HL Biological Approach to Understanding Behavior
The biological approach to studying behavior: there are physiological origins of many behaviors and that human beings should also be studied in terms of their biology.
Psychologists have found that the relationship between biological factors and behavior is bidirectional – biology may affect behavior and cognition, and the other way around.
Psychologists study how environmental factors interact with biological systems in both animals and humans.
Many physiological factors can play a role in behavior and cognition: neurotransmitters, hormones and genes.
However, physiology does not always work on its own; for example, physiology responds to environmental stimuli, such as a stressful or happy experience, or an attractive person walking by.
One of the major controversies in the history of psychology is the nature versus nurture debate: researchers debated whether human behavior is the result of biological or environmental factors.
At this point in the history of psychology, a more balanced approach has been adopted as scientific findings have demonstrated that it is not a question of either biology or environment, but that both nature and nurture play a role.
This is reflected in the interactionist approach used by modern psychologists who adopt a more holistic picture of human behavior.
An interactionist approach uses different approaches – biological, cognitive, and sociocultural – to get a richer understanding of behavior.
The biological approach is based on certain assumptions about human behavior.
There are biological correlates of behavior – complex human behaviors may be reduced to biological origins.
Biologists study the role that neurotransmitters, hormones, brain structure, and genetics – among other biological factors – may play in behavior.
A second assumption of the biological approach is that behaviors can be inherited.
A reductionist approach analyzes a complex behavior by studying the simplest, most basic mechanisms that are believed to be responsible for the behavior.
Since biological psychologists argue that biological factors are important in understanding the origins of behavior and our biology is the result of genes, this seems a logical argument.
The mapping of the human genome has led to the assumption that eventually, we will know how specific genes are related to behavior.
However, scientists already know the relationship between genes and behavior is complex.
Psychologists argue that there is not a single gene for a behavior, but a combination of gene expression may lead to physiological processes that result in a behavior.
Stress, and other environmental factors may play a key role in whether a gene related to a behavior is “expressed.”
A final assumption is that animal research can provide insight into human behavior; as a result, a significant amount of research is undertaken using animals.
As we will see in the HL extension, mammals have very similar physiology.
Our brains, nervous system, and endocrine systems work very much like other mammals.
In addition, our genetic makeup is also very similar to animals.
Charles Darwin (1809-1882) argued in his groundbreaking theory that there is a continuity of evolution, so not only do we share physiological traits with other organisms, but perhaps our behaviors are also related along this continuum.
Psychologists often use animals to carry out research that may not be possible with human beings.
Over the past thirty years, few areas of psychology have developed quite as rapidly as brain research. As technology has progressed, so has our ability to monitor and map out the brain’s activity. The brain is seen as the control center of human functioning.
Psychologists seek to understand how the brain matures over a lifetime and how it adapts to the environment.
Prior to the development of modern scanning technology, one of the most common ways to study the brain was through the use of case studies of brain damage.
Often such studies provide researchers with a situation that they could never ethically reproduce in a laboratory. Case studies of patients with a brain injury are done longitudinally, in order to observe both the short-term and long-term effects of damage.
Case studies use triangulation to be holistic in their approach, looking at a range of effects of the damage, rather than a single behavior.
In the case of a patient with brain damage, this may include interviews with the family, psychometric testing – for example, IQ or personality testing, experiments, and observations.
Limitations of Case Studies
As the researchers do not manipulate an independent variable, no cause-and-effect relationship can be determined.
Since case studies are of single individuals, from a single case study, we cannot generalize the findings to all human beings.
Since it is naturally occurring, the study cannot be replicated.
It may be very difficult to verify information about the patient before the accident took place.
Information about the individual’s IQ, problem-solving skills, memory, or interpersonal skills is often reliant on the memories of family members.
Besides the fact that this is not an accurate measure, the memories of the family members may not be accurate.
Data triangulation: When more than one source of data is used. For example, a case study of schools looked at stress in the IB program in five different schools. In this way, if we get consistent findings, it was not simply because of the school that we chose.
Method triangulation: When more than one research method is used. If we get consistent findings, that means that the choice of research method was not the reason for our findings.
Researcher triangulation: When more than one researcher studies a case. Researchers can compare their observations and interpretations in order to increase reliability and credibility.
Theory triangulation: When we look at a case from more than one theoretical perspective - e.g. biological, cognitive, and/or sociocultural.
In spite of these methodological limitations of a single case study, psychologists agree that they provide important information that can be used to study the effects of brain damage over time, as well as spark new research.
Psychologists do not use a single case study to draw definitive conclusions about the role of the brain on behavior.
Instead, they often use similar cases to verify their findings and they may even perform experiments with animals to investigate the hypothesized relationship between damage to a specific area of the brain and behavior.
If there are several case studies of damage to the same area of the brain that show the same consequences on behavior, biologists may conclude that damage to a specific part of the brain may cause a specific behavior.
This is the case with the famous case study of HM which has contributed to our understanding of the relationship between the brain and memory.
HM fell off his bicycle when he was aged 7 and sustained a serious head injury.
Epileptic attacks began when he was 10.
At the age of 27, he had become so incapacitated by his seizures that he could not lead a normal life and medication did not help him.
With the approval of the patient and his family, neurosurgeon William Scoville performed an experimental surgery where he removed tissue from the medial temporal lobe (including the hippocampus) on both sides of HM’s brain.
After the operation, HM remembered his childhood very well.
His personality appeared largely unchanged. However, HM suffered from anterograde amnesia–he could no longer transfer information from short-term memory to long-term memory.
In order to carry out her research, Milner used many strategies. This is an example of how method triangulation may be used in a case study:
Psychometric testing: IQ testing was given to HM.
His results were slightly above average, with an IQ of 104 before the operation and a slightly improved IQ of 112 after the operation because of the reduction in seizures.
Direct observation of his behavior;
Interviews with both HM and his family members.
Cognitive testing: memory recall tests and learning tasks - such as reverse mirror drawing.
HM could not acquire new episodic knowledge (memory for events) and new semantic knowledge (general knowledge about the world).
This suggests that the brain structures that were removed from his brain are important for long-term explicit memory.
Memories as motor skills, i.e. procedural memories, were well maintained, for example, he knew how to mow a lawn.
He also showed improvements in the performance of new skills, such as reverse mirror drawing in which he had to acquire new eye-hand coordination.
An MRI scan of HM’s brain was performed in 1997 and 2002, where Corkin analyzed the extent of the damage.
It was possible to see that parts of HM’s temporal lobe including the hippocampus, had the most damage.
Damage to the hippocampus explains the problem of transferring short-term memory to long-term memory.
The researchers concluded that the hippocampus plays a critical role in converting memories of experiences from short-term memory to long-term memory.
Since HM was able to retain some memories of events that happened long before his surgery it indicates that the hippocampus is not the site of permanent storage but rather plays a role in the organization and permanent storage of memories elsewhere in the brain.
Many early experiments on the brain involved invasive techniques—for example, removing (ablation) or scarring (lesioning) brain tissue in animals in order to study subsequent behavioral changes.
Behavior before and after lesioning was compared.
In a classic study, Hetherington and Ranson (1942) lesioned a part of the brain called the ventromedial hypothalamus (VHM) in rats, a part of the brain that is believed to control feeding.
As a result of the lesioning, the rats increased their food intake dramatically and often doubled their weight.
This led researchers to conclude that the hypothalamus acted as a brake on eating.
The use of invasive techniques raises serious ethical concerns and psychologists have to conform to codes of conduct for the use of non-human animals; for example, the Ethical Principles of Psychologists and Code of Conduct by the American Association of Psychologists.
This means that psychologists who engage in research with animals need to apply to an ethical committee for permission to carry out their research.
If the potential harm to the animal cannot be determined, permission will only be granted if the research is considered to add to current knowledge and there are no alternatives.
Modern technology is now extensively used in psychology because it provides an opportunity to study not only brain structures but also the active brain while avoiding many of the ethical concerns of animal experimentation.
This allows researchers to see the localization of function – that is, the functions of specific parts of the brain and how they relate to behavior.
One imaging technique is Magnetic Resonance Imaging [MRI].
The MRI gives a three-dimensional picture of the brain structures.
The MRI was used in the case study of HM to determine the extent of his brain damage.
An MRI scanner uses a magnetic field and radio waves to map the activity of hydrogen molecules, which are present in different brain tissue to different degrees.
The image can either be viewed as a slice of the brain from any angle, or it can be used to create a three-dimensional image of the brain.
There are several advantages to using an MRI scan.
First, the procedure is non-invasive, with minimal potential harm to the participant.
Secondly, the image has high resolution; this gives researchers a good sense of the actual structure of the brain.
However, the MRI only indicates structure; it does not map what is happening in the brain.
To observe the activity of the brain, other technologies are used.
Positron Emission Tomography – commonly known as PET scanning - is used to observe metabolic processes in the brain by detecting the gamma rays emitted indirectly by a tracer.
PET neuroimaging is based on the assumption that areas of high radioactivity are associated with brain activity.
Before a PET scan begins, a patient is given a safe dose of a radioactive tracer compound introduced into the body by a modified glucose molecule [FDG].
The injected FDG enters the bloodstream, where it can travel to the brain.
If a particular area of the brain is more active, more glucose will be needed there.
When more glucose is used, the radioactive tracer is detected by the PET scanner.
The scan, which usually takes between 30 minutes and two hours, produces a multi-colored image that shows which parts of the brain were the most active.
The color of each dot shows the intensity of the energy signal.
One of the key advantages of the PET scan is that it allows participants to perform psychological tasks while the researcher observes brain activity.
There are two key limitations of PET scanning.
First, it requires an injection with a small amount of radioactive material.
Although this will not cause harm to the participant, it is still an invasive practice and raises ethical concerns.
Secondly, PET scanning is quite slow and has relatively poor resolution.
So, although it does indicate where brain activity is taking place, it is not as clear as more modern technology like the fMRI.
Unlike the MRI, which shows the structure of the brain, an fMRI (functional magnetic resonance imaging) shows actual brain activity and indicates which areas of the brain are active when engaged in a behavior or cognitive process.
The fMRI measures changes in blood flow in the active brain.
These scans have a higher resolution than PET scans, and they are easier to carry out.
This is one of the most frequently used technologies in biopsychological research today.
It tracks changes in blood flow and oxygen level as a measurement of neural activity.
When a specific brain area is active, it uses more oxygen, and therefore the blood flow increases.
This can be detected by the fMRI scanner.
Unlike PET scanning, fMRIs are non-invasive.
There is no radioactive isotope necessary.
The quality of the image is also much better and rather than a static image, the fMRI produces a film that demonstrates a change in the brain over the period of the scan.
For both the MRI and the fMRI, there are certain precautions that must be taken to protect the safety of the participant.
Since the technology works with a powerful magnet, it is important that objects that contain iron be removed.
In rare cases, a participant may have to be removed from a sample because of a metal implant – for example, certain types of pacemakers or cochlear implants.
The fMRI scanner is not a natural environment for cognition.
Therefore, research may lack ecological validity.
There is a lot of noise in the tunnel and participants may experience anxiety due to the claustrophobic nature of the machine.
There is a question of artifacts in the imaging – that is, some of the activity may be related to anxiety or reaction to the machine, rather than the behavior being studied.
The use of colors may exaggerate the activity of the brain.
Much brain activity is spontaneous and is not a reaction to stimuli.
Therefore, it is difficult to know exactly which areas of the brain are active in a behavior.
Brain areas activate for various reasons – just because the amygdala lights up, doesn’t mean that fear is necessarily part of the response being observed.
Localization of function is the theory that specific parts of the brain are responsible for specific behaviors or cognitive processes.
The case study of HM is a good example of how a specific part of the brain has a specific function – that is, the hippocampus is responsible for transferring short-term memory to long-term memory.
Although we know that some parts of the brain do play specific roles in behavior, rarely does a part of the brain work in complete isolation.
For example, in memory research, we argue that the cognitive process is the result of distributive processing rather than localization of function – in other words, several parts of the brain have to work together in order to help us create and retrieve memories.
Today researchers continue to attempt to map the brain.
One of the ways that they are doing this is by looking at the neural connections in the brain and creating a map called a connectome.
When talking about the brain, we discuss four key areas:
the brain stem,
the cerebellum,
the cerebrum,
and the limbic system.
The brain stem is not usually studied by psychologists.
The brain stem is responsible for regulating life functions, such as breathing, heart rate, and blood pressure.
The cerebellum plays a key role in balance and motor function, including speech production.
It also plays a role in learning – specifically, in classically conditioned responses.
The cerebral cortex is the largest part of the human brain, associated with higher brain functions such as thought and action.
The cerebrum is divided into four sections, called lobes. Each of these lobes plays a key role in behavior:
· The Frontal Lobe is associated with executive functions – that is, planning, decision-making, and speech.
· The Occipital Lobe is associated with visual processing.
· The Parietal Lobe is associated with the perception of stimuli;
· The Temporal Lobe is associated with auditory processing and memory.
The Limbic System - often referred to as the emotional brain - is a major focus of psychological research for its role in memory and emotion.
In the table below, you will find the key components of the limbic system.
Amygdala - Plays a role in the formation of emotional memory and fear responses.
Basal ganglia- Plays a role in habit-forming and procedural memory.
Hippocampus - Responsible for the transfer of short-term memory to long-term memory
Hypothalamus - Involved in homeostasis, emotion, thirst, hunger, circadian rhythms, and control of the autonomic nervous system. In addition, it controls the pituitary gland.
Nucleus accumbens - Plays a role in addiction and motivation.
In the previous section, we looked at the case study of HM.
Researchers were able to determine through their long-term study of HM that the hippocampus plays a key role in the transfer of information from short-term memory to long-term memory.
A review of the study can be seen in the following video.
But as you can see, the answer to the question of how memory works was not complete from the study of HM.
Other studies have shown us more about how memory works, including the case study of Eugene Pauly.
In 1992 Larry Squire and his team were introduced to one of the most interesting cases of amnesia since the famous HM study.
At the age of 70, Eugene Pauly was diagnosed with viral encephalitis.
Both his amygdala and hippocampus were completely destroyed.
He demonstrated many of the same symptoms as HM.
Squire carried out a series of interviews with EP at his home.
During one interview he asked EP to draw a map of his home.
He was not able to do it.
However, EP excused himself and got up to go to the toilet.
How could a man who could not draw a map of his home find the bathroom on his own?
Several tasks that rely on procedural memories make this transition from involving an active frontal lobe to an active basal ganglia.
Although the actual process is complex and not fully understood, when we are learning to do a task it is often cognitive in nature.
So, when I first learn to drive a car, I need to think an awful lot about what I am doing.
But remember, thinking takes up a lot of energy.
Our brains have adapted in a way that minimizes the amount of energy that it needs to expend.
Over time, the task is no longer cognitive, but what is referred to as an associative task.
By chunking together a series of movements or behaviors, the task becomes automatic.
The more common word we use for associative tasks is "habits."
EP was also able to take a walk around the block by himself.
His wife would even follow him around the block to make sure that he was okay, but he was able to find his way home without any problems.
When he was asked from any point on his walk where he lived, he would say he didn't know, but since the task was associative - or a habit - he was able to simply walk home.
However, occasionally there was a problem.
If the sidewalk was being repaired and he had to leave his familiar path, EP would get lost.
Returning to our example of driving a car - even when we drive a long time, bad weather or heavy traffic forces us to concentrate more.
The task reverts from associative to cognitive.
When this happened to EP, he did not have the capacity to solve the problem as his memory was only procedural.
Once the familiar pattern was changed, he was unable to complete the task.
In this case study, Squire & his team carried out several different research methods including interviews with EP and his family, psychometric testing (IQ testing), and observational studies.
In addition, MRIs were used to determine the extent of the damage to EP's brain.
MRI indicated that EP's basal ganglia were undamaged.
It is believed that the basal ganglia are responsible for this type of procedural memory.
The brain is a dynamic system that interacts with the environment.
In a sense, the brain is physically sculpted by experience.
Not only can the brain determine and change behavior, but behavior and environment can change the brain.
Modern researchers argue that the brain is constantly changing as a result of experience throughout the lifespan.
Plasticity refers to the brain’s ability to alter its own structure following changes within the body or in the external environment.
Brain plasticity refers to the brain’s ability to rearrange the connections between its neurons - that is, the changes that occur in the structure of the brain as a result of learning or experience.
High levels of stimulation and numerous learning opportunities lead to an increase in the density of neural connections.
This means that the brain of an expert musician should have a thicker area in the cortex related to mastery of music when compared to the brain of a non-musician.
The same can be said about students who spend a lot of time studying, compared to students who do not.
Every time we learn something new, the neurons connect to create a new trace in the brain.
This is called dendritic branching because the dendrites of the neurons grow in numbers and connect with other neurons.
This can be illustrated by a series of studies of brain plasticity carried out by Rosenzweig, Bennett, and Diamond (1972).
The researchers conducted experiments where they placed rats into one of two environments to measure the effect of either enrichment or deprivation on the development of neurons in the cerebral cortex.
In the enriched environment, rats were placed in cages with up to 11 other rats.
In addition, there were stimulus objects for the rats to play with, as well as maze training.
In the deprived environment, the rat was alone with no stimulation.
The rats spent 30 or 60 days in their respective environments and then they were killed in order to measure the effect of the environment on their brain structures.
Post-mortem studies of their brains showed that those that had been in the stimulating environment had increased thickness in the cortex as a result of increased dendritic branching compared to the rats in the deprived environment.
The frontal lobe, which in humans is associated with thinking, planning, and decision-making, was heavier in the rats that had been in the stimulating environment.
The combination of having "friends" to play with and many interesting toys created the best conditions for developing cerebral thickness.
This raises the question of the importance of stimulation and education in the growth of new synapses.
If learning always results in an increase of dendritic branching, then the findings from animal studies that show increased dendritic branching in response to environmental stimulation are important for the human cortex as well.
This was seen in a key study done by Maguire et al (2000).
Unfortunately, environmental stressors can also have a negative effect on brain structures.
Carrion et al (2009) found that children who had been abused tended to show a smaller hippocampus than their same-age peers.
The aim of the study was to see whether the brains of London taxi drivers would be somehow different as a result of their exceptional knowledge of the city and the many hours that they spend behind the wheel navigating the streets of London.
All potential taxi drivers must learn “the Knowledge” – that is, they must form a mental map of the city of London.
The participants for this quasi-experiment were 16 right-handed male London taxi drivers.
The brains of the taxi drivers were MRI scanned and compared with the MRI scans of 50 right-handed males who did not drive taxis (the control group).
In order to take part in the study, the participants had to have completed the "Knowledge" test and had their license for at least 1.5 years.
The controls were taken from an MRI database.
The sample included a range of ages so that age would not be a confounding variable.
The study is correlational as the IV was not manipulated by the researcher but naturally occurring.
The researchers were looking to see if there was a relationship between the number of years of driving a taxi and the anatomy of one's brain.
It was also a single-blind study - that is, the researcher did not know whether she was looking at the scan of a taxi driver or a control.
There were two key findings of the study.
First, the posterior hippocampi of taxi drivers were significantly larger relative to those of control subjects and the anterior hippocampi were significantly smaller.
Secondly, the volume of the right posterior hippocampi correlated with the amount of time spent as a taxi driver.
No differences were observed in other parts of the brain.
Maguire argues that this demonstrates that the hippocampus may change in response to environmental demands.
The study of localization of function and brain plasticity are very much linked.
Studies from both abnormal and developmental psychology have demonstrated, for example, the way that stress has an effect on memory by interfering with the work of the hippocampus.
In addition, long-term stress appears to lead to hippocampal atrophy - that is, hippocampal cell death that leads to a smaller hippocampus.
This was found in a study by Bremner (2003).
Thirty-three women participated in this study, including women with early childhood sexual abuse and PTSD (N=10), women with abuse without PTSD (N=12), and women without abuse or PTSD (N=11).
The researchers used an MRI to measure the volume of the hippocampus in all of the participants - and a PET scan to measure its level of function during a verbal declarative memory test.
Women who were abused and showed symptoms of PTSD were found to have a 16% smaller volume of the hippocampus compared to women with abuse without PTSD.
In addition, these women showed a lack of activity in the hippocampus when carrying out the memory task.
Women with abuse and PTSD had a 19% smaller hippocampal volume relative to women without abuse or PTSD.
According to biologists, synaptic plasticity works by the maxim: use it or you lose it!
Synapses become stronger through repeated use.
This is known as long-term potentiation.
LTP leads to a greater level of response – that is, longer periods of depolarization - on the post-synaptic membrane.
Over time, this leads to protein synthesis and gene expression which will be the building blocks used for dendritic branching – a process called neural arborization.
When a synapse is not used or is under-stimulated, it may go through the process of synaptic pruning.
It is believed that this is the way for the brain to remove synapses that are no longer needed, making the functioning of the neural networks more efficient.
The process of pruning is still not fully understood.
If you are interested in an in-depth explanation of the process, you may want to watch the video below.
Simply being able to link the above information to a study like Draganski (2004) is all you need to be able to do to answer an SAQ on Paper 1.
Nerve cells, called neurons, are one of the building blocks of behavior.
It is estimated that there are between 10 and 100 billion neurons in the nervous system and that neurons make 13 trillion connections with each other.
The neurons send electrochemical messages to the brain so that people can respond to stimuli—either from the environment or from internal changes in the body.
The process by which these messages are sent is called neurotransmission.
The electrical impulse that travels along the body of the neuron is called an action potential.
When an action potential travels down the axon of the neuron, it releases neurotransmitters that are stored in the neuron’s terminal buttons.
The neurotransmitters are then released into the gap between the neurons – called the synapse.
The synaptic gap is an incredible one-millionth of a centimeter!
Neurotransmitters are the body’s natural chemical messengers that transmit information from one neuron to another.
After crossing the synapse, the neurotransmitters fit into receptor sites on the post-synaptic membrane, like a key in a lock.
Once the message is passed on, the neurotransmitters are either broken down by an enzyme or reabsorbed by the terminal buttons, in a process called reuptake.
Neurotransmitters have been shown to have a range of different effects on human behavior.
