Drossman’s focus on the psychosocial in gut disorders — a critique

One could consider that I received a symbolic birthday gift when I learnt that Douglas Drossman — the leading figure of the Rome foundation — is retiring this month.

For someone who proclaims to fight stigma against patients with “functional” gut disorders1, he has done an awful lot to repackage some older, now largely out of favour, controversial ideas (e.g. irritable bowel syndrome [IBS] being largely psychogenic) into discourse using terms and descriptions more palatable to the modern scientific discourse. His main “contribution” to the field of gastroenterology is taking the general biopsychosocial model of disease contrived by Engel — his mentor — extrapolating and refining it for use in the more underresearched conditions in gastroenterology; so called functional gut disorders, or disorders of gut-brain interaction, as they have more recently been dubbed.

Engel and his biopsychosocial model

The biopsychosocial model of disease, as invented by Engel, in short presents as follows:

Predicated on the systems approach, the biopsychosocial model dispenses with the scientifically archaic principles of dualism and reductionism and replaces the simple cause-and-effect explanations of linear causality with reciprocal causal models. Health, disease and disability thus are conceptualized in terms of the relative intactness and functioning of each component system on each hierarchical level. Overall health reflects a high level of intra- and intersystemic harmony. Such harmony may be disrupted at any level, at the cellular, at the organ system, at the whole person or at the community levels. Whether the resulting disturbance is contained at the level at which it is initiated or whether other levels become implicated is a function of the capacity of that system to adjust to change. For example, a modification in an individual’s social environment, impacting first on the psychological functions of perception and appraisal, may be successfully accommodated at the psychological level and hence give rise to no perceptible reverberations elsewhere. Similarly, a molecular substance introduced into the body might be broken down, excreted, neutralized or inactivated without implicating any but the particular molecular, cellular, tissue, or organ system required for its disposal. In both instances the systems involved have the capacity to handle the imposed change without disruption. Yet under different circumstances or with another individual with a different past history the very same social change or the very same molecules may induce profound disruptions involving many systems in the hierarchy. Such contrasts between smooth functioning and disruption provide the basis upon which health, disease, illness and disability may be differentiated. Central to this perspective are not only the dynamic interrelations that determine relative degrees of intra- and intersystemic harmony or disruption, but also the fact that every change becomes part of the history of each system, rendering it different at every successive point in time. In the biopsychosocial model there can be no return to status quo ante. Health restored is not the former state of health but represents a different intersystemic harmony than existed before the illness, with characteristics based on all the system changes incurred during the illness. By virtue of the illness not only is the individual changed as a person, but so too may be changed others in relationship to him, in the family as well as the community (FIGURES 2 and 3).2

For now, we just have to understand their intuitions behind this model of disease. Engel, and later Drossman, propose that biopsychosocial model of disease is more complete than the biomedical one. For the biomedical model only inspects the changes at the level of one person/body, as opposed to all the levels. They suggest that changes at different levels of the system (family, community, society-nation) may influence how a body responds to the same offending factor, which may be well-tolerated under some circumstances (well functioning family, community and other “systems”), but may cause disease under different circumstances. The figure below may better illustrate his argument:

Figure taken from Engel, G.L. (1978), THE BIOPSYCHOSOCIAL MODEL AND THE EDUCATION OF HEALTH PROFESSIONALS*†. Annals of the New York Academy of Sciences, 310: 169-181. https://doi.org/10.1111/j.1749-6632.1978.tb22070.x

So far, the difference between purely psychogenic disease and a “functional” disorder in this line of thought is unclear. This is because there really isn’t any. What Engel mainly succeeds to do in this paper is berate the biomedical model of disease; he gets angry, from a surprisingly humanistic perspective, at clinicians overinvestigating their patients, but he ultimately misdiagnoses where the problem lies.

I see this widespread adaptation of the BPS model of disease as a band-aid on the shortcomings of the current medical system, a biopolitical tool to justify redirecting patients, who have (poorly understood) physical conditions that poorly respond to current medical treatments, to various psychological specialists. Less so as a genuine addition to the understanding of the disease.
But let us play the devil’s advocate for a moment, and assume for the sake of the argument that the BPS model is at least clinically useful. Undoubtedly stress in family, society etc. have some effect on an individual, and it is not difficult to imagine that this may affect a person. As there are no biomarkers that would “show up” on tests available to a clinician, the presumed advantage of the model here would be pointing to perceptible changes in one of the other levels (family, community, state etc.) that could be considered a trigger of the disease.
These psychosocial factors still have no explanatory power on their own, not unless they are translated into clear-cut biological processes, as even evidenced by an overly long example given by Engel:

