Bingeing is another topic that generates tremendous anxiety and questions for those recovering from the restrictive eating disorder spectrum.
Experts have gone down some unfortunate rabbit holes using psychiatric definitions and treatments for eating disorders. It has resulted in treatment specialists encouraging patients to expend energy on suppressing the very things that would ensure their complete recovery.
“When treating those with eating disorders, the practitioners cannot be afraid of what the eating disorder is afraid of.”
Rebeckah Peebles (pediatrician), 2012
I cannot reinforce enough how brilliant that statement is in reflecting the problem we have in helping those with a restrictive eating disorder achieve a robust remission.
Who’s Afraid of the Big, Bad Wolf?
“Basically my GP laughed at my suggestion that exercise could be dangerous at certain weights. She asked me what I was doing (I have been doing running, cycling, etc. at the gym) and said this was all "really good". She also laughed when I asked if having a palpitation at the gym was any cause for concern, and said it was totally normal.” [roobear, forum post, 2012]
“As I said, initially she [dietician] encouraged me to eat more. However yesterday she told me to cut back and moderate my eating more. She said that any gain above 500g per week was "not recommended" and she was only telling me this because "she cares" and that "if she did it 4 weeks down the track I'd be angry".” [havecourage, forum post, 2012]
“I went to the doctor this morning and I told him about my thoughts about food and exercise but he thinks I'm ok because I don't look underweight and said that it's normal to be worried about food and weight. He thinks it's all in my head and told me to calm down.” [pat, forum post, 2012]
“She [psychologist] claims it is all part of my OCD, even though my family and I know it's not. She also warned me about becoming "obsessed with gaining weight"!” [hopeful12, forum post, 2012]
“However, I also was in a strange place for a long time, eating around 2000 calories under the supervision of a team that seemed to worry about me overeating.” [flor1234, forum post, 2012]
“Nutritionist, as I'm leaving: "Just remember, you don't need to gain any more weight." (and then blahblahblah about how I'm pretty much finished with recovery. After. A. Month.)” [kayebunny, forum post. 2012]
“By the way, I went to a nutritionist and she told me and my Mom that my behavior in the past few days shows that I have developed a binge eating disorder.” [paulad, forum post, 2012]
“I excitedly told my doctor all about what I had eaten and she looked extremely concerned, and essentially said that it was ok for a day or two to eat like that but that I need to eat 'healthier' and should be practicing moderation.” [laurenpoppy, forum post, 2012].
“When I first was restoring my weight, I ate a ton of peanut butter, my parents and the dietitians would get mad and say"eat more variety".” [owl-in-the-ocean, forum post, 2012]
“So I just got back from my first therapist appt (specializes in ED's and CBT)…"If you keep eating 3-4 thousand calories a day you will keep gaining weight. a normal diet is 2000."…she said it's not natural for me to be so tired after eating because apparently "the refeeding process is supposed to give you more energy so maybe it's your body’s way of telling you to not eat so much"...she was also "alarmed that you are swinging from one extreme to another, because that is what you do, and that one day soon you will weigh yourself and it will send you spiraling back into your restriction".” [prttyinpnk2, forum post, 2012]
Of course these quotes give the distinct impression that ED treatment specialists are all more afraid of weight gain, body image and food intake than your very own eating disorder might be! Later on in this post, I’ll discuss the fact that this is a fairly factual impression of the current state of treatment for restrictive eating disorders.
But first, we’ll investigate why eating during recovery is such a frightening prospect for both those with restrictive eating disorders and also often their entire treatment team as well.
Dogmatically Simple and Misguided-IV (soon to be V)
In the DSM-IV and the upcoming DSM-V (the diagnostic and statistical manual for mental illness—the tome used to identify and diagnose the entire suite of eating disorders as well as all other mental illness) anorexia nervosa and bulimia nervosa are defined as distinct and separate mental illnesses.
While they may be symptomatically distinct, they are not biologically distinct [DH Gleaves et al., 2000; RC Casper et al., 1980; K Eddy et al., 2002].
To try to clarify the confusion the DSM generates, I initially generated the new working classification of restrictive eating disorder spectrum in 2009, as it seemed better aligned with clinical trial data and genetic studies.