In fact, neurotransmission underlies behavior as varied as mood, sleep, learning and memory, sexual arousal, and mental illness.
The table below, which highlights just a few neurotransmitters, gives an idea of the variety of behaviors that are influenced by these neurochemicals.
Acetylcholine - Plays a role in the consolidation of memory in the hippocampus.
Dopamine - Controls the brain's reward and pleasure centers. Plays a key role in motivation; low levels are linked to addictive behavior.
Norepinephrine - Arousal and alertness.
Serotonin - Sleep, arousal levels, and emotion.
When discussing neurotransmitters, we categorize them by how they affect a neuron.
Excitatory neurotransmitters increase the likelihood of a neuron firing by depolarizing the neuron.
Excitatory neurotransmitters include acetylcholine.
Inhibitory neurotransmitters decrease the likelihood of a neuron firing by hyperpolarizing the neuron.
Inhibitory neurotransmitters include GABA.
Because neurotransmitters fit tightly into receptor sites, like a key in a lock, drugs have been developed to either simulate the neurotransmitter if there is not enough of a specific neurotransmitter or to block the site if it is excessive.
The application of such research has improved the lives of many people.
There has been criticism of reducing the explanation of behavior to the workings of neurotransmitters alone.
It is said to be reductionist.
Can a complex human behavior like falling in love with someone be attributed to a simple “love cocktail” of dopamine and norepinephrine?
Can your mood during the summer holidays be attributed simply to serotonin levels?
Once again, most psychologists consider that neurotransmitters play a role, but do not rely solely on neurotransmission to explain behavior.
Rogers & Kesner conducted an experiment to determine the role of acetylcholine in memory formation.
There is a significant number of acetylcholine receptors in the hippocampus.
The first group was injected with scopolamine, which blocks the acetylcholine receptor sites and thus inhibits any response.
The second group was the control, given a placebo injection of a saline solution.
This was done to make sure that the fact of getting an injection alone was not responsible for a change in memory.
After being injected, the rats were again placed into the maze to see how long it would take them to find the food that they had previously located.
The findings were that the scopolamine group took longer and made more mistakes, whereas the control group learned faster and made fewer mistakes.
It appears that acetylcholine may play an important role in memory consolidation.
There are many strengths to carrying out an experiment like the one by Rogers and Kesner.
First, the procedure is very simple.
In this way, the study can be easily replicated and the reliability of the results can be tested. In addition, the experiment was highly controlled.
The only difference in the conditions is the level of acetylcholine.
To make sure that receiving the injection was not the factor that influenced the rats’ ability to run the maze, the saline solution was injected.
In this way, the researchers could rule out the placebo effect as a reason for their results.
However, there are also limitations to the study.
It is not clear to what extent we can generalize the findings from rats to human beings.
However, researchers have found that there are lower levels of acetylcholine in Alzheimer’s patients.
In a study by Antonova et al (2011), researchers demonstrated that blocking acetylcholine receptors in the brain can affect spatial memory tasks in humans.
In their study, they used a sample of twenty healthy male adults, with a mean age of 28 years old.
The study used a double-blind procedure and participants were randomly allocated to one of two conditions.
They were injected with either Scopolamine or a placebo.
The participants were then put into an fMRI where they were scanned while playing the "Arena task."
This is a rather complex virtual reality game in which the researchers are observing how well the participants are able to create spatial memories.
The goal is for the participants to navigate around an "arena" with the goal of reaching a pole.
After they have learned where the pole is located, the screen would go blank for 30 seconds.
During this time, the participants were told to actively rehearse how to get to the pole in the arena.
When the arena reappeared, the participant was now at a new starting point in the arena.
The participants would have to use their spatial memory to determine how to get to the location of the pole.
The procedure was repeated three to four weeks later, each participant received the other treatment.
The researchers found that when participants were injected with scopolamine, they demonstrated a significant reduction in the activation of the hippocampus compared to when they received a placebo.
It appears that acetylcholine could play a key role in the encoding of spatial memories in humans, as well as in rats.
The most important inhibitory neurotransmitter is GABA - or Gamma-aminobutyric acid.
It appears that this neurotransmitter inhibits neural activity both in the hippocampus and in the frontal lobe.
This inhibition of neural activity allows us to increase our cognitive load - that is, how we are able to use our working memory.
When GABA levels are low, intrusive thoughts may make it difficult for us to concentrate and lay down new memories.
In a study by Porges et al (2017), the researchers looked at GABA concentrations in the frontal lobe in a sample of 94 older adults without a history of dementia.
The mean age was 73 years. The participants were asked to take the Montreal Cognitive Assessment to test their cognitive functioning.
The researchers found that there was a correlation between higher concentrations of GABA in the frontal lobe and superior cognitive performance.
This is significant because GABA concentrations decrease with age.
This research may lead to important treatments for people suffering from dementia.
For a modern study of how this treatment might work, see the key study by Prevot et al (2019).
When discussing the process of neurotransmission, biologists refer to chemicals as agonists or antagonists, depending on the effect they have on the post-synaptic receptor sites.
All neurotransmitters are agonists for receptor sites.
They are referred to as endogenous agonists since they are biologically already part of our nervous system.
So, acetylcholine is an agonist for ACh receptor sites.
Drugs can also be agonists.
Since they are external to our system, they are referred to as exogenous agonists.
For example, nicotine is an agonist for ACh receptor sites and in the short term appears to have some positive effects on memory.
(It should be noted, however, that long-term use of nicotine has a negative effect on memory!)
Antagonists are drugs that block the receptor site and do not allow the neurotransmitter to do its job, so no action potential is sent down the neuron.
For example, scopolamine is an antagonist for ACh.
Hormones are another class of chemicals that affect behavior.
Unlike neurotransmitters, hormones are not released by the terminal buttons of a neuron; instead, they are secreted by glands in the endocrine system.
So epinephrine (adrenaline) is released by the adrenal gland into the bloodstream as a hormone whereas norepinephrine (noradrenaline) is released by neurons in the brain as a neurotransmitter.
Hormones are released directly into the bloodstream; as a result, they take longer to produce changes in behavior than neurotransmitters.
However, they also produce effects that last a lot longer than an action potential.
Hormones can only produce reactions in certain cells – known as target cells - that have an appropriate receptor site for the hormone.
When the hormone binds to the target cell, it either increases or decreases its function.
Like neurotransmitters, hormones affect a wide range of behaviors.
There are at least fifty different types of hormones.
As you will see in the table of hormones, some hormones “act as neurotransmitters.”
This means that they work in the brain by targeting receptor sites on the neuron’s synaptic gap, even though the chemical is not stored in the terminal buttons, but is secreted by an endocrine gland.
When discussing the role of hormones, neuropeptide Y and oxytocin are definitely hormones, but they sometimes act as though they were neurotransmitters.
Adrenaline - Secreted by the adrenal glands; responsible for arousal and the "fight or flight" response. Plays a role in emotional memory formation.
Cortisol - Secreted by the adrenal glands; helps control blood sugar levels, regulate metabolism, reduce inflammation, and assist with memory formation.
Melatonin - Secreted by the pineal gland; signals the relaxation and lower body temperature that help with a night of restful sleep.
Neuropeptide Y - Produced by the hypothalamus; acts as a neurotransmitter in the brain. Stimulates food intake, reduces anxiety and stress, reduces pain perception, and affects the circadian rhythm. Higher levels of NPY appear to be linked to higher levels of resilience.
Oxytocin - Produced by the hypothalamus and secreted by the pituitary gland. When it affects the brain, it acts as a neurotransmitter. Plays a role in mother-child attachment; believed to play a role in social bonding and trust between people.
Testosterone - Produced by the testes; plays a facilitative role in aggressive behavior - that is, it doesn't cause aggression, but higher levels of testosterone result in higher levels of aggression.
Perhaps the most well-known hormone is adrenaline.
Adrenaline activates what is known as the Fight or Flight response.
The flight-or-fight response is what is known as a hormone cascade – that is, hormones triggering more hormones.
The release of adrenaline is part of the hypothalamic-pituitary-adrenal axis – or HPA axis for short.
When a stimulus threatens us – the hypothalamus responds by activating the pituitary gland.
The pituitary gland then releases a hormone that activates the adrenal glands, which are located on top of your kidneys.
As a result, both cortisol and adrenaline are released into the bloodstream.
Cortisol is responsible for dumping glucose into your bloodstream in order to provide energy, and adrenaline increases the heart rate, blood pressure, and respiration.
This reaction has evolved to help humans survive in the face of danger so that they can quickly escape an immediate threat.
However, many hormones have more than one function.
Adrenaline also plays a key role in memory formation, as seen in a study by Cahill & McGaugh (1995).
The aim of the study was to investigate the role of adrenaline and the amygdala on emotional memory.
Participants were divided into two groups.
Each group saw 12 slides that were accompanied by a very different story.
In the first condition, the participant heard a rather boring story about a woman and her son who paid a visit to the son’s father in a hospital where they witnessed the staff in a disaster preparation drill of a simulated accident victim.
In the second condition, the participant heard a story where the boy was involved in a car accident where his feet were severed.
He was quickly brought to the hospital where the surgeons reattached the injured limbs.
Then he stayed in the hospital for some weeks and then went home with his mother.
Two weeks after participating in the experiment the participants were asked to come back and their memory for specific details of the story was tested.
The test was a recognition task that consisted of a series of questions about the slides with three options for them to choose from.
For example, what was the job of the father of the boy in the story?
A. A janitor B. A lab technician C. A surgeon.
The researchers then did a follow-up study.
In the follow-up study, the above procedure was repeated, but this time the participants in the "traumatic story" condition were injected with a beta-blocker called propranolol.
Beta-blockers interfere with the release of adrenaline; in this study, it was used to prevent activation of the amygdala to prevent the formation of emotional memory.
In the original version of the experiment, the researchers found that the participants who had heard the more emotionally arousing story demonstrated better recall of specific details of the story.
They could also recall more details from the slides.
In the follow-up study, they found that those that had received the beta-blocker did no better than the group that had heard the "boring" story.
They, therefore, concluded that adrenaline and activation of the amygdala play a significant role in the creation of memories linked to emotional arousal.
By carrying out a well-controlled experiment, Cahill & McGaugh were able to deduce a cause-and-effect relationship between adrenaline and the activation of the amygdala in the creation of emotional memories.
But as the study was well controlled and rather simplistic, can we apply the findings to the “real world?”
The research has been applied to the treatment of accident victims with the goal of preventing PTSD.
Pitman et al (2002) carried out an experimental study where patients coming into emergency rooms after a traumatic injury were given either beta-blockers (propranolol) or a placebo.
One month after the traumatic event, people who had received the beta-blockers showed fewer symptoms of PTSD than those who had received no beta-blockers or a placebo.
It appears that Cahill & McGaugh’s findings may prove helpful in preventing the onset of PTSD in some patients following trauma.
A rather controversial area of psychological research is the role of pheromones on human behavior.
A pheromone is a chemical substance produced and released into the environment by an animal affecting the behavior or physiology of others of its own species.
Although pheromones are known to play a significant role in signaling between members of the same species among animals to affect various behaviors, it is not clear that this is also true in humans.
Some psychologists have argued that pheromones may affect the menstrual cycle in groups of women and the olfactory recognition of a newborn by its mother.
Some argue that individuals may exude different odors based on mood.
Although there is some evidence, nothing is conclusive on whether or not humans have functional pheromones.
In animals, we see two types of pheromones.
Primer pheromones that cause slow, long-term physiological changes, such as hormonal effects; and signaling pheromones that produce rapid behavioral effects, such as mating.
In humans, there is some evidence of primer pheromones.
However, for all the published research that shows these effects, there is an equal number of studies showing that there are no effects.
At this stage in the study of psychology, no human pheromone has yet been found.
Two potential human pheromones are Androstadienone (AND) – found in male semen and sweat – and Estratetraenol (EST), which is found in female urine.
Zhou et al (2014) carried out a study to see if AND or EST influences human mating behavior.
The sample was made up of 96 participants –
24 heterosexual men,
24 heterosexual women,
24 gay men,
and 24 lesbian women.
In the experiment, participants were asked to watch stick figures walking on a screen and to determine their gender.
While carrying out the task, the participants were exposed to the smell of cloves.
In the first condition, the cloves were mixed with androstadienone;
in the second condition, the cloves were mixed with estratetraenol;
and in the control condition, only cloves were used.
The findings showed that smelling androstadienone biased heterosexual females and gay males, but not heterosexual males or lesbian women, toward perceiving the walkers as more masculine.
By contrast, smelling estratetraenol systematically biases heterosexual males and, to some extent, lesbian women toward perceiving the walkers as more feminine.
The researchers concluded that pheromones influence the communication of gender information in a sex-specific manner.
Although the study showed a significant difference in behavior, there are some concerns with the study.
First, the participants were exposed to very high levels of pheromones; it is unclear if this response would happen in a naturalistic setting.
Secondly, although they identified the figure as masculine or feminine, this is not a clear study of sexual attraction but rather of whether participants perceived a person's walk as feminine or masculine.
It can be debated whether this is a reliable measure of sexual behavior.
Finally, the study is done on a relatively small sample.
The study would need to be replicated on a much larger sample in order to determine whether the results are reliable.
A more promising study was carried out by Doucet et al (2009) on the role of secretion of the areolar glands in suckling behavior in 3-day-old infants.
The areolar glands are located near the nipple.
The researchers administered the different secretions to the infants nasally and then measured their behavior and breathing rate.
The researchers compared the infants' reaction to seven different stimuli - including, secretions of areolar glands, human milk, cow milk, formula milk, and vanilla.
They found that the infants began sucking only when exposed to the secretions of the areolar glands.
In addition, there was a significant increase in their breathing rate.
The researchers argue that this stimulus of the areolar odor may initiate a chain of behavioral and physiological events that lead to the progressive establishment of attachment between the mother and the infant.
However, more research is necessary to definitively draw these conclusions.
There are several problems with the pheromone arguments.
First, the human sense of smell is very complex.
Richard Axel and Linda Buck shared the Nobel Prize in Medicine in 2004 for their discoveries of odor receptors and how the olfactory system is organized.
They found that we have about 400 different kinds of odor receptors - and each of the 400 receptors has genetic variations.
This makes it very difficult to see how pheromones would work in humans.
Another problem is that many body odors are actually not caused by secretions, but by bacteria that mix with our secretions - for example, in the armpits.
However, about 20% of the population does not have this bacteria and thus does not create the same scent.
This makes a universal finding of pheromones a bit less likely.
Finally, culture plays a key role in our sense of smell - we learn what smells bad and what smells good.
This could potentially be a confounding variable when trying to determine the role of pheromones on behavior.
Pheromones are chemical cues that are
released into the air, secreted from glands,
or excreted in urine and picked up by animals of the same species,
initiating various social and reproductive behaviors.
Although the perfume industry may be interested in the role of pheromones in human attraction,
psychologists are also interested in the potential role of human pheromones in human aggression and pro-social behavior.
In the animal kingdom, animals will often attack members of their own species if they feel threatened.
Males tend to do this to protect their territory and their mates.
They will attack other males that invade their territory, but they will not attack other females or, in lab conditions, neutered males.
To definitively demonstrate that a pheromone exists, one must design a repeatable experiment, a bioassay, that shows that a smell molecule (odorant) causes a particular effect on the receiver.
In this case, the effect would be an aggressive response.
In order to test this in mice, Chamero et al (2007) attempted to isolate molecules found in mouse urine.
They swabbed the backs of neutered male mice with various potential pheromone molecules and then introduced him as an intruder into the cage of a healthy male mouse.
Using this technique, they were able to narrow it down to a protein that may be a pheromone that provokes aggressive behavior.
Pheromones seem to be detected by a structure called the vomeronasal organ, a tube at the base of the nasal cavity directly behind the nostrils that is filled with sensory neurons.
It is found in most amphibians, reptiles, and nonprimate mammals, but is absent in birds and most primates.
Surgical removal of the VNO eliminates territorial aggression and territorial marking in male mice and male hamsters.
Humans do not have a functional VNO.
It is a big question whether humans even have pheromones - and to date, no human pheromone has been definitively identified.
However, Mishor et al. (2021) may have found a putative pheromone.
Hexadecanal is a putative (potential) pheromone linked to human aggression. It is a molecule that is emitted from the heads of babies.
It is, in fact, one of the most abundant molecules detected.
Could this provoke aggressive behavior from the baby's caretakers by acting as a pheromone?
Mishor et al. (2021) carried out two experiments to test the effect of hexadecanal on both male and female behavior.
In their first experiment, researchers used a volunteer sample of 67 men and 60 women (age range 21 - 34).
The researchers used a double-blind independent samples design. Each participant wore a sticky pad pasted to their upper lip - one group was exposed to hexadecanal, and the other group to a placebo.
The participants played computer games with a mysterious partner.
The participants were not aware that this “partner” was actually a computer algorithm designed to provoke them.
In each round of the game, both players were allocated money that they could keep if they agreed on how to divide it between themselves.
The "mysterious partner," however, never agreed if the participant would receive the greater sum.
After five rounds, it was clear that the participant was being discriminated against in the game.
The participants then began the second half of the experiment.
The participants were again deceived by believing that they were playing a computer game with the same "mysterious partner."
They competed to identify a change in the shape of a target.
The first person to react was then allowed to "blast" his/her opponent with a loud noise blast.
The volume of the "blast" was how the researchers chose to operationalize aggression.
The game was set up so that the participant "won" 16 out of 27 trials.
They were then able to set the volume before blasting the mysterious partner.
The researchers found a small but consistent difference between the two groups.
Women exposed to hexadecanal were more likely to "punish" the mysterious partner with severe noise blasts than women who had the placebo.
On the other hand, men who were exposed to hexadecanal opted for less intense noise blasts than those who weren’t.
Mishor proposed that the emission of hexadecanal from babies provokes protective tendencies in mothers.
However, how this mechanism actually works is not clear.
Mishor et al (2021) carried out a second experiment with a sample of 25 men and 24 women.
The goal was to determine how hexadecanal interacts with the brain to potentially cause aggression.
In this study, the participants would play a computer game while in an fMRI where their computer opponent occasionally stole money from them.
When this happened, they could choose to punish the mysterious partner by docking money from his/her account, without gaining any money themselves.
The design was a repeated measures design with either hexadecanal, a placebo, or simply clean air being infused through the fMRI.
The order of the conditions was counterbalanced.
Women showed more "punishment" activity than men when exposed to hexadecanal.
In addition, the researchers observed a difference in activity in the left angular gyrus - a part of the brain responsible for interpreting social cues.
Whereas men who were exposed to hexadecanal showed activity in the left angular gyrus synced with activity in brain areas involved in processing social information and aggression (such as the amygdala), women showed a decrease in activity.
Could this then mean that hexadecanal plays a role in women's protection of their infants?
The researchers used controls to increase the internal validity of the research and potentially identify a causal relationship.
These included double-blind controls and counterbalancing.
Although the researchers attempt to make the link between the scent emitted from an infant and the protective behavior of mothers, the experiments are highly artificial and do not reflect an infant/mother relationship.
It is not clear yet under what circumstances adults release hexadecanal or how humans would actually process the odorant.
The sample sizes of both studies are small.
The results of the study would have to be replicated with larger samples in order to determine the reliability of the findings.
Although the fMRI shows some brain activity, it was not able to demonstrate how this activity would lead to aggressive behavior.
Generalizations from animal research have not proven to be valid.
Human aggression is influenced by cognitive and sociocultural factors - including learned experience and social norms. It is a reductionist argument to propose that aggression can be attributed solely to pheromones.
Studies on pheromones have often not been replicated. In addition, many of the studies are low in ecological validity.
It is not possible to eliminate the effect of other variables that may influence human scent - eg. bacteria and diet.
Humans do not appear to have a functional VNO which other animals use to detect pheromones. The human process of scent detection is very complex and difficult to study. The human scent is complex and made up of many different molecules. No one has yet mapped all of those molecules.
Behavioral genetics deals with understanding how both genetics and the environment contribute to individual variations in human behavior.
We inherit our genetic material – that is, DNA – from our parents.
However, when psychologists argue that behavior may be inherited, what exactly does that mean?
What is inherited is the genes that give rise to the development of specific physiological processes that contribute to specific traits and behavior.
It is not probable that a single gene is responsible for such complex behaviors as intelligence, criminal behavior, altruism, or attachment.
Instead, what is inherited may be the building blocks for such complex behaviors.
Psychologists argue that an individual may have a genetic predisposition towards a certain behavior; however, without the appropriate environmental stimuli, the gene is not “turned on” and the behavior is not expressed.
For example, in the study of abnormal behavior, the diathesis-stress model is used to explain the origin of depression.
This model argues that depression may be the result of the interaction of a “genetic predisposition” and environmental stress.
The model predicts that an individual with certain genes, when exposed to a stressful environment, is more likely to develop depression than someone who does not have those genes.
This knowledge has been useful in understanding why not all people develop depression following a traumatic childhood, even if they have a sibling who becomes depressed.
It also illustrates the complexity of the problem and that there is no single cause-and-effect relationship between genes and behavior.
The Diathesis–Stress Model is a psychological theory that attempts to explain behavior as a predisposition to genetic vulnerability expressed as a result of stress from life experiences.
Genetic arguments of behavior are based on the principle of inheritance.
Genes and their DNA are passed down from parents to their offspring, with 50% of our genes being inherited from each parent.
Humans have 23 pairs of chromosomes, with approximately 20,000 – 25,000 genes.
We now know this number as a result of the worldwide research initiative started in 1990 called the Human Genome Project.
The goal of this project was to map and sequence the human genome.
This incredible project was completed in 2004.
However, although the mapping of human genes could be an important step in understanding the complexity of human behavior, as well as developing treatments for specific disorders, the exact role of specific genes in many behaviors remains unknown.
Although you can undergo genetic testing for some medical conditions, the same is not entirely true for a disorder like depression.
Genetic research in humans is to a large extent based on correlational studies.
This means that a researcher establishes that there is a relationship between variables, but the researcher does not manipulate an independent variable as in an experiment.
Therefore, no cause and effect can be determined.
