Part 1: Understanding an eating disorder

An Overview

What follows are a number of the mainstream technicalities that need introduction in order for you, as a patient, to be able to communicate with health care practitioners dedicated to diagnosing and treating eating disorders.

Definition

An eating disorder is best described as a chronic condition resulting from the misidentification of food as a threat; and as such it is best situated under the much larger umbrella of anxiety disorders. An eating disorder is currently defined as a mental illness within the Diagnostic and Statistical Manual of Mental Disorders (DSM) and psychiatrists are the only health care professionals tasked with submitting the clinical diagnosis that will be accepted by either private or national health insurance providers.

Classification

The DSM-5 divides eating disorders into three main classifications: anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED). This latest DSM edition has also added pica, rumination, and avoidant/restrictive food intake disorder (ARFID).

Additionally, there are these classifications: Other Specified Feeding and Eating Disorder (OSFED) and Unspecified Feeding and Eating Disorder (UFED), which ostensibly replace what was called Eating Disorder Not Otherwise Specified (EDNOS) as found in the DSM-IV.

Binge eating disorder (BED) was not identified as a stand-alone eating disorder by expert researchers 1 in the field and the symptoms are not related to eating disorders. It was identified as a condition needing further study within the DSM-IV. BED in the DSM-5 has no connection to its definition within the DSM-IV. Those with BED, prior to the 2013 release of the DSM-5, were diagnosed with EDNOS.

The current definition of BED within the DSM-5 reflects cycles of restriction and reactive eating behaviors that do not rise to the severity listed for a diagnosis of BN. For more details and thorough references explaining BED within the DSM-5, please refer to the Eating Disorder Institute website blog posts on the topic. 2, 3

The inclusion of BED in the DSM-5 was contentious and involved concerning conflicts of interest. 4, 5, 6

Out of the 18 panels tasked with developing recommendations for DSM-IV classifications, six had more than 80% of their members tied financially to the pharmaceutical industry. The eating disorder panel was one of those six, with 83% of its members tied to pharmaceutical industry support. 7 The number of panelists tied to pharmaceutical industries rose 14% overall from development of the DSM-IV to DSM-5. 8

There was a push from independent researchers in the field of eating disorders to move towards a transdiagnostic approach by merging the five distinct classifications of eating disorders from the DSM-IV into one broad classification of eating disorder in the DSM-5. Transdiagnosis would have accurately reflected the clinical evidence that anorexia and bulimia are not two distinct conditions, and that several other restrictive eating and compensatory behaviors are all part of the same neurobiological condition as well. 9, 10, 11 This appropriate merger of classifications did not occur perhaps because too many special interests groups were involved in the development of the DSM-5.

I have no use for the DSM as not only is its provenance highly suspect, given pharmaceutical industry ties, but also it fails to reflect much of the recent genetic and neurological research data that renders DSM symptom checklists overly simplistic, subjective, and often inapplicable. Nonetheless, patients struggling to receive a diagnosis that will allow for financial coverage of their treatment must familiarize themselves with the DSM because its classifications are the only ones recognized by most national and private medical insurance organizations in the world’s developed nations.

The International Classification of Diseases and Related Health Problems (ICD-10) is sometimes used in place of the DSM for diagnosis; however the classifications found within both tomes are essentially interchangeable with those of the DSM.

Symptomatology

Dr. Christopher Fairburn, a professor of psychiatry at Oxford University and a leader in the field eating disorder research and treatment, explains the symptoms associated with the eating disorder spectrum as follows:

…extreme dietary restraint and restriction, binge eating,

self-induced vomiting and the misuse of laxatives, driven exercising, body checking and avoidance, and the over-evaluation of control over eating, shape and weight. 12

Transdiagnosis recognizes the fact that those with an eating disorder can shift from one symptom to another or express several symptoms at the same time, and that these symptoms are also interchangeable.

The terminology I find more useful and accurate in describing eating disorder symptoms is as follows:

avoiding food intake

avoiding food intake and experiencing reactive eating sessions * in response to that restriction

in response to that restriction abuse of laxatives, diuretics, and purging to try to redress a reactive eating session

using exercise to alleviate anxiety associated with eating and validating eating through “burning off” food intake

abuse of prescription or illicit substances as a means to avoid food intake or reduce food absorption within the body

applying rigid adherence to eating “healthily” or “cleanly” to alleviate anxiety associated with eating.

