Tag Archives: eating disorder


The diagnosis of Trichotillomania (TM) is synonymous with the act of recurrently pulling one’s own body hair resulting in noticeable thinning or baldness.  (American Psychiatric Association, Diagnostic and statistical manual of mental disorders, 2000, p. 674)  Sites of hair pulling can include any area of the body in which hair is found, but the most common sites are the scalp, eyelashes, eyebrows, and the pubis area.  (Kraemer, 1999, p. 298)  The disorder itself is categorized in the DSM-IV-TR as an “Impulse Control Disorder Not Elsewhere Classified” along with disorders like Pathological Gambling, Pyromania, Kleptomania, and Intermittent Explosive Disorder.  Although TM was previously considered to be a rare disorder, more recent research indicates that prevalence rates of TM may be as high as 2% of the general population.  (Kraemer, 1999, p. 298)  This prevalence rate is significantly higher than the lifetime prevalence rate of .6% that is cited as a potential baseline among college students the DSM-IV-TR.  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 676)  The condition appears to be more common among women and the period of onset is typically in childhood or adolescence. (Kraemer, 1999, p. 298)  As is customary with most DSM-IV-TR diagnoses, the act of hair pulling cannot be better accounted for by another mental disorder (like delusions, for example) or a general medical condition.  Like every disorder in the DSM-IV-TR, the disturbance must cause significant distress or impairment in functioning.  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 675)

Alopecia is a key concept that must be understood in order to complete the differential diagnosis of TM.  Alopecia is a condition of baldness in the most general sense.  (Shiel, Jr. & Stoppler, 2008, p. 14)  Other medically related causes of alopecia should be considered in the differential diagnosis of TM, especially when working with an individual who deny pulling their hair.  The common suspects include male-pattern baldness, Discoid Lupus Erythematosus (DLE), Lichen Planopilaris (also known as Acuminatus), Folliculitis Decalvans, Pseudopelade of Brocq, and Alopecia Mucinosa (Follicular Mucinosis).  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 676)  Comprehensive coverage of these medical conditions is beyond the scope of this article – all of the aforementioned confounding variables can be eliminated by a general practitioner.

There are a number of idiosyncratic features associated with TM that bear mentioning.  Although the constellation of features covered here is not sufficient to warrant a diagnosis in isolation, they can aid in the differential diagnosis process.  Alopecia, regardless of the cause, has been known to lead sufferers to tremendous feats of avoidance so that the hair loss remains undetected.  Simply avoiding social functions or other events where the individual (and their attendant hair loss) might be uncovered is a common occurrence.  In cases where individual’s focus of attention is on the head or scalp, it is not uncommon for affected individuals to attempt to hide hair loss by adopting complimentary hair styles or wearing other headwear (e.g., hats, wigs, etc).  These avoidance behaviors will be the target of exposure and response prevention later in this article.

In addition to avoidant behavior and elaborate attempts to “cover it up,” individuals with TM frequently present with clinically significant difficulty in areas such as self-esteem and mood.  Comorbidity, or the presence of one or more disorders in the addition to a primary diagnosis, is the rule not the exception in the stereotypical presentation of TM.  Mood disorders (like depression) are the most common (65%) – anxiety (57%), chemical use (22%), and eating disorders (20%) round out the top four mostly likely candidates for comorbidity.  (Kraemer, 1999, p. 298)  These comorbidity rates are not overly surprising since they parallel prevalence rates across the wider population – perhaps with the notable exception of the high rate of comorbid eating disorders.  We can speculate about the source of comorbidity – one possible hypothesis is that a few people who suffer TM also suffer from a persistent cognitive dissonance associated with having happy-go-lucky personality trait which leads them “let the chips fall where they may.”  They are individuals prone to impulsivity, but they are subdued and controlled the shame, guilt, frustration, fear, rage, and helplessness associated with the social limitations placed on them by the disorder.  (Ingram, 2012, p. 269)  On the topic of personality, surprisingly enough, research suggests that personality disorders do not share significant overlap with TM.  This includes Borderline Personality Disorder (BPD) despite the fact that BPD is often associated with self-harming behavior.  (Kraemer, 1999, p. 299)

Differentiating TM from Obsessive-Compulsive Disorder (OCD) can be challenging in some cases.  TM is similar to OCD because there is a “sense of gratification” or “relief” when pulling the hair out.  Unlike individuals with OCD, individuals with TM do not perform their compulsions in direct response to an obsession and/or according to rules that must be rigidly adhered to.  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 676)  There are, however, observed similarities between OCD and TM regarding phenomenology, neurological test performance, response to SSRI’s, and contributing elements of familial and/or genetic factors.  (Kraemer, 1999, p. 299)  Due to the large genetic component contributions of both disorders, obtaining a family history (vis-à-vis a detailed genogram) is highly recommended.  The comprehensive genogram covering all mental illness can be helpful in the discovery the comorbid conditions identified above as well.