Since the completion of the Human Genome Project, we have seen a change in how genetic research is carried out.
One of the ways to study the possible correlation between genetic inheritance and behavior is through twin research.
Researchers study twins because they share common genetic material.
Prior to the Human Genome Project, it was the primary way that psychologists investigated the role of genetics in human behavior.
There are two types of twins: monozygotic (MZ) and dizygotic (DZ).
Monozygotic twins are genetically identical because they are formed from one fertilized egg that splits into two.
These twins are of the same sex and look very much alike. Dizygotic means “from two eggs.”
DZ twins will not be any closer genetically than brothers and sisters – on average, they will have about 50 percent of their genes in common.
These twins are not necessarily of the same sex.
Monozygotic twins: Also called identical twins; they develop from one fertilized egg, which splits and forms two embryos.
Dizygotic twins: Also called fraternal twins; they develop from two different fertilized eggs.
Psychologists use these different degrees of genetic relationship as a basis for their hypotheses about the contribution of genetic and environmental factors to behaviors such as psychiatric disorders or addictive behavior.
It should be the case that the higher the genetic relationship, the more similar individuals will be if the particular characteristic being investigated is inherited.
In twin research, the correlation found is called the concordance rate.
Twin research is based on a systematic analysis of the similarity between MZ and DZ twins and based on the assumption that any heritable trait will be more concordant in identical twins than in non-identical twins, and concordance rates will be even lower in siblings.
When carrying out twin research, if the concordance rate for MZ twins is significantly higher than for DZ twins or siblings, it is likely that there is a genetic component to the behavior.
If the concordance rate is high for both MZ and DZ twins it may be assumed that environmental factors play a large role in the observed behavior.
A concordance rate is the probability that the same trait will be present in both members of a pair of twins.
It makes sense for psychologists to first carry out twin studies to determine the concordance rate for a behavior between twins before carrying out more sophisticated genetic research, which is much more expensive.
However, there are limitations to twin studies.
First, twins are very rarely “raised apart,” so they tend to experience a very similar environment while growing up.
Therefore, it is difficult to isolate environmental influence as a variable.
That being said, we have to be careful not to overestimate the similarity of the environment for both twins.
Assuming that twins grow up in an equal environment is often called the equal environment fallacy.
Some research suggests that parents, teachers, peers, and others may treat identical twins more similar than fraternal twins.
Finally, twins are not highly representative of the general population, so it is difficult to generalize the findings.
Another way that behavioral genetics is studied is through family studies (also called pedigree studies).
Unlike twin research, this is a more representative sample of the general population.
A child inherits half its genes from the mother and half from the father.
It follows that ordinary brothers and sisters will share 50 percent of their genes with each other; grandparents will share 25 percent of their genes with their grandchildren, and first cousins will have 12.5 percent of their genes in common.
In family studies, these different degrees of genetic relatedness are compared with respect to specific traits or behavior.
The notion is that concordance rates will increase if heritability is high and vice versa.
For example, if the heritability of IQ Intelligence quotient is high, there should be a stronger correlation in IQ between children and their mothers than the correlation in IQ between second cousins, and very little, if any, between strangers.
One study that shows how family studies (what the IB refers to as "kinship studies") are used to study the role of inheritance of behavior was carried out by Weissman et al (2005).
The study looked at three generations over a 20-year period to determine the level of inheritance of depression and anxiety disorders.
The findings showed that depression in grandparents was a greater predictor of depression in grandchildren than depression in parents.
The link above will give you more details about the study.
When a behavior is suspected of being genetic within a family, psychologists use prospective studies, that is, the sample is selected and observed before certain behaviors are observed.
The researchers watch for outcomes, such as the development of a disorder.
For example, individuals who are considered “genetically vulnerable” to schizophrenia can be followed over many years to see if they actually develop the disorder.
However, there is an ethical concern that such research may cause undue stress to those who are labeled as vulnerable.
A final method used in traditional genetic research is adoption studies.
In principle, these allow the most direct comparison of genetic and environmental influences on behavior.
Adopted children generally share none of their genes with their adoptive parents, but they do share 50 percent of their genes with their biological parents.
It would be reasonable to suppose, therefore, that
if the heritability of behavior is high and the environment has little part to play,
then the behavior of adopted children should correlate more strongly with the behavior of their biological parents than their adoptive parents.
If, on the other hand, the environment has the strongest role to play, the reverse pattern should be found.
Adoption studies are often criticized as these children are not representative of the general population.
In addition, adoption agencies tend to use selective placement when finding homes for children, trying to place children with families who are similar in as many ways as possible to the natural parents.
Consequently, the effects of genetic inheritance may be difficult to separate from the influences of the environment.
Overall, these approaches to the study of the relative influence of genetic makeup and the environment allow researchers to determine if there is a potential genetic origin of behavior.
In spite of the weaknesses outlined here, it is clear that there is a correlation between several behaviors and genetic inheritance.
After the completion of the Human Genome Project, one of the key ways in which researchers study the heritability of a trait is through genetic mapping – also known as linkage analysis.
Genetic mapping indicates which chromosome contains the gene related to the behavior, as well as where the gene is located on that chromosome.
To create a genetic map, researchers collect blood samples from members of the families in which a behavior is common – for example, schizophrenia or aggression.
The researchers examine the DNA for polymorphism – the presence of genetic variation. These polymorphisms are referred to as genetic markers.
Association studies look to see if there is a correlation between these genetic markers and a certain behavior.
Although this is much more precise than the general twin study research outlined above, the results are still correlational in nature.
There would have to be a lot of research on these markers in order to see whether the effect is significant.
That is where GWAS comes in.
Once a particular gene is suspected of playing a role in human behavior, researchers today carry out Genome-wide association studies – known as GWAS.
These studies compare the DNA of two groups of participants: people with the behavior and similar people without, who serve as controls.
If a genetic marker is more frequent in people with the behavior, it is said to be "associated" with the disorder.
As you can see by its name, GWAS by definition is a very large study – often using data from hundreds of thousands of samples of both control and “target behaviors.”
By using such a large amount of data, the effect of outliers does not lead to false conclusions.
To make sense of the data, a graph called a “Manhattan Plot” is generated.
Along the x-axis, you can see the chromosomes and the genes that reside on each chromosome.
The y-axis indicates the level of significance for the association of a genetic variation with a behavior.
The red line is the required level of significance to determine whether a gene variation may exist between a control group and people living with schizophrenia.
By looking at the peaks, we can see that there are several genes that appear to differ between the two groups, indicating that a combination of these genes may lead to schizophrenia.
These are known as candidate genes - in other words, that does not mean that researchers now know which gene is the one that leads to schizophrenia, but they have identified genes that now require more research!
Adoption studies: Researchers investigate similarities between the adoptee and their biological and adoptive parents. Similarity with the biological parent is potentially the result of genetic inheritance, while similarity with the adoptive parent is more likely the result of environmental factors.
Association studies: Attempting to match a candidate gene with a specific behavior - for example, does the 5-HTT gene correlate with major depression?
Family studies: Researchers trace a phenotype over several generations in a family tree to determine the likelihood that a behavior is inherited.
Genome-wide Association Studies: an examination of a genome-wide set of genetic variants in a large sample to see if any variations are associated with a trait.
Twin studies: Researchers compare behavioral traits of monozygotic (MZ or identical) twins and dizygotic (DZ or fraternal) twins to evaluate the degree of genetic and environmental influence on a specific trait.
Historically, kinship studies - also known as family or pedigree studies - were a first step in determining whether a behavior or psychological disorder "runs in families."
When the risk of developing a disorder increases within a family, this indicates a potential genetic root of the behavior.
Although kinship studies are not used as frequently today, they have been useful in genetic research.
Today, kinship studies are more frequently part of larger linkage or association studies.
Kinship studies have several basic characteristics:
They measure the frequency of a behavior across generations.
They measure the frequency of a behavior within a generation.
They are often longitudinal.
They use case-control studies. Case-control studies are retrospective. They clearly define two groups at the start: one with the behavior/disorder and one without the behavior/disorder. They look back to assess whether there is a statistically significant difference in the rates of exposure to a defined risk factor between the groups - in this case, to potential genetic inheritance.
One kinship study took place in the 1960s in Colorado Springs.
Don Galvin was a respected member of the Air Force and the father of twelve children - 10 boys and two daughters.
Six of his sons would develop schizophrenia.
The story of the Galvin family is told in Hidden Valley Road by Robert Kolker.
Although a tragedy for the family, Lynn DeLisi was able to study the family and eventually was part of a team that used this data to determine a genetic link to schizophrenia.
Siddhartha Mukherjee, author of The Gene: An Intimate History, tells the story of his father's brother Jagu who suffered from schizophrenia, and Mukherjee's cousin, Moni, who would also go on to develop the disorder.
As Jagu had lived through the partition of India and Pakistan, the family believed that his illness was the result of the tragedy and loss that he had experienced.
However, Moni was the next generation and had not experienced this level of trauma.
This indicated that there must have been some other reason why these men developed schizophrenia.
The two stories above are a bit different.
The case of the Galvin family was studied by DeLisi and her team.
They collected empirical data, including blood samples that were eventually used for DNA testing.
Mukherjee's story, however, is anecdotal data.
Anecdotal data also has value in that it indicates that there is "something here to study."
However, it is not as reliable as empirical data.
Kinship studies limit the overall genetic variability of the sample which increases the statistical power of any ge discovery.
Kinship studies are more controlled than studies of unrelated people.
They have all lived in the same home, shared a common diet, and often have the same level of physical activity.
It is often difficult to obtain reliable data that goes back more than one generation.
Kinship studies are often reliant on anecdotal data with regard to the behavior of grandparents or great-grandparents.
This data may be open to memory distortion.
More importantly, it is only recently that a diagnosis of psychological disorders is obtained.
In many cases of past generations, there are assumptions made about potential diagnoses - but no clinical data that can be used.
Weissman et al (2005) carried out a longitudinal kinship study with a sample of 161 grandchildren and their parents and grandparents to study the potential genetic nature of Major Depressive Disorder.
The study took place over a twenty-year period, looking at families at high and low risk for depression.
The original sample of depressed patients (now, the grandparents) was selected from an outpatient clinic with a specialization in the treatment of mood disorders.
The non-depressed participants were selected from the same local community.
The original sample of parents and children was interviewed four times during this period.
The children are now adults and have children of their own - allowing for the study of the third generation.
Data was collected from clinicians, blind to past diagnoses of depression or to data collected in previous interviews.
Children were evaluated by two experienced clinicians - a child psychiatrist and a psychologist.
The researchers found high rates of psychiatric disorders in the grandchildren with two generations of major depression.
By 12 years old, 59.2% of the grandchildren were already showing signs of a psychiatric disorder - most commonly anxiety disorders.
Children had an increased risk of any disorder if depression was observed in both the grandparents and the parents, compared to children whose parents were not depressed.
In addition, the severity of a parent's depression was correlated with an increased rate of mood disorders in the children.
On the other hand, if a parent was depressed but there was no history of depression in the grandparents, there was no significant effect of parental depression on the grandchildren.
This study had a sample of 80 people living with OCD who were chosen from five different OCD clinics - and 73 control cases chosen by random-digit dialing within the same communities.
With their first-degree relatives (parents and siblings), the sample was 343 diagnosed participants and 300 control participants.
First-degree relatives were evaluated by psychiatrists using semi-structured interviews.
All interviews were done blindly to control for researcher biases.
The researchers found that the lifetime prevalence of OCD was significantly higher in diagnosed participants compared with control relatives (11.7% vs. 2.7%).
Case relatives had higher rates of both obsessions and compulsions; however, this finding is more robust for obsessions.
Lilienfield et al (1998) carried out a case-control study to determine if there is a potential genetic link to eating disorders.
The sample was made up of women living with anorexia nervosa (n = 26) or bulimia nervosa (n = 47) and a control group (n = 44).
First-degree female relatives were also interviewed (n = 460).
All interviews of the AN, BN, and control group were conducted face to face.
85% of the AN group had restored their weight at the time of the interview. Whenever possible, first-degree relatives were interviewed in person; otherwise, they were interviewed by telephone.
The mean number of relatives per group was 3.4 for AN, 3.5 for BN, and 4.3 for the control group.
Information was obtained on unavailable female relatives through family history interviews with all interviewed family members serving as informants.
Researchers carried out structured interviews.
One of the interview schedules was the Eating Disorders Family History Interview to determine eating disorders and disordered eating behaviors.
They also used the Family History Research Diagnostic Criteria, in order to determine the lifetime prevalence of depression, OCD, and other mental health concerns.
Relatives of anorexic and bulimic probands had an increased risk of disordered eating behaviors, but not a diagnosis of AN or BN.
The risk of obsessive-compulsive personality disorder was higher only among relatives of anorexic probands.
The prevalence of major depressive disorder and obsessive-compulsive disorder was independent of that of anorexia nervosa and bulimia nervosa - that is, there was no significant difference in the prevalence of these disorders between the eating disorder probands and the control group.
Modern biologists do not simply argue that a gene “causes” a behavior; instead, they recognize what is known as the gene-environment interaction.
This is part of a field of study known as epigenetics.
Epigenetics argues that for a behavior to occur, genes must be “expressed.” Genetic expression is a complex chemical reaction to environmental or physiological changes that allow a gene to “do its job.”
We do not need to understand the exact process of gene expression for IB psychology.
Still, it is important to know that environmental factors, such as stress, exercise, or diet, may result in genetic expression or the lack of genetic expression.
This also means that an individual may have a gene that could lead to a behavior, but if the gene is never expressed, this behavior will not occur.
When looking at twin research, the concordance rate of MZ twins is never 100%.
When we look at twin studies, we must remember that genes must be expressed.
So, MZ twins have the same genes, but they may not have been exposed to the same environmental stressors, and thus the same genes may not be expressed.
That concordance rates are higher for MZ than DZ twins also makes sense.
Twins do share some genes, so it is possible that DZ twins both share genes related to behavior like depression.
But not all DZ twins would.
In addition, some would not be expressed in the DZ twins that do share those genes.
This accounts for the significantly lower rate of concordance among DZ twins.
Depression – officially known as Major Depressive Disorder - is considered the common cold of mental health.
In the abnormal option, you may study this disorder in depth.
Here, we use it as an example of how genetic research is applied to understand human behavior.
Genetic researchers argue that genetic predisposition can partly explain depression.
We know that mood disorders tend to run in families, so one of the ways to investigate this is through twin studies.
Kendler et al. (2006) carried out a twin study of 15,493 complete twin pairs from the Swedish national twin registry to determine the level of heritability of depression.
They found that the average concordance rate for MZ male twins was 31 percent and for MZ female twins 44 percent, while for DZ twins, it was 11 and 16 percent, respectively.
Overall, Kendler concluded that the heritability of depression is estimated to be 38%.
The fact that the concordance rate for MZ twins is higher than the rate for DZ twins indicates that depression may be the result of a genetic predisposition - also called genetic vulnerability.
The fact that the concordance rate for MZ twins is below 100 % does not contradict the argument that depression is genetically inherited.
It may mean that the gene exists, but both twins have not experienced the same stress level and thus have not "expressed their genes."
The fact that some of the DZ twins also both had depression is also explained by the fact that they share some of the same genes.
Since twin studies leave many questions unanswered, modern genetics research focuses on genetic mapping.
Recent research has used DNA markers to try to identify the gene or genes involved in depression.
The Human Genome Project allowed us to see that up to 11 genetic markers—or variations—seem to be correlated with Major Depressive Disorder.
Caspi et al. (2003) examined the role of the 5-HTT gene in depression.
This gene plays a role in the serotonin pathways scientists believe are involved in controlling mood, emotions, aggression, sleep, and anxiety.
Caspi hypothesized that people who inherit two short versions of the 5-HTT gene are more likely to develop major depression after a stressful life event.
Caspi and his team examined a prospective, longitudinal sample of 847 26-year-old New Zealanders.
All were members of a cohort that had been assessed for mental health on an every-other-year basis until they were 21.
They were divided into three groups based on their 5-HTT alleles: Group 1 had two short alleles; Group 2 had one short and one long allele; Group 3 had two long alleles.
The mutation of the 5-HTT gene has shorter alleles.
The participants were asked to fill in a "Stressful life events" questionnaire about the frequency of 14 events - including financial, employment, health, and relationship stressors - between the ages of 21 and 26.
They were also assessed for depression.
People who had inherited one or more short versions of the allele demonstrated more symptoms of depression and suicidal ideation in response to stressful life events.
The effect was strongest for those with three or more stressful life events.
Simply inheriting the gene was not enough to lead to depression, but the genes interacting with stressful life events increased one's likelihood of developing depression.
The study is correlational, so no cause-and-effect relationship can be determined.
The study assumes that serotonin causes depression.
Information about life events was self-reported.
It may be the salience of the negative life events that play a role in depression - that is, those who recall them more easily may tend toward depression.
Those who are more resilient, may not recall negative life events as easily.
The theory acknowledges the interaction between both biological and environmental factors in depression.
This is a more holistic approach, not reductionist.
Some participants did not carry the gene mutation and became depressed; therefore, we cannot say that gene expression alone can cause depression.
Genetic arguments for depression have several strengths.
First, twin studies have been shown to be highly reliable.
Second, modern research has allowed us to locate genetic variations using very large sample sizes.
Third, modern research is not reductionist; it recognizes the interaction of environmental and biological factors in depression.
However, there are several limitations.
First, genetic arguments are correlational—they do not – and cannot—establish a cause-and-effect relationship.
Second, as mentioned earlier, twin studies have a problem with population validity.
The samples are not representative of the general population, and they tend to be small.
Population validity is a type of external validity that describes how well the sample can be generalized to a population.
In addition, it is impossible to isolate variables and separate the role of environmental factors.
Finally, although genetic markers have been identified, it is not clear how these genetic markers interact to produce the behaviors associated with depression.
Another assumption that underpins the biological approach is that the environment presents challenges to the individual.
This means that those who adapt best to the environment will have a greater chance of surviving, having children, and passing on their genes to their offspring.
This is Charles Darwin’s theory of natural selection.
Darwin’s theory of natural selection explains how species acquire adaptive characteristics to survive in an ever-changing environment.
According to the theory of natural selection, those members of a species who have characteristics that are better suited to the environment will be more likely to breed and thus pass on these traits.
An example of this was seen by Darwin when he traveled the Galapagos Islands. Finches on different islands had different types of beaks.
He found that the birds on each island had the beak that was most advantageous for the food available in that particular habitat.
Over several generations, the result of natural selection is that the species develop characteristics that make it more competitive in its environment.
This process is called adaptation.
When Darwin presented his theory in the book On the Origin of Species, he was not aware of the biological processes through which traits are inherited.
In addition to arguing that traits may be handed down, Darwin also laid the foundation for psychologists and biologists to study animals with the hope of gaining insight into human behavior.
In The Descent of Man (1871), Darwin noted that humans have a number of behaviors in common with other animals.
These include mate selection, the love of a mother for offspring, and self-preservation.
He also went on to catalog a number of facial expressions that people share with the apes.
He argued that humans also share many of the same feelings as animals.
Evolutionary psychology is grounded in the theory that as genes mutate, those that are advantageous are passed down through a process of natural selection.
Evolutionary psychologists attempt to explain how certain human behaviors are the result of the development of our species over time.
It is important to remember that natural selection cannot select for a behavior; it can only select for the genes that may produce behavior.
As you can see, there is another assumption made by evolutionary psychologists – that behaviors are genetic and may be inherited.
As we know from the first part of this chapter, this assumption is still being tested.
Price (1994) sees depressive behavior as part of an “involuntary subordinate strategy” that provides “a mechanism for yielding in competitive situations”.
Depressive behaviors in humans are likened to the submissive behaviors shown by other species to reduce aggression, signal defeat, and prevent physical injury during conflict.
Price suggests that we have evolved a mechanism that triggers a cascade of symptoms including reduced interest, motivation, and initiative when faced with a ‘no win’ situation.
These changes lead to submissive behaviors including social withdrawal which allows ‘losers’ to adjust to their reduced social status.
While these behaviors may have prompted our primitive ancestors to conserve energy and minimize injury, today they are viewed as maladaptive and often hinder our ability to cope in the face of difficulties.
Changes in social position are as common now as they were in our evolutionary past and depression as a result of loss, be it through personal bankruptcy, marital breakdown, or bereavement, is a widespread phenomenon.
Price refers to an animal’s awareness of its own fighting capacity (i.e. ability to know that it cannot win in certain situations) as its ‘resource holding potential’ (RHP) and sees this as an evolutionary precursor to self-esteem.
When animals come into conflict, it is their RHP that determines whether they attack (high self-esteem strategy) or become subordinate (low self-esteem strategy).
The animal accepts the loss of rank and communicates this to others in order to avoid further conflict and risk of injury.
These submissive behaviors are believed to be adaptive as they also serve to restore stability within the wider social group, allowing the group to continue to function successfully.
This, therefore, increases inclusive fitness - the ability of an individual organism to pass on its genes to the next generation.
Price’s theory is that it is able to explain the higher prevalence of depression in females than males.
Given that parental investment is greater for females than males, it makes sense that females are more likely to adopt behavioral strategies that ‘put their children first’ compared with males.
There is evidence from animal research to support the theory - see Raleigh et al (1984) below.
There is evidence that depressed patients are more likely to avoid competition than people with other disorders or healthy controls (see Kupferberg et al (2016)).
A weakness of Price’s theory is the rather dubious implications for attempts at treatment.
The theory argues that depression can be alleviated by adapting to a lower position in the social hierarchy.
The theory does not address the cognitive or biochemical origins of depression.
The theory can be seen as reductionist in its approach.
The theory is speculative with regard to the role of this behavior in inclusive fitness.
Aim:
To explore the relationship between social status and serotonin, a neurotransmitter believed to be associated with depressive symptoms, in Vervet monkeys.
Procedure:
The monkeys were in groups of three males and three females plus their offspring.
The researchers observed the adult males (captive for at least 5 months).
They were categorized as dominant or submissive using an observation schedule.
