It's well-known that exposure to psychological trauma (childhood/early life adversity, exposure to violence or assault, combat exposure, accidents, or natural disasters) can increase the risk of developing certain chronic physiological medical conditions (IBS, fibromyalgia, vascular disease, chronic pain, and cancer, among others).

Clinical and population studies provide evidence of systemic inflammatory activity in trauma survivors with various psychiatric and nonpsychiatric conditions. This transdiagnostic meta-analysis looks at the literature on the relationship of inflammatory biomarkers to trauma exposure and related symptomatology.

This article comes from Nature's Translational Psychiatry. It was published as open access,

Full Citation: 
Tursich M, Neufeld RWJ, Frewen PA, Harricharan S, Kibler JL, Rhind SG, and Lanius RA. (2014, Jul 22). Association of trauma exposure with proinflammatory activity: a transdiagnostic meta-analysis. Translational Psychiatry; 4, e413; doi:10.1038/tp.2014.56

Association of trauma exposure with proinflammatory activity: a transdiagnostic meta-analysis

M Tursich [1], R W J Neufeld [1,2,3], P A Frewen [1,2,3], S Harricharan [4], J L Kibler [5], S G Rhind [6] and R A Lanius [1,3]

1. Department of Psychiatry, University of Western Ontario, London, ON, Canada
2. Department of Psychology, University of Western Ontario, London, ON, Canada
3. Department of Neuroscience, University of Western Ontario, London, ON, Canada
4. Department of Biology, University of Western Ontario, London, ON, Canada
5. Center for Psychological Studies, Nova Southeastern University, Fort Lauderdale, FL, USA
6. Defence Research and Development Canada, Toronto Research Centre, Toronto, ON, Canada

Abstract

Exposure to psychological trauma (for example, childhood/early life adversity, exposure to violence or assault, combat exposure, accidents or natural disasters) is known to increase one’s risk of developing certain chronic medical conditions. Clinical and population studies provide evidence of systemic inflammatory activity in trauma survivors with various psychiatric and nonpsychiatric conditions. This transdiagnostic meta-analysis quantitatively integrates the literature on the relationship of inflammatory biomarkers to trauma exposure and related symptomatology. We conducted random effects meta-analyses relating trauma exposure to log-transformed inflammatory biomarker concentrations, using meta-regression models to test the effects of study quality and psychiatric symptomatology on the inflammatory outcomes. Across k=36 independent samples and n=14 991 participants, trauma exposure was positively associated with C-reactive protein (CRP), interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α (mean rs =0.2455, 0.3067, 0.2890, and 0.2998, respectively). No significant relationships were noted with fibrinogen, IL-2, IL-4, IL-8, or IL-10. In meta-regression models, the presence of psychiatric symptoms was a significant predictor of increased effect sizes for IL-1β and IL-6 (β=1.0175 and 0.3568, respectively), whereas study quality assessment scores were associated with increased effect sizes for IL-6 (β=0.3812). Positive correlations between inflammation and trauma exposure across a range of sample types and diagnoses were found. Although reviewed studies spanned an array of populations, research on any one specific psychiatric diagnosis was generally limited to one or two studies. The results suggest that chronic inflammation likely represents one potential mechanism underlying risk of health problems in trauma survivors.

Introduction

Chronic inflammation may be a hallmark of many chronic diseases, including cardiovascular disease (CVD), diabetes, and chronic pain disorders, among others. A history of exposure to traumatic events (for example, early life adversity, exposure to violence or assault, combat exposure, accidents, or natural disasters) is known to increase one’s risk of developing chronic medical problems,1,2 and research on inflammatory biomarkers has begun to elucidate some of the potential mechanisms underlying this increased risk.

Physiological mechanisms linking the experience of psychological stressors to immune functioning are complex, with influences exerted through various pathways. Briefly, in response to a traumatic stressor, the biological stress systems (including sympathetic/parasympathetic, catecholamine, hypothalamic-pituitary-adrenal axis, and immune system components) assist in promoting adaptive behavioral and physiological responses to the stressor.3, 4, 5 Severe, repeated and prolonged exposure to traumatic stressors, however, can lead to chronic dysregulation of these basic biological systems. Chronic, systemic inflammation has been posited as one mechanism underlying psychiatric symptomatology, across a range of disorders,6, 7, 8 as well as with increased risk of many physical health problems.2,9,10

Historically, research into the physiological mechanisms occurring within the context of psychopathology has been segregated according to diagnostic classification. However, despite differing symptom presentations, mounting evidence of neurobiological, genetic, and physiological mechanisms underlying a range of physical and psychological disorders has led to increasing recognition that current diagnostic classifications may no longer provide an adequate framework for psychobiological research or for translating this research into clinical practice.11,12 This awareness has led to transdiagnostic initiatives such as the US National Institutes of Mental Health (NIMH) Research Domain Criteria project.13 Indeed, studies of immune activity across multiple psychiatric disorders, including posttraumatic stress disorder (PTSD),5 major depression,14 and bipolar disorder15,16 have all identified disruptions in proinflammatory cytokines (such as interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-1β), among symptomatic individuals, as compared with healthy control participants. In addition, a convergence of evidence has identified lifetime trauma exposure, particularly early life adversity, as a major risk factor for a range of chronic physical and psychiatric conditions,1,2 and systemic inflammation has been suggested as one potential mechanism mediating this association.2,4,5,17

Despite a rapidly growing body of literature on the relationships between trauma exposure and inflammatory biomarkers (including cytokines and acute-phase proteins, such as C-reactive protein (CRP) and fibrinogen) in both clinical and nonclinical samples, few attempts have been made to quantitatively integrate this research. To our knowledge, all existing meta-analyses have been limited to disorder-specific comparisons of symptomatic vs asymptomatic individuals, such as in depressive disorders14,18, 19, 20, 21 or bipolar disorder.15,16 In addition to the narrow focus on specific psychiatric diagnoses, prior meta-analyses have faced methodological challenges, including skewed biomarker concentrations in primary studies, disparate statistical techniques used to evaluate data, and systematic exclusion of large, population-based regression studies, which are often better equipped to statistically control for covariates, such as body mass index (BMI), age, sex, and the use of medications or other substances, all of which have previously been identified as important in biobehavioral research.22 Using meta-analysis and meta-regression models, the present study therefore describes the relationships between trauma history and in vivo inflammatory biomarkers (that is, cytokines and acute-phase proteins) from a transdiagnostic perspective.

Materials and Methods

Protocol

This study adhered to PRISMA guidelines for meta-analysis.23 Search strategy and data extraction were informed by a preliminary review of the literature and further specified on the basis of data availability and methodological variation, including limiting the present analysis to unstimulated in vivo cytokines and acute-phase proteins.

Inclusion/exclusion criteria

To address the relevant transdiagnostic theoretical questions, we included all studies of adult participants that analyzed unstimulated, in vivo (circulating) inflammatory biomarkers in blood samples (that is, cytokines, CRP, or fibrinogen) in relation to measures of trauma exposure. We excluded child and adolescent samples due to evidence that cytokine production in children differs substantially from that of adults, even among healthy populations.24,25 Trauma exposure was defined either through self-report measures of trauma or abuse (for example, Adverse Childhood Experiences questionnaire26) or by exposure to events meeting criterion A for PTSD.27 Studies that only included pre-trauma cytokine measurements were excluded. The statistical analyses assessed the impact of trauma exposure, and meta-regression models assessed the impact of relevant covariates, including study quality and the presence or absence of psychiatric symptomatology within the samples. As trauma exposure can be assessed either as a continuous or dichotomous variable, our inclusion criteria were intentionally inclusive of either design. Because only a small number of studies had adequate data to test the relative contribution of posttraumatic symptomatology within trauma-exposed populations (that is, comparing trauma-exposed symptomatic individuals to trauma-exposed controls), such analyses were underpowered and are therefore reported solely as supplemental analyses (see Supplementary Material). Thus, we chose to exclude studies that did not include either a continuous measure of trauma exposure or a non-trauma-exposed comparison group.

Study selection

Studies were identified through systematic searches of PubMed, PsycInfo, PILOTS (Published International Literature on Traumatic Stress), and Ovid MEDLINE databases. Search criteria included peer-reviewed articles published in English, using terms related to inflammation (for example, interleukin, cytokine) and either traumatic event exposure (for example, trauma* stress, child* maltreatment) or psychiatric conditions commonly linked to trauma exposure (for example, PTSD, depression), limiting the results to human samples. Additional selected references were identified through limited update searches, citations in other papers, and personal communications with authors (see Supplementary Material for full search strategy).