The DSM-IV classifications rely (wrongly) on the presumption that distinct symptoms have distinct origins.
ED-NOS (eating disorder not otherwise specified) is that messy and inaccurate grab-bag classification in the DSM-IV that lumps together eating disorder facets that do not appear to match the observable symptoms of either anorexia nervosa or bulimia nervosa. However it is applied to conditions that end up having no genetic or biological commonality, namely true binge-eating symptoms with restrictive-eating symptoms.
Let’s first clarify the symptom groupings that are all a reflection of the same restrictive eating disorder spectrum:
Restrictive Eating Disorder Facets
- Anorexia Nervosa (meaning loss of appetite through severe emotional disturbance). As there is fundamentally no loss of appetite, but rather a denial of or disassociation from appetite due to various psychoneuroendocrine anomalies, a more accurate definition would be Self-Administered Starvation.
The DSM-IV will only recognize the severe version of self-administered starvation, yet sub-clinical self-administered starvation is more common, insidious and has poor long-term prognoses as well. Clinical starvation is anything less than 1000 calories a day and sub-clinical starvation rests between 1000-up to any amount that would still create daily energy deficits for the individual in question.
- Restriction/Reactive Eating Cycles: Often diagnosed as ED-NOS by psychiatrists and psychologists alike, the patient is encouraged to focus on lessening the bingeing episodes. Sadly, almost all patients enter into this cycle from a period of self-administered starvation and the bingeing is the body reacting to too-severe calorie restriction relative to its energy requirements. Recovery from all facets of a restrictive eating disorder requires focus on lessening restrictive behaviors.
- Bulimia Nervosa (meaning ox hunger, or ravenous hunger through severe emotional disturbance). Bulimia nervosa is actually Restriction/Reactive Eating/Purging Cycles.
Yet again, patients are often encouraged to put all their energy into curbing the bingeing (ravenous hunger) when the root cause is insufficient energy intake that results in reactive eating. 62% of all those who self-administer starvation will shift to this cycle within eight years of inadequate or partial recovery efforts [K Eddy et al., 2002].
- Orthorexia (Excessive Vigilance of Nutrient Intake) is not recognized in the DSM-IV. The Greek origins of the word combine orthodox (to seem right or true) with orexis (appetite). It has gotten a lot of attention in the media and that tends to generate a backlash of dogma within the expert communities who currently prefer to dismiss it out of hand. At present, a patient with orthorexia who must depend on a psychiatric assessment and diagnosis to receive medical coverage for treatment would be lucky to receive an ED-NOS diagnosis.
Essentially the focus of restriction shifts from frank starvation, or cycles of starvation and reactive eating, to pursuing perfect weight and body image through perfect energy intake. There are long lists of forbidden foods, weighing foods, attending to macronutrients and eating only foods considered healthy or pure.
Of note, male medical students have a statistically higher tendency for orthorexia, when compared to female medical students [T. Fidan et al., 2010]. Students of nutritional sciences restrict their food to control their weight more than students who are not majoring in those fields [A. Korinth et al., 2009; N. Reinstein et al., 1992].
- Anorexia Athletica, alternately referred to as Exercise Bulimia, (Excessive Energy Expenditure): Both excessive vigilance of nutrient intake and excessive energy expenditures are insidious facets of restrictive eating disorders because loved ones (and the patient herself/himself) can be easily swayed into believing the patient has recovered from his or her eating disorder and is only expressing a normal interest in being fit and eating healthily. Unfortunately, it is our society’s high anxiety over obesity that blinds our ability to see these facets as just as dangerous as self-administered starvation.
Sociocultural Framework and the Symptomatology of Neurobiological Conditions
A note on “drunkorexia” and why I have not currently included it in all the symptom groupings:
Drunkorexia is a term coined to suggest that the sufferer uses alcohol to suppress appetite.
It is not generally understood that alcohol abuse for women can lead to weight loss. The popular misconception is that alcohol is just empty calories and almost all restrictive diets recommend eradicating alcohol consumption to lose weight. For this reason, at the moment, few with a restrictive eating disorder have latched on to drinking alcohol as a way to prevent or hinder their appetite.
All psychoneuroendocrine disorders or conditions, anything from sleep disorders to schizophrenia, are heavily impacted by current social norms and influences.
