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[Disclosure - IAN a neurologist or MD of any kind. I am writing here as a parent who happens to be a clinical researcher.* ]

An interesting discussion on another thread (and in particular this comment) set me to thinking about the difficulties presented when our children have comorbid diagnoses. 

A general feature of serious brain illnesses is that having one increases the risks of being diagnosed with a second, and this is for a variety of reasons;
  1. The brain is an enormously complex organ, and if an important process or structure is seriously impaired, it is very probably going to have effects in many domains. For restricting disorders something like 60% of people have anxious & perfectionist temperaments that PREDATE the ED onset. So having Anxiety Disorder is very likely contributory to developing restricting EDs when combined with another exposure (the most likely candidate being undernutrition). The interaction between the biochemistry of elevated baseline anxiety and the biochemistry of the brain during undernutrition seems to create ED. It's one of the strongest causative scenarios emerging from the data we have and is a perfect example of how particularities in one domain can create risk for illness in another. (Yet it is by no means the ONLY causative scenario. )
  2. The brain controls our thoughts and behaviors. Even now, most people are diagnosed on the basis of their behavioral expressions. You "have" anorexia because you don't eat, bulimia because you throw up, orthorexia because you exercise, depression because you don't enjoy anything and don't leave the house, panic disorder because you exhibit panic attacks. And so forth. So if there is dysfunction of the brain that affects several domains of thoughts and behaviors, it is very likely that other diagnoses will be assigned.
  3. Socio-economic factors associated with mental illnesses increase the risks that there will be traumatic exposures - homelessness, impaired functionality, poverty, substance use are all common among those with serious mental illnesses, and each of these increases the person's vulnerability to violence, institutionalization, and addictions. Thus PTSD, substance abuse and depression are elevated among people who have OTHER "primary" (as in diagnosed prior to) mental illnesses, when compared to the general public w/o clinically significant mental health histories.
Now, turning more specifically to EDs - EDs ALL create malnutrition - yes, even BED. I recently had the privilege of talking with Chevese Turner, the founder of BEDA, who was gracious enough to share some of her own and the BED community's experiences and insights. One thing I came away with is an understanding that there is a substantial restrictive component for many (maybe most, in our diet-happy culture) people with BED; the restricting following binges - that restrict/binge cycle - can do as much harm for people with BED as it does in anyone else with ED. Although something like 50% of people with BED are at an "obese" BMI, they are in fact suffering many negative physical consequences of UNDER-nutrition. Say it with me again, and with feeling: BMI TELLS YOU NOTHING ABOUT HEALTH, ALL BY ITSELF.

Malnutrition affects the brain and the body GLOBALLY. In the Minnesota Semi-Starvation Study, the recruited subjects were fully grown (or just about), otherwise healthy men, who had to pass a battery of psychological tests for inclusion in the study. These 36 volunteers did not have (to the best of anyone's ability to tell) pre-existing mental illness. Yet after weeks of systematic, medically managed undernutrition they became anxious, irritable, compulsive, depressed. They showed cognitive impairments not there previously. Sleep disturbances were common. Some volunteers had to be terminated from the study - one subject became so distressed they self-harmed to the point of serious injury. JUST from malnutrition.

In a different setting, if one of these young men had walked into a doctor's office, they very likely would have been diagnosed on the basis of those other behaviors as HAVING Major Depression or Anxiety Disorder. In one of my favorite posts from Dr. O'Toole's blog The Many Disguises of An ED , Dr. O'Toole details some of her experiences with this property of EDs, and what that can mean in terms of treatment. We diagnose and treat mental illnesses on behaviors and thoughts exhibited. But the malnutrition that is secondary to ED affects the whole brain, and CAN look like pretty much any OTHER diagnosis in the DSM (the diagnositc manual used world wide for brain disorders - or maybe better said used to identify the particular flavor of neuro-diversity you are looking at, and to identify when that diversity has crossed into "needs clinical management" territory.)

Which begs the question "If ED can manifest as $_Diagnosis, does that meant that *standard treatments* for $_Diagnosis need to be added?"