Study characteristics and data extraction

Data extraction

A single effect size estimate was calculated from each fully independent sample of participants for each biomarker. Potential duplicate publications were identified (within each biomarker outcome) through cross-checking authors’ names and sample locations. Evaluation of inclusion/exclusion criteria and extraction of relevant data were conducted systematically by one of two coders, with a selection evaluated by both coders. Any disagreements (less than 5%) regarding eligibility or extracted data were settled by consensus.

Effect size and other study data were extracted from each of the published reports. Forms were piloted and revised as needed for extraction of relevant information. All assessments were made at the outcome level, with separate biomarkers analyzed independently. In the cases for which published data were insufficient, at least three attempts were made to contact authors. In total, the authors of 38 studies were contacted requesting information about sample independence, study eligibility or effect size calculation. Response rate was 76%, although some of these studies were not included in the present analyses (due to inclusion/exclusion criteria).

Data preparation and statistical analysis

Effect size preparation

A single effect size was calculated for each biomarker measured in an independent sample. Seven articles were confirmed by study authors to be duplicate samples, and one published report28 contained two independent subsamples (that is, African American and Caucasian participants), which were treated individually. Due to inclusion of both continuous and dichotomous predictors, we used correlation coefficients to synthesize the literature.29

As inflammatory biomarker distributions tend to be skewed, authors generally take one of three approaches to statistical testing and reporting of data: Use of nonparametric statistical methods, dichotomization according to clinically-relevant cut points (most frequently CRP>3 mg /L30), and logarithmic transformations to normalize the distributions before using parametric statistics.

Because data are log-transformed before statistical aggregation (individual data are converted into an exponent-scale before taking an arithmetic mean), effects based on log-transformed data cannot be mixed in the same analyses as raw (non-transformed) data. Log-transformed biomarker data are more likely to meet assumptions of normality than raw data; therefore, we chose to convert all raw effect sizes to estimated loge-transformed effect sizes,31 which were then converted to a log10 scale. When log-transformations were applied, any zero values were set to the smaller of the assay detection limit or a raw value of 1.0 (corresponding to a log-transformed value of 0), to allow for transformation and avoid artificially inflating the effect size estimate. Effect sizes for one study,32 for which we were unable to obtain effect size estimates by usual means, were extrapolated from a published scatterplot of individual participant data using WebPlotDigitizer, version 2.6 (http://arohatgi.info/WebPlotDigitizer/). Other effect size conversions were performed according to standard methods.29,33,34

Synthesis of results

We produced meta-analytic models for all analyses including at least three independent effect size estimates. Correlation coefficients were converted to Fisher’s Z-values for analyses and back-converted to correlations for interpretation. All meta-analysis and meta-regression models were fitted using Wilson’s meta-analysis macros for SPSS.35,36 Because we expected at least a moderate level of heterogeneity across studies, we used non-iterative method of moments random-effects models to integrate study findings. This approach produces wider confidence intervals and, thus, a more conservative estimate than either fixed- or other random-effects models.29 Forest plots were created,37 and heterogeneity analyses were conducted using the Q-test and I2 statistic.38

Publication bias and sensitivity analyses
Publication bias was assessed using funnel plots relating effect size to precision (inverse of standard error), two-tailed rank correlation tests,39 and trim and fill techniques,40 using the Comprehensive Meta-Analysis software, version 2.0. To provide protection against Type I error, publication bias was assessed only in those analyses which consisted of at least five studies. To evaluate the stability of results, we conducted sensitivity analyses by excluding samples consisting primarily of patients with known nonpsychiatric medical conditions (for example, CVD, migraine, pregnant samples), as the inflammatory processes could differ from those in the general population, despite study-level control. These post hoc models were fitted if there remained at least two studies for the analysis.

Study-level risk of bias

Risk of study-level bias was assessed with a checklist modeled after the Quality Assessment Tool for Quantitative Studies (QAT),41 modified slightly to fit our observational research question (see Supplementary Materials for details). We calculated both a categorical global rating (that is, high, moderate or low risk of bias), by using the QAT global rating instructions for relevant domains (selection bias, study design, control of relevant covariates, assessment validity, and use of appropriate data analysis techniques), and an average QAT score (average of the ordinal domain ratings). For each study, the percentage of recommended covariates (for example, age, sex, BMI, and the use of medications or other substances, among others)22 controlled either methodologically (that is, through exclusion or matching of subjects) or statistically was documented and entered as part of the QAT score (see Supplementary Material). Each domain was scored on a three-point likert scale (strong/moderate/weak); thus, both categorical and average QAT scores ranged between 1.0 and 3.0, with higher scores indicating greater potential for bias.

Meta-regression models

For each analysis, we tested the effect of average QAT scores using univariate models. We then conducted multivariate meta-regression models assessing the impact of a study’s inclusion of symptomatic individuals, while statistically controlling for study-level bias. Finally, we ran a series of dummy-coded meta-regression models to assess the effect of psychiatric diagnosis or symptom type. Due to the small number of studies of non-PTSD psychiatric populations, we used models comparing samples of non-comorbid PTSD participants to all other samples (including those using other psychiatric diagnoses and nonpsychiatric samples). Any models that displayed significant differences between the two groups (PTSD vs other samples) were then subjected to post hoc analyses to determine which symptom subgroups differed significantly from the PTSD samples. To increase power and interpretability, all meta-regression models were fitted only if at least four samples were included in the analysis.

Results

Study selection

A total of 3647 unique articles were identified through our searches, the majority of which were excluded through title or abstract screening (n=2919). Reasons for exclusion of full-text articles are shown in Figure 1. We identified 40 independent samples measuring 29 different cytokines, receptors or acute-phase proteins that met initial inclusion criteria. Of these, only biomarkers measured by at least three samples were included in our analyses. Three studies that failed to provide sufficient information to calculate log-transformed effect size estimates were not included. Thus, nine biomarkers from 36 independent samples were included in the meta-analysis (see Table 1).

Figure 1. Study screening and eligibility

 

Full figure and legend (142K)


Table 1 - Studies included in the meta-analysis.


Full table

None of the meta-analysis models for the anti-inflammatory cytokines (IL-4 and IL-10) was statistically significant (see Supplementary Figure 1), so we focus on presenting analyses of the acute-phase proteins (CRP and fibrinogen) and the proinflammatory cytokines (IL-1β, IL-2, IL-6, IL-8, and TNF-α).

The results of the baseline models, based on 36 independent samples, are presented in Figure 2. As expected, there was evidence of significant heterogeneity across studies for all biomarkers. Although rank correlation tests revealed a significant correlation between the standardized effect size and the standard error for IL-6 (τ=0.2963, z=2.1889, P=0.0302), no imputed ‘missing studies’ were identified using the trim and fill method.40

Figure 2. Meta-analysis summary statistics.

 
Full figure and legend (95K)

Acute phase proteins

CRP

Analyses for CRP included 16 studies and a total of 13 374 participants. As shown in Figure 2, a significant association between CRP concentration and trauma exposure was detected (mean r=0.2507, P=0.0030).

Fibrinogen
Analysis of four studies involving 1890 participants showed no significant correlation between trauma exposure and fibrinogen (mean r=0.0675, P=0.1860; see Figure 2).

Proinflammatory cytokines

IL-1β

Meta-analysis of four studies (304 participants) showed a significant relationship between IL-1β and trauma exposure (mean r=0.3169, P=0.0322), displayed in Figure 2.

IL-2

Overall analyses of four studies (362 participants) revealed no statistically significant association between IL-2 and trauma exposure (mean r=0.3627, P=0.1256; see Figure 2).

IL-6

As shown in Figure 2 analysis of 26 studies with 7295 participants showed a significant relationship between trauma exposure and IL-6 (mean r=0.3029, P<0.0001).

IL-8

No significant overall correlation relating trauma exposure to IL-8 was detected, based on five studies with 349 participants (mean r=0.4649, P=0.1609; see Figure 2).

TNF-α

As presented in Figure 2 TNF-α was significantly associated with trauma exposure in analysis of 11 studies with 1899 participants (mean r=0.2998, P=0.0288).

