574 CHAPTER 14
Causes of Schizophrenia
14.14 Evaluate the biological and environmental influences on schizophrenia.
When trying to explain the cause or causes of schizophrenia, biological models and theories
prevail, as it appears to be most likely caused by a combination of genetic and environmental
factors. This is captured by the neurodevelopmental model, or neurodevelopmental hypothesis,
of schizophrenia (Rapoport et al., 2005; Rapoport et al., 2012). Biological explanations of schizo-
phrenia have generated a significant amount of research pointing to genetic origins, prenatal
influences such as the mother experiencing viral infections during pregnancy, inflammation in
the brain, chemical influences (dopamine, GABA, glutamate, and other neurotransmitters), and
brain structural defects (frontal lobe defects, deterioration of neurons, and reduction in white
matter integrity) as the causes of schizophrenia (Brown & Derkits, 2010; Cardno & Gottesman,
2000; Gottesman & Shields, 1982; Harrison, 1999; Kety et al., 1994; Nestor et al., 2008; Rijsdijk
et al., 2011; Söderlund et al., 2009). Dopamine was first suspected when amphetamine users
began to show schizophrenia-like psychotic symptoms. One of the side effects of amphetamine
usage is to increase the release of dopamine in the brain. Drugs used to treat schizophrenia
decrease the activity of dopamine in areas of the brain responsible for some of the positive
symptoms. However, it is not that simple. The prefrontal cortex (an area of the brain involved
in planning and organization of information) of people with schizophrenia has been shown to
produce lower levels of dopamine than normal (Harrison, 1999), resulting in attention deficits
(Luck & Gold, 2008) and poor organization of thought, negative symptoms of the disorder.
Further support for a biological explanation of schizophrenia comes from studies
of the incidence of the disorder across different cultures. If schizophrenia were caused
mainly by environmental factors, the expectation would be that rates of schizophrenia
would vary widely from culture to culture. There is some variation for immigrants
and children of immigrants, but about 7 to 8 individuals out of 1,000 will develop
schizophrenia in their lifetime, regardless of the culture (Saha et al., 2005).
Family, twin, and adoption studies have provided strong evidence that genes are a
major means of transmitting schizophrenia. The highest risk for developing schizophrenia
if one has a blood relative with the disorder is faced by monozygotic (identical) twins, who
share 100 percent of their genetic material, with a risk factor of about 50 percent (Cardno &
Gottesman, 2000; Gottesman & Shields, 1976, 1982; Gottesman et al., 1987). Dizygotic twins,
who share about 50 percent of their genetic material, have about a 17 percent risk, the same
as a child with one parent with schizophrenia. As genetic relatedness decreases, so does the
risk (see Figure 14.3). Twin studies are not perfect tools, however; identical twins share the
same womb but are not necessarily exposed to the same exact prenatal or postnatal environ-
ments, causing some to urge caution in interpreting the 50 percent figure; and even twins
reared apart are often raised in similar childhood environments (Davis et al., 1995).
Adoption studies also support the genetic basis of schizophrenia (Sullivan, 2005;
Tienari et al., 2004). In one study, the biological and adoptive relatives of adoptees
with schizophrenia were compared to a control group of adoptees without schizophre-
nia but from similar backgrounds and conditions (Kety et al., 1994). The adoptees with
schizophrenia had relatives with schizophrenia but only among their biological relatives.
When the prevalence of schizophrenia was compared between the biological relatives of
the adoptees with schizophrenia and the biological relatives of the control group, the rate
of the disorder in the relatives of the group with schizophrenia was 10 times higher than in
the control group (Kety et al., 1994). It appears the strongest genetic risk may be associated
with a gene that plays a role in synaptic pruning during development. In individuals with
schizophrenia that have this gene, this process appears to go awry during adolescence,
leading to the removal of too many connections between neurons (Sekar et al., 2016).There’s something I don’t understand. If one identical twin has
the gene and the disorder, shouldn’t the other one always have it,
too? Why is the rate only 50 percent?Schizophrenia and depression have been
suggested as possible diagnoses that
may have been applicable for Mary Todd
Lincoln, the wife and widow of President
Abraham Lincoln. However, she reportedly
experienced a variety of medical conditions
that could also explain aspects of her
eccentric behavior, personality, and mood
changes.