8 Eating Disorders from the Perspective of Evolutionary Psychology – Meghan Dietrich

Disordered eating is a mysterious phenomenon from the perspective of evolutionary psychology, as it seems to work directly against the core evolutionary inclinations for humans to survive and to reproduce. Extreme patterns of disordered eating behaviors (DEB) are called eating disorders, which are more broadly regarded as mental disorders. Mental disorders may be regarded in evolutionary psychology as the improper functioning of evolved psychological mechanisms in such a manner that is harmful to the individual and/or others (Kardum et al., 2008). The three most researched eating disorders currently are anorexia nervosa, bulimia nervosa, and binge eating disorder. In this paper, the primary focus will be on anorexia and bulimia. These eating disorders are both significantly more prevalent in females than in males, they are marked by an unhealthy drive for thinness, and they are also significantly more prevalent in industrialized nations (Kardum et al., 2008). A good way to begin to understand the adapted evolutionary mechanisms behind eating disorders is to attempt to answer the questions of why these patterns exist. Many studies have been done on this topic that have led to multiple theories regarding the evolutionary explanations for disordered eating patterns and full-blown eating disorders, some of which will be explored in this paper. Reproductive suppression hypothesis will be briefly discussed as an important evolutionary theory of eating disorders. Sexual competition hypothesis will be discussed more in depth, since it currently is the most supported by research and boasts the most literature, and critiques, analyses, and future direction will be discussed.

The reproductive suppression hypothesis (RSH) posits that ancestral women developed a mechanism to alter their reproductive effort in response to harsh or undesirable environmental conditions by either shedding just a few pounds (about five to ten) or slowing their rate of weight gain during puberty. From this perspective, unnecessary and excessive restricting of food, as seen in anorexia, is seen as the result of the modern human environment triggering a disproportionately large response from the activation of the reproductive suppression mechanism in women (Salmon et. al, 2008). In this way, women can put off reproducing until the environment is more desirable by ridding their bodies of the fat necessary to do so; this is considered an unconscious strategy (Nettersheim et al., 2018). However, a critique of this theory is that it offers no explanation as to why body dissatisfaction, particularly a drive for thinness, as well as hyperactivity are key factors of modern eating disorders, nor their prevalence in industrialized cultures, or why less drastic measures are not taken (Kardum et al., 2008).

The sexual competition hypothesis (SCH) is an even more popular theory of eating disorders that fills some of the gaps left by RSH. According to SCH, the significant prevalence of eating disorders in women specifically, along with their notable drive for thinness, is caused by intense female intrasexual competition (ISC) (Abed et al., 2012; Faer et al., 2005; Nettersheim et al., 2018). Due to intrasexual selection, the mate preferences of the opposite sex determine a sex’s path of evolution, since those who do not possess the desired qualities of the opposite sex are less likely to acquire a mate and to reproduce than are those who do possess those qualities. In the case of the evolved preferences of males for female mates, there are significant preferences for youth and for physical attractiveness, as these have both historically been indicators of high reproductive value in females (Buss, 2019). Thus, intrasexual competition for mates consists of conforming to the mate preferences of the opposite sex, which leads women to place much more emphasis on their physical appearance than men do on theirs. SCH posits that female ISC has intensified in modern industrialized countries and westernized societies due to the increased ease at which older women of lower reproductive value can create a falsely youthful, sexually desirable appearance, as well as the increasing independence of women, increasing frequency of attractive women per capita, increasing portrayal of nubile women in the media, and the ease of access to nourishment in the general population. These factors lead to female ISC manifesting itself largely as a heavy emphasis on thinness (Faer et al., 2005; Abed et al., 2012). In societies where malnutrition is the norm, higher weight may indicate higher reproductive value, rather than the lower weight that people in nourished societies value, which has been partially proven by the fact that hunter-gatherer societies report a waist-to-hip ratio (WHR) that goes beyond the Western ideal WHR (Faer et al, 2005). Low WHR has evolved as a male preference due to its linkage to female fertility (Buss, 2019). This offers some evidence that ISC impacts DEB.

Life History Theory (LHT) is often used to explain why some women suffer with DEB or formal eating disorders, while others do not. LHT suggests that an organism’s resources are first invested into somatic effort (survival of the individual organism) and reproductive effort (production of offspring). Reproductive effort can further be divided into mating effort (finding, acquiring, and maintaining a sexual partner) and parental effort (investing resources into preexistent offspring). A slow life history strategy (SLH) is one that is focused on somatic and parental efforts, whereas a fast life history strategy (FLH) is one that is focused on reproductive and mating efforts (Abed et al., 2012; Nettersheim et al., 2018; Salmon et al., 2009). There have been many different hypotheses of how LHT correlates and interacts with ISC and DEB, and many studies have explored this relationship, some of which will be explored here.

