Login | Register

Anorexia Nervosa

Anorexia nervosa is an eating disorder characterized by extremely low body weight, distorted body image and an obsessive fear of gaining weight.

The term anorexia nervosa was established in 1873 by Sir William Gull, one of Queen Victoria’s personal physicians. The term is of Greek origin: a (α, prefix of negation), n (ν, link between two vowels) and orexis (ορεξις, appetite), thus meaning a lack of desire to eat.


Signs and Symptoms


A definition of anorexia nervosa was established by the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) and the World Health Organization’s International Statistical Classification of Diseases and Related Health Problems (ICD).

DSM-IV-TR criteria are:

  • Refusal to maintain body weight at or above a minimally normal weight for age and height (e.g. weight loss leading to maintenance of body weight less than 85% of that expected; or failure to make expected weight gain during period of growth, leading to body weight less than 85% of that expected).
  • Intense fear of gaining weight or becoming fat, even though underweight.
  • Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or denial of the seriousness of the current low body weight.
  • Amenorrhea (at least three consecutive cycles) in postmenarchal girls and women. Amenorrhea is defined as periods occurring only following hormone (e.g., estrogen) administration.

Furthermore, the DSM-IV-TR specifies two subtypes:

  • Restricting Type: during the current episode of anorexia nervosa, the person has not regularly engaged in binge-eating or purging behavior (that is, self-induced vomiting, or the misuse of laxatives, diuretics, or enemas). Weight loss is accomplished primarily through dieting, fasting, or excessive exercise.
  • Binge-Eating Type or Purging Type: during the current episode of anorexia nervosa, the person has regularly engaged in binge-eating or purging behavior (that is, self-induced vomiting, or the misuse of laxatives, diuretics, or enemas).

The ICD-10 criteria are similar, but in addition, specifically mention

  1. The ways that individuals might induce weight-loss or maintain low body weight (avoiding fattening foods, self-induced vomiting, self-induced purging, excessive exercise, excessive use of appetite suppressants or diuretics).
  2. Certain physiological features, including “widespread endocrine disorder involving hypothalamic-pituitary-gonadal axis is manifest in women as amenorrhea and in men as loss of sexual interest and potency. There may also be elevated levels of growth hormones, raised cortisol levels, changes in the peripheral metabolism of thyroid hormone and abnormalities of insulin secretion”.
  3. If onset is before puberty, that development is delayed or arrested.

The distinction between the diagnoses of anorexia nervosa, bulimia nervosa and eating disorder not otherwise specified (EDNOS) is often difficult to make in practice and there is considerable overlap between patients diagnosed with these conditions. Furthermore, seemingly minor changes in a patient’s overall behavior or attitude can change a diagnosis from “anorexia: binge-eating type” to bulimia nervosa. It is not unusual for a person with an eating disorder to “move through” various diagnoses as his or her behavior and beliefs change over time.

Signs and Symptoms

Back to Top

  • Weight changes
  • Obsession with food and eating
    • Unusual eating habits
    • Eating rituals
    • Excessive care in eating
    • Playing with food
    • Weighing foods
    • Intentional starvation
    • Cooking – some anorexics will prepare food for others but not eat it themselves
  • Obsession with weight
    • Fear of gaining weight
    • Desire to lose weight
    • Denial of hunger
    • Intense body dissatisfaction
    • Repeatedly checking weight
    • Distortion of body image
    • Believing too fat even when thin
    • Denial of low body weight
    • Wearing layered clothing – used to hide weight loss
  • Abusing other weight control methods
    • Excessive exercise
    • Purging
    • Vomiting
    • Laxative abuse
    • Enema abuse
    • Diuretic abuse
  • Menstrual abnormalities
    • Irregular menstrual periods
    • Absent menstrual periods
    • Delayed first period
  • Physical symptoms – mainly from malnutrition and starvation
    • Esophagus inflammation – from purging or vomiting
    • Dry skin
    • Thinning hair
    • Cold sensitivity
    • Vulnerable to infections
    • Anemia
    • Heart palpitations
    • Bone loss
    • Tooth decay
    • Soft body hair (lanugo)
    • Excess body hair
    • Excess facial hair
    • Hair loss
    • Balding scalp
    • Low breathing rate
    • Slow pulse
    • Low blood pressure
    • Low thyroid function
    • Low body temperature
    • Excessive thirst
    • Excessive urination
    • Dehydration
    • Constipation
    • Muscle mass loss
    • Swollen joints
    • Light-headedness
  • Emotional symptoms
    • Low self-esteem
    • Withdrawal
    • Isolation
    • Secrecy
    • Interpersonal conflict
    • Resistance to treatment
    • Denial that they are ill
    • Suicidal tendency
  • Excessive preoccupation with food
  • Consider themselves overweight despite being the contrary
  • Self-starvation
  • Binge eating
  • Absence of menstruation
  • Hyperactivity
  • Depression
  • Malnutrition


