TL;DR: Dopamine is built from the amino acid tyrosine through an enzyme pathway that requires iron, vitamin B6, folate, and vitamin C as cofactors. Protein-rich whole foods — eggs, fish, poultry, legumes, dairy — provide the raw materials. Ultra-processed foods cause exaggerated dopamine spikes that, over time, downregulate receptors and blunt motivation. The popular “dopamine detox” trend contains a kernel of truth but is wrapped in pseudoscience. Roughly 50% of the body’s dopamine is produced in the gut, making microbiome health directly relevant. For people with ADHD, dietary support for dopamine synthesis is especially important. The best strategy is not to chase dopamine highs but to maintain steady, adequate production through consistent whole-food nutrition.

Introduction

Dopamine has become one of the most talked-about molecules in popular health culture — and one of the most misunderstood. Social media is flooded with advice about “boosting your dopamine” through cold showers, fasting protocols, and supplement stacks. Much of this advice treats dopamine as a simple pleasure chemical: more is better, and the goal is to get as much of it firing as possible.

The reality is considerably more nuanced. Dopamine is not primarily a pleasure molecule. It is a motivation and prediction molecule — a neurotransmitter that drives you to pursue rewards, sustains your focus while working toward them, and helps your brain learn which behaviors are worth repeating. The distinction matters. A brain with healthy dopamine function is not one that is perpetually flooded with dopamine. It is one where dopamine signaling is responsive, well-calibrated, and supported by adequate substrate supply.

And that substrate supply depends, in large part, on what you eat. Dopamine is synthesized from dietary amino acids through an enzymatic pathway that requires specific vitamins and minerals as cofactors. The foods you choose — or fail to choose — directly affect how efficiently this pathway operates. Meanwhile, ultra-processed foods interact with the dopamine system in ways that go beyond simple nutrition, hijacking reward circuits in patterns that increasingly resemble, at the neurochemical level, the early stages of addiction.

This article covers the dopamine synthesis pathway from the ground up, identifies the nutrients and foods that support it, explains how modern diets disrupt it, evaluates the “dopamine detox” trend, explores the surprisingly large role of gut bacteria, and addresses the specific relevance of dopamine to ADHD.

The Dopamine Synthesis Pathway

Understanding how diet affects dopamine requires understanding how dopamine is made. The synthesis pathway is well-characterized and proceeds in a straightforward sequence.

Step 1: Tyrosine

The pathway begins with L-tyrosine, a non-essential amino acid found abundantly in protein-rich foods. Tyrosine can also be synthesized in the body from another amino acid, phenylalanine, via the enzyme phenylalanine hydroxylase. Under normal dietary conditions, most people obtain more than enough tyrosine from food to support dopamine production.

Tyrosine crosses the blood-brain barrier via large neutral amino acid transporters — a transport system it shares with several other amino acids, including tryptophan (the precursor to serotonin). This competition for transport is one reason why the macronutrient composition of a meal can influence neurotransmitter balance, a point we will return to.

Step 2: Tyrosine to L-DOPA

The rate-limiting step in dopamine synthesis is the conversion of tyrosine to L-DOPA (L-3,4-dihydroxyphenylalanine), catalyzed by the enzyme tyrosine hydroxylase. This is the bottleneck — the step that determines how fast the pipeline runs.

Tyrosine hydroxylase requires two critical cofactors: iron (specifically, a non-heme iron atom at the enzyme’s active site) and tetrahydrobiopterin (BH4), a cofactor whose own synthesis depends on folate and GTP. Without adequate iron, tyrosine hydroxylase activity drops, and dopamine production slows regardless of how much tyrosine is available. This is one of the mechanisms by which iron deficiency — even without overt anemia — can impair motivation, attention, and cognitive function.

Step 3: L-DOPA to Dopamine

The final step is the decarboxylation of L-DOPA to dopamine by the enzyme aromatic L-amino acid decarboxylase (AADC), which requires pyridoxal phosphate — the active form of vitamin B6 — as its cofactor.

