Evolutionary Psychology
www.epjournal.net – 2009. 7(4): 585-600
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Original Article
Life History Strategy and Disordered Eating Behavior
Catherine Salmon, Department of Psychology, University of Redlands, Redlands, CA, USA. Email:
Catherine_Salmon@redlands.edu.
Aurelio José Figueredo, Department of Psychology, University of Arizona, Tucson, AZ, USA. Email:
ajf@u.arizona.edu (Corresponding author).
Lindsey Woodburn, Department of Psychology, University of Arizona, Tucson, AZ, USA. Email:
woodburn@email.arizona.edu.
Abstract: A sample of female undergraduates completed a packet of questionnaires
consisting of the Arizona Life History Battery, a modified version of the Eating Disorders
Inventory, the Behavioral Regulation scales from the Behavior Rating Inventory of
Executive Function, and two measures of Female Intrasexual Competitiveness that
distinguished between competition for mates and competition for status. As predicted,
Executive Functions completely mediated the relation between Slow Life History Strategy
and Disordered Eating Behavior. Surprisingly, however, the relation between Female
Intrasexual Competitiveness (competition for mates and competition for status) and
Disordered Eating Behavior was completely spurious, with executive functions serving as a
common cause underlying the inhibition of both Disordered Eating Behavior and Female
Intrasexual Competitiveness. The protective function of Slow Life History Strategy with
respect to Disordered Eating Behavior apparently resides in a higher degree of Behavioral
Regulation, a type of Executive Function. The enhanced Behavioral Regulation or selfcontrol, of individuals with a Slow Life History Strategy is also protective against
hazardously escalated levels of Female Intrasexual Competitiveness.
Keywords: eating disorders, anorexia, bulimia, life history strategy, executive functions,
female intrasexual competition
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Introduction
A compelling puzzle of our modern world is the disturbing obsession of some
women with body image and dieting. Why do so many women in North America place
such an emphasis on being thin? Why do these desires lead to eating disorders in only some
women? It is commonly assumed that the desire for a thin female physique and its
Disordered Eating Behavior
pathological expression in eating disorders result from a social pressure for thinness. In
recent years, anorexia nervosa and bulimia have become the most attention grabbing eating
disorders with a multitude of studies being published from a variety of perspectives. With
all this attention, one would think that we would have a concrete understanding of the
causes of eating disorders and yet there have been a plethora of theories that have been
proposed in the literature. We will briefly review the predominant mainstream theories
before discussing evolutionary approaches to the study of dieting behavior and our own
research findings. We would also like to note that we use the term “disordered eating
behavior” to refer to a range of behaviors including various degrees of dieting from mild
restriction to anorexia as we are not considering only those who have a clinical diagnosis
but those women who are engaging in dieting that temporarily impairs their reproductive
function.
Psychoanalytic and Sociocultural Approaches
Early psychoanalytic approaches to anorexia focused on refusing to eat being part
of a struggle for psychological control and autonomy and emphasized the role overly
controlling parents might play in its development (Bruch, 1988). This also led to a family
systems approach and the belief that anorexics were trying to regress to a prepubertal state
(Crisp, 1980). The non-reproductive aspect of such a prepubertal state was not an early
emphasis but it returned to the spotlight in later evolutionary theorizing about the
reproductive impact of such excessive dieting.
Sociocultural theories have held the greatest influence in terms of public opinion on
eating disorders (and have also been the focus on many researchers and clinicians) in recent
years, attributing major risk to exposure to western ideals of female beauty that focus on a
thin form (Botta, 2003; Garner and Garfinkel, 1997; Groesz, Levine, and Murnen, 2002).
Excellent coverage of the sociocultural perspective can be found in reviews by Polivy and
Herman (2002) and Striegel-Moore and Bulik (2007). At the heart of the cultural models is
the idea that eating disorders develop from the internalization of a thin ideal of beauty.
