schizophrenia. However, the genetic link between dysbindin and schizophrenia has not been established in all the case control samples tested and this implies that there are different genetic subtypes of schizophrenia with different disease allele frequencies in different populations. This phenomenon is called genetic locus heterogeneity and is typical of all common disorders with a strong genetic component. A further complication is that it is highly likely that there are several or many different mutations within the dysbindin gene that are responsible for schizophrenia. This complexity is called 
disease allele heterogeneity and is a further reason that genetic associations are found with different markers in the dysbindin gene when different samples are studied.
Though the relationship between smoking and schizophrenia is well established, a factor to be considered in this relationship is the role of the tobacco industry. Research based on internal industry documents shows a concerted effort by the industry to promote belief that people with schizophrenia need to smoke and that it is dangerous for them to quit. Such promotion includes monitoring or supporting research that endorsed the idea that people with schizophrenia are uniquely immune to the health consequences of smoking (since proved false) and that tobacco is needed for people with schizophrenia to self-medicate. The industry also provided cigarettes to hospital wards and supported efforts to block hospital-based smoking bans. Although this does not discredit the effects of nicotine in schizophrenia, it is argued that the efforts of the tobacco industry slowed the decline in smoking prevalence in people with schizophrenia as well as the development of clinical policies to promote smoking cessation.
The term schizophrenia is commonly misunderstood to mean that affected persons have a "split personality". Although some people diagnosed with schizophrenia may hear voices and may experience the voices as distinct personalities, schizophrenia does not involve a person changing among distinct, multiple personalities; the confusion arises in part due to the literal interpretation of Bleuler's term "schizophrenia" (Bleuler originally associated schizophrenia with dissociation, and included split personality in his category of schizophrenia). Dissociative identity disorder (having a "split personality") was also often misdiagnosed as schizophrenia based on the loose criteria in the DSM-II. The first known misuse of the term to mean "split personality" was in an article by the poet T. S. Eliot in 1933. Other scholars have traced earlier roots. Rather, the term means a "splitting of mental functions", reflecting the presentation of the illness.
In their book, "Schizophrenia and the Family" (1965), Lidz, Fleck and Alice Cornelison compiled findings of what remains perhaps the most detailed clinical study of a series of patients with schizophrenia and their families. 
Several environmental factors, including perinatal complications and prenatal maternal infections could cause schizophrenia. These factors in a greater severity or frequency could result in an earlier onset of schizophrenia. Maybe a genetic predisposition is an important factor too, familial illness reported for childhood-onset schizophrenic patients.
Schizophrenia is a complex psychotic disorder in which symptoms include emotional blunting, intellectual deterioration, social isolation, disorganized speech and behavior, delusions, and hallucinations. The causes of schizophrenia are unclear, but it seems that genetics play a heavy role, as individuals with a family history are far more likely to suffer from schizophrenia. The disorder can be triggered and exacerbated by social and environmental factors, with episodes becoming more apparent in periods of high stress. Neurologists have found that the schizophrenic brain has larger ventricles (fluid-filled cavities) compared to a well brain. This is hypothesized to be due to loss of nerve cells. Symptoms usually appear around the onset of early adulthood. It is rare for a child to be diagnosed with schizophrenia, in part because of the difficulty in establishing what erroneous thoughts and beliefs can be attributed to childhood development and which thoughts and beliefs can be attributed to schizophrenia. With psychiatric medication (usually antipsychotics) and therapy, individuals with schizophrenia can live successful and productive lives.
From the 1940s to the 1970s prominent mental health professionals proposed trauma models as a means of understanding schizophrenia, including Harry Stack Sullivan, Frieda Fromm-Reichmann, Theodore Lidz, Gregory Bateson, Silvano Arieti and R.D. Laing. Based on their clinical work they theorised that schizophrenia appears to be induced by children's experiences in profoundly disturbed families and reflect victims attempts to cope with such families and live in societies that are inherently damaging to people's psychological well-being. In the 1950s Sullivan's theory that schizophrenia is related to interpersonal relationships was widely accepted in the United States. Silvano Arieti's book "Interpretation of Schizophrenia" won the American National Book Award in the field of science in 1975. The book advances a psychological model for understanding all the regressive types of the disorder.