Illness Anxiety Disorder (formerly Hypochondriasis)



Hypochondriasis, which is now known as illness anxiety disorder, and the other somatic symptom disorders (e.g., factitious disorder, conversion disorder) are among the most difficult and most complex psychiatric disorders to treat in the general medical setting. On the basis of many new developments in this field, the DMS-5 has revised diagnostic criteria to facilitate clinical care and research. While illness anxiety disorder is included in the category of "somatic symptom and related disorders" it continues to have much overlap with obsessive-compulsive disorder and related illness.

As with all psychiatric disorders, illness anxiety disorder demands creative, rich biopsychosocial treatment planning by a team that includes primary care physicians, subspecialists, and mental health professionals.

This article describes illness anxiety disorder, its diagnosis, and an overview of treatment approaches, with references for details beyond the scope of the article. Finally, the article reviews new developments in psychopharmacologic and psychotherapeutic treatments.

Case study

A 45-year-old white male engineer presents to a primary care clinic armed with multiple internet searches on the topic of cancer. He states that he “just knows” he has a GI cancer, "probably the colon or maybe the pancreas." When asked how long this concern has bothered him he says "for years I have been concerned that I have cancer." You ask about relevant symptoms and he is a bit vague, saying "I get some pain or pressure right here (he points to the left upper quadrant) but it is not there all the time." Upon asking about prior workups he says “I have had ultrasounds and colonoscopies but they couldn't find anything. I was initially relieved but a couple of weeks later started to think that they must have just missed something.”

When you ask about the patient's goals for today’s visit he is emphatic. "I think what I really need is another colonoscopy and abdominal CT scan." His examination is unrevealing. When you suggest a less invasive approach, he brings up error rates of the other evaluations and shows literature endorsing how abdominal CT is the criterion standard. He is anxious at baseline and increasingly irritable when you propose less invasive evaluation. He ends the encounter by stating that he will “find another doctor who sees my point and will get me what I need.”


Neurochemical deficits associated with illness anxiety disorder appear similar to those of mood and anxiety disorders. For example, Hollander et al posited an "obsessive-compulsive spectrum" to include hypochondriasis, obsessive-compulsive disorder (OCD), body dysmorphic disorder (BDD), anorexia nervosa, and Tourette syndrome, all of which were believed to have similarities in responsiveness to serotonin reuptake inhibitors and to demonstrate "hyperactivity" in areas of the frontal lobes.[4]  A more recent article highlights the effectiveness of fluoxetine (a serotonin reuptake inhibitor and a mainstay in the treatment of OCD), as effective in the treatment of hypochondriasis.[2, 3]

While the formulation of obsessive-compulsive (OC) spectrum disorders has been adopted by the DSM-5, this new clustering does not include illness anxiety disorder. It does include: OCD, BDD, hoarding disorder, trichotillomania, excoriation disorder, OCD and other related disorders that are substance induced or due to another medical condition. In addition, encountering a patient with more than one of the anxiety spectrum disorders comorbid with illness anxiety disorder is not unusual. Findings of neurochemical deficits in patients with illness anxiety disorder are only preliminary, but such deficits may explain why symptoms overlap, why the disorders are commonly comorbid, and why effective treatments for OC spectrum disorders are also effective for illness anxiety disorder (eg, selective serotonin reuptake inhibitors [SSRIs]).

In a study of biological markers, subjects who met DSM-IV-TR diagnostic criteria for hypochondriasis had decreased plasma neurotrophin 3 (NT-3) levels and platelet serotonin (5-HT) levels, compared to healthy control subjects. NT-3 is a marker of neuronal function and platelet 5-HT is a surrogate marker for serotonergic activity.[6]



United States

Based on the previously defined "hypochondriasis," the DSM estimates that the community 1–2 year prevalence is 1.3–10%, while the 6-month to 1-year prevalence in medical outpatients is 3–8%. Some degree of preoccupation with disease is apparently common, because 10–20% of people who are healthy and 45% of people without a major psychiatric disorder have intermittent unfounded worries about illness.[7, 8]

International/cultural effects

Efforts have been made to quantify international rates of illness anxiety disorder and other somatic symptom disorders. Those rates are heavily influenced by the diagnostic criteria involved (ie, somatization disorder versus abridged somatization disorder) and how studies are conducted.[9] Within the US, researchers have also worked to define how culture and ethnicity interact to determine "idioms" of distress and also how these factors influence the physician-patient relationship. This research has included the formulation of patterns of presentations that can be classified as "culture bound syndromes." A selective literature review recommends that culture be considered in idiopathic somatic symptom presentations, but also that caution be taken to not be overly generalizing about ethnicity.[9]


Illness anxiety disorder is usually episodic, with symptoms that last from months to years and equally long quiescent periods. Although formal outcome studies have not been conducted, one third of patients with illness anxiety disorder are believed to eventually improve significantly. A good prognosis appears to be associated with high socioeconomic status, treatment-responsive anxiety or depression, the absence of a personality disorder, and the absence of a related nonpsychiatric medical condition. Most children are believed to recover by adolescence or early adulthood, but empiric studies have not been carried out.

Epidemiological studies are few, but patients with illness anxiety disorder appear to have no differences in age or gender than patients without this disorder. There have been several studies that have found patients with illness anxiety disorder to have decreased educational and income levels and higher rates of childhood illness and abuse.[7] These individuals use medical care at high rates, making frequent visits to the emergency department, the doctor, and other health care providers and undergoing frequent physical examinations, laboratory testing, and other costly, invasive, and potentially dangerous procedures.[10]

Cognitive, social learning, and psychodynamic theories imply that patients have significant psychosocial disturbances in terms of relationships, vocations, and other endeavors. Exacerbations may occur with psychological stressors and in patients with comorbid psychiatric conditions.

