case study example pertaining to hypochondriasis

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Illness Anxiety Disorder: A Case Report and Brief Review of the Literature

Eduardo d espiridion.

1 Psychiatry, Drexel University College of Medicine, Philadelphia, USA

2 Psychiatry, West Virginia School of Osteopathic Medicine, Lewisburg, USA

3 Psychiatry, West Virginia University School of Medicine, Martinsburg, USA

4 Psychiatry, Philadelphia College of Osteopathic Medicine, Philadelphia, USA

5 Psychiatry, Reading Hospital Tower Health, West Reading, USA

6 Medicine, Drexel University College of Medicine, Philadelphia, USA

Adeolu O Oladunjoye

7 Critical Care Medicine, Boston Children's Hospital, Boston, USA

Illness anxiety disorder (IAD) is defined in the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-V) as the preoccupation with having or acquiring a serious illness, in the absence of somatic symptoms (or, if present, symptoms that are only mild in severity). Patients with IAD experience persistent anxiety or fear of having or acquiring a serious illness, which adversely affects their daily life. They remain unsatisfied with their physician’s reassurances to the contrary, mainly because their distress is created by the anxiety of the meaning, significance, and cause of the complaints and not necessarily due to the physical presentations. IAD remains a huge burden on both the health facility and for the managing healthcare provider. In this report, we present the case of a patient with IAD, which has been managed for the past five years with recurrent visits to the physician with no resolution of signs and symptoms. Despite extensive medical workup over this period, which repeatedly showed normal test results, the patient continued to have anxiety over his ill health and complained of recurrent mild somatic symptoms. After his most recent appointment, he got very upset and booked a flight to his home country to have a second opinion to validate his illness. Physicians are encouraged to build a therapeutic alliance with patients with IAD, rather than ordering expensive or unnecessary diagnostic tests or treatment.

Introduction

Illness anxiety disorder (IAD), previously known as hypochondriasis, is defined in the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-V) as the preoccupation with having or acquiring a serious illness, in the absence of somatic symptoms (or, if present, symptoms that are only mild in severity) [ 1 - 2 ]. Patients with IAD experience a high level of anxiety about their health and they are easily alarmed by their health status [ 1 ]. They experience persistent anxiety or fear of having or acquiring a serious illness, adversely affecting their daily life [ 2 - 3 ]. They remain unsatisfied with their physician’s reassurances, mainly because their distress arises from the anxiety of the meaning, significance, and cause of the complaints and not necessarily from the physical presentation. These individuals engage in excessive health-related behaviors (e.g., repeated checks on the body for signs of illness) or exhibit maladaptive avoidance (e.g., avoiding doctor appointments and hospitals) [ 1 ]. The diagnosis requires the existence of the preoccupation for at least six months, but specific illnesses may change over that period of time [ 1 ]. The illness is not better explained by other mental disorders. There are two types of IAD: care-seeking type and care-avoidant type [ 1 - 2 ]. The care-seeking type involves those who frequently utilize the healthcare system and medical resources, including physician visits and undergoing multiple tests and procedures [ 2 , 4 ]. The care-avoidant type, on the other hand, refers to patients with severe anxiety who hold the belief that their physician visit or laboratory test will reveal life-threatening illnesses such as cancer [ 2 , 4 ]. In this report, we present a patient with IAD whose disease course has been characterized by recurrent visits to the physician in the past five years with no resolution of signs and symptoms.

Case presentation

History of the presenting complaint

The patient was a 34-year-old male immigrant to the US from Asia who was admitted to the medical floor of a community hospital for the management of his medical problems. He had experienced a recurrent history of anxiety and mild somatic symptoms for the past five years. He reported sleeping difficulties, panic attacks, ruminative worries, muscle tension, body weakness, and chest discomfort. The patient had a prior psychiatric history and hospitalization for anxiety and depression. He had been admitted for anxiety and depression in a free-standing health facility five years ago and had been treated with medications. He had been prescribed sertraline and quetiapine but had self-discontinued because of tolerability issues. He had continued to be anxious with mild somatic symptoms. The patient denied any manic or psychotic symptoms or any neurological symptoms. The patient also denied any suicidal or homicidal ideations. He had no history of substance use or alcohol intake. He had a family history of anxiety disorder, described as an obsessive-compulsive disorder in his mother. In 2019, he had consulted a physician who had performed an extensive medical workup. All test results were unremarkable; he was reassured and his symptoms improved. During the two to three weeks prior to the current presentation, his anxiety and somatic symptoms had recurred and had subsequently worsened. He was then admitted for further investigation.

Examination

The mental status examination revealed a young man who was neat and well-groomed. He was cooperative, calm, and made appropriate eye contact. His speech was normal. He described his mood as anxious and his affect was constricted. His thought process was normal and linear. There was no suicidal or homicidal ideation. No delusions or hallucinations were reported. He was awake, alert, and oriented to time, place, people, and events. His judgment and insight were fair.

Investigation

He underwent a 12-lead electrocardiogram, which showed a ventricular rate of 80 beats/minute (reference range: 60-100 beats/minute), atrial rate of 80 beats/minute (reference range: 60-100 beats/minute), PR interval of 148 milliseconds (reference range: 120-200 milliseconds), QRS duration of 94 milliseconds (reference range: 80-100 milliseconds), QT interval of 350 milliseconds (reference range: 360-430 milliseconds), and QTC calculation (Bazett) of 403 milliseconds (reference range: ≤440 milliseconds) with normal sinus rhythm.

Other medical workups done revealed thyroid-stimulating hormone of 2.398 uIU/mL (reference range: 0.35-5.5 uIU/mL), hemoglobin A1c of 5.6% (reference range: <5.7%), and urinalysis showing no ketones or proteins. Lipid profile showed cholesterol of 182 milligrams per deciliter (reference range: <200 milligrams per deciliter), high-density lipoprotein of 39 milligrams per deciliter (reference range: <40 milligrams per deciliter), low-density lipoproteins of 103.8 milligrams per deciliter (reference range: <100 milligrams per deciliter), and a slightly elevated triglyceride of 196 milligrams per deciliter (reference range: <150 milligrams per deciliter). His basic metabolic panel was as follows: sodium of 140 millimoles per liter (reference range: 136-145 millimoles per liter), potassium of 4.1 millimoles per liter (reference range: 3.6-5.2 millimoles per liter), chloride of 104 millimoles per liter (reference range: 98-106 millimoles per liter), glucose of 93 milligrams per deciliter (reference range: 70-100 milligrams per deciliter), calcium of 9.3 milligrams per deciliter (reference range: 8.5-10.5 milligrams per deciliter), phosphorus of 4.0 milligrams per deciliter (reference range: 3.4-4.5 milligrams per deciliter), blood urea nitrogen of 9 milligrams per deciliter (reference range: 7-20 milligrams per deciliter), and creatinine of 1.0 milligrams per deciliter (reference range: 0.84-1.21 milligrams per deciliter). His complete blood count revealed a hematocrit of 48.9% (reference range: 38.3-48.6%), mean corpuscular volume of 84.7 femtoliters (reference range: 80-96 femtoliters), and red cell distribution width of 12.5% (reference range: 11.8-14.5%). All of these results were unremarkable. Also, an MRI of the brain without contrast was unremarkable. His vitamin B12 was unremarkable as well: 337 picograms per milliliter (reference range: 160-950 picograms per milliliter).

Both the hospitalist and cardiologist cleared him for any medical issues. Despite this reassurance, he got very upset and booked a flight to his home country to have a second opinion to validate his illness.