In four of the groups, a naturally arising change occurred in the dominance hierarchy, i.e. a previously subordinate monkey became dominant and the dominant monkey became subordinate.
Serotonin levels were measured at the beginning of the study and then after the changes in the dominance hierarchy were observed.
In order to do this, the monkeys were deprived of fruit for 48 hours and fasted overnight prior to measuring blood serotonin concentrations.
All samples were taken between 6.30 and 8.00 am.
Findings:
Serotonin levels increased by about 60% in monkeys that became dominant and decreased by about 40% in monkeys that became submissive.
Similar results occurred when the researchers deliberately elicited changes in the dominance hierarchies.
When they removed dominant monkeys, thus allowing one of the previously subordinate monkeys to become dominant, they noted that blood serotonin levels changed accordingly, i.e.
increasing in the subordinates that became dominant
and decreasing in dominants that were forced to become subordinate.
Conclusion:
Animals that become submissive and do not continue to fight when confronted with a stronger opponent reduce their risk of being mortally injured or being rejected by the group and therefore are more likely to survive and pass this trait to future generations,
thus showing how depressive behaviors may have been perpetuated as a product of natural selection.
This research supports the idea that loss, in this case, of status within the group, may trigger ‘depressive’ behaviors, such as
social withdrawal,
decreased motivation,
and acceptance of one’s lower social status, via the mechanism of reduced serotonin.
The researchers link their work to humans, suggesting that situations such as retirement or an extended personal crisis could similarly lead to reduced blood serotonin, and consequently trigger depressive symptoms.
One strength of Raleigh’s study is the use of a pre-test/post-test design - that is, they measured the serotonin levels of the male monkeys before the changes in the social hierarchy occurred.
This is a strength as it demonstrates that changes in serotonin levels occurred after changes in hierarchical position as opposed to the monkey’s losing one’s rank because of a drop in serotonin and this adds validity to the claim that depressive behaviors may be rooted in the loss of social status.
In other words, this eliminates the problem of bidirectional ambiguity.
There are several limitations to this research.
First, it is based on the assumption that serotonin is the cause of depression in humans. The serotonin hypothesis is highly contested.
The research does not look at the role of other neurotransmitters or hormones in depressive behavior, so the link to human depression may be limited.
Another limitation of Raleigh’s research is that the social lives of humans are far more complex than those of monkeys, suggesting the need for caution when generalizing the findings to human behavior.
It is unlikely that blood serotonin changes would be as dramatic in humans since they may occupy several dominant and subordinate status positions at any one time making the loss of one role less significant overall.
The study also does not address how cognitive factors may play a role when faced with a loss of position.
This is an important point as humans are capable of ‘reframing’ a social loss as gain.
For example, being turned down for a promotion at work could mean the person has more time for family, leading to an increase in self-esteem related to their ability to perform another role more effectively. Simply losing one's position in a hierarchy does not necessarily need to lead to depressive symptoms.
This theory was proposed by Raison and Miller (2012).
They argue that the genes that increase one’s risk for depression also increase one’s immune response to infections.
The depressive symptoms of social withdrawal, lack of energy, and loss of interest in once enjoyable activities may have actually played a key role in protecting our ancestors from infectious diseases.
Through GWAS studies, so far only two genetic variations have been identified as being linked to depression.
One is a gene for Neuropeptide Y – which is a neuropeptide associated with stress.
A variation of this gene results in lower levels of NPY – which makes it more difficult for the individual to cope with stress.
When this happens, the immune system is activated and there is more inflammation.
People with this variation are likely to pass it on to their offspring.
The researchers argue that the symptoms of depression also reflect this need to avoid disease.
For example, social withdrawal would remove an individual from an area with high concentrations of pathogens – the microorganisms that lead to disease.
To test their theory, Raison et al (2013) gave the drug infliximab to depressed patients. Infliximab is an anti-inflammatory drug.
They found that in depressed patients who showed elevated levels of inflammation, the drug reduced depressive symptoms.
This theory is relatively new, so more research is clearly needed.
In addition, although depressed patients with inflammation showed an improvement, depressed patients who did not show inflammation did not show any significant improvement.
This may mean that there are different types of depression and that the theory is not adequate for explaining all forms of depression.
It may also mean that our moods have an evolutionary root, but that does not necessarily mean that depression itself has an evolutionary basis.
However, as a result of such research, there is the potential that anti-inflammatory medication may play a role in the future treatment of people living with depression.
Evolutionary theories are based on the assumption that behaviors are inherited.
As we know from our study of genetics, it is difficult to know the extent to which certain behaviors are, in fact, genetically inherited.
Since it may be difficult to test empirically some evolution-based theories, researchers may be susceptible to confirmation bias—that is, they see what they expect to see.
Much of the research to test evolutionary theories is highly artificial and lacks ecological validity.
Research often involves animals as participants. It is debatable to what extent we can generalize from animals to human beings.
Little is known about the behavior of early humans, so statements about how humans “used to be” are hypothetical.
Evolutionary arguments often underestimate the role of cultural influences in shaping behavior.
Research in human genetics aims to identify particular genes involved in human behavior.
This kind of research may pose risks to participants because of the link between genetic inheritance and the potential for how people live their lives.
Genetic information obtained from such research can also be problematic for the participant’s family.
If misused, genetic information can be stigmatizing and may affect people’s ability to get jobs or insurance.
In any study, participants should always know how their privacy and confidentiality will be protected, and what will happen to any genetic material or information obtained as part of the study.
In addition, the aims and procedure of the study must be explained in plain language and participants must sign an informed consent paper to show that they have a clear understanding of the study they are participating in, and the implications, including any potential harm.
Confidentiality and privacy can be protected by coding information (where a code is assigned and only a small number of researchers have access to the codes)
or by fully anonymizing the sample (where researchers cannot link samples or information to particular people).
Anonymization protects confidentiality from insurance companies, employers, police, and others,
but it also can limit the scientific value of the study by preventing follow-up and further investigation.
Genetic research can reveal unexpected information that may result in undue stress or harm to the research participants.
Examples include evidence of misattributed paternity or unrevealed adoptions within a family.
Another example occurs when a person discovers from the study that he or she carries the gene for a particular genetic disorder.
This may cause undue stress as the participant then fears the potential onset of the disorder.
Wilhelm et al (2009) carried out a study to determine the effect of genetic testing for the 5-HTT gene which is believed to play a role in depression.
The researchers followed up by asking participants who had received genetic testing to fill out questionnaires.
When asked about the most important benefits of genetic testing, participants said that it allowed for early intervention, provided the potential to prevent the onset of depression, and helped people with the gene variation to avoid stressors that led to the onset of depression.
When asked to identify the most important limitations of receiving some information, participants said that it could lead to insurance discrimination, lead to discrimination from employers, and make people with the gene variation feel more stressed or depressed.
Regardless of which variation of the 5HTT gene was found, all participants reported more positive feelings than negative feelings.
However, the participants with two short alleles demonstrated significantly higher distress levels after learning their results compared with the other participants.
The study gives us some insight into the ethical considerations of genetic testing. However, the study has some limitations.
First, the sample had a mean age of 50 years old. 42% of the participants had suffered from depression during their lifetime – and those that had not had little chance of starting at such a late age. In addition, the sample was highly educated.
The sample is also made up of those who had agreed to have the testing in the first place.
Obviously, it is not possible to know the effect on those who refused to have the testing.
In order for this to be a more informative study, it would have been better to have the testing done before the participants were ever diagnosed with depression – in other words, a prospective study.
However, this raises other ethical concerns, especially if genetic testing is done on children.
Genetic testing could lead to a self-fulfilling prophecy, where people develop symptoms due to the expectation that they will get the disorder.
However, there is no evidence yet that this is, in fact, the case.
There is also a concern that genetic testing in children could change the parent-child relationship, with parents becoming overly protective of their child or disengaging from the child as a result of the test results.
A self-fulfilling prophecy is when a person unknowingly causes a prediction to come true, due to the simple fact that he or she expects it to come true.
Finally, the question of “genetic determinism” is an ethical concern in genetic testing.
It is important that those that receive genetic testing do not believe that their genetic makeup is their “destiny.”
It is possible that with effective counseling after test results are made available, people will understand that they are not passive victims of their genetic code, but that they can take specific actions – such as stress reduction, exercise, and changes to diet – that may help them to prevent the development of such disorders.
One of the most, if not the most, contentious issues in science is the use of animals in research.
Psychologists use animals to gain greater insight into human behavior and physiology because some research cannot be done with humans.
Over the past few decades, we have seen major changes in the way that this research is carried out.
Around 29 million animals per year are currently used in experiments in the US and European Union countries. Rats and mice make up around 80% of the total.
The good news is that the number of animals used in experiments has fallen by half in the past 30 years.
There are several reasons that we use animals to study human behavior.
First, procedures may be carried out – such as isolation and surgery – that would be unethical for humans.
In addition, the lifespan of an animal is significantly shorter than a human lifespan, so the effects of a variable – such as stress – can be studied over the course of a full lifetime and over several generations.
In addition, the behavior can be studied under controlled conditions in a way that would be impossible with humans.
For example, if we recall the study by Rogers & Kesner (2003), researchers were able to manipulate the levels of acetylcholine in order to see how this affected learning and memory.
This effect was temporary, so it caused no long-term harm to the animal.
In addition, the learning was highly controlled. This type of experiment would be very difficult to do on a human.
However, the research allows us to generate a hypothesis about the role of acetylcholine in human beings.
For example, modern research has shown depleted levels of acetylcholine in Alzheimer’s patients.
As a result of animal research, today drugs are used in the treatment of Alzheimer’s disease – such as Aricept or Exelon- that attempt to stabilize acetylcholine levels. This can be seen as a justification for the research carried out on animals.
Animal models of behavior are used when an animal has a similar behavior or disease to what is seen in humans.
This, however, can be problematic in some cases.
For example, when looking at animal models of depression, it is not possible to measure the typical human symptoms such as loss of self-esteem, pessimism, or suicidal thoughts.
However, psychologists argue that they can study animals with a specific endophenotype – that is, genetic markers – which are related to certain behaviors associated with depression.
An animal model helps us to understand the biochemical and genetic factors that may lead to depression – or any other disorder or behavior.
An endophenotype is the measurable biological, behavioral, or cognitive markers that are found more often in individual organisms with a disease than in the general population.
In 2002, geneticists completed the mapping of the rat genome.
Researchers found that rats and humans each have about 30,000 genes – only 300 are unique to either organism.
That means that the genes of the two species are 99% similar.
Much of the differences have to do with gene expression.
Both humans and rats have a gene that is responsible for the development of a tail – but only in rats is this gene expressed.
Another example of an animal model in research was used by LeDoux to understand what happens in the brain during the fear response.
By using lesioning in rats, LeDoux (1994) determined that the amygdala played a key role in the fear response.
He proposed a model based on his research with rats that argues that there are two paths in a fear response.
When we see something fearful, the visual thalamus sends a message to the amygdala.
This results in a fear response and blood pressure rises.
This is a quick response that is important for our survival.
He called this the low path. In the second path – the high path - the message from the thalamus passes through the visual cortex and the hippocampus and its meaning is interpreted.
If the stimulus is perceived to not be a threat, the amygdala lowers blood pressure and ceases the fear reaction.
Current techniques for examining the human brain are still not able to study the neural systems in the way that animal models allow.
Although researchers can study patients with brain lesions, these lesions often include damage to other structures and are not as precise as the animal models. In addition, because of the plastic nature of the brain,
If the lesions occurred a long time again,
the brain has changed in structure to compensate for the damage so it is difficult to determine the exact effect of the lesion.
There are several criticisms of the use of animal models in the study of human behavior. First, there is the question of external validity.
Especially with regard to drug therapies, it is often the case that what is observed in animals does not predict what will happen in humans.
It is questionable whether it is the physiology of the animal that leads to this lack of predictability, or whether it is a result of low ecological validity – that is, the highly controlled environment and the way that variables are operationalized.
External validity is the extent to which the results of a study can be generalized to other situations or, in the case of animal models, to people.
This leads us to question the extent to which animal research can be generalized to humans.
An animal model on its own cannot be generalized to humans.
It is important that the researchers find evidence in humans that can be explained through the animal model.
However, animal research might lead to inferences about human behavior.
This is called theoretical generalization.
Theoretical generalization is when the findings of a study contribute to the development of further theories.
A second criticism has to do with the quality of the data. Animals cannot readily communicate their responses, they can only be observed.
This means that we cannot know the cognitive processes of the animal.
This also means that research is open to researcher bias, where the researcher will see what is expected.
Animal research is not a research method.
When we discuss animal research, we are simply identifying the sample that is used.
All of the research methods that we use to study humans can be used to study animals.
Psychologists often use experiments to study behavior.
Unlike human experimentation, animal experimentation is often invasive – that is, it involves injecting drugs, removing part of the brain, or causing other permanent harm to the animal with the goal of establishing a cause-and-effect relationship.
In the study of the brain, Hetherington and Ranson (1942) lesioned the ventromedial hypothalamus [VMH] in order to see the role of this part of the brain on eating behavior.
The researchers found that the rats increased their food intake dramatically, and often doubled their weight.
This led researchers to believe that the hypothalamus acted as a brake on eating.
Later research showed that since lesioning can be imprecise, the actual part of the brain that was responsible for overeating was not the VMH.
Another study that used animals was Rosenzweig, Bennet & Diamond's (1972) study on the role of environmental stimuli on brain plasticity.
As the study was highly controlled, the researchers argued that there was a cause-and-effect relationship between stimuli and brain development.
However, in order to actually measure the effect, the researchers had to kill the animals and then measure the density of the brains.
Not all experiments in psychology use mice.
Even closer to us genetically than mice, primates have been used in several studies.
The following study is one of the classic studies in the psychology of stress.
Brady wanted to study the effect of stress on business executives.
In this experiment, monkeys were allocated to one of two conditions – either the “executive monkey” or the “yoked monkey.”
Both monkeys received an electric shock every 20 seconds for six hours at a time over a three-week period.
The executive monkey could pull a lever to stop the shock, but the yoked monkey, which was restrained in the cage, could not.
The executive monkeys developed ulcers and eventually died.
The yoked monkeys showed no negative health effects.
Brady concluded that high levels of stomach acid as the result of stress led to ulcers and the eventual death of the animal.
This study seemed to explain why some high-stress positions have problems with ulcers. However, this study has been highly criticized.
First, the monkeys were not randomly allocated to conditions.
The monkey that learned to pull the level faster was then given the position of the “executive.”
In addition, the study is highly unethical.
But most importantly, the study lacks external validity.
It assumes that being in charge is more stressful than not being in control of one’s environment.
Research in health psychology shows that those lower down the social hierarchy, people who often do not get to make the decisions, tend to have higher levels of heart disease and other health problems.
Later research (Warren & Marshall, 1983) showed that humans develop ulcers from bacteria, not from stress alone. Stress lowers one’s immune system.
This, in turn, increases the level of bacteria in the stomach – which then eats through the stomach lining, leading to ulcers.
Regardless of one’s level of stress, if you don’t have the bacteria, you won’t develop ulcers.
Not all research in psychology is experimental.
There have been many case studies of primate communities with the goal of understanding social hierarchies and stress.
Perhaps the most famous case study of this type was carried out by Robert Sapolsky.
In this case study, Sapolsky used observations, physiological tests, and experiments in a troop of baboons in order to find the role of one’s place in the hierarchy on cardiovascular health.
Sapolsky’s research was longitudinal and naturalistic.
The baboons were observed over a period of 25 years in their natural habitat in Western Kenya.
Sapolsky’s research showed the long-term effects of the hormones adrenaline and cortisol.
His findings showed that long-term exposure to stress, determined by being at the bottom of the baboon social hierarchy, leads to
higher levels of glucocorticoids (such as cortisol),
which results in
higher levels of heart disease,
lower rates of fertility,
and lower life expectancy.
Shively & Day (2015) carried out a longitudinal case study on the health of female macaque monkeys.
They found that those lower in the hierarchy suffered from twice the level of atherosclerosis – a plaque that builds up on the walls of the arteries – than higher-ranking monkeys.
Atherosclerosis is the usual cause of heart attacks, strokes, and cardiovascular disease.
As these studies were naturalistic and the animals were not manipulated in any way, the research is not only ecologically valid but also ethical.
This research has helped us to understand the role of stress on human health without causing undue stress or harm to the animals that were being studied.
The use of animals in research is highly debated with regard to ethical considerations.
Should procedures that are thought to be unethical for humans be carried out on animals?
If they are so similar to us that some argue that we can use animal models to understand human behavior, wouldn’t that also mean that such procedures could cause similar but undetectable suffering in animals?
Invasive research on animals also leads to permanent and irreversible damage.
Several countries have passed legislation in order to limit animal research and protect animal rights. In 1966 the USA passed the Animal Welfare Act.
The federal law requires that all animal dealers be registered and licensed. In addition, all animal labs must be overseen by a committee that includes one veterinarian and one person not affiliated with the facility.
The committee must regularly assess animal care, treatment, and practices during research, and is required to ensure that alternatives to animal use in experimentation would be used whenever possible.
A similar law, the Australian Code for the Care and Use of Animals for Scientific Purposes, was passed in 1969.
In 1986 the UK passed the Animal Act.
All research must take place in approved facilities; procedures must be approved by an ethics board; a minimal number of animals must be used, and it must be shown that the research cannot be carried out without using animals.
The most recent law passed by the EU was a directive in 2010.
The Directive is based on the principle of the “Three R’s”, to replace, reduce, and refine the use of animals used for scientific purposes.
Replace the use of animals with alternative techniques, or avoid the use of animals altogether.
Reduce the number of animals used to a minimum, to obtain information from fewer animals or more information from the same number of animals.
Refine the way experiments are carried out, to make sure animals suffer as little as possible.
This includes better housing and improvements to procedures that minimize pain and suffering and/or improve animal welfare.
One of the most debated areas of animal research is the use of primates in labs.
A great ape research ban is currently in place in the Netherlands, New Zealand, the United Kingdom, Sweden, Germany, and Austria.
These countries have ruled that chimpanzees, gorillas, and orangutans are cognitively similar to humans and that using them in experimentation is unethical.
The use of chimpanzees in research in the US has continued to decline, but the USA and Gabon are the only countries that still use chimpanzees for research purposes.
As of 2011 the USA still had over 1000 chimpanzees in six different laboratories around the country.
As chimpanzees may live for up to sixty years in captivity, the same chimps are often used for multiple experiments.
Wenka, a chimp that has been in captivity for over fifty years, has become the symbol of what happens to chimps in research facilities.
Wenka was born in 1954 and was removed from her mother to be used in a vision experiment.
Since then she has also been used in research on alcohol use, oral contraceptives, aging, and cognition.
Some researchers argue that since the chimp genome is so close to the human genome, it is essential to maintain the right to use them as subjects.
Some researchers have argued that we should use the same ethical standards that we use for human subjects who are unable to give consent – such as HM.
Animal advocates like Jane Goodall have put a lot of pressure on US labs to stop research on chimps and other primates.
In a 2011 report, the Institute of Medicine stated that “while the chimpanzee has been a valuable animal model in past research, most current use of chimpanzees for biomedical research is unnecessary.”
Although some may see this as a step in the right direction, the use of the term “most” leaves open the possibility that some primate research will continue.
One of the most controversial studies in psychology is the research done by Harlow on ‘the nature of love’ where he used monkeys to study how isolation affected social development.
Harry Harlow conducted many studies on rhesus macaque monkeys.
Harry Harlow established the USA’s first primate laboratory in 1932.
In one study he wanted to see the effect of isolation on infant monkeys.
Immediately after birth, he removed infant monkeys from their mother.
He kept these infants away from any contact with monkeys for three months to one year.
Then he put them in an environment with other monkeys to see what effect the lack of a “mother’s love” would have on their behavior.
He observed that the monkeys displayed abnormal behavior, including rocking compulsively and self-mutilation.
They were afraid of the other monkeys and often attacked them.
He also observed that they were unable to socialize with the other monkeys.
Those monkeys that were in isolation the longest never recovered.
Harlow’s research is definitely ethically problematic.
Some argue that this was important research in understanding the role of attachment in mental health and therefore justified.
However, others have argued that the studies were unnecessarily cruel.
One of the ways that animals are used in genetic research is through selective breeding experiments.
This is when animals are bred with the goal of producing a specific phenotype.
Modern research using selective breeding often uses transgenic mice – that is, a mouse that has had a single gene changed or removed.
In 2007 Mario Capecchi, Oliver Smithies, and Martin Evans won the Nobel Prize in Physiology for developing this procedure.
These mice are also sometimes referred to as “knockout mice.”
Cases et al (1995) carried out a study on the genetic origins of aggression.
For their study, they used a transgenic mouse where the gene that regulates the production of monoamine oxidase A (MAOA), an enzyme that breaks down serotonin and norepinephrine, was ‘knocked out” or deleted.
High levels of serotonin and norepinephrine were found in the offspring of the transgenic mice.
High levels of aggression were found in the male pups.
Does this animal model then help us to understand human behavior?
In a study carried out by Caspi et al (2002 ), the researchers carried out a 26-year longitudinal study of 1037 children born in Dunedin, New Zealand.
The study included 442 boys.
In their study, they looked at the genotype of the boys – particularly at the gene that controls the production of the MAOA enzyme – the same enzyme studied by Cases et al (1995).
The researchers wanted to see not only if the gene had an effect on the level of aggression in the children as they developed, but also whether environmental stressors may interact with the gene to determine behavior.
In other words, they were interested in the gene-environment interaction that is important to epigenetics.
By age 11, 36% of the children had been maltreated; this included rejection by the mother and physical and/or sexual abuse.
The results of the study showed that if the abused boy had the version of the MAOA gene that resulted in low levels of enzyme production, they were more likely to bully others and engage in aggressive and antisocial behavior.
As adults, 85 percent of the severely maltreated children who also had the gene for low MAOA activity developed anti-social outcomes, such as violent criminal behavior.
Boys who were abused but did not have this gene did not show any more aggression than boys who were not abused.
It appears that this study confirms the findings in the animal model, thus bringing support to the theory of genetic influence in aggressive behavior.
