The biomedical approach is based on the assumption that if a disorder like OCD is caused by a neurochemical imbalance, drugs can be used to alleviate the symptoms. For example, genetic abnormalities that affect the neurotransmitter serotonin can increase vulnerability to OCD, thus drugs that increase serotonin levels - such as SSRIs -  may be effective in reducing obsessive thoughts and compulsions.

Initially, tricyclic antidepressants were used to treat OCD by increasing levels of serotonin, noradrenaline, and dopamine. In one of the first detailed case studies of OCD, Rapoport (1989) describes the case of 12-year-old Charles, who spent hours a day engaged in ritualistic handwashing. The tricyclic clomipramine (Anafranil) gradually helped return his behaviour to normal, and he overcame his obsession with “stickiness”, which he described as a disease. Unfortunately, a year later, he developed tolerance, meaning higher and higher doses were needed in order to control his symptoms.

Despite the problems with tolerance, clomipramine is still used today as a first-line medication to alleviate obsessions.  Selective serotonin reuptake inhibitors (SSRIs) are also used, e.g. fluoxetine (Prozac). These drugs block the transporter molecules, or ‘pumps’, on the presynaptic cell membrane, meaning there is more serotonin available in the synapse, ready to bind to receptors on the postsynaptic cell.

Issari et al (2016) provides evidence to support the use of SSRIs; they carried out a meta-analysis of seventeen randomized control trials, including over 3000 participants. After just two weeks, Y-BOCS scores were significantly lower for the SSRI group than a matched, placebo group. This was a surprising but positive finding, as previous research suggests that SSRIs can be slow to take effect. On the downside, effects were reduced over the longer term, but this was moderated by increasing dosages.

Although SSRIs or clomipramine have been shown to be effective, at least 30% of patients do not show any significant improvement. Selective noradrenaline reuptake inhibitors [SNRIs], including venlafaxine, have been investigated as an alternative. These drugs have fewer side effects and have had positive outcomes for people with previously treatment-resistant symptoms. Yaryura-Tobias et al (1996) found that 43% of patients taking venlafaxine showed improvements compared to 0% in the placebo group. This said, many of the SNRIs studies have small samples and the trials sometimes lasted only 8 weeks. Much larger and longer studies are necessary in order to judge which drugs are most effective, especially in preventing relapse.

Overall, the picture regarding drug treatments is somewhat gloomy; although symptoms may be improved, patients are sometimes only 20 - 30% better off and, as stated above, many do not experience any improvement. Other drug treatments have been used with some success. For example, in a study by Selvi et al (2011), 72% of people who had received no benefit from SSRIs improved by at least 35% on the Y-BOCS when taking risperidone, an antipsychotic drug, usually used for people with schizophrenia, a disorder characterized by delusions and hallucinations. Interestingly, this drug decreases dopamine and serotonin levels.

Similarly, granisetron, a serotonin antagonist, was shown to be highly effective in a study by Askari et al. (2012). When patients took this drug in combination with an SSRI, all patients improved by at least 35%; in addition, 90% were in complete remission within just 8 weeks. It may seem paradoxical to take one drug that increases serotonin, only to take another that decreases its impact, but Askari explains that granisetron blocks 5HT-3 receptors and believe its therapeutic effect lies in its ability to indirectly reduce dopamine levels. This study demonstrates the complex interactions between neurotransmitters and highlights the importance of the treatment etiology fallacy - that is, just because a serotonin antagonist brings about improvement, this does not necessarily mean that an excess of serotonin was the cause of the disorder.

Evaluating drug treatments

The key strength of drug therapy is that for many people who suffer from OCD, it alleviates the symptoms that make day-to-day living difficult.

In spite of the strengths of drug treatments, there are also some rather serious limitations. One limitation is the problem of side-effects – the negative effect of using the drug itself. For example, SSRIs are known to have the following side effects in some patients: nausea, increased weight gain, loss of sexual desire, insomnia, blurred vision, constipation, dizziness, and anxiety.

Another limitation of drug therapy is that clinicians are still not sure how these drugs alleviate symptoms of OCD and why the treatment is not effective for all patients. Even though they boost levels of neurotransmitters in the brain within days or even hours of use, it usually takes several weeks of treatment before a therapeutic benefit results. And not all patients respond to them. 

Relying too heavily on drug treatments may lead to the neglect of important psychological or social factors that may play a significant role in the disorder. It can be argued that simply using a drug to treat OCD is a reductionist approach. An interesting study, carried out by Park et al (2020) combined measures of metacognitive beliefs and drug treatments. It was conducted on a sample of 132 Korean people with OCD, none of whom had taken medication prior to the study. Age and “positive beliefs about worry” both predicted early response to medication. Those who had the highest “positive beliefs about worry” were the latest to show any response to medication. These findings suggest that CBT that addresses beliefs about the role of worry may augment the effectiveness of drug treatments, particularly for older people. It also shows that cognitive factors may play a mediating role in the effectiveness of drug treatments.

Another limitation of drug treatment is the problem of developing a dependence on the drug. Anti-depressants and anti-anxiety drugs may lead to discontinuation syndrome – often known as “withdrawal symptoms.”  This is supported by Keuthen et al. (1994) who found that 39% of their sample suffered withdrawal symptoms at the end of their RCT examining the effectiveness of SSRI treatments for OCD.

Checking for understanding