In the time before space travel, those with hypnopompic sleep disorders were not abducted by small green aliens, but were rather attacked by small green hag-women who usually sat on the sufferers’ chests [K Frazier [ed.], The Hundredth Monkey: And Other Paradigms of the Paranormal, Prometheus Books, 1991].
In the time before off-the-rack and standardized clothing sizes, those with restrictive eating disorders hindered and prevented their appetites not for body image reasons or because they were sure they were too fat, but because God willed it so that they might transcend their putrid, sinful bodies [JJ Brumberg, Fasting Girls: The History of Anorexia Nervosa, First Vintage Books, 2000].
At present, if someone with a restrictive eating disorder is perhaps drinking too much alcohol, then it must first be determined whether the alcohol dependency is a distinct self-medicating process to modulate underlying anxiety or whether the alcohol intake is specifically driven by a desire to limit food intake.
However, as common understanding about alcohol’s ability to hinder appetite for some women grows, then drunkorexia could indeed become yet another facet of the restrictive eating disorder spectrum.
The facets of this condition have changed and will continue to change with environmental and societal pressures and inputs, but the underlying psychoneuroendocrine genotype remains the same.
Because this is a spectrum condition, individuals can have acute, chronic, sub-clinical or mild facets. Both the expression of the condition’s symptom groupings, and the progression and resolution of the condition are highly labile (fluid and inter-changeable) – meaning there is no certainty that someone who has a mild case will not develop a severe case at some point, or that someone who is restricting calories severely will not shift to expressing the restriction through excessive exercise instead, as just two examples.
Binge Eating Disorder and Night Eating Syndrome
So what of binge eating disorder or night eating syndrome? Problematically many experts in the field of eating disorders assume that these conditions are simply at the other end of the same spectrum of eating disorders that includes all the restrictive behavioral facets mentioned above. In other words if someone who is attempting to recover from a restrictive eating disorder is not vigilant towards any ‘excessive’ food intake, then they will develop a clinical case of binge eating disorder and become morbidly obese.
This misconception is monstrously unproven and not at all an evidence-based application of treatment for recovery. But, as you can see from our Big Bad Wolf section above, the attitude that unrestricted eating is dangerous is taken as known fact by many specializing in eating disorder treatment.
Please note that I use the term morbidly obese in its clinical sense. Obesity simply involves additional adipose (fat) tissue. Obesity is not a disease, nor is it a health risk. Metabolically healthy obese individuals are part of the normal variation of human heights and weights and their life expectancies are average to above-average [J Kuk et al., 2009; RP Wildman et al., 2008].
However, because adipose tissue is a hormone-producing organ, if it has been triggered into a kind of chronic malfunctioning state, then that condition is best described as inflammatory obesity.
And despite the public messaging hammering the concepts that overeating leads to obesity, numerous studies show absolutely no correlation between food intake and obesity onset [W. Kulesza, 1982; JA Baecke et al., 1983; RJ Myers et al., 1988; ML Johnson et al., 1956; L Lissner et al., 1989; AM Prentice et al., 1986].
There is, of course, equal emphasis on the concept that it is our inactivity that causes obesity. Yet energy expenditure was recently compared between office workers and a traditional hunter-gatherer tribe in Tanzania (the Hadza) and they were found to be indistinguishable [H Pontzer et al., 2012]. So much for Paleolithic perfection, as we appear to be able to create the same energy balance within cubicles and circulated air as we experience roaming barefoot searching for our food for hours every day.
If not food intake and exercise, then what causes inflammatory obesity? The answer is not definitive as yet, but the hints of causation reside much more with the critical role adipose tissue has in running our metabolism through hormone release and control than in its secondary role as an energy storage facility.
Fat is not our gas tank. Fat is more the point of origin of a trophic cascade of metabolic, homeodynamic dysfunction of which inflammatory obesity is the result. And, the causes of that trophic cascade are not food and exercise, but rather appear to be stress, sleep and (most critically) the introduction of endocrine-disruptors and mimickers in our environment.
Check out the blog post Binge Eating Disorder and Night Eating Syndrome for more information on these unrelated conditions. In that post I discuss the prevalence of misdiagnosis of binge eating disorder (BED); the symptom checklist that must be present for the condition to be correctly diagnosed; and how recovery from these rare conditions is actually not appreciably different from recovery from a restrictive eating disorder in any case.
