CLINICAL PSYCHOLOGY

2. KARUNA SINDHU JANA
SOHINI BHATTACHARJEE
SUKANYA DUTTA
DEPARTMENT OF PSYCHOLOGY
UNIVERSITY OF CALCUTTA

3. DIFFERENCE BETWEEN
MOOD AND AFFECT
AFFECT : AN AFFECT IS A TERM THAT ENCOMPASSES A BROAD
RANGE OF FEELINGS THAT PEOPLE CAN EXPERIENCE. IT BASICALLY
REFERS TO IMMEDIATE EXPRESSIONS OF EMOTION .
MOOD: A MOOD IS A STATE OF MIND THAT TENDS TO BE LESS
INTENSE THAN AN EMOTION AND DOES NOT NECESSARILY NEED A
CONTEXTUAL STIMULUS. MOODS LAST LONGER THAN EMOTIONS
FROM HOURS TO DAYS. THEREFORE WE CAN SAY THAT MOOD REFERS
TO EMOTIONAL EXPERIENCE OVER A MORE PROLONGED PERIOD OF
TIME.

4. MOOD DISORDER
DEFINITION:
 MOOD DISORDER ALSO KNOWN AS AFFECTIVE DISORDERS IS A GROUP
OF CONDITIONS WHERE A DISTURBANCE IN THE PERSON’S MOOD IS THE
MAIN UNDERLYING FEATURE. A PSYCHOLOGICAL DISORDER
CHARACTERIZED BY THE ELEVATION OR LOWERING OF A PERSON’S MOOD
SUCH AS DEPRESSION OR BIPOLAR DISORDER.
 MOST PEOPLE’S MOODS COME AND GO. THEIR FEELINGS OF ELATION OR
SADNESS ARE UNDERSTANDABLE REACTIONS TO DAILY EVENTS AND DO
NOT AFFECT THEIR LIVES GREATLY. THE MOODS OF PEOPLE WITH MOOD
DISORDERS, IN CONTRAST, TEND TO LAST A LONG TIME. BUT WHEN THE
MOOD COLORS ALL OF THEIR INTERACTIONS WITH THE WORLD AND
INTERFERES WITH NORMAL FUNCTIONING THIS CAN BE TERMED AS MOOD
DISORDER.

5. TYPES OF MOOD
DISORDERS
MAJOR DEPRESSIVE DISORDER
DYSTHYMIC DISORDER (DYSTHYMIA)
BIPOLAR DISORDER
CYCLOTHYMIA
SEASONAL AFFECTIVE DISORDER
PREMENSTRUAL DYSPHORIC DISORDER
DISRUPTIVE MOOD DYSREGULATION DISORDER

6. MAJOR DEPRESSIVE
DISORDER

8. MAJOR DEPRESSIVE DISORDER (MDD), ALSO KNOWN SIMPLY
AS DEPRESSION, IS A MENTAL DISORDER CHARACTERIZED BY
AT LEAST TWO WEEKS OF LOW MOOD THAT IS PRESENT
ACROSS MOST SITUATIONS. IT IS OFTEN ACCOMPANIED BY
LOW SELF-ESTEEM, LOSS OF INTEREST IN NORMALLY
ENJOYABLE ACTIVITIES, LOW ENERGY, AND PAIN WITHOUT A
CLEAR CAUSE.
SOME PEOPLE HAVE PERIODS OF
DEPRESSION SEPARATED BY YEARS IN WHICH THEY ARE
NORMAL, WHILE OTHERS NEARLY ALWAYS HAVE SYMPTOMS
PRESENT. MAJOR DEPRESSIVE DISORDER CAN NEGATIVELY
AFFECT A PERSON'S PERSONAL LIFE, WORK LIFE, OR
EDUCATION, AS WELL AS SLEEPING, EATING HABITS, AND
GENERAL HEALTH.
BETWEEN 2–8% OF ADULTS WITH MAJOR DEPRESSION
DIE BY SUICIDE (RICHARDS CS, O'HARA MW ,2014) AND
ABOUT 50% OF PEOPLE WHO DIE BY SUICIDE HAD DEPRESSION
OR ANOTHER MOOD DISORDER. (BACHMANN, S ,6 JULY 2018)

9. DIAGNOSTIC CRITERIA
(ACCORDING TO DSM-5)
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. NOTE: DO NOT
INCLUDE SYMPTOMS THAT ARE CLEARLY
ATTRIBUTABLE TO ANOTHER MEDICAL
CONDITION.

10. 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).
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).

11. 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.
NOTE: CRITERIA A-C REPRESENT A MAJOR DEPRESSIVE EPISODE

12. NOTE: RESPONSES TO A SIGNIFICANT LOSS (E.G., BEREAVEMENT,
FINANCIAL RUIN, LOSSES FROM A NATURAL DISASTER, A SERIOUS
MEDICAL ILLNESS OR DISABILITY) MAY INCLUDE THE FEELINGS OF
INTENSE SADNESS, RUMINATION ABOUT THE LOSS, INSOMNIA,
POOR APPETITE, AND WEIGHT LOSS NOTED IN CRITERION A,
WHICH MAY RESEMBLE A DEPRESSIVE EPISODE. ALTHOUGH SUCH
SYMPTOMS MAY BE UNDERSTANDABLE OR CONSIDERED
APPROPRIATE TO THE LOSS, THE PRESENCE OF A MAJOR
DEPRESSIVE EPISODE IN ADDITION TO THE NORMAL RESPONSE TO
A SIGNIFICANT LOSS SHOULD ALSO BE CAREFULLY CONSIDERED.
THIS DECISION INEVITABLY REQUIRES THE EXERCISE OF CLINICAL
JUDGMENT BASED ON THE INDIVIDUAL’S HISTORY AND THE
CULTURAL NORMS FOR THE EXPRESSION OF DISTRESS IN THE
CONTEXT OF LOSS.
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

13. EPIDEMIOLOGY
RECENTLY CONDUCTED WORLD MENTAL HEALTH SURVEYS INDICATE THAT MAJOR
DEPRESSION IS EXPERIENCED BY 10-15% PEOPLE IN THEIR LIFETIME (BROMET E,
ANDRADE LH, HWANG I,SAMPSON NA, ALONSO J, DE GIROLAMO G, ET AL. CROSS-
NATIONAL EPIDEMIOLOGY OF DSM-IV MAJOR DEPRESSIVE EPISODE. BMC MED
2011;9:90)AND ABOUT 5% SUFFER FROM MAJOR DEPRESSION IN ANY GIVEN YEAR.
(MURPHY JM, LAIRD NM, MONSON RR, SOBEL AM, LEIGHTON AH. A 40-YEAR
PERSPECTIVE ON THE PREVALENCE OF DEPRESSION: THE STIRLING COUNTY STUDY.
ARCH GEN PSYCHIATRY 2000;57:209-15.)
LIFETIME PREVALENCE OF ALL DEPRESSIVE DISORDERS TAKEN TOGETHER
IS OVER 20%, THAT IS ONE IN FIVE INDIVIDUALS. IN INDIAN CONTEXT, A RECENT
LARGE SAMPLE SURVEY WITH RIGOROUS METHODOLOGY REPORTED AN OVERALL
PREVALENCE OF 15.9% FOR DEPRESSION, (POONGOTHAI S, PRADEEPA R, GANESAN
A, MOHAN V. PREVALENCE OF DEPRESSION IN A LARGE URBAN SOUTH INDIAN
POPULATION - THE CHENNAI URBAN RURAL EPIDEMIOLOGY STUDY (CURES-70).
PLOS ONE 2009;4:E7185) WHICH IS SIMILAR TO WESTERN FIGURES. THERE IS SOME
SUGGESTION THAT PERHAPS THE PREVALENCE OF DEPRESSION HAS INCREASED
OVER PAST FEW DECADES. STUDIES DONE IN PRIMARY HEALTH CARE SETTINGS IN
INDIA HAVE FOUND DEPRESSION IN 21-84% OF THE CASES.(POTHEN M, KURUVILLA
A, PHILIP K, JOSEPH A, JACOB KS. COMMON MENTAL DISORDERS AMONG PRIMARY
CARE ATTENDERS IN VELLORE, SOUTH INDIA: NATURE, PREVALENCE AND RISK
FACTORS. INT J SOC PSYCHIATRY 2003;49:119– 25. )

14. THE AVERAGE AGE OF ONSET FOR MAJOR
DEPRESSION IS 24 YEARS AS PER THE RECENT
EPIDEMIOLOGICAL RESEARCH, THOUGH IT CAN BEGIN AT
ANYTIME THROUGHOUT THE LIFESPAN. (BROMET E,
ANDRADE LH, HWANG I,SAMPSON NA, ALONSO J, DE
GIROLAMO G, ET AL. CROSS-NATIONAL EPIDEMIOLOGY OF
DSM-IV MAJOR DEPRESSIVE EPISODE. BMC MED 2011;9:90.
). ONE OF THE CONSISTENT FINDINGS ACROSS ALMOST ALL
RESEARCH STUDIES IS THAT WOMEN ARE TWICE AS LIKELY
TO HAVE DEPRESSION COMPARED TO MALES.(BROMET E,
ANDRADE LH, HWANG I,SAMPSON NA, ALONSO J, DE
GIROLAMO G, ET AL. CROSS-NATIONAL EPIDEMIOLOGY OF
DSM-IV MAJOR DEPRESSIVE EPISODE. BMC MED 2011;9:90.
). DEPRESSION IS MUCH MORE LIKELY AMONG PEOPLE WHO
ARE UNMARRIED, WIDOWED, DIVORCED OR SEPARATED, OR
WITHOUT CLOSE INTER-PERSONAL RELATIONSHIPS. THOSE
RESIDING IN NUCLEAR FAMILIES AND URBAN AREAS ARE
POSSIBLY AT A HIGHER RISK. ELDERLY AGE AND PRESENCE
OF MEDICAL DISORDERS POSE AN EVEN HIGHER RISK OF

