1. Anorexia nervosa (AN) is just one variant of what is referred to as eating disorders. The other variants do not have anorexia as a major feature but EDs share other common features with each other (see below). AN patients are only a tiny minority of the much larger group of women/girls who show other variants (BN, EDNOS or subclinical ‘pursuit of thinness’). So while it is obviously important to understand the proximate causes of anorexia in AN patients (which is exactly what mainstream research has done but with little return in terms of new insights) this is unlikely to shed much light on the aetiology of EDs in general. It is possible, of course, that AN has a totally separate causation from other EDs but this is an empirical question that can only be answered through evidence.

2. Any explanatory theory for eating disorder must explain at a minimum the following common features: Why females? Why females of reproductive age? Why the particular geographical prevalence (high in western and westernised affluent societies; rare or even unknown in traditional societies) and why the rise in the last 50 years or so.

3. Theories of ultimate (evolutionary) causation of EDs in the current literature include:

a. Reproductive suppression (Voland & Voland, 1989)

b. Reproductive suppression of subordinates (Mealey, 2001)

c. Sexual competition hypothesis (SCH) (Abed, 1998)

d. Life History/Executive Functioning (Salmon et al, 2009)

The first 2 exclusively concern AN whereas the latter 2 are applicable to the whole range of EDs. Ultimate causation factors such are sexual competition, life history strategy and mismatch are not mutually exclusive. (See references below for a full discussion of the Sexual Competition Hypothesis (SCH) most of which are available for download from my researchgate entry). However, this area requires further research and the questions raised regarding the role played by each of these factors/processes should be answered through evidence.

4. A new variant of ED that disproportionately affects men (the drive for muscularity) would be impossible to accommodate within a theory framework that focuses on appetite/hunger/food etc. However, looking at this phenomenon through the prism of intra-sexual competition it is clear that while females compete with other females through the display of signs of youth, men compete with other men through the display of physical dominance and prowess where the display of the size and muscularity of the upper body is an important visual signal.

Looking at the available theoretical formulations evolutionary or otherwise, the only one that can account for all the female variants as well as this new male variant is the sexual competition hypothesis. In other words it’s the most parsimonious explanation of the whole range of eating disorders including this new male variant. I would suggest that the explanatory value of such a hypothesis which gives rise to a range of testable predictions far exceeds the alternatives (reproductive suppression for instance is completely irrelevant to this new male variant as well as all female EDs other than AN).

5. Given that appetite/eating/hunger and the need for nutrients are not sexually dimorphic, it will be difficult to explain the extreme lopsided gender difference in EDs based on a primary disorder in these systems. The solution that the non-evolutionary approach have used is the cultural norm or ideal hypothesis. This is fine but it leaves open the question as to why such a cultural ideal has arisen time and again in diverse western and westernised societies and if it is an arbitrary cultural norm why haven’t we witnessed some western societies that show the opposite sex ratio?

6. EDs here refers to patients who broadly show evidence of the following symptom clusters (extracted from DSM-5):

A. Restriction of energy intake relative to requirements (AN) or Bingeing and purging (BN)

B. Intense fear of gaining weight or of becoming fat,

C. Disturbance in the way in which one’s body weight or shape is experienced,

7. It is important to remember that explanations based on ultimate (evolutionary) causation may not have immediate therapeutic applications but can serve as a guide for further research which can lead to clinical applications.

Selected References for the Sexual Competition Hypothesis:

1. Abed, R. The sexual competition hypothesis for eating disorders. British Journal of Medical Psychology, 1998; 71: 525–547.

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

3. Abed, R., Mehta, S., Figueredo, A. J., Aldridge, S., Balson, H., Meyer, C., & Palmer, R. Eating disorders and intrasexual competition: Testing an evolutionary hypothesis among young women. TheScientificWorldJOURNAL 2012; http://www.tswj.com/2012/290813/

4. Li, N. P., Smith, A. R., Griskevicius, V., Cason, M. J., & Bryan, A. Intrasexual competition and eating restriction in heterosexual and homosexual individuals. Evolution and Human Behavior 2010; 31: 365–372.

