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 3: Some risks, complications and misdiagnoses
When I developed pneumonia, the doctor stated that for my age I should expect to get back to normal in six weeks’ time. I should have known better than to treat such a pronouncement as written in stone, and when I was still flaked out and exhausted two months in, I most certainly considered the possibility that something “was not normal.”
Our bodies are not machines. There are no mechanisms and no binary concepts of working or not working (with the exception of alive or dead, of course). Think of your body more as an ecosystem.
Imagine you are a forest, or a desert, or tundra, or perhaps a swamp. The absolute health and resilience of a forest or a desert are not measurable because each ecosystem has multivariate inputs. I can count the number of species; I can count the number of invasive species; I can measure temperatures, water levels, humidity, air pressure; I can identify which species seem healthy and which seem stressed; and I can even study these items over seasons and times to see if trends emerge. But none of those measurements will tell me the state of health and resiliency of the entire system.
When Mount St. Helens in Washington State (US) erupted in 1980, generating spectacular vertical and lateral explosions, a deadly pyroclastic flow, and subsequent landslides, it flattened an area of about 22 by 12 miles (35 by 20 km). Jimmy Carter, the US president at the time, was said to have described it as a moonscape when he flew over to inspect the damage. Scientific predictions initially suggested the area would take generations to recover. However, within just three years, 90% of the original species were found to be growing within the blast zone. 1
I use Mount St. Helens as an analogy for understanding two things about your body:
- Symptoms and screening tests will never accurately identify overall resilience, or lack thereof.
- What seems catastrophic may merely be a blip toward a new level of resilience.
Do not treat the Homeodynamic Recovery Method (HDRM) as a recipe or a set of exacting steps that will realize unequivocal and successful results. There are no assurances for any recovery effort, including this method.
Do not panic if you find some symptoms are not present, or seem to appear, disappear, and re-appear. Your entire recovery process may take you into full remission in as little as 3 months or as long as 79 months. The literature on time to remission is all over the map because there are no commonly agreed-upon definitions of remission for eating disorders at this time.
Three months is exceedingly rare. The median time to remission ranges from 14.4 months to 27 months. 2, 3 And in some studies the physical aspects of remission are disengaged from the psychological aspects. Drs. James Lock and Jennifer Couturier identified that the mean time to physical remission was 11.3 months, but the mean time to register remission on eating disordered thoughts and behaviors (using the Eating Disorder Examination score as the measurement tool) was 22.6 months. 4 One longitudinal study spanning 10–15 years noted that time to remission was protracted—ranging 57–79 months, depending on the definition of remission. 5
I know from experience that patients want concrete numbers: “Do I reach remission in 14 months or 79 months, based on my history of restriction?” The very disappointing answer to that question sounds like a riddle, but it is nonetheless ultimately true: “The recovery process is entirely what you make of it and is utterly unique for you.”
Pay attention to the small markers of progress along the way and celebrate them, rather than focusing on some imagined end state.
Like the post-eruption world around Mount St. Helens, your foundational goal in entering remission is to embrace a “new normal.” If you maintain an eating disorder–generated focus on eating the right foods at the right time, hitting and maintaining a certain weight, gaining to restore fertility, restoring enough weight to get people off your back, or restoring enough weight to lessen symptoms of starvation, then you are going to miss the forest for the trees.
Your mission, when pursuing remission, is to relish your new resilience and to live a life beyond an identity that has been tragically narrowed to numbers on a scale, or mileage on a pedometer, or shape in a mirror, or managing your anxiety with behaviors that impair your quality of life.
Recover fast or slow?
A recovery process is not without rare but potentially fatal risks. It’s not fair or accurate to assign these risks to the recovery process itself, because the brittleness of the living system has been caused by ongoing restriction.
No matter what facet of an eating disorder has had you in its grip (avoiding food, cycling through avoiding and reactively eating, using laxatives, diuretics and purging, applying exercise regimes to manage the anxiety of food intake, using prescription or illicit drugs to maintain a level of food avoidance that eases anxiety, or applying rigid concepts of so-called healthy diets and “pure” food choices) your current state has become akin to a well-crafted wizard doll I once received as a gift.