15. PERSISTENT DEPRESSIVE
DISORDER
(DYSTHYMIA)

16. PERSISTENT
DEPRESSIVE
DISORDER
(DYSTHYMIC
DISORDER)

17. DEFINITION
DYSTHYMIC DISORDER IS GENERALLY CONSIDERED TO BE OF MILD TO MODERATE
INTENSITY , BUT IT’S PRIMARY HALLMARK IS ITS CHRONICITY.
TO QUALIFY FOR A DIAGNOSIS OF DYSTHYMIC DISORDER A PERSON MUST HAVE A
PERSISTENTLY DEPRESSED MOOD FOR MOST OF THE DAY, FOR MORE DAYS THAN
NOT , FOR AT LEAST 2 YEARS. (1 YEAR FOR CHILDREN AND ADOLESCENTS).
IN ADDITION INDIVIDUALS WITH DYSTHYMIC DISORDER MUST HAVE AT LEAST TWO
OF SIX ADDITIONAL SYMPTOMS WHEN DEPRESSED . PERIODS OF NORMAL MOOD
MAY OCCUR BRIEFLY , BUT THEY USUALLY LAST FOR ONLY A FEW DAYS TO A FEW
WEEKS. THESE INTERMITTENTLY NORMAL MOODS ARE ONE OF THE MOST
IMPORTANT CHARACTERISTICS DISTINGUISHING DYSTHYMIA FROM MAJOR
DEPRESSIVE DISORDER , WHICH TYPICALLY OCCURS IN MORE DISCRETE MAJOR
DEPRESSIVE EPISODES. NEVERTHELESS IN SPITE OF THE INTERMITTENTLY
NORMAL MOODS, BECAUSE OF ITS CHRONIC COURSE PEOPLE WITH DYSTHYMIA
SHOW POORER OUTCOMES AND AS MUCH IMPAIRMENT AS THOSE WITH MAJOR
DEPRESSION (KLEIN , 2008 , 2010).

18. Diagnostic Criteria- (ACCORDING TO DSM-5)
This disorder represents a consolidation of DSM-lV-defined chronic major depressive
disorder
and dysthymic disorder.
A. Depressed mood for most of the day, for more days than not, as indicated by either
subjective account or observation by others, for at least 2 years.
Note: In children and adolescents, mood can be irritable and duration must be at least
1 year.
B. Presence, while depressed, of two (or more) of the following:
1. Poor appetite or overeating.
2. Insomnia or hypersomnia.
3. Low energy or fatigue.
4. Low self-esteem.
5. Poor concentration or difficulty making decisions.
6. Feelings of hopelessness.
C. During the 2-year period (1 year for children or adolescents) of the disturbance, the
individual
has never been without the symptoms in Criteria A and B for more than 2 months at a
time.

19. E. There has never been a manic episode or a hypomanic episode, and criteria have
never been met for cyclothymic disorder.
F. The disturbance is not better explained by a persistent schizoaffective disorder,
schizophrenia, delusional disorder, or other specified or unspecified schizophrenia
spectrum and other psychotic disorder.
G. The symptoms are not attributable to the physiological effects of a substance (e.g.,
a
drug of abuse, a medication) or another medical condition (e.g. hypothyroidism).
H. The symptoms cause clinically significant distress or impairment in social,
occupational,
or other important areas of functioning.
Note: Because the criteria for a major depressive episode include four symptoms that
are
absent from the symptom list for persistent depressive disorder (dysthymia), a very
limited
number of individuals will have depressive symptoms that have persisted longer than
2 years
but will not meet criteria for persistent depressive disorder. If full criteria for a major
depressive

20. EPIDEMIOLOGY
DYSTHYMIA IS ALSO QUITE COMMON , WITH A LIFETIME PREVALENCE
ESTIMATED AT BETWEEN 2.5 AND 6 PERCENT (KESSLER ET AL ., 1994 ;
KESSLER, BERGLUND, DEMLER ET AL., 2005). THE AVERAGE DURATION
OF DYSTHYMIA IS 4 TO 5 YEARS, BUT IT CAN PERSISTS FOR 20 YEARS OR
MORE (KELLER ET AL 1997; KLEIN ET AL ., 2006) . CHRONIC STRESS HAS
BEEN SHOWN TO INCREASE THE SEVERITY OF SYMPTOMS OVER 7.5- YEAR
FOLLOW UP PERIOD. (DOUGHERTY ET AL ., 2004). DYSTHYMIA OFTEN
BEGINS DURING THE TEENAGE YEARS, AND OVER 50 PERCENT OF THOSE
WHO PRESENT FOR TREATMENT HAVE AN ONSET BEFORE AGE 21. ONE 10
YEAR PROSPECTIVE STUDY OF 97 INDIVIDUALS WITH EARLY ONSET
DYSTHYMIA FOUND THAT 74 PERCENT RECOVERED WITH IN 10 YEARS
BUT THAT, AMONG THOSE WHO RECOVERED, 71 PERCENT RELAPSED,
WITH MOST RELAPSES OCCURRING WITHIN APPROXIMATELY 3 YEARS OF

21. ACCORDING TO THE NATIONAL INSTITUTE OF MENTAL HEALTH (NIMH),
DYSTHYMIA AFFECTS APPROXIMATELY 1.5% OF THE ADULT POPULATION IN THE
UNITED STATES. 49.7% OF THESE CASES ARE CONSIDERED “SEVERE” AND THE
AVERAGE AGE OF ONSET IS 31 YEARS. DYSTHYMIA CAN AFFECT CHILDREN AND
ADOLESCENTS. DATA FROM NIMH SHOWS THAT DEPRESSIVE DISORDERS (MAJOR
DEPRESSIVE DISORDER OR DYSTHYMIA) AFFECT APPROXIMATELY 11.2% OF 3O 18-
YEAR-OLDS AT SOME POINT DURING THEIR LIVES, AND THAT GIRLS ARE MORE
LIKELY THAN BOYS TO EXPERIENCE A DEPRESSIVE DISORDER.

22. DYSTHYMIC DISORDER
ONE YEAR PREVALENCE PERCENT 1.5–5.0%
FEMALE TO MALE RATIO: BETWEEN 3:2 AND 2:1
TYPICAL AGE AT ONSET (YEARS ) : 10–25
PREVALANCE AMONG FIRST DEGREE RELATIVES : ELEVATED
PERCENTAGE CURE,ENTLY RECEIVING TREATMENT : 36.8%
Source: González et al. 2010; Taube-Schiff & Lau, 2008; Kessler et al., 2005, 1994;
APA, 2000, 1994; Regier et al., 1993; Weissman et al., 1991.

23. BIPOLAR
DISORDER

24. DEPRESSION: A LOW, SAD STATE MARKED BY SIGNIFICANT LEVELS OF SADNESS,
LACK OF ENERGY, LOW SELF-WORTH, GUILT, OR RELATED SYMPTOMS.
MANIA: A STATE OR EPISODE OF EUPHORIA OR FRENZIED ACTIVITY IN WHICH
PEOPLE MAY HAVE AN EXAGGERATED BELIEF THAT THE WORLD IS THEIRS FOR
THE TAKING.
BIPOLAR DISORDER :A DISORDER MARKED BY ALTERNATING OR INTERMIXED
PERIODS OF MANIA AND DEPRESSION

25.  PEOPLE WITH A BIPOLAR DISORDER EXPERIENCE BOTH
THE LOWS OF DEPRESSION AND THE HIGHS OF MANIA.
 MANY DESCRIBE THEIR LIFE AS AN EMOTIONAL ROLLER COASTER, AS
THEY SHIFT BACK AND FORTH BETWEEN EXTREME MOODS.
 A NUMBER OF SUFFERERS EVENTUALLY BECOME SUICIDAL.
 THEIR ROLLER COASTER RIDE ALSO HAS A DRAMATIC IMPACT ON
RELATIVES AND FRIENDS (LEE ET AL., 2011;LOWE & COHEN, 2010

29. MANIC EPISODE
A. A DISTINCT PERIOD OF ABNORMALLY AND PERSISTENTLY ELEVATED,
EXPANSIVE, OR IRRITABLE MOOD AND ABNORMALLY AND PERSISTENTLY
INCREASED GOAL-DIRECTED ACTIVITY OR ENERGY, LASTING AT LEAST 1
WEEK AND PRESENT MOST OF THE DAY, NEARLY EVERY DAY (OR ANY
DURATION IF HOSPITALIZATION IS NECESSARY).
B. DURING THE PERIOD OF MOOD DISTURBANCE AND INCREASED ENERGY
OR ACTIVITY, THREE (OR MORE) OF THE FOLLOWING SYMPTOMS (FOUR IF
THE MOOD IS ONLY IRRITABLE) ARE PRESENT TO A SIGNIFICANT DEGREE
AND REPRESENT A NOTICEABLE CHANGE FROM USUAL BEHAVIOR:
1. INFLATED SELF-ESTEEM OR GRANDIOSITY.
2. DECREASED NEED FOR SLEEP (E.G., FEELS RESTED AFTER ONLY 3
HOURS OF SLEEP).
3. MORE TALKATIVE THAN USUAL OR PRESSURE TO KEEP TALKING.
4. FLIGHT OF IDEAS OR SUBJECTIVE EXPERIENCE THAT THOUGHTS ARE
RACING.
5. DISTRACTIBILITY (I.E., ATTENTION TOO EASILY DRAWN TO
UNIMPORTANT OR IRRELEVANT EXTERNAL STIMULI), AS REPORTED OR
OBSERVED

