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Prevalence of Viral Illness Immediately Prior to Presentation of
Anorexia Nervosa

Professor Mike Thomas,

University of Chester, UK


Purpose: The study investigated the prevalence of illness, particularly viral, immediately prior to the onset of anorexia nervosa during puberty.

Design and Method: A retrospective evaluation of clinical care records which identified viral onset illness. Two hundred records were scrutinised of which ninety-seven explicitly recorded the DSM-IV-TR (2000) criteria for Anorexia Nervosa diagnosis.

Findings: Thirteen individuals were identified as having experienced a viral illness during puberty and immediately prior to onset of Anorexia Nervosa presentation.

Implications: Further research should be undertaken to ascertain correlation between viral illness and pubescent onset of Anorexia Nervosa. Further work using a clinical inter-disciplinary approach should be undertaken to gain more knowledge regarding the potential for post-viral effects to influence digestion and psychological balance during puberty.


The study objective was to obtain the prevalence of adolescent onset viral-based illnesses prior to the development of severe and enduring eating disorders to provide additional data which builds upon earlier observations and which has practice implications for mental health interventions. Park et al. (1995) commented that the pathogenesis of eating disorders remains indistinct and fragmented and despite some advances in several areas the situation remains similar today. Their work is often cited as an interesting observation yet little further work has built upon their proposal that there may be a possible post-viral disruption involving corticotrophin-releasing hormones (CRH) regulation.

The influence of the hypothalamic-pituitary-adrenal axis in the regulation of eating patterns has been known for nearly half a century. There has been observation of anorexia nervosa symptoms amongst patients diagnosed with hypothalamic and mid-brain tumours (Lewin, Mattingly & Millis, 1972); whilst others discussed anorexia nervosa as a type of depressive illness closely mimicking post-viral depression (Cantwell, Struzenberger, Burroughs, Salkin & Green, 1977) or found a clear relationship between anorexia nervosa and other diagnostic criteria for physical illness (Patton, Wood & Johnson-Sabine, 1986); whilst Park et al. (1995) indicated a possible post-viral disturbance of neuroendocrine responses.

Others such as Maes, Goosens, Scharp, Metzer, D’Hondt and Cosyns (1994) have examined lowered serum prolyl-endopetidase enzyme activity amongst clients diagnosed with major depression and concluded that peptides play a part in the pathophysiology of depression. This is of interest because low mood is a known presenting symptom by clients experiencing anorexia nervosa and is considered by the Diagnostic and Statistical Manual of Mental Disorders IV (DSM IV 1994) as a co-morbid condition amongst clients experiencing bulimia nervosa. Park et al (1995) described four individuals with a diagnosis of severe restrictive anorexia nervosa who self-reported earlier episodes of glandular-fever like illnesses immediately before the onset of eating disorders. One was a nineteen year old woman who had presented with monospot positive glandular fever which caused loss of appetite, weight, menses and mood. Within three months of post-recovery she was diagnosed with anorexia nervosa (Body Mass Index (BMI) = 11.7). Neither she nor her immediate family had any previous psychiatric history and there was no previous history of dieting or of bingeing. At the age of seven years she reported a resolved case of “arthritis” but had no other relevant or significant physical ill-health. Despite regaining weight leading to discharge the woman was readmitted due to rapid relapse. The second client was a thirty-three year old woman with a twelve year history of sub-clinical eating disorder leading to a diagnosis of anorexia nervosa at the age of thirty years. The client had a co-morbid condition of multiple sclerosis and connective tissue disorder and recalled her eating disorder precipitating immediately after suffering glandular fever at the age of eighteen years. The woman was also diagnosed with irritable bowel syndrome. The third client, a woman age twenty-nine years, had a history of restrictive anorexia nervosa since the age of seventeen years following presentation of glandular fever-like symptoms when she was sixteen. Investigations demonstrated adenoviral infection but monospot was negative. There was no family history of mental health problems. The woman had a recurrent urinary tract infection at the age of twelve years which was treated with steroids. There were no other relevant or notable physical illnesses. At the time of the study she was admitted with a BMI of 10. The final case was a thirty-five year old woman with a history of restrictive anorexia nervosa. She recalled at the age of fifteen years a severe episode of pharyngitis and a loss of twelve kilograms in weight. Six months later she was referred to the mental health services and diagnosed with anorexia nervosa. At the age of twenty-nine years the client was diagnosed with a co-morbid obsessive-compulsive disorder and anorexia nervosa. For the past six years the client had spent all but nine months as an in-patient.

