IS THERE SUCH A THING AS A CURE FOR MENTAL ILLNESS?
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Transcript of IS THERE SUCH A THING AS A CURE FOR MENTAL ILLNESS?
IS THERE SUCH A THING AS A CURE FOR MENTAL ILLNESS?
TOM SENSKYAssurance Medical and Underwriting Society
March 2011
CURE versus REMISSION
CURE• The complete eradication of
the illnessREMISSION • State of absence of disease
activity (usually in someone with a chronic disease)
WHAT SORTS OF ILLNESSES CAN BE CURED?
Those which have ....• Clear-cut pathology• Simple aetiology (as opposed to
multifactorial)
Illnesses which have multifactorial causes or maintaining factors are likely to be chronic – cure here is unlikely
OVERVIEW – DIFFERENT TYPES OF CONDITIONS
CONDITION TYPE
EXAMPLES MANAGEMENT STRATEGY
Acute Common coldFractured humerus
• Remove pathology• Cure
Potentially Relapsing
Cerebro-vascular accident
• Self-management• Reduce risks where
possible• Contingency plan to
manage relapseChronic Diabetes
Rheumatoid arthritis
• Continue treatment indefinitely
• Shared decision-making• Self-management
OVERVIEW – DIFFERENT TYPES OF MENTAL HEALTH CONDITIONS
CONDITION TYPE
EXAMPLES MANAGEMENT STRATEGY
Acute Specific phobias
• Remove pathology• Cure
Potentially Relapsing
DepressionAnxiety
• Self-management• Reduce risks where
possible• Contingency plan to
manage relapseChronic Some cases
of schizophrenia and bipolar disorder
• Continue treatment indefinitely
• Shared decision-making• Self-management
OVERVIEW
• Focus on depression and anxiety, as common mental disorders
• Review of selective factors contributing to depression being best regarded as a chronic condition
• For anxiety, focus on some primitive psychological factors associated with the persistence of symptoms
DEPRESSION
Depression is often referred to as the common cold of psychiatry. But this analogy is wrong: although common, most depressive disorders are not mild and self limiting. It is time that we treated depression as the chronic disease that it is.
Jan Scott: Br Med J (editorial) (2006)
EPIDEMIOLOGY OF MENTAL DISORDERS (Health of the Nation)
• Of adults aged 16–64 years living in private households ,1 in 6 had suffered from some type of neurotic disorder in the week before the survey interview
• Half of these experienced anxiety and/or depression
Jenkins R et al: Br J Psychiatry (1998)
EPIDEMIOLOGY OF MENTAL DISORDERS (Health of the Nation)
Rates of common mental disorders higher among
• women• those who were separated, divorced and
widowed individuals of both genders, and among cohabiting women
• the unemployed• those with longstanding physical
complaints Jenkins R et al: Br J Psychiatry (1998)
PREVALENCE OF COMMON MENTAL DISORDERS (AGES 18-32 years)
Alcohol dependence
Depression
Anxiety
0 10 20 30 40 50
% Prevalence
1972-3 Dunedin birth cohort, followed up prospectively to age 32 years (95% follow-up)
Moffit TE et al: Psychological Medicine (2010)
Higher prevalence than previously reported attributed to prospective follow-up (likely to be more accurate)
DEPRESSION IN WOMEN : AETIOLOGICAL MODEL
DEPRESSION
PROVOKING AGENTS• Life events• Chronic difficulties VULNERABILITY FACTORS
• Maternal derivation• Parental separation• Social supports• Social circumstances
BACKGROUND• Personality• Genetics
After Brown GW & Harris T (1978)
COMMON MENTAL DISORDERS : AETIOLOGY
RATE OF LIFE EVENTS IMPACT OF
LIFE EVENTSONSET OFDISORDER
• Good parenting• Good marital relationship• Psychological factors
PROTECTIVE FACTORS
VULNERABILITY FACTORS
FAMILY• Parental loss• Lack of care• Child abuse
SOCIAL• Marital discord• Poor social support
SOCIAL ADVERSITY• Poor housing• Unemployment
PHYSIOLOGICAL• Genetic• Emotional reactivity
PERSONALITY• Neuroticism• Low self esteem• Low emotional strength
AETIOLOGICAL FACTORS RELEVANT TO DEPRESSION
Poor social support
Childhood abuse
Unsupportive work environment
Lack of control at work
Lifetime depression history
Discrimination
Anxiety
0 1 2 3 4 5 6
OnsetRecovery