A study conducted by Abed et. al in 2012 aimed to confirm whether or not ISC impacts DEB (as found by Faer et al., 2005), and to identify the extent to which life history strategy predicts female ISC, DEB, or both. Their findings matched those of the Faer et al. (2005) study, showing ISC as influencing DEB, thus supporting the SCH. In addition to confirming these original findings, Abed et al. uncovered a relationship between FLH strategy and DEB, indicating that those who pursue a FLH strategy are more likely to engage in DEB, and thus more likely to develop eating disorders (although this study was done in a nonclinical setting). SLH was instead found to have an inhibitory effect on DEB directly, as well as a separate and inhibitory effect on ISC, which only played a partial role in mediating the effect of slow life history on DEB. These findings leave an incomplete view of the mechanisms involved in mediating the effects of SLH on DEB, which urges research on what possible unidentified mechanisms may play roles in this relationship crucial to the SCH (Abed et al, 2012). Another study conducted by Salmon et al. in 2009 aimed to identify one such unknown mechanism, and they hypothesized it to be executive function, specifically in the form of behavioral regulation (self control). They tested the role of executive function as an indirect mechanism of lowering DEB by directly lowering ISC effects in a SLH strategy. Salmon et al. (2009) also tested a second model with executive function as a direct mechanism of inhibiting DEB, as well as directly (and separately) inhibiting ISC. To test the two alternative models, the researchers gathered self-report data from 100 female undergraduate students who completed a packet of five questionnaires directed at measuring life history strategies, DEB, behavioral regulation levels, ISC for mates, and ISC for status. Salmon et al. (2009) rejected Alternative Model 1 and accepted Alternative Model 2. The researchers detail the standardized path coefficients for Alternative Model 1 in four steps: (1) slow life history strategy predicted higher executive functions (p < 0.05); (2) higher executive functions predicted lower intrasexual competitiveness for mates (p < 0.05); (3) higher intrasexual competitiveness for mates predicted higher intrasexual competitiveness for status (p < 0.05); (4) higher intrasexual competitiveness for status failed to significantly predict lower DEB (p > 0.05). Alternative Model 2 maintains the same findings for steps 1-3, but differs on step 4, which found that higher executive functions directly lowered DEB (p < 0.05). Identifying this previously unmeasured mechanism in the research of mechanistic causes for DEB, as well as identifying its direct rather than indirect impact on the slow life history strategy which inhibits DEB, are two major strengths of this study. The results of this study may have larger implications on SCH, since executive function seems to operate against DEB through SLH far more powerfully than it does through ISC in this study, which is not a factor that has traditionally been considered in SCH. Perhaps the hypothesis should be adjusted to include executive function as an important proximate mechanism by which ISC is an ultimate cause for DEB.

Salmon et al. (2009) speculate that disordered eating behaviors are an individual’s response to natural desires to indulge in food when they perceive an inability in themselves to moderate their food intake. This connects to the findings of other research that have aimed to explain the prevalence of eating disorders in industrialized nations in particular and alludes to a mismatch hypothesis that has been explored by multiple researchers, such as Rantala et al. in 2019. Humans have complex arrays of evolved psychological mechanisms specific to food consumption, as well as mechanisms specific to mating efforts. These mechanisms were not designed for modern environments, where obtaining food takes minimal energy compared to the energy involved in consuming it, which often leads to obesity, since humans are naturally inclined to take complete advantage of any and all food supplies available to them. This mechanism was helpful in environments with scarce access to food, which were the types of environments our ancestors lived in. In addition to this mechanism to nourish, humans have evolved mechanisms to present themselves as having high reproductive value, which, for women, is signaled through physical appearance (as discussed earlier). In this way, cultural human evolution has led to a mismatch between these two major evolved psychological mechanisms, leading an individual to be torn between food rewards and mating rewards (Rantala et al., 2019).

In addition to all of these evolutionary and cultural reasons for DEB and eating disorders, hormones have also been found to be a biological contributor to the development of eating disorders. Bremser & Gallup (2012) refer to the “extreme female brain” when trying to explain the extreme prevalence of eating disorders in females, of which symptoms tend to arise at the start of puberty and fall at the end of puberty. In addition, animal studies have revealed that estrogen has a negative relationship with food intake, but a positive one with physical activity, which relates to the patterns of extreme caloric restriction and hyperactivity associated with eating disorders (particularly anorexia). In addition, the prevalence of autism in men and the uncovered link between testosterone and autism have led to the construction of a model for an extreme male brain that is based in social apathy, which would suggest that an extreme female brain, heavily influenced by estrogen, would be based in social anxiety. Social anxiety is common in those with eating disorders, especially negative evaluation anxiety, which refers to the anxiety surrounding others’ negative judgments of oneself (Bremser & Gallup, 2012).

All current studies and theories of the evolutionary attributions for eating disorders and, more broadly, disordered eating, offer great insight but still leave room for further research to be done in the future. SCH particularly provides great insight into a possible ultimate cause for eating disorders; in evolutionary psychology, ultimate (or functional) causes are results of a trait increasing an organism’s ability to survive or to reproduce (Lundy, 2020). Research for SCH has also attempted to explain proximate causes of eating disorders, which has largely been concluded to be female intrasexual competition, but only partially, with very little consensus on what further proximate causes influence DEB. Proximate (or mechanistic) causes are what drive the specific behaviors of an organism at a certain time; developmental (or ontogenetic) causes explain why one certain individual engaged in a specified behavior in a particular manner (Lundy, 2020). Life history strategies may be considered developmental causes, with a fast life history influencing the presence of DEB.