Park et al. (1995) suggested that there may be a possibility that viral infections could be a factor in many more cases of eating disorders but these may not be noted unless the infection is of such severity to invoke retention in the individuals memory or a referral to a medical practitioner who would record such illnesses in case notes. They postulated that the loss of appetite and weight commonly presented during a viral illness may precipitate anorexia nervosa in vulnerable individuals or that post-viral melancholy may precipitate a co-morbid depressive anorexia nervosa. Such a proposal replicates other similar conclusions by Cantwell et al. (1977) and Goodwin (1990) and additionally they put forward a further alternative that there may be viral induced alterations in neuroendocrine functions which precipitates restrictive eating disorders. The actual mechanism may be masked by clinical interventions to deal with weight loss and abnormalities in hypothalamic-pituitary results may be due to a primary post-viral cause or be caused by restricted food input and sudden weight loss. Weight gain causes a rebalance in results and may be hiding original sources. For example corticotrophin sensitivity to the inhibitory effects of free fatty acids is preserved in individuals experiencing anorexia nervosa despite persistent adrenal hyperactivity (Lanfranco, Giannotti, Picu, Giordano, Daga, Mondelli, Malfi, Fassino, Ghigo & Arvat, 2006) whilst plasma levels of homovanillic acid (pHVA) recover to within normal levels when individuals experiencing anorexia nervosa gain weight alongside psychopathological improvements suggesting a dopaminergic dysfunction amongst individuals with co-morbid depression (Castro, Deulofeu, Baeza, Casulai, Saura, Laizaro, Puig, Toro & Bernado, 2008). Interestingly Park et al’s (1995) study points out that similar abnormality had been found in the hypothalamic-pituitary-adrenal axis in patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). This is supported by Chia, Chia, Voeller, Lee and Changs’ (2009) more recent study demonstrating three patients with acute enterovirus infections who subsequently developed ME/CFS and who provided evidence of persistent viral infections through the presentation of VP1 and RNA found in the stomach.

Further studies by Patterson (2009) also highlight the difficulties regarding diagnosis. He states that following glandular fever at age thirteen years and a subsequent bout of depression and anorexia nervosa with self-harming behaviours until the age of twenty-one a young female was caught between her general practitioner diagnosing anorexia nervosa and the mental health professional diagnosing myalgic encephalomyelitis/chronic fatigue syndrome. A reduction in her BMI led to two admissions over the next five years and at age twenty-nine years ME/CFS was again queried due to possible Epstein-Barr virus.

The issue of co-morbidity arises frequently when working in the mental health field of eating disorders and disturbance around the hypothalamus implying corticotrophin-releasing hormone (CRH) hypersecretion (typically found in depression) is not uncommon and may explain co-morbid depression (Gold, Gwirtsman, Avgerinos, Nieman, Galluci, Kaye, Rittmaster & Loriaux, 1986). A similar conclusion was reached by Gordon, Laske, Bryant-Waugh, Christie and Timimi (1997) in a study into fifteen cases of child-onset anorexia nervosa. Thirteen children had unilateral temporal lobe hypoperfusion and three continued to present after a weight restoration programme suggesting an underlying primary functional abnormality.

This view is supported by Maes et al’s (1994) findings that serum prolyl-endopetidase (PEP) enzyme activity was lower amongst clients with severe depression. Prolyl-endopeptidase (PEP) is a cytosolic endopeptidase which cleaves peptide bonds on the carbonyl side of praline in proteins of relatively small molecular mass. PEP has substrates which equate to neuroactive peptites and include arginine vasopressin, luteinizing hormone-releasing hormone, thyrotrophin releasing hormone, a-melanocyte secreting hormone, substance P, oxytocin, bradykeinin, neurotensin and angiotensin (Ag) I and II.

