How does prozac help bulimia?

In some individuals, finding the correct antidepressant and dosage may take a trial phase, and your doctor may need to make adjustments to your prescription before finding a protocol that works best for you.

As with all medications, it is necessary to remain under the supervision of a physician, who can monitor signs and symptoms that you may be experiencing as a result of your prescription.

Addressing All of the Needs of the Individual

It is important to remember that since bulimia is a complex psychiatric illness, treatment must address various concerns on multiple levels: the physical/biological, emotional, and psychological.

Achieving total and complete healing involves work with a multi-disciplinary team, which can be one of the greatest tools for treatment and recovery.

Community Discussion – Share your thoughts here!

Why do you think medication for bulimia is more effective when used in conjunction with therapy?

Last Updated & Reviewed By: Jacquelyn Ekern, MS, LPC on November 19th, 2014
Published on EatingDisorderHope.com

How Medication Treats Eating Disorders

With eating disorders, there is no exact formula for treatment. Every patient is different, and what works for one may not work for another. Eating disorder treatment usually entails some type of nutritional therapy and psychotherapy. Medication, in the form of antidepressants, is often prescribed, depending on the type of eating disorder and patient’s needs.

Eating Disorder Treatment: When Medication May Help

“Particularly for bulimia nervosa and binge eating disorder, medications are often used, but are rarely the sole form of treatment,” says Michael Devlin, MD, professor of clinical psychiatry at Columbia University Medical Center in New York City and associate director of the eating disorders research unit at New York State Psychiatric Institute.

“Treatment should take into account nutritional considerations, such as weight gain for anorexia nervosa or weight management for overweight or obese individuals with binge eating disorder, and psychotherapy to address the issues that are driving the eating disorder,” Dr. Devlin continues.”

Eating Disorder Treatment: Medication for Anorexia

Medication is used less frequently to treat anorexia compared to other eating disorders because there is little evidence that shows it works, explains Devlin. “The best medicine for anorexia nervosa is food,” he says.

However, when medication is called for, antidepressants are typically prescribed to treat underlying mental health problems. Fluoxetine (Prozac) may help people with anorexia overcome their depression and maintain a healthy weight once they have gotten their weight and eating under control. Fluoxetine is in a class of drugs called selective serotonin uptake inhibitors (SSRIs). These drugs increase serotonin levels, a brain chemical connected to mood.

” have relatively few side effects and are pretty well-tolerated by most people,” says Devlin. The most common side effects reported include:

  • Loss of interest in sex
  • Drowsiness
  • Weight gain

SSRIs may cause some people to feel agitated and overexcited. While rare, some people taking SSRIs may be at an increased risk of hurting themselves.

If the patient does not do well on an SSRI, doctors may prescribe olanzapine (Zyprexa), an antipsychotic drug typically used to treat schizophrenia. This medication has been found to help some people with anorexia gain weight and change their obsessive thinking.

While SSRIs are generally safe and well tolerated by most people, antipsychotics have some risk of long-term side effects, such as tardive dyskinesia, a movement disorder. The most common side effects of olanzapine include dizziness, drowsiness, lightheadedness, and weakness. Still, many people tolerate this medication with relatively little difficulty, says Devlin.

Eating Disorder Treatment: Medication for Bulimia

Along with cognitive-behavior therapy (CBT), many people with bulimia respond well to SSRI antidepressants, even if they aren’t depressed. Fluoxetine can help people stop binging and purging when used alone or with CBT. In fact, fluoxetine is the only antidepressant approved by the U.S. Food and Drug Administration to treat bulimia. Other SSRI antidepressants may be helpful in treating bulimia and are often used, although scientific studies to support their use are limited.

Another possible bulimia medication is topiramate (Topamax), an anti-seizure drug. Topiramate may help people with bulimia suppress their urge to binge and reduce their preoccupation with eating and weight. However, topiramate can have troublesome side effects compared to the SSRIs, and some people do not tolerate it as well, says Devlin. The most common side effects include constipation or diarrhea, dizziness, drowsiness, trouble sleeping, flu-like symptoms, loss of appetite, and weight loss.