[…] Interview of this particular patient documented this indeed to have been the case.
The dogged persistence of the intern in perservering in his efforts to perform the
arterial puncture, without either explanation to the patient or attention to his distress
and pain, induced intense patient anger and frustration, an abrupt loss of confidence
in those providing care, followed by a growing sense of impotence to do anything
about the situation in which he found himself.‘
The occurrence of ventricular fibrillation at that point is in keeping with well-established
knowledge documenting the ability of increased autonomic activity and
catecholamine secretion to lower threshold for ventricular fibrillation in the presence
of an existing substratum of myocardial electrical instability, in this instance based
on myocardial infarction.3

In essence, stress in this example has biological (catecholamine surge etc.) correlates. The presence of stress and how it relates to other things, with the availability of appropriate tools, could be inferred by studying physiological changes in the body alone. Hence, biomedical model with advanced enough instruments should be no inferior to the BPS model, even if we assume that stress is one of the biggest players in disease.

I would, however, like to argue that this excessive focus on the psychosocial factors shifts attention from researching the actual pathophysiology (e.g. immune system overactivation) of some particular disease to obsessing over contributing factors (e.g. childhood trauma). Psychosocial factors alone will never explain why some patients will vomit, while others will have diarrhoea. Some will be constipated, others will have abdominal pain or early fullness. Some upper GI, some lower GI.

Drossman and DGBI

The whole edifice of disorders of gut-brain interaction rests on Drossman building upon this model, and conducting a couple of brain imaging studies:

The emerging evidence is that central processes, mediated by psychosocial distress, contribute to
pain perception, at least as much or more than visceral signals. Patients with more severe IBS
are distinguished from those with milder IBS by having greater psychological distress and disturbances yet with no differences in visceral sensation thresholds.4

The last sentence in the above quote is citing a different study, conducted by the same author, in which the results were much less unambiguous than suggested:

Patients with severe FBD were characterized by greater depression and psychological distress, poorer physical functioning and health-related quality of life, more maladaptive coping strategies, and greater health care utilization. There was a trend for patients with severe FBD to
have lower rectal sensation thresholds. Regression analysis indicated that severity was best predicted by behavioral features: poorer daily physical function, difficulties related to eating, more phone calls to the physician, and more days in bed for GI symptoms.5

The trend was very apparent:

But it did not reach statistical significance, so it was ignored by the authors. Their main focus were various psychosocial scores:

Patients with severe FBD reported significantly higher scores on the the Beck Depression Inventory (p , 0.005), the Overall Scale of the Sickness Impact Profile (p , 0.0001), and most subscales of the SIP (p , 0.01 to p , 0.0001). Patients with severe FBD also reported higher scores on the Catastrophizing Scale of the Coping Strategies Questionnaire (p , 0.0001), as well as less perceived ability to control (p , 0.05) or decrease (p , 0.01) symptoms. Finally, the severe FBD group showed significantly poorer quality of life on the Overall score on the IBS-QOL (p , 0.0003). There were no statistically significant differences with regard to SCL-90R GSI (trend at p , 0.07), neuroticism, social support, or dysfunctional attitudes. We also compared the frequency of physical and sexual abuse reported by questionnaire. There was a higher frequency of all types of abuse by the moderate group (57% vs 40%; p , 0.02). When evaluating the frequency of rape, the difference between groups was no longer statistically significant (22.2% vs 13%; p 5 0.13).

[…]

Patients with severe FBD reported more days in bed for GI symptoms (p , 0.0001), more overnight admissions for GI problems .3 months (p , 0.03), more physician visits for GI and other symptoms .3 months (p , 0.0001), more phone calls for GI symptoms .3 months (p , 0.0001), and more hospitalizations in the previous 2 yr (0.0001). There was a trend toward more nightly stays in the hospital (p , 0.08) and more lifetime surgeries (p , 0.10). There was no difference between groups for the number of endoscopic and surgical procedure over the previous 3 months.6

It is not difficult to see how increased symptoms and pain would lead to experiencing worse depression and anxiety. I do not want to go into an overlong segue here, but if one had the displeasure of dealing with medico-industrial complex with some serious disease in probably any country, they will know how harrowingly hellish and soul-sucking experience it is. It is pretty self-explanatory to such groups of people how one may succumb to “catastrophization” when being subject to constant abuse by the very ones whose help they are seeking (see the footnote for more).7
Drossman, however, think the causation works in the other direction, and that severe cases of FBDs are severe not because of worse physical symptoms. He seems to imply that their physical symptoms, in contrast to moderate patients, are “amplified” within the brain, and by and large seems to suggest that this kind of central sensitization is a result of various types of psychological trauma:

Patients with more severe IBS are distinguished from those with milder IBS by having greater psychological distress and disturbances yet with no differences in visceral sensation thresholds. Thus while chronic stress affects reports of pain perception, it does not appear to affect sensory thresholds. In fact, FGID patients with a history of sexual or physical abuse report greater pain but have higher visceral sensation thresholds.8

Again, the fragment about no different sensory tresholds feels like presenting findings from a different study in a way that would specifically support the conclusions they want to prove.

Overall, Drossman seems to recognize that there are often some pathophysiological processes going on within the viscera, but he seems to think stress is a “permissive factor”:

This is best demonstrated with post infectious IBS (PI-IBS) where the persistence of functional gastrointestinal symptoms for several months after a bacterial infection is associated not only with increased inflammation in the gut mucosa but also with increased psychological distress present at the time of the initial infection. In fact, these associations were present even when the abnormal motility and visceral hypersensitivity were similar between PI-IBS patients and those who became asymptomatic after the infection. Thus it was the CNS amplification of these peripheral signals in the psychologically distressed group that raised them to conscious awareness, thereby perpetuating the symptoms.9

Thus, imputing that for the symptoms to manifest, visceral pathology is not enough, and some problem within the brain is necessary.

I think we are finally getting to the heart of the matter. As, you may notice that Drossman often tends to move back and forth between using psychological and neurological terms, almost interchangeably.

The language that he chooses to speak about people with those diseases is also quite telling:

In a sample of 94 patients with acute gastroenteritis studied in an infectious disease unit, 22 (23%) were found three months later to fulfil Rome criteria for IBS. When comparing this group of symptomatic patients (IBS+) to the remaining sample (77%) who resolved their gut symptoms (IBS−), three major findings were noted. (1) Psychosocial difficulties were again shown to influence who with acute gastroenteritis would remain symptomatic. Specifically, in a regression analysis, pre-existent life stress and hypochondriasis were the strongest predictors of the IBS+ group, and the development of IBS-like symptoms was not explained by illness behaviours. (2) Acute gastroenteritis was associated with increased numbers (relative to biopsy samples taken from a healthy control group) of rectal inflammatory cells. However, three months later, only the IBS+ group continued to have increased mucosal inflammation. (3) When compared with healthy controls, those with the acute gastroenteritis went on at three months to develop physiological evidence of gut dysfunction— reduced whole gut transit time, decreased sensation threshold to rectal distension, decreased rectal compliance and reduced number of rectal contractions. However, there were no significant differences physiologically between the IBS+ and IBS− groups. One conclusion noted by the authors harmonises with a biopsychosocial understanding of IBS: “. . .physiological changes predispose to IBS, but psychological factors are required to bring out the perception of these physiological changes as symptoms.” So, the presence of dysmotility or visceral hypersensitivity is not sufficient to explain fully the symptoms of IBS;

I find these conclusions to be embarassingly simplistic, especially for such a heterogenous group of diseases as IBS. Aside from my reservations about the way they presented data about rectal tresholds, I want to point out that maybe measuring gut transit and inflating a balloon up someone’s ass is not the best model of a very complex bowel disorders (admittedly, I have no access to the cited study, so I am not able to verify Drossman’s report of the findings). Naturally, it won’t show all the changes at the level of enteric glia, coeliac plexus, mesenteric ganglia, pelvic nerves, spinal cord, or even the colon itself. The author seems to take quite a leap straight to the brain, ignoring all the intermediate processing neurological agents. Notably, increased input from any of those agents (which are not easily accessible to study in vivo), could explain subsequent increase in various brain regions they found on brain imaging:

With regard to IBS, several published studies indicate differences in levels of activation between patients with IBS and normal controls of these corticolimbic pain modulatory systems. Despite inconsistencies across the studies, in general there is an association of ACC activation to rectal distension in IBS relative to controls. Studies using both fMRI and PET show increases in activity of unspecified areas of the ACC compared with controls while others show increased activity of the aMCC or pACC compared with controls, thus linking emotion or fear with visceral pain in these patients, and others show increased pACC activity in controls relative to IBS Some of these studies also show an expected correlation between ACC activation and greater pain reports to rectal distension.10

