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

We welcome your use of this resource but please cite:

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

Low-income populations not only have nutrient depleted diets but higher levels of exposure to stress and/or trauma. Food insecurity is defined by:

‘the absence of sufficient, nutritionally adequate, safe foods, as well as the inability to acquire such foods in socially acceptable ways.’[1]

Food insecurity is a persistent problem in New Zealand.[2] Māori and Pasifika populations are most vulnerable to food insecurity in New Zealand, while women experience food insecurity more than men.[3] Consequent stress is not only nutrition-related, but psychological, despite for example, Māori communities working together to support community members who require additional care.[4]

Foodbanks cannot provide people with adequate nutrition.[5] [6] Food insecure individuals often have limited access to nutrient-rich foods including fruits, vegetables, and meat protein, and much greater access to highly processed foods which are high in refined carbohydrates and processed fats.

New Zealand has a large research cohort exploring the increased risk of substance abuse with poor mental health. Food addiction is yet to be integrated into research programmes and university curricula.

While people across all socio-demographic scales will experience food addiction, people and families experiencing food insecurity and poor mental health are likely to be uniquely susceptible to food addiction over the longer term:[7]

A similar pattern may exist with food addiction, such that individuals with food insecurity experience similar food addiction symptoms, but greater impairment and long-term negative consequences due to a lack of buffering from other socioeconomic supports. [8]

The chapter above demonstrates that in under-valuing dietary protein and over-emphasising dietary carbohydrates, dietary guidelines may be increasing risk for T2DM, obesity, and a spectrum of metabolic and mental illnesses, conditions which are disproportionately present in low socio-economic groups.

Diabetes Epidemic: The Ethics of Failing to Prevent T2DM in Children & Adolescents.

‘Type 2 diabetes is likely to be the biggest global epidemic in human history’.[9] [10]

Childhood T2DM, as with adult onset T2DM, is the result of insulin resistance. T2DM is preceded by a prediabetes state (impaired glucose tolerance and/or impaired fasting glucose). Disease onset and progression proceeds much more rapidly than in adults to frank T2DM.[11] [12] Cardiovascular disease risk is elevated in younger populations with T2DM.[13]

Figure 7. Pappachan JM, Fernandez CJ, Ashraf AP. (2024) Rising tide: The global surge of type 2 diabetes in children and adolescents demands action now. World J Diabetes.

Incidence rates of T2DM in children vary, between 285-734 per 100,000 population with 41,600 new cases confirmed in the year 2021. [14] Children who are diagnosed with T2DM are more likely to be obese. A global review and meta-analysis of 53 studies including 8942 participants in 2022, found that 75.27% of children with T2D had obesity, and 77.24% had obesity at diagnosis. [15]

The ethical dimensions arising from inadequate nutritional recommendations for children at risk of metabolic disease remain largely unexplored. Conventional reviews discussing the problem of obesity and diabetes do not generally discuss the aetiology of carbohydrates as an underlying factor in the development of these conditions. The role of bariatric surgery can be mentioned, but not carbohydrate restriction. [16] [17]

There are no formal guidelines recommending carbohydrate restriction in children to reduce or eliminate risk for elevated glucose and T2DM. A recent review by a U.S. based committee affiliated with the Indiana-based Riley Hospital, considered the potential risks of low-carbohydrate approaches, which included: growth deceleration, nutritional deficiencies, poor bone health, nutritional ketosis that cannot be distinguished from ketosis resulting from insulin deficiency, and disordered eating behaviours.[18]

Prevalence of Type 1 (T1DM) and Type 2 diabetes (T2DM) has been increasing. A recent study of adolescents found that T1DM was more prevalent in adolescent females, than males, while T2DM was more prevalent in adolescent males.[19] Increasing rates of T1DM suggest that environmental influences play a role. No single factor has been identified, and scientists have proposed that these may include nutrient insufficiency, impaired gut microbiota, psychosocial stress, and altered immune function.

The review did not consider the risk from long-term exposure to diabetes medication and health conditions that are tightly correlated with T2DM, particularly when it commences in childhood. These include higher risk for diabetic associated retinopathy, neuropathy and kidney disease; diabetic dyslipidaemia, hypertension and cardiovascular disease risk; cerebrovascular and peripheral vascular diseases; metabolic fatty liver disease; obstructive sleep apnoea, hyperandrogenism in females and/or polycystic ovary syndrome (PCOS). [20]

Prediabetes: The Quiet Threat Beneath the Surface.

