Anthropology & Aging Quarterly  2013: 34 (3) 61

Introduction
Anyone seeking to learn more about the subject of 
menopause1 will find standard clinical and public health 
policy interpretations readily and prominently available. 
A simple Internet search for the word “menopause” 
returns numerous websites from reputable online medical 
resources2, all of which provide roughly the same, 
narrow definition: menopause is the complete cessation 
of menstruation, and occurs twelve months after the final 
menstrual period, usually between 45-55 years of age. 
Along with these definitions, much of the accompanying 
health information addresses symptoms, risk for associated 
diseases, and treatment options. This information fits the 
overall medical paradigm that menopause is not simply 

A R T I C L E S

Postmenopausal Health and Disease from 
the Perspective of Evolutionary Medicine

Andrew W. Froehle
Department of Community Health

Boonshoft School of Medicine
Wright State University

a transition between physiologically distinct life history 
periods, but is instead a deficiency disease that calls for 
allopathic treatment (Marnocha et al. 2011; Meyer 2001; 
Meyer 2003)

 Epidemiological evidence indeed shows that the period 
surrounding and following menopause is associated with 
an increased prevalence of disease and disease risk factors, 
particularly those relating to the metabolic syndrome 
including weight gain, body composition change, obesity, 
hyperlipidemia, hypertension, and insulin resistance, all 
of which increase risk for heart attack, stroke, and type 2 
diabetes (Torrens et al. 2009; Enns and Tiidus 2010). In the 

Abstract

Menopause normally occurs between 45-55 years of age, marks the end of a woman’s reproductive 
lifespan, and is accompanied by a reduction in estrogen that has substantial physiological effects. The 
standard medical view is that these changes underlie high postmenopausal disease rates, defining 
menopause as an estrogen deficiency condition needing treatment. This view stems from the idea 
that extended postmenopausal longevity is a consequence of recent technological developments, 
such that women now outlive their evolutionarily-programmed physiological functional lifespan.
Increasingly, however, researchers employing an evolutionary medicine framework have used 
data from comparative demography, comparative biology, and human behavioral ecology to 
challenge the mainstream medical view. Instead, these data suggest that a two-decade human 
postmenopausal lifespan is an evolved, species-typical trait that distinguishes humans from 
other primates, and has deep roots in our evolutionary past. This view rejects the inevitability of 
high rates of postmenopausal disease and the concept of menopause as pathology. Rather, high 
postmenopausal disease risk likely stems from specific lifestyle differences between industrialized 
societies and foraging societies of the type that dominated human evolutionary history. Women 
in industrialized societies tend to have higher estrogen levels during premenopausal life, and 
experience a greater reduction in estrogen across menopause than do women living in foraging 
societies, with potentially important physiological consequences. The anthropological approach 
to understanding postmenopausal disease risk reframes the postmenopausal lifespan as an 
integral period in the human lifecycle, and offers alternative avenues for disease prevention by 
highlighting the importance of lifestyle effects on health. 

Keywords: **



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United States, 39.8% of women aged 45-64 years are obese, 
39.7% are hypertensive, and 11.3% are diabetic, whereas 
rates for the same conditions among women aged 20-44 
years are 33.2%, 6.9% and 3.2%, respectively(3) 3. Of all 
new type 2 diabetes diagnoses in U.S. adults over age 
20 years, 55% occur in the 45-64 year age range, with an 
additional 20% occurring after age 65 years (Centers for 
Disease Control and Prevention (CDC) 2011).

 The medical deficiency disease model attributes elevated 
disease prevalence to the substantial and permanent 
reduction in circulating levels of the reproductive steroid 
hormone 17β-estradiol (henceforth referred to as simply 
estrogen) that occurs within the four years surrounding 
the final menstrual period (Randolph et al. 2011; Sowers 
et al. 2008). Estrogen has multiple non-reproductive 
physiological functions including fat metabolism for 
energy, and is involved in numerous metabolic signaling 
pathways (Campbell and Febbraio 2001; Campbell et 
al. 2003; Spangenburg, Geiger et al. 2012; Sugiyama 
and Agellon 2012). Thus, increased rates of metabolic 
diseases in menopausal and postmenopausal women 
are thought to result in large part from the menopausal 
reduction in circulating estrogen and the ensuing 
hyposteroidal physiological environment (Carr 2003). In 
the medical model, the female body is poorly equipped 
to maintain normal metabolic function under reduced-
estrogen conditions, and the postmenopausal period 
represents a state of “…uncontrolled degenerative loss of 
homeostasis…” (Austad 1997).

 The idea that the female body is ill-prepared to function 
in the low-estrogen postmenopausal physiological 
environment derives from a specific view of the human 
lifespan, which holds that developments in hygiene, 
sanitation, and medical technology have only recently 
extended the normal human lifespan into the 6th and 7th 
decades of life, beyond the evolutionarily programmed 
physiological lifespan. In other words, these technological 
developments have resulted in humans “living too long”, 
and outlasting our intrinsic capacity for physiological 
self-maintenance. This perspective relies on the concept 
that somatic longevity, the lifespan of non-reproductive 
physiological systems, mirrors reproductive longevity, or 
the lifespan of germline cells that allow one to reproduce. 
Menopause represents the termination of reproductive 
longevity, which, implicit in the medical view, means that 
evolution has programmed the maintenance of somatic 
longevity to cease at this same point. In other words, somatic 
systems are expected not to have evolved to function past 
menopause, and are thus incapable of adapting to the 
hyposteroidal postmenopausal environment. This view 
lends a character of inevitability to the medical conception 

of postmenopausal disease, and suggests that women 
simply live longer than their bodies are built to handle.

 The main consequence of the medical deficiency disease 
model of menopause has been the extensive prescription 
of hormone replacement therapy (HT), with the intention 
of replacing lost estrogen to reduce symptoms and prevent 
development of disease. The promotion of HT as treatment 
serves as a thorough illustration of the medicalization 
of menopause, as demonstrated by a recent survey of 
HT-related pharmaceutical literature. Websites for HT 
generally cast menopause as having unnatural, negative 
effects and leading to suffering, not only physically, 
but also psychologically and socially, and present the 
physician’s perspective as privileged, versus women’s 
own experiences (Charbonneau 2010). Widespread 
prescription of HT as the solution to the medical problem 
of menopause in and of itself provides ample reason to 
seek alternative conceptions of the relationship between 
menopause and women’s health. This is because over 
the past decade, a series of papers reporting the results 
of the Women’s Health Initiative (WHI) and the Million 
Women Study have demonstrated an association between 
taking HT and increased risk of developing cardiovascular 
disease and breast cancer (Narod 2011; Rossouw et al. 
2002). Although these results have been debated since 
their publication (Tanko and Christiansen 2006; Utian 
2012; Shapiro 2004), the rate of women taking HT has since 
declined (Ettinger et al. 2012).

 While decreased HT use represents a modest shift 
away from the emphasis on pharmaceutical responses to 
menopause, it appears mainly to be due to women’s choices 
rather than a change in the medical model (Marnocha et 
al. 2011). Instead, the medical model appears to remain 
intact, as evidenced by the HT advertising discussed 
above (Charbonneau 2010), by the reflexive readiness of 
physicians to prescribe HT (Marnocha et al. 2011), and by 
efforts in the scientific community to promote HT by citing 
criticism of the WHI’s results (Nedergaard et al. 2013). 
Whereas women can reduce the physical consequences of 
the medical model by choosing not to fill HT prescriptions, 
the continued medicalization of menopause still has 
important and often negative social and psychological 
effects on women (Cimons 2008; Charbonneau 2010; 
Marnocha et al. 2011).

