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 Anorexia Nervosa: The Potential of Nonanimal Research

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Grand sage
Grand sage

Nombre de messages : 1490
Date d'inscription : 24/09/2011

MessageSujet: Anorexia Nervosa: The Potential of Nonanimal Research   Sam 23 Juin - 11:25

Beyond Animal Research
By Jonathan Balcombe, Ph.D.
November 2005

In last month’s column, I presented some examples of studies in which rats are starved and exercised in a futile attempt to model anorexia nervosa (AN), a uniquely human condition. As I researched these studies, I also encountered numerous human clinical studies. The following recent examples illustrate just some of the broad range of research strategies available for human-based research into eating disorders (ED).

At Israel’s Danek Gertner Institute of Human Genetics, a genetic component of AN was studied in 90 family groups with AN tendencies. Two suspect gene polymorphisms were found to be preferentially transmitted to AN offspring, suggesting a genetic predisposition to development of AN.1

At the University of Pittsburgh’s Department of Psychiatry, six traits (obsessionality, age at menarche, anxiety, lifetime minimum body mass index, concern over mistakes, and food-related obsessions) were selected for linkage analysis from patients suffering from AN. Strong linkages were found for a separate bulimia nervosa (BN) cohort, but only weakly suggestive linkages arose for AN.2

At the University of Mannheim, Germany, magnetic resonance imaging (MRI) was performed on 40 women who were long-term recovered from AN or BN and on 31 women with no history of ED. All groups had similar measures of cerebrospinal fluid volume and gray or white matter volume, suggesting that structural brain abnormalities are reversible with long-term recovery from AN.3

At the University of Minnesota, Department of Psychology, structured interviews and self-report assessments were conducted with a community-based sample of 620 adolescent girls, their 310 mothers, and 299 fathers. Data analysis revealed links between ED in mothers and daughters, but no cross-generational relationship between ED and substance use/abuse. The authors conclude that the addiction model of ED may be simplistic.4

At Yale University’s Department of Psychiatry, open-ended self-descriptions were obtained from 15 AN patients, 15 control psychiatric patients, and 48 control non-patients between age 14 and 24. AN patients had a significantly heightened and harsh self-reflectivity and they more openly expressed depression and anxiety in their self-descriptions.5

A “tempting, if rather speculative” proposal is forwarded that AN is associated with pre-existing biochemical vulnerabilities, rather than [or in addition to] psychological effects. The author argues that so-called “channelopathies” are associated with certain genetic, physiological, and pharmacological AN factors.6

Ongoing research into eating disorders like anorexia nervosa reminds us that they have no quick-fix solutions. The roots of these illnesses are as complex as the human psyche. But progress lies in working with and helping human patients, not studying starving rats.

As one dynamic AN survivor says: “The key to recovery is in finding other healthier things that bring you joy and happiness.”7 That’s a philosophy we can all live by.

1. Koronyo-Hamaoui M, Frisch A, Stein D, Denziger Y, Leor S, Michaelovsky E, Laufer N, Carel C, Fennig S, Mimouni M, Ram A, Zubery E, Jeczmien P, Apter A, Weizman A, Gak E Dual contribution of NR2B subunit of NMDA receptor and SK3 Ca(2+)-activated K(+) channel to genetic predisposition to anorexia nervosa. J Psychiatr Res. 2005 Sep 9; [Epub ahead of print]
2. Bacanu SA, Bulik CM, Klump KL, Fichter MM, Halmi KA, Keel P, Kaplan AS, Mitchell JE, Rotondo A, Strober M, Treasure J, Woodside DB, Sonpar VA, Xie W, Bergen AW, Berrettini WH, Kaye WH, Devlin B. Linkage analysis of anorexia and bulimia nervosa cohorts using selected behavioral phenotypes as quantitative traits or covariates. Am J Med Genet B Neuropsychiatr Genet. 2005 Sep 8; [Epub ahead of print]
3. Wagner A, Greer P, Bailer UF, Frank GK, Henry SE, Putnam K, Meltzer CC, Ziolko SK, Hoge J, McConaha C, Kaye WH. Normal Brain Tissue Volumes after Long-Term Recovery in Anorexia and Bulimia Nervosa. Biol Psychiatry. 2005 Aug 31 [Epub ahead of print]
4. Von Ranson KM, McGue M, Iacono WG. Disordered eating and substance use in an epidemiological sample: II. Associations within families. Psychol Addict Behav. 2003;17(3):193-201.
5. Bers SA, Blatt SJ, Dolinsky A. The sense of self in anorexia-nervosa patients: a psychoanalytically informed method for studying self-representation. Psychoanal Study Child. 2004;59:294-315.
6. Myslobodsky M. Phobic Memory and Somatic Vulnerabilities in Anorexia Nervosa: A perspective. Ann Gen Psychiatry. 2005;4(1):15.
7. Sargent, Judy. 1999. The Long Road Back: A Survivor’s Guide to Anorexia. Georgetown, Mass: Northstar Publications, Inc. (quoted October 2005 from
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Grand sage
Grand sage

