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Warrior-Worrier Model

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Warrior-Worrier model
Other namesWarrior-worrier hypothesis, COMT Val158Met polymorphism
(Left) Warrior figure and its characteristics, (Right) Worrier figure and its characteristics.
SpecialtyCognitive neuroscience, behavioral genetics
Causesrs4680 single-nucleotide polymorphism (Val158Met) in the COMT gene on chromosome 22q11.21
Key Characteristics
Gene Catechol-O-methyltransferase (COMT)
Chromosome 22q11.2[1]
Key genetic variant rs4680 (Val158Met)
Polymorphism type Single-nucleotide polymorphism (SNP), missense variant
Amino acid substitution Valine (Val) → Methionine (Met) at codon 158
Affected brain region Prefrontal cortex[2]
Phenotype labels Warrior (Val/Val)
Worrier (Met/Met)
Heterozygous (Val/Met)
Enzyme activity Val/Val: High
Met/Met: Low
Val/Met: Intermediate
Population frequency
(European ancestry)[3]		 Val/Val: ~25%
Met/Met: ~25%
Val/Met: ~50%
Primary limitations Polygenic trait, small effect size, sex differences,
population frequency variation, uncharacterised heterozygous majority


The Warrior-Worrier Model is a conceptual framework in cognitive neuroscience and behavioral genetics describing how a functional genetic polymorphism in the catechol-O-methyltransferase (COMT) gene influences individual differences in stress reactivity, emotional regulation, and cognitive performance.[4][5] COMT gene is responsible for prefrontal dopamine regulation by altering enzyme activity, the model proposes that two common variants of the COMT enzyme produce divergent psychological profiles, colloquially labeled the "warrior" with homozygous Valine (Val) allele and the "worrier" with homozygous Methionine (Met) allele.

The model has attracted significant interest in clinical psychiatry, evolutionary psychology, and personalised medicine as a potential explanation for naturally occurring variation in anxiety, resilience, and performance under pressure across human populations though criticism on oversimplification remains.

Mechanism

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Genetic Basis

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The warrior-worrier model is always associated with a common functional polymorphism in the COMT gene. The COMT gene is responsible for encoding the COMT enzyme, which plays a critical role in the brain by breaking down certain chemical messengers called neurotransmitters, mainly including dopamine, adrenaline, and noradrenaline, within the synapse.[6]

In humans, a common single-nucleotide polymorphism (SNP) is found in the COMT gene, known as rs4680. [7] A functional variation arises from a nonsynonymous substitution within the gene, where at codon 158, a missense mutation substitutes a guanine (G) nucleotide with an adenine (A) nucleotide, further translated to a substitution of the amino acid valine (Val) with methionine (Met) (Val158Met) in the amino acid sequence of the COMT enzyme.[8] This single Val158Met amino acid replacement results in significant differences in the COMT enzyme activity and has been proposed as a genetic basis for the variability in stress and emotion handling between individuals.

Individuals with the homozygous Val allele (Val/Val) produce more stable COMT enzyme with a generally higher enzymatic activity. The Val/Val genotype is called the “warrior” phenotype.[7]

Conversely, individuals with the homozygous Met allele (Met/Met) produce less stable COMT enzyme with a relatively lower enzymatic activity. This Met/Met genotype is described as the “worrier” phenotype.[7]

While the remaining heterozygous Met/Val individuals exhibit intermediate levels of enzymatic activity and are regarded as having a balanced phenotype between the “warrior” and “worrier”.[7]

Enzymatic Mechanism

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COMT enzyme in the synaptic cleft breaks down neurotransmitter like dopamine to regulate the level.

The major functional impact of the Val158Met polymorphism is on the COMT enzyme’s role in regulating neurotransmitters within the synapse. Their degradative function in catecolamine catabolism is dominant in the prefrontal cortex of the human brain, where the region governs decision-making, emotional regulation, and stress response, acting as the “personality centre” of a human.[7][9] Therefore, shaping individual differences in stress reactivity within the warrior-worrier framework.

