Science of Eating Disorders Tumblr
Tetyana here. I run the Science of Eating Disorders blog. This is the SEDs-associated Tumblr. I post about ED research, (mental) health, psychiatry, and medicine. I reblog pretty art and photography, promote critical thinking, and rant about stuff. Previously answered questions are here. Content is not always on topic and may be triggering.


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Anonymous:  I've believe I've read about AN possibly being related to an excess of serotonin which causes restriction to have a calming effect, whereas for someone with BN b/p behaviors can assuage a serotonin deficiency. But it also seems pretty common for people to be simultaneously diagnosed with anorexia and depression, and it seems like many anorexics are even prescribed SSRIs. Does that mean a completely different model of neurochemistry applies to those with AN and depression? Is this uncommon?

scienceofeds:

elizabeth—avenged:

edcynic:

I have no idea.

Seems like a question for scienceofeds!

What an astute observation anon! I will respond to this in more detail sometime today. 

Okay, I cheated. I outsourced this question to a friend of mine because I’m busy and because she’s more qualified than I am. I’ve been trying to a while to get her to write blog posts for SEDs with no luck. 

Here’s her answer (with my interjections in square brackets; all the bolding/italicizing/underlining and linking is also my doing)

5-HT = serotonin and 5-HT(1/2)R = serotonin receptor (that is, what serotonin binds to in the brain). 

I’m going to put her concluding paragraph in the beginning:

The simple answer in regards to depression and AN is that both illnesses are likely not just too little or too much serotonin and we really only have pieces of the puzzle in terms of understanding both illnesses. It’s too soon to say whether we can apply a completely different neurochemical model to AN vs. depression - for this we need better powered studies with many more people (both recovered and ill) and I think we also need to stop pooling AN-R and AN-BP, as we don’t know if these have completely similar neurochemical bases - However, this would be difficult given the cross-over rate between subtypes.

[Not only is focusing just on serotonin very simplistic, as there’s more to these illnesses than just serotonin and there are many serotonin receptors in different brain regions that have opposite effects on how neuronal activity — really, receptors, not the actual chemicals, are the important pieces of the puzzles — but the same behaviours or states (e.g., depression) could have different causes/causal factors. This would make sense, given that SSRIs don’t work for everyone with depression (LOL BY FAR). There’s no reason to think that just because person A and person B are both diagnosed with AN or BN or depression, that the underlying neurochemistry is the same. Very important point: There are also NO studies in AN and BN that look at the neurochemistry BEFORE the development of the ED, so the idea that these changes / differences are causal is a HUGE assumption.]

There is some evidence that AN is related to an excess of serotonin, but this is indirect (as we can’t actually measure serotonin in the brain, so anything we can do is indirect). Even with PET imaging [which is what’s used to study the levels of neurotransmitters in the brain, and the studies that have led to the hypotheses that anon mentions], at this point we have no good radioligands that are competitively displaced by serotonin which would give us an index of how much serotonin someone has in a certain state or after a certain challenge (i.e. administration of a hormone, starvation vs. recovery, etc.). There are groups working on this though and we do have a tracer like this for dopamine in which we can directly measure the amount of tracer displaced from a receptor by dopamine after a pharmacological/behavioural challenge or in a particular state of illness vs. recovery…

At the moment, one thing we can do is look at serotonin turnover, as measured by levels of its metabolite in CSF, which we assume is in equilibrium with serotonin synthesis so is an accurate measure of serotonin levels. However, this does not say anything about whether serotonin is elevated in some brain regions and not others and this is making a rather giant assumption.

In this respect, levels of 5-HIAA (a serotonin metabolite) have been found to be reduced in those with AN compared to healthy controls and elevated after recovery - supporting the hypothesis of a hypersertonergic state predisposing AN, leading to anxiety, harm avoidance, and a spiral of restriction etc. However, I’m not sure how well powered these studies were (i.e. in terms of sample size) and if they compared AN-R and AN-BP, recovered and healthy.

The second thing we can do is measure levels of various serotonin receptors (like the 5-HT1A receptor) using PET because these usually become desensitized upon repeated interaction with an agonist [something that activates the receptor] (i.e. serotonin) - so high states of serotonin should produce less 5-HT1A receptor binding as measured by PET and low states of serotonin should cause an upregulation of the 5-HT1AR, so greater 5-HT1AR levels.

There have been studies which have shown increased 5-HT1AR binding in AN as compared to health (i.e. less serotonin, anxiolytic, up-regulation of the 5-HT1AR), but some of these studies were grossly underpowered with sample sizes of 8 vs. 28 for ill and healthy participants, respectively  (Galusca et al., 2008). [Underpowered = the sample size is likely too small to detect any differences that have practical implications, for one, although it is more complex than that.]

In addition, this study included 9 recovered participants who also showed increased 5-HT1AR binding, which would not be expected if people recovered from AN have more available serotonin upon recovery (i.e. we would expect receptor down-regulation). [So, not all studies agree! There’s some conflicting findings.]

Also, the information can vary greatly depending on the tracer and how the data is analysed (researchers tend to use the analysis method which gives them the best results). 

Another study (Bailer et al., 2007) using a different tracer and method of analysis compared a larger sample of AN subjects - 15 (but 8 AN-R and 7 AN-BP) vs. 29 healthy controls and also found increased 5-HT1AR binding in AN vs. healthy subjects - so this does support the hypothesis of less serotonin during starvation leading to up-regulation of the 5-HT1A receptor and anxiolysis, but the jury is still out on what happens during recovery.

