The Warrior / Worrier Hypothesis
A biological explanation of stress

Travis Dixon Biological Psychology, Health Psychology

What gene do most MMA fighters have? Find out in this post.

The following is adapted from our textbook, Stress: A Student’s Guide for IB Health Psychology.

Are some people naturally more stressed than others? The Warrior / Worrier hypothesis says yes. This theory identifies the specific gene that explains stress levels. 

The Basic Theory

How do genes affect stress?

How you respond to stress could be based on your COMT gene. This is the basis of the warrior/worrier hypothesis. You might be a Met/Met homozygote (Met), a Val/Val homozygote (Val), or a Val/Met heterozygote (Val/Met). About 25% of people are Mets, 25% are Vals, and 50% are Val/Mets.

The Vals are the warriors. They have lower levels of stress. The Mets are the worriers. They have higher levels of stress. Predictably the Val/Mets fall in the middle.

Numerous studies have shown that the Mets have better cognitive skills, including executive functioning, working memory, and attentional control. However, this comes at a cost – the Mets also have a more reactive stress response, experience higher levels of stress, and feel pain more strongly. The Mets are the “worriers”. The Vals, on the other hand, are better at processing stressful stimuli, but have weaker cognitive skills. However, when under stress the Vals outperform the Mets in cognitive tasks. The Vals are the “warriors”. A majority of MMA fighters are Val/Val homozygotes – about 60% (Tartar et al., 2020).

Mets Vals
  • Worriers
  • Better cognition normally
  • More reactive to stress
  • Worse cognition under stress
  • Warriors
  • Poorer cognition normally
  • Less reactive to stress
  • Better cognition in stressful conditions

Tip: I remember which is which because Val reminds me of valiant (which means bold, brave and courageous like a warrior). A majority of MMA fighters are Val/Val homozygotes – about 60% (Tartar et al., 2020).

But why? 

So far our explanation is pretty basic. If you are a Val (Warrior) you’ll have lower stress than a Met (Worrier). Now let’s get deeper into the biological factors to understand why there’s a difference.

The COMT gene helps the body release the COMT enzyme. This enzyme breaks down neurotransmitters in the synapse. Depending on which variation of the gene you have, the levels of enzymes change and this affects levels of neurotransmitters in your brain. This then affects your stress levels.

File:Neuronal Synapse.jpg - Wikimedia Commons

After binding to the postsynaptic receptor, the neurotransmitters are either reabsorbed into the presynaptic membrane or broken down by enzymes like COMT and MAOA.

The Mets have reduced expression of the COMT gene, resulting in lower levels of the COMT enzyme, resulting in increased levels of some neurotransmitters. That makes sense if you think about it – with less enzyme to break down the neurotransmitters, they stay in the synapse and keep binding to the receptors. For example, noradrenaline, increases heart rate, blood sugar levels, and the restriction of blood vessels to increase blood pressure during acute stress. Mets have higher levels of noradrenaline because they have lower COMT activity. This means that there is less COMT enzyme breaking down the noradrenaline in the synapse, so noradrenaline levels remain high. This could explain their elevated stress response as shown in numerous studies.

Key term: Noradrenaline is also called norepinephrine. It’s a neurotransmitter released during times of stress and helps increase heart rate and blood pressure. Dopamine is the precursor to norepinephrine.

COMT and the Brain

The Hippocampus as a Neural Link between Negative Affect and Vulnerability for Psychostimulant Relapse | IntechOpen

The Hippocampus parts. Image Source from open access.

Another explanation for why the COMT gene is linked with stress is because of its relationship with the brain. Research using MRI has shown that the COMT genotypes are associated with differences in the brain, including the hippocampus, the prefrontal cortex (PFC), and amygdala. For example, one fMRI study found that the Vals had larger hippocampi compared with Val/Mets and another showed the Mets who experience adverse childhood experiences (ACEs) are more likely to have reduced hippocampal volume. This could explain the difference in stress because the hippocampus plays a role in inhibiting the activation of the HPA axis. The hippocampus has two parts – the dorsal (top) hippocampus and ventral (bottom) hippocampus. The dorsal hippocampus is important for memory. The ventral hippocampus helps in the regulation of the stress response. Animal studies have found that lesioning the hippocampus results in higher anticipatory stress responses and prolonged activation of the HPA axis following stress. Similarly, electrical stimulation of the hippocampus helps reduce cortisol levels following a stressor. This means someone with a Met genotype and who experiences ACEs is at risk for chronic stress and stress-related illnesses.

Note: You can learn more about the role of the PFC in stress in our blog article “The PFC and Stress”.

Regarding the amygdala, one fMRI study found that Mets had higher amygdala activity in response to unpleasant images. This suggests their amygdalae are more sensitive to perceiving potential threats. Increased amygdala activity could explain why the worriers (Mets) have a more reactive stress response following an acute stressor.

Note: They are called Val and Met after the amino acids Valine and Methionine respectively. The COMT and MAOA genes work in similar ways because they both produce enzymes that break down neurotransmitters.

The above post goes from a basic explanation that everyone can understand – Vals = low stress, Mets = high stress. It. then progresses into deeper explanations as to why those differences exist, using knowledge of neurotransmitters and the limbic system.


Bueller, J. A., Aftab, M., Sen, S., Gomez-Hassan, D., Burmeister, M., & Zubieta, J. K. (2006). BDNF Val66Met allele is associated with reduced hippocampal volume in healthy subjects. Biological psychiatry59(9), 812-815.; Frodl, T., Skokauskas, N., Frey, E. M., Morris, D., Gill, M., & Carballedo, A. (2014). BDNF V al66 M et genotype interacts with childhood adversity and influences the formation of hippocampal subfields. Human brain mapping35(12), 5776-5783.

Ebner, K., & Singewald, N. (2017). Individual differences in stress susceptibility and stress inhibitory mechanisms. Current Opinion in Behavioral Sciences14, 54-64.

Smolka, M. N., Schumann, G., Wrase, J., Grüsser, S. M., Flor, H., Mann, K., … & Heinz, A. (2005). Catechol-O-methyltransferase val158met genotype affects processing of emotional stimuli in the amygdala and prefrontal cortex. Journal of Neuroscience, 25(4), 836-842.

Chen, J., Lipska, B. K., Halim, N., Ma, Q. D., Matsumoto, M., Melhem, S., … & Weinberger, D. R. (2004). 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 Genetics75(5), 807-821.

Konopka, L. M. (2014). Genetic vulnerability in patients with psychiatric presentations: a neuroscience perspective. Croatian medical journal55(5), 545.

Dickinson, D., & Elvevåg, B. (2009). Genes, cognition and brain through a COMT lens. Neuroscience164(1), 72-87. ; Walder, D. J., Trotman, H. D., Cubells, J. F., Brasfield, J., Tang, Y., & Walker, E. F. (2010). Catechol-O-Methyltransferase (COMT) modulation of cortisol secretion in psychiatrically at-risk and healthy adolescents. Psychiatric genetics20(4), 166.; Buckert, M., Kudielka, B. M., Reuter, M., & Fiebach, C. J. (2012). The COMT Val158Met polymorphism modulates working memory performance under acute stress. Psychoneuroendocrinology37(11), 1810-1821.

*(COMT = catechol-O-methyltransferase).