Back to Top


Twin studies have estimated a high heritability of anorexia nervosa, ranging from 56% to as high as 84%. Subsequent association studies have shown polymorphisms in genes involved in regulation of eating behavior, motivation and reward mechanics, personality and emotion to be associated with the development of Anorexia Nervosa. Due to the low prevalence of anorexia nervosa, association studies published commonly have problems with low power due to small sample sizes. However, confirmed and consistent results have been published showing associations to polymorphisms associated with the genes encoding agouti related peptide, brain derived neurotrophic factor, catechol-o-methyl transferase, SK3 and opioid receptor delta-1. In one study, variations in the norepinephrine transporter gene promoter were associated with restrictive anorexia nervosa, but not binge-purge anorexia (though the latter may have been due to small sample size).


Anorexia may be linked to a disturbed serotonin system, particularly to high levels at areas in the brain with the 5HT1A receptor – a system particularly linked to anxiety, mood and impulse control. Starvation has been hypothesized to be a response to these effects, as it is known to lower tryptophan and steroid hormone metabolism, which might reduce serotonin levels at these critical sites and ward off anxiety. Other studies of the 5HT2A serotonin receptor (linked to regulation of feeding, mood, and anxiety), suggest that serotonin activity is decreased at these sites. There is evidence that both personality characteristics and disturbances to the serotonin system are still apparent after patients have recovered from anorexia.

Changes in brain structure and function are early signs often to be associated with starvation, and is partially reversed when normal weight is regained. Anorexia is also linked to reduced blood flow in the temporal lobes. It is possible that it is a risk trait rather than an effect of starvation.

Anorexia may be linked to an autoimmune response to melanocortin peptides which influence appetite and stress responses.


Zinc deficiency may play a role in Anorexia. It is not thought responsible for causation of the initial illness but there is evidence that it may be an accelerating factor that deepens the pathology of the anorexia. A 1994 randomized, double-blind, placebo-controlled trial showed that zinc (14 mg per day) doubled the rate of body mass increase compared to patients receiving the placebo.


Anorexic eating behavior is thought to originate from an obsessive fear of gaining weight due to a distorted self image and is maintained by various cognitive biases that alter how the affected individual evaluates and thinks about their body, food and eating. This is not a perceptual problem, but one of how the perceptual information is evaluated by the affected person. People with anorexia nervosa seem to more accurately judge their own body image while lacking a self-esteem boosting bias.

People with anorexia nervosa also have other psychological difficulties and mental illness. Clinical depression, obsessive compulsive disorder, substance abuse and one or more personality disorders may be the most likely conditions to be comorbid with anorexia. High-levels of anxiety and depression are likely to be present regardless of whether they fulfill diagnostic criteria for a specific syndrome.

Research into the neuropsychology of anorexia has indicated that many of the findings are inconsistent across studies and that it is hard to differentiate the effects of starvation on the brain from any long-standing characteristics. One finding is that those with anorexia have poor cognitive flexibility.

Other studies have suggested that there are some attention and memory biases that may maintain anorexia.

Social and environmental

Sociocultural studies have highlighted the role of cultural factors, such as the promotion of thinness as the ideal female form in Western industrialized nations, particularly through the media (see article). A recent epidemiological study of 989,871 Swedish residents indicated that gender, ethnicity and socio-economic status were large influences on the chance of developing anorexia, with those with non-European parents among the least likely to be diagnosed with the condition, and those in wealthy, white families being most at risk. People in professions where there is a particular social pressure to be thin (such as models and dancers) were much more likely to develop anorexia during the course of their career, and further research has suggested that those with anorexia have much higher contact with cultural sources that promote weight-loss.

There is a high rate of reported child sexual abuse experiences in clinical groups of who have been diagnosed with anorexia. Although prior sexual abuse is not thought to be a specific risk factor for anorexia, those who have experienced such abuse are more likely to have more serious and chronic symptoms.