These high-use patterns differ dramatically from those of nonsomatizing patients and remain true even when comorbid medical conditions and sociodemographic differences are accounted for.[11] The medically unexplained complaint is often a symptom of illness anxiety[12] and may well be a presentation of associated abnormal illness behavior.[13]

Patients with illness anxiety disorder have a high rate of psychiatric comorbidity.[14] In one general medical outpatient clinic, 88% of patients with hypochondriasis had one or more concurrent psychiatric disorders, the most common being generalized anxiety disorder (71%), dysthymic disorder (45.2%), major depression (42.9%), somatization disorder (21.4%), and panic disorder (16.7%). These patients are 3 times more likely to have a personality disorder than the general population.[14] Substance abuse or dependence is also a serious comorbid condition, particularly use of benzodiazepines, though epidemiological studies have not assessed the exact frequency of this problem. The long-term prognosis of patients with hypochondriasis is understudied due to the heterogeneity of the disorder. However, higher severity at baseline is likely associated with worse outcome.

Sex- and age-related demographics

Illness anxiety disorder appears to occur equally in men and women.

The disorder can begin at any age, but the most common age of onset is early adulthood.


Hypochondriasis is no longer a diagnosis according to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). Instead, approximately 75% of individuals previously diagnosed with hypochondriasis are subsumed under the diagnosis of somatic symptom disorder. The remaining 25% have high health anxiety in the absence of somatic symptoms and are classified as having illness anxiety disorder. Both somatic symptom disorder and illness anxiety disorder are classified in the DSM-5 under Somatic Symptom and Related Disorders.[73] The disorders in this class include somatic symptom disorder, illness anxiety disorder, conversion disorder, and factitious disorder.

The health preoccupation diagnostic interview has been determined to have sufficient inter-rater reliability for somatic symptoms disorder and illness anxiety disorder (kappa of 0.85; n=104).[79] According to the DSM-5, somatic symptom disorders all share a common feature: the prominence of somatic symptoms associated with significant distress and impairment.[73]

The core feature of somatic symptom disorder is the presence of one or more somatic symptoms that are distressing or result in significant disruption of daily life.

The core feature of illness anxiety disorder is a preoccupation with having or acquiring a serious, undiagnosed medical illness.

Diagnostic criteria (DSM-5)

The DSM-5 criteria for illness anxiety disorder are as follows:[73]


The absence of physical findings, particularly after serial examinations, supports the diagnosis of illness anxiety disorder. However, the patient must receive a physical examination to make the psychiatric intervention possible. A mental status examination complements the physical examination.

General appearance, behavior, and speech

See the list below:

Psychomotor status

See the list below:

Mood and affect

Mood is the pervasive and sustained emotion that colors the patient's perception of the world and affect is what the examiner observes.

Thought process

See the list below:

Thought content

See the list below:

Cognitive function

See the list below:


See the list below:


See the list below:


Developmental and other predisposing factors consistently indicate the importance of parental attitudes toward disease, previous experience with physical disease, and culturally acquired attitudes relevant to the etiology of the disorder.[15] Overall, however, few demographic and clinical differences have been found between patients with illness anxiety disorder and the general population. There are some findings that risk factors for illness anxiety disorder include a lower educational level, lower income, and a history of childhood illness or abuse.[7]

A cognitive model of illness anxiety disorder suggests that patients misinterpret bodily symptoms by augmenting and amplifying their somatic sensations. Patients also appear to have lower-than-usual thresholds for, and tolerance of, physical discomfort. For example, what most people normally perceive as abdominal pressure, patients with illness anxiety experience as abdominal pain. When they do sustain an injury (eg, ankle sprain), it is experienced with significant anxiety and is taken as confirmation of their worry about being ill. This may be due to a tendency among patients with illness anxiety to exaggerate their assessment of vulnerability to disease and their appraisal of the risk of serious illness.[11]

The social learning theory frames illness anxiety disorder as a request for admission to the sick role made by a person facing seemingly insurmountable and insolvable problems. This role may allow them to avoid noxious obligations, postpone unwelcome challenges, and be relieved from duties and obligations.[16]

The psychodynamic theory implies that aggressive and hostile wishes toward others are transferred via repression and displacement into physical complaints. The somatic symptoms serve to "undo" guilt felt about the anger and serve as a punishment for being "bad."

Neurochemical deficits with illness anxiety disorder and some other somatoform disorders (eg, body dysmporphic disorder [BDD]) appear similar to those of depressive and anxiety disorders. For example, in 1992, Hollander et al. posited an obsessive-compulsive spectrum that includes OCD, BDD, anorexia nervosa, Tourette syndrome, and impulse control disorders (eg, trichotillomania, pathological gambling).[4] Although only preliminary data have been reported on these neurochemical deficits, such deficits may explain why symptoms overlap, why the disorders are commonly comorbid, and why treatments may parallel one another (eg, SSRIs). Additionally, P-wave dispersion (the difference between the maximum and minimum P-wave duration on the electrocardiograph) has been found to be significantly higher in patients with panic disorder and in patients with illness anxiety, compared with healthy control subjects. The elevated P-wave dispersion may be an indicator of cardiac autonomic dysfunction in anxiety disorders.[17]

Laboratory Studies

In patients with hypochondriasis, the abnormal laboratory findings characteristic of the suggested physical disorder are absent.

Other Tests

Screening tools

Screening tools include the following:

Medical Care

Basic management principles

Basic management principles include the following:

Physician concerns and influence

The most powerful therapeutic tool is the physician and his or her team's attention, concern, interest, careful listening, and nonjudgmental stance, which can potentially break a pathological cycle of maladaptive interactions between the patient and movement from physician to physician (see the image below).[38]

View Image

Pathological cycle of bodily concern and anxiety in hypochondriasis.

