What can be gained from an integrative approach towards

various models of Anorexia Nervosa?

1. Introduction

Anorexia Nervosa is one of the more malleable of the

psychiatric disorders and its increase in incidence in

the last sixty years or so has brought with it concerns

of multiple possible causes in sociocultural contexts as

well as physiological ones (Szmukler et al 1995).

Sociocultural models of Anorexia Nervosa are often

concerned with desired body image in Western culture,

particularly as it is associated with fashion and beauty,

as well as changes in gender roles over the twentieth and

twenty first centuries. There have been shifts in broadly

desired and idealized weights in young women over the

past fifty to sixty years, and correspondingly incidents

of anorexia with symptoms such as fear of fatness have

increased, along with the emergence of Bulimia Nervosa in

the last thirty five years (Russell 1995).

Clearly, despite the need to accommodate such a

diverse range of phenomena in the psychological content

of anorexia patients today, in the whole history of

anorexia incidents, and possible future manifestations,

one also needs to maintain some kind of criteria for

diagnosis that can tell a case of anorexia from something

that need not fall under that category, such as

malnutrition in the case of severe poverty, or anaemia,

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for example. The current multiplicity in the recorded

character of Anorexia Nervosa displays a vast array of

differing theories that need not just some kind of

theoretical unity, but theoretical interaction. Sandra

Mitchell defends integrative pluralism in the 2004 paper

‘Why Integrative Pluralism?’. She argues that it is the

‘best description of the relationship of scientific

theories, models, and explanations of complex biological

phenomena’ (pg. 1). Her view is that biological theories

and methods must reflect the complexity of biological

systems; the representations that science deals with when

looking for single causal explanations for certain

phenomena are partial in their nature. She proposes an

integration of ‘models of variant possible contributing

factors … to yield the correct descriptions of the actual

constellation of causes and conditions that brought about

the event to be explained’ (Mitchell 2004).

Kendler (2012) recognizes that many want to move towards

a hard medical model for psychiatric disorder, which

means looking for a clear single level of explanation. He

ultimately opposes this move, arguing that identifying a

cause always responds to the purpose and interests of the

one doing the describing. He proposes two options; either

go for a hard medical model that will require consensus

of preferred explanation involving value judgments as

well as science, or move away from the hard medical

model, and start paying attention to cross level

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mechanisms rather than grounding diagnoses on single

biological mechanisms (Kendler 2012). The latter seems to

more realistically capture the nature of psychiatric

disorders, while the former might have better practical

use.

In the end Kendler argues that we are better off

moving away from the hard medical model for psychiatric

disorders. I want to review some possible explanations of

Anorexia Nervosa (AN) and then review Kendler and

Mitchell’s ideas to find adequate theories of such

phenomena. I will then apply them to AN as a paradigm

case. Psychiatric disorders are always going to be unique

in psychological content for the sufferer over time,

culture, and the individual, making diagnosis something

that needs to have accounted for the diverse array of

possibilities from the past and into the future. AN is a

good example of this because it is still very dubious as

to what causes it and whether a single cause ought to be

sought after.

It seems that an integrative pluralist approach to AN may

be necessary to accommodate the multiplicity of factors

that can lead to the development of AN in any individual.

I think an adequate model must encapsulate all levels of

explanation so as to reflect the process of this disorder

accurately. When it comes to applying such a model into

unique manifestations of AN, there needs to be

interaction between each level of explanation as well as

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a decision based on values and science as to which is the

best and most appropriate level of explanation for that

case. It is only by having a pluralist approach that one

can bracket an accurate theory of AN, and it is only by

integration of each level of explanation that this can

become a coherent model. This also supports Kendler’s

move away from the hard medical model into more complex

models.

2. Physiological Models

2.1 Gastric Physiology

Robinson and McHugh, in their contribution to The Handbook

of Eating Disorders (1995), argue that some of the

physiological features of AN act to ‘sustain the

behaviour of fasting in these conditions’ (pg. 109). They

form a hypothesis about the role of gastric physiology in

AN, particularly with respect to changes that occur in

gastric emptying that could have survival value during

times of natural starvation. One common complaint for

patients with AN is of bloating, stomach discomfort, and

lowered, if any, feelings of hunger. The idea here is

that during times of starvation, gastric emptying slows;

resulting in content staying in the stomach for longer,

which explains enhanced feelings of satiety in

anorectics.

