Chapter 4. The Carbohydrate-Dopamine Cycle: Amplified by Ultraprocessed Foods

We welcome your use of this resource but please cite:

PSGRNZ (2026) Reclaiming Health: Reversal, Remission & Rewiring. Understanding & Addressing the Primary Drivers of New Zealand’s Metabolic & Mental Health Crisis. Bruning, J.R., Physicians & Scientists for Global Responsibility New Zealand. ISBN 978-1-0670678-2-3

Hyperpalatability & Food Addiction.

While people do not become addicted to protein or vegetables, a high glycaemic carbohydrate intake (especially if spread over multiple meals/snacks) results in repeated postprandial glucose spikes. These glucose spikes are associated with dopamine release, and carbohydrate consumption impacts people differently.[1] Researchers are recognising that multifactorial drivers plausibly amplify health risk:

High glycemic index carbohydrates elicit a rapid shift in blood glucose and insulin levels, akin to the pharmacokinetics of addictive substances. Akin to drugs of abuse, glucose and insulin signals in the mesolimbic system to modify dopamine concentration. Sugar elicits addiction-like craving and self-reported problem foods are rich in high glycemic index carbohydrates. These properties make high glycemic index carbohydrates plausible triggers for food addiction.[2]

Uncertainty has prevailed over whether food addiction is behaviour-based or a function of exposure to substances (i.e. a substance use disorder). [3] [4] However the association of food addiction with industrially formulated ultraprocessed food consumption provides evidence for food addiction as a substance use disorder. Many addictive agents contain formulations of substances which reinforce the addictive potential. The combination of fat and refined carbohydrates in industrially formulated ultraprocessed foods, does not exist in naturally occurring foods. These factors may drive outcomes where:

consumption of ultraprocessed foods high in both fat and refined carbohydrates (e.g., Oreo cookies, M&Ms) leads to downregulation of dopamine receptors, binge eating, and willingness to obtain these foods despite negative consequences.[5]

Naturally occurring, minimally processed foods (fruits, vegetables, nuts, milk and meat protein) have not been associated with food addiction.

Ultraprocessed foods were first formally categorised as group four under the NOVA food classification system. The NOVA system is based on extent of processing and additives in the end food product. Work is being undertaken to validate the NOVA system in countries to account for cultural differences in food products.[6] [7] [8]

Many hyper-palatable ultraprocessed foods containing unnaturally high levels of refined carbohydrates or added fats, including sweets and salty snacks are strongly implicated in the behavioural indicators of addiction.[9] They consistently contain unnaturally high doses of reinforcing ingredients that are effective at activating reward and motivation systems. These calorie-dense foods are optimised; they lack ingredients which slow the rate of absorption, water, fibre and protein. This increases the speed of uptake and impact.[10] [11]

Diets high in ultraprocessed food are associated with an increase in free sugars, total fats, and saturated fats, as well as a decrease in fibre, protein, potassium, zinc, and magnesium, and vitamins A, C, D, E, B12, and niacin.[12] The proportion of ultraprocessed food in the diet increases the likelihood that people will gain weight.[13]

In a 2025 conference presentation[14] Dr Jen Unwin described the cycle of the ultraprocessed food addiction trap:

Suppression of frontal lobe activity.
Neurons that fire together, wire together.
Damage to the mitochondria, leading to energy deficits.
Negative reinforcement: a bad feeling state is temporarily relieved.

The Yale Food Addiction Scale (YFAS) is a clinical research tool that has been developed to measure food addiction by drawing from DSM-5 criteria for substance use disorder. In 2016, the YFAS 2.0 was released to reflect changes to the substance use disorder diagnostic criteria in the Diagnostic and Statistical Manual of Mental Disorders 5 (DSM-5).[15] Ultraprocessed foods include pizza, ice-cream, white bread biscuits and potato chips have been consistently associated with YFAS indicators.

Researchers have since progressed to develop a Food Addiction Symptom Inventory (FASI), a clinician-administered assessment of food addiction. This has been adapted from the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, fifth edition modules for diagnosing substance-use disorders.[16] Work has further been undertaken to develop simpler approaches to recognise food-related emotional expectancies including addiction that may be of benefit in clinical populations with high participant burdens.[17]

Scientists and researchers have recently moved closer to agreement on this issue.