Causes

An eating disorder is an inherited neurobiological condition.

The genetic markers are not fully identified, but the condition usually lies dormant and may be triggered by innumerable environmental factors. The genetic predisposition for the condition is present in all human populations and even exists in some animals. 13, 14 It has persisted within the human gene pool because it likely has, or once had, beneficial implications for survival.

All manner of fancy research has been investigating the tantalizing suggestion that the dopaminergic reward systems in the brains of those with eating disorders are different than those of healthy controls. 15, 16 There is also plenty of fascinating stuff on the brain structures that may or may not be involved in miscasting food as the enemy. However, there are far more comprehensive sites and books on these topics than this series on recovery. I will provide a layperson’s view of the cascade from the moment an eating disorder is activated.

While the environmental factors that might activate an eating disorder in someone with the genetic predisposition can be anything from simply starting a diet, to undergoing surgery, catching a stomach bug, experiencing traumatic life events, to any situation you might care to name, none of those factors causes the condition; however they all have the capacity to generate energy deficits in the body, and in so doing they activate the condition.

In other words, you won’t get an eating disorder because you’re exposed to pictures of thin models. However, if you have the genetic predisposition to misidentify food as a threat, then the exposure to pictures of thin models may indeed be one of several environmental factors that will activate the condition.

Evidence-based treatment

Most people are unaware that most treatments for an eating disorder are largely not evidence-based.

Evidence-based treatment requires that the following steps have been completed: 1) clinical trials where the treatment in question is measured against a control group and, 2) other researchers have duplicated the results. Ideally, the treatment has also been measured over a long period of time to further ensure the outcomes are not short-lived as well.

Today, only one treatment protocol qualifies as evidence-based treatment: Maudsley family-based treatment (FBT). FBT has controlled and duplicated trials along with published and confirmed five-year remission rates to support its classification as evidence-based treatment.

Two other protocols, Kartini (a family-based approach) and Mandometer (a technology-based approach), have self-published data but no independent corroboration of their findings as yet.

Problematically, FBT is specifically designed for child and adolescent sufferers of eating disorders and its design is difficult to translate into an adult patient environment.

Homeodynamic Recovery Method

The HDRM is the set of science-based guidelines for recovery from an eating disorder that are published here on the Eating Disorder Institute website. There have been no controlled trials or independent corroboration and therefore HDRM cannot be identified as evidence-based treatment at this point.

However, the guidelines are based on clinical trial data from FBT and the Minnesota Starvation Experiment, along with other published and peer-reviewed data, rather than merely being derived from empirical observation or practitioner philosophy. The name of the treatment program reflects the way in which the human body manages its own energy balance.

Homeodynamics is a way of viewing the human living system as defined by Martha Elizabeth Rogers (1914-1994) and often also called “nursing theory”. The three principles of homeodynamics are that human nature is dynamic, ever-changing and holistic. Within the space of functional medicine, homeodynamics captures the reality that there is no one homeostatic optimal state for a living system, but rather a range that dynamically adjusts in response to internal and external stimuli.

The HDRM for reaching remission from an eating disorder encompasses the fact that the human living system is optimized when most biological systems are actually running well above 100% and effectively clamped by key enzymes to remain at 100%. These clamping mechanisms are economical from an energy perspective rather than trying to rev the system up to be at 100% but no higher.

The HDRM includes the following key facets:

Unrestricted eating with minimum intakes that are set to reflect actual average consumption of non-restricting equivalents 17 No workouts or exercise, and no weighing or taking body measurements † 18 19 Applying specific training to address the misidentification of food as a threat ‡

Additionally, an omnivorous diet is highly recommended, although an ovo-lacto vegetarian diet can be accommodated. Ultra-processed foods are encouraged in the early phases of recovery as explained in the blog post Food, Family and Fear, found on the Eating Disorder Institute website. 20

Prevalence

One-third of all people who diet will end up on the eating disorder spectrum. 21, 22 While not all of develop clinical cases, if left untreated they will experience lifelong anxieties and compulsions around food and weight gain. The condition can develop into a clinical case at any point due to life stressors (anything from a cold to a break-up). Over time, those with the condition will often slide up and down the spectrum, or express multiple facets of the spectrum at once (anorexia, restrict/reactive eating cycles, bulimia, orthorexia [extreme focus on healthy foods], and anorexia athletica [over-exercise]).