The doll stood perhaps 18 inches (46 cm) in height and it had been designed with pale leather, wood fashioned for the staff, hand-stitching, the odd semiprecious stone, and white furs for the robes, hooded cloak, and boots, with white hair and beard—not a jolly Santa type; a wizard. The details were exquisite but I knew nothing of maintaining leathers and furs. Everything became brittle and fragile over time. As long as he was never touched or moved, he seemed fine. But move him, or try to deal with accumulating dust, and he shed as explosively as a cat visiting the vet. He still looked beautiful, but on close inspection the cracked, stressed leather and dull fur was apparent.
The conundrum with recovery from an eating disorder is that a go-low-and-slow approach to re-feeding has no clinical evidence to support its use, 6, 7 but it’s still often applied because common sense would suggest that trying to take the brittle, faded wizard back to a lustrous and resilient new state requires gingerly curating the restoration process. But as you already know, common sense is often nonsense when it comes to the ever-present research chasm. “Go low and slow” is the phrase often used to describe keeping a patient at low intake amounts and slowly increasing her intake over an extended period of time.
An eating disorder is, at its core, an anxiety disorder. The reward system in the brain is built to encourage us to approach the identified reward, and the threat system in the brain is built to drive us to avoid the identified threat. As food has been misidentified as a threat, then “go low and slow” for recovery doesn’t offer enough exposure to the threat to allow for the threat identification system to eventually stand down. Both patients and practitioners assume that by getting used to incremental increases over time that the process of recovery can be more comfortable. Instead, this approach continues to reinforce avoidance, thus strengthening the cycle of see food, avoid food. The tomorrow where you plan to try that much-feared food, or increase that intake just a bit more, never arrives.
The HDRM incorporates clinical trial data that demonstrates the treatment modality of exposure and response prevention (ERP), originally designed in the treatment of anxiety disorders (specifically phobias), is also suitable for eating disorder treatment as well. 8, 9, 10
Drs. Joanna Steinglass and Sarah Parker, researchers investigating the application of ERP therapy for treatment of both AN and BN patients, noted that the anxiety underpinnings, if not addressed, predispose a patient to relapse:
Anxiety has long been noted as a prominent feature of AN, and a high rate of comorbidity between AN and anxiety disorders has frequently been reported. Though generalized anxiety improves as weight is restored, it does not necessarily normalize. Instead, most AN patients continue to show significant psychopathology after successful weight restoration, including abnormal eating behavior, over-concern with weight, and fear of fat.
Individuals who have shown improvement in many psychological symptoms still significantly restrict their eating when observed in a laboratory situation. Furthermore, restrictive eating patterns consisting of a monotonous low-energy, low-density diet have been shown to predict relapse. These restrictive eating patterns may be driven by underlying fear and avoidance of foods, along with fear of certain eating situations, which may in turn be the manifestation of underlying traits of high anxiety and high obsessionality. 11
Keeping in mind that the brain is impaired due to the absence of energy required to keep it running smoothly, and it’s also caught in a threat identification system that ratchets to ever-increasing levels of strength as each avoidance maneuver is enacted and reinforced; there will never be a right time, enough information, or enough iron-clad assurances that will make re-feeding feel like a good choice or a sensible path forward.
You must rely on instinct. You will inherently know if this is the thing you must do, even when you don’t want to do it. But before you squeeze your eyes shut and just begin, we have to talk about medical risk. Understand that, on very rare occasions, the shedding wizard may not survive the restoration project.
Re-feeding syndrome
Dr. Laleeq Khan and colleagues provide a thorough systematic review of scientific literature that assessed the medical challenges of re-feeding after a period of starvation. The suite of symptoms is referred to as re-feeding syndrome and was first documented in the 1950s in malnourished prisoners of war:
RFS [re-feeding syndrome] is well recognised. It occurs after the reintroduction of feeding after a period of starvation or fasting. RFS describes a series of metabolic and biochemical changes that occur as a consequence of reintroduction of feeding after a period of starvation or fasting. This unfavorable metabolic response causes nonimmune-mediated harm to the body and can be mild, moderate, or severe. 12
In re-feeding, after a period of malnourishment, the body has to accommodate to a nutritional load that it has adapted to being without. The symptoms of that response include fluid and electrolyte imbalances with the most common (but not universal) imbalance being hypophosphatemia (low phosphate levels). 13
In one study, moderate hypophosphatemia occurred in 5.8% of eating disorder patients hospitalized for initial re-feeding. Mild hypophosphatemia with no other complications developed in 21.7% of these patients and it was resolved with supplementation. Patients with moderate hypophosphatemia were more malnourished at the outset. 14
Despite the fact that the underlying reasons for the condition and the treatment to resolve it are well understood, the circumstances in which RFS are likely to occur and, most importantly, the actual incidence and prevalence rates for those re-feeding from eating disorders, are absent from the research literature at present. As such, we have to go with an amalgamation of case reports where the details are sufficient to enable us to perhaps develop suitable guidelines for risk factors associated with RFS.