The biological approach to studying behavior: there are physiological origins of many behaviors and that human beings should also be studied in terms of their biology.
Psychologists have found that the relationship between biological factors and behavior is bidirectional – biology may affect behavior and cognition, and the other way around.
Psychologists study how environmental factors interact with biological systems in both animals and humans.
Many physiological factors can play a role in behavior and cognition: neurotransmitters, hormones and genes.
However, physiology does not always work on its own; for example, physiology responds to environmental stimuli, such as a stressful or happy experience, or an attractive person walking by.
One of the major controversies in the history of psychology is the nature versus nurture debate: researchers debated whether human behavior is the result of biological or environmental factors.
At this point in the history of psychology, a more balanced approach has been adopted as scientific findings have demonstrated that it is not a question of either biology or environment, but that both nature and nurture play a role.
This is reflected in the interactionist approach used by modern psychologists who adopt a more holistic picture of human behavior.
An interactionist approach uses different approaches – biological, cognitive, and sociocultural – to get a richer understanding of behavior.
The biological approach is based on certain assumptions about human behavior.
There are biological correlates of behavior – complex human behaviors may be reduced to biological origins.
Biologists study the role that neurotransmitters, hormones, brain structure, and genetics – among other biological factors – may play in behavior.
A second assumption of the biological approach is that behaviors can be inherited.
A reductionist approach analyzes a complex behavior by studying the simplest, most basic mechanisms that are believed to be responsible for the behavior.
Since biological psychologists argue that biological factors are important in understanding the origins of behavior and our biology is the result of genes, this seems a logical argument.
The mapping of the human genome has led to the assumption that eventually, we will know how specific genes are related to behavior.
However, scientists already know the relationship between genes and behavior is complex.
Psychologists argue that there is not a single gene for a behavior, but a combination of gene expression may lead to physiological processes that result in a behavior.
Stress, and other environmental factors may play a key role in whether a gene related to a behavior is “expressed.”
A final assumption is that animal research can provide insight into human behavior; as a result, a significant amount of research is undertaken using animals.
As we will see in the HL extension, mammals have very similar physiology.
Our brains, nervous system, and endocrine systems work very much like other mammals.
In addition, our genetic makeup is also very similar to animals.
Charles Darwin (1809-1882) argued in his groundbreaking theory that there is a continuity of evolution, so not only do we share physiological traits with other organisms, but perhaps our behaviors are also related along this continuum.
Psychologists often use animals to carry out research that may not be possible with human beings.
Over the past thirty years, few areas of psychology have developed quite as rapidly as brain research. As technology has progressed, so has our ability to monitor and map out the brain’s activity. The brain is seen as the control center of human functioning.
Psychologists seek to understand how the brain matures over a lifetime and how it adapts to the environment.
Prior to the development of modern scanning technology, one of the most common ways to study the brain was through the use of case studies of brain damage.
Often such studies provide researchers with a situation that they could never ethically reproduce in a laboratory. Case studies of patients with a brain injury are done longitudinally, in order to observe both the short-term and long-term effects of damage.
Case studies use triangulation to be holistic in their approach, looking at a range of effects of the damage, rather than a single behavior.
In the case of a patient with brain damage, this may include interviews with the family, psychometric testing – for example, IQ or personality testing, experiments, and observations.
Limitations of Case Studies
As the researchers do not manipulate an independent variable, no cause-and-effect relationship can be determined.
Since case studies are of single individuals, from a single case study, we cannot generalize the findings to all human beings.
Since it is naturally occurring, the study cannot be replicated.
It may be very difficult to verify information about the patient before the accident took place.
Information about the individual’s IQ, problem-solving skills, memory, or interpersonal skills is often reliant on the memories of family members.
Besides the fact that this is not an accurate measure, the memories of the family members may not be accurate.
Data triangulation: When more than one source of data is used. For example, a case study of schools looked at stress in the IB program in five different schools. In this way, if we get consistent findings, it was not simply because of the school that we chose.
Method triangulation: When more than one research method is used. If we get consistent findings, that means that the choice of research method was not the reason for our findings.
Researcher triangulation: When more than one researcher studies a case. Researchers can compare their observations and interpretations in order to increase reliability and credibility.
Theory triangulation: When we look at a case from more than one theoretical perspective - e.g. biological, cognitive, and/or sociocultural.
In spite of these methodological limitations of a single case study, psychologists agree that they provide important information that can be used to study the effects of brain damage over time, as well as spark new research.
Psychologists do not use a single case study to draw definitive conclusions about the role of the brain on behavior.
Instead, they often use similar cases to verify their findings and they may even perform experiments with animals to investigate the hypothesized relationship between damage to a specific area of the brain and behavior.
If there are several case studies of damage to the same area of the brain that show the same consequences on behavior, biologists may conclude that damage to a specific part of the brain may cause a specific behavior.
This is the case with the famous case study of HM which has contributed to our understanding of the relationship between the brain and memory.
HM fell off his bicycle when he was aged 7 and sustained a serious head injury.
Epileptic attacks began when he was 10.
At the age of 27, he had become so incapacitated by his seizures that he could not lead a normal life and medication did not help him.
With the approval of the patient and his family, neurosurgeon William Scoville performed an experimental surgery where he removed tissue from the medial temporal lobe (including the hippocampus) on both sides of HM’s brain.
After the operation, HM remembered his childhood very well.
His personality appeared largely unchanged. However, HM suffered from anterograde amnesia–he could no longer transfer information from short-term memory to long-term memory.
In order to carry out her research, Milner used many strategies. This is an example of how method triangulation may be used in a case study:
Psychometric testing: IQ testing was given to HM.
His results were slightly above average, with an IQ of 104 before the operation and a slightly improved IQ of 112 after the operation because of the reduction in seizures.
Direct observation of his behavior;
Interviews with both HM and his family members.
Cognitive testing: memory recall tests and learning tasks - such as reverse mirror drawing.
HM could not acquire new episodic knowledge (memory for events) and new semantic knowledge (general knowledge about the world).
This suggests that the brain structures that were removed from his brain are important for long-term explicit memory.
Memories as motor skills, i.e. procedural memories, were well maintained, for example, he knew how to mow a lawn.
He also showed improvements in the performance of new skills, such as reverse mirror drawing in which he had to acquire new eye-hand coordination.
An MRI scan of HM’s brain was performed in 1997 and 2002, where Corkin analyzed the extent of the damage.
It was possible to see that parts of HM’s temporal lobe including the hippocampus, had the most damage.
Damage to the hippocampus explains the problem of transferring short-term memory to long-term memory.
The researchers concluded that the hippocampus plays a critical role in converting memories of experiences from short-term memory to long-term memory.
Since HM was able to retain some memories of events that happened long before his surgery it indicates that the hippocampus is not the site of permanent storage but rather plays a role in the organization and permanent storage of memories elsewhere in the brain.
Many early experiments on the brain involved invasive techniques—for example, removing (ablation) or scarring (lesioning) brain tissue in animals in order to study subsequent behavioral changes.
Behavior before and after lesioning was compared.
In a classic study, Hetherington and Ranson (1942) lesioned a part of the brain called the ventromedial hypothalamus (VHM) in rats, a part of the brain that is believed to control feeding.
As a result of the lesioning, the rats increased their food intake dramatically and often doubled their weight.
This led researchers to conclude that the hypothalamus acted as a brake on eating.
The use of invasive techniques raises serious ethical concerns and psychologists have to conform to codes of conduct for the use of non-human animals; for example, the Ethical Principles of Psychologists and Code of Conduct by the American Association of Psychologists.
This means that psychologists who engage in research with animals need to apply to an ethical committee for permission to carry out their research.
If the potential harm to the animal cannot be determined, permission will only be granted if the research is considered to add to current knowledge and there are no alternatives.
Modern technology is now extensively used in psychology because it provides an opportunity to study not only brain structures but also the active brain while avoiding many of the ethical concerns of animal experimentation.
This allows researchers to see the localization of function – that is, the functions of specific parts of the brain and how they relate to behavior.
One imaging technique is Magnetic Resonance Imaging [MRI].
The MRI gives a three-dimensional picture of the brain structures.
The MRI was used in the case study of HM to determine the extent of his brain damage.
An MRI scanner uses a magnetic field and radio waves to map the activity of hydrogen molecules, which are present in different brain tissue to different degrees.
The image can either be viewed as a slice of the brain from any angle, or it can be used to create a three-dimensional image of the brain.
There are several advantages to using an MRI scan.
First, the procedure is non-invasive, with minimal potential harm to the participant.
Secondly, the image has high resolution; this gives researchers a good sense of the actual structure of the brain.
However, the MRI only indicates structure; it does not map what is happening in the brain.
To observe the activity of the brain, other technologies are used.
Positron Emission Tomography – commonly known as PET scanning - is used to observe metabolic processes in the brain by detecting the gamma rays emitted indirectly by a tracer.
PET neuroimaging is based on the assumption that areas of high radioactivity are associated with brain activity.
Before a PET scan begins, a patient is given a safe dose of a radioactive tracer compound introduced into the body by a modified glucose molecule [FDG].
The injected FDG enters the bloodstream, where it can travel to the brain.
If a particular area of the brain is more active, more glucose will be needed there.
When more glucose is used, the radioactive tracer is detected by the PET scanner.
The scan, which usually takes between 30 minutes and two hours, produces a multi-colored image that shows which parts of the brain were the most active.
The color of each dot shows the intensity of the energy signal.
One of the key advantages of the PET scan is that it allows participants to perform psychological tasks while the researcher observes brain activity.
There are two key limitations of PET scanning.
First, it requires an injection with a small amount of radioactive material.
Although this will not cause harm to the participant, it is still an invasive practice and raises ethical concerns.
Secondly, PET scanning is quite slow and has relatively poor resolution.
So, although it does indicate where brain activity is taking place, it is not as clear as more modern technology like the fMRI.
Unlike the MRI, which shows the structure of the brain, an fMRI (functional magnetic resonance imaging) shows actual brain activity and indicates which areas of the brain are active when engaged in a behavior or cognitive process.
The fMRI measures changes in blood flow in the active brain.
These scans have a higher resolution than PET scans, and they are easier to carry out.
This is one of the most frequently used technologies in biopsychological research today.
It tracks changes in blood flow and oxygen level as a measurement of neural activity.
When a specific brain area is active, it uses more oxygen, and therefore the blood flow increases.
This can be detected by the fMRI scanner.
Unlike PET scanning, fMRIs are non-invasive.
There is no radioactive isotope necessary.
The quality of the image is also much better and rather than a static image, the fMRI produces a film that demonstrates a change in the brain over the period of the scan.
For both the MRI and the fMRI, there are certain precautions that must be taken to protect the safety of the participant.
Since the technology works with a powerful magnet, it is important that objects that contain iron be removed.
In rare cases, a participant may have to be removed from a sample because of a metal implant – for example, certain types of pacemakers or cochlear implants.
The fMRI scanner is not a natural environment for cognition.
Therefore, research may lack ecological validity.
There is a lot of noise in the tunnel and participants may experience anxiety due to the claustrophobic nature of the machine.
There is a question of artifacts in the imaging – that is, some of the activity may be related to anxiety or reaction to the machine, rather than the behavior being studied.
The use of colors may exaggerate the activity of the brain.
Much brain activity is spontaneous and is not a reaction to stimuli.
Therefore, it is difficult to know exactly which areas of the brain are active in a behavior.
Brain areas activate for various reasons – just because the amygdala lights up, doesn’t mean that fear is necessarily part of the response being observed.
Localization of function is the theory that specific parts of the brain are responsible for specific behaviors or cognitive processes.
The case study of HM is a good example of how a specific part of the brain has a specific function – that is, the hippocampus is responsible for transferring short-term memory to long-term memory.
Although we know that some parts of the brain do play specific roles in behavior, rarely does a part of the brain work in complete isolation.
For example, in memory research, we argue that the cognitive process is the result of distributive processing rather than localization of function – in other words, several parts of the brain have to work together in order to help us create and retrieve memories.
Today researchers continue to attempt to map the brain.
One of the ways that they are doing this is by looking at the neural connections in the brain and creating a map called a connectome.
When talking about the brain, we discuss four key areas:
the brain stem,
the cerebellum,
the cerebrum,
and the limbic system.
The brain stem is not usually studied by psychologists.
The brain stem is responsible for regulating life functions, such as breathing, heart rate, and blood pressure.
The cerebellum plays a key role in balance and motor function, including speech production.
It also plays a role in learning – specifically, in classically conditioned responses.
The cerebral cortex is the largest part of the human brain, associated with higher brain functions such as thought and action.
The cerebrum is divided into four sections, called lobes. Each of these lobes plays a key role in behavior:
· The Frontal Lobe is associated with executive functions – that is, planning, decision-making, and speech.
· The Occipital Lobe is associated with visual processing.
· The Parietal Lobe is associated with the perception of stimuli;
· The Temporal Lobe is associated with auditory processing and memory.
The Limbic System - often referred to as the emotional brain - is a major focus of psychological research for its role in memory and emotion.
In the table below, you will find the key components of the limbic system.
Amygdala - Plays a role in the formation of emotional memory and fear responses.
Basal ganglia- Plays a role in habit-forming and procedural memory.
Hippocampus - Responsible for the transfer of short-term memory to long-term memory
Hypothalamus - Involved in homeostasis, emotion, thirst, hunger, circadian rhythms, and control of the autonomic nervous system. In addition, it controls the pituitary gland.
Nucleus accumbens - Plays a role in addiction and motivation.
In the previous section, we looked at the case study of HM.
Researchers were able to determine through their long-term study of HM that the hippocampus plays a key role in the transfer of information from short-term memory to long-term memory.
A review of the study can be seen in the following video.
But as you can see, the answer to the question of how memory works was not complete from the study of HM.
Other studies have shown us more about how memory works, including the case study of Eugene Pauly.
In 1992 Larry Squire and his team were introduced to one of the most interesting cases of amnesia since the famous HM study.
At the age of 70, Eugene Pauly was diagnosed with viral encephalitis.
Both his amygdala and hippocampus were completely destroyed.
He demonstrated many of the same symptoms as HM.
Squire carried out a series of interviews with EP at his home.
During one interview he asked EP to draw a map of his home.
He was not able to do it.
However, EP excused himself and got up to go to the toilet.
How could a man who could not draw a map of his home find the bathroom on his own?
Several tasks that rely on procedural memories make this transition from involving an active frontal lobe to an active basal ganglia.
Although the actual process is complex and not fully understood, when we are learning to do a task it is often cognitive in nature.
So, when I first learn to drive a car, I need to think an awful lot about what I am doing.
But remember, thinking takes up a lot of energy.
Our brains have adapted in a way that minimizes the amount of energy that it needs to expend.
Over time, the task is no longer cognitive, but what is referred to as an associative task.
By chunking together a series of movements or behaviors, the task becomes automatic.
The more common word we use for associative tasks is "habits."
EP was also able to take a walk around the block by himself.
His wife would even follow him around the block to make sure that he was okay, but he was able to find his way home without any problems.
When he was asked from any point on his walk where he lived, he would say he didn't know, but since the task was associative - or a habit - he was able to simply walk home.
However, occasionally there was a problem.
If the sidewalk was being repaired and he had to leave his familiar path, EP would get lost.
Returning to our example of driving a car - even when we drive a long time, bad weather or heavy traffic forces us to concentrate more.
The task reverts from associative to cognitive.
When this happened to EP, he did not have the capacity to solve the problem as his memory was only procedural.
Once the familiar pattern was changed, he was unable to complete the task.
In this case study, Squire & his team carried out several different research methods including interviews with EP and his family, psychometric testing (IQ testing), and observational studies.
In addition, MRIs were used to determine the extent of the damage to EP's brain.
MRI indicated that EP's basal ganglia were undamaged.
It is believed that the basal ganglia are responsible for this type of procedural memory.
The brain is a dynamic system that interacts with the environment.
In a sense, the brain is physically sculpted by experience.
Not only can the brain determine and change behavior, but behavior and environment can change the brain.
Modern researchers argue that the brain is constantly changing as a result of experience throughout the lifespan.
Plasticity refers to the brain’s ability to alter its own structure following changes within the body or in the external environment.
Brain plasticity refers to the brain’s ability to rearrange the connections between its neurons - that is, the changes that occur in the structure of the brain as a result of learning or experience.
High levels of stimulation and numerous learning opportunities lead to an increase in the density of neural connections.
This means that the brain of an expert musician should have a thicker area in the cortex related to mastery of music when compared to the brain of a non-musician.
The same can be said about students who spend a lot of time studying, compared to students who do not.
Every time we learn something new, the neurons connect to create a new trace in the brain.
This is called dendritic branching because the dendrites of the neurons grow in numbers and connect with other neurons.
This can be illustrated by a series of studies of brain plasticity carried out by Rosenzweig, Bennett, and Diamond (1972).
The researchers conducted experiments where they placed rats into one of two environments to measure the effect of either enrichment or deprivation on the development of neurons in the cerebral cortex.
In the enriched environment, rats were placed in cages with up to 11 other rats.
In addition, there were stimulus objects for the rats to play with, as well as maze training.
In the deprived environment, the rat was alone with no stimulation.
The rats spent 30 or 60 days in their respective environments and then they were killed in order to measure the effect of the environment on their brain structures.
Post-mortem studies of their brains showed that those that had been in the stimulating environment had increased thickness in the cortex as a result of increased dendritic branching compared to the rats in the deprived environment.
The frontal lobe, which in humans is associated with thinking, planning, and decision-making, was heavier in the rats that had been in the stimulating environment.
The combination of having "friends" to play with and many interesting toys created the best conditions for developing cerebral thickness.
This raises the question of the importance of stimulation and education in the growth of new synapses.
If learning always results in an increase of dendritic branching, then the findings from animal studies that show increased dendritic branching in response to environmental stimulation are important for the human cortex as well.
This was seen in a key study done by Maguire et al (2000).
Unfortunately, environmental stressors can also have a negative effect on brain structures.
Carrion et al (2009) found that children who had been abused tended to show a smaller hippocampus than their same-age peers.
The aim of the study was to see whether the brains of London taxi drivers would be somehow different as a result of their exceptional knowledge of the city and the many hours that they spend behind the wheel navigating the streets of London.
All potential taxi drivers must learn “the Knowledge” – that is, they must form a mental map of the city of London.
The participants for this quasi-experiment were 16 right-handed male London taxi drivers.
The brains of the taxi drivers were MRI scanned and compared with the MRI scans of 50 right-handed males who did not drive taxis (the control group).
In order to take part in the study, the participants had to have completed the "Knowledge" test and had their license for at least 1.5 years.
The controls were taken from an MRI database.
The sample included a range of ages so that age would not be a confounding variable.
The study is correlational as the IV was not manipulated by the researcher but naturally occurring.
The researchers were looking to see if there was a relationship between the number of years of driving a taxi and the anatomy of one's brain.
It was also a single-blind study - that is, the researcher did not know whether she was looking at the scan of a taxi driver or a control.
There were two key findings of the study.
First, the posterior hippocampi of taxi drivers were significantly larger relative to those of control subjects and the anterior hippocampi were significantly smaller.
Secondly, the volume of the right posterior hippocampi correlated with the amount of time spent as a taxi driver.
No differences were observed in other parts of the brain.
Maguire argues that this demonstrates that the hippocampus may change in response to environmental demands.
The study of localization of function and brain plasticity are very much linked.
Studies from both abnormal and developmental psychology have demonstrated, for example, the way that stress has an effect on memory by interfering with the work of the hippocampus.
In addition, long-term stress appears to lead to hippocampal atrophy - that is, hippocampal cell death that leads to a smaller hippocampus.
This was found in a study by Bremner (2003).
Thirty-three women participated in this study, including women with early childhood sexual abuse and PTSD (N=10), women with abuse without PTSD (N=12), and women without abuse or PTSD (N=11).
The researchers used an MRI to measure the volume of the hippocampus in all of the participants - and a PET scan to measure its level of function during a verbal declarative memory test.
Women who were abused and showed symptoms of PTSD were found to have a 16% smaller volume of the hippocampus compared to women with abuse without PTSD.
In addition, these women showed a lack of activity in the hippocampus when carrying out the memory task.
Women with abuse and PTSD had a 19% smaller hippocampal volume relative to women without abuse or PTSD.
According to biologists, synaptic plasticity works by the maxim: use it or you lose it!
Synapses become stronger through repeated use.
This is known as long-term potentiation.
LTP leads to a greater level of response – that is, longer periods of depolarization - on the post-synaptic membrane.
Over time, this leads to protein synthesis and gene expression which will be the building blocks used for dendritic branching – a process called neural arborization.
When a synapse is not used or is under-stimulated, it may go through the process of synaptic pruning.
It is believed that this is the way for the brain to remove synapses that are no longer needed, making the functioning of the neural networks more efficient.
The process of pruning is still not fully understood.
If you are interested in an in-depth explanation of the process, you may want to watch the video below.
Simply being able to link the above information to a study like Draganski (2004) is all you need to be able to do to answer an SAQ on Paper 1.
Nerve cells, called neurons, are one of the building blocks of behavior.
It is estimated that there are between 10 and 100 billion neurons in the nervous system and that neurons make 13 trillion connections with each other.
The neurons send electrochemical messages to the brain so that people can respond to stimuli—either from the environment or from internal changes in the body.
The process by which these messages are sent is called neurotransmission.
The electrical impulse that travels along the body of the neuron is called an action potential.
When an action potential travels down the axon of the neuron, it releases neurotransmitters that are stored in the neuron’s terminal buttons.
The neurotransmitters are then released into the gap between the neurons – called the synapse.
The synaptic gap is an incredible one-millionth of a centimeter!
Neurotransmitters are the body’s natural chemical messengers that transmit information from one neuron to another.
After crossing the synapse, the neurotransmitters fit into receptor sites on the post-synaptic membrane, like a key in a lock.
Once the message is passed on, the neurotransmitters are either broken down by an enzyme or reabsorbed by the terminal buttons, in a process called reuptake.
Neurotransmitters have been shown to have a range of different effects on human behavior.