First, this might be due to there being few researchers of eating disorders that are trained in evolutionary approaches; thus they are oblivious to considering sexual selection. Also, the few studies of disordered eating that come to mind have not considered patient populations, and have not been published in mental health outlets. As a result it is probably mainly people with special interest in evolutionary perspectives within the field of mental health in general who find a functional or selectionist approach relevant. Which might not be a very unusual state of affairs; apart from attachment (but rarely among contemporary researchers) and the functional understanding of fear that informs anxiety research and therapy few disorders are considered from an evolutionary perspective in mainstream mental health practice or research.

Stevens, A. & Price, J. (1996): Evolutionary Psychiatry; A new beginning. In this book, a brief chapter (9) is devoted to anorexia and bulimia nervosa. The evolutionary perspective is discussed on page 111-114. I haven't read it yet, so cannot summarize it.

Harry Smit (2010). Darwinisme, monisme & ziekte. The book is in Dutch. He also spends a chapter (8, p. 219-240) on Anorexia nervosa. One of the many things he discusses is the adaptive function of temporarily losing the capacity to become pregnant in circumstances of scarcity of food. This capacity is misused by AN patients in times of abundancy of food. However, such a relation between evolution and AN is too indirect to count as an evolutionary clarification, let alone explanation, of AN.

Of course, for all the functions and vulnerabilities of AN and BN that have been suggested by the experts, evolutionary roots can be shown, but this, again, can hardly be called evolutionary explanations of AN and BN. 

1. Anorexia nervosa (AN) is just one variant of what is referred to as eating disorders. The other variants do not have anorexia as a major feature but EDs share other common features with each other (see below). AN patients are only a tiny minority of the much larger group of women/girls who show other variants (BN, EDNOS or subclinical ‘pursuit of thinness’). So while it is obviously important to understand the proximate causes of anorexia in AN patients (which is exactly what mainstream research has done but with little return in terms of new insights) this is unlikely to shed much light on the aetiology of EDs in general. It is possible, of course, that AN has a totally separate causation from other EDs but this is an empirical question that can only be answered through evidence.

2. Any explanatory theory for eating disorder must explain at a minimum the following common features: Why females? Why females of reproductive age? Why the particular geographical prevalence (high in western and westernised affluent societies; rare or even unknown in traditional societies) and why the rise in the last 50 years or so.

3. Theories of ultimate (evolutionary) causation of EDs in the current literature include:

a. Reproductive suppression (Voland & Voland, 1989)

b. Reproductive suppression of subordinates (Mealey, 2001)

c. Sexual competition hypothesis (SCH) (Abed, 1998)

d. Life History/Executive Functioning (Salmon et al, 2009)

The first 2 exclusively concern AN whereas the latter 2 are applicable to the whole range of EDs. Ultimate causation factors such are sexual competition, life history strategy and mismatch are not mutually exclusive. (See references below for a full discussion of the Sexual Competition Hypothesis (SCH) most of which are available for download from my researchgate entry). However, this area requires further research and the questions raised regarding the role played by each of these factors/processes should be answered through evidence.

4. A new variant of ED that disproportionately affects men (the drive for muscularity) would be impossible to accommodate within a theory framework that focuses on appetite/hunger/food etc. However, looking at this phenomenon through the prism of intra-sexual competition it is clear that while females compete with other females through the display of signs of youth, men compete with other men through the display of physical dominance and prowess where the display of the size and muscularity of the upper body is an important visual signal.

Looking at the available theoretical formulations evolutionary or otherwise, the only one that can account for all the female variants as well as this new male variant is the sexual competition hypothesis. In other words it’s the most parsimonious explanation of the whole range of eating disorders including this new male variant. I would suggest that the explanatory value of such a hypothesis which gives rise to a range of testable predictions far exceeds the alternatives (reproductive suppression for instance is completely irrelevant to this new male variant as well as all female EDs other than AN).