 This paper presents an alternative approach to 
understanding menopause and postmenopausal health, 
that of evolutionary medicine, which follows from the 
principle that modern human health and disease are at 
least partially products of the evolutionary forces that have 
shaped modern human biology and variation (Nesse and 



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Williams 1994; Williams and Nesse 1991; Gammelgaard 
2000). As such, the following evidence serves as a critique 
of the medical model of menopause as a deficiency disease, 
supporting a different, evolutionary view that situates 
human menopause and the postmenopausal lifespan 
in its broader ecological and life history contexts. The 
evolutionary view derives from a wealth of comparative 
anthropological and biological evidence, incorporating 
cross-cultural and cross-species comparisons to more 
holistically understand the process of menopause and 
health expectations for the postmenopausal lifespan. 
Adopting the evolutionary perspective has the potential to 
change clinical practice in two key ways. The first is to further 
obviate the routine prescription of HT by establishing that 
extended maintenance of sound physiological function 
under low-estrogen postmenopausal conditions is the 
human norm. In other words, somatic and reproductive 
longevity are divorced, so that the human female body has 
evolved to function and remain healthy for a substantial 
period of time after menopause, despite the accompanying 
reduction in circulating estrogen.

 Second, comparisons of menopausal physiology, 
postmenopausal survival, and health across species and 
between human cultures allows for the identification of 
lifestyle and behavioral factors that may play a role in the 
etiology of metabolic diseases among women living in 
industrialized societies, presenting non-pharmacological 
and non-hormonal avenues for disease prevention. 
Although there is a vast literature on the physiology of 
metabolic disease, detailing the relevant physiochemical 
pathways and mechanisms of preventive strategies is 
beyond the scope of this paper. Instead, the following 
sections review the evidence for evolutionary medicine’s 
interpretation of menopause, which can point to 
promising areas of research into the specific physiological 
mechanisms that promote postmenopausal health. 
Overall, this paper contends that the medical paradigm of 
deficiency disease is out of step with the biological reality 
of human menopause, and that an evolutionary medicine 
approach has the potential to enhance medical, cultural, 
and individual understandings of menopause and the 
postmenopausal lifespan.

The Process of Menopause and its 
Relationship to Postmenopausal Health
An important aspect of the evolutionary medicine 
approach is the recognition that menopause is the 
culmination of a long-term, highly-variable process, 
rather than a brief transition or event, as sometimes 
characterized in the medical model. The length of the 
menopausal process contributes to its variability and also 

to variability in postmenopausal physiology, providing 
the raw material upon which natural selection acts. Also 
important to recognize is that menopause, defined as the 
end of menstruation, is better seen as the culmination 
of a larger and longer process wherein ovulation ceases 
and reduces fecundity, or reproductive potential, to zero. 
This larger process of the cessation of ovulation, in which 
menopause is the most readily observable outcome, 
places a limit on lifetime reproductive success, which 
is the key variable in natural selection. Evolutionary 
interpretations of menopause must therefore incorporate 
an understanding of variation in the process of menopause 
and its relationship to reproductive potential.

 The capacity to experience menopause is dependent 
on the property of semelgametogenesis, where all 
reproductive cells (in this case oocytes, or egg cells) are 
overwhelmingly produced only early in life, and are 
not replenished at any point later in the lifespan (Finch 
1990; Peccei 2001b; Ellison 2010). Human females are 
semelgametogenic, a trait they share with all other female 
mammals and birds (Bribiescas 2006), and human oocyte 
production occurs largely prior to birth (but see (White et 
al. 2012) with the number of egg cells peaking during the 
fifth month of gestation. Thereafter, due to atresia (a form 
of apoptosis, or programmed cell death) the population 
of oocytes decreases to roughly two million at birth, and 
400,000 at puberty. After puberty, ovulation and continued 
atresia cooperate to deplete the remaining store (Faddy 
et al. 1992; Hansen et al. 2008), eventually reaching a 
threshold of ~1000 surviving ova in the years leading up to 
menopause. Below this threshold, the remaining oocytes 
produce very little estrogen, which is required to stimulate 
uterine wall preparation in anticipation of implantation of 
the mature egg (Clancy 2009).

 Among other hormonal changes, the menopausal 
reduction in estrogen is thought to disrupt endocrine 
pathways responsible for ovulation and thus fecundity, 
leading to an average age at menopause between ~45-55 
years across human populations (O’Connor et al. 1998; 
Thomas et al. 2001; Greenspan and Gardner 2004; Johnson 
et al. 2004; Walker et al. 1984). The age at menopause 
does, however, vary on population and individual scales, 
owing to a combination of genetic, environmental and 
behavioral factors. On the whole, data from diverse human 
populations consistently fall within the aforementioned age 
range (see Figure 1). The three lowest population average 
ages at menopause (≤47 years), however, all come from 
subsistence farming or herding populations practicing 
natural fertility (i.e. non-contracepting), suggesting that 
nutritional and reproductive factors influence menopausal 
timing.



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 Andrew Froehle  Postmenopausal Health and Disease 

Whereas the medical model would tend to view such 
variation and deviations from the norm as pathological 
(Meyer 2001), the evolutionary perspective sees this 
variation as potentially adaptive (Gluckman and Beedle 
2007; Ellison 2010). Given that the process of oocyte 
depletion occurs over decades and across several very 
distinct life history periods, it is possible that variation in 
age at menopause and postmenopausal physiology may 
be optimized for an individual in the mode of a predictive 
adaptive response (Gluckman and Beedle 2007; Gluckman 
et al. 2005). The “predictive adaptive response” concept 
suggests that individual and population-level phenotypic 
variation reflects an evolved flexibility that responds to 
cues during development, influencing subsequent life 
history and geared towards maximizing lifetime fertility 
in the face of an unstable, yet to some extent predictable, 
environment. This approach has been used extensively 
to explain variation in menstrual cycle characteristics 

(Vitzthum 2008; Vitzthum 2009), and in a similar manner 
may be applicable to menopause and the postmenopausal 
lifespan (Ellison 2010). In this view, variation in the 
process of menopause and postmenopausal physiology 
represents the normal range of phenotypic expression, 
within constraints set by the specific evolutionary history 
of the human species.

 On top of population-level variation, there is also 
substantial inter-individual variation within populations 
in terms of the slowing of reproductive function and 
age at menopause (Treloar 1981; te Velde and Pearson 
2002). Some of this variation is inherited, with heritability 
estimates ranging from 30-85% (Torgerson, Thomas, 
Campbell et al. 1997; Torgerson, Thomas, and Reid 
1997; Peccei 1999; de Bruin et al. 2001; van Asselt et al. 
2004; Murabito et al. 2005; Snieder et al. 1998), but such 
estimates should be interpreted conservatively (Vitzthum 

Figure 1: Number of populations (total N=53) with average (mean and median) ages at natural menopause within each age 
range (Adekunle et al. 2000; Ayatollahi et al. 2003; Beall 1983; Castelo-Branco et al. 2005; Chim et al. 2002; Garrido-Latorre 
et al. 1996; Gonzales et al. 1997; Ku et al. 2004; Mohammad et al. 2004; Balan 1995; Okonofua et al. 1990; Reynolds 
and Obermeyer 2003; Walker et al. 1984; Castelo-Branco et al. 2006; Burch and Gunz 1967; Chow et al. 1997; Fuchs and 
Paskarbeit 1976; Greer et al. 2003; Hunt, Jr. and Newcomer 1984; Ismael 1994; Kapoor and Kapoor 1986; Karim et al. 1985; 
Kato et al. 1998; Kriplani and Banerjee 2005; Kono et al. 1990; Kwawukume et al. 1993; Luoto et al. 1994; Magursky et al. 
1975; McKinlay et al. 1985; Morabia et al. 1996; Ramoso-Jalbuena 1994; Reynolds and Obermeyer 2001; Rizk et al. 1998; 
Samil and Wishnuwardhani 1994; Tungphaisal et al. 1991; Walsh 1978; Carda et al. 1998; Hagstad 1988; Scragg 1973).



