Uncategorised

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

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Figure 10. Five Targets for the Health System. https://www.health.govt.nz/statistics-research/system-monitoring/health-targets#Thetargets

The key indicators of New Zealanders’ health and wellbeing include self-rated health, life expectancy, mortality rates across the population and maternity measures.[1] In contrast, the health targets that are published in the Government Policy Statement on Health 2024-2027 concern Ministry priorities and expectations for service care and delivery in the medical system.[2] No health targets exist for lowering the prevalence and incidence of diabetes, heart disease, the spectrum of problems driven by obesity (including pain and inflammation) and mental illness, in the public health directorate policies.

The targets are decoupled from the indicators, with no chain-of-logic that would support the integrative, health-protective approach that is necessary to sustain health and wellbeing. This policy–indicator misalignment means that targets do little to arrest upstream drivers of symptom clusters that precede diagnosis. Ministry targets instead centre on disease metrics and medical treatment.

This misalignment helps explain why metabolic and mental health burdens continue to rise despite expanded service access. The health targets do nothing to mitigate or stop the upstream drivers of the clusters of symptoms that drive complex illness and that precede a medical diagnosis, and produce declining health, wellbeing and life expectancy. The health targets are unable to address the drivers of chronic illness and multimorbidity and years lost due to illness.[3] [4]

Primordial prevention revolves around building and sustaining a healthy metabolism from the outset to prevent decline. Primordial prevention is absent from the current strategy. Instead, the health targets prioritise medically-focussed secondary and tertiary interventions. This structural misalignment helps explain why metabolic and mental health burdens continue to rise despite expanded service access.

Health targets include shorter stays in emergency departments, and shorter wait times for specialist assessments. Such policies can be presented in parallel with primordial and primary prevention strategies. The health targets focus on faster cancer treatment, yet there are no policies that prevent cancer arising in the first place.

The Ministry of Health maintains a page on multimorbidity, which is drawn from staff presentations at General Practice consultations.[5] The page includes a section on prevention, which includes:

lifestyle modification (increase physical activity, improve nutrition, smoking cessation, alcohol moderation)
motivational interviewing
referrals to community providers for support eg Green Prescriptions.
smoking cessation, treating hypertension and hypercholesterolemia.

It is not evident that primordial and primary prevention strategies have been clearly distinguished or prioritised by health officials. Current dietary guidelines appear to be treated as the extent of prevention in this domain. The current priority of screening and immunisation may also have, in practice, displaced earlier and more fundamental prevention strategies.

PUBLIC HEALTH FRAMEWORK

Primordial prevention:

Preventing the upstream social, environmental, cultural and dietary risk factors that disrupt the metabolic function of the individual. Risk factors can include factors that drive low-grade inflammation; dysregulate the endocrine and immune system; overload hepatic–renal clearance; and impair digestive, mitochondrial, cardiovascular, and neurodevelopmental function.

Primary prevention:

Reduce the risk of future disease by identifying and targeting modifiable risk factors in healthy people who are at risk of chronic disease through relevant support programmes. Nutritional and biomarker screening to identify e.g. methylation problems can identify personal vulnerabilities. Programmes may include doctor-patient and clinic-patient support, community support and local government and regional support. Programmes can increase knowledge, skills, and access to healthy food; reduce barriers to exercise and the natural environment; and promote connected communities.

Secondary prevention:

The identification of people with early/asymptomatic disease via the use of screening programmes in order to treat patients early, and ensure health status does not decline further. Programmes currently emphasise medical screening, and nutritional and biomarker screening can be more fully integrated to ensure an integrative approach to support optimum biological health.

Tertiary prevention:

Diagnosis of and treatment of people with the fully developed disease, so as to prevent recurrence and complications. Nutritional frameworks are yet to be adapted into tertiary prevention modalities.

Health Policy: A Prevention Framework That Sidelines Nutrition.

New Zealand health policy documents consistently emphasise central values of wellbeing, equity, and health. ‘Prevention’ in New Zealand health policy refers predominantly to health system interventions such as screening and early treatment. At times prevention refers to the need for a healthy diet. A healthy diet explicitly applies to Ministry of Health dietary guideline information.

