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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

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An extraordinary amount of scientific research reveals how conditions previously considered exclusively brain-related, commence as metabolic dysfunction. Metabolic dysfunction is inherent to the pathophysiology of mental illness.[1] [2] [3] [4] [5] [6] [7] [8]

The data arises from multiple levels of investigation, including cellular and mechanistic studies, case reports, cohort studies, and population-level (epidemiological) research.

High refined carbohydrate and/or ultraprocessed food diets are conventionally low in bioavailable nutrients, and the relative deficiency in these diets increases risk for cascading and overlapping metabolic, mental and immune system illnesses. Metabolic syndrome is a common correlate when these pressures converge, driving inflammation, and creating feedback loops that can overwhelm the body’s capacity to repair.

The central nervous system and the digestive tract are inter-dependent. A healthy microbiome is essential to optimise bi-directional neuroendocrine signalling, for sensory-motor reflexes, immune activation, gut brain cross-talk and hormonal signalling. [9] [10]

Biomarker studies have tracked relationships between diet quality, metabolic health, and risks for mental disorders including anxiety, depression, addiction and suicidality.[11] Risk factors can overlap, amplifying conditions or increasing the severity of symptoms and diseases.

Inadequate intake, systemic diseases, medical therapies, and genetic conditions can lead to deficiencies of specific nutrients, affecting both the central and peripheral nervous systems.[12]

Figure 4. Mayer EA, Nance K, Chen S. (2022). The Gut–Brain Axis. Annual Review of Medicine.

When these factors overlap and the stressors accrue over years and decades, brain function can be severely impacted. In a book on mental health and mitochondrial function, Harvard-based Chris Palmer has argued that:

mental symptoms are like the canary in the coal mine: they are sometimes the first indication of metabolic and mitochondrial failure.[13]

People with psychiatric diagnoses are rarely diagnosed with a single condition.

Multimorbidity is common in those with mental illness, and further deterioration of mental health, reduced quality of life, and premature mortality have been reported in those with multiple disorders.[14]

Symptoms of mental illnesses can overlap. Therefore, one person may be diagnosed for multiple brain disorders and receive prescriptions for multiple psychiatric medications.[15]

For example, while patients with schizophrenia die 20 years earlier than healthy populations, the mortality risk is predominantly associated with cardiovascular risks. As this paper will discuss below, treatment for individuals with major depressive disorder, bipolar disorder, and schizoaffective disorder can include metabolic and low-carbohydrate approaches.[16] [17] [18] [19] [20] [21]

The under-25 age group may be most severely affected. There is a:

‘greater burden of physical multimorbidity in people with severe mental illness compared with those without is higher for younger cohorts, reflecting a need for earlier intervention.[22]

Once a person is diagnosed with metabolic and psychiatric conditions, they will be prescribed a range of medical drugs for these conditions. The drugs may produce a range of side effects, which can necessitate additive prescriptions for other drugs. The drugs can also deplete the gut microbiome, which can create further disorder. Multiple drug regimens, or polypharmacy has substantially increased in recent decades.

In the US, for example, the prevalence of polypharmacy among adults aged 65 and older increased from 13% in 1998 to 43% in 2014,2425 with the most recent estimates from 2017-2018 at 45%.This increase was driven in particular by the growing use of cardioprotective and antidepressant drug treatments, and the highest prevalence of polypharmacy is seen among populations with heart disease.[23]

The gut-brain connection.

An impaired gut microbiome can produce cascading, interrelated metabolic and mental health outcomes.

Diet is a foundational factor in shaping the gut microbiota, influencing its composition, diversity, and functionality, which in turn affects a wide range of health outcomes through complex microbial-host interactions.[24]

Diet plays a central role in sustaining a healthy gut-brain-axis, the complex neuro-immuno-endocrine signalling pathway[25] that is fundamental for sustaining good mental health.[26]

Communication within this system is nonlinear, is bidirectional with multiple feedback loops, and likely involves interactions between different channels.[27]

Human bodies are complex and there are myriad ways poor diets and insufficient vitamin and mineral levels can affect brain function and mental health over time. Brain fog is associated with elevated glucose levels and gluten sensitivity.[28] Refined food diets and chemical exposures, genetic, and epigenetic stressors can increase risk for digestive disorders and impair nutrient processing and the synthesis of hormones, impair sleep patterns, cortisol regulation and promote fatigue and brain fog.

Key factors which contribute to inflammation and health decline include the following:

Insulin resistance (IR) which plays a crucial role in the development and progression of metabolism-related diseases including diabetes, hypertension, tumours, and non-alcoholic fatty liver disease.[29]
Frequent consumption of ultraprocessed foods that increase risk for insulin resistance.[30]
Gluten-heavy diets that can impair digestive tract function and result in a cascade of events which include symptoms which fit the criteria for many mental illnesses.[31] [32] [33]
Increasing burdens of synthetic chemicals that have toxic effects, which can be at higher levels in refined and ultraprocessed foods, including synthetically refined ingredients and additives, microplastics from packaging, and increasing use of pesticides in staple food crops.[34]
The inflammatory potential of chemically refined vegetable oils.[35] [36]
Suppression of ketone bodies which have anti-oxidative, anti-inflammatory, mitochondrial, neurological and cardio-protective features.[37] [38] [39]
Lower than optimum (insufficient) intakes of micronutrients which are physiologically indispensable for metabolic and/or immunological and/or physiological health, including mental health.

Mitochondria play a central role in metabolic function, and the systematic impact of metabolic stress can be observed at a microscopic level in the mitochondria.[40] Psychiatrists diagnose mental illness based on overactive, underactive or absent brain functions. However, the dysregulation of the mitochondria can drive these symptoms. Five distinct cellular processes are involved, whereby cells can either become overactive, underactive, abnormal, defunct or dead, or unable to function correctly and in disrepair. [41]

A spectrum of related processes such as chronic inflammation, altered gut integrity and dysbiosis, and dysregulation of the HPA axis (the body’s stress response system) can negatively affect metabolic homeostasis and mitochondrial function. They are all associated with risk for a psychiatric diagnosis. This includes impaired sleep and cortisol production.[42] [43] [44]

There is strong evidence that many if not most of the classic symptoms of depression[45] can be associated with a poor diet, metabolic syndrome and poor digestive tract functioning.[46] [47] [48] [49]

PSGRNZ do not downplay or underestimate the role of chronic stress, trauma and grief in driving temporary (ranging from weeks to years) poor mental health but instead draw attention to factors which may lead to a shortening, a reduction or reversal in the symptoms experienced by the person who is suffering. Evaluations of the role of higher-dose nutrients in times of trauma and stress, to identify whether people had improved outcomes, were more resilient and recovered more swiftly have been undertaken.

Following natural disasters of earthquake (Christchurch, Aotearoa/New Zealand, 2010–11) and flood (Calgary, Canada, 2013), controlled research showed statistically and clinically significant reductions in psychological distress for survivors who consumed minerals and vitamins (micronutrients) in the following months.[50]

Accumulation of toxins in the brain may also alter brain function. For example, people with autism spectrum disorder appear to have difficulty regulating mitochondria-related processes of apoptosis, which leads impaired autophagy. This can increase risk for an accumulation of toxic products in the brains of individuals with autism.[51]

Poor sleep can be associated with inadequate nutrition and high intakes of ultraprocessed food is associated with poor sleep-related outcomes.[52] [53] Sleep cycles play a key role in eliminating neurotoxic metabolites, waste products, that without clearing could contribute to dementia and poor brain health. Poor sleep cycles may lead to a reduction in the brain’s capacity to clear toxic waste, creating negative feedback loops that further impair mental health.[54] [55]

New Zealand government officials do not undertake this work that deepens public information and general practitioner knowledge on the relationship between nutrition and brain health. [56] [57] [58] Without an official effort review the scientific literature and update agency staff, nutrients critical for health can be poorly and incorrectly categorised due to out-dated legacy perspectives.

Introducing Nutritional Psychiatry.

Nutritional psychiatry is a growing sub-specialty of psychiatry. Mechanistic, observational and interventional data increasingly demonstrates that diet is a modifiable risk factor for mental illness.[59] Studies researching nutrition and psychiatry have exploded in the past 15 years.[60]

‘nutritional psychiatry encompasses the study of dietary and nutrient-based interventions for the prevention or treatment of mental disorders. The concept of nutraceuticals refers to non-toxic dietary extracts or supplements with scientifically validated benefits for promoting health and aiding in disease management.’[61]

PSGRNZ emphasise that psychotherapy, connection and support play an integral part of healing and management of brain and mind-related challenges. Human connection is central to the healthy functioning of all of us. The greater outcome from psychotherapy, friendship and community engagement includes deeper self-understanding, enhanced self-agency, and greater social engagement. [62]

Nutritional psychiatry which integrates nutritional and dietary changes, complements traditional psychotherapy, may play a key role for people who are treatment resistant and may assist with recovery. Dietary modifications may be an underutilised tool for people diagnosed with a psychiatric condition.[63]

An established and increasing scientific literature demonstrates that metabolic disruption and subclinical nutrient deficiency is a precursor and a companion to a wide range of metabolic and mental illness.[64] [65] [66] Deficiency across a spectrum of micronutrients, can follow months and years of inadequate intakes.[67] Studies consistently show that nutrient insufficiency is common in people with diagnosed with many brain-related conditions including depression and anxiety[68] [69] [70] and ADHD.[71] [72]

It is rarely one nutrient that bodies are missing and treatments with individual nutrients may result in inconsistent trial results. evidence is growing that dietary change and micronutrient supplementation which broadly raises nutrient intake levels may be more effective.[73] [74] [75]

Once ill, people are more likely to be diagnosed with multiple health conditions. Exposure to stressors such as trauma, can further promote systemic inflammation and disease risk, producing cascading harms for an individual.

Dietary shift exerts overlapping complex effects which can improve and repair gut microbiome function, lower the inflammatory burden, and increase nutrient intake. Practitioners in the field of metabolic and psychiatric nutrition, adopt a spectrum of flexible approaches that revolve around reducing carbohydrate intakes to reduce, mitigate and eliminate the markers of poor metabolic health which frequently underlie poor brain health. The approach necessarily involves psychological, behavioural and practical skills coaching.

Therefore, when people reduce ultraprocessed food intakes, glucose and gluten burdens, and shift to wholefood diets that are low in refined and chemically synthesised ingredients, reversal of multiple clinical parameters can occur. Dietary changes can include the elimination of foods that may play a triggering or mediating role in many chronic symptoms and conditions.[76] Biomarker testing, case studies and trials consistently report multiple positive outcomes across multiple clinical parameters.

Low-carbohydrate diets can upregulate endogenous ketone body production by shifting the metabolism toward increased fat oxidation. This may be a key mechanism underpinning many of the observed improvements in metabolic and mental functioning. Ketone bodies are produced when the body shifts from using glucose to mobilising stored fat for energy, have been consistently shown to provide important benefits for brain function and health.

From birth, humans are physiologically adapted to tolerate periods of fasting and food scarcity, and can flexibly transition into a state of nutritional ketosis when carbohydrate availability is low.[77]

Ketone bodies may be produced naturally by the body or provided through external supplements. Growing research is revealing how these molecules influence metabolism and brain function, making their therapeutic potential an exciting and fast-moving area of science. [78] [79] [80] [81] [82]

Ketone bodies not only function as fuel, but also as signalling metabolites with applications in health and disease. Scientists and clinicians are therefore regarding exogenous sources of ketone bodies, such as through infusion of beta-hydroxybutyrate (BHB), as a potential therapeutic treatment to reduce blood glucose, and improve performance, endurance/resilience and health outcomes. [83] A recent review found that dosing regimens of BHB produced more consistent results in healthy than non-healthy populations.[84] [85] [86]

Much of the early work in psychiatric nutrition was undertaken in an effort to improve health outcomes of treatment-resistant patients. For example, psychiatrist Georgia Ede’s approach was adopted after a French colleague, Dr Albert Danan, conducted a trial on 35 treatment resistant patients who were diagnosed with major depression, bipolar disorder (schizoaffective disorder). Patients were placed on a close supervision ketogenic diet. All were on multiple psychiatric medications, and all had been previously hospitalised. Many of the treatment resistant patients had high blood glucose, high blood pressure, high triglycerides and obesity and many could not work due to the psychiatric disability.[87]

By week three the 28 of the original 35 began improving metabolically and psychiatrically.
23 people with depression symptoms experienced substantial improvements in mood.
All 10 people with schizoaffective disorder experienced substantial reduction in psychosis symptoms.
12 people (44%) achieved full clinical remission.
18 people substantially reduced psychiatric medication.
All but one lost weight.