One difficulty with which physicians struggle is related to countertransference (ie, physicians' own emotional reactions to the patient). Typically, physicians feel angry, hopeless, and/or helpless because their assessments and interventions are not effective and efforts at reassuring the patient are usually met with resistance and even escalation of physical symptoms. These feelings may lead physicians to reject or withdraw from patients with illness anxiety disorder.

Psychiatric inpatient care

As with the other somatoform disorders, inpatient psychiatric hospitalization for the somatoform disorder itself is rarely necessary. As these patients are at risk for concurrent mood, anxiety, and personality disorders, a psychiatric admission may be necessary to manage episodic decompensation of the comorbid psychiatric conditions or suicidal ideation.

If the patient experiences suicidal ideation or makes a suicide act based on comorbid depression or personality disorder or develops uncontrollable anxiety, then an inpatient psychiatric hospitalization may be indicated. In such a case, an illness anxiety disorder diagnosis may be established in the context of an inpatient admission.

Formal psychometric testing may be of help.

The hypochondriacal patterns of behavior can be addressed in ward therapy interventions.

When patients are discharged following recovery of behavioral stability, the treatment model described below may be implemented.

General medical inpatient care

Patients with illness anxiety disorder should be admitted to general medicine and surgery services based on the medical and surgical acuity, not solely to facilitate work-up.

Due to the enigmatic nature of various physical symptoms, occasionally patients with illness anxiety disorder are admitted to the general medical-surgical hospital for an extensive work-up.

When illness anxiety disorder is suspected in a medical or surgical inpatient, a psychosomatic medicine consultation should be performed to elucidate the diagnosis and address psychiatric comorbidity.

If clinically recommended by the psychosomatic medicine consultant, psychotropic medication interventions can be started.

As in the outpatient care model, patients should not be exposed to high-risk invasive procedures.

Numerous other strategies appear to benefit patients with illness anxiety disorder or hypochondriasis (see the image below). These strategies may prevent potentially serious complications, including the effects of unnecessary diagnostic and therapeutic procedures.

View Image

Factors that maintain anxiety in patients with hypochondriasis.

Establish one primary care physician as the patient's main physician.

Review the patient's medical history to build an alliance and rule out medical disorders.

Premature reassurance, prescription of psychotropic medications, and referral for mental health services may suggest to the patient that he or she is not being taken seriously. Therefore, while such treatments may be indicated at some time (in the future), prematurely offering a diagnosis or psychiatric treatment may, in fact, impair the establishment of a trusting patient-physician relationship.

Acknowledge the patient's pain and suffering.

Couple reassurance statements of normal findings with statements that that the patient will not be abandoned. For example, “Mr. Smith, it appears that you are still having concern about having a “several medical disorder” despite all the workup, which, so far, has not showed any abnormal finding. I will continue to work with you to maximize you overall well-being and health.”

Reassure the patient that evaluation will be ongoing.

Understand the “the fear” of having an unknown medical disorder as a form of emotional communication.

Search for underlying medical and psychiatric disorders potentially amenable to treatment.

Seek consultation or refer the patient to a colleague if establishing an alliance proves difficult.

Allow for time-limited structured discussions about somatic concerns.

Spend sufficient time on health care maintenance issues such as diet, experience, smoking cessation, and cancer detection.

Treat comorbid psychiatric disorders concurrently.

Be aware of emotional reactions toward the patient (ie, anger, hopelessness, helplessness) and seek frequent informal consultation when possible.

Focus on care of the patient with illness anxiety disorder, not exclusively on “a cure” for the disorder.


Several authors have suggested a cognitive-educational approach to understand the development of the severe anxiety associated with illness anxiety disorder and the factors that maintain the long-term anxiety.[39] Randomized controlled trials now suggest that cognitive-behavioral therapy (CBT) is efficacious in the treatment of illness anxiety disorder[40, 41, 42, 43, 44] and may be the recommended treatment for patients with this disorder. Bibliotherapy, using CBT principles, may also be useful.

In a meta-analysis of outcomes using CBT for illness anxiety disorder, higher pre-treatment severity and great number of CBT sessions is associated with higher effect size.[75]

Cognitive and exposure therapy also seems promising for illness anxiety disorder.[76, 77]  Mindfulness-based cognitive therapy also appears to be effective when added to usual care.[78]

In clinical settings, both the availability of CBT and treatment adherence of patients with illness anxiety disorder to psychotherapy in general are major barriers to successful outcomes. It is possible that case management and integrated primary care and psychiatry programs may be especially suitable for patients with illness anxiety disorder and somatic symptom disorder. However, prospective treatment studies are urgently needed in this area.

Surgical Care

Psychosurgery is only recommended for patients with severe and intractable illness anxiety disorder.


Primary care physicians generally treat illness anxiety disorder, with psychiatrists providing consultation.


Patients with illness anxiety disorder should eat 3 meals per day to feel as healthy as possible. They should avoid substances that adversely affect mood, exacerbate anxiety symptoms, or reduce the quality of sleep (eg, caffeine, alcohol, nicotine).


Exercise increases psychological well-being. Patients who are hypochondriacal may be reluctant to follow this advice, but many patients greatly increase their physical activity as treatment progresses. Exercise helps to improve mood, reduce tension, and improve sleep in patients with associated depression, anxiety, or both.

Medication Summary

Pharmacotherapy is used as an adjunct to psychotherapy and educational treatments. The goals of pharmacotherapy are to reduce comorbid symptoms and disorders (eg, depression), to prevent complications, and, in a few circumstances, to reduce hypochondriacal symptoms. Each medication has advantages and disadvantages.[45]

There are no medications approved specifically for the treatment of hypochondriasis, somatic symptom disorder, or illness anxiety disorder. Medications are usually started to treat the comorbid depression or anxiety disorder. 

