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biological etiology of schizophrenia and mood disorders
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The document contains biological explanations for three disorders: schizophrenia, depression and bipolar disorders.
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UDPD- UNIT 1-Biological etiology-explanations and interventions for Mood disorders andSchizophrenia: Application in case of mood disorders and schizophrenia
What is the Biological etiology of schizophrenia? (18.75)
Schizophrenia is a complex mental disorder characterized by an array of diverse symptoms, including extreme
oddities in perceptions, hallucinations, delusions, disturbances in speech, and several other symptoms. As a
result of such fragmentation, persons with schizophrenia have serious problems in adjusting to the demands
of reality. Thus, the hallmark of schizophrenia is a significant loss of contact with reality, referred to as
psychosis.
Genetic Factors
There is a strong association between the closeness of the blood relationship (i.e., level of gene sharing or
consanguinity) and the risk for developing schizophrenia. For example, the prevalence of schizophrenia in the
first-degree relatives (parents, siblings, and offspring) of a proband (the diagnosed group of people who
provide the starting point for inquiry) with schizophrenia is about 10 percent. For second-degree relatives who
share only 25 percent of their genes with the proband (e.g., half-siblings, aunts, uncles, nieces, nephews, and
grandchildren), the lifetime prevalence of schizophrenia is closer to 3 percent. Interpretation of familial
concordance patterns is never completely straightforward, in part because of the strong relationship between
the sharing of genes and the sharing of the environments in which those genes express themselves. To
disentangle the contributions of genes and environment, twin and adoption studies are needed. One of the
strongest pieces of evidence that schizophrenia is a biological disorder is that it appears to be heritable. Both
adoption studies (Kety et al., 1968, 1994) and twin studies (Gottesman and Shields, 1982; Tsuang, Gilbertson,
and Faraone, 1991) indicate that schizophrenia is a heritable trait.
A) Twin Studies: Schizophrenia concordance rates for identical twins are routinely and consistently found to
be significantly higher than those for fraternal twins (sharing 50% genetic material) or ordinary siblings. E.
Fuller Torrey and his colleagues (1994) have published a review of the major literature worldwide on twin
studies of schizophrenia. The overall pairwise concordance rate is 28 percent in MZ twins and 6 percent in
DZ twins. This suggests that a reduction in shared genes from 100 percent to 50 percent reduces the risk of
schizophrenia by nearly 80 percent. Two conclusions can therefore be drawn: First, genes undoubtedly play a
role in causing schizophrenia. Second, genes themselves are not the whole story. Twin studies provide some
of the most solid evidence that the environment plays an important role in the development of schizophrenia
because if schizophrenia were exclusively a genetic disorder, the concordance rate for identical twins would,
of course, be 100 percent.
Fischer (1971, 1973) in an ingenious study pioneered the investigative strategy of studying MZ twins who are
discordant for schizophrenia. Fischer reasoned that genetic influences, if present, would be just as likely to
show up in the offspring of the twins without schizophrenia in discordant pairs as they would be to show up
in the offspring of the twins with schizophrenia (because they share all their genes in common). And, in a
search of official records in Denmark, Fischer found exactly that. Gottesman and Bertelson (1989) reported
an age-corrected incidence rate for schizophrenia of 17.4 percent for the offspring of the MZ twins without
schizophrenia (i.e., the well MZ twins). These results lend impressive support to the genetic hypothesis.
A problem with twin studies is the inherent assumption that the environments of MZ twins are similar to the
environments of DZ twins. But because MZ twins are identical (and always of the same gender), their
environments will actually be more similar than the environments of DZ twins. Therefore, twin studies will
overestimate the importance of genetic factors. To overcome this problem adoption studies have been done.
B) Adoption Studies: Here, concordance rates for schizophrenia are compared for the biological and adoptive
relatives of persons who have been adopted out of their biological families at an early age (preferably at birth)
and have subsequently developed schizophrenia. If concordance is greater among the patients’ biological than
adoptive relatives, a hereditary influence is strongly suggested. Heston (1966) followed up 47 children who
had been born to mothers who were in a state mental hospital suffering from schizophrenia. The children had
been placed with relatives or into foster homes within 72 hours of their birth. In his follow up study, Heston
found that 16.6 percent of these children were later diagnosed with schizophrenia. In contrast, none of the 50
,control children (selected from among residents of the same foster homes whose biological mothers did not
have schizophrenia) developed schizophrenia.
