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. 2025 Apr 15;186(4):e70041. doi: 10.1002/ajpa.70041

Early Life Stress and Long‐Term Survival in the Hamann‐Todd Collection

Allyson M Simon 1,✉, Mark Hubbe 1
PMCID: PMC11997635  PMID: 40230249

ABSTRACT

Objectives

The impact of physiological stress during growth and development on mortality has been a topic of intense interest in bioarchaeology and other disciplines. In this study, we analyze the association between survival and two markers of physiological stress, linear enamel hypoplasia (LEH) and adult stature, in a sample of 296 individuals from the Hamann‐Todd Osteological Collection (HTOC).

Materials and Methods

The HTOC is among the most well‐known osteological collections in the discipline, representing low socioeconomic status individuals from early 20th century Cleveland, Ohio. Ages‐at‐death and demographic identifiers (sex and socially ascribed race) were known for all individuals in the sample. The association between the skeletal and dental markers of early life stress and survival was evaluated through Kaplan–Meier survival analysis, using log rank tests to analyze the significance of differences in survival among demographic groups.

Results

Significant differences in survival were observed between demographic groups, regardless of LEH status or stature. However, there were no significant differences in survivorship by LEH presence in this sample, despite the expectation that periods of physiological stress during key stages of development contribute to long‐term health consequences such as suppressed immune function. For females, shorter statures were associated with a higher probability of survival, while there were no significant differences in survival for males based on stature.

Discussion

It is likely that differences in survival observed in this sample of the HTOC are the consequence of other factors, most likely related to adult environmental quality, as opposed to early life stress.

Keywords: historical skeletal collections, linear enamel hypoplasia, physiological stress, stature, survival

1. Introduction

Many studies have examined the impact that stress events during infancy and childhood have on the human body throughout the lifespan (see Cheverko 2020 for a review). During growth and development, a trade‐off takes place between the allocation of resources used for growth and those used to survive the stress episodes, often resulting in disruptions to homeostasis and the body's ability to develop and function properly (Edes and Crews 2017). There is strong evidence showing that this trade‐off during early life plays a significant role in immune development and function over the lifespan (McDade 2005; Padgett and Glaser 2003). During stress events, energy that would otherwise be invested in growth and maintenance is diverted to survival. Individuals that experience such stress episodes often develop non‐specific markers in their skeletal and dental tissues (Bogin 2020; Goodman et al. 1988), such as linear enamel hypoplasia, reduced stature, cribra orbitalia, and porotic hyperostosis.

Moreover, the impact of stressful events is not only restricted to the moments during which they occur, as systemic disruptions of homeostasis during key developmental periods can impact the long‐term ability to maintain or regulate homeostasis, often resulting in individuals being more susceptible to future insults (McDade 2005; McPherson 2021; Padgett and Glaser 2003). The developmental period during which the stress event occurs is related to the severity of outcomes, with accumulating evidence that individuals who experience frequent or prolonged stressors during the earliest stages of life, when high energy is required for rapid growth and development, experience higher mortality risk (Garland 2020; McPherson 2021). Therefore, while the trade‐off in resources during a stress event can increase the likelihood of individuals surviving it, stress events in early life can and often do have long‐term consequences to one's life experience and health (Worthman and Kuzara 2005), increasing overall frailty and the likelihood of premature death. There is also strong evidence that social and environmental conditions can further exacerbate or mitigate the outcomes of such developmental trade‐offs brought on by stress exposure (i.e., cultural buffering; Garland 2020; Schell 1997; Temple 2019; Worthman and Kuzara 2005). This body of research supports the Developmental Origins of Health and Disease (DOHaD) hypothesis, which suggests an association between early life stress and increased morbidity and mortality later in life.

