Once a single blog post, this is now a multi-part series on what to expect as you wend your way towards remission from an eating disorder. The series includes the following:
Part 1: Understanding an eating disorder
Part 2: Telltale dozen to uncover an eating disorder
Part 3: Some risks, complications and misdiagnoses
Part 4: Applying the Homeodynamic Recovery Method (HDRM) to get to remission
Part 5: Phases of recovery
Part 2: Telltale dozen to uncover an eating disorder
How can you tell if you have an eating disorder? Because it is a neurobiological condition and therefore rarely includes external, visible symptoms, it is the mindset you are forced to adopt toward food that is most telling.
Those dealing with this condition are two-thirds more likely to be of average or above-average weight than the emaciated icon that is commonly used to represent the condition in popular culture. 1 The fact that emaciation is not a definitive marker is yet another reason to pay particular attention to analyzing mindset, behaviors, and subjective reduction in quality of life.
- Family and friends have shifted from congratulating you on your weight loss and/or your healthier choices to making either careful or even blunt comments that you look unwell and generally don’t seem to eat enough. When workouts, runs, exercise and/or clean eating are dominant behaviors, then family and close friends start to make comments about how they feel you are unable to keep your commitments and priorities strait (meaning you put your behaviors ahead of your relationships).
- You are cold when others are not. You’ve started wearing sweaters (jumpers, pullovers) when others are in short sleeves. Sometimes you feel light-headed or dizzy. Other times you feel foggy-headed—like you are listening to others through cotton wool.
- You are tired and find your mind wanders. You struggle to focus in class or at work. You cannot remember things that others remember easily.
- You are prone to crying spells and/or explosive bouts of anger (more so than what might be usual). You alternate between wanting to be alone, snapping at family, and finding you are clingy and needy, seeking reassurance from loved ones.
- Not only do you find it hard to concentrate, but also you find you are absolutely consumed with thoughts of food: when you will eat; what you will eat; what you won’t eat.
- Facing social circumstances that involve food creates panic: family celebrations, lunches with friends at school, holiday gatherings…in the days leading up to such events you feel extremely anxious and spend a lot of time trying to figure out how to avoid it altogether.
- The number of rules you assign to when and how will eat keeps getting longer. You have become ritualistic to the point where any deviance causes massive anxiety (the wrong plate, the fork in the wrong place…).
- You have longer and longer lists of forbidden foods that you will not touch.
- If you indulge in any food that you consider unacceptable, you are wracked with shame, self-hatred, and loathing and usually “punish” yourself for the transgression (exercising to exhaustion, skipping yet another meal).
- As a woman, your regular menstrual cycle is irregular or has disappeared completely. * Whether you are a woman or man you notice your skin appears dull and dry. Your hair and nails are brittle and perhaps your hair loss seems more pronounced than usual (clumps in the bathtub drains or on your brush).
- You find yourself promising yourself and others more and more that tomorrow will be different. But it isn’t.
- You lie to loved ones about what you ate that day or how much you actually exercised and make excuses for why you cannot eat now. If they are friends, you often fabricate food allergies, intolerances, or other reasons why you cannot have the food being offered.
If the telltale dozen seems to ring true, then your next step is to determine whether these behaviors are impinging on your quality of life. If you feel you are missing out and are suffering, then it is time to seriously consider a recovery effort.
Why is the eating disorder mindset present?
When an eating disorder is activated, APNIE † changes occur in the patient’s body that presumably do not occur for those who don’t have the condition. Those changes and their exposure to various psychosocial and environmental reinforcements, make the telltale dozen feel like such a spiraling trap for those with an eating disorder.
When people restrict food intake, or experience an energy deficit in their bodies for whatever reason, leptin levels plummet in the body. Leptin is a gating hormone that manages metabolism, appetite, bone formation, immune function, and reproductive hormone function. 2, 3, 4, 5, 6, 7 When a person is energy balanced, leptin is at an optimal level. When leptin levels plummet two things happen: the metabolism is suppressed and the appetite increases. Describing the process in this way is a gross oversimplification of the complex hormonal and neurotransmitter cascades that occur when a person lowers his or her food intake, but the explanation will suffice for the purpose of this overview.