There is some suggestion that knowledge of events associated with onset is “intriguing, but unnecessary for successful treatment.”  (Kraemer, 1999, p. 299)  I call shenanigans.  There is a significant connection between the onset of TM and the patient enduring loss, perceived loss, and/or trauma.  Time is well spent exploring the specific environmental stressors that precipitated the disorder.  Although ignoring circumstances surrounding onset might be prudent when employing strict behavioral treatment paradigms, it seems like a terrible waste of time to endure suffering without identifying some underlying meaning or purpose that would otherwise be missed if we overlook onset specifics.  “Everything can be taken from a man but one thing: the last of human freedoms – to choose one’s attitude in any given set of circumstances, to choose one’s own way.”  (Frankl, 1997, p. 86)  If we acknowledge that all behavior is purposeful, then we must know and understand the circumstances around onset if we will ever understand the purpose of said behavior.  I liken this to a difference in professional opinion and personal preference because either position can be reasonably justified, but in the end the patient should make the ultimate decision about whether or not to explore onset contributions vis-à-vis “imagery dialogue” or a similar technique.  (Young, Klosko, & Weishaar, 2003, p. 123)  If such imagery techniques are unsuccessful or undesired by the client, a psychodynamic conversation between “internal parts of oneself” can add clarity to the persistent inability of the client to delay gratification.  (Ingram, 2012, p. 292)  Such explorations are likely to be time consuming, comparatively speaking, and should not be explored with patients who are bound by strict EAP requirements or managed care restrictions on the type and length of treatment.  Comorbid developmental disabilities and cognitive deficits may preclude this existential exploration.  I employ the exploration of existential issues of origin in the interest of increasing treatment motivation, promoting adherence, enhancing the therapeutic milieu, and thwarting subsequent lapses by anchoring cognitive dissonance to a concrete event.

TM represents a behavioral manifestation of a fixed action patterns (FAPs) that is rigid, consistent, and predicable.  FAPs are generally thought to have evolved from our most primal instincts as animals – they are believed to contain fundamental behavioral ‘switches’ that enhance the survivability of the human species.    (Lambert & Kinsley, 2011, p. 232)  The nature of FAPs that leads some researchers to draw parallels to TM is that FAPs appear to be qualitatively “ballistic.”  It’s an “all or nothing” reaction that is comparable to an action potential traveling down the axon of a neuron.  Once they are triggered they are very difficult to suppress and may have a tendency to “kindle” other effects.  (Lambert & Kinsley, 2011, p. 233)

There are some unique considerations when it comes to assessing a new patient with TM.  Because chewing on or ingesting the hair is reported in nearly half of TM cases, the attending clinician should always inquire about oral manipulation and associated gastrointestinal pain associated with a connected hair mass in the stomach or bowel (trichobezoar).  Motivation for change should be assessed and measured because behavioral interventions inherently require a great deal of effort.  Family and social systems should not be ignored since family dynamics can exacerbate symptomatlogy vis-à-vis pressure to change (negative reinforcement), excessive attention (positive reinforcement), or both.  (Kraemer, 1999, p. 299)

What remains to be seen is the role of stress in the process of “triggering” a TM episode.  Some individuals experience an “itch like” sensation as a physical antecedent that remits once the hair is pulled.  This “itch like” sensation is far from universal.  Some clinicians and researchers believe that the abnormal grooming behavior found in TM is “elicited in response to stress” with the necessary but not sufficient condition of “limited options for motoric behavior and tension release.”  (Kraemer, 1999, p. 299)  Although this stress hypothesis may materialize as a tenable hypothesis in some cases, it’s by no means typical.  Most people diagnosed with TM report that the act of pulling typically occurs during affective states of relaxation and distraction.  Most individuals whom suffer from TM do not report clinically significant levels of anxiety as the “trigger” of bouts of hair pulling.  We could attribute this to an absence of insight regarding anxiety related triggers or, perhaps anxiety simply does not play a significant role in the onset and maintenance of hair pulling episodes.  Regardless of the factors that trigger episodes, a comprehensive biopsychosocial assessment that includes environmental stressors (past, present and anticipated) should be explored.

The options for treatment of TM are limited at best.  SSRIs have demonstrated some potential in the treatment of TM, but more research is needed before we can consider SSRIs as a legitimate first-line treatment.  SSRIs are worth a shot as an adjunct treatment in cases of chronic, refractory, or treatment resistant TM.  I would consider recommending a referral to a psychiatrist (not a general practitioner) for a medication review due in part to the favorable risk profile of the most recent round of SSRIs.  Given the high rate of comorbidity with mood and anxiety disorders – if either is anxiety or depression are comorbid, SSRIs will likely be recommended regardless.  Killing two birds with one stone is the order of the day, but be mindful that some medication can interfere with certain treatment techniques like imaginal or in vivo exposure.  (Ledley, Marx, & Heimberg, 2010, p. 141)  Additional research is needed before anxiolytic medications can be recommended in the absence of comorbid anxiety disorders (especially with children).  Hypnosis and hypnotic suggestion in combination with other behavioral interventions may be helpful for some individuals, but I don’t know enough about it at this time to recommend it.  Call me skeptical, or ignorant, but I prefer to save the parlor tricks for the circus…