30. 6. INCREASE IN GOAL-DIRECTED ACTIVITY (EITHER SOCIALLY, AT
WORK OR SCHOOL, OR SEXUALLY) OR PSYCHOMOTOR
AGITATION (I.E., PUΦOSELESS NON-GOAL-DIRECTED
ACTIVITY).
7. EXCESSIVE INVOLVEMENT IN ACTIVITIES THAT HAVE A HIGH
POTENTIAL FOR PAINFUL CONSEQUENCES (E.G., ENGAGING IN
UNRESTRAINED BUYING SPREES, SEXUAL INDISCRETIONS, OR
FOOLISH BUSINESS INVESTMENTS).
C. THE MOOD DISTURBANCE IS SUFFICIENTLY SEVERE TO CAUSE
MARKED IMPAIRMENT IN SOCIAL OR OCCUPATIONAL
FUNCTIONING OR TO NECESSITATE HOSPITALIZATION TO
PREVENT HARM TO SELF OR OTHERS, OR THERE ARE
PSYCHOTIC FEATURES.
D. THE EPISODE IS NOT ATTRIBUTABLE TO THE PHYSIOLOGICAL
EFFECTS OF A SUBSTANCE (E.G., A DRUG OF ABUSE, A
MEDICATION, OTHER TREATMENT) OR TO ANOTHER MEDICAL

31. HYPOMANIC EPISODE
A. A DISTINCT PERIOD OF ABNORMALLY AND PERSISTENTLY ELEVATED,
EXPANSIVE, OR IRRITABLE MOOD AND ABNORMALLY AND PERSISTENTLY
INCREASED ACTIVITY OR ENERGY, LASTING AT LEAST 4 CONSECUTIVE DAYS
AND PRESENT MOST OF THE DAY, NEARLY EVERY DAY.
B. DURING THE PERIOD OF MOOD DISTURBANCE AND INCREASED ENERGY AND
ACTIVITY, THREE (OR MORE) OF THE FOLLOWING SYMPTOMS (FOUR IF THE
MOOD IS ONLY IRRITABLE) HAVE PERSISTED, REPRESENT A NOTICEABLE
CHANGE FROM USUAL BEHAVIOR, AND HAVE BEEN PRESENT TO A
SIGNIFICANT DEGREE:
1. INFLATED SELF-ESTEEM OR GRANDIOSITY.
2. DECREASED NEED FOR SLEEP (E.G., FEELS RESTED AFTER ONLY 3 HOURS OF
SLEEP).
3. MORE TALKATIVE THAN USUAL OR PRESSURE TO KEEP TALKING.
4. FLIGHT OF IDEAS OR SUBJECTIVE EXPERIENCE THAT THOUGHTS ARE RACING.
5. DISTRACTIBILITY (I.E., ATTENTION TOO EASILY DRAWN TO UNIMPORTANT OR
IRRELEVANT EXTERNAL STIMULI), AS REPORTED OR OBSERVED

32. 6. INCREASE IN GOAL-DIRECTED ACTIVITY (EITHER SOCIALLY, AT WORK OR SCHOOL, OR
SEXUALLY) OR PSYCHOMOTOR AGITATION.
7.. EXCESSIVE INVOLVEMENT IN ACTIVITIES THAT HAVE A HIGH POTENTIAL FOR PAINFUL
CONSEQUENCES (E.G., ENGAGING IN UNRESTRAINED BUYING SPREES, SEXUAL
INDISCRETIONS,
C. THE EPISODE IS ASSOCIATED WITH AN UNEQUIVOCAL CHANGE IN FUNCTIONING
THAT IS UNCHARACTERISTIC OF THE INDIVIDUAL WHEN NOT SYMPTOMATIC.
D. THE DISTURBANCE IN MOOD AND THE CHANGE IN FUNCTIONING ARE OBSERVABLE BY
OTHERS.
E. THE EPISODE IS NOT SEVERE ENOUGH TO CAUSE MARKED IMPAIRMENT IN SOCIAL OR
OCCUPATIONAL FUNCTIONING OR TO NECESSITATE HOSPITALIZATION. IF THERE ARE
PSYCHOTIC FEATURES, THE EPISODE IS, BY DEFINITION, MANIC.
F. THE EPISODE IS NOT ATTRIBUTABLE TO THE PHYSIOLOGICAL EFFECTS OF A
SUBSTANCE (E.G., A DRUG OF ABUSE, A MEDICATION, OTHER TREATMENTR FOOLISH
BUSINESS INVESTMENTS

35. CLINICAL FEATURES OF DEPRESSION
APPEARANCE: DRESS AND GROOMING MAY BE NEGLECTED. FACIAL
FEATURES ARE CHARACTERIZED BY A TURNING DOWNWARD
.
THE RATE OF BLINKING MAY BE REDUCED .
THE SOULDERS ARE BENT AND THE HEAD IS INCLINED
FORWARD SO THAT DIRECTION OF GAZE
DOWNWARD.
MOOD : THE MOOD OF THE PATIENT IS ONE OF MISERY. FEELING OF
SADNESS WOULD BE ALLEVIATED.
DEPRESSIVE COGNITION:
WORTHLESSNESS- THE PATIENT THINKS THAT HE IS FAILING INWHAT HE
DOES AND THAT OTHER PEOPLE SEE HIM AS FAILURE.HE NO LONGER
FEELS CONFIDENT, HE DISCOUNTS ANY SUCESESS AS A CHANCE

36. LACK OF INTEREST AND ENJOYMENT - ANHEDONIA IS FREQUENT.
THE PATIENT SHOWS NO ENTHUSIASM FOR ACTIVITIES AND HOBBIES
THAT HE WOULD NORMALLY ENJOY. HE FEELS NO ZEST FOR LIVING
AND NO PLEASURE IN EVERYDAY THINGS.
PSYCHOMOTOR CHANGES: PSYCHOMOTOR RETARDATION IS
FREQUENT . THE PATIENT WALKS SLOWLY.
ANXIETY IS FREQUENT , ALTHOUGH NOT INVARIABLY PRESENT , IN
SEVERE DEPRESSION. ANOTHER COMMON SYMPTOM IS IRRITABILITY,
WHICH IS THE TENDENCY TO RESPOND WITH UNDUE ANNOYANCE TO
MINOR DEMANDS.
PESSIMISTIC THOUGHTS CONCERNS HIS FUTURE PROSPECTS . THE
PATIENT EXPECT THE WORST . THIS IDEAS OF HOPELESSNES ARE OFTEN
ACCOMPANIED BY THE THOUGHT THAT LIFE IS NO LONGER WORTH
LIVING AND THAT DEATH WOULD COME AS A WELCOME RELEASE.
GUILT : FEELINGS OF GUILT OFTEN TAKE THE FORM OF UNREASONABLE
SELF BLAME ABOUT MINOR MATTERS, THE PATIENT MAY FEEL GUILTY
ABOUT PAST TRIVIAL ACTS OF DISHONESTY OR LETTING SOMEONE
DOWN.

37. BIOLOGICAL SYMPTOMS
SLEEP DISTURBANCE:
• EARLY MORNING WAKING, BUT DELAY IN FALLING SLEEP AND
WAKING DURING NIGHT.
• LOSS OF APPETITE OR EATING MORE THAN USUAL.
• LOSS OF WEIGHT OR GAINING OF EXCESSIVE WEIGHT.
• CONSTIPATION
• LOSS OF LIBIDO AND AMONG WOMEN AMENORRHOEA.
OTHER FEATURES:
 DEPERSONALIZATION
 OBSESSIONAL SYMPTOMS
 PANIC ATTACKS
 DISSOCATIVE SYMPTOMS
 POOR MEMORY[PSEUDODEMENTIA]
 DEFICITS ON A WIDE RANGE OF
NEUROPSYCHOLOGICAL TESTS

38. PSYCHOTIC FEATURES:
1. COMPLETE LOSS OF FUNCTION IN SOCIAL AND
OCCUPATIONAL SPHERES.
2. IN PSYCHOTIC DEPRESSION THERE MAY BE HALLUCINATION
AND DELUSION
3. DELUSION OF GUILT IS ALSO PRESENT.
DEPRESSIVE STUPOR
SLOWING OF MOVEMENT AND POVERTY OF SPEECH MAY
BECOME SO EXTREME THAT THE PATIENT IS MOTIONLESS AND
MUTE.

39. CLINICAL FEATURES OF MANIA
.
APPEARANCE:
THE PATIENT’S APPEARANCE IS CHEERFUL AND OPTIMISTIC.
THEIR CLOTHING MAY BE BRIGHTLY COLOURED AND ILL
ASSORTED.
MANIC PATIENTS ARE OVERACTIVE, SOMETIMES PERSISTENT
OVERACTIVITY LEADS TO PHYSICAL EXHAUSTION.

40. MANIC PATIENTS START MANY ACTIVITIES BUT LEAVE THEM UNFINISHED
AS NEW ONE ATTRACT THEIR ATTENTION.
APPETITE IS INCREASED AND FOOD MAY BE EATEN GREEDILY WITH
LITTLE ATTENTION TO CONVENTIONAL MANNER.
SEXUAL DESIRES ARE INCREASED AND SEXUAL BEHAVIOUR MAY BE
UNINHIBITED AND QUITE OUT OF CHARACTER. WOMEN MAY NEGLECT
PRECAUTIONS OF PREGNENCY.
SLEEP IS OFTEN REDUCED- PATIENTS WAKE EARLY, FEELING LIVELY AND
ENERGETIC.

41. SPEECH IS OFTEN RAPID AND COPIOUS (AS THOUGHT CROWDS IN
TO THEIR MINDS IN QUICK SUCCESSION.)
WHEN THE DISEASE IS MORE SEVERE,THERE IS FLIGHT OF
IDEAS.,WITH SUCH RAPID CHANGES THAT IT IS DIFFICULT TO
FOLLOW THE TRAIN OF THOUGHT.
[ HOWEVER THE LINKS ARE USUALLY UNDERSTANDABLE IF THE
SPEECH CAN BE RECORDED AND REVIEWED. THIS IS IN CONTRAST TO
THOUGHT DISORDER IN SCHIZOPHRENIA.,WHERE CHANGES IN THE
FLOW OF THOUGHT MAY NOT BE COMPREHENSIBLE EVEN ON
REFLECTION. ]
EXPANSIVE IDEAS ARE COMMON.PATIENTS BELIEVE THAT THEIR
OPINIONS ARE IMPORTANT, AND THEIR WORK IS OF
.