Relationship to autism

Following an initial suggestion of relationship between anorexia nervosa and autism, a longitudinal study of 102 participants into teenage onset anorexia nervosa conducted in Sweden found that 23% of people with a long-standing eating disorder are on the autism spectrum. Those on autism spectrum tend to have a worse outcome, but may benefit from the combined use of behavioral and pharmacological therapies tailored to ameliorate autism rather than anorexia nervosa per se. Other studies may suggest that autistic traits are common in people with anorexia nervosa. However, in one report it was concluded that these findings need to be replicated using larger samples with more sensitive measures.

It is also proposed that conditions on the autism spectrum make up the cognitive endophenotype underlying anorexia nervosa and appealed for increased interdisciplinary collaboration (see figure below). A pilot study into the effectiveness Cognitive Behavior Therapy, which based its treatment protocol on the hypothesized relationship between anorexia nervosa and an underlying autistic like condition, reduced perfectionism and rigidity in 17 out of 19 participants although further evaluation is needed.

A summary of the strategy Zucker et al. (2007) used to assess the relationship between anorexia nervosa and the autism spectrum.


Back to Top

Anorexia is thought to have the highest mortality rate of any psychiatric disorder, with anywhere from 6-20% of those who are diagnosed with the disorder eventually dying from related causes. The suicide rate of people with anorexia is also higher than that of the general population. In a longitudinal study women diagnosed with either DSM-IV anorexia nervosa (n = 136) or bulimia nervosa (n = 110) respectively who were assessed every 6 – 12 months over an 8 year period are at a considerable risk of committing suicide. Clinicians were warned of the risks as 15% of subjects reported at least one suicide attempt. It was noted that significantly more anorexia (22.1%) than bulimia (10.9%) subjects made a suicide attempt.


Back to Top

Treatment for anorexia nervosa tries to address three main areas. 1) Restoring the person to a healthy weight; 2) Treating the psychological disorders related to the illness; 3) Reducing or eliminating behaviors or thoughts that originally led to the disordered eating.

Drug treatments, such as SSRI or other antidepressant medication, have not been found to be generally effective for either treating anorexia, or preventing relapse although it has also been noted that there is a lack of adequate research in this area.

Family based treatment has also been found to be an effective treatment for adolescents with short term anorexia. At 4 to 5 year follow up one study shows full recovery rate of 60 – 90% with 10-15% remaining seriously ill. This compares favorable to other treatments such as inpatient care where full recovery rates vary between 33-55%.


Back to Top

The list of complications that have been mentioned in various sources for Anorexia Nervosa includes:


Back to Top

1. “PsychiatryOnline, Anorexia Nervosa”

2. Anorexia Nervosa (Apepsia Hysterica, Anorexia Hysterica) (1873) William Withey Gull, published in the ‘Clinical Society’s Transactions, vol vii, 1874, p22

3. Costin, Carolyn (1999). The Eating Disorder Sourcebook. Linconwood: Lowell House. p. 6. ISBN 0585189226.

4. Zucker, N. L; M. Losh, C. M Bulik, K. S LaBar, J. Piven, K. A Pelphrey (2007). “Anorexia nervosa and autism spectrum disorders: Guided investigation of social cognitive endophenotypes”. Psychological Bulletin 133 (6): 976–1006. doi:10.1037/0033-2909.133.6.976. PMID 17967091.

5. Klump KL, Miller KB, Keel PK, McGue M, Iacono WG (May 2001). “Genetic and environmental influences on anorexia nervosa syndromes in a population-based twin sample”. Psychological Medicine 31 (4): 737–40. doi:10.1017/S0033291701003725. PMID 11352375.

6. Kortegaard LS, Hoerder K, Joergensen J, Gillberg C, Kyvik KO (Feb 2001). “A preliminary population-based twin study of self-reported eating disorder”. Psychological Medicine 31 (2): 361-365. doi:10.1017/S0033291701003087. PMID 11232922.