Later studies by Maes, Goossens, Lin Ai-Hun, De Meester, Van Gastel and Sharpe, (1998) indicated a raised serum PEP and dipeptidyl peptidase IV amongst individuals engaged in stress-induced activities. Further results found alterations in serum PEP activity related to anxiety levels in early puerperium and post-partum depression (Maes, Libbrecht, Lin Ai-hun, Goossens, Ombelet, Stevens, Altamura, Cox, De Jongh & Sharpe, 2000). Raised serum PEP activity appears to influence post-partum anxiety whilst lowered serum PEP activity may be related to predisposition to major post-partum depression. Further work investigating whether anorexia nervosa and bulimia nervosa were accompanied by lower serum PEP activity suggests a similar picture (Maes, Monteleone, Bencivenga, Goossens, May, Van West, Bosmans & Sharpe, 2001). The serum PEP of sixty women split into three groups; (21 diagnosed with anorexia nervosa; 21 with bulimia nervosa and 18 who were non-symptomatic and within normal weight parameters as the control group) indicated that serum PEP activity was lower in both groups with anorexia nervosa and bulimia nervosa (irrespective of sub-types) compared to the control group. The conclusion was that lowered serum PEP activity takes part in the psychopathology of both anorexia nervosa and bulimia nervosa and the authors hypothesised that combined deregulation of PEP and neuroactive peptites, (the substrates of PEP), could be an integral component in eating disorder conditions. It is not clear how many of the sample in the study had histories of viral illnesses but nevertheless lowered serum prolyl-endopeptidase enzyme activity plays a part in both neuroendocrine and immune pathophysiology depression which is presented as a symptom of, or co-morbid with, eating disorder conditions.

An interesting effect of T-cells expressing high prolyl-endopeptidase activity (correlated with stress and anxiety) is that they are susceptible to cell death. Odaka, Mizuoshi, Shirasawa, Morain, Checler and Murine (2002) noted that immature thymotes are observed to have higher PEP activity and die before full maturation. This may, in part, explain the complex interaction between co-morbid obsessive-compulsive traits as a stress management strategy presented by some individuals living with anorexia nervosa or bulimia nervosa as both types of conditions have raised serum PEP activity. However when there is low serum PEP activity due to immature early cell death the client may present with symptoms of depression or low mood as a co-morbid condition. Individuals may therefore move along a continuum or swing between different co-morbid presentations in both types of severe and enduring eating disorders as condition deteriorates or improves.

A similar presentation to Park et al. (1995) but involving a younger age category was described by Sokol (2000) who presented four cases as infection-triggered anorexia nervosa. All were children and clinical results provided possible antecedent streptococcal infection in all four. Two were believed to have developed co-morbid OCD with possible infection-triggered anorexia nervosa. All four responded to conventional treatment with anti-biotics. The study concluded that there is a link between viral infection diseases and at least some individuals experiencing anorexia nervosa which was strong enough to raise the possibility that new treatment interventions may therefore be required.

Cases of viral infection-triggered eating disorders raise some other interesting issues; it is possible that such inflammatory conditions may have exposed the women in the above studies to susceptibility for eating disorders or viral entry, during adolescence, or entry was eased by earlier illnesses. The clients were also reported to have periods of depression interspersed with compulsive drives to exercise; both cognitive and behavioural psychopathology common amongst individuals with eating disorders but also mimicking differing levels of serum PEP activity. Little has been written about such links regarding eating disorders and Shapiro, Berkman, Brownley, Sedway, Lohr and Bulik et al (2007) concluded following a systematic review that more work is required to generate theory that encourages multi-disciplinary research.


The study objective was to gather evidence for viral and/or endocrinal disorders immediately prior to the onset of an eating disorder and to collect data regarding prevalence and incidence. A retrospective evaluation of data using the criteria of laboratory results and medical/pharmacological intervention for specific clinical diagnosis was carried out to gain data for analysis. Evaluative approaches are commonly applied in the social and health care fields (Gomm, 2004) and using an evaluative review method allows retrospective scrutiny of data and assessment of psychotherapeutic interventions. (Gill and Johnson (2006)). In this study the evaluative method with pre-set criteria enabled an interpretation of retrospective data within a contemporary context which provided analysis to take place (Robson, 2004).
Data relating to 95 consenting clients referred to three out-patient clinics specifically for interventions in severe and enduring or treatment resistant eating disorders (average 12 .6 years) were analysed to ascertain any pre-existing physical illnesses. Screening was undertaken to categorise diagnostic criteria for anorexia nervosa and bulimia nervosa. The review provided data for 62.1% (n=59) of the sample who had been diagnosed within DSMIV criteria 307.1 for anorexia nervosa (purging type n=39 and restrictive type n=20) and 37.8% (n=36) people who presented within the DSMIV criteria 307.51 for diagnosis of bulimia nervosa (purging type).