Danan’s diet protocol was adapted from a protocol developed by a Dr Eric Westman at Duke University.[88] [89] The diet consisted almost exclusively of meat, seafood, poultry, eggs, vegetables, nuts and cheese and was well tolerated by the patients.[90]

Multiple disease or symptom parameters (and multimorbidity) can regress, following a dietary shift.[91] [92] In a case of a 38-year-old female diagnosed with post-traumatic stress disorder, ADHD, binge eating disorder, bipolar II disorder, depression, anxiety, and premenstrual dysphoric disorder was placed on an insulin lowering ketogenic diet.:

By week 12, all psychiatric symptoms resolved evidenced by quantitative reductions to 0 across all validated instruments. The patient consistently reported optimal symptom control when blood ketone levels were maintained between 3 and 5 mmol/L. Qualitative reports substantiated marked functional gains, including improved occupational engagement and social functioning.[93]

The case above highlights the complex interplay between trauma, addictive behaviours and eating disorders. Diets high in rapidly absorbed carbohydrates can trigger sharp dopaminergic responses via mesolimbic reward pathways, while simultaneously driving spikes and crashes in blood glucose and insulin. Micronutrient insufficiency may play a significant role, particularly in younger adults.[94] [95] This combination of nutrient insufficiency, transient reward, followed by metabolic depletion and dysphoria, may heighten sensations of emptiness and reinforce repetitive seeking of the same foods. Compounding this, the widespread belief that dietary fat drives body fat can lead to unhealthy suppression of this essential macronutrient class, undermining satiety and further destabilising eating patterns. Vegetarianism may also be more commonly represented in eating disorder groups with the fat and protein intake under-represented.[96] Eating disorder literature rarely addresses the role of healthy saturated fats and proteins in supporting a return to adequate micronutrient status and in cutting short the addictive dopaminergic cycle.

When layered onto sociocultural pressures around body shape and health, pressures that disproportionately affect women, media influence and media, and the expansion of psychiatric categories, these interacting cultural, neurochemical, metabolic and psychosocial mechanisms may contribute meaningfully to the emerging pattern of eating-disorder vulnerability.[97] Low-carbohydrate and ketogenic diet researchers and clinicians have stepped into this field of research, with some success.[98] [99]

A cautionary approach is warranted. The person in the case study above carries a spectrum of risks and could revert to earlier dietary patterns and psychosis, or alternatively, the person may remain stable for the foreseeable future. Care involves navigation over time and people can be medication-supported and nutrition-supported and can taper off to drug-free states.

Nutritional psychiatry is stepping into the treatment void for many people who may choose not to take psychiatric drugs, and can address therapeutic gaps where people have found that conventional medical treatment has not suppressed symptoms (treatment failure), or where they have found adverse effects to be intolerable.

Are Symptoms of Inadequate Nutrition Misclassified as Psychiatric Disorders?

Psychiatric nutrition is a companion partner to conventional psychotherapy because nutrition enhances physiological health. Many of the ‘classic’ symptoms used to diagnose a psychiatric condition may have arisen due to insufficient nutrition or inadequate nutrient absorption over time, and poor mitochondrial (and cellular) health.

Many of the symptoms of depression[100], anxiety[101] and ADHD[102] that are listed in the Diagnostic and Statistical Manual of Mental Disorders[103], and that lead to a diagnosis and subsequent prescription, can be similarly attributable to dietary inadequacy, nutritional deficiencies and poor digestion.

The role of dietary nutrition in protecting from many of the symptoms of depression, including fatigue, insomnia, brain fog, is now well established.

Depressed mood.
Markedly diminished interest or pleasure in most or all activities.
Poor appetite, weight loss, or weight gain.
Insomnia or hypersomnia.
Slowing down of mental or physical activities (for example, sluggishness or diminished hand-eye coordination.
Fatigue or loss of energy.
Feelings of worthlessness or excessive or inappropriate guilt.
Diminished ability to think or concentrate ("brain fog"), or indecisiveness.
Recurrent thoughts of death; thinking about, planning, or attempting suicide.

Many of these categories might simply reflect inadequate nutrient intakes by age and/or gender, a differently functioning brain, a brain where discrete developmental periods mature at different stages (such as due to brain hemisphere differentiation) and/or deficiency in nutrients required for concentration and focus. These factors depend on complex interrelationships between diet, digestion, physical and social environmental exposures, genetics and methylation capacity.

Exercise is critical for optimum health, retention of healthy muscle and is associated with better mental health. However, fatigue, sleep loss, inadequate protein uptake and inadequate nutrition are often not factored in when people are urged to exercise. Over years, inadequate nutrition, although ’healthy’ may result in fatigue in groups that have nutrient requirements that are greater than, or that diverge from, current guideline recommendations.

The pathways, mechanisms and evidence of reversal following dietary shifts provide a compelling body of evidence that nutrition can be, and for some psychiatrists, already is, a first line treatment. [104] [105] [106] Results from trials show that people with major depressive disorder can be helped by making dietary changes, and ketogenic diets may provide one such pathway.[107]

Childhood and adolescent behaviour that is considered non-normative and behaviourally different, when teachers and practitioners clinically diagnose the behaviour of ADHD, sets that child on a path where medical treatment and behavioural strategies are first line treatments, and nutritional status is a minor order issue. The diagnostic criterion for ADHD is difficult to navigate [108] and ambiguous, and the quantity of criteria that are established to confirm an ADHD diagnosis has been arbitrary and flexible.[109]

Proportionately, these issues are not judged as equivalent factors, and there is a knowledge vacuum on the nutrition ‘side’ while the path is smoothed on the ‘medicalisation’ side. I.e. access to prescription drugs following a diagnosis of poor brain/mental health is non-controversial, but dietary changes to reverse or mitigate a brain-related syndrome or diagnosis is much more controversial.

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

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[65] Sarris J, Logan AC, Akbaraly TN. et al. (2015). Nutritional medicine as mainstream in psychiatry. The Lancet Psychiatry, 2(3):271 – 274.

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[69] Kris-Etherton PM, Petersen KS, Hibbeln JR (2025). Nutrition and behavioral health disorders: depression and Anxiety. Nutrition Reviews 79(3):247–260. DOI: 10.1093/nutrit/nuaa025.

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[72] Ryu SA, Choi YJ, An H, et al. (2022) Associations between Dietary Intake and Attention Deficit Hyperactivity Disorder (ADHD) Scores by Repeated Measurements in School-Age Children. Nutrients 2022, 14, 2919. DOI:10.3390/nu14142919

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[82] Kolb, H., Kempf, K., Röhling, M. et al. (2021) Ketone bodies: from enemy to friend and guardian angel. BMC Med 19:313. DOI: 10.1186/s12916-021-02185-0

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[84] Storoschuk KL, Wood TR, Stubbs BJ. (2023). A systematic review and meta-regression of exogenous ketone infusion rates and resulting ketosis—A tool for clinicians and researchers. Front. Physiol. 14:2023. DOI: 10.3389/fphys.2023.1202186

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RETURN TO CONTENTS PAGE.

This Reclaiming Health paper places a strong emphasis on cumulative carbohydrate burdens, because a growing body of international scientific and clinical literature identifies excess dietary carbohydrate intake of moderately processed and refined carbohydrates as a central driver of metabolic syndrome. Strong evidence suggests that this pattern has been reinforced by dietary guidelines that have historically encouraged carbohydrate consumption while understating the role of healthy fats and proteins.

As outlined in the Reform section, a key opportunity lies in recalibrating dietary guidelines to bring fats and proteins back into public view, alongside the integration of health coaching and substantial reinvestment in nutrition education. This would represent a shift away from guideline frameworks primarily designed to prevent nutrient deficiency toward approaches which may support satiety, appetite regulation, and metabolic stability, optimise metabolic health across the life course, and reduce risk for obesity.

Importantly, the paper does not argue that obesity is driven exclusively by carbohydrate intake. Excess energy consumption can and does contribute to weight gain. Rather, Reclaiming Health situates carbohydrate exposure within a broader scientific landscape. Multiple models seek to explain obesity pathogenesis. These include the energy balance model (EBM), the carbohydrate-insulin model (CIM), [1] and the more recently articulated REDOX model. [2] Taken together, the EBM, CIM and REDOX models offer complementary insights into the pathophysiology of obesity, rather than mutually exclusive explanations.

The EBM posits that changes in food environments, particularly the widespread availability and aggressive marketing of inexpensive, energy-dense, ultra-processed, and highly palatable foods, have driven obesity by increasing consumption beyond physiological energy requirements. Foods that are low in fibre and protein and offered in large portion sizes are thought to disrupt neural satiety signalling. The EBM highlights that external food-related cues, and the properties of the foods themselves, disrupt healthy neural signalling, and result in excess consumption and promoting excess accumulation of body fat. [3]

By contrast, the carbohydrate–insulin model (CIM) of obesity centres on the metabolic consequences of diets that are predominantly high in refined, rapidly digestible carbohydrate-containing foods, including fructose rich foods and beverages. This model proposes that such diets alter fuel partitioning, directing energy substrates away from oxidation and toward storage in adipose and other tissues, thereby promoting fat accumulation even in the absence of overt caloric excess.[4]

The REDOX model adds a further layer of explanation, proposing that obesity may arise from disturbances in cellular and systemic redox balance. Altered oxidation–reduction signalling can disrupt metabolic and hormonal regulation, interfere with insulin action and energy sensing, and impair adipose tissue function. In this framework, obesity emerges from perturbed signalling and feedback mechanisms shaped by environmental, dietary, and metabolic exposures, rather than from caloric excess alone. [5]

PSGRNZ’s emphasis on the carbohydrate-insulin model is not driven solely by obesity pathophysiology, but by the breadth of evidence linking excess carbohydrate intake to elevated insulin, triglycerides, blood pressure, and adverse mental-health outcomes. Accordingly, Reclaiming Health differs from conventional approaches by drawing on mechanistic studies alongside case series, cohort data, and real-world clinical evidence to illustrate the multifactorial nature of metabolic and mental ill-health. Obesity may precede the other markers of metabolic syndrome, but in many cases, the other markers precede obesity.

The paper also highlights an under-examined dimension: addictive eating patterns associated with cumulative refined carbohydrate exposure, including but not limited to ultra-processed foods. These patterns contribute substantially to non-adherence to dietary guidelines, often precede metabolic syndrome and obesity, yet remain poorly integrated into academic and policy frameworks. While fats and proteins have been progressively marginalised within dietary guidance, the EBM model of obesity offers limited insight into how individuals might sustainably manage hunger and satiety through caloric restriction, particularly in the presence of glycaemic volatility and reward-driven, addictive eating behaviours.

While there is sound scientific evidence supporting greater regulation of sugar, defaulting to an exclusive focus on ultra-processed foods (UPFs) as a discrete regulatory target risks creating a political quagmire, as not all UPFs are addictive.

As such, many of the recommendations for reform, outlined in Chapter 12, extend well beyond an individual-level approach. The proposed pathways for reform are intended to improve key metabolic parameters that increase risk across a spectrum of metabolic and mental health conditions. Evidence examined in the paper suggests that the approaches set out in the Reform section can deliver substantial metabolic and health benefits, again with particularly strong effects in lower-income populations.

