Whether you specialize in treating eating disorders, or not, you are trained to uncover your hidden biases so that you might best support your clients. If you’ve long held the belief that an eating disorder is “just taking things too far,” here’s an opportunity to uncover many things you may not have known were biases to begin with.
I am struggling with the dissent over diabetes I see across our forums. I have managed to alienate a dozen folk from the forums because they felt it was my obligation to include their anecdotal experience of taking very significant doses of insulin (under doctors’ orders) to bring their hyperglycemia in line and that this a) brought said elevated blood glucose in line and b) made them feel so much better.
When these kinds of things happen, I frankly don’t love being a patient advocate. But I’m going to attempt to explain why their first-person experiences have some important (and life endangering) caveats.
I had a colleague with a long list of male relatives who all had that first heart attack (many killed by it) in their 40s. He did the whole exercise and careful eating thing. He was also under close physician oversight and wore a holter monitor for a thorough screening of his heart function and all was in order. At 42 he keeled over on the street while on a lunchtime run. He survived his first massive heart attack. It took him a year to come back from that with a lot of fiddling around with various drugs and their side effects. That was 5 years ago or more now. Needless to say, it was life-changing. It was also, with hindsight bias, presumably inevitable.
Genetics aren't destiny, but they stack the odds in certain ways. At the end of the day we seem to have all lost an ability to be connected with our own mortality. We can do all the right things and be lucky. We can do all the wrong things and be lucky. Or whatever "things" we do that we think make the difference either way, end up not linked at all to the presence or absence of any luck.
We know from the literature that treated patients with diabetes, where the biomarkers are managed, do still develop diseases correlated with diabetes and die from those diseases. In fact, the mortality rates for diabetes are almost completely not impacted by the management of blood sugar levels. 1, 2 The good news is the mortality rates for those with diabetes (treated or untreated) are not that much different than for those without it. For the references on all of that, please look out these papers: Diabetes Mellitus Type II, Metformin, Disease Risk and You, Biomarkers and the Fear They Represent, Obesity Basic Facts II and Obesity Science in Context.
There’s a rather unfortunate side effect of diabetes diagnosis and treatment these days: patients develop anxiety and depression (to a clinical level) 3, 4 which negatively impacts blood glucose levels (and much more importantly negatively impacts the cardiovascular system through the influence of unrelenting levels of glucocorticoids). Interestingly, a systematic review and meta-analysis of those with diabetes and poorly managed glycemic control who were provided psychological interventions experienced improved glycemic outcomes. 5 Swallowing a spider to catch a fly (or taking more prescribed drugs to improve glycemic outcomes) may not be necessary when psychosocial and cultural influences are addressed.
But these things are phenomenally complex and even definitive books and research on the subject of personal models of health, illness perception, beliefs and feelings and their impacts on chronic illness experiences and outcomes, tend to overlook the inherent medical establishment bias that more medical intervention is unequivocally the desired outcome. 6 As a result much of the research assumes better treatment adherence is the desired outcome and patient quality of life is not measured at all. Today there are several medical practitioners who no longer adhere to that framework, but that doesn’t mean that all patients are aligned with the idea that less intervention may offer up better outcomes.
Quantum interplays of psychosocial and cultural framing for each patient, alongside actual observable symptoms as well as our new predilection to treat biomarkers as surrogates for clinical endpoints, all impact quality of life outcomes likely far more than any prescribed medical intervention.
Blood glucose level is a biomarker. A clinical endpoint would be, let’s say, peripheral neuropathy. A clinical endpoint is what a patient experiences as observable symptoms. Elevated blood glucose levels may or may not be responsible for observable symptoms in any given patient. But once a biomarker is made known to both doctor and patient, then it cannot be “un” known.
Living in a culture of medicalization and treating biomarkers as clinical endpoints means that you have a constant drain with any chronic condition of feeling and believing that you are not doing enough to treat it. Basically, you stress about having pre-diabetes or diabetes because it's framed as though you have Death himself watching your every move.
