The Trials and Tribulations of Doing a Systematic Review

Science is incremental, with every study – positive or negative – meant to contribute to a body of knowledge. Reviewing this body of knowledge is a key part of the process, to know what was done before and what still needs to be done. This is done as part of a ‘literature review’; to review the studies on a topic, find out how to advance our understanding, and design studies to address this.

This is what I did at the end of the first year of my PhD. I completed a project proposal which included a narrative literature review on the biopsychosocial factors of how social support affects mental health. Whilst I have technically already reviewed the literature, I’ve decided to re-do it in a ‘systematic’ way to ensure that I included all relevant research and to minimise bias. This is important for a topic that is multidisciplinary and incorporates both social and biological sciences, as different research fields use different terms for ‘social support’, such as ‘social connection’ or ‘social network’. To ensure that the remainder of my PhD research is based on an accurate view of the research that’s been conducted to date, I broadened my search terms and the databases used in my review of the literature.




Narrative reviews don’t always give the full picture of a topic. Often, someone will read a few influential papers in an area and use these as a base for finding other papers. This ultimately results in an echo chamber where the same or similar ideas are communicated. This also affects a person’s judgement of what they expect to find, making it more likely for them to dismiss ideas that do not fit. Although scientists try to be objective, we are ultimately human and are susceptive to our own cognitive biases to try and make sense of the world.

Another problem is publication bias, whereby positive findings tend to be published more than null or negative findings. Surveying the literature may suggest that an effect is robust and replicable, but this may be because the negative findings are buried away and never published, overestimating the likelihood that an effect is true in the world.


Systematic reviews address the pitfalls of standard reviews, which is why they are regarded as the gold standard of evidence. Systematic reviews require the researcher to pre-specify what they will search for, where they will search, how they will determine whether a study is suitable for inclusion in the review, and more. This process reduces the chance that a study will be ignored because it does not fit a particular narrative. This also increases accountability, as all stages of the review are documented, and another person can try to replicate the search if needed.

… But it isn’t as easy as it sounds.



The phrase ‘systematic review’ conjures up ideas of a rigid process of following strict guidelines. In reality, a systematic review has to be tailored to your research question and how much time you have to dedicate to it. Whilst there are excellent guidelines and tools available – such as resources from PRISMA and the Cochrane Collaboration – it takes a while to trawl through what is available to see what fits your project.

Luckily the University of Manchester library has online resources to help with knowing where to start, which provided a solid starting point for my review.


Before you can even think about searching for studies, you have to write a protocol stating what you will do and how you will do it, to prevent you from veering off track. I underestimated how long it would take to write the protocol and how much effort would go into constructing it, but ultimately it protects against questionable methods and biases. This planning also set me up nicely to pre-register my protocol on the online register PROSPERO.


Literature databases are all unique; some contain studies from one research discipline, others contain studies from multiple disciplines. Some databases use quotation marks around phrases, some have limits to the amount of terms you can enter, and almost all have different key terms that are tagged onto each study. The point is, it’s not as simple as copying and pasting your search strategy from one database to another, as you will most likely throw up an error in the process. You need to invest time in learning the intricacies of each database and adapt your terms accordingly.

This was made all the easier by the ‘Searching systematically’ course by the University of Manchester library, which shows how different databases work and gives an example of how to replicate search strategies across databases. I appreciated someone showing me how to navigate different databases step-by-step and helping me solve cryptic error messages that popped up.


When I was planning my review, I had the noble idea of wanting to find every study ever conducted on the topic. Whilst it is possible to find unpublished research, there is a trade-off between finding relevant studies and progressing with your review. You can search obscure journals and conference abstracts all day, but you also have to decide whether it is worth it just to find one potentially relevant study. It may be that you don’t find everything that’s ever been done but that’s okay – as long as you are systematic within your means, as defined by your protocol.



I have now conquered the behemoth of the systematic review protocol and registered this on PROSPERO – hooray! But this is probably just the beginning of the protocol, as it will evolve as the review unfolds and new challenges are presented (with updates being publicly available too, of course).

Systematic reviews are challenging. There is no one-size-fits-all guideline for it. I will probably run into many more problems during the process, but part of doing research is learning by doing and adapting to difficulties. As scientists, we do not have to be perfect, but we have to do the best we can with the resources that are available to us now.