‘Health promotion’ in New Zealand draws from the Ottawa Charter, the Bangkok Charter for Health Promotion and Māori models of health.[6] [7] These Charters recognise that a wide range of factors support health: peace, shelter, education, food, income, a stable eco-system, sustainable resources, social justice, and equity.

The Charters and corresponding Ministry of Health policy and health promotion literature under-emphasise the outsize role of diet in protecting the gut microbiome and digestive tract, supporting metabolic health to protect people from chronic metabolic diseases and syndromes, including mental illness. Papers outlining central role of nutrition in increasing resilience to the physical and emotional stresses of life, which includes supporting sleep, could not be identified. [8]

The Charters infer that current health information is correct. For example, the Bangkok Charter states:

‘Health promotion has an established repertoire of proven effective strategies which need to be fully utilised’.

In a response to an Official Information Act request regarding the Ministry’s Eating and Activity Guidelines (EAHs) Dr Nicholas Jones, Director of Public Health at the Public Health Agency confirmed that the primary documents for current guidelines consist of two background papers[9] [10] and the Australian Guide to Healthy Eating.[11] Dr Jones confirmed that the updated advice was ‘based on recent large international evidence reviews that: [12]

The updated advice in the EAGs is based on recent large international evidence reviews that were used to develop dietary guidelines for Australia, the United States and the Nordic countries. This multi-sourced evidence consistently describes a healthy eating pattern that is high in vegetables and fruit; includes whole grain cereals; low-fat milk products; legumes and nuts; fish and other seafood; and unsaturated oils. This eating pattern is low in processed meats, saturated fat, sodium (salt) and sugar-sweetened foods and drinks. The evidence shows that this way of eating is associated with a lower risk of heart disease, stroke and other health conditions.

The EAGs advice is also closely linked to evidence-based recommendations from the World Health Organization and the World Cancer Research Fund. The link between saturated fat consumption, blood cholesterol levels and heart disease are well established, with evidence building over the past 60 years.

In 2020 Health New Zealand updated its serving size advice, the first adjustment since 1991, to reflect Australian changes.[13] The Australian National Health and Medical Research Council (NHMRC) updated the Australian Guide to Healthy Eating[14], and this was adjusted to reflect data published in the 2006 Nutrient Reference Values for Australia and New Zealand.[15] These reference values as this paper discusses elsewhere, are based on the blood levels of healthy people from the 1980s- to the early 2000s.

The Health Promotion Directorate oversees public health campaigns; health promotion programmes and develops educational resources and publications. Nutrition and dietary information are based on Ministry of Health dietary guidelines which are then translated into promotional flyers and published on the HealthEd Resource database.[16]

Where food is mentioned in policy and health promotion literature, people are encouraged to consume more fruit and vegetables and consume less sugar. The scientific basis that high carbohydrate diets play a substantial role in increasing blood glucose levels and promote insulin resistance and inflammation is well established. However, New Zealand dietary guidelines do not communicate that cumulative dietary carbohydrate intakes elevate blood glucose and triglyceride levels and increase risk for insulin resistance. The government does not recommend paleo, detox or very low (e.g. ketogenic) diets, but does not show evidence of recently having undertaken reviews of the scientific literature to support this position.[17]

As we discussed in chapter 2, official recommendations that revolve around the reduction of saturated fat increasingly appear to be misdirected. The promotional PDFs discuss the benefits of all dietary categories with the exception of fat, and the guidelines recommend low-fat dairy products, and that fat is cut off meat. Although fat is an essential macronutrient, fat is regarded as a high-risk food. Children are advised to only consume foods high in fat, sugar or salt less than once a week.

Increasing evidence suggests that good quality dietary fats support metabolic including cardiac health.[18] Healthy minimally processed dietary fats play an important role in satiety, particularly for people reducing their fat to carbohydrate ratio, aiming to reverse a prediabetic or T2DM diagnosis.[19] [20] [21]

Important nuances in dietary intake are not addressed. This paper focusses on the challenge of refined, ultraprocessed food, yet, for example, official documents do not discern between the health potential of wholefood diets high in saturated foods but low in refined ingredients, versus diets that contain a high proportion of processed and refined products that might also include saturated fats.[22] [23]

There is no advice concerning the role of vitamins and minerals in preventing chronic and infectious disease (including respiratory illnesses). Despite the role of dietary nutrition in epigenetic, hormonal, neurotransmitter and immune regulation, and in moderating inflammation and oxidative stress, dietary nutrition is not prioritised in key health policies. Relatedly, guidance in the promotional flyers for stress, depression and anxiety does not educate or discuss the role of food and nutrition in contributing to improved or impaired mental health.[24]

Nutrition: The Missing Pillar in New Zealand’s Health Policy and Prevention Strategy.