Eating Disorder Treatment: Medication for Binge Eating Disorder

Researchers are still examining the best treatment approach for binge eating disorder. So far, combining psychotherapy and medication appears to be the best treatment strategy.

As with bulimia, antidepressants could help treat binge eating disorder. SSRIs, such as fluoxetine and sertraline (Zoloft), may help reduce binge eating and can improve mood in patients who are also struggling with depression or anxiety. However, antidepressants will in general not help much with weight loss.

If the patient needs to lose weight, she may be prescribed appetite suppressants like sibutramine (Meridia). While sibutramine can suppress hunger and help with weight loss, it can also cause dangerous changes in blood pressure, so patients need to have their blood pressure checked regularly when taking this medication. Other side effects, such as headache, dry mouth, and trouble sleeping, may occur.

Eating Disorder Treatment: Weighing the Pros and Cons

Every drug has side effects, so the potential benefits of taking medication must always be weighed against the potential risks. Most side effects of SSRI antidepressants are minimal and worth the risk, especially when weighed against the potential harm of having an uncontrolled eating disorder, says B. Timothy Walsh, MD, the Ruane professor of pediatric psychopharmacology at Columbia University and director of the division of clinical therapeutics at the New York State Psychiatric Institute.

“There is consensus that the benefits of antidepressant therapy outweigh the risk, even among young people,” explains Dr. Walsh, adding that no matter the drug, doctors and patients must keep an eye on potential adverse effects.

Always talk to your doctor about the pros and cons of a particular drug, and together you can decide if the medication is right for you.

Anorexia on Prozac

On the evening of 20th June 2008, I started taking Prozac. Halfway through the day’s single, extended meal, I described in my diary my fears about taking the drug. What frightened me most was the thought that doing so, just like beginning to eat more (which I hadn’t yet begun to do), might take my anorexic identity away from me. I admitted to my diary that I was scared

of turning into a different person even by this means, let alone by eating. They even look frightening, like green & yellow torpedoes of the unknown. But, well, I feel fine, & restored by all that starch & fat & salt (& veg); & now time for the ever-incredible luxuries of muesli & two sorts of milk

…and so on into a long discussion of calories and grams and the incomparable ecstasy of eating chocolate at dawn, which almost made me forget my fear.

I had recently visited an eating-disorders treatment centre and responded to a series of questions about my mood, and as a result had been prescribed 60 mg a day of fluoxetine, prior to the possible start of weight gain supported by cognitive-behavioural therapy. The hope was that the Prozac would improve my mood and motivation such that I’d be more likely to embark on treatment.

The essence of the experience of taking Prozac was for me a freeing-up of my mind, a loosening of the rigid bonds that kept my thoughts and actions tied in tight knots. But that change was mediated by extreme tiredness, weakness, and a sense of profound disconnection from myself. I’ll outline in the second half of this post reasons to suspect that the placebo effect may have played a large role in my experience of taking the drug, and I do think that the simple fact of having started taking medication, in acknowledgement of my illness and the need to do something about it (even if not eat more, yet), was a critical factor in making the foundations of my anorexia begin to shift. Another factor that may have played a significant role in the changes that occurred was setting off on a family holiday to a Greek island three days after I took the first pills. I’d been there often before and remained as ill as ever, but this time was a little different.

Part of that shift away from the depths of illness was the simple, crucial fact of feeling newly able to just eat more – not systematically, according to plan, or enough more to gain any significant weight; mainly just fragments of other people’s dinners. But, still, more. On the first evening in Greece, I ate more unplanned, unfamiliar foods than I had for years, and I felt the fear of wanting to eat more, along with exhilaration at the potential for fundamental change and conviction of the inevitable dead-end waiting for me otherwise:

Slept briefly but deliciously, got up to lie by pool then drink tawny port, walked to sunset restaurant with S. , tried the salmon mousse & the sea bream, & ordered expensive wine of which I also drank lots – & a fragment of bread – & felt a moment of terrifying longing just to be eating S.’s whole fish, & coming home & going to bed. But then told her some of the week’s events ; how things are converging. I feel I’m failing for not doing more – but fish x 2, + alcohol, + bread, is something. So much in that book rang – rings – true. In both the reasons for changing & the reasons I feel I can’t. If I don’t I probably never will change anything. It’ll probably always be like this. Only narrower & narrower. I feel that everywhere, in everything, now. Even the agonies of getting here – the terror as my bag failed to appear on the carousel, beginning to contemplate doing without all my food. My eyes are dizzy now. I went out to the pool & thought how terribly lucky I am to have a family that will let me come here, will tolerate me. I wonder what the hell my poor body really makes of all this.

