Unified Theory of Restrictive and Addictive Eating

How Two Developmental Pathways Share a Root, Diverge, and Converge Across the Life Course

David Wiss, PhD, RDN, FMCP
Founder, FxMed Mental Health

For decades, eating disorder specialists and addiction clinicians have worked from opposite playbooks — one blames restriction, the other blames ultra-processed foods. Patients who don’t fit neatly into either camp get caught in the middle, handed conflicting advice that erodes trust and stalls recovery. This session offers a different way of seeing it.

Some patients do not fit neatly into a box. Consider the person who restricted through their teens and twenties, then developed loss-of-control eating in their thirties, and later an alcohol use disorder. Or the adolescent who ate emotionally, then swung into rigid restriction, and eventually met criteria for anorexia nervosa with no overeating left in the picture at all. Or the person who got sober from a substance, moved into compulsive overeating, and only later developed purging. These are not exotic edge cases. They are common, and they expose the limits of a treatment landscape that was built around categories.

For roughly a decade, I have worked in the gray area between two fields that rarely talk to each other: the mainstream eating disorder world and the mainstream addiction world. Each has a philosophy it believes in deeply. Each has protected something real. And each, when it becomes too certain, starts to behave more like an ideology than a science. This post is the long-form companion to my recent webinar summarizing a paper I wrote with Dr. Alan Logan in the Journal of Eating Disorders — a unified, life-course theory of restrictive and addictive eating. It is written for clinicians trying to make sense of complex presentations, and for the patients and families who have lived in that gray area and felt unseen by both sides.

The argument is dialectical from the start: these two perspectives can both be true, for different people, and even within the same person across a lifetime. The goal is not to declare a winner. It is to think dimensionally — along continua and spectrums — instead of forcing people into one box or the other.

Estimated reading time: 31 minutes

The Patient Who Doesn’t Fit the Box

If you treat eating disorders or addictions, or if you have lived with disordered eating yourself, the gray area is familiar terrain. It is the person whose history bends across several diagnoses over time, whose family tree carries both compulsive traits and behavioral addictions, who processes sensory experience a little differently than the people around them. The presentation you see in the room is a snapshot. The story that produced it runs across decades and, often, across generations.

These are the people who fall through the cracks. Our treatment systems are designed for categorical diagnoses, not for dimensional phenotypes, so a patient with a mixed presentation gets routed to an eating disorder program or an addiction program and frequently receives conflicting advice from each. One provider emphasizes flexibility and self-acceptance. Another implements a more structured, targeted approach. The patient is left holding the contradiction, stuck between shame and relapse, and the discordant messaging itself can undermine the treatment.

I want to be careful here, because naming these patterns is not the same as prescribing them. Most people do have some phenotypic overlap between restrictive and addictive tendencies — but many people are also clearly one or the other, cleanly restrictive or cleanly along an addiction continuum. The point of describing the gray area is not to hand anyone a template to map onto themselves. It is to make the case that better assessment, rather than defaulting to a single model, is what these patients need. The National Institute of Mental Health’s Research Domain Criteria initiative made a version of this argument years ago when it challenged the categorical logic of the DSM [1]. I am extending that challenge into eating and addiction, where the categories have arguably done the most to obscure what is actually in front of us.

Our transdiagnostic models of eating disorders tend to assume very similar mechanisms across the diagnoses, yet anyone who works in the field knows that treatment response differs widely from person to person. A one-size-fits-all approach ignores that phenotypic heterogeneity. The DSM boundaries between overlapping phenomena are, to a real degree, artificial — useful for billing and research, less useful for understanding the person in front of you. My favorite assessment in functional medicine is simply the timeline: sitting with a patient and mapping an entire life-course context — biology, psychology, and social environment across the lifespan — and connecting the dots that a snapshot diagnosis leaves scattered. That is the frame this whole model lives inside.

Two Fields, Two Philosophies, One Impasse

There are two dominant perspectives, and each captures something true. The first holds that dietary restraint — whether actual or intended, nutritional or psychological — is the primary driver of loss-of-control eating. In this well-established view, restriction eventually produces the rebound: restrain long enough and you lose control [2]. The second perspective looks at the contemporary food environment, at ultra-processed foods engineered to be rewarding, and at the way they recruit brain circuitry to drive craving and overconsumption [3]. Importantly, the addiction model does not stop at access to rewarding substances; it also foregrounds the stress, trauma, and adversity that make those substances appealing in the first place. People reach for rewarding food, and rewarding substances of all kinds, partly because life is genuinely hard and these things briefly make the difficulty recede.

