You are a primary care physician, a general practitioner, or maybe a pediatrician or an internist. You spent far too much money and time, and lost a lifetime’s worth of sleep to sit across from a patient who has an eating disorder. Here’s all the stuff they never told you about this patient:
- First of all, it’s unlikely that the patient is actually clinically underweight—two-thirds of those with active eating disorders are never clinically underweight. Body mass index (BMI) is merely a bell-shaped curve of incidence across our entire population and there is no point or range along that curve that represents health for any one person. Weight is a highly heritable trait and trying to maintain it below its inherited point generates cumulative energy depletion throughout the body. What this means is that someone who is BMI 30 can be underweight as readily as someone who is BMI 20.
- Your patient will likely be average to well-above-average weight.
- The well-above average weight patient doesn’t have a problem with binges and the worst thing you could do is tell them to lay off the donuts and get to gym. That’s because all eating disorders are about not eating enough to support energy needs. A binge happens because of unending attempts to return to under eating relative to energy needs. 1
- Advising any patient to diet and exercise to ameliorate morbidity or mortality outcomes is not evidence-based medicine, 2 but to suggest these things to a patient with an eating disorder precipitates increased severity of the eating disorder. 3
- Your patient is probably not a 12-year-old middle-class white girl, even if you are a pediatrician. For most doctors your patient with an eating disorder will be a 20-to-70-something woman or man, or someone who will not self-identify using that binary classification. Their socioeconomic and/or racial backgrounds won’t help you to rule in or out the presence of an eating disorder.
- The upshot is that you cannot identify the eating disorder on sight. Worse still, the complaint(s) for which they are coming to see you will not even hint at the underlying cause: a system-wide energy deficit from years of not meeting the body’s energy needs.
- Now a quick detour to remind you of the standardized mortality ratio (SMR) of an eating disorder: somewhere in the range of 5.8, averaging out some wildly variable study results. The average looking patient in front of you has the deadliest of psychiatric conditions, and it kills young adults at 12 times the rate of any other cause of mortality (including car accidents) combined. 4
- But beyond the SMR and a reduced life expectancy of around 12 years, the patient sitting across from you will likely be fully disabled and unable to work, thanks to the eating disorder, by their mid to late 40s. And prevalence? Somewhere between 14-33% of the population at large. 5, 6, 7
- Your patient’s complaints will likely include:
- slow-to-heal injuries from workouts and distance running
- debilitating fatigue
- pruritus, rashes, skin conditions
- gastrointestinal distress (constipation, GERD, bloating etc.)
Obviously you’ll be faced with a differential diagnosis effort and the blood work will either tell you nothing (because it’s all good) or it will lead you down the garden path (because something shows up).
So before you get tripped up with all the common misdiagnoses (PCOS, IBS, anemia, MS, hypothyroidism (both antibody-driven and not), and etc.), here are some data to help you rule in or out the causative impact of an eating disorder:
- Know that average energy requirements for adult females and males are not 2000 and 2500 kcal/day respectively. Average intake for sedentary adult females is 2500 kcal/day and 3000 kcal/day for sedentary adult males. Between the ages of approximately 12-25 females require on average 3000 kcal/day and males 3500 kcal/day. Don’t hold back, and ask your patient to tell you what they eat on average each day and have in your mind a sense of what a 2500 or 3000 kcal/day meal plan would look like so you can compare and contrast. And don’t forget that net energy matters: if they are eating 3000 kcal/day but also work out an hour or two each day, then there will be a net energy deficit. 8
- Polycystic ovaries and/or the presence of oligomenorrhea or amenorrhea do not denote polycystic ovarian syndrome (PCOS). The presence of an eating disorder must be ruled out before PCOS can be definitively diagnosed because the reproductive system atrophies to mimic PCOS when the body has an energy deficit. 9, 10
- Under-eating relative to energy requirements drastically impacts gut motility, digestive enzyme production and the resilience of the gut mucosal layer. Symptoms of IBS, GERD, pruritus, skin rashes, distention, flatulence, severe constipation, so-called food sensitivities are all common signs of under eating relative to energy requirements. 11, 12