PSGRNZ’s recommendations involve structural changes designed to support dietary transition across New Zealand. The evidence reviewed indicates that these approaches deliver significant gains, particularly among lower-income groups.

The Carbohydrate-Insulin Model.

Nearly two billion people worldwide are now overweight or obese. [6] The conventional understanding holds that obesity drives type 2 diabetes mellitus (T2DM), and that together, these conditions set off a cascade of risks for a striking array of diseases and syndromes. In practice, insulin resistance develops first in obese and non-obese people. Beta cells are then unable to compensate.[7] However, as New Zealand doctors reversing diabetes have found, beta cell ‘relative’ failure is rare. Their experience aligns with other research which shows that pancreatic beta cell function and insulin secretion improves with dietary shifts.[8]

When eaten in quantities that exceed immediate energy demands and glycogen storage capacity, starchy carbohydrates are readily converted into body fat, fuelling weight gain and metabolic strain. An increasing range of randomised control trials support the suggestion that reductions in carbohydrate rather than low-fat intakes, may be more strongly associated with weight loss and reduction in risk for obesity.[9]

Dietary carbohydrates include sugars and starches, both of which are ultimately broken down in the digestive tract by enzymes into their simplest form, glucose. Starches vary in their digestibility: they may be rapidly digestible, slowly digestible, or resistant to digestion, and their characteristics can be significantly altered by domestic cooking methods and industrial processing. As with sugars, excessive consumption of rapidly digestible starches is associated with adverse health outcomes. Understanding differences in starch digestibility, and how quickly blood glucose levels rise after consuming starchy foods, is an important aspect of public health.[10]

The resultant glucose is absorbed into the bloodstream, raising blood sugar levels (reflected in HbA1c over time). In response, the pancreas releases insulin, a hormone that signals cells to take up glucose for immediate use or storage. Muscle and other body tissues use glucose as a rapid fuel source, particularly during physical activity, while liver and muscle cells store excess glucose as glycogen, a compact and readily mobilised energy reserve.

However, the body’s glycogen storage capacity is limited. Once these reserves are full, continued high glucose availability, especially from carbohydrate-based meals and snacks, triggers the liver to convert excess glucose into fatty acids through a process known as de novo lipogenesis (DNL). These fatty acids are combined with glycerol to form triglycerides, which are packaged by the liver into very-low-density lipoproteins (VLDL) and released into the bloodstream for transport as energy.

Triglycerides in the bloodstream are a normal component of metabolism, serving as a transport form of fat for energy use or storage. After a meal, dietary fats are absorbed by intestinal cells and packaged into chylomicrons, large, triglyceride-rich lipoprotein particles that enter the circulation via the lymphatic system. At the same time, the liver produces VLDL to carry triglycerides synthesised from excess carbohydrate or protein. These particles circulate through the bloodstream, where triglycerides may be delivered to adipose tissue for long-term storage as body fat or utilised by muscle tissue as an alternative energy source when required.[11] [12] [13] [14]

Summary papers addressing the physiological role of VLDL are scarce. Normal physiological function is typically treated as background knowledge and not considered worthy of synthesis. Journals, funding bodies, and regulators have historically prioritised disease endpoints, hazard identification, and modifiable risk factors. In physiological terms, VLDL secretion is a normal and essential hepatic function that protects hepatocytes from lipid overload, distributes endogenously synthesised energy substrates to peripheral tissues, and supports cellular membrane integrity and mitochondrial function; pathology arises primarily from chronic dysregulation of VLDL production and clearance rather than from VLDL itself.

VLDL is upstream of low-density lipoproteins (LDL). LDL is largely a metabolic product of VLDL following triglyceride removal. LDL play important physiological roles that are often downplayed. The primary cargo of LDL is cholesterol, and its principal physiological function is to deliver cholesterol for incorporation into cell membranes, synthesis of steroid hormones and bile acids, and support of myelin and synaptic function. There is no fixed biological amount of cholesterol per LDL particle and LDL particles vary widely in size and cholesterol content. An excess LDL burden will often reflect upstream VLDL dysregulation rather than a primary cholesterol excess.

The physiological roles of VLDL and LDL described here are foundational to lipid biochemistry and human metabolism and are widely accepted in the scientific literature; however, contemporary reviews overwhelmingly frame these lipoproteins through disease-risk paradigms rather than synthesising their normal biological functions.

Both injected insulin and pancreas-derived insulin promote the transport of triglycerides from the bloodstream into tissues, predominantly adipose tissue, even when the original dietary source is carbohydrate rather than fat. The precise mechanisms remain incompletely understood.

Insulin, the master regulator of energy metabolism, is central to this process. Insulin not only lowers blood glucose by facilitating its uptake, insulin also promotes fat storage by encouraging triglyceride uptake into fat cells, inhibiting fat breakdown. Under healthy conditions, this clearance is efficient, and triglyceride-rich lipoproteins do not remain elevated for long.

Over time, consistently high carbohydrate intakes, particularly from refined, high-glycaemic sources, can lead to chronically elevated compensatory insulin levels (hyperinsulinaemia), increased circulating triglycerides, and progressive fat accumulation. If carbohydrate intake (and thus hyperinsulinaemia) is not meaningfully reduced, this process can continue until pancreatic insulin secretion becomes impaired, resulting in persistently elevated blood glucose (HbA1c) and triglyceride levels.

As circulating triglyceride concentrations rise, the risk and severity of poorly controlled type 2 diabetes mellitus (T2DM) increase, alongside heightened risk of atherosclerotic disease, arterial occlusion, and myocardial infarction.[15] [16] Scientists have increasingly questioned the marginal benefits of many cholesterol-lowering drugs when cholesterol is treated as a surrogate marker for cardiovascular disease (CVD). In contrast, sustained elevations in blood glucose and insulin typically precede, and contribute to, rising triglyceride concentrations, increasing risk for both CVD and diabetes.[17]

A substantial and growing body of research indicates that glycaemic instability, insulin resistance, compensatory hyperinsulinemia, and associated low-grade inflammation underpin much of the contemporary burden of chronic disease. Together, these processes drive progressive metabolic dysfunction and neurodegeneration, limiting the ability of individuals and families to achieve and sustain optimal health. Pathophysiological injury begins at the mitochondrial level, where impaired mitochondrial function disrupts cellular energy production, increases oxidative stress, and propagates metabolic dysfunction across insulin-sensitive tissues.[18]

Genome-wide association studies have indicated that more than 65 genes are associated with an elevated risk of T2DM. These genes are involved in regulating the metabolic pathways of glucose homeostasis, insulin signalling, and sensitivity.[19] Generic dietary recommendations may be unsuitable for people with these genes, and such groups may benefit from dietary approaches that shield them from over-consumption of refined carbohydrates.

Some people (for example many South Asian populations) develop type 2 diabetes mellitus (T2DM) at a lower body mass index (BMI) and at lower levels of apparent adiposity than other groups.[20] People differ (including by ancestry) in how much subcutaneous fat they can safely store before ‘spillover’ to liver, pancreas, and muscle (ectopic fat) drives insulin resistance.[21] [22] [23]

When modern diets high in refined carbohydrates intersect with these biological differences, the tipping point into metabolic disease can be reached more rapidly. Health scholars have proposed that cutoff values for BMI may need to be revised to due to the risk that the current recommendations for obesity under-recognise the risk of developing T2DM in minority ethnic populations.[24]

Complementary interventions alongside dietary changes may further support the lowering of blood glucose. Dr Alpana Shukla has led trials on meal sequencing (also called food order, carbohydrate-last eating, or nutrient pre-loading) to control post-prandial blood glucose and insulin responses.[25] Time restricted eating (or fasting) in conjunction with a low carbohydrate diet is increasingly supported by studies[26] [27] [28], however, consideration needs to be given to the challenges inherent in transitioning to a fasted state and the intersecting challenge of food addiction (discussed in later chapters).

These processes also exert a distinct intergenerational impact. Infants born to mothers with T2DM or elevated insulin levels during pregnancy are more likely to be large for gestational age and to have increased adiposity at birth. Excess maternal glucose readily crosses the placenta, stimulating the foetal pancreas to increase insulin secretion. In the foetus, insulin functions as a potent growth factor, promoting accelerated growth and increased fat deposition. Although maternal insulin itself does not cross the placenta, maternal insulin resistance enhances placental transfer of glucose and lipids, indirectly driving foetal hyperinsulinaemia and adiposity, effectively acting as a metabolic amplifier across generations.[29] [30] [31]

An increasing range of studies, from mechanistic and biomarker studies to case studies and trials provide firm scientific evidence for carbohydrates as a primary driver of obesity and metabolic disease via this insulin pathway, rather than the historic consensus position that calorific consumption is the primary driver of obesity.[32] [33] A simple focus on calorie restriction may not be the most effective approach for reducing risk parameters when the carbohydrate-insulin pathway is taken into consideration.[34] Relatedly, most calorie-related research and policy does not address craving and food-addiction-related issues and the role of satiety and the regulation of appetite, when addressing dietary behaviour and health.

Insulin resistance is not driven by excess carbohydrate intake alone. Factors such as chronic stress, elevated cortisol and epinephrine, inadequate or disrupted sleep, exposure to environmental chemicals, and certain medications can contribute to the development of insulin resistance.

Metabolic Syndrome & Type Two Diabetes Mellitus (T2DM).

A growing scientific literature consistently associates insulin resistance and hyperinsulinaemia with a range of conditions that are increasingly prevalent in modern societies, including type 2 diabetes mellitus, cardiovascular disease, cellular senescence and cancer[35], and neurodegenerative diseases. [36] [37] [38] [39]
Metabolic syndrome describes a cluster of interrelated conditions: including hypertension, dyslipidaemia, obesity, type 2 diabetes mellitus, and chronic inflammation, that share common underlying mechanisms. The carbohydrate–insulin pathway represents a central mechanistic axis influencing the development and progression of metabolic syndrome.

Figure 2. Fazio S, Fazio V, Affuso F. The link between insulin resistance, hyperinsulinemia and increased mortality risk. Academia.

Hyperinsulinaemia, insulin resistance, and impaired metabolic function often precede a broad spectrum of inflammatory, metabolic, and brain-related conditions, contributing to microvascular dysfunction and increasing the risk of cardiovascular disease[40], cancer, visual impairment[41] [42] [43], neurodegeneration[44], and premature mortality. [45] [46] [47] Clinical features commonly associated with insulin resistance include acanthosis nigricans, metabolic-associated fatty liver disease (MAFLD), hyperandrogenism in females, and polycystic ovary syndrome (PCOS).[48]

People consuming diets high in sugars, refined carbohydrates, and ultra-processed foods are at increased risk of developing overlapping features of metabolic syndrome alongside a range of brain-related conditions.[49] [50] [51] An appreciation of the carbohydrate–insulin pathway helps explain why carbohydrate quality, quantity, and timing are critical not only for glycaemic control, but also for lipid regulation, adiposity, and overall metabolic health. [52] [53] [54]

T2DM is diagnosed when HbA1c is ≥ 50 mmol/L or fasting glucose is ≥ 7 mmol/L in repeated tests. Prediabetes is diagnosed when HbA1c is between 41 – 49 mmol/mol or fasting glucose 6.1 – 6.9 mmol/L or 2-hour glucose on GTT 7.8 – 11 mmol/L. [55] People with type 1 diabetes mellitus (T1DM) must contend with a pancreas that does not work, i.e. secrete insulin.