Fluoxetine (Prozac)

Clinical Context:  Selectively inhibits presynaptic serotonin reuptake with minimal or no effect on reuptake of norepinephrine or dopamine

Paroxetine (Paxil)

Clinical Context:  Potent selective inhibitor of neuronal serotonin reuptake. Also has weak effect on norepinephrine and dopamine neuronal reuptake

Sertraline (Zoloft)

Clinical Context:  Selectively inhibits presynaptic serotonin reuptake, minimal or no effect on reuptake of norepinephrine, and clinically insignificant inhibition of reuptake of dopamine.

Venlafaxine (Effexor XR)

Clinical Context:  Selectively inhibits presynaptic serotonin reuptake, norepinephrine (at doses of approximately 150 mg PO qam), and dopamine (at doses of approximately 150-225 mg qam).

Clomipramine (Anafranil)

Clinical Context:  Affects serotonin uptake while affecting norepinephrine uptake when converted into its metabolite desmethylclomipramine.

Fluvoxamine (Luvox)

Clinical Context:  Potent selective inhibitor of neuronal serotonin reuptake. Does not bind significantly to alpha-adrenergic, histamine, or cholinergic receptors and, thus, has fewer adverse effects than TCAs.

Imipramine (Tofranil)

Clinical Context:  Inhibits reuptake of norepinephrine or serotonin at presynaptic neuron.

Phenelzine (Nardil)

Clinical Context:  Usually reserved for patients who do not tolerate or respond to traditional cyclic or second-generation antidepressants.

Citalopram (Celexa)

Clinical Context:  Selectively inhibits presynaptic serotonin reuptake, minimal or no effect on reuptake of norepinephrine.

Escitalopram (Lexapro)

Clinical Context:  Selective serotonin reuptake inhibitor (SSRI) and S-enantiomer of citalopram. Used for the treatment of depression. Mechanism of action is thought to be potentiation of serotonergic activity in CNS resulting from inhibition of CNS neuronal reuptake of serotonin. Onset of depression relief may be obtained after 1-2 wk, which is sooner than other antidepressants.

Class Summary

These are typically used for depression or anxiety comorbid with hypochondriasis, although in some cases they alleviate hypochondriacal symptoms in the absence of another disorder. They are indicated for use in adults with depression, anxiety (eg, panic disorder, OCD, social phobia, generalized anxiety, posttraumatic stress disorders), and bulimia nervosa disorders.

Off-label uses include insomnia, attention-deficit/hyperactivity disorder, premenstrual dysphoric disorder, and other conditions. All SSRIs (eg, fluoxetine [Prozac], sertraline [Zoloft], paroxetine [Paxil], citalopram [Celexa], escitalopram [Lexapro], fluvoxamine [Luvox]), one selective norepinephrine and serotonin inhibitor (ie, venlafaxine [Effexor XR]), 2 TCAs (ie, clomipramine [Anafranil], imipramine [Tofranil]), and one MAOI (ie, tranylcypromine [Parnate]) have been listed; the latter should be used with care because of dietary restrictions and drug interactions. Data on bupropion (Wellbutrin) and mirtazapine (Remeron) are insufficient to warrant listing, but they may also be used.

Initial doses are listed below. The general principle in these patients is to start at a low dose and progress slowly, unless a psychiatric emergency (eg, suicidal ideation) is present. Once established, a well-tolerated and efficacious antidepressant should be continued as indicated for the comorbid condition (eg, 6-12 mo for a single depression or indefinitely for recurrent depression and an anxiety disorder). If used for hypochondriasis alone, for maintenance dosing, adjust the dose to maintain the patient on the lowest effective dosage, and reassess the patient periodically to determine the need for continued treatment.

Propranolol (Inderal)

Clinical Context:  Has membrane-stabilizing activity and decreases automaticity of contractions.

Class Summary

Compete with beta-adrenergic agonists for available beta-receptor sites. Propranolol inhibits beta-1 receptors (located mainly in cardiac muscle) and beta-2 receptors (located mainly in bronchial and vascular musculature), inhibiting chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation.

Alprazolam (Xanax)

Clinical Context:  For management of panic attacks. Binds receptors at several sites within CNS, including limbic system and reticular formation. Effects may be mediated through GABA receptor system.

Class Summary

Indicated for treatment of anxiety disorders and panic attacks, with or without agoraphobia, which are commonly comorbid with hypochondriasis. Use with caution because patients with hypochondriasis may have increased risk of substance abuse or dependence.

Pimozide (Orap)

Clinical Context:  Indicated for Tourette syndrome for suppression of motor and phonic tics. Off-label use for psychosis, hypochondriacal delusions and parasitosis, and Huntington chorea.

Risperidone (Risperdal)

Clinical Context:  Binds to dopamine D2 receptor with 20-times lower affinity than for serotonin receptor. Improves negative symptoms of psychoses and reduces incidence of EPS. Indicated for treatment of psychotic disorders, including schizophrenia and bipolar disorder mania; also used for sleep.

Olanzapine (Zyprexa)

Clinical Context:  Binds to dopamine D2 and serotonin receptors. Improves negative symptoms of psychoses and reduces incidence of EPS. Indicated for treatment of psychotic disorders, including schizophrenia and bipolar disorder mania; also used for sleep

Class Summary

Have been shown to reduce morbidity associated with this disorder, particularly in presence of comorbid anxiety or hypochondriacal worries that mimic obsessions or delusions. Because of potential for serious long-term adverse effects (eg, tardive dyskinesia), consultation with psychiatrist recommended to evaluate need for antipsychotic medication. Insufficient data to list other antipsychotics, although they have been used in patients with hypochondriasis.