There are possible evolutionary explanations for

this, for example slow gastric emptying might improve the

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efficiency of nutrient absorption when food is in short

supply, reducing metabolic rate during the emergency of

starvation. In this case the stomach might act as the

body’s larder when food is in short supply (1995, pg.

120). General levels of satiety in the organism are then

increased, and in the cases of AN, feelings of fullness

are generally felt much of the time by the sufferer.

After going through refeeding programmes in hospital,

gastric emptying rates generally return to normal,

however the anorectics in this condition still complain

of increased satiety much of the time, suggesting some

kind of misperception of stomach contents, or a sensation

according to expectation, not physiology.

Robinson and McHugh do not give a clear

physiological explanation for this phenomenon, although

it is suggested that there may be some disruption within

receptors of the cholecystokinin (CCK) peptide hormone,

which mediates digestion and satiety (1995). These

sensations of fullness states are also conducive to

conditioned emotional responses, such as feeling

depressed when one is full, leading to further efforts in

dieting. In the end, due to little evidence, Robinson and

McHugh were inconclusive with regard to abnormal CCK

function, such as having a predisposition for slow

gastric emptying or false perceptions of one’s gastric

content, as a causal factor for AN. Given that this

contribution was published close to twenty years ago and

this endeavour has been all but abandoned, it is unlikely

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that this might yield a physiological explanation for AN.

Despite this it is of course a useful section of

knowledge of the disorder in the organism.

2.2 Addiction

Szmukler and Tantam (1984) proposed a different kind of

explanation for a necessary mechanism acting in

conjunction with others in AN. They make it clear that

they do not propose this idea as a full explanation of

the cause of AN. They call AN an addiction to starvation,

analogous to alcohol dependency. They criticize attempts

to place features of AN under other previously

established diagnostic categories, such as depression and

phobias, arguing that there is a constancy of association

in the clinical features of AN. This is an important

point and similar to one side of the concern stipulated

by Gerard Russell (1995) in his essay ‘Anorexia through

Time’; that as much as diagnostic criteria needs to cater

for the differences in AN’s manifestation as a result of

different prevailing sociocultural norms, we also need

some balance in maintaining a diagnostic rectitude.

In the Szmukler/Tantam view, based on clinical

observation, the anorectic’s behaviour, like alcoholism,

is carried out under conscious control and it alters

their physiological and psychological state in a harmful

way (1984). As with the salience of drinking behaviour in

someone who is dependent on alcohol, the authors claim

that anorectics frequently admit to continuous thoughts

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of food (1984, pg. 2). Szmukler and Tantam point to

hedonic mechanisms as having an integral role in anorexic

behaviour, describing self starvation as causing some

kind of pleasurable, if harmful effect on the subject.

There are many other analogies between alcoholism and AN

that they describe, such as tolerance (dieting getting

more and more extreme to achieve the desired ‘hit’) and

it being a behaviour that disrupts the normal functioning

of the person’s life, such as social avoidance (1995).

Where Robinson and McHugh point to physiological changes

in gastric emptying, Szmukler and Tantam’s dependence

hypothesis directs us towards parts of the brain to do

with the experience of pleasure or tension relief. They

suggest that we approach AN as a dependence disorder even

if we don’t totally reduce it to that status. Because of

its reference to the brain, this might appeal to someone

who wants a hard medical model for psychiatry (Kendler

2012); we have a specific causal hypothesis that we can

consider to be a defining feature of the disorder,

perhaps in practice a dependency approach to AN might

prove effective, but it could also prove to be narrow and

it might rule out cases that should be considered

anorexic. Also where they set out to transcend differing

psychological reactions to a single physiological state,

dependency is arguably one choice of cognitive-

behavioural explanation of many others, such as phobia or

obsessive behaviour.