Body weights of BMI 19.9 or lower were involved in cases with RFS; however, one case involved a BMI of 35.2. The median BMI was 13.7. The onset of RFS occurred between 0.4 to 21 days with the median being 3 days. Of those who developed RFS, the mortality was 25%, with case reports dating back earlier in time (1940s) having higher mortality than those in more recent times. 15 Problematically, this data incorporates only 49 cases in the literature review—that’s very little to go on for developing risk assessment guidelines.
Electrolyte imbalances are a known outcome for those who purge or abuse diuretics and laxatives and yet these eating disorder patients are often average or above-average weight. The abrupt cessation of those maladaptive habits can cause heart and blood vessel damage. 16 While abrupt cessation of these behaviors is warranted, modest (but necessary) medical intervention will be required to support the body’s shift to an absence of purging and/or diuretic or laxative use.
We are all used to advisories to consult our doctor before we so much as comb our hair, but when it comes to a state of malnutrition* the advisory to consult your doctor before you begin re-feeding is a non-negotiable statement of urgency.
Incrementing food intake slowly does not necessarily reduce the chance of RFS—that is especially the case for patients with more enduring anorexia with few remaining physiological reserves (i.e., extremely low weight, other medical complications already present due to ongoing starvation, etc.). 17
Unfortunately symptoms of the possible progression of electrolyte imbalances toward full-blown RFS (leading to organ failure in the absence of immediate medical intervention) are also vague. It is wise to err very much on the side of caution within the first 21 days of incrementing food intake upward (usually by increasing 200 calories every other day until at 2000 kcal/day and then jump to the HDRM intake guidelines from there). If you have symptoms of muscle weakness, seizures, dizziness, nausea, vomiting, and feel as if you are coming down with a really bad flu, then visit an emergency department immediately. 18 Be closely monitored by medical professionals while you increase your intake amounts.
Specific deficiencies worth investigation
Supplementation of a diet necessarily means that the diet itself cannot be inadequate for overall energy needs. In other words, if you are actively restricting your food intake then you are not meeting your body’s basic energy requirements. A vitamin or mineral supplement is designed to supplement (add to) an existing energy-balanced level of food intake. Many with eating disorders lean toward using supplements as meal replacements and these supplements are not designed to replace meals.
Additionally, using supplements when there is no deficiency is at best wasteful and at worst could be dangerous to your health. First and foremost, confirm whether you have a vitamin or mineral deficiency with your doctor before you use supplements during your re-feeding efforts. Consider discussing with your medical practitioner screening for possible deficiencies in zinc 19, 20 magnesium 21, 22 and/or thiamine (vitamin B1) 23, 24 in advance of entering your recovery efforts. When deficiencies are correctly identified and then supplemented as you re-feed, it can lower the risk of serious complications during re-feeding as well as often ease many of the unpleasant symptoms that occur early in the recovery process.
Zinc, magnesium, and thiamine are by no means the only important minerals and vitamins that might require supplementation during early re-feeding, but they are the most likely deficiencies found in a reasonable minority of those undergoing re-feeding. However, using zinc, magnesium, or thiamine supplements in the absence of a confirmed deficiency could be dangerous in recovery, so play it safe and see your doctor first.
Other medical risks
Clinical levels of restrictive eating are defined as 1000 kcal/day or less. Subclinical levels of restrictive eating are set between >1000 kcal/day up to the total energy requirements as defined for the individual. Now of course those cutoffs are variable, depending on energy expenditure, sex, and age. For example, one comparative study identified subclinical eating disorder intake at 1989 kcal/day for female athletes. 25 Another study identified subclinical restrictive eating as 19% fewer calories along with higher than average Eating Disorder Inventory (EDI) scores compared to healthy controls. 26 Keep in mind that these cutoffs reflect net deficits. If you eat 1600 kcal/day (subclinical restrictive eating) but then are also a distance runner, your net energy deficit will actually result in you having clinical restrictive behaviors because you expend more than 600 calories during the exertion of your daily run (net ≥1000 kcal/day deficit).
