this presentation include causal factors of mood disorders

1. BY:
PAYAL SHARMA

2. What are mood disorders?
• Formerly known as “affective disorders”.
• Mood disorders are diverse in nature.
• Many different types of mood disorders recognized by DSM-5.
• In all mood disorders, extremes of emotion – soaring elation or
deep depression – dominate the clinical picture.
• Abnormal mood is the defining feature.

3. • 2 key moods involved in mood
disorders are:
MANIA – characterized by intense and unrealistic feelings of
excitement and euphoria.
DEPRESSION – feelings of extraordinary sadness and dejection.

4. •These mood states are often conceived to be at
opposite ends of a mood continuum with normal
mood in the middle.
•Though usually true, sometimes a person may have
symptoms of mania and depression during the same
time period – MIXED EPISODE cases.

5. Prevalence
•At least 15-20% higher frequency than schizophrenia.
•Almost same rate as all anxiety disorders taken
together.
•Unipolar major depression is much more common .
•Its occurrence has apparently increased in recent
decades to 17%.
•More frequent in women than in men – 2:1

6. DSM-5 lists Depressive disorders as:
• Major depressive disorder (including major depressive episode),
• Persistent depressive disorder (dysthymia),
• Disruptive mood dysregulation disorder,
• Premenstrual dysphoric disorder,
• Substance/medication-induced depressive disorder,
• Depressive disorder due to another medical condition,
• Other specified depressive disorder, and
• Unspecified depressive disorder.

7. MAJOR DEPRESSIVE DISORDER
•Diagnostic criteria – more symptoms than are
required for dysthymia and are more persistent.
•To receive the diagnosis, the person must be in a
major depressive episode – single or recurrent.
•Although few depressions occur without anxiety,
depression is the predominant feature.

8. Major Depressive Disorder – Diagnostic Criteria
A. Five (or more) of the following symptoms have been present during the
same 2-week period and represent a change from previous functioning: at
least one of the symptoms is either (1) depressed mood or (2) loss of interest
or pleasure.
1. Depressed mood most of the day, nearly every day, as indicated by either
subjective report (e.g., feels sad, empty, hopeless) or observation made by
others (e.g., appears tearful). (Note: In children and adolescents, can be
irritable mood.)
2. Markedly diminished interest or pleasure in all, or almost all, activities most
of the day, nearly every day (as indicated by either subjective account or
observation).
3. Significant weight loss when not dieting or weight gain (e.g., a change of
more than 5% of body weight in a month), or decrease or increase in appetite
nearly every day. (Note: In children, consider failure to make expected weight
gain.)
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day (observable by
others, not merely subjective feelings of restlessness or being slowed down).

9. 6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt (which may be
delusional) nearly every day (not merely self-reproach or guilt about being
sick).
8. Diminished ability to think or concentrate, or indecisiveness, nearly every
day (either by subjective account or as observed by others).
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal
ideation without a specific plan, or a suicide attempt or a specific plan for
committing suicide.
B. The symptoms cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
C. The episode is not attributable to the physiological effects of a substance or
to another medical condition.
D. The occurrence of the major depressive episode is not better explained by
schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional
disorder, or other specified and unspecified schizophrenia spectrum and other
psychotic disorders.
E. There has never been a manic episode or a hypomanic episode.

10. Causal Factors - BIOLOGICAL
• Genetic influences.
• Neurochemical factors
• Abnormalities of hormonal regulatory systems.
• Neurophysiological and neuroanatomical influences
• Sleep and other biological rhythms.

11. Genetic Influences
• Prevalence of mood disorders is three times higher among blood
relatives of unipolar depression.
• Twin studies provide a much more conclusive evidence.

12. • Adoption method studies have also shown that unipolar
depression occurred 7 times more often in biological
relatives of severely depressed adoptees than in the
biological relatives of control adoptees (Wallace et al.,2002;
Wender et al.,1986).
• Taken together, the result of family, twin and adoption
studies make a strong case for moderate genetic
contribution to the causal pattern of unipolar major
depression, although not as large a contribution as for
bipolar disorder.

13. •However, evidence of genetic contribution is much
less consistent for milder but chronic forms of
depression such as dysthymia.
•Some studies have found no evidence at all.
•Attempts to identify specific genes
that may be responsible for
these genetic influences have
not yet been successful, although
there are some promising leads.