DOHaD has been explored through analyzes of skeletal samples. Numerous studies have found that physiological stress during early life is related to poor health outcomes such as cardiovascular disease and increased morbidity in adulthood (Barker 2007; Barker et al. 2009; Suglia et al. 2020). Various models have been employed for measuring the impact of physiological stress on health throughout the lifespan, such as allostatic load and skeletal frailty (Edes and Crews 2017; Marklein et al. 2016). Regardless of the model used, higher mortality risk and reduced survivorship have been shown to be associated with markers of early life stress across various contexts (Armelagos et al. 2009; Boldsen 2007; DeWitte 2018; DeWitte and Hughes‐Morey 2012; DeWitte and Wood 2008; Ham et al. 2021; Kemkes‐Grottenthaler 2005; O'Donnell 2019; Yaussy et al. 2016). However, the link between stress exposure in early life and differential health outcomes or longevity is dependent on environmental context and experiences throughout the lifespan (Temple and Klaus 2022), showing that there are biocultural factors that may mitigate or accentuate the long‐term consequences of early life stress. In many cases, associations between early life stress and reduced survival are emphasized by experiences of marginalization and social inequality throughout life, which often exacerbate developmental compromises (for example Ham et al. 2021; O'Donnell 2019).

While the connection between early life stress and increased morbidity and mortality later in life has been studied in bioarchaeological and modern contexts, few studies have investigated whether these stressors are related to survival in historical anatomical skeletal collections such as the Robert J. Terry or Hamann‐Todd Collections. Such collections were amassed through state laws, the Anatomy Acts, which allowed the dissection of unclaimed cadavers by medical schools (Muller et al. 2017; Nystrom 2014). Following dissection, skeletal remains were curated in documented skeletal collections. This process resulted in a systematically unrepresentative sample of the larger population (Campanacho et al. 2021), as those likely to be “unclaimed” are those with relatives living far away (recent immigrants) or who cannot afford burial (low socioeconomic status) (Halperin 2007; Muller et al. 2017). Thus, historical anatomical skeletal collections typically consist of primarily poor and marginalized groups (de la Cova 2010, 2011, 2019, 2020). These collections have been well‐studied for the development of skeletal methods in biological anthropology that have been widely used to reconstruct life experiences in the past (Campanacho et al. 2021).

However, the “lived experiences,” defined as the conditions throughout life that significantly contribute to health and survival outcomes (Goodman 2016, 74), of people who constitute such collections are often made invisible in the historical record through structural violence (Klaus 2012). This has implications for how we study the lives of those who were incorporated in these collections, as well as an indirect impact on studies of other past populations that rely on methods developed from historical anatomical collections. While recent biocultural skeletal studies have brought to our attention the structural inequalities that characterize these collections (Mathena‐Allen and Zuckerman 2020; Rankin‐Hill 2016; Zuckerman et al. 2021), much discussion is still needed to properly contextualize and measure the consequences of historical marginalization in the populations that ultimately contributed to the collections we study today.

Although some studies have examined associations between early life stressors and measures of adult morbidity and mortality in historically documented skeletal samples (for example Amoroso et al. 2014; Weisensee 2013), the relationship between early life stress and mortality in historical populations cannot be assumed given temporal and regional differences in environment and lifestyle. Thus, this study examines the association between skeletal markers of stress during growth and development—namely, linear enamel hypoplasia (LEH) and stature—and survival in a known age‐at‐death sample from the Hamann‐Todd Osteological Collection (HTOC).

LEH are visible horizontal grooves across the crowns of teeth that form during acute periods of stress when enamel secretion subsides or stops (Goodman and Rose 1991; Guatelli‐Steinberg 2020; Hillson 2018). Enamel defects have been shown to correlate with periods of nutritional deficiency (Goodman et al. 1991), but are generally considered non‐specific markers of stress (Guatelli‐Steinberg 2020). Stature complements LEH as a measurement of stress, since for most populations, growth can be reduced due to exposure to stress during growth and development, resulting in shorter overall stature of adults (Vercellotti et al. 2014). When a period of stress occurs during growth and development, the body diverts energy away from musculoskeletal growth toward brain development and maintenance of key bodily functions (Saunders and Hoppa 1993). This can result in stunting, clinically defined as a height more than two standard deviations below the reference standard (Parsons et al. 2011). While growth deficits can be recovered in some circumstances when stress subsides (Vercellotti et al. 2014), stunted children typically have relatively shorter statures as adults, often due to continued exposure to poor environmental conditions (Dewey and Begum 2011; Martorell et al. 1994).

