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The assumption that the major types of drug used in psychiatry work by reversing or partially reversing the underlying disease process may be termed the ‘disease-centred’ model of drug action. There is little evidence to support this model, however. An alternative ‘drug-centred’ model states that psychiatric drugs produce a global state characterised by a range of physiological and psychological alterations, which are superimposed on, and interact with, the ‘symptoms’ of mental ‘disorders’ in ways that may or may not be perceived as beneficial.

2.2.1 The disease-centred model

The disease-centred model has been imported from general medicine, where most modern drugs are correctly understood in this way. Although most medical treatments do not reverse the original disease process, they generally act on the physiological processes that produce symptoms, or on specific physiological targets to reduce symptoms via an identified mechanism. Thus, chemotherapeutic agents counteract the abnormal cell division that occurs in cancer, while analgesics act on the physiological processes that produce pain. Some anti-hypertensives (medications for high blood pressure) relax blood vessels by acting on specific receptors to lower blood pressure, even though the cause of the hypertension may be unknown.

The disease-centred model of drug action is closely related to theories that mental health conditions are caused by abnormalities in particular brain chemicals, or a ‘chemical imbalance’. Chemicals that facilitate or inhibit the transmission of nervous impulses with the brain are called ‘neurotransmitters’. Following the observation that psychiatric drugs act on neurotransmitter systems, it started to be proposed that an abnormality in these systems might be the cause of psychiatric disorders. The best-known example of this way of thinking is the dopamine hypothesis of ‘schizophrenia’, which followed from the discovery that early antipsychotics reduce dopamine activity (dopamine is a brain-based neurotransmitter). The idea that depression is caused by a deficiency of the neurotransmitters serotonin or noradrenalin is another example sometimes referred to as the ‘monoamine theory’ of depression (serotonin and noradrenalin are both classified as monoamine-type brain chemicals or neurotransmitters).

Some researchers still support the dopamine hypothesis of ‘schizophrenia’3, and some antipsychotic drugs certainly affect dopamine transmission, although others have only weak effects on dopamine. However, evidence that there are dopamine abnormalities in people with psychosis or ‘schizophrenia’ prior to starting drug treatment is inconsistent.4,5 Few people now accept the idea that depression is caused by a serotonin or noradrenaline abnormality, and again the evidence is highly inconsistent.6

In fact, despite decades of intensive research on all sorts of aspects of biological science including various neurotransmitters, genetics and neural networks, definitive causes of mental health difficulties have not been established. Recently, the former head of the US National Institute of Mental Health admitted that $20 billion of funding for investigating the neuroscience and genetics of mental disorders, had produced no benefit to people suffering from mental health difficulties.7

There is also little evidence that drugs that are meant to have specific effects in certain conditions, according to the disease-centred model, are better than other sorts of drugs.8,9 For example, numerous drugs that are not considered to be antidepressants have been shown to have equivalent effects to antidepressants in people with depression, including anti-anxiety drugs like diazepam (Valium), stimulants and antipsychotics. Antipsychotics are not clearly distinguished from other sedatives in studies of people diagnosed with psychosis or schizophrenia10, and lithium is not superior to other drugs in studies in people diagnosed with acute bipolar or manic states.11 In addition, two studies that attempted to distinguish between the effects of lithium and antipsychotics in people with different diagnoses (bipolar or affective disorder versus non-affective psychosis or schizophrenia) failed to do so.12,13

Even if the mechanisms of mental health difficulties could be identified, however, we would still be uncertain whether or not psychiatric drugs impact symptoms by affecting those mechanisms. This is because to draw this conclusion, we somehow need to discount the effect of the general mental and behavioural alterations that these drugs are known to cause in anyone, regardless of whether or not they have an identified neurochemical abnormality.

The drug-centred model of drug action suggests it is these alterations that are significant.

