Understanding Why Recovery Takes So Long
I Only Restricted For A Very Short Time
Unless we suffer significant levels of chronic depression, we all tend to believe in our own exceptionalism, or illusory superiority. [1] Fully 80% of us believe ourselves to be above-average drivers and that’s a statistical impossibility given that the majority of us must be average drivers at best. [2] Given illusory superiority is the norm in human experience, it probably has some good evolutionary value.
Getting to a stable level of practicing remission from an active eating disorder takes a very long time and is usually measured in multiple years, not months. It’s tempting to assume that it’s a straightforward mathematical equation: number of months restricting equals number of months navigating active recovery. It’s also understandable to want to get beyond the recovery process because it’s very not fun. I’ve talked before about the elapse time to remission in the post: Time to Remission.
While many expect to sail through recovery in a matter of months, statistically it is not likely to happen that way. But should I be bursting the illusory superiority bubble? Well yes, because fostering what I would call flexible realism appears to increase success at persisting with remission as a practice, at least in my first-person experience with patients.
The first thing that crosses your mind when you are several months into recovery and nothing seems to be improving is to ask yourself “What am I doing wrong?” The conclusion that something must be wrong is at least partially based on many assumptions you made at the outset—assumptions that set you up for expecting an exceptional journey through recovery.
One common assumption is the time spent actually restricting food intake and exercising in a way that created cumulative net energy deficits in the body was measured in months, not years.
The eating disorder prodrome usually has a long duration. A prodrome is when the condition is active but doesn’t meet either the clinical criteria for a full-blown syndrome and/or the patient is unaware the behaviours are anything other than “healthy”. The clinical research on the eating disorder prodrome is sparse and fraught with arbitrary Diagnostic and Statistical Manual of Mental Disorders (DSM) categorizations. Dr. David Herzog and his colleagues undertook a prospective trial to identify conversion of sub-syndrome diagnosis to clinical diagnosis of anorexia nervosa (AN) and bulimia nervosa (BN). They found that conversion occurred within 2 to 4 years for half of all those with sub-syndrome AN and for two-thirds of those with sub-syndrome BN. [3]
Everyone has different behaviours during the prodromal period but some common ones are: lean-focused fitness and exercise behaviours, removing food groups and food types from the diet (anything from desserts to presumed food ‘intolerances’), adopting vegetarian or vegan diets, restricting food intake and/or food type to try to remediate symptoms due to chronic conditions, or looking to change the shape or size of the body believing it will confer greater health benefits. As you can see from Dr. Herzog’s results, not everyone engaged in these preoccupations will progress to a clinical case of an eating disorder. But for those now in recovery, clearly the behaviours worsened culminating in a period of clinical severity.
In this framework, patients tend to measure the time of active restriction at its worst and overlook the years of progressive worsening prior to that period, but damage was accumulating the entire time.
Another common assumption is that a period of weight restoration represents remission and a return to an energy balanced state. Given that so many treatment approaches equate remission with hitting a number on a scale, you’re not to blame for thinking that you were “recovered” when released from an inpatient treatment setting.
The weight restoration experienced after severe restriction is more commonly not sufficient to return to an energy-balanced state. Usually it merely lessens the grade of deterioration from cumulative net energy deficits in the body.
When any one of us doesn’t meet our energy requirements, then we are instantly thrown into catabolism and metabolic suppression. The body destroys its own cells (catabolism) to release energy into the system as a way to support crucial life functions (breathing, heart beating) and it shuts down/slows as many biological functions as it can (metabolic suppression) to try to delay death due to critical energy deficit failure.
To give you an overly simplified linear sense of what that looks like: when you eat 1200 kcal/day for six months (or use exercise to create an equivalent net energy intake) as a 28-year old female, then that removes 234,000 calories from your living system. A calorie is a unit that measures energy.
If you begin recovery and eat 4000 kcal/day (assuming a sedentary life) then 5.2 months would restore that deficit. However problematically that equation doesn’t include the additional energy needed to repair the damage caused by catabolism and metabolic suppression in the body. And I cannot stress enough that healing doesn’t work at all like a months-in-to-months-out equation.