The cause of IAD is largely unknown. However, several risk factors have been implicated in the development of IAD. These include an underlying anxiety disorder, excess amount of time spent reviewing health-related materials (e.g., on the internet), history of previous serious childhood illness or illness of the patient's caregiver, family history of anxiety, and discussions and experience that involve labeling normal body sensations as pathological [ 2 , 3 - 5 ]. Our patient did not present with any of these risk factors; however, he had a history of anxiety and depression. These patients usually present with comorbidities such as anxiety and depression and need to be treated for these conditions [ 6 ]. What is not known is whether psychiatric history was a trigger to IAD, or if these psychiatric conditions coexisted in our patient from the onset. This patient had discontinued treatment for his anxiety and depression, which may have also triggered IAD in him.

IAD is a diagnosis of exclusion. It is important that a comprehensive examination and testing be conducted to exclude any organic disease before establishing a diagnosis of IAD [ 2 , 4 ]. Patients with IAD typically utilize several medical facilities. They are seen by multiple physicians with repeated negative tests each time they visit a health facility [ 1 ]. Frequently, the physician will carry out unnecessary and costly tests without achieving satisfying results; though the patient is deemed healthy, the anxiety persists [ 7 ]. Therefore, patients continue to visit multiple physicians due to their frustration with repeatedly normal or negative test results and unsuccessful physician reassurance. In the case of our patient, after several visits with physicians in the US, he got upset with his management and decided to travel to see another physician in his home country for a second opinion.

Patients with IAD are more often found in primary care centers than in mental health clinics, resulting in a delay in treatment and subsequent worsening of their psychiatric condition [ 7 , 8 ]. The primary care provider (PCP) is typically trained to identify physical symptoms that are not found in patients with IAD. This results in excessive use of scarce medical resources, worsening the depletion of the health resources apart from wasting the physician’s time and efforts [ 9 ]. It is not known how much money has been spent on this patient in total, but it is expected to run into several thousands of US dollars. It was estimated that 10-20% of the US medical budget is spent on patients with some form of somatization or IADs [ 10 ].

The most important aspect in the management of IAD is for the physician to establish a longitudinal trust relationship with the patient [ 11 ]. Communication should focus on empathy, open dialog, coordination of testing, and consistent delivery of messages [ 3 ]. The physician should first acknowledge their fears and concerns with the patient. Patients need to be reassured that although there is no specific treatment for the unexplained symptoms, the symptom is not fatal or catastrophic and that the physician will continue to work with patients on their path back to health and well-being. Holder-Perkins et al. have proposed that the physician should focus on psychosocial problems instead of the somatic concerns of the patient [ 8 ]. Patients can have regular follow-up visits with their PCP and psychiatrist to address new complaints, triggers, or stressors [ 4 ]. This will ultimately reduce unnecessary visits to the emergency department or other physicians.

Psychotherapy is the first-line treatment for IAD and has been shown to reduce symptoms associated with the condition [ 2 ]. This includes cognitive-behavioral therapy, which focuses on eradicating dysfunctional maladaptive cognitive beliefs by means of behavioral modification strategies [ 2 , 4 ]. Other therapy options include mindfulness-based cognitive therapy, group-therapies, attention training, and acceptance and commitment therapy [ 2 , 7 ]. Psychotropic medications have also been helpful in treating marked comorbidity of anxiety and depressive symptoms in patients with IAD [ 8 ]. Antidepressants such as selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) have been proven to be effective in patients with IAD [ 2 ]. However, the challenges of prescribing these drugs include the patient’s misinterpretation of this as an attempt to dismiss their unexplained symptoms, as well as the side effects of these medications. Patients should be reassured about using medications and given very detailed information about the management plan during scheduled visits.

Conclusions

Physicians are encouraged to build a therapeutic alliance with patients with IAD as they work with them on their path back to health. This is essential to reduce the tremendous burden on the healthcare system caused by the wastage of physician resources and ordering of expensive or unnecessary investigations while caring for patients with IAD.

The content published in Cureus is the result of clinical experience and/or research by independent individuals or organizations. Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein. All content published within Cureus is intended only for educational, research and reference purposes. Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional. Do not disregard or avoid professional medical advice due to content published within Cureus.

The authors have declared that no competing interests exist.

Human Ethics

Consent was obtained or waived by all participants in this study

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New Insights on the Treatment of Hypochondriasis

• Katharine A. Phillips , M.D.

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Treating patients with hypochondriasis, who worry that they have a serious disease when in fact they do not, can be challenging. Many seek nonpsychiatric medical treatment, even though their illness fears and beliefs are unwarranted. Indeed, these patients have substantially elevated rates of medical care utilization, and psychosocial functioning is often impaired ( 1 , 2 ).

In this issue, Fallon, Barsky, and colleagues—leading researchers on this disorder—report a landmark treatment study of this often difficult-to-treat condition ( 3 ). They randomly assigned 195 patients with DSM-IV hypochondriasis to one of four treatments: fluoxetine, cognitive-behavioral therapy (CBT), pill placebo, or joint treatment with both fluoxetine and CBT. This is the first study to examine the effects of combined CBT and a serotonin reuptake inhibitor (SRI) for hypochondriasis. CBT and SRIs have each been shown to be efficacious, although only two prior randomized controlled SRI trials have been done ( 2 , 4 ).

The results supported the predicted pattern of response (p=0.036); response rates were 47.2% for joint therapy (fluoxetine plus CBT), 41.8% for single active treatment, and 29.6% for placebo. There was no significant difference in the proportion of responders across groups. However, secondary analyses showed that on one of two continuous measures of hypochondriasis, treatment group was significant overall (p=0.049); pairwise contrasts revealed that fluoxetine was significantly more effective than placebo and had a significantly faster rate of improvement than placebo. CBT was not more effective than placebo, however. When considering those participants who completed the study (a secondary analysis), the fluoxetine group had the highest response rate (81.3%) compared with 62.2% for joint treatment, 51.7% for CBT, and 44.0% for placebo.

It is somewhat surprising that joint treatment with both fluoxetine and CBT showed only a small incremental advantage over fluoxetine alone in intention-to-treat analyses and actually yielded a lower response rate than fluoxetine alone in secondary completer analyses. As the authors note, a possible explanation is that the mean endpoint fluoxetine dose in the joint treatment group was lower than that of the fluoxetine group. Consistent with this explanation, on one outcome measure improvement was significantly greater for those receiving ≥40 mg/day than for those receiving less than 40 mg/day.

It is possible that response rates would have been even higher if patients had received higher doses of fluoxetine. The mean doses of 40 mg/day in the fluoxetine group and 31 mg/day in the joint treatment group are lower than those used in a prior study of fluoxetine for hypochondriasis ( 4 ); they are also lower than doses often used and needed to successfully treat disorders with similarities to hypochondriasis, such as obsessive-compulsive disorder and body dysmorphic disorder (distressing or impairing preoccupation with nonexistent or slight defects in appearance) ( 5 , 6 ). In fact, the American Psychiatric Association Practice Guideline for Obsessive-Compulsive Disorder states that doses as high as 120 mg/day of fluoxetine are occasionally used for obsessive-compulsive disorder ( 5 ), as is also the case for body dysmorphic disorder ( 6 ).

SRI dosing for obsessive-compulsive disorder and body dysmorphic disorder may be relevant to hypochondriasis because these three conditions share obsessional preoccupation and excessive repetitive behaviors (i.e., rituals, compulsions), such as checking one’s body for signs of illness in hypochondriasis ( 2 , 7 ). Furthermore, hypochondriasis is often conceptualized as an obsessive-compulsive or related disorder (also known as an obsessive-compulsive spectrum disorder) ( 7 ). During the development of DSM-5, the controversial question of where to classify hypochondriasis was carefully examined ( 7 ). Some research evidence supported moving it to DSM-5′s new chapter “Obsessive-Compulsive and Related Disorders”; however, evidence for its placement in this chapter was more mixed and less persuasive than for other disorders, such as body dysmorphic disorder ( 7 ). Ultimately, hypochondriasis was not moved to this chapter, although the upcoming 11th edition of the International Classification of Diseases will likely classify hypochondriasis in a chapter on obsessive-compulsive and related disorders ( 8 )—a reflection of these disorders’ similarities, including, perhaps, their treatment response.