Individuals are exposed to such ideals, which they then internalize. When they experience
an inevitable discrepancy between their self and the ideal, the result is body dissatisfaction
and extreme dieting behavior. Other factors such as social pressure, class, and
perfectionism are also used to explain why this cultural ideal affects some young women
but not all. However, most of these models focus too much on western media images and
do not take into account the role played by interactions between female reproductive roles
and the social environment. There is an assumption that the western media has created a
thin standard of beauty. However, cross-cultural explorations of ideal body type suggest
that the role of women in a society (valued in traditional reproductive roles vs. modern
workplace roles) is an excellent predictor of whether a society has a thin or heavier
standard of female beauty (Anderson, Crawford, Nadeau, and Lindberg, 1992). The social
dominance of women outside the home is a better predictor of a thin standard of beauty
than exposure to media images of thinness.
Biological approaches
There has also been some attention paid to the possible influence of genetics,
particularly in terms of susceptibility to such cultural forces. Twin studies have suggested
some genetic contribution is likely to play a role, though the specifics remain very unclear
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(Klump, Miller, Keel, McGue, and Iacono, 2001, Striegel-Moore and Bulik, 2007). Studies
of treated twin samples and twin samples from the general population suggest a heritability
of close to 70% and also implicate certain alleles as risk factors for anorexia nervosa
specifically (Gorwood, Kipman, and Foulon, 2003).
Evolutionary approaches
There have been a number of evolutionary approaches to eating disorders, most
focusing on reproductive suppression or female competition for mates or status (for a
recent overview of evolutionary approaches to eating disorders, see Kardum, Gracanin, and
Hudek-Knezevic, 2008). Much of the work in this area has focused on the reproductive
suppression hypothesis (RSH) which suggests that natural selection shaped a mechanism
for adjusting female reproduction to sociological conditions by altering the amount of body
fat (Anderson and Crawford, 1992; Surbey, 1987; Wasser 1990; Wasser and Barash, 1983).
Since female body fat stores significant amounts of estrogen and converts androgens to
estrogen, adjusting body fat in response to environmental stress is an effective mechanism
for adjusting women’s reproduction (Frisch, 1990, 1996). While the threshold varies from
woman to woman, and others factors also contribute, most women require adipose tissue to
make up about 22% of their body weight to maintain ovulation. In female athletes, for
example, who are close to this threshold, menstruation can be turned off or on by the loss
or gain of only a few pounds. Thus, alterations in the rate of adolescent weight gain or
weight control in adult lean women (Ellison, 2008; Rippon, Nash, Myburgh, and Noakes,
1988) could have been an efficient mechanism for adjusting ancestral reproductive effort in
response to environmental conditions.
In contemporary western culture, social and ecological cues (such as high levels of
social competition among women and stressful sexual attention from undesirable males),
which would have signaled the need for temporary postponement of reproduction in
ancestral environments, may now be experienced to an unprecedented intensity and
duration, leading to fears related to fatness and body image (Salmon, Crawford, Dane, and
Zuberbier, 2008). Such a mechanism could also serve to delay puberty in response to
conditions indicative of a currently poor environment for reproduction (Surbey, 1987).
Several studies (Juda, Campbell, and Crawford, 2004; Salmon et al., 2008) have suggested
that high levels of female competition, as well as perceived low levels of social support,
may increase dieting behavior, as both may be indications that the conditions for
reproduction are not as good as they might be in future. Mealey (2000) took the RSH in a
slightly different direction, arguing that modern anorexia is the consequence of intrasexual
competition, a manipulative strategy in which dominant females suppress the reproduction
of subordinate females (hijacking the existing mechanism for reproductive control). The
majority, over 95%, of eating disorders are found in women, which should not be
surprising from an evolutionary perspective as reproduction is more closely linked to body
fat in women than in men.
Other evolutionary minded approaches have included the AFFH, or adapted to flee
famine hypothesis (Guisinger, 2003), which suggests that anorexia’s characteristic
restriction of food, denial of weight loss, and hyperactivity are evolved mechanisms that
would have aided nomadic foragers in leaving depleted environments. In this model,
genetic susceptibility is also raised as the reason some people are more likely to develop
anorexia. Another recent study (Li, Smith, Griskevicius, Cason, and Bryan, 2009; cited
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with permission) looked at the relationship between intrasexual competition (in the form of
exposure to high status and competitive same sex individuals) and unhealthy eating in
heterosexual and homosexual individuals. They found exposure to cues of intrasexual
competition resulted in unhealthy attitudes and body image in women but not men and that
for homosexuals, only the men were negatively influenced in terms of attitudes and body
image by such exposure. The lesbian participants were not impacted. This study
emphasizes the role intrasexual competition may be playing in the development of eating
disorders, in particular cues of high status competitors.