And I think the evidence and Dr. O'Toole's blog post points to "It depends". Because a LOT of the time, the symptoms of $_Diagnosis resolve when you correct the malnutrition. And in the case of Anxiety Disorders, they appear to be a part of the structure of the ED themselves, so it seems plausible that your overall treatment plan needs to address BOTH.

But what if $_Diagnosis is NOT pre-existing, or isn't resolving with nutrition, or nutritional rehabilitation is not progressing for whatever reasons? Does it make sense to apply the treatment as usual (TAU)? And the intuitive answer might seem to be "yes", but well, THAT is what I started wondering about. Specifically about Major Depression- because it is really common, and definitely complicates the course and treatment of ED.

I was not sure that ED + depression is the same animal as major depression. I think the emerging science indicates that while the behaviors and thoughts look similar enough to warrant the diagnoses in each case, while similar neural processes may be involved, the Depression is arising from different causes. 

One thing that the literature shows, and I think the parent reports on this forum have borne out over the years, is that SSRIs are ineffective with underweight AN. Anecdotally, a lot of parents have reported here that their kid was an "atypical responder". But SSRIs have a good track record on depression (and anxiety) in the absence of ED. I wondered what might be the difference making the difference - what gives?

The next bit is an over-simplification - I'm no molecular biochemist for one thing! - but this is the general gist of my reading of the medical literature.

The first thing to understand, is that in randomized clinical trials (RCTs) for a given condition, having a "competing" diagnosis is generally an exclusion criteria. An RCT is designed to ISOLATE the effect of your treatment, on the people you are treating, so they are typically designed to exclude anything that might confuse the issue & muddy the waters. In short, SSRIs were developed for and tested on people with Depression, but NO ED.

A quick primer on brain structure and function: brain cells communicate electro-chemically. When a cell is stimulated, an electrical impulse is carried down to the end of the cell. Nerve cells don't connect directly to each other (or muscle or gland cells) - there is a gap - the "synapse" between the two. Neurotransmitters are the chemicals that go from the end of one cell, across the synapse to the next cell. On the receiving end of the second cell, there are receptors. The receptors are like loading docks that are shaped to accept only specific neurotransmitters. When an electrical impulse comes to the end of the cell, the neurotransmitter is released. It floats across the synapse, lands in any appropriately shaped receptor, and that is how the signal starts in the receiving cell. Once all the docks are filled, the neurotransmitters remaining kinda just hang out until they are reabsorbed by the sending cell - this is the REUPTAKE. 

Depression is well associated with dysregulation of the neurotransmitter serotonin. Selective Serotonin Reuptake Inhibitors work by stopping the sending cell from reabsorbing the serotonin. This means the chemical stays around in the synapse - so when the first bunch of serotonin that landed in the receptors on the receiving cell has been absorbed, this lingering serotonin can ALSO dock. SSRIs effectively extend the bang for the buck on the serotonin released. Why this works, is because it appears that people with Major Depression have cell in parts of their brain (amygdala & midbrain) that produce much less of a protein needed to transport serotonin in the synapse to the receptors, when compared to healthy controls[1]. Having the serotonin linger in the synapse means that the transporters can do "double duty". In contrast, work by Kaye et al [2] suggest that the serotonin problem in restricting EDs is twofold. First, there appear to be differences in howl the serotonin receptors work prior to onset of ED - and these differences are in different parts of the brain from the ones implicated in major depression. These differences are implicated in the pre-existing traits of anxiousness and harm-avoidance. Malnutrition then creates difficulties in serotonin *production*. 

But the depression of malnutrition is not an issue of transport or reception, it's an issue of PRODUCTION. Also, this effect is global, not just in select areas of the brain. SSRIs cannot ameliorate this problem - they work on a different problem altogether![3]

When too few cells are receiving serotonin messages, depression may well be the result. But because the system is complex, there can be varied reasons for why messages aren't getting through. This is the conundrum that psychiatric medicine & psychology are in. For the most part, all we have to go on are self-reported and observed thoughts and behaviors. But these lack specificity - they don't tell us very much about exactly WHY they are happening. We do but see through the glass darkly, when it comes to mental health, though much progress is being made.