Habit reversal is no parlor trick.  My goal isn’t to heal the patient; that would create a level of dependence I am not comfortable with… my goal is to teach clients how to heal themselves.  Okay, but how?  The combination of Competing Response Training, Awareness/Mindfulness Training, Relaxation Training, Contingency Management, Cognitive Restructuring, and Generalization Training is the best hope for someone who seeks some relief from TM.  Collectively I will refer to this collection of techniques as Habit Reversal.

Competing Response Training is employed in direct response to hair pulling or in situations where hair pulling might be likely.  In the absence of “internal restraints to impulsive behavior,” artificial circumstances are created by identifying substitute behaviors that are totally incompatible with pulling hair.  (Ingram, 2012, p. 292)  Just like a compulsive gambling addict isn’t in any danger if spends all his money on rent, someone with TM is much less likely to pull hair if they are doing something else with their hands.

Antecedents, or triggers, are sometimes referred to as discriminative stimuli.  (Ingram, 2012, p. 230)  “We sense objects in a certain way because of our application of priori intuitions…”  (Pirsig, 1999, p. 133)  Altering the underlying assumptions entrenched in maladaptive priori intuitions is the core purpose of Awareness and Mindfulness Training.  “There is a lack of constructive self-talk mediating between the trigger event and the behavior. The therapist helps the client build intervening self-messages: Slow down and think it over; think about the consequences.”  (Ingram, 2012, p. 221)  The connection to contingency management should be self evident.  Utilizing a customized self-monitoring record, the patient begins to acquire the necessary insight to “spot” maladaptive self talk.  “Spotting” is not a new or novel concept – it is central component of Abraham Low’s revolutionary self help system Recovery International.  (Abraham Low Self-Help Systems, n.d.)  The customized self-monitoring record should invariably include various data elements such as precursors, length of episode, number of hairs pulled, and a subjective unit of distress representing the level of “urge” or desire to pull hair.  (Kraemer, 1999)  The act of recording behavior (even in the absence of other techniques) is likely to produce significant reductions in TM symptomatlogy.  (Persons, 2008, p. 182-201)  Perhaps more importantly, associated activities, thoughts, and emotions that may be contributing to the urge to pull should be codified.  (Kraemer, 1999, p. 300)  In session, this record can be reviewed and subsequently tied to “high risk circumstances” and “priori intuitions” involving constructs such as anger, frustration, depression, and boredom.

Relaxation training is a critical component if we subscribe to the “kindling” hypothesis explained previously.  Relaxation is intended to reduce the urges that inevitably trigger the habit.  Examples abound, but diaphragmatic breathing, progressive relaxation, and visualization are all techniques that can be employed in isolation or in conjunction with each other.

Contingency Management is inexorably tied to the existential anchor of cognitive dissonance described above.  My emphasis on this element is where my approach might differ from some other clinicians.  “You are free to do whatever you want, but you are responsible for the consequences of everything that you do.”  (Ingram, 2012, p. 270)  This might include the client writing down sources of embarrassment, advantages of controlling the symptomatlogy of TM, etc.  (Kraemer, 1999)  The moment someone with pyromania decides that no fire worth being imprisoned, they will stop starting fires.  The same holds true with someone who acknowledges the consequences of pulling their hair.

How do we define success?  Once habit reversal is successfully accomplished in one setting or situation, the client needs to be taught how to generalize that skill to other contexts.  A hierarchical ranking of anxiety provoking situations can be helpful in this process since self-paced graduated exposure is likely to increase tolerability for the anxious client.  (Ingram, 2012, p. 240)  If skills are acquired, and generalization occurs, we can reasonably expect a significant reduction in TM symptomatlogy.  The challenges are significant, cognitive behavioral therapy is much easier said than done.  High levels of treatment motivation are required for the behavioral elements, and moderate to high levels of insight are exceptionally helpful for the cognitive elements.  In addition, this is an impulse control disorder… impulsivity leads to treatment noncompliance and termination.  The combination of all the above, in addition to the fact that TM is generally acknowledged as one of the more persistent and difficult to treat disorders, prevents me from providing any prognosis other than “this treatment will work as well as the client allows it to work.”


Abraham Low Self-Help Systems. (n.d.). Recovery international terms and definitions. Retrieved August 2, 2012, from http://www.lowselfhelpsystems.org/system/recovery-international-language.asp

American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). Washington, DC: Author.

Frankl, V. E. (1997). Man’s search for meaning (rev. ed.). New York, NY: Pocket Books.

Ingram, B. L. (2012). Clinical case formulations: Matching the integrative treatment plan to the client (2nd ed.). Hoboken, NJ: John Wiley & Sons.

