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Blue Genes? Understanding and Mitigating Negative Consequences of Personalized Information about Genetic Risk for Depression

  • Original Research
  • Published:
Journal of Genetic Counseling

Abstract

Personalized genetic testing for vulnerability to mental disorders is expected to become increasingly common. It is therefore important to understand whether learning about one’s genetic risk for a mental disorder has negative clinical implications, and if so, how these might be counteracted. Among participants with depressive symptoms, we administered a sham biochemical test purportedly revealing participants’ level of genetic risk for major depression. Participants told that they carried a genetic predisposition to depression expressed significantly lower confidence in their ability to cope with depressive symptoms than participants told they did not carry this predisposition. A short intervention providing education about the non-deterministic nature of genes’ effects on depression fully mitigated this negative effect, however. Given the clinical importance of patient expectancies in depression, the notion that pessimism about one’s ability to overcome symptoms could be exacerbated by genetic information—which will likely become ever more widely available—represents cause for concern. Education and counseling about the malleability of genetic effects may be an important tool for counteracting clinically deleterious beliefs that can be evoked by genetic test results. Genetic counselors may be able to help patients avoid becoming demoralized by learning they have a genetic predisposition to depression by providing education about the non-deterministic role of biology in depression, and a brief audiovisual intervention appears to be an effective approach to delivering such education.

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Notes

  1. Our modified version of the BDI-II demonstrated high internal consistency (reliability), Cronbach alpha = .94.

  2. Participants could have provided low ratings of the saliva test’s accuracy and reliability for reasons other than suspicion of the test being fake—such as people’s tendency toward defensive processing of threatening health information (Etchegary and Perrier 2007), which may lead individuals to reject personalized messages that suggest they may be at risk for health problems. If this had been the reason some participants did not rate the saliva test as credible, though, there would likely have been more participants endorsing the credibility of the saliva test in the Gene-Absent condition than in the Gene-Present conditions (because the gene-absent feedback did not contain threatening information). On the contrary, among participants who scored at least 13 on the BDI-II there was no significant difference by condition in credibility ratings, F(2, 256) = .65, p = .53. Nonetheless, the present study did not directly measure the reasons people might have discredited the saliva test, and future research examining the causes of such reactions in depth would be highly valuable.

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Acknowledgements

This work was supported (via grant number R01-HG007653) by the National Institutes of Health. The first author also received support from National Institutes of Health grant P50-HG007257. The funding agency had no role in the design of the study, the collection, analysis, and interpretation of data, or in writing the manuscript.

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Correspondence to Matthew S. Lebowitz.

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Matthew S. Lebowitz declares no conflict of interest.

Woo-kyoung Ahn declares no conflict of interest.

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All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1975, as revised in 2000 (5). Informed consent was obtained from all patients for being included in the study.

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This article does not contain any studies with animals performed by any of the authors.

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Lebowitz, M.S., Ahn, Wk. Blue Genes? Understanding and Mitigating Negative Consequences of Personalized Information about Genetic Risk for Depression. J Genet Counsel 27, 204–216 (2018). https://doi.org/10.1007/s10897-017-0140-5

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