Psychopathology Sum-Up: Bulimia Nervosa

[This is a guest post by Tetyana Pekar]

Tetyana is about to defend her MSc in Neuroscience at the University of Toronto. She is passionate about making eating disorder research more accessible to the public. She writes the Science of Eating Disorders blog where she aims to make sense of the latest findings in eating disorder research for lay audiences. She can be reached at tetyana@scienceofeds.org.

What is bulimia nervosa?

Bulimia nervosa (BN) is a serious eating disorder (ED) characterized by cycles of bingeing and compensatory behaviors. The most common compensatory behaviour is self-induced vomiting, but others include laxatives, diuretics, fasting, and excessive exercise. It is a common misconception that all BN patients self-induce vomiting—not so, while most do, there is a sizeable minority that does not (Keski-Rahkonen et al, 2009).

Individuals with BN are typically normal weight or overweight. This isn’t by chance; it is almost by definition. If someone binges and purges but is underweight, they will most likely be diagnosed with anorexia nervosa (AN) binge/purge subtype. Importantly, these diagnostic categories are not static, distinct groups, as over 50% of those diagnosed with restricting type AN cross over to bingeing/purging type within 5 years of ED onset, and about one-third cross over to BN (Eddy et al. 2008). So, take these diagnostic categories with a grain of salt.

Prevalence & Mortality

EDs have a high mortality rate, but keep in mind that prevalence and mortality statistics always depend on the duration of the study, the study size, and the population studied (among other things). However, most studies converge on a lifetime prevalence of BN somewhere between 1-2% (0.9-1.5 among women and 0.1-0.5% among men) (Smink et al., 2012).

The standardized mortality ratio (bulimia patients/normal, age-controlled population) for BN varies from ~2-5 (Arcelus et al., 2011). In one study of 906 individuals with BN, 3.9% died in the mean follow-up of 19 years, with suicide accounting for 23% of those deaths (Crow et al., 2009).

Causes

As much as people like the point the finger at the media and ‘thin culture,’ this explanation cannot be the whole story. After all, we are all exposed to images of thin models, and yet only 1-2% of women experience BN at some point in their lives. What is it about this percentage of women that makes them susceptible to BN?

Certainly, genetics plays a role.

Family studies are useful for determining if a particular disorder aggregates in families, though they cannot decipher if that aggregation is due to genetic risk factors of shared environmental factors (such as an over-emphasis on weight and appearance). These studies have shown that first-degree relatives of BN patients have a 4.4-9.6 higher likelihood of having BN than relatives of healthy controls (Kassett et al., 1989; Stein et al., 1999; Strober et al., 2000; ).

Twin studies are another good way to delineate the effects of genes and environment. These studies have shown that between 54-83% of the variation we see in BN is accounted for by genetic effects (Bulik et al. 1998, 2010; Kortegaard et al. 2001; Wade et al. 1999). (Note, this DOES NOT mean genes cause 54-83% of the disorder.)

This does not mean there are genes for BN (genes code for proteins, after all). However, commonly occurring temperament and personality traits might account for some of the genetic risk factors. Traits such as perfectionism, obsessionality, sensitivity to reward and punishment, and impulsivity often occur before ED onset and persist following recovery for many patients (Kump et al., 2004).

In addition, neurotransmitter systems, such as serotonin and dopamine, appear to modulate a lot of the traits associated with eating disorders. Indeed, serotonin might play an important function in the development of BN (and, along with the effects of estrogen, might partly explain why females are much more likely to suffer from EDs than males.)

It is almost important to emphasize that EDs are not “Western” disorders that arise solely due to an overemphasis on thinness. To provide just a few examples, blind women are not immune to EDs, and Iranian women living in Tehran exhibit similar levels of disordered eating behaviours as their counterparts in Los Angeles.

Behaviour does not occur in a vacuum. Genetics and environment both play a role. (For more on causes, see this post.)

Comorbidities

Eating disorders are generally highly comorbid with depression and anxiety disorders (Blinder et al., 2006). As mentioned earlier, patients with eating disorder tend to score high on perfectionism, neuroticism, impulsivity (particularly for BN patients), harm avoidance and obsessive-compulsive disorder. Among BN patients, the most common personality disorder appears to be borderline personality disorder (Sansone et al., 2005).

Treatment & Outcomes

Treatment for BN can include outpatient, inpatient, and/or residential treatments, among other things. As readers of FtB are well aware, any hard to treat diseases and disorders always attract pseudoscientific treatments. So, what treatments are evidence-based?

SSRIs, interestingly enough, have been shown to be effective in reducing the frequency of bingeing and purging in BN patients compared to placebo, particularly fluoxetine/Prozac (reviewed in Flament et al., 2012 and Hay et al., 2012). Cognitive-behavioural therapy is also widely considered to be an evidence-based treatment for BN (though, I have my reservations) (Murphy et al., 2010). In the end, the most important thing is to have a strong therapeutic alliance between the patient and the treatment team/therapist, as well as motivation to change.

