biological approach to explaining ocd essay

The Biological Approach To Explaining OCD – (Genetic And Neural Explanations)

March 5, 2021 - paper 1 introductory topics in psychology | psychopathology.

Recap the general principles of the  Biological Approach  before learning specifically about how it can be used to explain the onset of OCD

A popular explanation for mental disorders is that they are  inherited.  This would mean that individuals inherited specific  genes  from their parents that are related to the onset of OCD.

(2) The SERT Gene:

Also called 5-HTT, the SERT gene is thought to affect the transport of  serotonin  creating lower levels of the neurotransmitter. These changed levels of serotonin are also implicated in OCD.

High Dopamine levels  are thought to be associated with OCD.  Szechtman, 1998  conducted animal studies and found that high doses of drugs that enhanced levels of dopamine induced stereotyped movements that resembled the compulsive behaviours witnessed in OCD patients.

Low Serotonin levels  are associated with OCD.  Pigott, 1990  found that anti-depressant drugs (which increase serotonin activity) have been shown to reduce the symptoms of OCD. 

A feature that is often witnessed on PET scans of OCD sufferers, The Obofrontal Cortex (associated with higher level thought and conversion of sensory information into thoughts.) This brain area is thought to help initiate activity upon receiving impulses to act and then stop the activity when the impulses lessen. A non-sufferer may have an impulse to wash dirt from their hands; once this is done, the impulse to perform the activity stops as does the behaviour. It may be that those with OCD have difficulty switching off or ignoring impulses so that they turn into obsessions resulting in compulsive behaviour.

Evaluation, AO3 of Biological Explanations of OCD:

(1) POINT:  The biological explanations of OCD can be criticised for being deterministic:  EVIDENCE:  For example, the biological explanation states that if an individual has the presence of COMT or SERT gene, or a lower level of serotonin in the brain than they are pre-programmed to develop OCD  EVALUATION:  This is a weakness because this theory of OCD ignores individual free will and the fact that an individual’s free choice can also have an influence on their behaviour.

(2) POINT:  The biological explanations of OCD can be criticised for being reductionist. EVIDENCE:  For example, the biological explanation suggests that OCD is caused by the presence of the SERT or COMT gene or by a lower level of serotonin in the brain, it states that OCD is a product of just an individual’s nature.  EVALUATION:  This is a problem because the biological approach to explaining OCD can be seen to be too simplistic as it ignores the role of other factors such as our childhood experiences, everyday stressors and the role of learning in the development of abnormality.

Biological Explanations of OCD ( AQA A Level Psychology )

Revision note.

Head of Humanities & Social Sciences

Biological Explanations of OCD: Genetic Explanations

The biological approach is known as the medical model as it explains all behaviour through our biology. The biological approach sees OCD and other abnormalities in the same way it sees a physical illness, explaining it by abnormal biological processes.

Genetic explanations 

These are hereditary influences transmitted from parent to offspring by genetic transmission.

• Researchers have identified Candidate genes as genes that create vulnerability to OCD 
• OCD seems to be polygenic; this means OCD is not caused by one single gene but by a combination of genetic variations that together cause significantly increased vulnerability
• There are different types of genes that cause OCD and one gene variation or group of genes may cause it in one person, but another sufferer of OCD could have a different variation of genes
• Taylor (2013) found evidence from previous studies that there are up to 230 different genes which may be involved with OCD
• Genes studied in relation to OCD include those involved in the action of  dopamine  and serotonin and both neurotransmitters are believed to have a role in regulating mood
• Tukel et al. (2013) suggested a variation of the COMT gene may contribute to OCD as it is more common in patients who suffer from OCD than in those that do not. This variation produces higher levels of dopamine and lower activity of the COMT gene
• The 5-HTT gene has also been linked with OCD as it affects the levels of serotonin, making them less and these lower levels of the neurotransmitter are linked with OCD

Evaluation of genetic explanations

Biological Explanations of OCD: Neural Explanations

• OCD can also be explained through neural connections and the imbalance or damage these can have.
• The neural damage may have been caused by illnesses that affect the immune system, such as different bacterias, and the explanation links to the genetic difference that has been found in OCD sufferers, where the gene, influences the levels of key neurotransmitters and the structures in the brain.

Neural explanations

• Serotonin is known to play a role in regulating mood, if a person has low levels of serotonin , the person can have low moods and other mental processes are often affected
• The reduction of serotonin can explain some cases of OCD
• Dopamine levels are thought to be abnormally high in people who suffer from OCD 
• The orbital Frontal Cortex (OFC), sends signals to the thalamus about things that are worrying you, this area of the brain is overactive in people who suffer from OCD
• The thalamus, which is the part of the brain that instructs the person to do a certain activity or behaviour, in OCD sufferers, this would be the ODC behaviour
• The caudate nucleus  is the part of the brain that in non-OCD suffers, surprises the messages from the OFC, and normalises the worry, however, in OCD suffers, this part of the brain is not completing this job and allows the OFC to make the sufferer worry. This could be due to damage or overstimulation
• Some forms of OCD have been linked with poor decision-making , which could be down to abnormal functioning in the lateral parts of the frontal lobes. (the parts of the brain responsible for logical thinking and making decisions)

Evaluation of neural connections 

Biological explanations are reductionist, looking at and breaking down specific parts and ignoring the holistic approach. Be careful in the exam to address the actual question. If the examiner asks about genes, do not wander into a discussion of neurotransmitters (even though there is a slight risk). The examiner wants you to address the question asked and not the one you actually wanted.