Interestingly, the author is well-aware of all the problems with brain imaging, but this disclaimer is not often given in works based on Drossman’s hypotheses:

(a) activations often involve neural circuitry of several interacting regions (which for simplicity are not discussed) which make it difficult to target single sites,

(b) there may be imaging differences between PET and fMRI,

(c) sex differences exist,

(d) there are confounding effects on the registration of images to rectal distension with anticipation of that event,

(e) there may be confounding central influences, such as placebo effects,11

(f) there is clinical heterogeneity among patients with regard to diagnosis and severity of the disorders, and

(g) there are methodological issues in technique, lack of instrument and protocol standardisation, low ‘‘signal to noise’’ ratios, and limitations in measuring functionally heterogeneous regions of the cingulate and other brain regions.12

This does not even take into account the fact, that once an etiology of some condition is established, it suddenly stops being a “disorder of gut-brain interaction” and starts functioning as a well-defined disease with precise pharmacological targets (see bile acid malabsorption‘s case) and is not called IBS-D anymore.

All of the above unfortunately fuels a lot of uninteresting research about those disorders, and lends some credence to specialists showing you a picture of a naked squatting goblin as a treatment device for bowel disorders.

Footnotes

  1. Feingold JH, Drossman DA. Deconstructing stigma as a barrier to treating DGBI: Lessons for clinicians. Neurogastroenterol Motil. 2021 Feb;33(2):e14080. doi: 10.1111/nmo.14080. Epub 2021 Jan 23. PMID: 33484225; PMCID: PMC8091160. ↩︎
  2. Engel, G.L. (1978), THE BIOPSYCHOSOCIAL MODEL AND THE EDUCATION OF HEALTH PROFESSIONALS*†. Annals of the New York Academy of Sciences, 310: 169-181. https://doi.org/10.1111/j.1749-6632.1978.tb22070.x ↩︎
  3. Engel, G.L. (1978), THE BIOPSYCHOSOCIAL MODEL AND THE EDUCATION OF HEALTH PROFESSIONALS*†. Annals of the New York Academy of Sciences, 310: 169-181. https://doi.org/10.1111/j.1749-6632.1978.tb22070.x
    Afterwards, he goes on to draw some bizarre, if not outright laughable, conclusions that are not worth invoking here. ↩︎
  4. Drossman, D. A. (2005). Brain imaging and its implications for studying centrally targeted treatments in irritable bowel syndrome: a primer for gastroenterologists. Gut, 54(5), 569-573. ↩︎
  5. Drossman, D. A., Whitehead, W. E., Toner, B. B., Diamant, N., Hu, Y. J., Bangdiwala, S. I., & Jia, H. (2000). What determines severity among patients with painful functional bowel disorders?. Official journal of the American College of Gastroenterology| ACG, 95(4), 974-980. ↩︎
  6. Drossman, D. A., Whitehead, W. E., Toner, B. B., Diamant, N., Hu, Y. J., Bangdiwala, S. I., & Jia, H. (2000). What determines severity among patients with painful functional bowel disorders?. Official journal of the American College of Gastroenterology| ACG, 95(4), 974-980. ↩︎
  7. The term “catastrophization” seems to suggest some maladaptive mechanism that is not grounded in reality. As mentioned, when you’ve been failed time after time, with no improvement in your condition, or you are stuck in a medical limbo of referrals, diagnostics, underwhelming treatments for years with no answers and no end in sight, it it difficult to see lack of hope for improvement as unfounded. ↩︎
  8. Drossman, D. A. (2005). Brain imaging and its implications for studying centrally targeted treatments in irritable bowel syndrome: a primer for gastroenterologists. Gut, 54(5), 569-573. ↩︎
  9. Drossman, D. A. (2005). Brain imaging and its implications for studying centrally targeted treatments in irritable bowel syndrome: a primer for gastroenterologists. Gut, 54(5), 569-573. ↩︎
  10. Drossman, D. A. (2005). Brain imaging and its implications for studying centrally targeted treatments in irritable bowel syndrome: a primer for gastroenterologists. Gut, 54(5), 569-573. ↩︎
  11. See the fragment on neural correlates of visceral analgesia in my article about gut-directed hypnotherapy. ↩︎
  12. Drossman, D. A. (2005). Brain imaging and its implications for studying centrally targeted treatments in irritable bowel syndrome: a primer for gastroenterologists. Gut, 54(5), 569-573. ↩︎