In terms of outcomes, the results depend on length of follow-up, duration of illness, and sample population (i.e., how sick are the patients?). However, one large review found that about 45% of BN patients fully recovered, 27% improved, and 23% had a chronic course (Steinhausen et al., 2009).

Problems with the DSM

Compared to the problems with anorexia nervosa (AN), there are not as many. However, here are two things that annoy me:

  • Arbitrary frequency and duration criteria (2x/week for 3 months) (This will be reduced to 1x/week in the DSM-V.)
  • Too focused on weight (“compensatory behavior in order to prevent weight gain” and “self-evaluation is unduly influenced by body shape and weight”). These can certainly be true, but they don’t have to be. Bingeing and purging can just be a tool to regulate emotions.

Common Myths

Here are some other common myths that I haven’t mentioned yet:

  • BN patients throw up everything they eat. No, but some do, sometimes. The frequency and extent of behaviours varies a lot.
  • BN patients should just eat 5-small meals a day. Well, yes, but the problem has got nothing to do with not knowing how to eat well in theory.
  • BN is on the increase. Actually, studies suggest is pretty stable or even decreasing.
  • It is an effective weight control method (i.e., it is safe). I suppose, if you are okay with the plethora of medical complications (including death).

And one that bothers me the most:

  • BN is just about vanity. Actually, for me, bingeing and purging is incredibly anxiety reducing, and I’m usually symptomatic when I’m stressed, overwhelmed, or feel like crap about myself (not productive enough, for example). A sense of calmness and tranquility often follows self-induced vomiting (and I’m not alone in feeling this way).

Hopefully I’ve covered the basics. If you want to know more about BN, feel free to ask me questions in the comments, send me an email or check out BN-related posts on my blog here.


Tetyana was diagnosed with restricting type anorexia when she was in grade 10, started bingeing and purging at the end of first year in university. Her eating disorder has been all over the place, and she enrolled in outpatient treatment in high-school. She will be attending Women in Secularism conference. (Where I finally get to meet her!) You can follow her on Twitter.

Previous Psychopathology-Sum Ups:

Specific Phobias
Bipolar Disorder
Types of Antidepressants

Psychopathology Sum-Up: Types of Antidepressants

Weekly series! As per previous discussion, I will be publishing a big information blog on each Friday. Unfortunately, it’s midterms for me, which means a shorter post for you. Blame the paper(s) and exams and readings and stuff. I promise to be back on schedule next week. Also, I’ve commissioned a post on bulimia from Tetyana, who runs the spectacular Science of Eating Disorders blog, a skeptical look at research on ED’s.

Anyways, today we look at the types of antidepressants.

Selective Serotonin Reuptake Inhibitors (SSRI’s)

[Note to neurobiologists: I am simplifying massively here. I know that.]

These are the most popular medications for depression, and include a bunch of names you probably recognize: Zoloft, Prozac, Paxil, Celexa, Lexapro.

How do they work?

A general sketch of two neurons.

A general sketch of two neurons.

Neurons don’t connect directly to each other–they have a very tiny space (the synaptic cleft) between each end of one and beginning of the next. Neurotransmitters (like serotonin, dopamine, GABA, etc) are released from the presynaptic neuron, and partially absorbed by the postsynaptic neuron. The neurotransmitter that isn’t absorbed is mainly taken back by the presynaptic neuron. SSRI’s work by blocking the reuptake mechanism for serotonin, leaving more available serotonin in the brain, which seems to relieve depression in some people.

But, this is grossly oversimplified, and depression is not as basic as not having enough serotonin. In the words of Ozy, brain chemicals are not fucking magic.

Side effects of SSRI’s can include lack of sex drive, hyperactivity or lowered energy, etc. In some, these are so life-disrupting that other medications are preferred.

Serotonin-Norepinephrine Reuptake Inhibitors (SNRI’s)

SNRI’s include Cymbalta, Effexor, and Pristiq. They work very much like SSRI’s, except they inhibit both the reuptake mechanism for norepinephrine and serotonin.

The effectiveness of SSRI’s lends support to the Monoamine Hypothesis–an incomplete explanation for depression, suggesting that several neurotransmitter systems (including serotonergic) are responsible.  The hypothesis does hold up to scrutiny, but doesn’t explain why many antidepressants also help with anxiety and obsessive-type disorders.

Tricyclic Antidepressants

Color me happy to have done my research before publishing–turns out I didn’t have all of my facts straight. Tricyclics are antidepressants that operate somewhat like SSRI’s by inhibiting the reuptake of serotonin–but they also have a laundry list of possible side effects, and, like MAOI’s, are used more and more rarely.

Monoamine Oxidase Inhibitors (MAOI’s)

MAOI’s can be super effective! However, they come with hefty diet restrictions, and resultingly, are used rarely–mostly as a last resort.

