Genes shape almost every trait we possess, from the color of our eyes to the quirks of our temperament. Among the thousands we inherit, a handful can be downright unsettling. Below we explore the 10 scary genes that slip into our DNA from our parents, each with its own eerie back‑story and surprising science.
Why 10 Scary Genes Shape Our Lives
Understanding these genetic hitchhikers helps us see why certain behaviors or health issues run in families, and it offers clues on how environment and lifestyle can tip the balance.
10 Violence Genes
Variants of the MAOA gene and the cadherin‑13 (CDH13) gene are popularly dubbed “warrior genes” because they have been linked to heightened aggression. A 2014 Finnish study showed that offenders carrying these variants accounted for roughly five to ten percent of all crimes recorded in Finland.
The same research revealed that individuals with the warrior genes are about 13 times more likely to reoffend compared with those lacking the variants. The study examined 900 convicted participants who together committed 1,154 murders, attempted murders, manslaughters, and violent assaults.
Importantly, possessing these genes does not guarantee violent conduct. Most carriers never engage in criminal activity, and proper upbringing can mitigate their influence. Some scientists even argue that, because up to half of the Finnish population may carry them, attributing violent acts solely to these genes would be misleading.
9 Suicide Gene
Researchers have linked the RGS2 gene to both depression and suicidal tendencies. A 2011 investigation led by John Mann at the New York State Psychiatric Institute identified one RGS2 variant that predisposes individuals to depression, while another variant appears to increase the likelihood of suicide.
The study suggested that the RGS2 gene could help explain why suicidal behavior sometimes clusters within families. Notably, the famous writer Ernest Hemingway’s family—who suffered multiple suicides, including his own in 1961—has been hypothesized to carry the high‑risk variant.
Out of 412 participants with severe depression, 154 had a history of suicide attempts. Among those, 43 percent possessed the aggressively suicidal RGS2 variant, while roughly 20 percent carried a less risky version.
Although Mann acknowledged that detecting this gene might serve as a risk indicator, he cautioned that the findings remain inconclusive and further research is essential before drawing firm conclusions.
8 Trauma Gene
Groundbreaking work has shown that parents can transmit the biological imprint of severe trauma to their children via genetic mechanisms. This phenomenon has been observed in descendants of enslaved peoples, Holocaust survivors, and Vietnam‑war veterans, where post‑traumatic stress disorder (PTSD) appears to echo across generations.
Dr Rachel Yehuda of the Icahn School of Medicine at Mount Sinai led the research, explaining that a profoundly traumatic event can alter gene expression, and these epigenetic changes are inherited. She sampled Jewish neighbors who were grandchildren of Holocaust survivors and found hormone profiles matching those of PTSD‑affected Vietnam veterans, along with hyper‑active amygdalae.
Parallel findings among African‑American descendants of enslaved ancestors prompted sociologist Dr Joy DeGruy to coin the term “Post‑Traumatic Slave Disorder,” underscoring how historic oppression can leave a lingering genetic signature.
7 Infidelity Gene
The dopamine‑regulating DRD4 gene influences reward pathways that drive motivation and sexual satisfaction. A 2010 investigation by Justin Garcia at Binghamton University uncovered a DRD4 variant that appears to heighten the propensity for cheating and one‑night stands.
Garcia’s team surveyed 181 young adults and discovered that carriers of this variant were statistically more inclined toward infidelity compared with non‑carriers.
Nevertheless, Garcia emphasized that the presence of the gene does not excuse unfaithful behavior; it merely signals a potential predisposition, and many carriers remain faithful throughout their lives.
6 Death Genes
Studies across humans and animals consistently show that women outlive men by five to six years on average. Researchers attribute part of this gap to a set of mitochondrial DNA variants dubbed the “Mother’s Curse.”
These mitochondrial genes are passed exclusively from mother to child. While both sexes inherit them, the variants exert a detrimental effect on males, accelerating aging and shortening lifespan, yet they leave females unaffected, allowing the genes to persist through generations.
5 Back Pain Genes
In 2018, a massive genetic analysis involving 29,000 chronic‑back‑pain sufferers (drawn from a broader cohort of 158,000 Europeans) identified three genes associated with persistent spinal discomfort.
The most influential of these is the SOX5 gene, which plays a pivotal role during embryonic development. Earlier rodent experiments showed that disabling SOX5 resulted in skeletal malformations, highlighting its importance.
The remaining two genes influence spinal‑cord formation and susceptibility to intervertebral disc herniation—commonly known as a “slipped disc”—both of which can underlie chronic back pain.
4 Pessimistic Gene
A research team headed by Rebecca M. Todd at the University of British Columbia pinpointed the ADRA2B gene as a contributor to a naturally pessimistic outlook. For the gene to promote negativity, it must lack certain amino‑acid segments.
Individuals missing these segments tend to focus more readily on adverse stimuli, noticing threatening cues—such as a menacing figure on a street—more quickly than neutral or pleasant ones.
The discovery emerged from a study of 200 participants who were briefly shown two words and asked to attend to the second. While most struggled to recognize the second word, carriers of the altered ADRA2B gene consistently identified it when it carried emotionally charged content like “rape” or “orgasm.” Some scholars, including Ahmad R. Hariri of Duke University, argue that pessimism likely stems from a constellation of genes rather than a single culprit.
3 The Lung Problem Gene
Archaeological evidence from Viking latrines in Denmark revealed that these seafaring peoples suffered massive intestinal worm infestations, exposing them to proteases capable of damaging vital organs, including the lungs.
The Vikings’ immune systems were shielded by a mutation in the alpha‑1‑antitrypsin (A1AT) gene. While the standard A1AT protein guards tissues from our own proteases, the Viking‑specific mutation also neutralized worm‑derived enzymes.
Modern descendants—estimated at over 300 million—inherit this mutated A1AT variant, which, unlike the original, offers weaker protection against our internal proteases. Consequently, they face heightened risks of chronic obstructive pulmonary disease (COPD) and emphysema, especially if they smoke.
2 Sleeplessness Genes
A massive survey of 113,006 participants uncovered seven distinct genes that predispose individuals to insomnia. Several of these genes overlap with conditions such as depression, anxiety, and restless‑legs syndrome (RLS), which often co‑occur with sleep disturbances.
One notable gene, MEIS1, is linked not only to insomnia but also to RLS and periodic limb movements during sleep (PLMS). Affected individuals experience an irresistible urge to move their legs, disrupting rest and leaving them fatigued the following day.
1 Talking Gene
Popular belief holds that women are more talkative than men, a claim supported by data showing women average around 20,000 spoken words daily versus roughly 7,000 for men. Women also tend to acquire languages faster and begin reading earlier.
A University of Maryland School of Medicine study traced this disparity to the FOXP2 gene, a key regulator of speech and language development. The gene produces a specialized protein that appears in greater quantities in female brains.
The investigation involved ten children—five girls and five boys—and revealed that girls possessed about 30 percent more of the FOXP2‑derived protein than boys. While the researchers consider the sample size modest, the findings hint at a genetic contribution to the observed vocal differences.