Exclusion criteria included data which did not meet DSMIV criteria such as binge eating disorders, bulimic patterns amongst individuals diagnosed as morbidly obese and data indicating differential uncertainty; for instance acute weight loss due to undisclosed drug use. Inclusion data were incidences of viral-type infections and significant endocrinological conditions prior to onset, or which were found during development of severe and enduring eating disorder presentations. These were collated and analysed to ascertain incidence and prevalence and the results compared with existing literature.


Gender ratio was 98:2 female: male. Age ranged from 23.2 to 47.8 years. All individuals had co-morbid psychopathological conditions; some individuals had more than two co-morbid conditions. The most common were bulimia nervosa and depression (all clients n=36); anorexia nervosa and depression (all clients n=59); anorexia and anxiety/depression 83% (n=49); anorexia nervosa and obsessive-compulsive traits 46% (n=27); bulimia nervosa and borderline personality disorder 36.4% (n=13); bulimia nervosa and anxiety/depression 14% (n=5). Within the BN group a further 16.6% (n=6) regularly took chemical substances such as amphetamine and cocaine whilst 36.4% (n=13) of clients diagnosed with severe and enduring BN regularly drank alcohol to excess.

Individuals with a diagnosis of anorexia nervosa presented low weight (BMI 15.1 to 17). Common recorded pathophysiological results amongst the group experiencing AN were low potassium, low calcium/phosphate levels, frequent bouts of opportunistic infections, dental problems, (particularly shrunken and bleeding gums) and sleep disturbances.
For individuals diagnosed with bulimia nervosa the data indicated that they were within or above normal weight (BMI average 24.1) and all had chronic physical complaints ranging from joint aches, poor dental health, gastro-intestinal bloating and spasms due to laxative abuse, opportunistic infections and all had been prescribed anti-depressants for a number of years.

Amongst the whole group (=95); 5.2% (n=5) had histories of glandular fever, 4.2% (n=4) reported flu-like illnesses during adolescence, 2.1% (n=2) had diagnosis of hypothalamic tumour whilst one individual was found to have a pituitary microadenoma and one other had a co-morbid diagnosis of Type- 1 diabetes; a total of 13.6% (n= 13).
The data for microadenoma diagnosis are of interest. DSMIV (1994) refer to such conditions generally for differential diagnosis but these incidences appear to be co-morbid conditions. They include a mid-thirties female who presented with a fifteen year history of severe and enduring restrictive type anorexia nervosa and a co-morbid diurnal mood disorder. The retained records show no significant viral infections or childhood illnesses but the client recalled frequent rates of opportunistic infections during periods of depression throughout late adolescence. During her twenties she experienced bouts of over-activity and elation which became progressively longer and despite many years of psychotherapy with regular periods of remission her condition was considered treatment resistive as her eating disorder worsened. On referral and admission to a general hospital following severe anxiety symptoms, extreme thirst and low urine SG, laboratory tests and scan revealed a pituitary tumour. Two year follow-up indicated continuing irregularity of mood and presentation of restrictive type anorexia nervosa, a BMI of 15 and continuing difficulties with maintaining potassium levels.
The data for another female in her twenties with a diagnosis of restrictive type anorexia nervosa and severe co-morbid depression indicated that she had a history of glandular fever at age fourteen after which she had “lost” her appetite, became severely depressed and presented with low BMI of 14.7. She had a history of three previous mental health in-patient episodes and as her condition worsened she was admitted to hospital where laboratory results indicated a hypothalamic tumour. Her condition continued to deteriorate and she was admitted to a specialist unit with severe depression and a BMI of 13.