Study results for CBT were relatively weak compared with those in prior studies ( 9 ). An alternative way of viewing the results, however—the “glass half full” perspective—is that 52% of study completers responded to CBT, a high proportion after only six sessions. As the investigators note, the relatively low response rate in intention-to-treat analyses may be explained by the fairly high dropout rate (one-third of participants did not complete at least six sessions) and the brevity of CBT treatment. Lengthening treatment, which clinicians would likely do if response were insufficient after six sessions, may have improved outcomes. Indeed, a meta-analysis found that more CBT sessions were associated with larger effect sizes at posttreatment (number of sessions varied from 3 to 16) ( 9 ). CBT could be lengthened and perhaps strengthened by further practicing already-learned CBT skills during additional sessions or by adding other cognitive or behavioral approaches. Additional approaches might include exposure to reduce avoidance of anxiety-provoking situations and ritual prevention to decrease repetitive behaviors such as body checking or reassurance seeking if present (approaches used for obsessive-compulsive disorder and body dysmorphic disorder) ( 2 ). The relatively high dropout rate suggests that strategies to enhance treatment retention might be valuable. Approaches such as motivational interviewing—developed for treatment of substance use disorders and subsequently adopted for a broad range of conditions—might facilitate patient engagement and retention in treatment ( 2 , 10 ). Motivational interviewing may be especially well suited to hypochondriasis because insight—although not well studied in this condition—appears to often be poor, which may decrease patients’ willingness to receive psychiatric treatment.

DSM-5 made changes to hypochondriasis after this study began ( 11 ). DSM-5 does not use the name “hypochondriasis,” and it classifies DSM-IV hypochondriasis either as somatic symptom disorder or as illness anxiety disorder; both are in DSM-5′s chapter on somatic symptom and related disorders. Somatic symptom disorder highlights distressing or disruptive somatic symptoms (it also corresponds closely to DSM-IV’s somatization disorder). In contrast, illness anxiety disorder emphasizes preoccupation with having or acquiring a serious physical illness; it puts less emphasis on physical symptoms, requiring them to be only mild or not present at all. DSM-5′s definition of illness anxiety disorder overlaps with that of obsessive-compulsive disorder, especially when physical symptoms are absent, concerns focus on a fear of acquiring rather than actually having a serious illness, and excessive repetitive behaviors (compulsions) are present. This overlap suggests use of higher doses of fluoxetine (if needed and tolerated) for this form of illness anxiety disorder in particular. The study findings likely apply to illness anxiety disorder and somatic symptom disorder, but studies are needed to ascertain that this is the case.

No study is perfect, and the authors are to be congratulated for successfully conducting this important trial. Studies like this one—large randomized efficacy trials with multiple treatment arms that use state-of-the-art methodology—are difficult to do. Recruiting a large number of patients who meet all inclusion/exclusion criteria and are willing to accept their assigned treatment, retaining them in the study, and implementing and adhering to quality assurance procedures require tremendous effort and expertise. An additional recruitment and retention challenge is that patients with hypochondriasis may not readily recognize the potential value of psychiatric care ( 1 , 2 ).

There is a pressing need for additional treatment studies of somatic symptom and related disorders. These conditions cause patients to suffer, and they challenge clinicians and health care systems. In the meantime, for patients with clinically significant illness worries, this study offers valuable insights about helpful treatment approaches.

In the past 36 months Dr. Phillips has received support from the National Institute of Mental Health (grant reviews), Oxford University Press (royalties), American Psychiatric Publishing (royalties), Merck Manual (honoraria), UpToDate (royalties), International Creative Management (royalties), Guilford Press (royalties), Royal Pharma (honorarium for a presentation), Abbott Pharmaceuticals (honorarium for a presentation), AstraZeneca (honorarium for a presentation), American Society for Clinical Psychopharmacology (honorarium and travel funds for a presentation), American Psychiatric Association (honorarium for a presentation), B. Braun Medical (travel funds), and academic institutions (speaking honoraria and/or travel reimbursement). Grant support in the past 36 months: National Institute of Mental Health (R01 MH091023 and 1R25 MH101076), National Institute of General Medical Sciences (2P20GM103430), Brown University Division of Biology and Medicine, and Brown Institute for Brain Science and Norman Prince Neurosciences Institute. Dr. Freedman has reviewed this editorial and found no evidence of influence from these relationships.

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• Cited by None

• Hypochondriasis
• illness anxiety disorder

Metacognitive Therapy in the Treatment of Hypochondriasis: A Systematic Case Series

• Original Article
• Published: 11 April 2014
• Volume 38 , pages 541–550, ( 2014 )

Cite this article

• Robin Bailey 1 , 2 &
• Adrian Wells 1  

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Hypochondriasis is a debilitating condition which can have profound psychological and functional effects. The most effective psychological treatments are cognitive and behavioural therapies. However, the degree of improvement across these treatments is variable, often with modest recovery and a high dropout rate. The aim of this study was to provide a preliminary investigation of effects associated with metacognitive therapy (MCT) applied to DSM-IV hypochondriasis. Four consecutively referred patients were treated using established A–B single case series methodology. Following MCT all patients demonstrated large and clinically meaningful improvements in specific hypochondriacal symptoms and more general negative affect measures. Treatment gains were maintained at 6-month follow-up. Substantial changes were also observed in metacognitive beliefs. Overall this case series provides preliminary evidence that MCT can be applied to hypochondriasis and it supports a move towards a more definitive evaluation of the treatment in this group.

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Acknowledgments

The data have been presented at the 2nd International Conference of Metacognitive Therapy, Manchester, UK, 2013. The study did not receive external funding.

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Robin Bailey and Adrian Wells declare that they have no conflict of interest.

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Informed consent was obtained from all patients for being included in the study.

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Bailey, R., Wells, A. Metacognitive Therapy in the Treatment of Hypochondriasis: A Systematic Case Series. Cogn Ther Res 38 , 541–550 (2014). https://doi.org/10.1007/s10608-014-9615-y

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Hypochondriasis: an overview with reference to medical students

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• Oliver Howes , Maudsley Hospital 1

Oliver Howes provides the medical background to a seemingly very common condition

“For each ailment that doctors cure with medications (as I am told they do occasionally succeed in doing) they produce 10 others in healthy individuals by inoculating them with that pathogenic agent 1000 times more virulent than all the microbes--the idea that they are ill.” Marcel Proust, The Guermantes Way

Hypochondriasis is common in primary care and general hospital settings. The diagnosis is frequently missed, and it causes considerable morbidity and a large burden to health services. Transient hypochondriasis has been reported in 70% of medical students. The definition of hypochondriasis is a persistent, unrealistic preoccupation with the possibility of having a serious disease. Common, normal sensations and appearances are often misinterpreted as abnormal and signs of disease. The diagnostic criteria for hypochondriacal disorder in the ICD-10 (international classification of diseases, 10th revision) require the following to be present 1 :

* persistent belief in the presence of at least one serious physical illness underlying the presenting symptom or symptoms; and

* persistent refusal to accept the reassurance of several different doctors that there is no physical illness.