T2DM constitutes up to 96% of diabetes cases globally. A 2021 The Lancet analysis reported that more than 90% of the age-standardised diabetes prevalence rate across major regions was due to type 2 diabetes.[56]

T2DM is increasing in prevalence. Current New Zealand data on diabetes is based on estimates held with the Virtual Diabetes Register (VDR). In 2024, about 348,500 people were estimated to have diabetes in Aotearoa New Zealand. The estimated age-standardised prevalence of diabetes has increased from 36.6 (in 2013) to 47.0 per 1000 population, with the highest prevalence in Pasifika (137.2 per 1000 Pasifika population), Indian (103.6 per 1000 Indian population) and Māori (82.4 per 1000 Māori population) communities.[57] The register does not discern between T1DM and T2DM, nor does it disclose shifts in prevalence by age group over time.

It is that thought that the prevalence of diabetes has been increasing by 7% per year.[58] A 2025 paper calculated that:

Aotearoa New Zealand will experience a significant increase in the absolute volume of prevalent diabetes, rising by nearly 90% to more than 500,000 by 2044. The age-standardised prevalence of diabetes will increase from around 3.9% of the population (268,248) to 5.0% overall (502,358). The prevalence and volume of diabetes diagnoses will increase most drastically for Pacific peoples, most notably Pacific females for whom diabetes prevalence is projected to increase to 17% of the population by 2044.[59]

The current annual cost of T2DM in New Zealand is estimated to be $2.1 billion. PWC calculated that the annual cost would increase by 63% to $3.5 billion in the next 20 years.[60] PWC drew attention to the additive costs of a diagnosis in youth:

the personal and economic impact of the disease is most detrimental when a person is diagnosed early in life. When comparing the lifetime cost of someone diagnosed with type 2 diabetes at age 25 years ($565k) to the lifetime cost of someone diagnosed at age 75 years ($44k), the cost differential is $521k or a factor of 13. This is significant given the shift towards younger cohorts of New Zealanders developing type 2 diabetes. [61]

Coronary Artery / Heart Disease Risk.

Cardiovascular risk is only one aspect of the broader metabolic risk landscape. Coronary artery disease (a form of cardiovascular disease) occurs when these processes take place within the coronary arteries supplying the heart.

A diagnosis of T2DM represents the tip of a ‘risk iceberg’, signalling a spectrum of disease risks that stem from chronically elevated HbA1c and triglyceride levels, including vascular, renal, hepatic, and neurological complications. An increasing range of studies consistently demonstrate that carbohydrate restrictive diets improve cardiovascular health, reducing triglyceride levels, blood pressure and other inflammatory markers.[62]

A high triglyceride-to-high-density lipoprotein ratio predicts cardiovascular risk and is a recognised surrogate marker of insulin resistance. This ratio often improves rapidly with carbohydrate reduction. By contrast, low-density lipoprotein cholesterol (LDL-C), the cholesterol content within LDL particles, does not reliably reflect cardiometabolic risk in isolation and may poorly predict cardiovascular disease in the presence of insulin resistance and metabolic dysfunction. Individuals with identical LDL-C values can have markedly different particle numbers and risk profiles, which helps explain why LDL-C often tracks poorly with outcomes when insulin resistance and inflammation are present.

Cardiac problems arise when triglycerides remain chronically elevated due to excessive production (often from high carbohydrate diets, insulin resistance, or liver overactivity) or impaired clearance (as in metabolic syndrome or genetic lipid disorders). Persistently high triglycerides mean a constant presence of triglyceride-rich lipoproteins and their remnants in circulation. These remnants are particularly dangerous because they can penetrate the arterial wall, where they contribute to the build-up of atherosclerotic plaque.

The heart disease risk grows as fatty deposits in the blood (atheroma) attach to artery walls which over time, become hardened and stiff. In the arterial wall, remnants are taken up by macrophages, forming lipid-laden ‘foam cells’. Over time, this accumulation of fat, cholesterol, and inflammatory cells creates plaques that narrow and stiffen arteries, a process called atherosclerosis. Triglyceride-rich particles also promote low-grade inflammation, oxidative stress, and endothelial dysfunction (damage to the artery’s inner lining), all of which accelerate plaque growth and instability.

Unstable atherosclerotic plaques can rupture, exposing their lipid-rich contents to the bloodstream and triggering clot formation (thrombosis). If such a clot develops in a coronary artery, it can abruptly block blood flow to part of the heart muscle, resulting in a myocardial infarction (heart attack).

Elevated triglycerides are not merely markers of metabolic imbalance; they actively contribute to the pathological cascade underlying coronary artery disease. Triglycerides and blood pressure rise in parallel because they share upstream metabolic drivers, particularly insulin resistance, endothelial dysfunction, and vascular inflammation. Managing triglycerides is therefore a central component of cardiovascular risk reduction, alongside controlling blood pressure, blood glucose, and insulin instability.

Saturated Fats and Cholesterol – guilty by association?

Cholesterol has been used as a surrogate target for the prevention of heart disease. The heart-disease hypothesis postulates that reducing dietary saturated fat lowers serum cholesterol, thereby reducing cardiovascular risk. [63] Keeping LDL-C low by restricting saturated fat was an underpinning rationale for low-fat and low-saturated-fat diets. Carbohydrate-restricted diets may be associated with higher cholesterol levels but typically occur in a context of otherwise low metabolic risk.[64] [65]

New Zealand’s dietary guidelines directly influence the scope and framing of the questions officials include in national dietary surveys. A New Zealand Ministry of Health report, Adults’ Dietary Habits (2022), illustrates the Ministry’s disproportionate emphasis on dietary fat reduction, alongside a relative lack of attention to adequate protein intake and an absence of consideration of cumulative carbohydrate intake.

The report refers to ‘fat’ fifty-seven times predominantly in the context of promoting low-fat alternatives, while ‘protein’ is mentioned only three times, each instance limited to noting that nuts, seeds, and legumes are protein sources, with no discussion of animal-derived protein. The carbohydrate macronutrient class is not discussed at all. In addition, no differentiation is made between vegetable classes (for example, starchy vegetables such as potatoes versus leafy green vegetables such as silverbeet), and total daily protein intake is not estimated or reported. [66]

Insulin is a tiny but highly potent molecule, while cholesterol is a much larger molecule. Gary Taubes meticulous research has shed light on why and how the more easily detectable cholesterol created the heart disease risk, while the invisible insulin was neglected. [67] Contemporary beliefs that cholesterol is the driving factor for heart disease risk, rather than carbohydrate-mediated lipidosis (high triglyceride levels), may be a consequence of the limitation of early testing technologies and later studies which may have exaggerated the relationship of high cholesterol with mortality risk. [68]

This was the origin of the belief that high saturated-fat diets contribute to heart disease risk. It wasn’t until after 1960 that researchers would appreciate how insulin levels in individuals with T2DM would spike far higher than that of healthy populations after consuming carbohydrates.[69]

Reviews consistently highlight the lack of robust evidence supporting an association between saturated fat intake and adverse cardiovascular outcomes, emphasising inconsistent findings and the context-dependent nature of reported effects.[70] [71] [72] [73]

In 2014 a U.K. based group assessed the relative risk of consumption of saturated, monosaturated, and polyunsaturated fats. The group concluded:

Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.[74]

In A 2015 review identified that saturated fats were not associated with all-cause mortality, CVD, CHD, ischemic stroke, or T2DM, while finding that trans fats were associated with all-cause mortality, total CHD, and CHD mortality.[75] A later Cochrane review (2015, updated 2020) determined that reducing saturated fat intake for at least two years causes a potentially important reduction in combined cardiovascular events.[76] New Zealand researchers evaluated that review, finding that the relative risk became non-significant when using more robust assumptions. [77]

Two 2025 reviews have further confirmed the absence of convincing evidence implicating saturated fat in cardiovascular disease. Steen et al. found only low to moderate certainty, i.e. no significant evidence that that reducing saturated fat intake might reduce risk for at-risk groups. For people with low baseline risk, absolute reductions were below the threshold of importance.[78] Yamada et al. concluded that:

The findings indicate that a reduction in saturated fats cannot be recommended at present to prevent cardiovascular diseases and mortality. [79]

Studies may fail to adequately control for dietary fat quality and carbohydrate burdens, which may act as significant confounders of outcomes.[80] The health effects of fats depend not just on their type (saturated, monounsaturated, polyunsaturated), but on the extent of processing and refining. Unprocessed or minimally processed fats, such as those found in extra virgin olive oil, nuts, seeds, avocados, and oily fish, consistently show protective effects for heart and metabolic health. Evidence also suggests that replacing refined carbohydrates with unprocessed fats yields better outcomes than simply reducing fat intake.

The example of eggs illustrates how public health messaging can become misdirected. From the 1970s through the early 1990s, dietary cholesterol was widely portrayed as a driver of elevated blood cholesterol, and eggs were framed as directly harmful to heart health. These restrictions peaked in the 1980s and early 1990s, before being revised as evidence showed that dietary cholesterol has only a modest and variable effect on serum cholesterol and cardiovascular risk; however, the associated cultural risk perception has persisted. More recent evidence increasingly highlights the nutritional value of eggs, with a large Australian cohort study of older adults finding that frequent egg consumption was associated with a lower risk of cardiovascular disease and all-cause mortality.[81]

Cholesterol is a sterol (lipid) that plays metabolic key roles, including cell signalling and hormone synthesis. Cholesterol is present in all vertebrates, while most invertebrates (including insects, molluscs and crustaceans) do not synthesize cholesterol but source it from their diet.[82] [83] This fundamental role of cholesterol across all systems suggests that early diagnostic testing for plaque in sclerotic arteries would naturally, consistently detect elevated cholesterol levels. This did not mean that cholesterol was the driver of heart disease.

Cholesterol is synthesized from acetyl-CoA in a multi-step pathway and cholesterol is most concentrated in organs involved in membrane biogenesis, hormone synthesis, cellular signalling and lipoprotein assembly. Lipoproteins are the shipping containers that carry cholesterol to where it is required.[84] The membrane of every cell requires cholesterol to make and maintain them. The liver controls homeostasis, and the main sites are in the liver, intestine and brain but the adrenal glands, gonads, skin, kidney, lungs, spleen and muscle can also synthesise cholesterol.[85] [86] [87] [88] [89]

Cholesterol’s fundamental role in the brain is well established. Cholesterol is the major building block of myelin sheaths and cholesterol is essential to maintain its compact structure. Cholesterol is crucial for synapse formation and function, influencing neurotransmitter release and receptor organisation, and hence plays a key role in plays a central role in early brain development.[90] [91] [92]

Higher HDL-cholesterol is associated with greater longevity.[93] Low low-density lipoprotein cholesterol (for example below 70 mg/dL) may be associated with health risks including mortality while high levels (such as over 200 mg/dL) may be health promoting.[94] [95]

Statins are HMG-COA reductive inhibitors and are taken to reduce cholesterol levels, with the impression that this will reduce cardiovascular-related mortality. However, primary and secondary prevention trials suggest that the median postponement of death for may be only 3.2 and 4.1 days, respectively.[96] Statins may be associated with reduced cholesterol levels that are detrimental to brain health. Trials that failed to demonstrate that by lowering cholesterol coronary heart disease would be prevented, may have been downplayed,[97] excluded and suppressed.[98] Animal studies have revealed that statins can lower cholesterol levels in the brain.[99] [100] [101]

The Inflammatory Cascade that Drives Multimorbidity, & High Sensitivity C-reactive Protein.

Inflammation can be provoked by an acute injury, or accrue slowly over time from toxic exposures which, if they occurred rarely, would not build up to inflammation at the system level, whether an organ, tissue or a whole-body response.

Persistent high refined carbohydrate exposures drive inflammation in the body. As the cascade diagram below shows, it does not happen all at once but builds over time. The cascade occurs from a convergence of hyperinsulinemia, glycaemic volatility, ectopic fat accumulation, adipocyte stress and macrophage infiltration. [102] [103] [104]

High blood glucose (hyperglycaemia) is toxic to cells and to the mitochondria. T2DM is recognised as an inflammatory disease and glycation plays an important role. The frequent intake of sugary or starchy foods over time results in high glucose levels, which then stick to proteins in the blood and tissues in a process called glycation. This is somewhat like a slow biological version of caramelisation, where sugars react with proteins without enzymes. These altered proteins, known as advanced glycation end products (AGEs), can build up in tissues and bind to special receptors on cells called RAGE (Receptors for Advanced Glycation End Products).

