See discussions, stats, and author profiles for this publication at: https://www.researchgate.

net/publication/249342068

Life History Evolution

Article · May 2012

CITATIONS READS

76 8,234

2 authors:

Daniel K. Fabian Thomas Flatt

University of Cambridge Université de Fribourg
29 PUBLICATIONS 940 CITATIONS 159 PUBLICATIONS 7,220 CITATIONS

SEE PROFILE SEE PROFILE

Some of the authors of this publication are also working on these related projects:

Evolution and Mechanisms of Life History Adaptation and Aging in Drosophila View project

SNEV/Prp19/Pso4 is a DNA repair factor modulating cellular and organismal lifespan View project

All content following this page was uploaded by Daniel K. Fabian on 05 June 2014.

The user has requested enhancement of the downloaded file.

 http://www.nature.com/scitable/knowledge/library/life-history...

Life History Evolution

By: Daniel Fabian (Institute of Population Genetics, Vetmeduni Vienna Veterinaerplatz 1, A-1210
Vienna, Austria) & Thomas Flatt (Institute of Population Genetics, Vetmeduni Vienna
Veterinaerplatz 1, A-1210 Vienna, Austria) © 2012 Nature Education

Citation: Fabian, D. & Flatt, T. (2012) Life History Evolution. Nature Education
Knowledge 3(10):24

To explain the remarkable diversity of life histories among species we must

understand how evolution shapes organisms to optimize their reproductive
success.

What is Life History Evolution?

A female North Pacific Giant Octopus (Enteroctopus dofleini) lives three to four years; it lays
thousands of eggs in a single bout and then dies. By contrast, a mature Coast Redwood Tree
(Sequoia sempervirens) lives for many hundreds of years and produces millions of seeds each year
(Figure 1). As these two examples illustrate, organisms differ dramatically in how they develop, the
time they take to grow, when they become mature, how many offspring of a particular size they
produce, and how long they live. Together, the age-, size-, or stage-specific patterns of
development, growth, maturation, reproduction, survival, and lifespan define an organism's life
cycle, its life history.

1 von 13 4/28/13 11:20 AM

 http://www.nature.com/scitable/knowledge/library/life-history...

Figure 1: Diversity of life histories.

Top: A female North Pacific Giant Octopus (Enteroctopus
dofleini). Bottom: A Coast Redwood Tree (Sequoia
sempervirens).
Photos courtesy of (top) Bachrach44 via Wikimedia
Commons, (bottom) Bernt Rostad via Flickr.

The principal aim of life history theory, a branch of evolutionary ecology, is to explain the
remarkable diversity in life histories among species. But there is another, more compelling reason
for why life history evolution is important: adaptation by natural selection is based on variation in
Darwinian fitness among individuals, and since life history traits determine survival and
reproduction they are the major components of fitness. The study of life history evolution is thus
about understanding adaptation, the most fundamental issue in evolutionary biology.

Here we introduce the basics of life history theory and review what biologists have learned about
life history evolution. For more in-depth coverage we refer to Stearns (1992), Roff (1992, 2002),

2 von 13 4/28/13 11:20 AM

 http://www.nature.com/scitable/knowledge/library/life-history...

Charlesworth (1994), and Flatt and Heyland (2011). Also see the Nature Education Knowledge
articles by Shefferson (2010), Young (2010), and Fabian and Flatt (2011).

The Basics of Life History Theory

Life history theory seeks to explain how natural selection and other evolutionary forces shape
organisms to optimize their survival and reproduction in the face of ecological challenges posed by
the environment (Stearns 1992, Roff 1992, Stearns 2000), or as David Reznick has recently put it:
"Life history theory predicts how natural selection should shape the way organisms parcel their
resources into making babies" (Reznick 2010, p. 124). The theory does so by analyzing the
evolution of fitness components, so-called life history traits, and how they interact: size at birth;
growth pattern; age and size at maturity; number, size, and sex of offspring; age-, stage- or
size-specific reproductive effort; age-, stage- or size-specific rates of survival; and lifespan.