Those small additions to my daily diet – little bits of bread and fish and wine – were momentous to me, and they made a difference to my family too:

frightened at delighting in all that, & craving more, even while hating the uncertainty of accepting as opposed to denial’s pure simplicity. But S.’s sadness as she told the owner that I “live on air”, & her shrug of the shoulders, made me persist; she said yesterday how it does feel very different, even just bread, as opposed to only wine – there being something on a plate, getting smaller.

Another interesting thing that happened very quickly was that my ecstatic night-time eating became distinctly less ecstatic. That could have been the heat and the change in ingredients, but I’d been on holiday many times before without it happening, and it was as frightening to me as anything else:

3:57 a.m. It was nice, but not all-encompassingly, mind-weakeningly so as at home. Maybe it’s just everything messed up in time & temperature – or is the magic really waning?

2:55 a.m. I don’t know how much it’s the food itself, how much the temperature, how much myself, my mood or attitudes or what – but it just isn’t nice in the way it is at home – not nice at all, mostly. Let alone fabulous. Rather a dull chore, it feels, working through lettuce & salted cucumber.

3:56 a.m. was lovely – creamy, cool, crunchy. But nothing quite delights as it did.

The physical side-effects were quite frightening at first: the day after ingesting those first coloured capsules, I wrote of how

Today has been really terrifying. Dizziness, weakness, mental distance & confusion. I really didn’t know whether I could – or should try to – manage my ride; all the way I felt nervous about the next little hill. Just walking has been hard. Decision-making has been terrifying.

I wanted to stop taking them, and I blamed them for physical clumsiness I’d never had before:

Oh, my body rebels against three more of those pills.

4:19 a.m. I feel a bit better, but not as wholly as food usually makes me – & much of it tasted oddly bitter. I realize how wrong something is with me, everything: just upturned my whole bowl of All Bran. Thank God it was dry, thank God it wasn’t yesterday’s muesli with yoghurt; & I think I’ve retrieved most of it. But all is not well. I’ve never done anything like it before – just turned, moved my arm, absolutely without looking. Anyway, ten minutes’ sleep lost. But little more than that, I hope. Except confidence.

When everything’s as fragile as anorexia makes it, even upturning a bowl of cereal makes for confusion and feverish self-recrimination. And even though I blamed the drugs for it, there being things like this to blame on them was just one way in which the drugs, or the placebo effect, or mere coincidence, forced me to acknowledge that things couldn’t remain as they were. No trivial accident should make one feel like that.

The general mental loosening-up manifested itself as a softening almost to jelly of both my rigid mind and my wasted muscles:

A frightening day in so many conflicting directions. Fear at the mental flaccidness . And then eating a bit, again, of chocolate & biscuit sandwich – both bits today, not just biscuit. Frightened at feeling so weak, lying on my verandah sofa at 3 p.m., that I couldn’t walk at all, couldn’t drag myself up to put on my shoes & work out a picnic, couldn’t even read more than a page of Vile Bodies, before sinking back into torpor – yet then, after two hours’ walking, feeling I could still carry on indefinitely.

The old illusion of invincibility crept back in the end, but while it was gone, it was utterly gone, and this brief absence constituted just one more little reason to take illness and hence the idea of recovery (through eating more) seriously:

If you decide on the treatment it’ll be more than this. Every day till I start getting fatter. Don’t think. Eyes swimming.

More immediately, it was also just a reason to dare to eat a little more, a little earlier:

I’ve felt really dreadful today. So weak & vacant that I dared eat some oats & a nibble of chocolate before setting off .

Perhaps the most striking, though far from the most significant, effect was the awareness of my own heartbeat, which stayed with me for a few days, and made me a little more aware of my body in general, and its fragility in particular.

