IB Psychology HL Paper 2
1. Biological Etiologies in Affective Disorder: MDD (GENETIC): Zubenko
Aim: to investigate genetic inheritance involved in MDD and whether or not there
was a common gene associated with the onset of MDD
Method: scanned the genomes of 81 families that had one member suffering from
MDD and looked for commonalities.
Results: 19 regions of chromosomes found to be common throughout the 81
families associated with MDD (4 of which were only found in women including CREB
1 that is associate with estrogen production and, 1 of 19 where only found in men)
Conclusion: Zubenko concluded that there are more genes that cause the onset of
MDD in females than males. Thus providing genetic explanations for the higher
prevalence of MDD in females than males
Critical Analysis:
1. Reductionist: genetics are not the only factor contributing to the onset of MDD
(sociocultural factors / cognitive factors)
2. Ethical vs. Applicability Issues
- what to do with the results
- may result in the selective breeding
- may inflict prejudice and high stigmatisation
- may influence the individuals with families with MDD perception of illness to
change (self-fulfilling prophecy)
3. Further studies have supported this by showing that the prevalence of MDD in
females and males in children are the same until puberty whereby the
prevalence of MDD in females increase
4. Results may not be applicable to other types of depression
2. Biological Etiologies in Affective Disorder: MDD (HORMONAL
ABNORMALITIES): MDD is linked to the hyperactivity of the HPA axis
(hyperthalamic - pituitary - adrenal axis), a system that manages stress through the
secretion of the hormone cortisol. During stressful life events, the hyperactivity of
the HPA-axis results in the constant production of cortisol that stimulates the flight
or fight response.
Sapolsky
, IB Psychology HL Paper 2
Aim: to investigate the effects of hierarchical stress on baboons in Kenya
Method: took blood sample from the baboons and measured it for levels of
glucose and cortisol. Also observed the social hierarchies and interactions
between baboons.
Results: baboons with of lower hierarchical status was shown to have
significantly higher levels of stress hormones than their higher hierarchal
counterparts. As a result, they displayed higher blood pressure, weaker immune
systems, higher susceptibility to disease and were less productive.
Conclusion: sapolsky concluded that the consequences and effects of the hyper-
activity of the HPA-axis in baboons can be applicable to human depression.
Critical Analysis
1. Animal testing (extrapolation of data): may not be applicable to human behaviour
(baboons experience a different type of stress than humans do in everyday life) 2.
Synthesis: Kendler et al investigated the associations between childhood sexual
abuse and depression. Observed 1404 female twin siblings who had experienced
childhood sexual abuse. Found that they have a higher chance in the onset of
depression and greater sensitivity to depressogenic events (stress coping) to
stressful life events.
- although not everyone who has experienced childhood sexual abuse has
depression (linked to stress-diathesis model; non-reductionist explanation for
depression whereby it may increase the vulnerability but biological factors are also
contributory) 3. Study has bi-directional ambiguity (cause and effect relationship
cannot be established)
3. Biological Etiologies for Affective Disorder: MDD (BIOCHEMICAL
ABNORMALITIES): Permissive Hypothesis suggests by Prange Jr
- in opposition to Schildkraut's Catecolamine Hypothesis
- low serotonin allows for a drop in norephephrine and onsets depression
Prange Jr.
Aim: to investigate the correlation between depression and serotonin
Method: evaluated and compared 100's of correlational studies that investigate the
effectiveness of SSRI's (selective serotonin re-uptake inhibitors) on the onset of
depression.
Results: showed that biochemical imbalances can be attributed to the onset of
depression
, IB Psychology HL Paper 2
Critical Analysis
1. Third-variable effect (due to bi-directional ambiguity)
- Neurogenisis theory (intake of SSRI's cause a growth of
extra brain cells that cause the onset of depression)
2. Reductionist theory
3. Correlational studies on SSRI's show only a 60% success rate. Furthermore, the
studies are usually funded by the multi-million dollar psychopharmeceutical
companies that may result in researcher bias
4. Stress Diathesis Model: non-reductionist theory for the onset of depression
(Nemeroff et al)
- suggests that new environment and biology interact to cause the onset of
depression
- biological factors are contributory but stressors are needed to increase the
vulnerability and cause the onset of the illness
5. Biological Etiologies of Anxiety Disorder: PTSD (NEUROBIOLOGICAL):
Neurobiological (HIPPOCAMPUS):
studies have suggested that the smaller than average size of the hippocampi due
to the experiencing of traumatic life events results in the onset of PTSD
Williams et al
Aim: investigate the neurobiological etiologies of anxiety
Method: participant volunteers asked to play a game of pacman where they were
being chased by a red dot. If caught, an electrical shock was administered to their
leg. During this process, an fmri was administered.
Results: the fmri showed that the visual and muscle control centers in the brain
were active during the time of anxiety and shock. Furthermore the hippocampus
was shown to be highly stimulated
Conclusion: thus showcasing that the hippocampus is highly involved in the
management and onset of anxiety
Critical Analysis:
1. Bi-directional ambiguity (FMRI)
2. Reductionist
3. Application: allow for new anxiety drugs that target the hippocampus to be
established
1. Biological Etiologies in Affective Disorder: MDD (GENETIC): Zubenko
Aim: to investigate genetic inheritance involved in MDD and whether or not there
was a common gene associated with the onset of MDD
Method: scanned the genomes of 81 families that had one member suffering from
MDD and looked for commonalities.