The Government Policy Statement on Health (July 2024)[25] and the New Zealand Health Plan (August 2025)[26] [27] do not carry substantive policy content that provides pathways for health agencies to assess and address dietary inadequacies and nutritional deficiencies. The Statement notes:

The Government is particularly focused on accelerating action to address five non communicable diseases: cancer, cardiovascular disease, respiratory disease, diabetes and poor mental health. Together, these conditions account for around 80% of deaths from non-communicable diseases in New Zealand and considerable health loss experienced by New Zealanders.

Improved prevention of these non-communicable diseases will be achieved through addressing five modifiable risk factors: alcohol, tobacco, poor nutrition, physical inactivity, and adverse social and environmental factors. [28]

The action, or target, of ‘poor nutrition’, which directly relates to nutrition and diet, is the Policy Statement aim to increase the:

Percentage of people eating the recommended daily intake of vegetables and fruit (five or more servings of vegetables, and two or more servings of fruit).[29]

This insubstantial lever cannot address the increasing non-communicable disease burden. This aim drafts out and downplays the role of non-carbohydrate macronutrient groups in supporting health, micronutrients in supporting health and the problem of refined food intakes.

When the policy language consistently fails to prioritise dietary and nutritional drivers, officials are unlikely to launch into related policy development. More opaque outcomes might improve health outcomes in the long term, but direct policy focusing on diet and nutrition might improve health outcomes more swiftly.

Social determinants and environmental factors such as education, employment, income, housing, transport and climate account for the majority of health loss, but when strengthened, these same factors also provide a significant opportunity to improve health outcomes. [30]

The Policy Statement lists seven key health strategies over the next 5-10 years in providing the direction to guide health entities in protecting, promoting, and improving specific health outcomes. As with the overarching document, these key policy papers neglect or downplay the role of diet and nutrition, effectively amplifying the silence around the dietary drivers of New Zealand’s burden of disease.:

Pae Tū: Hauora Māori Strategy (2023): No mention of diet, nutrition or diabetes. Wellbeing mentioned 81 times, equity mentioned 40 times, health mentioned 628 times.
Whakamaua: Māori Health Action Plan 2020–2025 (2020): No mention of diet or nutrition. Diabetes mentioned 5 times, regarding an action plan to prevent and manage gout and diabetes. Wellbeing mentioned 61 times, equity mentioned 54 times, health mentioned 760 times.
New Zealand Health Strategy (2023): Dietary risk factors (mentioned once), and notes (once) need for better access to healthy food and nutrition. Refers to the work of Healthy Families NZ. Wellbeing mentioned 104 times and equity mentioned 32 times.
Te Mana Ola: The Pacific Health Strategy (2023): Notes Pasifika people are three times more likely to have diabetes than European. Mentions dietary risk factors. This policy recommends an expansion of healthy school lunches and a food reformulation target work programme to reduce sodium and sugar in processed food.
Health of Disabled People Strategy (2023): Report mentions higher rates of heart disease, diabetes, respiratory disease and mental health experienced by disabled people. No mention of diet or nutrition. Wellbeing mentioned 129 times, equity mentioned 12 times, health mentioned 780 times.
Women’s Health Strategy (2023): Mentions poor nutrition and that women spend more of their life in poorer health. Priorities 1-3 focus on health system support and pregnancy care. Priority 4 ‘living well and ageing well’ concerns prevention and early intervention but does not mention diet or nutrition.
Rural Health Strategy (2023): No mention of diet or nutrition. One case study discusses a poor diet and diabetes. Wellbeing is mentioned 51 times, equity 28 times, and health 770 times.