With the deep weariness that I felt the drugs brought to the surface in me came the feeling of being powerfully disconnected from my own mind and body, from myself altogether. Back in England, I described how

I’ve been so unbelievably tired all day; terrifyingly incapable of waking up, or feeling connected to myself. I stared at myself for minutes in the mirror after getting up; my eyes looked insane. Not mine.

This self-disconnect was bound up with feeling hungrier and eating more, even if not the 500 calories extra I knew I’d have to eat every day if I embarked on recovery:

And I’ve been so hungry, & eaten so many tiny things; more oats & chocolate for “breakfast”, a fragment of biscuit to keep R. company when I made him a walker’s biscuit sandwich; some crumbs of the chocolate & biscuits from the bags from which I created them for him. But not 500, is it? I just wish I could feel myself, or feel alive, or awake. How much is it the drugs doing all this, how much just my eternal weakness, my tired readjustment to England?

The weakness and disconnection seemed to get worse and worse, so that two weeks after starting to take the Prozac, trying to do some testing of participants for a reading experiment, I was describing how

I’m terrified. All day I’ve wanted to do nothing but sleep. Battling against lethargy, or succumbing to it; lying listening to the Archers & Front Row not knowing how I’d ever get up again. Getting up at 2 pm having slept so long yet feeling so awful. Eating more oats & chocolate; but walking to the department & doing all I had to there with a terrifying sense of distance, & fragility, & dazed inability to be present & have any confidence in any single act or decision. It’s awful. And though I have done some transcriptions now, after the third I felt so completely dreadful I could only wander stiltedly around the garden, breathing in the cold air, & then sink into the armchair with a book . I just long to wake up feeling better, different, tomorrow. Slight nausea, too, to make it all worse. Shaking with weakness.

Above all, the Prozac – or my response to it as placebo, or as something that might support my growing conviction of the need for change, or whatever else it was that made it effective – took away my ability to deceive myself into believing everything was all right:

It’s just so much harder to pretend with these pills. Everything’s more violent, more obvious, more irrefutable.

3:30 a.m. Funny how the magic of the plate of food was suddenly lost in Corfu, for a few meals, & now is as intensely powerful as ever. Of course, setting, temperature, the variations on the ingredients, matter a good deal – but it’s weird to think how hollow all this felt, briefly, when the magic didn’t work.

The magic of food had come back, but the fact that it had been absent, if only for a week or so, meant it could never quite be the same again.

So, the question persists: how much of all this was the drug’s direct chemical action? What is the clinical logic behind prescribing Prozac to someone not-yet recovering (or still recovering) from anorexia? There isn’t a straightforward answer, because the connections and distinctions between anorexia and depression are not entirely clear. The symptoms of being severely underweight are similar in some respects to those of clinical depression: low mood, impaired concentration, lack of energy, irritability, poor sleep, loss of interest in sex, and obsessive thoughts and actions. And other aspects of eating disorders (including anorexia) which may not be attributable directly to the underweight state are the same as those observed in depression, notably low self-esteem and self-critical thinking (see Fairburn, 2008, p. 246). It can therefore be difficult to assess whether clinical depression is present comorbidly (simultaneously) with anorexia, or whether the anorexia is manifesting traits highly similar to those of depression – or whether this is a sustainable distinction. There are, however, some symptoms more likely to indicate ‘semi-independent’ depression, such as extreme negative thinking beyond food- and body-related matters, impaired decision-making, neglect of personal appearance, hygiene, or everyday activities, and other impairments in sociability or cognitive functioning beyond what would be expected or had previously been manifested as part of the eating disorder.

If clinical depression is diagnosed, there may be significant benefits to be gained from treating it with antidepressants, because this can make the eating disorder easier to overcome. The cognitive-behavioural treatment programme outlined by Chris Fairburn (2008) recommends a moderate to high dose (40-60 mg as standard) of fluoxetine for around 4-6 weeks in most cases, followed by treatment of the eating disorder using CBT-E (‘enhanced’ cognitive behavioural therapy, developed specifically for eating disorders). Fairburn also notes that antidepressants can reduce the frequency of binge eating, which can in turn have positive secondary effects like reducing the fear of losing control over eating. However, he also acknowledges that recovery from depression, although it can motivate the patient to engage more fully in recovery, can in some cases have the effect of heightening restrictive eating habits because of increased drive and determination. In other words, even if the treatment of a comorbid depression is successful in people with anorexia, it can be risky.