Therefore, valuable future research should consist of studies aimed to further identify proximate causes of DEB and eating disorders other than ISC, as well as identify the extent to which each proximate cause operates on these food behaviors. The relationship between executive function and ISC should be further explored, since the scarce studies currently examining executive function (particularly self control) as a variable are inconsistent in their conclusions regarding the level of influence this mechanism has. Such a study would be structured similarly to studies reviewed in this paper. Self report surveys aimed at measuring DEB, ISC, and executive function would be distributed to participants, and it may be helpful to include males as well as females, which many past studies have neglected to include. If executive function is observed to impact the ISC behaviors of males as well as females, then the relationship between the two factors may be further supported. ISC measures for males would differ from those of females, since females value different traits in potential male mates, thus creating a different form of ISC for men. In addition, a study of executive function’s influence on DEB without any sort of mediation from ISC should be studied as well, since some studies studying both have found that executive function actually plays a larger role than ISC (which contradicts many other studies of the same topic).

In conclusion, many hypotheses and theories regarding the evolutionary causes for eating disorders in women have recently been explored. While disordered eating behaviors at first seem counterintuitive to the primary evolutionary inclination to survive and reproduce, some researchers have attempted to explain this phenomenon using the reproductive suppression hypothesis, which posits that this sort of behavior would make sense for an ancestral woman trying to inhibit her body’s ability to produce offspring in an unsupportive or otherwise undesirable environment. While possible, this explanation doesn’t offer reasonings for the significant prevalence of such behavior in women, in industrialized societies, and around the time of puberty; sexual competition hypothesis fills in these blanks by attributing these facts to female intrasexual competition, which is driven by a beautiful, youthful physical appearance with a low WHR as preferred by potential male mates. The mismatch between this adaptive mechanism acting in the current industrial climate of easy access to nutritionally dense foods creates stress for modern Western and Westernized women who feel both an instinct to eat a lot of food (also an evolved psychological mechanism) and to be thin to attract mates; in this case, disordered eating is an overcompensatory reaction to the stress of this mismatch. Besides intrasexual competition, differences in executive function also likely affect an individual’s susceptibility to disordered eating behaviors. Life history strategy can be used to explain such susceptibilities. More research is required for there to be total certainty in any of these concepts and to further identify other important mechanisms and evolutionary contributors to the issue of eating disorders.

References

Abed, R., Mehta, S., Figueredo, A. J., Aldridge, S., Balson, H., Meyer, C., & Palmer, R. (2012). Eating disorders and intrasexual competition: Testing an evolutionary hypothesis among young women. The Scientific World Journal, 2012, https://doi.org/10.1100/2012/290813

Bremser, J. A., & Gallup, G. G. (2012). From one extreme to the other: Negative evaluation anxiety and disordered eating as candidates for the extreme female brain. Evolutionary Psychology, 10(3), 457-486.

Buss, D. M. (2019). Evolutionary psychology: The new science of the mind (6th ed.). Routledge.

Faer, L. M., Hendriks, A., Abed, R., and Figueredo, A. J. (2005). The evolutionary psychology of eating disorders: Female competition for mates or for status? Psychology and Psychotherapy: Theory, Research and Practice, 78, 397-417.

Kardum, I., Gračanin, A., & Hudek-Knežević, J. (2008). Evolutionary explanations of eating disorders. Psychological Topics, 17(2), 247-263.

Lundy, D. (2020). Evolutionary psychology: An introduction [PowerPoint slides]. Department of Psychology, Indiana University East.

Nettersheim, J., Gerlach, G., Herpertz, S., Abed, R., Figueredo, A., & Brüne, M. (2018). Evolutionary psychology of eating disorders: An explorative study in patients with anorexia nervosa and bulimia nervosa. Frontiers in Psychology, 9, https://doi.org/10.3389/fpsyg.2018.02122

Rantala, M. J., Luoto, S., Krama, T., & Krams, I. (2019). Eating disorders: An evolutionary psychoneuroimmunological approach. Frontiers in Psychology, 10, https://doi.org/10.3389/fpsyg.2019.02200

Salmon, C., Crawford, C. B., & Walters, S. (2008). Anorexic behavior, female competition, and stress: Developing the female competition stress test. Evolutionary Psychology, 6(1), 96-112. https://journals.sagepub.com/doi/pdf/10.1177/147470490800600112

Salmon, C., Figuerdo, A. J., & Woodburn, L. (2009). Life history strategy and disordered eating behavior. Evolutionary Psychology, 7(4), 585-600. https://journals.sagepub.com/doi/pdf/10.1177/147470490900700408