Despite diverse early life environments (Cobb 1935), a high proportion of individuals in the HTOC exhibit skeletal markers of stress that form during growth and development such as LEH (Simon et al. 2023). Individuals in the HTOC died in the Cleveland area between 1911 and 1938, and are from predominantly low socioeconomic backgrounds (Cobb 1935). Most were employed as laborers or in “unskilled” trades (Alioto 2020). Many were subjected to overcrowded housing or homelessness with limited access to healthcare, resulting in overall poor living environments (Alioto 2020; de la Cova 2010, 2011, 2020). Previous research has shown a high prevalence of skeletal indicators of physiological stress and poor health among individuals in the collection (de la Cova 2011; Simon et al. 2023, 2025). A large percentage of Black Americans in the HTOC came to Cleveland during the Great Migration and many White Americans were immigrants or descendants of immigrants from European countries, meaning they were born in different regions of the US or in other countries (Cobb 1935).

Given that many of the people in the HTOC are thought to have experienced moderate to severe physiological stress during growth and development and poor adult environmental conditions (Simon et al. 2023), this collection represents one of the best samples to explore the degree of impact that early stressors have on longevity in low socioeconomic populations from urban contexts. Considering the evidence accumulated in previous studies, we expect to find significant differences in survival between individuals that exhibit skeletal markers of early life stress, specifically LEH and short stature, compared to those that do not. It is hypothesized that LEH presence and relatively shorter stature will be related to increased mortality and consequently to lower survival rates during adulthood.

In addition, we expect differences in survival, and possibly differences in how early life stress is related to survival, between demographic groups represented in the sample. In the HTOC, individuals were labeled as Black or White when integrated into the collection. However, these descriptors may not reflect how they would have identified during life. Thus, we use the term “socially ascribed race” to describe these categories. Although race is socially constructed (Blakey 1999; Jablonski 2017), it can have substantial effects on the lived experiences of different groups (for example Kuzawa and Sweet 2009). These social inequalities can be embodied biologically (Gravlee 2009; Krieger 2005, 2012; Krieger and Davey Smith 2004; O'Donnell and Edgar 2021), due to unequal exposure to physiological stress throughout life (Kuzawa and Gravlee 2016; Zarenko 2020). Historical accounts document differential opportunities in employment, housing, and resources between Black and White Americans throughout American history, including in early 20th century Cleveland (Alioto 2020; de la Cova 2010, 2011; Giffin 2005; Phillips 1996). These circumstances undoubtedly contributed to additional psychosocial and physiological stressors for Black Americans (Rankin‐Hill 2016).

2. Materials and Methods

The sample for this study (n = 296) was generated randomly from individuals with known age‐at‐death of 20 years or older in the HTOC and stratified for sex and socially ascribed race. The sample constitutes approximately 10% of the HTOC, and as such can be considered representative of the collection and the portion of the Cleveland population represented by it. Two skeletal markers of stress during early life were analyzed in this study: linear enamel hypoplasia (LEH) and stature.

Previous analyzes of this sample found that LEH were most common on the incisors and canines (Simon et al. 2023), as expected given the structure of enamel growth in these teeth (Goodman and Armelagos 1985), as well as their age of formation. The crowns of the anterior teeth typically begin forming around birth and are fully developed between three and seven years of age (Hillson 2018). Thus, the analysis of LEH prevalence explores exposure to stress episodes during early childhood. The presence of LEH was recorded for all individuals with at least four anterior teeth in any combination of incisors or canines. Teeth with significant tooth wear affecting more than half of the crown and teeth with crown replacements or caps were scored as present (that is not lost antemortem or missing postmortem) but unobservable. Individuals with pathological conditions were not excluded unless the pathology interfered with the observation of LEH. Based on these exclusion criteria, the sample for LEH analysis included 58 Black females, 27 White females, 63 Black males, and 47 White males. The smaller sample size for White females is attributed to higher frequencies of antemortem tooth loss (Simon et al. 2023). LEH were recorded by macroscopic observation as “present” or “absent” for each tooth available. Information about the timing and age of formation of LEH was not recorded in the study, and therefore, the age of onset of the stressful event that resulted in the hypoplasia was not considered in the analyzes presented here. Individuals that displayed at least one LEH on any tooth were considered to be affected by LEH (referred to as “LEH‐present”).