Much as we’d like a mechanistic math equation to determine how long it might be considered acceptable to be wiped out, in pain and exhausted in recovery, the body is much more quantum weirdness than simple math.
2500 kcal/day is what an energy balanced woman over the age of 25 needs on average to support her living system (for the references on that, look out this post). Our bodies are designed to be optimized when we run at over 100% with specific metabolic clamping enzymes and hormones keeping everything right at the 100% level. The minute we diet, we send that entire system into chaos. We have short-term emergency functions that can come online as soon as we’re not providing at (or above) 100% energy input (i.e. we’re dieting) but it’s at a high cost as these functions are not as efficient as those that support us when we are not restricting energy intake.
Non-exercise induced thermogenesis (NEAT) can account for up to 2000 kilo calories’ worth of expenditure (it varies from one person to the next). [4] NEAT is a subconscious and automatic expenditure of unneeded energy in the system. NEAT is one of the primary reasons that over feeding humans in experimentation results in the subjects returning to pre-experiment mass, often within weeks of the completion of the over-feeding period. [5] It should be noted that over feeding experimentation also involves prohibiting NEAT throughout the active experimentation phase to determine how mass increases when NEAT is suppressed.
NEAT is the bane of recovery from an active eating disorder, but it is also a central nervous system- and fat-derived hormone-directed process to maintain energy balance (and inherited mass) when excess energy is taken into the system for those with no history of an eating disorder. [6] I’ve discussed the problem of NEAT as it relates to hyperactivity and fidgetiness for those with a history of an eating disorder in the post: Exercise Two.
Without any further consideration, we all tend to accept the cultural adage that we are optimized for famine and that it’s the massive availability of food today that means our bodies expand in mass indefinitely. Human populations across the planet have not faced, on an evolutionary scale, any serious famine pressures in a timeframe that would have acted on our gene pool. Famines are predominantly an unfortunate outcome of the move from hunter/gatherer and pastoralist lifestyles, to settled agriculture. [7]
If you choose to delve into the scientific hypotheses for the presence of a range of fat organ sizes within human populations, there are none that presuppose fatness has any adaptive evolutionary value. To review this literature is a great lesson in the limits of scientific inquiry. Science is undertaken and enacted by human beings. Those human beings are optimized to communicate efficiently through culture—often referred to as “memes” or “viruses of the mind”. [8] Memes are efficient for human communication and greatly enhance our ability to live in complex societies and large settlements filled with strangers (cities). Memes also hobble scientific inquiry as we have a tendency to accept the concepts within a meme without any further examination or critical thought. Just as a virus is able to evade our immune systems’ natural defences, so too does a virus of the mind evade our conscious immunity.
The dominant scientific discourse generating hypotheses for the presence of fatness in our populations is that the fat organ is just a storage unit for preventing death during famine and that in our modern food-laden cultures, the storage unit is over-filled. About the only scientist who has veered at all from this philosophy is Dr. John Speakman and even he assumes “obesity epidemic bad” is an incontrovertible truth. [9]
Speakman coined the term “drifty gene” (a play on the original “thrifty gene” hypothesis for the presence of ‘obesity’ in our populations):
“I have suggested an alternative scenario that subsections of the population have a genetic predisposition to obesity due to an absence of selection, combined with genetic drift. The scenario presented earlier was based on evidence from prehistory concerning the release of our ancestors from heavy predation pressure around 2 million years ago. I suggest here that this is one of a number of potential scenarios based on random genetic drift that may explain the specific aetiology of the obesity epidemic.”
Apart from the fact that there is no fatness epidemic at all (prevalence has remained either flat or decreasing for approximately the past 15 years in developed nations across the globe) [11] and the fact that one could argue that neither presence nor absence of heavy predation would necessarily act upon metabolic function in human populations either way, Speakman fails to incorporate important “known knowns” in his drifty gene hypothesis.