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3. Cognitive-Behavioural Models

Padmal De Silva emphasizes reinforcement as a significant

factor for the development and maintenance of anorexic

behaviour (1995). AN can be described as a learned

behaviour, for example an individual might want to lose

weight and so they go on an excessive diet to lose this

weight. This can be reinforced positively with praise

from one’s peers, on the reverse it can be reinforced

negatively by seeing being overweight as being met with

ridicule or disapproval. Even the attention one gets with

concern from friends and family after excessive dieting

can reinforce this behaviour, the individual might

actually get pleasure from this, claims De Silva (1995).

He criticizes other behavioural theories, including

Szmukler and Tantam’s, saying that they don’t account for

the possible origins of the problem, which can be related to

various different prior conditions, such as family

conflicts, social pressure, loss of control, and many

more (1995).

What is crucial to understanding AN, says De Silva,

is the antecedent triggering factors. He gives further

behavioural explanation, citing Slade’s (1982) theory of

the conditions and predisposing factors for AN. For

example, problems in the family combined with

interpersonal problems can lead to a state of

dissatisfaction with oneself and others. This, combined

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with a predisposition for perfectionist tendencies might

lead the person to need some control and success in one

area of her life. Control of one’s own body is the

perfect candidate for this. The comments of friends and

peers are then the triggers for dieting behaviour which

becomes maintained and intensified by reinforcement

(1995, pg. 144).

This brings our attention to a central puzzling feature

of AN. It seems paradoxical to consider anorexic

behaviour to involve a calculated and controlled

regulation of food intake and also to be a mental

disorder, which insinuates a certain loss of control for the

person with respect to the associated behaviour. To avoid

positing it as behaviour according to the free will of

the person, a delusional pathology might be considered.

Another possibility is that despite AN being caused by an

attempt to gain control by the person, it is maintained by

either physiological changes, such as delayed gastric

emptying, or perhaps distorted cognitions of body weight

and image, coinciding with other reinforcements that are,

to some extent, beyond the person’s control.

Perhaps, despite AN developing according to

controlled behaviour, there is a point at which the

person loses some degree of wilful control to her

choices. Therefore different stages might be

distinguished in the development of AN. If these

distinctions can be made then perhaps multiple levels of

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explanation can account for different stages in the

development of AN as well as the diverse possibilities

for its manifestation. For example sociocultural theories

might better explain predisposing factors for developing

AN while physiological or cognitive theories might be of

better use for stages when the condition has become more

severe in individuals.

4. Different Levels of Explanation for Distinct Stages of Development?

The main idea of the cognition behind anorexic behaviour

refers to distorted ideas about body weight. Other

features can then be understood in terms of this. The

person suffering from AN has distorted and dysfunctional

cognitions such as selective abstraction (getting a

better sense of control from not eating), extreme and

dichotomous thinking, overgeneralizing meaning from

specific events into rules over other ones, and

interpreting things in a self centred way (De Silva

1995). These maladaptive thought patterns play a crucial

role in determining the behaviour of the anorectic,

claims De Silva, and the complex of anorexic beliefs

become more autonomous leading to further isolation

exposing the subject to more of these dysfunctional

thoughts (1995).

It appears that a cognitive behavioural model has to

appeal to distinct stages of development in AN. De Silva

wants to view all features of AN in terms of what he

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considers to be crucial aspects, like reinforcement and

distorted cognitions. However, the predisposing features

of the person and the types of situations and life events

that would reliably lead to the development of AN might

sometimes be better viewed in terms of other

explanations, like sociocultural ones for example.

Viewing all of the features of anorexia in terms of

distorted cognitions of body weight will not encapsulate

the full extent to which it can vary. For example there

will be differences in socialization processes that may

affect the severity of the misperceptions of body weight

and thus the severity of the condition. For example

Western culture reinforces specific desires to be thin

where cases of AN in other cultures might contain

different crucial cognitions. There may also be cases in

which the sufferer has pretty accurate cognitions about

their body and then we might look to physiological

changes that may sustain their fasting behaviour, for

example. All stages are equally as important for a

complete understanding of AN.