Inpatient & Outpatient Medications

Continue successful long-term trials of medications for patients with illness anxiety disorder.

For patients with comorbid disorders, consider maintenance of those trials because these disorders can initiate and/or exacerbate hypochondriacal symptoms.


Physician-to-physician dialogue on the nature of the patient's problems and successful management strategies is useful.


Patients who are hypochondriacal may be significant consumers of medical care, undergoing repetitive doctor visits, physical examinations, laboratory testing, and other costly, invasive, and potentially dangerous procedures.

Physician concerns regarding workups for somatic complaints also may preclude diagnosis of common comorbid disorders (eg, depression) that are quite treatable.


Hypochondriasis is a common disorder in primary care settings.

The differential diagnosis includes other somatoform, depressive, anxiety (eg, generalized anxiety disorder, OCD), and psychotic disorders.

Biopsychosocial treatment is required to manage this complex disorder, and further research is required to better understand its pathophysiology and interface with other psychiatric conditions. Recognizing the biological similarities between these seemingly disparate disorders may be a useful starting point to begin a more systematic study of novel treatments for hypochondriasis.[46]

A systematic review of six studies on hypochondriasis indicated that 30-50% of patients achieve recovery.[47]

A good prognosis appears to be associated with high socioeconomic status, treatment-responsive anxiety or depression, the absence of a personality disorder, and the absence of a related nonpsychiatric medical condition.

Most children recover by adolescence or early adulthood.

There is a dearth of long-term follow-up studies examining outcomes of patients with hypochondriasis. In a prospective study that examined 58 patients with hypochondriasis who had participated in selective serotonin reuptake inhibitor (SSRI) treatment for 4-16 years (mean 8.6±4.5 y), 40% continued to meet the diagnosis of hypochondriasis. Predictors of continued diagnosis of hypochondriasis include longer duration of hypochondriasis prior to treatment, history of childhood physical punishment, and lower use of SSRI during the treatment period. A large portion of patients with hypochondriasis who received SSRI treatment were able to achieve remission.[48]

Patient Education

Educational approaches provide accurate information, allowing the patient to realize somatic symptoms are exceedingly common, with only a small proportion caused by disease and most compatible with physical health.

Accurate information about the relationship of a threatening stimulus and its somatic consequences can influence the severity of autonomic responses, subjective distress, and behavior.

Maladaptive iatrogenic beliefs must be countered. Providing a small amount of information at a time and repeating it is best.

For excellent patient education resources, visit eMedicineHealth's Mental Health Center and Depression Center.

For mild and short-lived symptoms, the primary medical provider could provide detailed education (symptoms, course, monitoring, diagnosis, and treatment) about the medical condition about which the patient is concerned.

Education should additionally focus on the role of anxiety and how anxiety could increase autonomic activity or arousal and, thereby, cause the body to misattribute certain physical sensations and symptoms.

For more persistent and chronic hypochondriasis, especially in situations where the patient has already failed treatment with multiple providers, education needs be delivered in small “doses,” when the time is right, and after the establishment of a firm patient-provider relationship.

The tailoring of education delivery as applied to mild versus severe symptoms has not been systematically studied.

Since hypochondriasis may be precipitated by psychosocial stress, family support is likely to be additionally helpful. However, the role of family education requires further investigation.

Even in the absence of formal research into family education for hypochondriasis, several practical pointers are recommended:

Given that these patients are often comfortable with computer searches, websites specific to hypochondriasis may be helpful to recommend to patients and families:


Debra Kahn, MD, Associate Clinical Professor, Director of Psychosomatic Medicine Service, Director of Psychosomatic Fellowship, Director of Transplant Psychiatry, Department of Psychiatry and Behavioral Sciences, University of California, Davis, School of Medicine

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Otsuka Pharmaceutical Development & Commercialization, Inc.


Glen L Xiong, MD, Associate Clinical Professor, Department of Psychiatry and Behavioral Sciences, Department of Internal Medicine, University of California, Davis, School of Medicine; Medical Director, Sacramento County Mental Health Treatment Center

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Doctor On Demand<br/>Received income in an amount equal to or greater than $250 from: Blue Cross Blue Shield Federal Employee Program<br/>Received royalty from Lippincott Williams & Wilkins for book editor; Received grant/research funds from National Alliance for Research in Schizophrenia and Depression for independent contractor; Received consulting fee from Blue Cross Blue Shield Association for consulting. for: Received book royalty from American Psychiatric Publishing Inc.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

David Bienenfeld, MD, Professor, Departments of Psychiatry and Geriatric Medicine, Wright State University, Boonshoft School of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Donald M Hilty, MD, Associate Chief of Staff, Mental Health, Northern California VA Healthcare System; Vice-Chair of VA Mental Health Services

Disclosure: Nothing to disclose.

James A Bourgeois, MD, OD, MPA, Chair, Department of Psychiatry, Baylor Scott and White Health, Central Texas Division; Clinical Professor, Department of Psychiatry, Texas A&M University Health Science Center College of Medicine

Disclosure: Nothing to disclose.

Peter M Yellowlees, MD, MBBS, Professor of Psychiatry, Director of Health Informatics Program, University of California, Davis, School of Medicine

Disclosure: Received consulting fee from Medscape for independent contractor.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Shayna L Marks, BA, MA; Dandan Liu, BA; and Celia Chang, MD to the development and writing of this article.