14. • One promising candidate – serotonin transporter gene.
• Central seronergic dysfunction has been implicated in
negative mood states.
• There are two different kinds of versions or alleles are
involved- the short alleles (s) and the long alleles (l). And
people may have two short alleles (ss), two long alleles (ll),
and one of each (sl)
• Researchers have studied the possibility of gene-
environment interaction.

15. •STUDY – 847 people in New Zealand were followed
from birth until 26 years of age (Caspi, et al. 2003).
•Assessed occurrence of major depression in the past
one year and stressful life events in the previous 5 yrs.
•ss allele – twice as likely to develop depression
following 4 or more stressful life events.
•Severe maltreatment as children also increased the
rate.

17. Neurochemical Factors
•Since 1960’s, view that depression may arise from
disruptions in the delicate balance of
neurotransmitter substances that regulate and
mediate the activity of brain’s nerve cell.
•Early attention focused on three neurotransmitter
substances of monoamine class – norepinephrin,
dopamine, and serotonin.

18. •Observation by researchers – antidepressant
medication seems to have an effect of increasing their
availability at synaptic junctions.
•This led to the influential monoamine hypothesis –
that depression was at least sometimes due to the
absolute or relative depletion of one or all of these
neurotransmitters at important receptor sites in the
brain.

20. • The depletion could be due to:
- impaired synthesis of these neurotransmitters in the
presynaptic neuron,
- increased degradation once they have been released into the
synapse,
- altered functioning of the postsynaptic receptors.

21. •However, by the 1980’s it was clear that explanation is
not so simple and straight-forward.
•Some studies found increases in norepinephrine
activity in some depressed patients – especially those
with severe or melancholic depression.
•Only a minority of depressed patients have lowered
serotonin activity.

22. •However, no compelling alternative to the monoamine
theory.
•Clear evidence that altered neuro-transmitter activity
in several systems is associated with major
depressions.
•A number of integrative theories have been proposed
which include the role of neuro-transmitters, not
alone but as they interact with other disturbed
hormonal and neurophysiological patterns and
biological rhythms.

23. Abnormalities Of Hormonal Regulatory
Systems
•Most research on hormonal causes of mood disorders
has focused on the role of hypothalamic-pituitary-
adrenal (HPA) axis, and in particular, on the hormone
cortisol, which is regulated through a complex
feedback loop.
•Human stress response is associated with elevated
activity of the HPA axis, which is partly controlled by
norepinephrine and serotonin.

24. HPA Axis

25. •Norepinephrine activity in hypothalamus causes
release of corticotrophin releasing hormone (CRH)
from hypothalamus.
•CRH triggers release of adreno-corticotrophin
releasing hormone (ACTH) from anterior pituitary.
•ACTH then travels through the blood to adrenal
cortex where cortisol is released.

26. • Levels of cortisol are seen to be elevated in patients of depression.
• Sustained levels of cortisol can result from:
- increased CRH activation (e.g. sustained stress or threat),
- increased secretion of ACTH,
- failure of feedback mechanisms.

27. • Other findings – stress in infancy and early childhood can promote
long-term changes increasing the reactivity of HPA axis.
• This may help to explain the higher risk for depression in children
reared in adversity.

28. •The other endocrine system that has relevance to
depression – hypothalamic-pituitary-thyroid axis.
•Disturbance to this axis also linked to mood disorders.
•People with low thyroid levels (hypothyroidism) often
become depressed.
•Findings that some patients who have not responded
to traditional antidepressants, may show
improvement with thyrotropin-releasing hormone.

29. Neurophysiological and
Neuroanatomical Influences
•Recent research findings – damage to the left but not
to the right, anterior, or prefrontal cortex often leads
to depression.
•EEGs have shown asymmetry in the activity of the two
sides of the prefrontal regions of the brain – low
activity in the left hemisphere and high activity in the
right hemisphere.

30. •Relatively lower activity on the left side of the
prefrontal lobe in depression is thought to be related
to symptoms of reduced positive affect and approach
behavior to rewarding stimuli.
•Increased right side activity is thought to underlie
increased anxiety symptoms and increased negative
affect associated with increased vigilance for
threatening information.

31. • One of the other areas of the brain showing abnormalities –
anterior cingulate cortex – extremely low levels of activation.
• Orbitofrontal cortex shows decreased volume in individuals
with recurrent depression.
• Prolonged depression often leads to decreased volume of the
hippocampus.
• Finally, the amygdala tends to show decreased activation,
which may be related to the individual’s biased attention to
negative emotional information.