Although Fairburn makes it clear that antidepressants should be used only if the depression is diagnosed as at least ‘semi-independent’ from the eating disorder, the distinction between depression-like symptoms resulting from the underweight state and ‘semi-independent’ clinical depression may not be meaningful. Depressive symptoms may or may not be identified as predating the onset of the eating disorder, or as extending significantly beyond the scope of the eating disorder’s symptoms, but treatment of anorexia-as-depression could still be warranted and beneficial. There are several grounds for drawing connections between the two, including their comparable neurobiological basis, their frequent comorbidity, their shared genetic risk and associated personality traits, and their experiential similarities, like low mood, loss of interest and motivation, social isolation, and obsessive-compulsive behaviours.

On the question of whether antidepressants may have a role to play in recovery from anorexia regardless of whether depression is diagnosed as an independent or semi-independent condition, one perspective comes from the neurobiology of anorexia in relation to that of depression. (Here I base my discussion on Claudino et al., 2006, pp. 3-4) Abnormalities have been identified in anorexic patients during the acute phase of illness in specific neurotransmitters like serotonin, dopamine, and norepinephrine/noradrenaline (involved, broadly speaking, in pleasure, reward-motivated and interpretive behaviour, and concentration/anxiety respectively) as well as in neuropeptides (neuronal signalling molecules) and neuroendocrine hormones and the hormone leptin (key to regulating energy intake and expenditure).

Most of these abnormalities have been attributed to the starved state and disturbed eating behaviours. Some researchers have claimed that the differences may persist after recovery: for instance, Walter Kaye and colleagues (1999‎) found persistent differences in dopamine metabolism in people who had maintained at least 90% of a population average body weight for at least a year after their anorexia. But I’ve written elsewhere about the widespread problem in anorexia research of setting this kind of implausibly low threshold for ‘recovery’. The authors of this study even admit that because of ‘the difficulty of finding recovered AN subjects’ (p. 504), they included four who hadn’t reached even this obvious underestimate of what a post-anorexic healthy weight is. Meanwhile, another of Kaye and colleagues’ studies (1991) found that functional activity of central serotonin systems seems to be diminished in the underweight state but then abnormally increased in long-term weight-restored patients, from which they concluded that those who develop anorexia may have high levels of serotonin activity before the onset of illness.

Decreased levels of cerebrospinal fluid (CSF) 5-HIAA, the main product of serotonin metabolism, in underweight anorexia patients may be related to their low dietary intake of tryptophan. (Tryptophan is an essential amino acid found in eggs, dairy, red meat, and some nuts and seeds, and is (amongst other things) the precursor of serotonin.) So the unusually elevated levels of (CSF) 5-HIAA found in the weight-restored participants relative to healthy controls may also be a result of the nutritional normalisation process, and/or hormonal changes accompanying recovery (ovarian steroids are thought to increase serotonin neuronal activity). Throughout, the same caveats apply to their definition of ‘weight-restored’: here, participants had to have maintained only 85% of population average bodyweight for six months (where their prior anorexia involved having been at less than 75% – an oddly narrow gap), and in interviews reported ‘mild to moderate concerns with body image’ (p. 557); that is, they were categorically not recovered, and any findings about their physiological state should be interpreted as reflecting the phase of partial not full recovery.

Some of the same neurobiological abnormalities found in anorexia are also manifested in depression, especially in dysfunction related to serotonin activity and the activity of the neurotransmitters adrenaline, noradrenaline, and dopamine. We might therefore expect antidepressants to act on anorexia similarly to how they do on depression. But different classes of antidepressants can be expected to act in different ways when treating anorexia (or depression). Serotonergic drugs (including fluoxetine, aka Prozac) are expected to re-establish homeostasis between the neurotransmitters dopamine, noradrenaline, and GABA (gamma-aminobutyric acid, the main inhibitory neurotransmitter), all of which are involved in bodyweight control and food intake. The reduction of noradrenergic activity has also been considered potentially treatable by tricyclic antidepressants that stimulate alpha-noradrenergic receptors in the hypothalamus. Clinical researchers have also been interested in using antidepressants to treat anorexia because of the capacity of some of them, particularly the tricyclics, to induce weight gain (Pope and Hudson, 2013, pp. 78-79, give a brief overview; see also Corwin et al., 1995, who found no difference in weight gain between tricyclics and fluoxetine). But tricyclics also have side-effects which seem to be particularly pronounced in anorexic patients – and of course, experiencing chemically induced weight gain not mediated also by increased nutrition might induce more panic than progress in someone with anorexia.

