The leading contemporary cognitive-behavioral model of excessive health anxiety (HA) emphasizes the importance of environmental factors, such as learning experiences. The model has little to say about the role of genetic factors and, by ignoring these factors, seems to imply that they are unimportant. In contrast, results from the University of British Columbia Twin Study, using a sample of 88 monozygotic and 65 dizygotic twin pairs, indicated that various facets of HA, such as excessive disease fear, unrealistic beliefs that one has a serious disease, and HA-related interference in functioning, are moderately heritable. The present study extended the analyses of this data set by investigating the extent to which the various facets of HA are due to genetic or environmental factors that are common to all facets versus specific to each facet. Results indicated that all facets of HA are influenced by a common set of genes-there was very little evidence of facet-specific genetic influences. There was considerably stronger evidence for facet-specific environmental influences, where each facet is strongly influenced by environmental experiences that are specific to that facet. However, there was also evidence that particular environmental influences-especially those that shape disease conviction-also influence some of the other HA facets (fear and interference). The importance of environmental factors is consistent with the cognitive-behavioral model of HA, although the model needs to be refined to account for the role of genetic factors. Possibilities for refining the model are discussed, along with promising research directions to better understand the role of genes and the environment in HA.
Keywords: health anxiety; hypochondriasis; behavioral genetics; twins
Anxiety about one's health is a common occurrence. Our focus in this article is on excessive health anxiety (HA), which is anxiety that is disproportionate to one's objectively defined physical condition. There are several facets of HA, including health-related fears (i.e., fear of disease, pain, or death), disease conviction (belief that one has a serious disease), excessive health-related behaviors (e.g., repetitive reassurance seeking from physicians), and functional impairment (e.g., impairment in occupational functioning because of preoccupation with bodily sensations). HA ranges on a continuum of severity and chronicity; the more severe and persistent forms meet the diagnostic criteria of the Diagnostic and Statistical Manual of Mental Disorders for hypochondriasis (American Psychiatric Association, 2000), whereas the milder, more transient forms have been referred to as subclinical or abridged hypochondriasis (Looper & Kirmayer, 2001; Taylor & Asmundson, 2004).
HA often arises when a person is under stress, is seriously ill, is recovering from a serious illness, or has suffered the loss of a family member (Barsky & Klerman, 1983). Some health-anxious people may have a coexisting general medical condition that fuels their excessive anxiety. The most well-developed, empirically supported model is the cognitive-behavioral approach, which has led to effective treatment (Salkovskis, Warwick, & Deale, 2003; Taylor & Asmundson, 2004). HA is posited to arise from dysfunctional beliefs about sickness, health, and health care, including beliefs that lead the person to misinterpret the significance and dangerousness of benign bodily changes and sensations. Benign bodily changes and sensations arise from any number of sources, including benign bodily perturbations, minor diseases, and autonomic arousal associated with anxiety or other emotional states (Taylor & Asmundson, 2004). Many of these sensations are mild or transient and are not associated with disease. The dangerousness of these sensations tends to be overestimated by people who are excessively anxious about their health.
The cognitive-behavioral model is supported by a good deal of empirical research (for a review, see Taylor & Asmundson, 2004), yet the question arises as to whether it neglects the role of genetic factors. …