For the person with an eating disorder, the appearance of an energy deficit presumably activates genes that affect normal function of neurotransmitters in the brain. It is these neurotransmitters that are believed to generate the anxious and compulsive thoughts, feelings, and behaviors around food. 8, 9
A woman without an eating disorder will say she feels irritated, fatigued, hungry, and moody when dieting. The lowered leptin level is creating unpleasant moods and extreme hunger to signal to the brain that it is time to go find more food to eat.
A person with an eating disorder will say she’s not hungry. Although experts dispute whether she actually does feel hunger or not, it’s clear she initially feels calmer, more energized, and dissociated from negative feelings (emotionally blunted) as a result of avoiding food intake. 10, 11, 12 The eating disorder–skewed neurotransmitters appear to interact with the lowered leptin level in a way that is distinct from the norm: the usually unpleasant moods are replaced with positive emotional outcomes (short term). Even as the irritation, mood swings, exhaustion, and deep hunger may begin to override that initial positive outcome of creating energy deficits in the body, now the brain’s threat identification system is also locked into keeping food avoidance in place.
If someone essentially feels better when she avoids food, then that can be a powerful reinforcement to continue with the avoidance. Activation of an eating disorder should have a period in which either extinction or habituation might occur—meaning the avoidance behavior may or may not stick, depending on the presence of other positive or negative influences in the patient’s life at that time. But it’s quite likely that this window of opportunity is too short and too subtle to be accessible to tangible intervention.
Other researchers suggest that the perseveration of behaviors is not due to the positive mood modulation effect of starvation, but rather the pursuit of removing ambiguity through the application of rules. 13 But, as with almost everything to do with these complex neurological conditions, likely both the positive mood modulation due to neurotransmitter-based anomalies and the drive to avoid unpleasant arousal or ambiguity quickly allow behaviors to take root. This conditioning will occur for those with the genetic underpinning who also face those necessary psychosocial inputs to reinforce and prolong the application of food avoidance behaviors.
What is really going on?
Most patients are profoundly puzzled when I inform them that their condition is essentially a misidentification of food as a threat. The common response is “But I’m not afraid of food, I just________.” The fill-in-the-blank usually includes fattist statements in one form or another but occasionally fat phobia is absent from the post-hoc explanations as well.
The prefrontal cortex in our brains, responsible for our conscious thought processes, is habitually underestimated for its imaginative and creative capability. It is perceived as the seat of logical thought and in Western culture that logical capability is considered the essence of human superiority. It is the prefrontal cortex that generates that fill-in-the-blank best guess after the fact when the internal system (both brain structures and the body as a whole) has been placed into a fight/flight/freeze state of arousal. The more accurate phrase would be: “I believe (fill-in-the-blank) because my threat identification system in my brain has typecast food as a threat.”
Our threat identification system is a powerful system distributed throughout several brain structures that, evolutionarily speaking, are much older structures than our prefrontal cortex. We share this threat identification system with essentially all other animals on the planet.
Any brain structure responsible for our survival works with extreme efficiency and doesn’t concern itself too much with accuracy. The threat identification system is our lightning-fast yet somewhat dirty system (reflecting that efficiency trumps accuracy for survival). Our prefrontal cortex, conversely, tries to concern itself more with accuracy and that means it ends up working as a slower yet cleaner system. It has little influence on, or neural oversight of, the threat identification system. The way I view these complementary systems in our brain is that the evolutionarily older structures in our brain largely excuse and indulge the overblown sense of importance that our prefrontal cortex believes it has in running our lives.
If you are walking across a field and out of the corner of your eye you see a snake about to strike, the prefrontal cortex is blissfully uninvolved in all the reactions you enact to jump back and avoid the strike. However, once you are hopefully standing to the side watching the snake slither away, your prefrontal cortex will now consciously frame the experience that you were about to be bitten by a snake: “Whew! We avoided that one! Way to go, team!” Of course the rest of the brain that was really responsible for that lightning-quick response rolls its collective “eyes,” knowing full well that the prefrontal cortex was most certainly not part of the team—it arrived late, as usual, and full of itself.