Although stature is influenced by many factors besides stress, including the genetic growth potential of the individual, relatively short stature is associated with long‐term stress exposure for individuals that have lived in poor environments for long periods of time during childhood through adolescence (approximately 3–18 years old for females and 3–22 years old for males, Bogin 2020). Stature at the time of death (i.e., cadaveric stature) was available from collection records (Holland 1995; data collection procedures described by Todd and Lindala 1928) for all but 11 individuals in the sample, resulting in 140 females and 145 males for stature analyzes. It has been found that cadaveric statures may slightly overestimate living stature (Trotter and Gleser 1952); however, cadaveric statures are often more reliable than stature estimated from long bones, as limb proportions vary by population and time (Jantz and Jantz 1999), compromising the accuracy of regression formulae (Ousley 1995). Moreover, comparisons between Todd's cadaveric statures and statures estimated from long bones in the HTOC have found both measures to be very similar reconstructions of living stature (Dupertuis and Hadden 1951). Males and females were analyzed separately to account for sexual dimorphism. Relative stature was assessed by separating individuals into three quantile groups: the shortest 25%, middle 50%, and tallest 25%.

Before testing the relationship between LEH or stature and survival of the sample, the effects of demographic information (i.e., sex and socially ascribed race) on survivorship were tested using Kaplan–Meier survival analysis. Log rank (Mantel–Cox) tests were used to test for significant differences between survival curves. The associations between age‐at‐death and LEH presence and stature on survival were then analyzed using the same tests, within each demographic group. All analyzes were computed in Prism 10.1.2 (https://www.graphpad.com/).

3. Results

Survivorship curves differed significantly among the four sub‐groups represented in the sample (p < 0.001, Figure 1a), with over 10 years difference in median age of survival between some sub‐groups (Table 1). Significant differences in survival exist between Black and White Americans in this sample (χ 2 = 22.30, p < 0.001), with Black Americans dying at earlier ages than White Americans (Figure 1b). In addition, log rank test results showed that there were significant differences in survival curves between males and females (χ 2 = 3.921, p = 0.048, Figure 1b). Given the survival differences identified between Black and White Americans and between males and females (Figure 1b, Table 1), the impacts of LEH presence and stature on survival were assessed separately for Black and White Americans, and for males and females.

FIGURE 1.

FIGURE 1

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Kaplan–Meier survival curves for each demographic sub‐group (a) and group (b).

TABLE 1.

Survival statistics summary by group and sub‐group.

Sample size Median survival time (years) Standard deviation (years) 95% Confidence interval
Black Americans 147 41 15.04 21.7–76.5
White Americans 149 50 16.42 24.5–81.5
Females 148 46.5 18.41 22–84.1
Males 148 45 14.21 21.73–80
Black Females 73 40 16.98 22–87.3
White Females 75 52 17.87 24.8–83.6
Black Males 74 42 12.96 20.88–73.25
White Males 74 49.5 14.60 22–81
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LEH frequency ranged from 42.6% to 45.9% across the groups analyzed (Table 2). There were no statistically significant differences in LEH prevalence between females and males (χ 2 = 0.194, p = 0.660), and between Black and White Americans (χ 2 = 0.012, p = 0.914). There were also no significant differences in survival curves between those for which LEH were present and absent (Table 3, Figure 2a–d).

TABLE 2.

LEH prevalence.

LEH prevalence Total
Females 39 (45.9%) 85
Males 47 (42.7%) 110
Black Americans 53 (43.8%) 121
White Americans 33 (44.6%) 74
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TABLE 3.

Results of log rank tests for survival by LEH status.