The criteria defined in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV), include the additional qualifiers that the preoccupation lasts at least 6 months and causes clinically significant impairment or distress. 2 The belief should not be delusional in intensity. It is almost unique in medicine as it is a diagnosis that requires other doctors to have seen the patient and failed to reassure him or her; the first doctor to see the patient cannot make the diagnosis. Epidemiological evidence suggests that this diagnosis is not made often enough.

The term hypochondriasis has a long and complex history. It derives from hypochondrium (“below the cartilage”), an anatomical description for the abdominal area below the ribs first used by Hippocrates in the fourth century BC. “Humours” (fluids) presumed to be emanating from the hypochondrium were thought to cause disturbances in the psyche and soma and lead to disease. 3 In the 18th century, “hypochondria” was referred to as the “English malady,” because it was said to be so common in England, and was linked to disorders of many organs, particularly the spleen and uterus. 4 The many famous sufferers include Immanuel Kant, Beethoven, and Samuel Johnson. Charles Darwin began a lifetime of suffering as a medical student. “Hypochondriac,” derived from the same root as hypochondriasis, has acquired pejorative connotations and become associated with malingering. These connotations should, however, not be attached to hypochondriasis, which is a distinct medical condition associated with considerable suffering. Hypochondriasis is used as a term both for a symptom describing fears of illness and for a distinct condition. 5 6

Classification

Hypochondriasis traditionally fits into the group of neurotic disorders. The extent to which hypochondriasis overlaps with these other disorders is subject to ongoing debate. 1 2 6 The ICD-10 category of somatoform disorders includes somatisation disorder, and somatoform autonomic dysfunction as well as hypochondriacal disorder. The table highlights the main differences between the disorders. Patients, however, often have somatic symptoms as well as worries about disease. The somatoform disorders may be best thought of as a continuum, with fear of serious disease at one end and preoccupation with somatic symptoms at the other.

Hypochondriasis may be primary when it exists independently from other psychiatric conditions. Hypochondriacal symptoms, however, are often secondary to other conditions such as depression, anxiety disorders, and delusional disorders. Treatment should be only for the primary disorder; secondary hypochondriacal symptoms will usually resolve as the primary disorder is treated. Shortlived hypochondriacal ideas are common in the general population, particularly in patients who have just received a medical diagnosis with a poor prognosis. Forms of hypochondriasis have been described in specific subpopulations. Hypochondriacal concerns are reportedly associated among people in certain occupations; these occupations include actors, musicians, doctors, and medical students. 4 Although the reports of hypochondriacal concerns in these occupations are largely based on anecdotal reports, the association of shortlived hypochondriacal reactions with medical students has been more formally studied. Transient hypochondriacal concerns seen in these groups and the general population, however, are clearly distinct from ICD-10 hypochondriacal disorder in form and severity.

“Medical studentitis”

Clinical teachers have long reported that medical students frequently develop groundless fears and symptoms of illness. 7 This has been termed “medical student's disease,” “hypochondriasis of medical students,” “nosophobia,” and “medical studentitis.” 8 Such reactions rarely reach the strict ICD-10 or DSM-IV criteria for hypochondriasis. 9 The reactions are often comparatively shortlived, although repeated, and associated with a disease being studied at the time ( box 1 ).

Box 1 - Case study

A student on a neurology placement reported interpreting minor aches and twinges as being early symptoms of multiple sclerosis. She woke up every morning for two weeks convinced that she would be paralysed by an acute attack. This health anxiety interfered with study and caused considerable distress. It resolved when she finished the attachment, but it recurred in other forms during later courses.

There has been little research into this phenomenon, although early studies suggest that 70-80% of medical students experienced it. 7 8 These studies were uncontrolled and based on case records or small samples. Less than 1% of the students displayed “true hypochondriasis.”

The first controlled study matched medical students with law students (60 in each group) for age and sex. 10 Responses to questionnaires assessing hypochondriacal concerns were compared. The medical students attended to their health and somatic symptoms more, but there was no significant difference in the prevalence of hypochondriacal tendencies. Law students are highly selected, however, and may not be a good comparison group. More recently, a controlled study in the United Kingdom assessed rates of hypochondriasis in clinical medical students and compared them with other students and the general population. 9 Sixty per cent of clinical students replied. The medical students showed non-significantly lower rates of hypochondriasis than the other students and non-students.

These results question the widely held view that medical students are more hypochondriacal than others. Two factors may have resulted in this idea. Firstly, the phenomenon of hypochondriasis in trainee doctors may receive more attention from tutors and student doctors than the same phenomenon in, say, a history student. Secondly, early claims of very high prevalence in uncontrolled studies may have resulted in selective attention and a lowered threshold for recognition of the phenomenon.

Epidemiology

Most healthy people--60-80% in studies--experience somatic symptoms regularly. 11 It is likely that only a very small proportion of these would meet the full diagnostic criteria for hypochondriasis. In primary care settings in 14 countries throughout four continents, 0.5-1.0% of patients meet the ICD-10 criteria for hypochondriasis. 11 About 2.2% meet criteria for an abridged version that is based on all the major criteria except the failure to accept medical reassurance. 11 12 Many of these patients go on to be seen in general hospitals. The prevalence of hypochondriasis in general medical clinics has been reported at 4.2-13.8%. 13 There are no clear differences of sex, age, or geographical location in the prevalence of the condition.

Physiological, psychological, and sociological factors are implicated in the cause and maintenance of hypochondriasis. There is little firm evidence of specific genetic factors. Hypochondriacal patients may be more prone to anxiety and tend to perceive their bodily functions more accurately than others. 11 The emotional arousal associated with anxiety may lead to physiological changes and increased activity in the autonomic nervous system, endocrine changes, and even biochemical disturbances--for example, hypocapnia following hyperventilation. These may cause or increase somatic symptoms. 14

Maladaptive behaviours, such as bodily checking, feed into the cycle of anxiety, leading to greater arousal and increased symptoms. For example, a man who feared that he had testicular cancer repeatedly checked his testicles. This caused testicular pain, which he interpreted as the early signs of cancer and led to increased checking.

The reactions of others may serve to establish and maintain behaviour. 6 A number of childhood experiences, especially of illness, may predispose individuals to develop hypochondriasis. Adult hypochondriasis has been found to be associated with the following childhood experiences 15 :

* serious or chronic medical illness in the individual or family members;

* being sick and missing school; and

* traumatic experiences, particularly physical and sexual trauma.

Certain parental characteristics may predispose children to develop hypochondriasis as adults. In particular, parental overprotectiveness, neuroticism, and selective responses to physical complaints, such as showing more sympathy and being more likely to call the doctor when the child was ill, are more common in patients with hypochondriasis than controls. 16 Interestingly, although medically unexplained symptoms in childhood may be a precursor to those symptoms in adulthood, the largest follow up study to date found they were more strongly associated with psychiatric disorder generally, such as depression and anxiety, than physical symptoms. 17

Course and prognosis

Hypochondriasis is considered to be a chronic, stable condition that causes long term disability, and this is supported by a recent prospective case control study. 18 Over 200 subjects and controls were recruited from the medical outpatient department in a big teaching hospital. At follow up, 4-5 years later, there had been an improvement in hypochondriacal symptoms, but two thirds of the patients still met diagnostic criteria.