One researcher at the forefront of BED and night eating syndrome (NES) is Albert Stunkard. His research indicates that BED not only is rare but also is likely a marker of other psychopathological disorders and not a distinct disorder in and of itself.
Unfortunately both BED and NES are being identified and diagnostically defined through the observation of measurable symptoms and self-reported questionnaire responses, rather than determining what, if any, neuroendocrine genotypes may underpin these unrelated conditions.
Both are defined in the appendices of the DSM-IV but must be classified as ED-NOS for the purpose of diagnosing patients at present.
Stunkard may be on the right track but rather than being markers of psychopathology, both BED and NES may actually be markers for endocrine disorders.
The field of chronobiology has identified that NES may indeed be a sleep disorder [AJ Stunkard et al., 2009]. Adipose tissue (fat) is actually our largest endocrine producing organ in the body and the hormones it produces impact circadian rhythms and metabolism.
Controlled studies also suggest that people with diagnosed sleep disorders of narcolepsy or cataplexy have a higher than anticipated rate of binge eating.
NES and BED are far more prevalent in the obese rather than non-obese populations.
There may be specific melanocortin-4 receptor gene variants (MCR4) in patients with BED. MCR-4 mediates the central nervous system’s response to leptin (a critical gating hormone associated with appetite, metabolism, bone formation and reproductive hormone function)[T Gotoda et al., 2003; Y-X Tao et al., 2005]. Genetic variants near MCR-4 are also associated with insulin resistance and obesity as well.
Will I Become A Binge-Eater?
Does someone who recovers from the restrictive eating disorder, no matter the restrictive facets they experience, develop a binge eating disorder?
The answer is “no”. However, it is important to note that the process of recovery from an energy deficient state most certainly involves a period of extreme hunger and eating. It is a transient condition that disappears once energy balance is restored.
Here are the likely reasons why those who reach a complete remission from a restrictive eating disorder do not develop binge eating disorder:
- The candidate genes associated with inflammatory obesity, cholesterol, insulin and glucose levels are unrelated to the genes identified thus far for restrictive eating disorders [R Stöger, 2012; AW Drong et al., 2012; CJ Nolan et al., 2011; A. Hinney et al., 1999 and 2000].
- Patients fully recovered from the restrictive eating disorder rarely reach final restored weights above BMI 25. 2% of the recovered population does go above BMI 25, however ALL return to weights at or below BMI 25 after one full year beyond recovery (with no relapse of restriction involved) [CM Bulik et al., 2006].
- Leptin resistance is not a factor in either the activation or resolution of a restrictive eating disorder. Yet, leptin resistance is often present in patients with inflammatory obesity. [P. Dandona et al., 2004; JF Caro et al., 1996; S Herpertz et al., 1998 and 2000]
Responding to Hunger is Vital
Why do we think that the sensation of hunger is suspect?
There are a plethora of studies, all conducted in the field of psychology, that suggest eating for any other purpose than for the replenishment of energy, to allow for the correct functioning of your body, is “emotional eating”. Presumably “emotional eating” is bad because addressing “emotional eating” appears to allow for more success with weight loss [S. Dalton, Overweight and Weight Management, Aspen Publishers, 1997, p. 447]. This is a profoundly circular argument that actually offers no scientific data that emotional salience in the human consumption of food has any negative affect whatsoever unless weight loss is a paramount goal.
Given that I have already shown that fat tissue is not a storage unit, but a hormone-producing organ, losing weight is actually a process of organ destruction and damage and therefore hardly an ideal pursuit for any human being to undertake willfully and purposefully.
I have described in other posts our profound misunderstanding of the value of emotional eating in this way:
When you struggle with a restrictive eating disorder, so much of the social/emotional connections with food consumption have been hijacked by eating disorder-related anxieties. This disconnect is also heavily reinforced by our society’s current preoccupation with the presumed superiority of what I once called autistic eating (referencing parallel nomenclature used in economics, namely autistic economics). However, it is an incorrect term to use because autism is not a condition lacking in an emotional landscape, rather it is a variation on the usual development of theory of mind.