A similar picture was found with a twenty-six year old diagnosed with severe and enduring bulimia nervosa purging sub-type having first presented with over activity compensatory behaviours at age fifteen. Assessments results for both post-traumatic stress (PTSD) and personality disorder (PD) were significant. Laboratory results indicated latent vaginal candida albicans infection and amenorrhea had been present for several years. Referral to endocrinology resulted in the discovery of a pituitary microadenoma. Following treatment she showed a marked improvement in the psychopathology of bulimia nervosa with cessation of regular bingeing and laxative use, an increase in more appropriate physical activity and a decrease in associated features, particular anxiety symptoms whilst PD scores were lowered although PTSD remained relevant.

Other endocrinal conditions also appear to complicate the presentation of eating disorders. For example a woman in her forties with a history of severe and enduring bulimia nervosa purging type since the age of nineteen years old. Purging occurred several times daily irrespective of the amount of intake. The woman had a co-morbid depression with anxiety. At the age of twenty-eight she was diagnosed late with Type- 1 diabetes mellitus which alongside her bulimic condition disrupted the influence of insulin and has led to severe retinopathy in the right eye and polyneuropathy with particular degeneration in the right thigh. It is highly likely based on the client history that the original diagnosis of bulimia nervosa was incorrect and that she was self-regulating the somatic effects of hypoglycaemia and hyperglycaemia swings through carbohydrate intake and purging. By the time diagnosis of diabetes mellitus occurred it appeared that she had developed a deeply ingrained, habitual, self-management of the underlying condition to cope with co-morbid depression and anxiety. One year follow up following cognitive behavioural and maintenance therapy showed no alteration in depression which remained low; anxiety levels had however lowered and purging was less but still at least once a day. The physical deterioration caused by an uncontrolled diabetes condition slowed but was still significant. The endocrinological disturbances appeared to have a bearing on the bulimic condition itself although it remains unclear which condition precipitated the other or maintained the other.

A typical history of individuals with viral illness can be demonstrated through one individual aged twenty-six years with a diagnosis of treatment resistive severe and enduring BN since the age of fourteen. There were several episodes of opportunistic infections during adolescence, frequent colds and herpes simplex outbreaks which was self-reported as anxiety and stress induced. Immediately following a bout of influenza at age twenty-three the client began to binge and purge several times a day, sometimes on immediate awakening in the morning. The client reported that she was convinced her thought patterns and her ability to self-manage the eating disorder deteriorated due to physical alterations in her brain which she believed were precipitated by the influenza. Follow-up after one year showed persistent low mood and bingeing/purging continued at least once daily. The family reported that the management of the bulimia nervosa condition deteriorated significantly after the influenza illness and that there had been observable deterioration in mood and coping abilities.

The evaluative data analysis suggests that a proportion of individuals who experienced viral illnesses or metabolic disorders may have had a vulnerability to the development of eating disorders classified as anorexia nervosa and bulimia nervosa. In some individuals there appeared to be a pathogenic intervention in normal hypothalamic-pituitary-adrenal function. The structural post-viral damage supported co-morbid conditions which may have presented as actual criteria for diagnosis or may have masked conditions such as post-viral depression (Cantwell et al. 1977), hypothalamic-pituitary adenoma (Lewin et al. 1972), gastrointestinal problems or diabetes. The overall incidences were relatively small but further research on larger samples using dot testing and DNA/RNA tracking for viral relics or post-viral residue may provide a clearer picture.

The work around protein and carbohydrate conversion and the relevance of protein and prion chains to auto-immunology may also provide further links to post-viral effects in relation to neuroendocrine performance and mental health (Goodwin, 1990). The input from endocrinology/virology when carrying out a mental health assessment should be considered as a valuable and standard procedure when relevant and before case formulations and treatment programmes are undertaken.
The evaluations of retrospective data based on specific criteria related to post-viral onset and endocrinological conditions indicates support for earlier studies regarding post-viral onset (Park et al. 1995) and for a possible defect in, or around the hypothalamus related to corticotrophin-releasing hormones (CRH) hypersecretion (Maes et al. 2001). It is interesting to note that like lowered serum prolyl-endopeptidase activity a raised CRH is correlated with depression and can be confounded with co-morbidity in eating disorders. Similar findings have been found amongst clients experiencing myalgic encephalomyelitis/chronic fatigue symptoms and are thought to be due to damage from long-term yet common viral infections (Ablashi, 1994).
Other studies indicate that such long-term damage not only contributes to psychopathological functional presentations but also impacts directly on the physiological structure; for example by reducing cortical blood flow (Yoshiuchi, Farkas & Natelson, 2006). There is evidence that women who experience persistent low weight due to anorexia nervosa present with abnormal brain alterations such as larger lateral ventricles whilst amenorrhea or irregular menses over a long time period appears to have a significant negative effect on cognitive functions (Chui, Christensen, Zipursky, Richards, Hanratty, Kabani, Mikulis & Katzman, 2008).