In Met/Met “worrier”, the Met substitutions result in a less stable and less active COMT enzyme. With lower functional levels of COMT enzymes in the brain, the breakdown of catecholamine neurotransmitters is less efficient. Consequently, leading to a prolonged synaptic accumulation, receptor activation, and sustained neuronal stimulation. Accumulated neurotransmitters like noradrenaline, recognised as the primary stress chemical[10], contribute to physiological changes under stress, such as accelerated heart rate, increased blood glucose level, and vasoconstriction to increase blood pressure.[11] Over time, these individuals will tend to become highly sensitive to stress signals and show elevated levels of anxiety and worry in response to stress.[12]

By contrast, Val/Val “warrior” individuals benefit from the more stable form of the COMT enzymes with higher enzymatic activity. Catecholamine neurotransmitters within their synapse are being broken down more rapidly and efficiently.[13] With the accelerated clearance of noradrenaline and other stress-related chemicals, nerves are less activated and stimulated by a lower level of neurotransmitters. As a result, “warriors” are usually less prone to stress-induced physiological changes, thereby increasing their resilience to stress.[12]

Meanwhile, heterozygous Met/Val individuals experience a normal level of COMT enzymes, a moderate neurotransmitter clearance rate, and show adaptable responses to stress.

Phenotype Expression

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Warrior (Val/Val)

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Individuals with the Val/Val gene have high COMT activity, which lowers dopamine levels in the prefrontal cortex.[14][15] This neurochemical profile is associated with traits of lower baseline anxiety and greater emotional resilience. [16] People with the gene have better working memory and cognitive functions in acute stress conditions.[17] The term “warrior” is a metaphorical description of people with an advantage in stressful situations, having the ability for rapid robust response.

However, in conditions with low stimulation, the Val/Val phenotype reduces dopamine tone and impairs sustained attention, increasing susceptibility to impulsive or anti-social behaviours. These individuals are considered less cognitively efficient in a low stress environment compared to Met/Met phenotype.[15]

Worrier (Met/Met)

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Individuals with the Met/Met gene have low COMT activity, which raises dopamine levels in the prefrontal cortex.[14] This profile confers advantages in working memory, complex problem solving and other cognitively demanding tasks performed in low stress conditions. [18] The “worrier” term describes sensitivity to potential risks and tendency to ruminative cognition.[19]

But in intense stress conditions, excessive catecholamine accumulation increases dopamine levels in the prefrontal cortex beyond optimal range on the inverted-U curve. This worsens cognitive functions that are enhanced at rest and increases vulnerability to anxiety disorders.[20][21]

Heterozygous

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Individuals with Val/Met genes demonstrate intermediate COMT activity and moderate prefrontal dopamine levels. This profile, represented by 50% of the population, has a stable cognitive performance and stress response. There is no specific colloquial label in the literature for this group and are sometimes described as an “adaptable” stress-response profile.

Evolutionary Context

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Both Val and Met alleles appear to be close to equal across human populations. Its frequency varies by ancestral background based on historical selection pressures, reflecting a balanced polymorphism. [3] The core argument is that the two phenotypes represent complementary survival strategies. “Warrior” benefits in rapid processing tasks, while “worrier” confers advantage on tasks involving memory and sustained attention. [22]

In an ancestral environment requiring quick physical responses to predation or intergroup conflict, the Val/Val stress resilient phenotype would have been selectively favoured. Conversely, in a stable social environment demanding forward planning, threat detection and cooperative problem-solving, the vigilance and enhanced working memory of the Met/Met phenotype would have been favoured.

History

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The theoretical underpinning of the inverted-U curve dopamine curve was developed by Goldman-Rakic and colleagues (2000), whose work on prefrontal dopamine dynamics established that too much or too little dopamine can impair cognitive performance.[23]

Then the formal coinage of warrior worrier framework is generally attributed to Stein et al. (2006), who summarized the (COMT) literature and proposed that the warrior strategy from Val158 alleles are associated with an advantage in processing aversive stimuli, while the worrier strategy from Met158 alleles are associated with an advantage in memory and attention tasks.[7]

A notable extension of the evolutionary argument came from combat sports research. A study of mixed martial arts fighters found that Val/Val “warrior” homozygotes occurred at greater frequencies in Mixed Martial Arts (MMA) athletes relative to controls.[23] The model also invites a group level selection interpretation. A population composed of both warriors and worriers may be collectively more adaptive than one dominated by either phenotype alone. Warriors providing decisive action under threat, warriors providing analytical caution and memory based planning under calm. This mix of traits would have ensured adaptability in complex and changing environments.[24][25]

Implication

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The relationship between dopamine level and the working memory performance shows a inverted-U shape. Too low and too high dopamine level show poor performances while medium and normal level shows the best performance.[26]