The classical theory treats life history evolution as an optimization problem: given particular
ecological factors (e.g., predators, nutrition) that affect an organism's probability of survival and
reproduction, and given limiting constraints and trade-offs intrinsic to the organism, what are the
optimal values and combinations of life history traits that maximize reproductive success? To find
the solution to this problem we need to understand its "boundary conditions" (Stearns 2000): (1)
how extrinsic, environmental factors affect survival and reproduction; and (2) how intrinsic
connections among life history traits (trade-offs) and other constraints limit whether and how life
history traits can evolve. Once these conditions have been understood and defined, life history
models can be used to answer questions such as: How small or large should an organism grow? At
what age and size should it mature? How many times should it reproduce? How many offspring
should it produce and what size should they be? For how long should it reproduce and how long
should it live?

Life history optimization problems are typically modeled by using the Euler-Lotka equation, which
describes population growth rate (i.e., fitness) of a clonal genotype (or allele substitution) in
continuous generation time as a function of its age at maturity, age at last reproduction,
age-specific survival probability, and the expected age-specific number of offspring (Stearns 1992,
Roff, 1992, Brommer 2000):

where α is the age at first reproduction, ω the age at last reproduction, lx the probability of
surviving from birth to age class x, mx the expected number of offspring in age class x, and r the
population growth rate or Malthusian parameter. The equation sums the probabilities of survival
and reproduction over the entire lifetime of the individuals in the population and can then be
solved for r. Note that in the context of life history theory r measures the growth rate or fitness of
a clone or, in sexually reproducing organisms, the rate of spread of an allele that affects life
history. Thus, the implicit assumption is that the modeled population consists of phenotypically
and genetically identical individuals. If the population described by the Euler-Lotka equation is
stationary (non-growing), r is zero and the equation becomes

3 von 13 4/28/13 11:20 AM

 http://www.nature.com/scitable/knowledge/library/life-history...

or, if generation time is discrete,

where R0 is the expected number of daughters per female per lifetime (net reproductive rate). This
equation is simpler than the continuous-time version and can be used whenever r is zero or close
to zero; for stable populations that do not change in size, R0 is the appropriate fitness measure
(Stearns 1992, Roff 1992, Brommer 2000). Using this framework, one can ask what particular
combination of life history traits maximizes fitness, or how much fitness is affected when one of
the traits is changed. This approach has been used with great success to predict the evolution of
life history traits.

Genetic Variation for Life History Traits

The evolution of life history traits by natural selection depends upon genetic variation on which
selection can act to produce adaptations in response to the environment. The models mentioned
above implicitly assume that life history evolution is not limited by a lack of genetic variation.
Interestingly, however, the heritability (h2 = VA/VP = additive genetic variance divided by
phenotypic variance), i.e. the proportion of phenotypic differences among individuals in a
population that is explained by additive genetic differences among them, is usually small for life
history traits. This low heritability could be caused by low amounts of additive genetic variance;
yet, there exists ample genetic variation for life history traits in natural and laboratory populations.
Consistent with the notion that fitness components harbor lots of genetic variation, many artificial
selection experiments in the laboratory have successfully managed to cause evolutionary changes
in life history traits in the predicted direction (Stearns 1992, Roff 1992, Houle 2001). One reason
for the large VA of life history traits may be that they are highly complex, quantitative, polygenic
traits influenced by many loci (Houle 1992).

But how can we reconcile the fact that VA is large while at the same time h2 is small? A likely
reason for the low heritability of life history traits is that, although VA (the numerator) is large, VP
(the denominator) is much larger than VA. Note that the phenotypic variance VP consists of VA, the
additive genetic variance, plus a remainder, VR, that itself consists of all non-additive genetic
sources of variation (i.e., due to dominance, epistasis, etc.) and phenotypic variation engendered
by the environment (i.e., phenotypic plasticity, genotype by environment interactions; see below).
Thus, life history traits probably have low heritability because they are influenced by many loci
(which inflates both VA and VP) while at the same time harboring substantial amounts of residual
variation VR, for example variation due to changes in the environment (which inflates VP but not
VA) (Houle 1992, Houle 2001).