Increasing rates of prediabetes may be one of the earliest and under-recognised symptoms of the chronic disease epidemic. Prediabetes is a sign of early pathophysiology that precedes T2DM, and prediabetic diagnosis is a condition associated with elevated glucose and inflammation which can be associated with poor mental health. Prediabetes and diabetes are associated with an elevated risk for depression and anxiety.[21] [22] [23] [24]

Professor Caryn Zinn recently highlighted that prediabetes risk is effectively downplayed by existing clinical approaches, arguing that the term signals a waiting room instead of a treatment window. Zinn argued that instead, prediabetes should be retitled early type 2 diabetes, which would then enable practitioners to refer for tailored dietary and lifestyle intervention.:

prediabetes is often a footnote in primary care, flagged inconsistently on lab reports, mentioned briefly or ignored for ‘watchful waiting’. This passive approach fails to reflect the biological reality. Long before HbA1c reaches the diagnostic threshold for type 2 diabetes (T2D) (≥48 mmol/mol or ≥6.5%), the disease process is active: insulin resistance, hyperinsulinaemia and β-cell stress drive early microvascular and cardiovascular damage.[25]

Prediabetes in children and adolescents is increasingly common.[26] [27] The U.S. Centre for Disease Control (CDC) recently identified that 32% of U.S. adolescents between 12-17 years had prediabetes.[28] [29] The CDC used 2023 data from CDC's National Health and Nutrition Examination Survey (NHANES). The CDC advised that the change in methodology had increased the recognised rates of the condition. Only 4 years before, the CDC had identified that 1 in 5 adolescents and 1 in 4 young adults were diagnosed with prediabetes. [30]

New Zealand Ministry of Health data on the prevalence of prediabetes and diabetes in children is difficult to find. New Zealand lacks national data on prediabetes,[31] however, data suggests that prediabetes in children is more prevalent in Pasifika and South Asian children.[32] Doctors and clinicians lack knowledge about prediabetes, and prediabetes is relatively understudied.[33]

New Zealand may have higher rates of prediabetes in children and adolescents than has been formally recognised.[34] A 2021 New Zealand study measured blood glucose (HbA1c) in 451 children, aged 8-11 years. Pre-diabetes was present in 71 (16%) children and was greatest in South Asian (n=13, 30%), Pacific Island (n=29, 27%) and Māori (n=10, 18%) children, compared with European children (n=10, 6.0%) (P< 0.001).[35]

The prevalence of prediabetes increases with age and approximately 67% of people regulatory take hypoglycaemic medication.[36] New Zealand’s Ministry of Health ‘Data Explorer’ indicates that the prevalence of diabetes in 2023/2024 was 6.4% of the adults (over age 15) excluding pregnant women.[37]

Prediabetes and diabetes are more easily reversed at an early stage. When young people are diagnosed with prediabetes and T2DM, this sets the metabolic ‘stage’ for a spectrum of illnesses at an earlier stage than previous generations, which can then undermine health, wellbeing and productivity in the years to come.

Not Only Nutrition: Environmental Toxins and the Human Exposome.

While this paper focuses primarily on diet and nutrition, acute and chronic exposures beyond diet and nutrition form an essential part of the wider environmental-health framework shaping metabolic and mental wellbeing. Environmental and dietary exposures frequently interact, amplifying risk across the life course. Exposures occurring pre-conception, during pregnancy, infancy and youth can produce long-term deficits in cognition, health and earning capacity, contributing to increased disability, lower lifetime income and reduced quality of life.