I think what happens with a lot of clinicians, is that when they see depressive symptoms continuously in a patient, they think to themselves "Aha! Depression!" but without thinking "Aha! This patient is so malnourished, they have depression from it!" I think historical models of ED as being the consequence of trauma and poor parenting, aid in creating the impression for many clinicians that the ED therefore is a result of underlying depression. And no doubt, there are at least some patients who fit this profile as well. But MOST restricting patients, have a different brain biochemical profile from this - their depression is BECAUSE of the ED. As a result, as Dr. O'Toole hnted in her blog post, the point where Depression gets added as a diagnosis can be the point where one enters Dante's 13th Circle of Treatment Hell - Psychiatric Whack-A-Mole.

The burden and the treatment problems of depression vs depression + malnutrition are each severe and affect every aspect of the patient's quality of life. Major Depression symptoms in ED patients are not to be ignored - far from it. The evidence suggests that the mortality of the latter scenario is considerable, maybe up to  1/2 of the total excess mortality associated with ED! But it seems to me that in practice, what happens is a focus on the depression that somehow winds up "de-emphasizing", if you will, the primary issue: Starved brains are depressed brains.  Starved brains alter personality, cognitive abilities, and mood.

My take home from all of this is this: Physically and psychologically, the deficits caused by malnutrition really ought to be on the top of the Problem List, when it comes to ED.
  • Research and development of medication therapies need to account for malnutrition.
  • Treatment paradigms need to center correcting malnutrition.
  • The inability to self nourish needs to be weighted more heavily when developing treatment plans, and when considering questions of autonomy.
  • The special circumstances of malnutrition need to be considered: we cannot assume that "off label" use of any TAU in a malnourished ED patient is going to have the predictable & beneficial effects seen for those same symptoms in different populations.
I think that looking for pharmacotherapies which help patients eat better and/or suppress compensatory behavior urges is a really important avenue for exploration.

But we KNOW what works to reverse malnutrition. The questions I see are: As a community of people interested in helping patients recover, can we figure out better ways to center and prioritize a patient's INABILITY to maintain their own nutritional status, as part of their care plan? Can we understand this inability in the same ways we consider other serious challenges to autonomy? Can we figure out ways to meet the medical ethics standards of Beneficence, Autonomy, and Respect for Persons while acknowledging that EDs frequently will cross into the same incapacitating territory as the other biggie Serious Mental Illnesses?


1. Parsey et al, 2006. http://ajp.psychiatryonline.org/doi/10.1176/appi.ajp.163.1.52
2. http://eatingdisorders.ucsd.edu/research/pdf_papers/2005/kaye2005serotoinin.pdf
3. http://eatingdisordersreview.com/nl/nl_edr_10_3_1.html

This is completely intriguing to me. I've been thinking so much about what many of you have told me - get the weight up on my D a few more pounds, close gaps and see how the depression goes. However, at the same time, my D has had her period for nearly three years straight and so her ED RD and ED T - and me to some degree - haven't really stressed the aspect of gaining more because why? All the metrics seem ok.  But your post and her behavior - being down a few pounds for about 6 months - has got me thinking a lot. I'm going to put a call into her T tonight and leave a message on that since we have a session tomorrow. 

As you talk about all of this being interconnected in the brain, it just gets me thinking more. What if a healthy weight is determined by the elimination/lessening of depressive symptoms and anxiety and not only a period returning or a certain number? How do we know that's not the fact? For many here, it was definitely helpful with their children to up the weight and many of the symptoms resolved quite a bit.

My D definitely has emotional deregulation, and I'm hoping that DBT skills training and counseling will help her find better coping mechanisms while she does have anxiety and depression, but if we could find an organic solution to them, that would be amazing.