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• > Theoretical Approaches to Obsessive-Compulsive Disorder
• > Biological approaches to OCD

Book contents

• Frontmatter
• Synopsis of Theoretical approaches to obsessive-compulsive disorder
• Acknowledgments, and provenance of Theoretical approaches to obsessive-compulsive disorder
• 1 The natural history and definition of obsessive-compulsive disorder
• 2 Behavioural/learning accounts of OCD
• 3 Accounts of OCD based upon personality theories derived from the work of Pavlov
• 4 Janet on OCD
• 5 Psychodynamic approaches to OCD
• 6 Cognitive style/deficit approaches to OCD
• 7 Biological approaches to OCD
• 8 Concluding remarks
• Author index
• Subject index

7 - Biological approaches to OCD

Published online by Cambridge University Press:  07 May 2010

Introduction

An increase of interest has recently been shown in biological approaches to OCD, and there are available a number of reviews/discussions of the findings from genetic, neuroanatomical, neurophysiological, neuropsychological and biochemical studies of OCD, as well as from studies of what have been presented as animal models of the disorder (for example, Turner, Beidel and Nathan, 1985; Rapoport and Wise, 1988; Insel, 1988; Pitman, 1989). This chapter will attempt to offer neither detailed comments on the quality of these biological findings, nor a comprehensive review of them. Instead, some of what have been claimed to be the most important of these findings will be briefly outlined, along with some of the suggestions biological theorists have offered regarding the psychological processes at work in OCD. Discussion will then focus on how powerful an argument in favour of a biological account of OCD these findings, if sound, could sustain.

Given the use of supposed animal models of OCD in some biological research, a few remarks concerning such models are in order here. (Animal models of OCD are also offered in other types of research – for example, de Silva, 1988, pp. 206–7). Reed (1985, p. 11) objects to the use of animal models in the study of OCD on the basis of his belief that the defining criteria for the disorder are phenomenological – for a thought or action to be symptomatic of the disorder, according to Reed, it must be experienced as senseless and be resisted, and it is unclear, in the case of any animal behaviour, on what grounds it could be argued that such behaviour has been experienced in this way (although see de Silva, 1988, p. 207).

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• Biological approaches to OCD
• Ian Jakes , University of London
• Book: Theoretical Approaches to Obsessive-Compulsive Disorder
• Online publication: 07 May 2010
• Chapter DOI: https://doi.org/10.1017/CBO9780511721793.009

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Study Notes

Explaining OCD

Last updated 22 Mar 2021

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In this and related study notes we focus on biological explanations and treatments for obsessive compulsive disorder (OCD).

Biological explanations are divided into genetic explanations and neural explanations .

Genetic explanations for OCD

Genetic explanations suggest OCD is inherited and that individuals inherit specific genes which cause OCD

Genetic explanations have focused on identifying particular genes which are implicated in OCD and two genes have been linked to OCD, including the COMT gene and SERT gene .

The COMT gene is associated with the production of , which regulates the neurotransmitter dopamine. One variation of the COMT gene results in higher levels of dopamine and this variation is more common in patients with OCD, in comparison to people without OCD.

A second gene which has been implicated in OCD is the SERT gene (also known as the 5-HTT gene). The SERT gene is linked to the neurotransmitter serotonin and affects the transport of the serotonin (hence SERotonin Transporter), causing lower levels of serotonin which is also associated with OCD (and depression)

Neural explanations for OCD

Neural explanations of OCD focus on neurotransmitters as well as brain structures .

Neural explanations suggest that abnormal levels of neurotransmitters , in particular serotonin and dopamine , are implicated in OCD.

Neural explanations also suggest that particular regions of the brain, in particular the basal ganglia and orbitofrontal cortex , are implicated in OCD.

Neurotransmitters

The neurotransmitter serotonin is believed to play a role in OCD. Serotonin regulates mood and lower levels of serotonin are associated with mood disorders, such as depression. Furthermore, some cases of OCD are also associated with the reduced levels of serotonin, which may be caused by the SERT gene (see above). Further support for the role of serotonin in OCD comes from research examining anti-depressants, which have found that drugs which increase the level of serotonin are effective in treating patients with OCD.

In addition, the neurotransmitter dopamine has also been implicated in OCD, with higher levels of dopamine being associated with some of the symptoms of OCD, in particular the compulsive behaviours.