Problematically, all clinical trials identifying the prevalence of eating disorders use the narrow, and largely unrepresentative, symptom checklists found in the DSM for identifying those with eating disorders.

When Dr. Daniel Le Grange and his colleagues reviewed and analyzed community-based surveys to uncover eating disorder prevalence, they offered the following conclusions:

Although the lifetime prevalence estimates of eating disorders from population-based studies of adults are relatively low (0.5%–1.0% for anorexia nervosa [AN] and 0.5%–3.0% for bulimia nervosa [BN])…community studies that used dimensional measures in youths have also yielded far greater prevalences of disordered eating behaviors (ie, 14%–22%) than those found in studies that applied strict DSM-IV diagnostic criteria. 23

The prevalence of eating disorders in infertile women is also five times higher than the population-wide lifetime prevalence rate. 24 While you may have been used to seeing prevalence rates for distinct DSM categories (AN, BN, EDNOS, or the more recent DSM-5 category equivalents) that suggest lifetime rates of between 0.3% to 2%, as an entire spectrum disorder that can impact quality and length of life, it is conservative to apply the much broader range of 20% to 33%.

The reason for the disparity between diagnosed prevalence and community-based prevalence is two-fold: the DSM categories are narrow, and many with the condition are unaware their behaviors would constitute the presence of an eating disorder and thus never seek treatment.

Here are the criteria for diagnosing AN in the DSM-5:

Persistent restriction of energy intake leading to significantly low body weight (in context of what is minimally expected for age, sex, developmental trajectory, and physical health)

Either an intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain (even though significantly low weight)

Disturbance in the way one's body weight or shape is experienced, undue influence of body shape and weight on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight. 25

As you can see from the above criteria, someone with a drive to be fit (and not thin) who spends significant amounts of time working out and attending to optimal macronutrient intake would not self-identify as having AN, nor would she receive such a diagnosis through psychiatric evaluation. However there is a classification in the DSM-5 called unspecified feeding or eating disorder (UFED) that will allow for a clinician to identify that a person is experiencing significant distress or impairment of quality of life due to eating or feeding behaviors that do not meet the exact criteria for AN, BN, etc. However in order for a patient to be diagnosed with an eating disorder she must first self-identify as experiencing distress and a reduction in quality of life such that she will seek psychiatric evaluation. Given we live in a society where the pursuit of fitness and so-called healthy eating is unlikely to be seen as impairing quality of life (although it most certainly does for those with an eating disorder), a large number of those with active eating disorders remain unidentified and untreated in the community as their behaviors are almost indistinguishable from the accepted norm.

Within our current sociocultural fattist environment we need to ensure that we avoid underdiagnosis of eating disorders to avoid the commensurate harm that failing to diagnose and treat will entail for individual patients.

Statistics and prognosis

Between the ages of 15 and 24, eating disorders are 12 times more deadly than all other leading causes of death combined for that age group, including car accidents. 26

The rates of remission range from 3% to 96% 27 and relapse rates range from 35% to 50%. 28, 29 Remission rates for FBT at 12- and 36-month follow-ups are 75%. 30, 31, 32

Standardized mortality ratios (SMRs) for eating disorders range from 1.92 to 10.5. 33, 34, 35 A standardized mortality ratio is a scientific way of identifying the increased risk of death associated with a particular condition when compared to a random healthy group of human beings. The standardized mortality ratio for a random healthy group is set at 1.00.

Because causes of death for those with eating disorders can range from heart failure to suicide, it is not always possible to extract accurate data if their underlying contributing condition (namely the eating disorder) is not identified on the death certificate. That is why SMRs vary from one trial to the next.

Reframing the SMR ranges into something more tangible, eating disorders have approximately a 1 in 4 to 1 in 5 fatality rate over a 20-year period.

The prognosis is that 50% will achieve full remission and generally maintain that remission, and the remaining 50% struggle with chronicity, social decline, progressive ill health, and early death. 36 This data applies no matter the treatment program applied.