42. MANY PATIENT BECOME EXTRAVAGANT , SPENDING MORE THAN THEY CAN
AFFORD.
OTHERS MAKE RECKLESS DECISIONS TO GIVE UP GOOD JOBS, OR EMBARK ON
PLANS OF ILL CONSIDERED AND RISKY BUSINESS VENTURES.
SOMETIMES EXPANSIVE THEMES ARE ACCOMPANIED BY GRANDIOSE DELUSIONS.
SOME PATIENTS MAY BELIEVE THAT THEY ARE RELIGIOUS PROPHETS OR DESTINED
TO ADVISE STATESMEN ABOUT MAJOR ISSUES.
AT TIMES THERE ARE DELUSIONS OF PERSECUTION WHEN THE PATIENTS BELIEVE
THAT PEOPLE ARE CONSPIRING AGAINST THEM BECAUSE OF THE SPECIAL
IMPORTANCE.
DELUSIONS OF REFERENCE AND PASSIVITY FEELINGS ALSO OCCURS. INSIGHT IS
ALSO IMPAIRED IN MORE SEVERE MANIC PATIENT.

43. HYPOMANIA IS DIFFERENTIATED FROM MANIA ON THE BASIS
OF DURATION OF SYMPTOMS, ABSENSE OF PSYCHOTIC
FEATURES, AND LESSER DEGREE OF OCCUPATIONAL AND
SOCIAL IMPAIRMENT.

44. CAUSAL FACTORS OF AFFECTIVE
DISORDERS (ETIOLOGY)

45. THE BIOLOGICAL VIEW
GENETIC FACTORS
TWIN STUDIES SHOW THAT WHEN ONE TWIN OF A MONOZYGOTIC (IDENTICAL) PAIR HAS
MDD, THE OTHER TWIN HAS A RISK OF ALSO DEVELOPING THE DISORDER THAT IS FOUR
TIMES HIGHER THAN WHEN THE TWINS ARE DIZYGOTIC (FRATERNAL; BOWMAN &
NURNBERGER, 1993; KENDLER, KARKOWSKI, & PRESCOTT, 1999). BECAUSE MONOZYGOTIC
TWINS BASICALLY SHARE ALL OF THEIR GENES BUT DIZYGOTIC TWINS SHARE ONLY HALF OF
THEIR GENES, THESE RESULTS POINT TO A ROLE FOR GENETICS IN THE ETIOLOGY OF THIS
DISORDER. ONE POSSIBILITY IS THAT GENES INFLUENCE HOW A PERSON RESPONDS TO
STRESSFUL EVENTS (COSTELLO ET AL., 2002; KENDLER ET AL., 2005).
ADOPTION STUDIES: HAVE ALSO IMPLICATED A GENETIC FACTOR, AT LEAST IN CASES OF
SEVERE DEPRESSION. ONE STUDY LOOKED AT THE FAMILIES OF ADOPTED PERSONS WHO HAD
BEEN HOSPITALIZED FOR THIS DISORDER IN DENMARK. THE BIOLOGICAL PARENTS OF THESE
ADOPTEES TURNED OUT TO HAVE A HIGHER INCIDENCE OF SEVERE DEPRESSION (BUT NOT
MILD DEPRESSION) THAN DID THE BIOLOGICAL PARENTS OF A CONTROL GROUP OF
NONDEPRESSED ADOPTEES . SOME THEORISTS INTERPRET THESE FINDINGS TO MEAN THAT
SEVERE DEPRESSION IS MORE LIKELY THAN MILD DEPRESSION TO BE CAUSED BY GENETIC
FACTORS.

46. IF A PERSON IS SENSITIVE TO STRESSFUL EVENTS, THE SENSITIVITY COULD LEAD TO
INCREASED HPA AXIS ACTIVATION (HASLER ET AL., 2004), WHICH IN TURN COULD
CONTRIBUTE TO DEPRESSION. HOWEVER, GENES ARE NOT DESTINY. THE ENVIRONMENT
CLEARLY PLAYS AN IMPORTANT ROLE IN WHETHER A PERSON WILL DEVELOP
DEPRESSION (ELEY ET AL., 1998; HASLER ET AL.,2004; RICE, HAROLD, & THAPER, 2002;
WENDER ET AL., 1986). EVEN WITH IDENTICAL TWINS, IF ONE TWIN IS DEPRESSED, THIS
DOES NOT GUARANTEE THAT THE CO-TWIN WILL ALSO BE DEPRESSED—IN SPITE OF
THEIR HAVING BASICALLY THE SAME GENES. WHETHER A PERSON GETS DEPRESSED
DEPENDS PARTLY ON HIS OR HER LIFE EXPERIENCES, INCLUDING THE PRESENCE OF
HARDSHIPS AND THE EXTENT OF SOCIAL SUPPORT.
THE ENVIRONMENT PLAYS A KEY ROLE NOT ONLY IN WHETHER THE GENES
CONTRIBUTE TO DEPRESSION, BUT ALSO IN HOW THE GENES HAVE THEIR EFFECTS. IN
SOME CASES, GENETIC FACTORS MAY AFFECT DEPRESSION INDIRECTLY—BY
DISRUPTING SPECIFIC ASPECTS OF NORMAL FUNCTIONINGTHAT IN TURN TRIGGER THE
DISORDER. FOR EXAMPLE, RESEARCHERS HAVE FOUND THAT GENETICS MAY INFLUENCE

47. GENETIC INFLUENCES IN CASE OF BIPOLAR DISORDERS :
STUDIES SUGGEST THAT ABOUT 8 TO 9 % OF FIRST
DEGREE RELATIVES OF A PERSON WITH BIPOLAR DISORDER
CAN BE EXPECTED TO HAVE BIPOLAR DISORDER RELATIVE
TO ONE PERCENT OF GENERAL POPULATION.(PLOMIN ET
AL. 2001)
STUDIES ALSO SUGGEST THAT FIRST DEGREE RELATIVES
OF BIPOLAR DISORDER ALSO ARE ELEVATED RISK FOR
MAJOR DEPRESSIVE DISORDER , ALTHOUGH REVERSE IS
NOT TRUE. (AKISKAL AND BENAJJIN, 2005).

48. NEUROCHEMICAL FACTOR
DEPRESSION ARISES FROM DISRUPTIONS IN THE DELICATE BALANCE OF
NEUROTRANSMITTER SUBSTANCES THAT REGULATE AND MEDIATE THE ACTIVITY OF
THE BRAIN’S NERVE CELLS .
PREVIOUSLY ATTENTION WAS FOCUSED PRIMARILY ON TWO NEUROTRANSMITTER
SUBSTANCES OF THE MONOAMINE CLASS- NOR EPINEPHRINE AND SEROTONIN-
BECAUSE RESEARCHES OBSERVED THAT ANTIDEPRESSANT MEDICATIONS SEEMED TO
HAVE THE EFFECT OF INCREASING THESE NEUROTRANSMITTERS AVAILABILITY AT
SYNAPTIC JUNCTIONS (EG THASE AND DENKO 2008; THASE ET AL., 2002). THESE
OBSERVATION LED TO THE ONCE INFLUENTIAL MONOAMINE THEORY OF
DEPRESSION- THAT DEPRESSION WAS AT LEAST SOMETIMES DUE TO AN ABSOLUTE
OR RELATIVE DEPLETION OF ONE OR BOTH OF THESE NEUROTRANSMITTERS AT
IMPORTANT RECEPTOR SITES IN THE BRAIN (SCHINDKRAUT , 1965).

49. FOR YEARS IT WAS THOUGHT THAT LOW ACTIVITY OF EITHER NOREPINEPHRINE OR SEROTONIN WAS
CAPABLE OF PRODUCING DEPRESSION, BUT INVESTIGATORS NOW BELIEVE THAT THEIR RELATION TO
DEPRESSION IS MORE COMPLICATED (GOLDSTEIN ET AL., 2011). SOME STUDIES HINT, FOR EXAMPLE,
THAT DEPRESSED PEOPLE HAVE AN OVERALL IMBALANCE IN THE ACTIVITY OF THE
NEUROTRANSMITTERS SEROTONIN, NOREPINEPHRINE, DOPAMINE, AND ACETYLCHOLINE. IN A
VARIATION OF THIS THEORY, SOME RESEARCHERS BELIEVE THAT SEROTONIN IS ACTUALLY A
NEUROMODULATOR, A CHEMICAL WHOSE PRIMARY FUNCTION IS TO INCREASE OR DECREASE THE
ACTIVITY OF OTHER KEY NEUROTRANSMITTERS. IF SO, PERHAPS LOW SEROTONIN ACTIVITY SERVES
TO DISRUPT THE ACTIVITY OF THE OTHER NEUROTRANSMITTERS, RESULTING IN DEPRESSION.
 THE ENDOCRINE GLANDS THROUGHOUT THE BODY RELEASE HORMONES, CHEMICALS THAT IN
TURN SPUR BODY ORGANS INTO ACTION . PEOPLE WITH UNIPOLAR DEPRESSION HAVE BEEN FOUND
TO HAVE ABNORMALLY HIGH LEVELS OF CORTISOL, ONE OF THE HORMONES RELEASED BY THE
ADRENAL GLANDS DURING TIMES OF STRESS (GAO & BAO, 2011; VEEN ET AL., 2011). THIS
RELATIONSHIP IS NOT ALL THAT SURPRISING, GIVEN THAT STRESSFUL EVENTS OFTEN SEEM TO
TRIGGER DEPRESSION. ANOTHER HORMONE THAT HAS BEEN TIED TO DEPRESSION IS MELATONIN ,
SOMETIMES CALLED THE “DRACULA HORMONE” BECAUSE IT IS RELEASED ONLY IN THE DARK.