5. Given that appetite/eating/hunger and the need for nutrients are not sexually dimorphic, it will be difficult to explain the extreme lopsided gender difference in EDs based on a primary disorder in these systems. The solution that the non-evolutionary approach have used is the cultural norm or ideal hypothesis. This is fine but it leaves open the question as to why such a cultural ideal has arisen time and again in diverse western and westernised societies and if it is an arbitrary cultural norm why haven’t we witnessed some western societies that show the opposite sex ratio?

6. EDs here refers to patients who broadly show evidence of the following symptom clusters (extracted from DSM-5):

A. Restriction of energy intake relative to requirements (AN) or Bingeing and purging (BN)

B. Intense fear of gaining weight or of becoming fat,

C. Disturbance in the way in which one’s body weight or shape is experienced,

7. It is important to remember that explanations based on ultimate (evolutionary) causation may not have immediate therapeutic applications but can serve as a guide for further research which can lead to clinical applications.

Selected References for the Sexual Competition Hypothesis:

1. Abed, R. The sexual competition hypothesis for eating disorders. British Journal of Medical Psychology, 1998; 71: 525–547.

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

3. Abed, R., Mehta, S., Figueredo, A. J., Aldridge, S., Balson, H., Meyer, C., & Palmer, R. Eating disorders and intrasexual competition: Testing an evolutionary hypothesis among young women. TheScientificWorldJOURNAL 2012; http://www.tswj.com/2012/290813/

4. Li, N. P., Smith, A. R., Griskevicius, V., Cason, M. J., & Bryan, A. Intrasexual competition and eating restriction in heterosexual and homosexual individuals. Evolution and Human Behavior 2010; 31: 365–372.

We must be really careful when talking about natural and sexual selection in modern humans. Namely, selection presumes the presence of genes that are favoured (or have a tendency towards elimination) and that are connected with a trait of interest. In eating disorders, there are no specific genes that could be associated with these characters and it is highly probable that the genetic background of these traits is very complex and related, even more directly, with many other psychological characteristics of individuals. And, finally, the influence of social environments on developing such behaviour is extremely large. Even though thin body could be sexually preferable during the last few decades, it was not the case in times before that. Cultural influences on changing preferences are very variable on a long-term scale. Also, in order to talk about effects of sexual or natural selection on any trait, we should calculate the difference in reproductive fitness between individuals with different characters. I am not sure that we would find anything interesting here. Or, we could find that thin figure is attractive, but it lowers down the fecundity. This cannot be, in a Darwinian sense, the trait exposed to evolutionary changes in a way that it could be favoured.

The importance of extrinsic factors (culture) in occurrence of eating disorders could be illustrated by the estimation of heritability parameter for anorexia that is very high (approx. 70%) in modern western populations. On the other hand, 40 or 50 years ago this disorder was completely unknown and there is no way that selection could have any effect on a trait that effectively did not exist. This leads to a conclusion that anorexia is a disorder connected to some other human characteristics and that in novel environmental (sociological, cultural) context these strange results on heritability appeared (genotype by environment interactions).

The Sexual Competition Hypothesis (SCH) for eating disorders is based on two Darwinian processes namely intra-sexual competition and the idea of mismatch where a novel environment uncovers a vulnerability that may not have existed in the environment of evolutionary adaptedness. So there no assumption that eating disorders are adaptive or useful. Therefore, the fact that anorexia nervosa reduces fecundity does not argue against such a formulation. The question is : does the hypothesis make testable predictions and if so it can be supported or refuted by data.

Are slimness and muscularity  in women and men respectively,  taken to a moderate level ,theoretically signs of fitness?  but taken to extreme become dangerous,  a handicap or fitness reducing?. This may be   especially  worrying if  accompanied by drug abuse to  achieve  the states  e.g. amphetamines or laxatives for slimness and  Gamma hydroxyl Butyric acid or Anabolic Steroids to achieve muscular bulk?

(I also recognise non-drug strategies may be harmful too!)