Meta-regression models and sensitivity analyses

As shown in Table 2, risk of study-level bias (defined as the average of the applicable QAT domains: selection bias, study design, covariate control, assessment reliability/validity, and statistical analysis) was a significant predictor of heterogeneity in meta-regression models for the proinflammatory cytokines IL-6 and IL-8, such that higher risk of bias was associated with larger effect size estimates. In models controlling for risk of bias, studies that included participants with psychiatric disorders yielded larger effects for IL-1β and IL-6.

Table 2 - Meta-regression models.


Full table

None of the meta-regression models comparing PTSD samples with all other samples was statistically significant, with the exception of fibrinogen (which did not include any psychiatric samples) and IL-6 (see Supplementary Table 2). Post hoc comparisons coding non-PTSD psychiatric samples separate from asymptomatic samples revealed no differences in effect sizes for IL-6 between non-comorbid PTSD vs other types of psychiatric disturbance.

Sensitivity analyses showed that the findings were robust to exclusion of medical samples, which did not significantly change the pattern or significance of findings for any of the biomarkers except TNF-α (see Supplementary Figure 1). Although of increased magnitude, the TNF-α mean effect size was no longer statistically significant, once medical samples were excluded (k=6, mean r=0.4579, P=0.0857).

Discussion

To our knowledge, this is the first meta-analysis of trauma exposure as a risk factor for inflammation to utilize a transdiagnostic perspective. We integrated all available studies measuring trauma exposure, rather than limiting the analysis to a single diagnostic category. Further, to reflect the true status of the current literature, we incorporated both continuous and categorical measures. Although this procedure is likely to increase the observed heterogeneity in effect sizes across studies, it is essential to represent the diversity of study designs to obtain an accurate and comprehensive review of inflammation in trauma survivors. A growing body of evidence suggests that there may be a dose-response relationship between physical health problems and increased levels of exposure to traumatic events.75,76 Within the field of trauma research, however, it has been difficult to arrive at a single adequate method of quantifying cumulative trauma exposure, taking into account differences in number, frequency and severity of potentially traumatic experiences. As a result, there was insufficient literature to assess the potential impact of continuous vs categorical measures or to assess variability across different continuous measures of trauma exposure.

As expected, increased inflammation in trauma-exposed samples was found across a range of biomarkers. In particular, we noted moderate-to-large correlations relating trauma exposure to circulating concentrations of the proinflammatory cytokines IL-1β, IL-6, and TNF-α and of the acute-phase protein CRP. On the basis of our meta-regression models, the relationship between trauma exposure and the proinflammatory cytokines IL-1β and IL-6 was especially pronounced in samples that included, at least in part, clinical populations, as compared with samples which did not specifically recruit symptomatic individuals. No significant differences were observed as a function of the specific psychiatric diagnosis, although the statistical power was likely insufficient, at least in most analyses, to detect such relationships if they exist.

Because it was not possible to obtain log-transformed effect sizes for all studies, we produced log-transformed effect size estimates following accepted techniques.31 When we were unable to confirm with authors the base of the logarithm applied, we assumed the use of log-10 transformations, in accordance with similar studies. In keeping with prior recommendations for biomarker research,77 we advocate for greater consistency in reporting of methods, including transformations applied, sample demographics and characteristics, and covariates controlled in statistical analyses. Although it is beyond the scope of this study to recommend specific statistical techniques, other authors have endorsed the use of log-transformation when data are log-normally distributed, due to its flexibility in allowing for the use of traditional (parametric) statistical techniques and due to the ability to back-transform (exponentiate) geometric means to facilitate interpretation and comparison.77

Despite recent interest in these questions, research on the relationships among trauma exposure, psychiatric symptomatology, and inflammatory biomarkers has historically been limited to the PTSD literature. Thus, our power to detect differences between diagnostic groups was somewhat limited by a relative scarcity of reporting or measurement of trauma histories in non-PTSD psychiatric samples. Given the evidence that trauma exposure, particularly when prolonged and/or occurring early in life, is associated with a wide range of chronic medical and psychological health problems2,26 even after accounting for the effects of psychiatric disorders,75,76 it would be useful for future research to routinely include measures of trauma exposure in both medical and psychiatric populations.

Our analyses were also limited by the number of published biomarker studies providing information on participants’ trauma history. Although the numbers of studies included in our meta-analyses are comparable with other early meta-analyses on inflammation and psychiatric disorders,14, 15, 16, 18, 19,20, 21 further research is necessary to determine whether replicable relationships exist between trauma exposure and those biomarkers with relatively few published studies (for example, fibrinogen, IL-1β, IL-2, and IL-8).

Our findings suggest that the risk of study-level bias, especially related to the control of relevant covariates,22 such as medication use, BMI, and comorbid medical conditions, was significantly related to heterogeneity of effect sizes observed across studies. That is, higher QAT scores (indicating greater risk of bias) were associated with larger correlations between trauma exposure and IL-4, IL-6, IL-8 and IL-10. We therefore advocate for wider adoption of accepted standards for control of these potentially relevant covariates in future studies.

Another important question concerns the longitudinal course of inflammation in trauma-exposed individuals. We were unable to evaluate the effects of treatment or to examine the longitudinal course of inflammation following traumatic events in our analyses. However, there is preliminary evidence56,72,78,79 to suggest that successful treatment of trauma-related psychopathology may lead to improvements in the chronic immune dysregulation observed in our analyses, although results to date have been somewhat contradictory and unclear. This lack of consistency may be due, at least in part, to methodological differences among studies. Further research is needed to better understand the time course of inflammatory biomarkers following successful psychological or pharmacological treatment.

Conclusions

The relevance of inflammation in the pathophysiology and consequences of psychiatric disorders and general medical conditions has been increasingly recognized within research, clinical and public health arenas.9,10,80,81 The results of this meta-analysis are in keeping with a growing body of cross-disciplinary evidence11,12,82 which provides a framework for examination of transdiagnostic relationships among psychiatric risk factors (such as trauma exposure) and both psychological and physiological dysfunction. In our review of 36 samples with 14 991 participants, we found moderate correlations between inflammatory biomarker concentrations (IL-1β, IL-6, TNF-α, and CRP) and trauma exposure (mean rs=0.2455, 0.3067, 0.2890, and 0.2998, respectively) across 36 independent samples with a total of 14 991 participants. Further research is needed to confirm this association in a broader range of psychiatric and general medical populations, and to determine whether these findings extend to other inflammation-related biomarkers.

Although prior systematic reviews on inflammatory biomarkers in PTSD have provided a qualitative synthesis of the literature,4,5,81,83, 84, 85 to our knowledge, this is the first meta-analysis to examine the relationship of trauma to proinflammatory cytokines and acute-phase proteins. Meta-analyses of inflammatory activity observed within other psychiatric disorders (for example, depression14,18, 19, 20, 21 and bipolar disorder15,16) have found evidence of systemic inflammation, but none have yet examined the impact of trauma on these relationships. Our findings are also consistent with the results of two recent studies59,61 (included within our analysis), which found significantly higher inflammatory biomarkers only in those psychotic patients with a trauma history, as compared with healthy control participants. In both studies, patients without a trauma history did not significantly differ from controls. However, the majority of studies in psychiatric populations that we screened did not assess participants’ histories of trauma exposure, so further research is needed to confirm and clarify these findings. We therefore endorse routine assessment and reporting of trauma exposure within immunological research studies.

Conflict of interest

The authors declare no conflict of interest.

References at the Nature Translational Psychiatry page.