LEH status Sample size Median survival time (years) Standard deviation (years) 95% Confidence interval χ 2 p
Females Absent 46 37 14.48 22–79.13 0.373 0.541
Present 39 40 15.87 22–76
Males Absent 63 43 12.43 21.6–72.8 < 0.001 0.992
Present 47 42 11.94 20.2–68.8
Black Americans Absent 68 39.5 12.30 21.73–69.92 0.299 0.585
Present 53 40 13.86 20.35–71.30
White Americans Absent 41 45 14.52 22.05–80 0.009 0.923
Present 33 44 13.08 25–76
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FIGURE 2.

FIGURE 2

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Kaplan–Meier survival curves for females (a), males (b), Black Americans (c), and White Americans (d) by LEH status.

Log rank test results indicate significant differences in survival for females based on stature group (Table 4). The shortest 25% of females in this sample have a higher probability of survival at all ages and a larger median survival time (Figure 3a). There were significant differences between survival curves for the shortest 25% and middle 50% (χ 2 = 6.848, p = 0.009) and the shortest 25% and tallest 25% (χ 2 = 13.78, p < 0.001). However, there was no difference between the survival curves for the middle 50% and the tallest 25% (χ 2 = 2.056, p = 0.152).

TABLE 4.

Results of log rank tests for survival by stature group.

Stature group Sample size Median survival time (years) Standard deviation (years) 95% Confidence interval χ 2 p
Females Shortest 25% 37 59 19.41 25–89 13.450 0.001
Middle 50% 68 46.5 18.67 22–84.65
Tallest 25% 35 43 15.07 22–77
Males Shortest 25% 36 44.5 14.96 21–88 3.776 0.151
Middle 50% 73 50 14.28 20.85–80
Tallest 25% 36 41.5 11.73 25–71
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FIGURE 3.

FIGURE 3

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Kaplan–Meier survival curves for females (a) and males (b) by stature group.

When survival curves for all three stature groups are compared for males, there are no significant differences (Table 4, Figure 3b). However, when longevity is compared across pairs of stature cohorts, log‐rank tests show that the tallest 25% of males has a significantly lower mean age‐at‐death than the middle 50% (χ 2 = 4.175, p = 0.041). Differences between survival curves for the shortest 25% and middle 50%, and the shortest 25% and tallest 25%, were not significant (χ 2 = 0.095, p = 0.758; χ 2 = 1.462, p = 0.227, respectively).

4. Discussion

Our results link early life stress and longevity in this sample from the HTOC. However, their observed relationship in this sample is contrary to expectations. We found no measurable impact of the presence of LEH, which represents stress experienced during early childhood and survival, on the survival curve of the samples. There are differences in age‐at‐death between stature cohorts, but these differences contradict expectations, with shorter females showing longer average lifespans and the tallest males showing lower mean age‐at‐death than the mid‐stature cohort. Overall, these findings suggest that adult environment prevails over early life conditions in shaping resiliency and susceptibility to physiological stress throughout the lifespan, or that individuals who experience early life stress become more resilient to stressors later in life.

Given similarities in prevalence of early life stress markers (Simon et al. 2023), differences in survival between Black and White Americans also support this conclusion, as the lived experiences of Black Americans in this environment contributed to significantly lower survival probability or younger average ages‐at‐death. Historical records also report higher mortality among Black Americans living in Ohio during this period (Giffin 2005). The skeletal data combined with the historical record offer a good example of how social inequality based on racial identity becomes embodied biologically (Gravlee 2009; Krieger 2005, 2012; Krieger and Davey Smith 2004). There are significant differences in frailty and mortality according to socially ascribed race in our sample, which reflects other studies showing the embodiment of social inequality in differential outcomes in longevity (for example O'Donnell and Edgar 2021). While this is unsurprising, as systemic racism likely exacerbated the economic stressors faced by many individuals in the HTOC, our results help us to qualify the ways through which stressors are embodied in the overall life experience of the individuals studied here.