So now we’ve made our way round to the central question: do any antidepressants actually work in the treatment of anorexia?

The review study ‘Antidepressants for anorexia nervosa’ by A.M. Claudino and colleagues (2006) is a Cochrane Collaboration meta-analysis of randomised controlled trials of antidepressants prescribed as part of the treatment of acute anorexia. The authors found only seven trials – from an original total of 1303 citations – that fulfilled their stringent quality criteria relating to type of intervention, outcome measures, and the potential for bias in the results. There is clearly a serious lack of high-quality research in this area, with very few studies testing antidepressants against a placebo, sample sizes typically being very small, total intervention duration being very short without follow-up, and completion rates – an important factor when it comes to medication with potentially serious side-effects – not always being given. There’s also significant variability between trials in factors like reporting of weight gain and secondary outcome measures, the treatment packages provided alongside the medication, and the age and acuteness of illness in the patients treated. In addition, the trials were all were carried out in inpatient settings, which doesn’t accurately reflect the treatment structure for many people with anorexia.

With those shortcomings in mind, however, the randomised controlled trials included in the review study were unable to demonstrate any effect of antidepressants compared with placebo in the majority of outcomes considered. The two positive findings concerned comparisons between types of antidepressant, but the authors stress that these should not be taken as evidence of efficacy of a specific drug or class of drugs. Correspondingly, the regulatory agencies in the UK and US, for example, have not approved any medication for the treatment of anorexia. There have been more promising results using fluoxetine to contribute to preventing relapse in weight-restored patients, by helping reduce residual symptoms and prevent weight loss at follow-up (e.g. Kaye et al., 1991), so this may be a better point at which to consider incorporating antidepressants into recovery from anorexia. But proper replications are needed. Meanwhile medical practice takes its own course: given the absence of evidence for efficacy, there has been a worryingly rapid increase in the prescription of psychotropic medications (including antidepressants and antipsychotics) to people with anorexia over the past twenty years: double the number were reported as having been used between 2003 and 2009 compared to 1997-2002 (Fazeli et al., 2012).

There are various possible reasons why, in the context of severe anorexia, the drugs might not work. The malnourished state of anorexia may reduce the efficacy of the antidepressants: for example, low oestrogen levels and low intake of nutrients (including essential fatty acids and zinc) that seem to influence serotonin pathway function may impair the release of serotonin in the brain, which would lead to a down-regulation of its receptor and a reduction in antidepressant function. Inadequate nutrition has, however, been challenged as a reason for lack of response to selective serotonin reuptake inhibitor (SSRI) medications like fluoxetine, in a trial (Barbarich et al., 2004) that added nutritional supplements (tryptophan, vitamins, minerals, and essential fatty acids) or placebo to fluoxetine, finding no effect. But this was a small trial (26 participants) with a high drop-out rate (only nine participants completed the 26-week study).

As with any drug, there is also a risk of side-effects. The tricyclic class of antidepressants are associated with more discomfort than newer, safer classes of drugs with better side-effect profiles such as SSRIs, and also with increased cardiac risks due to their ability to alter the heart rhythm (QT interval), which can be a problem for anorexic patients in any case. A possible heightened suicide risk is also associated with the use of antidepressants, and only fluoxetine has been found to have on balance a positive effect – fluoxetine is therefore the only approved drug in the UK and US for treating depression in under-18s (Claudino et al., 2006, p. 16). All antidepressants carry the risk of withdrawal symptoms including dizziness, nausea, lethargy, and headaches, and more serious symptoms such as mania or hypomania (see a blog post by Gwyneth Olwyn). I never experienced any withdrawal symptoms at all, though, as it happens; when I came off the Prozac it wasn’t even a significant enough event to record in my diary.