The policies repeatedly stress prevention, however, consistent with the Policy Statement on Health, these papers predominantly view health promotion as timely access to health services including screening and immunisation services.

The seven health strategies frequently refer to chronic illness being driven by the broader social determinants of disease, and acknowledge that fast-food businesses will cluster geographically near low-income communities.

New Zealand’s relatively recent mental wellbeing plan does not address the role of nutrition in supporting brain health, despite the He Ara Oranga Report of the Government Inquiry into Mental Health and Addiction (2018) consistently acknowledging associations between poor nutritional status and poor mental health outcomes. The Inquiry was informed by more than 5,200 public submissions and over 400 engagement meetings with communities, clinicians, and sector stakeholders. [31]

‘He Ara Oranga translates as Pathways to Wellness’

The Inquiry was therefore explicitly tasked with examining systemic pathways that support mental wellbeing across the life course. However, despite repeated recognition of nutrition as a contributing factor, the Inquiry did not recommend the allocation of public resources to systematically evaluate the role of diet and nutrition in brain health by age, sex, developmental stage, or multimorbidity status.

As a consequence, no policy mandate exists that might address nutrition and embed nutrition and dietary health as a core consideration in subsequent policy development. Neither the ten-year strategy Kia Manawanui Aotearoa: the Long-term pathway to mental wellbeing’,[32] nor a recent update[33], includes a coherent policy framework for integrating nutrition into mental health service design, prevention strategies, or therapeutic pathways.

Policies that highlight the problem of insufficiency, suggest ways to identify insufficiency, and which tangibly increase access to nourishing food do not exist in the strategies. Some policies have wish-lists and most policies hope for people to eat healthier diets, however healthy diets are aligned with Ministry of Health guideline recommendations which do not address optimum nutritional status.

PSGRNZ could locate only one only consistently funded programme by the Ministry of Health and Health New Zealand that is directly related to improving dietary nutrition and health in New Zealand communities. Healthy Families NZ commenced in 2014. It has received $10 million annually to provide resources to encourage ‘community-up’ leadership and collaboration to leverage activities which support health and equity. The programme has worked across ten locations, primarily Māori communities, with the aim of preventing the rise of chronic disease.[34]

Healthy Families NZ adopted a ‘six conditions of systems change’ approach (aimed at shifting conditions which hold a problem in place[35]) coupled with Kaupapa Māori and mātauranga Māori to drive purpose and impact in local communities. Projects supported by Health Families NZ include the Papatoetoe Food Hub initiative and a Tupu Tahi Whangaroa Growing Together Initiative.[36]

The programme is funded by the Ministry of Health. However, this initiative is not mentioned in Ministry Annual Reports, nor is the allocated funding referred to in the past two Vote Health appropriations. It is not known if funding will extend after 2026.

It is unlikely that other similar projects are funded from the Ministry of Health’s $31 billion budget, other than this $10 million per annum project, that increase access in local communities to high quality wholefoods and which support nutrition and dietary education (including cooking education).

Chapter 8. Health, Research & Academic Sector: No Pathways for Knowledge.

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REFERENCES

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

[1] Ministry of Health. 2024. Health and Independence Report 2023 - Te Pūrongo mō te Hauora me te Tū Motuhake 2023. Wellington: Ministry of Health.

[2] Delivery Plan A summary of the plan to improve healthcare and achieve the Government’s priorities. March 2025 – June 2026

[3] Ministry of Health (September 2024). Achieving the Health Targets. High Level Implementation Plans. July 2024 – June 2027. ISBN 978-1-99-106778-4

[4] Minister of Health (July 2024). Government Policy Statement on Health 2024 – 2027. HP9076. ISBN 978-1-991075-77-2 Wellington: Ministry of Health.