In fact, neurotransmission underlies behavior as varied as mood, sleep, learning and memory, sexual arousal, and mental illness.
The table below, which highlights just a few neurotransmitters, gives an idea of the variety of behaviors that are influenced by these neurochemicals.
Acetylcholine - Plays a role in the consolidation of memory in the hippocampus.
Dopamine - Controls the brain's reward and pleasure centers. Plays a key role in motivation; low levels are linked to addictive behavior.
Norepinephrine - Arousal and alertness.
Serotonin - Sleep, arousal levels, and emotion.
When discussing neurotransmitters, we categorize them by how they affect a neuron.
Excitatory neurotransmitters increase the likelihood of a neuron firing by depolarizing the neuron.
Excitatory neurotransmitters include acetylcholine.
Inhibitory neurotransmitters decrease the likelihood of a neuron firing by hyperpolarizing the neuron.
Inhibitory neurotransmitters include GABA.
Because neurotransmitters fit tightly into receptor sites, like a key in a lock, drugs have been developed to either simulate the neurotransmitter if there is not enough of a specific neurotransmitter or to block the site if it is excessive.
The application of such research has improved the lives of many people.
There has been criticism of reducing the explanation of behavior to the workings of neurotransmitters alone.
It is said to be reductionist.
Can a complex human behavior like falling in love with someone be attributed to a simple “love cocktail” of dopamine and norepinephrine?
Can your mood during the summer holidays be attributed simply to serotonin levels?
Once again, most psychologists consider that neurotransmitters play a role, but do not rely solely on neurotransmission to explain behavior.
Rogers & Kesner conducted an experiment to determine the role of acetylcholine in memory formation.
There is a significant number of acetylcholine receptors in the hippocampus.
The first group was injected with scopolamine, which blocks the acetylcholine receptor sites and thus inhibits any response.
The second group was the control, given a placebo injection of a saline solution.
This was done to make sure that the fact of getting an injection alone was not responsible for a change in memory.
After being injected, the rats were again placed into the maze to see how long it would take them to find the food that they had previously located.
The findings were that the scopolamine group took longer and made more mistakes, whereas the control group learned faster and made fewer mistakes.
It appears that acetylcholine may play an important role in memory consolidation.
There are many strengths to carrying out an experiment like the one by Rogers and Kesner.
First, the procedure is very simple.
In this way, the study can be easily replicated and the reliability of the results can be tested. In addition, the experiment was highly controlled.
The only difference in the conditions is the level of acetylcholine.
To make sure that receiving the injection was not the factor that influenced the rats’ ability to run the maze, the saline solution was injected.
In this way, the researchers could rule out the placebo effect as a reason for their results.
However, there are also limitations to the study.
It is not clear to what extent we can generalize the findings from rats to human beings.
However, researchers have found that there are lower levels of acetylcholine in Alzheimer’s patients.
In a study by Antonova et al (2011), researchers demonstrated that blocking acetylcholine receptors in the brain can affect spatial memory tasks in humans.
In their study, they used a sample of twenty healthy male adults, with a mean age of 28 years old.
The study used a double-blind procedure and participants were randomly allocated to one of two conditions.
They were injected with either Scopolamine or a placebo.
The participants were then put into an fMRI where they were scanned while playing the "Arena task."
This is a rather complex virtual reality game in which the researchers are observing how well the participants are able to create spatial memories.
The goal is for the participants to navigate around an "arena" with the goal of reaching a pole.
After they have learned where the pole is located, the screen would go blank for 30 seconds.
During this time, the participants were told to actively rehearse how to get to the pole in the arena.
When the arena reappeared, the participant was now at a new starting point in the arena.
The participants would have to use their spatial memory to determine how to get to the location of the pole.
The procedure was repeated three to four weeks later, each participant received the other treatment.
The researchers found that when participants were injected with scopolamine, they demonstrated a significant reduction in the activation of the hippocampus compared to when they received a placebo.
It appears that acetylcholine could play a key role in the encoding of spatial memories in humans, as well as in rats.
The most important inhibitory neurotransmitter is GABA - or Gamma-aminobutyric acid.
It appears that this neurotransmitter inhibits neural activity both in the hippocampus and in the frontal lobe.
This inhibition of neural activity allows us to increase our cognitive load - that is, how we are able to use our working memory.
When GABA levels are low, intrusive thoughts may make it difficult for us to concentrate and lay down new memories.
In a study by Porges et al (2017), the researchers looked at GABA concentrations in the frontal lobe in a sample of 94 older adults without a history of dementia.
The mean age was 73 years. The participants were asked to take the Montreal Cognitive Assessment to test their cognitive functioning.
The researchers found that there was a correlation between higher concentrations of GABA in the frontal lobe and superior cognitive performance.
This is significant because GABA concentrations decrease with age.
This research may lead to important treatments for people suffering from dementia.
For a modern study of how this treatment might work, see the key study by Prevot et al (2019).
When discussing the process of neurotransmission, biologists refer to chemicals as agonists or antagonists, depending on the effect they have on the post-synaptic receptor sites.
All neurotransmitters are agonists for receptor sites.
They are referred to as endogenous agonists since they are biologically already part of our nervous system.
So, acetylcholine is an agonist for ACh receptor sites.
Drugs can also be agonists.
Since they are external to our system, they are referred to as exogenous agonists.
For example, nicotine is an agonist for ACh receptor sites and in the short term appears to have some positive effects on memory.
(It should be noted, however, that long-term use of nicotine has a negative effect on memory!)
Antagonists are drugs that block the receptor site and do not allow the neurotransmitter to do its job, so no action potential is sent down the neuron.
For example, scopolamine is an antagonist for ACh.
Hormones are another class of chemicals that affect behavior.
Unlike neurotransmitters, hormones are not released by the terminal buttons of a neuron; instead, they are secreted by glands in the endocrine system.
So epinephrine (adrenaline) is released by the adrenal gland into the bloodstream as a hormone whereas norepinephrine (noradrenaline) is released by neurons in the brain as a neurotransmitter.
Hormones are released directly into the bloodstream; as a result, they take longer to produce changes in behavior than neurotransmitters.
However, they also produce effects that last a lot longer than an action potential.
Hormones can only produce reactions in certain cells – known as target cells - that have an appropriate receptor site for the hormone.
When the hormone binds to the target cell, it either increases or decreases its function.
Like neurotransmitters, hormones affect a wide range of behaviors.
There are at least fifty different types of hormones.
As you will see in the table of hormones, some hormones “act as neurotransmitters.”
This means that they work in the brain by targeting receptor sites on the neuron’s synaptic gap, even though the chemical is not stored in the terminal buttons, but is secreted by an endocrine gland.
When discussing the role of hormones, neuropeptide Y and oxytocin are definitely hormones, but they sometimes act as though they were neurotransmitters.
Adrenaline - Secreted by the adrenal glands; responsible for arousal and the "fight or flight" response. Plays a role in emotional memory formation.
Cortisol - Secreted by the adrenal glands; helps control blood sugar levels, regulate metabolism, reduce inflammation, and assist with memory formation.
Melatonin - Secreted by the pineal gland; signals the relaxation and lower body temperature that help with a night of restful sleep.
Neuropeptide Y - Produced by the hypothalamus; acts as a neurotransmitter in the brain. Stimulates food intake, reduces anxiety and stress, reduces pain perception, and affects the circadian rhythm. Higher levels of NPY appear to be linked to higher levels of resilience.
Oxytocin - Produced by the hypothalamus and secreted by the pituitary gland. When it affects the brain, it acts as a neurotransmitter. Plays a role in mother-child attachment; believed to play a role in social bonding and trust between people.
Testosterone - Produced by the testes; plays a facilitative role in aggressive behavior - that is, it doesn't cause aggression, but higher levels of testosterone result in higher levels of aggression.
Perhaps the most well-known hormone is adrenaline.
Adrenaline activates what is known as the Fight or Flight response.
The flight-or-fight response is what is known as a hormone cascade – that is, hormones triggering more hormones.
The release of adrenaline is part of the hypothalamic-pituitary-adrenal axis – or HPA axis for short.
When a stimulus threatens us – the hypothalamus responds by activating the pituitary gland.
The pituitary gland then releases a hormone that activates the adrenal glands, which are located on top of your kidneys.
As a result, both cortisol and adrenaline are released into the bloodstream.
Cortisol is responsible for dumping glucose into your bloodstream in order to provide energy, and adrenaline increases the heart rate, blood pressure, and respiration.
This reaction has evolved to help humans survive in the face of danger so that they can quickly escape an immediate threat.
However, many hormones have more than one function.
Adrenaline also plays a key role in memory formation, as seen in a study by Cahill & McGaugh (1995).
The aim of the study was to investigate the role of adrenaline and the amygdala on emotional memory.
Participants were divided into two groups.
Each group saw 12 slides that were accompanied by a very different story.
In the first condition, the participant heard a rather boring story about a woman and her son who paid a visit to the son’s father in a hospital where they witnessed the staff in a disaster preparation drill of a simulated accident victim.
In the second condition, the participant heard a story where the boy was involved in a car accident where his feet were severed.
He was quickly brought to the hospital where the surgeons reattached the injured limbs.
Then he stayed in the hospital for some weeks and then went home with his mother.
Two weeks after participating in the experiment the participants were asked to come back and their memory for specific details of the story was tested.
The test was a recognition task that consisted of a series of questions about the slides with three options for them to choose from.
For example, what was the job of the father of the boy in the story?
A. A janitor B. A lab technician C. A surgeon.
The researchers then did a follow-up study.
In the follow-up study, the above procedure was repeated, but this time the participants in the "traumatic story" condition were injected with a beta-blocker called propranolol.
Beta-blockers interfere with the release of adrenaline; in this study, it was used to prevent activation of the amygdala to prevent the formation of emotional memory.
In the original version of the experiment, the researchers found that the participants who had heard the more emotionally arousing story demonstrated better recall of specific details of the story.
They could also recall more details from the slides.
In the follow-up study, they found that those that had received the beta-blocker did no better than the group that had heard the "boring" story.
They, therefore, concluded that adrenaline and activation of the amygdala play a significant role in the creation of memories linked to emotional arousal.
By carrying out a well-controlled experiment, Cahill & McGaugh were able to deduce a cause-and-effect relationship between adrenaline and the activation of the amygdala in the creation of emotional memories.
But as the study was well controlled and rather simplistic, can we apply the findings to the “real world?”
The research has been applied to the treatment of accident victims with the goal of preventing PTSD.
Pitman et al (2002) carried out an experimental study where patients coming into emergency rooms after a traumatic injury were given either beta-blockers (propranolol) or a placebo.
One month after the traumatic event, people who had received the beta-blockers showed fewer symptoms of PTSD than those who had received no beta-blockers or a placebo.
It appears that Cahill & McGaugh’s findings may prove helpful in preventing the onset of PTSD in some patients following trauma.
A rather controversial area of psychological research is the role of pheromones on human behavior.
A pheromone is a chemical substance produced and released into the environment by an animal affecting the behavior or physiology of others of its own species.
Although pheromones are known to play a significant role in signaling between members of the same species among animals to affect various behaviors, it is not clear that this is also true in humans.
Some psychologists have argued that pheromones may affect the menstrual cycle in groups of women and the olfactory recognition of a newborn by its mother.
Some argue that individuals may exude different odors based on mood.
Although there is some evidence, nothing is conclusive on whether or not humans have functional pheromones.
In animals, we see two types of pheromones.
Primer pheromones that cause slow, long-term physiological changes, such as hormonal effects; and signaling pheromones that produce rapid behavioral effects, such as mating.
In humans, there is some evidence of primer pheromones.
However, for all the published research that shows these effects, there is an equal number of studies showing that there are no effects.
At this stage in the study of psychology, no human pheromone has yet been found.
Two potential human pheromones are Androstadienone (AND) – found in male semen and sweat – and Estratetraenol (EST), which is found in female urine.
Zhou et al (2014) carried out a study to see if AND or EST influences human mating behavior.
The sample was made up of 96 participants –
24 heterosexual men,
24 heterosexual women,
24 gay men,
and 24 lesbian women.
In the experiment, participants were asked to watch stick figures walking on a screen and to determine their gender.
While carrying out the task, the participants were exposed to the smell of cloves.
In the first condition, the cloves were mixed with androstadienone;
in the second condition, the cloves were mixed with estratetraenol;
and in the control condition, only cloves were used.
The findings showed that smelling androstadienone biased heterosexual females and gay males, but not heterosexual males or lesbian women, toward perceiving the walkers as more masculine.
By contrast, smelling estratetraenol systematically biases heterosexual males and, to some extent, lesbian women toward perceiving the walkers as more feminine.
The researchers concluded that pheromones influence the communication of gender information in a sex-specific manner.
Although the study showed a significant difference in behavior, there are some concerns with the study.
First, the participants were exposed to very high levels of pheromones; it is unclear if this response would happen in a naturalistic setting.
Secondly, although they identified the figure as masculine or feminine, this is not a clear study of sexual attraction but rather of whether participants perceived a person's walk as feminine or masculine.
It can be debated whether this is a reliable measure of sexual behavior.
Finally, the study is done on a relatively small sample.
The study would need to be replicated on a much larger sample in order to determine whether the results are reliable.
A more promising study was carried out by Doucet et al (2009) on the role of secretion of the areolar glands in suckling behavior in 3-day-old infants.
The areolar glands are located near the nipple.
The researchers administered the different secretions to the infants nasally and then measured their behavior and breathing rate.
The researchers compared the infants' reaction to seven different stimuli - including, secretions of areolar glands, human milk, cow milk, formula milk, and vanilla.
They found that the infants began sucking only when exposed to the secretions of the areolar glands.
In addition, there was a significant increase in their breathing rate.
The researchers argue that this stimulus of the areolar odor may initiate a chain of behavioral and physiological events that lead to the progressive establishment of attachment between the mother and the infant.
However, more research is necessary to definitively draw these conclusions.
There are several problems with the pheromone arguments.
First, the human sense of smell is very complex.
Richard Axel and Linda Buck shared the Nobel Prize in Medicine in 2004 for their discoveries of odor receptors and how the olfactory system is organized.
They found that we have about 400 different kinds of odor receptors - and each of the 400 receptors has genetic variations.
This makes it very difficult to see how pheromones would work in humans.
Another problem is that many body odors are actually not caused by secretions, but by bacteria that mix with our secretions - for example, in the armpits.
However, about 20% of the population does not have this bacteria and thus does not create the same scent.
This makes a universal finding of pheromones a bit less likely.
Finally, culture plays a key role in our sense of smell - we learn what smells bad and what smells good.
This could potentially be a confounding variable when trying to determine the role of pheromones on behavior.
Pheromones are chemical cues that are
released into the air, secreted from glands,
or excreted in urine and picked up by animals of the same species,
initiating various social and reproductive behaviors.
Although the perfume industry may be interested in the role of pheromones in human attraction,
psychologists are also interested in the potential role of human pheromones in human aggression and pro-social behavior.
In the animal kingdom, animals will often attack members of their own species if they feel threatened.
Males tend to do this to protect their territory and their mates.
They will attack other males that invade their territory, but they will not attack other females or, in lab conditions, neutered males.
To definitively demonstrate that a pheromone exists, one must design a repeatable experiment, a bioassay, that shows that a smell molecule (odorant) causes a particular effect on the receiver.
In this case, the effect would be an aggressive response.
In order to test this in mice, Chamero et al (2007) attempted to isolate molecules found in mouse urine.
They swabbed the backs of neutered male mice with various potential pheromone molecules and then introduced him as an intruder into the cage of a healthy male mouse.
Using this technique, they were able to narrow it down to a protein that may be a pheromone that provokes aggressive behavior.
Pheromones seem to be detected by a structure called the vomeronasal organ, a tube at the base of the nasal cavity directly behind the nostrils that is filled with sensory neurons.
It is found in most amphibians, reptiles, and nonprimate mammals, but is absent in birds and most primates.
Surgical removal of the VNO eliminates territorial aggression and territorial marking in male mice and male hamsters.
Humans do not have a functional VNO.
It is a big question whether humans even have pheromones - and to date, no human pheromone has been definitively identified.
However, Mishor et al. (2021) may have found a putative pheromone.
Hexadecanal is a putative (potential) pheromone linked to human aggression. It is a molecule that is emitted from the heads of babies.
It is, in fact, one of the most abundant molecules detected.
Could this provoke aggressive behavior from the baby's caretakers by acting as a pheromone?
Mishor et al. (2021) carried out two experiments to test the effect of hexadecanal on both male and female behavior.
In their first experiment, researchers used a volunteer sample of 67 men and 60 women (age range 21 - 34).
The researchers used a double-blind independent samples design. Each participant wore a sticky pad pasted to their upper lip - one group was exposed to hexadecanal, and the other group to a placebo.
The participants played computer games with a mysterious partner.
The participants were not aware that this “partner” was actually a computer algorithm designed to provoke them.
In each round of the game, both players were allocated money that they could keep if they agreed on how to divide it between themselves.
The "mysterious partner," however, never agreed if the participant would receive the greater sum.
After five rounds, it was clear that the participant was being discriminated against in the game.
The participants then began the second half of the experiment.
The participants were again deceived by believing that they were playing a computer game with the same "mysterious partner."
They competed to identify a change in the shape of a target.
The first person to react was then allowed to "blast" his/her opponent with a loud noise blast.
The volume of the "blast" was how the researchers chose to operationalize aggression.
The game was set up so that the participant "won" 16 out of 27 trials.
They were then able to set the volume before blasting the mysterious partner.
The researchers found a small but consistent difference between the two groups.
Women exposed to hexadecanal were more likely to "punish" the mysterious partner with severe noise blasts than women who had the placebo.
On the other hand, men who were exposed to hexadecanal opted for less intense noise blasts than those who weren’t.
Mishor proposed that the emission of hexadecanal from babies provokes protective tendencies in mothers.
However, how this mechanism actually works is not clear.
Mishor et al (2021) carried out a second experiment with a sample of 25 men and 24 women.
The goal was to determine how hexadecanal interacts with the brain to potentially cause aggression.
In this study, the participants would play a computer game while in an fMRI where their computer opponent occasionally stole money from them.
When this happened, they could choose to punish the mysterious partner by docking money from his/her account, without gaining any money themselves.
The design was a repeated measures design with either hexadecanal, a placebo, or simply clean air being infused through the fMRI.
The order of the conditions was counterbalanced.
Women showed more "punishment" activity than men when exposed to hexadecanal.
In addition, the researchers observed a difference in activity in the left angular gyrus - a part of the brain responsible for interpreting social cues.
Whereas men who were exposed to hexadecanal showed activity in the left angular gyrus synced with activity in brain areas involved in processing social information and aggression (such as the amygdala), women showed a decrease in activity.
Could this then mean that hexadecanal plays a role in women's protection of their infants?
The researchers used controls to increase the internal validity of the research and potentially identify a causal relationship.
These included double-blind controls and counterbalancing.
Although the researchers attempt to make the link between the scent emitted from an infant and the protective behavior of mothers, the experiments are highly artificial and do not reflect an infant/mother relationship.
It is not clear yet under what circumstances adults release hexadecanal or how humans would actually process the odorant.
The sample sizes of both studies are small.
The results of the study would have to be replicated with larger samples in order to determine the reliability of the findings.
Although the fMRI shows some brain activity, it was not able to demonstrate how this activity would lead to aggressive behavior.
Generalizations from animal research have not proven to be valid.
Human aggression is influenced by cognitive and sociocultural factors - including learned experience and social norms. It is a reductionist argument to propose that aggression can be attributed solely to pheromones.
Studies on pheromones have often not been replicated. In addition, many of the studies are low in ecological validity.
It is not possible to eliminate the effect of other variables that may influence human scent - eg. bacteria and diet.
Humans do not appear to have a functional VNO which other animals use to detect pheromones. The human process of scent detection is very complex and difficult to study. The human scent is complex and made up of many different molecules. No one has yet mapped all of those molecules.
Behavioral genetics deals with understanding how both genetics and the environment contribute to individual variations in human behavior.
We inherit our genetic material – that is, DNA – from our parents.
However, when psychologists argue that behavior may be inherited, what exactly does that mean?
What is inherited is the genes that give rise to the development of specific physiological processes that contribute to specific traits and behavior.
It is not probable that a single gene is responsible for such complex behaviors as intelligence, criminal behavior, altruism, or attachment.
Instead, what is inherited may be the building blocks for such complex behaviors.
Psychologists argue that an individual may have a genetic predisposition towards a certain behavior; however, without the appropriate environmental stimuli, the gene is not “turned on” and the behavior is not expressed.
For example, in the study of abnormal behavior, the diathesis-stress model is used to explain the origin of depression.
This model argues that depression may be the result of the interaction of a “genetic predisposition” and environmental stress.
The model predicts that an individual with certain genes, when exposed to a stressful environment, is more likely to develop depression than someone who does not have those genes.
This knowledge has been useful in understanding why not all people develop depression following a traumatic childhood, even if they have a sibling who becomes depressed.
It also illustrates the complexity of the problem and that there is no single cause-and-effect relationship between genes and behavior.
The Diathesis–Stress Model is a psychological theory that attempts to explain behavior as a predisposition to genetic vulnerability expressed as a result of stress from life experiences.
Genetic arguments of behavior are based on the principle of inheritance.
Genes and their DNA are passed down from parents to their offspring, with 50% of our genes being inherited from each parent.
Humans have 23 pairs of chromosomes, with approximately 20,000 – 25,000 genes.
We now know this number as a result of the worldwide research initiative started in 1990 called the Human Genome Project.
The goal of this project was to map and sequence the human genome.
This incredible project was completed in 2004.
However, although the mapping of human genes could be an important step in understanding the complexity of human behavior, as well as developing treatments for specific disorders, the exact role of specific genes in many behaviors remains unknown.
Although you can undergo genetic testing for some medical conditions, the same is not entirely true for a disorder like depression.
Genetic research in humans is to a large extent based on correlational studies.
This means that a researcher establishes that there is a relationship between variables, but the researcher does not manipulate an independent variable as in an experiment.
Therefore, no cause and effect can be determined.