50. IF DEPRESSION IS CAUSED BY DEFICIENCIES OF NOR EPINEPHRINE / SEROTONIN
, THEN PERHAPS MANIA IS CAUSED BY EXCESS OF THESE NEURO
TRANSMITTERS.
 HOWEVER SEROTONIN ACTIVITY APPEARS TO BE LOW IN BOTH DEPRESSIVE
AND MANIC PHASES.(MANJI AND LENOX,2000)
 INCREASED DOPAMINERGIC ACTIVITY IN SEVERAL BRAIN AREAS MAY BE
RELATED TO MANIC SYMPTOMS OF HYPER ACTIVITY , GRANDIOSITY ,
EUPHORIA ( HOWLAND AND THESE , 1999)

51. BRAIN SYSTEMS
STUDIES OF DEPRESSED PEOPLE HAVE SHOWN THAT THEY HAVE UNUSUALLY LOW ACTIVITY IN A
PART OF THE FRONTAL LOBE THAT HAS DIRECT CONNECTIONS TO THE AMYGDALA (WHICH IS
INVOLVED IN FEAR AND OTHER STRONG EMOTIONS) AND TO OTHER BRAIN AREAS INVOLVED IN
EMOTION (KENNEDY ET AL., 1997). THIS FINDING HINTS THAT THE DEPRESSED BRAIN IS NOT AS
ABLE AS THE NORMAL BRAIN TO REGULATE EMOTION. MOREOVER, THIS PART OF THE FRONTAL
LOBE HAS CONNECTIONS TO THE BRAIN AREAS THAT PRODUCE THE NEUROTRANSMITTER
SUBSTANCES DOPAMINE, SEROTONIN, AND NOREPINEPHRINE. THUS, THIS PART OF THE FRONTAL
LOBE MAY WELL BE INVOLVED IN REGULATING THE AMOUNTS OF SUCH SUBSTANCES. THIS IS
IMPORTANT BECAUSE THESE SUBSTANCES ARE INVOLVED IN REWARD AND EMOTION, WHICH
AGAIN HINTS THAT THE BRAINS OF THESE PEOPLE ARE NOT REGULATING EMOTION NORMALLY.
RESEARCHERS HAVE REFINED THIS GENERAL OBSERVATION AND REPORTED THAT ONE ASPECT OF
DEPRESSION—LACK OF MOTIVATED BEHAVIOR—IS SPECIFI CALLY RELATED TO REDUCED ACTIVITY
IN THE FRONTAL (AND PARIETAL) LOBES (MILAK ET AL., 2005). IN ADDITION, THESE RESEARCHERS
REPORT THAT DEPRESSION DOES NOT SIMPLY REFLECT THAT THE BRAIN AS A WHOLE HAS BECOME
SLUGGISH.
RATHER, THEY FOUND THAT MORE SEVERE DEPRESSION IS ASSOCIATED WITH GREATER ACTIVITY
IN THE EMOTION-RELATED LIMBIC SYSTEM, WHICH FITS WITH THE IDEA THAT EMOTIONS ARE NOT
BEING EFFECTIVELY REGULATED. MOREOVER, THESE RESEARCHERS FOUND THAT SOME OF THE
BRAIN AREAS INVOLVED IN ATTENTION (IN PARTICULAR, THE THALAMUS) AND IN CONTROLLING
MOVEMENTS(BASAL GANGLIA) ARE OVERACTIVE IN DEPRESSED PEOPLE, WHICH AGAIN SUGGESTS

52. Prefrontal
cortex
Brodmann
Area 25
Amygdala
Hippocamp
usThe biology of depression: Researchers believe that the
brain circuit involved in depression includes the
prefrontalcortex, hippocampus, amygdala, and Brodmann
Area 25.

53.  BIOLOGICAL RESEARCHERS NOW BELIEVE THAT THE ROOT OF PSYCHOLOGICAL DISORDERS
IS MORE COMPLICATED THAN A SINGLE NEUROTRANSMITTER OR SINGLE BRAIN AREA.
THEY HAVE DETERMINED THAT EMOTIONAL REACTIONS OF VARIOUS KINDS ARE TIED TO
BRAIN CIRCUITS—NETWORKS OF BRAIN STRUCTURES THAT WORK TOGETHER, TRIGGERING
EACH OTHER INTO ACTION AND PRODUCING A PARTICULAR KIND OF EMOTIONAL
REACTION.
 AN ARRAY OF BRAIN-IMAGING STUDIES POINT TO SEVERAL BRAIN AREAS THAT ARE LIKELY
MEMBERS OF THIS CIRCUIT, PARTICULARLY THE PREFRONTAL CORTEX, THE HIPPOCAMPUS,
THE AMYGDALA,AND BRODMANN AREA 25, AN AREA LOCATED JUST UNDER THE BRAIN
PART CALLED THE CINGULATE CORTEX.
 NOT SURPRISINGLY, THIS CIRCUIT IS FILLED WITH SEROTONIN TRANSPORTERS, OR 5-HTTS,
THOSE PROTEINS THAT HELP SEROTONIN CARRY MESSAGES FROM ONE NEURON TO
ANOTHER (SELVARAJ ET AL., 2011). WE KNOW PEOPLE WITH AN ABNORMAL 5-HTT GENE
ARE MORE PRONE TO DEVELOP DEPRESSION.
 THE PREFRONTAL CORTEX IS LOCATED WITHIN THE FRONTAL CORTEX OF THE BRAIN.
BECAUSE IT RECEIVES INFORMATION FROM A NUMBER OF OTHER BRAIN AREAS, THE
PREFRONTAL CORTEX IS INVOLVED IN MANY IMPORTANT FUNCTIONS,INCLUDING MOOD,
ATTENTION, AND IMMUNE FUNCTIONING. SEVERAL IMAGING STUDIES HAVE FOUND LOWER
ACTIVITY AND BLOOD FLOW IN THE PREFRONTAL CORTEX OF DEPRESSED RESEARCH
PARTICIPANTS THAN IN THE PREFRONTAL CORTEX OF NON DEPRESSED INDIVIDUALS

54.  HOWEVER, OTHER STUDIES, FOCUSING ON SELECT AREAS OF THE PREFRONTAL
CORTEX, HAVE FOUND INCREASES IN ACTIVITY DURING DEPRESSION ( LEMOGNEET
AL., 2010; DREVETS , 2001, 2000). CORRESPONDINGLY, RESEARCH FINDS THAT THE
PREFRONTAL CORTEX ACTIVITY OF DEPRESSED INDIVIDUALS INCREASES AFTER
SUCCESSFUL TREATMENT BY SOME ANTIDEPRESSANT DRUGS, BUT DECREASES
AFTER SUCCESSFUL TREATMENT BY OTHER KINDS OF ANTIDEPRESSANT DRUGS
(COOK & LEUCHTER, 2001). GIVEN THESE VARIED FINDINGS, RESEARCHERS
CURRENTLY BELIEVE THAT THE PREFRONTAL CORTEX PLAYS A CRITICAL ROLE IN
DEPRESSION BUT THAT THE SPECIFIC NATURE OF THIS ROLE HAS YET TO BE CLEARLY
DEFINED (LIM ET AL.,2011; GOLDSTEIN ET AL., 2011).
 THE PREFRONTAL CORTEX HAS STRONG NEURAL CONNECTIONS WITH ANOTHER PART
OF THE DEPRESSION BRAIN CIRCUIT, THE HIPPOCAMPUS. THE HIPPOCAMPUS IS ONE OF
THE FEW BRAIN AREAS TO PRODUCE NEW NEURONS THROUGHOUT ADULTHOOD, AN
ACTIVITY KNOWN AS NEUROGENESIS. SEVERAL STUDIES INDICATE THAT SUCH
HIPPOCAMPAL NEUROGENESIS DECREASES DRAMATICALLY WHEN INDIVIDUALS BECOME
DEPRESSED (KUBERA ET AL., 2011; AIRAN ET AL., 2007). CORRESPONDINGLY, WHEN
DEPRESSED INDIVIDUALS ARE SUCCESSFULLY TREATED BY ANTIDEPRESSANT DRUGS,
NEUROGENESIS IN THE HIPPOCAMPUSRETURNS TO NORMAL (MALBERG & SCHECHTER,
2005). MOREOVER, SOME IMAGING STUDIES HAVE DETECTED A REDUCTION IN THE SIZE
OF THE HIPPOCAMPUS AMONG DEPRESSED PERSONS (GOLDSTEIN ET AL., 2011;
CAMPBELL ET AL., 2004). HIPPOCAMPUS HELPS TO CONTROL THE BRAIN’S AND BODY’S
REACTIONS TO STRESS AND PLAYS A ROLE IN THE FORMATION AND RECALL OF

55.  THE AMYGDALA IS A BRAIN AREA THAT REPEATEDLY SEEMS TO BE INVOLVED IN THE EXPRESSION
OF NEGATIVE EMOTIONS AND MEMORIES. IT HAS BEEN FOUND TO BE A KEY AREA IN EACH OF
THE BRAIN CIRCUITS TIED TO GENERALIZED ANXIETY DISORDER, PANIC DISORDER, AND
POSTTRAUMATIC STRESS DISORDER APPARENTLY, IT ALSO PLAYS A ROLE IN DEPRESSION. PET
AND FMRI SCANS INDICATE THAT ACTIVITY AND BLOOD FLOW IN THE AMYGDALA IS 50 PERCENT
GREATER AMONG DEPRESSED PERSONS THAN NONDEPRESSED PERSONS (GOLDSTEIN ET AL.,
2011; DREVETS, 2001). IN FACT, ONE STUDY SUGGESTS THAT AS A PATIENT’S DEPRESSION
INCREASES IN SEVERITY, THE ACTIVITY IN HIS OR HER AMYGDALA INCREASES PROPORTIONATELY
(ABERCROMBIE ET AL., 1998).
 THE FOURTH PART OF THE DEPRESSION BRAIN CIRCUIT, BRODMANN AREA 25, HAS RECEIVED
ENORMOUS ATTENTION OVER THE PAST DECADE (HAMANI ET AL., 2011; MAYBERG ET AL., 2005,
2000, 1997). THIS AREA TENDS TO BE SMALLER IN DEPRESSED PEOPLE THAN NON DEPRESSED
PEOPLE.MOREOVER, LIKE THE AMYGDALA, IT IS SIGNIFICANTLY MORE ACTIVE AMONG
DEPRESSED PEOPLE THAN AMONG NON DEPRESSED PEOPLE. IN FACT, BRAIN SCANS REVEAL
THAT WHEN A PERSON’S DEPRESSION SUBSIDES , THE ACTIVITY IN HIS OR HER AREA
25 DECREASES SIGNIFICANTLY. BECAUSE ACTIVATION OF AREA 25 COMES AND GOES WITH
DEPRESSION, SOME THEORISTS BELIEVE THAT IT MAY IN FACT BE A “DEPRESSION SWITCH,”
A KIND OF JUNCTION BOX WHOSE MALFUNCTION MIGHT BE NECESSARY AND
OCCUR.