Both camps acknowledge developmental trauma as a predisposing factor [4], though trauma is far better established in the addiction literature than in the eating disorder literature, where it has only more recently been described in depth. And this is where the impasse sets in. In the eating disorder field, the refrain has often been that “it’s not about the food” — that dietary restraint is the core driver, and that emphasis belongs on societal pressure toward thinness, internalized weight stigma, body image, and the work of self-acceptance. The addiction field, meanwhile, is more interested in neurobiology: the vulnerability to ultra-processed foods and other substances, measured with tools like the Yale Food Addiction Scale, which applies substance use disorder criteria to food [5], and studied with the funding and neuroimaging resources that field commands.

You can frame the difference as a dialectic between change and acceptance. Addiction models tend to emphasize changing something; eating disorder models tend to emphasize acceptance. In dialectical behavior therapy, that exact tension — change versus acceptance — is the central dialectic, and the clinical skill is holding both as simultaneously true. Instead, what I have often seen is fear on both sides. Eating disorder clinicians fear messages that promote restriction and moralize food, and that fear is valid and hard-won. Addiction clinicians fear ongoing exposure to a triggering substance. Both fears are legitimate. But when each hardens into orthodoxy, the patient in the middle pays the cost. And the cost is measurable: a meta-regression spanning four decades of psychological treatment for bulimia nervosa and binge eating disorder found no improvement in abstinence rates over that time, and by some measures a decline [6]. Protecting people with restrictive eating disorders has sometimes come at the expense of people with binge-type presentations and ultra-processed food use disorder, who can feel marginalized or even harmed by models that treat their experience as nothing more than a downstream effect of restriction. Sometimes that is exactly what it is. Sometimes it is not. The clinical failure is deciding in advance.

It helps to zoom out and name the cultural weather around all of this. The anti-diet movement is powerful and was a genuinely needed response to real harm — think of the patient whose doctor only ever tells them to lose weight, who then stops going to the doctor at all. The protective instincts behind that movement, especially on behalf of people with restrictive eating disorders, are genuine and necessary. But protecting one group has, at times, marginalized another: the people with binge-type presentations and ultra-processed food use disorder, whose lived experience gets waved off as merely their restrictive history in disguise. When belonging-forces in a culture break down and separation-forces get amplified, fields dig into their trenches, and the patients caught in the crossfire are the ones with complex presentations. What is missing is not another manifesto for one side. It is conceptual alignment — enough shared language to coordinate care — without forcing a false uniformity that pretends every patient is the same.

What Both Sides Get Right — and the Shared Root

The way out of the impasse is to notice what both fields already agree on and follow it upstream. Both acknowledge early adversity. And when you take that seriously, a shared origin comes into view beneath the two philosophies.

That shared soil is generational trauma and adverse childhood experiences. I use the term ACEs broadly here — not only the ten items from the original study or the expanded and community versions, but childhood adversity as a whole, including the food-specific adversity around the family table that standard instruments never capture. ACEs predict psychiatric outcomes in a dose-response fashion, and the same graded relationship shows up for chronic disease [7]. Elevated ACE exposure is a consistent finding across both eating disorder and addiction samples [8]. In my own clinical research, the relationship between ACEs and eating disorder symptoms was mediated by PTSD — the trauma, not merely the adversity, carried the effect [9].

Underneath that sits the biology, and I want to keep this brief rather than mechanistic. Early adversity becomes biologically embedded: it shapes the stress system, the immune system, epigenetic expression, and brain development, and one of its more consistent effects is to prime the brain for reward-seeking — for more addictive tendencies later in life [10]. This is what “generational trauma” points at. I use the phrase because there is research behind it, but what I really mean is generational mental health: adversity transmitted through the germ line and through the social environment, legacies that cannot be ignored when you are trying to understand a behavioral health outcome [11]. There is also a food-specific layer of adversity that standard tools miss entirely. A great deal of what happens around the dinner table growing up — the conflict, the scarcity, the control, the chaos — never shows up on the original ten-item ACE questionnaire or even its expanded and community versions. I have long wanted an adverse food-related childhood experiences measure precisely because this dimension is so clinically important and so poorly captured. The absence of a tool does not mean the absence of the exposure.