Photo by saeed mhmdi on Unsplash

Photo by AbsolutVision on Pixabay.

Originally published on the Research Hive at


Exercising the Blues

Exercise. The word alone is enough to instil a feeling of dread in a lot of people. I am lucky enough to have gotten into a good exercise routine these last few years, so I don’t mind it. I was introduced to weightlifting from a course at my gym and it’s remained a staple in my exercise routine ever since. Before that, I associated physical activity with repetitive, strenuous cardio that required a lot of effort to get any better at. Lifting weights opened up a different world to me, allowing me to make progress quickly and marvel at how strong I could be. It motivated me to stick to a routine, which is the key part of any exercise regime. 

However, recently I haven’t been able to stick to my routine as well as I wanted to. Injuries coupled with the boredom of solo activity are the main reasons for this, so I’ve decided to try and switch it up and try new things. From trying various things – tennis, netball, high intensity exercises – I realised that I missed the feeling of sweating and breathing hard at the gym. Of course, you still sweat when lifting weights, but it’s a different feeling than the continuous grind of cardio. There is something that is cathartic and physically liberating about it – if I’m having a bad day, going for a run makes me feel a lot better.  

This led me to look at the evidence of how exercise – both aerobic and anaerobic – benefits mental health. Much of the research looks at trials to improve mental health in people with depression, which is what I will focus on. A recent review by Farris and colleagues in 2019 [1] looked at aerobic and anaerobic exercise interventions for improving mood for people with depression. The main points were that both aerobic and anaerobic exercise interventions produced an antidepressant effect compared to no intervention. It was also found that people in the aerobic interventions were just as likely to stick at it compared to non-exercise interventions such as psychotherapy and antidepressants. However, for anaerobic exercise interventions, there is currently not much research into how well people stick to the intervention. So, it appears as though aerobic and anaerobic exercise are equally as good at alleviating mood, with evidence showing that people stick to aerobic exercise regimes. This does not mean that people are not as good at sticking to anaerobic exercise, rather we don’t have the evidence yet to say for sure either way. 

What about the specifics of exercise, such as for how long people exercise for and at what intensity? Longer sessions did not produce a greater antidepressant effect; sessions more than an hour were less effective in alleviating depression. This may be because participants get tired and less motivated with longer sessions which blunts any potential mood improvements. Interestingly, some studies even found that short-term mood relief can be achieved from as little as 5 minutes per day. In terms of the length of the trials, shorter trials (e.g. two months long) were found to have a stronger antidepressant effect than longer trials (e.g. eight months long). This was thought to be due to people getting used to exercise over the weeks and it losing the novelty aspect. Higher intensity training was also better than lower intensity in mood alleviation, but this depended on the mood of the participant; depressed people are less likely to feel good after a hard workout if they weren’t feeling great to begin with.  

One thing that stands out to me from this review is how the effectiveness of an intervention largely depends on a person’s preference and their own individual symptoms. Trials that evaluate exercise interventions mainly focus on exercise as having a purely physical effect – which it does – but a person’s attitude towards exercise and whether they are likely to implement it into their routine seems to be down to other contextual factors. 

As alluded to in the review, whether an intervention is successful depends on the individuals’ symptoms, with factors such as fatigue and lack of motivation in depression being a barrier to entry in starting an exercise program. A person is unlikely to want to do high intensity exercise if they are already feeling low, even if this has been shown to have a strong antidepressant effect. Negative thoughts about exercise could also blunt mood improvements if a person dreads being active or fears being embarrassed. As mentioned by Farris and colleagues, trials which combine cognitive behavioural skills with exercise programs could address these mental barriers. 

But it all counts for nothing if the person doesn’t like the exercise that they are doing, if they are bored of it or feel like it isn’t going anywhere. Study participants are often randomly allocated to exercise groups or control groups. Whilst this is important in showing the effect of the intervention in an unbiased way, if a person is stuck in an aerobic group and they absolutely despise running, it’s unlikely that they are going to get much of it. In a similar vein, these trials often get the participants to do the same exercises over several weeks – 16 weeks of walking or jogging several times a week in the case of Blumenthal and colleagues’ study mentioned in the review [2]. Whilst it is important to establish a routine, this does not have to be monotonous. This may be contributing to why longer trials have a smaller antidepressant effect – perhaps participants are just getting bored of the lack of variation in the exercises that they are doing. Periodically changing the types of interventions could capitalise on the novelty aspect and stronger antidepressant effect of short interventions, whilst encouraging physical activity over the long term. 