Kraemer, P. A. (1999). The application of habit reversal in treating trichotillomania. Psychotherapy: Theory, Research, Practice, Training, 36(3), 298-304. doi: 10.1037/h0092314

Lambert, K. G., & Kinsley, C. H. (2011). Clinical neuroscience: Psychopathology and the brain (2nd ed.). New York: Oxford University Press.

Ledley, D. R., Marx, B. P., & Heimberg, R. G. (2010). Making cognitive-behavioral therapy work: Clinical process for new practitioners (2nd ed.). New York, NY: Guilford Press.

Persons, J. B. (2008). The case formulation approach to cognitive-behavior therapy. New York, NY: Guilford Press.

Pirsig, R. M. (1999). Zen and the art of motorcycle maintenance: An inquiry into values (25th Anniversary ed.). New York: Quill.

Shiel, W. C., Jr., & Stoppler, M. C. (Eds.). (2008). Webster’s new world medical dictionary (3rd ed.). Hoboken, NJ: Wiley Publishing.

Young, J. E., Klosko, J. S., & Weishaar, M. E. (2003). Schema therapy: A practitioner’s guide. New York: Guilford Press.

Eating Disorders (EDs) and Substance Use Disorders (SUDs): Shared and Causal Etiology

The etiologies of both Eating Disorders (EDs) and Substance Use Disorders (SUDs) are perceived to be complex and multidimensional in nature.  No simple etiological path is indicated in either category.  Many contemporary theories “implicate a ‘collision’ among biological factors (e.g., genetic influences on neurotransmitter and hormonal function), psychological tendencies (problems with mood, temperament, and impulse controls), and social pressures (promoting body consciousness or generalized self-definition problems, and developmental processes (conducive to self-image or adjustment problems).”  (Blaney & Millon, 2009, p. 436)  The current model of SUD risk factors would not be complete without all of the above, perhaps with a few minor modifications.  This essay will attempt to address and discuss the common etiological factors between EDs and SUDs, as well an explore concepts of causal etiology that suggest that having one disorder predispositions an individual to succumb to another.

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Causal etiology has suggested that having one disorder (an eating disorder, for example) may put an individual at risk for developing another disorder (like substance abuse, or vice versa).  The statistics surrounding the comorbidity of substance abuse and eating disorders is considerable.  “Substance abuse and eating disorders have the highest mortality risks of all mental disorders and half of all clients with eating disorders abuse alcohol or illicit drugs.”  (Carbaugh & Sias, 2010, p. 125)  Shared or causal etiological factors between the substance abuse and eating disorders include psychological, environmental, and biological antecedents.  Both disorders are influenced by specific personality type (lack of control, craving, denial, impulsiveness), similar developmental issues (societal and familial pressures), as well as common family history (genetic predisposition) and specific biological vulnerability.  (Carbaugh & Sias, 2010)  Whether causal or shared, it is increasingly evident that SUDs and EDs share common etiological pathways, even to the extent that they may be causal in their relationship.

Common personality factors play a significant role in the onset and maintenance of both eating disorders and their comorbid conditions.  However, the personality of people whom suffer from AN tend to qualitatively different from the personalities of people whom suffer from BN.  Individuals whom suffer from AN have been found to be approval seeking, self-doubting, conflict-avoidant, excessively dependent, socially anxious, and have a tendency to be described as “perfectionists.”  Individuals whom suffer from bulimia often experience significant affective instability including highly variable mood states, impulsive behavior, low frustration tolerance, and high anxiety.  (Netherton, Holmes, & Walker, 1999, p. 401)  Differences in the underlying personality deficiencies can account for differences in comorbidity when comparing EDs among themselves, although EDs and SUDs generally continue to demonstrate remarkable comorbidity regardless of the type of ED we examine.

The news media frames obesity as a “moral problem.”  Obese populations are condemned by the media as engaging in gluttony and sloth while society overwhelmingly blames “bad individual choices” (despite increasing discussion of social-structural factors over time).  (Saguy & Gruys, 2010, p. 247)  The above statements easily could have been rewritten to drive home a different message.  The news media frames drug abuse as a “moral problem.”  Drug abusers are condemned by the media as engaging in greed and apathy (synonyms for gluttony and sloth) while society overwhelming blames “bad individual choices” (despite increasing discussing of social structural factors over time).  Obesity and drug abuse are 21st Century witches.  Will you join the hunt?