Hazard RatioSample of 10,045 primary care patients, from 7 countries, followed up at 6 and 12 months Bottomley C et al: Br J Psychiatry (2010)
AFFECTIVE DISORDERS : GENETICS
• Genetic loading : bipolar (BP)>unipolar (UP)• Concordance (MZ twins) : BP=70%,
UP=40%• Risk of mood disorder in 1st degree
relatives : BP=30%, UP=15%• Close relative with BP disorder =
increased lifetime risk of both BP and UP disorder
• Close relative with UP disorder = increased risk of UP disorder only
EFFECT OF 5HT TRANSPORTER POLYMORPHISM ON SUSCEPTIBILITY TO LIFE EVENTS
Individuals homozygous for the short allele of the 5HT Transporter gene [s/s] were significantly more likely to develop a major depressive episode in response to stressful life events than those homozygous for the long allele [l/l]
Caspi A et al: Science (2003)
AUTOBIOGRAPHICAL MEMORY
AUTOBIOGRAPHICAL MEMORY IN DEPRESSION
CONSEQUENCES
• Depressed people recall fewer autobiographical memories (40% cf 70% for non-depressed people)
• Impairment most noticeable for positive events
• Autobiographical memory for negative events less impaired
• Depressed people have difficulty remembering events or activities that give pleasure or satisfaction
• Remember details of unhappy events
• Poor autobiographical memory leads to impaired problem-solving
The ability to recall specific memories in response to cues
ATTRIBUTIONS: AN EXAMPLEBeing criticised for a piece of work
STABLE
She’s right – I don’t think I’m up to this work
UNSTABLE
She must have got out of bed the wrong side today
GLOBAL
Nothing I do is ever good enough SPE
CIFIC
I didn’t put as much effort into this piece of work as I usually do
INTERNA
L
It’s all my faultEXTERNAL
If she hadn’t overloaded me with other assignments, I could have spent more time on this one
REFORMULATION OF THE LEARNED HELPLESSNESS MODEL: ATTRIBUTION TYPES
Abramson LY, Seligman K, Teasdale J: J Abnormal Psychology (1978)
UNSTABLE STABLE
INTERNAL
EXTERNAL
GLOBAL
SPECIFIC
Attributions by depressed people for
NEGATIVE events
Attributions by depressed people for
POSITIVE events
ASSOCIATION OF STRESS AT WORK WITH DEPRESSION: SYSTEMATIC REVIEW
Demand-control model
• High psychological demands
• Low degree of control over one’s tasks
• Combination of factors that prevents the experience of autonomy
• 8 studies• 44,114 respondents• Depression
associated with high demands plus low control
Effort reward imbalance model
• Usually expect reciprocity of contractual exchange at work – efforts compensated by adequate rewards (money, career opportunity, job security and esteem
• Imbalance occurs if rewards are not commensurate with efforts
• 4 studies• 81,582 respondents• Depression
assoiciated with effort-reward imbalance
Sigrist J: Eur Arch Psychiatry Clin Neurosci (2009)
ASSOCIATION OF STRESS AT WORK WITH DEPRESSION: SYSTEMATIC REVIEW
Demand-control model
• High psychological demands
• Low degree of control over one’s tasks
• Combination of factors that prevents the experience of autonomy
• 8 studies• 44,114 respondents
• Depression associated with high demands plus low control
Effort reward imbalance model
• Usually expect reciprocity of contractual exchange at work – efforts compensated by adequate rewards (money, career opportunity, job security and esteem
• Imbalance occurs if rewards are not commensurate with efforts
• 4 studies• 81,582 respondents
• Depression associated with effort-reward imbalance
Sigrist J: Eur Arch Psychiatry Clin Neurosci (2009)
WORK-RELATED FACTORS CONTRIBUTING TO DEPRESSION ONSET
• Longitudinal study examining onset of depression in 7 countries (6 European)
• Examined influence of 39 potential risk factors
• Sample: 7558 people not depressed at baselineFactor Adjusted
HR95% CI of
HR
Discrimination 1.94 1.46-2.58
Distress at work without respect 2.02 1.56-2.63
Difficulties at work without support 2.01 1.49-2.72
Lack of control at work 2.09 1.44-3.02
Bottomley C et al. British Journal of Psychiatry 196 (1):13-17, 2010
OFFSPRING OF SEVERELY DEPRESSED PARENTS
