Is an essay with studies better?

Do we need studies or not? This is an interesting dilemma in the new IB Psychology course. In my previous post, I wrote an example essay with no studies. I found it difficult, but not impossible. It didn’t surprise me, however, that I found it hard to talk about the concept. The Big Six are all about research. Or maybe that’s just me. In this post, I’ll tackle the same question without the “no studies” shackles. 

Question: In the context of health and well-being, discuss the concept of bias in relation to one or more biological explanations of one mental health disorder.

The Plan:

• Intro
• BP 1: Monoamine and serotonin hypothesis
• BP: Publication bias and placebo effects (researcher bias)
• BP 3: 5-HTT Gene
• BP 4: Cultural bias
• BP 5: Diathesis-stress model and the Dunedin study
• BP 6: Bias – not sure yet?
• Conclusion

Edit: You’ll notice how the plan is different to the real essay. That’s because when I write these examples I do it under exam-like conditions. Fast plan, no heavy re-writes and minimal editing.

 

The Essay

In the context of health and well-being, discuss the concept of bias in relation to one or more biological explanations of one mental health disorder.
One mental health disorder that can be explained by biological factors is depression, or major depressive disorder (MDD). However, a variety of biases can distort what we know about depression and its biological causes, as will be discussed in this essay.	Examiner-style annotations Simple intro that addresses the concept, the area of study and the context.
The first biological explanation of depression is the monoamine hypothesis. This originated in the 1950s after it was discovered that depression symptoms were a side-effect of some medications. Similarly, other medications reduced patients symptoms. For example, one drug was used to treat tuberculosis and it was found that patients had reduced depressive symptoms. These medications were monoamine oxidase inhibitors (MAOIs) – they prevent the enzyme monoamine oxidase from breaking down neurotransmitters, which means they stay in the synaptic cleft longer. This increases the amount of monoamines (like dopamine and serotonin) to bind to receptors. Since these medications were shown to improve depression, it was suggested that low monoamine levels were the cause of depression.	Biological explanation is summarised with specific terminology.
However, studies on this hypothesis might have suffered from researcher bias and the placebo effect. Early studies didn’t use randomised clinical trials. Instead they just gave participants the medication and measured their change in depressive symptoms. The placebo effect could have been biasing the participants responses – they might have felt better because they were expected to get better. Similarly, since there was no control group there might have been researcher bias – the researchers might have expected the drugs to work so they were unconsciously biased in their recording of depression symptoms. This can be avoided with a double-blind placebo controlled trial.	Transitional phrase (However) links the bias to the area of study directly. The relevant bias is explained and linked to the content directly.
Interestingly, double-blind, placebo controlled trials have been run on selective serotonin reuptake inhibitors because serotonin is also hypothesised to be a biological cause of depression. From the monoamine hypothesis emerged the serotonin hypothesis – low levels of serotonin are thought to be the cause of depression. If that’s the case, then SSRIs which block reuptake and increase available serotonin in the synapse for binding should reduce depression. In order for these SSRIs to get prescribed they need to go through clinical trials. However, meta-analyses have shown that there’s weak evidence for the serotonin hypothesis of depression. So why are SSRIs still being prescribed? It could be because of publication bias. Research journals publish positive and significant results more than others. This means if a drug is tested in a study and there are no effects (or even worse it makes the depression worse) then these results are less likely to be published. This researcher bias may be why SSRIs continue to be prescribed despite a lack of evidence for the serotonin hypothesis.	Another transition phrase keeps the points connected. There’s a balance between summarising facts (using terminology to show knowledge) and then explaining the issue with bias. The answer keeps redirecting to the explanation rather than going off topic with SSRIs.
A related biological explanation is genetics. Specifically, the 5-HTT gene (aka the serotonin transporter gene) has been identified as a risk for depression. This gene affects gene expression and the production of serotonin transporters – proteins on the presynaptic neuron that reabsorb serotonin from the synaptic cleft. There are two variants – the S variant (two short alleles) and the L variant (two long alleles), and some people are a combination SL (one short, one long). In Western people the S variant is the risk variant – people with this variant are more likely to be diagnosed than others. However, the opposite is true for East Asians – in those populations it’s the people with the L variant who are at risk. This shows one reason why cultural bias is important to consider in biological explanations of disorders. If we only use our knowledge from one group and apply it around the world, this biased perspective might be incorrect. It also shows how cross-cultural replication of studies can reduce cultural bias from distorting our knowledge of biological explanations.	Biological explanation provided in-depth.  Link with cultural bias is made explicit.
Depression probably isn’t caused by biological factors alone. It’s more likely due to a combination of environment plus biology, nature via nurture. This is where the diathesis-stress model is valuable. This model suggests that depression is caused by the combination of stress and existing vulnerabilities (like genetics or serotonin levels).	This paragraph seems tacked on – because it is – ran out of time and oomph. Probably better without this paragraph.
In conclusion, the serotonin and genetic explanations for depression are two biological explanations that are closely related, but these hypotheses might suffer from a number of biases. The original research into monoamines didn’t control for placebo or researcher biases, while the serotonin hypothesis and SSRIs are probably affected by publication bias. Thankfully, cross-cultural studies comparing genetic risks for depression have shown that it’s important to replicate research in different cultures so our knowledge isn’t impacted by Western cultural biases. (732 words)	A detailed conclusion that shows the biological explanations but how and why they might be limited by specific biases.

The Mark

This essay shows the same level of knowledge of the area of study as my previous one. Where it differs is the development of the concept. More examples of biases throughout the essay elevates it to the top mark band. That’s because it better matches phrases in the rubric like “Links between the area of study and the concept are included throughout the response” and “knowledge and understanding of the area of study/concept are fully explained.”

The essay is 200 words longer. This extra detail is all from defining different types of biases and linking them to the topic. Is this that much extra content to cover? I’d hope not for students aiming for a 7. Remember they also need to discuss concepts in Paper 2, both for the practicals and the unseen study. Knowing terms like publication bias and cultural bias will be helpful for these exams.

The Problem?

The above essay includes a lot of quite nuanced and esoteric knowledge about depression. Would most IB Psych students be able to replicate that essay? Probably not. Many would, but not most. I like to make exemplars and templates that nearly every student could adapt if they just work hard enough. So…let me write another example essay since it’s Monday afternoon and I love doing it so much. In my next essay I’ll put my money where my mouth is – I’ve been encouraging teachers to consider using hypothetical research scenarios in their teaching. Let’s put them in an essay and see what happens.