Am I right that Sexual selection components of any evolved trait are nearly always paradoxically fitness and reproduction reducing beyond an optimum as is the case with  peacocks'  tails?

Paul, as to your last question: it seems most likely to me that sexual selection of potentially suboptimal  features (like the peacock tail and the elk or moose antlers) only takes place when the conditions for survival are not very challenging for a prolonged period. If these become more challenging, the sexual appetite of both sexes will probably evolve in the direction of preference for signs of physical fitness again, and the sub-optimal features and traits will gradually disappear. Rhiad can probably give you a more decisive, better informed answer about this issue.

Maybe considering two types of sexual selection is relevant: Intrasexual competition might cause same-sex competition on traits in such a manner that one moves away from the preferences of the opposite sex; and this might manifest in male and female models in magazines for either men or women being either slimmer/curvier or fit/very muscular. NB: sexually selected traits will be selected by increasing reproductive success, not the opposite.

What is adaptive in one environmment (in this case, social environment) may not be so in another. So we can think of the extremes of sexually selected traits in the organism's natural environment which will always be counter-balanced by the effects on survival. Hence, tails that are too large or antlers that are too heavy in the natural environment will be weeded out through reproductive failure. However, they  can survive in the protection of captivity (mismatch). Hence human sexually selected traits when they interact with the 'unnatural' urban environment with ubiquitous media images (and availability of chemicalsand nutrients  that were not available in the EEA) can become dysregulated and no longer be adaptive due to mismatch. The occurence of such dysregulation in the EEA was either extremely rare or non--existant.

Sexual selection is a mode of natural selection where members of one biological sex choose mates of the other sex to mate with (intersexual selection), and compete with members of the same sex for access to members of the opposite sex (intrasexual selection). These two forms of selection mean that some individuals have better reproductive success than others within a population, either from being more attractive or preferring more attractive partners to produce offspring. Darwin conjectured that some heritable traits such as appearances e.g. beards and hairlessness, significant in the geographical differentiation of human appearance, are results of sexual selection. Human styles are clearly influenced by culture and fashion. This may result in activities that taken to extremes result in a distribution of fitness which is decreased at the more extreme values e.g. thinness and excess weight

Much human behaviour is not clearly tied to survival benefits. Abilities that result in music, visual art, verbal creativity, and some forms of altruism, are courtship adaptations that have been favoured through sexual selection. Many human artefacts can be considered subject to sexual selection as part of the extended phenotype, for instance clothing that enhances sexually selected traits. Some argue that the evolution of human intelligence is a sexually selected trait, as it would not confer enough fitness in itself relative to its high maintenance costs.

 For Darwin, the important form of (genetic) variation for evolution is continuous in nature and small in effect. Variations, as Darwin recognized, were of two types. There was what we now know as single autosomal or Mendelian traits. These involved phenotypically large discontinuous variations, and were relatively rare. Secondly there were the less obvious but more pervasive and common minor variations which occurred in every character of the organism. The nature of genetic variation can be thought of both at the individual level (Are most important differences in individuals the result of single genes of large effect or many genes of small effect?) and at the population level (Is the distribution of genetic liability normal or very bumpy with a small proportion of individuals at high risk and the rest at low risk?). Kendler 2015. The phenotypic products of evolution viewed by Darwin may now be considered to be adaptations or by-products, exaptations, spandrels or even just random variation. Not all traits of organisms improve survival or reproduction or “fitness” or are to be considered evolutionary adaptations. Traits may also be exaptations, by-products of adaptations (sometimes called "spandrels"), or random variation between individuals. Some traits are trade-offs, design constraints and mismatches to modem environments. Complex issues like sexual selection and other related forms of signalling also complicate the issues.

Intrasexual selction may lead to increasing physical strength of the males, as it did/does with the sea-elephant, not (anymore) because of female preference but because of getting in a position to monpolize the females in a herd. If so, only endangering of the species as a result of inbreeding is able to reverse this direction in the evolution of this particular species.