• Prospective 20-year follow-up of offspring of severely depressed patients
• Matched comparison group – offspring of parents without psychiatric morbidity
• Mean age of offspring at follow-up was 35 years
Weissman MMet al: Am J Psychiatry (2006)
DIAGNOSISCumulative Rate (%)
Relative RateDepresse
d Control
Any mood disorder 80 50 3.3Major depressive disorder 65 27 3.3Any anxiety disorder 67 34 2.9Any substance abuse 21 18 1.1Any physical illness 78 60 2.5Overweight 51 70 0.4
OFFSPRING OF SEVERELY DEPRESSED PARENTS
• Prospective 20-year follow-up of offspring of severely depressed patients
• Matched comparison group – offspring of parents without psychiatric morbidity
• Mean age of offspring at follow-up was 35 years
Weissman MMet al: Am J Psychiatry (2006)
DIAGNOSISCumulative Rate (%)
Relative RateDepresse
d Control
Any mood disorder 80 50 3.3Major depressive disorder 65 27 3.3Any anxiety disorder 67 34 2.9Any substance abuse 21 18 1.1Any physical illness 78 60 2.5Overweight 51 70 0.4
ADVERSE EVENTS IN CHILDHOOD AND ADULT DEPRESSED MOOD
4+
3
2
1
0
0 1 2 3 4 5
Adjusted Odds Ratio
Num
ber
of a
dver
se
child
hood
eve
nts
•Survey of 9508 adults registered with a health maintenance organisation•Assessed a variety of adverse childhood events, including abuse, violence against mother, parent in prison, etc•Assessed the odds of having at least 2 weeks of depressed mood in the past 12 months
Felitti VJ et al: Am J Prev Med (1998)
ETHNIC DENSITY AND COMMON MENTAL DISORDERS
• Random community sample (N=4281)• After adjusting for confounders, as own-
group ethnic density rose, the prevalence of common mental disorders decreased in (a) the whole ethnic minority sample; (b) the Irish group; (c) the Bangladeshi group
• This was despite areas of high minority ethnic density being socially deprived
• These results were not explained by discrimination, social support or social networks
Das-Munshi J et al : Br Med J (2010)
WILL THE INCIDENCE OF DEPRESSION RISE IN MEN?
• All research to date indicates higher incidence of depression in women
• Women tend to derive their self-esteem from reflected appraisals, while men focus on social comparisons, particularly regarding ‘traditional’ male roles
• Women are increasingly the primary household earners (4% in 1970, 22% in 2007)
• Male jobs are arguable more sensitive to the effects of recession than female jobs
Dunlop BW & Mietzko T: Br J Psychiatry (2011)
DEPRESSION RELAPSE RATES – ANTIDEPRESSANTS vs PLACEBO
6 12 18 24 36 Total0
1020304050607080
Antide-pressant
Months follow-up
S Reid & C Barbui. Long term treatment of depression with selective serotonin reuptake inhibitors and newer antidepressants. BMJ 340 (mar26_1):c1468, 2010.
4.5* 5.0*3.1*
3.1*2.4*
4.2*
* Number Needed to Treat
EFFICACY OF ANTIDEPRESSANT TREATMENT FOR DEPRESSION IN PRIMARY CARE
Arroll B et al. Antidepressants versus placebo for depression in primary care. Cochrane Database Syst Rev (3):CD007954, 2009
UK PRESCRIPTION OF ANTIDEPRESSANT MEDICATIONS
From www.tuesday1st.blogspot.com/ (dated 28 January 2010)
VARIATIONS IN ANTIDEPRESSANT PRESCRIBING IN ENGLAND
http://www.guardian.co.uk/news/datablog/2011/mar/05/data-store-pharmaceuticals-industry?intcmp=239#
Northern doctors prescribe more antidepressants, study revealsPatients in areas such as Blackpool are prescribed up to three times as many antidepressants as those in parts of LondonJames Ball and Sarah Boseley guardian.co.uk, Friday 4 March 2011 21.30 GMT
GP DIAGNOSIS OF DEPRESSION• Meta-analysis of 41 studies involving 50,371
patients• Weighed sensitivity = 50%• Weighed specificity = 81%• GPs tend to rule out non-cases more
effectively than recognising cases, but the modest prevalence of depression means that there are more false positives than missed cases
• For every 100 unselected cases seen, 10 true cases of depression are identified, 10 cases missed, and 15 people diagnosed as false positives Mitchell AJ et al. Lancet 374 (9690):609-619, 2009.