This step is generally not rate-limiting under normal conditions, meaning that once L-DOPA is produced, conversion to dopamine proceeds efficiently as long as B6 status is adequate. However, in individuals with marginal B6 status — which is more common than often recognized, particularly among older adults, people on restrictive diets, and heavy alcohol consumers — this step can become a functional bottleneck.

The Cofactor Summary

To synthesize dopamine efficiently, the brain needs:

  • Tyrosine (from dietary protein or conversion from phenylalanine)
  • Iron (for tyrosine hydroxylase activity)
  • Folate (for BH4 synthesis, which tyrosine hydroxylase also requires)
  • Vitamin B6 (for the final conversion of L-DOPA to dopamine)
  • Vitamin C (protects dopamine from oxidation and supports the recycling of BH4)

A deficiency or insufficiency in any one of these creates a potential chokepoint in the pathway. This is not a theoretical concern — subclinical deficiencies in iron, folate, and B6 are common in the general population and significantly more prevalent in certain groups, including menstruating women, vegetarians, older adults, and individuals with ADHD.

Tyrosine-Rich Foods

Because tyrosine is the foundational building block, ensuring adequate intake is the first dietary priority for dopamine support. Fortunately, tyrosine is abundant in high-protein foods.

Top sources per typical serving:

  • Soy products (tofu, tempeh, edamame): ~1,400–2,000 mg per cup cooked
  • Cheese (Parmesan, Swiss, Gruyere): ~1,200–1,600 mg per 100 g
  • Turkey and chicken breast: ~1,000–1,200 mg per 3 oz cooked
  • Pork loin: ~900–1,100 mg per 3 oz cooked
  • Fish (salmon, tuna, cod): ~800–1,000 mg per 3 oz cooked
  • Eggs: ~250 mg per large egg
  • Legumes (lentils, black beans): ~400–600 mg per cup cooked
  • Pumpkin seeds: ~1,000 mg per ounce
  • Dairy (milk, yogurt): ~300–500 mg per cup

A study by Fernstrom and Fernstrom (2007) in the Journal of Nutrition demonstrated that plasma tyrosine levels rise predictably after protein-containing meals, and that this increase is sufficient to enhance brain tyrosine availability and, under conditions of demand, dopamine synthesis. The researchers noted that meals containing at least 20–25 grams of protein provide enough tyrosine to meaningfully influence the precursor pool.

This does not mean that more protein always equals more dopamine. Tyrosine hydroxylase — the rate-limiting enzyme — is tightly regulated by end-product inhibition (dopamine itself inhibits the enzyme) and by neuronal firing rates. Under resting conditions, extra tyrosine has limited effect. But under conditions of sustained cognitive demand, stress, or high dopaminergic activity, extra tyrosine availability has been shown to prevent the depletion that would otherwise occur.

Research by Jongkees et al. (2015), published in Neuroscience & Biobehavioral Reviews, conducted a meta-analysis of tyrosine supplementation studies and concluded that acute tyrosine administration reliably enhances cognitive performance under demanding conditions — particularly working memory and cognitive flexibility — without meaningful effects under low-demand conditions. The practical interpretation: tyrosine from diet matters most when you need it most.

How Ultra-Processed Food Hijacks the Dopamine System

If steady-state tyrosine from whole foods represents the healthy way to fuel dopamine, ultra-processed food represents its pathological counterpart. The problem is not that ultra-processed foods contain too much tyrosine — they often contain less protein per calorie than whole foods. The problem is that they trigger exaggerated dopamine responses through a different mechanism entirely: supranormal reward signaling.

The Supranormal Stimulus

Ultra-processed foods are engineered to combine sugar, fat, salt, and texture in ways that do not exist in nature. This combination produces a reward signal that exceeds anything the dopamine system evolved to handle. A study by Gearhardt et al. (2011), published in the Archives of General Psychiatry, used fMRI to demonstrate that highly processed foods — particularly those combining high sugar and high fat — activate the same striatal dopamine circuits, in the same patterns, as drugs of abuse in susceptible individuals.

This is not a metaphor. The neuroimaging data show overlapping activation in the nucleus accumbens, ventral tegmental area, and prefrontal cortex — the core circuitry of the mesolimbic dopamine pathway. The magnitude of the response is proportional to the degree of food processing, not to caloric content or macronutrient composition per se.