The contribution of the family only begins with biological disturbances in the serotonin, dopamine, gamma-aminobutyric acid and endogenous opioid peptide systems that may underlie both disorders.  (Pearlstein, 2002, p. 70)  Despite the fact that The Academy for Eating Disorders (AED) has specifically condemned statements that implicate family influences “as the primary cause of AN or BN,” they have acknowledged that particular styles of family behavior and biological vulnerability may increase risk for psychopathology in general, including eating disorders.  (“Role of Family in EDs”, 2009)  Dieting is one example of a behavior that is frequently encouraged by well intentioned families.  Research supports the positive association between the dieting behaviors (not just eating disorders themselves) and increased risk for alcohol use problems.  (Heidelberg & Correia, 2009)  Families who promote dieting in their children may inadvertently be promoting substance abuse.  Add latent genetic influence (like a parent with an eating disorder or who abuses substances) to that encouragement we may have a ‘perfect storm’ of predispositions that could potentially result in a full blown eating disorder comorbid with a substance abuse problem.  Be it through the environmental impact of familial behavior, or by latent genetic influence, family plays a significant role in the development of both disorders.

EDs and SUDs can be viewed through the same lens.  Shared etiology, including familial contributions, media influences, and personality factors; all play a role in the perpetuation of the stereotype.  If we perpetuated the image of common people drinking wate,r instead of hard bodies drinking alcohol, perhaps the association between substance abuse and eating disorders could be severed.

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American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). Washington, DC: Author.

Blaney, P. H., & Millon, T. (2009). Oxford textbook of psychopathology (2nd ed.). New York, New York: Oxford University Press.

Carbaugh, R. J., & Sias, S. M. (2010, Apr). Comorbidity of bulimia nervosa and substance abuse: Etiologies, treatment issues, and treatment approaches. Journal of Mental Health Counseling, 32(2), 125-138. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=2026599321&sid=1&Fmt=3&clientId=4683&RQT=309&VName=PQD

Heidelberg, N. F., & Correia, C. J. (2009, Dec). Dieting behavior and alcohol use behaviors among national eating disorders screening program participants. Journal of Alcohol and Drug Education, 53(3), 53-64. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1959547071&sid=9&Fmt=3&clientId=4683&RQT=309&VName=PQD

Netherton, S. D., Holmes, D., & Walker, C. E. (1999). Child and adolescent psychological disorders: A comprehensive textbook. Oxford, NY: Oxford University Press.

Paper stresses important role of family in eating disorders. (2009, Nov). Journal of Psychosocial Nursing & Mental Health Services, 47(11), 11. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1908060671&sid=9&Fmt=3&clientId=4683&RQT=309&VName=PQD

Pearlstein, T. (2002, Mar). Eating disorders and comorbidity. Archives of Women’s Mental Health, 4(3), 67-78. Retrieved from http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?index=24&did=687270031&SrchMode=2&sid=11&Fmt=6&VInst=PROD&VType=PQD&RQT=309&VName=PQD&TS=1274809726&clientId=4683

Saguy, A. C., & Gruys, K. (2010, May). Morality and health: News media constructions of overweight and eating disorders. Social Problems, 57(2), 231-250. doi: 10.1525/sp.2010.57.2.231


Like so many other mental disorders, eating disorders project people who are really “out of balance.”  I don’t think anyone would be an obesity advocate… after all; obesity presents as many or more health problems as being overly thin.  In the end, it’s all about balance.

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1 in 5 women have an eating disorder.  Kids start dieting as early as 4th grade.  I can actually see this, I see a bit of it in my daughter… she is age 8 (2nd grade) and has shown concerns about “being too heavy.”  We have turned the focus onto “being healthy” not “being thin.”  80% of 13 year olds have tried to lose weight… this doesn’t surprise me, considering the “ideal image” that western culture projects to children.  1 in 5 anorexics die?  Our text indicates it was closer to 1-10, that’s nearly double NHW’s estimate.  I know it’s a real problem, but having good epidemiological data would be a good start to “justifying” expending resources to extinguish it.

With regard to what a clinican should know or ask about eating disorders, the following questions are at the top of my list.

1)      Clinicians should know your subtypes of Anorexia Nervosa (AN):

  1. Restricting Type describes presentations in which weight loss is accomomplished primarily through dieting, fasting, or excessive exercise.
  2. Binge-Eating/Purging Type describes presentations where the individual engages in binge eating, purging, or both.  They may employ self induced vomiting, misuse of laxative, diuretics, or enemas.  (American Psychiatric Association, Diagnostic and statistical manual of mental disorders, 2000, p. 585)

2)      Probe for comorbid disorders and associated features, especially depression, anxiety disorders, dissociative disorders, substance abuse, and personality disorders (particularly borderline personality disorder).  (Netherton, Holmes, & Walker, 1999, p. 401)

3)      Clinicians should know that, while these disorders predominantly effect females, males can also suffer from either AN or BN.  “There is some evidence that ED prevalences are recently increasing in males.”  (Blaney & Millon, 2009, p. 433)

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American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). Washington, DC: Author.

Blaney, P. H., & Millon, T. (2009). Oxford textbook of psychopathology (2nd ed.). New York, New York: Oxford University Press.

Netherton, S. D., Holmes, D., & Walker, C. E. (1999). Child and adolescent psychological disorders: A comprehensive textbook. Oxford, NY: Oxford University Press.