An alternative approach involves locating adult patients with schizophrenia who were adopted early in life
and then looking at rates of schizophrenia in their biological and adoptive relatives. A large-scale and
multifaceted adoption study of this type was undertaken in Denmark, with Danish and American investigators
working in collaboration. As would be expected on the basis of a genetic model, the data showed a
preponderance of schizophrenia and “schizophrenia-spectrum” problems (e.g., schizotypal and paranoid
personality disorder) in the biological relatives of adoptees with schizophrenia. More specifically, 13.3 percent
of the 105 biological relatives had schizophrenia or schizophrenia-spectrum disorders themselves. In contrast,
only 1.3 percent of the 224 adoptive parents showed such problems.
* GENETIC MUTATION- So far, researchers have not located a single “schizophrenia gene,” although
researchers have found many genes that appear to increase the likelihood of this disease. A review by Crow
(2007) notes that evidence for linkage to susceptibility for schizophrenia has been reported for twenty-one of
the twenty-three pairs of chromosomes, but many of the findings have not been replicated. So far, no single
gene has been shown to cause schizophrenia. For example, Walsh et al. (2008) suggest that a large number of
rare mutations play a role in the development of schizophrenia. One rare mutation involves a gene known as
DISC1 (disrupted in schizophrenia 1). This gene is involved in the regulation of embryonic and adult
neurogenesis, neuronal migration during embryonic development, function of the postsynaptic density in
excitatory neurons, and function of mitochondria (Brandon et al., 2009; Kim et al., 2009; Park et al., 2010;
Wang et al., 2010). Mutations of this gene have been found in some families with a high incidence of
schizophrenia (Chubb et al., 2008; Schumacher et al., 2009). Although the incidence of DISC1 mutation is
very low, its presence appears to increase the likelihood of schizophrenia by a factor of 50 (Blackwood et al.,
2001). This mutation also appears to increase the incidence of other mental disorders, including bipolar
disorder, major depressive disorder, and autism (Kim et al., 2009).
The effect of paternal age provides further evidence that genetic mutations may affect the incidence of
schizophrenia (Brown et al., 2002; Sipos et al., 2004). Several studies have found that children of older fathers
are more likely to develop schizophrenia. Most investigators believe that the increased incidence of
schizophrenia is caused by mutations in the spermatocytes, the cells that produce sperms. These cells divide
every sixteen days after puberty, which means that they have divided approximately 540 times by age thirty-
five. In contrast, women’s oocytes divide twenty-three times before the time of birth, and only once after that.
The likelihood of a copying error in DNA replication when a cell divides increases with the number of cell
divisions and an increase in copying errors may cause an accumulation of mutations that are responsible for
an increased incidence of schizophrenia.
Several researchers (for example, Tsankova et al., 2007; Swerdlow, 2011) suggest that epigenetic
mechanisms, as well as mutations, may contribute to the development of schizophrenia. Epigenetic (“on top
of the genes”) mechanisms control the expression of genes. The long strands of DNA that constitute the
chromosomes are wound around a series of proteins known as histones. Groups of atoms can attach to the
amino acids in the histone proteins and change their characteristics. For example, when methyl groups (–CH3)
attach to histone proteins, the regions of DNA wound around them draw in more tightly, which prevents these
regions from being translated into messenger RNA. Thus, methylation of histone proteins prevents the
expression of particular genes. (Other groups of atoms can also bind with histone proteins and either inhibit
or promote gene expression.) Many epigenetic changes are initiated by environmental events such as exposure
to toxins, and some epigenetic changes can be transmitted to offspring.