Morbidity and cost

Patients with hypochondriasis suffer considerable emotional and psychological stress, and impairment of social and occupational functioning. In a general practice sample they were at least twice as likely to have moderate to severe occupational disability than patients without hypochondriasis. 12 They were also nearly three times more likely to be referred for further investigation. They show as much or more impairment on standard physical functioning scales than patients with chronic conditions such as diabetes or arthritis, and are limited to bed two to three times more than patients with most major medical illnesses. 18 19

Where the diagnosis is not made, they can suffer major iatrogenic morbidity. There is a risk of complications from investigations, and side effects from symptomatic or inappropriate treatments. Both severe cases and less extreme cases illustrate the considerable morbidity and the resource burden on health services ( box 2 ). 20 A study focusing on “mild” cases found that somatising patients had mean annual medical costs of US $3185 (£2016). 19

Box 2 - Case study

A 48 year old woman had 77 admissions, 11 operations, and 996 investigations in 25 years. She has been seen in 10 hospital specialties but, other than her psychiatric diagnosis, she has not received a diagnosis that explains her symptoms. She has suffered from a number of serious iatrogenic complications, including: opiate dependence; opiate induced respiratory arrest; Cushing's syndrome after a trial of steroids; and a pulmonary embolism after a period of immobility.

The interventions and investigations used repeatedly led to further deterioration in her condition. The total financial cost has been about £250 000. After psychiatric intervention her healthcare use decreased, graphically shown by costs dropping from £10 000 to £2000 a year.

The treatment of hypochondriasis has traditionally been difficult. Where it is secondary to another condition it usually resolves with treatment of the primary disorder. For example, hypochondriasis which is secondary to depression will usually resolve when the depression is successfully treated.

Recognition and early diagnosis are important. Reassurance, combined with a serious appraisal of symptoms and an explanation of psychological factors may then be effective. 5 6 It is not enough simply to tell the patient that there is nothing wrong. It is important to acknowledge the patient's distress and provide an alternative model, introducing psychological factors. A dismissive attitude that “it is all in your head” is counterproductive. 6 Management regimes based on regular, brief appointments with one key doctor, and avoiding admissions to hospital are useful. They have been found greatly to improve physical functioning and cut costs on investigations and hospital admissions by one third. 19

Various drug treatments and talking therapies are beginning to be evaluated with controlled trials. Even in chronic cases 50% of patients improve with treatment. 11

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Psychotherapies (talking therapies)

Models have been developed for use in primary care based on understanding, and reattribution of symptoms and associated worries to a psychological explanation. 6 Anxiety management techniques, and other behavioural treatments have also been used, but the best evidence is for cognitive behavioural therapy. 21 This was developed to treat depression but subsequent trials have shown its efficacy in many psychiatric conditions. It is a structured therapy based on a scientific model that aims to alleviate psychological problems and improve coping skills. Cognitive behavioural therapy for hypochondriasis addresses both the thoughts and the beliefs (the cognitive element) that the patient has about bodily sensations and illness, and the associated behaviours (the behavioural part). Maladaptive automatic thoughts and assumptions are worked upon, such as “all bodily sensations are signs of serious illness” and “if I don't worry about health I'll get a serious illness.” Perpetuating behaviours, such as repeated checking for symptoms or reassurance seeking, are identified and alternative behaviours developed and tested by the patient and therapist. Patients given cognitive behavioural therapy show significant improvements, up to 80%, on a number of indicators of hypochondriasis compared with controls. 22

Pharmaceutical treatment

Case reports suggest tricyclic antidepressants are helpful. 23 There is better evidence for the efficacy of selective serotonin reuptake inhibitors. Preliminary results from a controlled trial indicate a better response to fluoxetine (66.7% virtual remission) than placebo (50%), although the placebo effect is large. 24

Hypochondriasis is common and can cause considerable distress, iatrogenic illness, and costs to health services. Diagnosis is often delayed, which exacerbates the condition. Greater awareness and the expansion of liaison psychiatry should correct this. There is growing evidence for the efficacy of treatments, particularly for cognitive behavioural therapy and selective serotonin reuptake inhibitors. Finally, it seems that medical students are not any more hypochondriacal than the general population. So you have one less thing to worry about.

Originally published as: Student BMJ 1999;07:410

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• Introduction
• Conclusions
• Article Information

The shaded areas indicate 95% CIs.

Models adjusted for birth year, sex, county of residence, country of birth, latest recorded education, civil status, and family income.

eFigure. Flow Chart of Study Participants and Cohort Selection

eTable 1.  International Classification of Diseases ( ICD ) Codes Used to Group Specific Causes of Death in the Study

eTable 2. Groups of Psychiatric Comorbidities and their Corresponding International Classification of Diseases ( ICD ) Codes

eTable 3. Psychiatric Comorbidities Restricted to Those Recorded Before the First Diagnosis of Hypochondriasis or Index Date for the Matched Unexposed Individuals

eTable 4. Hazard Ratios (HRs) With 95% Confidence Intervals (CIs) for All-Cause and Cause-Specific Mortality Among Women With Hypochondriasis, Compared to Their Matched Unexposed Individuals

eTable 5. Hazard Ratios (HRs) With 95% Confidence Intervals (CIs) for All-Cause and Cause-Specific Mortality Among Men With Hypochondriasis, Compared to Their Matched Unexposed Individuals

eTable 6. Results Statified According to Whether the Participants Were First Diagnosed With Hypochondriasis in Inpatient vs Outpatient Settings in a Subcohort From 2001 (n=4,006 Exposed and 40,060 Matched Unexposed Individuals)

eTable 7. Hazard Ratios (HRs) With 95% Confidence Intervals (CIs) for All-Cause and Cause-Specific Mortality Among Individuals With Hypochondriasis, Compared to Their Matched Unexposed Individuals, Further Adjusted for Different Groups of Psychiatric Comorbidities (Restricted to Comorbidities Recorded Before the First Diagnosis of Hypochondriasis or Index Date for the Matched Unexposed Individuals)

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Mataix-Cols D , Isomura K , Sidorchuk A, et al. All-Cause and Cause-Specific Mortality Among Individuals With Hypochondriasis. JAMA Psychiatry. 2024;81(3):284–291. doi:10.1001/jamapsychiatry.2023.4744

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All-Cause and Cause-Specific Mortality Among Individuals With Hypochondriasis

• 1 Department of Clinical Neuroscience, Centre for Psychiatry Research, Karolinska Institutet and Stockholm Health Care Services, Region Stockholm, Stockholm, Sweden
• 2 Department of Clinical Sciences, Lund University, Lund, Sweden
• 3 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
• 4 School of Medical Sciences, Örebro University, Örebro, Sweden
• 5 Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway
• 6 Department of Biomedicine, Aarhus University, Aarhus, Denmark
• 7 Division of Psychology, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden

Question   Are individuals with hypochondriasis at increased risk of death due to natural and unnatural causes?

Findings   In this Swedish nationwide matched-cohort study of 4129 individuals with a diagnosis of hypochondriasis and 41 290 demographically matched individuals without hypochondriasis, those with hypochondriasis had an increased risk of death from both natural and unnatural causes, particularly suicide.

Meaning   This study suggests that individuals with hypochondriasis have an increased risk of mortality, mainly from potentially preventable causes.

Importance   Hypochondriasis, also known as health anxiety disorder, is a prevalent, yet underdiagnosed psychiatric disorder characterized by persistent preoccupation about having serious and progressive physical disorders. The risk of mortality among individuals with hypochondriasis is unknown.

Objective   To investigate all-cause and cause-specific mortality among a large cohort of individuals with hypochondriasis.

Design, Setting, and Participants   This Swedish nationwide matched-cohort study included 4129 individuals with a validated International Statistical Classification of Diseases and Related Health Problems, Tenth Revision ( ICD-10 ) diagnosis of hypochondriasis assigned between January 1, 1997, and December 31, 2020, and 41 290 demographically matched individuals without hypochondriasis. Individuals with diagnoses of dysmorphophobia (body dysmorphic disorder) assigned during the same period were excluded from the cohort. Statistical analyses were conducted between May 5 and September 27, 2023.

Exposure   Validated ICD-10 diagnoses of hypochondriasis in the National Patient Register.