[Here are links to blog posts where I expand on this and talk about serotonin levels in AN, or at least, what we know/don’t know: here and here

1. Benefits of Starving and Why You Don’t Have a “Chemical Imbalance” 

2. The Benefits of Starving – Part II (Restricting Reduces Anxiety in Anorexia Nervosa)]]

In terms of depression and treatment of AN with SSRIs, my guess would be that since the literature points to the fact that people with acute AN have less serotonin (and also display many depressive symptoms during the acute phase of the illness), it’s not necessarily a bad thing to prescribe SSRIs to alleviate some of the depressive symptoms. However, I’m not aware of any research supporting their use once an individual is in recovery. 

In terms of BN, there is evidence of elevation of the serotonin transporter (again, using PET, but with a crappy radiotracer) and the serotonin transporter reduces the amount of available serotonin. SSRIs are antagonists of the serotonin transporter so increase extracellular serotonin - therefore, it makes sense that SSRIs would be an effective treatment for BN, and at the moment, I believe SSRIs are the only evidence-based pharmacological treatment for eating disorders (BN specifically). [This is true, 60mg has been shown to be somewhat effective at reducing binge eating and especially purging in patients with BN.] Low serotonin can also affect appetite (which is why weight loss can be a side effect of some SSRIs which elevate serotonin), so this might also play into the b/p behaviours seen in BN - but again, this is an overly simplistic answer to a complex question. 

[Here’s my post on serotonin in bulimia nervosa:Serotonin Function in Bulimia Nervosa – Brain Circuits & Behaviour]

Prevalence, types and comorbidity of mental disorders in a Kenyan primary health centre.

scienceofeds:

And I still hear people say that mental disorders or depression are just a thing that exists in Western countries. Yeah, okay… eyeroll. Just because you don’t research it doesn’t mean it doesn’t exist. 

Do childhood anxiety trajectories predict adolescent disordered eating?

The goal of the present article was to examine whether childhood anxiety trajectories predict eating psychopathology.

We predicted that girls with trajectories of increasing anxiety across childhood would have significantly greater risk of disordered eating in adolescence in comparison to girls with stable or decreasing trajectories of anxiety over childhood.

Method

Data were collected as part of the prospective longitudinal [study of 450 girls]. Childhood anxiety was assessed yearly (54 months through 6th grade) via maternal report on the Child Behavior Checklist. Disordered eating behaviors were assessed at age 15 via adolescent self-report on the Eating Attitudes Test (EAT-26). …

Results

The best fitting model included three trajectories of childhood anxiety, the low-decreasing class (22.9% of girls), the high-increasing class (35.4%), and the high-decreasing class (41.6%).

Mothers with more symptoms of depression and separation anxiety had girls who were significantly more likely to belong to the high-increasing anxiety trajectory.

There were no significant differences in adolescent disordered eating for girls across the three childhood anxiety trajectories.

Discussion

Childhood anxiety, as captured by maternal report, may not be the most robust predictor of adolescent disordered eating and may be of limited utility for prevention programs that aim to identify children in the community at greatest risk for disordered eating.

(Source)

I was surprised at the results! Turns out Stephanie Zerwas, the lead author, was as well:

Anonymous:  I've believe I've read about AN possibly being related to an excess of serotonin which causes restriction to have a calming effect, whereas for someone with BN b/p behaviors can assuage a serotonin deficiency. But it also seems pretty common for people to be simultaneously diagnosed with anorexia and depression, and it seems like many anorexics are even prescribed SSRIs. Does that mean a completely different model of neurochemistry applies to those with AN and depression? Is this uncommon?

elizabeth—avenged:

edcynic:

I have no idea.

Seems like a question for scienceofeds!

What an astute observation anon! I will respond to this in more detail sometime today. 

❝ To date, despite significant progress in modifying risk factors for EDs and depression, the field still lacks a public health study that has been appropriately designed and/or adequately powered to assess true ED/depression prevention effects. Further, although several programs show promise, many widely disseminated approaches lack empirical support, raising concerns about the potential for waste of limited resources.

— 

Changing the course of comorbid eating disorders and depression: what is the role of public health interventions in targeting shared risk factors?

This paper is open access.

elizabeth—avenged:

ohanniepo:

Despite having a long list of tags, phrases, and specific URL’s blacklisted, my dash continues to be filled with drama, misinformation (or information presented without appropriate conditions), self-importance, and often an infuriating lack of critical thinking. Tumblr is an important outlet and means of interaction for me (it’s almost my only interaction), but it’s hard to enjoy it anymore.

I apologize for bringing such unpleasantries onto your dash, dear friend. I’m also extremely frustrated by the amount of self-importance and ignorance I’ve seen today, but I hope I haven’t contributed to the self-important aspect. I am definitely going to be making an effort to avoid negativity on Tumblr, even if I see something that really angers me.

Internet “fights” are so tiring sometimes, eh. 

Anonymous:  I liked your reply re fat talk...I do think it can be detrimental &it is really hard to go against the status quo. How do you think one should respond when faced with that kind of talk from other women? Recovering from AN, I never join in bc I feel horribly awkward & also acutely aware of how harmful body preoccupation can be. But then I feel like people think I'm stuck up (ha so far from the truth). &I really don't want to invalidate but also don't want to give it airtime/reinforce it...?

That’s a very good question. I am not sure I have an answer (or any answers). I am, fortunately, almost never surrounded by fat talk. Indeed, the last I can think of hearing someone talk negatively about their body was one of my students (a pre-teen). Other than that, and outside of people with AN, I can’t think of the last time I heard people talking negatively about their bodies. Sooo I am not sure I have an answer! 

I think it would depend on context and the relationships you have with the people engaging in the fat talk. Co-workers? Students? Boss(es)? Friends? Family members? 

Anyone want to provide some advice/suggestions for anon?