Exposures can be tiny, in trace amounts, at parts per million, billion and/or trillion yet can have biologically meaningful effects. Environmental epigenetic factors modulate gene expression through interconnected mechanisms such as DNA methylation, histone modification and non-coding RNA regulation.[38] [39] Endocrine-disrupting chemicals, even at hormonally relevant low doses, can mimic or block normal hormone action, disrupt cellular signalling networks and alter transcriptional patterns. These processes intersect with metabolic pathways including glycolysis, oxidative phosphorylation and fatty-acid oxidation, all of which govern cellular phenotype and function. Exposures at sensitive developmental stages, particularly those affecting the central nervous system, can lead to long-lasting impairments and reduce quality of life.[40] [41] [42] These pathways can directly interfere with the control of food intake and metabolism:

including metabolic efficiency via effects on the development of the adipose tissue, pancreas, liver, gastrointestinal tract, brain and/or muscle, thereby resulting in an altered body weight set point or sensitivity for developing obesity across the lifespan and generations. In utero and early development may be a highly sensitive time for the programming of fat storage due to permanent effects on gene expression and adipose tissue differentiation. [43]

Importantly, these environmental, nutritional, inflammatory, endocrine and epigenetic influences are not isolated. They frequently dovetail: nutritional insufficiency can heighten vulnerability to environmental toxins; endocrine-disrupting exposures can intensify metabolic instability; and chronic inflammation can magnify epigenetic and neurological impacts. Together, these interacting factors may precipitate or exacerbate both metabolic and mental-health conditions. This integrative view does not imply that mental health challenges are solely genetic, chemical or psychological; rather, they often emerge from a complex constellation of interrelated processes.

As a consequence, the simple excess energy balance theory of obesity is being replaced by a more complex approaches which encompass carbohydrate and obesogen exposure across the lifespan and which increasingly appear to provoke excess consumption. Personal and dietary changes including shifts away from refined and ultraprocessed foods consequently reduce exposure to obesogenic substances. [44]

Socially and environmentally mediated exposures are now recognised as far more influential drivers of chronic disease than discrete genetic traits. Genome-wide association studies (GWAS) demonstrate that genetic contributions to affect, behaviour and cognition arise from thousands of variants, each exerting extremely small effects. [45] In response to the limited explanatory power of genetics alone, the concept of the ‘exposome’ was proposed in 2005, the ‘lifetime environmental exposures (physical, chemical, biological, psychosocial, social, behavioral, etc.) from conception to death’ was defined. This was further refined and expanded to the:

classification of the exposome into three overlapping domains that can change over time: the internal exposome (e.g., aging, oxidative stress, metabolism, gut microbiome), the general external exposome (e.g., climate, built environment), and the specific external exposome (e.g., chemical exposure, lifestyle, occupations). [46]

Socially and environmentally mediated exposures are a far greater driver of chronic disease than discrete genetic traits. The genome-wide association (GWA) studies demonstrated that:

‘genetic influences on individual differences in affect, behavior, and cognition are driven by thousands of DNA variants, each with very small effect sizes.’

In 2005, after recognising the relatively small contribution of genetics to cancer risk, the concept of the human exposome, the ‘lifetime environmental exposures (physical, chemical, biological, psychosocial, social, behavioral, etc.) from conception to death’ was defined. This was further refined and expanded to the:

classification of the exposome into three overlapping domains that can change over time: the internal exposome (e.g., aging, oxidative stress, metabolism, gut microbiome), the general external exposome (e.g., climate, built environment), and the specific external exposome (e.g., chemical exposure, lifestyle, occupations). [47]

Industrial, agricultural and urban pollution drives early childhood deaths and promotes gastrointestinal diseases and non-communicable disease in children.[48] Health effects from pesticides,[49] [50] electromagnetic-fields,[51] [52] [53] [54] [55] , plastics,[56] [57] remain relatively unresearched and therefore unknown in New Zealand. General practitioners and clinicians lack clinically approved and funded pathways for testing and funded pathways for research are lacking. Priorities may not reflect real risks. Heavy metal poisoning may cause more heart disease than high cholesterol, but testing for cholesterol is normal while testing for heavy metals is not normal.[58] [59] [60]

People can be exposed to pollutants and toxins via industrial, agricultural, urban and workplace exposures. These exposures can then not only result in chronic illness, but can provoke and amplify poor mental health and neurodegenerative disorders.[61] Heavy metals[62] [63] [64] [65], particulate matter[66] [67], common pesticides[68] [69] and household and general use substances have been identified as neurodevelopmental toxicants which increase risk to brains, from preconception onwards. [70]

This facet of health care is largely unrecognised in conventional medical practice. Integrative or functional medical practitioners often have a greater ‘toolkit’ to address the environmental contributors to poor health. These doctors have elected to pursue continuing professional development (CPD) outside the conventional ‘mainstream’, to gain a broader appreciation of the drivers of toxicity. This includes further education to support their capacity to evaluate and address the complex interrelationships between diet, digestion, physical and social environmental exposures, genetics and methylation capacity. When presented with complex, chronic conditions, functional medicine practitioners run serum and biomarker screening tests in addition to conventional screening to evaluate genetic variation and methylation capacity, and toxic stressors and work to eliminate toxicity, improve absorption in the digestive tract and enhance nutrition.