Once activated, these receptors trigger a chain reaction: the release of oxidative molecules, the activation of inflammatory cytokines, and the recruitment of immune cells to the site.

Health authorities that urge populations to shift away from saturated fats have often failed to adequately assess the inflammatory potential of processed fats. Processed fats including industrial trans fats, hydrogenated oils, and refined seed oils commonly used in ultra-processed foods, are consistently associated with increased risk of cardiovascular disease, metabolic syndrome, and chronic inflammation. These fats frequently undergo chemical processing or high-heat treatment, generating harmful by-products that can disrupt lipid metabolism and impair endothelial function.

Context is important: saturated fats derived from heavily processed meats and packaged foods may confer greater risk than saturated fats from whole-food sources such as dairy and fresh meat. The role of high-quality, minimally processed fat sources in supporting metabolic health has been under-recognised in nutrition policy.[105] [106]

Low-grade systemic inflammation is increasingly recognised as a clinically relevant contributor to cardiovascular risk. High-sensitivity C-reactive protein (hsCRP) is a well-validated acute-phase inflammatory biomarker, synthesised by the liver in response to pro-inflammatory cytokines (notably interleukin-6). While hsCRP rises rapidly following acute infection or trauma, persistent elevation is thought to reflect ongoing low-grade inflammation. Elevated CRP concentrations are consistently associated with an increased risk of coronary heart disease and broader cardiovascular events.

Dietary patterns influence inflammatory status. Diets characterised by a high carbohydrate burden and a high intake of ultra-processed foods are associated with higher CRP concentrations, whereas low-carbohydrate dietary patterns are generally associated with reductions in CRP and other inflammatory markers. [107] [108] [109] [110] [111] In 2009, researchers developed and validated the Dietary Inflammatory Index (DII), demonstrating that shifts toward a more anti-inflammatory dietary pattern were associated with significant reductions in hs-CRP.[112]

In September 2025, the American College of Cardiology updated their guidance, with new ACC recommendations including universal screening of C-reactive protein levels in all patients.:

Measurement of hsCRP (>3 mg/L) can be used in routine clinical practice to identify primary prevention individuals at increased inflammatory risk as long as the patient is not acutely ill.[113]

Inflammation, as assessed by hsCRP, may not only be a more accurate predictor of risk for future cardiovascular events and death than hyperlipidaemia assessed by low-density lipoprotein cholesterol (LDLC), it may highlight risk in populations currently overlooked by standard screening approaches. Contemporary preventive cardiology frameworks, focussed on hypertension, dyslipidaemia, diabetes mellitus, and smoking, do not routinely account of the inflammatory status of the individual.[114]

Evidence from large population studies supports this position. A United Kingdom study, the largest analysis to date, involving 448,653 UK Biobank participants without known atherosclerotic cardiovascular disease, found that:

hsCRP independently enhances CV risk stratification, and the predictive performance of hsCRP was comparable to or greater than traditional risk factors such as systolic blood pressure or LDL-C.

…individuals with hsCRP levels >3 mg/L had a 34% higher risk of MACE, a 61% and 54% increased risk of CV death and all-cause death compared to those with hsCRP <1 mg/L.

Notably, ‘the association of hsCRP with all endpoints was consistent across subgroups.’[115] A separate U.K. cohort study investigating the usefulness of baseline serum hsCRP as a predictor of long-term cardiovascular events in stable patients with hypertension, found that participants in the top third of hsCRP experienced a substantially greater incidence of cardiovascular events and all-cause mortality, compared to the lowest third.[116]

Comparable findings have been reported in the U.S. In a prospective cohort study of 12,530 initially healthy women followed for 30 years, women with persistently elevated hsCRP concentrations had a significantly higher risk of future cardiovascular events, independent of traditional risk factors.[117]

Figure 3. Kurt B, Reugels M, Schneider KM, et al. (2025). C-reactive protein and cardiovascular risk in the general population. European Heart Journal.

In New Zealand, high-sensitivity CRP (hsCRP) is available, however, it is used more selectively, predominantly for cardiovascular risk stratification, and is not universally ordered. It may be requested by GPs or specialists, but it is not part of routine population screening in NZ.

HYPERINSULINAEMIA & INFLAMMATORY CASCADE – can precede obesity.

High refined carbohydrate intake.

Frequent intake of high-glycaemic carbs leads to large postprandial glucose spikes.
Pancreas releases large insulin pulses to bring glucose down.
No inflammation yet. Sets the hormonal scene (high insulin → low glucagon → low fat oxidation).
Sensitive individuals may show transient oxidative stress and low-grade inflammatory markers.

Chronically elevated insulin levels (hyperinsulinemia).

Even in normoglycaemia, insulin may remain elevated for hours.
Over time, tissues become less responsive → early insulin resistance.
Early signs of inflammation begin here: Chronic hyperinsulinemia suppresses autophagy (mTOR) and, together with hyperglycaemia/FFAs, increases ROS, altering immune cell signalling.
Acceleration of non-enzymatic glycation of circulating proteins.
Endothelial dysfunction and low-grade inflammation (e.g., IL-6, CRP) can precede fat gain.

Insulin promotes fat storage (visceral adiposity).

Inhibits lipolysis (fat breakdown) and stimulates lipogenesis (fat creation) in adipose tissue, especially visceral fat. Preferential deposition impacted by genetics, gender, stress etc.
Inflammation ramps up here. Repeated postprandial hyperglycaemia accelerates AGE formation; glycated proteins activate RAGE receptors, triggering NF-κB and downstream inflammatory cytokine release, which exacerbates tissue hypoxia.
Immune cells (esp. macrophages) infiltrate visceral fat. Adipose remains endocrine but becomes increasingly pro-inflammatory (from macrophage infiltration, cytokine.).
Macrophage infiltration reinforces adipose inflammation, amplifying insulin resistance.

Weight gain and metabolic inflexibility

Persistent hyperinsulinemia shifts caloric partitioning toward fat storage.
Appetite regulation can be disrupted via leptin and ghrelin and hypothalamic inflammation.
Ongoing inflammation fuels impaired mitochondrial function, exacerbates insulin resistance, and promotes hepatic steatosis (fatty liver).
Glycation accelerates in liver, muscle, and vascular tissues; AGEs crosslink extracellular matrix proteins, increasing vascular stiffness. Repeated postprandial hyperglycaemia accelerates glycation.
Immune cells in adipose and vessel walls respond with inflammatory amplification.

Obesity emerges & glycation drives inflammation — downstream of insulin load

Hyperinsulinemia precedes and drives weight gain in many individuals; obesity is often an outcome, not the origin. Especially in youth, where beta-cell resilience is limited.
Chronic exposure to glycation products increases oxidative stress, stiffens the vasculature, and damages renal filtration structures and pancreatic β-cells.
Inflammation is now systemic: -
– Endothelial cells, liver (via NAFLD), skeletal muscle (via lipotoxicity), kidney and β-cells.
– Adipose tissue macrophages release increase IL-6 levels, stimulating hepatic CRP production.

T2DM develops once beta-cell function falters

In youth, β-cell decline can be more rapid and often severe.
Persistent hyperglycaemia entrenches glycation, vascular injury, and chronic inflammation.
Glucotoxicity, lipotoxicity, and immune-mediated inflammation drive β-cell apoptosis and multi-organ complications (retinopathy, nephropathy, neuropathy, CVD).

While blood testing remains the conventional standard, urine and saliva present promising, less resource-intensive alternatives, especially for screening inflammatory markers in vulnerable populations, who may be reluctant or unable to undergo venipuncture.[118] [119]

People diagnosed with type 2 diabetes mellitus (T2DM) are substantially more likely to develop multiple co-existing conditions, and multimorbidity is the norm rather than the exception in this population. Increasingly, scientific research identifies a shared spectrum of upstream risk factors and overlapping pathophysiological pathways that drive the range of conditions commonly associated with a T2DM diagnosis.[120]

Glycation is thought to be a key contributor to the development of diabetes-related complications, contributing to the increased risk of multiple, overlapping health conditions. In parallel, recent meta-analyses and pooled evidence consistently demonstrate that elevated hsCRP is associated with an increased risk of incident type 2 diabetes and cardiometabolic events. The development of T2DM and cardiovascular disease share common inflammatory aetiologies, for which hsCRP serves as a well-validated biomarker. Elevated hsCRP concentrations are associated with a higher risk of both prediabetes and established T2DM.[121] [122] [123] [124]

Over time, this persistent low-grade inflammatory milieu, effectively captured by hsCRP, contributes to progressive microvascular damage, particularly affecting the eyes, kidneys, and peripheral nerves.[125] [126] [127] [128]

Without such an appreciation, guidelines may over-emphasise downstream correlates, such as obesity as a primary driver, and under-emphasise the contribution of the cumulative carbohydrate burden to elevated blood glucose, inflammation, insulin resistance and eventual diabetes.

Chapter 3. Brain Health: Consistently Associated With Metabolic Dysfunction.

RETURN TO CONTENTS PAGE.

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[111] Field R, Field T, Pourkazemi F, Rooney K. (2023). Low-carbohydrate and ketogenic diets: a scoping review of neurological and inflammatory outcomes in human studies and their relevance to chronic pain. Nutr Res Rev. 36(2):295-319. DOI: 10.1017/S0954422422000087.

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[116] Hartley A, Rostamian S, Kaura A et al. (2025). The relationship of baseline high-sensitivity C-reactive protein with incident cardiovascular events and all-cause mortality over 20 years. eBioMedicine 2025;117:105786. DOI: 10.1016/j.ebiom.2025.105786

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We welcome your use of this resource but please cite:

‘The voice of nutrition in New Zealand is alarmingly quiet’.[1]

PSGRNZ advances this Report as a catalyst for informed discussion and constructive debate on the health-reform responses required to address New Zealand’s metabolic and mental-health challenges. The Report has two central aims: first, to synthesise the evidence identifying the key drivers of the global surge in metabolic and mental-health disorders; and second, to outline evidence-based pathways capable of restoring individuals, families, and communities to health.

A substantial body of scientific research now demonstrates that much of today’s chronic disease burden is preventable and, in many cases, reversible. This is a consequential finding. It restores agency to individuals and communities and offers clinicians renewed purpose at a time when health systems remain heavily oriented toward symptom management rather than causal prevention.

Yet despite medical advances and increasing health system investment, public agencies and medical practitioners have been unable to reduce the burden of metabolic and mental illness. These conditions are now most commonly expressed as multimorbidity, the co-existence of multiple, interacting conditions. Legacy approaches, and the ‘best international evidence’ routinely relied upon by government, are increasingly contradicted by contemporary scientific literature that integrates nutrition, metabolism, inflammation, and neurobiology. This disconnect has material consequences for health outcomes, workforce participation, and public expenditure.

Nutrition is foundational to protecting metabolic and mental health, and nutrition plays a key role in recovery from common conditions. Both functions remain marginal in government health strategy. This Report examines the evidence showing that cumulative carbohydrate burdens, high intakes of ultra-processed foods, and widespread micronutrient insufficiencies play an outsized role in promoting New Zealand’s chronic-disease epidemic. These factors contribute directly to hyperglycaemia, hypertension, systemic inflammation, and impaired brain function, operating upstream of many commonly diagnosed conditions.

The cumulative carbohydrate burden emphasises daily exposures to rapidly digestible starches, often in the form of processed carbohydrates, which affects not only the body but also the brain. A consistent body of evidence shows that reducing blood glucose and triglyceride levels, primarily through lowering carbohydrate intake, reduces risk not only of type 2 diabetes and cardiovascular disease, as well as many psychiatric and neurocognitive conditions. This evidence remains largely absent from official dietary policy.