ARE ANTIDEPRESSANTS EFFECTIVE IN TREATING DEPRESSION?
•Meta-analysis of all clinical trials submitted to the US (FDA for licensing of the four new-generation antidepressants for which full datasets were available
•35 clinical trials involving 5,133 patients (3,292 randomised to antidepressants, 1,841 to placebo)
Kirsch I et al: Plos Medicine (2008)
COMPARATIVE EFFICACY OF ANTIDEPRESSANT MEDICATIONS
Data from Cipriani et al (2009) – table from Bandolier (http://www.medicine.ox.ac.uk/bandolier)
META-ANALYSIS OF COMPUTER CBT FOR DEPRESSION AND ANXIETY
DIAGNOSIS STUDIES EFFECT SIZE (g) NNT
Major depression 6 0.78 2.39
Social phobia 8 0.92 2.07
Panic disorder 6 0.83 2.26
Generalised anxiety 2 1.12 1.75
All combined 22 0.88 2.15
Andrews Get al : PLoS ONE (2010)
DEPRESSION TREATMENT: SHORT-TERM EFFECTS OF ANTIDEPRESSANT MEDICATION OR COGNITIVE THERAPY
DeRubeis R et al: Nature Reviews Neuroscience (2008)
•Severely depressed patients (n=240) were randomized to ADM (n = 120), CT (n = 60) or a (pill) placebo control (n = 60) treatment. •ADM involved paroxetine, augmented with lithium or desipramine as needed. •Treatment phase lasted 16 weeks.•The clinicians providing either ADM or CT were experienced practitioners who received feedback and supervision throughout the period of the study.
CBT vs ANTIDEPRESSANTS: CHANGE IN COGNITIONS I
40
60
80
100
120
Baseline Week 4 Week 8 EndAuto
mat
ic T
houg
hts Q
uest
ionn
aire
CBTDrugs
Simons AD et al (1984) Arch Gen Psych 41:45-51
CBT vs ANTIDEPRESSANTS: CHANGE IN COGNITIONS II
110
120
130
140
150
160
170
Baseline Week 4 Week 8 End
Dysf
unct
iona
l Att
itude
s Sca
le
CBTDrugs
Simons AD et al (1984) Arch Gen Psych 41:45-51
PROGNOSIS OF PEOPLE DIAGNOSED WITH DEPRESSION
% FOLLOW-UP MONTHS
Episodes of depression 30%
Symptoms of depression 52%
Antidepressant prescription 59%
• Prospective cohort study of people diagnosed with depression
• 8-11 year follow-up (N=61)
Kennedy N et al: Br J Psychiatry (2005)
• 18% of the cohort never achieved asymptomatic status
DEPRESSION TREATMENT: DIFFERENCES WITH/WITHOUT ANXIETY PRESENT
Intolerance
Severe side-effects
Response
Remission
0 10 20 30 40 50 60
Anxiety-Anxiety+
% Patients
Data from STAR*D trial – 2,876 adults with major depressive disorder, started initially on treatment with citalopram
Fava M et al: Am J Psychiatry (2008)
EFFECTS OF PAST HISTORY AND SUBTHRESHOLD DEPRESSIVE SYMPTOMS ON LATER DEPRESSION INCIDENCE
• Prospective cohort study from the Netherlands
• N=1167• Community
sample• 2-year follow-up• Those who had
depression within 6 months of baseline assessment were excluded
Karsten J et al: Br J Psychiatry (2011)
FACTORS PREDICTING LESS FAVOURABLE PROGNOSIS IN PEOPLE DIAGNOSED WITH DEPRESSION
FACTOR Adjusted Odds Ratio
Female gender 5.45
Severe index episode 5.70
Index anxiety 3.64Depression prior to index episode 3.50
Kennedy N et al: Br J Psychiatry (2005)
DEPRESSION: RELAPSE FOLLOWING ANTIDEPRESSANT MEDICATION OR COGNITIVE THERAPY
DeRubeis R et al: Nature Reviews Neuroscience (2008)
•After 16 week treatment phase, patients on ADM were randomised to continuation with ADM or placebo•Patients who had CBT were allowed no more than 3 booster sessions after acute treatment
ANXIETY - AETIOLOGY
PSYCHOLOGICAL FACTORS
• Classical conditioning• Operant conditioning• Social learning
GENETIC FACTORS
• Modest genetic contribution overall• Sensitivity of CO2 inhalation ?related to
polymorphism of lactate dehydrogenase gene
• Panic attacks more common in people who have joint hypermotility
NEURO-TRANSMITTERS
• Serotonin and GABA receptors important• Serotonin depletion increases susceptibility
