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Unravelling the Inflammation Hypothesis

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Most people feel down, tired and inactive when they鈥檙e injured or ill. This 鈥渟ickness behaviour鈥� is caused by the activation of the body鈥檚 immune response. It鈥檚 the brain鈥檚 way of conserving energy so the body can heal.

This immune response can also occur in people with depression. This has prompted some researchers and clinicians to hypothesise that depression is actually a side effect of the inflammatory process.

But while there may be a connection between inflammation and depression, one doesn鈥檛 necessarily lead to the other. So it鈥檚 too simplistic to say depression is a physical, rather than a psychiatric, illness.

The inflammation hypothesis

University of California clinical psychologist and researcher is one of the key recent proponents of depression as a physical illness. He hypothesises that social threats and adversity trigger the production of pro-inflammatory 鈥渃ytokines鈥�. These are messenger molecules of the immune system that play a critical role in orchestrating the host鈥檚 response to injury and infection.

This inflammatory process, Slavich argues, can initiate profound behavioural changes, including the induction of depression.

The idea that the activation of the immune response may trigger depression in some people is by no means a new one. Early descriptions of post-influenza depression appeared in the 19th century in the writings of English physician Daniel Tuke.

But it was not until the , published by veterinarian Benjamin Hart, that the phenomenon of acute 鈥渟ickness behaviour鈥� caught the interest of the scientific community.

Hart described his detailed observations of the 鈥渂ehaviour of sick animals鈥�. During acute infection, and in response to fever, the animals sought sleep, lost their appetite, showed a reduction in activity, grooming and social interactions, as well as showing signs of 鈥渄epression鈥�.

Just like the immune response itself, these changes reflect an evolved survival strategy that shifts priorities toward energy conservation and recovery.

Putting the theory into practice

Cytokine-induced sickness behaviour has subsequently been as an example of communication between the immune system and the brain.

The behavioural changes during sickness resemble those associated with depression, so it didn鈥檛 take long for between the phenomenon of sickness behaviour and mental disorders.

Such speculation was strengthened by that depressive states can be experimentally induced by administering cytokines and other immunogenic agents (such as vaccines) that cause an inflammatory response.

Depression is frequently associated with inflammatory illnesses such as heart disease and rheumatoid arthritis. It鈥檚 also a of treatment with cytokines to enhance the immune system.

Over recent decades, researchers have made progress in understanding how inflammation may impact on the activity of signalling pathways to and from the brain, as well as on the involved in mood regulation.

But there鈥檚 not always a link

From the available evidence it鈥檚 clear, however, that not everyone who suffers from depression has evidence of inflammation. And not all people with high levels of inflammation develop depression.

Trajectories of depression depend on a complex interplay of a spectrum of additional risk and resilience factors, which may be present to varying degrees and in a different combination in any individual at different times. These factors include the person鈥檚:

• 
  affecting the intensity of our inflammatory response


• other medical conditions


• acquired hyper-vigilance in the stress response systems due to early life trauma, current adversities, or physical stressors


• coping strategies, including social support


• health behaviours, such as sleep, diet and exercise.

Implications for treatment

In line with the notion that inflammation drives depression, some researchers have the effectiveness of anti-inflammatory therapy as a treatment for depression.

While some recipients (such as those with high levels of inflammation) showed benefit from the treatment, others without increased inflammation did not. This supports the general hypothesis.

However, in our desire to find more effective treatments for depression, we should not forget that the immune response, including inflammation, has a specific purpose. It protects us from infection, disease and injury.

Cytokines act at many different levels, and often in subtle ways, to fulfil their numerous roles in the orchestration of the immune response. Undermining their vital role could have negative consequences.

Mind versus body

The recent enthusiasm to embrace inflammation as the major culprit in psychiatric conditions ignores the reality that 鈥渄epression鈥� is not a single condition. Some depressive states, such as melancholia, are diseases; some are reactions to the environment; some are existential; and some normal.

Such separate states have differing contributions of biological, social and psychological causes. So any attempt to invoke a single all-explanatory 鈥渃ause鈥� should be rejected. Where living organisms are concerned it is almost never that simple.

In the end, we cannot escape the reality that changes must occur at the level of the brain, in regions responsible for mood regulation, for 鈥渄epression鈥� to be experienced.

is Associate Professor, School of Psychiatry at .
is Scientia Professor at .

This article was originally published on .
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