Finding the neuro-social city

Kwame McKenzie, Professor of Psychiatry, University of Toronto CEO, Wellesley Institute

The Neurosocial City

Fitzgerald and Rose (2015) have eloquently outlined the need for the concept of the neuro-social city. As new biological mechanisms are discovered and bold claims are made about their ability to help us understand how adversity gets under the skin we are in desperate need of a truly interdisciplinary approach if we are to move forwards. Here, I will discuss three questions, where is the neuro-social city, what is the neuro-social city and are there any other things we need to know about it relation to the causes of mental illness?

But, first I should explain my approach to the causation of illness. I use multi-level theory (Susser and Susser 1996). One metaphor for this is the concept of Russian dolls or Matryoshkas. In that design paradigm there is an object within a similar object. Applying this to causation, each doll represents a different biological or social level. For instance; the centre doll could be molecular theory, the next doll up may be cellular theory, the next level up the organ and then through progressively larger fields of study to the individual, and again through a number of levels to the city. Each level has its own science; it would be difficult to try to understand the molecular level using Freudian theory. The degree to which one level can predict cause or risk is bounded by the next level up. Different levels interact. (Susser and Susser 1996, Shah et al 2011)

I believe that ordering and understanding how sciences at each level fit together is essential if we are to make progress on causation. If we want to move forwards our knowledge needs to be at least the sum, if not more than the sum, of the different scientific parts.

Though researcher often stay within a specific scientific paradigm, the need is to understand how different levels of causation inter-relate and interact.

Where is the neuro-social city?

The neuro-social city lies in the space between individual and environmental levels of risk and causation. In Fitzgerald and Rose’s position paper (2015) the individual is a complex amalgamation of biological and psychological processes. The individual spans a number of level from the cell to the person. These levels will be characterised in different ways and to different extents by different philosophical and scientific approaches to sciences and understanding. There will be varied levels of sophistication and accuracy. The environment is also complex. The city is a material, geographical, psychological, interpersonal, cultural, perceptual and political space that we are still aiming to understand (Brenner and Schmid 2015). In some ways, both the city are illusions. We can see them, we experience them, we think we know what they are, but when we try to describe them, they seem to become conceptual.

What is the neuro-social city?

The neuro-social city is a commons which may enable different sciences to communicate.   It attempts to describe the processes through which the individual and the city interact. These processes or mechanisms may be neurological, may be linked to an individual’s non brain based biology, but are likely, at least in part, to be psychological in nature. Some of the toxins and pollutants found in cities may be linked to changes in anxiety and depression themselves. But if stress is considered an important factor in the impact of the city on the individual, then perception becomes important.

What more do we need to know?

The neuro-social city aims to build a bridge between two points which are ill defined. We do not know how sure the ground is at either side. But a further issue is we need to consider is how the neuro-social city deals with the issue of time. An expansion of multi-level theory argues that time is important but neglected factor in understanding causation. Time may be thought of as different chronologies of vulnerability, for instance the differing impact of exposure to risks in childhood compared to adulthood. It could be the time of exposure needed to cause a problem. It could be a latency period between exposure and developing an illness. It could be the differing chronologies or different processes at different levels that need to line up to lead to illness. It could be history. We usually ignore time, though your history is one of the better predictors of your future. (Shah et al 2011).

It is unclear how the neuro-social city can deal with the problem of psychiatric diagnoses. Fitzgerald and Rose’s task is made more difficult by the choice of using mental illness as the pathology to investigate. Mental illness by definition is faulty environmental adaptation (van os et al 2010). Not all of the brain interacts with the social environment. For ease I will call the part that does, the mind. The mind’s job is to optimise our ability to live in the world. The mind starts to develop when we are in utero and keeps developing through our life. It adapts to what our environment throws at it. If this adaptation is ineffective, either by causing psychological distress or through problems in functioning we may say we have a mental health problem. But whether adaptation is called a mental health problem, and whether adaptation has to be aberrant for it to be so labeled, is culturally determined. Mental illness is a cognitive adaptation to an environmental stressor which is then perceived and adjudicated on by a group of people who have gone through similar adaptive processes. Whether the cognitive adaptation has to have a brain substrate is not known and whether the processes by which any physical adaptation takes place – such as neurogenesis, neuroplasticity or epigenetics, offer us useful information on the nature of the disorder is not clear.

Mental illnesses are concepts that are slowly being refined. They are theories linked to data. Our current diagnostic schemes are problematic. The National Institutes of Mental Health in the US has launched a major scheme which tries to rebuild our diagnostic systems based on research data. They are looking at dimensional as opposed to categorical diagnoses. They think that the American Psychiatric Association’s Diagnostic Statistical Manual (DSM5) is flawed. They also do not think that our diagnoses have clear brain pathology to back them (NIMH 2015).

In summary, the neuro-social city aims to link two contested concepts by ill-defined mechanisms to help us understand a difficult to describe group of conditions. As such the neuro-social city is a bridge from somewhere to somewhere else in order to understand something – but none of this is well defined. This may sound vague and flippant, but it is not a criticism. It is a reflection of the state of the different disciplines that inhabit the space. Yes, we are increasing our knowledge about the city and about the individual level causes of mental illness. But we are starting from a very low base and we are a long way behind other disciplines. And, of course, more is not always better. If it is not intentional, action does not always lead to progress. Instead of aiming to find false solace in the minutia of their science researchers may do better by mapping out the territory and plotting a course that will move us forwards. Asking fundamental questions and using the answers to develop a more comprehensive understanding of causation may make academic pursuits less academic. As a clinician, policy maker and researcher, I wonder sometimes if we are learning more and more about less and less. I wonder if bold efforts to try to outline the architecture of causation may move us forwards quicker. I believe that the neuro-social city offers us a lens that we can use to make faster progress.

If your identical twin develops schizophrenia, you will have a 50-50 chance of developing it yourself. Some biologists will claim this proves the genetic basis of the disease, some social scientists will say it demonstrates the importance of the environment. Neither is anywhere near understanding schizophrenia well enough to convince a Government to launch a prevention strategy. But what if biology and the social environment worked together? Could we better understand the biggest risk factor for schizophrenia – urban birth and residence (Van os et al 2010). If the neuro-social city can help us with that, it is a fabulous addition.

 

References

Brenner M , Schmid C.,Seeking ‘a new epistemology of the urban.’ City April 2015: http://www.tandfonline.com/doi/pdf/10.1080/13604813.2015.1014712 ]

Fitzgerald and Rose 2015…

National Institutes of Mental Health   Research Domain Criteria accessed at http://www.nimh.nih.gov/research-priorities/rdoc/index.shtml on July 23

Shah J, Mizrahi R, McKenzie K. The four dimensions: a model for the social aetiology of psychosis. Br J Psychiatry. 2011 Jul;199:11-4.

Susser M1Susser E. Choosing a future for epidemiology: II. From black box to Chinese boxes and eco-epidemiology. Am J Public Health. 1996 May;86(5):674-7.

Van os, j, Kenis G, Rutten B The environment and schizophrenia Nature 2010 468, 203–212

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