Moreover, although life history traits are under strong selection, which should exhaust genetic
variance, several factors can maintain genetic variation for these traits, including mutation-
selection balance, environmental heterogeneity and genotype by environment interactions, and
negative genetic correlations (Stearns 1992, Roff 1992, Houle 2001). However, despite typically

4 von 13 4/28/13 11:20 AM

 http://www.nature.com/scitable/knowledge/library/life-history...

large amounts of life history variation, life history evolution is also subject to constraints.

Life History Trade-Offs and Other Constraints

Fitness would obviously be maximal if survival and reproduction would be maximal at all ages,
stages, or sizes of an organism. In principle then, the basic problem of life history evolution is
trivial: all life history traits should always evolve so as to maximize survival and reproduction and
thus fitness (Houle 2001). This would very rapidly lead to the evolution of "Darwinian demons"
(Law 1979) that would take over the world, i.e. organisms that start to reproduce as soon as they
are born, produce an infinite number of offspring, and live forever. Such organisms, however, do
not exist in the real world: Resources are finite, and life history traits are subject to intrinsic
trade-offs and other types of constraints, so natural selection cannot maximize life history traits —
and thus fitness — beyond certain limits. We call such limits evolutionary constraints (Stearns
1992, Houle 2001); as mentioned above, they represent the intrinsic "boundary condition" we must
understand to predict life history evolution.

One of the most important types of constraint are life history trade-offs (Stearns 1992, Roff 1992,
Flatt and Heyland 2011). A trade-off exists when an increase in one life history trait (improving
fitness) is coupled to a decrease in another life history trait (reducing fitness), so that the fitness
benefit through increasing trait 1 is balanced against a fitness cost through decreasing trait 2
(Figure 2A). (Note that trade-offs can also involve more than two traits.) At the genetic level, such
trade-offs are thought to be caused by alleles with antagonistic pleiotropic effects or by linkage
disequilibrium between loci.

Trade-offs are typically described by negative phenotypic or genetic correlations between fitness
components among individuals in a population (Figure 2A). If the relationship is genetic, a
negative genetic correlation is predicted to limit (i.e. to slow down or prevent) the evolution of the
traits involved. Thus, a genetic trade-off exists in a population when an evolutionary change in a
trait that increases fitness is linked to an evolutionary change in another trait that decreases
fitness. The existence of genetic correlations can be established through quantitative genetic
breeding designs or through correlated phenotypic responses to selection. For example, direct
artificial selection for extended lifespan in genetically variable laboratory populations of fruit flies
(Drosophila melanogaster) causes the evolution of increased adult lifespan (sometimes in 10 or
fewer generations), but this evolutionary increase in longevity is coupled to decreased early
reproduction (e.g., Zwaan et al. 1995). This suggests that lifespan and early reproduction are
genetically negatively coupled, e.g. through antagonistic pleiotropic alleles (e.g., Flatt 2011, Fabian
and Flatt 2011).

At the physiological level, trade-offs are caused by competitive allocation of limited resources to
one life history trait versus the other within a single individual, for example when individuals with
higher reproductive effort have a shorter lifespan or vice versa (Figure 2B). A helpful way to think
resource allocation trade-offs is to imagine a life history as being a finite pie, with the different
slices representing how an organism divides its resources among growth, storage, maintenance,
survival, and reproduction (Reznick 2010; Figure 2C). The essential problem is this: given the
ecological circumstances, and the fact that making one slice larger means making another one
smaller, what is the best way to split the pie? Note that since resource allocation trade-offs might
have a genetic basis, and since different genotypes may differ in aspects of resource allocation, the
genetic and physiological views of trade-offs are not necessarily incompatible. However,
physiological trade-offs at the individual level do not always translate into genetic (evolutionary)
trade-offs at the population level. For instance, when the physiological (within-individual)
trade-off is genetically fixed ("hard-wired") among all individuals within the population, all
individuals will exhibit the same negative physiological relationship between two life history traits
but the genetic correlation among individuals would be zero (Stearns 1989, Stearns 1992).