Current dietary guidelines place disproportionate emphasis on carbohydrate intake while understating the physiological importance of fat and protein. As a result, many officials and members of Parliament remain insufficiently aware of the extent to which high-carbohydrate dietary patterns drive insulin spikes, hyperinsulinemia, and chronic inflammation. This omission persists despite clear evidence that insulin resistance and inflammatory pathways sit upstream of type 2 diabetes, hypertension, cardiovascular disease, periodontal disease, and many mental-health conditions, often concurrently.

Multimorbidity is the defining crisis. More New Zealanders now live with multiple chronic conditions than with any single diagnosis, and the associated costs, clinical, social, and economic, are super-additive. As metabolic and neurobiological dysfunction has intensified, prescribing rates have risen sharply. Yet polypharmacy is rarely associated with improved health or wellbeing and frequently compounds harm where medications address symptoms without resolving underlying dysfunction.

New Zealand’s health system is increasingly out of step with the evidence base. Laws, policies, institutional cultures, and regulatory frameworks have not been systematically updated to reflect advances in metabolic and nutritional science. Officials have frequently relied on offshore ‘consensus’ positions that stabilise existing approaches rather than interrogate them. Independent, comprehensive reviews of the scientific literature have not occurred at scale, while science-policy and funding frameworks have created barriers to public-good research capable of addressing these gaps.

There is, however, significant scope for reform. One purpose of this Report is to contrast the breadth of evidence in the scientific literature with current Ministry of Health approaches. While health targets emphasise service access and utilisation, performance indicators increasingly focus on wellbeing. This policy-indicator misalignment leaves upstream prevention, particularly nutrition, largely out of scope. This is visible across white papers, ministerial briefings, consultation documents, and official responses to public inquiry.

PSGRNZ, as a New Zealand charitable trust, lays down a challenge:

New Zealand can reverse its metabolic and mental-health crisis, but doing so requires rewiring health policy, general practice, and research systems.

Reform cannot occur if problems are acknowledged abstractly, without understanding how existing systems perpetuate them. Human biology is fundamentally dependent on vitamins and minerals, and officials have the discretion and responsibility to identify obstructive legislation and evaluate contemporary nutritional evidence. Accordingly, this Report identifies outdated scientific assumptions that no longer serve New Zealanders; highlights the absence of targeted biomarker screening that limits clinicians’ ability to assess metabolic dysfunction, nutrient deficiency, or toxicity; and examines legislative settings that automatically classify nutrients as drugs once biochemical pathways are identified, an approach that can impede health-promoting interventions.

Reform is already underway in homes, clinics, and communities. The burden imposed by carbohydrate-rich diets has been scientifically and politically difficult to address, yet clinicians, health coaches, researchers, and patients have developed practical strategies for adopting nutrient-dense whole-food diets that are not burdensome, do not spike glucose or insulin and frequently reverse insulin resistance.

Effective reform must be multifaceted.

Health coaches provide personalised dietary support, recognising that individuals vary in their metabolic response to carbohydrates. Daily dietary decisions can mitigate, and often reverse, conditions long considered permanent, including type 2 diabetes. As glucose and insulin stabilise, a wide range of symptoms frequently subside, challenging the orthodoxy of ‘one medication per symptom’. Health coaches can be integrated into clinical, hospital, and community settings, supporting individuals to navigate addictive food patterns that undermine health.

A broader reform agenda also requires the restoration and protection of academic and research freedom public good research for human and environmental health, alongside a willingness to challenge entrenched assumptions. Contemporary, interdisciplinary evidence from nutrition, metabolism, and neurobiology must be permitted to inform public policy. Biological and health-science curricula at primary, secondary, and tertiary levels require updating to reflect the central role of diet and metabolic health.

This Report concludes with recommendations for reform, including paradigm-shifting changes in how New Zealand approaches carbohydrate-heavy diets, insulin resistance, and hyperinsulinemia. The Reform section is structured in four parts: (1) diet-first approaches in local communities; (2) educational reform; (3) institutional and regulatory reform and (4) science-system reform.

Chapter 1. The Problem. Cascading Impairment Driving Multimorbidity.

REFERENCES

[1] Coad J and Pedley K. (2020). Nutrition in New Zealand: Can the Past Offer Lessons for the Present and Guidance for the Future? Nutrients, 12:3433; DOI:10.3390/nu12113433

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PART I. FOUNDATIONS: METABOLIC DYSFUNCTION & THE RISE OF MULTIMORBIDITY

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RETURN TO CONTENTS PAGE.

The Global Burden of Disease Study calculates years lived with disability (YLDs), and years of life lost (YLLs) to arrive at disability-adjusted life-years (DALYs). The data continue to show escalating metabolic and mental health disease burdens across the world.

Globally between 2010 and 2021, among the 25 leading Level 3 causes, age-standardised DALY rates increased most substantially for anxiety disorders (16·7%), depressive disorders (16·4%), and diabetes (14·0%).[1]

This is the first of two PSGRNZ Reports which lay a groundwork to suggest that dietary stressors play a major role in driving the unpredictable, complicated and complex outcomes that are prevalent in modern society, and which lead to over-burdened medical systems.

Diets high in refined carbohydrates and ultraprocessed food, which directly elevate blood glucose and lipid levels. The addiction-provoking impact on dopamine receptors can result in these diets being prioritised over nourishing foods which promote metabolic, including digestive tract health.
Insufficient levels of dietary micronutrients that are key cofactors in metabolic and mental processes.

PSGRNZ’s Reports outline pathways for reform, highlighting prominent case studies, that can lead to reversal and mitigation of the complex conditions that individuals present with, when they visit their clinician or general practitioner (GP).

The metabolic and mental health crisis is global. But what does metabolic mean? The human metabolism is the coordinated network of chemical, cellular, and mitochondrial processes that sustain life and maintain the body’s internal balance. Human metabolic function changes and adapts across the lifespan, influenced by developmental, hormonal, and physiological shifts.

Diet plays a key role in sustaining a healthy metabolism. Disruptions in gut function influence the metabolism through immune activation, altered microbial metabolites, and changes in nutrient absorption, affecting both brain function and mitochondrial health. Mitochondria are central regulators of cellular energy metabolism and redox balance, and emerging research increasingly links mitochondrial dysfunction to the pathophysiology of mental disorders.

These factors interact to suppress or provoke inflammatory and oxidative stress responses, which can also produce knock-on, cascading effects, further amplifying metabolic impairment across body systems.

The interrelated factors rarely result in the diagnosis of a single condition. It is more common to have multiple conditions (multimorbidity) than a single condition.[2] People across the Western world are diagnosed at younger and younger ages with multiple conditions.

Multimorbidity, the co-occurrence of three or more chronic conditions[3], occurs a decade earlier in deprived communities.[4] [5] The societal cost of multimorbidity is super-additive.[6]

Metabolic syndrome is one example of how metabolic disturbances drive multimorbidity. Yet people who present with metabolic syndrome, which includes the overlapping conditions of hypertension, dyslipidaemia, type 2 diabetes mellitus, obesity, and inflammation, also are more likely to be diagnosed with a mental illness or brain-related disorder.[7] [8] [9] [10] Metabolic dysfunction is strongly correlated with risk for brain-related conditions and periodontal disease, yet these associations are rarely raised by health agencies.[11] [12]

In many individuals, metabolic disturbances precede the onset of psychiatric symptoms and formal diagnosis. Clinical presentation in a doctors’ clinic by a patient, can reflect the complex interplay of genetic and epigenetic predispositions, dietary nutrient status, toxic exposures, and familial patterns. Lifestyle factors such as sleep disruption and physical inactivity further modulate this relationship, and the interaction is bidirectional: mental disorders can exacerbate metabolic dysfunction via neuroendocrine and behavioural pathways.[13]

Emerging lines of evidence indicate that the metabolic and mental-illness crisis is amplified by a class of food products, ultra-processed foods, that are engineered to be hyper-palatable and addictive. Ultra-processed foods can layer on top of diets that are already high in rapidly digestible starches.

Carbohydrate processing exists along a continuum, from minimally processed (e.g. unpeeled, cooked potatoes, rolled oats, and brown rice), to moderately processed (e.g. white rice or sourdough bread), and highly processed, refined carbohydrates, such as breakfast cereals, snack bars, crackers, and reconstituted breads (where the grain has been fractionated into refined flour, starch, bran, and germ).

Refinement increases glycaemic volatility, the risk of hyperinsulinaemia, and downstream metabolic stress, even when calorie content is similar. While minimally processed carbohydrate-based foods are generally compatible with health, regular intakes of moderately processed and refined carbohydrates create a cumulative metabolic burden, increasing the frequency of blood-glucose spikes. Ultra-processed foods are most strongly associated with food addiction.

Food addiction was first described in 1956. Food addiction is associated with dependency behaviours relating ultra-processed, refined, or high-glycaemic index carbohydrates. [14] [15]

Medical doctors often lament that their patients do not stick to a ‘healthy diet’. Some foods, particularly those high in sugar and refined carbohydrates, can activate the brain’s reward circuitry in ways that parallel mechanisms observed in substance addiction. This occurs in part through stimulation of the mesolimbic dopamine pathway, extending from the ventral tegmental area (VTA) to the nucleus accumbens, thereby reinforcing craving and repeated intake. Separately, chronic metabolic dysregulation (like sustained high insulin levels and associated leptin resistance) can impair normal appetite and reward signalling, potentially exacerbating dysfunctional eating behaviours; but the latter mechanism is part of broader metabolic research and is not established as one of the core addiction mechanisms.[16]

Ultraprocessed foods that are high in fats and refined carbohydrates, are the foods that are most closely associated with food addiction. Ultraprocessed foods are formulations of low-cost ingredients, mostly of exclusive industrial use, that result from a series of industrial processes. These processes involve the fractioning of whole foods into substances which are often derived from a few high-yield crops. Some of the substances can undergo hydrolysis, or hydrogenation, or other chemical modifications. Colours, flavours, emulsifiers and other additives are frequently added to make the final product palatable or hyper-palatable and ensure a long shelf life.[17]

Human bodies are not so much complicated as complex. The overlapping drivers work synchronistically to set human bodies on an illness trajectory: Systemic metabolic dysfunction gives rise to a cascade of symptoms and drives multimorbidity. Like any system with compromised structural integrity, the body’s metabolic network becomes unstable and susceptible to cascading failures.

Ultraprocessed foods are not uniformly addictive, and treating them as one regulatory category is poorly supported by evidence and easily exploited by industry. A focus which reduces the cumulative burden of moderately processed and refined carbohydrates, to improve blood-sugar and insulin level, which takes account of individual insulin sensitivity, will concurrently result in less consumption of the ultraprocessed food groups that are most addictive, those that are high in sugar and refined carbohydrates.[18]

This Report draws from multiple levels of investigation, including cellular and mechanistic studies, case reports, cohort studies, audits of clinical data and population-level (epidemiological) research. The consistency and strength of findings are supported by systematic reviews and meta-analyses, which evaluate the consistency and strength of findings across studies. Meta-analyses help to determine whether the accumulated evidence supports, refutes, or remains inconclusive regarding a particular hypothesis.

Traditional dietary guidelines have not drawn from such a broad base of evidence, instead relying primarily on population-level epidemiological studies and randomised controlled trials.

Carbohydrate consumption as a driver of unstable blood glucose, elevated triglycerides (fat molecules in the blood), hyperinsulinemia and, ultimately, insulin resistance (the insulin pathway) is well established in the scientific literature. Insulin resistance is a byproduct of elevated insulin. This knowledge has prompted researchers and doctors to study or adopt low-carbohydrate approaches aimed at stabilising blood glucose and insulin and reducing triglyceride levels.[19] These insulin lowering diets, of which the ketogenic diet may be the most well-characterised, are based on low-carbohydrate, high-fat and moderate-protein foods. The ketogenic diet induces the production of ketone bodies by mimicking the breakdown of a fasting state.[20] [21]

From 2015 Onwards – Escalating Evidence.