Although we are certain that schizophrenia has a genetic basis, we are still a long way from understanding
which genes are involved and what effects they have. To simplify things, researchers are now focusing on less
complex and more homogenous phenotypes (such as specific symptom clusters) that may potentially be under
the control of a smaller number of genes. They are also exploring endophenotypes—discrete, stable, and
measurable traits that are thought to be under genetic control. By studying different endophenotypes,
researchers hope to get closer to specific genes that might be important in schizophrenia
Prenatal Exposures
, Whether or not a genotype is expressed depends on biological and environmental triggers, therefore, it is
important to discuss some environmental risk factors that might either cause schizophrenia or trigger it in a
genetically vulnerable person.
A) Viral infection: In 1957 there was a major epidemic of influenza in Finland. Studying the residents of
Helsinki, Mednick, and colleagues (1988) found elevated rates of schizophrenia in children born to mothers
who had been in their second trimester of pregnancy at the time of the influenza epidemic. The link between
maternal influenza and subsequent schizophrenia in the grown offspring has now been well replicated using
influenza epidemic information from other countries. The risk of schizophrenia seems to be greatest when the
mother gets the flu in the fourth to seventh month of gestation.
B) Rhesus Incompatibility: Rhesus (Rh) incompatibility occurs when an Rh-negative mother carries an Rh-
positive fetus. (Rhesus-positive or -negative is a way of typing a person’s blood.) Incompatibility between the
mother and the fetus is a major cause of blood disease in newborns. Interestingly, Rh incompatibility also
seems to be associated with an increased risk for schizophrenia. Hollister, Laing, and Mednick (1996) have
shown that the rate of schizophrenia is about 2.1 percent in males who are Rh-incompatible with their mothers.
For males who have no such incompatibility with their mothers, the rate of schizophrenia is 0.8 percent—very
near the expected base rate found in the general population.
C) Pregnancy and Birth Complications: Patients with schizophrenia are much more likely to have been
born following pregnancy or delivery that was complicated in some way (Cannon et al., 2002). Although the
type of obstetric complication varies, many delivery problems (for example, breech delivery, prolonged labor,
or the umbilical cord around the baby’s neck) affect the oxygen supply of the newborn (hypoxia). The research
points toward damage to the brain at a critical time of development.
D) Early nutritional deficiency: In October 1944, a Nazi blockade resulted in a severe famine that affected
people living in Amsterdam and other cities in the west of the country. The population was severely
malnourished and many died of starvation. Children who were conceived at the height of the famine had a
twofold increase in their risk of later developing schizophrenia (Brown, 2011). Early prenatal nutritional
deficiency seems to have been the cause.
E) Maternal Stress: If a mother experiences an extremely stressful event late in her first trimester of
pregnancy or early in the second trimester, the risk of schizophrenia in her child is increased (King e al., 2010).
In a large population study conducted in Denmark, the death of a close relative during the first trimester was
associated with a 67% increase in the risk of schizophrenia in the child (Khashan et al., 2008).
Brain abnormalities
Positron emission tomography (PET), magnetic resonance imaging (MRI), and other sophisticated approaches
are revealing abnormalities in the structure and function of the brain as well as in neurotransmitter activity in
people who suffer from schizophrenia.
A) Structural Abnormalities:
● One of the most well-replicated findings concerns the brain ventricles. These are fluid-filled spaces
that lie deep within the brain. Compared with controls, patients with schizophrenia have enlarged brain
ventricles, with males possibly being more affected than females. Enlarged brain ventricles are
important because they are an indicator of a reduction in the amount of brain tissue. MRI studies of
patients with schizophrenia show about a 3 percent reduction in whole-brain volume relative to that in
controls (Hulshoff Pol & Kahn, 2008).
● Cahn and colleagues (2002) measured changes in the overall volume of gray matter (which is made up
of nerve cells) in patients who were experiencing their first episode of schizophrenia. Thirty-four
patients and 36 matched, healthy comparison subjects received MRI brain scans at the start of the study
and then again 1 year later. The results showed that the volume of gray matter declined significantly
over time in the patients but not in the controls. More specifically, there was almost a 3 percent
decrease in the volume of gray matter in the patients in the 1-year period between the first and the
second scans.
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