Brain Structures

Two brain regions have been implicated in OCD, including the basal ganglia and orbitofrontal cortex.

The basal ganglia is a brain structure involved in multiple processes, including the coordination of movement. Patients who suffer head injuries in this region often develop OCD-like symptoms, following their recovery. Furthermore, Max et al. (1994) found that when the basal ganglia is disconnected from the frontal cortex during surgery, OCD-like symptoms are reduced, providing further support for the role of the basal ganglia in OCD.

Another brain region associated with OCD is the orbitofrontal cortex , a region which converts sensory information into thoughts and actions. PET scans have found higher activity in the orbitofrontal cortex in patients with. One suggestion is that the heightened activity in the orbitofrontal cortex increases the conversion of sensory information to actions (behaviours) which results in compulsions. The increased activity also prevents patients from stopping their behaviours.

One strength of the biological explanation of OCD comes from research from family studies. Lewis (1936) examined patients with OCD and found that 37% of the patients with OCD had parents with the disorder and 21% had siblings who suffered. Research from family studies, like Lewis, provide support for a genetic explanation to OCD, although it does not rule out other (environmental) factors playing a role.

Further support for the biological explanation of OCD comes from twin studies which have provided strong evidence for a genetic link. Nestadt et al. (2010) conducted a review of previous twin studies examining OCD. They found that 68% of identical twins and 31% of non-identical twins experience OCD, which suggests a very strong genetic component.

Support for the neural explanations of OCD come from research examining biological treatments including anti-depressants.

Anti-depressants typically work by increasing levels of the neurotransmitter serotonin . These drugs are effective in reducing the symptoms of OCD and provide support for a neural explanation of OCD.

Extension: However, no twin study has found a concordance rate of 100% in identical twins, which means that biological factors are not the only factor contributing to OCD and there must be environmental factors which also contribute to this disorder.

One weakness of the biological explanation for OCD is that it ignores other factors and is reductionist. For example, the biological approach does not take into account cognitions (thinking) and learning. Some psychologists suggest that OCD may be learnt through classical conditioning and maintained through operant conditioning stimulus (for example, dirt) is associated with anxiety and this association is then maintained through operant conditioning, where a person avoids dirt and continually washes their hands. This hand washing reduces their anxiety and negatively reinforces their compulsions.

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• Nestadt et al. (2010)
• Lewis (1936)
• Max et al. (1994)

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• Revision notes >
• A-Level Psychology Revision Notes >
• Psychopathology

The biological approach to explaining OCD - A-Level Psychology

Genetic explanations:.

-is a biological explanation

-diathesis-stress model suggests certain genes leave some people more likely to suffer a mental disorder but is not certain-some environmental stress is necessary to trigger the condition.

-Candidate genes create vulnerability for OCD ,some of these genes are involved in regulating the serotonin system.

-OCD is polygenic so has several genes that are involved such as those associated with the action of dopamine and serotonin,both neurotransmitters that are believed to regulate mood.

-There are different types of OCD based on different groups of genes.

Neural explanations:

The role of serotonin-serotonin regulates mood and is a neurotransmitter.Neurotransmitters are responsible for relaying information from one neuron to another.Low levels of serotonin means that the normal transmission of mood-relevant information does not take place,so mood is affected.Some cases of OCD may be explained by a reduction in the functioning of the serotonin system in the brain.

Decision making systems-Some cases of OCD seem to be associated with impaired decision making due to abnormal functioning of the frontal lobes of the brain.The frontal lobes are responsible for logical thinking and making decisions.There is evidence that suggests that the left parahippocampal gyrus associated with processing unpleasant emotions,functions abnormally in OCD.

Evaluation:

Twin studies-supports the genetic explanation.Nestadt et al found that in previous twin studies 68% of identical twins shared OCD as opposed to 31% of non-identical twins.This suggests a genetic influence on OCD.However,twin studies are flawed ,the fact that identical twins may be more similar in terms of shared environments may be overlooked.

Lacks clarity-it is not clear exactly what neural mechanisms are involved in OCD.

The biological approach suggests that OCD has a physical basis, such as genetics, brain chemistry, and neuroanatomy. This approach views OCD as a disorder of the brain rather than a psychological or environmental issue.

Studies suggest that OCD is hereditary, meaning that genetics play a significant role in its development. People with a first-degree relative with OCD have a higher chance of developing the disorder themselves.

Research has shown that imbalances in neurotransmitters, such as serotonin, dopamine, and glutamate, can contribute to OCD. These chemicals are responsible for transmitting messages in the brain, and when they are not functioning properly, they can lead to obsessive and compulsive behaviors.

Studies have shown that people with OCD have structural differences in certain areas of the brain, such as the basal ganglia, orbitofrontal cortex, and anterior cingulate cortex. These differences can lead to problems with decision-making, impulse control, and emotional regulation.

Yes, medication can be effective in treating OCD by targeting imbalances in neurotransmitters. Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed to treat OCD and have been shown to be effective in reducing symptoms.