Faer, Hendriks, Abed, and Figueredo (2005) studied the relationship between eating
disorders and female intrasexual competitiveness, predicting that female intrasexual
competitiveness for mates would be the strongest predictor of bulimia (BN), and that, in
contrast, female intrasexual competitiveness for status would be the strongest predictor of
anorexia (AN). The resulting structural equations model demonstrated that intrasexual
competitiveness for mates was the driving factor that ultimately contributed to female
competitiveness for status, general competitiveness, perfectionism, body dissatisfaction,
drive for thinness, and both bulimia and anorexia. Contrary to initial expectations, the
results indicated a mostly spurious causal relationship between female competitiveness for
status and anorexia, with the only indirect causal effect being through the influence of
Perfectionism, which was uniquely on anorexia and not on bulimia. The role of perceived
personal and ideal partner mate value was also explored. Although strongly positively
related to each other, perceived personal and ideal partner mate value had nearly equal and
opposite effects on body dissatisfaction.
Abed, Mehta, Figueredo, Aldridge, Balson, Meyer, and Palmer (2009) recently
performed a constructive replication in the United Kingdom, which included several
measures of reproductive life history strategy. These measures permitted a close
examination of possible evolutionary sources of female intrasexual competitiveness. This
hypothesis was derived from Life History Theory, which is a mid-level theory from
evolutionary biology that describes the allocation of limited bioenergetic and material
resources to the twin goals of survival and reproduction. According to this theory,
resources are first partitioned into somatic effort, invested in the survival of the individual
organism, and reproductive effort, invested in the production of offspring. Reproductive
effort is further partitioned into mating effort, invested in the acquisition and retention of
sexual partner, and parental effort, invested in the survival of existing offspring. A slow
life history strategy (K-selected) is one that emphasizes somatic and parental effort,
whereas a fast life history strategy (r-selected) is one that instead emphasizes reproductive
and mating effort (Bogaert and Rushton, 1989; Figuerdo et al, 2005; Stearns, 1992). Thus,
a slower life history strategy would be inconsistent (and a faster life history strategy would
be consistent) with the increased expenditure of mating effort entailed in heightened levels
of female intrasexual competitiveness (Geary, 2005).
As in the original (Faer et al., 2005) study, the respondents completed the Female
Competitiveness for Mates Scale, the Female Competitiveness for Status Scale, the General
Competitiveness Scale, and the Eating Disorders Inventory. In addition, respondents also
completed the Eating Disorders Examination. All of the measures of life history converged
upon a single common Slow Life History factor, all of the measures of competitiveness
converged upon a single common Intrasexual Competitiveness factor, and both of the
outcome measures converged upon a single Disordered Eating Behavior Factor. As
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predicted by Life History Theory, the Slow Life History factor had a negative (inhibitory)
effect upon the Intrasexual Competitiveness factor. The Intrasexual Competitiveness factor
partially mediated the effect of the Slow Life History factor upon Disordered Eating
Behavior, but Slow Life History had a negative direct effect on Disordered Eating
Behavior, indicating that Slow Life History inhibits Disordered Eating Behavior by an
unmeasured mechanism as well as by the suppression of intrasexually competitive behavior
for mates or for status.
The purpose of the present study is to identify one possible neuropsychological
mechanism for this inhibitory effect. Executive functions include the abilities entailed in
planning for the future, inhibiting or delaying responding, initiating behavior, and shifting
between activities flexibly. The ability to set goals, plan, sequence, prioritize, organize,
initiate, inhibit, pace, shift, monitor, control, and complete actions all involve executive
functions (Lezak, Howieson, and Loring, 2004).
We therefore hypothesized that enhanced Executive Functions, and more
specifically Behavioral Regulation (Self-Control), would mediate the effects of Slow Life
History Strategy on female intrasexually competitive behavior and on disordered eating
behavior. However, we were uncertain as to whether the enhanced Executive Functions
possessed by slower life history strategists would serve to reduce disordered eating
behavior indirectly by inhibiting the heightened intrasexually competitive behavior for
mates and for status that has been associated with it in previous research, or whether
enhanced Executive Functions would directly inhibit disordered eating behaviors as well as
intrasexually competitive behavior for mates and for status. Thus, based on the results of
the Abed, Mehta, Figueredo, Aldridge, Balson, Meyer, and Palmer (2009) study, we also
tested the possibility that enhanced Executive Functions would also have a direct effect
upon disordered eating behavior that was not mediated by inhibited intrasexually
competitive behavior either for mates or for status.