Most studies examining the relationship between early life stress and survival have found skeletal stress indicators are associated with increased mortality risk or decreased likelihood of survival (Armelagos et al. 2009; Boldsen 2007; DeWitte 2018; DeWitte and Hughes‐Morey 2012; DeWitte and Wood 2008; Ham et al. 2021; Kemkes‐Grottenthaler 2005; O'Donnell 2019; Yaussy et al. 2016), as was hypothesized here. Stress events that disrupt the development of the immune system may contribute to weakened immune responses later in life (McDade 2005; Padgett and Glaser 2003). Per the DOHaD model, this is explained by biological trade‐offs during the period of metabolic stress, which affect the body's ability to invest in healthy growth and maintain homeostasis during key developmental stages (McDade 2005; McPherson 2021; Padgett and Glaser 2003; Worthman and Kuzara 2005), and can therefore be reflected in the formation of LEH and/or reduced stature (Bogin 2020; Goodman et al. 1988).

Yet, our results show no significant difference in survival based on LEH presence in the samples analyzed. One possible explanation may be the timing of the stress episode (King et al. 2005; Temple 2014). Timing or age at which the stress episode occurred was not examined in the current study, and therefore could not be properly explored here. However, these data may provide insight to the findings presented here in the future since there are periods during development when the body is more vulnerable to growth disruptions (Garland 2020; McPherson 2021), and accumulating evidence shows that individuals with younger ages‐at‐death have an earlier age of first occurrence of enamel hypoplasia (King et al. 2005; Temple 2014). Considering the window when the crowns of the anterior teeth form, approximately from birth to the first few years of life (Hillson 2018), the timing of stress events between individuals in our sample may vary, obscuring clear differences in survival. However, it is also possible that exposure to other more prolonged stressors later in life effectively erases the signature of early childhood stress events. It is challenging to evaluate the relative weight that stress events experienced at different stages in life have on long‐term frailty and allostatic load in individuals from this sample of the HTOC. Yet, as suggested by survival differences among stature cohorts, it is possible that early life stress exposure, which was common in the HTOC (Simon et al. 2023), was later offset by exposure to prolonged stressors throughout life.

As previously stated, differences in survival by relative stature diverge from expected patterns, since there is a significantly higher probability of survival for the shortest females in the sample. This pattern is also seen to a lesser degree among males. The tallest males show lower survival relative to average stature (middle 50%) males. In addition, Simon et al. (2023) reported significantly shorter statures for females with at least one LEH in this sample, showing an association between multiple markers of physiological stress during growth and development. However, shorter stature may be an adaptive mechanism (Kuzawa et al. 2007; Temple 2019), allowing lower caloric intake for maintenance and survival, to buffer against environmental stressors such as limited availability of nutrients (Ham 2018). Thus, shorter stature may have allowed individuals to survive longer in a food‐scarce environment (Ham 2018), which is likely among low socioeconomic groups living in urban environments during the early 20th century (Alioto 2020; de la Cova 2011; Giffin 2005; Phillips 1996; Simon et al. 2023, 2025). A higher likelihood of surviving stress events during early childhood for shorter individuals could explain why we see taller individuals in this sample with lower average longevity, and this could be a compounding factor for this population. It is also possible that our sample includes individuals of genetically determined short stature that have not been affected by stress during growth and development. In addition, other studies have reported evidence that taller stature is associated with higher mortality in some populations, suggesting that in some circumstances tall individuals can represent more frail individuals (Samaras et al. 2003).

Socioeconomic status and poor adult environment have also been suggested as meaningful factors in survival and may obscure a significant pattern or account for variation in mortality within this sample (Amoroso et al. 2014). Amoroso et al. (2014) found a significant association between LEH and age‐at‐death, consistent with the findings of others; however, the relationship between childhood stress and survival was not significant when controlling for socioeconomic status. As discussed previously, most individuals in the HTOC belonged to low socioeconomic backgrounds (Cobb 1935), owing to the processes that targeted marginalized groups for anatomization during the collection's formation (Halperin 2007; Muller et al. 2017). Thus, considering low socioeconomic background is believed to be predominantly shared among individuals in the HTOC, it is possible that differences in survival are more strongly related to other factors such as the adult environment, as opposed to developmental stress.