Results: 19 regions of chromosomes found to be common throughout the 81
families associated with MDD (4 of which were only found in women including CREB
1 that is associate with estrogen production and, 1 of 19 where only found in men)
Conclusion: Zubenko concluded that there are more genes that cause the onset of
MDD in females than males. Thus providing genetic explanations for the higher
prevalence of MDD in females than males
Critical Analysis:
1. Reductionist: genetics are not the only factor contributing to the onset of MDD
(sociocultural factors / cognitive factors)
2. Ethical vs. Applicability Issues
- what to do with the results
- may result in the selective breeding
- may inflict prejudice and high stigmatisation
- may influence the individuals with families with MDD perception of illness to
change (self-fulfilling prophecy)
3. Further studies have supported this by showing that the prevalence of MDD in
females and males in children are the same until puberty whereby the
prevalence of MDD in females increase
4. Results may not be applicable to other types of depression
2. Biological Etiologies in Affective Disorder: MDD (HORMONAL
ABNORMALITIES): MDD is linked to the hyperactivity of the HPA axis
(hyperthalamic - pituitary - adrenal axis), a system that manages stress through the
secretion of the hormone cortisol. During stressful life events, the hyperactivity of
the HPA-axis results in the constant production of cortisol that stimulates the flight
or fight response.
Sapolsky
, IB Psychology HL Paper 2
Aim: to investigate the effects of hierarchical stress on baboons in Kenya
Method: took blood sample from the baboons and measured it for levels of
glucose and cortisol. Also observed the social hierarchies and interactions
between baboons.
Results: baboons with of lower hierarchical status was shown to have
significantly higher levels of stress hormones than their higher hierarchal
counterparts. As a result, they displayed higher blood pressure, weaker immune
systems, higher susceptibility to disease and were less productive.
Conclusion: sapolsky concluded that the consequences and effects of the hyper-
activity of the HPA-axis in baboons can be applicable to human depression.
Critical Analysis
1. Animal testing (extrapolation of data): may not be applicable to human behaviour
(baboons experience a different type of stress than humans do in everyday life) 2.
Synthesis: Kendler et al investigated the associations between childhood sexual
abuse and depression. Observed 1404 female twin siblings who had experienced
childhood sexual abuse. Found that they have a higher chance in the onset of
depression and greater sensitivity to depressogenic events (stress coping) to
stressful life events.
- although not everyone who has experienced childhood sexual abuse has
depression (linked to stress-diathesis model; non-reductionist explanation for
depression whereby it may increase the vulnerability but biological factors are also
contributory) 3. Study has bi-directional ambiguity (cause and effect relationship
cannot be established)
3. Biological Etiologies for Affective Disorder: MDD (BIOCHEMICAL
ABNORMALITIES): Permissive Hypothesis suggests by Prange Jr
- in opposition to Schildkraut's Catecolamine Hypothesis
- low serotonin allows for a drop in norephephrine and onsets depression
Prange Jr.
Aim: to investigate the correlation between depression and serotonin
Method: evaluated and compared 100's of correlational studies that investigate the
effectiveness of SSRI's (selective serotonin re-uptake inhibitors) on the onset of
depression.
Results: showed that biochemical imbalances can be attributed to the onset of
depression
, IB Psychology HL Paper 2
Critical Analysis
1. Third-variable effect (due to bi-directional ambiguity)
- Neurogenisis theory (intake of SSRI's cause a growth of
extra brain cells that cause the onset of depression)
2. Reductionist theory
3. Correlational studies on SSRI's show only a 60% success rate. Furthermore, the
studies are usually funded by the multi-million dollar psychopharmeceutical
companies that may result in researcher bias
4. Stress Diathesis Model: non-reductionist theory for the onset of depression
(Nemeroff et al)
- suggests that new environment and biology interact to cause the onset of
depression
- biological factors are contributory but stressors are needed to increase the
vulnerability and cause the onset of the illness
5. Biological Etiologies of Anxiety Disorder: PTSD (NEUROBIOLOGICAL):
Neurobiological (HIPPOCAMPUS):
studies have suggested that the smaller than average size of the hippocampi due
to the experiencing of traumatic life events results in the onset of PTSD
Williams et al
Aim: investigate the neurobiological etiologies of anxiety
Method: participant volunteers asked to play a game of pacman where they were
being chased by a red dot. If caught, an electrical shock was administered to their
leg. During this process, an fmri was administered.
Results: the fmri showed that the visual and muscle control centers in the brain
were active during the time of anxiety and shock. Furthermore the hippocampus
was shown to be highly stimulated
Conclusion: thus showcasing that the hippocampus is highly involved in the
management and onset of anxiety
Critical Analysis:
1. Bi-directional ambiguity (FMRI)
2. Reductionist
3. Application: allow for new anxiety drugs that target the hippocampus to be
established