We all have Death watching our every move -- but not because those moves are how Death identifies when it's our time; Death is just interested in watching all living things.
And that's just creepy, so human beings have a long history of creating all manner of complex rituals that they hope will get Death to look the other way.
Many will deny any existential threat when treating a chronic condition. They are focused on wanting the symptoms to go away and don’t really concern themselves with mortality. Or so they think. The emotional salience we place on any symptom is psychosocial and cultural in origin and usually stands on existential threat whether we realize it or not.
Let’s use my chronic condition as an example. I have migraines. My risk of stroke in later life is not too terribly elevated as I am not prone to auras (a migraine symptom more strongly correlated with elevated stroke risk) but whether I treat a migraine or not, my mortality risk associated with any possible stroke in later life, is unchanged. Well in fact, if I do decide to treat a migraine it’s quite possible I am directly increasing my risk of heart attacks and stroke thanks to the risks of using triptans (a class of serotonin agonist used to treat migraines). Now that risk isn’t easily uncovered and it’s murky because longitudinal studies are always few and far between. Then there’s also gastrointestinal complications directly attributable to the use of triptans, and/or subsequent inability of triptans to abort a migraine altogether due to gastrointestinal paresis directly attributable to longer term triptan use. 7
My decision-making list for treatment of migraines for me is as follows:
- Of primary concern is quality of life in the presence of debilitating pain.
- The risks of triptan treatment are known to me, but not made readily available to most who are prescribed this drug.
- I choose to use triptans even as this likely elevates my risk of either extreme impaired quality of life (post a cardiac event/stroke that I survive in late life) or earlier-than-expected death from a cardiac event/stroke I don’t survive.
- There are no psychosocial or cultural moral issues around treating or not treating migraines (unlike the issues around diabetes these days); although there are plenty of cultural moral issues around the belief that such pain is “not real.”
- Triptans work to abort migraines for those who have migraines responsive to triptans. And that outcome is definitively proven through research-based double-blinded randomized-controlled trials (RCTs). Therefore, placebo influence is unlikely to be involved in the relief I experience associated with their ability to abort my migraines.
In the final decision, I am choosing to increase my risk of disease and early death (albeit we’re talking statistical and not necessarily actual clinical increased risk) as a tradeoff for quality of life function in the near- to mid-term. That means I have to navigate an increased presence of existential threat in return for the immediate benefits I experience of not being in pain. If I experience a lot of anxiety over that increased existential threat then I either seek psychological interventions, or I choose to stop taking triptans in favor of navigating the pain of migraine.
I would suggest that anyone treating symptoms associated with a chronic condition is making the same tradeoffs and that the decision to favor one tradeoff over another can also change over time for anyone too.
But my concern as a patient advocate is that individuals are actually made aware of those tradeoffs so that they might make the right decision for themselves. What are the tradeoffs of treating symptoms of elevated serum glucose levels and/or the presence of insulin resistance?
Well first of all, what are the symptoms? We are all given the list constantly: excessive thirst/urination, dark coloration of skin (armpits, groin etc.) and fatigue. We also know that elevated serum glucose levels and insulin resistance can be present with absolutely no observable symptoms, but let’s assume we are only speaking of those with actual symptoms that impact their current quality of life.
What are the risks of using prescriptions to treat these symptoms? Well close management of blood glucose levels leads to macro and microvascular complications, pancreatitis in some, and increased risk of cancer in others. 8, 9, 19, 11 The most serious risk from insulin treatment will be a single hypoglycemic event (low blood sugar) which can lead to seizures, unconsciousness and death. Any hypoglycemic episode increases risk of cardiovascular death and stroke. 12 In fact, some research investigation now suggests that risks of cardiovascular death correlated with the presence of diabetes mellitus type 2 is confounded by a greater risk of cardiovascular death correlated with management of diabetes mellitus type 2 through the control of blood glucose levels triggering episodes of hypoglycemia. The risk of cardiovascular disease due to hypoglycemia was found to be greater in one systematic review and meta-analysis than that of the presence of hyperglycemia/diabetes mellitus type 2. 13
And yes, successful treatment of elevated serum glucose levels does lower thirst/urination levels, improves dark discoloration of skin, quality of life perception, sleep and cognitive function (although that was not blinded given subjects had access to blood glucose readings at home).14 Such improvements were registered in only the first 12 weeks and longitudinal data is still lacking from the literature. One study spanning 6 months actually has the word “longitudinal” in its title and suggests that improved quality of life following insulin therapy is weak yet significant. 15
For the dozen people I referenced at the beginning of this post who believe that early and aggressive blood sugar management (though for those in question it took a while before it was aggressively managed) is responsible for their improved quality of life, short term research confirms their subjective experience.