7. Wade TD, Bulik CM, Neale M, Kendler KS (March 2000). “Anorexia nervosa and major depression: shared genetic and environmental risk factors”. Am J Psychiatry 157 (3): 469–71. PMID 10698830

8. Rask-Andersen M, Olszewski PK, Levine AS, Schiöth HB (November 2009). “Molecular mechanisms underlying anorexia nervosa: Focus on human gene association studies and systems controlling food intake”. Brain Res Rev. doi:10.1016/j.brainresrev.2009.10.007. PMID 19931559

9. Urwin RE, Bennetts B, Wilcken B, et al. (2002). “Anorexia nervosa (restrictive subtype) is associated with a polymorphism in the novel norepinephrine transporter gene promoter polymorphic region”. Molecular Psychiatry 7 (6): 652–7. doi:10.1038/sj.mp.4001080. PMID 12140790

10. Kaye WH, Frank GK, Bailer UF, et al. (May 2005). “Serotonin alterations in anorexia and bulimia nervosa: new insights from imaging studies”. Physiology & Behavior 85 (1): 73–81. doi:10.1016/j.physbeh.2005.04.013. PMID 15869768

11. Kaye WH, Bailer UF, Frank GK, Wagner A, Henry SE (September 2005). “Brain imaging of serotonin after recovery from anorexia and bulimia nervosa”. Physiology & Behavior 86 (1-2): 15–7. doi:10.1016/j.physbeh.2005.06.019. PMID 16102788

12. Palazidou E, Robinson P, Lishman WA (August 1990). “Neuroradiological and neuropsychological assessment in anorexia nervosa”. Psychological Medicine 20 (3): 521–7. doi:10.1017/S0033291700017037. PMID 2236361

13. Lask B, Gordon I, Christie D, Frampton I, Chowdhury U, Watkins B (2005). “Functional neuroimaging in early-onset anorexia nervosa”. The International Journal of Eating Disorders 37 Suppl: S49–51; discussion S87–9. doi:10.1002/eat.20117. PMID 15852320

14. Fetissov SO, Harro J, Jaanisk M, et al. (October 2005). “Autoantibodies against neuropeptides are associated with psychological traits in eating disorders”. Proceedings of the National Academy of Sciences of the United States of America 102 (41): 14865–70. doi:10.1073/pnas.0507204102. PMID 16195379

15. Shay NF, Mangian HF (May 2000). “Neurobiology of zinc-influenced eating behavior”. The Journal of Nutrition 130 (5S Suppl): 1493S–9S. PMID 10801965

16. Rosen JC, Reiter J, Orosan P (January 1995). “Assessment of body image in eating disorders with the body dysmorphic disorder examination”. Behaviour Research and Therapy 33 (1): 77–84. doi:10.1016/0005-7967(94)E0030-M. PMID 7872941

17. Skrzypek S, Wehmeier PM, Remschmidt H (December 2001). “Body image assessment using body size estimation in recent studies on anorexia nervosa. A brief review”. European Child & Adolescent Psychiatry 10 (4): 215–21. doi:10.1007/s007870170010. PMID 11794546

18. Jansen A, Smeets T, Martijn C, Nederkoorn C (March 2006). “I see what you see: the lack of a self-serving body-image bias in eating disorders”. The British Journal of Clinical Psychology / the British Psychological Society 45 (Pt 1): 123–35. doi:10.1348/014466505X50167. PMID 16480571

19. O’Brien KM, Vincent NK (February 2003). “Psychiatric comorbidity in anorexia and bulimia nervosa: nature, prevalence, and causal relationships”. Clinical Psychology Review 23 (1): 57–74. doi:10.1016/S0272-7358(02)00201-5. PMID 12559994

20. Tchanturia K, Campbell IC, Morris R, Treasure J (2005). “Neuropsychological studies in anorexia nervosa”. The International Journal of Eating Disorders 37 Suppl: S72–6; discussion S87–9. doi:10.1002/eat.20119. PMID 15852325

21. Cooper MJ (June 2005). “Cognitive theory in anorexia nervosa and bulimia nervosa: progress, development and future directions”. Clinical Psychology Review 25 (4): 511–31. doi:10.1016/j.cpr.2005.01.003. PMID 15914267

22. Lindberg L, Hjern A (December 2003). “Risk factors for anorexia nervosa: a national cohort study”. The International Journal of Eating Disorders 34 (4): 397–408. doi:10.1002/eat.10221. PMID 14566927

23. Garner DM, Garfinkel PE (November 1980). “Socio-cultural factors in the development of anorexia nervosa”. Psychological Medicine 10 (4): 647–56. doi:10.1017/S0033291700054945. PMID 7208724

24. Toro J, Salamero M, Martinez E (March 1994). “Assessment of sociocultural influences on the aesthetic body shape model in anorexia nervosa”. Acta Psychiatrica Scandinavica 89 (3): 147–51. doi:10.1111/j.1600-0447.1994.tb08084.x. PMID 8178671