The warrior-worrier model has introduced a critical implication for understanding individual differences in stress vulnerability. The relationship between dopamine and noradrenaline levels that are affected by the Val158Met polymorphism, and the cognitive and emotional functioning, is often described as an inverted-U shaped curve: either too little or too much neurotransmitters in the prefrontal cortex can lead to underperformance of cognitive ability, while an optimal level enhances it.[27][17] Research has suggested that, Met/Met ("worrier") individuals may show more optimal performance on measures of working memory, whereas Val/Val ("warrior") individuals may perform less well.[26]

Based on individual's COMT genotype, individualized therapies are also rapidly developing to maximize the cognitive performance. Therapies such as dietary interventions can associate with greater memory improvement in Val/Val individuals. Catechol-containing polyphenols present in caffeine and tea, and oleacein in extra virgin olive oil are called the natural COMT inhibitors. This substances will lower COMT enzyme activity, thereby reducing the breakdown of dopamine in Val/Val ("warrior") individuals.[28][29]

Criticisms and Limitations

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Single-gene explanation for polygenic trait

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The warrior worrier model rests on a SNP, rs4680, to account for individual differences in stress reactivity and cognitive performance. However, both traits are substantially polygenic. There are additional genetic variations that interact with COMT to influence cognitive phenotypes.[30] The rs4680 polymorphism alone explains only a small proportion of variance in any behavioural measure, but genome-wide association studies of traits such as anxiety and executive function implicate hundreds of loci rather than one.[31]

Small and inconsistently replicated effect sizes

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Meta analysis of Val158Met across psychiatric phenotypes report that effect sizes, while sometimes statistically significant, are small in magnitude and associations have been inconsistently replicated across individual studies.[31]Significant trends have emerged only when results from many studies are pooled, which is consistent with a small additive contribution rather than a determinative one.[31] Several independent studies of working memory and executive function have reported no significant association with COMT genotype, and the direction of observed effects varies across populations and experimental conditions.[32]

Sex differences and the role of oestrogen

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COMT activity in the human prefrontal cortex is measurably higher in males than in females, independent of Val158Met genotype.[33] Oestrogen appears to down-regulate COMT enzyme transcription, where female Met allele carriers may experience a compounding reduction in enzyme activity and male Met carriers do not. [34] This creates a genotype-by-sex interaction that the binary warrior worrier framework does not accommodate. In addition, the Met allele has been associated with obsessive-compulsive disorder in males but not in females, while the Val allele shows links to impulsivity-related phenotypes in male only.[31] Studies that do not stratify by sex risk conflating effects that operate differently across biological sexes.[35]

Population allele frequency variation

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The frequencies of the Val and Met alleles vary substantially across ancestral populations, with some populations showing markedly different distributions from the roughly 25:50:25 (Val:Val/Met:Met) split observed in European-ancestry samples.[3][36] Because most foundational warrior worrier studies were conducted using predominantly European-ancestry cohorts, the generalisability of their findings to other populations is unclear. Meta-analyses that include diverse samples have identified heterogeneity in effect sizes by ancestry.[31]

The heterozygous majority lacks defined phenotype

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Approximately 50% of the population carries one Val and one Met allele. The warrior worrier model assigns this group an “intermediate” profile but offers no distinct characterisation, no agreed label and limited predictive content. In practice this group is often treated as a statistical residual between the two named phenotypes, despite comprising the largest portion of the population.[19]