Multidirectional system

The conditions listed in the DSM as mental disorders are identified with separate symptom checklists that bypass common genetic underpinnings. As just one example, bipolar disorder and schizophrenia are distinct conditions within the DSM, but genetic studies indicate these conditions are one and the same, based on proband and genotyping investigations. 37, 38 Eating disorders are another example where proband, twin, and genotyping studies all confirm that discrete symptoms are merely variations of the same underlying genetic presdisposition to misidentify food as a threat. 39, 40

Of course a genetic predisposition tells us nothing of the individual’s likelihood of developing an active state of any of these conditions. Nor can we identify how the sociocultural, familial, and environmental factors will shape not only the activation of the condition, but also its expression and progression. Genetic predisposition also tells us nothing of how the condition may perseverate, worsen, or resolve to full remission.

A multidirectional system of environmental inputs linked with genetic predispositions for all eating disorders will mean that there is never one single cause for the presence of an eating disorder.

Thus psychiatry, as a specialty, should be sidelined from the exclusive diagnosis and management of these conditions and instead the newer cross-disciplinary area of psycho-neuro-immuno-endocrinology (PNIE) should take up the research, examination, diagnosis, management, and resolution of these conditions.

Perhaps despite its own best efforts, psychiatry will indeed morph to become the field of PNIE. However, human beings cannot be treated in isolation from the community in which they reside, and that suggests anthropology should also be included: APNIE.

The interactions between the patient’s psychological state, her sociocultural space, and her neurological, immune, and endocrine (hormone) functions will reinforce or ultimately change the expression of genes prone misidentify food as a threat.

The four Ws and an H

While patients must navigate the silos of medical and psychiatric specialties today, the framework of the Homeodynamic Recovery Method rests on an as-yet-to-be mainstreamed APNIE discipline. The questions who, what, when, where, and how, rather than DSM symptom checklists, are the foundation of the HDRM.

Identifying an eating disorder becomes a patient-driven exercise the moment she determines her quality of life does not meet her expectations due to the invasive interference of the restrictive behaviors on her life. Those five questions frame the unique specifics of the condition’s expression and impact on the patient’s life. The answers frame the psychotherapeutic options that will best suit the patient involved. We will look at those psychotherapeutic options in more depth in chapter five.

The brain is a social organ, and it therefore physically changes with all APNIE inputs. These changes are rarely signs of disease. They occur constantly in each of us and predominantly create increased resilience in brain function and heighten overall individual survival. What we call learning is realized as physical changes within the brain.

Mental illness may be the result of progressive brain disease or it may be merely a transitory dip in function followed by increased function, or it might entail a shift into a chronic altered state of function.

Is an eating disorder a mental illness?

Individuals with this condition rarely lose their connection to what is referred to as consensus, or consensus-based, reality. 41

Consensus-based reality can, and often does, include many technically unreal thoughts that are held to be true by the majority. Therefore, there is majority agreement that those thoughts are sane. As one example, we do not classify those who believe in one all-seeing, all-knowing deity as insane, however that belief could not be said to be a sensory-based reality. Sensory-based reality—what we can identify through our senses—can cause all manner of cognitive contortions to try to single out someone with psychosis who constantly hears the voice of God as needing treatment without inadvertently treating everyone with a belief in a god as well—hence the usefulness of using consensus-based reality as way to identify psychosis.

Those with eating disorders are usually well aware they have a problem, even if they are applying denial tactics to avoid having to come to terms with the problem. They are grounded in consensus-based reality. Starvation does cause significant cognitive impairment that parallels what we might see in patients with physical trauma to the brain; only rarely, due to severe starvation, will a patient develop psychotic breaks with reality and, in those rare cases, re-feeding will usually resolve the attack.

But even the judicious use of consensus reality to identify those who are mentally ill among those who are mentally healthy still represents a binary concept that does not reflect the continuum of mental states. We are used to thinking of ourselves as being well or sick, but at what point does refusing to use a public washroom reflect mental illness vs. culturally normative expressions of hygiene? How many times does hand washing in a single day reflect the presence of an obsessive-compulsive disorder (OCD)?

Mental states do not have a clear marker of wellness and illness and they are fluid and changing throughout our lives, even throughout a single day.