There is now an example of a distinction that should be

acknowledged for AN theories because they may require

separate explanations. When together and complete, the

various levels of explanation will contribute to a more

realistic picture of the various processes going on in

AN.

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Finally, no explanation should be regarded as

fundamental in explaining AN. The different stages might

be better understood as being causally intertwined; in

theory they can be distinguished but in reality they

interact and modify each other. Murphy (2008) recognizes

that theories in psychiatry represent exemplars of what

they set out to explain; they are partial accounts of

such entities. One choice of explanation should not

eliminate another, argues Murphy; instead different

levels of explanations should be understood in ways that

interact causally with each other rather than by

isolating them and attributing crucial significance to

certain ones.

These ideas will be continued further on in the paper.

First we are going to look at some sociocultural

considerations, which might be best attributed to broader

issues within the predisposing phase of AN’s development. It

should also highlight where further issues of complexity

and diversity within AN might arise for our theories

about it.

5. Some Sociocultural Considerations

Sociocultural models are generally concerned with local

female ideals and the pressures that Western culture

exerts on women to look a certain way (Russell 1995).

Russell explores how incidence rates of anorexia

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seemingly correspond to ideals of thinness; cases of

anorexia seem to prevail where ideals of thinness do. We

have also seen a rise in admission rates of AN over the

20th century, a time when fashion and beauty have become

preoccupied with a thin body image (1995, pg. 9).

Russell points to studies measuring the average

waistlines of women in beauty pageants and fashion

magazines over the 20th century, noticing that women

partaking in beauty pageants have weights far below their

national norms and sharp falls of waistline sizes over

the 20th century. Between 1959 and 1978 we see an average

decline in weight in Western populations, which suggests

a clear shift for ideal weights for women (1995, pg. 9).

Studies have also shown that there have been increased

rates of incidence of AN in the West over the 20th

century, this evidence supports a rising incidence

between the 1950’s and the 1980’s (pg. 11).

Investigators tend to attribute this to culturally

determined attitudes or behaviours over time. This

correspondence is hardly coincidental and it can be seen

how vulnerable young girls might respond to these local

norms combined with other personal problems highlighted

in the cognitive-behavioural model, and take on rigorous

dieting. Persistence in harsh dieting can be a factor in

disposing the individual to the risk of developing AN,

and Russell suggests that AN could even be seen as an

extension to harsh and determined dieting in the context

of these cultural considerations (1995). These models

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might be best viewed as having a pathoplastic effect,

however, rather than constituting a cause of AN. Ideals

to be thin will play a major role in influencing the

preoccupations of people who might become predisposed to

AN.

Szmukler and Patton’s essay (1995) also suggests that

dieting might be a significant factor in the development

of AN. However, although a lot of cases of anorexia have

resulted from dieting, it is not the case that a lot of

dieters have ended up with AN. They also suggest that the

rise in incidence rates of AN since 1960 undermines it as

a mental disorder (1995, pg. 181). However, the increase

of AN since then is mostly among adolescent girls, it

isn’t so much recognized as being a phenomenon among

women of older ages and particularly not with men. Also,

they highlight that links between being obsessive,

experiencing social stress, and dissatisfaction with body

weight are much closer connected with dieting than with

anorexic behaviour in general (1995, pg. 182).

This suggests that there needs to be a

predisposition toward anorexic behaviour in combination

with dieting to increase the chance of becoming anorexic.

Affective disturbances might, for example, help us to

understand the cross from dieting to disorder.

Individuals might be more predisposed in either cognitive

or physiological responses to dieting behaviour, in fact.

Someone might be more sensitive to a delay in gastric

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emptying after a period of very little food intake, for

example. Someone might be more predisposed to

dysfunctional cognitive thinking, such as thinking one

has self control if one is dieting excessively. However,

just like with Russell, we can determine that an emphasis

on slimness causes higher rates of AN in a population.