to panic• Treated with benzodiazepines/SSRIs
BRAIN CHANGES
• Anxiety associated with changes in amygdala, cingulate gyrus and prefrontal/anterior temporal cortex
THE EXPERIENCE OF ANXIETY
• Many people who experience anxiety recognise their fears as unwarranted
• Such people know (“intellectually”) that they have no need to be anxious, yet the anxiety persists
• Very simple psychological factors contribute to this persistence• Conditioning (classical and
operant)• Social learning
CLASSICAL CONDITIONING (PAVLOV’S DOG)
Context egplayground
CLASSICAL CONDITIONING
Bullying Anxiety
Context egplayground
Anxiety
Unconditioned stimulus
Unconditioned response
Conditioned stimulus
Conditioned response
Waterway
CLASSICAL CONDITIONING
Accident in boat in water
Anxiety
Waterway Anxiety
Unconditioned stimulus
Unconditioned response
Conditioned stimulus
Conditioned response
PROBLEMS WITH REGARDING SPECIFIC PHOBIAS AS CLASSICALLY CONDITIONED
• There isn’t always a past history of a traumatic event
• If there is a past history of trauma, it does always lead to development of a phobia
Mineka S & Zinbarg R: American Psychologist (2006)
VICARIOUS CONDITIONING
• In ‘normal’ classical conditioning, the individual is exposed directly to the fearful stimulus
• Laboratory-reared rhesus monkeys (not afraid of snakes) became afraid of snake by seeing wild-reared monkeys reacting fearfully to snakes
• Humans can develop fears by watching videotapes of other people reacting fearfully
INDIVIDUAL DIFFERENCES IN VULNERABILITY TO ACQUIRE SPECIFIC PHOBIAS
• Modest genetic vulnerability for phobias (?mediated by genetic contribution to fear conditioning)
• Phobias more likely with certain personality variables• High trait anxiety• Behavioural inhibition (shyness,
timidity)• Differences in life experience (before,
during and after the conditioning event(s))
EXPERIENCES PRIOR TO CONDITIONING EVENT(S)
Exposure to the conditioned stimulus (2) before this is paired with the unconditioned stimulus (3) reduces the extent to subsequent conditioningExample: children visiting the dentistUnlike experimental animals, humans are seldom naïve to any conditioning stimulus
EXPERIENCES DURING CONDITIONING
• Fear is less likely to be conditioned when the aversive event is seen as• escapable• controllable
EXPERIENCES AFTER CONDITIONING
Mild fear (previously conditioned)
Exposure to a more intense but unrelated traumatic experience
Increased fear to the original conditioned
stimulusINFLATION
EFFECT
EXAMPLE• Mild driving phobia after
car accident• Subsequent personal
assault• Driving phobia then
becomes much worse
CONDITIONING OF PHOBIAS – OTHER FACTORS
• In monkeys, easier to condition fears for snakes or crocodiles than for flowers or toy rabbits
• Similar findings in humans – fears are selectively conditioned (people fear spiders more frequently than guns)
• Such prepared fears are probably similar now to the experience of prehistoric man
• Prepared fears more easily acquired, and more difficult to get rid of
EXAMPLES OF SOCIAL LEARNING IN SOCIAL PHOBIA
VICARIOUS LEARNING
Observing someone else being humiliated or ridiculed may be sufficient to generate social phobia
SOCIAL REINFORCEMENT
Parents of anxious children are more likely than other parents to support their childrens’ wishes to avoid social situations
CULTURAL NORMS
In Western cultures, social phobia commonly involves a fear of being scrutinised, while in Japan, it commonly involves a fear of causing offence by staring inappropriately, blushing, etc
OPERANT CONDITIONING