Materials and Methods
Participants
Participants included one hundred female undergraduate students who received
course credit in return for completing the questionnaires. Their mean age was 18.8 years
(range 18-47). Ninety-five percent were heterosexual, while 92% were single, 6% living
together, and 2% were married. Eighty-six percent came from middle or upper middle class
backgrounds, while 6% came from high income families and 9% came from lower income
family backgrounds. In addition, the mean age at which they reached menarche was 12.6
years (range 5-16).
Procedures
Respondents completed a packet of questionnaires consisting of the Arizona Life
History Battery (ALHB), a modified version of the Eating Disorders Inventory (EDI-2), the
Behavioral Regulation scales from the Behavior Rating Inventory of Executive Function
(BRIEF-A), and two measures of Female Intrasexual Competitiveness: the Female
Intrasexual Competitiveness for Status Scale and the Female Intrasexual Competitiveness
for Mates Scale.
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Measures
The Arizona Life History Battery (ALHB; Figueredo, 2007; Gladden, Figueredo, and
Jacobs, 2009) is a battery of cognitive and behavioral indicators of life history strategy
compiled and adapted from various original sources. These self-report psychometric
indicators measure graded individual differences along various complementary facets of a
coherent and coordinated life history strategy, as specified by Life History Theory, and
converge upon a single multivariate latent construct. They are scored directionally to
indicate a “slow” (K-selected) life history strategy on the “fast-slow” (r-K) continuum. The
Cronbach’s alphas for these subscales were .63 for the Mini-K Short Form, .83 for Insight,
Planning, and Control, .76 for Mother/Father Relationship Quality, .88 for Family Social
Contact and Support, .85 for Friends Social Contact and Support, .90 for Secure Romantic
Partner Attachment, .87 for General Altruism, and .96 for Religiosity.
The Eating Disorders Inventory (EDI-2; Garner, 1991) includes 11 subscales
measuring several different aspects of disordered eating behavior, and was expanded to
include a twelfth subscale with seven items specific to Anorexia (restriction of eating
behavior) taken from the Oral Control subscale of the Eating Attitudes Test (EAT)
developed by Garner and Garfinkel (1979), as had been done in a previous study (Faer et
al., 2005). The Cronbach’s alphas for these subscales were .92 for Drive for Thinness, .75
for Bulimia, .74 for Body Dissatisfaction, .91 for Ineffectiveness, .79 for Perfectionism, .81
for Interpersonal Distrust, .80 for Interoceptive Awareness, .82 for Maturity Fears, .61 for
Asceticism, .77 for Impulse Regulation, .75 for Social Insecurity, and .60 for Anorexia.
The Female Intrasexual Competitiveness Scales (Faer et al., 2005) distinguished
between intrasexual competitiveness for mates and intrasexual competitiveness for status.
These two scales each contained several third-person vignettes, which consisted of
questions in which participants read a situation and rated the behavior of the fictional
character named Mary. Both measures contained statements requiring participants to rate
their level of endorsement on 7-point Likert scales of the behavior of the hypothetical
protagonist (“Mary”) on how likely, how appropriate, and how understandable her behavior
was for each of the given scenarios. In the previous (Faer et al., 2005; Abed et al., 2009)
studies, only a single rating was taken on a 6-point Likert scale from “Completely
Inappropriate” to “Completely Appropriate”, but the present study expanded upon that
procedure to enhance the density of measurement. The Cronbach’s alphas for these scales
were .70 for Female Intrasexual Competitiveness for Mates and .69 for Female Intrasexual
Competitiveness for Status.
The Behavioral Regulation Scales of the Behavior Rating Inventory of Executive
Function - Adult version (BRIEF-A; Gioia, Isquith, Retzlaff, and Espy, 2002) were used to
measure Executive Functions. This portion of the BRIEF-A is a 30-item self-report
instrument of adult executive functions or self-regulation in everyday environments that
assess Inhibition (e.g., “I tap my fingers or bounce my legs”), Set Shifting (e.g., “I have
trouble changing from one activity or task to another”) and Emotional control (e.g., “I
overreact emotionally”). The Cronbach’s alpha for this scale was .94.