56.  BLOOD FLOW TO THE LEFT PREFRONTAL CORTEX IS REDUCED
DURING DEPRESSION, DURING MANIA IT IS REDUCED TO RIGHT
FRONTAL AND TEMPORAL REGIONS (HOWLAND AND THESE ,1999).
 CORTISOL LEVELS ARE ELAVATED IN BIPOLAR DEPRESSION AND
THEY ARE ALSO ELAVATED IN MANIC EPISODE.
 DEFICITS IN ACTIVITY IS PRESENT IN DLPFC IN BIPOLAR DISOREDR,
AND DEFICIT IN ANTERIOR CINGULATE CORTEX IS PRESENT IN
DEPRESSION.
 SUBCORTICAL STRUCTURES ARE ENLARGED IN BIPOLAR DISORDER
BUT REDUCED IN SIZE IN DEPRESSION.

57. PSYCHODYNAMIC THEORY
ACCORDING TO FREUD, THE CONSCIOUS AND UNCONSCIOUS PARTS
OF THE MIND CAN COME INTO CONFLICT WITH ONE ANOTHER,
PRODUCING A PHENOMENA CALLED REPRESSION (A STATE WHERE
YOU ARE UNAWARE OF HAVING CERTAIN TROUBLING MOTIVES,
WISHES OR DESIRES BUT THEY INFLUENCE YOU NEGATIVELY JUST THE
SAME). IN GENERAL, PSYCHODYNAMIC THEORIES SUGGEST THAT A
PERSON MUST SUCCESSFULLY RESOLVE EARLY DEVELOPMENTAL
CONFLICTS (E.G., GAINING TRUST, AFFECTION, SUCCESSFUL
INTERPERSONAL RELATIONSHIPS, MASTERING BODY FUNCTIONS,
ETC.). IN ORDER TO OVERCOME REPRESSION AND ACHIEVE MENTAL
HEALTH. MENTAL ILLNESS, ON THE OTHER HAND, IS A FAILURE TO
RESOLVE THESE CONFLICTS.

58.  FREUD AND KARL ABRAHAM (1924, 1927 ) BOTH HYPOTHESIZED THAT WHEN A
LOVED ONE DIES THE MOURNER REGRESSES TO THE ORAL STAGE OF
DEVELOPMENT AND INTROJECTS THE LOST PERSON, FEELING ALL THE SAME
FEELING TOWARDS SELF AS TOWARDS THE LOST PERSON . THIS FEELINGS WERE
THOUGHT TO INCLUDE ANGER AND HOSTILITY BECAUSE HE BELIEVED THAT WE
UNCONSCIOUSLY HOLD NEGATIVE FEELINGS TOWARDS THOSE WE LOVE
BECAUSE OF THEIR POWER OVER US.
 PSYCHOANALYSTS HISTORICALLY BELIEVED THAT DEPRESSION WAS CAUSED BY
ANGER CONVERTED INTO SELF-HATRED ("ANGER TURNED INWARD). NEUROTIC
PARENTS WHO ARE INCONSISTENT (BOTH OVERINDULGENT AND DEMANDING),
LACKING IN WARMTH, INCONSIDERATE, ANGRY, OR DRIVEN BY THEIR OWN
SELFISH NEEDS CREATE A UNPREDICTABLE, HOSTILE WORLD FOR A CHILD. AS A
RESULT, THE CHILD FEELS ALONE, CONFUSED, HELPLESS AND ULTIMATELY,
ANGRY. HOWEVER, THE CHILD ALSO KNOWS THAT THE POWERFUL PARENTS ARE
HIS OR HER ONLY MEANS OF SURVIVAL. SO, OUT OF FEAR, LOVE, AND GUILT,
THE CHILD REPRESSES ANGER TOWARD THE PARENTS AND TURNS IT INWARDS
SO THAT IT BECOMES AN ANGER DIRECTED TOWARDS HIM OR HERSELF.

59. A "DESPISED" SELF-CONCEPT STARTS TO FORM, AND THE CHILD
FINDS IT COMFORTABLE TO THINK THOUGHTS ALONG THE LINES OF
"I AM AN UNLOVABLE AND BAD PERSON." AT THE SAME TIME, THE
CHILD ALSO STRIVES TO PRESENT A PERFECT, IDEALIZED (AND
THEREFORE ACCEPTABLE) FACADE TO THE PARENTS AS A MEANS OF
COMPENSATING FOR PERCEIVED WEAKNESSES THAT MAKE HIM OR
HER "UNACCEPTABLE".
CAUGHT BETWEEN THE BELIEF THAT HE OR SHE IS UNACCEPTABLE,
AND THE IMPERATIVE TO ACT PERFECTLY TO OBTAIN PARENTAL
LOVE, THE CHILD BECOMES "NEUROTIC" OR PRONE TO
EXPERIENCING EXAGGERATED ANXIETY AND/OR DEPRESSION
FEELINGS. THE CHILD ALSO FEELS A PERPETUAL SENSE THAT HE OR
SHE IS NOT GOOD ENOUGH, NO MATTER HOW HARD HE OR SHE
TRIES.

60. ACCORDING TO OBJECT RELATIONS THEORY, DEPRESSION IS CAUSED BY
PROBLEMS PEOPLE HAVE IN DEVELOPING REPRESENTATIONS OF HEALTHY
RELATIONSHIPS.
DEPRESSION IS A CONSEQUENCE OF AN ONGOING STRUGGLE THAT DEPRESSED
PEOPLE ENDURE IN ORDER TO TRY AND MAINTAIN EMOTIONAL CONTACT WITH
DESIRED OBJECTS. THERE ARE TWO BASIC WAYS THAT THIS PROCESS CAN PLAY
OUT: THE ANACLITIC PATTERN, AND THE INTROJECTIVE PATTERN. EVEN
THOUGH THESE TERMS ARE NOT CURRENTLY USED IN THE DSM, SOME
THERAPISTS MAY STILL USE THEM TO LABEL DIFFERENT TYPES OF DEPRESSION .
ANACLITIC DEPRESSION IS CAUSED BY THE DISRUPTION OF A CAREGIVING
RELATIONSHIP WITH A PRIMARY OBJECT AND IS CHARACTERIZED BY FEELINGS
OF HELPLESSNESS AND WEAKNESS. A PERSON WITH ANACLITIC DEPRESSION
EXPERIENCES INTENSE FEARS OF ABANDONMENT AND DESPERATELY STRUGGLES
TO MAINTAIN DIRECT PHYSICAL CONTACT WITH THE NEED-GRATIFYING
OBJECT.
INTROJECTIVE DEPRESSION ARISES FROM A HARSH, UNRELENTING, HIGHLY
CRITICAL SUPEREGO THAT CREATES FEELINGS OF WORTHLESSNESS, GUILT AND

61.  MANIC PATIENTS LIKE NORMAL CONTROL, SEEMED TO SHOW HIGH SELF
ESTEEM AND AN OPTIMISTIC ATTRIBUTIONAL STYLE, WHERE AS
DEPRESSED PATIENT SHOWS LOW SELF ESTEEM AND PESSIMISTIC
ATTRIBUTIONAL STYLE.
 FREUD IN TOTEM AND TABOO [579], GAVE A PHYLOGENETIC
HYPOTHESIS AS TO HOW THIS CYCLE MIGHT HAVE COME INTO BEING.
 THE MANIC-DEPRESSIVE CYCLE IS A CYCLE BETWEEN PERIODS OF
DECREASED AND INCREASED GUILT FEELINGS, BETWEEN FEELINGS OF
ANNIHILATION AND OMNIPOTENCE, OF PUNISHMENT AND NEW DEED.
 IN DEPRESSIONS , THE EGO IS NO LONGER LOVED BY SUPEREGO;IT HAS
BEEN DESERTED,ITS ORAL WISHES UNREALIZED. IN MANIA, THE FOGIVING
ORAL LOVE UNION WITH THE SUPEREGO IS RESTORED.[1107]

62.  MANIC AND DEPRESSIVE REACTIONS MAY BE VIEWED AS TWO DIFFERENT
BUT RELATED DEFENCE ORIENTED STRATEGIES FOR DEALING WITH SEVERE
STRESS. IN THE CASE OF MANIA, THE INDIVIDUAL TRIES TO ESCAPE HIS
DIFFICULTIES BY A FLIGHT INTO REALITY.
 THE PERSON TRIES TO FORGET A BROKEN AFFAIR , OR TRIES TO ESCAPE
FROM A THREATENING LIFE SITUATION BY RESTLESS ACTIVITY IN WHICH
HE OCCUPIES EVERY MOMENT WITH WORK, SEXUAL AFFAIRS AND
COUNTLESS OTHER CROWDED ACTIVITIES- ALL PERFORMED WITH LITTILE
ENJOYMENT.
 WITH A TREMENDOUS EXPENDITURE OF ENERGY, THE MANIC TRIES TO
DENY HIS FEELINGS OF HELPLESSNESS AND HOPELESSNESS AND TO PLAY A
ROLE OF COMPETENCE. IT CONTINUES UP TO EMOTIONAL EXHAUSTION
AND FINALLLY THE PERSON ADMITS HIMSELF TO THE ONLY OTHER
ALTERNATIVE THAT IS DEFEAT AND INEVITABLE DEPRESSION.