The effects of growth and neuroendocrine regulation during puberty may expose vulnerable adolescents to common viral sources which may precipitate structural or functional alterations in the immune system which distorts either prion function or the normal enzyme and amino acids processes particularly if there is associated psychopathological distress during this period of maturation (Gold et al. 1986; Sokol, 2000 and also Chui et al. 2008). It is likely that only a minority of individuals may be affected in this way, possibly due to genetic predisposition but the picture is blurred. There may also be a role for sex-characteristics hormonal changes during puberty which may account for the predominance of female presentations with eating disorders but this is speculative at present.

Work continues in the area of cellular prion protein mediates in other fields such as dementia demonstrating links between pathophysiological disease processes at genetic levels which predisposes vulnerable members of the population to synaptic receptor dysfunctions (Lauren, Gimbrel, Nygaard, Gilbert & Strittmatter, 2009). Others have found differences in the influence of the hypothalamic-pituitary-adrenal function on stress responses associated with individuals who have experienced child abuse, particularly in the hippocampal glucocorticoid receptor NR3C1 (McGowan, Sasaki, D’Alessio, Dymov, Labonte, Szyf, Turecki & Meaney, 2009).

There is growing evidence that there may be a subtle relationship between gastrointestinal function and the hypothalamic-pituitary-adrenal axis which crosses the boundaries between psychopathological and pathophysiological presentations. For instance Bohmelt, Nater, Franke, Hellamer and Ehlert (2005) focused on 30 patients diagnosed with irritable bowel syndrome or non-ulcer dyspepsia and compared corticotrophin-releasing hormone (CRH) results alongside salivary cortisol results against 24 healthy individuals and found that there was lower pituitary and adrenocortical activity amongst patients with functional gastrointestinal disorders. CRH appears to be disinhibited in the brain as lower adrenocortical activity is affected by pituitary-adrenal reaction to chronic gastrointestinal disorders and may mimic poor mental health symptoms.

The data suggests that there is at the very least the possibility that some people diagnosed with eating disorders, particularly severe and enduring conditions with co-morbidity, may have a pathophysiological viral precipitator which may have damaged the hypothalamic-pituitary-adrenal axis, possibly through disturbance at the prion-protein-amino acid level. If so then it has repercussions for treatment interventions.
Implications for treatment interventions;
Post-viral damage causing psychopathological presentations should be considered a possibility for some individuals with an eating disorder condition and possibly amongst other general mental health conditions. In such cases that support a viral basis the most fundamental impact on psychotherapeutic treatment programmes would be the introduction of physiological interventions to support the management of the condition. The use of antibiotics as a pharmaceutical option would currently have no place in viral damage but the potential to use new pharmaceutical products incorporating vitamin and protein therapy, adapted to suit the diagnosis may be an interesting avenue for further exploration. More input from dieticians and nutritionists, trained to plan programmes for people who may have complex absorption and metabolic processes, in tandem with mental health nursing, anti-depressants and other medication to control prolyl-peptide activity should be considered and researched. A dietary plan may need to be individualised and support implemented to help the person cope with lifestyle alterations. In many ways there are lessons in this area from colleagues who work with individuals with Type-1 diabetes mellitus.