  1. Barsky AJ, Klerman GL. Overview: hypochondriasis, bodily complaints, and somatic styles. Am J Psychiatry. 1983 Mar. 140(3):273-83. [View Abstract]
  2. Fallon BA, Petkova E, Skritskaya N, et al. A double-masked, placebo-controlled study of fluoxetine for hypochondiasis. J Clin Psychopharmcol. December 2008. 6:638-45.
  3. Ravindran AV, da Silva TL, Ravindran LN, Richter MA, Rector NA. Obsessive-compulsive spectrum disorders: a review of the evidence-based treatments. Can J Psychiatry. 2009 May. 54(5):331-43. [View Abstract]
  4. Hollander E, Stein DJ, Decaria CM, Cohen L, Islam M, Frenkel M. Disorders related to OCD--neurobiology. Clin Neuropharmacol. 1992. 15 Suppl 1 Pt A:259A-260A. [View Abstract]
  5. Wooley SC, Blackwell B, Winget C. A learning theory model of chronic illness behavior: theory, treatment, and research. Psychosom Med. 1978 Aug. 40(5):379-401. [View Abstract]
  6. Brondino N, Lanati N, Barale F, et al. Decreased NT-3 plasma levels and platelet serotonin content in patients with hypochondriasis. J Psychosom Res. 2008 Nov. 65(5):435-9. [View Abstract]
  7. Magarinos M, Zafar U, Nissenson K, Blanco C. Epidemiology and treatment of hypochondriasis. CNS Drugs. 2002. 16(1):9-22. [View Abstract]
  8. Kellner R. Hypochondriasis and somatization. JAMA. 1987 Nov 20. 258(19):2718-22. [View Abstract]
  9. Barsky AJ, Ettner SL, Horsky J, Bates DW. Resource utilization of patients with hypochondriacal health anxiety and somatization. Med Care. 2001 Jul. 39(7):705-15. [View Abstract]
  10. Barsky AJ, Ahern DK, Bailey ED, Saintfort R, Liu EB, Peekna HM. Hypochondriacal patients' appraisal of health and physical risks. Am J Psychiatry. 2001 May. 158(5):783-7. [View Abstract]
  11. Holder-Perkins V, Wise TN, Williams DE. Hypochondriacal Concerns: Management Through Understanding. Prim Care Companion J Clin Psychiatry. 2000 Aug. 2(4):117-121. [View Abstract]
  12. Lipowski ZJ. Somatization: a borderland between medicine and psychiatry. CMAJ. 1986 Sep 15. 135(6):609-14. [View Abstract]
  13. Barsky AJ, Wyshak G, Klerman GL. Psychiatric comorbidity in DSM-III-R hypochondriasis. Arch Gen Psychiatry. 1992 Feb. 49(2):101-8. [View Abstract]
  14. Ball RA, Clare AW. Symptoms and social adjustment in Jewish depressives. Br J Psychiatry. 1990 Mar. 156:379-83. [View Abstract]
  15. Jones LR, Mabe PA 3rd, Riley WT. Illness coping strategies and hypochondriacal traits among medical inpatients. Int J Psychiatry Med. 1989. 19(4):327-39. [View Abstract]
  16. Atmaca M, Korkmaz H, Korkmaz S. P wave dispersion in patients with hypochondriasis. Neurosci Lett. 2010 Nov 26. 485(3):148-50. [View Abstract]
  17. Smith RC. Somatization disorder: defining its role in clinical medicine. J Gen Intern Med. 1991 Mar-Apr. 6(2):168-75. [View Abstract]
  18. Stefansson JG, Messina JA, Meyerowitz S. Hysterical neurosis, conversion type: clinical and epidemiological considerations. Acta Psychiatr Scand. 1976 Feb. 53(2):119-38. [View Abstract]
  19. Toone BK. Disorders of hysterical conversion. Bass C, ed. Physical Symptoms and Psychological Illness. London, UK: Blackwell Scientific; 1990. 207-34.
  20. de Leon J, Bott A, Simpson GM. Dysmorphophobia: body dysmorphic disorder or delusional disorder, somatic subtype?. Compr Psychiatry. 1989 Nov-Dec. 30(6):457-72. [View Abstract]
  21. Bienvenu OJ, Samuels JF, Wuyek LA, Liang KY, Wang Y, Grados MA, et al. Is obsessive-compulsive disorder an anxiety disorder, and what, if any, are spectrum conditions? A family study perspective. Psychol Med. 2011 May 13. 1-13. [View Abstract]
  22. van den Heuvel OA, Mataix-Cols D, Zwitser G, Cath DC, van der Werf YD, Groenewegen HJ, et al. Common limbic and frontal-striatal disturbances in patients with obsessive compulsive disorder, panic disorder and hypochondriasis. Psychol Med. 2011 May 5. 1-12. [View Abstract]
  23. Hollifield M, Tuttle L, Paine S, Kellner R. Hypochondriasis and somatization related to personality and attitudes toward self. Psychosomatics. 1999 Sep-Oct. 40(5):387-95. [View Abstract]
  24. Fallon BA, Harper KM, Landa A, Pavlicova M, Schneier FR, Carson A. Personality disorders in hypochondriasis: prevalence and comparison with two anxiety disorders. Psychosomatics. 2012 Nov-Dec. 53(6):566-74. [View Abstract]
  25. Xiong GL, Bougeois JA, Chang CH, Liu D, Hilty DM. Hypochondriasis: common presentations and treatment strategies in primary care and specialty settings. Therapy. 2007. (4):3:323-38.
  26. Salkovskis PM, Rimes KA, Warwick HM, Clark DM. The Health Anxiety Inventory: development and validation of scales for the measurement of health anxiety and hypochondriasis. Psychol Med. 2002 Jul. 32(5):843-53. [View Abstract]
  27. Campo JV, Di Lorenzo C, Chiappetta L, et al. Adult outcomes of pediatric recurrent abdominal pain: do they just grow out of it?. Pediatrics. 2001 Jul. 108(1):E1. [View Abstract]