Eating Disorders = BIG BUSINESS

“Weight discrimination and the resulting obsession with thinness are rampant and recalcitrant.  I believe that, in order to make any kind of a dent in this field, we all need to combat these pernicious influences.”  (Netherton, Holmes, & Walker, 1999, p. 412)  Amen.  The weight of the media, the “diet food industry,” and the purveyors of a “healthy lifestyle” propagate this issue… without a doubt.  Losing weight is BIG BUISINESS, and there are huge profits to be made for those that offer obese people the glimmer of a stereotypically thin body.

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I also appreciated the acknowledgement on the pressure exerted by managed care.  Eating disorders appear to be particularly “deep seated” and ill suited for half a dozen one hour sessions.  Correcting inaccurate perceptions, relabeling cognitions of visceral and affective states, and redrawing boundaries… this kind of work takes time… more time than managed care often provides.  This is yet another example of the effect managed care will continue to have for as long as it is the primary method of seeking out psychological assistance.

I was suitably surprised at the long-term mortality rate… suggested to be over 10%.  (Netherton et al., 1999, p. 399)  With a roughly 1 in 10 shot of succumbing to starvation, suicide, or electrolyte imbalance; you would think this particular set of disorders would get more research attention.  The fact that there is still limited epidemiological data is frustrating… perhaps the difficulty obtaining the data is related to the relative secrecy and shame associated with the disorders themselves?

Like the BM text, NHW jumps on the multi-determined etiology bandwagon.  It’s hard to disagree with since biological, familial, sociocultural, and personality factors all seem to be plausible.  The differences in family characteristics were particularly interesting.  “Bulimic families tend to be characterized as disengaged, chaotic, and highly conflictual and as having a high degree of life stress.”  Conversely, “anorexic families tend to be characterized as enmeshed, overprotective, and conflict avoidant.”  (Netherton et al., 1999, p. 400)  That’s a strange clinical picture that seems to suggest that there might be a single underlying biological cause for EDs in general, but that familial and personality factors may play a role in its manifestation.

The list of comorbid disorders we need to consider during the assessment process is long and fairly inclusive.  “Depression, anxiety disorders, dissociative disorders, substance abuse, and personality disorders” are on the forefront of the disorders we should be checking for.  (Netherton et al., 1999, p. 401)  Furthermore, NHW suggest we assess treatment history, as well as suicide attempts and self mutilative behaviors (cutters).

Pharmacological interventions employing antidepressants have been particularly successful.  This text only cites 3 studies that have employed SSRI class antidepressants, but they report “significant improvement with 60-80 mg dosages (of Prozac) compared to placebo.”  (Netherton et al., 1999, p. 407)  I think I am going to dig deep into some more recent research to see of this trend holds up, there has to be more than three studies on it by now.

I like the idea of a behavioral contract… not just for eating disorders, but for any disorders which involve “behavior.”  I am inclined to agree with the statement “the contract provides structure and predictability.  Expectations, rewards, and consequences are delineated so that all people involved (patient, treaters, families) know what is expected at all stages of treatment.”  (Netherton et al., 1999, p. 407)  My question is this… realistically, what “consequences” are there if we are dealing with outpatient treatment?

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Netherton, S. D., Holmes, D., & Walker, C. E. (1999). Child and adolescent psychological disorders: A comprehensive textbook. Oxford, NY: Oxford University Press.

Eating Disorders

“Eating disorders (EDs) are polysymptomatic syndromes, defined by maladaptive attitudes and behaviors around eating, weight, and body image.”  (Blaney & Millon, 2009, p. 431)  The primary disorders in this category are anorexia nervosa (AN), bulimia nervosa (BN), and eating disorders no otherwise specified (EDNOS).  Examples of EDNOS might include “AN-like” with preoccupations with thinness, normal-weight people purging food without binging or simply binging without purging (Binge Eating Disorder, or BED).  (Blaney & Millon, 2009, p. 432)

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Epidemiological data suggests that EDs occur more often in women than in men (by a factor of roughly 10); although there is some evidence indicating that the gender gap is closing.  Although AN/BN tend to be most prevalent in late adolescence and early adulthood, BED defies the stereotype by manifesting in an older age group (typically around 40 years of age).  There is also little linkage to socioeconomic status, despite the common belief that Eds are disorders of the affluent.  (Blaney & Millon, 2009, p. 433)  This totally astounds me… how can people who are already undernourished give up what sustenance they are offered?

