The Fluid Spectrum: Why People Move Between Different Eating Disorders

Why does someone with anorexia for years begin binging one day? Then, almost overnight, abscond into a bulimia frenzy? For decades, clinicians have been puzzled by these transitions. 

Eating disorders (EDs) are severe mental health conditions characterised by persistent disturbances in eating behaviour that impair both physical health and psychosocial functioning (Psychiatry.org, 2025). They manifest in a myriad forms, including the aforementioned anorexia nervosa, bulimia nervosa, and binge eating disorder—but exist as several other presentations. Traditional models treat these disorders as separate illnesses, each with its own diagnostic criteria in the DSM. Yet lived experience rarely fits neatly into those categories. Patients often migrate across diagnoses, leaving families and doctors asking one question: why?

A growing body of research suggests that the answer lies not in the outward behaviours that constitute the eating disorders themselves, but in the neurobiology beneath them. The emerging thesis is that EDs are not separate diseases at all. Rather, they may be maladaptive coping mechanisms designed to alleviate serotonin dysfunction-related stress and anxiety, an insight which could potentially explain why people transition between different ED types. This article will explore why those transitions occur, how serotonin dysfunction provides a unifying framework, and what this perspective reveals about improving treatment.

The Serotonin Paradox: When More Becomes Less

One of the most prominent differences seen in the brains of people with eating disorders as compared to healthy people lies in the serotonin system. Serotonin, chemically known as 5-hydroxytryptamine, is a neurotransmitter synthesised in a cluster of tiny regions called the raphe nuclei in the brainstem. Its molecular precursor, tryptophan, is unique in that it can only be obtained through diet—that means what (and whether) you eat can directly influence serotonin availability—creating a direct and fragile link between nutrition and brain chemistry.

Here’s the paradox: in people with eating disorders, the serotonin system seems to be dysregulated in a consistent way—higher serotonin activity doesn’t soothe, but rather intensifies anxiety. In this light, disordered eating behaviours emerge as a form of biological self-medication—improvised strategies to quiet an overactive and hyper serotonin system. Behaviours such as restriction, bingeing, and purging may look different on the surface, but at their core, may just be functioning as coping mechanisms to modulate the same neurochemical imbalance. 

Two receptors, in particular, help explain this paradox:

• 5-HT1A receptors: These are often considered inhibitory in the serotonin system. When serotonin binds to 5-HT1A, it tends to reduce neural excitability or tone down signalling. In the Kaye et al. study, individuals recovered from bulimic or anorexic-bulimic subtypes showed increased binding potential of a 5-HT1A radiogland (i.e. elevated 5-HT1A receptor activity) in multiple brain regions; frontal, temporal, cingulate areas, and even in the raphe itself (KAYE et al., 2005).

• 5-HT2A receptors: These are often considered excitatory in the serotonin system, meaning they help regulate perception, mood, and flexibility in thinking. The same Kaye et al. group found reduced binding potential of a 5-HT2A radioligand in individuals recovered from anorexia and bulimia (KAYE et al., 2005). Reduced activity of 5-HT2A receptors, commonly seen in EDs, can contribute to rigid thought patterns, perfectionism, and difficulty adapting. 

Taken together, this receptor imbalance helps explain why serotonin feels anything but “happy” in the context of eating disorders.

The Brain’s Value System: Why Food Feels Wrong

If serotonin dysfunction sets the stage, then the brain's valuation system explains why food itself becomes the villain. At the heart of this system is the ventral limbic network; a set of cortical and subcortical regions that work together to assign meaning and emotional weight to experiences. In healthy individuals, this circuitry helps integrate signals about hunger, taste, and reward into a balanced decision: to eat, or not to eat, that is the question. But in EDs, this same system misfires, turning food into a source of dread.

Several cortical regions play key roles. The orbitofrontal cortex helps evaluate the emotional and motivational value of food, often overanalysing “should I eat this?” The insula integrates internal bodily states (like hunger or fullness) with taste and emotional signals. The ventral anterior cingulate contributes to assigning value judgments that normally guide adaptive decision making. 

On the subcortical side, the amygdala amplifies fear and anxiety responses around food, while the striatum (including the nucleus accumbens) normally drives motivation and reward-based learning. When dysregulated, this system makes eating feel unrewarding—or even threatening—reinforcing avoidance instead of approach when it comes to food.

The Neurochemical Loop: Why Eating Behaviours Get Stuck

Even with serotonin dysfunction and a misfiring valuation system, ultimately, it’s the interplay of dopamine and serotonin that locks in eating disorder behaviours. Eating disorders manifest in a few common patterns: restriction,  where someone severely limits the amount of food they eat; binging, which involves consuming large amounts of foods in a short period of time; and purging, which can include vomiting, excessive exercise, or laxative use to try to “undo” a binge.

When someone restricts, binges, or purges, each action triggers a cascade in the brain: dopamine rewards the behaviour, serotonin reacts to amplify anxiety and the amygdala heightens fear. Over time, these patterns become reinforcing loops. Binging can feel addictive because dopamine tells the brain “this feels good” while serotonin-driven anxiety pushes the person to purge, restrict, or plan their next episode.

This perspective also explains why transitions happen: someone might start with restrictive anorexia to dampen anxiety, but the same brain circuitry can later drive a binge-purge cycle when dopamine signals become overwhelming. Understanding this loop makes the “fluid spectrum” of eating disorders much less mysterious; a neurochemical tug-of-war is, alas, happening before our eyes.

Recovery and Rebalancing the Brain

Eating disorders hijack the brain’s reward and fear circuits, but the same circuits can be rewired. Recovery is essentially a form of neuroplasticity; training the brain to feel safe, curious, rewarded, and joyous around food again. Small consistent steps matter. Below are some neuroscience-informed strategies:

1. Structured eating: Eat at regular intervals to stabilise blood sugar and provide a steady supply or tryptophan, helping serotonin levels normalise.

2. Reward retraining: Pair meals with small positive experiences (music, company, self-care) to retrain the striatum and orbitofrontal cortex to replace previous negative associations of eating with pleasurable ones.

3. Therapy support: Cognitive-behavioural therapy (CBT) or other evidence-based therapies have been shown to be effective in helping reshape thought patterns and break maladaptive loops.

4. Movement and self-care: Gentle exercise and relaxation techniques such as medication and yoga may help regulate dopamine and serotonin balance, reducing overall anxiety.

5. Mindful exposure: Gradually reintroduce feared foods while noticing thoughts and feelings, teaching the amygdala that food is not a threat.

Food is unlike any other; it is integral to survival, and the body cannot endure without it. This is what makes eating disorder recovery all the more difficult; unlike drugs or alcohol, complete abstinence is not an option. Yet, within this necessity lies its power: every bite becomes a chance to rewire the brain, to teach fear to dampen, reward to return, and the body to be trusted again, once more. If you or a loved one is struggling, neuroplasticity is on your side. With appropriate professional support, a freer relationship with food is not only possible—it’s waiting for you.

Reference list

Jancke, D., Herlitze, S., Kringelbach, M.L. and Deco, G. (2021). Bridging the gap between single receptor type activity and whole‐brain dynamics. ˜The œFEBS journal, 289(8), pp.2067–2084. doi:https://doi.org/10.1111/febs.15855.

KAYE, W., FRANK, G., BAILER, U., HENRY, S., MELTZER, C., PRICE, J., MATHIS, C. and WAGNER, A. (2005). Serotonin alterations in anorexia and bulimia nervosa: New insights from imaging studies. Physiology & Behavior, [online] 85(1), pp.73–81. doi:https://doi.org/10.1016/j.physbeh.2005.04.013.

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