[5] Health New Zealand (January 2024). Multimorbidity. https://www.tewhatuora.govt.nz/for-health-professionals/clinical-guidance/diseases-and-conditions/long-term-conditions/management-of-multimorbidity

[6] Health New Zealand. Models of Health. https://www.tewhatuora.govt.nz/health-services-and-programmes/public-health/models-of-health

[7] WHO. The 1st International Conference on Health Promotion, Ottawa, 1986. https://www.who.int/teams/health-promotion/enhanced-wellbeing/first-global-conference

[8] Sierra P. Feeney et al. (2025) Sleep loss is a metabolic disorder. Sci.Signal. 18,eadp9358. DOI:10.1126/scisignal.adp9358

[9] Ministry of Health. 2012. Food and Nutrition Guidelines for Healthy Children and Young People (Aged 2–18 years): A background paper. Partial revision February 2015. Wellington: Ministry of Health. HP 5480. https://www.health.govt.nz/system/files/2012-08/food-nutrition-guidelines-healthy-children-young-people-background-paper-feb15-v2.pdf

[10] Ministry of Health. 2013. Food and Nutrition Guidelines for Healthy Older People: A background paper. Wellington: Ministry of Health. HP 5574. https://www.health.govt.nz/system/files/2011-11/food-nutrition-guidelines-healthy-older-people-background-paper-v2.pdf

[11] Ministry of Health Official Information Act Request response. September 4, 2024. H2024048401 https://fyi.org.nz/request/27933/response/107134/attach/9/H2024048401%20Response%20Letter.pdf

[12] Ministry of Health Official Information Act Request response. September 4, 2024. H2024048401

[13] Health New Zealand (December 2020). New Serving Size Advice. https://www.tewhatuora.govt.nz/assets/Health-services-and-programmes/Nutrition/new-serving-size-advice-dec20-v3.pdf

[14] NHMRC. 2013. Australian Dietary Guidelines. Canberra: National Health and Medical Research Council. URL: www.eatforhealth.gov.au/sites/default/files/files/the_

guidelines/n55_australian_dietary_guidelines.pdf

[15] NHMRC. 2006. Nutrient Reference Values for Australia and New Zealand including Recommended Dietary Intakes. Canberra: National Health and Medical Research Council; Wellington: Ministry of Health.

[16] Healthed. Healthy Eating. https://healthed.govt.nz/collections/topic-healthy-eating

[17] Health New Zealand (July 2025). Popular diets review. https://info.health.nz/keeping-healthy/eating-well/popular-diets-review

[18] Wu JH, Micha R & Mozaffarian D. Dietary fats and cardiometabolic disease: mechanisms and effects on risk factors and outcomes. Nat Rev Cardiol 16:581–601 (2019). DOI: 10.1038/s41569-019-0206-1

[19] Masood W, Annamaraju P, Khan Suheb MZ, et al. (June 2023). Ketogenic Diet. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499830/

[20] Dashti HM, Mathew TC, Hussein T, et al (2004) Long-term effects of a ketogenic diet in obese patients. Exp Clin Cardiol. 2004 Fall;9(3):200-5. PMID: 19641727; PMCID: PMC2716748.

[21] Kelly, T, Unwin, D, Finucane, F. (2020). Low-Carbohydrate Diets in the Management of Obesity and Type 2 Diabetes: A Review from Clinicians Using the Approach in Practice. Int. J. Environ. Res. Public Health 2020, 17, 2557. DOI: 10.3390/ijerph17072557

[22] Hendriksen RB, van der Gaag EJ (2022). Effect of a dietary intervention including minimal and unprocessed foods, high in natural saturated fats, on the lipid profile of children, pooled evidence from randomized controlled trials and a cohort study. PLOS ONE 17(1): e0261446. https://doi.org/10.1371/journal.pone.0261446

[23] Astrup, A, Magkos, F, Bier, D. et al. (2020) Saturated Fats and Health: A Reassessment and Proposal for Food-Based Recommendations: JACC State-of-the-Art Review. JACC. 76 (7) 844–857. DOI: 10.1016/j.jacc.2020.05.077

[24] Health New Zealand (2025). There is a way through. A guide for people experiencing stress, depression and anxiety. HE2570. https://healthed.govt.nz/cdn/shop/files/HE2570_There_is_a_way_through_booklet_JAN_25-WEB_d4285d44-ddac-4dc8-af38-2b30d5d3432e.pdf?