The difference between clinical and subclinical levels of restriction is the angle of the grade of deterioration in your health
An adult woman (biologically speaking, that would be women at or over the age of 25 27) with subclinical restrictive eating could be consuming a maximum of 2025 kcal/day (or 19% of confirmed average intake of 2500 kcal/day for healthy controls). Yet unscientific and confusing government-published recommended calorie intake levels would suggest that this woman is meeting her energy needs.
There is no clear understanding within the practitioner or research communities as to whether activation of the eating spectrum disorder can really appear for the first time in a mature adult, or whether it was activated in child or adolescent years but maintained a subclinical presence until later life. Dr. Kathryn Zerbe, MD, psychiatrist and clinical professor at Oregon Health and Sciences University, wrote a short article on the current understanding of eating disorders that appear in mature adults within the psychiatric and medical communities:
In the 1980s, examples of “late life eating disorders” in the literature were intriguing but rare, and for the most part a biological explanation was given for their etiology and resistance to intervention. In the 21st Century, clinicians see more patients who have maintained full-blown or subclinical eating and body image problems for decades… No matter the cause, eating disorders in the older population are dangerous illnesses that beguile practitioners who must be alert to the myriad of medical “rule outs” that must be made before the diagnosis of eating disorder is given. 28
Subclinical restrictive eating behaviors manifest negative health impacts over decades, whereas clinical restrictive eating behaviors manifest negative health impacts over mere months or years. Remembering that restrictive eating behaviors are cumulative in their impacts on the body, many patients who are diagnosed with late-onset eating disorders have actually experienced a long-running subclinical condition that has met the threshold for clinical diagnosis in later life just because the medical complications are compounding due to years of cumulative damage.
One of the main reasons that the dangerous illnesses caused by ongoing restrictive eating behaviors in older adult patients “beguile” medical practitioners is that patients fail to divulge their long history of such behaviors. In many cases, they are not even aware that their behaviors constitute the presence of an eating disorder. And unfortunately, even if they are forthcoming, often physicians are not as aware as Dr. Kathryn Zerbe (quoted above) that such behaviors are indeed responsible for numerous and often seemingly unrelated serious medical illnesses:
- Moderate to severe osteoporosis
- Kidney, liver, heart damage
- Likely both clinical depression and/or anxiety—intractable and progressively unresponsive to treatment
- Sexual dysfunction due to organ atrophy and low reproductive hormone levels
- Digestive tract issues: constipation, malabsorption, gastroesophageal reflux disease, multiple intolerances due to insufficiency of digestive enzymes, gastroparesis, etc.
- Anemia
- Susceptibility to serious complications with infection
- Damage to key areas of the brain that manage memory and retention, possibly leading to early-onset dementia
- A reduced life expectancy of 12 years (approximately)
- Usually disabled from work when the patient reaches mid to late 40s
- Severely reduced quality of life requiring on average six or more prescriptions to remediate various painful and debilitating symptoms in the patient’s 40s and 50s.
If you pursue a recovery effort after a decade or more of subclinical restrictive eating behaviors, then just as with those who are attempting the process after many months or a few years of clinical restrictive eating behaviors, there is still cumulative latent damage present.
All patients undertaking recovery from an undernourished state are moving a brittle living system into a new state of resiliency. That process stresses a fragile system.
The vast majority will experience unpleasant but essentially benign and temporary symptoms: exhaustion, swelling, pain, etc. The symptoms are not due to re-feeding and resting, but rather the body’s process of healing the damage that accrued during the active eating disorder period.
For a very small minority, the body has underlying damage that will be exacerbated by the recovery effort. In those circumstances, medical intervention is a necessity. Beyond the very rare instances of RFS, the heart, gastrointestinal organs, and kidneys are most vulnerable to serious medical emergencies (again in those rare cases where underlying damage is severe due to prior restriction).
Unfortunately hyper-intervention is the common framework applied by the medical community today—the result of mounting fears regarding medical malpractice and ever-more questionable application of standards of care developed by administrative specialists within medical and hospital corporations that remove the individual physician’s autonomy and expertise from the diagnosis and treatment options.