So, I’m going to rename this issue in our society: the reverence attributed to consciousness eating (sometimes misattributed as mindful eating).
Consciousness eating presumes that having our emotions active and interacting with our hunger and satiation cues is inferior to the process of applying our conscious, or logical mind, to the assessment of whether the desire we feel to eat is in fact something that must be addressed for logical reasons.
We cannot eat logically. Our logical minds are too late to the evolutionary party, by millennia, to actually offer any value to how we pursue and stay optimally energized.
This reverence of the logical mind and twinned disdain of the emotional mind is, from an evolutionary perspective, ludicrous. The structures within your brain that support your emotional landscape are robust, distributed and ensure your survival to a level that your logical mind couldn’t even hope to achieve on its best coffee-upped day!
I often mention the patients with lesions and trauma to the emotional centers of the brain (you’ll find one in particular who is referenced by multiple neuroscientists and neurologists in their bestseller books) who are institutionalized despite the fact that they have fabulous and intact IQs; have completely intact memory, retention and retrieval faculties; and can sustain a conversation on any topic pertaining to the past (historical and personal) to the present and future (current affairs, debate, analyses etc.). Ask them what they would like to have for lunch and then you see why they need the 24/7 oversight and care. Without emotional salience, their logical mind is completely stymied by what might be the better option: lasagna or burger and fries.
How you feel about your food is how you not only survive, but also thrive.
Minnesota Starvation Experiment
This study was conducted in 1944-1945, at the end of WWII, by lead researcher Ancel Keys and his colleagues. The participants were all conscientious objectors who volunteered for the study. Their normal eating patterns were studied for 3 months; their rations were then cut in half for 6 months (averaging approximately 1500+ calories a day); and then their rations were slowly increased back to pre-study levels over a final 3 months. Several subjects agreed to stay on past the final re-feeding period. They all ate huge amounts of food and found it hard to stop eating, and felt hunger even when they couldn’t physically eat any more.
These study subjects were not anorexic patients, although it appears the experiment itself triggered anorexia in a few of them, as they compulsively continued to restrict food intake beyond the completion of the study.
Apart from those who resisted recovery by continuing to restrict intake, all returned to pre-starvation weights and mental health status. However it took longer and required far more energy than was predicted.
The extreme hunger phase is normal in recovery and as long as you respond to the hunger and continue to avoid any restriction, complete recovery will be forthcoming.
Please read Extreme Hunger: What is it? and Extreme Hunger: Profoundly Disturbing to understand much more about the necessity of responding to your extreme hunger in recovery and that doing so will not result in the appearance of pathological binge eating behaviors. Restrictive eating behaviors are, and remain, the maladapted anxiety-modulating response that must be replaced with well-adapted anxiety modulating behaviors.
The Dreaded Overshoot
Oh, the hand wringing of those in recovery who face the possibility that they may temporarily overshoot their optimal weight set point during recovery!
As most of you know, all those subjects in the Minnesota Starvation Experiment temporarily overshot their pre-study weights and all returned to their pre-study weights in the 12-18 months following the end of the study [A. Keys et al., 1950]. For most subjects they initially gained about 10% above their pre-study weights in the re-feeding period.
And many an ED specialist is adamant that such an overshoot is unnecessary and also dangerous. However, yet again, there is no clinical evidence on which they can base that belief. We don’t actually know if the temporary overshoot in weight is or is not necessary. However we can say, with some clinical authority, that it is not dangerous as the subjects of the Minnesota Starvation Experiment were all healthy post-study and many were interviewed 50 years later and attested to there having been no long-lasting impacts to their health: physical, mental or emotional.
As for whether the temporary overshoot is necessary, there is some evidence that it may indeed have value in ensuring the return of an optimal fat-mass to fat-free-mass ratio. In fact, Abdul Dulloo and colleagues re-examined the Minnesota trial data and discovered that the depletion of fat-free mass and fat mass (occurring during starvation) separately trigger hyperphagia (excessive eating) in post-starvation subjects and that the hyperphagia will persist until both fat and fat-free mass are restored [A Dulloo et al., 1997].