- Fatigue, anemia, depression, hypothyroidism and neuropathies all represent various ways in which the body catabolizes itself to release energy from living cells into the blood stream and suppresses all non-essential biological functions to stay alive as long as possible when faced with an ongoing energy deficit. If you treat these symptoms in the absence of getting the patient to re-energize with enough food to rectify the energy deficit, then you will be pushing the living system and overriding its inherent life-saving energy usage reduction mechanisms. 13
- The brain is disproportionately affected by energy deficits as it requires 20% of the energy coming in despite its making up only 3% of the body by weight. Obsessive compulsive behaviors, depression, phobias, anxieties, memory retention issues and rumination may not represent “dual diagnosis”, but rather reflect how poorly all brains function when under nourished. And as you well know from head injuries, hypoxia and diabetic crises, the brain is exquisitely ill equipped to identify its own impairment. 14, 15
- Most of you will know this, but oral contraceptives do not reverse the bone mineral density impacts of oligomenorrhea and amenorrhea. They slow the rate of deterioration somewhat, but functional hypothalamic amenorrhea/oligomenorrhea and its impacts on bone mineral density can only be successfully reversed with rest and adequate re-feeding. 16
- And with all this talk of female reproductive function 17, it’s easy to overlook that reproductive atrophy and dysfunction are common signs of an eating disorder in men as well. Eating disorders take up residence as readily in men as women. If there’s erectile dysfunction, lowered or absent libido, and/or lowered volume of ejaculate, then ask about food intake and exercise regimes. 18
- Bradycardia does not reflect athletic health in those with eating disorders. If your patient has an enviable resting heart rate at or below 66 bpm, do take the time to investigate corrected Q-T interval prolongation and dispersion. As there are no correlations with either BMI or potassium levels and the longest values of a corrected Q-T interval, proof of any risk of cardiac arrhythmia and sudden death from an eating disorder that will necessitate cessation of all exertion while the patient pursues re-feeding depends upon your investigation of the Q-Tc. 19, 20 Investigating whether orthostatic hypotension or postural orthostatic tachycardia are present can also help to uncover a hidden eating disorder.
- An optimal homeodynamic state cannot be realized by treating average energy requirements (as listed in item 1 in this section) as a maximum intake value for someone trying to recover from the cumulative energy deficits of an eating disorder. Your patient will have to rectify energy deficits and repair the damage associated with catabolism by eating more than average and the body may overshoot its optimal weight set point temporarily during that recovery process.
- Doctors get eating disorders too—very commonly expressed as “healthy” eating and athletic compulsions. Be gentle with your patient if you have fallen victim to the cultural and unscientific norms of fattism and healthism. Realize that if you have a blown out knee from years of triathlons and you’re still clocking in your regular runs each week and/or you believe that “junk” food causes illness then you are going to have to recuse yourself from treating a patient with an eating disorder. You are a doctor and a human being and to be the best doctor you can be, you have to know when your card carrying membership as a human being impedes your impartiality and professionalism as a medical doctor.
Please note that the references for the above include both the blog posts providing review and analysis as hyperlinks below as well as the original peer-reviewed published data referenced within those blog posts.
1. Binge Eating Disorder Part I and II
direct references for analysis as follows:
Stunkard, A. J., & Allison, K. C. (2003). Binge eating disorder: disorder or marker?. International Journal of Eating Disorders, 34(S1), S107-S116.
Cosgrove, L., Krimsky, S., Wheeler, E. E., Kaitz, J., Greenspan, S. B., & DiPentima, N. L. (2014). Tripartite conflicts of interest and high stakes patent extensions in the DSM-5. Psychotherapy and psychosomatics, 83(2), 106-113.
Appelbaum, P. S., & Gold, A. (2010). Psychiatrists’ relationships with industry: the principal-agent problem. Harvard review of psychiatry, 18(5), 255-265.
Elliott, C. (2010). White coat, black hat: adventures on the dark side of medicine. Beacon Press.
Cassidy, S. B., & Driscoll, D. J. (2009). Prader–Willi syndrome. European Journal of Human Genetics, 17(1), 3-13.
Stunkard, A. J. (1959). Eating patterns and obesity. Psychiatric Quarterly, 33(2), 284-295.