Thank you for sharing this - I find it very thought provoking. 
19 yo D. AN - since about 15 years old. WR quickly - but the last four years have been tough. Since Sept. 2017, two residential stays, now in IOP, fighting a relapse. ED is hanging on, mental state not great, can't get her to remain at a weight long enough or high enough to see mental healing. She's on a gap year that will likely now turn into two.
There is a great book on the topic of the brain and nutritional status.  It is more than weight - it is also micro nutrients missing, etc.

It is called "Answers for Anorexia."  It is complicated - but we followed some of it and we felt it helped to supplement during refeeding.  His claim is that zinc in particular is needed by most anorexics.  It is a tricky mineral because you can overdose on it - but anyway, this book is a good read on the subject.  I found it very helpful.

When we gave our daughter some of the recommended nutrient supplements in this book, we saw a huge turn around in her mental status within days.  She was like a different person.  We had to go off them to get a GI test done and her crying/yelling/flipping out/ED behaviors came back in full force.  The supplements were started again - and within a day or two, we had a relatively functioning and somewhat normal d back.  She still struggles, but the mood is much more stable and she is more reasonable person when she is supplemented. 

If you go on PubMed and look at research on zinc and anorexia, it has been known for a long time that zinc is helpful to anorexics in terms of relapse prevention and weight gain.  Almost all the research I found suggested that it should be standard treatemnt for anorexics to supplement with zinc.  But, my doctor did not know about it at all (she is the main doctor in an eating disorder specialty group!).  So, just putting that out there - should check out this book - I think it is really helpful.
One day at a time...

daughter diagnosed 8/15 when she was 16,
wr through maudesly method 1/16,
currently in potential first relapse
IrishUp wrote:
...I was not sure that ED + depression is the same animal as major depression. I think the emerging science indicates that while the behaviors and thoughts look similar enough to warrant the diagnoses in each case, while similar neural processes may be involved, the Depression is arising from different causes. ...

IrishUp, Thanks for your interesting post.

I'm really not convinced that person A's depression is necessarily the same illness as person B's depression, even if neither person suffers from an ED. I think it might be more like viral vs bacterial pneumonia in that the symptoms look very similar, but antibiotics will only help those suffering from the bacterial type. 

My hope is that they will eventually be able to do much better in predicting which (and whether) antidepressant will be effective instead of taking shots in the dark, which seems to be pretty much what happens with the present state of knowledge regarding treatment for depression. Surely there is some rhyme and reason for why Person A responds well to Drug A but not Drug B, etc. My guess is that among the causes of confusion is that "depression" is not one illness, but rather a collection of quite different animals.

Add in an ED (on top of depression) and the water just gets muddier. 


"We are angels of hope, of healing, and of light. Darkness flees from us." -YP 
Thanks so much IrishUp.

Such a clever, scientific portrait of my D!

Earlier I was 'chatting' with another parent via email and I commented that the horrible, violent relationship my D had with me when she was ill was resolved at the dinner table, not at the therapist's office.  Her mood is directly related to her weight.   Her anxiety never goes away completely, but is more manageable at a higher BMI.

Whilst in the thick of it, it seemed unbelievable to me that such a deep hatred could be resolved with nutrition alone. And I'm sure she would never have believed that I was 'horrible' only because she was underweight.

This is another nail in the coffin of the whole 'They have to want to get better/It's all about control' philosophy.'


D in and out of EDNOS since age 8. dx RAN 2013. WR Aug '14. Graduated FBT June 2015 at 18 yrs old. [thumb]
This is really interesting. My son definetly has the pre dating perfectionist, anxiety personality, but it was made much, much worse by the malnutrition. It magnified all the most difficult parts of him and minimised all the lovable parts. Other effects we saw were on sleep, relaxation - legs were in constant motion when malnourished, even when sitting, depression, emotional disregulation - unable to control rages, stopping communication, lack of interest in things which used to give him pleasure, irrational thought processes, particularly regarding food and inability to cope with change.
As weight increased anxiety and depression have very slowly improved, as has sleep (with medication), is now able to relax, became more chatty, started to do things he enjoyed again, stopped raging, last thing to conquer is irrational thoughts on food! Progress seems to happen in tiny increments, and then all of a sudden we must hit the right weight to trigger a big improvement, and something else is switched back on within him. It's like watching his personality come back to life.
13 yr old son diagnosed April 2015 with Anorexia.
Fascinating post Irish.