Main Outcome and Measures   All-cause and cause-specific mortality in the Cause of Death Register. Covariates included birth year, sex, county of residence, country of birth (Sweden vs abroad), latest recorded education, civil status, family income, and lifetime psychiatric comorbidities. Stratified Cox proportional hazards regression models were used to estimate the hazard ratios (HRs) and 95% CIs of all-cause and cause-specific mortality.

Results   Of the 4129 individuals with hypochondriasis (2342 women [56.7%]; median age at first diagnosis, 34.5 years [IQR, 26.3-46.1 years]) and 41 290 demographically matched individuals without hypochondriasis (23 420 women [56.7%]; median age at matching, 34.5 years [IQR, 26.4-46.2 years]) in the study, 268 individuals with hypochondriasis and 1761 individuals without hypochondriasis died during the study period, corresponding to crude mortality rates of 8.5 and 5.5 per 1000 person-years, respectively. In models adjusted for sociodemographic variables, an increased rate of all-cause mortality was observed among individuals with hypochondriasis compared with individuals without hypochondriasis (HR, 1.69; 95% CI, 1.47-1.93). An increased rate was observed for both natural (HR, 1.60; 95% CI, 1.38-1.85) and unnatural (HR, 2.43; 95% CI, 1.61-3.68) causes of death. Most deaths from unnatural causes were attributed to suicide (HR, 4.14; 95% CI, 2.44-7.03). The results were generally robust to additional adjustment for lifetime psychiatric disorders.

Conclusions and Relevance   This cohort study suggests that individuals with hypochondriasis have an increased risk of death from both natural and unnatural causes, particularly suicide, compared with individuals from the general population without hypochondriasis. Improved detection and access to evidence-based care should be prioritized.

Hypochondriasis, also known as health anxiety disorder, is a prevalent psychiatric disorder 1 characterized by persistent preoccupation about having 1 or more serious and progressive physical disorders. 2 The preoccupation is accompanied by hypervigilance and a catastrophic interpretation of bodily signs, resulting in repetitive and excessive checking and reassurance-seeking behavior or maladaptive avoidance. The symptoms are clearly disproportionate and cause significant distress and impairment. 3 Hypochondriasis is thought to be severely underdiagnosed due to the condition not being properly recognized or taken seriously by health professionals as well as to the negative connotations associated with the diagnostic label. 4 , 5 However, as a symptom, health anxiety is highly prevalent in health care settings 6 and is associated with a substantial use of health care resources. 1 , 4 Hypochondriasis is widely regarded as a chronic disorder, with a low probability of remission without specialized treatment. 7 , 8

Individuals with hypochondriasis have high rates of medical consultations, typically leading to a chain of laboratory and other tests, which are often unnecessary from a medical perspective and conceptualized as counterproductive from a psychological viewpoint. 9 Theoretically, this high degree of vigilance may lead to the early detection and timely management of serious health conditions, potentially reducing mortality. However, there are several reasons to believe that this may not be the case. First, some individuals with hypochondriasis experience such high levels of health anxiety that they actually avoid contact with medical services altogether, risking the oversight of potentially serious illnesses. 7 , 10 , 11 Second, chronic anxiety and depression, which are characteristic of the disorder, are known to be associated with a range of adverse health consequences, such as cardiovascular disorders and premature mortality. 12 - 14 A longitudinal Norwegian cohort study of 7052 individuals found that those with self-reported symptoms of health anxiety were 73% more likely to develop ischemic heart disease after a 12-year follow-up compared with individuals with low health anxiety scores. 15 Finally, suicide has not been formally investigated among individuals with hypochondriasis, but it could contribute to increased mortality among this group. To our knowledge, no studies have examined the risk of all-cause and cause-specific mortality among individuals with a clinical diagnosis of hypochondriasis.

This nationwide matched-cohort study linked several Swedish registers to investigate all-cause and cause-specific mortality among a large cohort of individuals with hypochondriasis. Unlike its international version, the Swedish version of the International Statistical Classification of Diseases and Related Health Problems, Tenth Revision ( ICD-10 ) includes separate diagnostic codes for hypochondriasis and dysmorphophobia (body dysmorphic disorder), 16 resulting in a unique resource for nationwide cohort studies.

The Swedish Ethical Review Authority approved this study without requiring informed consent from participants because the study was register based and the included individuals were not identifiable at any time. This study followed the Strengthening the Reporting of Observational Studies in Epidemiology ( STROBE ) reporting guideline.

We linked several Swedish population-based registers using the unique national identification numbers assigned to Swedish citizens. 17 Sociodemographic data were extracted from the Census register, containing data from 1960; the Swedish Total Population Register, containing data on all Swedish inhabitants since 1968 18 ; and the Longitudinal Integration Database for Health Insurance and Labour Market Studies, which, since 1990, annually integrates data on the labor market, education, and social sectors from all individuals living in Sweden. 19 Dates of immigration into and emigration out of Sweden were extracted from the Migration Register. 18 The National Patient Register includes diagnostic information on individuals admitted to a Swedish hospital since 1969, with complete data coverage for psychiatric disorders from 1973. From 2001, the National Patient Register also contains data on outpatient consultations in specialized care. 20 Diagnoses are based on the International Classification of Diseases, Eighth Revision (1969-1986), International Classification of Diseases, Ninth Revision (1987-1996), and ICD-10 (1997-onward) classification systems. The Cause of Death Register contains a record of all deaths in Sweden since 1952, with compulsory reporting nationwide. 21 Each record contains the date of death and ICD codes for underlying and contributory causes of death. The Cause of Death Register covers more than 99% of all deaths among Swedish residents, including those occurring abroad, resulting in minimal loss of information.

A matched-cohort design was used to estimate the risk of all-cause and cause-specific mortality among individuals with a diagnosis of hypochondriasis compared with individuals from the general population without hypochondriasis. The study population included individuals who lived in Sweden at any time between 1997 and 2020 at the age of 6 years or older. Individuals who died or emigrated prior to 1997 or their sixth birthday, whichever occurred last, and individuals who were born after December 31, 2014 (ie, <6 years before the study end on December 31, 2020), were excluded.

Exposed individuals were defined as those who received a diagnosis of hypochondriasis between January 1, 1997, and December 31, 2020, at the age of 6 years or older. They entered the cohort on the date of their first registered hypochondriasis diagnosis. Each exposed individual was matched on sex, birth year, and county of residence at the time of the first hypochondriasis diagnosis with 10 individuals from the study population who lived in Sweden but had not received a diagnosis of hypochondriasis by the date when the exposed individual received such diagnosis (ie, index date). At the time of matching, we further excluded all individuals who had emigrated and then returned to Sweden between their sixth birthday or 1997, whichever came later, and the index date to allow for a more complete register coverage. Individuals with and without hypochondriasis were followed up from the index date until the date of the outcome (ie, death), emigration from Sweden, or the end of the study (ie, December 31, 2020), whichever occurred first. For individuals without hypochondriasis, the follow-up was additionally censored at the date they changed the exposure status (ie, if they received a diagnosis of hypochondriasis during the study period), if relevant.

Individuals with at least 1 inpatient or outpatient diagnosis of hypochondriasis according to the Swedish ICD-10 (code F45.2) were identified from the National Patient Register between January 1, 1997 (introduction of the ICD-10 in Sweden), and December 31, 2020 (end of the study period). In line with previous register-based studies in related disorders, 22 , 23 a lower age limit of 6 years was used to minimize the risk of misdiagnoses. The validity and reliability of the hypochondriasis ICD code in the National Patient Register are acceptable for register-based research (80% true positives; interrater reliability, 95%). 16 As per previous validation work, we excluded individuals with a lifetime diagnosis of dysmorphophobia (Swedish ICD-10 code F45.2A) from the entire cohort to limit the risk of misdiagnosis due to the close proximity of these codes. 16

For all individuals who died during the study period, we extracted all-cause mortality data and the specific underlying cause of death from the Cause of Death Register. We analyzed specific causes of death if the number of deaths in the group of exposed individuals was larger than 10. Specific causes of death with 10 or fewer individuals and causes of death classified under the “Codes for Special Purposes” chapter were grouped together under an “other causes of death” category. Causes of death were further grouped into natural and unnatural (ie, “external causes of morbidity and mortality”). From the group of unnatural causes, we also extracted the specific deaths due to suicide. See eTable 1 in Supplement 1 for the ICD codes.