EDs frequently co-occur with mood, anxiety, substance-abuse, personality, and other psychiatric disorders.  There are so many comorbid mood disorders noted in individuals with EDs that it is easier to exclude mood disorder (singular) that is unrelated… bi-polar disorders.  Personally, I believe the single mood disorder that is currently excluded should be considered.  “The disorders are believe to depend on similar family/developmental determinants (e.g., attachment problems or trauma), and both have been thought to have similar neurobiological substrates.”  (Blaney & Millon, 2009, p. 434)  Social phobias and OCD were among the most prevalent anxiety related comorbid disorders.  Since anxiety disorders often precede ED onset, it has been suggested that an anxious or obsessive-compulsive attitude predisposes an individual to ED development.  (Blaney & Millon, 2009, p. 435)

Not only are PTSD and substance abuse disorders often comorbid with EDs, but they are often comorbid with each other.  “Substance abusers in an eating-disordered population show significantly more Social Phobia, Panic Disorder, and Personality Disorders.  In addition, comorbid substance abuse was found to predict elevations in Major Depression, Anxiety Disorders, Cluster B personality disorders, as well as greater impulsivity and perfectionism.”  (Blaney & Millon, 2009, p. 435)

Finally, personality disorders are frequently present in individuals whom suffer from EDs.  Restrictive type EDs seem to be associated with Anxious-Fearful PD diagnosis (anxiousness, orderliness, introversion, preference for sameness and control).  Binge-purge types have a pronounced affinity for the dramatic-erratic PDs including attention/sensation seeking, extroversion, mood lability, and proneness to excitability or impulsivity.  (Blaney & Millon, 2009, p. 435)

EDs are assumed to be multiply determined by complex interactions including constitutional factors, psychological/developmental processes, social factors, and secondary effects in the biological, psychological and social spheres of maladaptive eating practices themselves.  (Blaney & Millon, 2009, p. 443)  All of the above features generally manfest in eating-specific cognitions related to bodily appearance and appetite regulation, body image or weight considerations, and social values that heighten concerns with all of the above.  As a result, it is currently conceived that EDs represent a “tightly woven” expression of causes and symptoms that have an interrelationship between and among each other.

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Blaney, P. H., & Millon, T. (2009). Oxford textbook of psychopathology (2nd ed.). New York, New York: Oxford University Press.

Comorbidity: Substance Abuse Disorders (SUDs)

Comorbid, or comorbidity, is literally defined as “recurring together.”  (Shiel, Jr. & Stoppler, 2008, p. 94)  For our purposes, comorbidity will refer to cases where two or more psychiatric conditions coexist, and where one of the conditions is a substance abuse disorder (SUD).  “There are 11 groups of substances specifically discussed in the DSM-IV: alcohol; amphetamines and related sympathomimetics; caffeine; cannabis; cocaine; hallucinogens; inhalants; nicotine; opiates; phencyclidine and related drugs (PCP); and sedatives, hypnotics, and anxiolytics.”  (Colman, 2009, p. 741)  Any one of the above substances, or combination of the above substances, can contribute to and be related this discussion of comorbidity with SUDs.

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Although this list is by no means exhaustive, “long-term substance use is related to psychiatric conditions such as suicide and depression, affective disorders, eating disorders (ED), and personality disorders (PD).”  (Netherton, Holmes, & Walker, 1999, p. 248)  Increased risk of mood disorders has been documented across all substance categories and across all mood related diagnoses.  (Blaney & Millon, 2009, p. 287)  Substance-Related Disorders are commonly comorbid with many mental disorders, including Conduct Disorder in adolescents; Antisocial and Borderline Personality Disorders, Schizophrenia, Bipolar Disorder.  (American Psychiatric Association, Diagnostic and statistical manual of mental disorders, 2000, p. 204)   Schneier et al. (2010) also concluded that alcohol use disorders and social anxiety disorder (SAD) is a prevalent dual diagnosis, associated with substantial rates of additional co-morbidity.

ADHD represents a risk factor for substance abuse.  ADHD patients with a high degree of nicotine consumption may be consuming large quantities as a form of self-medication.  Nicotine and alcohol, when combined, pose a markedly greater risk for the development of other addictions.  (Ohlmeier et al., 2007, p. 542)  There is “high comorbidity between heavy drinking and heavy smoking.”  (Blaney & Millon, 2009, p. 266)  These admissions seem to support the premise that alcohol and nicotine continue to serve as “gateway drugs” for people whom suffer from ADHD.

“In terms of clinical presentation, a concurrent Personality Disorder (PD) diagnosis is associated with an earlier age of onset of alcohol-related problems, increased addiction severity, more secondary drug use, more psychological distress, and greater impairment in social functioning.  As for course in addiction treatment, a concurrent PD diagnosis has been associated with premature discontinuation of treatment, earlier relapse, poorer treatment response, and worse long-term outcome.”  (Zikos, Gill, & Charney, 2010, p. 66)  Cluster B (Antisocial, Borderline, Histrionic, and Narcissistic) Personality Disorders (PDs) appear to be particularly prevalent, perhaps because the link between substance dependency and antisocial behavior can be found genetically.  (Blaney & Millon, 2009, p. 263)

