The Progression of Schizophrenia, Onset, Genetic Susceptibility, and Environmental Risk

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The Progression of Schizophrenia, Onset, Genetic Susceptibility, and Environmental Risk

Abnormal Psychology · Chapter 19: Psychotic Disorders and Disruptions to RealitySection 19.3 · lesson 72 of 9717 min · free with a free account

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In this lesson

Phases, genetic susceptibility, and environmental factors - at population level.

  • Describe the phases, from premorbid to long-term course
  • Explain clinical high-risk criteria and their ethical problem
  • Describe genetic and environmental contributions accurately
  • Distinguish clinical from personal recovery

Transcript

Everything said in the video, section by section (2,321 words). Read along, or search it.

Psychotic Disorders and Disruptions to Reality

Course, Onset, and Risk

This section follows the progression of schizophrenia, from long before onset to the long-term course. We look at the phases, at the clinical high-risk idea and its ethical problem, and at what genetic and environmental findings do and do not mean. And we separate two senses of recovery, finishing with two composite cases.

Before You Begin

Population Facts Don't Transfer to Individuals

This material is educational. It is not a basis for diagnosis, and not a basis for estimating anyone's personal risk, including your own or a relative's. Everything here is population-level information, and population-level information does not transfer to individuals. If you are concerned about yourself or someone close to you, please speak with a qualified professional. Two statements from the genetics material belong right here, because they are the ones most often needed. Most people who develop this condition have no affected close relative. And most relatives of an affected person do not develop it.

The Phase Model

Premorbid, Prodrome, First Episode, Course

Thinking about the condition in phases changed research and services substantially. The phases are premorbid, prodromal, first episode, and subsequent course. Before that, the condition was studied and treated largely as established illness. Research samples came from people who had been unwell for years, and services were organized around managing that state. Two consequences followed. Research could study the period before onset, which is where the developmental questions can actually be answered. And services gained a rationale for intervening early, producing the specialist early intervention model.

Figure 19.3.1

Where Functioning Is Lost

Here is a schematic of functioning across the phases. Functioning is broadly maintained in the premorbid period. It declines through the prodrome. It drops sharply at the first episode, and then recovers to a variable degree in the later course. Look at the shape of the line through the prodromal and first-episode bands, rather than the end point. Much of the decline happens before the first episode. That is the entire basis of the early intervention argument, and why the early intervention window sits where it does.

Premorbid and Prodromal Periods

Informative for Science, Useless for Screening

Large birth-cohort studies have found subtle average differences in the childhood development of people who later develop the condition. Small delays in motor milestones, and differences in cognition and social functioning, years before any symptom. The predictive value for any individual is very low, and that must be stated plainly. The distributions overlap almost completely, and the great majority of children with any of these features never develop the condition. They inform the science of origins, and are useless as a screening tool. The prodrome is the period before a first episode. Function declines, attenuated experiences and beliefs appear, held with some doubt, and the person withdraws socially. It is usually identified in hindsight. Telling it apart from ordinary adolescent change is genuinely difficult. Withdrawal, changing friendships, falling grades, altered sleep, and unusual preoccupations all occur in typically developing adolescents. They also occur in depression, anxiety, adversity, and substance use. A withdrawn teenager with falling grades is something extremely common, with an extremely uncommon possible outcome, and no feature reliably separates them.

Clinical High-Risk Criteria

Most Who Meet Them Don't Transition

Clinical high-risk criteria are a research and service construct. They identify people with attenuated psychotic symptoms, brief intermittent symptoms, or genetic risk combined with functional decline. They exist to make the prodromal period studiable, and to define a group who might be offered early intervention. The honest statement is that most people meeting these criteria, do not go on to develop a psychotic disorder. Transition rates are a minority, and they fell as the criteria were applied more widely, just as base-rate reasoning predicts. The ethical problem is real. Consider a label indicating risk of a severely stigmatized condition, applied to a group most of whom will not develop it. It brings altered self-concept, altered treatment by others, and anxiety about a future most will never face. Against that, the group is already help-seeking and distressed, and most have something treatable regardless. So the defensible position depends on what is offered. Providing support to a distressed group is easier to justify than applying a designation to them.

First Episode and Untreated Psychosis

A Period That Matters Disproportionately

Onset typically falls in late adolescence and early adulthood. On average it is somewhat later in women than in men, with a second, smaller peak in women in mid-life. No explanation for that is established. This period matters disproportionately, because it coincides with finishing education, establishing work, and forming adult relationships. Disruption then removes foundations that are hard to rebuild. The duration of untreated psychosis is the interval, between the onset of psychotic symptoms and the start of adequate treatment. Longer duration is consistently associated with poorer outcome. The usual interpretation is that untreated psychosis is actively harmful. But there is an equally compatible alternative. An insidious onset with prominent negative symptoms both delays presentation and independently predicts poorer outcome. So duration may be a marker of the type of illness, rather than a cause of the outcome. The association supports early intervention, without establishing that the delay itself does the damage.

