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On the surface, it may not be so clear where war, health, and evolution intersect. From the perspective of biological anthropology, many have called for a holistic, transdisciplinary approach to human biology and health which considers the environment as the totality of its evolutionary, ecological, and social components, including social inequality (Little and Haas 1989; Thomas et al. 1989; Wiley 2004).

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More than a decade ago, Leatherman and Goodman (1998) suggested that biological anthropologists put more effort toward better understanding what they termed the ‘biology of poverty.’ In this sense, poverty is an ‘environment’ that may induce consistent, but obviously varying, biological responses depending upon local circumstances. Similarly, war can be conceived as a biological environment. At least in the short term from an evolutionary point of view, wartime conditions may be as biologically challenging as some of the classic ecologically extreme environments faced by humans (circumpolar, tropical, high-altitude, desert, etc.) (Clarkin 2010).

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Though war is sometimes portrayed solely as a contest between competing militaries, the reality is that it almost always has repercussions that extend beyond the battlefield, imposing an array of stressors (physical trauma, psychological stress, malnutrition, infection, etc.) on non-combatants as well. As the British General Rupert Smith (2005:271) wrote about modern war: “We fight amongst the people, not on the battlefield.” This pattern extends far back in history. For example, in his best-selling book “1776” David McCullough (2005) described the siege of Boston during the American Revolution:

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On November 25 (1775), the British sent several boatloads of the ragged poor of Boston, some 300 men, women, and children, across the Back Bay, depositing them on the shore near Cambridge for the rebels to cope with. They were a heartrending sight. Many were sick and dying, ‘the whole in the most miserable and piteous condition,’ wrote Washington” (p. 61-2).

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The poor of Boston, like civilians caught up in wars throughout the world, were likely faced with some of the aforementioned stressors, dramatically exacerbating health conditions. This can be seen in many places in the world today, including the Democratic Republic of Congo, Darfur, Afghanistan, Iraq, Yemen, and likely others with large-scale population displacements (Philippines, Kyrgyzstan). Tangentially, the suffering of the North Korean population could be considered a result of a war that never ended (though bad government also seems an obvious culprit).

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Where this overlaps with an evolutionary perspective is that immediate stressors (i.e., proximate factors) induced by war may trigger developmental plasticity instilled in us by natural selection (ultimate factors) as a way to meet challenging circumstances. This makes sense because genes that are flexible and can work in multiple environments should have higher survival value (i.e., fitness) than ones which ‘fit’ in a straight-jacket manner to only one set of environmental conditions. In Matt Ridley’s words, plasticity may be natural selection’s ‘master stroke’ (2003: 174).

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There is a research agenda in here somewhere.

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While epidemiological studies (Burnham et al 2006; Salama et al 2004) describing the ways war influences health are essential, it is also important to have a better understanding why war predictably leads to deterioration in health. What are the mechanisms, why do they exist, and how did they evolve? (Tinbergen 1963). The classic studies stemming from the Dutch Hunger Winter, caused by a Nazi embargo during WWII, illustrate this well (Painter et al 2005). Multiple studies have documented that the famine had long-term developmental effects on those persons exposed in utero, leading to greater risk for various chronic diseases decades later. Because such fetal responses are fairly consistent, and are sometimes seen in other species, it is likely that these are at least somewhat adaptive and have been favored by natural selection in our evolutionary past (Gluckman and Hanson 2005). These responses are likely to enhance survival in early life, but with costs later in life (Kuzawa and Quinn 2009).

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Therefore, ontogenetic development during war seems an important area of study. It can help us understand how stressful events ‘out there’ get inside our bodies during growth, sometimes embedding themselves permanently for fundamental biological reasons. For a fuller understanding of any biological outcome, including war and health, Richard Lewontin reminded us of the necessity of a big picture approach (2002: 17-18):

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There exists, and has existed for a long time, a large body of evidence that demonstrates that the ontogeny (growth and development) of an organism is the consequence of a unique interaction between the genes it carries, the temporal sequence of external environments through which it passes during its life, and random events of molecular interactions within individual cells. It is these interactions that must be incorporated into any proper account of how an organism is formed.

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It is also possible that such research has the potential to serve as a reminder that war’s effects do not end immediately. People literally carry them around in their bodies.

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Related Posts

The Logic of War: Iraq, Afghanistan, and Pakistan  (Sep 24, 2011)

Reconciliation, Biology, and the Second Indochina War  (Mar 11, 2011)

Meeting to Ban Cluster Munitions, Vientiane Laos (Nov 8, 2010, with photos)

War and Child Growth: Iraq and WWII Germany (June 17, 2010)

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References

Burnham G, Lafta R, Doocy S, Roberts L. 2006. Mortality after the 2003 invasion of Iraq: a cross-sectional cluster sample survey. Lancet 368:1421-28.

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Clarkin PF. 2010. The echoes of war: effects of early malnutrition on adult health. In The War Machine and Global Health: The Human Costs of Armed Conflict and the Violence Industry, M Singer and GD Hodge (eds). Alta Mira Press, Lanham, MD, pp. 31- 58.

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Gluckman PD, Hanson MA. 2005.  The Fetal Matrix: Evolution, Development and Disease. Cambridge: Cambridge University Press.

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Kuzawa CW, Quinn EA. 2009. Developmental origins of adult function and health: evolutionary hypotheses. Annual Reviews of Anthropology 38:131-47.

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Leatherman T and AH Goodman. 1998. Expanding the biocultural synthesis toward a biology of poverty. American Journal of Physical Anthropology 102(1):1-3.

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Lewontin R. 2002. The Triple Helix: Gene, Organism, and Environment. Harvard University Press.

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Little MA, Haas JD. 1989.  Introduction: human population biology and the concept of transdisciplinarity. In Human Population Biology: A Transdisciplinary Science. MA Little and JD Haas, eds., eds. Pp. 3-12. New York: Oxford University Press.

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McCullough D. 2005. 1776. Simon & Schuster.

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Painter RC, Roseboom TJ, Bleker OP. 2005. Prenatal exposure to the Dutch famine and disease in later life: an overview. Reproductive Toxicology 20: 345-352.

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Ridley M. 2003. Nature Via Nurture: Genes, Experience, and What Makes Us Human. New York: Harper Collins.

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Salama P, Spiegel P, Talley L, Waldman R. 2004. Lessons learned from complex emergencies over past decade. Lancet 364(9447): 1801-13.

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Smith R. The Utility of Force: The Art of War in the Modern World. Knopf.

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Thomas RB, Gage TB, Little MA. 1989. Reflections on adaptive and ecological models. In Human Population Biology: A Transdisciplinary Science. MA Little and JD Haas, eds. Pp. 296-319. New York: Oxford University Press.

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Tinbergen, N. 1963. On aims and methods of ethology. Zeitschrift für Tierpsychologie 20:410-433.