People taking MAOI’s need to avoid all sorts of things, like pickled foods, most cheeses, wine, decongestants, and SSRI’s. Failure to do so can cause a stroke–the result of buildup of tyramine in the brain. Since other antidepressants are available, MAOI’s have fallen out of favor.

Norepinephrine and dopamine reuptake inhibitors (NDRIs)

Wellbutrin! NDRI’s are good because they usually don’t have the sexual side effects. They too, lend support to the Monoamine Hypothesis, by altering the dopaminergic and norandronergic pathways.

St. Johns Wort

Okay. This is alt-med, but it’s been gaining mainstream popularity. It’s one of those that might work on mild to moderate depression. And if taken without doctor supervision and with other medications it can cause you all sorts of problems. In combination with SNRI’s, it can cause Serotonin Syndrome–an excess of the neurotransmitter which overloads the central nervous system. It also appears to decrease the effectiveness of oral contraceptives, might cause problems if you’re breast-feeding, and oh, right, as an herbal supplement, isn’t all that regulated. What I’m saying is, self-prescribing this stuff is not a great idea, and right now, there’s not evidence that it works for major depression. But some people do use it, so I’ll include it.

Psychopathology Sum-Up: Specific Phobias

It’s Friday, which means a mental health summary. This post is about so called ‘specific’ phobias, which excludes social phobia. Another Sum-Up will deal with that. 

The Overview:

Specific phobias are a category of anxiety disorders. (Anxiety disorders also include OCD, Post-Traumatic Stress Disorder, and Generalized Anxiety Disorder, among others.) Specific phobias are can be seen as the Mad Libs of anxiety: “fear of [insert a noun here]“. The fear is paralyzing, and often interferes with normal functioning, but most are easily cured. In fact, this makes them unusual–one of the only disorders where upon discovery, we know what to do, and we know you’ll most likely be cured.

Specific phobias are also fairly common, and occur most often in adolescence. When the phobia interferes with functioning, people are quite good about seeking treatment. Otherwise, most people avoid the trigger (sometimes going to great lengths), and live their lives. Common phobias include flying, enclosed places, heights, dogs, escalators, spiders, and snakes. (NIMH)

Phobia Treatment:

Blood/Injury/Injection Treatment: Fear of needles, blood, wounds, injuries, or some combination thereof is known as BII. In severe cases, just reading about injuries, even in fiction, can cause wooziness. Treatment is actually different from other phobias, because it’s hard to unlearn fainting. Clients are taught to tense all of their muscles at once when triggered, which raises blood pressure.

Exposure Therapy: Exposure therapy can work in a single day, which is kinda cool. Of course, it takes all day, but no other therapy is quite so simple. Client and therapist both decide on a series of experiences from mild to very scary, and work through each. For instance, looking at a picture of a snake, then talking about snakes, imagining a snake, being in the same room as a snake, being near a snake, and finally, holding a snake. Update: Cuttlefish expands on this very very well–there’s a few types of ET, and they’re very different from each other.

Cognitive therapy: Talking through excessively fearful thought processes and challenging them. This is often combined with exposure therapy.

Medication: Never been shown to be effective.

Important Note: Just because phobias are irrational fears and easily treated does not mean you should badger, mock, or otherwise force someone to face their phobia. It’s rude and callous. Don’t do it.

Things Specific Phobias are Not:

Disliking things: hating dogs is not the same as being scared of them.

Rational fear: I think we can all agree that it’s rational to fear the idea of a plane crash, or developing a terminal illness. However, it’s slightly less rational to refuse to look at planes because of a fear of plane crashes. Phobias are irrational fears.

If any information is incorrect, please note it in the comments! However, I am going to ask for citations. I have access to journals as a student, so no worries if it appears behind a paywall. Also, please chime in with your own experiences, misconceptions, myths you’ve heard, and any book suggestions!

Previous Psychopathology Sum-Ups:
Bipolar Disorder

Psychopathology Sum-Up: Bipolar Disorder

[Content note: brief discussion of suicide]

Weekly series! As per previous discussion, I will be published a big information blog about a specific mental illness on each Friday.

I know, today is not Friday. I’m publishing early because I’m excited, and also I want to get lots of feedback. Tell me what I’m not including, what other things you want to know, etc. If there’s enough questions, I’ll do a second follow-up post. Lastly, tell me if there’s terms I’m not defining that I should be. I really really don’t want to get wrapped around jargon here–it helps nobody.

The idea is to talk about what the diagnoses are and aren’t, common misconceptions, what treatment and outcomes look like, and so on. Though not all therapeutic orientations (the theory and approach behind a course of treatment) depend on or use diagnoses–and there’s some very good arguments against using the medical model of diagnosis–we do use labels to conduct research, and it’s worth learning what a mental illness is. I’m going to try to include any changes to diagnostic criteria as well as current debates.

This post is massive and organized in informational sections, so I’ve put it behind a jump.

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