Since the completion of the Human Genome Project, we have seen a change in how genetic research is carried out.
One of the ways to study the possible correlation between genetic inheritance and behavior is through twin research.
Researchers study twins because they share common genetic material.
Prior to the Human Genome Project, it was the primary way that psychologists investigated the role of genetics in human behavior.
There are two types of twins: monozygotic (MZ) and dizygotic (DZ).
Monozygotic twins are genetically identical because they are formed from one fertilized egg that splits into two.
These twins are of the same sex and look very much alike. Dizygotic means “from two eggs.”
DZ twins will not be any closer genetically than brothers and sisters – on average, they will have about 50 percent of their genes in common.
These twins are not necessarily of the same sex.
Monozygotic twins: Also called identical twins; they develop from one fertilized egg, which splits and forms two embryos.
Dizygotic twins: Also called fraternal twins; they develop from two different fertilized eggs.
Psychologists use these different degrees of genetic relationship as a basis for their hypotheses about the contribution of genetic and environmental factors to behaviors such as psychiatric disorders or addictive behavior.
It should be the case that the higher the genetic relationship, the more similar individuals will be if the particular characteristic being investigated is inherited.
In twin research, the correlation found is called the concordance rate.
Twin research is based on a systematic analysis of the similarity between MZ and DZ twins and based on the assumption that any heritable trait will be more concordant in identical twins than in non-identical twins, and concordance rates will be even lower in siblings.
When carrying out twin research, if the concordance rate for MZ twins is significantly higher than for DZ twins or siblings, it is likely that there is a genetic component to the behavior.
If the concordance rate is high for both MZ and DZ twins it may be assumed that environmental factors play a large role in the observed behavior.
A concordance rate is the probability that the same trait will be present in both members of a pair of twins.
It makes sense for psychologists to first carry out twin studies to determine the concordance rate for a behavior between twins before carrying out more sophisticated genetic research, which is much more expensive.
However, there are limitations to twin studies.
First, twins are very rarely “raised apart,” so they tend to experience a very similar environment while growing up.
Therefore, it is difficult to isolate environmental influence as a variable.
That being said, we have to be careful not to overestimate the similarity of the environment for both twins.
Assuming that twins grow up in an equal environment is often called the equal environment fallacy.
Some research suggests that parents, teachers, peers, and others may treat identical twins more similar than fraternal twins.
Finally, twins are not highly representative of the general population, so it is difficult to generalize the findings.
Another way that behavioral genetics is studied is through family studies (also called pedigree studies).
Unlike twin research, this is a more representative sample of the general population.
A child inherits half its genes from the mother and half from the father.
It follows that ordinary brothers and sisters will share 50 percent of their genes with each other; grandparents will share 25 percent of their genes with their grandchildren, and first cousins will have 12.5 percent of their genes in common.
In family studies, these different degrees of genetic relatedness are compared with respect to specific traits or behavior.
The notion is that concordance rates will increase if heritability is high and vice versa.
For example, if the heritability of IQ Intelligence quotient is high, there should be a stronger correlation in IQ between children and their mothers than the correlation in IQ between second cousins, and very little, if any, between strangers.
One study that shows how family studies (what the IB refers to as "kinship studies") are used to study the role of inheritance of behavior was carried out by Weissman et al (2005).
The study looked at three generations over a 20-year period to determine the level of inheritance of depression and anxiety disorders.
The findings showed that depression in grandparents was a greater predictor of depression in grandchildren than depression in parents.
The link above will give you more details about the study.
When a behavior is suspected of being genetic within a family, psychologists use prospective studies, that is, the sample is selected and observed before certain behaviors are observed.
The researchers watch for outcomes, such as the development of a disorder.
For example, individuals who are considered “genetically vulnerable” to schizophrenia can be followed over many years to see if they actually develop the disorder.
However, there is an ethical concern that such research may cause undue stress to those who are labeled as vulnerable.
A final method used in traditional genetic research is adoption studies.
In principle, these allow the most direct comparison of genetic and environmental influences on behavior.
Adopted children generally share none of their genes with their adoptive parents, but they do share 50 percent of their genes with their biological parents.
It would be reasonable to suppose, therefore, that
if the heritability of behavior is high and the environment has little part to play,
then the behavior of adopted children should correlate more strongly with the behavior of their biological parents than their adoptive parents.
If, on the other hand, the environment has the strongest role to play, the reverse pattern should be found.
Adoption studies are often criticized as these children are not representative of the general population.
In addition, adoption agencies tend to use selective placement when finding homes for children, trying to place children with families who are similar in as many ways as possible to the natural parents.
Consequently, the effects of genetic inheritance may be difficult to separate from the influences of the environment.
Overall, these approaches to the study of the relative influence of genetic makeup and the environment allow researchers to determine if there is a potential genetic origin of behavior.
In spite of the weaknesses outlined here, it is clear that there is a correlation between several behaviors and genetic inheritance.
After the completion of the Human Genome Project, one of the key ways in which researchers study the heritability of a trait is through genetic mapping – also known as linkage analysis.
Genetic mapping indicates which chromosome contains the gene related to the behavior, as well as where the gene is located on that chromosome.
To create a genetic map, researchers collect blood samples from members of the families in which a behavior is common – for example, schizophrenia or aggression.
The researchers examine the DNA for polymorphism – the presence of genetic variation. These polymorphisms are referred to as genetic markers.
Association studies look to see if there is a correlation between these genetic markers and a certain behavior.
Although this is much more precise than the general twin study research outlined above, the results are still correlational in nature.
There would have to be a lot of research on these markers in order to see whether the effect is significant.
That is where GWAS comes in.
Once a particular gene is suspected of playing a role in human behavior, researchers today carry out Genome-wide association studies – known as GWAS.
These studies compare the DNA of two groups of participants: people with the behavior and similar people without, who serve as controls.
If a genetic marker is more frequent in people with the behavior, it is said to be "associated" with the disorder.
As you can see by its name, GWAS by definition is a very large study – often using data from hundreds of thousands of samples of both control and “target behaviors.”
By using such a large amount of data, the effect of outliers does not lead to false conclusions.
To make sense of the data, a graph called a “Manhattan Plot” is generated.
Along the x-axis, you can see the chromosomes and the genes that reside on each chromosome.
The y-axis indicates the level of significance for the association of a genetic variation with a behavior.
The red line is the required level of significance to determine whether a gene variation may exist between a control group and people living with schizophrenia.
By looking at the peaks, we can see that there are several genes that appear to differ between the two groups, indicating that a combination of these genes may lead to schizophrenia.
These are known as candidate genes - in other words, that does not mean that researchers now know which gene is the one that leads to schizophrenia, but they have identified genes that now require more research!
Adoption studies: Researchers investigate similarities between the adoptee and their biological and adoptive parents. Similarity with the biological parent is potentially the result of genetic inheritance, while similarity with the adoptive parent is more likely the result of environmental factors.
Association studies: Attempting to match a candidate gene with a specific behavior - for example, does the 5-HTT gene correlate with major depression?
Family studies: Researchers trace a phenotype over several generations in a family tree to determine the likelihood that a behavior is inherited.
Genome-wide Association Studies: an examination of a genome-wide set of genetic variants in a large sample to see if any variations are associated with a trait.
Twin studies: Researchers compare behavioral traits of monozygotic (MZ or identical) twins and dizygotic (DZ or fraternal) twins to evaluate the degree of genetic and environmental influence on a specific trait.
Historically, kinship studies - also known as family or pedigree studies - were a first step in determining whether a behavior or psychological disorder "runs in families."
When the risk of developing a disorder increases within a family, this indicates a potential genetic root of the behavior.
Although kinship studies are not used as frequently today, they have been useful in genetic research.
Today, kinship studies are more frequently part of larger linkage or association studies.
Kinship studies have several basic characteristics:
They measure the frequency of a behavior across generations.
They measure the frequency of a behavior within a generation.
They are often longitudinal.
They use case-control studies. Case-control studies are retrospective. They clearly define two groups at the start: one with the behavior/disorder and one without the behavior/disorder. They look back to assess whether there is a statistically significant difference in the rates of exposure to a defined risk factor between the groups - in this case, to potential genetic inheritance.
One kinship study took place in the 1960s in Colorado Springs.
Don Galvin was a respected member of the Air Force and the father of twelve children - 10 boys and two daughters.
Six of his sons would develop schizophrenia.
The story of the Galvin family is told in Hidden Valley Road by Robert Kolker.
Although a tragedy for the family, Lynn DeLisi was able to study the family and eventually was part of a team that used this data to determine a genetic link to schizophrenia.
Siddhartha Mukherjee, author of The Gene: An Intimate History, tells the story of his father's brother Jagu who suffered from schizophrenia, and Mukherjee's cousin, Moni, who would also go on to develop the disorder.
As Jagu had lived through the partition of India and Pakistan, the family believed that his illness was the result of the tragedy and loss that he had experienced.
However, Moni was the next generation and had not experienced this level of trauma.
This indicated that there must have been some other reason why these men developed schizophrenia.
The two stories above are a bit different.
The case of the Galvin family was studied by DeLisi and her team.
They collected empirical data, including blood samples that were eventually used for DNA testing.
Mukherjee's story, however, is anecdotal data.
Anecdotal data also has value in that it indicates that there is "something here to study."
However, it is not as reliable as empirical data.
Kinship studies limit the overall genetic variability of the sample which increases the statistical power of any ge discovery.
Kinship studies are more controlled than studies of unrelated people.
They have all lived in the same home, shared a common diet, and often have the same level of physical activity.
It is often difficult to obtain reliable data that goes back more than one generation.
Kinship studies are often reliant on anecdotal data with regard to the behavior of grandparents or great-grandparents.
This data may be open to memory distortion.
More importantly, it is only recently that a diagnosis of psychological disorders is obtained.
In many cases of past generations, there are assumptions made about potential diagnoses - but no clinical data that can be used.
Weissman et al (2005) carried out a longitudinal kinship study with a sample of 161 grandchildren and their parents and grandparents to study the potential genetic nature of Major Depressive Disorder.
The study took place over a twenty-year period, looking at families at high and low risk for depression.
The original sample of depressed patients (now, the grandparents) was selected from an outpatient clinic with a specialization in the treatment of mood disorders.
The non-depressed participants were selected from the same local community.
The original sample of parents and children was interviewed four times during this period.
The children are now adults and have children of their own - allowing for the study of the third generation.
Data was collected from clinicians, blind to past diagnoses of depression or to data collected in previous interviews.
Children were evaluated by two experienced clinicians - a child psychiatrist and a psychologist.
The researchers found high rates of psychiatric disorders in the grandchildren with two generations of major depression.
By 12 years old, 59.2% of the grandchildren were already showing signs of a psychiatric disorder - most commonly anxiety disorders.
Children had an increased risk of any disorder if depression was observed in both the grandparents and the parents, compared to children whose parents were not depressed.
In addition, the severity of a parent's depression was correlated with an increased rate of mood disorders in the children.
On the other hand, if a parent was depressed but there was no history of depression in the grandparents, there was no significant effect of parental depression on the grandchildren.
This study had a sample of 80 people living with OCD who were chosen from five different OCD clinics - and 73 control cases chosen by random-digit dialing within the same communities.
With their first-degree relatives (parents and siblings), the sample was 343 diagnosed participants and 300 control participants.
First-degree relatives were evaluated by psychiatrists using semi-structured interviews.
All interviews were done blindly to control for researcher biases.
The researchers found that the lifetime prevalence of OCD was significantly higher in diagnosed participants compared with control relatives (11.7% vs. 2.7%).
Case relatives had higher rates of both obsessions and compulsions; however, this finding is more robust for obsessions.
Lilienfield et al (1998) carried out a case-control study to determine if there is a potential genetic link to eating disorders.
The sample was made up of women living with anorexia nervosa (n = 26) or bulimia nervosa (n = 47) and a control group (n = 44).
First-degree female relatives were also interviewed (n = 460).
All interviews of the AN, BN, and control group were conducted face to face.
85% of the AN group had restored their weight at the time of the interview. Whenever possible, first-degree relatives were interviewed in person; otherwise, they were interviewed by telephone.
The mean number of relatives per group was 3.4 for AN, 3.5 for BN, and 4.3 for the control group.
Information was obtained on unavailable female relatives through family history interviews with all interviewed family members serving as informants.
Researchers carried out structured interviews.
One of the interview schedules was the Eating Disorders Family History Interview to determine eating disorders and disordered eating behaviors.
They also used the Family History Research Diagnostic Criteria, in order to determine the lifetime prevalence of depression, OCD, and other mental health concerns.
Relatives of anorexic and bulimic probands had an increased risk of disordered eating behaviors, but not a diagnosis of AN or BN.
The risk of obsessive-compulsive personality disorder was higher only among relatives of anorexic probands.
The prevalence of major depressive disorder and obsessive-compulsive disorder was independent of that of anorexia nervosa and bulimia nervosa - that is, there was no significant difference in the prevalence of these disorders between the eating disorder probands and the control group.
Modern biologists do not simply argue that a gene “causes” a behavior; instead, they recognize what is known as the gene-environment interaction.
This is part of a field of study known as epigenetics.
Epigenetics argues that for a behavior to occur, genes must be “expressed.” Genetic expression is a complex chemical reaction to environmental or physiological changes that allow a gene to “do its job.”
We do not need to understand the exact process of gene expression for IB psychology.
Still, it is important to know that environmental factors, such as stress, exercise, or diet, may result in genetic expression or the lack of genetic expression.
This also means that an individual may have a gene that could lead to a behavior, but if the gene is never expressed, this behavior will not occur.
When looking at twin research, the concordance rate of MZ twins is never 100%.
When we look at twin studies, we must remember that genes must be expressed.
So, MZ twins have the same genes, but they may not have been exposed to the same environmental stressors, and thus the same genes may not be expressed.
That concordance rates are higher for MZ than DZ twins also makes sense.
Twins do share some genes, so it is possible that DZ twins both share genes related to behavior like depression.
But not all DZ twins would.
In addition, some would not be expressed in the DZ twins that do share those genes.
This accounts for the significantly lower rate of concordance among DZ twins.
Depression – officially known as Major Depressive Disorder - is considered the common cold of mental health.
In the abnormal option, you may study this disorder in depth.
Here, we use it as an example of how genetic research is applied to understand human behavior.
Genetic researchers argue that genetic predisposition can partly explain depression.
We know that mood disorders tend to run in families, so one of the ways to investigate this is through twin studies.
Kendler et al. (2006) carried out a twin study of 15,493 complete twin pairs from the Swedish national twin registry to determine the level of heritability of depression.
They found that the average concordance rate for MZ male twins was 31 percent and for MZ female twins 44 percent, while for DZ twins, it was 11 and 16 percent, respectively.
Overall, Kendler concluded that the heritability of depression is estimated to be 38%.
The fact that the concordance rate for MZ twins is higher than the rate for DZ twins indicates that depression may be the result of a genetic predisposition - also called genetic vulnerability.
The fact that the concordance rate for MZ twins is below 100 % does not contradict the argument that depression is genetically inherited.
It may mean that the gene exists, but both twins have not experienced the same stress level and thus have not "expressed their genes."
The fact that some of the DZ twins also both had depression is also explained by the fact that they share some of the same genes.
Since twin studies leave many questions unanswered, modern genetics research focuses on genetic mapping.
Recent research has used DNA markers to try to identify the gene or genes involved in depression.
The Human Genome Project allowed us to see that up to 11 genetic markers—or variations—seem to be correlated with Major Depressive Disorder.
Caspi et al. (2003) examined the role of the 5-HTT gene in depression.
This gene plays a role in the serotonin pathways scientists believe are involved in controlling mood, emotions, aggression, sleep, and anxiety.
Caspi hypothesized that people who inherit two short versions of the 5-HTT gene are more likely to develop major depression after a stressful life event.
Caspi and his team examined a prospective, longitudinal sample of 847 26-year-old New Zealanders.
All were members of a cohort that had been assessed for mental health on an every-other-year basis until they were 21.
They were divided into three groups based on their 5-HTT alleles: Group 1 had two short alleles; Group 2 had one short and one long allele; Group 3 had two long alleles.
The mutation of the 5-HTT gene has shorter alleles.
The participants were asked to fill in a "Stressful life events" questionnaire about the frequency of 14 events - including financial, employment, health, and relationship stressors - between the ages of 21 and 26.
They were also assessed for depression.
People who had inherited one or more short versions of the allele demonstrated more symptoms of depression and suicidal ideation in response to stressful life events.
The effect was strongest for those with three or more stressful life events.
Simply inheriting the gene was not enough to lead to depression, but the genes interacting with stressful life events increased one's likelihood of developing depression.
The study is correlational, so no cause-and-effect relationship can be determined.
The study assumes that serotonin causes depression.
Information about life events was self-reported.
It may be the salience of the negative life events that play a role in depression - that is, those who recall them more easily may tend toward depression.
Those who are more resilient, may not recall negative life events as easily.
The theory acknowledges the interaction between both biological and environmental factors in depression.
This is a more holistic approach, not reductionist.
Some participants did not carry the gene mutation and became depressed; therefore, we cannot say that gene expression alone can cause depression.
Genetic arguments for depression have several strengths.
First, twin studies have been shown to be highly reliable.
Second, modern research has allowed us to locate genetic variations using very large sample sizes.
Third, modern research is not reductionist; it recognizes the interaction of environmental and biological factors in depression.
However, there are several limitations.
First, genetic arguments are correlational—they do not – and cannot—establish a cause-and-effect relationship.
Second, as mentioned earlier, twin studies have a problem with population validity.
The samples are not representative of the general population, and they tend to be small.
Population validity is a type of external validity that describes how well the sample can be generalized to a population.
In addition, it is impossible to isolate variables and separate the role of environmental factors.
Finally, although genetic markers have been identified, it is not clear how these genetic markers interact to produce the behaviors associated with depression.
Another assumption that underpins the biological approach is that the environment presents challenges to the individual.
This means that those who adapt best to the environment will have a greater chance of surviving, having children, and passing on their genes to their offspring.
This is Charles Darwin’s theory of natural selection.
Darwin’s theory of natural selection explains how species acquire adaptive characteristics to survive in an ever-changing environment.
According to the theory of natural selection, those members of a species who have characteristics that are better suited to the environment will be more likely to breed and thus pass on these traits.
An example of this was seen by Darwin when he traveled the Galapagos Islands. Finches on different islands had different types of beaks.
He found that the birds on each island had the beak that was most advantageous for the food available in that particular habitat.
Over several generations, the result of natural selection is that the species develop characteristics that make it more competitive in its environment.
This process is called adaptation.
When Darwin presented his theory in the book On the Origin of Species, he was not aware of the biological processes through which traits are inherited.
In addition to arguing that traits may be handed down, Darwin also laid the foundation for psychologists and biologists to study animals with the hope of gaining insight into human behavior.
In The Descent of Man (1871), Darwin noted that humans have a number of behaviors in common with other animals.
These include mate selection, the love of a mother for offspring, and self-preservation.
He also went on to catalog a number of facial expressions that people share with the apes.
He argued that humans also share many of the same feelings as animals.
Evolutionary psychology is grounded in the theory that as genes mutate, those that are advantageous are passed down through a process of natural selection.
Evolutionary psychologists attempt to explain how certain human behaviors are the result of the development of our species over time.
It is important to remember that natural selection cannot select for a behavior; it can only select for the genes that may produce behavior.
As you can see, there is another assumption made by evolutionary psychologists – that behaviors are genetic and may be inherited.
As we know from the first part of this chapter, this assumption is still being tested.
Price (1994) sees depressive behavior as part of an “involuntary subordinate strategy” that provides “a mechanism for yielding in competitive situations”.
Depressive behaviors in humans are likened to the submissive behaviors shown by other species to reduce aggression, signal defeat, and prevent physical injury during conflict.
Price suggests that we have evolved a mechanism that triggers a cascade of symptoms including reduced interest, motivation, and initiative when faced with a ‘no win’ situation.
These changes lead to submissive behaviors including social withdrawal which allows ‘losers’ to adjust to their reduced social status.
While these behaviors may have prompted our primitive ancestors to conserve energy and minimize injury, today they are viewed as maladaptive and often hinder our ability to cope in the face of difficulties.
Changes in social position are as common now as they were in our evolutionary past and depression as a result of loss, be it through personal bankruptcy, marital breakdown, or bereavement, is a widespread phenomenon.
Price refers to an animal’s awareness of its own fighting capacity (i.e. ability to know that it cannot win in certain situations) as its ‘resource holding potential’ (RHP) and sees this as an evolutionary precursor to self-esteem.
When animals come into conflict, it is their RHP that determines whether they attack (high self-esteem strategy) or become subordinate (low self-esteem strategy).
The animal accepts the loss of rank and communicates this to others in order to avoid further conflict and risk of injury.
These submissive behaviors are believed to be adaptive as they also serve to restore stability within the wider social group, allowing the group to continue to function successfully.
This, therefore, increases inclusive fitness - the ability of an individual organism to pass on its genes to the next generation.
Price’s theory is that it is able to explain the higher prevalence of depression in females than males.
Given that parental investment is greater for females than males, it makes sense that females are more likely to adopt behavioral strategies that ‘put their children first’ compared with males.
There is evidence from animal research to support the theory - see Raleigh et al (1984) below.
There is evidence that depressed patients are more likely to avoid competition than people with other disorders or healthy controls (see Kupferberg et al (2016)).
A weakness of Price’s theory is the rather dubious implications for attempts at treatment.
The theory argues that depression can be alleviated by adapting to a lower position in the social hierarchy.
The theory does not address the cognitive or biochemical origins of depression.
The theory can be seen as reductionist in its approach.
The theory is speculative with regard to the role of this behavior in inclusive fitness.
Aim:
To explore the relationship between social status and serotonin, a neurotransmitter believed to be associated with depressive symptoms, in Vervet monkeys.
Procedure:
The monkeys were in groups of three males and three females plus their offspring.
The researchers observed the adult males (captive for at least 5 months).
They were categorized as dominant or submissive using an observation schedule.