25. Carter JC, Bewell C, Blackmore E, Woodside DB (March 2006). “The impact of childhood sexual abuse in anorexia nervosa”. Child Abuse & Neglect 30 (3): 257–69. doi:10.1016/j.chiabu.2005.09.004. PMID 16524628

26. Gillberg, Christopher (1985). “Autism and anorexia nervosa: Related conditions?”. Nordic Journal of Psychiatry 39: 307. doi:10.3109/08039488509101911

27. Rothery DJ, Garden GM (November 1988). “Anorexia nervosa and infantile autism”. The British Journal of Psychiatry 153: 714. doi:10.1192/bjp.153.5.714. PMID 3255470

28. Gillberg, C.; Rastam, M. (1992). “Do some cases of anorexia nervosa reflect underlying autistic-like conditions?”. Behavioural neurology 5 (1): 27–32.

29. Gillberg IC, Råstam M, Gillberg C (1995). “Anorexia nervosa 6 years after onset: Part I. Personality disorders”. Comprehensive Psychiatry 36 (1): 61–9. doi:10.1016/0010-440X(95)90100-A. PMID 7705090

30. Gillberg IC, Gillberg C, Råstam M, Johansson M (1996). “The cognitive profile of anorexia nervosa: a comparative study including a community-based sample”. Comprehensive Psychiatry 37 (1): 23–30. doi:10.1016/S0010-440X(96)90046-2. PMID 8770522

31. Råstam, M.; Gillberg, C.; Gillberg, I. C. (1996). “A six-year follow-up study of anorexia nervosa subjects with teenage onset”. Journal of Youth and Adolescence 25: 439. doi:10.1007/BF01537541

32. Nilsson EW, Gillberg C, Gillberg IC, Råstam M (November 1999). “Ten-year follow-up of adolescent-onset anorexia nervosa: personality disorders”. Journal of the American Academy of Child and Adolescent Psychiatry 38 (11): 1389–95. PMID 10560225

33. Wentz E, Gillberg C, Gillberg IC, Råstam M (July 2001). “Ten-year follow-up of adolescent-onset anorexia nervosa: psychiatric disorders and overall functioning scales”. Journal of Child Psychology and Psychiatry, and Allied Disciplines 42 (5): 613–22. doi:10.1017/S0021963001007284. PMID 11464966

34. Råstam M, Gillberg C, Wentz E (2003). “Outcome of teenage-onset anorexia nervosa in a Swedish community-based sample”. European Child & Adolescent Psychiatry 12 (Suppl 1): I78–90. doi:10.1007/s00787-003-1111-y. PMID 12567219

35. Wentz E, Lacey JH, Waller G, Råstam M, Turk J, Gillberg C (December 2005). “Childhood onset neuropsychiatric disorders in adult eating disorder patients. A pilot study”. European Child & Adolescent Psychiatry 14 (8): 431–7. doi:10.1007/s00787-005-0494-3. PMID 16341499

36. Wentz E, Gillberg IC, Anckarsäter H, Gillberg C, Råstam M (February 2009). “Adolescent-onset anorexia nervosa: 18-year outcome”. The British Journal of Psychiatry 194 (2): 168–74. doi:10.1192/bjp.bp.107.048686. PMID 19182181

37. Fisman S, Steele M, Short J, Byrne T, Lavallee C (July 1996). “Case study: anorexia nervosa and autistic disorder in an adolescent girl”. Journal of the American Academy of Child and Adolescent Psychiatry 35 (7): 937–40. PMID 8768355

38. Kerbeshian, Jacob; Burd, Larry (2009). “Is anorexia nervosa a neuropsychiatric developmental disorder? An illustrative case report”. World Journal of Biological Psychiatry 10: 648. doi:10.1080/15622970802043117

39. Gillberg IC, Råstam M, Wentz E, Gillberg C (February 2007). “Cognitive and executive functions in anorexia nervosa ten years after onset of eating disorder”. Journal of Clinical and Experimental Neuropsychology 29 (2): 170–8. doi:10.1080/13803390600584632. PMID 17365252

40. Lopez C, Tchanturia K, Stahl D, Booth R, Holliday J, Treasure J (March 2008). “An examination of the concept of central coherence in women with anorexia nervosa”. The International Journal of Eating Disorders 41 (2): 143–52. doi:10.1002/eat.20478. PMID 17937420