But in the absence of double-blinded trials and longitudinal studies that at least make an attempt at a decade-long (rather than 6-month) review, we don’t know if sleeping better and thinking more clearly is a direct result of the psychosocial and cultural impact of seeing a blood glucose reading that is “acceptable,” or whether it is actually attributable to the lower blood glucose level itself.
Ultimately for those dozen people, it doesn’t matter because subjective quality of life improvements are very important markers of success for any patient. But my job as a patient advocate isn’t to reinforce what we already all have a great tendency to do – treat anecdotal evidence and proof of ultimate validity for all – my job is to have each individual develop their own decision-making list for treatment.
Unfortunately, there is little research data on the presence of hyperglycemia during recovery from an eating disorder. Pancreatic function is impaired due to starvation and its ability to return to full function is a work in progress during recovery. 16, 17 And such limited research as there is on the topic suggests that many metabolic anomalies resolve with continued recovery efforts in the absence of any treatment intervention. 18
It is not my job to tell you how to address any specific symptoms or how to arrive at developing your decision-making list for treatment. It is my job to try, to the best of my ability, to provide you with the research and the strengths and limitations of that research so that you can determine, alongside the advice from your actual medical advisers, whether the benefits of treatment outweigh the risks in your specific case—to develop your own decision-making list that works for you.
And it needs to be said that “to the best of my ability” isn’t without bias because no one is without bias. I have a bias that treating anxiety is fundamental to treating all chronic conditions. There is no way to navigate all the existential threat of illness without having an intimate relationship with that threat response and there’s no way to limit iatrogenic harm of aggressive medical intervention if you don’t first get a handle on what exactly you are treating about the condition and why.
Secondly, you own your treatment decision. If you are influenced by my writing, or conversely anecdotal suggestion, or heaps of drug-company-supported illness associations and foundations and their “informational” materials, or your own medical practitioner’s reasoned advice…no matter how you arrive at your treatment decision it’s yours and no one else’s.
I resisted using triptans for almost a decade. That was a lot of days lost to excruciating pain that didn’t respond to any over-the-counter analgesics. I could lay blame on my mother (who had been successfully treating her migraines with triptans throughout that time). I could lay blame on my family physician who knew a) my mother was being successfully treated, and b) I had migraines as did my mother. Nope. I own it. Did I suffer needlessly? Well I’m not sure any suffering is needful for anyone ever. But I choose to make use of what I learned about myself and pain during that time. I made the decision to avoid triptans because I was quite frankly afraid. I wasn’t prepared to take on the drug’s side effects and risks when compared to the known impact of the pain. That is, until the pain simply got to be too much, too frequent and too debilitating. Quality of life is important; but we don’t all get quality of life bumps by taking a drug. Plenty of people don’t respond to triptans for migraine treatment; some have very negative side effects; and a few die (directly attributable to the impacts of the drug on the heart).
Finally, I remember the inimitable words of Elizabeth Watson and her farewell advice to all: “trust no bitches” (on shuttering her MinnieMaud Skeptic Tumblr subscriber site). That’s likely the best advice you can carry forward in your own recovery journey.
1. Liu, Jiali, Ling Li, Ke Deng, Chang Xu, Jason W. Busse, Per Olav Vandvik, Sheyu Li, Gordon H. Guyatt, and Xin Sun. "Incretin based treatments and mortality in patients with type 2 diabetes: systematic review and meta-analysis." bmj 357 (2017): j2499.