Balanced Inventory of Desirable Responding (BIDR-6; Paulhus, 1991) is a 40-item
measure that includes two subscales commonly used to statistically control for socially
desirable responding: Self-deceptive Enhancement (e.g., “I am fully in control of my own
fate”) and Impression Management (e.g., “I never swear”). The Cronbach’s alphas for the
two scales were 0.54 for Self-deceptive Enhancement and 0.75 for Impression
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Management.
Statistical Analyses
All univariate and multivariate analyses were performed using SAS 9.1. Because it
was not possible to analyze all of the individual subscales within a single multivariate
model simultaneously due to the limitations of our sample size, a hierarchical analytical
strategy was employed. Unit-weighted common factor scores (Gorsuch, 1983) were
estimated, using SAS PROC STANDARD and DATA, as the means of the standardized
scores for all non-missing subscales on each factor (Figueredo, McKnight, McKnight, and
Sidani, 2000).
Also computed were both the Cronbach’s alphas and the covariance matrices of the
subscales using SAS PROC CORR. The loadings (scale-factor correlations) of the unitweighted factors on the subscales are presented in Tables 1 and 2.
Table 1. The Arizona Life History Battery.
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Subscales
Slow LH Factor
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Mini-K
.80*
Insight, Planning, Control
.51*
Parent Relationship Quality
.57*
Family Contact/Support
.67*
Friends Contact/Support
.48*
Partner Attachment
.25*
General Altruism
.60*
Religiosity
.55*
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*p < 0.05
All the unit-weighted factor scales were entered as manifest variables for
multivariate causal analysis within a single structural equation model. Structural equation
modeling was performed by SAS PROC CALIS. Structural equation modeling between
these constructs then provided a multivariate causal analysis of the structural relations
between them. Structural equations models were evaluated by use of chi-square, the
Bentler-Bonett Normed Fit Index (NFI), the Bentler-Bonett Comparative Fit Index (CFI),
and the Root Mean Squared Error of Approximation (RMSEA). Index values of the NFI and
CFI greater than 0.90 are considered satisfactory levels of practical goodness-of-fit (Bentler
and Bonett, 1980; Bentler, 1995), whereas RMSEA values of 0.05 or less are considered
indications of good fit, values between 0.08 and 0.10 are considered indications of a
mediocre fit, and values greater than 0.10 are considered indications of a poor fit (Steiger
and Lind, 1980; Browne and Cudeck, 1993). The CFI was selected because it is adjusted
for model parsimony and performs well with moderate to small sample sizes (N < 250),
especially with Maximum Likelihood estimation (Bentler, 1990; Hu and Bentler, 1995).
Alternative fit indices, such as the Bentler-Bonett Non-Normed Fit Index (NNFI), provide
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poor estimates of model fit with smaller samples (Hu and Bentler, 1995).
Prior to these structural analyses, all the variables were residualized on both SelfDeceptive Enhancement and Impression Management to statistically control for any
socially desirable responding.
Table 2. The Eating Disorders Inventory.
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Subscales
Disordered Eating Behaviors
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Drive for Thinness
.72*
Bulimia
.63*
Body Dissatisfaction
.65*
Ineffectiveness
.87*
Perfectionism
.48*
Interpersonal Distrust
.60*
Interoceptive Awareness
.77*
Maturity Fears
.53*
Asceticism
.73*
Impulse Regulation
.64*
Social Insecurity
.74*
Anorexia
.59*
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*p < 0.05
Statistical Power
A sample size of N = 100 is considered a “small” sample for the purposes of
structural equations modeling. However, the absolute size of the sample must also be
considered in terms of the relative complexity or parsimony of the model. Bentler (1995)
has recommended a ratio of at least five cases for every structural parameter freely
estimated in confirmatory models. A sample size of N = 100 could therefore in principle
support k = 20 parameter estimates according to this ratio. Both alternative models tested
with the present data, however, only contained 4 structural path coefficients to be
estimated.