Russell observes that a Hong Kong study of AN hardly

involves reports of fear of fatness (1995). This suggests

that where in some cases sociocultural concerns are

necessary for providing one aspect of understanding for

AN (like in Western cases), other levels of explanation

are also required, like if there is a consistency of

physiological disturbance in cases of AN but sometimes no

fear of fatness. What it does suggest is that cultural

context is another significant, if rather more

contingent, level of causality that contributes towards

AN.

6. Integrative Pluralism; A Philosophical Analysis of Differing Theories

6.1 Multi-Level Explanation

Kendler, in the paper ‘Levels of Explanation in

Psychiatric and Substance Use Disorders’ (2012), points

out that there is a fundamental difference between

classifying and explaining a classical medical disorder

like cystic fibrosis than something like alcohol

dependency. We can have absolute causal confidence in a

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mutation that will cause cystic fibrosis, no matter what

the environmental exposures are. With alcohol dependency,

like with many other psychiatric disorders, there isn’t

the same possibility because of the variety of

precipitating factors that can contribute to its

development. There isn’t an obvious candidate for most

psychiatric disorders that can be used for a nosology.

The status of our science and the nature of psychiatric

disorders will not help us to yield unambiguous choices

for etiological explanations of psychiatric disorders.

This is clearly evident in AN, for which I’ve given

a range of possible and legitimate contributing factors

and causes, but most if not all of these will be given

and understood as partial accounts. For anorexia there

might be genetic factors that play a role in predisposing

someone towards excessive dieting, perhaps these are

given expression in personality traits, like someone

being a perfectionist or having a tendency to follow and

form rules. Or perhaps one’s physiology is predisposed to

reacting faster than others to changes in behaviour, such

as dieting, and delayed gastric emptying occurs quicker

in some individuals leading to AN. Of course cognitive-

behavioural models give us a good, evidence based and

likely story for the cognitions and behaviour development

leading to anorexic behaviour and give us possible

reasons why. Also environmental factors cannot be ignored

because these will manifest the most diverse array of

possible factors leading to AN.

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Murphy wants us to view levels of explanation in

psychiatry as representing qualitatively different causal

processes (2008, pg. 104). Rather than each level

involving different epistemic perspectives, as if we were

considering multi-level explanation as a variety of

perspectives and types of knowledge on the same process,

each level of explanation represents substantively

different causal processes. The difference between

sociocultural and physiological theories of AN, for

example, is not to be attributed to different types of

knowledge on a process known as AN, but they are

representations of distinct processes that collectively

contribute to AN.

Kendler wants to say that the criteria for choosing one

level of explanation over another will vary according to

the individual who is choosing (2012). Different

interests and purposes of the individual behind an

explanation will help determine the level at which it is

given. Alone these levels of explanation don’t correlate

to the complexity of the process of the disorder and so

hardly capture a realistic picture of it. Kendler

suggests that there isn’t an a priori way of picking out

the correct criteria for explanation, but it is a

normative question that we can draw out on pragmatic

grounds (2012). Science alone cannot unambiguously lead

this process and values will need to be considered, we

just need an agreed upon set of criteria for choosing

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appropriate levels of representation from a diverse range

of perspectives. Disorders need definitions in more

realistic terms and in mutually reinforcing networks of

causal mechanisms, he argues.

Therefore a hard medical model that may be

appropriate for medical conditions like cystic fibrosis

is inappropriate for psychiatric disorders. Psychiatry

requires a shift of focus from single etiological agents,

like the serotonin theory in depression, to disordered

multi-level models (Kendler 2012). This means that all of

the factors that might come into consideration in broad

theorizing about AN must come into consideration in its

definition so as to try and capture its ‘real nature’ in

theory, rather than attempt to narrow down diverse

theories into a single aetiology. This puts psychiatric

definitions back into complex, fuzzy boundaries of

mechanical relations, and means that it involves the

requirement of value-laden agreement as well as

scientific guidance.

6.2 Integration

Sandra Mitchell also recognizes the need for theories to

capture something more realistic about complex biological

processes in her defence of integrative pluralism (2004).

