Skip to content

Reference topic 31: The Mind That Cannot Find Its Village

Why is anxiety on the rise? An evolutionary view of mood

ProbableEvidence grade: Probable. Good observational evidence with a plausible mechanism, or small or few trials.17 sources5 graded recommendationsTopic hub: Stress and the mind

Published Updated

In 2008 four researchers published body measurements and DNA samples from the Ariaal of northern Kenya, a people who live by their herds. Sixty-five of the men they measured were still nomads, moving with the animals across dry country. Another 87 came from communities of the same people that had recently settled down. The Ariaal are chronically underfed, so the team read body mass index (BMI), weight scaled to height, as a gauge of how well a man's world fed him.1

The gene they studied, DRD4, is the code for one of the brain's receptors for dopamine, a chemical messenger tied to reward and drive. It comes in several lengths. One, the seven-repeat version, had been linked in other populations to the traits that get diagnosed as attention deficit hyperactivity disorder (ADHD): restlessness, impulsivity, a pull toward novelty. Among the nomads, men who carried it had a higher BMI than men who did not. Among the settled men, from the same people and carrying the same variant, the carriers had a lower BMI.1

Mismatch card

The system

The defensive emotions, low mood, anxiety and vigilance, plus the attention systems that tune exploring against exploiting.

What it expects

Threats that are physical, local and resolvable; problems a small group can help solve; a world where scanning and moving pay.

What it gets

Unresolvable threats delivered continuously, thin social support, and settings that reward long stillness and narrow focus.

What happens in the gap

Alarms built to over-fire go off constantly and stop resetting, and trait variation that once paid in one environment is diagnosed as pathology in another.

The handrail

Treatment first, movement as an adjunct, and repair of sleep, daylight and company (●●○)

Strength of evidence

●●○ Treatment effects and the diagnosis-rate findings rest on large trials and registries; the evolutionary explanations of why these systems exist remain hypotheses.

What this topic covers

  • ·The Alarm Built to Fire Early
  • ·Three Stories About Low Mood
  • ·The Inputs That Went Missing
  • ·The Serotonin Story, and What It Did Not Settle
  • ·Exercise Earns Its Place
  • ·The Hunter in the Classroom, Measured

The practical version is in the book: Chapter 13, Stress and the Mind.

The handrail

The first item is not optional and carries no caveat. If you are depressed, anxious or struggling with attention, get assessed and treated. Medication, psychotherapy and environmental change are complements, not rivals. Never stop or alter a psychiatric medication on the strength of a book chapter; any change belongs in a conversation with the clinician who prescribed it.

If you are supporting a child who was among the youngest in their class when the question of ADHD first came up, raise that with the clinician. It is not a reason to dismiss the diagnosis, but it is one more piece of information.15

Each recommendation carries the strength of the evidence behind it. How the grades work.

  1. Take treatment seriously

    StrongEvidence grade: Strong. Multiple randomized controlled trials, or consistent large cohort studies with a well-understood mechanism.

    Across 522 randomized trials and 116,477 participants, all 21 antidepressants studied beat placebo for acute major depression, with a small-to-moderate average effect.11 The chemical-imbalance explanation being wrong does not make the treatment wrong.

  2. Add movement, as an adjunct

    ProbableEvidence grade: Probable. Good observational evidence with a plausible mechanism, or small or few trials.

    In a 2024 network meta-analysis, walking or jogging, yoga and strength training each produced moderate drops in depressive symptoms against active controls, with the last two the best tolerated. Nearly all of those trials carried a high risk of bias, and that is why the grade is not higher.12 Topic 40 sets the weekly dose. Start where you are; a depressed body does not begin at a runner's baseline.

  3. Restore sleep, daylight and darkness

    EmergingEvidence grade: Emerging. Early, small, animal-only, or actively contested.

    Disrupted sleep and reduced sunlight sit on the list of modern changes tracking rising depression, though the evidence is observational and tangled.9 Topic 23 holds the sleep program.

  4. Put people back in

    EmergingEvidence grade: Emerging. Early, small, animal-only, or actively contested.

    Weaker social capital appears on the same list.9 Topics 29 and 42 hold the evidence on connection and health, and what to do about it.