It is important to have an engaged physician for whom both the risk of life threatening complications and iatrogenic complications (i.e., illness or damage exclusively caused by medical intervention) are kept front of mind.
Common misdiagnoses either prior to or during recovery
Many patients with active eating disorders will be diagnosed with hypothyroidism or autoimmune hypothyroidism (Hashimoto’s thyroiditis).
Given that Hashimoto’s thyroiditis (Hashimoto’s) has a prevalence of 2 in 100, 29 the rate at which I see this condition diagnosed in those with eating disorders who are of average or above-average weight at the time of diagnosis is staggeringly higher than what it should be.
There are many ways in which we can over treat patients both when they are actively restricting food intake and when they undergo recovery from an eating disorder. Prescribing thyroid replacement hormone is one of the most common ways in which we interfere too quickly in a process that is most likely going to resolve with absolutely no intervention, given time and continued re-feeding and rest.
The prescribing of thyroid hormone treatment has increased approximately 30% in the UK in the past 10 years. 30 That is largely due to new lower cutoff points for the classification of hypothyroidism, even though there is no good data to confirm that treating patients at these cutoff points yields measurable long-term benefit. Instances of autoimmune hypothyroidism overdiagnosis may also be due to transient repair of the thyroid misdiagnosed as antibody-generated pathology. 31
In other words, misdiagnosis is quite possible for those with a history of an eating disorder. Almost all physicians and endocrinologists overlook the fact that a hypothyroid state is often entirely resolvable were the patient merely encouraged to reverse the energy deficit within her body.
There is insufficient clinical data to confirm whether restrictive eating behaviors activate autoimmune hypothyroidism; however, a parallel circumstance seen in postpartum women may indicate that the presence of autoimmune hypothyroidism in patients with an eating disorder is not, in fact, Hashimoto’s thyroiditis.
Postpartum patients can develop transient autoimmune hypothyroiditis, suggesting that dropping reproductive hormone levels have something to do with the activation of this transient state. Resolution of transient autoimmune hypothyroiditis likely coincides with reproductive hormone levels returning to their optimal state. 32 Given that patients who restrict food take the boots to their reproductive hormone levels, then it’s possible that there are transient autoantibodies present due to fluctuating reproductive hormone levels and that these autoantibodies are not destroying thyroid tissue just as is the case with postpartum autoimmune hypothyroiditis as well. As such, no treatment intervention would be required beyond resting and re-feeding.
As for hypothyroidism that appears in the absence of any antibodies, it’s a known outcome of even intermittent fasting, such as is found in subjects adhering to daytime fasting for Ramadan†. 33 For those with eating disorders, low triiodothyronine (T3) is common, and during re-feeding both T3 and tetraiodothyronine (T4) may drop even further before returning to match healthy control levels after a sustained period of rest and re-feeding. 34
If your practitioner diagnoses you with hypothyroidism, autoimmune or otherwise, then consider discussing a wait-and-see approach while you pursue your recovery effort. Keep in mind that each patient is different and it will be for you and your doctor to determine together whether your particular results indicate immediate intervention is necessary or not.
Another common misdiagnosis for those with eating disorders is polycystic ovarian syndrome (PCOS). PCOS may include increased facial hair, weight gain, and a lack of a regular menstrual cycle. However, PCOS should not be diagnosed in a patient with a coexisting eating disorder unless and until the patient is in a full remission.
If a patient were diagnosed with PCOS prior to the onset of an eating disorder, then she would need to have been older than at least 21 at the time of the PCOS diagnosis as prior to that age, immature ovaries can lead to misdiagnosis. Polycystic ovaries are common in maturing females and can also appear transiently in mature females without signifying any syndrome in need of medical intervention. 35, 36
Clinical studies suggest that approximately 50% PCOS diagnoses are incorrect for a variety of reasons. There is both a level of overdiagnosis and lack of reproducibility in the screening and clinical criteria used, that suggest that the entire condition is hard to identify and it has many phenotypic variables.
The data suggest that there is considerable uncertainty of all measurements and lack of clarity of the definition of the term “hyperandrogenaemia” which can lead to misdiagnosis. The current diagnostic strategies for PCOS are defined too vaguely to ascertain that individuals fit the definition of the syndrome. 37
Therefore an “official” PCOS diagnosis should be approached with extreme skepticism.