Kendler proposes a pluralist approach to psychiatry

(2012), but Mitchell’s notion of integration is useful

for understanding how different levels of explanation

(sociocultural, cognitive, and physiological) might

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interact, rather than separately explain, in an overall

explanation of psychiatric disorders. She criticizes

reductionism because it doesn’t capture the complex

picture of processes that won’t ever fully correspond to

the chosen perspectival representations that form

idealized theories of things.

Reductionism works on the principle that ultimately

there is one maximally accurate description from which

others can be derived and it requires replacing higher

level abstractions by lower level ones (Mitchell 2004).

However, if each level of explanation is partial,

capturing only a portion of the full process in question,

a ‘fundamental’ explanation is not going to capture the

same part of the process as a different level of

explanation would. Therefore different levels of

explanation do not stand in any ‘straightforward

derivability or intertranslatability relation’ (2004, pg.

83). For Murphy there cannot be any ‘fundamental’ level

of explanation either: each level causally interacts with

and modifies another (2008).

Like Kendler, Mitchell thinks a pluralist approach

is necessary to capture a better (if harder to

understand) theory that represents more accurately the

process it stands to describe. Again, she agrees with

Kendler that no single theoretical framework or algorithm

will suffice. Mitchell appeals to the idealized structure

of scientific models; they are abstract and developed

partially, much like Murphy’s (2008) understanding of

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each level as representing a generalized exemplar of what

it aims to explain. Mitchell argues that the realistic

and concrete nature of explanation of specific phenomena

entails integration; when models are applied to

phenomena, which have their own contingent historical

causal pathway, it must be done so in a piecemeal and

local fashion; we must be able to extract from our model

what is appropriate for specific cases. Pluralist models

must co-exist with integration in the generation of

explanation of ‘complex and varied biological phenomena’

(2004, pg. 89).

7. Applied to Anorexia Nervosa

Applying this to the paradigm case of anorexia, each

level of explanation is as valuable as the next. As long

as an explanation captures a correct, if partial, aspect

of the disorder then it is valuable. It is apparent that

many of the changes and processes correspond to each

other, such as sociocultural reports that anorectics over

time seem to consistently complain of a complete loss of

hunger and physical discomfort is complimentary to a

physiological explanation of delayed gastric emptying

that increases levels of satiety. Both explanations have

different purposes, the former is looking for

similarities and differences over time and culture

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perhaps to find what might be essential to a definition,

the latter is looking for treatable and consistent

symptoms across cases of AN.

What one might look for in an integrative pluralist

definition of AN is a theoretical encapsulation of all

levels of explanation. Because of the multiplicity of

causal pathways that each individual with anorexia will

bring with her, there needs to be a way of localizing our

explanation out of a pluralist definition that may

contain features that don’t apply to each and every

specific case. For example, sometimes a sociocultural

fear of fatness may be applicable and significant but in

other cases it won’t. This suggests the need for values

to be put to use in such a practice; science alone will

not suffice to provide a decision on what levels of

explanation are adequate in specific cases. What an

integrative pluralist approach to models of AN can bring

is better accommodation for a multiplicity of possible

circumstances according to sociocultural and individual

diversity, whilst still providing the necessary

diagnostic rectitude. Fear of fatness need not be a

necessary criterion for all cases of AN, but it certainly

will remain a possible and even probable one.

8. Conclusion

What can be gained from an integrative approach to

various models of AN is a larger and more complex multi-

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level model to better understand it. Because each theory

works with some idealized and partial exemplar of AN,

they cannot alone explain it as an entire entity and no

level of explanation can achieve a ‘fundamental’ status.

Therefore we need multiple models and a pluralist

framework to think about AN. Integration of each level

would enable a complete model to capture the interaction

between the multitude of factors that cause the complex

variety of features that are seen in cases of AN. There

must then be a way to extract the applicable elements

from the complete model to specific cases of AN. To do so

Kendler proposes the use of values as well as science and

Mitchell suggests the use of some piecemeal fashion to

piece together an accurate picture.

Word Count: 4,710

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