1.1 Appears to run in families &
studies claim that the risk of
someone developing SZ is
proportional to the amount
of genes they share.
1.1.1 MZ twins
126.96.36.199 DZ twins
188.8.131.52.1 Children of 2
have 46% risk.
have 5% risk.
1.1.2 Gottesman found in several twin studies higher
concordance rates for MZ twins than for DZ twins, supporting
the claim that risk is higher if more genes are shared.
184.108.40.206 Concordance rates
vary widely depending
on the methods used
to calculate them.
220.127.116.11.1 sample sizes are small due to
MZ twin occurrence being rare
and only 1% chance of SZ
occurrence in the population.
18.104.22.168.1.1 lowers external validity
22.214.171.124 Assumes that environments of MZ&DZ twins
are the same, so must mean greater
concordance rates are due to greater genetic
126.96.36.199.1 Others point out MZ twins have different
environments to DZ twins, often treated as
'the twins' not individuals.
188.8.131.52.1.1 Difference in concordance rates
may only reflect environmental
difference of the twin types.
1.1.3 Adoption studies have tried to distinguish
effects of heredity from environmental effects.
184.108.40.206 Research found high rates of SZ in
individuals whose bio parents had SZ even
though they were adopted by healthy parents.
220.127.116.11.1 Tienari studied 155 adopted children whose bio mothers had SZ. They
were compared with a healthy matched group & found 10% had developed
SZ compared to 1% from the control.
18.104.22.168.1.1 Offers strong evidence for genetic component in development of SZ.
22.214.171.124.1.1.1 However, such studies are plagued by methodological problems
such as the bias of the researches in favour of genetic conclusions.
2.1 Messages from
dopamine fire too
easily & too often.
2.1.1 SZ's have abnormally high
numbers of D2 receptors so
more dopamine binds. They
play an important role in
guiding attention, perception
& thought so disturbance in
the functions leads to SZ
126.96.36.199 Phenothiazines that
block dopamine at the
synapse are successful
at alleviating symptoms.
188.8.131.52.1 but they don't work
for everyone so
dopamine may not
account for all types
of SZ, suggesting
184.108.40.206 L-dopa for treating
dopamine levels, resulting
in SZ episodes in the
highlighting a link between
SZ & excess dopamine.
220.127.116.11.1 Amphetamines also increase
availability of dopamine and have made
symptoms worse in those already
affected, causing characteristic
symptoms such as hallucinations.
18.104.22.168.1.1 however, this has not
happened to all individuals.
22.214.171.124 This explanations is over
simplified and does not take
into account that other
neurotransmitters such as
serotonin and glutamate
influence development of SZ.
126.96.36.199.1 Recent research
deficits as secondary
to altered cortical
glutamate levels may
play more important
role in onset of SZ.
188.8.131.52.1.1 research found glutamate agonists
reversed SZ symptoms supporting the
glutamate theory & its involvement in SZ
suggesting dopamine alone is not
184.108.40.206.2 high levels of
dopamine were not
found in all SZ's &
drugs such as
effectively against the
disorder yet have little
been found to be
may be involved.
220.127.116.11.3 new theories suggest high levels in
mesolimbic dopamine system are associated
with positive symptoms & high levels in
mesocortical system associated with negative.