[25] Minister of Health. 2024. Government Policy Statement on Health 2024 – 2027. https://www.health.govt.nz/system/files/2024-06/government-policy-statement-on-health-2024-2027-v4.pdf

[26] Health New Zealand (August 2025). New Zealand Health Plan | Te Pae Waenga 2024-2027. Wellington: Health New Zealand. https://www.tewhatuora.govt.nz/assets/Publications/New-Zealand-Health-Plan/New-Zealand-Health-Plan-Te-Pae-Waenga.pdf

[27] Health New Zealand (March 2025). Delivery Plan. A summary of the plan to improve healthcare and achieve the Government’s priorities March 2025 – June 2026. ISBN 978-1-991139-27-6 (online)

[28] Minister of Health. 2024. Government Policy Statement on Health 2024 – 2027. Page 4.

[29] Minister of Health. 2024. Government Policy Statement on Health 2024 – 2027. Page 48.

[30] Minister of Health. 2024. Government Policy Statement on Health 2024 – 2027. Page 8. https://www.health.govt.nz/system/files/2024-06/government-policy-statement-on-health-2024-2027-v4.pdf

[31] He Ara Oranga, Report of the Government Inquiry into Mental Health and Addiction. Published in November 2018 by the Government Inquiry into Mental Health and Addiction

978-0-9941245-2-4 (print) https://mentalhealth.inquiry.govt.nz/__data/assets/pdf_file/0024/20868/he-ara-oranga.pdf

[32] Ministry of Health. 2021. Kia Manawanui Aotearoa: Long-term pathway to mental wellbeing. Wellington: Ministry of Health. https://www.health.govt.nz/system/files/2021-08/kia-manawanui-aotearoa-companion-document-sep21.pdf

[33] Ministry of Health. 2023. Kia Manawanui Aotearoa: Update on implementation of a mental wellbeing approach. Wellington: Ministry of Health.

[34] Matheson A, Wehipeihana N, Gray R, et al. (2022). Community-up system change for health and wellbeing Healthy Families NZ Summative Evaluation Report 2022. Te Whatu Ora — Health New Zealand. Wellington.

[35] Kania J, Kramer M, & Senge P, 2018. The Water of Systems Change. FSG. https://inspiringcommunities.org.nz/wp-content/uploads/2019/04/The-Water-of-Systems-Change-FSG-2018.pdf

[36] Healthy Families NZ. 10 Years of Impact. Reshaping our Systems for A Healthier Aotearoa New Zealand. https://www.healthyfamiliesnz.org/_files/ugd/44d27c_bb65d9af249949bc9d114e432cc26b0e.pdf

PART II. GOVERNMENT AGENCIES ‘DRAFT OUT’ INDIVIDUAL BIOLOGY & MULTIMORBIDITY

We welcome your use of this resource but please cite:

Chapter 6. New Zealand's Carbohydrate-Rich Guidelines.

Part II reviews Ministry of Health and Health New Zealand policies to identify the extent to which nutrition and diet is prioritised across the policy spectrum. The public health role of primordial and primary prevention is outlined and contrasted against secondary and tertiary prevention interventions.

This rapid review of government health policies and white papers reveals that New Zealand’s health policies may mention diet or nutrition but consistently lack substantive content reflecting contemporary scientific knowledge and individual risk factors. Contemporary health policies have not translated into tangible outcomes that have lowered the prevalence of poor, and frequently comorbid mental and metabolic health outcomes.

New Zealand’s legislation emphasises the role of officials in the protection of health. Ministry of Health entities and officials are granted powers under the Health Act 1956 and the Pae Ora (Healthy Futures) Act 2022. At all times they are required to ‘improve, promote and protect public health’.

New Zealand acknowledges that poor nutrition is a modifiable risk factor for poor health.

New Zealand’s health budget is considerable, but the percentage dedicated for the research to update existing knowledge bases, to reflect new findings in the scientific literature, to ensure that our policies reflect best scientific evidence, is negligible. Funding to support practitioner and community education for diet and nutrition is negligible. The 2025/2026 budget for the Ministry of Health is $31,052,217,000. Of the $31 billion, $15.7 is budgeted for hospital and specialist services, $9.7 billion is budgeted primary, community, public and population health services and $1.77 billion is targeted for pharmaceutical medicines.[1]

The 2025/2026 budget allocated $6 million for the PHA and the NPHS and $95.3 million to public health and population health leadership.:

‘This category is limited to providing leadership on policy, strategy, regulatory, intelligence, surveillance and monitoring related to public and population health’.[2]

Current New Zealand dietary guidelines for adults recommend 6 servings of grain foods a day and two servings of fruit a day.[3] Pregnant women are advised to consume diets low in only unsaturated fat and eat at least eight servings of cereals a day[4]. The guidelines for children and young people urge four servings of breads and cereals for preschoolers, five servings for children and six to seven servings of breads and cereals per day for young people.[5] Older people are advised to ‘eat plenty of breads and cereals’, 3 servings for women and 5 servings for men a day.[6] Cereals are describe as ‘the best source of energy for the body.’[7]

The guidelines describe T2DM as:

A condition associated with insulin resistance, leading to a relative insulin deficit. It usually develops in adulthood and is caused by lifestyle factors, including obesity. Treatment includes changes to diet, physical activity, weight loss, tablets and/or insulin injections. Sometimes referred to as adult-onset diabetes mellitus or non insulin-dependent diabetes mellitus.[8]

The dietary guidelines do not describe the association of elevated blood glucose levels with risk for insulin resistance, a diagnosis of T2DM and the strong association of elevated insulin levels with obesity. The guidelines simply describe insulin resistance as:

‘The reduced sensitivity of cells to insulin.’[9]

Government guidelines broadly recommending high carbohydrate dietary intakes, do not take into account individual insulin sensitivity, particularly in genetically or metabolically sensitive (e.g. ageing) individuals.

A 2024 Official Information Act request asked two questions regarding carbohydrates and cardiac risk:[10]

Question: Has the Ministry of Health ever reviewed the evidence that partial substitution of carbohydrate with either protein and fats can lower blood pressure, improve lipid levels, reduce estimated cardiovascular risk and reduce pre-diabetes and diabetes incidence?

Response: The Ministry undertook a review of popular diets in 2017 including paleo and very low-carbohydrate diets. The information in this review has now been transferred to Health New Zealand – Te Whatu Ora and can be found on their website at: https://info.health.nz/keeping healthy/popular-diets-review.

Question: Has the Ministry of Health reviewed evidence that current dietary guidelines relating to current recommended levels of breads and cereals in the diet may have potential to increase serum lipids and contribute to the development of pre-diabetes and diabetes? - Pre-schoolers: at least 4 servings - Children: at least 5 servings - Young people: at least 6 servings.

Response: This question was not directly addressed, with Dr Jones instead referring to the 2020 update of current serving sizes which was based on Australian nutrition data from 2013 and earlier. [11]

The government has not reviewed the potential for the cumulative burden of recommended carbohydrate intakes to drive risk for prediabetes and diabetes, and the potential for this to be amplified by ultraprocessed food intake. In a similar vein, New Zealand has been disinclined to identify, regulate and tax ultraprocessed foods and sugar.[12] [13] Ministry of Health guidelines for type 2 diabetes mellitus (T2DM) do not recommend low-carbohydrate approaches.[14] The term ‘metabolic syndrome’ is not recognised by the Ministry of Health.

PSGRNZ’s review of government websites and white pages was unable to identify any budgeted area of policy or policy deployment which were directly concerned with the role of diet and nutrition beyond the production of promotional literature. There are no established bioethics publications specifically addressing whether panels should be ethically required to revisit paediatric carbohydrate guidelines in light of rising prediabetes, T2DM risk and the associated comorbidities. Consensus reviews acknowledge a lack of paediatric carbohydrate alternatives, but they stop short of ethical examination.

As we discuss below in chapter 7-9, neither health policy, health agencies nor science policies build in obligations and explicitly fund ongoing research to keep abreast of the evidence on elevated glucose and unstable insulin levels as a driver of chronic disease, the role of nutrition and toxic exposures to inform policy.

Finally, a series of examples are provided that demonstrate how current policies do not work scientifically or practically, underserving both clinicians and patients.

Chapter 7. Health Targets Decoupled From Policies. No Power to Stop Rising Disease Rates.

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REFERENCES

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

[1] Treasury. Vote Health. The Estimates of Appropriations 2025/26 - Health Sector B.5 Vol.5 https://budget.govt.nz/budget/pdfs/estimates/v5/est25-v5-health.pdf

[2] [2] Treasury. Vote Health. The Estimates of Appropriations 2025/26 - Health Sector B.5 Vol.5 Page 4.