For something to become part of your routine, you need to like it enough to do it consistently. For people who already have depression, just starting exercise may be the hardest part. But finding something that fits with the person, which has variation and progression, may help build their self-belief. This coupled together with the obvious physical benefits of exercise could be a powerful way of promoting good mental health. 


  1. Farris, S. G., Abrantes, A. M., Uebelacker, L. A., Weinstock, L. M., & Battle, C. L. (2019). Exercise as a Nonpharmacological Treatment for Depression. Psychiatric Annals49(1), 6-10. 
  2. Blumenthal, J. A., Babyak, M. A., Moore, K. A., Craighead, W. E., Herman, S., Khatri, P., … & Doraiswamy, P. M. (1999). Effects of exercise training on older patients with major depression. Archives of Internal Medicine159(19), 2349-2356. 

The Errors of our Measurement

One of the issues with studying psychology is that we do not have direct access to the contents of people’s minds. Unlike other biological measurements, such as blood pressure, we rarely have ‘objective’ measures of people’s mood and thinking skills that we can get reliable recordings of over several occasions. We often have to make really good guesses based on the questions we ask.

math lady confused
Image from

If you have ever been to your GP about anxiety, you may have been asked questions about how often you have felt ‘nervous, anxious or on edge’ in the last week. This question is trying to measure your level of ‘anxiety’ but, because we cannot directly reach into your mind and pull out your level of anxiety, it is inferred from how you have answered the question. But your answer to the question is not a one-to-one representation of your anxiety. Other factors such as how you are feeling in the moment, how you remember events over the last week or even how you interpret the question can influence what your score is on the questionnaire. These factors are known as measurement error.

This does not mean that it is hopeless to try and measure the concept of anxiety. Often studies factor in what is thought to affect reported levels of anxiety, such as current levels of anxiety. Also, even though the name suggests so, measurement error also does not mean that someone has made an ‘error’ with measurement (although this sometimes can be the case!) It refers to all the unmeasured, sometimes random factors that affect what you are interested in measuring.

I didn’t really think much about measurement error before attending the National Centre for Research Methods (NCRM; masterclass at the University of Manchester last week. Harvey Goldstein, a distinguished Professor of Statistics at the University of Bristol and a speaker at the event, asserts that measurement error is a problem that does not get enough attention in research. If a questionnaire has high measurement error, then we will have less reliability in our findings. Going back to the anxiety example, this means that we will not get a consistent score on the anxiety scale, even if levels of anxiety remain the same. Therefore, it is important to model and make adjustments for a test’s reliability, which is often not done in research.

Goldstein provides a cautionary tale to illustrate this point. A paper by Feinstein (2003) analysed test scores and socio-economic status (SES) for children between the ages of 2 and 6. The results suggested that children who were grouped into the “high educational ability but low SES” at age 2 scored worse than the “low ability but high SES” children at age 6. This suggests that deprivation and inequality blunt educational achievement, even when the child was capable to begin with. Goldstein mentioned that this study was presented to Parliament to illustrate the damaging effects of poverty on educational achievement, revealing the powerful impact that studies can have to shape policy.

Feinstein 2003
Graph from Feinstein (2003)

Needless to say, the study was flawed. There was no consideration of the reliability of the ability test at age 2, which provides the baseline for the follow-up analysis. Therefore, we cannot determine how much of the score was due to the child’s ability and how much was due to measurement error. Goldstein and French (2015) addressed these issues in a follow-up paper by comparing scores across time and by factoring in reliability estimates. They found that high SES children scored better than low SES children across time, but the estimates were less dramatic than what was found by Feinstein (2003) depending on what reliability criteria were used. The implications were not completely refuted; SES is still important in educational ability, but it is less clear whether low SES can hinder a child’s future progress. The latter point was probably what got it noticed by Parliament in the first place but it may not be reflective of reality, which is what we want our policies to be based on.