5 von 13 4/28/13 11:20 AM

 http://www.nature.com/scitable/knowledge/library/life-history...

Figure 2: Life history trade-offs.

Top (A): A negative genetic (or phenotypic) correlation, i.e. a
trade-off, between reproduction (e.g., number of eggs
produced) and adult survival, one of the most commonly
found negative relationships between life history traits.
Middle (B): The so-called Y-model of resource allocation
trade-offs. In this example, a limited resource (e.g., a
nutrient) is acquired and differentially (competitively)
allocated (invested) into physiological processes that affect
survival at the expense of investment into reproductive
functions (e.g., egg production, fecundity). Bottom (C): A
useful way of thinking about resource allocation trade-offs is
to imagine the life history as being a finite pie. See text for
further details.
© 2012 Nature Education All rights reserved.

The book by Stearns (1992) lists 45 possible trade-offs among 10 major life history traits, and
many more can be envisaged to exist. Those trade-offs that have received most attention include
(1) current reproduction versus survival; (2) current versus future reproduction; (3) current
reproduction versus parental growth; (4) current reproduction versus parental condition; and (5)
number versus size of offspring.

Some of the best evidence for genetically based life history trade-offs comes from artificial
selection and experimental evolution experiments carried out in Drosophila (see reviews in Stearns
and Partridge 2001, Flatt and Schmidt 2009, Flatt 2011). In summary, many experiments have

6 von 13 4/28/13 11:20 AM

 http://www.nature.com/scitable/knowledge/library/life-history...

found: a negative correlation between early fecundity and adult lifespan; a positive correlation
between developmental time and body size; a positive correlation between either developmental
time or body size with early fecundity; and a negative correlation between early and late fecundity.

Other constraints on life histories that prevent natural selection from attaining a particular fitness
optimum can involve biophysical, biochemical and structural factors, developmental properties of
the organism, phylogenetic and historical contingencies, or simply a lack of genetic variation
(Stearns 1992, Houle 2001).

Phenotypic Plasticity in Life History Traits

Genetic variation and constraints are not the only factors affecting the expression and evolution of
life history traits. Another important issue is that life history variation is often strongly influenced
by the environment (e.g., temperature, nutrition, predators,), a phenomenon called phenotypic
plasticity, i.e. the ability of a single genotype (or clone) to produce different phenotypes across
different environments (Stearns 1992, Roff 1997, Pigliucci 2001, DeWitt and Scheiner 2004). The
plasticity of a specific genotype can be conceptually described by a mathematical function called a
reaction norm, i.e. a line or curve that relates the phenotypes produced by this genotype to
changes in the environment it experiences (Figure 3A).

Figure 3: Life history plasticity.

Top (A). Phenotypic plasticity is often visualized using
so-called reaction norms, curves that relate phenotypes and
environments for a specific genotype. An example of a single
reaction norm for body size in fruit flies (Drosophila),
relating changes in ambient temperature during development
to the adult body size phenotypes produced by a single fly
genotype. Bottom (B): Genetic variation among genotypes in
phenotypic plasticity manifests itself as a bundle of reaction
norms with different slopes, i.e. the reaction norms are on

7 von 13 4/28/13 11:20 AM

 http://www.nature.com/scitable/knowledge/library/life-history...

average non-parallel. Such a pattern is also called genotype

by environment interaction (GxE). Shown here is a case of
particularly strong GxE, with the reaction norms of three
genotypes crossing each other, a pattern that changes the
relative ranking of the phenotypes across environments.
© 2012 Nature Education All rights reserved.