63. BEHAVIORAL THEORIES
 PETER LEWINSOHN ARGUED THAT DEPRESSION IS CAUSED BY A COMBINATION
OF STRESSORS IN A PERSON'S ENVIRONMENT AND A LACK OF PERSONAL
SKILLS. MORE SPECIFICALLY, THE ENVIRONMENTAL STRESSORS CAUSE A
PERSON TO RECEIVE A LOW RATE OF POSITIVE REINFORCEMENT. ACCORDING
TO LEARNING THEORY, RECEIVING POSITIVE REINFORCEMENT INCREASES THE
CHANCES THAT PEOPLE WILL REPEAT THE SORTS OF ACTIONS THEY HAVE
TAKEN THAT LED THEM TO RECEIVE THAT REINFORCEMENT. SO PEOPLE
BECOME DEPRESSED EITHER WHEN THEIR RESPONSES NO LONGER PRODUCE
POSITIVE REINFORCEMENT OR WHEN THEIR RATE OF NEGATIVE
REINFORCEMENT INCREASES . (LEWINSOHN AND GOTLIB , 1995).
 ACCORDING TO LEWINSOHN, DEPRESSED PEOPLE ARE PRECISELY THOSE
PEOPLE WHO DO NOT KNOW HOW TO COPE WITH THE FACT THAT THEY ARE
NO LONGER RECEIVING POSITIVE REINFORCEMENTS LIKE THEY WERE BEFORE.
IN ADDITION, DEPRESSED PEOPLE TYPICALLY HAVE A HEIGHTENED STATE OF
SELF-AWARENESS ABOUT THEIR LACK OF COPING SKILLS THAT OFTEN LEADS
THEM TO SELF-CRITICIZE AND WITHDRAW FROM OTHER PEOPLE.

64. • DEPRESSED PERSONS DO INDEED RECEIVE FEWER POSITIVE VERBAL AND SOCIAL
REINFORCEMENTS FROM THEIR FAMILIES AND FRIENDS THAN DO NON
DEPRESSED PERSONS AS WELL AS EXPERIENCE MORE NEGATIVE EVENTS (
LEWINSOHN AND GOTLIB , 1995 ).

65. COGNITIVE VIEWS
COGNITIVE THEORISTS BELIEVE THAT PEOPLE WITH UNIPOLAR
DEPRESSION PERSISTENTLY VIEW EVENTS IN NEGATIVE WAYS AND THAT
SUCH PERCEPTIONS LEAD TO THEIR DISORDER . THE TWO MOST
INFLUENTIAL COGNITIVE EXPLANATIONS ARE THE THEORY OF NEGATIVE
THINKING AND THEORY OF LEARNED HELPLESSNESS.
NEGATIVE THINKING : AARON BECK BELIEVES THAT NEGATIVE
THINKING, RATHER THAN UNDERLYING CONFLICTS OR A REDUCTION IN
POSITIVE REWARDS, LIES AT THE HEART OF DEPRESSION (BECK
&WEISHAAR, 2011; BECK, 2002, 1991, 1967). OTHER COGNITIVE
THEORISTS—ALBERT ELLIS, FOR ONE—ALSO POINT TO MALADAPTIVE
THINKING AS A KEY TO DEPRESSION. ACCORDING TO BECK,
MALADAPTIVE ATTITUDES, A COGNITIVE TRIAD, ERRORS IN THINKING,
AND AUTOMATIC THOUGHTS COMBINE TO PRODUCE DEPRESSION.

66. BECK BELIEVES THAT SOME PEOPLE DEVELOP MALADAPTIVE ATTITUDES AS CHILDREN.
THE ATTITUDES RESULT FROM THEIR OWN EXPERIENCES , THEIR FAMILY
RELATIONSHIPS, AND THE JUDGMENTS OF THE PEOPLE AROUND THEM. BECK
SUGGESTS THAT LATER IN THESE PEOPLE’S
LIVES, UPSETTING SITUATIONS MAY TRIGGER AN EXTENDED ROUND OF NEGATIVE
THINKING THAT THINKING TYPICALLY TAKES THREE FORMS, WHICH HE CALLS THE
COGNITIVE TRIAD :THE INDIVIDUALS REPEATEDLY INTERPRET (1) THEIR EXPERIENCES,
(2) THEMSELVES , AND (3) THEIR FUTURES IN NEGATIVE WAYS THAT LEAD THEM TO
FEEL DEPRESSED.
ACCORDING TO BECK, DEPRESSED PEOPLE ALSO MAKE ERRORS IN THEIR THINKING. IN
ONE COMMON ERROR OF LOGIC, THEY DRAW ARBITRARY INFERENCES—NEGATIVE
CONCLUSIONS BASED ON LITTLE EVIDENCE.
DEPRESSED PEOPLE EXPERIENCE AUTOMATIC THOUGHTS, A STEADY TRAIN OF
UNPLEASANT THOUGHTS THAT KEEP SUGGESTING TO THEM THAT THEY ARE
INADEQUATE AND THAT THEIR SITUATION IS HOPELESS.
MANY STUDIES HAVE PRODUCED EVIDENCE IN SUPPORT OF BECK’S
EXPLANATION (REHM, 2010). SEVERAL OF THEM CONFIRM THAT DEPRESSED PEOPLE
HOLD MALADAPTIVE ATTITUDES AND THAT THE MORE OF THESE MALADAPTIVE
ATTITUDES THEY HOLD, THE MORE DEPRESSED THEY TEND TO BE (EVANS ET AL.,

67. LEARNED HELPLESSNESS-
SINCE THE MID-1960S SELIGMAN HAS DEVELOPED THE LEARNED HELPLESSNESS
THEORY OF DEPRESSION. IT HOLDS THAT PEOPLE BECOME DEPRESSED WHEN
THEY THINK (1) THAT THEY NO LONGER HAVE CONTROL OVER THE
REINFORCEMENTS (THE REWARDS AND PUNISHMENTS) IN THEIR LIVES AND (2)
THAT THEY THEMSELVES ARE RESPONSIBLE FOR THIS HELPLESS STATE.
SELIGMAN NOTED THAT THE EFFECTS OF LEARNED HELPLESSNESS GREATLY
RESEMBLE THE SYMPTOMS OF HUMAN DEPRESSION, AND HE PROPOSED THAT
PEOPLE IN FACT BECOME DEPRESSED AFTER DEVELOPING A GENERAL BELIEF
THAT THEY HAVE NO CONTROL OVER REINFORCEMENTS IN THEIR LIVES.
IN NUMEROUS HUMAN AND ANIMAL STUDIES, PARTICIPANTS WHO UNDERGO
HELPLESSNESS TRAINING HAVE DISPLAYED REACTIONS SIMILAR TO DEPRESSIVE
SYMPTOMS. WHEN, FOR EXAMPLE, HUMAN PARTICIPANTS ARE EXPOSED TO
UNCONTROLLABLE NEGATIVE EVENTS, THEY LATER SCORE HIGHER THAN OTHER
INDIVIDUALS ON A DEPRESSIVE MOOD SURVEY (MILLER & SELIGMAN, 1975).

68. ACCORDING TO A NEW VERSION OF THE THEORY, THE ATTRIBUTION-
HELPLESSNESS THEORY, WHEN PEOPLE VIEW EVENTS AS BEYOND THEIR CONTROL,
THEY ASK THEMSELVES WHY THIS IS SO (TAUBE-SCHIFF & LAU, 2008; ABRAMSON
ET AL., 2002, 1989, 1978). IF THEY ATTRIBUTE THEIR PRESENT LACK OF
CONTROL TO SOME INTERNAL CAUSE THAT IS BOTH GLOBAL AND STABLE (“I AM
INADEQUATE AT EVERYTHING AND I ALWAYS WILL BE”), THEY MAY WELL FEEL
HELPLESS TO PREVENT FUTURE NEGATIVE OUTCOMES AND THEY MAY EXPERIENCE
DEPRESSION. IF THEY MAKE OTHER KINDS OF ATTRIBUTIONS, THIS REACTION IS
UNLIKELY.

69. PSYCHOSOCIAL FACTORS
GROWING AWARENESS OF BIOLOGICAL FACTORS IN THE
AETIOLOGY OF UNIPOLAR DEPRESSIVE DISORDERS DOES NOT
IMPLY THAT PSYCHOSOCIAL FACTORS ARE IRRELEVANT.
• RECENT LIFE EVENTS- METHODOLOGICALLY RELIABLE
RESERACH HAS SHOWN THAT-
1. -THERE IS A SIXFOLD EXCESS OF ADVERSE LIFE EVENTS IN
THE MONTHS BEFORE THE ONSET OF DEPRESSIVE DISORDER.
2. -AN EXCESS OF SIMILAR EVENTS ALSO PRECEEDS SUICIDE
ATTEMPTS.
3. -IN GENERAL, LOSS EVENTS ARE ASSOCIATED WITH
DEPRESSION.
EVENTS THAT LEAD TO FEELINGS OF ENTRAPMENT
AND HUMILIATION MAY BE PARTICULARLY RELEVANT TO
THE ONSET OF DEPRESSION.

70. VULNERABILITY FACTORS AND LIFE DIFFICULTIES
BROWN AND HARRIS(1978) DIVIDED PREDISPOSING EVENTS INTO 2
CATEGORIES- THE FIRST KIND ARE PROLONGED STRESSFUL
CIRCUMSTANCES WHICH CAN THEMSELVES CAUSE DEPRESSION AS WELL AS
ADDING TO THE EFFECTS OF SHORT TERM LIFE EVENTS.
THE SECOND KIND OF PREDISPOSING CIRCUMSTANCES ACTS BY
INCREASING THE EFFECTS OF SHORT TERM LIFE EVENTS, KNOWN AS
VULNERABILITY FACTORS.
THERE IS A GOOD EVIDENCE THAT POOR SOCIAL SUPPORT ,
MEASURED AS LACK OF INTIMACY OR SOCIAL INTEGRATION , IS
ASSOCIATED WITH AN INCREASED RISK OF DEPRESSION.