See also

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References

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  1. ↑ Hall, Kathryn T; Loscalzo, Joseph; Kaptchuk, Ted J (2019-05-24). "Systems Pharmacogenomics – Gene, Disease, Drug and Placebo Interactions: A Case Study in COMT". Pharmacogenomics. 20 (7): 529–551. doi:10.2217/pgs-2019-0001. ISSN 1462-2416. PMC 6563236. PMID 31124409.
  2. ↑ Dean, Brian; Parkin, Georgia M.; Gibbons, Andrew S. (2020-02-01). "Associations between catechol-O-methyltransferase (COMT) genotypes at rs4818 and rs4680 and gene expression in human dorsolateral prefrontal cortex". Experimental Brain Research. 238 (2): 477–486. doi:10.1007/s00221-020-05730-0. ISSN 1432-1106.
  3. 1 2 3 "rs4680 (COMT Val158Met): Complete Guide to the Worrier-Warrior Gene". Ask My DNA. 14 November 2025. Retrieved 30 March 2026.
  4. ↑ Goldman, David; Weinberger, Daniel R.; Malhotra, Anil K.; Goldberg, Terry E. (2009-05-08). "The Role of COMT Val158Met in Cognition". Biological Psychiatry. 65 (1): e1–e2. doi:10.1016/j.biopsych.2008.07.032. PMC 2679368. PMID 18838132.
  5. ↑ Dickinson, D.; Elvevåg, B. (2009-11-24). "Genes, cognition and brain through a COMT lens". Neuroscience. 164 (1): 72–87. doi:10.1016/j.neuroscience.2009.05.014. ISSN 0306-4522. PMC 2760675. PMID 19446012.
  6. ↑ "COMT gene: MedlinePlus Genetics". medlineplus.gov. Retrieved 2026-04-12.
  7. 1 2 3 4 5 6 Stein, Dan J; Newman, Timothy K; Savitz, Johnathan; Ramsear, Rajkumar (October 2006). "Warriors Versus Worriers: The Role of COMT Gene Variants". CNS Spectrums. 11 (10). Cambridge University Press: 745–748. Retrieved 22 March 2026.
  8. ↑ Smolka, Michael N.; Schumann, Gunter; Wrase, Jana; Grüsser, Sabine M.; Flor, Herta; Mann, Karl; Braus, Dieter F.; Goldman, David; Büchel, Christian; Heinz, Andreas (2005-01-26). "Catechol-O-Methyltransferase val158met Genotype Affects Processing of Emotional Stimuli in the Amygdala and Prefrontal Cortex". Journal of Neuroscience. 25 (4): 836–842. doi:10.1523/JNEUROSCI.1792-04.2005. ISSN 0270-6474. PMC 6725630. PMID 15673663.
  9. ↑ Hathaway, William R.; Newton, Bruce W. (2026), "Neuroanatomy, Prefrontal Cortex", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 29763094, retrieved 2026-04-12
  10. ↑ Glavin, Gary B. (1984-08-06). "Stress and brain noradrenaline: A review". Neuroscience & Biobehavioral Reviews. 9 (2): 233–243. doi:10.1016/0149-7634(85)90048-X.
  11. ↑ Ibragimov, Sherzod; Rustamova, Dilafruza; Ganieva, Aziza; Zubaydilloeva, Zarina; Raiimzhanova, Kamilla (2021-11-03). "ADRENALINE, AND WHAT PROCESSES OCCUR UNDER ITS ACTION IN OUR BODY". ГРААЛЬ НАУКИ: 398–401. doi:10.36074/grail-of-science.22.10.2021.71. ISSN 2710-3056.
  12. 1 2 Serrano, Jose Martinez; Banks, Jonathan B.; Fagan, Thomas J.; Tartar, Jaime L. (2019-03-04). "The influence of Val158Met COMT on physiological stress responsivity". Stress. 22 (2): 276–279. doi:10.1080/10253890.2018.1553949. ISSN 1025-3890.
  13. ↑ Chen, Jingshan; Lipska, Barbara K.; Halim, Nader; Ma, Quang D.; Matsumoto, Mitsuyuki; Melhem, Samer; Kolachana, Bhaskar S.; Hyde, Thomas M.; Herman, Mary M.; Apud, Jose; Egan, Michael F.; Kleinman, Joel E.; Weinberger, Daniel R. (2004-07-15). "Functional Analysis of Genetic Variation in Catechol-O-Methyltransferase (COMT): Effects on mRNA, Protein, and Enzyme Activity in Postmortem Human Brain". The American Journal of Human Genetics. 75 (5): 807–821. doi:10.1086/425589. PMC 1182110. PMID 15457404.
  14. 1 2 Akil, Mayada; Kolachana, Bhaskar S.; Rothmond, Debora A.; Hyde, Thomas M.; Weinberger, Daniel R.; Kleinman, Joel E. (2003-03-15). "Catechol- O -Methyltransferase Genotype and Dopamine Regulation in the Human Brain". The Journal of Neuroscience. 23 (6): 2008–2013. doi:10.1523/JNEUROSCI.23-06-02008.2003. ISSN 0270-6474.