Figure 8. Petit, P., Vuillerme, N. (2025) Global research trends on the human exposome: a bibliometric analysis (2005–2024). Environ Sci Pollut Res.

This dimension of health care remains only partially recognised within conventional medical practice and health agencies. Integrative and functional medicine practitioners tend to work with a broader clinical ‘toolkit’ that allows them to engage more directly with environmental contributors to ill health. Many pursue additional continuing professional development outside standard CPD pathways through organisations such as Australasian College of Nutritional and Environmental Medicine, to deepen their understanding of the interrelated drivers of toxicity, metabolic instability and chronic inflammation. This training supports a more integrated evaluation of diet, digestion, physical and social environmental exposures, genetic variation and methylation capacity. When faced with complex, multi-system conditions, functional practitioners commonly use targeted serum and biomarker assessments to identify toxic stressors, address digestive-tract function, and optimise nutritional status.

In New Zealand, however, most functional medicine practitioners are required to send clinical samples overseas for toxicity and biomarker analysis, as no domestic infrastructure exists to provide these services. There is currently no Ministry of Health support or coordinated framework in the research sector to assist clinicians who manage complex chronic or acute presentations that may be initiated or exacerbated by toxic, endocrine, inflammatory or epigenetic environmental exposures.

The practical effect is that both physicians and patients are constrained by cost, and the public system has not provided affordable pathways to support appropriate metabolic or toxicity screening. This produces inequity: individuals on low incomes are often unable to investigate complex or chronic conditions, while those with greater financial means can access comprehensive testing. Although there is a recognised risk that repeated testing may at times be driven by health anxiety or diagnostic uncertainty, resulting in low-value or low-yield investigations, many functional medicine practitioners use a defined, evidence-guided panel of tests that they adjust according to the patient’s history, exposures and clinical presentation.

Figure 9. Escobedo-Monge M, Lustig RH, Suchkov S, et al.(2025). Personalized Nutrition in Pediatric Chronic Diseases. Metabolites.

The absence of a national research programme assessing human toxicity patterns has also constrained scientific innovation. As international awareness of environmental exposures, nutrition and metabolic health grows, consumer demand for affordable and accessible biomarker and toxicity-screening technologies is increasing rapidly. Without investment in local research, health practitioners and agencies will be unable to address health inequities over the longer term as these technologies become more sophisticated and affordable.

A recent paper, Personalized Nutrition in Pediatric Chronic Diseases, reviewed Omics technologies which can increasingly precisely analyse gene–diet interactions, gut microbiome compositions, and metabolic responses. Multi-omics integration combines microbiome, metabolomics, and genomics diagnostics. The data can play an important role in revealing inter-individual variability in nutrient processing.[71] While there are many challenges, which include concerns about privacy, this interdisciplinary area is an exciting field of development that could support health clinicians with future diagnostics.

Oral Health Opportunity: Correlates with common metabolic conditions.

If one looks at teeth as a window to overall systemic health, an absence of both dental caries and gingival bleeding in the absence of oral hygiene could be regarded as a potentially sensitive marker for an overall healthy diet.[72]

An increasing weight of evidence suggests that that the modern epidemics of dental caries and periodontal disease are correlates of a broader chronic disease spectrum that includes metabolic syndrome and poor mental health.[73] [74] [75] Oral disease does not occur in isolation; it frequently reflects broader metabolic and inflammatory pressures operating across the body.

As such, the modern oral health epidemic may be primarily mediated by diets high in refined carbohydrates. These foods exert cascading effects on the oral microbiome, local immune responses, epithelial integrity, and the mineralisation of bone and teeth. The cluster of risks that undermine oral health (poor diet, smoking, stress, low socioeconomic status, metabolic dysfunction) are the same modifiable determinants that drive most chronic diseases. The cluster of risks that undermine oral health (poor diet, smoking, stress, low socioeconomic status, metabolic dysfunction) are the same modifiable determinants that drive most chronic diseases. In a landmark paper, Sheiham and Watt argued that ‘a collaborative approach is more rational than one that is disease specific’.[76]

Oral health, like mental health, does not exclusively begin above the neck. The state of the mouth is intricately associated with the health of the human body. The most commonly encountered dental diseases and conditions in New Zealand include tooth decay (dental caries), chalky teeth (molar hypomineralisation), gum disease (periodontal disease), and oral cancer.