Receptor Downregulation

The critical downstream consequence is receptor downregulation. When any stimulus — a drug, a food, a behavior — repeatedly produces supranormal dopamine surges, the brain protects itself by reducing the number and sensitivity of dopamine D2 receptors in the striatum. This is a well-characterized adaptive response, documented extensively in both substance abuse research and, more recently, in obesity research.

Wang et al. (2001), publishing in The Lancet, demonstrated that obese individuals had significantly lower striatal D2 receptor availability compared to lean controls — a finding strikingly similar to the pattern seen in cocaine and methamphetamine users. Johnson and Kenny (2010), in a landmark study published in Nature Neuroscience, showed that rats given unrestricted access to a “cafeteria diet” of ultra-processed foods developed compulsive eating behavior and progressive D2 receptor downregulation. When the processed food was removed and replaced with standard chow, the animals initially refused to eat — despite being hungry — because their reward system had been recalibrated to a higher threshold.

The human implication is straightforward. A diet dominated by ultra-processed food progressively raises the bar for what registers as rewarding. Whole foods — with their more moderate dopamine signaling — become less appealing. Motivation for everyday activities that produce modest dopamine responses (exercise, focused work, social interaction) can diminish. The subjective experience is a vague sense of anhedonia: nothing feels quite satisfying enough.

Sugar and Dopamine: The Acute-Chronic Paradox

Sugar occupies a special position in the dopamine conversation because its effects are time-dependent and directionally opposite depending on the consumption pattern.

The Acute Response

Consuming sugar triggers a reliable, measurable dopamine release in the nucleus accumbens. Rada et al. (2005), working in Bart Hoebel’s laboratory at Princeton, demonstrated this elegantly in rodent models: intermittent sugar access produced dopamine surges in the nucleus accumbens that were comparable in magnitude — though shorter in duration — to those produced by drugs of abuse. The acute dopamine release from sugar is real, robust, and partly explains why sugar cravings can feel so compelling.

In humans, this acute response is amplified by the speed of delivery. A can of soda delivers 39 grams of sugar in liquid form with zero fiber to buffer absorption. The resulting glucose spike triggers a correspondingly rapid insulin response and a sharp dopamine peak. By contrast, the equivalent amount of sugar locked within a whole apple — accompanied by fiber, water, and polyphenols — produces a slower, more moderate dopamine response that does not trigger the same reward learning.

The Chronic Consequence

The problem emerges with repeated, frequent consumption. Colantuoni et al. (2002), also from Hoebel’s group, showed that rats given daily intermittent sugar access developed neurochemical changes resembling opioid dependence: increased dopamine release followed by progressive tolerance, withdrawal symptoms (anxiety, teeth chattering, tremor) upon sugar removal, and eventual bingeing behavior when access was restored.

In the chronic state, the dopamine system adapts. D2 receptors are downregulated. Baseline dopamine levels between sugar exposures may actually fall below normal — creating a state where the individual needs sugar to feel normal, rather than to feel good. This is the precise neurochemical pattern that underlies tolerance and dependence in substance use disorders.

A systematic review by Jacques et al. (2019), published in Neuroscience & Biobehavioral Reviews, evaluated the “sugar addiction” hypothesis and concluded that while the full clinical syndrome of addiction is not clearly established for sugar in humans, the neurobiological parallels are substantial and the behavioral patterns — cravings, loss of control, continued use despite consequences — are frequently observed.

The practical implication for diet design is clear: the goal is not to achieve zero sugar intake (that is neither necessary nor realistic) but to avoid the pattern of frequent, rapid, high-dose sugar delivery that drives reward system recalibration. Whole fruit is fine. A daily soda habit is not.

The “Dopamine Detox” Trend: What Is Real and What Is Not

The concept of a “dopamine detox” has gained enormous popularity, primarily through social media and productivity culture. The basic premise is that by abstaining from highly stimulating activities — social media, video games, junk food, pornography — for a defined period (typically 24 to 72 hours), you can “reset” your dopamine system and restore normal sensitivity to everyday rewards.