Polycystic ovaries occur in several circumstances where treatment is not required and, for those who are under-eating relative to their energy requirements, the presence of polycystic ovaries reflects the atrophy of the entire reproductive system as the body’s way to keep going despite cumulative energy deficits. Facial hair growth indicates hyperandrogenism. However its presence, in conjunction with the presence of an active eating disorder, reflects low levels of estradiol and other female reproductive hormone levels relative to androgen levels, rather than confirming true elevated levels of androgens.
Such symptoms, when they are the result of an eating disorder, will resolve with rest and re-feeding. Again, many practitioners will assume in error that someone of average or above-average weight cannot have an eating disorder. Many misdiagnosed cases of PCOS are the result of this profound misconception that patients who just “don’t look anorexic” cannot have an active eating disorder. It will be up to you to apprise your health care provider of your energy deficit status and to decide to move on if you determine that they are too steeped in cultural fattism to familiarize themselves with the scientific data.
Clinical data is readily available regarding the reproductive and fertility impacts of an eating disorder for women, however there are equivalent reproductive and fertility impacts in men with eating disorders. 38 The same is also true for anyone undergoing any kind of gender reassignment as well.
One further area of misdiagnosis for those with a history of an eating disorder that is not quite as straightforward as hypothyroidism or PCOS in recovery will involve blood glucose issues. Seriously out-of-range blood glucose results can occur in re-feeding and may require medical intervention until your pancreas is receiving enough energy to get back up to speed. A dietician can be very helpful for those dealing with either hypo- or hyperglycemia in early re-feeding to keep the recovery process moving forward safely. Yet again, however, there is a marked prejudice against average- and above average–sized patients when non-threatening and modest shifts in blood glucose management occur and health practitioners may advise aggressive treatment with, most commonly, use of the drug metformin.
Hypercortisolism (elevated cortisol levels) may also develop for some in recovery, as with blood glucose issues, tends to resolve with continued rest and re-feeding. Watchful waiting removes the possibility of unnecessary treatment but it may not always possible to go that route and keep the patient safe at the same time. Make your case for watchful waiting but then listen closely to your doctor’s assessment and recommendations when it comes to your unique situation.
Thankfully most physicians will be willing to take a wait-and-see approach if warranted, but they may not always offer it as an option. Asking if it’s possible to retest in three months’ time often allows for enough time to reveal a trend towards the norm. Waiting to reveal the trend will allow everyone to feel confident that either nature can take its course or perhaps intervention is warranted to support the recovery effort over the long term.
In part 4 we’ll look at how the HDRM is applied for the recovery effort.
* Please note that malnutrition is not a state that is purely developed through restriction of food intake. If you have been applying a lot of exercise with insufficient rest and food intake, or if you have been purging or using laxatives and diuretics, then these warnings apply.
† Please note that the leaders of all religions that include religion-based pursuits of fasting or food restriction are familiar with extending medical dispensation for individual followers. Not only that, they are demonstrably supportive of those who are not able to partake for health reasons and refute all arguments that not partaking is in any way a faithless act.
1. Franklin, Jerry F. "Ecosystem responses to the eruption of Mount St. Helens." National Geographic Research 1 (1985): 198-216.
2. Bergh, Cecilia, Ulf Brodin, Greger Lindberg, and Per Södersten. "Randomized controlled trial of a treatment for anorexia and bulimia nervosa." Proceedings of the National Academy of Sciences 99, no. 14 (2002): 9486-9491.
3. Von Holle, Ann, Andréa Poyastro Pinheiro, Laura M. Thornton, Kelly L. Klump, Wade H. Berrettini, Harry Brandt, Steven Crawford et al. "Temporal patterns of recovery across eating disorder subtypes." Australian and New Zealand Journal of Psychiatry 42, no. 2 (2008): 108-117.
4. Couturier, Jennifer, and James Lock. "What is recovery in adolescent anorexia nervosa?" International Journal of Eating Disorders 39, no. 7 (2006): 550-555.
5. Strober, Michael, Roberta Freeman, and Wendy Morrell. "The long‐term course of severe anorexia nervosa in adolescents: Survival analysis of recovery, relapse, and outcome predictors over 10–15 years in a prospective study." International Journal of Eating Disorders 22, no. 4 (1997): 339-360.