In 2015 Richard Feinman and colleagues proposed that dietary carbohydrate restriction should be the first approach in diabetes management[22], arguing that a fundamental reappraisal of dietary recommendations was overdue. They cited several reasons:

General failure to halt the epidemic of diabetes under current guidelines.
The specific failure of low-fat diets to improve obesity, cardiovascular risk, or general health.
Constant reports of side effects of commonly prescribed diabetic medications, some quite serious.
Most importantly, the continued success of low carbohydrate diets to meet the challenges of improvement

Feinman et al. reasoned that this approach would lower blood glucose and reduce the risk of hyperglycaemia. They highlighted the role of increasing carbohydrate consumption in promoting obesity, weight loss is not the central issue (i.e. many people with type 2 diabetes are not overweight), yet when weight loss is required low-carbohydrate diets consistently outperformed low-fat diets for weight reduction. The authors further noted that replacing carbohydrates with protein is ‘generally beneficial’, and they challenged long-standing assumptions about dietary fat, arguing that total and saturated fat intake do not correlate with cardiovascular disease risk. They emphasised that ‘plasma saturated fatty acids are controlled by dietary carbohydrate more than by dietary lipids’ pointing to a metabolic rather than dietary origin. Crucially, the authors emphasised:

Adherence to low-carbohydrate diets in people with type 2 diabetes is at least as good as adherence to any other dietary interventions and is frequently significantly better.

Despite presenting a substantial evidence base and identifying multiple downstream benefits, the conclusions of Feinman et al. have not been incorporated into major clinical guidelines. In the decade 2015-2025, their position has been corroborated by an expanding body of trials and mechanistic studies that demonstrate that people experience improved glycaemic control, reduced insulin requirements, and favourable lipid profiles under low-carbohydrate and ketogenic dietary patterns.

The Feinman paper does not appear to be referenced in Ministry of Health guidance or related agency documents. Yet New Zealand researchers did recognise the potential for a different approach to diabetes management and population health. Notably, Professor Grant Schofield and colleagues at Auckland University of Technology published a paper in the New Zealand Medical Journal supporting a low-carbohydrate approach and challenging the prevailing high-starch, low-fat dietary guidelines. The paper concluded:

We suggest that clinical dietary advice for the treatment of diabetes, as well as population prevention guidelines, be urgently revised.[23]

New Zealand researchers have tried to raise attention to the carbohydrate (or starch) burden as a driver of poor metabolic health. Low-carbohydrate dietary responses to high blood glucose and triglyceride levels first reached mainstream media attention in New Zealand when Professor Grant Schofield and Dr Caryn Zinn, and chef Craig Dodger published the book What The Fat (WTF) book in 2015. The book was controversial, yet received critical acclaim, and has since been republished in various formats. The book remains widely available.

A few years earlier, New Zealand researchers theorised that carbohydrate cravings were associated with the dopaminergic pathway and food addiction. [24] [25] [26] In a groundbreaking paper, New Zealand researchers also explored the role of dopamine in reward and psychosis, considering the potential use of food as a substitute to induce dopamine release, which would then contribute to the weight gain that commonly follows antipsychotic drug use, in people with psychotic illness. The authors speculated that:[27]

‘food may be a key stimulant of this disordered pathway, and altering diet may improve psychosis and reduce the need for antipsychotic treatment. If blocking the effects of free dopamine reduces psychotic symptoms, then reducing dopamine release is likely to induce a similar effect.’

Although low-carbohydrate and food addiction research were identified as promising fields for investigation from 2008 onwards, and received a major ‘injection’ in 2015, some ten years later, these lines of research have not been extensively pursued by New Zealand’s public universities, including public health and medical faculties, despite advancing population-level burdens of metabolic disease.

A substantial and robust body of research now reveals that type 2 diabetes mellitus (T2DM) is neither inevitably chronic nor irreversible, and that early reversal of prediabetes and T2DM is both feasible and associated with wider health benefits.[28] [29] [30] As poor diets frequently precede multimorbidity and multifactorial disease states, when diet and nutrition is addressed, a serendipitous, domino effect can occur and other health markers can improve, as blood glucose levels improve.

Studies consequently show that health coaching can be integrated into everyday clinical practice, to support shifts away from poor dietary habits and addictive patterning that can overwhelm and hinder the best of intentions. Health coaching interventions apply a three-pronged approach: whole food, carbohydrate reduction; a health coach, behaviour-change-based delivery approach; and community- or peer-based initiatives.[31] Health coaching has been integrated into New Zealand Primary Health Organisations (PHOs). However, the current PHO work-scope does not extend to diet and nutrition coaching. In contrast, the health coaching that is discussed in this paper, explicitly integrates diet and nutrition support and education, with the central objective of improving metabolic, including mental health.

The January 2026 U.S. Dietary Guideline Shift.

Dietary guidelines not only shape the everyday choices of the general public; they also guide public-sector catering decisions and clinical advice, with effects that reverberate across society. Menus developed for government institutions, including schools, hospitals, and the military, are typically designed to align with guideline directives, while dietary recommendations by medical practitioners will, by convention, adhere to guidelines.

On 7 January 2026, the United States (US) Department of Health and Human Services (HHS) and the US Department of Agriculture (USDA) released substantially revised dietary guidelines, the ‘most significant reset of federal nutrition policy in decades’.[32]

American households must prioritize diets built on whole, nutrient-dense foods—protein, dairy, vegetables, fruits, healthy fats, and whole grains. [33]

HHS and USDA scientific and promotional materials draw attention to important but historically under-examined issues relating to macronutrient (protein, fat and carbohydrate) intake and the health impact of industrial processing. The Overview of Evidence Accepted and Rejected from the Dietary Guidelines Advisory Committee (DGAC) Report illustrates the extent to which many previously taken-for-granted ‘healthy options’ were rejected by the Advisory Committee as inconsistent with current evidence.[34]

The Scientific Foundation for the Dietary Guidelines for Americans, 2025–2030 clarifies several concepts that have previously been under-represented or downplayed. It notes, for example, that many foods described as ‘healthy carbohydrates’ are more accurately classified as refined grains, and that many low-fat products are highly processed and may therefore be less nourishing than less-processed alternatives. The Scientific Foundation paper acknowledges that legacy guidelines and health claims may have inadvertently directed people away from healthier products to less healthy products. They cited the example of minimally processed, full-fat yoghurt with no additives, which, when reformulated as ‘low-fat’ or ‘fat-free’, typically incorporates added sugars, starches, and other chemical additives. The document advises against artificial ingredients and advocates against added sugars, including their widespread inclusion in grain-based snack foods that were formerly viewed as healthy.

The U.S. guideline shift marks a constructive departure from the historic over-emphasis on carbohydrates and the relative under-recognition of the health benefits of protein and healthy fats. Historically, the U.S. acceptable macronutrient distribution range (AMDR) was established to balance competing metabolic considerations within a physiologically acceptable range. For example, in the 2005 dietary reference intake discussion, diets very high in carbohydrates were acknowledged to increase risk for coronary heart disease (CHD) and T2DM:

High carbohydrate diets frequently cause greater insulin and plasma glucose responses than do low carbohydrate diets. These excessive responses theoretically could predispose individuals to the development of type 2 diabetes because of prolonged overstimulation of insulin secretion’; versus the risk of weight increase from excess fats in the diet. [35]

At the same time, concerns were raised in the 2005 paper about excessive dietary fat contributing to weight gain.

As the Scientific Foundation states, the recommended daily allowance/intake levels and the AMDR serve complementary purposes:

The RDA prevents deficiency (e.g., preventing loss of lean body mass or negative nitrogen balance), while the AMDR identifies a range of intakes compatible with health and nutrient adequacy. [36]

Importantly, they distinguish between the longstanding objective of preventing nutrient deficiency and the emerging evidence on intake levels, by age, sex, and life stage, that support optimal health. The AMDR framework recognises that intakes above minimum deficiency-prevention thresholds may confer additional health benefits.

The revised guidelines place renewed emphasis on protein as an essential macronutrient and re-establish a broad intake range compatible with health. This represents a subtle but important shift. These shifts provide U.S. government institutions and medical practitioners with greater latitude in dietary planning and clinical guidance.

Historically, attention has tended to focus on the lower end of the acceptable macronutrient distribution range (AMDR) for protein, around 10% of total energy intake. The updated position recognises that protein intakes across a wider range, from 10–35% of total energy, can support maintenance of lean mass and metabolic health. [37] (New Zealand dietary guidelines do not appear to specify a comparable macronutrient distribution range.)

In practice, adults roughly consume 1.0 g/kg per day of protein. By comparison the recommended daily allowance for protein for U.S. adults 18 years and over has historically been set at 0.8 g/kg[38], while the New Zealand and Australian reference values range from 0.84-0.94 g/kg.[39]

The new guidelines place heightened emphasis on distinguishing whole grains from refined grain products, explicitly outlining the health risks associated with refined carbohydrates that often contain added sugars and industrial additives. They recommend substantial reductions in highly processed carbohydrates and reduce recommended whole-grain intake to 2-4 servings per day.

The Scientific Foundation provides practical clarity on how whole grains may be differentiated from less healthy refined carbohydrate products, noting that ‘most true whole-grain foods contain at least 1 gram of fibre for every 8 grams of carbohydrate.’ [40] Notably, neither the Dietary Guidelines for Americans nor the Daily Servings by Calorie Level reference ‘cereal’ as a recommended category. [41] [42] Instead, breakfast cereals are more commonly characterised as refined or processed foods to be limited or avoided.

Importantly, the Appendices recognise that a low-carbohydrate dietary pattern is scientifically justified option for people who are overweight or obese with metabolic syndrome or T2DM.[43]

Unrefined saturated fats are increasingly positioned as compatible with health. The new guidelines endorse full-fat milk and more generally frame unprocessed fats as health-supportive.:

‘Healthy fats are plentiful in many whole foods, such as meats, poultry, eggs, omega-3-rich seafood, nuts, seeds, full-fat dairy, olives, and avocados. When cooking with or adding fats to meals, prioritize oils with essential fatty acids, such as olive oil. Other options can include butter or beef tallow.

Despite this shift in framing, the formal recommendations remain constrained by legacy limits.:

In general, saturated fat consumption should not exceed 10% of total daily calories.

This threshold reflects the position in the 2020–2025 Dietary Guidelines, which encouraged substitution of meats, butter, and dairy with a wide range of plant-based alternatives.[44] However, the 10% limit appears inconsistent with the evidence reviewed by the Advisory Committee and with Scientific Foundation statements and the analyses presented in the appendices.[45] For example, The Scientific Foundation states:

Overall, the RCT evidence does not provide causal support for reducing saturated fat below 10% of energy or replacing saturated fat with linoleic acid–rich oils to prevent CHD or death. [46]

The information contained in the Appendices provide the scientific evidence that underpins guidelines positions. Two separate views in the Appendices found that current saturated fat recommendations which limit intake to below 10% of total daily calories have little scientific foundation. The first review (Appendix 4.6) analysed randomised controlled trials to identify causal evidence that saturated fat intakes below 10% of total energy prevent coronary heart disease or all-cause mortality. The authors found no convincing evidence to support this hypothesis. [47]

The second review (Appendix 4.7) adopted a different approach, using Bayesian methods to examine whether saturated fat intake influenced all-cause mortality or cardiovascular disease (CVD) risk, including stroke. This latter review found that analyses and systematic reviews consistently conflated the more atherogenic trans fats, which are known to increase CVD risk, with saturated fats, and that the evidence base could not distinguish saturated fat effects from those of trans fatty acids. [48]

Following the release of the new guidelines, nutritionist Nina Teicholz, founder of the U.S.-based Nutrition Coalition, argued that retention of the 10% saturated-fat cap may disproportionately affect populations reliant on government food programmes, as these settings are most likely to restrict saturated fats while continuing to rely on refined seed oils. Teicholz further notes that the guidelines’ positive framing of unprocessed fats is difficult to reconcile in practice, i.e., in the daily diet. For example, she observes that consuming one cup of full-fat yoghurt together with a chicken thigh cooked with the skin on in a tablespoon of butter would bring daily saturated-fat intake close to the recommended ceiling.