Nombre de messages : 1490
Date d'inscription : 24/09/2011

MessageSujet: Re: Anorexia Nervosa: The Potential of Nonanimal Research   Sam 23 Juin - 11:26

Beyond Animal Research
By Jonathan Balcombe, Ph.D.
October 2005

Anorexia Nervosa and Animal Experiments
A childhood family friend developed anorexia nervosa as a teenager while studying at an elite ballet school. She nearly died. Anorexia is a terrible illness that afflicts some two million Americans, mostly young women.

Not surprisingly, there is a concerted effort to understand and address anorexia and other eating disorders. A search for “anorexia nervosa” on the NIH’s PubMed online database yielded more than 8,600 studies. Most are human clinical studies—but not all. Many researchers are being funded to perform experiments on animals, usually (male) rats. But because rodents don’t spontaneously develop eating disorders, experimenters must create “animal models” of the condition.

One such model is the “activity-based anorexia” (ABA) or “semi-starvation-induced hyperactivity” (SIH) model, which combines starvation with exercise. Experimenters place rats on a starvation diet and place an activity wheel in their shoebox cage. Perhaps because they are desperate to find food, starved rats show excessive use of the wheel, which accelerates weight loss. This mimics the excessive physical activity common among self-starving human patients.

Here are some recent examples of ABA model studies:

■In a study from the University Medical Center Utrecht, starved/exercised rats exercised less and ate less after leptin (a blood protein) was injected into their brains.1
■At Florida State University, rats were starved by restricting food access to two hours per day. Rats given running wheels developed ABA. During recovery (resumption of normal food access), food consumption rose and exercise dropped.2
■At the University of British Columbia, 200 rats were forced into a tight-fitting cylinder tube for one of three periods of time—20 minutes, two hours, or two hours per day for five days—to investigate the role of restraint stress on uptake of dietary fat, carbohydrate, and protein.3
■At Memorial University, Newfoundland, rats starved on the ABA model were confined to running wheels except during a 90-minute meal per day period. A control group (animals not confined to a running wheel) didn’t lose weight, whereas the wheel group consumed less food, lost weight, and ran increasingly farther during the study.4
■In another Memorial University study, starved rats were kept in one of three different environments—a flat, circular alley; a running wheel; or a shoebox cage—to see if the alley also produces ABA (it didn’t).5
These studies subject rats to the grinding misery of starvation while frustrating their frenetic efforts to seek and find food. And to what end? Anorexia is a complex syndrome, unique to humans, of primarily psychological origin. Trying to understand it by forcing rats to starve in their cages is rather like trying to understand suicide by giving a gun to a depressed guinea pig. My next column will explore more applicable, human clinical approaches to anorexia nervosa.

1.Hillebrand JJ, Koeners MP, de Rijke CE, et al. Leptin treatment in activity-based anorexia. Biol Psychiatry. 2005;58(2):165-171.
2.Dixon DP, Ackert AM, Eckel LA. Development of, and recovery from, activity-based anorexia in female rats. Physiol Behav. 2003;80(2-3):273-279.
3.Wang SW. Effects of restraint stress and serotonin on macronutrient selection: a rat model of stress-induced anorexia. Eat Weight Disord. 2002;7(1):23-31.
4.Lett BT, Grant VL, Smith JF, et al. Preadaptation to the feeding schedule does not eliminate activity-based anorexia in rats. Q J Exp Psychol B. 2001;54(3):193-199.
5.Koh MT, Lett BT, Grant VL. Activity in the circular alley does not produce the activity anorexia syndrome in rats. Appetite. 2000r;34(2):153-159.
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