  5. For ADHD, treat and adjust the environment together, not one instead of the other

    ProbableEvidence grade: Probable. Good observational evidence with a plausible mechanism, or small or few trials.

    Registry data link medication to lower two-year mortality and to fewer criminal convictions.1617 The evidence that specific changes to a child's day alter ADHD outcomes is much thinner; Topic 34 covers what is known about structure, recess and play.

The skeptic's corner

The case against this topic, from the research itself.

Evolutionary psychiatry has a testability problem, and this chapter has been living inside it. The three evolutionary accounts of depression (social defeat, problem-solving rumination, infection defense) were each fitted to existing observations after the fact, and none has been set against the others in an experiment that could rule any of them out.678 Adaptive stories are cheap to build and expensive to test. Treat them as frames for asking questions, not as findings.

The hunter-in-the-classroom story carries its own risk. The rigorous evidence behind it is real but narrow: one field study of a gene in two settings, one online foraging game, one natural experiment in diagnosis rates.11415 None of it shows that ADHD symptoms were a net advantage for most Paleolithic (Old Stone Age) foragers. It shows only that particular traits interact with particular settings in ways you can measure. Popular hunter-versus-farmer accounts came before this evidence and go far beyond it; do not cite them as though they were the same body of work.

The framing can also do harm. The 2021 consensus statement was written to counter myths that stigmatize people with ADHD and delay their treatment.13 That matters, because untreated ADHD is associated with outcomes, including death, that treatment appears to reduce.16 Knowing why a trait cluster exists says nothing about whether a given person needs support.

On serotonin, hold two things at once. The umbrella review found no consistent evidence for the shortage model, and it drew published rebuttals of its methods.10 Neither fact is about whether antidepressants work; the trial evidence on that is separate and reasonably strong.11