Not all adversity points the same direction, either. Some specific experiences are linked more strongly to addiction than to restriction — childhood sexual abuse is one of them — and in my own work I have argued that this kind of exposure is better understood as a biological process shaping reward circuitry than as a purely psychodynamic one. As always, it is a both/and rather than an either/or. The clinical upshot is that the shared root does not erase the divergence to come; it seeds it. Two people can carry high adversity and, depending on the flavor of that adversity and the neurodevelopmental soil it lands in, grow toward very different presentations.

Siloed models fail precisely because they cannot integrate a shared developmental origin. Two pathways that look nothing alike at the surface can grow from the same root, and missing that root is how a field ends up treating the branches in isolation.

Two Pathways Diverge: OCD/Restrictive and ADHD/Addictive

From that shared root, two developmental pathways tend to diverge, and the fork is shaped by neurodevelopmental risk. This is the core of the model.

The Restrictive Eating Pathway more often runs through parental traits on the obsessive-compulsive spectrum — rigid or disordered eating patterns, OCD or OCPD features. Layer childhood adversity onto that predisposition, and you get conditions conducive to dieting, food rules, and rigidity, which can culminate in restrictive eating disorders such as anorexia and the restrictive variants of bulimia. The Addictive Eating Pathway more often runs through parental substance use disorders and ADHD-type traits, characterized by impulsivity. Layer adversity onto that predisposition, and you get conditions conducive to hedonic eating — eating for reward and for relief from negative affect — which can progress to ultra-processed food use disorder and other addictive processes. Substance use disorder shows up frequently in both, but as a comorbidity and a potential crossover point, not as a prerequisite for either trajectory.

The cleanest way I have found to describe the psychological signatures is compulsivity versus impulsivity. Compulsivity is repetitive behavior that persists despite adverse consequences; it has roots in OCD, where it is right there in the name, and in the restrictive context it tends to be avoidant — organized around not doing, not eating, imposing order on an unpredictable world [12]. Impulsivity is action without forethought, the rash decision made under distress; it is more approach-oriented, more reaching, and it tracks the addictive pathway [13]. One patient is, in a sense, over-ordered, trying to impose control. The other is under-ordered, contending with a loss of control. Their coexistence is exactly what produces mixed presentations and diagnostic crossover, and they can shift across the trajectory of an illness rather than sitting at fixed poles.

The genetics support distinct but overlapping liabilities. Eating disorders and substance use disorders are each substantially heritable — roughly 40 to 60 percent of the liability for eating disorders and 43 to 53 percent for substance use disorders [14,15]. Genome-wide work has shown anorexia nervosa correlating with OCD and, strikingly, negatively correlating with metabolic traits — anorexia and OCD cluster together at the level of genetic architecture [16,17]. On the other side, ADHD and substance use disorder cluster strongly, with roughly a quarter of people in addiction treatment meeting criteria for ADHD [18], sharing a hypodopaminergic state with reduced reward responsiveness and steep delay discounting, the tendency to favor smaller immediate rewards over larger later ones [19]. The overlap between ADHD and eating disorders is real and weighted toward the binge-type presentations — binge eating disorder and bulimia far more than restrictive anorexia [20]. It helps to see the model as a sequence of stages rather than a single snapshot: a historical layer (generational trauma, epigenetic and prenatal influence), a predisposing layer (parental mental health leaning OCD/eating-disorder or SUD/ADHD), a developmental layer where the endophenotypes emerge, a behavioral layer where patterns cement into food rules and rigidity or hedonic loss of control, a mental-health layer where clinical diagnoses appear, and a metabolic layer. I want to be clear that the metabolic layer is not necessarily last — metabolic derangements can precede psychiatric symptoms, a point becoming better described all the time. The staging is a scaffold for thinking, not a conveyor belt everyone rides in the same direction.

Parental influence operates well before conscious food choices. There is good data that parental disordered eating predicts offspring eating disorders, that maternal eating disorders predict offspring emotional, conduct, and hyperactivity problems, and that these patterns show up across grandmother-mother-daughter triads [21,22]. On the addictive side, maternal addictive eating is associated with problematic infant eating and elevated overweight risk, and a family history of substance use disorder raises the odds of offspring eating pathology. There is even a reward-expectancy mechanism worth naming: a brain primed to expect reward from ultra-processed food becomes, in effect, less likely to reach for minimally processed food — hedonic eating displacing whole foods by way of how reward is anticipated. Pathway divergence can begin before a child makes a single food choice, which is why family history and parental mental health are such useful clues.