In the Clinic

Early Intervention Services

Specialist early intervention services are among the better-evidenced service innovations in this field. Their rationale rests on the association with untreated psychosis, and on the observation that much functional loss happens early. It also rests on the timing of onset in the years when education, work, and relationships are being built. They are multi-component by design, combining medication, psychological therapy, family work, and vocational support. They usually run for a defined period after a first episode, and the loss of benefit after discharge to standard services is a recognized problem. They only work if people reach them, so pathways through schools, primary care, and families matter as much as the service itself. And note that intervening after a first episode raises none of the ethical difficulty of intervening before one.

Genetic Contribution

Polygenic, Not Deterministic

Three findings define the current position on genetics. Familial aggregation is well established. The condition occurs more often among biological relatives of affected people, and more often the closer the relationship. The architecture is polygenic. Many variants each have a very small effect, with rarer variants of larger effect in a small minority of cases. There is no single causal gene, no genetic test, and nothing that identifies an individual. And relatives share environments as well as genes. Family aggregation alone establishes less than it appears to, which is why twin, adoption, and genomic designs are needed. One more point, against fatalism. A person told a condition is genetic often concludes the outcome is fixed, and that psychological and social help is beside the point. Neither follows. Genetic contribution to liability is compatible with a course that can change substantially, and the treatments that work do not depend on the condition being non-genetic.

Table 19.3.3

Statements About Familial Risk, Corrected

Here are five common statements about familial risk, with their corrections. Schizophrenia is genetic. Correction: genetic variation contributes to differences in liability across a population, and determines no individual's outcome. If a parent has it, the child will get it. Correction: having an affected parent raises risk, but the great majority of such children never develop the condition. If it does not run in my family, I cannot get it. Correction: most people who develop it have no affected close relative. High heritability means the environment does not matter. Correction: heritability says nothing about whether an outcome can be changed. And a genetic test could tell me my risk. Correction: no such test exists. Notice that four of the five errors apply a population statistic to a person. Correcting that is a routine clinical task.

In the Clinic

Talking With a Worried Relative

Relatives often ask about their own risk, or their children's. The question deserves an accurate answer, rather than either reassurance or a number. Lead with the two statements that are true, and rarely heard. Most people who develop the condition have no affected close relative, and most relatives of an affected person do not develop it. Do not supply a personal risk figure. Population figures do not transfer to individuals, and the request is usually for reassurance rather than arithmetic. Ask what prompted the question. Something specific has often happened, and addressing that is more useful than a statistics lesson. Correct fatalism explicitly where it appears. And where there is genuine concern about a specific person, the answer is assessment by a clinician, not an estimate.

Table 19.3.4

Environmental Associations - No Established Cause

Several environmental factors are associated with later risk, and each has competing explanations. Obstetric complications might affect early brain development directly. Or a shared genetic liability might affect both the pregnancy and later risk. Or maternal health and circumstances might confound both. Prenatal infection and nutrition might act directly, or through the mother's immune response, or be confounded by season, crowding, and socioeconomic position. Advanced paternal age might work through new mutations, or through social and selection factors. Season and place of birth is robust, and poorly understood. Urban upbringing faces the question of social causation versus social selection. And childhood adversity and cannabis each have direct, shared-vulnerability, and confounding explanations still live. Every row has at least two competing explanations, and none contains an established cause. Yet these factors are routinely reported as causes.

Migration and Minority Status

A Finding About Social Context

Elevated rates of psychotic disorders have been found among migrant and ethnic minority populations in several countries. The elevation is often larger in the second generation than the first. The finding is robust. The leading explanations concern social experience. Discrimination is the most frequently cited. Social defeat is proposed as a mechanism, and exclusion from housing, work, and services compounds both. Two patterns support the social reading. Rates are higher where a minority group forms a smaller share of the local population. That is a finding about social context, not about the people. And the second-generation elevation argues against explanations resting on migration itself. Any genetic-group interpretation is explicitly rejected. Rates are not elevated in the countries of origin, the second-generation pattern runs the wrong way for it, and the local-density finding cannot be explained that way at all. An observed group difference is a starting point for investigation. It is never evidence of a group deficit.

Stress, Family, and Interaction

Triggers, Relapse, and Combined Risk

Stressful life events are associated with the timing of episodes, rather than with whether the condition develops. They are triggers, not causes. An episode that follows a stressor does not mean the stressor produced the condition. Households rated high on criticism, hostility, or emotional over-involvement show higher relapse rates. Three qualifications apply. The direction is not settled, since a more severe presentation is harder to live with. High expressed emotion arises in relatives who are frightened, exhausted, and uninformed. It is what care looks like without information. And the response is family psychoeducation. The finding directs help toward families, never blame at them. Finally, gene-environment interaction is the framework the field would like to use. But specific interactions have often failed to replicate, and current work with polygenic scores still operates at group level.