Anthropology & Aging Quarterly  2013: 34 (3) 65

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2003; Voorhuis et al. 2010). Thus, the genetic basis for 
menopause remains incompletely understood (Voorhuis 
et al. 2010) despite extensive research on the genetics of 
aging more generally (Finch 1990; Finch and Kirkwood 
2000). Still, the inconsistency between samples can be 
taken to mean that age at menopause is a complex (non-
Mendelian) trait, under the influence of multiple genetic 
and environmental factors.

 The effects of environmental, behavioral, and 
developmental influences on the age at menopause are 
somewhat better-known. Cigarette smoking is associated 
with an earlier age at menopause (Zenzes 2000; Mishra 
et al. 2010), whereas women who experience fewer 
menstrual cycles throughout life due to greater parity or 
more irregular cycles tend to have a later age at menopause 
(Soberon et al. 1966; Kaufert et al. 1987; Stanford et al. 
1987; Whelan et al. 1990; Dahlgren et al. 1992; Torgerson 
et al. 1994; Cramer et al. 1995; vanNoord et al. 1997). 
Socioeconomic indicators including level of education 
and income may affect age at menopause, but results are 
highly inconsistent, likely owing to a large number of 
uncontrolled confounding variables (Mohammad et al. 
2004; Flint 1974; Beall 1983; Kaufert et al. 1987; Weinberg et 
al. 1989; Torgerson et al. 1994; Garrido-Latorre et al. 1996; 
Gonzales et al. 1997; vanNoord et al. 1997; Chim et al. 2002; 
Ku et al. 2004; Castelo-Branco et al. 2005; Walker et al. 
1984; Okonofua et al. 1990; Gonzales et al. 1997; Reynolds 
and Obermeyer 2003; Mohammad et al. 2004; Kriplani and 
Banerjee 2005). Studies of birth weight and early postnatal 
growth suggest that developmental conditions can also 
affect age at menopause, but again, the aggregate results 
fail to point to a consistent relationship (Mishra et al. 2007; 
Cresswell et al. 1997; Hardy and Kuh 2002; Hardy and Kuh 
2005; Tom et al. 2010; Sloboda et al. 2011; Elias et al. 2003).

 Although continued research is needed to precisely 
define the major factors that influence menopause, it 
is clear that the timing and process of menopause are 
quite variable, and receive inputs from both external 
and internal environmental factors. The variability and 
heritability of the timing of menopause provide the raw 
material from which adaptations evolve, and part of the 
menopausal adaptation in humans appears to have been 
the retention of flexibility as part of an overall ovulatory 
predictive adaptive response mechanism, aimed at 
maximizing reproductive success. This flexibility may 
predispose different women to varying metabolic profiles 
after menopause, differentiating between levels of function 
and disease risk in the low-estrogen postmenopausal 
environment. As seen below, however, the evolutionary 
evidence also points to selection for extended somatic 
maintenance well-into the postmenopausal period, which 

may have also evolved as a method of increasing lifetime 
reproductive success.

Evolutionary Views of the Postmenopausal 
Lifespan: Paradox or Adaptation?
Before discussing the postmenopausal lifespan 
specifically, it is important to understand how biologists 
conceptualize the more general issue of aging, defined not 
simply as the accrual of time spent living, but as the loss 
of function in physiological systems with increasing age 
(Gavrilov and Gavrilova 2006). Aging in and of itself has 
long been a problematic concept for evolutionary biology 
(Weismann 1889; Medawar 1952), since theoretically 
the most reproductively successful organisms should 
be those that live forever and never cease to reproduce. 
Why should selection allow for functional deterioration 
and the regular occurrence of intrinsic causes of mortality 
(i.e. death due to failure of internal physiological systems 
rather than succumbing to extrinsic sources of mortality 
such as predation), rather than favoring self-maintenance 
in perpetuity, so long as organisms can avoid extrinsic 
mortality factors?  Reproductive decline, in particular, 
requires explanation from the standpoint of natural 
selection (Williams 1957), since reducing fecundity to 
zero curtails reproductive success and is of no apparent 
selective value.

 The prevailing theory of aging posits that the rate of 
intrinsic senescence in physiological systems results 
from the interaction between the population-specific 
rate of extrinsic-cause mortality (e.g., predation) and 
age-specific fertility potential (Medawar 1952; Williams 
1957; Hamilton 1966; Charlesworth 1994). For any age 
cohort, the number of individuals left alive at a particular 
age to pass on genes, and the offspring those remaining 
individuals will potentially produce as a fraction of total 
offspring production for that cohort, will determine the 
force of selection of any gene acting at that particular 
age. At ages where most individuals are still alive and 
only a small proportion of potential offspring have been 
produced (such as shortly after puberty), selection to 
minimize intrinsic mortality is very high. In contrast, at 
ages where many individuals from a cohort have fallen 
to accidental death, predation, disease, or other extrinsic 
factors, and when most of the likely offspring for that 
cohort have already been produced, then the strength of 
selection to maintain somatic integrity against intrinsic 
sources of mortality is much lower, since it has little effect 
on subsequent generations’ ability to reproduce (Williams 
1957; Hamilton 1966; Kirkwood 1977; Kirkwood 1980; 
Kirkwood and Holliday 1979).



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 Intrinsic challenges to somatic integrity arise as inborn 
biochemical byproducts of multiple physiological 
processes. For example, errors in cellular division, DNA 
replication, and protein synthesis (Kirkwood 1977; 
Kirkwood and Holliday 1979; Kirkwood 1980) can occur 
easily and challenge somatic viability, so that organisms 
invest considerable energy in mechanisms that increase 
accuracy in these processes. Such mechanisms are, 
however, only maintained as long as required to ensure 
that genes are successfully passed on to offspring at a 
population-specific rate. With increasing age, higher 
error rates in these processes lead to accumulation of 
dysfunction, disruption of physiological systems, and 
ultimately death (Kirkwood and Shanley 2010).

Challenges to somatic integrity can also arise as a result 
of antagonistic pleiotropy, where individual genes have 
positive effects early in life prior to and during the peak 
reproductive period, but have detrimental effects later 
in life (Williams 1957). This occurs because genes that 
promote viability and reproductive success early in 
life, when much reproductive potential remains, will be 
strongly selected for, but will be only weakly selected 
against if they exert negative effects later in life, when fewer 
individuals remain alive and little if any reproductive 
potential remains. In fact, menopause itself and the 
resultant low estrogen environment may be products of 
antagonistic pleiotropy (Crews 2003). Genes that promote 
higher circulating estrogen levels during the reproductive 
years have likely been selected for, since they play a major 
role in stimulating ovulation and thus raise fecundity. This 
same process, however, leads to more rapid depletion of 
oocyte stores, and therefore menopause, after which the 
ovary drastically reduces estrogen production and poses 
significant challenges to maintaining the somatic integrity 
of metabolic and cardiovascular systems.

 This sharp increase in disease risk after menopause is 
in agreement with the overarching biological perspective 
on aging. Maintaining somatic viability after menopause 
is anathema to the evolutionary process, so much so that 
Hamilton (Hamilton 1966) predicted a so-called “wall of 
death”, where intrinsic mortality would increase sharply 
upon the loss of reproductive capacity. In the same 
paper, however, Hamilton also noted that humans fail 
to meet the “wall of death” prediction, with much more 
gradual mortality rates past the age of menopause than 
expected from theory. Thus, the human postmenopausal 
lifespan and its relative rarity in the living world present a 
theoretical paradox for evolutionary biology. The problem 
lies in the apparent disconnect between the reproductive 
lifespan and somatic longevity: if differential reproductive 
success is the key functional outcome of evolution, then 

why would human females have evolved to maintain 
non-reproductive physiological function for decades 
past the termination of ovulation? The assumption that 
somatic and reproductive longevity are closely linked is 
at least implicit in the medical model of menopause and 
postmenopausal health.