Where the Pathways Converge

Two trajectories that diverge in childhood can arrive at similar destinations later, and the convergence tends to happen in the body. Both pathways ultimately meet at metabolic dysfunction, by different routes. Restrictive eating is generally associated with low body weight, nutritional deficiencies, hormonal disruption, and, over time, later-life weight regain. The addictive pathway is more associated with metabolic syndrome, cardiometabolic disease, and inflammatory phenotypes [23,24]. Different roads, overlapping endpoints — and this is part of why reframing eating pathology through a metabolic lens opens up new subtyping possibilities rather than collapsing everyone into one mechanism [25].

The two pathways are also biochemically distinguishable in a way that has clinical traction. The restrictive pathway is better characterized by serotonergic dysfunction, which is part of why serotonergic medications feature in the treatment of restrictive eating disorders and OCD. The addictive pathway carries more of its patterning through the dopamine system [26]. The animal literature makes the generational piece vivid: when dams are fed ultra-processed food, their offspring show heightened preference for ultra-processed foods and for drugs of abuse, and maternal nicotine exposure produces offspring with greater addiction vulnerability and shared dopaminergic dysfunction [27,28]. These preclinical models are one of the few ways to study maternal influence rigorously, and they point toward transmission of addictive-eating vulnerability by way of dopamine, among other neurotransmitters.

Substance use disorder sits in the middle of the model deliberately. Placing it there avoids reductionism — it is not the hub around which everything else turns — while still acknowledging that introducing addictive processes changes the brain and raises clinical complexity wherever it appears. It is a bridge, connecting and reflecting trajectories, not a mandatory station on either line. And I cannot leave the convergence zone without a brief word on the gut, even though I kept the mechanism light in the talk. Early-life stress alters the microbiome, which in turn influences neurotransmitter systems; ultra-processed foods reduce bacterial diversity and compromise the gut lining [29,30]. There are threads here connecting eating patterns, adversity, and psychiatric outcomes that are only beginning to be mapped — including biomarkers like uric acid, which has been linked to impulsivity and eating pathology and which I have started folding into my own assessment [31].

Seeing eating disorders partly as metabolic disorders opens genuinely new possibilities rather than closing them down. Some of the most interesting research right now sits exactly here: ketogenic and lower-carbohydrate approaches being studied for anorexia nervosa and for binge-type presentations, and emerging psychedelic-assisted approaches such as psilocybin being explored for eating disorders [32,33,34]. I raise these not as recommendations — they are emerging, not established — but to make a point about the frame. Once you stop treating eating pathology as purely a story about diet culture and the pursuit of thinness, and start also asking what is happening in the brain and the metabolism, the menu of testable interventions expands. The whole purpose of the model is to generate more clues for better case conceptualization, not fewer.

Pathways Aren’t Fixed: Fluidity and Crossover

The model describes two pathways, but it is emphatically dimensional, not categorical. The arrows — especially on the behavioral end — are largely bidirectional, and they represent likely tendencies, not deterministic tracks. Individuals can occupy both pathways at once, and they can move between them across the lifespan. Certain kinds of adversity can nudge someone from a more compulsive, over-ordered presentation toward a more impulsive, under-ordered one. People who are over-ordered in one season of life become under-ordered in another. Most people live somewhere in the crossover space between the two poles, which is exactly why a categorical system keeps producing patients who look like noise. In a dimensional frame, their mixed and shifting presentations become predictable rather than confusing.

One finding deserves particular emphasis because it unsettles a deeply held assumption in the eating disorder field. The prevailing view has been that addictive eating is downstream of restriction — that the loss of control is a rebound from restraint, so the “real” problem is always the dieting. But work I and others have done points the other way for a meaningful subset of people: the addictive eating comes first, and the restriction develops as a byproduct — people become dieters in response to their addictive eating [9,35]. In one of my own samples, made up largely of older, socially advantaged white women, ACEs predicted food addiction more strongly than they predicted eating disorder symptoms. This is not an argument that restriction never drives loss of control; it often does. It is an argument that the causal arrow runs in both directions depending on the person, and that assuming a single direction is how we get the sequence wrong. Temporal sequencing — asking honestly which came first, and being willing to hear that loss of control sometimes preceded restraint — is clinical information we routinely discard.

Crossover is a feature of the model, not a bug. Certain kinds of adversity can move someone from a more compulsive endophenotype toward a more impulsive one. Recovery from one pattern can precipitate the emergence of another — the phenomenon of addiction transfer, where resolving one behavior opens the door to a substitute. Substance use disorder, sitting in the middle, is frequently where these shifts get expressed, without being required for either trajectory. Thinking dimensionally also creates space for the presentations that never reach diagnostic threshold at all — the subclinical patterns, the pre-addiction states — which categorical systems tend to render invisible until they become severe. Keeping people out of boxes is not vagueness; it is what lets you see the whole range of possibility, and intervene earlier, before a pattern hardens into a diagnosis.

