OCD is a fairly well-known, but also a very misunderstood mental health condition, often
people who are exceptionally organised and tidy, or like to do things a certain way will
say, oh I’m a bit OCD.
But that's simply not true.
That kind of comment minimises how badly people with obsessive-compulsive disorder suffer
from their illness.
Repetitive and intrusive thoughts dominate the internal mental world of someone with
OCD causing constant and crippling anxiety.
The need to repeat the same behavioural compulsions, again and again, leaves little time for the
rest of your life.
In this video, we will discuss the biological approach to explaining, and treating OCD.
Of course, if you want to brush up on biological terminology, you can check out my biological
psychology video in the approaches unit, but I will cover everything you need for this
section, from the areas of the brain to candidate genes and drug treatments, as well as evaluations
right here.
The biological approach to explaining and treating OCD
reword each paragraph in the style of a knowledgeable expert, and keep paragraphs numbered
You likey remember what obsessive-compulsive disorder is from my characteristics video,
but as a quick reminder, OCD is a common mental health condition affecting around one in fifty
people, these individuals have obsessive thoughts and compulsive behaviours.
The repetitive and unpleasant obsessive thoughts are mental images, worries or urges that cause
anxiety.
The compulsion are the behaviours that the individual feels they need to act out to relieve
discomfort caused by the obsessive thought, unfortunately, this relief is only temporary,
and the obsessive thoughts soo n return
Obsessions around dirt and contagon are common, leading to repetitive cleaning, there are
obsessions about burglary, leading to repetitive checking of locks, and obsessions about causing
a fire, leading to repetitive checking of power switches.
These are just some of the more common symptoms, but there are many many other obsessions and
compulsions.
There are a range of explanations for why people develop OCD, but in this video we need
to focus on the biological, including genetic and neural explanations
The biological approach to explaining OCD: the genetic explanation
The Genetic explanation suggests that a vulnerability or predisposition to OCD is inherited from
our parents, while there certainly isn't one single OCD gene that causes OCD, there are
some individual genes, called candidate genes that are found more frequently in those people
who have OCD, these include gene 9, COMT gene, SERT gene and 5HT1-D beta gene.
However in total there are as many as 230 separate genes that could be involved in some
way in the development of OCD, this means OCD is polygenic.
Family studies also indicate a genetic origin to OCD, the prevalence rate of OCD in the
general population is 2%, however if an individual has OCD, the likelihood that their first degree
relatives, has OCD, known as the concordance rate, rises to 10%, this increased risk is
arguably due to shared genetics, with first degree relatives sharing 50% of their genes.
Identical twins, who share 100% of their genetic makeup, also known as monozygotic twins have
been shown to have a 68% concordance rate for OCD, while non identical, or dizygotic
twins have a 31% concordance rate.
The presence of genes isn't the whole story, because these genes have functions, the role
of your genes is to code for aspects of your biology, and it's thought these candidate
genes might influence the functioning of certain neural systems in your brain, especially the
serotonin system.
The biological approach to explaining OCD: the neural explanation.
Neural explanations for OCD include both biochemical causes, this is an imbalance of neurotransmitters,
chemicals that communicate information between neurons, and the large structures in the brain
that are made of many neurons.
Serotonin is the neurotransmitter most associated with OCD.
Low levels of serotonin is thought to cause obsessive thoughts, and the low level of serotonin
is likely due to it being removed too quickly from the synapse, before it has been able
to transmit its signal.
If you haven't studied neurons and synapses yet, that probably sounded like a pretty weird
sentence, when it comes to synapse and synaptic transmission, I’m going to tell you what
you need to know for OCD in this video, but I did make an entire video on synapses you
may want to watch..
Serotonin and other neurotransmitters are chemical messengers, presynaptic neurons release
neurotransmitters, these are detected by receptors on the postsynaptic neuron, if the signal
is strong enough then the message is passed on, the neurotransmitters detach from the
receptors are taken back to the presynaptic neuron through a process called reuptake.
It seems this process happens too quickly in people with OCD, leading to reduced levels
of serotonin in the synapse.
The SERT gene mentioned in the previous section is the gene responsible for serotonin transportation
in the synapse.
Looking at the larger structures in the brain, the communication between a set of brain structures
termed the “worry circuit” is overactive in people with OCD, leading to an inability
to filter out small worries.
The structures that forms the worry circuit are the orbito-frontal cortex, the part of
the brain responsible for rational decision making, the basal ganglia system, in particular
a part called the caudate nucleus, and the thalamus.
In normal functioning the basal ganglia filters out minor worries coming from the orbito-frontal
cortex, but if this area is hyperactive even small worries get to the thalamus, which are
then passed back to the OFC forming a loop, this is the recurring obsessive thoughts.
This abnormal activity is ultimately responsible for the repetitive motor functions, the compulsions,
these are an attempt to break this loop.
While carrying out the compulsion may give temporary relief, the hyperactive basal ganglia
will soon resume the worry circuit.
There is another brain area linked to OCD called the parahippocampal gyrus, its an area
of cortex on the underside of the brain, close to the hippocampus, its responsible for regulating
and processing unpleasant emotions, and has been seen to function abnormally in cases
of OCD.
The biological approach to explaining OCD: Evaluations
The fact that there is a high concordance rate between close family members, shown by
the data provided by Nestadt, suggests that there is a genetic origin to OCD.