41. Russell TA, Schmidt U, Doherty L, Young V, Tchanturia K (August 2009). “Aspects of social cognition in anorexia nervosa: affective and cognitive theory of mind”. Psychiatry Research 168 (3): 181–5. doi:10.1016/j.psychres.2008.10.028. PMID 19467562

42. Zastrow A, Kaiser S, Stippich C, et al. (May 2009). “Neural correlates of impaired cognitive-behavioral flexibility in anorexia nervosa”. The American Journal of Psychiatry 166 (5): 608–16. doi:10.1176/appi.ajp.2008.08050775. PMID 19223435

43. Harrison A, Sullivan S, Tchanturia K, Treasure J (2009). “Emotion recognition and regulation in anorexia nervosa”. Clinical Psychology & Psychotherapy 16 (4): 348–56. doi:10.1002/cpp.628. PMID 19517577

44. Hambrook D, Tchanturia K, Schmidt U, Russell T, Treasure J (September 2008). “Empathy, systemizing, and autistic traits in anorexia nervosa: a pilot study”. The British Journal of Clinical Psychology 47 (Pt 3): 335–9. doi:10.1348/014466507X272475. PMID 18208640

45. Herzog DB, Greenwood DN, Dorer DJ, et al. (July 2000). “Mortality in eating disorders: a descriptive study”. The International Journal of Eating Disorders 28 (1): 20–6. doi:10.1002/(SICI)1098-108X(200007)28:13.0.CO;2-X. PMID 10800010

46. Pompili M, Mancinelli I, Girardi P, Ruberto A, Tatarelli R (July 2004). “Suicide in anorexia nervosa: a meta-analysis”. The International Journal of Eating Disorders 36 (1): 99–103. doi:10.1002/eat.20011. PMID 15185278

47. Franko DL, Keel PK, Dorer DJ, et al. (July 2004). “What predicts suicide attempts in women with eating disorders?”. Psychological Medicine 34 (5): 843–53. doi:10.1017/S0033291703001545. PMID 15500305

48. “National Institute of Mental Health, Anorexia Nervosa”

49. Claudino AM, Hay P, Lima MS, Bacaltchuk J, Schmidt U, Treasure J (2006). “Antidepressants for anorexia nervosa”. Cochrane Database of Systematic Reviews (1): CD004365. doi:10.1002/14651858.CD004365.pub2. PMID 16437485

50. Walsh BT, Kaplan AS, Attia E, et al. (June 2006). “Fluoxetine after weight restoration in anorexia nervosa: a randomized controlled trial”. JAMA 295 (22): 2605–12. PMID 16772623

51. Whitney J, Easter A, Tchanturia K (September 2008). “Service users’ feedback on cognitive training in the treatment of anorexia nervosa: a qualitative study”. The International Journal of Eating Disorders 41 (6): 542–50. doi:10.1002/eat.20536. PMID 18433016

52. Lock J, le Grange D (2005). “Family-based treatment of eating disorders”. The International Journal of Eating Disorders 37 Suppl: S64–7; discussion S87–9. doi:10.1002/eat.20122. PMID 15852323

53. le Grange D, Eisler I (January 2009). “Family interventions in adolescent anorexia nervosa”. Child and Adolescent Psychiatric Clinics of North America 18 (1): 159–73. doi:10.1016/j.chc.2008.07.004. PMID 19014864

54. “WrongDiagnosis, Complications of Anorexia Nervosa”

, , ,

6 Responses to “Anorexia Nervosa”

  • […] Alphalipoproteinemia Anorexia Nervosa […]

  • TomPier says:

    great post as usual!

  • scat says:

    Having been through it and lived to read articles on it….Interesting. Many years later, seems so silly now. Not at the time, though. Sonething close to a living hell….articles like these are needed to educate the ill informed and reassure the desperate.

  • Anorexia says:

    It took me years to get over it. My teenage and young adult years were hell. This is the most difficult to treat.

  • Anorexia says:

    It took many years to overcome anorexia, and I know how to eat well, live well, and I live a very normal very productive life. It does leave a scar in your psyche-it’s kind of there, because I had it for many years-and I sometimes (rarely) think about it. That doesn’t mean it can’t happen again. I mean if something catastrophic happens to me and I won’t be able to deal with it, I could end up starving myself. I suppose that can happen. I hope not. I hope not. But I have learned to become a surviver and I think good coping mechanisms, so chances are it won’t happen again.

  • missfatty says:

    helloooooo! els hier

Leave a Reply

Your email address will not be published. Required fields are marked *