What the Trend Gets Right

The underlying neuroscience is partially valid. Chronic overstimulation of the dopamine system does lead to receptor downregulation, as described above. Reducing the frequency and intensity of supranormal dopamine stimuli can, over time, allow receptor density and sensitivity to partially recover. This has been demonstrated in the addiction literature: sustained abstinence from drugs of abuse is associated with gradual recovery of D2 receptor availability, as shown by Volkow et al. (2001) using PET imaging.

The behavioral insight is also sound. Deliberately stepping away from hyperpalatable food and compulsive digital stimulation often results in people rediscovering that simpler activities — cooking a meal, reading, walking in nature — are more enjoyable than they remembered. This is consistent with what receptor recovery would predict.

What the Trend Gets Wrong

The term “dopamine detox” is itself misleading. You cannot “detox” from dopamine — it is an endogenous neurotransmitter essential for movement, motivation, learning, and survival. A brain without dopamine signaling would be profoundly impaired, as seen in Parkinson’s disease.

The timeframe claimed by most proponents — 24 to 72 hours — is almost certainly too short for meaningful receptor recovery. Neuroimaging studies in substance abuse populations suggest that significant D2 receptor recovery takes weeks to months of sustained abstinence, not a single weekend. A one-day dopamine detox is unlikely to produce measurable neurochemical changes; the benefits people report are more likely attributable to behavioral novelty, reduced decision fatigue, and the placebo effect.

Furthermore, the concept is often applied indiscriminately. Advocates sometimes recommend avoiding all pleasurable activities, including exercise, meaningful social interaction, and creative work — activities that produce healthy, moderate dopamine signaling and are part of normal reward circuit functioning. There is no scientific basis for abstaining from these.

A More Accurate Framework

A better way to think about it is not “dopamine detox” but “reward recalibration.” The goal is to reduce exposure to supranormal stimuli — ultra-processed food, excessive social media, and other inputs engineered to exploit the dopamine system — while maintaining and even increasing engagement with activities that produce moderate, sustained dopamine signaling (exercise, creative work, social connection, nature exposure). This is not a weekend project but an ongoing lifestyle pattern.

Gut Bacteria and Dopamine Production

One of the more surprising findings in recent neuroscience is the extent to which dopamine is produced outside the brain. Approximately 50% of the body’s total dopamine is synthesized in the gastrointestinal tract, primarily by enterochromaffin cells and certain bacterial species (Eisenhofer et al., 1997, Journal of Clinical Endocrinology & Metabolism). While gut-derived dopamine does not cross the blood-brain barrier directly, it influences brain dopamine signaling through several indirect but important pathways.

Bacterial Dopamine Production

Specific bacterial genera — including Bacillus, Serratia, and Escherichia — possess the enzymatic machinery to synthesize dopamine and its precursor L-DOPA from tyrosine. Strandwitz (2018), writing in Brain Research, documented the capacity of various gut commensals to produce neuroactive compounds, including dopamine, GABA, and serotonin. The quantities produced are not trivial and contribute to the enteric nervous system’s signaling capacity.

Vagal and Immune Signaling

The gut communicates with the brain primarily through the vagus nerve and through immune-mediated signaling. Gut-derived dopamine modulates vagal afferent activity, which in turn influences central dopamine circuits. Inflammation originating in the gut — driven by dysbiosis, increased intestinal permeability, or pathogenic overgrowth — can also impair central dopamine synthesis. Pro-inflammatory cytokines such as interferon-gamma and TNF-alpha have been shown to reduce tetrahydrobiopterin (BH4) availability, directly limiting the rate-limiting step of dopamine synthesis (Felger and Treadway, 2017, Neuropsychopharmacology).

Dietary Implications

This means that dietary factors affecting gut microbiome composition indirectly affect dopamine signaling. Diets high in fiber, fermented foods, and polyphenols support microbial diversity and reduce gut inflammation — creating a favorable environment for dopamine precursor availability and reducing cytokine-mediated inhibition of central synthesis. Conversely, ultra-processed diets that deplete microbial diversity and increase gut permeability create conditions that impair dopamine production at multiple levels simultaneously.