Cognitive-behavioral therapy (CBT) is often used to treat OCD. This therapy involves teaching individuals coping skills to manage their obsessive and compulsive behaviors. Exposure and response prevention (ERP) is a type of CBT that involves gradually exposing individuals to their fears and teaching them how to resist the urge to engage in compulsive behaviors.

While there is no cure for OCD, treatment can help manage symptoms and improve quality of life. It is important for individuals with OCD to seek professional help to develop an individualized treatment plan that works for them.

OCD affects around 1-2% of the population, and it is more common in women than men. It often begins in childhood or adolescence and can persist throughout adulthood if left untreated.

Common OCD symptoms include obsessive thoughts, such as a fear of germs or harm coming to oneself or others, and compulsive behaviors, such as excessive cleaning or checking. These behaviors can interfere with daily life and cause significant distress.

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OCD: Biological Approach

Genetic and neural explanations of ocd.

It is possible that OCD may be partially caused by a genetic tendency for the condition, and that the neural OCD circuit may play an important role. But there is a lack of research in both areas.

Genetic statistics

• The results of family and twin studies suggest that OCD has a moderate genetic component.
• The disorder is five times more frequent in the first-degree relatives of people with OCD than in people without the disorder.
• If a pair of twins are concordant, both are affected by the disorder.

• Studies have found about two dozen potential genes that may be involved in OCD. These genes regulate the function of three neurotransmitters: serotonin, dopamine, and glutamate.
• Many of these studies included small sample sizes and have yet to be replicated.
• So additional research needs to be done in this area.

Orbitofrontal cortex

• The orbitofrontal cortex is a brain region believed to play a critical role in OCD. It is an area of the frontal lobe involved in learning and decision-making.
• In people with OCD, the orbitofrontal cortex becomes especially hyperactive when they are provoked with tasks in which, for example, they are asked to look at a photo of a toilet or of pictures hanging crookedly on a wall.

OCD circuit

• The orbitofrontal cortex is part of a series of brain regions that, collectively, is called the OCD circuit. The OCD circuit is made up of several interconnected regions that influence the perceived emotional value of stimuli and the selection of both behavioural and cognitive responses.
• As with the orbitofrontal cortex, other regions of the OCD circuit show heightened activity during symptom provocation. This suggests that abnormalities in these regions may produce the symptoms of OCD.
• People with OCD also show a substantially higher degree of connectivity of the orbitofrontal cortex and other regions of the OCD circuit than those without OCD.

Limitations of neural findings

• The findings on the neural bases of OCD were based on imaging studies, and they highlight the potential importance of brain dysfunction in OCD.
• But one important limitation of these findings is that they don't explain differences in obsessions and compulsions.
• Another limitation is that the correlational relationship between neurological abnormalities and OCD symptoms cannot imply causation.

Biological Approach to Treating OCD

The biological approach treats OCD using anti-anxiety and anti-depressant drugs.

Biological approach

• The biological approach tries to treat psychological disorders directly by influencing the chemistry of the body and the brain.

Anti-anxiety drugs

• Some anti-anxiety drugs, or ‘anxiolytics’, treat OCD by tackling anxiety directly.
• Drugs such as Valium increase levels of GABA in the brain — a neurotransmitter responsible for inhibiting other neurons. This helps to calm people down.

Mood modifiers

• Other forms of medication try to tackle people’s thoughts and mood.
• A drug called sertraline was initially developed as an anti-depressant, but is widely prescribed for OCD because it helps to boost mood and reduce the tendency to worry.

Limitations of anti-depressant drugs

• A limitation of anti-depressant drugs, such as sertraline, is that they can take four to six weeks to take effect.
• One person may find the side effects mild, while another person may need to switch to a different medication.

