[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 [email protected].

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.