The first known he overlooks is that fatness confers tremendous morbidity and mortality protection—known in the scientific literature as the “obesity paradox.” [12] Even that term reinforces the meme that fatness must necessarily be harmful and therefore its known protective value is paradoxical (pffft). The second known element that is left unexamined in the Speakman hypothesis is the fact that fat is not a storage unit, but an endocrine organ driving much our metabolic clamping and optimization. [13],[14]
What does all this fat talk have to do with time spent grinding through recovery from an eating disorder? It’s fundamental to the time spent in recovery on two counts: 1) memes associated with the assumed badness of fatness impact your ability to feed freely and 2) we don’t know (because no one has moved beyond circular memes in fat research) how much time such a critical metabolic-driving organ needs to fix (or adjust to) the damage associated with having the bottom drop out of all the clamping mechanisms designed to work with us being in over-energized rather than under-energized states.
Basically, putting our populations under discretionary famines (diet-as-lifestyle) through memetic infection is a strange experiment with very little conscious and critical thought reviewing and assessing the outcomes of the experiment.
In order to develop flexible realism such that you can practice remission from an eating disorder, it helps to engage in psychoeducational and therapeutic treatment wherein you stop letting the fatness-is-bad meme evade your conscious and critical immunity. At the same time, your therapist can help you practice constantly approaching and eating food despite mounting anxiety (whether that anxiety has been linked to fat phobia or not). It also helps to incorporate the fact that your fat deserves some serious respect as a very complex and important organ responsible for metabolic optimization. Give it the time it needs to restore energy balance and provide it with the energy it needs to do so.
Allan, Lorraine G., Shepard Siegel, and Samuel Hannah. “The sad truth about depressive realism.” The Quarterly Journal of Experimental Psychology 60, no. 3 (2007): 482-495.
McCormick, Iain A., Frank H. Walkey, and Dianne E. Green. “Comparative perceptions of driver ability—a confirmation and expansion.” Accident Analysis & Prevention 18, no. 3 (1986): 205-208.
Herzog, D. B., J. D. Hopkins, and C. D. Burns. “A follow-up study of 33 subdiagnostic eating disordered women.” The International journal of eating disorders 14, no. 3 (1993): 261.
Levine, James A. “Non-exercise activity thermogenesis.” Proceedings of the Nutrition Society 62, no. 03 (2003): 667-679.
Pasquet, Patrick, and Marian Apfelbaum. “Recovery of initial body weight and composition after long-term massive overfeeding in men.” The American journal of clinical nutrition 60, no. 6 (1994): 861-863.
Teske, J. A., C. J. Billington, and C. M. Kotz. “Neuropeptidergic mediators of spontaneous physical activity and non-exercise activity thermogenesis.” Neuroendocrinology 87, no. 2 (2007): 71-90.
Berbesque, J. Colette, Frank W. Marlowe, Peter Shaw, and Peter Thompson. “Hunter–gatherers have less famine than agriculturalists.” Biology letters 10, no. 1 (2014): 20130853.
Greene, Penelope J., and Richard Dawkins. “From genes to memes?” (1978): 706-709.
Speakman, John R. “Thrifty genes for obesity, an attractive but flawed idea, and an alternative perspective: the ‘drifty gene’hypothesis.” International journal of obesity 32, no. 11 (2008): 1611-1617.
ibid.
Ogden, Cynthia L., Margaret D. Carroll, Brian K. Kit, and Katherine M. Flegal. "Prevalence of childhood and adult obesity in the United States, 2011-2012." Jama 311, no. 8 (2014): 806-814.
Romero-Corral, Abel, Victor M. Montori, Virend K. Somers, Josef Korinek, Randal J. Thomas, Thomas G. Allison, Farouk Mookadam, and Francisco Lopez-Jimenez. "Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: a systematic review of cohort studies." The Lancet 368, no. 9536 (2006): 666-678.
Trayhurn, P. "Endocrine and signalling role of adipose tissue: new perspectives on fat." Acta Physiologica Scandinavica 184, no. 4 (2005): 285-293.
Harwood, H. James. "The adipocyte as an endocrine organ in the regulation of metabolic homeostasis." Neuropharmacology 63, no. 1 (2012): 57-75.