Gábor Máté MD - Attachment = Wholeness and Health or Disease, ADD, Addiction, Violence

 

In depth interview with Gábor Máté MD by Michael Mendizza. The topic is attachment (the parent-child bond type of attachment) and the two basic outcomes:

• Secure = Wholeness and Health
• Insecure = ADD, addiction, disease, mental illness

Here is a brief outline of the basic attachment patterns from Wikipedia:

Attachment patterns

Much of attachment theory was informed by Mary Ainsworth's innovative methodology and observational studies, particularly those undertaken in Scotland and Uganda. Ainsworth's work expanded the theory's concepts and enabled empirical testing of its tenets.[4] Using John Bowlby's early formulation, she conducted observational research on infant-parent pairs (or dyads) during the child's first year, combining extensive home visits with the study of behaviours in particular situations. This early research was published in 1967 in a book entitled Infancy in Uganda.[4] Ainsworth identified three attachment styles, or patterns, that a child may have with attachment figures: secure, anxious-avoidant (insecure) and anxious-ambivalent or resistant (insecure). She devised a procedure known as the Strange Situation Protocol as the laboratory portion of her larger study, to assess separation and reunion behaviour.[37] This is a standardised research tool used to assess attachment patterns in infants and toddlers. By creating stresses designed to activate attachment behaviour, the procedure reveals how very young children use their caregiver as a source of security.[8] Carer and child are placed in an unfamiliar playroom while a researcher records specific behaviours, observing through a one-way mirror. In eight different episodes, the child experiences separation from/reunion with the carer and the presence of an unfamiliar stranger.[37]

Ainsworth's work in the United States attracted many scholars into the field, inspiring research and challenging the dominance of behaviourism.[38] Further research by Mary Main and colleagues at the University of California, Berkeley identified a fourth attachment pattern, called disorganized/disoriented attachment (insecure). The name reflects these children's lack of a coherent coping strategy.[39] The type of attachment developed by infants depends on the quality of care they have received.[40]

Anyway, this is a nice discussion.

,

Thomas Schramme - On the Autonomy of the Concept of Disease in Psychiatry

 

Via the open access Frontiers in Theoretical and Philosophical Psychology, Thomas Schramme examines the disease concept of mental illness and the philosophical implications of implying a Cartesian account of the mind-body relation or the need to give up a notion of mental disorder in its own right.

The disease model has reframed itself with the word "disorder" - or with "mental health problems." This is still the same belief system with different words inserted. There is still the implication of a "healthy" norm by which to judge a disordered brain. Yet no one has EVER identified this norm.

This is flawed and reductionist approach.

My preference is to see a more organism-based model of psychological distress. All of the things we call "symptoms" are better understood as behavioral adaptations or survival strategies to deal with situations we generally refer to as trauma. I think of this as the trauma model.

For example, depending on who one listens to, hoarding is either an anxiety disorder (minority position) or an obsessive compulsive disorder (the model developed by Randy Frost, who is the leading expert on hoarding). However, a very large percentage of those who hoard have been sexually, physically, or emotionally abused or neglected as children.

In a trauma model, hoarding is a behavior that makes a certain amount of sense (from a child-mind perspective). The person who hoards likely has a part of themselves stuck in the trauma that was experienced, and that child part might think that if it is surrounded by a LOT of "stuff," kind of like barricading a door, s/he might be safe from the abuse.

Or if the child was severely neglected, not having had adequate food or clean clothing, hoarding might be an adaptive response to deprivation, a behavior that was seen in some adults who were children during the Great Depression or during the bombing of London. Throwing things away might feel like being deprived, or the desire to collect stuff might be a way to ensure that one will never go without. I would suspect this behavior might also be seen in those who experienced emotional neglect.

Keep this in mind as you read the article below - there a variety of ways to conceptualize psychological distress. The question for me is which one best explains the situation and honors the experience of the client.

Full Citation:
Schramme T (2013, Jul 19). On the autonomy of the concept of disease in psychiatry. Frontiers in Theoretical and Philosophical Psychology, 4:457. doi: 10.3389/fpsyg.2013.00457

On the autonomy of the concept of disease in psychiatry

Thomas Schramme
Department of Philosophy, Hamburg University, Hamburg, Germany

Does the reference to a mental realm in using the notion of mental disorder lead to a dilemma that consists in either implying a Cartesian account of the mind-body relation or in the need to give up a notion of mental disorder in its own right? Many psychiatrists seem to believe that denying substance dualism requires a purely neurophysiological stance for explaining mental disorder. However, this conviction is based on a limited awareness of the philosophical debate on the mind-body problem. This article discusses the reasonableness of the concept of mental disorder in relation to reductionist and eliminativist strategies in the philosophy of mind. It is concluded that we need a psychological level of explanation that cannot be reduced to neurophysiological findings in order to make sense of mental disorder.

For some time, especially in the 60s and 70s of the twentieth century, psychiatry was under pressure because it did not seem capable of showing that mental illness actually exists. Can there really be such a thing as a “disease of the mind”? At the time skeptics such as Thomas Szasz (1974) wrote against the “myth of mental illness.” The emphasis of this debate lay for a long time in the scrutiny of the associated norms, i.e., the question whether one can differentiate between sick or healthy mental phenomena. One still visible effect of this debate, which has more or less reached its conclusion, is the avoidance of the term “disease” in the official nomenclature of psychiatric medicine. Nowadays we speak of disorders, not diseases, for example in the Diagnostic and Statistic Manual of Mental Disorders (DSM), or in the International Statistical Classification of Diseases and Related Health Problems (ICD), in which the psychiatric classification is also described as “mental and behavioral disorders.” One cannot help feeling that the attempt had been to avoid a definition that is already all too close to somatic medicine, which would have required a corresponding “hard” validation of the respective categories, or at least a set of explanations of the nosological units in these classification systems. Because contemporary psychiatry barely meets this idea, one could get out of this whole affair with a “weaker” term1.

The downside of this difficulty is visible in the likewise wide-spread somatization of psychopathology, which—put briefly—is the identification of mental disorders as diseases of the brain, a practice that has a long tradition in the history of psychiatry. All efforts are undertaken to establish psychopathological phenomena as “real,” precisely because many psychiatrists share the view that psychiatry has to be scientifically demonstrable and ought to put in place generally testable criteria for pathological conditions, and because it is somewhat embarrassing for them to separate “disorder” from the disease concept in such a way. Because the real is in turn considered to be one and the same as the observable, from this point on the material disorder of the brain counted as what ideally should be proven. The move had some initial plausibility, in that one more aspect of the original skepticism toward the concept of disease in psychiatry could be undermined. This doubt was fed by the supposedly non-existing location of the disturbance: the spirit or the psyche. How can one rationally assume scientifically valid criteria of pathology when the impaired or damaged object apparently does not exist, or at the very least cannot be affected by disorders? The answer lay in tossing away significant reference to the psyche, the mind, or to mental objects, and talking mainly about neurophysiology, the nervous system, and the brain; for instance when schizophrenia was regarded as a disorder of dopamine and serotonin levels. The somatization could therefore solve both problems of psychiatry: its ostensibly poor scientific grounding and the supposed lack of reality of its phenomena. One astonishing result of this development lay furthermore in the fact that leading proponents of psychiatry now claim—just as their strongest critics once had—that mental illnesses do not actually exist, because only brain disease exists. From a philosophical perspective such a conclusion seems unreasonable2.

The proponents of the concept of disease in psychiatry, however, seem to be left indeed in an uncomfortable dilemma: If they emphasize the bodily manifestation of mental diseases, then they save the analogy to somatic disease and therefore the medical terminology. At the same time they stand to lose through this strategy the uniqueness of mental disease, which is reduced to somatic disease. If one wants on the other hand to keep the distinctive manner of speaking of mental disease (or disorder), then this is apparently only possible when one at the same time postulates a sphere of the mind that is distinct from the body. This strategy, again, seems to lead to a mind-body-duality in the mode that has become unpopular in philosophy. The supposed dilemma for proponents of the concept of mental disease therefore consists in the choice between the Scylla of reduction and the Charybdis of dualism. “Psychiatry is left with two seeming alternatives: either to say that personal, psychological, and emotional disorders are really states of the body, objective features of brain-tissue, the organism-under-stress, the genes or what have you; or else to deny that such disorders are illnesses at all” (Sedgwick, 1973).

As already indicated, there are authors, especially on the side of psychiatry, who are ready to solve this dilemma by consistent somatization and consequentially abandoning the concept of mental disease. One prominent example for this is Robert Kendell (1993, 3), a well-known British psychiatrist: “[…] it follows that there is, strictly speaking, no such thing as disease of the mind or mental disorder and that Griesinger was right—mental illnesses are diseases of the brain, or at least involve disordered brain function—because all mental events are accompanied by and dependent on events in the brain. (Thomas Szasz was also right; mental illness is a myth, though not for the reasons he believed.).” A surprising alliance between biological psychiatrists and skeptics has been formed; in the end both positions are ready to give up the concept of mental illness.