We also know from numerous other studies that anorexics often maintain a higher proportion of fat mass post-re-feeding [CI Orphanidou et al., 1997; M Probst et al., 2001; C Mantzoros et al., 1997] and this is likely due to the prevailing attitudes that hyperphagia must be avoided during recovery at all costs as it is considered a marker of “bingeing”. Instead, what these post-recovery data may show is that the prohibition of hyperphagia in recovery from restrictive eating disorders serves to halt the body’s ability to return to an optimal fat mass to fat-free mass ratio.
Furthermore researchers have shown there is a significant increase in trunk adiposity (fat deposits around the mid-section of the body) in recovery [S Grinspoon et al., 2001; L Mayer et al., 2005] and this fat mass is evenly redistributed in the optimization period after weight restoration only if the patient continues to eat in an unrestricted fashion [ibid., ibid.]
In other words, the initial trunk adiposity and disproportionate fat mass ratio in the early period of re-feeding may not resolve unless and until a patient successfully supports the period of hyperphagia that is part and parcel of the process of reaching a healthy remission. We also know that trunk adiposity in particular is correlated with cardiovascular disease in older men and women [RE Van Pelt et al., 2001; JP Després et al., 1990] which is all the more reason to encourage those in recovery to allow their bodies to complete the re-feeding process fully to allow for a return to optimal fat mass to fat-free mass ratios.
The overshoot in weight during a re-feeding process is not present for all patients, but it is assuredly temporary for those who do experience it.
We Cannot Be Afraid of Food
We are going to revisit Dr. Peebles’ very astute observation that treatment specialists cannot fear the same thing that an eating disorder fears, namely food. It bears repeating.
When a treatment specialist reinforces concepts of “good” food and “bad” food, of “healthy” food choices and sticking to a “balanced” meal plan, then how might someone in the grips of a restrictive eating disorder titrate the level of anxiety such that he magically remains anxious about consuming food, but not so much so that he applies maladaptive anxiety modulating techniques such as self-administered starvation, excessive exercise, restriction and reactive eating cycles etc.?
Surely the more suitable approach is to help a patient embrace the fact that food is not something that should trigger fear for anyone? Why is anxiety over food choice and consumption accepted as not only a normative response, but also an ideal response in humans?
The dominant treatment approach for restrictive eating disorders today is equivalent to attempting to de-sensitize someone with a severe phobia of sunflowers by telling them a) it’s not about the sunflower at all in any case, b) there are good sunflowers and bad sunflowers and so the sufferer still needs to be vigilant, and c) as long as the sufferer does not flip into becoming a full-blown sunflower lover, then it will be possible to recover from the phobia and live a normal and balanced life where the person neither yearns for nor overly fears sunflowers.
In that entire scenario no one thought to suggest that sunflowers are not a threat to anyone and therefore the treatment specialist will set out to provide opportunities to reinforce the inherent benign nature of sunflowers such that the patient is able to recalibrate his or her threat response. If they end up loving sunflowers, then how nice is that? They are pretty cheery flowers after all.
And unlike sunflowers, food is critical for life. None of us can fear what an eating disorder fears.
Weight Restoration Does Not Necessarily Equal Remission
Many will visit Your Eatopia after several months of conscientiously working on recovery from a restrictive eating disorder. Because there are so many treatment programs that are not evidence-based, many are eating far too little to dependably restore their optimal weight and repair damage. I discuss these realities in several blog posts, however you will likely find I Need How Many Calories?!! a good place to get evidence on actual intake requirements.
Some in recovery have continued to exercise, restrict foods, and avoid going over the calorie allotment even though they are hungry for far more.
Many patients in this circumstance have lingering issues that concern them enough to have them seek out further advice and support.
Some continue to have amenorrhea (lack of a regular menstrual cycle); others are frustrated that if they eat even just a bit above the sub-optimal level they have been following, they gain more weight; others may have continuing hypothyroidism, issues of fatigue and feeling the cold; restrictive eating disorder-based thoughts continue to plague them; many are frustrated that heroic efforts to starve and/or over-exercise, do not result in weight loss; others complain of a disproportionate amount of weight that won’t budge around the mid-section; and finally almost all continue to be hungry but resist responding to the hunger because they are “weight recovered” and they don’t want to become obese (if they succumb at all to the hunger, then they tend to cycle through restriction and reactive eating/sometimes purging).
