Stress and CR history produces binges?

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Hi All,

Related to discussing the pdf-available:

Hagan MM, Chandler PC, Wauford PK, Rybak RJ, Oswald KD.

The role of palatable food and hunger as trigger factors in an animal model of

stress induced binge eating.

Int J Eat Disord. 2003 Sep;34(2):183-97.

PMID: 12898554

OBJECTIVE: Dieting and stress are etiological factors in eating disorders,

and

dieting strongly predicts stress-induced overeating in the nonclinical

population.

We developed an animal model of binge eating in sated rats that is evoked by

stress,

but only in rats with a history of caloric restriction and only if highly

palatable

food (HPF) is available after stress. This study investigated the effect of

known

binge triggers, a taste of HPF and of hunger, on this type of binge eating.

METHOD:

Female rats were cycled through the R/S protocol but this time were given just a

taste of HPF with ad lib regular chow. After another R/S cycle, rats were

stressed

during restriction (while hungry) and were given HPF and chow. RESULTS: Although

binge eating did not occur if only chow was available after stress, just a taste

of

HPF sufficed to increase chow intake to more than 160% (p < 0.001) of rats with

a

history of restriction only, stress-only, or neither. Hunger increased the

proportion of chow consumed by both restricted groups, but stress magnified this

hunger-induced overeating by increasing HPF intake to 137% of restriction-only

rats

(p < 0.001). DISCUSSION: These effects suggest that binge eating in this model

is

motivated by reward, not metabolic need, and parallels observations of binge

triggers described in clinical binge-eating disorders. This strengthens the

validity

of using this animal model to target the physiology and treatment of eating

disorders preceded by dieting and stress.

is:

Geary N.

A new animal model of binge eating.

Int J Eat Disord. 2003 Sep;34(2):198-9. No abstract available.

PMID: 12898555

COMMENTARY

In contrast to the widespread use of animal models of the neural and genetic

mechan-isms

underlying psychiatric disorders, there is only modest enthusiasm for animal

models of the psychological processes involved in psychiatric disorders. This

lack

of

interest stems largely from the belief that animals simply do not possess the

cognitive

and emotional processes that underlie human behavior. This is an expression of

what

de

Waal (2002) referred to as ‘‘human-animal’’ dualism in experimental psychology.

The

idea is that because humans possess some psychological capacities that animals

do

not,

none of our psychological processes is shared. The logic is faulty. Many studies

indicate

that animals possess at least rudimentary forms of psychological processes

important

in

humans. The danger of animal-human dualism in psychiatry is that it can be a

prejudice

that prevents research aimed at determining whether psychological processes that

are

manifest in animals are relevant to the etiology, course, or treatment of

psychiatric

disorders.

These issues are brought into sharp focus by the new rat model of binge eating

presented by Hagan and her colleagues (Hagan, Chandler, Wauford, Rybak, &

Oswald, 2003; Hagan, Wauford, Chandler, Jarrett, Rybak, & Blackburn, 2002). They

showed that following a history of food restriction, electric shock elicited

transient and

dramatic overeating if rats were offered even a taste of palatable food. The

parallels to

bulimia nervosa are striking. For example, individuals with bulimia almost

always

have

a history of dieting, stress can precipitate binges, and binges typically

involve

preferred

foods. However, the model may apply better to binge eating disorder (BED)

because

the

rats did not engage in behaviors to compensate for their overeating.

This model, like any other scientific model, will ultimately be judged by its

ability to

produce new knowledge (Keller, 2002). Its potential seems rich. Perhaps, the

most

unexpected outcome would be the identification of etiology. Could it be that

food

restriction, stress, and limited access to certain foods alone are sufficient to

produce

binges in humans? Are our vaunted phylogenetic differences with rats irrelevant

to

this process? Would such binges be accompanied by the feelings of loss of

control

and

guilt that occur in bulimia and BED patients? Or, do humans possess

psychological

processes that prevent these contingencies alone from producing binging?

Experiments

to address these questions directly are ethically inappropriate. However, any

number

of

more feasible, and probably more clinically useful, investigations of the

psychological,

neural, and genetic parallels between the rat model and the human syndrome are

easy

to

imagine. These experiments would provide indirect answers to these questions as

well

as

establish the model’s predictive value for the development of therapeutic

strategies. The

results of the new rat model of binging are anticipated eagerly.

Finally, even if dietary restriction, stress, and palatable foods are sufficient

for

binge

eating in humans, they are unlikely to account for all instances of binge

eating. A

genetic

cause was reported recently by Branson et al. (2003), who sequenced the region

of

the

POMC gene that encodes the Melanocortin 4 receptor (MC4R) in a large sample of

severely obese patients (mean body mass index 44). They found that 5% of the

obese

patients carried MC4R mutations and that 100% (20 of 20) of the patients with

MC4R

mutations met the criteria for BED as outlined in the 4th ed. of the Diagnostic

and

Statistical Manual of Mental Disorders (DSM-IV; American Psychiatric

Association,

1994). Only 14% of the obese patients with normal MC4R genes met the DSM-IV

criteria.

The inclusion of molecular genetic and experiential manipulations in the

development

of

animal models of binge eating should increase our understanding of the

interactions

between genes and environment that lead to human eating disorders.

Al Pater, PhD; email: old542000@...

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