The importance of such plasticity in life history evolution is at least three-fold (Stearns and Koella
1986, Stearns et al. 1991, Stearns 1992, Nylin and Gotthard 1998, DeWitt and Scheiner 2004, Flatt
2005): (1) since plasticity modulates the phenotypic expression of genetic variation for single life
history traits and of genetic correlations for pairs of traits, it affects the genetic response to
selection across environments; (2) if there exists adaptive variation among genotypes for the
plastic response, selection can produce an optimal reaction norm that maximizes fitness across
environments; and (3) plasticity of a specific trait may homeostatically buffer the organism against
environmentally-induced changes in other traits so that organismal performance and thus fitness
is optimized.

Many life history traits (e.g., age at maturity, fecundity) exhibit a high degree of plasticity, and
there is often significant genetic variation for plasticity in natural populations, i.e. genotypes have
different reaction norms, a phenomenon called genotype by environment interaction (GxE) (Figure
3B). Moreover, not only single traits but also correlations between traits can be plastic, and
different environments can change the slope and/or sign of the trait correlation (Stearns et al.
1991, Stearns 1992). In spadefoot toads (Scaphiophus couchii), for example, individuals that
develop in ponds of short duration have a shorter larval period and a smaller body size at
metamorphosis (with the traits being negatively correlated) than individuals that develop in ponds
of long duration (with the traits being positively correlated) (Newman 1988, Stearns et al. 1991).

Having discussed the optimality modeling approach and the factors that influence the expression
of life history traits, we turn now to discussing some major predictions for the evolution of life
histories (for details see Stearns 1992, Roff 1992, Charlesworth 1994, Stearns 2000, Roff 2002).

Predictions for the Evolution of Life History Traits

At what age and size should an organism mature? A genotype's reproductive success depends
strongly on its growth rate and — as a consequence of growth — on its age and size at maturity.
To predict the optimal age and size at maturity we must understand the relative costs and benefits
(in terms of mortality and reproduction) of either maturing early or late and of either growing large
or staying small. The benefits of one "strategy" are the costs of the other, and vice versa. The
benefits of maturing earlier and at a smaller size (i.e., the costs of maturing later and at larger
size) include: (1) a higher probability of survival to maturity because of a shorter duration of the
risky developmental and juvenile period, and (2) a shorter generation time which allows parents to
produce offspring that are born earlier and that start to reproduce sooner. Thus, high juvenile
mortality, for example, should favor the evolution of earlier maturity. Conversely, the benefits of
maturing later and at a larger size (i.e., the costs of maturing earlier and at a smaller size) include:
(1) longer growth which leads to larger size at maturity and thus increased fecundity (since
fecundity often increases with size), (2) lower adult mortality (and thus potentially higher lifetime
fecundity) due to a larger size (mortality due to predators is often lower for larger individuals), and
(3) higher quality offspring (e.g., increased investment per offspring, better parental care) which
improves survival of the offspring produced.

How many offspring should an organism produce? A good starting point to address this question is
the "Lack clutch", a concept that goes back to the ornithologist David Lack (1947). Lack's basic
insight was that birds should optimize their clutch size by maximizing the number of fledged
(surviving) offspring. Deviations from this optimal clutch size would lower reproductive success: if
parents produce too large a clutch, they may not be able to support and rear all their offspring,

8 von 13 4/28/13 11:20 AM

 http://www.nature.com/scitable/knowledge/library/life-history...

with some or all of them dying, whereas if they produce too small a clutch, the number of fledged
offspring may be lower than what the parents could support (Figure 4). Although Lack was correct
in his assertion that fitness is often maximized at intermediate investment, clutch sizes are
typically smaller than what the Lack clutch predicts. This is because the concept ignores several
factors that can reduce clutch size, including parental mortality, future reproduction, the rate of
grandchildren production, and parent-offspring conflict. For example, the existence of trade-offs
between current reproduction and parental survival, current and future reproduction, or the
number and size of offspring can cause deviations from the Lack clutch, and models that take such
factors into account usually yield a better fit with observed clutch size than the Lack clutch. For an
excellent empirical study of optimal clutch size see the study by Daan et al. (1990) on European
kestrels.