  28. Noyes R Jr, Stuart S, Langbehn DR, Happel RL, Longley SL, Yagla SJ. Childhood antecedents of hypochondriasis. Psychosomatics. 2002 Jul-Aug. 43(4):282-9. [View Abstract]
  29. Fiddler M, Jackson J, Kapur N, Wells A, Creed F:. Childhood adversity and frequent medical consultations. Gen Hosp Psychiatry. 2004. 26:367-77.
  30. Durso FT, Reardon R, Shore WJ, Delys SM:. Memory processes and hypochondriacal tendencies. J Nerv Ment Dis. 1992. 179(5):279-83.
  31. Gottlieb GL. Hypochondriasis: A psychosomatic problem in the elderly. Adv Psychosom Med. 1989. 19:67-84.
  32. Stein EM. When is hypochondriasis not hypochondriasis? Geriatrics. 2003. 58(3):41-2.
  33. Tyrer P, Cooper S, Tyrer H, et al. CHAMP: Cognitive behaviour therapy for health anxiety in medical patients, a randomised controlled trial. BMC Psychiatry. 2011 Jun 14. 11:99. [View Abstract]
  34. Kellner R, Abbott P, Pathak D, Winslow WW, Umland BE. Hypochondriacal beliefs and attitudes in family practice and psychiatric patients. Int J Psychiatry Med. 1983-1984. 13(2):127-39. [View Abstract]
  35. Speckens AE, Spinhoven P, Sloekers PP, Bolk JH, van Hemert AM. A validation study of the Whitely Index, the Illness Attitude Scales, and the Somatosensory Amplification Scale in general medical and general practice patients. J Psychosom Res. 1996 Jan. 40(1):95-104. [View Abstract]
  36. Janca A, Isaac M, Bennett LA, Tacchini G. Somatoform disorders in different cultures--a mail questionnaire survey. Soc Psychiatry Psychiatr Epidemiol. 1995 Jan. 30(1):44-8. [View Abstract]
  37. Harrington P. Obsessive compulsive disorder with associated hypochondriasis. BMJ. 2008 May 10. 336(7652):1070-1. [View Abstract]
  38. Weck F, Neng JM, Richtberg S, Stangier U. Dysfunctional beliefs about symptoms and illness in patients with hypochondriasis. Psychosomatics. 2012 Mar-Apr. 53(2):148-54. [View Abstract]
  39. Looper KJ, Kirmayer LJ. Behavioral medicine approaches to somatoform disorders. J Consult Clin Psychol. 2002 Jun. 70(3):810-27. [View Abstract]
  40. Visser S, Bouman TK. The treatment of hypochondriasis: exposure plus response prevention vs cognitive therapy. Behav Res Ther. 2001 Apr. 39(4):423-42. [View Abstract]
  41. Kroenke K, Swindle R. Cognitive-behavioral therapy for somatization and symptom syndromes: a critical review of controlled clinical trials. Psychother Psychosom. 2000 Jul-Aug. 69(4):205-15. [View Abstract]
  42. Visser S, Bouman TK. Cognitive-behavioural approaches in the treatment of hypochondriasis: six single case cross-over studies. Behav Res Ther. 1992 May. 30(3):301-6. [View Abstract]
  43. McManus F, Surawy C, Muse K, Vazquez-Montes M, Williams JM. A randomized clinical trial of mindfulness-based cognitive therapy versus unrestricted services for health anxiety (hypochondriasis). J Consult Clin Psychol. 2012 Oct. 80(5):817-28. [View Abstract]
  44. Medical Economics Staff. Medical Economics. Physicians' Desk Reference. 58th ed. Monvale, NJ; 2004.
  45. Kellner R. Prognosis of treated hypochondriasis. A clinical study. Acta Psychiatr Scand. 1983 Feb. 67(2):69-79. [View Abstract]
  46. olde Hartman TC, Borghuis MS, Lucassen PL, van de Laar FA, Speckens AE, van Weel C. Medically unexplained symptoms, somatisation disorder and hypochondriasis: course and prognosis. A systematic review. J Psychosom Res. 2009 May. 66(5):363-77. [View Abstract]
  47. Schweitzer PJ, Zafar U, Pavlicova M, Fallon BA. Long-term follow-up of hypochondriasis after selective serotonin reuptake inhibitor treatment. J Clin Psychopharmacol. 2011 Jun. 31(3):365-8. [View Abstract]
  48. Adler G. The physician and the hypochondriacal patient. N Engl J Med. 1981 Jun 4. 304(23):1394-6. [View Abstract]
  49. Avia MD, Ruiz MA, Olivares ME, Crespo M, Guisado AB, Sánchez A. The meaning of psychological symptoms: effectiveness of a group intervention with hypochondriacal patients. Behav Res Ther. 1996 Jan. 34(1):23-31. [View Abstract]
  50. Barsky AJ. Hypochondriasis. Medical management and psychiatric treatment. Psychosomatics. 1996 Jan-Feb. 37(1):48-56. [View Abstract]
  51. Bouman TK. A community-based psychoeducational group approach to hypochondriasis. Psychother Psychosom. 2002 Nov-Dec. 71(6):326-32. [View Abstract]
  52. Bursztajn H, Barsky AJ. Facilitating patient acceptance of a psychiatric referral. Arch Intern Med. 1985 Jan. 145(1):73-5. [View Abstract]
  53. Cetin M, Ebrinç S, Agargün MY, Yigit S. Risperidone for the treatment of monosymptomatic hypochondriacal psychosis. J Clin Psychiatry. 1999 Aug. 60(8):554. [View Abstract]
  54. Fallon BA, Javitch JA, Hollander E, Liebowitz MR. Hypochondriasis and obsessive compulsive disorder: overlaps in diagnosis and treatment. J Clin Psychiatry. 1991 Nov. 52(11):457-60. [View Abstract]