The individual learns by ‘operating’ appropriately on the environmentExampleMouse learns that pressing lever in response to red light results in getting a food pellet, while pressing lever in response to green light leads to electric shock
OPERANT CONDITIONING – EXAMPLE OF A CHILD HAVING A TANTRUM
Mother gives child immediate
attentionPOSITIVE
REINFORCEMENTTantrums repeated
Mother withdraws
NEGATIVE REINFORCEMENT
Tantrum ends
Mother gives attention when tantrum ended
POSITIVE REINFORCEMENTTantrums reduce
OPERANT CONDITIONING IN ANXIETY: EXAMPLES
• Avoidance of phobic stimuli or of vicarious conditioning• Child avoids dogs because mother
is afraid of them• Persistent ‘safety’ behaviours
• Always going out accompanied• Taking alcohol before going out
SAFETY BEHAVIOURS INHIBIT IMPROVEMENT IN PATIENTS WITH SOCIAL PHOBIA
0
10
20
30
40
50
% Im
prov
emen
t
Keep SB Drop SB
BeliefsAnxiety
Wells A et al: Behavior Therapy (1995)
• Case series (N=8)• Within-subjects
crossover design• One therapy
session with safety behaviours, one session without
• Monitored in-session anxiety and thoughts
CONCLUSIONS
• Chronic conditions can seldom be cured
• Disorders like schizophrenia and bipolar disorder are often considered chronic
• However, even common mental disorders (depression and anxiety) are best understood and managed as chronic conditions
CONTACT DETAILS
PTSD and subsyndromal PTSD, and change of diagnoses over three years (N=90)
5
19
66 624
134
223
2 weeks post accident1
4
9
7773
4
44
21
78
10
2
1
1
3 yearfollow-up
1 yearfollow-up
SubsyndromalPTSD
PTSD
no PTSD
1 Time criterion for PTSD not fulfilled
Psychiatric comorbidity at one-year follow-up (N=106)
Schnyder et al. (2001) Am J Resp Crit Care Med 164: 653-656
PTSDfull or subsyndromal
Anxiety(HADS)
Depression(HADS)
3 + 3*
8
4
421
2
PERSONALITY DISORDER versus NEUROSIS
PERSONALITY DISORDER NEUROSIS
ONSET Childhood/ adolescence
May be in adulthood
ENVIRONMENTAL PRECIPITANTS ?? Present
DISCRETE SYMPTOMS
No (except transiently) Yes
SYMPTOMS CHANGE OVER
TIMENo Usually
DURATION Always chronic May be brief
Affective disorders : prognosis• UNIPOLAR DEPRESSIVE DISORDER
• First episode lasts 4-6 months• 25% recurrence after 1 year• 75% recurrence within 10 years, 93% within 20 years• Average gap is 65 months• Typically 4-6 episodes over 20 years• 10% will eventually have hypomanic / manic episode (diagnosis then =
Bipolar Disorder)
• BIPOLAR DISORDER• Recurrence common (depression or mania)• Average gap is 48 months• Remission periods become shorter• Average 6.5 episodes in lifetime
Suicide rate in severe affective disorder = 10 - 15%
DEPRESSION : AETIOLOGY
GENETIC Family history
Emotional deprivation Early maternal separation Parental discord
EARLY DEVELOPMENT
Childhood abuse
PERSONALITY Neuroticism
Loss events Chronic difficulties
SITUATIONAL FACTORS
Lack of social supports
PROGNOSIS OF PEOPLE DIAGNOSED WITH DEPRESSION
• Prospective cohort study of people diagnosed with bipolar affective disorder, symptomatic at baseline (N=1469)
• 24-month follow-up
Perlis RH et al: Arch Gen Psychiatry (2006)
• 58% achieved recovery• 48% had a recurrence (depression 34%, other 13%)
FACTORS INDEPENDENTLY ASSOCIATED WITH TIME TO RECURRENCERELAPSE TYPE FACTOR HAZARD
RATIO
Depression Residual manic symptoms 1.22% days depression (past yr) 1.02% days anxiety (past yr) 1.01
Mania/Mixed Episodes depression (past yr) 1.07% days depression (past yr) 0.99% days elevated mood (past yr) 1.02
SELECTIVE PUBLICATION OF ANTIDEPRESSANT TRIALS
Turner EH et al. N Engl J Med 358 (3):252-260, 2008
• Obtained reviews from FDA for studies of 12 antidepressants (12,564 patients)
• Identified relevant published papers