 Evolutionary biologists, on the other hand, have 
addressed several key questions in attempting to explain 
this paradox, the evidence for which is summarized below. 
First, are aging patterns in human somatic and reproductive 
systems disjointed only under conditions like those of 
industrialized societies, or is the pattern shared across 
diverse socioeconomic environments? Second, do humans 
differ from other animals, especially closely-related 
primate species, in the process of menopause and the 
postmenopausal lifespan? If the pattern of postmenopausal 
survival seen among women in industrialized society is in 
fact shared by women in other types of societies, and if 
this differs from other primates, how and why might the 
unique human pattern have arisen? Most importantly, 
what are the consequences of the answers the evidence 
provides for health expectations among postmenopausal 
women living today and in the future, and what do these 
data mean for the current prevailing medical model?

Comparative Demography
Demographic data show clearly that a high rate of 
multi-decade postmenopausal survival occurs in human 
populations living under non-industrialized conditions, 
and lacking access to medico-technological developments, 
thus challenging the medical model’s notion that a long 
postmenopausal lifespan is only a recent, technological 
development. Changes in mortality and survivorship 
from 1850 to 2000 among females in the United States 
illustrate this point well. Whereas major changes in 
sanitation, hygiene and medical technology that occurred 
from the late 19th century to the present (Cutler and 
Miller 2005) have dramatically increased infant and 
childhood survivorship (Gray 1976), they have had much 
more modest effects on the postmenopausal lifespan. 
Survivorship rates from birth to age 15 years (a proxy for 
sexual maturity) and from birth to age 45 years (a proxy 
for age at menopause) have risen from ~ 65% to ~100% 
and from ~50% to ~95%, respectively, over the past 150 
years (Figure 2). The proportion of women living to age 
15 that then also survived to age 45, meanwhile, increased 
from ~70% to ~95%. Whereas life expectancy at birth has 
doubled over that same time period, the average amount 
of life remaining at age 45 has only increased from ~25 
years to ~35 years, with most of the increase occurring after 
1940 (Figure 3). Thus, despite modest gains in the past 150 



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 Andrew Froehle  Postmenopausal Health and Disease 

Figure 2: Survivorship from birth 
to age 15 years (solid gray 
line) and birth to age 45 years 
(dashed gray line); conditional 
survivorship from 15-45 years 
(black line: rate at which 
individuals who survived to 
age 15 also survived to age 45). 
Life table data for 1850-1890 
(Haines 1994) and for 1900-
2000 (Bell and Miller 2005).

Figure 3: L.E. = Life expectancy, 
or average years of life 
remaining at a specific age. 
Life table data for 1850-1890 
(Haines 1994) and for 1900-
2000 (Bell and Miller 2005).



Anthropology & Aging Quarterly  2013: 34 (3) 68

 Andrew Froehle  Postmenopausal Health and Disease 

years, even in 1850 prior to greater sanitation, hygiene and 
medical technology, over two-thirds of women fortunate 
enough to live to age 15 could expect to live to age 45, and 
to then survive an average of another 25 years, or 35% of 
the total lifespan.

Demographic data from five hunter-gatherer groups 
(Gurven and Kaplan 2007) support the idea that this 
pattern of postmenopausal survival is a widely-shared 
human trait. Despite immense diversity (Kelly 1995; 
Panter-Brick et al. 2001), hunter-gatherer societies share 
general characteristics that make them good models 
for mortality and survivorship in non-industrial, non-
agricultural people. Although hunter-gathers are modern 
humans living in the modern world, and are thus not our 
“ancestors”, the manner in which they live approximates 
in some critical ways the activity patterns and nutritional 
and reproductive conditions that may have prevailed over 
the vast majority of human evolutionary history. Hunter-
gatherers obtain food from seasonally fluctuating wild 
plant and animal supplies, practice natural fertility, and 
lack reliable access to antibiotics, immunizations, water 

treatment, and other developments that increase life 
expectancy at birth in industrialized societies (Wood 1994; 
Panter-Brick 2002; Blurton Jones et al. 2002; Gurven and 
Kaplan 2007). As such, hunter-gatherers are expected to 
differ in terms of mortality and survivorship rates from 
populations living under agricultural and industrialized 
conditions.

Nonetheless, hunter-gatherer survivorship and life 
expectancy patterns are remarkably similar to the 
pre-industrial United States (Figure 4). In both cases, 
high rates of infant and juvenile mortality result in life 
expectancy at birth of less than 40 years and 57-65% 
survivorship from birth to age 15. For those who live to 
sexual maturity, however, ~65% will also reach age 45 
and on average survive for another two decades. The 
data therefore strongly suggest that even under divergent 
socioeconomic conditions, a substantial proportion of all 
females born, and an even greater proportion of those who 
live to reproductive adulthood, share the expectation of 
multi-decade postmenopausal survival, amounting to on 
average a third of the total lifespan.

Figure 4: Survivorship from birth to age 15 years (black bars) and birth to age 45 years (dark gray 
bars); conditional survivorship from 15-45 years (light gray bars); and PM/LS ratio, the average 
postmenopausal lifespan (PM) remaining at age 45 years as a percentage of total lifespan (LS), 
calculated as e45/(e45+45), where e45 is the life expectancy at age 45 years. United States (US) 
data for 1850 (Haines 1994) and for 2000 (Bell and Miller 2005); hunter-gatherer (H-G) and 
chimpanzee data (Gurven and Kaplan 2007).



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Comparative Biology
Whereas comparative demography points to biological 
similarities between all humans, regardless of 
socioeconomic environment, comparative biology can 
place the human pattern of postmenopausal survival 
in its proper evolutionary context. Note that Figure 4 
also includes survivorship data from wild and captive 
chimpanzees (addressed in detail below). As our closest 
living relatives (Goodman et al. 1998), the panins (common 
chimpanzees: Pan troglodytes spp.; bonobos: Pan paniscus 
spp.) provide critical information as to which traits 
humans share with other primates, and which traits likely 
evolved since the split with our last common ancestor. 
Comparative biological data can address whether the 
human pattern of postmenopausal survival is unique or 
common among some larger taxonomic grouping. As 
shown below, although a few individual animals in many 
species may briefly outlive menopause (Cohen 2004) and 
some whale species exhibit a postmenopausal lifespan 
similar to humans (Kasuya and Marsh 1984; Marsh and 
Kasuya 1984; Marsh and Kasuya 1986; Olesiuk et al. 1990; 
Bloch et al. 1993; Martin and Rothery 1993; McAuliffe 
and Whitehead 2005; Foote 2008), overall humans are 
unique among mammals, including primates, and are 
evolutionarily derived relative to panins in having species-
wide, common, multi-decade survival past menopause 
(Caro et al. 1995; Packer et al. 1998; Bronikowski et al. 2002; 
Pavelka and Fedigan 1999; Bellino and Wise 2003; Cohen 
2004; Fedigan and Pavelka 2006).

 The first question is whether human postmenopausal 
longevity has been achieved by foreshortening the 
reproductive lifespan, or by extension of the somatic lifespan 
relative to our last common ancestor. Overwhelmingly, 
the evidence supports the latter conclusion: modern 
humans share an average age at menopause with panins, 
but have the capacity to live well beyond menopause 
due to an extension of somatic longevity. Evidence for 
a shared human/panin menopausal process, and an age 
range for the cessation of ovulation of 45-55 years (Walker 
and Herndon 2008), comes from studies of both wild and 
captive chimpanzees and bonobos, with data on ovarian 
histology and reproductive hormones, menstruation and 
sexual swellings (swellings of the anogenital region that 
signify ovulation and are a proxy for estrogen activity), 
and age-specific fertility. First, from examinations of 
ovarian histology, humans and panins share a similar 
trajectory of oocyte reduction (Gould et al. 1981; Leidy 
et al. 1998; Hansen et al. 2008; Videan et al. 2008; Jones et 
al. 2007) that proceeds at essentially the same rate in both 
taxa (Jones et al. 2007). As in humans, the reduced oocyte 
population is related to hormonal changes in panins, and 

reproductive hormone profiles of panins from their late 
30s to age 50 resemble those of pre- and perimenopausal 
women of the same age (Gould et al. 1981; Jurke et al. 
2000; Videan et al. 2006). In terms of the effects of oocyte 
depletion on estrogenic stimulation of ovulation and 
fecundity, panin menstrual bleeding and sexual swellings, 
which reach peak frequency, regularity, and duration of 
maximal tumescence in the 20s, gradually become less 
frequent, more irregular, and shorter until eventually 
ceasing altogether in the 40s and 50s (Graham 1979; Gould 
et al. 1981; Jurke et al. 2000; Videan et al. 2006; Lacreuse 
et al. 2008). Thus, it appears that humans and panins 
share an ancestral pattern of oocyte reduction and a 
similar ovulatory “dose-response” to the small remaining 
population of sex cells during the fifth and sixth decades 
of life (Hawkes and Smith 2010).