The task of this article is therefore to search for compelling arguments in favor of a distinctive concept of mental illness. As already indicated, I cast doubt on the presented dilemmatic structure as a defense of this concept. Rather, I shall try to show that there are well-reasoned positions somewhere between the two horns of the dilemma. The question—can we see “mental illness” as an autonomous concept without relying upon unpleasant theoretical premises?—is, as I have said, based on an important philosophical issue: the mind-body problem. This problem can be formulated as follows: Are there really mental phenomena, and if so, how can they be explained and how are they connected with physical phenomena? The first part of this question may sound rather strange, since what are we more sure of than that mental states such as pain, wishes and beliefs exist?3 In the course of this investigation it will become clearer—so I hope at least—why questioning the existence of mental phenomena is not as strange as it seems. The second part of the mind-body problem, the question of the nature of mental phenomena and their relation to physical states, has of late, with the study of the brain and the nervous system, received a strong empirical orientation and even a new twist. The idea that the nervous system and especially the brain are the basis of mental states is nowadays no longer seriously disputed. For this reason the mind-body problem is sometimes reformulated as the “mind-brain problem.” The assumption that mental phenomena are based upon physiological processes suggested itself after the observation of people with brain injuries. Since the introduction of new imaging techniques to study the brain's physiological processes, this theory has been strengthened and refined. Today we can identify connections between regions in the brain and specific mental capabilities, even if definitive relationships between them are not yet possible. And ultimately we are still far away from being able to formulate a generally accepted solution to the mind-body problem.

In this article I will first briefly focus on Thomas Szasz, the main critic of the concept of mental illness. Here I will examine especially his arguments that are related to the mind-body problem4. Second, I will apply reductionist and eliminative theories in the philosophy of mind in order to find out whether they might rule out the concept of mental illness.

The Sceptical Arguments of Thomas Szasz

Like no other theorist, Szasz has dealt with the concept of disease in psychiatry in a very intensive way, and has attempted to demonstrate particularly the different disanologies between the concept of disease in somatic medicine and psychiatry. The concept of disease—as Szasz has put it in the argument that interests us—cannot be applied to mental phenomena, because the expressions “body” and “mind” belong to different logical categories. When we speak of mental illness, we are merely using the term as a metaphor.

In this argument Szasz relies upon the British philosopher Gilbert Ryle (1949), who, in his book The Concept of Mind, attacked the “official doctrine” of Cartesianism, in which every human being possesses both a body and a mind, which exist as independent entities. Ryle also called this position the “dogma of the ghost in the machine.” He wanted to refute this position by showing that it is based on a so-called category mistake. Szasz uses Ryle's approach in order to demonstrate that the “official doctrine” of psychiatry commits an identical category mistake, in virtue of assuming that there is both bodily illness and mental illness. The mistake consists in the claim that the mind can, just like the body, be affected by illness.

Ryle explains his conception of a category mistake by way of several examples. Suppose that a student comes to Oxford for the first time. There she is given a tour of the many colleges, libraries, and administrative offices. After the tour she says: “I now know the individual colleges and where the books are kept, and I have also seen where the administrators work. But now I want to be shown the university.” Naturally this wish cannot be fulfilled, because colleges, libraries, etc. are the university. There is no other point of interest that is called “university.” Apparently the student does not know that “university” belongs to a category separate from “New College,” “Bodleian Library,” etc. It would be a similar mistake to ask, after one had been shown the functions of the defender, the forward, and the goalkeeper etc., whose function it was to contribute the team spirit in a football team.

The mistake of Cartesianism is given, according to Ryle, in such a mixing of categories, in that “mind” is classified in the same logical category as “body.” Only in this way could it be claimed that a human being has both a mind and a body. But one could only combine expressions in linguistically correct conjunctions when they belong to the same category. Therefore, one cannot, from a linguistic point of view, state, for example that one has seen New College, Bodleian Library, and Oxford University.

Ryle does not claim that the mind cannot be said to exist as a matter of principle. But if this claim is made, one would need another meaning of “exist” than in the assertion that bodies exist. Because mind and body belong to different categories, it cannot be reasonably claimed that mind and body exist in the same way. Nor can it be expressed in a logically compelling way that either the mind or the body exists, because this disjunction is just as inadmissible when expressing different categories. To say, “Either I have visited the New College, the Bodleian Library etc. or seen the university” is patently absurd.

At this point Szasz (1974) wants to show that because “body” and “mind” belong to different logical categories, in principle there can be no such thing as a mental illness. This theory and its basis—the category mistake argument—are important for Szasz's work and are mentioned again and again, even when there is no direct relation to Ryle, such as when Szasz says that an illness can only affect the body.

As previously mentioned, Ryle's category mistake argument is directed at the “official doctrine” that had prevailed after Descartes and that postulated two distinct entities: the body and the mind. The special feature of Ryle's argument as compared to other critiques of dualism is his claim that asking about the relationship between mind and body is already by itself non-sensical (Ryle, 1949, 23). But even if this view is correct, the category mistake argument alone does not support Szasz's theory, because the mere suggestion that “mind” and “body” belong to different categories does not allow the conclusion that a mental illness cannot exist. The argument does not express whether mental phenomena exist or not, but rather casts doubt on Cartesianism.

Moreover, illness does not exist independent from organisms. If one abandons the notion of an independent existence for illness, the idea of actual mental illness is no longer implausible, because we need not claim that the mind has an illness, but rather, as one could say for example, a disorder of mental capacities—however specified—is a mental illness. In order to make this claim one would not have to postulate a separation between mind and body. Substance dualism is not required for the maintenance of the concept of mental illness. Therefore, Szasz cannot show the absurdity of this concept in principle through casting doubt on the Cartesian separation of mind and body.

The Mind-Body Problem

There are many different theories about the relationship between mental and physiological states. These theories range from strict separation of the two spheres to their identification, or lead all the way to the claim that the mind-body problem is principally unsolvable. This situation and the enormous scale that the respective literature has since reached make it necessary to restrict this examination to a cursory treatment and to keep as strictly as possible to the issue at stake. For this reason I will largely restrict myself to negative statements in order to defend the concept of mental illness, and will attempt to show accordingly that the theories that doubt the explanatory independence of mental phenomena are not adequately justified to reject such an autonomy5. Positive criteria of such evaluation of theories would be their scientific adequacy—this spoke against Cartesian dualism—but also their philosophical plausibility, of course. Still, I cannot deal with all of the many contributions in this area of research.

Theories of the relation between mind and body that lead to a questioning of the mental disease concept are largely of two kinds: Either they are reductive—they lead to an explanation of mental phenomena through reference to physiological states; or else they are eliminative—they relegate mental phenomena to the sphere of myth that is, dispute the very existence of mental states. I naturally do not want to claim that the respective authors actually want to discard the notion of mental illness. Ultimately their theories are aimed at a different question. But it is possible to scrutinize the independence of the mental disease concept on the basis of such theories and in doing so to ultimately scrutinize the identity of psychology and psychiatry. And I think furthermore that implicit or explicit theories about the connection between mind and body can have an impact on psychiatry's research focuses, its methods of treatment, and its classifications.

From this point on I will take it for granted that the problems of substance dualism, such as those exemplified in Descartes, are already well-known. In the following I will first analyse the reductive theories on the mind-body problem. Then I will examine the eliminative theories. The result will show that the rejection of an independent concept of mental illness does not succeed. A conceptualization of mental disease by referring to mental states is possible without having to advocate an awkward dualism. Nevertheless, we should not go so far as to generally repudiate somatic approaches in psychiatry, but rather emphasize their one-sidedness and their need to be complemented. Psychiatry should be neither “mindless” nor “brainless”.6

Identity-Theory

The mind-body identity theory makes reference to mental states, which underlie our actions, and therefore it does not reduce them to observable behavior, as behaviorism had done previously, ultimately leading to a theoretical dead end. Identity theory permits explanations of behavior that appeal to desires, beliefs, pain, etc., and seems in this regard adequate to work as a basis for an explication of the mental illness concept. However, the theory posits the ontological identity of mental states and neurophysiological states. In this way identity theory rules out substance-dualistic assumptions. Mental states are identical to physiological states of the nervous system and the brain. There are not two different substances, only one, namely matter. The mental does not have any properties that go beyond the physiological7. One often cited example for this is the identity of pain with the stimulation of C-fibers.