What This Means for Treatment

If the model is right that presentations differ by pathway, then treatment has to be matched to pathway rather than applied uniformly. The advanced clinician resists the pressure to adopt one food philosophy for everyone and instead asks a better question: which approach, for which patient, at which point in time. Abstinence, moderation, harm reduction, “all foods fit” — each is right for some people and wrong for others. The skill is discernment, and in the gray area it cannot be fully manualized; it requires genuine fluency in both orientations.

Here I need to state something plainly, because it is where the greatest potential for harm lives. For a patient on the restrictive pathway, further dietary restriction is not a neutral default — it can be actively harmful, and it can worsen the restrict-binge cycle. Restriction is frequently the accelerant, not the remedy, and imposing more of it on someone whose problem is rigidity and control can deepen exactly the pattern you are trying to relieve. This is a large part of why the addictive-eating conversation has been treated as dangerous by the eating disorder field: the worry that naming food addiction will license restriction in people who are already harmed by it. That worry is legitimate and I share it. The clinical response is to think at the level of philosophy rather than prescription. For the restrictive-predominant patient, the orientation is toward liberalization — expanding variety, loosening rules, reducing the moral weight attached to food. For the addictive-predominant patient, the orientation may involve reducing exposure to the specific ultra-processed foods that drive the loss of control, alongside addressing the underlying trauma and the hedonic drivers. I am describing directions of clinical reasoning, not diets, targets, or numbers, and nothing here should be read as a self-administered protocol. When restrictive and addictive features coexist, the answer is a hybrid held with ongoing clinical judgment, not a rule applied from a manual. And it is worth noting that recent work suggests introducing the concept of addictive eating, and using dimensional assessment tools, is not inherently harmful even in higher levels of care — a reassuring counterweight to the fear that the conversation itself does damage [36].

Two guardrails hold this together. The first is that dimensional, non-binary assessment is the safer path; forcing people into binaries is, in my view, the more clinically harmful move. The second is that pathology and nourishment are not the same thing. We can put real guardrails against dietary restraint for people at eating disorder risk while still declining to pathologize nutritious food. Encouraging someone to heal their gut and their brain does not have to mean handing them an eating disorder.

It follows that the framing of “abstinence versus moderation” is the wrong question stated in absolute terms. The better question is which approach, for which patient, and why. For the addictive pathway, recovery leans on community and social support, and harm-reduction models are common and often appropriate; psychoeducation about the neurobiology of reward, mindfulness, and other practices that help rewire circuits over time all have a place. For the restrictive pathway, the serotonergic emphasis of OCD-oriented care and the work of exposure to feared foods look nothing like that. And a subtlety that gets missed: when someone screens positive for addictive eating, it is sometimes restraint-driven craving rather than true addiction, which points toward liberalization rather than reduction. Part of the clinician’s job is to help the patient work out which one they are looking at — not to crack the code for them, but to bring the wisdom of both camps into the room and let the person locate themselves within it. That is a conversation, held over time, not a verdict delivered at intake.

You don’t have to fit into a box to get help. If you or someone you love has lived in the gray area between restrictive and addictive eating — and felt handed conflicting advice by every provider — a more integrated, whole-person assessment may be the missing piece. Schedule a free 15-minute discovery call to explore whether the FxMed Mental Health approach is the right fit.

A Comprehensive, Whole-Person Approach

Matching treatment to pathway requires actually seeing the whole person, which is where a functional medicine orientation earns its place. The foundation is trauma-informed care — foundational, not adjunctive — because unresolved trauma is so often the upstream cause. When PTSD is present, evidence-based trauma therapies belong at the center of the plan, and microbiome-targeted and other systems-level interventions are an emerging area of investigation as complements in the context of trauma [37]. On the restrictive pathway, trauma frequently expresses as control-seeking through restriction; on the addictive pathway, as reward dysregulation and self-medication. Same upstream cause, different downstream shape.

From there, assessment is a biopsychosocial timeline. I build a life-course history and look for the clues the model tells me matter: parental psychiatric history, and whether it leans toward an OCD/eating disorder spectrum or a substance use disorder/ADHD spectrum. I screen for PTSD. I pay attention to temporal sequencing — restriction first, or loss of control first — because sometimes it changes the plan and sometimes it does not. And I look at neurodivergent traits like sensory processing, impulsivity, rigidity, and delay discounting, because they are part of the picture more often than our diagnostic categories admit. This is the emerging spirit of precision neurodiversity: treating cognitive variability as clinical signal rather than noise.