“Among individuals with schizophrenia, between 40% and 50% also meet criteria for one or more substance use disorders.”  (Blaney & Millon, 2009, p. 288)  Comorbid substance use complicates adherence to sometimes complex schizophrenia treatment regimens.  Poor adherence to treatment results in worsening of schizophrenia symptoms, relapse, worsening of overall condition, increased utilization of health care facilities, re-hospitalization, reduced quality of life, social alienation, increased substance abuse, unemployment, violence, high rates of victimization, incarceration, and death.  (Hardeman, Harding, & Narasimhan, 2010, p. 405-406)  The compounding effect of substance abuse on the quality of life for individuals with schizophrenia can’t be understated.  Substance abuse is particularly common and also worsens the course of schizophrenia.  (Buckley, Miller, Lehrer, & Castle, 2009, p. 396)

Differential diagnosis and treatment can sometimes be a troublesome proposition.  Comorbidity complicates the diagnosis, treatment, and clinical course of Substance Abuse Disorders (SUDs).  (Blaney & Millon, 2009, p. 287)  “If symptoms precede the onset of substance use or persist during extended periods of abstinence from the substance, it is likely that the symptoms are not substance induced.”  (4th ed., text rev.; DSM-IV-TR; American Psychiatric Association, 2000, p. 210)  Carbaugh and Sias (2010) concluded that successful outcomes can be increased through proper diagnosis and early intervention, at least in the case of comorbid Bulimia Nervosa and substance abuse.  Prevention of substance use disorders can help alleviate or decrease much impairment in psychiatric patients in particular.  (Powers, 2007, p. 357)  Furthermore, a review of treatments for patients with severe mental illness and comorbid substance use disorders concluded that mental health treatment combined with substance abuse treatment is more effective than treatment occurring alone for either disorder or occurring concurrently without articulation between treatments.  (Hoblyn, Balt, Woodard, & Brooks, 2009, p. 54)

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American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text rev.). Washington, DC: Author.

Blaney, P. H., & Millon, T. (2009). Oxford textbook of psychopathology (2nd ed.). New York, New York: Oxford University Press.

Buckley, P. F., Miller, B. J., Lehrer, D. S., & Castle, D. J. (2009, Mar). Psychiatric comorbidities and schizophrenia. Schizophrenia Bulletin, 35(2), 383-402. doi: 10.1093/schbul/sbn135

Carbaugh, R. J., & Sias, S. M. (2010, Apr). Comorbidity of bulimia nervosa and substance abuse: Etiologies, treatment issues, and treatment approaches. Journal of Mental Health Counseling, 32(2), 125-138. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=2026599321&sid=2&Fmt=3&clientId=4683&RQT=309&VName=PQD

Colman, A. M. (2009). Oxford dictionary of psychology (3rd ed.). Oxford, NY: Oxford University Press.

Hardeman, S. M., Harding, R. K., & Narasimhan, M. (2010, Apr). Simplifying adherence in schizophrenia. Psychiatric Services, 61(4), 405-408. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=2006767471&sid=3&Fmt=3&clientId=4683&RQT=309&VName=PQD

Hoblyn, J. C., Balt, S. L., Woodard, S. A., & Brooks, J. O. (2009, Jan). Substance use disorders as risk factors for psychiatric hospitalization in bipolar disorder. Psychiatric Services, 60(1), 50-55. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1654365811&sid=6&Fmt=3&clientId=4683&RQT=309&VName=PQD

Netherton, S. D., Holmes, D., & Walker, C. E. (1999). Child and adolescent psychological disorders: A comprehensive textbook. Oxford, NY: Oxford University Press.

Ohlmeier, M. D., Peters, K., Kordon, A., Seifert, J., Wildt, B. T., Weise, B., … Schneider, U. (2007, Aug). Nicotine and alcohol dependence in patients with comorbid attention-deficit/hyperactivity disorder (ADHD). Alcohol and Alcoholism : International Journal of the Medical Council on Alcoholism, 42(6), 539-543. doi: 10.1093/alcalc/agm069

Powers, R. A. (2007, May). Alcohol and drug abuse prevention. Psychiatric Annals, 37(5), 349-358. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1275282831&sid=5&Fmt=3&clientId=4683&RQT=309&VName=PQD

Schneier, F. R., Foose, T. E., Hasin, D. S., & Heimberg, R. G. (2010, Jun). Social anxiety disorder and alcohol use disorder co-morbidity in the National Epidemiologic Survey on Alcohol and Related Conditions. Psychological Medicine, 40(6), 977-988. doi: 10.1017/S0033291709991231

Shiel, W. C., Jr., & Stoppler, M. C. (Eds.). (2008). Webster’s new world  medical dictionary (3rd ed.). Hoboken, NJ: Wiley Publishing.

Zikos, E., Gill, K. J., & Charney, D. A. (2010, Feb). Personality disorders among alcoholic outpatients: Prevalence and course in treatment. Canadian Journal of Psychiatry, 55(2), 65-73. Retrieved from http://ezproxy.bellevue.edu:80/login?url=http://proquest.umi.com.ezproxy.bellevue.edu/pqdweb?did=1986429431&sid=1&Fmt=3&clientId=4683&RQT=309&VName=PQD