1 Social Influence

1.1 Social Influence

1.1.1 Conformity

1.1.2 Asch (1951)

1.1.3 Sherif (1935)

1.1.4 Conformity to Social Roles

1.1.5 BBC Prison Study

1.1.6 End of Topic Test - Conformity

1.1.7 Obedience

1.1.8 Analysing Milgram's Experiment

1.1.9 Agentic State & Legitimate Authority

1.1.10 Variables of Obedience

1.1.11 Resistance to Social Influence

1.1.12 Minority Influence & Social Change

1.1.13 Minority Influence & Social Impact Theory

1.1.14 End of Topic Test - Social Influences

1.1.15 Exam-Style Question - Conformity

1.1.16 Top Grade AO2/AO3 - Social Influence

2.1.1 Multi-Store Model of Memory

2.1.2 Short-Term vs Long-Term Memory

2.1.3 Long-Term Memory

2.1.4 Support for the Multi-Store Model of Memory

2.1.5 Duration Studies

2.1.6 Capacity Studies

2.1.7 Coding Studies

2.1.8 The Working Memory Model

2.1.9 The Working Memory Model 2

2.1.10 Support for the Working Memory Model

2.1.11 Explanations for Forgetting

2.1.12 Studies on Interference

2.1.13 Cue-Dependent Forgetting

2.1.14 Eye Witness Testimony - Loftus & Palmer

2.1.15 Eye Witness Testimony Loftus

2.1.16 Eyewitness Testimony - Post-Event Discussion

2.1.17 Eyewitness Testimony - Age & Misleading Questions

2.1.18 Cognitive Interview

2.1.19 Cognitive Interview - Geiselman & Fisher

2.1.20 End of Topic Test - Memory

2.1.21 Exam-Style Question - Memory

2.1.22 A-A* (AO3/4) - Memory

3 Attachment

3.1 Attachment

3.1.1 Caregiver-Infant Interaction

3.1.2 Condon & Sander (1974)

3.1.3 Schaffer & Emerson (1964)

3.1.4 Multiple Attachments

3.1.5 Studies on the Role of the Father

3.1.6 Animal Studies of Attachment

3.1.7 Explanations of Attachment

3.1.8 Attachment Types - Strange Situation

3.1.9 Cultural Differences in Attachment

3.1.10 Disruption of Attachment

3.1.11 Disruption of Attachment - Privation

3.1.12 Overcoming the Effects of Disruption

3.1.13 The Effects of Institutionalisation

3.1.14 Early Attachment

3.1.15 Critical Period of Attachment

3.1.16 End of Topic Test - Attachment

3.1.17 Exam-Style Question - Attachment

3.1.18 Top Grade AO2/AO3 - Attachment

4 Psychopathology

4.1 Psychopathology

4.1.1 Definitions of Abnormality

4.1.2 Definitions of Abnormality 2

4.1.3 Phobias, Depression & OCD

4.1.4 Phobias: Behavioural Approach

4.1.5 Evaluation of Behavioural Explanations of Phobias

4.1.6 Depression: Cognitive Approach

4.1.7 OCD: Biological Approach

4.1.8 Evidence for the Biological Approach

4.1.9 End of Topic Test - Psychopathy

4.1.10 Exam-Style Question - Phobias

4.1.11 Top Grade AO2/AO3 - Psychopathology

5 Approaches in Psychology

5.1 Approaches in Psychology

5.1.1 Psychology as a Science

5.1.2 Origins of Psychology

5.1.3 Reductionism & Problems with Introspection

5.1.4 The Behaviourist Approach - Classical Conditioning

5.1.5 Pavlov's Experiment

5.1.6 Little Albert Study

5.1.7 The Behaviourist Approach - Operant Conditioning

5.1.8 Social Learning Theory

5.1.9 The Cognitive Approach 1

5.1.10 The Cognitive Approach 2

5.1.11 The Biological Approach

5.1.12 Gottesman (1991) - Twin Studies

5.1.13 Brain Scanning

5.1.14 Structure of Personality & Little Hans

5.1.15 The Psychodynamic Approach (A2 only)

5.1.16 Humanistic Psychology (A2 only)

5.1.17 Aronoff (1957) (A2 Only)

5.1.18 Rogers' Client-Centred Therapy (A2 only)

5.1.19 End of Topic Test - Approaches in Psychology

5.1.20 Exam-Style Question - Approaches in Psychology

5.2 Comparison of Approaches (A2 only)

5.2.1 Psychodynamic Approach

5.2.2 Cognitive Approach

5.2.3 Biological Approach

5.2.4 Behavioural Approach

5.2.5 End of Topic Test - Comparison of Approaches

6 Biopsychology

6.1 Biopsychology

6.1.1 Nervous System Divisions

6.1.2 Neuron Structure & Function

6.1.3 Neurotransmitters

6.1.4 Endocrine System Function

6.1.5 Fight or Flight Response

6.1.6 The Brain (A2 only)

6.1.7 Localisation of Brain Function (A2 only)

6.1.8 Studying the Brain (A2 only)

6.1.9 CIMT (A2 Only) & Postmortem Examinations

6.1.10 Biological Rhythms (A2 only)

6.1.11 Studies on Biological Rhythms (A2 Only)

6.1.12 End of Topic Test - Biopsychology

6.1.13 Top Grade AO2/AO3 - Biopsychology

7 Research Methods

7.1 Research Methods

7.1.1 Experimental Method

7.1.2 Observational Techniques

7.1.3 Covert, Overt & Controlled Observation

7.1.4 Self-Report Techniques

7.1.5 Correlations

