BIOLOGICAL
EXPLANATIONS
Bio chemical changes
Genetic inheritance
Metabolic &
hormonal changes
MAOI’S
• In the 1950’s, using
Monoamine oxidising
inhibitors for TB, they
discovered that patients
were remarkably euphoric
Yippee,
I’m ill!
Qu. Therefore, what neurotransmitters
are likely to be involved with mood?
• Monoamines are = ?
• Serotonin – Noradrenaline – Dopamine
•
• catecholamine" hypothesis
• Schildkraut (1965) believed that too high a
level of noradrenaline led to mania and too
little to depression.
Qu. What happens if you change
the level of one monoamine?
• Prange, 1974
• A deficit in serotonin ‘permits’ (not causes) the
symptoms of depression.
• Changes in serotonin levels affect the nature
and intensity of the symptoms.
• If monoamine activity is increased = mania
• If monoamine activity is decreased = depression
Kety, 1975 – Permissive Amine Theory
• Both Serotonin and noradrenaline levels change in
mood disorders.
• It is serotonin that controls the levels of noradrenaline.
• High levels of serotonin keep levels of noradrenaline
constant which prevents mood swings.
• There is a serotonin deficit in depressives = is genetic.
• Qu. Therefore, according to this theory, what happens
if there are low serotonin levels?
Kety, 1975 – Permissive Amine Theory
Mania
Noradrenaline
Serotonin
Depression
Qu. What if Serotonin levels drop to a very low level?
Supporting evidence for the
permissive amine theory?
• Teuting et al (1981)
• Examined the urine of
depressed patients
• Found by-products
that suggest lowered
levels of both
serotonin and
noradrenalin.
Supporting evidence for the
permissive amine theory?
• McNeal & Cimbolic
(1986)
• Examined the cerebo spinal fluid of depressed
suicidal patients
• Found reduced amount of
by-product.
• Suggests low level of
serotonin in the brain
Qu. If this theory is true, what would happen
if you take drugs to increase serotonin
levels?
• Drugs treatments that concentrate on raising
serotonin levels (SSRI’s) do improve the
depressed mood in the majority of patients
• Newer anti-depressants (like Effexor) are
actually targeted at both serotonin and
noradrenaline, and are even more effective in
treating depression.
Qu. Can this theory explain gender
differences in prevalence rates?
• Diksic et al (1997)
• Found that men make
52% more serotonin than
women.
• Qu. Conclusion?
• This could make men far
less prone to depression
than women.
Qu. Any criticisms of theory?
• 1. Not all depressives show reduced levels of
these neurochemicals.
• Qu. Would these benefit from drug treatments?
• No, not all patients benefit from drugs
treatments.
• Qu. What does this imply about the causes?
• Are other biological factors involved?
• Cortisol, oestrogen, diet?
Qu. Any criticisms of theory?
• Deakin & Graeff (1991)
• 2. Even following recovery from depression
the deficits in serotonin and noradrenalin
levels still remain.
• Qu. What does this imply?
• Another neurochemical involved perhaps?
Qu. Any criticisms of theory?
• 3. Anti-depressives such as MAOIs
(monoamine oxidase inhibitors) increase the
levels of noradrenalin and serotonin within
minutes.
• However, they have no effect on mood for
many weeks (normally two weeks).
• This suggests that they are not working simply
by increasing the levels of chemical in the brain.
• Qu. What does this imply about the cause?
Conclusion:
Depression is a
complex issue
We don’t really
understand the full
interaction between
neurotransmitters.
Other biological
factors are clearly
involved.
Genetics & Depression
Qu. How do you ‘prove’ a
genetic argument for any
behaviour?
Twin studies:
McGuffin
et al, 1996
MZ
46%
Bertelsen 1977
Qu. Problems?
59%
DZ
20%
30%
Genetics & Depression
Family concordance rates
Gen Pop
Family
Gershon 1990
Wender 1986
15%
15%
40-50%
70% if adopted
Qu. Problems?
Essay Preparation
• Biological Aetiologies
• Using PPt and handout group A01 and AO2
material for Neurotransmitter Explanations
• Do the same for genetic explanations