  15. 1 2 Egan, Michael F.; Goldberg, Terry E.; Kolachana, Bhaskar S.; Callicott, Joseph H.; Mazzanti, Chiara M.; Straub, Richard E.; Goldman, David; Weinberger, Daniel R. (7 August 2000). "Effect of COMT Val108/158 Met genotype on frontal lobe function and risk for schizophrenia". Proceedings of the National Academy of Sciences. 98 (12). The National Academy of Sciences: 6917–6922. doi:10.1073/pnas.111134598. Retrieved 22 March 2026.
  16. ↑ Enoch, Mary-Anne; Xu, Ke; Ferro, Erica; Harris, Claudia R.; Goldman, David (March 2003). "Genetic origins of anxiety in women: a role for a functional catechol-O-methyltransferase polymorphism". Proceedings of the National Academy of SciencessPsychiatric Genetics. 13 (1). Wolters Kluwer Health: 33–41. doi:10.1097/00041444-200303000-00006. Retrieved 22 March 2026.
  17. 1 2 Buckert, Magdalena; Kudielka, Brigitte M.; Reuter, Martin; Fiebach, Christian J. (2012-11-01). "The COMT Val158Met polymorphism modulates working memory performance under acute stress". Psychoneuroendocrinology. 37 (11): 1810–1821. doi:10.1016/j.psyneuen.2012.03.014. ISSN 0306-4530.
  18. ↑ Goldberg, Terry E.; Egan, Michael F; Gscheidle, Tonya; Coppola, Richard; Weickert, Thomas; Kolachana, Bhaskar S.; Goldman, David; Weinberger, Daniel R. (September 2003). "Executive subprocesses in working memory: relationship to catechol-O-methyltransferase Val158Met genotype and schizophrenia". JAMA Psychiatry. 60 (9). Arch Gen Psychiatry: 889–896. doi:10.1001/archpsyc.60.9.889. Retrieved 22 March 2026.
  19. 1 2 Goldman, David; Oroszi, Gabor; Ducci, Francesca (1 August 2006). "The Genetics of Addictions: Uncovering the Genes". Focus. 4 (3). American Psychiatric Publishing: 401–415. doi:10.1176/foc.4.3.401. Retrieved 22 March 2026.
  20. ↑ Stein, Murray B.; Fallin, Margaret Daniele; Schork, Nicholas J.; Gelernter, Joel (2005-06-08). "COMT Polymorphisms and Anxiety-Related Personality Traits". Neuropsychopharmacology. 30 (11): 2092–2102. doi:10.1038/sj.npp.1300787. ISSN 1740-634X.
  21. ↑ Baumann, C.; Klauke, B.; Weber, H.; Domschke, K.; Zwanzger, P.; Pauli, P.; Deckert, J.; Reif, A. (2013-10-03). "The interaction of early life experiences with COMT val158met affects anxiety sensitivity". Genes, Brain and Behavior. 12 (8): 821–829. doi:10.1111/gbb.12090. ISSN 1601-1848.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  22. ↑ Rajkumar, Ravi P (28 August 2020). "Warriors, Worriers, and COVID-19: An Exploratory Study of the Catechol O-Methyltransferase Val158Met Polymorphism Across Populations". Cureus. 12 (8) e10103. Cureus. doi:10.7759/cureus.10103. Retrieved 22 March 2026.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  23. 1 2 Tartar, Jaime L; Cabrera, Dominick; Thomas, Julius D; Antonio, Jose; Peacock, Corey A (24 February 2020). "The "Warrior" COMT Val/Met Genotype Occurs in Greater Frequencies in Mixed Martial Arts Fighters Relative to Controls". Journal of Sports Science and Medicine. 19 (1). PubMed: 38–42. Retrieved 22 March 2026.
  24. ↑ "COMT: The Warrior/ Worrier Gene". My Gene. 25 August 2025. Retrieved 30 March 2026.
  25. ↑ Oh, Jamie; Fernando, Amali; Muffley, Lara; Honari, Shari; Gibran, Nicole S. (2022-03-24). "Correlation Between the Warrior/Worrier Gene on Post Burn Pruritus and Scarring: A Prospective Cohort Study". Annals of Surgery. 275 (5): 1002–1005. doi:10.1097/SLA.0000000000004235. ISSN 0003-4932.
  26. 1 2 Fang, Yi-Jia; Tan, Chun-Hsiang; Tu, Shao-Ching; Liu, Chien-Yu; Yu, Rwei-Ling (2019-03-21). Moccia, Marcello (ed.). "More than an "inverted-U"? An exploratory study of the association between the catechol-o-methyltransferase gene polymorphism and executive functions in Parkinson's disease". PLOS ONE. 14 (3): e0214146. doi:10.1371/journal.pone.0214146. ISSN 1932-6203. PMC 6428400. PMID 30897147.{{cite journal}}: CS1 maint: article number as page number (link) CS1 maint: unflagged free DOI (link)