7.1.6 Exam-Style Question - Research Methods

7.1.7 End of Topic Test - Research Methods

7.2 Scientific Processes

7.2.1 Aims, Hypotheses & Sampling

7.2.2 Pilot Studies & Design

7.2.3 Questionnaires

7.2.4 Variables & Control

7.2.5 Demand Characteristics & Investigator Effects

7.2.6 Ethics

7.2.7 Limitations of Ethical Guidelines

7.2.8 Consent & Protection from Harm Studies

7.2.9 Peer Review & The Economy

7.2.10 Validity (A2 only)

7.2.11 Reliability (A2 only)

7.2.12 Features of Science (A2 only)

7.2.13 Paradigms & Falsifiability (A2 only)

7.2.14 Scientific Report (A2 only)

7.2.15 Scientific Report 2 (A2 only)

7.2.16 End of Topic Test - Scientific Processes

7.3 Data Handling & Analysis

7.3.1 Types of Data

7.3.2 Descriptive Statistics

7.3.3 Correlation

7.3.4 Evaluation of Descriptive Statistics

7.3.5 Presentation & Display of Data

7.3.6 Levels of Measurement (A2 only)

7.3.7 Content Analysis (A2 only)

7.3.8 Case Studies (A2 only)

7.3.9 Thematic Analysis (A2 only)

7.3.10 End of Topic Test - Data Handling & Analysis

7.4 Inferential Testing

7.4.1 Introduction to Inferential Testing

7.4.2 Sign Test

7.4.3 Piaget Conservation Experiment

7.4.4 Non-Parametric Tests

8 Issues & Debates in Psychology (A2 only)

8.1 Issues & Debates in Psychology (A2 only)

8.1.1 Culture Bias

8.1.2 Sub-Culture Bias

8.1.3 Gender Bias

8.1.4 Ethnocentrism

8.1.5 Cross Cultural Research

8.1.6 Free Will & Determinism

8.1.7 Comparison of Free Will & Determinism

8.1.8 Reductionism & Holism

8.1.9 Reductionist & Holistic Approaches

8.1.10 Nature-Nurture Debate

8.1.11 Interactionist Approach

8.1.12 Nature-Nurture Methods

8.1.13 Nature-Nurture Approaches

8.1.14 Idiographic & Nomothetic Approaches

8.1.15 Socially Sensitive Research

8.1.16 End of Topic Test - Issues and Debates

9 Option 1: Relationships (A2 only)

9.1 Relationships: Sexual Relationships (A2 only)

9.1.1 Sexual Selection & Human Reproductive Behaviour

9.1.2 Intersexual & Intrasexual Selection

9.1.3 Evaluation of Sexual Selection Behaviour

9.1.4 Factors Affecting Attraction: Self-Disclosure

9.1.5 Evaluation of Self-Disclosure Theory

9.1.6 Self Disclosure in Computer Communication

9.1.7 Factors Affecting Attraction: Physical Attributes

9.1.8 Matching Hypothesis Studies

9.1.9 Factors Affecting Physical Attraction

9.1.10 Factors Affecting Attraction: Filter Theory 1

9.1.11 Factors Affecting Attraction: Filter Theory 2

9.1.12 Evaluation of Filter Theory

9.1.13 End of Topic Test - Sexual Relationships

9.2 Relationships: Romantic Relationships (A2 only)

9.2.1 Social Exchange Theory

9.2.2 Evaluation of Social Exchange Theory

9.2.3 Equity Theory

9.2.4 Evaluation of Equity Theory

9.2.5 Rusbult’s Investment Model

9.2.6 Evaluation of Rusbult's Investment Model

9.2.7 Relationship Breakdown

9.2.8 Studies on Relationship Breakdown

9.2.9 Evaluation of Relationship Breakdown

9.2.10 End of Topic Test - Romantic relationships

9.3 Relationships: Virtual & Parasocial (A2 only)

9.3.1 Virtual Relationships in Social Media

9.3.2 Evaluation of Reduced Cues & Hyperpersonal

9.3.3 Parasocial Relationships

9.3.4 Attachment Theory & Parasocial Relationships

9.3.5 Evaluation of Parasocial Relationship Theories

9.3.6 End of Topic Test - Virtual & Parasocial Realtions

10 Option 1: Gender (A2 only)

10.1 Gender (A2 only)

10.1.1 Sex, Gender & Androgyny

10.1.2 Gender Identity Disorder

10.1.3 Biological & Social Explanations of GID

10.1.4 Biological Influences on Gender

10.1.5 Effects of Hormones on Gender

10.1.6 End of Topic Test - Gender 1

10.1.7 Kohlberg’s Theory of Gender Constancy

10.1.8 Evaluation of Kohlberg's Theory

10.1.9 Gender Schema Theory

10.1.10 Psychodynamic Approach to Gender Development 1

10.1.11 Psychodynamic Approach to Gender Development 2

10.1.12 Social Approach to Gender Development

10.1.13 Criticisms of Social Theory

10.1.14 End of Topic Test - Gender 2

10.1.15 Media Influence on Gender Development

10.1.16 Cross Cultural Research

10.1.17 Childcare & Gender Roles

10.1.18 End of Topic Test - Gender 3

11 Option 1: Cognition & Development (A2 only)

11.1 Cognition & Development (A2 only)

11.1.1 Piaget’s Theory of Cognitive Development 1

11.1.2 Piaget's Theory of Cognitive Development 2

11.1.3 Schema Accommodation Assimilation & Equilibration