2.2.2 The drug-centred model

This model highlights that psychiatric drugs can be considered to be ‘psychoactive’ drugs in the sense that they are substances that cross the blood/brain barrier and affect brain functioning. By doing so they produce an altered global state characterised by a range of physiological, psychological and behavioural changes. There is no essential distinction, according to this view, between drugs used for psychiatric treatment and recreational psychoactive drugs like alcohol and cocaine. All psychoactive drugs produce altered physical and mental states that can influence the way people think, feel and act, with different sorts of substances having different sorts of effects. The effects of recreational drugs are experienced as desirable by at least some people, but some drugs produce mental and physical changes that are generally experienced as unpleasant (e.g. antipsychotics and lithium). The drug-centred model suggests that it is these psychoactive properties that explain the changes seen when drugs are given to people with mental health difficulties. Drugs like benzodiazepines and alcohol, for example, reduce arousal and induce a usually pleasant state of calmness and relaxation. This state may be experienced as a relief for someone who is intensely anxious or agitated. But taking a drug like this does not return the individual to ‘normal’, or to their ‘pre-symptom’ state. The drug-induced state is superimposed on the ‘symptoms’ and is found to be preferable, either by the sufferer themselves, or by others.

In psychiatry, an accepted example of a drug-centred treatment is the recognised benefits of alcohol in social anxiety (also referred to as social phobia). Alcohol can help people with social anxiety because a state of mild intoxication is associated with a lessening of social inhibitions. Rather than reversing an underlying biochemical imbalance, alcohol works because it substitutes the alcohol-induced behavioural and emotional state, with its characteristic lessening of inhibitions, for the previous anxious state.

The brain reacts to the presence of a drug in various ways, and often adapts to the drug in ways that counteract the drug’s effects. Therefore, the effects that a drug has when it is first taken may wear off and increasing doses may be required to sustain the initial effects. Sometimes this is referred to as ‘tolerance’. Biological adaptations to the presence of a drug are also responsible for withdrawal symptoms. When a drug that has been taken for some time is stopped, the body’s adaptations are no longer opposed by the presence of the drug and can give rise to unpleasant and debilitating sensations and experiences.

Whereas the disease-centred model assumes that psychiatric drugs help to restore normal brain functioning, the drug-centred model stresses that taking a drug creates an abnormal biological state. Some effects associated with this altered state may be perceived as worthwhile in certain situations. Often however, by distorting normal bodily function, drugs have an adverse impact. They may therefore do more harm than good, particularly in the long term.

Much of the material in this section is a condensed and updated version of material contained in A Straight Talking Introduction to Psychiatric Drugs by Joanna Moncrieff, published by PCCS Books, and used with the publisher’s kind permission.

3. Howes, O.D., McCutcheon, R., Owen, M.J. & Murray, R.M. (2017). The role of genes, stress, and dopamine in the development of schizophrenia. Biological Psychiatry 81(1): 9–20.
4. Kendler, K.S. & Schaffner, K.F. (2011). The dopamine hypothesis of schizophrenia: An historical and philosophical analysis. Philosophy, Psychiatry & Psychology, 18(1), 41–63.
5. Moncrieff, J. (2009). A critique of the dopamine hypothesis of schizophrenia and psychosis. Harvard Review of Psychiatry, 17(3), 214–25.
6. Healy, D. (2015). Serotonin and depression. BMJ. 350:h1771.
7. Henriques, G. (2017). Twenty billion fails to ‘move the needle’ on mental illness Thomas Insel admits to misguided research paradigm on mental illness. Psychology Today, 23 May 2017, https://www.psychologytoday.com/gb/blog/theory-knowledge/201705/twenty-billion-fails-move-the-needle-mental-illness. (Accessed 7 July 2019.)
8. Moncrieff, J. (2008). The myth of the chemical cure: A critique of psychiatric drug treatment. Basingstoke: Palgrave Macmillan.
9. Moncrieff, J. & Cohen, D. (2005). Rethinking models of psychotropic drug action. Psychotherapy and Psychosomatics 74(3), 145–53.
10. Wolkowitz, O.M. & Pickar, D. (1991). Benzodiazepines in the treatment of schizophrenia: A review and reappraisal. The American Journal of Psychiatry 148(6), 714–726.
11. Prien, R.F., Caffey Jr., E.M. & Klett, C.J. (1972). Comparison of lithium carbonate and chlorpromazine in the treatment of mania. Report of the Veterans Administration and National Institute of Mental Health Collaborative Study Group. Archives of General Psychiatry 26(2), 146–153.
12. Braden, W. et al. (1982). Lithium and chlorpromazine in psychotic inpatients. Psychiatry Research 7(1), 69–81.
13. Johnstone, E.C. et al. (1988). The Northwick Park ‘functional’ psychosis study: Diagnosis and treatment response. Lancet 2(8603), 119–125.

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