 Observations of panin age-specific fertility are consistent 
with the data on oocyte counts, hormone profiles, and 
ovulatory cycling, also suggesting an end to reproductive 
capacity occurring between the mid-40s and mid-50s. Past 
age 35, fertility declines substantially, and the proportion 
of pregnancies terminating in stillbirth or spontaneous 
abortion increases among captive chimpanzees (Graham 
1979; Roof et al. 2005; Atsalis and Videan 2009b; Atsalis 
and Videan 2009a). Across a large sample from multiple 
wild chimpanzee study sites, there is a sharp drop-off in 
number of births per female per year between 40-44 years 
old, with a tiny fraction of females reproducing up to age 
55 (Emery et al. 2007). 

 As in humans (den Tonkelaar et al. 1998; Vitzthum 
2009), there is substantial individual and population-level 
variation among panins in the process of reproductive 
aging, the age at which ovulation ceases, and the 
termination of fertility (Boesch and Boesch-Achermann 
2000; Videan et al. 2006; Emery et al. 2007; Lacreuse et al. 
2008). For example, there are isolated reports of live captive 
births in the late 40s (Puschmann and Federer 2008). 
Whether this site-based variation is physiological or due to 
social differences in age-related mating behavior remains 
undetermined, but it is entirely possible that ecological 
factors affect reproductive parameters similarly in both 
panins and humans (Atsalis and Videan 2009b; Atsalis 
and Videan 2009a). Although this hypothesis has not been 
extensively explored (Herndon and Lacreuse 2009), it 
points to the possibility of a shared capacity for predictive 
adaptive responses in the reproductive systems of the 
human-panin clade, and thus the variability necessary for 
evolutionary differentiation by natural selection.

 Overall, however, due to mortality patterns, menopause 
occurs in a very small proportion of all female panins 



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 Andrew Froehle  Postmenopausal Health and Disease 

born, and then usually only very late in life (Herndon 
and Lacreuse 2009; Lacreuse et al. 2008), but there is 
also variation in the rate at which panins survive past 
menopause (Hill et al. 2001; Videan et al. 2006; Emery et al. 
2007; Atsalis and Videan 2009b; Atsalis and Videan 2009a; 
Herndon and Lacreuse 2009). To some extent, mortality 
differences between captive and wild chimpanzees mirror 
differences between human populations living under 
different socioeconomic circumstances (i.e. reduced infant 
mortality and greater survivorship due to nutritional 
security and decreased risk of extrinsic mortality). Even 
in captivity, however, most benefits of reduced extrinsic-
cause mortality accrue as increased survivorship to age 15 
(a good proxy for sexual maturity in chimpanzees as in 
humans: (Hill et al. 2001), with a relatively small proportion 
of females born survive past menopause, and then only 
briefly (see Figure 4). At wild sites, only 5% of all females 
born survive to age 45-50, with adult mortality rates rising 
between 25-30 years and spiking at and beyond age 40 
(Hill et al. 2001). Of those surviving to sexual maturity, less 
than 10% survive to age 45, at which point they have only 
10% of their total lifespan remaining (Gurven and Kaplan 
2007)2007).

 Although extrinsic mortality risk likely differs between 
wild panins and human hunter-gatherers, much of the 
inter-species difference in survivorship and longevity past 
menopause may result from differences in the rate of aging 
in somatic physiological systems. Critically, although 
overall mortality rates are lower in captive chimpanzees, 
they too experience a major increase in adult mortality 
at roughly the same age as wild populations, implicating 
intrinsic rather than extrinsic causes of death (Hill et al. 
2001). While adult mortality rates increase exponentially 
and at roughly the same rate in both chimpanzees and 
hunter-gatherers, the increase in mortality due to intrinsic 
senescence begins ≥10 years earlier in chimpanzees 
(Gurven and Kaplan 2007). Wild chimpanzees begin to 
show signs of somatic aging beginning in their mid-30s, 
and though these outward signs of deterioration do not 
always correlate with incapacitation (Tarou et al. 2002; 
Finch and Stanford 2004), it seems plausible that they 
tend to succumb to intrinsic somatic senescence at earlier 
average ages than do humans. Possible mechanisms that 
explain these apparent species-level differences in intrinsic 
mortality and somatic longevity are discussed below.

Mechanisms for Extension of the Somatic 
Lifespan
In seeking explanations for the extension of somatic 
maintenance past menopause in humans, is it important 
to consider both the proximate physiological mechanisms 

by which cellular viability and functional integrity is 
maintained, as well as the ultimate evolutionary pressures 
most likely to have driven selection for an extended 
lifespan. The two main proximate causes of aging are the 
metabolic production of free radicals, which can oxidize 
and damage tissues and DNA (HARMAN 1956), and the 
accumulation of errors in DNA and its macromolecular 
end-products due to poor replicative control, leading 
to malfunctioning cells and the eventual interruption 
of physiological pathways (Orgel 1963; Orgel 1970; 
Kirkwood 1977; Kirkwood and Holliday 1979; Kirkwood 
1980). Extending somatic longevity can be achieved by 
investing energy in mechanisms that reduce free radical 
production or activity, and that enhance the accuracy of 
protein synthesis and cellular replication.

 Although somewhat limited, existing data on 
differences between humans and other primates in the 
expression of such mechanisms tends to point to greater 
maintenance of somatic integrity among humans. On 
a large scale, a reduced metabolic rate may limit free 
radical production and thus reduce oxidative damage 
(Ku and Sohal 1993; Barja et al. 1994), and humans have 
slightly lower than expected mass-specific metabolic rates 
compared to chimpanzees (Froehle and Schoeninger 
2006). On a more molecular scale, blood levels of the free 
radical scavenger uric acid (Ames et al. 1981) tend to be 
higher in primates than in most mammals (Friedman 
et al. 1995), and are especially high in apes and humans 
(Wu et al. 1992; Oda et al. 2002). Humans and apes, to the 
exclusion of monkeys, also share mutations in the genes 
responsible for another group of free radical scavengers, 
the superoxide dismutases (Fukuhara et al. 2002), which 
are more active in longer-lived primate species and are 
most active in human organ tissues (Tolmasoff et al. 1980). 
In terms of DNA and fidelity in macromolecular synthesis 
and cellular replication, humans have higher rates of 
DNA repair than apes (Cortopassi and Wang 1996). 
Overall, then, in keeping with a longer lifespan, humans 
appear to have a greater physiological capacity for somatic 
maintenance via free-radical management and accuracy in 
macromolecule transcription and translation compared to 
other primates.