Goldstein’s words after presenting this ‘cautionary tale’ resonated with me: “If you are using quantitative methods in your research, you are ethically bound to use best practice. You shouldn’t play with tools without understanding them.” I might write this on a post-it and stick it on my screen, so I am reminded of it whenever I am working on my PhD.



Feinstein, L. (2003). Inequality in the early cognitive development of British children in the 1970 cohort. Economica70(277), 73-97.

Goldstein, H. & French, R., Differential educational progress and measurement error. In Feinstein, L., Jerrim, J. & Vignoles, A., Goldstein, H. & French, R., Washbrook, E. & Lee, R. & Lupton, R. (2015). Social class differences in early cognitive development debate. Longitudinal and Life Course Studies, 6, 331-376.

Social Networks and Brain Networks

I have three brothers and two sisters. “Wasn’t it strange, growing up with so many siblings?” I’m often asked. Not at all – it was normal for me and we all got along well! I have fond memories of us growing up together; playing rounders and dodgeball outside, watching my brothers play video games, starting a pop group with my sister (called the Twosome Two).  

Throughout my life, my family has been a strong source of support for me. Being part of my family feels like I am part of a club with exclusive rewards. Obviously, it’s the same for other people in their family, but I feel like this is amplified for me due to the size of my immediate family network. We give each other both practical and emotional support – money, advice, consolation, sharing in each other’s achievements. We all want each other to do well in life, so we will help in whatever way we can. 

Unsurprisingly, social support is a strong predictor of psychological wellbeing [1]. As social animals, being part of a group and engaging in reciprocity is pivotal to surviving and thriving. Social groups give us access to resources that we wouldn’t otherwise have and provide emotional support during difficult times; a concept known as social capital [2]Those with more social connections have been found to live longer, have better mental health and are more resistant to illness and disease [3]But how can social connections ‘get under the skin’ to affect health? The mediating factor may be the role of the brain. 

According to a review by Eisenberger (2013), the benefits of receiving support works on two systems in the brain: by activating neural regions relating to safety and attenuating regions related to threat [3]. In other words, social support works by making us feel safe and buffering us against stress.  

The safety network is housed in the ventromedial prefrontal cortex (VMPFC) and the posterior cingulate cortex (PCC). These regions are involved in processing reward and actively inhibiting activity in threat-related regions. Essentially, the VMPFC is the “phew” centre of the brain, creating feelings of relief after a period of stress. 

Conversely, the threat reduction network contains the amygdala, dorsal anterior cingulate cortex (dACC), anterior insula (AI) and periaqueductal gray (PAG). These regions are involved in processing threat and pain. As mentioned before, the VMPFC actively reduces activity in these areas in response to social support, reducing threat and fear. 

Experimental studies, where people are provided with social support during a social exclusion task, have found increased activity in the VMPFC and PCC, and decreases in activity such as the amygdala and insula (for the specific studies, see reference 3)This is true even when people are just shown pictures of loved ones; highlighting that the representation and perception of a relationship with a support figure is enough to elicit this salutary activity. 

Interestingly, studies where people report their general levels of social support only tend to find support for attenuation in threat-related areas in stressful tasks, not the safety activity. It may be that the top-down VMPFC activity only becomes online when a specific person is envisioned or a person is actively present in a situation, compared to reporting general feelings of social support. The latter of which may be influenced by other cognitive, personality or emotional factors. For example, people who have more symptoms of depression may erroneously perceive a lack of social support in their lives due to a clouded view of the world. It may also be more related to a person’s attachment style, which is thought to be shaped in early childhood. Probing the exact conditions for activation of these hypothesised social support networks is a next step for future research.  

Additionally, the nature of social support is changing with the advent of social media, with online communication replacing much of the physical contact that we have with people in our daily lives. This provides huge benefits, such as being able to contact loved ones who are far away almost instantaneously. But it is still unclear whether virtual support provides the same benefits of physically interacting with someone, and whether it affects the same neural systems mentioned earlier. Thus, another avenue for investigation could be the importance of a physical presence of social support compared to virtual support in the differences in outcomes for safety-related VMPFC activity. 

