Asymmetrical genetic attributions for the presence and absence of health problems

Abstract

Objective

Recent research has suggested that people more readily make genetic attributions for positively valenced or desirable traits than for negatively valenced or undesirable traits—an asymmetry that may be mediated by perceptions that positive characteristics are more ‘natural’ than negative ones. This research sought to examine whether a similar asymmetry in genetic attributions would emerge between positive and negative health outcomes.

Design

Across seven experiments, participants were randomly assigned to read a short vignette describing an individual experiencing a health problem (e.g. hypertension) or a corresponding healthy state (e.g. normal blood pressure).

Main Outcome Measures

All participants provided ratings of naturalness and genetic attributions for the outcome described in their assigned vignette.

Results

For diagnoses other than addictive disorders, participants rated the presence of a diagnosis as less genetically caused than its absence; for addictive disorders, the presence of a diagnosis was rated as more genetically caused than its absence. Participants consistently rated the presence of a health problem as less natural than its absence.

Conclusion

Even within a single domain of health, people ascribe differing degrees of ‘naturalness’ and genetic causation to positive versus negative health outcomes, which could impact their preferences for treatment and prevention strategies.

Keywords:

• Genetics
• social cognition
• health beliefs
• psychological essentialism
• causal attribution
• motivated reasoning

Disclosure statement

No potential conflict of interest was reported by the authors.

Data availability statement

The data that support the findings of this research, as well as the vignettes used in the experimental procedures, are available at https://osf.io/b4wec/?view_only=3e315ec7306a49a7bb5bef1696de187e (hosted via the Open Science Framework).

Additional information

Funding

This work was supported by funding from the Genetics & Human Agency Initiative of the John Templeton Foundation and from the National Human Genome Research Institute (grants RM1HG007257 and R00HG010084).