• Examined papers to determine whether their conclusions agreed with FDA decision, or conflicted with it
ETHNIC DENSITY, PHYSICAL ILLNESS AND ANTIDEPRESSANT PRESCRIBING
• Data from 8515 GP practices in England
• Performance data from Quality and Outcomes Framework (QOF) (2004-5)
• Sociodemographic data from 2001 census
• Prescribing from Prescribing Analysis and CosT (PACT) data
• Multiple regression analysis
Walters P et al: Br J Psychiatry (2008)
ANTIDEPRESSANT PRESCRIBING – UNIVARIATE ASSOCIATIONSVARIABLE VARIANCE
EXPLAINEDUNADJUSTED
BETA
Chronic respiratory disease 25% 574
Coronary heart disease 22% 329% Black ethnic patients 12% -52% Chinese ethnic patients 9% -179% S Asian ethic patients 7% -19% White ethnic patients 15% 20Index of multiple deprivation 4% 12
Group practice 4% 465List size 3% -0.2
ETHNIC DENSITY, PHYSICAL ILLNESS AND ANTIDEPRESSANT PRESCRIBING
• Data from 8515 GP practices in England
• Performance data from Quality and Outcomes Framework (QOF) (2004-5)
• Sociodemographic data from 2001 census
• Prescribing from Prescribing Analysis and CosT (PACT) data
• Multiple regression analysis
Walters P et al: Br J Psychiatry (2008)
ANTIDEPRESSANT PRESCRIBING – UNIVARIATE ASSOCIATIONSVARIABLE VARIANCE
EXPLAINEDUNADJUSTED
BETA
Chronic respiratory disease 25% 574
Coronary heart disease 22% 329% Black ethnic patients 12% -52% Chinese ethnic patients 9% -179% S Asian ethic patients 7% -19% White ethnic patients 15% 20Index of multiple deprivation 4% 12
Group practice 4% 465List size 3% -0.2
EPIDEMIOLOGY OF MENTAL DISORDERS (Health of the Nation)
DisorderPoint
Prevalence
Lifetime Risk
Schizophrenia 0.2-0.5% 0.7-0.9%
Bipolar affective disorder 0.1-0.5% 1%
Depressive disorder 3-6% 20%
Dementia at age >65 years 5%
Dementia at age >80 years 20%
Jenkins R et al: Br J Psychiatry (1998)
PANIC DISORDER: REDUCTION IN GABA RECEPTOR BINDING
GABAA receptor binding measured by positron emission tomography (PET) imaging with 11C-flumazenil (benzodiazepine antagonist)
Malizia AL et al: Arch Gen Psychiatry (1998)
Marked reduction noted in GABAA receptor binding throughout the brain, with greatest decrease in orbitofrontal and temporal cortex (?involved in the experience of anxiety)
THE BURDEN OF DEPRESSION
• Depression is the third most common presentation among GP referrals
• 20% of those with depression will not recover fully from the index episode
• 70-80% of those achieving remission will have at least 1 recurrence
• 15% will eventually commit suicide Scott J: Br Med J (2006)
WORLDWIDE DISABILITY BY DISEASE
Source: WHO Collaborative Project on Psychological Problems in General Health Care
DEPRESSION : AETIOLOGY
GENETIC Family history
Emotional deprivation Early maternal separation Parental discord
EARLY DEVELOPMENT
Childhood abuse
PERSONALITY Neuroticism
Loss events Chronic difficulties
SITUATIONAL FACTORS
Lack of social supports
DEPRESSION AND THE RESPONSE OF OTHERS
• Female undergraduates (N=45) randomised to 3 groups to have phone conversations with:• Depressed people (N=15)• People with a history of
depression (N=15)• Controls with no history of
depression (N=15)
Coyne JC: J Abnormal Psychology (1976)
DEPRESSION AND THE RESPONSE OF OTHERS
• Those subjects talking to depressed patients reported:• more depression, anxiety and hostility• increased reluctance to re-engage
• The speech of the depressed patients contained more self-references, particularly of negative personal and private events
Coyne JC: J Abnormal Psychology (1976)
Depression is not a social skills deficit but depressed patients tend to alienate others, leading to less positive reinforcement