6. Garber, Andrea K., Nobuaki Michihata, Katherine Hetnal, Mary-Ann Shafer, and Anna-Barbara Moscicki. "A prospective examination of weight gain in hospitalized adolescents with anorexia nervosa on a recommended refeeding protocol." Journal of Adolescent Health 50, no. 1 (2012): 24-29.
7. Whitelaw, Melissa, Heather Gilbertson, Pei-Yoong Lam, and Susan M. Sawyer. "Does aggressive refeeding in hospitalized adolescents with anorexia nervosa result in increased hypophosphatemia?." Journal of Adolescent Health 46, no. 6 (2010): 577-582.
8. Steinglass, Joanna E., Robyn Sysko, Deborah Glasofer, Anne Marie Albano, H. Blair Simpson, and B. Timothy Walsh. "Rationale for the application of exposure and response prevention to the treatment of anorexia nervosa." International Journal of Eating Disorders 44, no. 2 (2011): 134-141.
9. Hildebrandt, Tom, Terri Bacow, Mariana Markella, and Katharine L. Loeb. "Anxiety in anorexia nervosa and its management using family‐based treatment." European Eating Disorders Review 20, no. 1 (2012): e1-e16.
10. Carter, Frances A., Virginia VW McIntosh, Peter R. Joyce, Patrick F. Sullivan, and Cynthia M. Bulik. "Role of exposure with response prevention in cognitive–behavioral therapy for bulimia nervosa: Three‐year follow‐up results." International Journal of Eating Disorders 33, no. 2 (2003): 127-135.
11. Steinglass, Joanna, and S. Parker. "Using exposure and response prevention therapy to address fear in anorexia nervosa." Eating Disorders Review 22, no. 5 (2011).
12. Khan, Laeeq UR, Jamil Ahmed, Shakeeb Khan, and John MacFie. "Refeeding syndrome: a literature review." Gastroenterology Research and Practice 2011 (2010).
13. Boateng, Akwasi Afriyie, Krishnan Sriram, Michael M. Meguid, and Martin Crook. "Refeeding syndrome: treatment considerations based on collective analysis of literature case reports." Nutrition 26, no. 2 (2010): 156-167.
14. Ornstein, Rollyn M., Neville H. Golden, Marc S. Jacobson, and I. Ronald Shenker. "Hypophosphatemia during nutritional rehabilitation in anorexia nervosa: implications for refeeding and monitoring." Journal of Adolescent Health 32, no. 1 (2003): 83-88.
15. Boateng, Akwasi Afriyie, Krishnan Sriram, Michael M. Meguid, and Martin Crook. "Refeeding syndrome: treatment considerations based on collective analysis of literature case reports." Nutrition 26, no. 2 (2010): 156-167.
16. Mehler, Philip S., Cynthia Crews, and Kenneth Weiner. "Bulimia: medical complications." Journal of Women's Health 13, no. 6 (2004): 668-675.
17. Mehanna, Hisham M., Jamil Moledina, and Jane Travis. "Refeeding syndrome: what it is, and how to prevent and treat it." BMJ: British Medical Journal 336, no. 7659 (2008): 1495.
18. Coldwell, Amy. “Refeeding Syndrome Symptoms”, Eating Disorders Online (article), September 12, 2011, http://www.eatingdisordersonline.com/articles/anorexia/refeeding-syndrome-symptoms/
19. Birmingham, C. Laird, and S. Gritzner. "How does zinc supplementation benefit anorexia nervosa?" Eating and Weight Disorders-Studies on Anorexia, Bulimia and Obesity 11, no. 4 (2006): e109-e111.
20. Golden, Barbara E., and M. H. Golden. "Effect of zinc on lean tissue synthesis during recovery from malnutrition." European Journal of Clinical Nutrition 46, no. 10 (1992): 697-706.
21. Birmingham, C. L., D. Puddicombe, and J. Hlynsky. "Hypomagnesemia during refeeding in anorexia nervosa." Eating and Weight Disorders-Studies on Anorexia, Bulimia and Obesity 9, no. 3 (2004): 236-237.