All these disparate complaints have a common origin: sub-optimal weight recovery that generated a persistent hypo-metabolic rate coupled with lingering unresolved starvation-induced physiological damage.
The answer to getting out of this quasi-recovered state and reaching full recovery is to eat to the recovery guideline amounts (and more) every single day. Responding to any extreme hunger is as critical now as it is all throughout the recovery process.
Despite restrictive eating disorder-based fears that there is no way to eat this much and not become obese when you are already ‘weight restored’, no clinical evidence supports those fears.
Your metabolism will ensure that your body adjusts to its optimal weight set point and the excess energy is necessarily needed to complete the lingering repair and to finally push the metabolism back to its optimal functioning rate. And no, your metabolism is not broken and your brain responds accurately to leptin levels.
Non-ED men and women ‘overeat’ regularly and it is not bingeing in any clinical sense nor does it impact optimal weight stability.
Between the ages of 10-16 it is common for the body to store extra energy in anticipation of physical growth requirements. It is difficult for anyone in our obese-fearing and weight-obsessed culture to not react to these phases of extra weight with immediate restriction. Sadly, for those with the restrictive eating disorder genotype, it is usually this very circumstance that catapults them into years of cycling through restrictions and quasi-recoveries.
Between the ages of 16-25, the body will occasionally store extra energy, but usually it is using the extra energy coming in (through natural overeating sessions) as it happens. However, if a restrictive eating disorder patient hijacked his or her normal development as a child with self-administered starvation and/or excessive exercise, then the recovery process may mimic the energy storage/growth spurt that was supposed to happen but was stalled by the onset of the eating disorder. Give it time and it works itself out.
Finally, women eat more in the post-ovulation phase relative to the pre-ovulation phase of the menstrual cycle [SP Dalvit, 1981]. This too does not result in progressive weight gain [ibid.] and it appears the extra energy is involved in serotonin modulation [SE Møller, 1992]. Basal metabolic rate varies significantly throughout the menstrual cycle [SJ Solomon et al., 1982] and carbohydrates (serotonergic nutrients) are the preferred nutrient that increases in the post-ovulation period [SP Dalvit-McPhillips, 1983].
Bingeing in the true clinical sense only occurs for the tiny group suffering what appear to be rare circadian rhythm and endocrine disorders that result in binge eating disorder or night eating syndrome.
Critically, those with BED are not able to apply any restrictive responses to their overeating. The condition appears in pre-pubescent childhood and usually involves being classified as ‘obese’ by age 11.
I’m going to repeat that:
Binge eating as a clinical disorder involves an inability to apply any restriction.
That means, if you are on the restriction eating disorder spectrum, you are unable to develop BED. Your bingeing experience is an expression of required energy needs in reaction to restrictive eating behaviors. It is why I call this behavior reactive eating and not bingeing.
Restriction is the enemy. Be vigilant against restriction and put your trust in your body’s ability to find it’s optimal weight set point if you just give it the energy it is demanding (no matter your current weight).
No one keeps gaining and gaining. We each have an optimal weight set point [RE Keesey et al., 1997; RE Keesey, 1988]. On average 70% of adult females reside between BMI 21-27 [Statistics Canada, 1978] but our heights and weights exist on a bell curve and you are only going to be healthy at your particular optimal weight set point.
You will find all manner of mainstream articles professing some miracle way in which optimal weight set points can be lowered permanently. They cannot. As Albert Stunkard and Daryth Stallone pointed out in their review of the regulation of body weight : appetite suppressant medication must be used long-term or not at all if body weight set points are to be manipulated successfully. That is not to suggest that permanent suppression of appetite is healthy by any means!
In fact, the only permanent manipulation of optimal weight set points that has been achieved thus far is in rats and mice by creating lesions in the hypothalamic region of the brain [JK Elmquist et al., 1999; LE Harrell et al., 1975]
Given that our extreme fat-hating society has not yet reached a point where we are gleefully searing parts of people’s brains to ‘cure’ them of fat, the epitome of a full remission from a restrictive eating disorder is the ability to not merely accept your body’s optimal weight set point, but to embrace the fact that it has no bearing on your life and the potential within you to live a meaningful existence.
Excise the word “binge” from your vocabulary. You won’t need it any more.
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