Ultimately, changes to our social landscape are inevitable and largely welcomed. However, it is important for us to understand the neural mechanisms of social connections, so that the benefits of social connections can prevail with the advancing times. 

  1. Portela, M., Neira, I., & del Mar Salinas-Jiménez, M. (2013). Social capital and subjective wellbeing in Europe: A new approach on social capital. Social Indicators Research114(2), 493-511.  
  2. Kawachi, I., & Berkman, L. (2014). Social cohesion, social capital and health. In: Berkman, L., & Kawachi I. (eds). Social Epidemiology (pp. 174-90) Oxford: Oxford University Press. 
  3. Eisenberger, N. I. (2013). An empirical review of the neural underpinnings of receiving and giving social support: implications for health. Psychosomatic Medicine75(6), 545-556. doi  

Nurturing our Nature

Learning about behavioural genetics through Robert Plomin’s book Blueprint (1) has transformed my thinking about psychology and the brain.

The fact that most psychological factors show between 30-50% heritability – with no factors at all showing a lack of heritability – has shown that our genetic blueprint plays a major role in shaping our personalities, cognitive abilities and risk or resilience to psychopathology. A misconception I previously had was what was actually meant by heritability. For example, weight has been found to have a heritability of 70%. This does not mean that for any given person 70% of their weight is determined by genetics. Rather, the individual differences in weight between individuals in a particular population (mostly Western populations) at a particular time (in the last few decades) are governed by genetics. This also does not mean that we are slaves to our genetics; heritability describes what is but not does not say anything about what could be.

In both psychology research and everyday thinking, the environment is heralded as the main driver in shaping who we are. For example, in a podcast I was listening to this morning, the hosts were talking about how men who learned wrestling when they were younger had more ‘toughness’ when fighting in mixed martial arts (MMA) tournaments compared to other men who did not. They attribute this to the taxing and gruelling nature of wrestling in shaping their approach to fighting in the current day. But it may be that their ‘tough’ personalities attracted them to wrestling when they were young, and it’s those same personality traits that make them unrelenting in the ring.

This is related to another main point in Plomin’s Blueprint that I was not expecting: measures of the environment show genetic influence. Rather than a person being a passive sponge to experiences, people amplify the aspects of the environment that are aligned with their genetic blueprint and diminish parts that are not. Tough people are attracted to tough sports, more so than tough sports shaping someone to be tough.

This is my understanding of it: we are all born with a genetic blueprint which defines aspects such as our temperament, preferences and character. This blueprint is translated to the brain to execute this template. We are then placed in environments which give myriad ways to fulfil our preferences in line with our temperament and character. In different environments this could look different depending on the resources available and it could be executed to varying degrees.

It is also important to note that building our environment would only be possible for events which are controllable. Uncontrollable events – such as an unexpected death of a family member – would also have a profound impact on us, so we cannot just rule them out. The point is that, in terms of trying to change who we are, we can only focus on our genetics and experiences which are controllable. This is relevant to designing interventions for behaviour change or attenuating risk for psychopathology.

There has been a big drive to personalise medicine to improve outcomes. If we know the genetic pulls for people, we can use this to design interventions and engineer the environment specific to the person to maximise chances of success. Now that it is easier to collect and analyse genetic data in large scale studies – such as those part of CLOSER (2) – perhaps this reality is closer than we realise.


Brains and Navigation in Games

Whenever you learn something new or practice a skill, your brain changes too. People don’t realise that the same is true with playing video games.

Video games are a training ground; full of motivational pulls to navigate worlds, solve puzzles, form strategies, react quickly, empathise with characters, and plan to beat bosses. Depending on the type of game, we can use our memory, attention and problem-solving skills to win. Using these skills shapes our brain so that it becomes more proficient and efficient in these skills. It’s an area with a great amount of potential – especially because video games are so engaging – but we still know little about the specific brain changes that occur with prolonged video game play.

A study by West and colleagues in 2017 (1) sought to investigate how navigation strategies used in video games affect the structure of a brain region called the hippocampus.

The hippocampus (from the Greek for ‘seahorse’, because it looks like a seahorse) is an area that is often implicated in memory. You may have heard that it is one of the areas that is affected in Alzheimer’s disease (2).


Proof that the hippocampus looks like a seahorse. From Wikipedia Commons.