The best legacy (apart from the fact that thanks to them she's still alive) that my daughter gained from treatment in a specialist ED unit was her knowledge of the Minnesota Starvation Study. As d is an adult professionals tend to tune out to anything I might say (if indeed they let me into the room in the first place to pose the question) but I am proud to say that she is now perfectly capable of teaching clueless professionals about it herself.

All that is not to say that she doesn't have genuine co-morbid, indeed pre-morbid conditions. We both believe that she does. I also believe that the fact that, as you say, "in randomized clinical trials (RCTs) for a given condition, having a "competing" diagnosis is generally an exclusion criteria. An RCT is designed to ISOLATE the effect of your treatment, on the people you are treating, so they are typically designed to exclude anything that might confuse the issue & muddy the waters" tends to apply to ED treatments like FBT and CBT-E as much as it does for drugs, has complicated her treatment so far (all claiming to be evidence-based).

So my dream for 2016 would be for all clinicians (particularly general mental health ones who we seem to have had the most difficulty with) to read and understand the Minnesota Starvation Study and include its lessons in their work. I'm happy to say that my daughter will be one of the most vocal, and I hope persuasive, advocates for this with the people she meets along the way
Fiona Marcella UK
Very interesting thoughts to consider.

One question that I think we really need to find an answer for is: when is malnutrition no longer present? 

I think that there is ample evidence that malnutrition leads to depression. It is able to be reproduced in other circumstances. That being said, we cannot use BMI or weight to assess when that malnutrition has been reversed.

Neurologically my reading tells me that the depression of malnutrition is caused by a severe reduction in serotonin precursors. This in turn leads to down regulation and increased sensitivity of serotonin receptors. (What would seem a wise response to help keep those synapses still working). SSRI's lead to more serotonin sitting there waiting to be taken up, because the uptake is reduced. If there is no serotonin to be found then this is ineffective. Hence the reduced effect of SSRI in ED's. 

When malnutrition is reversed there can be an increase in serotonin precursors and an increase in serotonin present now with an increased sensitivity of receptors. This is thought to be the cause of a marked increase in anxiety and seen in many ED sufferers with refeeding. Their neurons are now being flooded.

So this then leads to, when has malnutrition been reversed sufficiently that SSRI's would be effective. Many professionals use a 90% of EBW. Biologically since malnutrition can occur at any weight it would seem unlikely that this fixed number would be reliable. Is it more to do with the micronutrients? When should we expect depression to naturally lift if it is all due to malnutrition. How do we assess malnutrition of the brain anyway?

If we are trying alternative treatments how do we assess the efficacy? Depression after all is based on those symptoms that are being expressed, it is the subjective experience of those with the illness. (We have no idea what is biologically happening in those with similar or slightly differing experiences.) Do we look for biological markers? Are there any?

Much of this then goes into how do we decide when someone is weight restored? I am not a great believer that the brain knows a precise number in weight that our loved one's need to be to get rid of ED thoughts or co-morbids. Body fat is a complex glandular organ. There are genetic and environmental influences on weight that we are still only learning about. We know that calorie restriction and weight loss sets causes the release of glandular changes that persist for well over 12 months post weight loss, and continue even if weight is being regained. (This comes from papers on those treating obesity). There is no reason to believe that our loved one's with ED don't have similar hormonal changes. What is the effect of these hormonal changes on ED thoughts? The role of nutrition on ED thoughts? Percentage body fat? Exercise? What is their role in depression or other co-morbids?

D diagnosed restrictive AN June 2010 age 13.5. Weight restored July 2012. Relapse and now clawing our way back. Treatment: multiple hospitalisations and individual and family therapy.
Sometimes I think you have to stop looking for causes and just treat what you see.  Ed + depression may not be the same as major depression but that does not mean that the treatment will be less effective.  The DSM does not stipulate how someone got the collection of symptoms he/she has.  That can be both a pitfall and a bonus.