The exact same reaction can occur when out of the corner of your eye you see a stick on the ground that looks like a snake moving toward you. And when I say “you see,” in fact the part of your brain registering what is coming in through the retina is really not accessible to the conscious “you” in the story. You will likely jump back immediately and full seconds may elapse before you (as in prefrontal cortex “you”) recognize and confirm that it is just a stick. The prefrontal cortex then might sheepishly laugh but the rest of the brain responsible for that reaction doesn’t care because it runs on a better-safe-than-sorry track. That is your fast-and-dirty neural processing system at its finest. That the stick was not a snake is an irrelevant error—efficient response, but not necessarily accurate.
Now let’s get back to what is happening for the threat identification system in someone with an activated eating disorder.
Because eating disorders are essentially a type of anxiety disorder, they have close links to the kinds of neural responses we see in patients with both specific phobias as well as obsessive-compulsive disorder. In all expressions of anxiety disorders, the threat identification system is too sensitively calibrated or what I would call “twitchy,” or what another Eating Disorder Institute forum member called “trigger-happy.”
How does this system become twitchy in the first place? Well, we can be born predisposed to have a sensitively calibrated threat response system. Both low cardiac vagal tone and high startle response at birth predisposes the individual to the development of anxiety disorders in later life. 14 However, much of the subsequent infant-mother postpartum interactions can greatly dampen or heighten these predispositions.15, 16
There is also a fair amount of research data on the measurable differences in the serotonergic and dopaminergic system functions in the brains of those with an eating disorder when compared to healthy controls. 17, 18, 19 These neurotransmitter systems are implicated in our reward identification system, which balances the threat identification system in our brain. The reward identification system, too, is distributed across several evolutionarily older brain structures.
Think of this process as: reward = approach; threat = avoid.
When these two systems are well attuned, releases of neurotransmitters frame what types of things in our environment we want more of and what things we want less of. It creates a nice positive spiral of increased survival and improved quality of life.
While we know that there is dampened function of the reward identification system in those with eating disorders, this reduced activity may actually be the result of heightened threat identification responses dampening the reward system. In other words, the facets that researcher Walter Kaye investigates (serotonin and dopamine function 20) may be the result of preexisting anomalous amygdala function (a brain structure that is intimately involved in threat identification). And anomalous amygdala function, perhaps combined with persistent low vagal tone and high startle responses, may subsequently all act upon the reward identification system to dampen its activity overall in the brain.
Walter Kaye and his colleagues have identified that anxiety disorders are a common precursor for the development of an eating disorder. 21 And while much of the neuroscientific focus on the study of anxiety rests with the amygdala-cortical interactions, the involvement of the orbitofrontal cortex is equally relevant and may also explain why sociocultural framing of mental illnesses change throughout history.
The frontal lobes are one of four main areas in our brains. Within the frontal lobes (left and right hemisphere) are three main areas: prefrontal cortex, the premotor area, and motor area. The orbitofrontal cortex resides within the prefrontal cortex, the area responsible for complex thought. The orbitofrontal cortex provides an important connection between the frontal lobes and the temporal lobes, where auditory, visual and emotional perceptions are interpreted. Our decision-making ability is inextricably linked to memory and emotional salience (importance). 22 The orbitofrontal cortex supports the complex decision-making skills that occur within the prefrontal cortex through its connection to the temporal lobes, where the entire limbic system resides.
In overly simplistic terms, the orbitofrontal cortex is bidirectional in its ability to receive messages from other structures in the brain as well as send messages to the amygdala. It scans your surrounding environment all the time. If it identifies a concern or threat, it communicates with the amygdala, an area within the brain’s limbic system. However, the amygdala can also inform the orbitofrontal cortex that there are interoceptive (internal body) inputs that suggest a problem is present, and the orbitofrontal cortex is then instructed to scan the environment more closely for a likely source of the problem. This facet of the orbitofrontal cortex is likely why a patient with anorexia nervosa living in the 1700s explained her avoidance of food as an attempt to get closer to God and a patient with the same condition today states that she is avoiding food to stay “healthy,” thin, and fit. In both cases there are interoceptive changes that activate the pattern to find the source of the problem in the surrounding environment. To make meaning of the internal distress, the mind latches onto dominant sociocultural norms.