Because a structural equation model is ultimately no more than a system of crosslinked multiple regressions, another approach to estimating the statistical power available
for a given sample size is to estimate the power available to test the significance of the
model parameters that were omitted in the restricted structural models. In the case of the
present data, the most complex regression one could specify within a fully saturated model
would contain four predictors of disordered eating behaviors: Slow Life History, Executive
Functions, Competition for Mates, and Competition for Status. Using G*Power (Erdfelder,
Faul, and Buchner, 1996), we estimated the post hoc statistical power to detect a
“moderate” increment in the squared multiple correlation (f2 = 0.15) of a prediction
equation using 100 cases, 4 predictors, and α = 0.05. The results were a non-centrality
parameter (λ) of 15.00, a critical F-ratio of 3.94, and a power (1 - β) of 0.97. We therefore
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concluded that we indeed had sufficient statistical power to detect any additional effects of
“moderate” magnitude (f2 = 0.15) that had not been specified in either of the alternative
restricted structural equation models. Thus, rather than estimate the power available to
reject an entire alternative model, which we clearly had because we in fact rejected one of
them, we applied and we satisfied the more stringent criterion of whether we would have
had sufficient statistical power to detect any of the effects that were omitted in either or
both of our restricted structural models.
Results
Descriptive Statistics
Garner, Olmstead, and Polivy (1983) claim that the presence or absence of bulimia
differentiates subtypes of anorexia. These two subtypes are termed “restricters” and “bingeeating/purging” by DSM-IV (1994). In the EDI-2 Professional Manual (Garner, 1991),
means are reported for each EDI subscale for “anorexic” females versus “comparison”
group females (university students without a diagnosed ED). In comparing EDI subscale
means from the EDI manual with EDI means from the present sample, the approximate
location of the present sample on the eating disorder continuum can be examined. The
present sample scored lower than the clinical anorexic group on all subscales, except for
bulimia, which was higher in our sample than for the clinical anorexic restricting sample
and the college non-anorexic comparison group(AN diagnosed: M = 1.8, SD = 3.5,
comparison: M = 1.2, SD = 1.9, present sample: M = 2.2, SD = 0.7). The present sample
had lower mean scores than the clinical sample and higher mean scores than the
“comparison non-anorexic” group on Ineffectiveness (AN diagnosed: M =11.4, SD = 8.4,
comparison: M = 2.3, SD = 3.6, present sample: M = 2.5, SD = 0.8), Interpersonal Distrust
(AN diagnosed: M = 6.9, SD = 5.3, comparison: M = 2.0, SD = 3.1, present sample: M =
2.6, SD = 0.7), and Maturity Fears (AN diagnosed: M = 4.8, SD= 5.1, comparison: M =
2.7, SD = 2.9, present sample: M = 3.0, SD = 0.8).
A frequency analysis was also conducted to see how many women in the present
sample exceeded the cut off for clinical screening purposes suggested by Garner. For the
present sample, no women exceeded a score of 14 on Drive for Thinness, or a score of 11
on Bulimia, or a score of 14 on Body Dissatisfaction.
From a combination of these descriptive analyses, we may conclude the following.
First, although some of our sample means were higher than the “comparison” group means,
overall they were closer to the “comparison” group means than to the means of women
who had been specifically diagnosed as “anorexic.” This is reasonable because our sample
was composed of university students who had not been screened for either presence or
absence of anorexia. On the other hand, our sample did contain a small proportion of
women who had scores on subscales that were greater than the means of the women
diagnosed with “anorexia”, whether they were restricters or bulimics, in these previous
studies.
Structural Equation Models
In both alternative structural models, we hypothesized that enhanced Executive
Functions, and more specifically Behavioral Regulation (Self-Control), would mediate the
effects of Slow Life History Strategy on female intrasexually competitive behavior and on
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disordered eating behavior. However, in Alternative Model 1, the enhanced Executive
Functions possessed by slower life history strategists were hypothesized to reduce
disordered eating behavior indirectly by inhibiting the heightened intrasexually competitive
behavior for mates and for status. In Alternative Model 2, the enhanced Executive
Functions possessed by slower life history strategists were hypothesized to directly inhibit
disordered eating behaviors as well as to directly inhibit intrasexually competitive behavior
for mates and for status.