Country of birth (Sweden or abroad) was extracted from the Swedish Total Population Register. Other sociodemographic variables were retrieved from the Census register or the Longitudinal Integration Database for Health Insurance and Labour Market Studies, using records corresponding to the end of the follow-up (ie, latest registered). These included the highest level of education (elementary education, ≤9 years; secondary education, 10-12 years; and higher education, >12 years), civil status (single, married or cohabiting, and divorced or widowed), and family income (lowest 20%, middle 60%, and top 20%).

Lifetime records of other psychiatric disorders were obtained from the National Patient Register and grouped into (1) neurodevelopmental disorders, (2) psychotic disorders, (3) bipolar disorders, (4) depressive disorders, (5) anxiety-related disorders, (6) eating disorders, and (7) substance use disorders ( ICD codes in eTable 2 in Supplement 1 ). A lifetime approach to comorbidity was chosen because the time of recorded diagnosis in the registers often does not correspond to the date of disorder onset. Data on race and ethnicity are not collected as part of the Swedish registers and were therefore not available.

Statistical analyses were conducted between May 5 and September 27, 2023. Mortality rates per 1000 person-years for individuals with and without hypochondriasis were calculated. Survival curves by exposure status were calculated using Kaplan-Meier survival estimates. Stratified Cox proportional hazards regression analyses were used to estimate hazard ratios (HRs) with 95% CIs for mortality among individuals with a diagnosis of hypochondriasis compared with matched individuals without hypochondriasis, with time in years since the start of the follow-up as the underlying time scale. The analysis was first conducted for all causes of mortality and then separately for each specific cause (ie, individuals who died of other causes than the cause of interest were censored at the time of death). The initial model (model 1) adjusted for the matching variables, including birth year, sex, and county of residence at the index date. A second model (model 2) further adjusted for socioeconomic variables: country of birth and latest recorded educational level, civil status, and income. Missing data were coded as unknown and included in the models as nominal variables. Models 1 and 2 were repeated stratifying by sex. Additional models were used to assess whether further adjustment for lifetime psychiatric comorbidities (1 separate model for each comorbidity group) influenced the magnitude of the associations between hypochondriasis and mortality.

Data management and analyses were performed using SAS, version 9.4 (SAS Institute Inc). All tests used 2-tailed significance set at P  < .05.

We identified 13 534 945 individuals living in Sweden between January 1, 1997, and December 31, 2020. After applying several exclusion criteria (eFigure in Supplement 1 ), we matched 4129 individuals with a diagnosis of hypochondriasis (2342 women [56.7%]; median age at first diagnosis, 34.5 years [IQR, 26.3-46.1 years]) with 41 290 individuals without hypochondriasis (23 420 women [56.7%]; median age at matching, 34.5 years [IQR, 26.4-46.2 years]) on sex, birth year, and county of residence at the time of diagnosis ( Table 1 ).

The demographic and clinical characteristics and mean follow-up times of the study cohorts are reported in Table 1 . Individuals with hypochondriasis were significantly more likely than those without hypochondriasis to be born in Sweden, to be less educated, to be single, and to have a lower family income. Most individuals with hypochondriasis (3537 [85.7%]) had received at least 1 other lifetime psychiatric diagnosis, primarily anxiety-related and depressive disorders, compared with 8213 individuals in the group without hypochondriasis (19.9%; P  < .001). These proportions were substantially lower (2222 individuals with hypochondriasis [53.8%] vs 5027 individuals without hypochondriasis [12.2%]; P  < .001) if comorbidities were limited to those preceding the first diagnosis of hypochondriasis (eTable 3 in Supplement 1 ).

A total of 268 individuals with hypochondriasis and 1761 individuals without hypochondriasis died of all causes during the follow-up (crude mortality rates, 8.5 and 5.5 per 1000 person-years, respectively). Individuals with hypochondriasis died at an earlier mean (SD) age than the individuals without hypochondriasis (70.0 [16.8] years vs 75.1 [15.8]; t  = 4.81; P  < .001). Figure 1 displays the survival curves by exposure status.

The minimally adjusted risk estimates (model 1) showed that individuals with hypochondriasis had an 84% higher risk of all-cause mortality during the follow-up compared with individuals without hypochondriasis (HR, 1.84; 95% CI, 1.60-2.10) ( Table 2 ; Figure 2 ). This risk remained significant when adjusting for all sociodemographic variables in model 2 (HR, 1.69; 95% CI, 1.47-1.93). Model 2 also showed significantly higher risks for both natural (HR, 1.60; 95% CI 1.38-1.85) and unnatural causes of death (HR, 2.43; 95% CI, 1.61-3.68).

Regarding specific natural causes of death, the general pattern was one of increased risk for all causes except neoplasms. Most deaths from unnatural causes were attributed to suicide, with a 4-fold increased risk (HR, 4.14; 95% CI, 2.44-7.03) in model 2 ( Table 2 ; Figure 2 ). The risk of all-cause and cause-specific mortality was generally similar among women and men with hypochondriasis (eTables 4 and 5 in Supplement 1 ).

In a post hoc analysis including a subcohort of 4006 individuals diagnosed from 2001 (when outpatient diagnoses were included in the register), we estimated, separately, the risks of death among individuals who first received a diagnosis of hypochondriasis in inpatient (n = 316) and outpatient settings (n = 3690). The risks were significantly higher in the inpatient group vs the outpatient group for all-cause mortality and for natural causes, but not for unnatural causes of death (eTable 6 in Supplement 1 ).

Analyses further controlling for various groups of lifetime psychiatric comorbidities showed that the risks of all-cause mortality and death from any natural causes remained statistically significant ( Table 3 ). The risk of death from suicide was no longer statistically significant after adjustment for depressive and anxiety-related disorders. In a post hoc analysis limiting comorbidities to those recorded before the first diagnosis of hypochondriasis (and the corresponding date for individuals without hypochondriasis), the overall estimates were broadly unchanged, with suicide risk being attenuated but remaining statistically significant (eTable 7 in Supplement 1 ).

To our knowledge, this was the first study to examine the causes of death among individuals with clinically diagnosed hypochondriasis. Several key findings emerged. First, individuals with a diagnosis of hypochondriasis had a significantly higher mortality rate than their counterparts without hypochondriasis and an 84% higher risk of all-cause mortality compared with individuals from the general population. The risks were broadly comparable for women and men with the disorder. Risks remained largely unchanged (with slightly attenuated estimates) after adjusting for socioeconomic variables known to be associated with life expectancy. 24 The increased risk of death was already apparent early in the follow-up ( Figure 1 ).