 Recent research has expanded beyond the above domains 
to include comparative studies of other biomarkers of aging 
in primates. Perhaps the most extensive body of work has 
focused on dehydroepiandrosterone sulfate (DHEAS), 
an important androgen hormone with a wide variety of 
physiological roles, and protective effects against several 
metabolic and cardiovascular diseases (Lane et al. 1997). 
Multiple studies in rhesus monkeys (Macaca mulatta) 
and humans have demonstrated a decline in serum 



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 Andrew Froehle  Postmenopausal Health and Disease 

concentrations of DHEAS with age (Kemnitz et al. 2000; 
Roth et al. 2002), and an association between higher levels 
of circulating DHEAS and slower rates of aging (Roth et al. 
2002; Lane et al. 1997). Compared to chimpanzees, human 
serum levels of DHEAS decline more rapidly with age, 
but overall concentrations are two-to-three times higher 
in humans at any age, and only begin to drop into the 
high end of the chimpanzee range at ages older than 65 
years (Blevins et al. 2013). Other great ape species exhibit 
even lower DHEAS concentrations (Bernstein et al. 2012), 
consistent with the idea that higher human levels have 
evolved since our split with the apes and promote a unique, 
extended period of somatic viability. Additional research 
in these areas should help to clarify additional proximate 
physiological mechanisms by which the human lifespan is 
extended compared to our close primate relatives.

 In terms of ultimate evolutionary mechanisms for the 
extension of the somatic lifespan past menopause in 
humans, multiple theorists (Williams 1957; Hamilton 
1966) have proposed the existence of a critical breach in 
the so-called “wall of death”. In species with relatively 
low lifetime fertility and high levels of long-term parental 
care, infant and childhood survivorship can be enhanced 
by traits that increase the delivery of energy to offspring. 
This reproductive strategy is common to most primates, 
and mother-child food sharing is not uncommon among 
panins (Ueno and Matsuzawa 2004). Humans, however, 
represent an extreme version of the primate pattern, with 
offspring that are slow-developing, energy-needy, and 
highly nutritionally-dependent for a much longer period 
of time than panins. Thus, successfully raising human 
offspring to sexual maturity is an exceptionally energy-
expensive endeavor (Gurven and Walker 2006). To address 
this challenge, humans also diverge from other primates 
in the frequency of food sharing, the quantity of calories 
shared, and the breadth of regular, dyadic food sharing 
relationships (Kaplan and Gurven 2005).

 This pattern of food sharing greatly expands the 
range and frequency of opportunities to indirectly boost 
reproductive success (i.e., through means other than 
producing more of one’s own children), since a proportion 
of one’s genes are shared with even distant kin. Because of 
these potential inclusive fitness benefits via broad-based 
food sharing, the human lifespan is socially selected rather 
than individually selected. In other words, the human 
lifespan serves not only to facilitate one’s own direct 
reproductive success, but also facilitates the reproductive 
success of close relatives, opening up the possibility of 
lifespan extension via kin selection and inclusive fitness 
effects (Carey and Judge 2001).

 This is the crack evolution requires to pry open a hole 
in the “wall of death”: in humans, long-term parental 
care as well as “…altruistic contributions due to post-
reproductives…” (Hamilton 1966) serve as methods by 
which infant and childhood survivorship are increased 
(Williams 1957; Hamilton 1966; Lee 2008; Lee 2003). The 
importance of food sharing to human reproduction has 
thus likely added reproductive value to older adults, 
driving the evolution of extended somatic longevity and 
generating a self-reinforcing feedback loop with adult 
mortality. Increased fitness via food sharing at older ages 
would promote lower age-specific intrinsic mortality, 
which would in turn increase age-specific reproductive 
value as more individuals of older age would survive 
to obtain inclusive fitness benefits. This feedback would  
further increase the force of selection to maintain 
physiological function into later life (Carey and Judge 
2001).

 Providing for the reproductive success of offspring via 
food sharing plays a prominent role in hypotheses for the 
evolution of human longevity through effects on selective 
fitness.  The “Mother Hypothesis” (Williams 1957; 
Hamilton 1966; Peccei 1995a; Peccei 1995b; Peccei 2001a; 
Peccei 2001b; Peccei 2005) and “Grandmother Hypothesis” 
(Blurton Jones et al. 2005; Hawkes et al. 1989; Hawkes et al. 
1997; Hawkes et al. 1998; Hawkes 2003; O’Connell et al. 1999) 
both propose that the postmenopausal lifespan evolved 
because it allowed women to boost lifetime reproductive 
success.  In the former, postmenopausal mothers benefit 
directly by eschewing risky new pregnancies that could 
jeopardize the survival of existing dependent offspring.  
In the latter, postmenopausal women indirectly increase 
fitness by sharing food to promote grandchild production 
and survival.

 Several lines of evidence support the positive effect of 
postmenopausal women on the reproductive success, 
growth, development, and survival of their children 
and grandchildren. In pre-industrial and modern non-
industrial agricultural societies, a maternal grandmother’s 
presence promotes weight gain in grandchildren and 
increases lifetime fertility in daughters (Mayer 1981; 
Mayer 1982; Turke 1988; Sear et al. 2000; Sear et al. 2002; 
Voland and Beise 2002; Lahdenpera et al. 2004; Fox et al. 
2010). Hadza hunter-gatherer grandmothers target hard-
to-obtain, valuable resources that their reproductively-
active daughters are not as able to procure due to the 
constraints of pregnancy, nursing, and childcare (Hawkes 
et al. 1989; Hawkes et al. 1997; Hawkes et al. 1995; 
Crittenden et al. 2009). As such, childhood weight gain is 
positively correlated with the amount of time maternal 
grandmothers living in the same camp spend foraging 



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 Andrew Froehle  Postmenopausal Health and Disease 

(Hawkes et al. 1989; Hawkes et al. 1997).

 Mathematical models also tend to find both the mother and 
grandmother hypotheses evolutionarily plausible. Maternal 
mortality has a strong enough effect on the survivorship of 
unweaned children, for example, to drive the extension of 
the lifespan past the end of fertility (Shanley and Kirkwood 
2001; Sousa 2003). The mother hypothesis is, however, 
weakened when other potential offspring providers 
(e.g., fathers, aunts, uncles) are present to feed weaned 
children (Shanley and Kirkwood 2001; Shanley et al. 2007; 
Lahdenpera et al. 2011). Inclusive fitness effects accruing to 
grandmothers who participate in intergenerational food-
sharing could also have driven lifespan extension (Shanley 
and Kirkwood 2001; Lee 2008; Lee 2003), with the greatest 
contributions to grandchild survival occurring during the 
critical period of 1-2 years old when infants are still nursing 
and on the cusp of being weaned (Shanley et al. 2007). This 
suggests that provisioning of adult daughters to subsidize 
nursing energy needs may have served as the primary role 
for postmenopausal women that initially selected for a 
longer lifespan.

 Though many of the specific tenets of these two 
hypotheses differ, they share one crucial argument: 
active foraging and food sharing in support of offspring 
production and viability have imbued humans with the 
potential for reproductive value at much older ages than 
expected from theory, or from comparative data on panins.  
By extension, these hypotheses predict that selection has 
favored human phenotypes that retain the capacity for 
somatic maintenance at those older ages.  As such, the 
human postmenopausal period is interpreted as an evolved, 
species-typical life history stage, as integral to the human 
life course as adolescence or childhood, and characterized 
by low rates of intrinsic senescence in physiological 
systems, at least into the seventh decade of life (Gurven and 
Kaplan 2007). This life-history interpretation informs the 
study of menopause and the postmenopausal lifespan from 
the perspective of evolutionary medicine.  Following these 
evolutionary hypotheses, it seems reasonable to expect that 
the evolutionary extension of somatic maintenance should 
foster low rates of chronic and degenerative diseases, and 
overall good health during the postmenopausal life history 
period, at least into the seventh decade of life. Given this 
expectation, it becomes critical to evaluate the potential 
lifestyle and behavioral patterns among women in industrial 
society that may predispose them to postmenopausal 
disease by diverging sharply from conditions under the 
natural fertility foraging regime that has likely dominated 
human evolutionary history.