Figure 4: The Lack clutch.

The "Lack clutch" is defined as the clutch size that maximizes
the number of fledged (surviving) offspring, assuming that
offspring mortality is a function of clutch size. The trade-off
between clutch size and offspring survival leads to an
intermediate optimum in reproductive effort.
© 2012 Nature Education All rights reserved.

How often should an organism reproduce? Should it be semelparous (i.e., reproduce only once) or
iteroparous (i.e., reproduce several times) (Figure 5; also see Young 2010)? Theory suggests that
iteroparity and the evolution of increased reproductive lifespan are favored when adult survival is
high and when adult fecundity or juvenile survival is low: high (or non-variable) adult survival
increases the number of reproductive events per lifetime, and low (or variable) fecundity or juvenile
survival cause fitness losses that select for increased compensatory reproductive effort.
Conversely, semelparity and the evolution of decreased reproductive lifespan are favored when
adult survival is low and juvenile survival is high. Thus, high (or non-variable) adult relative to
juvenile survival favors iteroparity and lengthens reproductive lifespan while high (or variable)
adult relative to juvenile mortality favors semelparity and shortens reproductive lifespan.
Semelparous organisms typically have higher reproductive effort than iteroparous organisms.

9 von 13 4/28/13 11:20 AM

 http://www.nature.com/scitable/knowledge/library/life-history...

Figure 5: Semelparity versus iteroparity.

Top: Organisms such as the octopus, the agave, or the marsupial mammal Antechinus reproduce only once per life
and are therefore semelparous. From left to right: Octopus vulgaris, Agave tequilana, Antechinus agilis. Bottom:
Organisms that reproduce more than once in their life are called iteroparous, a common life history strategy for
example among birds, mammals including humans, insects, and many other species. From left to right: a small
ground finch (Geospiza fuliginosa), a Madagascan family, and a yellow fever mosquito (Aedes aegypti).
© 2012 Nature Education All rights reserved.

The above considerations are aspects of a more general issue called the "general life history
problem" or "reproductive effort model" (Schaffer 1983, Stearns 1992, Roff 1992, Charlesworth
1994): given that reproduction has both benefits (i.e., offspring production) and costs (e.g.,
decreased future reproduction, increased parental or offspring mortality), what is the optimal
reproductive investment that maximizes fitness? Many theoretical and empirical studies have
addressed this problem; some of the major conclusions from this work are (see Stearns 1992, Roff
1992, Charlesworth 1994): (1) reproductive effort often, but not always, increases with age
because the cost of current reproduction in terms of future reproduction is expected to decrease
with age (since the number of future reproductive events where costs may manifest themselves
declines with age); (2) if reproductive effort yields decreasing returns or if mortality increases as
the effort increases, intermediate reproductive investment and iteroparity are favored; otherwise,
maximal reproductive effort and semelparity are favored; (3) if mortality increases in all age
classes, reproductive effort increases early in life and age at maturity decreases; similarly, if adult
mortality increases, age at maturity should decrease; and (4) if mortality increases after a particular
age (or in one specific age class), reproductive effort increases before and decreases after that age.
As particularly beautiful tests of such reproductive effort models we refer the reader to the field
and laboratory experiments of David Reznick and colleagues on Trinidad guppies (e.g., Reznick et
al. 1990).