Second, individuals with hypochondriasis had increased risk of death due to both natural and unnatural causes compared with individuals without hypochondriasis. Among natural causes of death, the most common were circulatory system diseases, respiratory diseases, and “symptoms, signs and abnormal clinical and laboratory findings not elsewhere classified” (mainly including individuals whose death was due to unknown reasons). Our study could not address the mechanisms behind the findings. Multiple factors, probably acting in tandem, are likely to be associated with the increased risks. The avoidance of medical consultations that has been described for some individuals with severe hypochondriasis 7 , 10 , 11 seems a less plausible explanation, given the observation that the risk of death from neoplasms was comparable in the groups with and without hypochondriasis. Other possible explanations appear more plausible, such as chronic stress leading to dysregulated hypothalamic-pituitary-adrenal axis function, immune dysfunction, chronic inflammation, 25 - 28 lifestyle factors (eg, alcohol and substance use), the underrecognition of hypochondriasis as a genuine psychiatric disorder that requires treatment, and/or limited access to evidence-based treatment.

Third, individuals with a diagnosis of hypochondriasis had a more than 4-fold higher risk of death by suicide compared with individuals from the general population. To our knowledge, the risk of suicide in this group had not been previously quantified. A systematic review concluded that suicide attempts may be less frequent among individuals with hypochondriasis than among individuals without, although the included studies had methodological limitations. 29 Clinicians should be aware that individuals with hypochondriasis are at risk of death by suicide, particularly if they have a lifetime history of depression and anxiety.

Fourth, the risks of death from all causes and natural causes were higher among individuals who first received a diagnosis in inpatient settings compared with individuals who first received a diagnosis in outpatient settings, suggesting that patients with more severe or complex symptoms requiring hospitalization are more likely to die. The risk of death from unnatural causes was not significantly different between groups, potentially due to limited statistical power.

Fifth, systematic adjustment for lifetime psychiatric disorders attenuated the magnitude of the risks, but, overall, these remained statistically significant. Suicide risk was no longer statistically significant after adjustment for depressive and anxiety-related disorders. However, these findings should be interpreted with caution given the high proportion of exposed individuals with these lifetime comorbidities and the resulting power issues. In a post hoc analysis limiting comorbidities to those recorded before hypochondriasis, suicide risk was attenuated but remained statistically significant. Even if the finding of increased mortality were not entirely specific to hypochondriasis, it is clear that hypochondriasis is not associated with protection from death.

Taken together, these findings illustrate a paradox, whereby individuals with hypochondriasis have an increased risk of death despite their pervasive fears of illness and death. In this study, most deaths could be classified as potentially preventable. Dismissing these individuals’ somatic symptoms as imaginary may have dire consequences. More should be done to reduce stigma and improve detection, diagnosis, and appropriate integrated (ie, psychiatric and somatic) care for these individuals. 30 Evidence-based psychological treatments for hypochondriasis exist 31 and, in some countries, are even available as low-threshold, guided self-help via the internet, 32 , 33 substantially increasing access to treatment. The hope is that increased detection and access to evidence-based treatment will reduce somatic morbidity, suicidality, and mortality in this group.

This study has some strengths; it was possible due to a unique quirk of the Swedish ICD-10 , which has a separate code for hypochondriasis. 16 Other strengths are the nationwide cohort design with a mean follow-up time of nearly 8 years and the adjustment for important sociodemographic variables and lifetime psychiatric comorbidities. Furthermore, to our knowledge, this cohort was probably the largest cohort of individuals with a formal diagnosis of hypochondriasis ever studied.

This study also has some limitations. First, hypochondriasis is underdiagnosed in Sweden, with only approximately 4000 cases registered in specialist services in 2 decades. Some reasons for this low number include that hypochondriasis symptoms are often wrongly considered secondary to other psychiatric disorders (eg, depression or anxiety), individuals are not taken seriously by health professionals, and the fact that the diagnosis carries stigma. 4 , 7 These reasons mean that many individuals with this disorder are likely to be in the cohort without hypochondriasis, thus diluting the estimates; the true excess mortality among individuals with hypochondriasis may be even higher than reported. Second, we did not have data from primary care, where most individuals with hypochondriasis present for consultation. However, in Sweden, hypochondriasis is rarely diagnosed in primary care. Third, we controlled for sociodemographic variables at the end of follow-up, when they are most relevant for the outcome of interest. We acknowledge that this choice has some limitations, such as the difficulty of knowing if the covariate is a confounder or a mediator. However, we also reported a minimally adjusted model that did not include sociodemographic variables with broadly comparable results. Fourth, we could not adjust for somatization disorder because the code was not included in our database. However, our validation study showed that the risk of misdiagnosis is small. 16 Fifth, while it is common practice in register studies to include undetermined causes of death as suicides, 34 - 37 it is not possible to know if all were indeed suicides. Sixth, limited statistical power meant that we had to group several specific causes of death, and we could not conduct a co-sibling analysis, which would have helped rule out potential familial confounding.

This cohort study is the first, to our knowledge, to suggest that individuals with hypochondriasis have an increased risk of all-cause mortality. The excess mortality was attributed to both natural and unnatural causes, particularly suicide, which can be generally classed as preventable.

Accepted for Publication: October 10, 2023.

Published Online: December 13, 2023. doi:10.1001/jamapsychiatry.2023.4744

Open Access: This is an open access article distributed under the terms of the CC-BY License . © 2023 Mataix-Cols D et al. JAMA Psychiatry .

Corresponding Author: David Mataix-Cols, PhD, Department of Clinical Neuroscience, Karolinska Institutet, Child and Adolescent Psychiatry Research Centre, Gävlegatan 22B, 8th Floor, 113 30 Stockholm, Sweden ( [email protected] ).

Author Contributions: Dr Isomura had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: Mataix-Cols, Isomura, Sidorchuk, Rück, Hedman-Lagerlöf, Fernández de la Cruz.

Acquisition, analysis, or interpretation of data: Mataix-Cols, Isomura, Sidorchuk, Rautio, Ivanov, Österman, Lichtenstein, Larsson, Kuja-Halkola, Chang, Brickell, Hedman-Lagerlöf, Fernández de la Cruz.

Drafting of the manuscript: Mataix-Cols.

Critical review of the manuscript for important intellectual content: Isomura, Sidorchuk, Rautio, Ivanov, Rück, Österman, Lichtenstein, Larsson, Kuja-Halkola, Chang, Brickell, Hedman-Lagerlöf, Fernández de la Cruz.

Statistical analysis: Isomura, Lichtenstein, Kuja-Halkola.

Obtained funding: Mataix-Cols, Fernández de la Cruz.

Administrative, technical, or material support: Lichtenstein, Kuja-Halkola, Chang, Hedman-Lagerlöf, Fernández de la Cruz.

Supervision: Mataix-Cols, Lichtenstein, Larsson, Fernández de la Cruz.

Conflict of Interest Disclosures: Dr Mataix-Cols reported receiving personal fees from UpToDate Inc outside the submitted work. Mr Rautio reported receiving grants from the International OCD Foundation and the Jane and Dan Olsson Foundation outside the submitted work. Dr Larsson reported receiving grants from Shire/Takeda; and personal fees from Shire/Takeda, Evolan, and Medici outside the submitted work. Dr Fernández de la Cruz reported receiving grants from the Heart and Lung Foundation (Hjärt-Lungfonden), the Swedish Research Council (Vetenskapsrådet), Folksam’s Research Foundation (Folksams Forskningsstiftelse), and Karolinska Institutet; and personal fees from Elsevier, UpToDate, and Wolters Kluwer Health outside the submitted work. No other disclosures were reported.

Funding/Support: The study was supported by grants from the Swedish Research Council for Health, Working Life and Welfare (FORTE; grants 2015-00569 and 2021-00132), Region Stockholm (ALF funding; grants 20160143 and 20180078), the Swedish Society of Medicine ( Svenska Läkaresällskapet ; grant SLS-879801), Region Stockholm (clinical postdoc appointment; grant 963608), and Karolinska Institutet (grant FS-2018:0007).

Role of the Funder/Sponsor: The funding sources had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.

Data Sharing Statement: See Supplement 2 .

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