A study by Tillisch et al. (2013), published in Gastroenterology, demonstrated that consumption of a fermented milk product containing probiotics over four weeks altered brain activity in regions controlling emotion and sensation processing, as measured by fMRI. While this study did not measure dopamine directly, it established proof of concept that dietary modification of the microbiome can produce measurable changes in brain function.

The ADHD Connection

Attention-deficit/hyperactivity disorder is fundamentally a disorder of dopamine signaling. The dopamine hypothesis of ADHD — supported by decades of genetic, pharmacological, and neuroimaging evidence — posits that ADHD involves reduced dopaminergic tone in the prefrontal cortex and striatum, leading to impaired executive function, working memory, motivation, and impulse control.

Pharmacological Evidence

The first-line medications for ADHD — methylphenidate (Ritalin) and amphetamine-based compounds (Adderall) — work by increasing synaptic dopamine availability. Methylphenidate blocks the dopamine transporter (DAT), preventing reuptake; amphetamines both block reuptake and promote active dopamine release. The efficacy of these medications in improving ADHD symptoms is among the most replicated findings in psychiatry, and their mechanism of action underscores dopamine’s central role.

Nutritional Vulnerabilities in ADHD

Several nutritional factors relevant to dopamine synthesis are disproportionately affected in people with ADHD. Iron deficiency is significantly more prevalent among children and adults with ADHD than in the general population. Konofal et al. (2008), publishing in the Archives of Pediatrics and Adolescent Medicine, found that serum ferritin levels — a marker of iron stores — were abnormally low in 84% of children with ADHD compared to 18% of controls. Since iron is required for tyrosine hydroxylase activity, this deficiency directly constrains dopamine synthesis capacity.

Zinc, another mineral relevant to dopaminergic function (it modulates dopamine transporter activity), is also more frequently deficient in ADHD populations. Bilici et al. (2004), in the Journal of Child and Adolescent Psychopharmacology, conducted a randomized controlled trial showing that zinc supplementation improved ADHD symptoms in zinc-deficient children, with the effect being additive to stimulant medication.

There is also evidence that dietary patterns affect ADHD symptom severity. A randomized controlled trial by Pelsser et al. (2011), published in The Lancet, demonstrated that a restricted elimination diet (removing common food additives, refined sugars, and allergenic foods) significantly reduced ADHD symptoms in 64% of children. While the mechanism is not exclusively dopaminergic — immune-mediated and gut-brain pathways are likely involved — the results support the broader principle that what children with ADHD eat matters for their neurochemistry.

Practical Considerations for ADHD

For individuals with ADHD, the dietary strategies that support dopamine function are not different in kind from those recommended for the general population — they are simply more important (for a comprehensive overview, see best foods for ADHD). Ensuring adequate protein at every meal (to supply tyrosine), monitoring iron and ferritin status, maintaining B6 and folate intake, minimizing ultra-processed food, and supporting gut health through fiber and fermented foods address multiple bottlenecks in the dopamine pathway simultaneously.

This is not a substitute for medical treatment where indicated. But it is a complementary strategy that addresses the underlying biochemistry rather than merely managing symptoms.

Practical Takeaway

Healthy dopamine function is not about chasing peaks — it is about maintaining a well-supplied, well-calibrated system. Here is how to do that through diet:

  1. Eat adequate protein at every meal. Aim for 20–30 grams per meal from whole food sources — eggs, fish, poultry, legumes, dairy, or soy. This ensures a steady supply of tyrosine without relying on supplements.

  2. Prioritize cofactor-rich foods. Red meat, lentils, and spinach for iron. Leafy greens, legumes, and liver for folate. Poultry, fish, and potatoes for vitamin B6. Citrus fruits, bell peppers, and broccoli for vitamin C. These are the enzymatic tools your brain needs to convert tyrosine into dopamine.

  3. Reduce ultra-processed food, especially items combining sugar and fat. These engineered combinations hijack the reward system and drive receptor downregulation. The goal is not perfection but a meaningful reduction in the frequency and quantity of supranormal reward stimuli.