How long should an organism live (also see Fabian and Flatt 2011)? The evolution of lifespan can
be viewed as a balance between selection for increased reproductive lifespan (and thus potentially
increased reproductive success) and aging (i.e., intrinsic age-dependent increase in mortality). The
benefits of evolving a longer reproductive lifespan include (also see above): (1) a higher number of
reproductive events (and thus offspring) per lifetime if extrinsic adult mortality is low, (2) sufficient
time to reproductively compensate for offspring lost due to high juvenile mortality, and (3)
decreased reproductive uncertainty due to high variation in juvenile mortality from one round of
reproduction to the next, again by being able to compensate for lost offspring. These effects are

10 von 13 4/28/13 11:20 AM

 http://www.nature.com/scitable/knowledge/library/life-history...

counteracted by those that increase adult mortality (e.g., survival costs of reproduction; aging)
relative to juvenile mortality. Thus, increases in the mean (and/or variance) of adult relative to
juvenile mortality tend to favor a shorter reproductive lifespan and semelparity, whereas decreases
in the mean (and/or variance) of adult relative to juvenile mortality tend to favor longer
reproductive lifespan and iteroparity.

Today many of these predictions of life history theory are well supported by evidence; we shall end
this article by giving an example of a particularly elegant experiment that has confirmed the major
predictions of the "general life history problem".

An Example of an Empirical Test of the Theory

To test the basic tenets of life history theory, Stearns et al. (2000) used an outbred population of
fruit flies (D. melanogaster) to establish two sets of replicate "experimental evolution" lines: three
lines were exposed to a high adult mortality treatment (HAM; by randomly killing 90% of the flies
twice per week) and three lines to a low adult mortality treatment (LAM; by killing 10% of the flies
twice per week). After four years of experimental evolution under these conditions in the lab,
Stearns and collaborators measured the life history phenotypes of all lines in both treatments to
examine the flies' evolutionary responses to high versus low extrinsic mortality. The results of this
long-term experiment were both clear-cut and intriguing, confirming the theoretical predictions:
fruit flies that had evolved under HAM conditions developed more rapidly as larvae, eclosed earlier
and at a smaller size as adults, had higher early peak fecundity, and showed a shorter lifespan
than the LAM flies which evolved the opposite suite of adaptations. In other words, flies evolving in
a highly dangerous environment responded evolutionarily by speeding up their development,
decreasing their age and size at maturity, laying more eggs earlier, and living shorter: they
adapted to high levels of random mortality by shifting their reproductive effort to earlier ages and
by compressing their entire life history into a shorter lifespan. Thus, similar to the findings by
Reznick et al. (1990) in guppies, these results confirm the major predictions of life history theory,
in particular the major role of extrinsic adult mortality in shaping the evolution of growth,
maturation, reproduction, and aging.

Summary
Here we have introduced the basics of life history theory. Life history theory attempts to
understand how natural selection designs organisms to achieve reproductive success, given
knowledge of how selective factors in the environment (i.e., extrinsic mortality) and factors
intrinsic to the organism (i.e., trade-offs, constraints) affect survival and reproduction. By using a
variety of theoretical and empirical methods, and in particular by applying optimality thinking, life
history theorists have derived major predictions about the evolution of the major life history traits,
including age and size at maturity, the number and size of offspring, age- or size-specific
reproductive effort, reproductive lifespan, and aging. Based on these predictions, and by testing
them in field and laboratory experiments, for example in flies, fish, or birds, life history biologists
have provided us with some compelling answers to fundamental questions such as: How fast
should an organism develop? At what age and size should it mature? How many offspring should it
have and how large should they be? Should it reproduce once or more than once? And how long
should it live? Through addressing these problems life history theory has made a major impact on
our understanding of adaptation by natural selection, the most fundamental issue in all of
evolutionary biology.

References and Recommended Reading

Brommer, J.E. The evolution of fitness in life-history theory. Biological Reviews of the Cambridge Philosophical
Society 75, 377-404 (2000).

11 von 13 4/28/13 11:20 AM

 http://www.nature.com/scitable/knowledge/library/life-history...

Charlesworth, B. Evolution in Age-Structured Populations. Cambridge: Cambridge University Press (1994).

Daan, S. et al. Family planning in the kestrel (Falco tinnunculus): the ultimate control of covariation of laying date and clutch
size. Behavior 114, 83-116 (1990).