Much more high-quality research needs to be done, but for now there’s little basis for confidence in the efficacy of antidepressants in treating anorexia. I was surprised to discover this when researching this post, because for me, starting to take Prozac really felt like the beginning of the end of my illness. I may in fact have responded unusually well to the drug neurochemically, or its effects may all have been those of a placebo (whose power shouldn’t be underestimated), in that I was ready at last to face up to my physical and cognitive dysfunction and the drug was what I needed to give me a feeling of change. There was also, of course, that powerful confounding factor, the holiday in Corfu beginning at almost the same time. But whatever the causal factors, it really felt like it did things to me.

It was a long road from there to living without anorexia, taking in the milestones of a second visit to the clinic, the decision to start eating those 500 calories more in order to make the minimum weight for admittance to the clinical trial, the start of therapy, the coping with everything that weight gain brought with it, and the reconstruction of a life that wasn’t all about eating and not eating. But I’ve always felt that those green and yellow torpedoes of the unknown were a necessary stage on that journey. Embracing the unknown is, after all, what abandoning anorexia is all about, and putting those pills into my mouth, that first night five years ago, felt like embracing it in the bravest way I knew how: by eating something new.

Source: Козыбаков Александр, via Wikimedia Commons CC 3.0

PMC

Accumulating evidence suggests that antidepressants in combination with psychotherapy can be effective in the treatment of bulimia nervosa. Clinical experience supports the use of most selective serotonin reuptake inhibitors (i.e., fluoxetine, sertraline and citalopram) as well as some of the newer antidepressants (i.e., venlafaxine). The following case illustrates some of the factors that must be taken into account when considering pharmacological treatment for bulimia nervosa.

Ms. A. is a normal weight 28-year-old woman with a 5-year history of daily bingeing and self-induced vomiting. She describes recurrent seasonal depressions, generalized anxiety, mood lability, impulsivity and mild obsessive–compulsive symptoms. She admits to frequent dizziness, sporadic pinkish blood in her vomitus, heartburn and occasional leg cramps. She uses ecstasy once per week and caffeine pills daily to promote diuresis. Recent laboratory investigations and electrocardiogram were unremarkable except for sinus bradycardia with a rate of 58 beats/min.

A trial of sertraline, gradually increased to 125 mg and combined with cognitive-behaviour therapy, was successful in decreasing binge–purge frequency and in preventing seasonal depressive episodes. Within a few weeks of starting medication, the patient also reported decreased anxiety, irritability and mood lability.

This case illustrates that it is not unusual to find patients who fulfill criteria for other concomitant disorders in addition to bulimia nervosa. Studies have documented higher rates of major depression, bipolar disorder, anxiety disorders, obsessive–compulsive disorder, personality disorders and alcohol and substance abuse disorders among eating disorder sufferers. Although antidepressants tend to be effective for bulimia and several of its associated conditions, other conditions such as bipolar disorder or severe personality disorders may require the use of drugs from other classes, such as mood stabilizers and neuroleptics. The choice of medication should take into account the high prevalence of impulsivity in this population, even in the absence of borderline personality disorder; drugs that are potentially toxic in overdose should therefore be avoided. In addition, the high prevalence of recreational drug use as well as the tendency to abuse appetite suppressants, stimulants, fat burners, laxatives and diuretics, invites caution to avoid unexpected drug interactions or adverse effects.

Medical complications that arise from bingeing and purging must also be considered in the choice of medications. Drugs that prolong the QT interval (e.g., tricyclic antidepressants, some neuroleptics) may result in fatal arrhythmias in the context of intermittent hypokalemia induced by vomiting or laxative abuse. Drugs excreted by the kidney, such as lithium, should be avoided because of risk of toxicity due to recurrent dehydration and electrolyte disturbances. Bupropion is contraindicated because of the increased risk for seizures; patients should also be warned against its use for smoking cessation.

Finally, drugs that can increase appetite or cause weight gain (e.g., olanzapine, mirtazapine, paroxetine) are not recommended. In the context of the weight phobia, increasing appetite will not only affect compliance but also likely intensify the vicious cycle of dietary restriction, bingeing and purging.