In 2025 international clinicians and academics in the field conducted a consensus exercise and concluded that the term ultra-processed food addiction (UPFA) appropriately describes the disorder.[18] The consensus statements agreed to by the majority of participants were:

There is enough evidence to justify the classification of new substance use disorder.
The disorder should be referred to as ultra-processed food addiction (UPFA).
The symptoms that comprise addiction to other substances of abuse in the DSM and ICD describe UPFA symptoms.
Given that UPFA is a substance use disorder: abstinence from a person’s ‘drug foods’ will form the mainstay of therapy.
FA exists on a continuum and can co-occur with eating disorders but is a distinct disorder.
Recognition of the disorder will lead to more research and treatment options.

Figure 5. Unwin J, Giaever H, Avena N, Kennedy C, Painschab M and LaFata EM (2025) Toward consensus: using the Delphi method to form an international expert consensus statement on ultra-processed food addiction. Front. Psychiatry

The ‘dose’ of both carbohydrate and fat appears to drive the addictive potential of an ultraprocessed food formulation. Di Feliceantonio et al. (2018) analysed neural responses to ultraprocessed foods containing fat and carbohydrate and equicaloric foods containing primarily fat or carbohydrate. The study found that reward-related activation peaked with foods high in both fats and carbohydrate, that the neural response was supra-additive, and that the effect was independent of liking.[19]

Prevalence of food addiction may more common than recognised. A recent review finding that 14% of adults and 12% of children, (a reported prevalence that is similar to alcohol addiction) struggle with refined and ultraprocessed food addiction.[20] Food addiction symptoms appear to better fit criteria for substance use disorder than behavioural addiction,[21] yet it is important to note that food addiction is higher in groups with other behavioural addictions. [22]

Individual risk factors interact with the addictive potential of a substance to determine the likelihood that a specific individual will become addicted. Individual risk factors that increase a propensity for addiction include a family history of addiction, cognitive control difficulties, trauma exposure, and depression.[23] [24]

Many groups, including children and adolescents, may struggle to limit consumption levels. A spectrum of challenges face children and adolescents if they are to reduce their dependency on high carbohydrate intakes. These not only concern the role of dopamine feedback in young minds, the prevalence of food addiction but relate to the risk of attrition. In a 12-week whole food, carbohydrate restricted dietary trial, drop-out rates were high (48%) with children’s adherence influenced, positively and negatively, by levels of support from friends and family.[25]

Current Ultraprocessed Food Intakes Associated with Poor Health Outcomes.

While carbohydrates were always in diets, ultraprocessed foods drive addictive actions which further displace nutrient dense foods. Poor diets drive mental illness risk and western populations can on average consume 50% of their diets as ultraprocessed foods which are low in bioavailable nutrients. The proportion of the diet that is ultra-processed has grown markedly:

New Zealand toddlers and pre-schoolers: Ultra-processed foods contributed to the 45% (12 months), 42% (24 months), and 51% (60 months) of energy intake to the diets of children.[26]
U.S. young people under age 19 consume on average 67% ultraprocessed food in their diet.[27]
U.S. adults consume around 60% of their diet in ultra-processed food.[28]
British children consume more than 60% of their calories as ultra-processed food.[29]
Canadian children and adolescents consumed over half their dietary calories as ultra-processed food.[30]
Australian children consume more than 42% of their calories as ultra-processed food, processed culinary ingredients (6.8% and minimally or unprocessed foods (35.4%).[31]

The addictive potential of these foods seems to present the challenge that generally accompanies dopamine-inducing technologies. For many people, stopping at a designated ‘safe’ level may not be feasible. Ultraprocessed food intakes which form more than 30% of daily calorie intake seems to increase risk.[32] While lower intakes (e.g., in the lowest quintile, often <10–20% of energy) generally serve as the reference group with no excess risk, a universal ‘safe’ threshold has not been established.