It also plays a central role in spatial navigation – knowing how to get from one place to another. If you have heard of the hippocampus before, you have perhaps heard of the London taxi driver study (3), which found that London taxi drivers have an enlarged hippocampus, which is related to the vast amount of spatial information they need to remember to transport their passengers.

West and colleagues found something similar but with two differences: hippocampal volume change was found when navigating a virtual environment (via video games) and the differences in hippocampal grey matter gains depended on the type of spatial navigation strategy used.

We have two main navigation systems that are represented in our brain. The first one is spatial and relies on learning the relationship between landmarks in an environment, which is housed in the hippocampus. The other is a response learning strategy that involves memorising actions from a starting point, which is governed by the caudate nucleus.

Here’s an easier way to think about it: say you wanted to go to the hospital from your house. A spatial strategy (using the hippocampus) would navigate using the landmarks on the way – go north to the post office then turn right until you get to the shoe shop, turn left and keep on going until the hospital is on the right. A response learning strategy would just use directions – go north two blocks, right two blocks, left five blocks then the hospital is on the right.

> Hospital
Post office ^
^ > > Shoe shop

Spatial navigation strategy

> Hospital
^ > >

Response-learning strategy

Both systems are useful and necessary to navigate the world. But the two brain regions underpinning these navigation strategies have an inverse relationship to each other; that means that an increase in structure or activity in one leads to a decrease in the other. Over-relying on one navigation system could cause the other one to shrink, which could have repercussions for other thinking and emotional skills that these regions are implicated in. One potential finding is that decreased hippocampal grey matter (a structural part of the brain composed of neuron bodies) has been implicated in the development of psychiatric disorders such as depression (3). The implication is that if you use over-use response-learning navigation strategies, your hippocampus may shrink, which could put you at risk for cognitive or mental health difficulties.

This is where West and colleagues’ study comes in. One of the experiments in the paper trained participants in a lab for 90 hours (over an average of 59 days) on either an action video game (which encourages the use of response-learning strategies) or a 3D platform video game (which encourages spatial strategies). Just focusing on the hippocampus, it was found that the action video game group had significantly decreased grey matter in the right hippocampus compared to the 3D-platform group. On the other hand, the 3D-platform group had increased grey matter in the left hippocampus compared to the action video game group.

Before training, participants were tested on a separate task to see whether they spontaneously prefer response-learning or spatial navigation strategies. It was found that, in the action video game group, people who preferred spatial strategies had an increased volume in the hippocampus after training compared to those who preferred response-learning strategies.

These findings suggest that the nature of the video game and the preferred navigation system interact to alter the structure of the brain in as little as two months. Findings like this may cause concern for people who enjoy action video games, but it’s not just playing action video games that will cause your brain to shrink. Action video games may encourage use of one navigation strategy but ultimately it depends on whether the person will use that strategy when playing the game.

First, I want to emphasise how well-designed this study is. Usually research into the effect of video games is correlational. Information at one time point on video game playing habits, measures of thinking and emotional skills and brain imaging is collected and related to each other. But in order to show that video game playing causes changes in thinking/emotional skills and the brain, we need to track this over time and carefully match who is playing games, what they are playing and how much they are playing it. With this study, the participants in each group were similar, randomly assigned to each group and played the game for roughly the same amount of time. From this, we can see that the changes in the brain are due to the type of game that they were playing.

One area that I am sceptical of that needs further research is whether the hippocampal changes associated with action video game play lead to cognitive and emotional difficulties. The researchers did not measure cognitive ability or psychiatric symptoms before or after video game play, so even though they assert that it may cause these types of difficulties, there is a lack of evidence whether it will. The action video game group had decreased grey matter in the right hippocampus but a meta-analysis (a large analysis combining results from many studies) found that people with depression have a reduced amount of grey matter in the left hippocampus (3). Regional grey matter changes provide a general view but the fine-level changes may be what is important here to relate it to cognition and emotion.

There is also a practical question of what this means for the design of video games. Many people play action video games worldwide, such as Call of Duty which was used in the current study. If response-learning strategies have a negative effect on brain structure, the navigation strategies in-game may need to be adapted to encourage use of spatial strategies. This could be achieved by removing the mini-map or by designing maps that change regularly. Of course, this will be met with contention in the gaming community, as many players rely on knowing a map well in order to git gud. Either way, if these findings are replicated in future studies and are shown to have effects on how we think and feel, there needs to be a conversation on how to address this.