Goel, N., Stunkard, A. J., Rogers, N. L., Van Dongen, H. P., Allison, K. C., O'Reardon, J. P., ... & Dinges, D. F. (2009). Circadian rhythm profiles in women with night eating syndrome. Journal of Biological Rhythms, 24(1), 85-94.
Dingemans, A. E., Bruna, M. J., & Van Furth, E. F. (2002). Binge eating disorder: a review. International Journal of Obesity, 26(3), 299-307.
Ramacciotti, C. E., Coli, E., Paoli, R., Gabriellini, G., Schulte, F., Castrogiovanni, S., ... & Garfinkel, P. E. (2005). The relationship between binge eating disorder and non-purging bulimia nervosa. Eating and Weight Disorders-Studies on Anorexia, Bulimia and Obesity, 10(1), 8-12.
Pike, K. M., Dohm, F. A., Striegel-Moore, R. H., Wilfley, D. E., & Fairburn, C. G. (2014). A comparison of black and white women with binge eating disorder. American Journal of Psychiatry.
Wonderlich, S., (2005). Eating Disorders Review, Part I, Radcliffe Publishing, UK, p.40.
2. Systematic Review of Weight Gain Correlates in Literature Parts I and II
direct references for analysis as follows:
MJ Franz, JJ VanWormer, AL Crain, JL Boucher, T Histon, W Caplan, JD Bowman, NP Pronk, Weight-loss outcomes: a systematic review and meta-analysis of weight-loss clinical trials with a minimum 1-year follow-up, Journal of the American Dietetic Association, Vol.107(10), pp.1755-1767, 2007.
AG Tsai, TA Wadden, Systematic review: an evaluation of major commercial weight loss programs in the United States, Annals of internal medicine, Vol.142(1), pp.56-66, 2005.
VS Malik, MB Schulze, FB Hu, Intake of sugar-sweetened beverages and weight gain: a systematic review, The American journal of clinical nutrition, Vol.84(2), pp.274-288, 2008.
MG Tordoff, AM Alleva, Effect of drinking soda sweetened with aspartame or high-fructose corn syrup on food intake and body weight, The American journal of clinical nutrition, Vol.51(6), pp. 963-969, 1990.
DP DiMeglio, RD Mattes, Liquid versus solid carbohydrate: effects on food intake and body weight." International journal of obesity, Vol.24(6), pp.794-800, 2000.
J James, P Thomas, D Cavan, D Kerr, Preventing childhood obesity by reducing consumption of carbonated drinks: cluster randomised controlled trial, Bmj, Vol.328(7450), p.1237, 2004.
CB Ebbeling, HA Feldman, SK Osganian, VR Chomitz, SJ Ellenbogen, DS Ludwig, Effects of decreasing sugar-sweetened beverage consumption on body weight in adolescents: a randomized, controlled pilot study, Pediatrics, Vol.117(3), pp.673-680, 2006.
A Stevens, C Hamel, K Singh, MT Ansari, E Myers, P Ziegler, B Hutton, A Sharma LM Bjerre, S Fenton, R Gow, S Hadjiyannakis, K O’Hara, C Pound, E Salewski, I Shrier, N Willows, D Moher, M Tremblay, Do sugar-sweetened beverages cause adverse health outcomes in children? A systematic review protocol, Systematic Reciews, Vol 3.(1), p.96, 2014.
R Rosenheck, Fast food consumption and increased caloric intake: a systematic review of a trajectory towards weight gain and obesity risk, Obesity Reviews, Vol.9(6), pp. 535-547, 2008.
TJ Parsons, C Power, S Logan, CD Summerbelt, Childhood predictors of adult obesity: a systematic review, International Journal of Obesity, Vol.23, 1999.
Fogelholm, M., and K. Kukkonen‐Harjula. "Does physical activity prevent weight gain–a systematic review." Obesity reviews 1, no. 2 (2000): 95-111.
Proper, Karin I., Amika S. Singh, Willem Van Mechelen, and Mai JM Chinapaw. "Sedentary behaviors and health outcomes among adults: a systematic review of prospective studies." American journal of preventive medicine 40, no. 2 (2011): 174-182.