22. Boateng, Akwasi Afriyie, Krishnan Sriram, Michael M. Meguid, and Martin Crook. "Refeeding syndrome: treatment considerations based on collective analysis of literature case reports." Nutrition 26, no. 2 (2010): 156-167.
23. McCray, Stacey, Sherrie Walker, and Carol Rees Parrish. "Much ado about refeeding." Practical Gastroenterology 29, no. 1 (2005): 26-44.
24. Winston, A. P., C. P. Jamieson, W. Madira, N. M. Gatward, and R. L. Palmer. "Prevalence of thiamin deficiency in anorexia nervosa." International Journal of Eating Disorders 28, no. 4 (2000): 451-454.
25. Beals, Katherine A., and Melinda M. Manore. "Nutritional status of female athletes with subclinical eating disorders." Journal of the American Dietetic Association 98, no. 4 (1998): 419-425.
26. Cobb, KRISTIN L., Laura K. Bachrach, G. A. I. L. Greendale, R. O. B. E. R. T. Marcus, ROBERT M. Neer, J. E. R. I. Nieves, Mary Fran Sowers et al. "Disordered eating, menstrual irregularity, and bone mineral density in female runners." Medicine & Science in Sports & Exercise 35, no. 5 (2003): 711-719.
27. Kreitner, K-F., F. J. Schweden, T. Riepert, B. Nafe, and M. Thelen. "Bone age determination based on the study of the medial extremity of the clavicle." European Radiology 8, no. 7 (1998): 1116-1122.
28. Zerbe, K. J. "Late life eating disorders." Eating Disorders Review 24, no. 6 (2013): 3-5.
29. Chistiakov, Dimitry A. "Immunogenetics of Hashimoto's thyroiditis." Journal of Autoimmune Diseases 2, no. 1 (2005): 1.
30. Taylor, Peter N., Ahmed Iqbal, Caroline Minassian, Adrian Sayers, Mohd S. Draman, Rosemary Greenwood, William Hamilton et al. "Falling threshold for treatment of borderline elevated thyrotropin levels—balancing benefits and risks: evidence from a large community-based study." JAMA Internal Medicine 174, no. 1 (2014): 32-39.
31. Wakasa, Tomoko, Masayuki Shintaku, Shinzo Tanaka, Koichiro Yamada, Yaqiong Li, and Kennichi Kakudo. "Morphological Changes of Follicular Cells in Hashimoto’s disease: A Possible Cause of Overdiagnosis in Cytology." Journal of Basic and Clinical Medicine 2, no. 1 (2013).
32. Amino, Nobuyuki, Kiyoshi Miyai, Toshio Onishi, Takuma Hashimoto, Kayoko Arai, Kaichiro Ishibashi, and Yuichi Kumahara. "Transient hypothyroidism after delivery in autoimmune thyroiditis." The Journal of Clinical Endocrinology & Metabolism 42, no. 2 (1976): 296-301.
33. Sajid, Khan Mohammad, Mehfooz Akhtar, and Ghulam Qadir Malik. "Ramadan fasting and thyroid hormone profile." J Pak Med Assoc 41, no. 9 (1991): 213-6.
34. Nedvidkova, Jara, Hana Papezová, Martin Haluzik, and Vratislav Schreiber. "Interaction between serum leptin levels and hypothalamo-hypophyseal-thyroid axis in patients with anorexia nervosa." Endocrine Research 26, no. 2 (2000): 219-230.
35. Clayton, R. N., V. Ogden, J. Hodgkinson, L. Worswick, D. A. Rodin, S. Dyer, and T. W. Meade. "How common are polycystic ovaries in normal women and what is their significance for the fertility of the population?" Clinical Endocrinology 37, no. 2 (1992): 127-134.
36. Azziz, Ricardo. "Diagnosis of polycystic ovarian syndrome: the Rotterdam criteria are premature." The Journal of Clinical Endocrinology & Metabolism 91, no. 3 (2006): 781-785.
37. Barth, Julian H., Ephia Yasmin, and Adam H. Balen. "The diagnosis of polycystic ovary syndrome: the criteria are insufficiently robust for clinical research." Clinical Endocrinology 67, no. 6 (2007): 811-815.
38. Carlat, Daniel J., Carlos A. Camargo, and David B. Herzog. "Eating disorders in males: A report on 135 patients." American Journal of Psychiatry 154, no. 8 (1997): 1127-1132.