Brains in a Space: Mental Health

Not a day goes by where I don’t see someone mentioning mental health on social media. Then again, my sample is pretty biased – being a PhD student who is interested in mental health, with friends and colleagues who are in the same field – but it’s welcome nonetheless. Most days when I’m perusing my Facebook timeline, I see someone openly talking about their struggles with anxiety or I read an article advising how to help someone who has depression. It’s not weird to talk about your mental health anymore, which helps us all to connect and to create the culture of openness that will encourage others to do the same. One in six people in England report mental health difficulties in a given week (1). It’s a scary thing to deal with alone.

The problem I have is with people treating mental health difficulties as solely the result of biological processes, whether it be due to factors such as a genetic predisposition (2), a disruption in serotonin (3) or dysregulation of neural activity associated with emotional regulation (4). Although these play a part, our lives are too rich to be reduced to only these factors.

We are brains existing in a physical world, so mental health difficulties do have a biological basis, similar to other psychological processes such as learning or reasoning. I understand that people are trying to ‘legitimise’ mental health difficulties such as depression as a problem on par with other physical illnesses, such as heart disease or a fracture (see Robot Hugs’ comic for a commentary on this – 5). And it’s true that the structure and function of the brain can change following multiple episodes of depression (6). To some people, focusing on the biological basis of mental health difficulties may be empowering, as they are able to show to people that it isn’t just “all in their head” and that there is a physical basis for it.

But this leaves out a multitude of reasons why someone could be depressed, for example: family or work issues, a negative self-image, living life that does not align with one’s values or even small stressors that have built up over months. If someone simply treats their depression as a purely physical illness, it may be that they are less likely to tackle aspects of their lives which are perpetuating their distress. There are practical things a person with depression can do to alleviate their symptoms. But if we focus purely on the neurochemical side of it, they may feel that they are at the mercy of their biology, which can only be corrected with medication.

On the flip side, there are people who declare that a person does not “deserve” to be depressed based on their privileged life. A few weeks ago I came across a Twitter post that presented the following:

@renoomokri Sep 24
“Are you depressed? Ask yourself these questions:
* Do you have a home?
* Do you have food?
* Are you healthy?
* Do you have family?

It people who dont have these can be happy, then what reason do you have to be depressed? You are more blessed than half of humanity #RenosNuggets”
(* The tweet has since been removed from the account, but I do have a screenshot I could upload if anyone is interested.)

A person may have a seemingly perfect life – food, shelter, family – but they may have suffered a painful and traumatic event, or they may have a toxic relationship with their family and have no social support. Sometimes people may not know the reason themselves – they may just realise that something is not right; their life feels meaningless because the needs important to them aren’t being met. People’s reasons for depression vary greatly. Comparing and shaming people for their depression does no good and a whole lot of harm. There is evidence that the act of gratitude can help people who are feeling depressed and can increase social support (7), but the nature of the gratitude would be for the person to figure out for themselves, not thrust upon them through shame.

My point is that strictly prescribing to either ends of the nature or nurture debate is unhelpful in learning about a person as a whole. On one particular day, a person may be more sensitive to stressors or negative events. But that does not mean that they will definitely feel low, as that depends on the environment that day and how they conceptualise and interact with it. It’s not a one-way street – our social environment, thoughts, feelings and brain all interact both ways. Our brains can change according to experience, a phenomenon known as neuroplasticity (8).

Mental health clinicians often utilise the bio-psycho-social approach (integrating biological, psychological and social factors) to understanding and treating mental health difficulties and I believe the public discourse should adopt the same framework. It’s all about putting the whole person back into the focus of mental health difficulties. We are our brains, but in our day-to-day lives we live in a social and cognitive context where we can make choices. This may be more difficult for some people whose base level of mood is highly variable, but ultimately there is always something a person can do to help themselves. Sometimes it may only help a little or it may only help sometimes, but it’s better to do something. And it’s a better way to live than to do nothing.


Views and comments are encouraged and welcomed!