2. Wulffelé, ele MG, A. Kooy, D. de Zeeuw, C. D. A. Stehouwer, and R. T. Gansevoort. "The effect of metformin on blood pressure, plasma cholesterol and triglycerides in type 2 diabetes mellitus: a systematic review." Journal of internal medicine 256, no. 1 (2004): 1-14.
3. Nouwen, Arie, Kirsty Winkley, J. Twisk, C. E. Lloyd, Mark Peyrot, K. Ismail, F. Pouwer, and European Depression in Diabetes (EDID) Research Consortium. "Type 2 diabetes mellitus as a risk factor for the onset of depression: a systematic review and meta-analysis." (2010): 2480-2486.
4. Smith, Kimberley J., Mélanie Béland, Matthew Clyde, Geneviève Gariépy, Véronique Pagé, Ghislaine Badawi, Rémi Rabasa-Lhoret, and Norbert Schmitz. "Association of diabetes with anxiety: a systematic review and meta-analysis." Journal of psychosomatic research 74, no. 2 (2013): 89-99.
5. Ismail, Khalida, Kirsty Winkley, and Sophia Rabe-Hesketh. "Systematic review and meta-analysis of randomised controlled trials of psychological interventions to improve glycaemic control in patients with type 2 diabetes." The Lancet 363, no. 9421 (2004): 1589-1597.
6. Martin, Leslie R., and M. Robin DiMatteo, eds. The Oxford handbook of health communication, behavior change, and treatment adherence. Oxford University Press, 2013.
7. Newman, Lawrence C. "Why triptan treatment can fail: focus on gastrointestinal manifestations of migraine." Headache: The Journal of Head and Face Pain 53, no. S1 (2013): 11-16.
8. UK Prospective Diabetes Study (UKPDS) Group. "Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33)." The lancet 352, no. 9131 (1998): 837-853.
9. Meier, Juris J., and Michael A. Nauck. "Risk of pancreatitis in patients treated with incretin-based therapies." Diabetologia 57, no. 7 (2014): 1320-1324.
10. Franciosi, Monica, Giuseppe Lucisano, Emanuela Lapice, Giovanni FM Strippoli, Fabio Pellegrini, and Antonio Nicolucci. "Metformin therapy and risk of cancer in patients with type 2 diabetes: systematic review." PloS one 8, no. 8 (2013): e71583.
11. Action to Control Cardiovascular Risk in Diabetes Study Group. "Effects of intensive glucose lowering in type 2 diabetes." N Engl j Med 2008, no. 358 (2008): 2545-2559.
12. Zoungas, Sophia, Anushka Patel, John Chalmers, Bastiaan E. de Galan, Qiang Li, Laurent Billot, Mark Woodward et al. "Severe hypoglycemia and risks of vascular events and death." New England Journal of Medicine 363, no. 15 (2010): 1410-1418.
13. Goto, Atsushi, Onyebuchi A. Arah, Maki Goto, Yasuo Terauchi, and Mitsuhiko Noda. "Severe hypoglycaemia and cardiovascular disease: systematic review and meta-analysis with bias analysis." Bmj 347 (2013): f4533.
14. Testa, Marcia A., and Donald C. Simonson. "Health economic benefits and quality of life during improved glycemic control in patients with type 2 diabetes mellitus: a randomized, controlled, double-blind trial." Jama 280, no. 17 (1998): 1490-1496.
15. Hajos, Tibor RS, F. Pouwer, R. de Grooth, F. Holleman, Jos WR Twisk, M. Diamant, and Frank J. Snoek. "The longitudinal association between glycaemic control and health-related quality of life following insulin therapy optimisation in type 2 diabetes patients. A prospective observational study in secondary care." Quality of Life Research 21, no. 8 (2012): 1359-1365.
16. Brown, Nigel W., Anne Ward, Richard Surwit, Jane Tiller, Stafford Lightman, Janet L. Treasure, and Iain C. Campbell. "Evidence for metabolic and endocrine abnormalities in subjects recovered from anorexia nervosa." Metabolism 52, no. 3 (2003): 296-302.