If you are sitting in front of a plate of pasta and you are hungry, then you begin eating. But what if, along with hunger, your heart rate has increased, your hands are clammy, and your breathing is shallow? You are likely not even consciously aware just yet that your internal state is not relaxed. But soon the signals become more insistent. You feel jittery and you want to leave the table. You identify that you are anxious. At this point there is frantic firing between the amygdala and the orbitofrontal cortex creating a “Check again!” loop. The internal setting is most definitely suggesting there is a threat present and nearby, but the orbitofrontal cortex is scanning and sees a plate of pasta.
That’s when the impasse reaches the conscious mind because there is no clear logical or identifiable threat. So the prefrontal cortex does what it does best: tries to make meaning of it all. And in the absence of any clear threat it will have to guess using its lifetime exposure to sociocultural and environmental inputs.
Patients do not experience food avoidance as the misidentification of food as a threat because the prefrontal cortex has to make meaning out of a nonsensical situation: “The plate of pasta cannot be a threat, so what am I missing?" In today’s culture, a patient will likely frame the avoidance of food as concern for the types of ingredients in the pasta that may be “unhealthy” or perhaps worry that the amount of calories in the pasta will make her fat (and therefore socially abhorrent). And of course our patient back in the 17th century was framing her avoidance of pasta as an expression of religious adherence and godliness.
The threat identification and reward systems in the brain of someone with an eating disorder are misaligned or imbalanced, but experts cannot fully explain all the reasons why that happens or why it is food that gets miscast as a threat. Both our reward and threat identification systems work as positive feedback systems, so any imbalance between these two systems quickly spirals out of control. A reward identification system unleashed can lead to pathological levels of addiction. A threat identification system unleashed can lead to pathological levels of aversion.
For those with an eating disorder, an aversion to food is the fundamental life-threatening result of a threat identification system that has lost its way.
In Part 3 we will look at the challenges of embarking on a recovery effort.
* An absent menstrual cycle is a marker of ill health but its presence is not a marker of health. It is a one-way marker only.
† APNIE: anthropologically-framed psycho-neuro-immuno endocrinology as explained in Part 1 of this series
1. Whitelaw, Melissa, Heather Gilbertson, Katherine J. Lee, Mick B. Creati, and Susan M. Sawyer. "A new phenotype of anorexia nervosa: The changing shape of eating disorders." Journal of Eating Disorders 1, no. 1 (2013): 1-1.
2. Elefteriou, F., S. Takeda, K. Ebihara, J. Magre, N. Patano, C. Ae Kim, Y. Ogawa et al. "Serum leptin level is a regulator of bone mass." Proceedings of the National Academy of Sciences of the United States of America 101, no. 9 (2004): 3258-3263.
3. Carbone, Fortunata, Claudia La Rocca, and Giuseppe Matarese. "Immunological functions of leptin and adiponectin." Biochimie 94, no. 10 (2012): 2082-2088.
4. Friedman, Jeffrey M. "The function of leptin in nutrition, weight, and physiology." Nutrition Reviews 60, no. suppl 10 (2002): S1-S14.
5. Méndez‐Ferrer, Simón, and Paul S. Frenette. "Hematopoietic Stem Cell Trafficking." Annals of the New York Academy of Sciences 1116, no. 1 (2007): 392-413.
6. Meier, Ursula, and Axel M. Gressner. "Endocrine regulation of energy metabolism: review of pathobiochemical and clinical chemical aspects of leptin, ghrelin, adiponectin, and resistin." Clinical Chemistry 50, no. 9 (2004): 1511-1525.