DeWitt, T. J. & Scheiner, S. M. eds. Phenotypic Plasticity: Functional and Conceptual Approaches. Oxford: Oxford
University Press (2004).

Fabian, D. & Flatt, T. The evolution of aging. Nature Education Knowledge, 2(11):9 (2011).

Flatt, T. The evolutionary genetics of canalization. Quarterly Review of Biology 80, 287-316 (2005).

———. Survival costs of reproduction in Drosophila. Experimental Gerontology 46, 369-375 (2011).

Mechanisms of Life History Evolution. The Genetics and Physiology of Life

Flatt, T. & Heyland A. eds.
History Traits and Trade-Offs. Oxford: Oxford University Press (2011).

Flatt, T. & Schmidt, P. S. Integrating evolutionary and molecular genetics of aging. Biochimica et Biophysica Acta 1790,
951-962 (2009).

Houle, D. Comparing evolvability and variability of quantitative traits. Genetics 130, 195-204 (1992).

———. "The character problem in life history evolution", in The Character Concept in Evolutionary Biology, 109-140,
eds G. P. Wagner. Academic Press, 2001.

Lack, D. The significance of clutch size. Ibis 89, 302-352 (1947).

Law, R. Optimal life histories under age-specific predation. American Naturalist 114, 399-417 (1979).

Newman, R. A. Adaptive plasticity in development of Scaphiopus couchii tadpoles in desert ponds. Evolution 42, 774-783.

Nylin, S. & Gotthard, K. Plasticity in life-history traits. Annual Review of Entomology 43, 63-83 (1998).

Pigliucci, M. Phenotypic Plasticity: Beyond Nature and Nurture. Baltimore: The Johns Hopkins University Press (2001).

Reznick, D. N. et al. Experimentally induced life-history evolution in a natural population. Nature 346, 357-359 (1990).

Reznick, D. N. The Origin Then and Now. An Intepretative Guide to the Origin of Species. Princeton:
Princeton University Press (2010).

Roff, D. A. The Evolution of Life Histories. Theory and Analysis. New York: Chapman and Hall, 1992.

———. Evolutionary Quantitative Genetics. New York: Chapman and Hall, 1997.

———. Life History Evolution. Sunderland: Sinauer Associates, Inc., 2002.

Schaffer, W. M. The application of optimal control theory to the general life history problem. American Naturalist 121, 418-431
(1983).

Shefferson, R. P. Why are life histories so variable? Nature Education Knowledge 1(12):1 (2010).

Stearns, S. C. The evolution of life histories. Oxford: Oxford University Press, 1992.

———. Trade-offs in life-history evolution. Functional Ecology 3, 259-268 (1989).

———. Life history evolution: successes, limitations, and prospects. Naturwissenschaften 87, 476-486 (2000).

Stearns, S. C. et al. The effects of phenotypic plasticity on genetic correlations. Trends in Ecology and Evolution 6,
122-126 (1991).

et al. Experimental evolution of aging, growth, and reproduction in fruitflies, Proceedings of the National
Stearns, S. C.
Academy of Sciences USA 97, 3309-3313 (2000).

Stearns, S. C. & Koella, J. C. The evolution of phenotypic plasticity in life-history traits - predictions of reaction norms for age and

12 von 13 4/28/13 11:20 AM

 http://www.nature.com/scitable/knowledge/library/life-history...

size at maturity. Evolution 40, 893-913 (1986).

Stearns, S. C. & Partridge, L. "The genetics of aging in Drosophila", in Handbook of the Biology of Aging, S. 5th ed.,
353-368. Academic Press, 2001.

Young, T. P. Semelparity and Iteroparity. Nature Education Knowledge 1(9), 2 (2010).

Zwaan, B. et al. Direct selection on life span in Drosophila melanogaster. Evolution 49, 649-659 (1995).

13 von 13 4/28/13 11:20 AM

View publication stats