Long-Term Course and Recovery

Clinical and Personal Recovery

Long-term outcomes are heterogeneous, and often better than historically assumed. Clinical recovery is defined by symptom remission and restored functioning, judged against criteria. Personal recovery is defined by the person. Living a meaningful life with agency and hope, whether or not symptoms have fully remitted. The idea of personal recovery came from the service-user movement. Its elements are usually connectedness, hope, identity beyond the diagnosis, meaning, and empowerment. The tension between the two is real. A person may meet criteria for remission while their life feels diminished. Another may have persistent symptoms and be living well. A service measuring only clinical recovery gets both cases wrong. Protective factors include social support, early access to treatment, stable housing, work or education, family understanding of the condition, and no continued substance use. Notice how many of those lie outside anything a clinic delivers in an appointment. And all outcome factors are group associations. None predicts an individual course.

Case Vignette 1 (Composite)

Yusuf: A Possible Prodrome

Now two composite cases, constructed for instruction. Yusuf is seventeen. His school referred him after about eight months of decline. He has withdrawn from friends and from a sport he played for years. His grades have fallen, and he sleeps by day and is awake at night. He describes some unusual experiences, which he himself finds puzzling and does not fully believe. This is genuinely difficult. Every feature occurs in typically developing adolescents, and in depression, anxiety, adversity, and substance use. Even the doubted experiences are reported by teenagers who never develop any condition. Psychotic disorders are uncommon, and this presentation is common. So even a feature that is more frequent among those who will transition produces mostly false positives. Most young people like Yusuf do not develop a psychotic disorder. Telling him he is at risk of schizophrenia, would apply a severely stigmatized label that most likely will not arrive. Saying nothing risks missing the minority for whom early help matters most. The resolution turns on what is offered. He is distressed and declining now. So help is framed around the present, sleep, mood, school, and substance history, with follow-up that lets the picture declare itself.

Case Vignette 2 (Composite)

Fiona: 24 Years On

Fiona is forty-six. She had a first episode at twenty-two, in her final year of study, and two more episodes in her twenties. That was twenty-four years ago. She still has some attenuated symptoms most weeks. On a strict clinical definition, she is not in full remission, and a service counting symptoms alone would record a poor outcome. But she has worked for the same organization for eleven years. She lives with her partner, has a settled circle of friends, and is in contact with her family. She manages her treatment together with her prescriber, recognizes her early warning signs, and has not been admitted to hospital in fourteen years. Asked if she considers herself recovered, she says yes. The symptoms, she explains, are a feature of her life, not the substance of it. What supported that was sustained work, stable housing, a partner and friends who understand the condition, and continuity of care. Most of those are not clinic appointments. And a prognosis given at twenty-two, based on group associations, would have been wrong. Recovery is defined by the person, as well as by criteria.

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FAQ

Questions students ask us

About The Progression of Schizophrenia, Onset, Genetic Susceptibility, and Environmental Risk

Is schizophrenia hereditary?
Genes contribute to schizophrenia, but they do not determine it. The condition clusters in families and is polygenic, involving many variants that each have a very small effect, so there is no single gene and no genetic test for individual risk. Most people who develop schizophrenia have no affected close relative, and most relatives of an affected person never develop it. Genetic contribution also does not mean the course cannot change.
What is the prodromal phase of schizophrenia?
The prodrome is the period before a first psychotic episode, when functioning declines, attenuated unusual experiences or beliefs appear but are held with some doubt, and the person withdraws socially. It is usually identified only in hindsight. Telling it apart from ordinary adolescent change, depression, anxiety, or substance use is very difficult, and most people meeting clinical high-risk criteria do not go on to develop a psychotic disorder.
What is the duration of untreated psychosis?
The duration of untreated psychosis is the interval between the onset of psychotic symptoms and the start of adequate treatment. Longer duration is consistently associated with poorer outcomes, which supports specialist early intervention services. The direction is debated, though: a gradual onset with prominent negative symptoms can both delay help-seeking and predict a poorer course, so the delay may partly mark the type of illness rather than cause the outcome.
What is the difference between clinical recovery and personal recovery?
Clinical recovery is judged against criteria, meaning symptom remission and restored functioning. Personal recovery is defined by the person: living a meaningful life with agency and hope, whether or not symptoms have fully remitted. The idea came from the service-user movement and stresses connectedness, hope, identity beyond the diagnosis, meaning, and empowerment. Someone with persistent mild symptoms may still be working, in close relationships, and recovered by their own account.

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