11.1.4 Piaget & Inhelder’s Three Mountains Task (1956)

11.1.5 Conservation & Class Inclusion

11.1.6 Evaluation of Piaget

11.1.7 End of Topic Test - Cognition & Development 1

11.1.8 Vygotsky

11.1.9 Evaluation of Vygotsky

11.1.10 Baillargeon

11.1.11 Baillargeon's studies

11.1.12 Evaluation of Baillargeon

11.1.13 End of Topic Test - Cognition & Development 2

11.1.14 Sense of Self & Theory of Mind

11.1.15 Baron-Cohen Studies

11.1.16 Selman’s Five Levels of Perspective Taking

11.1.17 Biological Basis of Social Cognition

11.1.18 Evaluation of Biological Basis of Social Cognition

11.1.19 Important Issues in Social Neuroscience

11.1.20 End of Topic Test - Cognition & Development 3

11.1.21 Top Grade AO2/AO3 - Cognition & Development

12 Option 2: Schizophrenia (A2 only)

12.1 Schizophrenia: Diagnosis (A2 only)

12.1.1 Classification & Diagnosis

12.1.2 Reliability & Validity of Diagnosis

12.1.3 Gender & Cultural Bias

12.1.4 Pinto (2017) & Copeland (1971)

12.1.5 End of Topic Test - Scizophrenia Diagnosis

12.2 Schizophrenia: Treatment (A2 only)

12.2.1 Family-Based Psychological Explanations

12.2.2 Evaluation of Family-Based Explanations

12.2.3 Cognitive Explanations

12.2.4 Drug Therapies

12.2.5 Evaluation of Drug Therapies

12.2.6 Biological Explanations for Schizophrenia

12.2.7 Dopamine Hypothesis

12.2.8 End of Topic Test - Schizoprenia Treatment 1

12.2.9 Psychological Therapies 1

12.2.10 Psychological Therapies 2

12.2.11 Evaluation of Psychological Therapies

12.2.12 Interactionist Approach - Diathesis-Stress Model

12.2.13 Interactionist Approach - Triggers & Treatment

12.2.14 Evaluation of the Interactionist Approach

12.2.15 End of Topic Test - Scizophrenia Treatments 2

13 Option 2: Eating Behaviour (A2 only)

13.1 Eating Behaviour (A2 only)

13.1.1 Explanations for Food Preferences

13.1.2 Birch et al (1987) & Lowe et al (2004)

13.1.3 Control of Eating Behaviours

13.1.4 Control of Eating Behaviour: Leptin

13.1.5 Biological Explanations for Anorexia Nervosa

13.1.6 Psychological Explanations: Family Systems Theory

13.1.7 Psychological Explanations: Social Learning Theory

13.1.8 Psychological Explanations: Cognitive Theory

13.1.9 Biological Explanations for Obesity

13.1.10 Biological Explanations: Studies

13.1.11 Psychological Explanations for Obesity

13.1.12 Psychological Explanations: Studies

13.1.13 End of Topic Test - Eating Behaviour

14 Option 2: Stress (A2 only)

14.1 Stress (A2 only)

14.1.1 Physiology of Stress

14.1.2 Role of Stress in Illness

14.1.3 Role of Stress in Illness: Studies

14.1.4 Social Readjustment Rating Scales

14.1.5 Hassles & Uplifts Scales

14.1.6 Stress, Workload & Control

14.1.7 Stress Level Studies

14.1.8 End of Topic Test - Stress 1

14.1.9 Physiological Measures of Stress

14.1.10 Individual Differences

14.1.11 Stress & Gender

14.1.12 Drug Therapy & Biofeedback for Stress

14.1.13 Stress Inoculation Therapy

14.1.14 Social Support & Stress

14.1.15 End of Topic Test - Stress 2

15 Option 3: Aggression (A2 only)

15.1 Aggression: Physiological (A2 only)

15.1.1 Neural Mechanisms

15.1.2 Serotonin

15.1.3 Hormonal Mechanisms

15.1.4 Genetic Factors

15.1.5 Genetic Factors 2

15.1.6 End of Topic Test - Aggression: Physiological 1

15.1.7 Ethological Explanation

15.1.8 Innate Releasing Mechanisms & Fixed Action Pattern

15.1.9 Evolutionary Explanations

15.1.10 Buss et al (1992) - Sex Differences in Jealousy

15.1.11 Evaluation of Evolutionary Explanations

15.1.12 End of Topic Test - Aggression: Physiological 2

15.2 Aggression: Social Psychological (A2 only)

15.2.1 Social Psychological Explanation

15.2.2 Buss (1963) - Frustration/Aggression

15.2.3 Social Psychological Explanation 2

15.2.4 Social Learning Theory (SLT) 1

15.2.5 Social Learning Theory (SLT) 2

15.2.6 Limitations of Social Learning Theory (SLT)

15.2.7 Deindividuation

15.2.8 Deindividuation 2

15.2.9 Deindividuation - Diener et al (1976)

15.2.10 End of Topic Test - Aggression: Social Psychology

15.2.11 Institutional Aggression: Prisons

15.2.12 Evaluation of Dispositional & Situational

15.2.13 Influence of Computer Games

15.2.14 Influence of Television

15.2.15 Evaluation of Studies on Media

15.2.16 Desensitisation & Disinhibition

15.2.17 Cognitive Priming

15.2.18 End of Topic Test - Aggression: Social Psychology