Conversely, the improved environment since the completion of growth and development has been thought to explain a lack of differences in survival between those with and without skeletal stress indicators in other contexts (Ham et al. 2021). The sociocultural and physical environment can buffer against, or further exacerbate, the impact of developmental stress on health during adulthood (Garland 2020; Schell 1997; Temple 2019). Many historical documents and studies on the experience of White immigrants and Black Americans during the Great Migration in Cleveland have pointed to increased reliance on community ties for survival (de la Cova 2010; Phillips 1996), which would constitute cultural buffering. Among several US cities in 1900, including Cleveland, Ohio, nearly half of deaths were due to infectious disease; however, this figure drops to approximately 18% in 1936 largely in response to public health improvements such as water filtration (Cutler and Miller 2005). Thus, the long‐term consequences of early life stressors may not have led to reduced survival in adulthood if environmental conditions improved. At the same time, these environmental improvements may not have reached low socioeconomic and marginalized communities until much later, which is supported by the high frequency of causes of death attributed to infectious disease in the HTOC (Simon et al. 2025).

Moreover, a tradeoff of “mortality for morbidity” could explain the higher probability of survival for individuals with markers of early life stress (Crimmins et al. 1994; Crimmins and Beltrán‐Sánchez 2010; DeWitte 2018, 2). In this way, people may have survived longer but amassed the impact of stressful events throughout their lifetimes. Individuals that were susceptible to chronic stress events during early life but survived to adulthood exhibit markers of stress during development and subsequently poor overall health and increased morbidity (DeWitte 2018; Weisensee 2013). Concurrently, it may also be that short stature, often considered an indicator of skeletal frailty (Crews and Marklein 2023; Marklein et al. 2016), is representative of resiliency in this sample (McFadden and Oxenham 2020), given its association with higher survival.

Despite the possibility of an improved environment during adulthood, there would have been sources of ongoing physiological stress stemming from the predominantly low socioeconomic status of those that make up the HTOC, including overcrowded housing, a high prevalence of infectious disease, discriminatory hiring policies, sporadic and unreliable employment opportunities for manual and unskilled laborers (de la Cova 2011; Giffin 2005; Phillips 1996). Thus, while the effects of developmental stress on survival may have been reduced by support networks and improved public health systems, evidence for the negative impact of poor living conditions on morbidity and mortality in this collection persists (de la Cova 2011; Simon et al. 2023).

In sum, although it was expected that LEH presence and shorter statures would be associated with lower survivorship, no significant difference in survival was found, as LEH presence and shorter statures were associated with higher survival for females in this sample from the HTOC. Poor adult environmental quality may be a more important variable shaping differences in survival within this sample than exposure to early‐life stress. Alternatively, social networks (that is cultural buffering) may have mitigated the impact of developmental stress on long‐term health. Given the historical and sociocultural context surrounding the HTOC, the former explanation appears more likely. These findings provide support for a tradeoff of mortality for morbidity taking place, in which individuals that would have likely died at young ages survived to adulthood but accumulated the poor outcomes of physiological stress during development.

In conclusion, the association between early life stress markers and survival rates in the HTOC is not consistent with previous skeletal studies (Armelagos et al. 2009; Boldsen 2007; DeWitte 2018; DeWitte and Hughes‐Morey 2012; DeWitte and Wood 2008; Ham et al. 2021; Kemkes‐Grottenthaler 2005; O'Donnell 2019; Yaussy et al. 2016). While there is strong support for the long‐term impact of stress during growth and development, as is captured by literature relating to DOHaD, our analyzes suggest that other factors may mask these effects. As such, when studying the relationship between skeletal stress markers and survival in past populations, the environment they experienced as adults must be factored into the interpretation of patterns related to cumulative stress responses, health, and mortality of individuals.

Author Contributions

Allyson M. Simon: conceptualization (lead), data curation (lead), formal analysis (lead), investigation (lead), methodology (equal), visualization (equal), writing – original draft (lead), writing – review and editing (equal). Mark Hubbe: conceptualization (supporting), formal analysis (supporting), methodology (equal), visualization (equal), writing – review and editing (equal).

Conflicts of Interest

The authors declare no conflicts of interest.

Permissions Statement

Permission to conduct this research was granted by the Cleveland Museum of Natural History in 2021 under the guidelines in place at that time.

Acknowledgments

The authors would like to thank Lauren Hayden for her helpful feedback during the writing of this manuscript.

Data Availability Statement

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.

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