  27. ↑ Farrell, Sarah M.; Tunbridge, Elizabeth M.; Braeutigam, Sven; Harrison, Paul J. (2012-03-15). "COMT Val158Met Genotype Determines the Direction of Cognitive Effects Produced by Catechol-O-Methyltransferase Inhibition". Biological Psychiatry. 71 (6): 538–544. doi:10.1016/j.biopsych.2011.12.023. PMC 3314969. PMID 22364739.
  28. ↑ Cuyàs, Elisabet; Verdura, Sara; Lozano-Sánchez, Jesús; Viciano, Ignacio; Llorach-Parés, Laura; Nonell-Canals, Alfons; Bosch-Barrera, Joaquim; Brunet, Joan; Segura-Carretero, Antonio; Sanchez-Martinez, Melchor; Encinar, José Antonio; Menendez, Javier A. (2019-06-01). "The extra virgin olive oil phenolic oleacein is a dual substrate-inhibitor of catechol-O-methyltransferase". Food and Chemical Toxicology. 128: 35–45. doi:10.1016/j.fct.2019.03.049. ISSN 0278-6915.
  29. ↑ DNALabs (2022-02-01). "Are You a Worrier, or a Warrior? - DNALabs". dnalabs.ca. Retrieved 2026-04-12.
  30. ↑ Wishart, heather A; Roth, Robert M; Saykin, Andrew J; Rhodes, C Harker; Tsonggalis, Gregory J; Pattin, Kristine A; Moore, Jason H; Mcallister, Thomas W (10 December 2010). "OMT Val158Met Genotype and Individual Differences in Executive Function in Healthy Adults". Journal of the International Neuropsychological Society. 17 (1). PubMed: 174–180. Retrieved 22 March 2026.
  31. 1 2 3 4 5 Taylor, Steven (13 June 2017). "Association between COMT Val158Met and psychiatric disorders: A comprehensive meta-analysis". Am J Med Genet Part B. 177 (2). Wiley Periodicals, Inc.: 199–210. doi:10.1002/ajmg.b.32556. Retrieved 22 March 2026.
  32. ↑ El-Hage, Wissam; Cléry, Helen; Andersson, Frederic; Filipiak, Isabelle; Thiebaut de Schotten, Michel; Gohier, Benedicte; Surguladze, Simon (9 August 2017). "Sex-specific effects of COMT Val158Met polymorphism on corpus callosum structure: A whole-brain diffusion-weighted imaging study". Brain and Behavior. 7 (9). Wiley Periodicals, Inc. doi:10.1002/brb3.786. Retrieved 22 March 2026.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  33. ↑ Mione, Valentina; Canterini, Sonia; Brunamonti, Emiliano; Pani, Pierpaolo; Donno, Federica; Fiorenza, Maria Teresa; Ferraina, Stefano (19 May 2015). "Both the COMT Val158Met single-nucleotide polymorphism and sex-dependent differences influence response inhibition". Front. Behav. Neurosci. 9 (127). Frontiers. doi:10.3389/fnbeh.2015.00127. Retrieved 22 March 2026.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  34. ↑ Lamb, Yvette N; McKay, Nicole S; Singh, Shrimal S; Waldie, Karen E; Kirk, Ian J (27 June 2016). "Catechol-O-methyltransferase val158met Polymorphism Interacts with Sex to Affect Face Recognition Ability". Front. Psychol. 7 (965). Frontiers. doi:10.3389/fpsyg.2016.00965. Retrieved 22 March 2026.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  35. ↑ Sindermann, Cornelia; Luo, Ruixue; Zhang, Yingying; Kendrick, Keith M; Becker, Benjamin; Montag, Christian (3 August 2018). "The COMT Val158Met Polymorphism and Reaction to a Transgression: Findings of Genetic Associations in Both Chinese and German Samples". Front. Behav. Neurosci. 12 (148). Frontiers. doi:10.3389/fnbeh.2018.00148. Retrieved 22 March 2026.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  36. ↑ González-Castro, Thelma Beatriz; Tovilla-Zárate, Carlos; Juárez-Rojop, Isela; Pool García, Sherezada; Genis, Alma; Nicolini, Humberto; López Narváez, Lilia (2013-09-10). "Distribution of the Val108/158Met polymorphism of the COMT gene in healthy Mexican population". Gene. 526 (2): 454–458. doi:10.1016/j.gene.2013.05.068. ISSN 0378-1119.
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