Professor Mike Thomas,
University of Chester, UK
Abstract
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.
Background
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.