Acute risk factors, such as high free-sugar intake and frequent consumption of acidic beverages, directly contribute to dental hard-tissue erosion and the development of dental caries. Dental erosion may also result from certain medications or repeated exposure to gastric acid.

In contrast, poor overall dietary quality drives more complex, chronic metabolic responses that act systemically to increase the risk of common dental diseases and conditions. Many factors are implicated in oral health decline, and numerous confounders, oral-hygiene practices, stress, smoking, socioeconomic status, genetics have historically made direct attribution difficult. Yet these interacting factors are themselves influenced, up- or down-regulated, by diet quality. Nutrient-dense diets can buffer genetic vulnerabilities and support stress resilience, whereas inferior diets promote a cascading effect across body systems, increasing susceptibility to inherited conditions, inflammation, and stress-related disorders. Before the widespread availability of processed foods, periodontal disease was recognised as a manifestation of scurvy, caused by inadequate vitamin C intake, illustrating how diet and nutrient status directly affect gum and bone health. [77]

Clinicians in hospitals, dental clinics and general practice now routinely encounter patients with multimorbidity, a pattern that includes elevated risk of tooth decay and periodontal disease. The scientific literature demonstrates consistent associations between oral disease and both free sugars (added to processed foods and beverages, and naturally present in syrups, honey, fruit concentrates and juices) and rapidly digestible starchy foods.

Persistent exposure to refined carbohydrates, including high-glycaemic starches and ultra-processed foods, is strongly implicated in the aetiology of dental caries, hypomineralisation, periodontal disease and, to some extent, oral cancer. These risks converge around several mechanisms: diets that sustain an environment conducive to bacterial replication; persistent local or systemic inflammation; deficiencies in essential vitamins and minerals; and reduced immune competence. However, these interrelated drivers of dysbiosis, chronic inflammation[78] [79] and poor mineralisation of bone and teeth are rarely examined in combination in landmark oral-health papers (such as Venturelli et al (2019)[80]) or reflected in health-promotion materials.

Dental caries arise primarily from sustained exposure to fermentable carbohydrates. Both simple sugars and rapidly digestible starches possess similar capacities to increase caries risk. Historically, populations consuming minimal refined carbohydrates experienced far lower rates of dental caries. [81] [82]

Frequent consumption of refined carbohydrates across the day, including meals and snacks, creates an oral environment conducive to caries, gingivitis (a reversible early-stage gum inflammation), and periodontal disease. Periodontitis is a progressive, destructive condition involving irreversible damage to gum tissue, the periodontal ligament and the alveolar bone. Progression from gingivitis to periodontitis depends on a range of interacting factors, including metabolic health, immune function, smoking, stress, and genetic susceptibility.

Refined starches and their breakdown products lower plaque pH, shift the oral microbiome, and promote bacterial fermentation. Highly processed starches adhere to the tooth surface and are readily metabolised by oral bacteria. Increased sugar intake promotes plaque accumulation and is associated with heightened gingival inflammation, producing a biofilm-induced inflammatory response. Gingivitis can develop even in the presence of good oral hygiene if dietary pressures are persistent.[83] The persistence of refined starch in the mouth promotes dental decay but also sets the scene for the development of gingivitis and/or periodontal disease.[84] [85] A recent (2025) paper reported that increased intake of sugars in study participants resulted in increased plaque accumulation, and was associated with higher levels of gingival inflammation, producing a biofilm-induced inflammatory response on the gingival tissue.[86]

Ingredients in ultra-processed foods which include sugars, refined starches and refined seed oils, are associated with increased risk for periodontal disease, and early-life exposure may predispose to earlier onset of disease.[87] [88] [89] [90]

Excess intake of refined carbohydrates and ultra-processed foods not only harms oral tissues directly but also displaces nutrient-dense foods that support epithelial integrity, immune function, bone mineralisation and periodontal health. [91] [92] [93] [94] Key mechanisms include:

B-vitamins for cellular metabolism, repair and proliferation
Vitamin A for epithelial health and antioxidant defence
Vitamin C for collagen formation and oxidative-stress protection
Vitamin D for calcium absorption, bone and tooth mineralisation, and prevention of hypomineralisation
Minerals such as calcium and magnesium for bone and tooth structure; iron for preventing ulceration and oxidative stress; zinc for epithelial repair and immune function

Together, these findings indicate that oral health is a sensitive indicator of broader metabolic and nutritional status, and that contemporary diets dominated by refined and ultra-processed foods create conditions that undermine both.

A recent white paper by the New Zealand Dental Association (NZDA), Roadmap Towards Better Oral Health[95] highlighted the poor oral health of the New Zealand population and the barriers to adequate dental treatment. The paper reported that in 2023/2024 an estimated 321,000, or 7.4% of the adult population had one or more teeth removed due to decay, abscess, infection or gum disease, while 31,000, or 3.3% of children had one or more teeth removed over the same period. The report highlighted the progressive and severe implications of chronic progressive dental disease, and emphasised that low-income groups and that Pasifika populations were most at risk of deteriorating oral health.

The report recommended expanding care to young adults and the implementation of dental service models to meet the needs of local communities and high-need population groups. The Roadmap continued the advocacy of the NZDA in increasing the affordability of oral health related prescriptions and laboratory screening services:

That pharmacy charges to patients for prescriptions issued by a dentist should be the same as those for prescriptions issued by a medical practitioner in primary care.
That patients attending a dentist should have access to funded laboratory services for histology and routine blood tests on the same basis as primary care.

PSGRNZ supports many of the Roadmap’s positions. The following paragraphs explain why, in our view, the NZDA missed an important opportunity by downplaying the role of diet and nutrition while giving substantial weight to a compound that may pose risks to children’s brain health.

The Roadmap identifies several risk factors for poor oral health that are shared with other chronic conditions such as diabetes, cardiovascular disease and respiratory disease. The recognised obstacle of excess sugar consumption, tobacco use and alcohol is addressed, however, the Roadmap does not discuss the broader role of refined carbohydrates, i.e. the cumulative carbohydrate burden as an underlying driver of tooth decay (dental caries), chalky teeth (molar hypomineralisation), gum disease (periodontal disease) and oral cancer. The Roadmap does not devote attention to nutritional determinants of oral health, particularly the roles of essential vitamins and minerals in supporting epithelial integrity, immune function, bone mineralisation and periodontal tissue health. Instead, six pages are dedicated to community water fluoridation and topical fluoridation.

The Roadmap does not disclose the ongoing scientific controversy surrounding community water fluoridation or the ethical considerations relating to fluoride exposure in children under ten years of age, a population exquisitely vulnerable to neurodevelopmental toxicants. Recently, a 2024 Cochrane review found only the low-certainty evidence for the potential for water fluoridation to reduce socioeconomic disparities in dental caries. For clinicians committed to achieving the best health outcomes for children, low-certainty evidence raises a reasonable ethical question about cost–benefit trade-offs, particularly given emerging concerns about neurodevelopmental risks. New Zealand has not conducted a risk assessment examining the combined exposure of fluoridated drinking water and fluoride toothpaste in children under ten. At present, no lower safe threshold has been established for these early developmental age groups.[96] The Roadmap cited papers by the Prime Minister’s Chief Science Adviser and the Royal Society Te Aparangi. These reviews did not conform to any standards for a methods-based risk assessment which are appropriate for the formation of government policy.

The findings published in the U.S. National Toxicology Program monograph[97], an influential document that has intensified international debate regarding the safety of community water fluoridation were also omitted from the report, and evidence that was disclosed in a U.S. court case (2024) [98] which found that the U.S. Environmental Protection Agency had failed to follow their own risk assessment guidelines. [99]

PSGRNZ recognises that, over time, the NZDA will place greater emphasis on the multifactorial dietary and nutritional drivers of poor oral health, including the substantial overlaps with metabolic and mental health. A stronger focus on micronutrients, central to epithelial integrity, immune function, bone mineralisation and periodontal health, would support a more comprehensive, evidence-informed approach to improving oral health outcomes in New Zealand.

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