The foundation of the HDRM is that the subjective assessment of quality of life defines the necessity of treatment. The label-first approach to identifying mental illness is not a defining factor for determining whether or not the HDRM is applicable for a patient.

Assessing quality of life allows you to step outside the clinical straitjackets of specialization and labels to determine for yourself whether you have lost critical facets of your quality of life to the behaviors and compulsions that drive the way you live your day-to-day existence (as you define it).

Ultimately it does not matter where one draws a line in the sand to identify behaviors beyond that line as expressions of mental illness; the issue is not the definition, but the self-defined level of distress that accompanies the expression of those behaviors.

Starving brain afraid of food

Fundamentally, the misidentification of food as a threat in any animal is not conducive to supporting life. That fact alone will be a definitive marker of a severe reduction in quality of life.

Keep in mind that the vast majority of those with eating disorders do not identify the drive to restrict as a misidentification of food as a threat. The drive to misidentify food as a threat resides in areas of the brain to which the conscious mind has almost no access. This threat is actually experienced as the conscious mind’s post-hoc evaluation (i.e., a guess) of why the patient is dealing with uncomfortable levels of arousal (anxiety, jitteriness, shallow breathing, twitchiness, clamminess, drive to move, etc.). I will explain how sociocultural frameworks shape these post-hoc evaluations in later sections of this blog series.

Restoring energy balance within the body (through rest and re-feeding) most certainly resolves many starvation-generated behaviors, which can also include anxiety, paranoia, depression, withdrawal, and extremely labile (changing) emotional states. However, in the absence of proactive learning and practicing of non-restrictive behaviors, remission from this deadly chronic condition is unlikely.

The application of behavior change is somewhat comparable to a desensitization program for a patient who has developed a severe allergy to peanuts. With a peanut allergy, the immune system misidentifies the proteins found within that legume as dangerous and it mounts an extreme response to rid the system of the foreign invader. It is that immune response that is potentially fatal to the patient rather than the proteins within the peanut itself. Recent research to help those with severe peanut allergies, using peanut flour to incrementally retrain the immune system to lower its response to those proteins, has met with success. 42

With an eating disorder, several areas distributed throughout the brain that are responsible for identifying environmental threats, have misidentified food consumption as a threat. Retraining the threat identification system with various psychological treatment modalities has met with clinical success for both eating disorders and a host of other related anxiety disorders.

Most importantly, as a chronic neurological condition, learning and practicing new and non-restrictive patterns improve both the symptoms and expression of an eating disorder within the mind and body. The question of whether the mind, or consciousness, is an artifact of brain function, or is inherently an expression of brain function, it not critical for the purpose of understanding the value of retraining the mind in reaching complete remission from an eating disorder.

Clinicians and patients have wrongly assumed that labeling these conditions as genetic in origin would remove the stigma associated with having a mental illness.

In fact several studies have shown that people’s responses are surprisingly more judgmental in their interactions when another’s behavior is framed as genetic in origin, and less judgmental and more patient when the behavior is framed as the result of environmental conditions or situations the patient has faced in her past or is facing today. 43, 44, 45

An eating disorder is treatable primarily because the brain is a social organ capable of structural changes due to factors that are both within and outside of the owner’s control. The outcomes of such treatments are ultimately unpredictable precisely because not all of the influencing factors are modifiable.

However it is important to reinforce the fact that an energy-depleted brain cannot function at all. Therefore, in the absence of adequate rest and re-feeding to reverse the energy deficit in the body, moving an eating disorder toward remission will have no hope of success.

In part 2 we’ll investigate how to determine whether an eating disorder is present or not.

* "Binge eating" is an inappropriate term for those with an eating disorder, for whom such eating sessions never occur in the absence of overall energy deficits within the body.

† Numerous inpatient environments resort to “blind weigh-ins” (standing on the scale backward) so that they can monitor the patient’s progress while ensuring the patient isn’t triggered to relapse by knowing his or her weight. But the larger issue of why we must know our weight is overlooked in this approach. Weighing oneself is counterproductive to accepting that optimal weight set points are maintained without cognitive interference.

‡ The training involves synthesizing and practicing natural behavior that is at odds with the dominant cultural environments in which we live today.