32. Sleep and Other Biological Rhythms
• Sleep – depressed patients, especially those with melancholic
features, show a variety of sleep problems:
# early morning awakening
# periodic awakening during the night
# difficulty falling asleep
• EEG recordings have also found to have a 20 min earlier
occurrence of REM sleep.
• Intensity and frequency of their rapid eye movement is also
greater

34. • Result – depressed person gets lower-than-normal amount of deep
sleep.
• Both the reduced latency to REM sleep and decreased amount of deep
sleep often precede the onset of depression and persist following
recovery.
• They may be vulnerability markers for some forms of major depression.

35. •Circadian rhythm – (24-hr cycles other than sleep)
body temperature, secretion of cortisol, TSH, growth
hormone etc.
•Research has found abnormalities in most of these
rhythms in depressed persons.
•Although the exact nature of circadian rhythm
dysfunction is not known, it may play a causal role in
many of the clinical features of depression.

36. •Sunlight and seasons – most patients seem to be
responsive to total quantity of available light in the
environment.
•A vast majority become depressed in fall and winter.
•Research on animals has also documented the
variations in basic functions related to seasons.

37. PSYCHOLOGICAL CAUSAL FACTORS
• Evidence for psychological causes as strong as that for biological causes.
• However, high degree of likelihood that certain psychological factors
(like stress) have their effects due to their interaction with the biological
factors.

38. Stressful Life Events
• Severely stressful life events often serve as precipitating factors for
unipolar depression.
• Stressful life events involved:
- loss of loved one
- threat to important relationships
- loss of occupation
- severe economic or health problems

39. DEATH OF
LOVED ONE
DIVORCE
LOSS OF JOB

40. • Losses that involve an element of humiliation is an important causal
factor.
• Another important stress factor associated with the onset of both major
depression and generalized anxiety is that of a caregiver to a spouse
with a debilitating disease.

41. • Important to distinguish between stressful life events that are
independent of person’s life and personality (independent life events),
and events that have been at least partly generated by the individual’s
own behavior and personality (dependent life events).
• Dependent life events play a stronger role in the onset of major
depression.

42. • Recent review have shown that severely stressful life events play an
important role, especially for persons having their first onset of
depression – 70%.
• Only 40% people with recurrent episodes have had a recent major life
event.

43. Mildly stressful events and chronic stress:
•Studies have found conflicting results regarding the
role of mildly stressful events.
•Not found to have a role in the onset of initial episode
of clinical depression, but may have a role to play in
the onset of recurrent episodes.
•No conclusive results due to difference in the usage of
the terms stress and chronic stress.

44. Individual differences in response to stressors:
• Persons at genetic risk for depression were found to be three times
more likely than those who were not, to develop depression following
severely stressful life events.
• Greater genetic vulnerability – 2 ss alleles of the serotonin-transporter
gene.

45. • Brown and Harris (1978) – 4 factors associated with not becoming
depressed:
(i) having an intimate relationship with a spouse or lover.
(ii) having no more than three children still at home.
(iii) having a job outside the home.
(iv) having a serious religious commitment.

46. • 4 factors strongly associated with the onset of depression following a
major life event:
(i) not having a close relationship with a spouse or lover.
(ii) having three children under the age of 5 at home.
(iii) not having a job.
(iv) having lost a parent by death before the age of 11years.

47. Different Types of Vulnerabilities
• Important vulnerability factors that may increase the risk for depression
– whether or not they interact with stress.
(1) Personality and cognitive diathesis.
(2) Early adversity and parental loss.

48. Personality and cognitive diathesis:
• ‘Neuroticism’ is the primary personality variable associated with
depression.
• Neuroticism or negative affectivity refers to a stable and heritable
personality trait that involve a temperamental sensitivity to negative
stimuli.

49. • People with high levels of this trait are more prone to experiencing a
broad range of negative emotions like sadness, guilt, and hostility.
• Also associated with worse prognosis for complete recovery.

50. •Limited evidence that high level of introversion may
also serve as a vulnerability factor for depression –
either alone or when combined with neuroticism.
•Low level of positive affectivity is also a factor.
•Cognitive diathesis – negative patterns of thinking –
make people who are prone to depression more likely
to become depressed when faced with stressful life
events

51. Early adversity and parental loss:
• Early evidence suggested that parental loss through death or permanent
separation created a vulnerability for depression.

