I have noticed a recent trend in bioarchaelogy referring to odontoskeletal stress markers as measures of allostatic load. Allostatic load was first described by McEwan and Stellar in 1993. They argue (quite well and rightly) that the concept of homeostasis (or internal maintenance of system functioning) fails to consider the complex biological negotiations over time within a body between internal systems (e.g., cardiovascular, immune, etc) and external forces (e.g., disease, socio-economic disparity)–a point Selye also raised in his work on stress. They specifically point to the well-established relationship between chronic stress (and stressors) and disease. They further point out that homeostasis fails to incorporate an understanding of allostatic load
“fluctuating or heightened neural or neuroendocrine response resulting from repeated or chronic environmental challenge that an individual reacts to as being particularly stressful”
and the environmental factors and genetic predispositions that contribute to/shape allostatic load–these things combined form individual susceptibility to disease (in bioarch, part of assessment of ‘frailty’ or elevated risk of death). The neural/neuroendocrine response which defines allostatic load is prolonged systemic exposure to endogenous cortisol (a hormone produced in response to stress). Cortisol levels (and our ability to recover from episodes of stress) vary significantly with age in humans. For a popular science review of cortisol levels and stress over the human lifespan, see this as a starting point then explore the rich body of lit on human cortisol.
Human biologists evaluate allostatic load relative to disease susceptibility in studies of living human populations for which they have data on cortisol levels alongside biological, cultural, and psychosocial stresses contemporaneous to actual disease incidence. Bioarchaeologists certainly benefit from their work on the theoretical level because it elucidates an area of human biology that cannot be captured in the archaeological record but may inform our interpretation of stress markers in similar contexts. The use of the term in bioarchaeology to describe stress markers, however, is highly problematic. Certain techniques and methods sometimes allow estimation of duration and timing of disease and/or nutritional episodes that contribute to generalized stress but we cannot measure allostatic load (cortisol levels). The implication of calling traditional odontoskeletal markers (for which we have limited information on causation and other factors that are undetectable in the archaeological record) a measure of allostatic load (as described by McEwan and Stellar) is that these markers are direct proxies for elevated cortisol (allostatic load)–we have no evidence of this nor an idea of the scale of the relationship. The term is clearly interpreted broadly rather than as originally described (and currently used in human biology). Rather, allostatic load, for now, appears to be a synonym for stress markers.
A key point McEwan and Stellar make is that allostatic load is very precisely determined on an individual level–this then can be taken to the level of the population with a robust dataset in living humans. We simply do not have experimental data that allow us to extrapolate allostatic load from a few odontoskeletal makers. And, the final piece of the disease process system discussed by McEwan and Stellar, genetic predispositions, is barely given consideration in interpreting stress markers in the archaeological record. In the past, one could mention there is a genetic component to a process but then move past it by by arguing that it is immeasurable in the record. The mushrooming of new genetics technology and DNA recovery and repair techniques now allow us to examine these contributions (look at Saqqaq and Denisova) but few are doing so yet (hopefully that will increase as the analysis cost decreases more and more). Bone chemistry is a possible avenue of examining cortisol levels but the caveats that apply to stable isotope studies (a general search in google scholar for stable isotope anthropology will turn up papers that raise the issues) would come into play if it were even possible.
Bioarchaeology is a rich field and informs us about past population health and disease process relative to the archaeological record (among many other things) but it has its limitations, ones that are discussed in the literature and at conferences regularly. The dialogue about problems in bioarchaeology and improving and new technologies have allowed us to resolve or fine tune some old problems (e.g., aDNA to find instances of plague or TB) even as new ones crop up. That said, every field has its limits; most life scientists lack contextual approaches and many have limited understanding of cultural and evolutionary context. The movement in the field of bioarchaeology toward taking terms from other biological disciplines is sometimes a move in the right direction because it makes our work more accessible outside our specialization. Sometimes, however, it appears to be an attempt to legitimize our work to another community rather than celebrating the difference, recognizing the limits, and highlighting the legitimate contribution we make. I’ll end with by referring to anyone whose read this far to a great abstract from Rachel Leahy and Doug Crews from the 2013 AAPAs that critically considers the issue and draws a bridge a between skeletal frailty and living human frailty and allostatic load: In sickness and in death: What do age, stress, and illness in life tell us about skeletal remains?
The Smell of Evolution 