  4. Avoid frequent, rapid-delivery sugar. Whole fruit is not the problem. Sodas, energy drinks, candy, and sweetened coffee drinks consumed multiple times daily are the problem. The pattern matters more than the total amount.

  5. Support your gut microbiome. Eat fermented foods (yogurt, kefir, sauerkraut, kimchi), high-fiber vegetables, and legumes. Gut bacteria contribute directly to dopamine precursor availability and influence central dopamine synthesis through immune and vagal pathways.

  6. If you have ADHD, check your iron and ferritin levels. Suboptimal iron status is common in ADHD and directly limits the rate-limiting step of dopamine synthesis. This is a simple, testable, and correctable factor that is frequently overlooked.

  7. Skip the weekend “dopamine detox.” Pursue reward recalibration instead. Sustained reduction of supranormal stimuli (hyper-processed food, compulsive social media, excessive gaming) combined with regular engagement in naturally rewarding activities (exercise, creative work, meaningful social interaction) is more effective than any short-term fast.

Frequently Asked Questions

Can you boost dopamine with tyrosine supplements?

Tyrosine supplements (typically 500–2,000 mg) can increase brain tyrosine availability and have been shown to improve cognitive performance under demanding conditions, including stress, sleep deprivation, and high cognitive load (Jongkees et al., 2015). However, under resting conditions or low demand, supplemental tyrosine has limited effect because the rate-limiting enzyme, tyrosine hydroxylase, is tightly regulated by end-product inhibition. For most people eating adequate protein, supplementation is unnecessary. It may have specific utility for individuals facing acute cognitive demands — a long exam, a high-pressure workday — but it is not a substitute for consistent dietary protein intake.

Does coffee affect dopamine?

Yes. Caffeine increases dopamine signaling, primarily by blocking adenosine A2A receptors in the striatum, which has an indirect potentiating effect on D2 dopamine receptor activity (Ferre, 2008, Journal of Alzheimer’s Disease). This is one reason coffee improves alertness, mood, and motivation. The effect is moderate and does not produce the supranormal surges associated with ultra-processed food or drugs of abuse. Regular moderate coffee consumption (2–4 cups daily) is not associated with meaningful dopamine receptor downregulation and may in fact be neuroprotective, as suggested by the lower Parkinson’s disease risk consistently observed among coffee drinkers.

Is the “dopamine detox” backed by science?

The concept is partially grounded in real neuroscience — chronic overstimulation does cause receptor downregulation, and reducing supranormal stimuli can allow gradual recovery. However, the popular version overpromises and oversimplifies. Receptor recovery takes weeks to months, not 24 hours. You cannot “detox” from an essential endogenous neurotransmitter. And avoiding all pleasurable activities, including healthy ones like exercise and social connection, is counterproductive. A more accurate and effective approach is sustained “reward recalibration” — consistently reducing exposure to engineered superstimuli while maintaining engagement with naturally rewarding activities.

What is the connection between dopamine and serotonin in diet?

Tyrosine (dopamine precursor) and tryptophan (serotonin precursor) compete for the same blood-brain barrier transporter. High-protein meals tend to favor tyrosine transport (because protein foods contain more tyrosine than tryptophan), while high-carbohydrate meals favor tryptophan transport (because the insulin response drives competing amino acids into muscle, leaving proportionally more tryptophan available for brain entry). This is why a protein-rich meal can promote alertness and focus (dopamine-favoring), while a carbohydrate-heavy meal can promote relaxation and drowsiness (serotonin-favoring). A balanced meal with both protein and complex carbohydrates supports both systems without dramatically skewing either.

Should people with ADHD eat differently?

People with ADHD should prioritize the same whole-food, dopamine-supportive dietary principles described in this article — adequate protein at every meal, sufficient iron and cofactor intake, minimal ultra-processed food — but the stakes are higher because their dopaminergic system is already operating with reduced headroom. Iron status should be monitored and corrected if low. Elimination of artificial food colorings and preservatives has shown benefit in some controlled trials. These dietary strategies complement, but do not replace, evidence-based medical treatment where indicated.

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