However, diets that are high in carbohydrates, even where ultraprocessed food component is less than 30% can promote repeated elevations in blood glucose levels, increasing risk for insulin resistance and T2DM. Other carbohydrate foods that are less processed, cumulatively add to the cumulative burden, increasing blood glucose and therefore triglyceride levels in the body. These can include rice, bread, pasta, starchy vegetables and fruits. The body burden of sugars and starches potentially cumulatively contribute to the potential for hyperinsulinemia and insulin resistance to present in an individual.

Current consumption levels of ultraprocessed foods are strongly associated with escalating harms which impair quality of life, well into adulthood. Most studies report a dose–response between ultra-processed food intake and adverse metabolic and mental-health outcomes. Diets high in ultraprocessed food are associated with premature mortality, inflammatory bowel diseases, impaired reproductive health and metabolic fitness, obesity, non-alcoholic fatty liver disease, wheezing, poor sleep, metabolic syndrome (including T2DM) obesity, male and female fertility and cardiovascular risks.[33] [34] [35] [36] [37] [38] [39] [40] [41] [42]

Ultraprocessed food consumption increases health risk from conception on. For example, the greater intake of ultraprocessed food in pregnancy, the increased potential for T2DM.[43]

Ultraprocessed food intakes are associated with a broad range of neuropsychiatric outcomes. Studies correlate ultraprocessed food consumption with neurodegeneration, cognitive decline, dementia, and mood disorders.[44] Eight cohort studies now demonstrate a strong association of depression with ultraprocessed food intake.[45] Increasing evidence links aggression and antisocial behaviour with a poor diet.[46]

Scientists increasingly observe associations of poor dietary intakes with anxiety,[47] obsessive compulsive disorder (OCD)[48] and conditions involving psychosis.[49]

Dietary carbohydrates may be more associated with inflammation than has been formally recognised. In a 20-year cohort study, the follow-up in 2022 identified that chronic systemic inflammation appeared to affect the CVD risk of participants who had a higher carbohydrate intake more substantially, as compared to those with low intake. [50]

Satiety, Glycaemic Volatility and the Drivers of Addictive Eating.

Unlike meals based on refined carbohydrates where food is rapidly absorbed and individuals more swiftly experience symptoms of hunger, an optimum diet will assure between-meal satiety and support the regulation of appetite. It will not elicit addiction-like cravings, and it will prevent glucose ‘lows’. These discrete differences are rarely discussed in depth, and it is possible that children and adults misinterpret or conflate homeostatic hunger (regulation of energy balance) with addictive cravings or a glucose ‘lows’.[51]

Satiety is known to be associated with the inter-meal period, through the suppression of hunger and the inhibition of further eating.

Satiation describes within-meal inhibition and can be said to determine meal size and bring a particular eating episode to an end. [52]

A glucose ‘low’, or reactive or postprandial hypoglycaemia can occur 2-5 hours after a high carbohydrate meal. Reactive hypoglycaemia is defined as: recurrent episodes of hypoglycaemia occurring after consumption of carbohydrate-containing meals.[53] Symptoms include fatigue, shakiness, irritability and cravings. This can occur independently of obesity or a T2DM diagnosis.[54] For people with T2DM, metformin alone may be insufficient. Continuous glucose monitoring (CGM) technology may help predict and prevent these events.[55]
Food addiction is recognised as a substance use disorder with ultraprocessed foods recognised as an addictive agent that triggers neurobiological and behavioural responses including loss of control, craving, withdrawal, and tolerance that are similar to other addictive substances.[56] [57]
Guidelines that provoke a glycaemic response and under-recommend protein may be particularly problematic for children and adolescents, as these groups often have underdeveloped yet hyperactive inhibitory control systems in the brain, factors that mediate motor impulsivity and dietary restraint. These issues may amplify addictive-like eating behaviours.[58] [59] [60]

People who consume high quantities of starchy carbohydrates including breakfast cereals, supermarket bread (including ‘whole-grain’ when this only forms a limited portion of the bread ingredients), white rice, and ultraprocessed food are exposed to big glucose swings, known as reactive hypoglycaemia, which people who consume a relatively small amount of starchy carbohydrates each day, who are ‘metabolically flexible’, including people who consume a ketogenic diet, do not experience.

