1) The Biochemistry Of Depression
The amine hypothesis is still our starting point for understanding the biology of depression. The idea is that depression is the consequence of imbalances in the key neurotransmitters, noradrenaline and serotonin. It’s an idea that has been around for the best part of half a century and one which is easy to challenge. Antidepressant drugs address the availability of serotonin as soon as people start taking them but the symptoms of depression take rather longer to disappear. There must be more to depression than lack of serotonin. The question then is why this myth has persisted. Part of the answer may lie in the way in which drugs are marketed. This article however suggests that the myth has survived because it is convenient for both patients and doctors to believe it.
It’s in patients’ interest to believe that they have an illness like any other which can be treated with pills. I’m reminded here of how the former pastor of the church my wife goes to spoke about his depression in this way. It’s easier to deal with it as a simple illness than admit that it was in part brought about by a complex mix of factors: faith, hierarchy, support need. It’s also in doctor’s interests for patients to believe this in order for them to comply with medication which has been shown to do them at least a bit of good. The problem, however, with believing myths is that reality eventually intervenes.
A second link which deals with the biology of depression is here.
A standard claim when we study biological therapies is that antidepressants are not narcotics. They do not produce some sort of high in brains which are functioning normally but they can address imbalances in brains which are not working well. This article is important because it challenges this idea. It suggests that in some people without depression, about 25% of the sample, antidepressants had a positive effect. This is important because the researchers claim to know which part of the brain is being affected in these people. The difficulty is to understand why the other 75% of participants were unaffected in this way.
2) Rewards And The Adolescent Brain
When we look at age as a risk factor in addictive behaviour, we look at the claim that adolescents are bad at dealing with risk because the part of their brain which deals with inhibiting risk is not fully developed. This piece of research goes further.
It suggests that the problem isn’t in the bit which inhibits behaviour but instead in the bit which experiences reward. Adolescents simply experience the pleasure of reward or success for longer than adults and are less likely to give rewarding behaviour up.
3) Publishing Negative Findings
When we look at the way in which research is published and validated in PSYA4, we adopt the traditional approach. Research which has statistically significant results gets peer reviewed and published, enabling science to move on. This way of doing things is being increasingly questioned because it leads to the file drawer problem where research which challenges published findings by suggesting that they cannot be replicated gets put away and forgotten about. There is a move towards open access publishing where everything gets published whether significant or insignificant, positive or negative. We tried something like this with our studies into attitudes to mental health late last year at DHSG. There are however problems with this approach too. This article suggests some ways forward.
4) Amnesia – The Reality
Cases of amnesia interest psychologists studying the structure of memory. They seem important because they tell us how memory works and what it is for. They are also human stories. Here is one such story.
The fascination with these is what is left after catastrophic memory loss. In common with other such cases, John in this story knows who his family is and retains a high level skill, playing chess. It’s what is lost which is both difficult and sad.
5) Using Mobile Technology To Promote Well Being
In psychological therapies for depression, we look at the impact of online therapies as treatments for depression. At a simpler level, mobile technology can be used to help people stay well and adhere to their medication.
Here’s a link explaining how this works. The same principle applies to adherence to diets. We saw in last week’s post that some researchers claim that it doesn’t matter too much what diet you are on as long as you can stick to it. Apps are being developed which encourage people to stick to a diet.
The evidence so far is that this technology improves adherence to a diet. In this study, the control groups did not lose significantly less weight. However, these control groups had access to nutritional counselling. This suggests that apps work as well as face to face counselling but they are much cheaper.
6) Critically evaluate
Much of what we do in A Level Psychology. We evaluate core research in order to work out what the problems are and often look at how contemporary research addresses these problems and moves the field on. The exam moves us away from generic evaluation points which do not relate to the specific topic and studies in which we are engaged.
In this article, Tom Stafford identifies three levels of criticism of psychological research. I think we generally get beyond level 1 but level 3 is mostly beyond us at A Level. That’s what undergraduate Psychology is for.
7) Mental Health – The Global Dimension
Most of what we do in our A Level course is done from the perspective of Psychology based in affluent, western society. Mental health represents a substantial global disease burden. The video on this website powerfully challenges us to think about what we might do about it.