This is also where systems biology comes in, and where FxMed Mental Health fits. In my practice I run a suite of specialty lab tests across blood, stool, urine, and saliva to map the biological terrain — dopamine and serotonin metabolites, hormones, gut bacteria, inflammation — and then map those biomarkers onto the person’s own narrative so the data becomes a story rather than a pile of numbers. The driving premise is simple: mental health is physical health, and much of what gets labeled treatment-resistant is more accurately undertested. It is the reason our orientation is to test, don’t guess.

In practice that means a full suite of specialty tests — seven of them — across blood, stool, urine, and saliva, chosen to leave no stone unturned across dopamine and serotonin metabolism, hormones, gut bacteria, inflammation, and more. The value is not the volume of data; it is the pattern recognition. A finding in the gut connects to a marker in the urine, connects to a hormone in the saliva, and the biomarkers get mapped onto the person’s own life story so the picture coheres instead of fragmenting. The care itself is coordinated across the whole team — psychiatry by referral, psychology, nutrition — because discordant messaging confuses patients, and every team member needs fluency in both eating disorder and ultra-processed food use disorder science for a pathway-matched plan to hold together. The nutrition approach is individualized to the pathway orientation, never applied uniformly. And because the gray area cannot be manualized, the discipline is to keep monitoring, keep following the literature, and hold more questions than answers — which is exactly the posture the emerging field of precision neurodiversity asks of us as it learns to treat cognitive variability as a clinical guide rather than a deviation.

Frequently Asked Questions

Conclusion

The unified theory of restrictive and addictive eating is, at bottom, a call to stop choosing sides. Generational trauma and adverse childhood experiences are shared upstream risks for both pathways. Parental OCD-spectrum traits tilt toward the restrictive pathway; parental ADHD-spectrum traits tilt toward the addictive one. Substance use disorder is a frequent comorbidity and a bridge, not a required component of either. And the presentations are dimensional and fluid, not categorical and fixed. Held together, these commitments ask us to serve the whole person in a life-course context — which is exactly what functional medicine, at its best, is built to do. The right clinical question is never which philosophy wins, but which approach fits which patient at which point in time, and the advanced clinician resists the pull toward any single answer in favor of integrating wisdom from across the continuum while staying agnostic to food ideologies.

None of this dissolves the hard-won wisdom on either side. Shame is counterproductive. Weight stigma causes real harm. Patients deserve informed consent and genuine options. Not all eating disorders share the same biology. Trauma-informed care is foundational. Food is more than calories. And “all foods fit,” harm reduction, and abstinence are each right for some people and not for all. Holding those truths at once is not fence-sitting; it is the dialectical stance the work actually requires, and it means being willing to set your own story aside — because sometimes it is not about you. The way we treat the other eventually becomes the treatment we receive. Together we can accomplish what none of us can alone, but only if we stop the infighting long enough to risk belonging to each other, and put patient care first. That is the real-world clinic I want to practice in — one that combines the research, our expertise, and the patient’s own preferences.

If you are navigating these questions for yourself, a loved one, or a patient, schedule a free 15-minute discovery call to explore whether a comprehensive, whole-person assessment is the right next step.

About the Author

Dr. David Wiss, PhD, RDN, FMCP, is a functional medicine practitioner and researcher specializing in the intersection of nutrition, addiction, and mental health. He completed his doctorate at UCLA, founded the practices Nutrition in Recovery and FxMed Mental Health, and created the Wise Mind Nutrition app, which brings addiction and restriction concepts together in a trauma-informed model. His research integrates trauma, neurodevelopment, eating disorder, and addiction science, with a particular focus on adverse childhood experiences and ultra-processed food use disorder. His work has been published in the Journal of Eating Disorders and other peer-reviewed journals.

Disclaimer

This article is provided for educational purposes only and does not constitute medical advice, diagnosis, or treatment. It is a conceptual and clinical overview, not a guide for self-diagnosis or self-directed dietary change. Nothing here should be used to start, stop, or change any eating pattern, treatment, or medication. Eating disorders and addictive disorders are serious conditions; decisions about assessment and care should always be made in consultation with qualified medical and mental health professionals who know your individual history. If you are struggling with disordered eating or thoughts of self-harm, please reach out to a licensed clinician or an appropriate helpline for support.

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