Biological Etiology of Major Depressive Disorder

Biological Etiology of Major Depressive Disorder

1. Biochemdical

   • Neurotransmitter
     • serotonin hypothesis
       • Lacasse and Leo (2005)
         • lack of evidence that any depressed person has low levels of serotonin
           • no baseline balanced level of serotonin to measure against
             • Cannot compare the level of serotonin before and after having depression
         • common analogy for what is wrong with using the e ectiveness of a treatment as support for a causal explanation
           • headaches are successfully treated by aspirin, but we do not have any theory suggesting that headaches are caused by a lack of aspirin
       • Sarek, 2006
         • tianeptine, a drug commonly used in Europe and South America to treat depression
           • opposite action to fluoxetine
             • prevention of neuronal damage due to stress
       • significant in the pharmaceutical industry
         • medical treatment
   • Hormone
     • cortisol
       • reactivity to stress
         • Burke et al., 2005
           • meta- analysis of studies connecting cortisol with depression
           • difference in reactivity to stress between depressed and non-depressed people
             • non- depressed people
               • cortisol levels rise and fall rapidly
             • depressed people
               • more blunt reaction and remain under stress for longer
         • Hormone--> reactivity to stress--> depression
         • Depression--> change in hormone--> more reactive to stress
       • history of many negative life events
         • Cutuli et al., 2010
           • homeless children
           • age: 4-7
           • significant correlation between high levels of cortisol and a history of many negative life events
           • Negative life event--> Hormone~> Depression
     • Correlation does not indicate causation
       • Change in hormone --> depression
       • Depression --> change in hormone
     • Provide medical treatment
       • easy to measure
       • synthetic
       • can be directly injected into bloodstream

2. Genetics

   • Evolution
     • Hagen et al. (2004)
       • signal need
       • elicit help from others in the social group
     • Logical
       • e.g. the point that most suicides by depressed individuals are preceded by the threat of suicide, which therefore signals a need for help and attention
     • impossible to test experimentally
     • genetic basis of this evolved behaviour
   • Genes
     • Twin Study
       • Kendler et al., 2006
         • Swedish
         • over 42 000 participants
           • Large Sample Size
         • telephone interviews
           • Self-reporting bias
           • Participants may not have the insight to symptoms
         • diagnose depression on the basis of (a) the presence of most of the DSM-IV symptoms or (b) having had a prescription for antidepressants
         • concordance rates among monozygotic twins of 44% for female and 31% for male, compared with 16% and 11% for female and male dizygotic twins respectively
         • indicate a strong genetic component
           • Not purely genetic (if yes,monozygotic concordance rates would be much higher)
     • Gene Mapping
       • Caps et al. (2003)
         • Relationship between 5-HTT gene and depression after stressful events
           • Both genes and environmental factors are under investigation
             • Difficult to conclude the gene is a major contribution to depression
             • Unclear how environmental factors influence genes
           • Compared participants with normal 5-HTT genes and a mutation with shorter alleles
             • Large proportion of population carries the mutation of 5-HTT gene
               • 43%
             • Participant with shorter alleles: more likely to become depressed after stressful event
               • Vulnerability to depression after stress events
         • 847 Caucasian New Zealanders
           • large sample size
         • Self-report on depression
           • Cross checking with friends
     • Ethics
       • Having the genes does not equal having the disorder
     • Confusing
       • Levinson (2005)
         • short allele on 5-HTT acts in a similar way of drugs improve the symptoms of depression (e.g. Prozac); it hinders reuptake of serotonin
     • Predict who is vulnerable to depression
       • Provide special treatment to prevent having the disorder
     • Levinson (2005)
       • the gene is more likely to make individuals more sensitive to stressful life events
     • Diathesis–stress model
       • explain behavior as a predispositional vulnerability together with stress from life experiences
         • Lazarus (1993)
           • if the combination of the predisposition and the stress exceeds a threshold, the person will develop a disorder

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