Closer relations share more DNA, and have a higher concordance rate, this is because
if you share more DNA you have a higher chance of sharing the parts of DNA that causes OCD.
Both MZ and DZ twins grow up sharing very similar environments like food, upbringing
and education, and life events like bereavement or parental divorce.
But there is a significant difference in concordance rate, 68% MZ and 31% DZ, suggesting its the
additional shared DNA is what’s responsible for the increased concordance.
But as you can imagine, there are issues with assuming its the DNA that results in the high
concordance rates, closer family members also share similar environments, and even when
it comes to twins, who do have similar experiences, it could be argued that identical monozygotic
twins are treated more similarly, on the basis that they look identical, compared to dizygotic,
non identical twins.
Also the concordance rate even for identical twins at 68%, is not 100%, the level we would
expect for a feature that was entirely genetically determined, so there is likely a role for
the environment.
This means the diathesis stress model may be a more valid explanation than biology alone,
individuals inherit a genetic vulnerability to OCD, a diathesis, however the disorder
does not develop unless there is a stressor, an environmental factor such as a traumatic
life experience.
This is supported by research from Cromer, who showed 54% of 265 participants with OCD
reported at least one traumatic life event, and those with traumatic life events reported
increased severity of OCD symptoms, this demonstrates an environmental aspect to OCD.
A number of neuroimaging studies using PET scanners have shown hyperactivity in the OFC
and the caudate nucleus in people with ocd both while scanning the brain at rest and
when symptoms are stimulated, but there is a problem with this neural evidence, it is
correlational, researchers cannot be sure if the hyperactivity in these areas are the
cause of OCD, or a consequence of having OCD.
We can evaluate the biological explanation for OCD based on the effectiveness of drug
therapies, A meta-analysis by Soomro demonstrated SSRI’s are more effective than placebos,
suggesting there is a biological aspect to OCD, however despite altering levels of serotonin
in the synapse within hours, these drugs take weeks to reduce symptoms and 40% to 60% of
patients show no or just partial symptom improvement.
These findings suggest low levels of serotonin have a role to play in OCD, but are not the
sole cause of OCD.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181958/
The main type of drug used to control the symptoms of OCD are a group of antidepressant
drugs called SSRIs, one example is Fluoxetine, also known as prozac.
I think these SSRI’s are really well named because the name explains exactly what this
class of drugs do in the brain, they are selective serotonin, meaning they only influence serotonin
in the brain, reuptake inhibitors, meaning they inhibit, so slow down the process of
reuptake in the synapse this means the serotonin continues to stimulate the postsynaptic neuron.
This decreases anxiety by normalising the activity of the worry circuit.
Going back to this image, we can see the process of reuptake, SSRI’s by blocking the reuptake
of serotonin, keep serotonin in the synapse for longer, increasing its effectiveness.
It can take three to four months for SSRIs to impact symptoms, however for some patients
SSRIs are not effective, the dosage can be increased, or there are other treatment options,
anti-anxiety drugs like benzodiazepines enhance a neurotransmitter called GABA, slowing the
central nervous system resulting in general relaxation.
Tricyclics and SNRIs work by increasing serotonin and noradrenaline; these drugs can be effective
when SSRIs fail, but because they work on multiple neurotransmitters, they tend to have
more intense side effects.
Evaluations of biological treatments for OCD
There is research evidence by Soomro that compared SSRI’s to placebos, placebos are
sugar pills that make the patient think they are receiving drug therapy.
Soomro combined the data from 17 studies, including 3097 participants into a meta-analysis.
The results showed that SSRI’s significantly reduced the symptoms of OCD placebos between
6 and 17 weeks post treatment.
This suggests drug therapy is effective, at least in the short term.
There are criticisms that this type of research may not be as reliable as it appears, Goldacre
points out that the vast majority of the research studies on drug therapies are conducted by
the pharmaceutical companies who created them.
This means they have a financial interest in showing they are effective, this along
with the file drawer problem, the fact that many negative results stay unpublished, means
that drug therapies may not actually be as effective as drug companies claim they are.
On a related point, Dr Ben Goldacre has two book’s Bad Science and Bad Pharma.
They are interesting and well written, any student considering medicine, or just interested
in how science is conducted poorly and misrepresented in the media should read them.
economics of drug therapy and alternatives An advantage of drug therapy is its a relatively
inexpensive treatment, as well as potentially more convenient for the patient, this is in
comparison to psychological therapies like CBT, which require multiple sessions with
a trained therapist, as CBT is much more expensive, from an economic perspective health services
like the NHS are more likely to provide drug therapy before CBT.
A disadvantage of drug therapy is it is not the preferred treatment plan for many patients,
with many preferring a course of cognitive behavioural therapy, this is because drug
therapy can have a range of potential side effects, in the Soomro meta-analysis Nausea,
headache and insomnia were the most common side effect for each drug tested.
There are other reasons drug therapy are not preferred by patients, the desired effects
of the drugs, the symptom reduction can take up to three to four months and patients can
ultimately become dependent on the drugs.
And finally, drug therapies may actually be only treating the symptoms of OCD, not the
cause, serotonin imbalance could be due to other biological processes, or the origin
of OCD may not be biological at all, but be due to a traumatic experience.
Remember research by Cromer showed 54% of 265 participants with OCD reported at least
one traumatic life event, and those with traumatic life events reported increased severity of
OCD symptoms.
This suggests drug therapy may only be a temporary solution, and psychological therapy may be
a more effective long term treatment.