52. • No such evidence in subsequent studies.
• What follows the loss, i.e how loss is dealt with, is more
important.

53. • Range of other adversities in the early environment can also create long
term vulnerability to depression.
- family turmoil
- parental psychopathology
- physical or sexual abuse
- harsh or coercive parenting
• Long-term effects of such early adversities may be mediated by biological
variables.

54. • Important to realize that certain individuals remain resilient in the face
of adversity.
• If exposure to early adversity is moderate, it works as a form of stress
inoculation that makes the individual less susceptible to the effects of
later stress.

55. 5 MAJOR PSYCHOLOGICAL THEORIES
• PSYCHODYNAMIC THEORIES
• BEHAVIORAL THEORIES
• BECK’S COGNITIVE THEORY
• HELPLESSNESS AND HOPELESSNESS THEORIES
• INTERPERSONAL EFFECTS OF MOOD DISORDERS

56. PSYCHODYNAMIC THEORIES
•Oral fixation: Depends on others
for self-esteem.
•Bereavement, introjection, and
mourning .
•Symbolic loss – loss of mother or
lack of fulfillment of need for
love and caring.

57. • Klein (1934) and Jacobson (1971) emphasized
- the importance of quality of early mother and child relationship
- decrease in or threat to self esteem as a critical issue.
• Bowlby (1973, 1980) also emphasized child’s need for secure
attachment.

58. BEHAVIORAL THEORIES
•Reduction in reinforcement leads to a reduction in
activity.
•Depressive behaviors are reinforced.
•Depressed people have taken part in fewer pleasant
events.
•Modeling of depressive behavior of parents and
significant others.

59. BECK’S COGNITIVE THEORY
•AARON BECK (1967)
•One of the most significant
theories of depression.
•Cognitive aspects often precede and cause the
affective symptoms.
•CENTRAL FEATURE – Negative cognitions

60. Aspects of the Theory
• Depressogenic Schemas – dysfunctional beliefs that are rigid,
extreme, and counter-productive.
• These beliefs develop during childhood and adolescence.
• Cause – negative experiences with ones parents and significant
others.
• Stay as negative automatic thoughts.

62. • The negative triad tends to be maintained by a variety of negative
cognitive biases and errors:
(i) Dichotomous or all-or-none reasoning
(ii) Selective abstraction
(iii) Arbitrary inference

63. Beck’s theory:
Character of pessimism (Negative Triad)
Habits of negativity (Negative schemas)
Erroneous thinking (Characteristic biases)
DEPRESSION

64. HELPLESSNESS AND HOPELESSNESS THEORIES
•Learned helplessness theory emerged out of
observations in animal research labs.
•MARTIN SELIGMAN (1974, 1975) – First to use it as a
model of depression.
•STUDY – dogs exposed to uncontrollable shocks later
acted in passive and helpless manner.

65. Reformulated Helplessness Theory
•Some research with humans led to major
reformulation of the theory by ABRAMSON
et.al.(1978).
•Proposed that when people are exposed to
uncontrollable events, they ask themselves – WHY.
•Kind of attributions they make are central to
becoming depressed.

66. •Attributional reformulation (Abramson, Seligman &
Teasdale, 1978) – 3 critical dimensions:
• Personal/Environmental (Internal/External)
• Stable/Unstable
• Global/Specific
•Proposed that depressogenic attribution is internal,
stable, and global.

67. • Pessimistic attributional style – diathesis for depression.
• This kind of cognitive style develops through:
- social learning
- parent communication
- negative parenting

68. Hopelessness Theory of Depression
• Revision of the helplessness theory, presented by ABRAMSON
et.al.(1989).
• Not sufficient to have a pessimistic attributional style to develop
depression.
• A state of hopelessness was also an important factor.

69. • HOPELESSNESS EXPECTANCY – defined by :
- perception that one has no control over what was going to happen
- absolute certainty that an important bad outcome was going to
occur
- highly desired good outcome was not going to occur.

70. • Also proposed that internal/external dimension was not important.
• Instead proposed 2 other dimensions as being important components of
cognitive diathesis:
- global attributions
- stable attributions
- negative inferences about events
- negative implications for self

71. INTERPERSONAL EFFECTS OF MOOD
DISORDERS
• Reduced interpersonal support
• Experiences of rejection
• Due to social structure
• Inadequate social networks
• Others may dislike them
• Elicited by patient
• Consequences of behavioral choices
• Critical comments by spouse
• Poor social skills and seeking reassurance