Identity theory is superior to behaviorism not only thanks to its appeal to inner states, but also through its ability to acknowledge different mental phenomena in cases of identical observable behaviors. For identical behaviors can have many different underlying mental states, which are themselves identical to specific neurophysiological states. Therefore, for instance the same behavioral abnormality could in one case be accompanied by a neurophysiological irregularity that is completely missing in another case. On the basis of such a theory this suggests searching for the boundaries between mental normality and illness on a neurophysiological level, because on this level different mental states manifest themselves. The first step to a theory about mental illness as a brain illness is therefore fulfilled. Identity theory also solves Descartes's problem of explaining mental causation, for instance the causation of the action of going to the fridge by a desire to drink and a belief that there is a drink in the fridge. On the basis of substance dualism such a straightforward explanation becomes quite difficult to achieve, because mental phenomena are regarded as non-material in Cartesianism, and non-material things lack the force to cause anything physical. However, if mental states are identical to neurophysiological states, then there is no need to postulate an obscure non-mental causality. Mental states can cause material changes to the body in virtue of their material existence.

We should clarify what the identity theorists mean by “identity.” J. J. C. Smart (1959, 171), one of the prominent proponents of identity theory, speaks of “strict identity” and uses the identity of lightning and electric discharge as explanatory example. The thesis is stronger than a mere claim to a correlation between brain states and mental phenomena. This type of identity is often explained using Leibniz's law of the identity of indiscernibles: X is strictly identical to Y if they are indiscernible from one another, i.e., if every property of X is also a property of Y, and vice versa. In the present case of an identity claim, this means that there are no properties of the mental that are not also properties of the nervous system. Hence there is no unique property of the mental.

The proposition of identity theorists is not tantamount to the claim that statements about mental and neurophysiological states have the same meaning, and are therefore synonymous. The identity theory merely claims that the state being referred to is one and the same. We can elucidate this distinction with the following example: The Evening Star is identical with the Morning Star (both have the same properties of the planet Venus, and so refer to the same object), although the terms have different meanings, because there are “different modes of presentation” at hand (Frege, 1892).

Smart (1959) emphasizes the difference between synonymity and identity in order to avoid one obvious objection to identity theory. For there's room to claim that mental and physical states are not identical, because someone who has no idea of neurophysiology can nonetheless refer to his mental condition. If the two states were identical, so this argument goes, then we could substitute the proposition in a statement such as “I know that my foot hurts” with the proposition “my brain is in state X” while retaining the truth value. Since this clearly does not work, the states cannot be identical. This only shows, however, that statements about mental states have a different meaning than statements about physical states, not that they are not ontologically identical. Therefore, this kind of argumentation against identity theory is invalid.

In the distinction between meaning and reference there is also the implication that the postulated identity of mental and physical statements is informative (i.e., not a priori). In its differentiation between types of identity statements such as “a bachelor is an unmarried man,” “a square is an equilateral rectangle,” and the like, identity theory contains an assertion of a contingent, empirically verifiable fact. Mental states could also be identical with completely different states, but it has been established by science that they are identical with neurophysiological states.

Still, the critique of identity theory was not hard to come by. At this point two variations of objections can be distinguished8. Firstly, the neurophysiological side of the identity proposition has been the starting point for objections. Here the argument of “multiple realizability” is especially pertinent. In the case that indistinguishable mental states could each be realized through different brain states, they would not, contrary to the proposition of identity theory, be identical to specific neurophysiological states after all. Secondly, it is questionable whether mental states in their usual taxonomy can be rendered at all as identical with any underlying brain states. The terminology, with which we categories mental states as desires, hopes, etc., has been around long before anyone ever had any insight into brain processes, and it seems therefore unlikely that clear equivalents can be found.

The identity theorists postulate a strict identity of mental states and neurophysiological states. The proposition is that indistinguishable mental phenomena each correspond to the same physiological states. But, as the objection goes, it is not only conceivable, but even extremely likely that many animals experience states of consciousness such as for example pain. Yet the nervous system and brains of many animals vary widely from those of humans. Therefore, it is completely unlikely to ever be able to identify specific neurophysiological states with mental states. A bird's feeling of pain, or that of a perhaps unknown creature, could be based on radically different physiological states. This is one possible way of formulating the argument of “multiple realizability.”

The objection itself was first advanced by Hilary Putman (1967). For strong forms of identity theory it has proven to be fatal, but not necessarily for weaker ones. Putnam supports identity theory with a strong proposition. He claims that the theory has to show, for example that a feeling of pain can always be identified with a specific neurophysiological state. If, however, different physical states can accompany the same mental state (feelings of pain), then this proposition falls apart. “Consider what the brain-state theorist has to do to make good his claims. He has to specify a physical-chemical state such that any organism (not just a mammal) is in pain if and only if (a) it possesses a brain of a suitable physical-chemical structure; and (b) its brain is in that physical-chemical state. This means that the physical-chemical state in question must be a possible state of a mammalian brain, a reptilian brain, a mollusc's brain (octopuses are mollusca, and certainly feel pain), etc. At the same time, it must not be a possible (physically possible) state of the brain of any physically possible creature that cannot feel pain” (Putman, 1967, 53).

The philosophers that support identity theory have only inadequately explained what they understand as mental states. It would be, for example, conceivable not to simply identify unspecified feelings of pain with one neurophysiological state, but rather “sharp” pain, “dull” pain, etc. It would be equally possible, naturally, to realize the classification of species-specific mental states. Then human pain could be identified with the neurophysiological state X, octopus pain with mollusc state Y, etc. Such species-oriented reduction seems to weaken Putman's argument. But even if we restrict ourselves to examples of mental phenomena in humans, it remains unlikely to be able to carry out identification at a higher level of mental states. Consider, for example, a desire to travel to London. This desire realizes itself clearly within an entire web of other mental states: for instance the belief that London lies in England; the belief that London is beautiful; the knowledge that one has an important appointment there. Even given all that we know about the brain, it appears hopeless ever to be able to match such a state one-for-one with a neurophysiological state. The brain (and also the respective mental state) is simply too complex to be able to ascribe such identities9.

There is still the alternative of weakening statements of identity by making the classification of mental states more finely granulated. Hence it could be the case, for example that we can identify a specific neurophysiological state with the mental state “sensing an orange in a veiled and darkened room.” Yet here it would be unclear what advantage would come of this kind of reduction. The more that identity theory specifies the types of mental states that they want to identify, the more they lose its original advantage, namely its simplicity. But it does not necessarily follow from the lack of plausibility of such type-identification that mental phenomena are not, on particular levels, after all identical with physical events. This is the proposition of the so-called token-identity. This theory attributes the identity of every single mental event (token), for example the belief of person X at time t that it will rain today, to a single neurophysiological event. This is admittedly an extremely weak identity thesis, but it guarantees the maintenance of a non-dualistic position. Still, it apparently prevents any reasonable reduction of the explanation of mental states to physiological states, and is therefore inadequate as an argument against the autonomy of the concept of mental illness.

There is a yet another way to understand type-identity: If every realization of a type of mental states could be subsumed to a class of neurophysiological states, then the argument of multiple realization would be defeated. Suppose the belief that Berlin is the capital of Germany would be realized in the respective neurophysiological states N1, N2, N3, etc. Due to this assumption multiple realizability would be safeguarded, because the belief would not always be identical to one and the same neurophysiological state. If, however, N1, N2, N3, etc. could be subsumed to a class, then a kind of type-identity would be saved (Rosenthal, 1994, 351; Hannan, 1994, 21f.).

Maybe we could identify particular mental illnesses with distinct classes of neurophysiological states, in the sense that all realizations of a mental illness would fall under a neurophysiological class. The following is an example: Suppose that schizophrenia in person X were realized in neurophysiological state N(X), in person Y in state N(Y), etc. Now it appears that N(X), N(Y), etc. all belong to a distinct class S. Then it would evidently be possible to reduce the explanation for schizophrenia to the class S. Whether we can show that I cannot say, but the chances seem (theoretically) not so bad10. On the other hand the question remains whether through S we have really explained and reduced the mental phenomena-type schizophrenia completely. This is arguably not the case. One important reason to me seems to be the following: To subsume such mental phenomena as “schizophrenia” assumes that they have in common a particular property, namely that they are cases of disorders of “normal” mental states. Even if it were indeed the case that S underlies all these states, the mere reference to S does not explain the pathology of the schizophrenic realizations (see also Margolis, 1991). We only show that there is a correlation between the mental states and a type of neurophysiological states. The claim that all instances of S have the property of realizing a disordered neurophysiological process is only possible on the psychological level of explanation. The fact that specific mental phenomena count as a mental illness cannot therefore be explained exclusively through brain physiology. In this respect I take the assertion that mental illnesses are brain illnesses (or diseases, for that matter) to be truncated. The assertion conceals that being ill is explained and only recognizable on the psychological level. A psychological explanation of mental illness is in this regard autonomous in relation to physiological attempts at explanation.