16 Option 3: Forensic Psychology (A2 only)

16.1 Forensic Psychology (A2 only)

16.1.1 Defining Crime

16.1.2 Measuring Crime

16.1.3 Offender Profiling

16.1.4 Evaluation of Offender Profiling

16.1.5 John Duffy Case Study

16.1.6 Biological Explanations 1

16.1.7 Biological Explanations 2

16.1.8 Evaluation of the Biological Explanation

16.1.9 Cognitive Explanations

16.1.10 Moral Reasoning

16.1.11 Psychodynamic Explanation 1

16.1.12 Psychodynamic Explanation 2

16.1.13 End of Topic Test - Forensic Psychology 1

16.1.14 Differential Association Theory

16.1.15 Custodial Sentencing

16.1.16 Effects of Prison

16.1.17 Evaluation of the Effects of Prison

16.1.18 Recidivism

16.1.19 Behavioural Treatments & Therapies

16.1.20 Effectiveness of Behavioural Treatments

16.1.21 Restorative Justice

16.1.22 End of Topic Test - Forensic Psychology 2

17 Option 3: Addiction (A2 only)

17.1 Addiction (A2 only)

17.1.1 Definition

17.1.2 Brain Neurochemistry Explanation

17.1.3 Learning Theory Explanation

17.1.4 Evaluation of a Learning Theory Explanation

17.1.5 Cognitive Bias

17.1.6 Griffiths on Cognitive Bias

17.1.7 Evaluation of Cognitive Theory (A2 only)

17.1.8 End of Topic Test - Addiction 1

17.1.9 Gambling Addiction & Learning Theory

17.1.10 Social Influences on Addiction 1

17.1.11 Social Influences on Addiction 2

17.1.12 Personal Influences on Addiction

17.1.13 Genetic Explanations of Addiction

17.1.14 End of Topic Test - Addiction 2

17.2 Treating Addiction (A2 only)

17.2.1 Drug Therapy

17.2.2 Behavioural Interventions

17.2.3 Cognitive Behavioural Therapy

17.2.4 Theory of Reasoned Action

17.2.5 Theory of Planned Behaviour

17.2.6 Six Stage Model of Behaviour Change

17.2.7 End of Topic Test - Treating Addiction

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A-Level Psychology - THE BIOLOGICAL APPROACH TO EXPLAINING OCD [Psychopathology Topic]

Subject: Psychology

Age range: 16+

Resource type: Lesson (complete)

Last updated

24 March 2024

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This lesson was created using the latest AQA A-Level Specification (published June 2019) although content and activities may be useful for other specifications.

Key content covered in this Lesson:

• Key Questions
• The Biological Approach to Explaining OCD
• Genetic Explanations of OCD
• Family Studies
• Candidate Genes
• OCD is Polygenic
• Different types of OCD
• Neural Explanations of OCD
• The Role of Serotonin
• Decision-Making Systems
• Activity: Concepts - Jack
• Evaluation worksheet
• Evaluation points
• Exam Practice with Mark Scheme: 16 Mark Essay with Application
• Activity: Planning worksheet
• Plenary: Consolidation Question

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A bundle is a package of resources grouped together to teach a particular topic, or a series of lessons, in one place.

OCD LESSON BUNDLE: Includes Characteristics, Biological Explanations and Biological Treatments (A-Level Psychology - Psychopathology Topic)

*** This bundle was created using the latest AQA A-Level Specification (published June 2019) although content and activities may be useful for other specifications. *** The three lessons included in this bundle are: 1. Characteristics of OCD 2. Biological Explanations for OCD 3. Biological Treatments for OCD *** Please refer to individual lessons for further details of included content. ***

A-LEVEL PSYCHOLOGY - PSYCHOPATHOLOGY TOPIC [COMPLETE TOPIC]

*** This bundle was created using the latest AQA A-Level Specification (published June 2019) although content and activities may be useful for other specifications. *** This bundle includes a complete lesson and activities for the A-Level Psychopathology Topic. *** The 10 lessons included in this bundle are: 1. Definitions of Abnormality 2. Characteristics of Phobias 3. The Behavioural Approach to Explaining Phobias 4. The Behavioural Approach to Treating Phobias 5. Characteristics of Depression 6. The Cognitive Approach to Explaining Depression 7. The Cognitive Approach to Treating Depression 8. Characteristics of OCD 9. The Biological Approach to Explaining OCD 10. The Biological Approach to Treating OCD *** Please see individual lessons for further details of the content included. ***

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