71. PERSONALITY FACTORS-
CERTAIN KINDS OF PERSONALITY DEVELOPMENT COULD BE ASSOCIATED WITH
PREDISPOSITION TO MOOD DISORDER-GENERALLY IT IS OBSERVED THAT PATIENTS WITH
DEPRESSION OFTEN SEEM TO HAVE HIGH LEVELS OF PREMORBID ANXIETY.
A COGNITIVE STYLE THAT IS CHARACTERIZED BY SOCIOTROPY (ASTRONG
NEED FOR APPROVAL) IS ASSOCIATED WITH INCREASED RISK OF DEPRESSION AFTER
ADVERSE LIFE EVENTS. (MAZURE AND MACIEJEWSKI, 2003)
NEUROTICISM , AS MEASURED BY EPQ, PREDISPOSES TO MAJOR DEPRESSION
BUT TWIN STUDIES SUGGEST THAT NEUROTICISM AND MAJOR DEPRESSION HAVE
GENES IN COMMON. (FANOUS AND KENDLER, 2004).
EFFECTS OF PHYSICAL ILLNESS-
ALL MEDICAL ILLNESS AND THEIR TREATMENT CAN ACT AS NON- SPECIFIC
STRESSORS WHICH MAY LEAD TO MOOD DISORDER IN PREDISPOSED INDIVIDUALS.

72. SOME PEOPLE ARE CONSTITUTIONALLY MORE PRONE THAN
OTHERS TO DEVELOP MOOD DISORDERS- IT WOULD SEEM REASONABLE TO
SUPPOSE THAT SUCH HIGH –RISK PERSONS WOULD BE MORE SUSCEPTIBLE
TO THE EFFECTS OF SEVERELY STRESSFUL EVENTS. (KENDLER ET AL.,
1995).
A LARGE PERCENTAGE OF THE POPULATION IS AT RISK
FOR DEPRESSION IF THEY ARE EXPOSED TO ONE OR MORE SEVERE LIFE
EVENTS. (MONROE AND SIMONS, 1991)
AMONG DEPRESSED WOMEN, MORE THAN 60% HAD ONE
OR MORE SEVERE LIFE EVENTS IN THE PAST TWO TO SIX MONTHS. (BROWN
AND HARRIS, 1978).
RESEARCHERS SUGGESTED THAT PSYCHOSOCIAL
STRESSORS MAY CAUSE LONG –TERM CHANGES IN BRAIN FUNCTIONING
AND THESE CHANGES MAY PLAY A ROLE IN THE DEVELOPMENT OF MOOD
DISORDERS.(THASE ET AL, 1985; WHYBROW, 1997).
BECAUSE OF GENETIC FACTORS SOME PEOPLE SEEM TO
BE MORE PRONE TO RISKY ENVIRONMENTS, AND IT ALSO PLAY AN
IMPORTANT ROLE IN HOW LIFE EVENTS ARE PERCEIVED BY PARTICULAR
INDIVIDUAL.

73. EARLY ENVIRONMENT
PARENTAL DEPRIVATION
PSYCHOANALYSTS HAVE SUGGESTED THAT CHILDHOOD DEPRIVATION OF
MATERNAL AFFECTION THROUGH SEPERATION OR LOSS PREDISPOSES TO DEPRESSIVE
DISORDERS IN ADULT LIFE. THE KEY FACTOR HERE APPEARS TO BE DISCORD AND
DIMINISHED CARE.(HARRIS, 2011)
RELATIONSHIPS WITH PARENTS
GROSS- DISRUPTION OF PARENT –CHILD RELATIONSHIP ACTS (IN PHYSICAL AND
SEXUAL ABUSE) AS A RISK FACTOR FOR SEVERAL KINDS OF ADULT PSYCHIATRIC
DISORDER INCLUDING MAJOR DEPRESSION.
IT APPEARS THAT BOTH NON-CARING AND OVER-PROTECTIVE PARENTING
STYLE ARE ASSOCIATED WITH NON-MELANCHOLIC DEORESSION IN ADULTHOOD.
(PARKER ET. AL., 1992)
MOTHERS WITH POSTNATAL DEPRESSION MAY MANIFEST A REARING STYLE THAT
IS CHARACTERIZED BY NEGLECT AND EMOTIONAL INDIFFERENCE, WHICH INCREASE THE
RISK OF DEPRESSION IN THE SUBSEQUENT GENERATION. SIMILAR EFFECT OCCURS WHEN
A FATHER IS DEPRESSED. (RAMCHANDANI ET.AL. ,2005)

74. SOCIOCULTURAL VIEWS
THERE ARE TWO KINDS OF SOCIOCULTURAL VIEWS—THE FAMILY-SOCIAL PERSPECTIVE,
WHICH LOOKS AT THE ROLE PLAYED BY INTERPERSONAL FACTORS IN THE DEVELOPMENT
OF DEPRESSION, AND THE MULTICULTURAL PERSPECTIVE, WHICH TIES DEPRESSION TO
FACTORS SUCH AS GENDER, RACE, AND ECONOMIC STATUS.
THE FAMILY-SOCIAL PERSPECTIVE:-
THE CONNECTION BETWEEN DECLINING SOCIAL REWARDS AND DEPRESSION IS A TWO-
WAY STREET. ON THE ONE HAND, RESEARCHERS HAVE FOUND THAT DEPRESSED PERSONS
OFTEN DISPLAY WEAK SOCIAL SKILLS AND COMMUNICATE POORLY (TAUBE-SHIFF & LAU,
2008; JOINER, 2002).
CONSISTENT WITH THESE FINDINGS, DEPRESSION HAS BEEN TIED REPEATEDLY TO
THE UNAVAILABILITY OF SOCIAL SUPPORT SUCH AS THAT FOUND IN A HAPPY
MARRIAGE (WHISMAN & SCHONBRUN, 2010; KENDLER ET AL., 2005). PEOPLE WHO
ARE SEPARATED OR DIVORCED DISPLAY AT LEAST THREE TIMES THE DEPRESSION
RATE OF MARRIED OR WIDOWED PERSONS AND DOUBLE THE RATE OF PEOPLE
WHO HAVE NEVER BEEN MARRIED (SCHULTZ, 2007; WEISSMAN ET AL., 1991).

75. THE MULTICULTURAL PERSPECTIVE :-
TWO KINDS OF RELATIONSHIPS HAVE CAPTURED THE INTEREST OF
MULTICULTURAL THEORISTS: (1) LINKS BETWEEN GENDER AND DEPRESSION AND
(2) TIES BETWEEN CULTURAL AND ETHNIC
BACKGROUND AND DEPRESSION.
GENDER AND DEPRESSION:- A STRONG LINK EXISTS BETWEEN GENDER AND
DEPRESSION.
THE ARTIFACT THEORY HOLDS THAT WOMEN AND MEN ARE EQUALLY PRONE TO
DEPRESSION BUT THAT CLINICIANS OFTEN FAIL TO DETECT DEPRESSION IN MEN
(EMMONS, 2010; BROMMELHOFF ET AL., 2004). PERHAPS MEN FIND IT LESS
SOCIALLY ACCEPTABLE TO ADMIT FEELING DEPRESSED OR TO SEEK TREATMENT.
PERHAPS DEPRESSED WOMEN DISPLAY MORE EMOTIONAL SYMPTOMS, SUCH AS
SADNESS AND CRYING, WHICH ARE EASILY DIAGNOSED, WHILE DEPRESSED MEN
MASK THEIR DEPRESSION BEHIND TRADITIONALLY “MASCULINE” SYMPTOMS SUCH
AS ANGER.

76. THE LIFE STRESS THEORY SUGGESTS THAT WOMEN IN OUR SOCIETY EXPERIENCE MORE
STRESS THAN MEN (ASTBURY, 2010; KEYES & GOODMAN, 2006). ON AVERAGE THEY FACE
MORE POVERTY, MORE MENIAL JOBS, LESS ADEQUATE HOUSING, AND MORE
DISCRIMINATION THAN MEN—ALL FACTORS THAT HAVE BEEN LINKED TO DEPRESSION.
THE BODY DISSATISFACTION EXPLANATION STATES THAT FEMALES IN WESTERN SOCIETY
ARE TAUGHT, ALMOST FROM BIRTH, TO SEEK A LOW BODY WEIGHT AND SLENDER BODY
SHAPE—GOALS THAT ARE UNREASONABLE, UNHEALTHY, AND OFTEN UNATTAINABLE.
HOWEVER, IT IS NOT CLEAR THAT EATING AND WEIGHT CONCERNS ACTUALLY CAUSE
DEPRESSION; THEY MAY INSTEAD BE THE RESULT OF DEPRESSION.
THE LACK-OF-CONTROL THEORY PICKS UP ON THE LEARNED HELPLESSNESS RESEARCH
AND ARGUES THAT WOMEN MAY BE MORE PRONE TO DEPRESSION BECAUSE THEY FEEL
LESS CONTROL THAN MEN OVER THEIR LIVES. (LE UNES, NATION, & TURLEY, 1980).
A FINAL EXPLANATION FOR THE GENDER DIFFERENCES FOUND IN DEPRESSION IS THE
RUMINATION THEORY. RESEARCH SHOWS THAT PEOPLE WHO RUMINATE WHENEVER THEY
FEEL SAD ARE MORE LIKELY TO BECOME DEPRESSED AND STAY DEPRESSED LONGER. IT
TURNS OUT THAT WOMEN ARE MORE LIKELY THAN MEN TO RUMINATE WHEN THEIR
MOODS DARKEN, PERHAPS MAKING THEM MORE VULNERABLE TO THE ONSET OF CLINICAL
DEPRESSION (NOLEN-HOEKSEMA & CORTE, 2004; NOLEN-HOEKSEMA, 2002, 2000).