Hu, Frank B., Michael F. Leitzmann, Meir J. Stampfer, Graham A. Colditz, Walter C. Willett, and Eric B. Rimm. "Physical activity and television watching in relation to risk for type 2 diabetes mellitus in men." Archives of internal medicine 161, no. 12 (2001): 1542-1548.
Hu, Frank B., Tricia Y. Li, Graham A. Colditz, Walter C. Willett, and JoAnn E. Manson. "Television watching and other sedentary behaviors in relation to risk of obesity and type 2 diabetes mellitus in women." Jama 289, no. 14 (2003): 1785-1791.
Dunstan, D. W., E. L. M. Barr, G. N. Healy, J. Salmon, J. E. Shaw, Beverley Balkau, D. J. Magliano, A. J. Cameron, P. Z. Zimmet, and N. Owen. "Television viewing time and mortality the australian diabetes, obesity and lifestyle study (AusDiab)." Circulation 121, no. 3 (2010): 384-391.
3. Gaining Weight Despite Calorie Restriction
direct references for analysis as follows:
Manninen, A. H. (2004). Is a calorie really a calorie? Metabolic advantage of low-carbohydrate diets. Journal of the International Society of Sports Nutrition, 1(2), 1-6.
Feinman, R. D., & Fine, E. J. (2004). A calorie is a calorie" violates the second law of thermodynamics. Nutr J, 3(9), 10-1186.
Redman, L. M., Heilbronn, L. K., Martin, C. K., De Jonge, L., Williamson, D. A., Delany, J. P., ... & Pennington CALERIE Team. (2009). Metabolic and behavioral compensations in response to caloric restriction: implications for the maintenance of weight loss. PloS one, 4(2), e4377
Lowe, M. R., Annunziato, R. A., Markowitz, J. T., Didie, E., Bellace, D. L., Riddell, L., ... & Stice, E. (2006). Multiple types of dieting prospectively predict weight gain during the freshman year of college. Appetite, 47(1), 83-90.
Pietiläinen, K. H., Saarni, S. E., Kaprio, J., & Rissanen, A. (2012). Does dieting make you fat? A twin study. International Journal of Obesity, 36(3), 456-464.
Field, A. E., Austin, S. B., Taylor, C. B., Malspeis, S., Rosner, B., Rockett, H. R., ... & Colditz, G. A. (2003). Relation between dieting and weight change among preadolescents and adolescents. Pediatrics, 112(4), 900-906.
Wardle, J. (1987). Compulsive eating and dietary restraint. British Journal of Clinical Psychology, 26(1), 47-55.
Wardle, J., Chida, Y., Gibson, E. L., Whitaker, K. L., & Steptoe, A. (2011). Stress and Adiposity: A Meta‐Analysis of Longitudinal Studies. Obesity, 19(4), 771-778.
Wyse, C. A., Selman, C., Page, M. M., Coogan, A. N., & Hazlerigg, D. G. (2011). Circadian desynchrony and metabolic dysfunction; did light pollution make us fat?. Medical hypotheses, 77(6), 1139-1144.
Stevens, R. G. (2009). Light-at-night, circadian disruption and breast cancer: assessment of existing evidence. International journal of epidemiology, 38(4), 963-970.
Van Drongelen, A., Boot, C. R., Merkus, S. L., Smid, T., & Van Der Beek, A. J. (2011). The effects of shift work on body weight change—a systematic review of longitudinal studies. Scandinavian journal of work, environment & health, 263-275.
Nedeltcheva, A. V., Kilkus, J. M., Imperial, J., Schoeller, D. A., & Penev, P. D. (2010). Insufficient sleep undermines dietary efforts to reduce adiposity. Annals of internal medicine, 153(7), 435-441.
Patel, S. R., & Hu, F. B. (2008). Short sleep duration and weight gain: a systematic review. Obesity, 16(3), 643-653.
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8. Homeodynamic Recovery Method, Doubly-Labeled Water Method Trials and Temperament-Based Treatment
direct references for analysis as follows:
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Public Health England, Food Standards Agency, National diet and nutrition survey: results from years 1-4 (combined) of the rolling programme (2008/2009 – 2011/12) Executive Sumary, p.11
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