Even if all counterarguments up to now are not sufficient for a complete repudiation of identity theory, can the theory ever show itself to be true? The second of the objections to be presented here focuses on the mental side of the identity thesis in replying to the question introduced, i.e., the question about the possibility of reducing the mental to the physical level11. Mental states are normally grouped into so-called propositional attitudes (for example desires, beliefs, hopes, which all have propositional content) and sensations (pain, sensual perception, etc.). We use this classification in order to make actions comprehensible. If we see someone running in the train station, then we understand this behavior in that we ascribe to the person certain beliefs—for example that the train is about to leave—and desires—that he wants to board the train before it leaves. We can even make our own actions comprehensible with these categories, such as in the following example: “I took my hand away because I suddenly felt a sharp pain.” At the same time there are certain principles that guide our explanations, such as, for instance, if a person would carry out action A when she has the chance, because she has the desire X and believes that A will achieve X. Together these categories and principles amount to an apparently useful basis for the explanation and prediction of behavior. This is not an especially complicated psychological theory that requires its own field of study, but rather an accumulation of concepts and rules, which are regularly used on an everyday basis. This tool has been given the short-hand name “folk-psychology”12. Already for hundreds of years—and long before anyone ever knew about brain processes—this has been used by people, at least in a similar form, in order to interpret their behaviors. Yet identity theory claims that there is a one-to-one correspondence between neurophysiological processes—any knowledge about which we have only ever gathered in the last few decades—and the taxonomy of folk-psychology. It seems more than unlikely, however, that categories that originated long before our knowledge of the brain and nervous system can be precisely identified with corresponding neurophysiological types of processes. It would be just about as likely as a correspondence between the disease taxonomy of Paracelsus and the newest insights into physiological processes in the human body.

Eliminative Materialism

The results of this examination up to now suggest a certain skepticism toward reductive theories in philosophy of the mind. To be sure, mental states are not on the one hand non-physiological states, since they are apparently realized through physiological processes in the brain. On the other hand the world of the mental is not entirely physiologically explicable. “The desire to drink a beer causes him to go into the pub.” “The detective followed the murderer because he believed he wanted to hide the weapon of the crime.” It is questionable how such complex situations could be described meaningfully on a purely physical level. In this regard we have levels of explanation that are independent and irreducible. Folk-psychology works on this level. But are its explanations correct? Proponents of Eliminative Materialism (EM) answer this question in the negative13. Going further, they actually come to the radical conclusion that these states, which we and other creatures are ascribed to within the framework of folk-psychology, do not exist. There are no desires, beliefs, fears, etc. This thesis contains the eliminative side of EM. Propositional attitudes (and even states of experience like feelings of pain, here depending on what EM exactly sees as elements of folk-psychology)14 are removed of their ontological legitimation, whereby they are relegated to the sphere of myth.

This is a truly radical proposition, and I will try to illustrate why it is not as unintelligible as it may at first seem. Certainly it should be clear that—if EM is right—it would have equally radical consequences for our conception of mental illness. If the sphere of the mental, in the way that we describe and explain it every day, is non-existent in the strictest sense, then this would really revolutionize its conceptualization as well as the categorization of single types of illnesses. Whether the mental disease concept in its own independent framework would also be lost depends on which level of explanation is chosen for the corresponding phenomena. If there were a (future) scientific psychology that would then replace the eliminated folk psychology, then talk of mental disease would—in my opinion—still be warranted15. However, because the main supporters of EM want to see folk psychology eliminated to the benefit of a (future) neurophysiology, it is questionable whether there could still be mental illnesses in the strictest sense16.

The discussion concerning EM's persuasiveness is therefore linked primarily to the status of folk psychology. Ironically the latter's irreducibility becomes a symptom of its superfluity. Because mental states are based on physical states, a neurophysiological explanation should support the folk-psychological explanation. That was also the claim of identity theory. Now it has been shown, however, that explanations on the level of folk psychology cannot be reduced to a neurophysiological level. And precisely because this irreducibility relation exists, it can be shown that folk psychology and neurophysiology are incommensurable. Temperature could be successfully reduced to molecular kinetic energy, and therefore can continue to be seen as existing. Conversely, no one could find a scientific explanation for witches that were commensurable with superstition, and so witches count as non-existing. The more we learn about the functionality of the brain the clearer it becomes that there are practically no equivocations to be made from the folk-psychologically explained mental states to neurophysiological levels. But when two approaches of explanation are incompatible, then it is to be taken that at least one is false, in which case it should be discarded. The claim of EM is naturally that folk psychology is false and therefore has to disappear. To this degree mental states go the way of witches: They are expelled from the scientific ontology.

In short, EM consists of two premises and one conclusion (cf. Stich, 1996, 4). Premise 1: Folk psychology is a theory. Premise 2: Folk psychology is false. Conclusion: The mental states postulated by folk psychology do not exist and can play no role in any future explanation of behavior.

Which objections are addressed toward EM?17 Its first premise pertains to the form of folk psychology: Does it really represent a theory? This claim is essential for EM's proposition, for otherwise it would be questionable why we should drop folk psychology. The assumption of EM is that folk psychology aims to provide explanations and predictions of behavior, and therefore contains certain claims and supports certain principles, etc. If this were not the case, then it would not compete with a neurological explanation of the same issue, and would therefore not be an eligible candidate for elimination. It seems to me, on the basis of the already discussed need for a psychological perspective to establish distinct mental disorders that we cannot abandon the corresponding vocabulary and its related theoretical constructs.

The second premise of EM states that folk psychology as a theory is false, because it leaves many phenomena unexplained and is therefore incompatible with the underlying natural sciences: “(…) what we must say is that FP [folk psychology, TS] suffers explanatory failures on an epic scale that it has been stagnant for at least twenty-five centuries, and that its categories appear (so far) to be incommensurable with or orthogonal to the categories of the background physical science whose long term claim to explain human behavior seems undeniable. Any theory that meets this description must be allowed a serious candidate for outright elimination” (Churchland, 1981, 212).

Churchland sees shortcomings to the explanations of folk psychology in the areas of, e.g., creativity, intelligence, sleep, memory, sensory illusions, and—especially interesting for our analysis—in relation to mental illness. This suggestion of Churchland's is not easy to counter. It seems true that we can learn fairly little about mental illness through the help of folk-psychological conceptions and principles. But does folk psychology even have this aim? A theory can only be untrue in that area where it claims to have explanatory value. Otherwise it does not at all seek to compete with other theories such as neurophysiology or a “scientific” psychology.

Churchland's claim that folk psychology breaks down or fails as a theory apparently stems from the assumption that it does compete with neurophysiology. Then it would be an appropriate candidate for elimination. But this assumption is not straightforward. First the role and aim of folk psychology would have to be clarified. There is much to indicate that even when it is not all that successful as a theory, neither is it so false that it has to be eliminated, nor does it have to be replaced by a (future) neurophysiology. Even if it is replaced, it would be done so by a scientific theory that is situated on the same level of explanation—that is, a psychological one. Folk psychology works on a macro level, and neurophysiology on a micro level. In this regard the irreducibility of folk psychology does not necessarily lead to its incommensurability with neurophysiology. Each explains phenomena, but simply on two different levels of abstraction.

Psychiatric explanations of disease phenomena would not manage without psychological conceptions. Which role folk psychology will keep in the process is still undecided; but to eliminate it is neither necessary on theoretical grounds nor advisable on practical grounds, for it is through its coarse grain that in the end the psychological perspective facilitates our access to the mental world.

Conclusion

The reductive and eliminative theories of the mind-body problem are not convincing. The reductive versions largely fail for the lack of correlation between types of mental and neurophysiological states. Identity theory seems to apply on the level of single mental events. Thereby, however, only an ontologically non-dualistic position is implied, and not at all the superfluity of mental terminology. On the contrary, mental illness is one of the very phenomena that would be unexplainable on an exclusively neurophysiological level, because here no explanation of a single event (token) is being sought, and because the ascription of pathology itself can only happen by taking the mental level into account. The eliminative position fails largely due to its ascription to unreasonably high expectations on the part of folk psychology. Sure it is unlikely that we can adequately explain mental illness with folk-psychological terminology alone. But this finding neither makes folk psychology as such superfluous nor excludes the possibility of a scientific and therefore psychological (and specifically psychiatric) explanation of mental illness.