In four of the groups, a naturally arising change occurred in the dominance hierarchy, i.e. a previously subordinate monkey became dominant and the dominant monkey became subordinate.
Serotonin levels were measured at the beginning of the study and then after the changes in the dominance hierarchy were observed.
In order to do this, the monkeys were deprived of fruit for 48 hours and fasted overnight prior to measuring blood serotonin concentrations.
All samples were taken between 6.30 and 8.00 am.
Findings:
Serotonin levels increased by about 60% in monkeys that became dominant and decreased by about 40% in monkeys that became submissive.
Similar results occurred when the researchers deliberately elicited changes in the dominance hierarchies.
When they removed dominant monkeys, thus allowing one of the previously subordinate monkeys to become dominant, they noted that blood serotonin levels changed accordingly, i.e.
increasing in the subordinates that became dominant
and decreasing in dominants that were forced to become subordinate.
Conclusion:
Animals that become submissive and do not continue to fight when confronted with a stronger opponent reduce their risk of being mortally injured or being rejected by the group and therefore are more likely to survive and pass this trait to future generations,
thus showing how depressive behaviors may have been perpetuated as a product of natural selection.
This research supports the idea that loss, in this case, of status within the group, may trigger ‘depressive’ behaviors, such as
social withdrawal,
decreased motivation,
and acceptance of one’s lower social status, via the mechanism of reduced serotonin.
The researchers link their work to humans, suggesting that situations such as retirement or an extended personal crisis could similarly lead to reduced blood serotonin, and consequently trigger depressive symptoms.
One strength of Raleigh’s study is the use of a pre-test/post-test design - that is, they measured the serotonin levels of the male monkeys before the changes in the social hierarchy occurred.
This is a strength as it demonstrates that changes in serotonin levels occurred after changes in hierarchical position as opposed to the monkey’s losing one’s rank because of a drop in serotonin and this adds validity to the claim that depressive behaviors may be rooted in the loss of social status.
In other words, this eliminates the problem of bidirectional ambiguity.
There are several limitations to this research.
First, it is based on the assumption that serotonin is the cause of depression in humans. The serotonin hypothesis is highly contested.
The research does not look at the role of other neurotransmitters or hormones in depressive behavior, so the link to human depression may be limited.
Another limitation of Raleigh’s research is that the social lives of humans are far more complex than those of monkeys, suggesting the need for caution when generalizing the findings to human behavior.
It is unlikely that blood serotonin changes would be as dramatic in humans since they may occupy several dominant and subordinate status positions at any one time making the loss of one role less significant overall.
The study also does not address how cognitive factors may play a role when faced with a loss of position.
This is an important point as humans are capable of ‘reframing’ a social loss as gain.
For example, being turned down for a promotion at work could mean the person has more time for family, leading to an increase in self-esteem related to their ability to perform another role more effectively. Simply losing one's position in a hierarchy does not necessarily need to lead to depressive symptoms.
This theory was proposed by Raison and Miller (2012).
They argue that the genes that increase one’s risk for depression also increase one’s immune response to infections.
The depressive symptoms of social withdrawal, lack of energy, and loss of interest in once enjoyable activities may have actually played a key role in protecting our ancestors from infectious diseases.
Through GWAS studies, so far only two genetic variations have been identified as being linked to depression.
One is a gene for Neuropeptide Y – which is a neuropeptide associated with stress.
A variation of this gene results in lower levels of NPY – which makes it more difficult for the individual to cope with stress.
When this happens, the immune system is activated and there is more inflammation.
People with this variation are likely to pass it on to their offspring.
The researchers argue that the symptoms of depression also reflect this need to avoid disease.
For example, social withdrawal would remove an individual from an area with high concentrations of pathogens – the microorganisms that lead to disease.
To test their theory, Raison et al (2013) gave the drug infliximab to depressed patients. Infliximab is an anti-inflammatory drug.
They found that in depressed patients who showed elevated levels of inflammation, the drug reduced depressive symptoms.
This theory is relatively new, so more research is clearly needed.
In addition, although depressed patients with inflammation showed an improvement, depressed patients who did not show inflammation did not show any significant improvement.
This may mean that there are different types of depression and that the theory is not adequate for explaining all forms of depression.
It may also mean that our moods have an evolutionary root, but that does not necessarily mean that depression itself has an evolutionary basis.
However, as a result of such research, there is the potential that anti-inflammatory medication may play a role in the future treatment of people living with depression.
Evolutionary theories are based on the assumption that behaviors are inherited.
As we know from our study of genetics, it is difficult to know the extent to which certain behaviors are, in fact, genetically inherited.
Since it may be difficult to test empirically some evolution-based theories, researchers may be susceptible to confirmation bias—that is, they see what they expect to see.
Much of the research to test evolutionary theories is highly artificial and lacks ecological validity.
Research often involves animals as participants. It is debatable to what extent we can generalize from animals to human beings.
Little is known about the behavior of early humans, so statements about how humans “used to be” are hypothetical.
Evolutionary arguments often underestimate the role of cultural influences in shaping behavior.
Research in human genetics aims to identify particular genes involved in human behavior.
This kind of research may pose risks to participants because of the link between genetic inheritance and the potential for how people live their lives.
Genetic information obtained from such research can also be problematic for the participant’s family.
If misused, genetic information can be stigmatizing and may affect people’s ability to get jobs or insurance.
In any study, participants should always know how their privacy and confidentiality will be protected, and what will happen to any genetic material or information obtained as part of the study.
In addition, the aims and procedure of the study must be explained in plain language and participants must sign an informed consent paper to show that they have a clear understanding of the study they are participating in, and the implications, including any potential harm.
Confidentiality and privacy can be protected by coding information (where a code is assigned and only a small number of researchers have access to the codes)
or by fully anonymizing the sample (where researchers cannot link samples or information to particular people).
Anonymization protects confidentiality from insurance companies, employers, police, and others,
but it also can limit the scientific value of the study by preventing follow-up and further investigation.
Genetic research can reveal unexpected information that may result in undue stress or harm to the research participants.
Examples include evidence of misattributed paternity or unrevealed adoptions within a family.
Another example occurs when a person discovers from the study that he or she carries the gene for a particular genetic disorder.
This may cause undue stress as the participant then fears the potential onset of the disorder.
Wilhelm et al (2009) carried out a study to determine the effect of genetic testing for the 5-HTT gene which is believed to play a role in depression.
The researchers followed up by asking participants who had received genetic testing to fill out questionnaires.
When asked about the most important benefits of genetic testing, participants said that it allowed for early intervention, provided the potential to prevent the onset of depression, and helped people with the gene variation to avoid stressors that led to the onset of depression.
When asked to identify the most important limitations of receiving some information, participants said that it could lead to insurance discrimination, lead to discrimination from employers, and make people with the gene variation feel more stressed or depressed.
Regardless of which variation of the 5HTT gene was found, all participants reported more positive feelings than negative feelings.
However, the participants with two short alleles demonstrated significantly higher distress levels after learning their results compared with the other participants.
The study gives us some insight into the ethical considerations of genetic testing. However, the study has some limitations.
First, the sample had a mean age of 50 years old. 42% of the participants had suffered from depression during their lifetime – and those that had not had little chance of starting at such a late age. In addition, the sample was highly educated.
The sample is also made up of those who had agreed to have the testing in the first place.
Obviously, it is not possible to know the effect on those who refused to have the testing.
In order for this to be a more informative study, it would have been better to have the testing done before the participants were ever diagnosed with depression – in other words, a prospective study.
However, this raises other ethical concerns, especially if genetic testing is done on children.
Genetic testing could lead to a self-fulfilling prophecy, where people develop symptoms due to the expectation that they will get the disorder.
However, there is no evidence yet that this is, in fact, the case.
There is also a concern that genetic testing in children could change the parent-child relationship, with parents becoming overly protective of their child or disengaging from the child as a result of the test results.
A self-fulfilling prophecy is when a person unknowingly causes a prediction to come true, due to the simple fact that he or she expects it to come true.
Finally, the question of “genetic determinism” is an ethical concern in genetic testing.
It is important that those that receive genetic testing do not believe that their genetic makeup is their “destiny.”
It is possible that with effective counseling after test results are made available, people will understand that they are not passive victims of their genetic code, but that they can take specific actions – such as stress reduction, exercise, and changes to diet – that may help them to prevent the development of such disorders.
One of the most, if not the most, contentious issues in science is the use of animals in research.
Psychologists use animals to gain greater insight into human behavior and physiology because some research cannot be done with humans.
Over the past few decades, we have seen major changes in the way that this research is carried out.
Around 29 million animals per year are currently used in experiments in the US and European Union countries. Rats and mice make up around 80% of the total.
The good news is that the number of animals used in experiments has fallen by half in the past 30 years.
There are several reasons that we use animals to study human behavior.
First, procedures may be carried out – such as isolation and surgery – that would be unethical for humans.
In addition, the lifespan of an animal is significantly shorter than a human lifespan, so the effects of a variable – such as stress – can be studied over the course of a full lifetime and over several generations.
In addition, the behavior can be studied under controlled conditions in a way that would be impossible with humans.
For example, if we recall the study by Rogers & Kesner (2003), researchers were able to manipulate the levels of acetylcholine in order to see how this affected learning and memory.
This effect was temporary, so it caused no long-term harm to the animal.
In addition, the learning was highly controlled. This type of experiment would be very difficult to do on a human.
However, the research allows us to generate a hypothesis about the role of acetylcholine in human beings.
For example, modern research has shown depleted levels of acetylcholine in Alzheimer’s patients.
As a result of animal research, today drugs are used in the treatment of Alzheimer’s disease – such as Aricept or Exelon- that attempt to stabilize acetylcholine levels. This can be seen as a justification for the research carried out on animals.
Animal models of behavior are used when an animal has a similar behavior or disease to what is seen in humans.
This, however, can be problematic in some cases.
For example, when looking at animal models of depression, it is not possible to measure the typical human symptoms such as loss of self-esteem, pessimism, or suicidal thoughts.
However, psychologists argue that they can study animals with a specific endophenotype – that is, genetic markers – which are related to certain behaviors associated with depression.
An animal model helps us to understand the biochemical and genetic factors that may lead to depression – or any other disorder or behavior.
An endophenotype is the measurable biological, behavioral, or cognitive markers that are found more often in individual organisms with a disease than in the general population.
In 2002, geneticists completed the mapping of the rat genome.
Researchers found that rats and humans each have about 30,000 genes – only 300 are unique to either organism.
That means that the genes of the two species are 99% similar.
Much of the differences have to do with gene expression.
Both humans and rats have a gene that is responsible for the development of a tail – but only in rats is this gene expressed.
Another example of an animal model in research was used by LeDoux to understand what happens in the brain during the fear response.
By using lesioning in rats, LeDoux (1994) determined that the amygdala played a key role in the fear response.
He proposed a model based on his research with rats that argues that there are two paths in a fear response.
When we see something fearful, the visual thalamus sends a message to the amygdala.
This results in a fear response and blood pressure rises.
This is a quick response that is important for our survival.
He called this the low path. In the second path – the high path - the message from the thalamus passes through the visual cortex and the hippocampus and its meaning is interpreted.
If the stimulus is perceived to not be a threat, the amygdala lowers blood pressure and ceases the fear reaction.
Current techniques for examining the human brain are still not able to study the neural systems in the way that animal models allow.
Although researchers can study patients with brain lesions, these lesions often include damage to other structures and are not as precise as the animal models. In addition, because of the plastic nature of the brain,
If the lesions occurred a long time again,
the brain has changed in structure to compensate for the damage so it is difficult to determine the exact effect of the lesion.
There are several criticisms of the use of animal models in the study of human behavior. First, there is the question of external validity.
Especially with regard to drug therapies, it is often the case that what is observed in animals does not predict what will happen in humans.
It is questionable whether it is the physiology of the animal that leads to this lack of predictability, or whether it is a result of low ecological validity – that is, the highly controlled environment and the way that variables are operationalized.
External validity is the extent to which the results of a study can be generalized to other situations or, in the case of animal models, to people.
This leads us to question the extent to which animal research can be generalized to humans.
An animal model on its own cannot be generalized to humans.
It is important that the researchers find evidence in humans that can be explained through the animal model.
However, animal research might lead to inferences about human behavior.
This is called theoretical generalization.
Theoretical generalization is when the findings of a study contribute to the development of further theories.
A second criticism has to do with the quality of the data. Animals cannot readily communicate their responses, they can only be observed.
This means that we cannot know the cognitive processes of the animal.
This also means that research is open to researcher bias, where the researcher will see what is expected.
Animal research is not a research method.
When we discuss animal research, we are simply identifying the sample that is used.
All of the research methods that we use to study humans can be used to study animals.
Psychologists often use experiments to study behavior.
Unlike human experimentation, animal experimentation is often invasive – that is, it involves injecting drugs, removing part of the brain, or causing other permanent harm to the animal with the goal of establishing a cause-and-effect relationship.
In the study of the brain, Hetherington and Ranson (1942) lesioned the ventromedial hypothalamus [VMH] in order to see the role of this part of the brain on eating behavior.
The researchers found that the rats increased their food intake dramatically, and often doubled their weight.
This led researchers to believe that the hypothalamus acted as a brake on eating.
Later research showed that since lesioning can be imprecise, the actual part of the brain that was responsible for overeating was not the VMH.
Another study that used animals was Rosenzweig, Bennet & Diamond's (1972) study on the role of environmental stimuli on brain plasticity.
As the study was highly controlled, the researchers argued that there was a cause-and-effect relationship between stimuli and brain development.
However, in order to actually measure the effect, the researchers had to kill the animals and then measure the density of the brains.
Not all experiments in psychology use mice.
Even closer to us genetically than mice, primates have been used in several studies.
The following study is one of the classic studies in the psychology of stress.
Brady wanted to study the effect of stress on business executives.
In this experiment, monkeys were allocated to one of two conditions – either the “executive monkey” or the “yoked monkey.”
Both monkeys received an electric shock every 20 seconds for six hours at a time over a three-week period.
The executive monkey could pull a lever to stop the shock, but the yoked monkey, which was restrained in the cage, could not.
The executive monkeys developed ulcers and eventually died.
The yoked monkeys showed no negative health effects.
Brady concluded that high levels of stomach acid as the result of stress led to ulcers and the eventual death of the animal.
This study seemed to explain why some high-stress positions have problems with ulcers. However, this study has been highly criticized.
First, the monkeys were not randomly allocated to conditions.
The monkey that learned to pull the level faster was then given the position of the “executive.”
In addition, the study is highly unethical.
But most importantly, the study lacks external validity.
It assumes that being in charge is more stressful than not being in control of one’s environment.
Research in health psychology shows that those lower down the social hierarchy, people who often do not get to make the decisions, tend to have higher levels of heart disease and other health problems.
Later research (Warren & Marshall, 1983) showed that humans develop ulcers from bacteria, not from stress alone. Stress lowers one’s immune system.
This, in turn, increases the level of bacteria in the stomach – which then eats through the stomach lining, leading to ulcers.
Regardless of one’s level of stress, if you don’t have the bacteria, you won’t develop ulcers.
Not all research in psychology is experimental.
There have been many case studies of primate communities with the goal of understanding social hierarchies and stress.
Perhaps the most famous case study of this type was carried out by Robert Sapolsky.
In this case study, Sapolsky used observations, physiological tests, and experiments in a troop of baboons in order to find the role of one’s place in the hierarchy on cardiovascular health.
Sapolsky’s research was longitudinal and naturalistic.
The baboons were observed over a period of 25 years in their natural habitat in Western Kenya.
Sapolsky’s research showed the long-term effects of the hormones adrenaline and cortisol.
His findings showed that long-term exposure to stress, determined by being at the bottom of the baboon social hierarchy, leads to
higher levels of glucocorticoids (such as cortisol),
which results in
higher levels of heart disease,
lower rates of fertility,
and lower life expectancy.
Shively & Day (2015) carried out a longitudinal case study on the health of female macaque monkeys.
They found that those lower in the hierarchy suffered from twice the level of atherosclerosis – a plaque that builds up on the walls of the arteries – than higher-ranking monkeys.
Atherosclerosis is the usual cause of heart attacks, strokes, and cardiovascular disease.
As these studies were naturalistic and the animals were not manipulated in any way, the research is not only ecologically valid but also ethical.
This research has helped us to understand the role of stress on human health without causing undue stress or harm to the animals that were being studied.
The use of animals in research is highly debated with regard to ethical considerations.
Should procedures that are thought to be unethical for humans be carried out on animals?
If they are so similar to us that some argue that we can use animal models to understand human behavior, wouldn’t that also mean that such procedures could cause similar but undetectable suffering in animals?
Invasive research on animals also leads to permanent and irreversible damage.
Several countries have passed legislation in order to limit animal research and protect animal rights. In 1966 the USA passed the Animal Welfare Act.
The federal law requires that all animal dealers be registered and licensed. In addition, all animal labs must be overseen by a committee that includes one veterinarian and one person not affiliated with the facility.
The committee must regularly assess animal care, treatment, and practices during research, and is required to ensure that alternatives to animal use in experimentation would be used whenever possible.
A similar law, the Australian Code for the Care and Use of Animals for Scientific Purposes, was passed in 1969.
In 1986 the UK passed the Animal Act.
All research must take place in approved facilities; procedures must be approved by an ethics board; a minimal number of animals must be used, and it must be shown that the research cannot be carried out without using animals.
The most recent law passed by the EU was a directive in 2010.
The Directive is based on the principle of the “Three R’s”, to replace, reduce, and refine the use of animals used for scientific purposes.
Replace the use of animals with alternative techniques, or avoid the use of animals altogether.
Reduce the number of animals used to a minimum, to obtain information from fewer animals or more information from the same number of animals.
Refine the way experiments are carried out, to make sure animals suffer as little as possible.
This includes better housing and improvements to procedures that minimize pain and suffering and/or improve animal welfare.
One of the most debated areas of animal research is the use of primates in labs.
A great ape research ban is currently in place in the Netherlands, New Zealand, the United Kingdom, Sweden, Germany, and Austria.
These countries have ruled that chimpanzees, gorillas, and orangutans are cognitively similar to humans and that using them in experimentation is unethical.
The use of chimpanzees in research in the US has continued to decline, but the USA and Gabon are the only countries that still use chimpanzees for research purposes.
As of 2011 the USA still had over 1000 chimpanzees in six different laboratories around the country.
As chimpanzees may live for up to sixty years in captivity, the same chimps are often used for multiple experiments.
Wenka, a chimp that has been in captivity for over fifty years, has become the symbol of what happens to chimps in research facilities.
Wenka was born in 1954 and was removed from her mother to be used in a vision experiment.
Since then she has also been used in research on alcohol use, oral contraceptives, aging, and cognition.
Some researchers argue that since the chimp genome is so close to the human genome, it is essential to maintain the right to use them as subjects.
Some researchers have argued that we should use the same ethical standards that we use for human subjects who are unable to give consent – such as HM.
Animal advocates like Jane Goodall have put a lot of pressure on US labs to stop research on chimps and other primates.
In a 2011 report, the Institute of Medicine stated that “while the chimpanzee has been a valuable animal model in past research, most current use of chimpanzees for biomedical research is unnecessary.”
Although some may see this as a step in the right direction, the use of the term “most” leaves open the possibility that some primate research will continue.
One of the most controversial studies in psychology is the research done by Harlow on ‘the nature of love’ where he used monkeys to study how isolation affected social development.
Harry Harlow conducted many studies on rhesus macaque monkeys.
Harry Harlow established the USA’s first primate laboratory in 1932.
In one study he wanted to see the effect of isolation on infant monkeys.
Immediately after birth, he removed infant monkeys from their mother.
He kept these infants away from any contact with monkeys for three months to one year.
Then he put them in an environment with other monkeys to see what effect the lack of a “mother’s love” would have on their behavior.
He observed that the monkeys displayed abnormal behavior, including rocking compulsively and self-mutilation.
They were afraid of the other monkeys and often attacked them.
He also observed that they were unable to socialize with the other monkeys.
Those monkeys that were in isolation the longest never recovered.
Harlow’s research is definitely ethically problematic.
Some argue that this was important research in understanding the role of attachment in mental health and therefore justified.
However, others have argued that the studies were unnecessarily cruel.
One of the ways that animals are used in genetic research is through selective breeding experiments.
This is when animals are bred with the goal of producing a specific phenotype.
Modern research using selective breeding often uses transgenic mice – that is, a mouse that has had a single gene changed or removed.
In 2007 Mario Capecchi, Oliver Smithies, and Martin Evans won the Nobel Prize in Physiology for developing this procedure.
These mice are also sometimes referred to as “knockout mice.”
Cases et al (1995) carried out a study on the genetic origins of aggression.
For their study, they used a transgenic mouse where the gene that regulates the production of monoamine oxidase A (MAOA), an enzyme that breaks down serotonin and norepinephrine, was ‘knocked out” or deleted.
High levels of serotonin and norepinephrine were found in the offspring of the transgenic mice.
High levels of aggression were found in the male pups.
Does this animal model then help us to understand human behavior?
In a study carried out by Caspi et al (2002 ), the researchers carried out a 26-year longitudinal study of 1037 children born in Dunedin, New Zealand.
The study included 442 boys.
In their study, they looked at the genotype of the boys – particularly at the gene that controls the production of the MAOA enzyme – the same enzyme studied by Cases et al (1995).
The researchers wanted to see not only if the gene had an effect on the level of aggression in the children as they developed, but also whether environmental stressors may interact with the gene to determine behavior.
In other words, they were interested in the gene-environment interaction that is important to epigenetics.
By age 11, 36% of the children had been maltreated; this included rejection by the mother and physical and/or sexual abuse.
The results of the study showed that if the abused boy had the version of the MAOA gene that resulted in low levels of enzyme production, they were more likely to bully others and engage in aggressive and antisocial behavior.
As adults, 85 percent of the severely maltreated children who also had the gene for low MAOA activity developed anti-social outcomes, such as violent criminal behavior.
Boys who were abused but did not have this gene did not show any more aggression than boys who were not abused.
It appears that this study confirms the findings in the animal model, thus bringing support to the theory of genetic influence in aggressive behavior.