Evolutionary expectations for 
postmenopausal health
In seeking lifestyle factors that might underlie 
postmenopausal disease risk in industrialized societies, it 
is important to first examine the prevalence of the same 
diseases among older women in hunter-gatherer societies. 
Overwhelmingly, hunter-gatherers without access to 
medical care appear not to experience the high rate of 
decline in early postmenopausal somatic maintenance 
seen in industrialized populations. Degenerative diseases 
in foraging populations (as far as they can be diagnosed) 
are extremely rare, accounting for less than 3% of deaths 
before age 60 (Howell 1979; Hill and Hurtado 1996; Gurven 
and Kaplan 2007). Although degenerative diseases become 
more common as causes of death after age 60, obesity, 
hypertension, heart attack and stroke are still very much 
the exception (Eaton et al. 1988; Gurven and Kaplan 2007). 
Anthropometric work among the Hadza demonstrates 
that average body fat percentage remains constant at 
about 19% in women from age 18-75 (Sherry and Marlowe 
2007), in stark contrast to the increase in body fat with age 
in postmenopausal women from industrialized societies 
(Heymsfield et al. 1994). Anecdotal and empirical evidence 
also points to the maintenance of physical vigor in old age 
in foragers (Blurton Jones et al. 2002; Hawkes et al. 1989; 
Walker and Hill 2003), including the observation that older 
Hadza women tend to work longer and perform difficult 
foraging tasks more frequently than women of reproductive 
age (Hawkes et al. 1989; Hawkes et al. 1997). These data 
show that the metabolic syndrome is rare among hunter-
gatherers, likely related to an absence of age-related body 
composition change and continued physical activity. 
Maintenance of somatic physiological systems well past 
menopause appears to be the hunter-gatherer norm, with 
an absence of the related high mortality rates that would be 
present in industrialized society without advanced medical 
treatment (e.g., insulin for diabetes).

 The potential cause(s) of postmenopausal health 
differences between women living in industrialized vs. 
hunter-gatherer societies must be understood from a 
biocultural and evolutionary perspective as a consequence 
of the divergent conditions under which they live. As stated 
previously, probably the most important physiological 
change with menopause is the reduction in estrogen levels. 
This “hyposteroidal” physiological environment is thought 
to cause disease by undermining the proper functioning 
of various somatic physiological systems, especially those 
related to metabolic health. This hypothesis, however, 
is contrary to expectations if the postmenopausal 
lifespan indeed represents an evolved life history period. 
According to Austad (Austad 1997), “… if menopause is 



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 Andrew Froehle  Postmenopausal Health and Disease 

an adaptive physiological state molded by evolution…
then natural selection would presumably have tailored 
postreproductive physiology to the hyposteroidal state…” 
[emphasis in the original]. In other words, if selection 
has promoted the extension of somatic maintenance past 
menopause, then one would expect postmenopausal 
physiology to retain functional capacity despite reduced 
estrogen levels.

 Rather than see this necessarily as a contradiction, 
it is possible that factors other than just a reduction in 
steroid hormone levels affect the ability of metabolic 
systems to maintain their operations after menopause. 
Alternatively, if lifestyle factors elevate estrogen levels 
during the premenopausal period in women living under 
industrialized conditions, the magnitude of hormonal 
change across the menopausal transition may be greater 
than in women living in subsistence-level societies, 
with possibly important physiological consequences 
(Pollard 2008). Given that physiological systems act not 
in isolation, but interact and affect one another, it seems 
reasonable that the physiological effects of behavior and 
experiences during pre-menopausal life could extend 
into the postmenopausal period. In the same way that 
it is reasonable to suspect that selection would have 
molded human postmenopausal physiology to operate 
under hypersteroidal conditions, it is also reasonable to 
predict that the environment (both internal and external) 
under which individual metabolic physiological systems 
develop and operate across the reproductive lifespan 
might predispose those systems to function better or 
worse in the postmenopausal environment. If this is the 
case, we might then expect the prevailing conditions of 
hunter-gatherer life to be integral in preparing metabolic 
physiological systems for operation in the low-estrogen 
postmenopausal milieu. From this perspective, cultural 
variation in subsistence practices and reproduction may 
be particularly important.

 The experience of women in industrialized countries 
differs in a variety of ways from women’s lives in 
modern hunter-gatherer societies, and many of these 
same differences likely distinguish industrialized life 
from conditions during the initial evolution of the 
postmenopausal life history period. For one, decreased 
infant and childhood mortality may remove biological 
filters on survival, thereby promoting higher adult disease 
risk if phenotypes prone to pre-adult mortality also tend 
to be prone to chronic disease (Hawkes 2010; Forbes 1997).  
Reproductive history also diverges between women 
in low-fertility industrialized populations vs. women 
practicing natural fertility. In the latter, higher birthrates, 
longer nursing, and more frequent lactational amenorrhea 

(Wood 1994) mean fewer lifetime ovulatory cycles and 
lower exposure to estrogens, possibly related to decreased 
risk for reproductive cancers (Henderson et al. 1985; Eaton 
et al. 1994; Bernstein 2002; Yang and Wu 2005; Yang and 
Jacobsen 2008). The same factors, given their relationship 
to estrogen levels, could also relate to metabolic function 
in the low-estrogen, postmenopausal physiological 
environment (Xue and Michels 2007). 

 Diets in industrialized societies, too, differ greatly 
from the seasonally-variable wild plants and animals 
that constitute hunter-gatherer diets, which generally 
tend to be higher in fiber and low in fat (Cordain et al. 
2000; Cordain et al. 2002; Eaton and Konner 1985; Eaton 
et al. 1997; Konner and Eaton 2010). Disparities in 
consumption of fiber, simple carbohydrates, and fat likely 
relate to higher metabolic disease risk in industrialized 
populations, partly through effects on estrogen levels and 
related metabolic processes. Contrary to the estrogen-
deficiency model of postmenopausal metabolic disease, 
however, characteristics of the typical hunter-gatherer 
diet actually tend to decrease estrogen levels. Greater 
dietary fiber intake, for example, is correlated with lower 
concentrations of estrogen and estrogen metabolites in the 
blood (Sowers et al. 2006; Wayne et al. 2008; Gaskins et al. 
2012), as are low fat diets (Gencel et al. 2012; Nagata et al. 
2005; Turner 2011). In addition to greater estrogen from low-
fiber/high-fat diets, women in industrialized societies may 
add more estrogen to the circulation from consumption 
of dairy products, in particular from dairy cattle bred to 
lactate year-round (Davoodi et al. 2013). According to the 
model of low estrogen as a deficiency disease, a typical 
low-fat, high-fiber, and dairy-free hunter-gatherer diet 
should increase risk for metabolic disease vs. a high-fat, 
low-fiber Western diet. This is, however, demonstrably 
not the case, and the evolutionary perspective suggests 
that dietary elevation of circulating estrogen during the 
premenopausal period may in fact have a carry-over effect 
on postmenopausal metabolic physiology that increases 
disease risk.

 A fourth factor is the substantial difference in physical 
activity between hunter-gatherer women, who engage 
in regular, vigorous physical activity to obtain food, vs. 
the generally more sedentary women of industrialized 
societies (Hayes et al. 2005). Low exercise levels result 
in generalized health problems (Cordain et al. 1997; 
Eaton and Eaton 2003; Chakravarthy and Booth 2004), 
but the particular relationship between exercise, 
estrogen, and metabolic physiology may put inactive 
postmenopausal women at even greater risk for metabolic 
and cardiovascular diseases (Major et al. 2005; Torrens 
et al. 2009). In premenopausal women, higher levels of 



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 Andrew Froehle  Postmenopausal Health and Disease 

exercise correlate with suppression of estrogen levels 
(Jasienska et al. 2006), and in extreme cases lead to athletic 
amenorrhea and interruption of ovulation (Mcardle et 
al. 2001). Higher overall levels of estrogen compared to 
men, however, mean that women tend to burn more fat 
for energy both at rest and during exercise (Tarnopolsky 
2008). This metabolic difference fades with menopausal 
hormone changes (Isacco et al. 2012), possibly making 
postmenopausal women prone to fat gain. Low activity 
combined with low estrogen levels after menopause may 
also limit the body’s ability to build cardiovascular and 
muscular adaptations to exercise (Grounds 1998; Grounds 
2002; Harris 2005), potentially blunting the health benefits 
of exercise interventions in sedentary postmenopausal 
women. These factors suggest that postmenopausal 
women are more susceptible to metabolic diseases 
regardless of exercise levels. Recent work shows, however, 
that resting energy expenditure, a fundamental indicator 
of metabolic function, has a dose-response relationship 
with exercise in postmenopausal women (Froehle et al. 
2013). Thus, exercise after menopause appears to have 
metabolic effects that can compensate for the consequences 
of lowered estrogen (Spangenburg et al. 2012).