7. Barash, Ilona A., Clement C. Cheung, David S. Weigle, Hongping Ren, Emilia B. Kabigting, Joseph L. Kuijper, Donald K. Clifton, and Robert A. Steiner. "Leptin is a metabolic signal to the reproductive system." Endocrinology 137, no. 7 (1996): 3144-3147.
8. Kaye, Walter H., Guido K. Frank, Ursula F. Bailer, Shannan E. Henry, Carolyn C. Meltzer, Julie C. Price, Chester A. Mathis, and Angela Wagner. "Serotonin alterations in anorexia and bulimia nervosa: new insights from imaging studies." Physiology & Behavior 85, no. 1 (2005): 73-81.
9. Fumeron, F., D. Betoulle, R. Aubert, B. Herbeth, G. Siest, and D. Rigaud. "Association of a functional 5-HT transporter gene polymorphism with anorexia nervosa and food intake." (2001).
10. Guisinger, Shan. "Adapted to flee famine: Adding an evolutionary perspective on anorexia nervosa." Psychological Review 110, no. 4 (2003): 745.
11. Espeset, Ester, Kjersti S. Gulliksen, Ragnfrid HS Nordbø, Finn Skårderud, and Arne Holte. "The link between negative emotions and eating disorder behaviour in patients with anorexia nervosa." European Eating Disorders Review 20, no. 6 (2012): 451-460.
12. Berg, Kathleen Mary, Dermot J. Hurley, James A. McSherry, and Nancy E. Strange. “Eating disorders: a patient-centered approach” (United Kingdom: Radcliffe Medical Press, 2002)
13. Merwin, Rhonda M., C. Alix Timko, Ashley A. Moskovich, Krista Konrad Ingle, Cynthia M. Bulik, and Nancy L. Zucker. "Psychological inflexibility and symptom expression in anorexia nervosa." Eating Disorders 19, no. 1 (2010): 62-82.
14. Beauchaine, Theodore. "Vagal tone, development, and Gray's motivational theory: Toward an integrated model of autonomic nervous system functioning in psychopathology." Development and Psychopathology 13, no. 02 (2001): 183-214.
15. Porter, Christin L. "Coregulation in mother-infant dyads: links to infants’ cardiac vagal tone." Psychological Reports 92, no. 1 (2003): 307-319.
16. Porter, Christin L., Melissa Wouden‐Miller, Staci Shizuko Silva, and Adrienne Earnest Porter. "Marital harmony and conflict: Links to infants' emotional regulation and cardiac vagal tone." Infancy 4, no. 2 (2003): 297-307.
17. Kaye, Walter H., Julie L. Fudge, and Martin Paulus. "New insights into symptoms and neurocircuit function of anorexia nervosa." Nature Reviews Neuroscience 10, no. 8 (2009): 573-584.
18. Kaye, Walter H., Guido KW Frank, and Claire McConaha. "Altered dopamine activity after recovery from restricting-type anorexia nervosa." Neuropsychopharmacology 21, no. 4 (1999): 503-506.
19. Frank, Guido K., Ursula F. Bailer, Shannan E. Henry, Wayne Drevets, Carolyn C. Meltzer, Julie C. Price, Chester A. Mathis et al. "Increased dopamine D2/D3 receptor binding after recovery from anorexia nervosa measured by positron emission tomography and [11 C] raclopride." Biological Psychiatry 58, no. 11 (2005): 908-912.
20. Kaye, Walter H., Julie L. Fudge, and Martin Paulus. "New insights into symptoms and neurocircuit function of anorexia nervosa." Nature Reviews Neuroscience 10, no. 8 (2009): 573-584.
21. Kaye, Walter H., Cynthia M. Bulik, Laura Thornton, Nicole Barbarich, Kim Masters, and Price Foundation Collaborative Group. "Comorbidity of anxiety disorders with anorexia and bulimia nervosa." American Journal of Psychiatry (2014).
22. Bechara, Antoine, Hanna Damasio, and Antonio R. Damasio. "Emotion, decision making and the orbitofrontal cortex." Cerebral Cortex 10, no. 3 (2000): 295-307.