Teicholz also highlights an internal tension in the guidelines, arguing that the 10% threshold creates a paradox: meeting higher protein targets through commonly consumed whole-food sources such as beef, pork, or chicken thighs with skin would exceed the saturated-fat limit early in the day.[49]

The new U.S. guidelines, and the scientific evaluations that accompany them, provide renewed analytical attention to issues that have previously received limited emphasis and that are relevant to individual and population health outcomes. The release of the U.S. guidelines immediately prior to the launch of PSGRNZ’s Reclaiming Health paper is notable, as the underlying Scientific Foundation analyses in many respects both reflect and independently corroborate key elements of the evidence base and reasoning advanced in this New Zealand-based work.

Chapter 2. The Total Carbohydrate Burden & Individual Vulnerability

RETURN TO CONTENTS PAGE.

REFERENCES

NB: Number order differs from the original Reclaiming Health publication (PDF).

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[2] Russell et al (2019). Multimorbidity in Early Childhood and Socioeconomic Disadvantage: Findings From a Large New Zealand Child Cohort. Academic Pediatrics, 20(7),P619-627.

[3] Skou ST, Mair FS, Fortin M. et al. (2022). Multimorbidity. Nat Rev Dis Primers 8, 48. DOI: 10.1038/s41572-022-00376-4

[4] Head A, Fleming K, Kypridemos C, et al. (2021). Multimorbidity: the case for prevention J Epidemiol Community Health 2021;75:242–244. DOI:10.1136/jech-2020-214301

[5] Skou ST, Mair FS, Fortin M. et al. (2022). Multimorbidity. Nat Rev Dis Primers.

[6] Blakely T, Kvizhinadze G, Atkinson J, Dieleman J, Clarke P. (2019). Health system costs for individual and comorbid noncommunicable diseases: An analysis of publicly funded health events from New Zealand. PLoS Med. 16(1):e1002716. DOI: 10.1371/journal.pmed.1002716. PMID: 30620729.

[7] Otokunefor O, & Atoe K. (2025). The Nexus Between Metabolic Syndrome and Mental Health Disorders: A review. Open Journal of Medical Research (ISSN: 2734-2093), 6(1), 15-32. https://doi.org/10.52417/ojmr.v6i1.824

[8] John AP, Koloth R, Dragovic M, Lim SCB. (2009) Prevalence of metabolic syndrome among Australians with severe mental illness. MJA 2009; 190: 176–179

[9] Kim, JR., Kim, HN. & Song, SW. Associations among inflammation, mental health, and quality of life in adults with metabolic syndrome. Diabetol Metab Syndr 10, 66 (2018). DOI: 10.1186/s13098-018-0367-9

[10] Penninx, B. W. J. H., & Lange, S. M. M. (2018). Metabolic syndrome in psychiatric patients: overview, mechanisms, and implications. Dialogues in Clinical Neuroscience, 20(1), 63–73. Doi: 10.31887/DCNS.2018.20.1/bpenninx

[11] Palmer CM. (2025) Beyond comorbidities: metabolic dysfunction as a root cause of neuropsychiatric disorders. BJPsych Advances. Published online 2025:1-3. doi:10.1192/bja.2024.74

[12] Gobin R, Tian D Liu Q Wang J. (2020). Periodontal Diseases and the Risk of Metabolic Syndrome: An Updated Systematic Review and Meta-Analysis. Front. Endocrinol. Volume 11. DOI:10.3389/fendo.2020.00336

[13] Palmer CM. (2025) Beyond comorbidities: metabolic dysfunction as a root cause of neuropsychiatric disorders.

[14] Unwin J, Delon C, Giæver H, Kennedy C, et al. (2022). Low-carbohydrate and psychoeducational programs show promise for the treatment of ultra-processed food addiction. Front. Psychiatry 13:1005523. DOI: 10.3389/fpsyt.2022.1005523

[15] Sethi Dalai S, Sinha A, Gearhardt A. (2020). Low carbohydrate ketogenic therapy as a metabolic treatment for binge eating and ultraprocessed food addiction. Curr Opin Endocrinol Diabetes Obes. 27:275–82. DOI: 10.1097/MED.0000000000000571

[16] Lustig RH (2025). The battle over “food addiction”. Front. Psychiatry 16:1621742. DOI:10.3389/fpsyt.2025.1621742

[17] Monteiro CA, Cannon G, Levy RB (2019). Ultra-processed foods: what they are and how to identify them. Public Health Nutrition, 22(5):936–941. DOI:10.1017/S1368980018003762.

[18] Ludwig DS (2025). Ultraprocessed Food on an Ultrafast Track. NEJM 393:1046-1049. DOI: 10.1056/NEJMp250869

[19] Unwin D. (2024). Reducing overweight and obesity; so how are we doing? BMJ Nutrition, Prevention & Health. 2024;:e000836. DOI:10.1136/bmjnph-2023-000836

[20] Nojek P, Zawół M, Zimonczyk M, et al. (2024) Ketogenic diet and metabolic health: A review of its impact on type 2 diabetes and obesity. Analysis of research on the ketogenic diet in the context of treating metabolic disorders. J Educ Health Sport. 2024;71:55923. DOI: 10.12775/JEHS.2024.71.55923.

[21] Baylie T, Ayelgn T, Tiruneh M, Tefsa KH (2024). Effect of Ketogenic Diet on Obesity and Other Metabolic Disorders: Narrative Review. Diabetes, Metabolic Syndrome and Obesity, 17:1391–1401, DOI: 10.2147/DMSO.S447659.

[22] Feinman RD, Pogozelski WK, Astrup A et al. (2015). Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base. Nutrition, 31:1-13. DOI: /10.1016/j.nut.2018.12.002

[23] Schofield G, Henderson G, Thornley S, Crofts C. (2016) Very low-carbohydrate diets in the management of diabetes revisited. NZMJ, 129:1432. ISSN 1175-8716.

[24] Thornley, S.; McRobbie, H.(2009). Carbohydrate withdrawal: is recognition the first step to recovery? N. Z. Med. J., 2009, 122, 133-134.

[25] Thornley, S.; McRobbie, H.; Eyles, H.; Walker, N.; Simmons, G. (2008). The obesity epidemic: is glycemic index the key to unlocking a hidden addiction? Med. Hypotheses, 71, 709-714.

[26] Thornley, S, McRobbie H. (2011). Sickly Sweet: Sugar, Refined Carbohydrate, Addiction and Global Obesity (Nutrition and Diet Research Progress). Nova Novinka.

[27] Thornley S, Russell B and Kydd R. (2011) Carbohydrate reward and psychosis: an explanation for neuroleptic induced weight gain and path to improved mental health? Curr Neuropharmacol. 9(2):370-5

[28] Unwin D, Khalid AA, Unwin J, Crocombe D, Delon C, Martyn K, et al. (2020). Insights from a general practice service evaluation supporting a lower carbohydrate diet in patients with type 2 diabetes mellitus and prediabetes: a secondary analysis of routine clinic data including HbA1c, weight and prescribing over 6 years. BMJ Nutr Prev Health. 3:285–94, DOI:10.1136/bmjnph-2020-000072

[29] Unwin D, Delon C, Unwin J, et al. (2023). What predicts drug- free type 2 diabetes remission? Insights from an 8- year general practice service evaluation of a lower carbohydrate diet with weight loss. BMJ Nutrition, Prevention & Health 2023;0:e000544. DOI:10.1136/bmjnph-2022-000544

[30] Zinn C, Campbell JL, Fraser L, Davies G, Hawkins M, Currie O, Cannons J, Unwin D, Crofts C, Stewart T, et al. (2025) Carbohydrate Reduction and a Holistic Model of Care in Diabetes Management: Insights from a Retrospective Multi-Year Audit in New Zealand. Nutrients.17(24):3953. DOI:10.3390/nu17243953

[31] Zinn C, Campbell JL, Fraser L. et al. (2025) Carbohydrate Reduction & a Holistic Model of Care in Diabetes Mngmnt.

[32] HHS (January 7, 2026). Kennedy, Rollins Unveil Historic Reset of U.S. Nutrition Policy, Put Real Food Back at Center of Health. https://www.hhs.gov/press-room/historic-reset-federal-nutrition-policy.html

[33] HHS & USDA (Jan 2026). Dietary Guidelines for Americans, 2025–2030. Page 2. https://cdn.realfood.gov/DGA.pdf

[34] HHS & USDA (2026). The Scientific Foundation for the Dietary Guidelines for Americans, 2025–2030. P.iii-viii. https://cdn.realfood.gov/Scientific%20Report_1.8.26.pdf

[35] Institute of Medicine. 2005. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. Washington, DC: The National Academies Press. DOI: 10.17226/10490. p.784.

[36] HHS & USDA (2026). The Scientific Foundation for the Dietary Guidelines for Americans, 2025–2030. P.37.

[37] HHS & USDA (2026). The Scientific Foundation for the Dietary Guidelines for Americans, 2025–2030. P.37-40.

[38] Wolfe RR, Cifelli AM, Kostas G, Kim IY. (2017). Optimizing protein intake in adults: Interpretation

and application of the Recommended Dietary Allowance compared with the Acceptable Macronutrient Distribution Range. Adv Nutr. 8(2):266–275. DOI:10.3945/an.116.013821

[39] NHMRC (2005). Nutrient Reference Values for Australia and New Zealand Including Recommended Dietary Intakes. Protein. https://www.eatforhealth.gov.au/sites/default/files/2022-10/n35-protein_0.pdf

[40] HHS & USDA (2026). The Scientific Foundation for the Dietary Guidelines for Americans, 2025–2030. P.20.

[41] USDA (January 2026). Dietary Guidelines for Americans, 2025–2030. https://cdn.realfood.gov/DGA.pdf

[42] HHS & USDA (2026). Daily Servings By Calorie Level. https://cdn.realfood.gov/Daily%20Serving%20Sizes.pdf

[43] HHS & USDA (2026). The Scientific Foundation For The Dietary Guidelines For Americans. Appendices. P.199 https://cdn.realfood.gov/Scientific%20Report%20Appendices_1.8.26.pdf

[44] 2025 Dietary Guidelines Advisory Committee. 2024. Scientific Report of the 2025 Dietary Guidelines Advisory Committee: Advisory Report to the Secretary of Health and Human Services and Secretary of Agriculture. U.S. Department of Health and Human Services. Page 5. DOI: 10.52570/DGAC2025   

[45] HHS & USDA (2026). The Scientific Foundation For The Dietary Guidelines For Americans. Appendices. P.22-40.

[46] HHS & USDA (2026). The Scientific Foundation for the Dietary Guidelines for Americans, 2025–2030. Page 30. https://cdn.realfood.gov/Scientific%20Report_1.8.26.pdf

[47] HHS & USDA (2026). The Scientific Foundation For The Dietary Guidelines For Americans. Appendices. P.230.

[48] HHS & USDA (2026). The Scientific Foundation For The Dietary Guidelines For Americans. Appendices. P.248-259.

[49] Teicholz N (Jan 7, 2026). Butter Is Not Back: The Broken Promise on Saturated Fats. Substack.

Physicians and Scientists for Global Responsibility New Zealand Charitable Trust (NZ Charities no.CC29935) has been successfully operating for 25 years.

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