 Researchers have only recently begun to focus on how 
these lifestyle and behavioral factors affect metabolic 
disease risk and prevalence specifically in the low-estrogen 
postmenopausal physiological context. The combined 
evidence provides some interesting leads, though, and 
points to potentially promising avenues for continued 
research. A common feature of the reproductive, dietary, 
and activity differences between women in industrialized 
societies and women in subsistence-level, natural fertility 
societies, is their effects on premenopausal estrogen 
levels. High lifetime fertility and breastfeeding, a diet 
high in fiber and low in fat, and greater levels of activity 
all characterize the hunter-gatherer lifestyle, and all 
have the common effect of suppressing estrogen levels 
during the reproductive years. The opposite is true of the 
typical lifestyle in industrialized societies, where women 
are subject to much higher estrogen exposure over the 
premenopausal lifespan. The difference may be critical 
to postmenopausal physiological functioning given the 
key role of estrogen in metabolism. It is possible that low 
estrogen levels during the premenopausal period “prime” 
metabolic systems to function under that hormonal 
regime, so that after the menopausal reduction in estrogen 
the body maintains greater capacity to function normally, 
even in the presence of low circulating estrogen.

 In contrast, if the body adapts to high estrogen levels 
prior to menopause, the magnitude of the menopausal 
drop in estrogen and subsequent low-estrogen 

postmenopausal environment may more greatly disrupt 
metabolic pathways, resulting in higher disease risk 
without substantial intervention. This hypothesis has 
already been presented with regard to bone disease 
(Pollard 2008; Galloway 1997), and may very well also 
extend to metabolic disease. Additionally, if the degree 
of hormonal change around the time of menopause 
is important to postmenopausal metabolic function, 
then lifestyle interventions that seek to lower estrogen 
levels need to begin as far before menopause as possible 
(Spangenburg, Wohlers et al. 2012; Appt and Ethun 2010; 
DiPietro 2010). Some speculations as to possible areas of 
non-pharmacological, behavioral modes of prevention are 
discussed below.

Conclusion
Overwhelmingly, the evidence from comparative 
demography and comparative biology contradict the 
tenets of the medical model of menopause and the 
postmenopausal lifespan. Rather than being a recent 
technological development in industrialized societies 
that extends the lifespan past its evolutionarily intended 
endpoint, the postmenopausal period is shared broadly 
across a wide range of human societies living under 
widely varying nutritional and medical conditions. The 
shared age at menopause between humans and panins, 
coupled with greatly reduced mid-life adult mortality 
rates in the former vs. the latter, also suggest strongly that 
the postmenopausal lifespan has evolved not by early 
termination of the reproductive period, but instead by 
lengthening the lifespan of somatic physiological systems 
beyond a retained ancestral age range for menopause. 
In short, multi-decade postmenopausal survival that 
accounts for roughly one-third of the total lifespan is an 
evolved, species-defining trait in humans, and should be 
considered a normal life history phase akin to childhood, 
adolescence, or reproductive adulthood.

 Whereas the postmenopausal lifespan is universally 
experienced across societies, however, it does not 
universally represent the initiation of a period of metabolic 
disease risk and decline. Given evidence that the lifespan 
has been selected to last past menopause, the low-estrogen 
deficiency disease model that prevails in Western medicine 
is flawed. Rather than a period of uncontrolled disruption 
to metabolic homeostasis, the evolutionary approach 
proposes that metabolic physiological systems have 
evolved to maintain sound function after menopause, 
despite decreased circulating estrogen. Instead of focusing 
on prescribing estrogen to cure a perceived deficiency, 
more effective strategies to minimize postmenopausal 
metabolic disease among women in industrialized 



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 Andrew Froehle  Postmenopausal Health and Disease 

countries should follow from a better understanding of 
the conditions under which human physiology largely 
evolved. Four key areas of continued research can 
potentially contribute to developing preventive strategies 
by addressing the effects of lifestyle and behavioral 
factors on estrogen levels during premenopausal life, their 
effect on the magnitude of the menopausal reduction in 
circulating estrogen, and the consequences for metabolic 
function after menopause. These areas are: 1) the effects of 
decreased infant and child mortality on adult disease risk; 
2) the effects of reproductive patterns on estrogen levels; 
3) the effects of diet on body composition and metabolic 
function in relation to estrogen; and 4) the effects of 
physical activity on metabolic function, again with regard 
to estrogen physiology. 

 First, there are clearly ethical concerns with advocating 
greater childhood mortality or interfering with individual 
women’s choices about reproduction, contraception, or 
family planning, and so preventive strategies deriving 
from the first two areas above are unlikely to be developed 
(nor should they be, in this author’s opinion). Studying 
the effects of early life experiences on later life physiology, 
however, as well as genetic predisposition to certain 
conditions, may be fruitful in identifying women who 
may be at greater risk of developing metabolic diseases 
after menopause. Such information would be useful in 
tailoring preventive exercise and dietary programs early 
in life so as to maximize postmenopausal health.

 Certainly, advocating diets higher in fiber and lower in 
many kinds of fat, along with greater levels of physical 
activity is important not only to general health, but also 
specifically for metabolic health after menopause. Initiating 
these habits as early as possible in the lifespan may be 
critical to developing a metabolic adaptation to lower levels 
of estrogen, which may then prime these physiological 
systems to maintain function after menopause. There is 
already some interesting thought in this direction (Pollard 
2008; Spangenburg et al. 2012), and continued work in this 
vein has great promise in reducing the prevalence of mid-
life metabolic disease among women in industrialized 
societies. Overall, it is critical to understand menopause 
in its broader evolutionary and biological context so as to 
recognize that life past menopause is not a disease, but has 
likely been an integral part of the lifespan of most women 
for millennia (Blurton Jones et al. 2002; Caspari and Lee 
2004). Using the framework of evolutionary medicine 
to study menopause offers the opportunity to develop 
lifelong preventive strategies that ensure postmenopausal 
health, and that have the potential to change societal, and 
perhaps more importantly for health, medical perceptions 
of menopause.

Notes

1  This paper focuses on “natural menopause,” the result of innate 
physiological processes, as opposed to surgical menopause, 
which is a consequence of various surgical procedures, 
including hysterectomy and oophorectomy.

2 National Library of Medicine: http://www.nlm.nih.gov/
medlineplus/menopause.html (May 21, 2013); National 
Institute on Aging: http://www.nia.nih.gov/health/
publication/menopause (May 21, 2013); Mayo Clinic: 
http://www.mayoclinic.com/health/menopause/DS00119 
(May 21, 2013).

3 National Health and Nutrition Examination Survey, obtained 
from National Center for Health Statistics, Health Data 
Interactive, http://www.cdc.gov/nchs/hdi.htm, accessed 
May 21, 2013.

Acknowledgements

The author thanks Margaret Schoeninger, Jim Moore, 
Sue Hopkins, Loki Natarajan, Katerina Semendeferi, and 
two anonymous reviewers for their helpful comments on 
various incarnations of this manuscript.

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