Terms this topic defines

Related topics

Sources cited above

  1. 1.Eisenberg, D.T.A., Campbell, B., Gray, P.B., and Sorenson, M.D. (2008). "Dopamine receptor genetic polymorphisms and body composition in undernourished pastoralists: an exploration of nutrition indices among nomadic and recently settled Ariaal men of northern Kenya." BMC Evolutionary Biology, 8, 173. https://doi.org/10.1186/1471-2148-8-173 (Field genetic-association study, 65 nomadic and 87 recently settled men; exploratory, reporting associations. BMI was higher in nomadic men with one or two DRD4 7R alleles and lower in settled men with the same alleles; a post-hoc analysis attributed the difference mainly to fat-free mass.)
  2. 6.Sloman, L., and Gilbert, P. (Eds.) (2000). Subordination and Defeat: An Evolutionary Approach to Mood Disorders and Their Therapy. Lawrence Erlbaum. The involuntary defeat strategy is usually traced to J.S. Price in 1967, by analogy with ritualized yielding in animal dominance contests; this volume develops it. Price's original paper was not consulted directly for this chapter.
  3. 7.Andrews, P.W., and Thomson, J.A. (2009). "The bright side of being blue: depression as an adaptation for analyzing complex problems." Psychological Review, 116(3), 620-654. https://doi.org/10.1037/a0016242 (Theoretical synthesis, not new trial data.)
  4. 8.Raison, C.L., and Miller, A.H. (2013). "The evolutionary significance of depression in Pathogen Host Defense (PATHOS-D)." Molecular Psychiatry, 18(1), 15-37. https://doi.org/10.1038/mp.2012.2 (Hypothesis paper synthesizing epidemiological, genetic and immunological evidence.)
  5. 14.Barack, D.L., Ludwig, V.U., Parodi, F., Ahmed, N., et al. (2024). "Attention deficits linked with proclivity to explore while foraging." Proceedings of the Royal Society B, 291(2017), 20222584. https://doi.org/10.1098/rspb.2022.2584 (About 457 online participants.)
  6. 15.Layton, T.J., Barnett, M.L., Hicks, T.R., and Jena, A.B. (2018). "Attention deficit-hyperactivity disorder and month of school enrollment." New England Journal of Medicine, 379(22), 2122-2130. https://doi.org/10.1056/NEJMoa1806828 (In states with a September 1 cutoff, August-born children were diagnosed at 85.1 per 10,000 against 63.6 for September-born children, a difference of 34%.)
  7. 13.Faraone, S.V., Banaschewski, T., Coghill, D., Zheng, Y., et al. (2021). "The World Federation of ADHD International Consensus Statement: 208 evidence-based conclusions about the disorder." Neuroscience and Biobehavioral Reviews, 128, 789-818. https://doi.org/10.1016/j.neubiorev.2021.01.022 (Prevalence 5.9% in youth and 2.5% in adults; 80 authors from 27 countries, with the contents endorsed by a further 366 readers; the statement holds that ADHD diagnosed by a licensed clinician is well defined and valid at all ages. This corrects the first edition's "5-7% of children and 2-5% of adults.")
  8. 16.Li, L., Zhu, N., Zhang, L., Kuja-Halkola, R., et al. (2024). "ADHD pharmacotherapy and mortality in individuals with ADHD." JAMA, 331(10), 850-860. https://doi.org/10.1001/jama.2024.0851 (Swedish national registry, n=148,578, analyzed as a target trial emulation: two-year all-cause mortality 39.1 versus 48.1 deaths per 10,000, hazard ratio 0.79; unnatural-cause mortality hazard ratio 0.75; natural-cause mortality hazard ratio 0.86, confidence interval crossing 1. Observational.)
  9. 10.Moncrieff, J., Cooper, R.E., Stockmann, T., Amendola, S., et al. (2022). "The serotonin theory of depression: a systematic umbrella review of the evidence." Molecular Psychiatry, 28(8), 3243-3256. https://doi.org/10.1038/s41380-022-01661-0 (Published online July 2022; print issue 2023.) The review drew several published replies in the same journal in 2023 disputing its methodology and interpretation; this chapter does not adjudicate that dispute. (Databases searched to December 2020. The five strands were serotonin and its metabolites in body fluids, 5-HT1A receptor binding, serotonin transporter levels measured by imaging or after death, tryptophan depletion experiments, and studies of the serotonin transporter gene and its interaction with stressful life events.)
  10. 11.Cipriani, A., Furukawa, T.A., Salanti, G., Chaimani, A., et al. (2018). "Comparative efficacy and acceptability of 21 antidepressant drugs for the acute treatment of adults with major depressive disorder: a systematic review and network meta-analysis." The Lancet, 391(10128), 1357-1366. https://doi.org/10.1016/S0140-6736(17)32802-7 (522 double-blind randomized trials, 116,477 participants; odds ratios for response versus placebo about 1.37 to 2.13 across drugs; commentary cites an overall standardized mean difference near 0.30.)
  11. 12.Noetel, M., Sanders, T., Gallardo-Gómez, D., Taylor, P., et al. (2024). "Effect of exercise for depression: systematic review and network meta-analysis of randomised controlled trials." BMJ, 384, e075847. https://doi.org/10.1136/bmj-2023-075847 (218 trials, 14,170 participants. Effects versus active controls, Hedges' g: walking or jogging -0.62, yoga -0.55, strength training -0.49, mixed aerobic exercise -0.43, tai chi or qigong -0.42. One trial met the Cochrane low-risk-of-bias criteria; CINeMA confidence was low for walking or jogging and very low for the other modalities. Correction: BMJ (2024), 385, q1024, https://doi.org/10.1136/bmj.q1024) (The correction concerned the standard deviation used to calculate the effect sizes.)
  12. 9.Hidaka, B.H. (2012). "Depression as a disease of modernity: explanations for increasing prevalence." Journal of Affective Disorders, 140(3), 205-214. https://doi.org/10.1016/j.jad.2011.12.036 (Review of associations.)
  13. 17.Lichtenstein, P., Halldner, L., Zetterqvist, J., Sjölander, A., et al. (2012). "Medication for attention deficit-hyperactivity disorder and criminality." New England Journal of Medicine, 367(21), 2006-2014. https://doi.org/10.1056/NEJMoa1203241 (Swedish registry, n=25,656, comparing medicated and unmedicated periods within the same individuals: criminal convictions 32% lower in men and 41% lower in women during medicated periods.)

This topic carries 17 notes in the research manuscript; the 13 above are those behind the material on this page. Full source register.