Is Suicide Hereditary?
Updated: Jul 11
There's evidence that bio-genetics play a significant role in suicidal activity.
Heredity, environmental factors, and epigenetics contribute to suicide risk.
There is a 2.1 to 2.7-fold increase of suicide risk in relatives of suicide victims.
Family suicide history should be considered a strong risk factor and heavily inform one's overall level of risk and safety planning.
A family history of suicide is correlated with a 2.1 to 2.75-fold risk increase in relatives (e.g., Qin, 2003; Jang et al., 2002). When presented with this information, students and concerned parents have asked me, “Is suicide something genetic?” My answer is, “It depends.” As noted by Hoehne et al. (2015), “The heritability of suicide is well-established.” If, however, by “genetic,” one means the inheritance of a specific, self-destructive gene that pointedly leads to suicide, then no, that’s not been discovered. If someone means suicide is influenced by genetics, that’s a different story.
A multifactorial blueprint To start, one might figure that such genetic influence is rooted in, say, depression, a disorder known for genetic factors that are highly correlated with suicidal activity. For example, Zai et al. (2012) wrote, “In a study of suicide records dating from 1880 to 1980 in an Amish community, Egeland and Sussex (1985) found 26 reported suicides that aggregated within four families who also had a high incidence of mood disorders….” They continued, however, “The authors also found other families that were affected by multiple mood disorders but had no history of suicidal behavior.” Next, add to this the statement from Diblasi et al. (2021), “Broadly, molecular studies suggest a complexity of suicide etiology that cannot simply be accounted for by depression.”
Based on the above two researchers’ statements, it’s clear that genetics influence depression, and while some depressed people become suicidal, it’s more complicated than the influence of any inherited mood alone. The “ingredients” are perhaps best encapsulated by Kouter et al. (2019), who wrote, “[Suicide] is a result of the interplay between hereditary and environmental factors, tied together by epigenetics.”
A survey of biogenetic factors In more recent years, increasingly-sophisticated medical technology has allowed researchers to examine specific aspects of brain anatomy and genes that contribute to suicidal activity. For example, Cha et al. (2017), citing Gosnell et al. (2016), provided: “The hippocampus, which is connected with the body’s stress response system and important in mood regulation and memory, has been found to be structurally abnormal in suicide attempters. The [dorsolateral prefrontal cortex] is involved in goal-directed behavior, decision-making, and emotion regulation and is also found to be structurally abnormal in suicide attempters.” Further, there is the ventral prefrontal cortex (VPC), which is important in “binding together the large-scale networks that subserve emotional processing, decision-making...” (Gage & Baars, 2018). The VPC seems influenced by molecular-level complications, illustrating the role of biological or genetic intricacies underlying some people’s suicidal activity.
To expand, Leonard (2005), for example, noted postmortem studies of depressed people found that the VPC showed serotonin deficits. Serotonin is believed to be essential in controlling aggressive or impulsive behaviors (e.g., Popova, 2008). Leonard surmised this implies a dysfunction in the serotonergic system, for which “there is increasing evidence of a genetic basis.”
This said, biological contributions quickly become more complicated, going from gray matter to microbiology. Readers interested in an in-depth review of molecular contributions may be interested in reading Turecki’s 2014 paper, The Molecular Bases of the Suicidal Brain. In brief, the author explained how early-life adverse environmental factors (epigenetics) can alter gene expression, which influences stress response associated with a lifetime susceptibility to suicidal behavior. As for the suicide-stress response link, O’Connor (2020) pointed out that hypothalamic-pituitary-adrenal (HPA) axis dysregulation is a particular culprit, which, as noted by Berardelli et al. (2020), disrupts healthy neurotransmission. To add to this more specifically, Oquendo et al. (2014) observed that an altered stress response seems responsible for downstream effects in the form of the aforementioned serotonin system abnormalities.
If this seems overwhelming, bear in mind that it is only a glimpse of the research on the bio-genetic factors of suicide. In addition, is it chicken or egg? Do people with the above complications have more proneness to being depressed, a state of being that then interacts with those factors for a dangerous cocktail? Or does being depressed initiate some of the bio-genetic abnormalities that are correlated with suicide attempts? Clinical implications
Outside of psychiatrists prescribing antidepressants, clinicians likely aren’t able to change someone’s bio-genetics. Further, antidepressants alone likely cannot alter such a complicated equation to eradicate bio-genetic risk factors entirely. There may also be cultural factors related to the family for clinicians to consider. For instance, Jang et al. (2022) discovered that South Korean survivors of suicide victims were three times more likely to die by suicide. Interestingly, this was especially true for wives whose husbands died by suicide.
The best that clinicians can do is: 1) Always ask about a family history of suicide, and 2) if present, weigh it as a significant factor when deciding someone’s level of risk or the observation or safety planning required.
If you or someone you love is contemplating suicide, seek help immediately. For help 24/7, dial 988 for the National Suicide Prevention Lifeline, or reach out to the Crisis Text Line by texting TALK to 741741. Disclaimer: The material provided in this post is for informational purposes only and is not intended to diagnose, treat, or prevent any illness or suicide in readers or people they know. The information should not replace personalized care or intervention from an individual’s provider or formal supervision if you’re a practitioner or student.
Anthony D. Smith, LMHC - Blog