Although medications can play a beneficial role in the treatment of bulimia nervosa, the choice of agent should be guided by a careful consideration of concomitant psychological characteristics, as well as by potential medical complications that may modify drug response.

Can Antidepressants Treat Binge Eating Disorder?

When you have binge eating disorder, you often eat large amounts of food and have trouble stopping. You don’t eat because you’re hungry, but because you feel empty or sad inside.

Researchers are increasingly learning that binge eating disorder, like other eating disorders, is a mental health condition. People who binge often have anxiety, depression, or other mental health issues.

Binge eating disorder often responds to antidepressant medicines because of its roots in mental health. Here’s a look at the link between depression and binge eating, and how medicines used to treat depression might also help binge eaters.

What’s the Link Between Depression and Binge Eating Disorder?

Binge eating disorder and depression share a strong connection. Up to half of people who binge are either currently depressed or were depressed in the past. Anxiety and stress are also linked to binge eating.

How Can Antidepressants Help with Binge Eating Disorder?

Antidepressants may help reduce binge-eating episodes in one of a few ways. Lower-than-normal levels of chemical messengers in the brain, such as serotonin, dopamine, and norepinephrine may affect appetite, mood, and impulse control. This can contribute to binge eating. Antidepressants increase levels of these brain chemicals, which may help control binge eating.

A side effect of some antidepressants is a decrease in appetite. Research has also shown that antidepressants may help people with bulimia binge less often. Binge eating disorder is similar to bulimia, except that people with bulimia purge the food afterward by vomiting.

People with binge eating disorder often have other conditions, like depression, panic disorder, or generalized anxiety disorder. Antidepressants can be used to treat these conditions.

Types of Antidepressants Used to Treat Binge Eating Disorder

Selective serotonin reuptake inhibitors (SSRIs), a class of antidepressants, are sometimes used to treat binge eating disorder. SSRIs increase the amount of a chemical messenger called serotonin in the brain. Serotonin helps boost mood.

SSRIs used for binge eating include:

  • fluoxetine (Prozac)
  • paroxetine (Paxil)
  • sertraline (Zoloft)

Other types of antidepressants, including tricyclic antidepressants and serotonin and norepinephrine reuptake inhibitors (SNRIs), have been studied for treating bulimia. In bulimia, these drugs help with both bingeing and purging. It is not yet clear if they help people with binge eating disorder.

How Effective Are Antidepressants at Treating Binge Eating Disorder?

People who’ve taken antidepressants for binge eating disorder have reported that they feel less of an urge to binge while on the medication. A review of studies found that people who took antidepressants were more likely to stay in binge eating remission than those who didn’t take the medicine. Antidepressants also relieved depression in people with binge eating disorder.

Not enough studies have been done to prove that these drugs work long term for binge eating, though. Existing studies have only lasted for a few weeks or months, so researchers have not been able to see whether people started to binge again after the studies ended.

The authors of the review didn’t recommend using antidepressants alone as a first treatment for binge eating disorder. They concluded that more research is needed to find out exactly how antidepressants can help with binge eating and how these drugs should be used.

What Are the Side Effects of Antidepressants?

Just like any other medicine, antidepressants can cause side effects. One potential side effect, appetite loss, can actually be helpful for those who binge eat. But sometimes antidepressants can have the opposite effect, increasing appetite and leading to weight gain, which can make them counterproductive for people with binge eating disorder.

Other side effects of antidepressants include:

  • dizziness
  • dry mouth
  • fatigue
  • headache
  • nausea or vomiting
  • nervousness
  • reduced sexual desire
  • trouble sleeping

Ask Your Doctor About Antidepressants

You have a few different options for treating binge eating disorder. Your doctor might start you on cognitive behavioral therapy (CBT), which helps you overcome the negative thoughts that cause you to binge eat. Or, you could try the medicine lisdexamfetamine dimesylate (Vyvanse), the only drug that’s approved by the FDA to treat binge eating.

If these treatments don’t work for you, antidepressants may be another option. Discuss with your doctor whether depression might be a factor in your binge eating. Also talk about the possible benefits and side effects of antidepressants to decide whether they’re right for you.

Pharmacological Treatment of Bulimia Nervosa: Page 2 of 4

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