people can become
depressed though several
different routes, such as
genetics, trauma, hormones,
substance abuse and head
injuries etc...
MAJOR DEPRESSIVE
DISORDER
major depression more intense and
pro-longed. DSM-IV (APA) sad and helpless
everyday for weeks at a time, ABSENCE
OF HAPPINESS more reliable symptom
than sadness.
ROTTENBERG ET AL. (2002)
- examined films and
individuals with depression
acted normally to negative
films but laughed less at
comedies or smiled at happy
pictures.
5% of adults in
the US are
majorly
depressed. 10%
of people have it
at some point in
their life. no lab
tests confirm
such a diagnosis
however.
beyond age
14 there is a
distinctive
pattern that
depression is
more common
in females.
It is more common to have
episodes of depression
separated by periods of a
normal mood. the first
episode in depression is
likely to be triggered by an
event but for later episodes
it gets less and less likely to
be triggered, it's as if brain
learns to be depressed.
GENETICS
twin and adoption studies
indicate a moderate degree of
heritability for depression, no
one gene shows a strong link to
depression.
people with early onset
depression (before 30) have
a high probability of
relatives with depression
and anxiety disorders.
whereas people with a late
onset of depression have a
high probability of relatives
with circulatory problems.
distinguishing between
early and late onset may
lead to progress in
identifying genes and
therapies.
CAPSI et al. (2003) - the effect of a
gene might interact with the
environment. one gene controls the
serotonin transporter, two short forms of
this gene combined with increasing
numbers of stressful experiences led to
higher probability of depression than
people with two long forms where the
risk was only slight with increased
events. HOWEVER this study has failed
replications since
OTHER BIOLOGICAL INFLUENCES
a few cases of
depression are linked to
VIRAL INFECTIONS -
such as BORNA disease
in farm animals, 100% of
people tested positive for
BORNA disease were also
depressed. viruses might
PREDISPOSE depression.
HORMONES might
be another trigger for
depression, stress
increases release of
cortisol. postpartum
(after birth)
depression,
hormones are a
contributing factor. In
older men a decline in
TESTOSTERONE
was associated with
increased probability
of depression.
LINKS TO HEMISPHERIC DOMINANCE -
studies have found link between a happy
mood and increased activity in the
prefrontal cortex. Furthermore, most
people with depression have
DECREASED ACTIVITY in the LEFT and
INCREASED IN THE RIGHT.
ANTIDEPRESSANT DRUGS
early antidepressants were
discovered by accident. there are
THREE TYPES OF
ANTIDEPRESSANT, TRICYLICS,
SELECTIVE SEROTONIN
REUPTAKE INHIBITORS AND
MONOAMINE OXIDASE
INHIBITORS
TRICYLICS - block the transporter proteins that reabsorb
SEROTONIN, DOPAMINE AND NOREPINEPHRINE into the
presynaptic neuron after their release. this PROLONGS the
presence of neurotransmitters in the synaptic cleft, where
they continue to stimulate the postsynaptic cell. HOWEVER
TRICYLICS ALSO block histamine receptors (causes
drowsiness), acetylcholine receptors (which causes dry
mouth) and sodium channels (which causes heart
irregularities)
SSRIs - similar to TRICYCLICS but
specific to the neurotransmitter
serotonin. blocks reuptake of
serotonin, milder side effects than
tricyclics.
MAOIs - MONOAMINE OXIDASE
INHIBITORS - block the enzyme
monoamine oxidase, which
metabolizes serotonin into active
forms.
ATYPICAL
ANTIDEPRESSANTS -
e.g. ST. JOHN'S WORT
- a herb, less
expensive, not
prescribed (+ or -) snd
effectiveness is the
same as an
antidepressant drug.
HOWEVER, the
enzyme breaks down
other medicines taken
at the same time.
moat antidepressants increase the presence of serotonin
so it would seem that the problem in depression is too little
neurotransmitter. HOWEVER people with depression have a
normal neurotransmitter release. There is no clear evidence
that ANY ANTIDEPRESSANT DRUG PRODUCES ANY
DIFFERENT EFFECTS from any other.
TODAY research focuses on neurotrophins,
which aid in the survival, growth and
connections of neurons. most people with
depression have lower than average levels
of a neurotrophin called BNDF. people with
LOW BDNF have a smaller than average
hippocampus, impaired learning etc.. BDNF
by itself does not automatically elevate /
raise mood, but it helps facilitate new
learning that builds new synapses.
HOW EFFECTIVE ARE
ANTIDEPRESSANTS? depression occurs in
episodes, giving someone medication
produces expectation of improvement,
enhancing probability of recovery,
researchers compare the drug influence to a
placebo. many people respond well to
placebos.for patients with mild to moderate
depression, results for placebos overlap with
drugs, the only group where drugs produce
an advantage is for severe depression.
AN ALTERNATIVE TO ANTIDEPRESSANTS and PSYCHOTHERAPY IS
ELECTROCONVULSIVE THERAPY (ECT) - which is an ELECTRICALLY
INDUCED SEIZURE. seizures WERE PREVIOUSLY induced with a large dose
of insulin. HOWEVER NOWADAYS seizures are induced with an ELECTRIC
SHOCK. ECT is quick and most people awaken calmly. it is used today mostly
for people who haven't responded to therapy or drugs. A COMMON SIDE
EFFECT OF ECT IS MEMORY LOSS and there is a HIGH RISK OF
RELAPSING. not sure how ECT relieves depression.
a similar
treatment is
repetitive
transcranial
magnetic
stimulation.
ALTERNATIVE TO DRUGS IS PSYCHOTHERAPY -
drugs and psychotherapy are about equally effective.
HOWEVER drugs work better for life-long unhappiness,
secondly drugs are often of little use to people who
have suffered childhood abuse. thirdly, psychotherapy
is more likely to have long-term benefits
SLEEP PATTERNS - almost all people with depression
have sleep problems, awaken early, unable to get
back to sleep, sleep goes straight into REM sleep
after 45 minutes. people who are depressed have
more than average eye movements. ALTERED
SLEEP is a life-long trait of people predisposed to
depression.
SEASONAL AFFECTIVE DISORDER
- DEPRESSION that recurs during a
particular season. people with SAD
have phase-delayed sleep and
temperature rhythms. it is rarely as
severe as normal depression. can
cure SAD with very bright lights.
BIPOLAR DISORDER
UNIPOLAR DISORDER vary between
depression and normality, people with
BIPOLAR vary between depression and
mania.was previously known as
MANIC-DEPRESSIVE DISORDER.
MANIA is characterised by restless
activity, laughter, confidence, loss of
inhibitions.
BIPOLAR 1 MORE
FULL-BLOWN EPISODES OF
MANIA COMPARED TO
BIPOLAR 2
GENETICS IN BIPOLAR DISORDER -
genetic predisposition for bipolar disorder,
two genes increase the probability of it,
some of the same genes that predispose
major depression.
TREATMENTS for bipolar disorder include
LITHIUM SALTS. lithium stabilises mood.
antidepressant drugs are risky for people with
bipolar disorder as they sometimes provoke a
switch from one end of the scale to the other.
FURTHERMORE, getting
people to maintain a constant
sleep-wake cycle reduces the
risk of intense mood swings