The use of cognitive-behavioural (CBT) interventions may require more focus on immediate problems in the context of a chronic and enduring physical illness and less on mental health psychopathologies. This would be in line with CBT work carried out within clinical neuro-cognitive units and their treatment of clients presenting with neurological damage. Case formulations may therefore need to account for a different approach to negative automatic thoughts in view of the possibility that symptoms may have been precipitated by structural or functional hypothalamic-pituitary alterations. This would indicate that there would need to be more emphasis on maintenance interventions alongside traditional CBT interventions and more support from symptom-specific self-help groups. Maintenance interventions in such cases would need to be based on chronic disease management models and again there are lessons from the work done with individuals who live with myalgic encephalomyelitis/chronic fatigue syndrome.
The particular emphasis on the hypothalamic-pituitary-adrenal axis as the symptomatic presentation supports work in physiological and endocrinal areas. These together raise some potential fields of study on the role of monoamines, protein chains and prions in response to immune system alterations and later damage to structure or function. Pathophysiological research should continue around serum prolyl-endopeptidase activity and the correlation between monoamine acids and the immune system. The age of vulnerability appears to be a factor and adolescent hormonal processes could be affected by even earlier impact on the developing hypothalamic loop and endocrinal processes. It is of significance that the pattern of eating adopted by some clients as a coping method is severely disrupted after a viral-based illness with particular decrease in mood state and motivation but not in cognitive functioning suggesting further viral attacks causes a relapse in the eating disorder condition. Underlying, obstinate, treatment-resistive infections also appear to cause deterioration in severe and enduring conditions. They appear to play a disruptive influence over attempts to manage an eating disorder during periods of relapse but disappear as immunological responses take effect giving a presentation of poor lability and inconsistency in self-management for some individuals. Physical alterations such as tumours in the hypothalamic-pituitary area appears to have a more direct influence on the progression of an eating disorder and can be masked by other co-morbid presentations making diagnosis difficult. The importance of referrals for endocrinological assessments when compiling treatment strategies based on co-morbid or differential diagnosis cannot be underestimated. Eating disorder symptoms can present in line with DSM IV 307.1 and 307.5 criteria and the ICD-10 539 code (DSMIV (1994)) and may therefore mask underlying hypothalamic-pituitary structural alterations which may be co-morbid or have substantial influence on the progression of severe and enduring eating disorders.
The analysis has some limitations due to the methodological approach. Case records may not adequately provide diagnostic criteria so records that were screened for exclusion from the evaluative analysis may actually be relevant. The data collection relied on good data records of physical illnesses and diagnostic testing which were not always archived or legible so some data which may have relevance could have been lost. Continuity notes had to be relied upon to gather self-reporting of past illnesses and recall may not always be reliable. Laboratory tests were sometimes insufficiently detailed regarding endocrinological results and some individuals had no referrals to endocrinology so past lab results based on different hospital admissions had to be carefully followed to gather data. The containment of many treatment approaches between the general practitioner and the mental health services restricted the opportunity for archived records to hold sufficient data regarding past illnesses purely because referral outside mental health was only warranted when clear physical problems arose from the eating disorder itself.

The physical elements of mental health conditions and the subsequent case management need to be more interdisciplinary with a wider remit than the current tiered UK Step Care pathway model. This restricts mental health interventions within its own field and gives little room for colleagues from the physical disciplines to be more fully involved in therapeutic interventions apart from a referral system.


The objectives of the study were achieved and the results appear to support previous studies in this area. The analysis of ninety-five individuals presenting with severe and enduring eating disorders with the aim of updating earlier work on physiological observations indicates that 13.6% had a history of viral illness immediately prior to diagnosis. The symptoms deteriorated into a severe and enduring condition with co-morbidity associated with endocrinal alterations. In some cases foodstuff and alcohol seemed to be a self-administered form of crude pharmacological intervention to manage psychopathological symptoms.

This study suggests three potential areas for further mental health research. One is to ascertain the level of viral incidences on a larger population of individuals with severe and enduring bulimia nervosa and anorexia nervosa, particularly when associated with co-morbidity or more complexed due to somatic diagnosis. The second is to study outcomes based on a higher priority and acknowledgement of the physical co-morbid illnesses associated with severe and enduring eating disorders. Thirdly, the study suggests more work should be undertaken to ascertain the success outcomes of more interdisciplinary physical treatments provided alongside psychotherapeutic interventions. There study also has implications for other presentations of psychopathology and may have to be considered for more general mental health conditions.


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First Published February 2011

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