Alternative Model 1 was rejectable by all statistical and practical indicators of
goodness-of-fit (X2(6) = 15.795, p = 0.0149, CFI = 0.853, RMSEA = 0.1291). These results
are displayed graphically in Figure 1.
Figure 1. Alternative Structural Equations Model 1 (see text for details).
Slow Life
History
(ALHB)
.23*
Executive
Functions
-.24*
Competition
for Mates
.62*
Competition
for Status
.11ns
Eating
Disorders
The standardized path coefficients for Alternative Model 1 were as follows: (1)
Slow Life History Strategy predicted higher Executive Functions (β = 0.23, t = 2.38, p <
0.05); (2) Higher Executive Functions predicted lower Intrasexual Competitiveness for
Mates (β = -.24, t = -2.46, p < 0.05); (3) Higher Intrasexual Competitiveness for Mates
predicted higher Intrasexual Competitiveness for Status (β = 0.62, t = 7.89, p < 0.05); and
(4) Higher Intrasexual Competitiveness for Status failed to significantly predict lower
Disordered Eating Behaviors (β = 0.11, t = 1.14, p > 0.05).
In contrast, Alternative Model 2 was acceptable by all statistical and practical
indicators of goodness-of-fit (X2(6) = 4.205, p = 0.6490, CFI = 1.000, RMSEA = 0.0000).
These results are displayed graphically in Figure 2.
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Figure 2. Alternative Structural Equations Model 2 (see text for details).
Slow Life
History
(ALHB)
.23*
-.35*
Executive
Eating
Disorders
Functions
-.24*
Competition
for Mates
.62*
Competition
for Status
The standardized path coefficients for Alternative Model 2 were as follows: (1)
Slow Life History Strategy predicted higher Executive Functions (β = 0.23, t = 2.38, p <
0.05); (2) Higher Executive Functions predicted lower Intrasexual Competitiveness for
Mates (β = -0.24, t = -2.46, p < 0.05); (3) Higher Intrasexual Competitiveness for Mates
predicted higher Intrasexual Competitiveness for Status (β = 0.62, t = 7.89, p < 0.05); and
(4) Higher Executive Functions predicted lower Disordered Eating Behaviors (β = -0.35, t
= -3.71, p < 0.05).
We therefore accepted Alternative Model 2 as superior to Alternative Model 1 by
all criteria applied.
Discussion
As predicted, Executive Functions completely mediated the relation between Slow
Life History and Disordered Eating Behaviors. The relation between Intrasexual
Competitiveness (competitiveness for mates and competitiveness for status) and the
Disordered Eating Behaviors, however, was completely spurious. This means that although
Executive Functions indeed served to inhibit both Intrasexual Competitiveness and
Disordered Eating Behaviors, the inhibition of Disordered Eating Behaviors was not even
partially mediated by Intrasexual Competitiveness, as it had been represented to be in
previous studies. The data were most consistent with Executive Functions serving as a
common cause underlying the inhibition of both Disordered Eating Behaviors and
Intrasexual Competitiveness.
These data patterns suggest that the function of a Slow Life History strategy in
protecting against Disordered Eating Behaviors resides in the higher degree of Behavioral
Regulation exhibited by individuals with a Slow Life History Strategy. Enhanced
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Behavioral Regulation, or self-control, is also protective against escalated levels of
intrasexual competitiveness. Previous work, looking at both intrasexual competitiveness for
mates and intrasexual competitiveness for status, has suggested that some women may be
more vulnerable to the pressures of intrasexual competition than others and indicated that
this increased vulnerability might pose a health hazard (Salmon et al., 2008; Li et al., 2009;
cited with permission), whether or not it is directly causal to disordered eating behavior.
For example, subjects who rated low in susceptibility were less affected by the stressful
scenarios in this study than subjects who rated high in susceptibility (Salmon et al., 2008).
Because some women were more vulnerable to cues of intrasexual competition, a clearer
understanding of why they are more susceptible may point the way toward developing
more effective prevention and intervention methods for those at risk. Salmon et al.
suggested that the factors that might play a role in the development of susceptibility,
deserving of further examination, included rearing environment, sexual experience, and
social support. It may be that, in addition to these, slow life history strategy, or more
specifically enhanced executive functioning, is another major factor influencing such
susceptibility to intrasexually competitive pressures.