Reactive hypoglycaemia, post-prandial hyperinsulinaemia, or exaggerated insulin secretion after high-glycaemic meals involve pancreatic ‘overshoot’ responses. Importantly, reactive hypoglycaemia can precede insulin resistance, not just result from it, can occur in people with prediabetes and may predict diabetes.[61] [62] [63]

People who shift away from starchy carbohydrate-based diets, find that these swings reduce, ketones then counter-regulate in low-intake periods, as insulin secretion becomes extremely low and steady. This may also occur over time for people who have been diagnosed with T2DM, particularly in the early years of diagnosis.

Satiety is a multifactorial concept, but nutritionally rich food and macronutrient balance are integral to achieving satiety and reducing snacking and hunger cravings between meals. Studies consistently show that higher protein foods or meals deliver better satiety than energy matched foods with lower levels of protein which inhibit appetite in the period after consumption lessen the effect of sensations of hunger on motivation and mood. The order of fat and carbohydrate is contested, but as this paper discusses elsewhere, the degree of processing of these macronutrients, and the adherence to carbohydrate levels that do not spike blood sugar may be more important than prescribed ratios.[64]

Recent papers have shed light on the differential postprandial glycaemic responses (PPGRs) to carbohydrates (including pasta, rice and bread). A small study analysed the association between carbohydrate response type and metabolic traits to demonstrate how people vary in their response. Responses were associated with the level of insulin resistance presenting in those people.[65]

A two-week continuous glucose monitoring (CGM) study in young adults showed that identical meals (varying in carbohydrate content) produced distinct PPGR patterns across individuals, linked to differences in glycaemic variability, these results were not necessarily related to BMI or age. [66]

The physio-neurological effects of sustained carbohydrate exposure, including its potential to provoke unstable satiety, glycaemic volatility, and complex, neurobiologically mediated responses may precede and accompany food addiction. These patterns are increasingly associated with the development of obesity and T2DM.

Increasing diet-related chronic conditions may not so much be a reflection of simple ‘noncompliance’ to dietary recommendations, but the fundamental unsuitability of the guidelines for a significant portion of the population.

Dietary fibre plays a key role in satiety and health maintenance, protecting colonic health, supporting gut microflora, metabolite and hormone synthesis and preventing and suppressing inflammation.[67] Fibre is thought to contribute to satiety via affect satiety in many ways, depending on the fibre type, and relating to its ability to bulk foods, increase viscosity, gel in the stomach and ferment in the gut.

However, controversy and lack of consistency in study outcomes fail to elucidate which dietary fibres most clearly confer inflammatory risk or anti-inflammatory benefit, and dietary recommendations fail to make allowance for and protect individuals from gastrointestinal disorders.[68] [69]

Personal responsibility in ‘healthy eating’ which accords to current dietary guidelines may be discordant when people consume insufficient protein and higher levels of ‘low fat’ carbohydrates which do not assure between-meal satiety. High carbohydrate dietary recommendations may dovetail with food addiction, disordered sleep patterns and lack of energy.

Figure 6. The Problem of Carbohydrate Addiction.

The language of ‘personal responsibility’ and ‘lifestyle choice’ may require revisiting if the addictive potential of ultraprocessed food is widely understood. [70]

Practitioners are not only stepping in to offer health coaching and community programmes to support individuals in navigating the addictive potential and shift away from habitual patterns of food consumption, they are publishing case studies in the scientific literature to encourage other groups to offer similar services. [71]

These can allow people to address food addiction personally in their communities. Studies show, as we discuss below, that supportive environments can assist with addictive cravings, and facilitate skills development to navigate change away from ultraprocessed food consumption.

Policies that implement advertising restrictions, improve data capture, increase access to nutritious food for lower income groups and that deter lobbying will be amplified by the integration of practitioner-led and wrap-around community-based programmes.

Chapter 5. Ethical Catastrophe: The Greater Burden on Low-Income Groups & Young People.

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