Understanding depression and anxiety
Understanding depression and anxiety

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Understanding depression and anxiety

6  Genes and environment: bringing it all together

Earlier in this OpenLearn course you saw that heritability values suggest that genetic and environmental factors both affect whether people develop mental disorders. Identical twins share the same genes, but if one identical twin develops schizophrenia, there is just a 50–70% chance of the other one developing it too. This suggests a role for the environment in determining behaviour. On the other hand, it is also clear that experiences, or environment, alone cannot explain the aetiology of disorders. For instance, stressful or traumatic events can trigger clinical depression. But not all people who suffer such events become seriously depressed.

Thus, how an individual looks and behaves, including whether or not they have a mental disorder (their phenotype), is the product of an interaction between their inherited genetic make-up (their genotype) and environmental factors. Increasingly, psychologists are coming round to the idea, well-established amongst developmental biologists since the 1950s, that there is no question of it being ‘nature versus nurture’ – nature (our genotype) is in intimate interaction at all levels with nurture (our environment) to produce us (our phenotype) (See Box 2).

By environment we mean all the things outside our genes that can interact with them. This could be the environment of the cell in which the gene resides; it could be the environment in your mother’s womb, where you could hear her heartbeat, and where chemicals from her blood passed into your blood. It could be the way in which you were treated as a baby, or the infections that you caught and the kind of food that you ate.

You might be wondering how such things could possibly interact with our genes, which are safely enclosed in the cells in our bodies. This is a very good question. In some cases, there is data to suggest that gene–environment interactions may be important, but it is not yet known how any effects are actually brought about. In other cases, an understanding of what may be happening in gene–environment interactions at the molecular level is beginning to emerge, though the picture is still far from complete. We consider some studies that are shedding light in this very important and exciting area in Box 2.

Box 2  Nature–nurture, diathesis–stress, gene–environment: what’s the difference?

The short answer is that there is none. All these ideas or formulations address the same issue, the interaction between some kind of ‘predisposition’ – represented by nature, the diathesis (which is often seen as a pre-existing vulnerability), or a gene, and something outside the predisposition that interacts with it – represented, respectively, by nurture, a stressful environment or stressor, and the environment. Is it useful to have three different models of much the same thing? Quite possibly, the idea of nature – nurture is rather vague and bucolic, and while it might be good for arguments in the pub, it does not allow much precision in the discussion.

The greatest precision is allowed by the gene–environment model – there is no question here about what ‘nature’ might be. It is the activity of a gene. However, this precision itself could be a limitation in some respects, as becomes clearer when we consider the diathesis–stress formulation (Nemeroff, 1998). In essence this is a model that postulates interaction between biological factors and environmental factors. The term ‘diathesis’ is used to mean an inborn, genetic vulnerability or a predisposition to a particular disorder. The model assumes that exposure to a stressful environment can trigger behavioural disorder in an individual who is vulnerable, while individuals who are not vulnerable may experience similar stressors and not succumb. It allows some precision; however, it appears that the usage has evolved to allow changes in the phenotype – for instance, due to early animal handling or child abuse – to become diatheses themselves. Thus ‘neuroticism’ could be seen as a diathesis for the development of emotional disorders – although neuroticism itself may be a product of gene–environment interactions and hence a phenotype. As you will by now have realised, it is not easy to draw clear lines in this area!


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