  55. Fallon BA, Liebowitz MR, Salman E, Schneier FR, Jusino C, Hollander E. Fluoxetine for hypochondriacal patients without major depression. J Clin Psychopharmacol. 1993 Dec. 13(6):438-41. [View Abstract]
  56. Fallon BA, Schneier FR, Marshall R, et al. The pharmacotherapy of hypochondriasis. Psychopharmacol Bull. 1996. 32(4):607-11. [View Abstract]
  57. Ford CV, Long KD. Group psychotherapy of somatizing patients. Psychother Psychosom. 1977. 28(1-4):294-304. [View Abstract]
  58. Greeven A, van Balkom AJ, Visser S, et al. Cognitive behavior therapy and paroxetine in the treatment of hypochondriasis: a randomized controlled trial. Am J Psychiatry. 2007 Jan. 164(1):91-9. [View Abstract]
  59. Hamann K, Avnstorp C. Delusions of infestation treated by pimozide: a double-blind crossover clinical study. Acta Derm Venereol. 1982. 62(1):55-8. [View Abstract]
  60. Hiller W, Leibbrand R, Rief W, Fichter MM. Predictors of course and outcome in hypochondriasis after cognitive-behavioral treatment. Psychother Psychosom. 2002 Nov-Dec. 71(6):318-25. [View Abstract]
  61. House A. Hypochondriasis and related disorders. Assessment and management of patients referred for a psychiatric opinion. Gen Hosp Psychiatry. 1989 May. 11(3):156-65. [View Abstract]
  62. Kellner R. Psychotherapeutic strategies in hypochondriasis: a clinical study. Am J Psychother. 1982 Apr. 36(2):146-57. [View Abstract]
  63. Klimes I, Mayou RA, Pearce MJ, Coles L, Fagg JR. Psychological treatment for atypical non-cardiac chest pain: a controlled evaluation. Psychol Med. 1990 Aug. 20(3):605-11. [View Abstract]
  64. Lidbeck J. Group therapy for somatization disorders in primary care: maintenance of treatment goals of short cognitive-behavioural treatment one-and-a-half-year follow-up. Acta Psychiatr Scand. 2003 Jun. 107(6):449-56. [View Abstract]
  65. Pearce MJ, Mayou RA, Klimes I. The management of atypical non-cardiac chest pain. Q J Med. 1990 Sep. 76(281):991-6. [View Abstract]
  66. Phillips KA. Body dysmorphic disorder: clinical features and drug treatment. CNS Drugs. 1995. 3:30-40.
  67. Reilly TM, Jopling WH, Beard AW. Successful treatment with pimozide of delusional parasitosis. Br J Dermatol. 1978 Apr. 98(4):457-9. [View Abstract]
  68. Stone AB. Treatment of hypochondriasis with clomipramine. J Clin Psychiatry. 1993 May. 54(5):200-1. [View Abstract]
  69. Thomson A, Page L. Psychotherapies for hypochondriasis. Cochrane Database of Systematic Reviews 2007, Issue 4. Art. No.: CD006520. DOI: 10.1002/14651858.CD006520.pub2.
  70. Walker J, Vincent N, Furer P, Cox B, Kjernisted K. Treatment preference in hypochondriasis. J Behav Ther Exp Psychiatry. 1999 Dec. 30(4):251-8. [View Abstract]
  71. Wesner RB, Noyes R Jr. Imipramine an effective treatment for illness phobia. J Affect Disord. 1991 May-Jun. 22(1-2):43-8. [View Abstract]
  72. American Psychiatric Association. Somatic Symptom and Related Disorders. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Washington, DC: American Psychiatric Association; 2013. 310-318.
  73. Escobar JI, Gureje O. Influence of Cultural and Social Factors on the Epidemiology of Idiopathic Somatic Complaints and Syndromes. Psychosomatics. 2007. 69:841-845.
  74. Olatunji BO, Kauffman BY, Meltzer S, Davis ML, Smits JA, Powers MB. Cognitive-behavioral therapy for hypochondriasis/health anxiety: a meta-analysis of treatment outcome and moderators. Behav Res Ther. 2014 Jul. 58:65-74. [View Abstract]
  75. Weck F, Neng JM. Response and Remission After Cognitive and Exposure Therapy for Hypochondriasis. J Nerv Ment Dis. 2015 Nov. 203 (11):883-5. [View Abstract]
  76. Weck F, Neng JM, Schwind J, Höfling V. Exposure therapy changes dysfunctional evaluations of somatic symptoms in patients with hypochondriasis (health anxiety). A randomized controlled trial. J Anxiety Disord. 2015 Aug. 34:1-7. [View Abstract]
  77. McManus F, Surawy C, Muse K, Vazquez-Montes M, Williams JM. A randomized clinical trial of mindfulness-based cognitive therapy versus unrestricted services for health anxiety (hypochondriasis). J Consult Clin Psychol. 2012 Oct. 80 (5):817-28. [View Abstract]
  78. Axelsson E, Andersson E, Ljótsson B, Wallhed Finn D, Hedman E. The health preoccupation diagnostic interview: inter-rater reliability of a structured interview for diagnostic assessment of DSM-5 somatic symptom disorder and illness anxiety disorder. Cogn Behav Ther. 2016 Jun. 45 (4):259-69. [View Abstract]

Pathological cycle of bodily concern and anxiety in hypochondriasis.

Factors that maintain anxiety in patients with hypochondriasis.

Pathological cycle of bodily concern and anxiety in hypochondriasis.

Mood, cultural, developmental, and environmental factors that influence hypochondriasis.

Factors that maintain anxiety in patients with hypochondriasis.

A cognitive model of the development of anxiety with hypochondriasis.