The concept of mental illness was drawn into question on the basis of reductive and eliminative theories. As a consequence the rejection of these accounts leads to the possibility of an independent conceptualization of mental illness—so long as no further, more convincing objections are brought forward. To be sure, the difficulties of substance dualism prevent any possible explanation of mental illness to be completely independent of physiological knowledge. Mental and bodily phenomena do not belong to principally separate areas. In this regard both the general rejection and the one-sided restriction to brain-physiological explanations of mental illness fail. In brief, even if we have accepted that theories of mental illness are not allowed to be in conflict with the knowledge of neurophysiology, it does not follow that the single (let alone the best) explanation of mental illness can exist on a neurophysiological level.

Even if for many disorders of the mental apparatus no corresponding disorders of brain-physiological processes were found, the language of mental illness does not seem to me to have necessarily failed. The desire for “objective” signs of disease, as they are supposed to be in the brain or in observable behaviors, is understandable. Nevertheless, this is in the end a methodological problem that is posed for a future scientific study of mental illness. It should not lead to discounting any of the two—neurophysiological or mental—perspectives. Mental illness is not reducible to brain illness, even when mental phenomena have their basis in the brain.

The recent publication of the fifth version of the Diagnostic and Statistical Manual of Mental Disorders should cause occasion for the underlying philosophical aspects of the language of mental disorder to make itself clear within the psychiatric trade. The chairpersons of the working committee that put together the DSM-IV had still formulated the following misgivings: “There could arguably not be a worse term than mental disorders to describe the conditions classified in DSM-IV. Mental implies a mind-body dichotomy that is becoming increasingly outmoded (…)” (Frances, 1994, VIII). We should have expected that such mistaken misgivings—which are after all concerning the very foundations of psychiatry—would be resolved by now. A cursory look at current psychiatric publications, however, gives us cause to fear that the same error in reasoning will be made as before: “‘Mental’ implies a Cartesian view of the mind-body problem that minds and brains are separable and entirely distinct realms, an approach that is inconsistent with modern philosophical and neuroscientific views” (Stein et al., 2010, 1760) (18). In this respect we surely have to be skeptical that psychiatric thinking will have seriously progressed. Instead the cure will very likely be looked for in neurobiology. In this article I have attempted to show why psychiatry will not find here what it is looking for and that there is no need to look for a supposed cure, since the concept of mental illness is autonomous from somatic medicine. For philosophers this is no surprising realization; for many psychiatrists, however, the insight seems to remain closed off.

Conflict of Interest Statement

The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Footnotes

¹^In this paper I use “disease,” “illness” and “disorder” synonymously.

²^In this contribution I draw on considerations that were published first in German in my book Schramme (2000).

³^This assumption in reference to the existence of the mental on the basis of its experiential aspects has also once again gained some weight recently in philosophy of psychiatry. To this end new phenomenological approaches, such as those from Fuchs (2004), Gallagher and Vaever (2004), or Ratcliffe (2008), have taken up the experiential attributes of mental disorders. From this perspective we could claim that the challenge of the mental by somatization is itself drawing upon a dualistic starting-point. In virtue of doubting distinct properties of the mental realm, somatization accordingly even results in a rejection of one aspect of human existence, i.e., the mental, which, however, cannot be separated from human corporeality. The contrasting holistic perspective becomes prominent in the concept of Leib (lived body), which accordingly plays an important role in the phenomenological tradition.

⁴^A more extensive critical evaluation of Szasz's position, and of other critics of the concept of mental illness, can be found in Schramme (2004).

⁵^Unfortunately there is still very little cooperation between philosophy and psychiatry regarding this specific issue as well as the underlying mind-body problem. The psychiatric literature is relatively unaffected by the elaborate debates in philosophy. In turn, a theory in philosophy will still seldom be examined against concrete examples, such as those found in psychiatry. It would be important to achieve stronger cooperation here, and on the whole I see this article to be an attempt at mediation. There are in the meantime some interesting publications that are headed in this direction. To highlight just a few: Wilkes (1988); Graham and Stephens (1994); Griffiths (1994); Northoff (1997); Ghaemi (2003); Radden (2004); Murphy (2006); Bolton (2008); Kendler and Parnas (2008); Graham and Stephens (2010), and Graham and Stephens (1994) founded periodical Philosophy, Psychiatry & Psychology; see also Schramme and Thome (2004).

⁶^Eisenberg and Lipowski coined the terms “mindless” and “brainless” psychiatry (compare Sullivan (1990), p. 271).

⁷^It is meant thereby that every mental state can in principle be fully explained exclusively in reference to neurophysiological processes. Compare for example Smart (1959) p. 54.

⁸^Here I ignore a whole line of objections, which deal with so-called qualia that is, the specific, felt qualities of a mental state. These objections are not limited to the identity theory introduced here, but rather are in part turned in general against physicalism, disputing therefore that mental states possess exclusively physical attributes. The best known versions of these objections come from Nagel (1974) and Jackson (1982, 1986).

⁹^Beckermann (1996, 6) points out that after injuries to the brain many mental processes of other parts of the brain, which previously were not involved, can be realized. To an extent this would be an intrapersonal variation of the argument of multiple realization. In my opinion the neuroplasticity of the brain is a general argument against the possibility of simple identification, which, however, I will ignore.

¹⁰^Practically there are certainly significant problems, for in order to show that the single neurophysiological processes actually fall under a certain type one has to acquire a detailed knowledge of them. However, “The more precisely one wants to establish neural state N as the origin of a behavior, the greater does one change the brain and the overall situation of the test subject … ” (Tetens, 1992, p. 121). Tetens describes this as a “fuzziness relation” of neurobiology, and argues “Already for this reason naturalistic descriptions of the human being are not practically realizable alternatives to the mental-psychological descriptions.”

¹¹^It can be found for example in Churchland (1988 p. 27 f.) This objection is, as it will later become clear, not merely advanced against the plausibility of identity theory, but also serves as an argument for eliminative materialism.

¹²^Sometimes common-sense-psychology is also being used, because the expression “folk psychology” has a pejorative connotation.

¹³^The term “eliminative materialism” stems from Cornman (1968). It was already used earlier in the sixties by Feyerabend (1970) and Rorty (1965) in a similar form. The main supporters of a “modern” EM are Patricia and Paul Churchland.

¹⁴^Sometimes only propositional attitudes are attributed to folk psychology. Hannan (1994, p. 45) points out that supporters of EM are often less critical of qualitative states. But Churchland (1994, (308) explicitly specifies pain for example as a component of folk psychology).

¹⁵^Naturally I do not want to claim that the future psychology will manage without any reference to physiological and chemical processes in the brain. Already today the borders are fluid. The independence of the concept of mental illness would be kept alive in the maintenance of a genuine psychological terminology in this science. An attempt to discuss the theory of EM from a psychiatric point of view is undertaken by Harrison (1991).

¹⁶^In this regard EM as such is not a threat to the mental illness concept (even if for today's existing classification of mental illnesses), but rather only in a certain version. Some arguments for why a future science of mental phenomena should not be exclusively located on a neural level can be found in Kitcher (1996). To be sure, it is not always clear from the Churchlands' writings whether they expect the elimination of psychology in general or of only folk psychology.

¹⁷^One objection to EM that I do not find convincing, but will mention for the sake of thoroughness, is that it is self-defeating: The theory of EM contains the premise that beliefs, etc. do not exist. It is objected that one can only sensible formulate this premise, however, with recourse to the affected states themselves, for example beliefs. To me this objection seems to be begging the question, because it assumes the same manner of speaking that is put in question. An expression of the theses of EM may very well radically change, once folk psychology is eliminated. Hannan (1994, p. 62 ff.) puts more faith in this objection. For a defense against this charge see Churchland (1986, p. 397 f.); Churchland (1988, p. 48).

¹⁸^This article was mentioned on the DSM-5 website as background for the planned revision of the definition of “mental disorder”: http://www.dsm5.org/proposedrevision/Pages/proposedrevision.aspx?rid=465# [Accessed 14. September 2012]. The reference has since been deleted from the website.

References available at the Frontiers site