Abnormal Psychology

546 CHAPTER 12

the fi nding that women with schizophrenia who had higher levels of estrogen also had

better cognitive functioning (Hoff et al., 2001). The other is the fi nding that providing

constant doses of estrogen through a skin patch (in addition to antipsychotic medica-

tion) reduced the positive symptoms of women with severe schizophrenia more than

did antipsychotic medication without supplementary estrogen (Kulkarni et al., 2008).

Genetics

Various twin, family, and adoption studies indicate that genes play a role in schizo-

phrenia (Gottesman, 1991; Kendler & Diehl, 1993; Tienari, Wahlberg, & Wynne,

2006; Wynne et al., 2006). The more genes that a person shares with a relative who

has schizophrenia, the higher the risk that that person will also develop

schizophrenia (see Table 12.7). However, even for those who have a close

relative with schizophrenia, the chance of developing the disorder is still

relatively low: More than 85% of people who have one parent or one

sibling (who is not a twin) with the disorder do not go on to develop

it themselves (Gottesman & Moldin, 1998), and this percentage is even

lower for people with a grandparent, aunt, or uncle (second-degree rela-

tives) with the disorder (Gottesman & Erlenmeyer-Kimling, 2001). None-

theless, a family history of schizophrenia is still the strongest known risk

factor for developing the disorder (Hallmayer, 2000).

If the cause of schizophrenia were entirely genetic, then when one

identical twin developed the disorder, the co-twin would also develop the

disorder; that is, the co-twin’s risk of developing schizophrenia would

be 100%—if schizophrenia were entirely caused by genes. But this is

not what happens; the actual risk of a co-twin developing schizophrenia

ranges from 46 to 53% (in different studies), as shown in Table 12.7.

However, identical twins have the same predisposition for develop-

ing schizophrenia, although only one of them may develop it. This means

that even if only one twin in a pair develops the disorder, the children of

both twins (the one with the disorder and the one without) have the same

risk of developing it. That is, both the affected and the unaffected twin transmit the

same genetic vulnerability to their offspring (Gottesman & Bertelsen, 1989).

Another risk factor that may be related to genes does not involve the usual pat-

terns of inheritance, but may hinge on genetic defects in the sperm of older fathers

(Tsuchiya et al., 2005; Wohl & Gorwood, 2007; Zammit et al., 2003): Children

whose fathers were over 45 years old when they were born were almost three times

as likely to develop schizophrenia as children whose fathers were between the ages

of 20 and 24 when they were born. One possibility is that mutations in the sperm

of older fathers may be responsible for this increased rate, but there is no solid evi-

dence yet that such mutations are in fact responsible for this effect.

Researchers have begun to make inroads in identifying specifi c genes that cre-

ate various vulnerabilities for schizophrenia (Craddock, O’Donovan, & Owen,

2005; Stefansson et al., 2008; Xu et al., 2008). However, the results of studies that

examine specifi c genes thought to be related to schizophrenia have generally been

disappointing—any given gene accounts for only a small minority of cases of schizo-

phrenia (Hamilton, 2008; Sanders et al., 2008). Nevertheless, some aspects of the

disorder have been linked to specifi c genes; for example, some patients with schizo-

phrenia exhibit symptoms of agitation, and a specifi c mutation of one gene has been

linked to this symptom (Sachs, 2006).

Clearly, genes alone do not determine whether someone will develop schizophre-

nia. In order to examine the influences of both genes and environment, a Finnish

adoption study tracked two groups of adopted children: those whose biological moth-

ers had schizophrenia, and those whose mothers did not (the control group). None of

the adoptive parents of these children had schizophrenia, but some adoptive families

were dysfunctional (Tienari et al., 1994, 2006). In the control group, the incidence of

schizophrenia was no higher than in the general population, regardless of the charac-

teristics of the adoptive families. In contrast, the children whose biological mothers had

schizophrenia and whose adoptive families were dysfunctional were much more likely

P S

N

Table 12.7 • Degree of Relatedness and Risk

of Developing Schizophrenia

Family Member(s) with

Schizophrenia

Risk of Developing

Schizophrenia

First cousin 2%

Half-sibling 6%

Full sibling 9%

One parent 13%

Two parents 46%

Fraternal twin 14–17%

Identical twin 46–53%

Sources: Gottesman, 1991; Kendler, 1983.