In the past, there has been a great deal of emphasis in non-evolutionary explanations
of eating disorders on the role of rearing environment in the development of disordered
eating behavior. In particular, the focus has been on the impact of mother-daughter
relationships on the development of eating disorders in young women (Ogden and Steward,
2000). This relationship might facilitate the development of anorexic behavior if the
mother’s perceptions of female competition or other stressors is exacerbated (through the
media or other sources) and then communicated, perhaps through overprotection, to a
daughter. In the absence of high executive function, this might result in a greater likelihood
of developing eating disordered behavior. More research needs to be done in this area to
clarify exactly how this relationship can contribute (in a positive or negative way) to the
susceptibility of young women to eating disorders.
A majority of the sociocultural approaches to eating disorders have focused on the
internalization of a thin standard of beauty and the role the media plays in fostering this.
And while body dissatisfaction is surely increased by heavy exposure to individuals with
ideal bodies such approaches fail to explain why eating disorders are not significantly more
prevalent clinically than they appear to be. Current prevalence estimates of anorexia and
bulimia among young females are 0.3% and 1% respectively with little change over the
past twenty years (Hoek, 2006). Our theory, which suggests that executive function
(specifically behavioral regulation) mediates the effects of slow life history strategy on
disordered eating behavior, accounts for such a pattern. High levels of executive
functioning serve to buffer young women against the impact of intrasexual competition
while at the same time slow life history tends to suppress the intrasexually competitive
behavior itself. The women who will be most at risk of developing an eating disorder will
be those who have lower executive function and who experience environments with more
abundant cues of intrasexual competition.
Thus, our results are somewhat counterintuitive in the context of the common
conception that eating disorders are pathologies of excessive self-control rather than the
result of deficient behavioral regulation. It might be that disordered eating behaviors
represent extreme attempts to control tendencies towards overeating when the mechanisms
of moderation used by normal individuals are perceived to be failing. This might be
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analogous to the plight of alcoholics. Most non-alcoholics are able to drink moderately and
avoid the pathological consequences associated with drinking to excess. In fact, many
studies have revealed that moderate intake of alcohol may instead have some salubrious
effects. Alcoholics, on the other hand, are apparently unable to drink moderately and must
instead abstain altogether or risk losing control and drinking to excess.
By analogy, individuals with disordered eating behaviors might be unable to eat in
moderation due to insufficient competencies in behavioral regulation, as in the cyclical
binging of bulimics, who rely on purging afterwards to control their weight. Anorexics
instead restrict their food intake to unhealthy and even life-threatening levels, possibly as a
paradoxical overreaction to tendencies towards overeating. These adverse health
consequences may be seen as unintended side-effects of these alternative weight-control
strategies in girls who perceive themselves to be under high degrees of competitive
pressure from other girls. Although the reproductive suppression hypothesis considers
amenorrhea and infertility as the ultimate function of anorexic behavior, the present results
indicate that they might also represent unintended and fitness-reducing consequences of
disordered eating behavior. The present results indirectly associate disordered eating
behaviors with faster life history strategies, instead of the slower ones that might be
expected to correlate with adaptive reproductive suppression. The present results are
therefore inconsistent with the reproductive suppression hypothesis, because sacrificing
present reproduction in favor of potential future reproduction is a tactic more aligned with
slow life history strategy (Ellis, Figueredo, Brumbach, and Schlomer, 2009).
Limitations of the Study
We recognize that the major limitation of this study is the reliance on data collected
from a non-clinical population with an average age of 18.8. The lack of clinically
diagnosed bulimics and anorexics probably accounted for the relatively small effect sizes
found in this study. Presumably, the effect sizes would be much larger with more severe
cases than with a non-clinical population. In addition, childhood and adult onset eating
disorders cannot be examined in this study due to the restricted participant age range. We
only had the power to detect effects of moderate magnitude. Our findings, therefore, await
replication in future studies using clinical populations of anorexics and bulimics with a
more diverse age range.
Conclusion
Our results indicate that a slow life-history strategy is indicative of greater
executive function, which indicates enhanced self control and manifests as increased
behavioral regulation, serving as a protective factor against both escalated female
intrasexual competitiveness and the development of disordered eating behaviors.
Received 27 July 2009; Revision submitted 13 October 2009; Accepted 13 November
2009
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