17. Kinzig, Kimberly P., Janelle W. Coughlin, Graham W. Redgrave, Timothy H. Moran, and Angela S. Guarda. "Insulin, glucose, and pancreatic polypeptide responses to a test meal in restricting type anorexia nervosa before and after weight restoration." American Journal of Physiology-Endocrinology and Metabolism 292, no. 5 (2007): E1441-E1446.
18. Modan-Moses, Dalit, Daniel Stein, Clara Pariente, Amit Yaroslavsky, Anka Ram, Michal Faigin, Ron Loewenthal, Eleanor Yissachar, Rina Hemi, and Hannah Kanety. "Modulation of adiponectin and leptin during refeeding of female anorexia nervosa patients." The Journal of Clinical Endocrinology & Metabolism 92, no. 5 (2007): 1843-1847.
Biomarkers are increasingly meant to foretell actual patient experience (if left untreated). Biomarker screening thus ends up creating a serious dilemma for the patient with an eating disorder. Here, we take a closer look at how someone with an eating disorder might navigate biomarkers.
Hypercortisolism (or Cushing’s syndrome) is sometimes present in those with an eating disorder. This state can occur either during active restriction or in the early phases of re-feeding.
Metabolic anomalies are common during recovery from an eating disorder and therefore the diagnosis of diabetes mellitus type 2 and treating it using metformin comes up enough in discussion threads on the Eating Disorder Institute forums that makes sense to synthesize the material here.
Understanding how to pull together a treatment team as an adult looking to reach remission from an eating disorder or to manage an active state while maximizing quality of life and minimizing complications.
Misophonia, Tourette's, eating disorders, OCD...they have so much more in common than you might think possible. If these conditions coexist then it doesn't mean "comorbidity", rather it means commonality and leveraged options for regaining quality of life too.
Eating disorders are mostly invisible. They are also great deceivers: able to mimic all manner of common chronic conditions and ailments. Some patients may have been told they were cured in their teens, but many more will have never been treated for an eating disorder at any time in their lives. So it won't occur to your patient that the cause of their symptoms is an eating disorder. Given the prevalence of eating disorders, here's a primer on how to identify them as a physician.
Second of two parts looking at binge eating disorder BED and its inclusion as a standalone eating disorder in the DSM-5 and what this means for those sure that bingeing causes BED.
First of two parts looking at binge eating disorder BED and its inclusion as a standalone eating disorder in the DSM-5 and what this means for those sure that bingeing causes BED.
The reality of gaining weight despite calorie restriction is dogmatically put down to a lack of control and not adequately ensuring the calorie restriction is consistently in place. Trouble is, the science thoroughly disproves that dogma.
A multi-part series to look at the scientific literature in depth on the topics of obesity onset and perseveration. Part II: Inactivity
How the scientific literature on obesity is regularly misinterpreted.
A multi-part series to look at the scientific literature in depth on the topics of obesity onset and perseveration. Part I: Food Intake
A closer and updated look at the Homeodynamic Recovery Method in relation to temperament-based treatment and calorie intake guidelines.
The level of organization and investment necessary in our health care systems when we instigated massive immunization and inoculation programs in the first half of the 20th century were very successful in developed nations. But of course now we have massive health care systems left in the wake of that effort...
I will not be able to address all the facets of this topic completely, but I must touch on them in some way because nothing is more difficult to navigate than the presence of both identifiable symptoms due to food intake and an anxiety disorder...
Not only is obesity not a disease; it does not cause disease. In fact, it is very likely that becoming fat (i.e. the fat organ increases in size) is the body’s protective response to the appearance of chronic disease for completely distinct and far more complex reasons than burgers and couches...
As soon as it is roughly understood that a body can maintain its weight and it’s not seen as a theory as in “theoretically, faeries could exist”...
Supplementation: not unless your medical team says so and even then you may want to discuss with them that such interventions are based on very narrow clinical trial data...