[3] Health New Zealand (2020) Healthy eating, active living. Food and Activity Advice for Adults from 19-64 years. HE code HE1518 https://cdn.accentuate.io/5313685192862/11408390422661/HE1518-healthy_eating_active_living-web_0_Sep2020-v1603943673274.pdf

[4] Health New Zealand (2023). Safe and Healthy Eating in Pregnancy. HE code HE1805 https://cdn.accentuate.io/5313672904862/11408390422661/1.0-HE1805-Healthy-healthy-for-pregnancy_Aug-2023-(1)-v1695958003663.pdf

[5] Healthy Eating for Young People - HE1230 https://healthed.govt.nz/products/healthy-eating-for-young-people

[6] Health New Zealand (2021). Eating for Healthy Older People. https://cdn.accentuate.io/5313672052894/11408390422661/HE1145-HealthyEatingOlderPeople-WEB-Apr-21-v1621897274164.pdf HE1145

[7] Health New Zealand (2023). Eating for healthy children from 2-12 years. Code HE1302 https://cdn.accentuate.io/5313671594142/11408390422661/1.1_he1302_healthy_children_apr_2023_web_0-v1685674014232.pdf

[8] Ministry of Health. 2012. Food and Nutrition Guidelines for Healthy Children and Young People (Aged 2–18 years): A background paper. Partial revision February 2015. Wellington: Ministry of Health. P.181.

[9] Ministry of Health. 2012. Food and Nutrition Guidelines for Healthy Children and Young People. P.177

[10] Ministry of Health Official Information Act Request response. September 4, 2024. H2024048401 https://fyi.org.nz/request/27933/response/107134/attach/9/H2024048401%20Response%20Letter.pdf

[11] Health New Zealand (December 2020). New Serving Size Advice. https://www.tewhatuora.govt.nz/assets/Health-services-and-programmes/Nutrition/new-serving-size-advice-dec20-v3.pdf

[12] Lustig R (2021). Ultraprocessed Food: Addictive, Toxic, and Ready for Regulation. Nutrients 12, 3401; DOI:10.3390/nu12113401

[13] Warhurst L. (October 9, 2019). Jacinda Ardern 'rules out' introduction of sugar tax despite rising numbers of diabetes. Stuff. https://www.newshub.co.nz/home/lifestyle/2019/10/jacinda-ardern-rules-out-introduction-of-sugar-tax-despite-rising-numbers-of-diabetes.html

[14] Ministry of Health and New Zealand Society for the Study of Diabetes. Type 2 Diabetes Management Guidelines Healthy eating and weight loss. https://t2dm.nzssd.org.nz/Section-88-Healthy-eating-and-weight-loss

We welcome your use of this resource but please cite:

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Hyperpalatability & Food Addiction.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Current Ultraprocessed Food Intakes Associated with Poor Health Outcomes.

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

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

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

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

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

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

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

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

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

Satiety, Glycaemic Volatility and the Drivers of Addictive Eating.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Figure 6. The Problem of Carbohydrate Addiction.

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

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

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

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

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

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REFERENCES

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

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[61] Hofeldt FD. (1989) Reactive hypoglycemia. Endocrinol Metab Clin North Am. 18(1):185-201. PMID: 2645126.

[62] Shanik MH, Xu Y, Skrha J, Dankner R, Zick Y, Roth J. (2008). Insulin resistance and hyperinsulinemia: is hyperinsulinemia the cart or the horse? Diabetes Care. 31 Suppl 2:S262-8. DOI: 10.2337/dc08-s264. PMID: 18227495.

[63] Altuntaş Y. (2019) Postprandial Reactive Hypoglycemia. Med Bull Sisli Etfal Hosp 53(3):215–220. DOI: 10.14744/SEMB.2019.59455

[64] Chambers L, McCrickerd K, Yeomans MR. (2015). Optimising foods for satiety. Trends in Food Science & Technology, 41(2):149-160. DOI: 10.1016/j.tifs.2014.10.007

[65] Wu, Y., Ehlert, B., Metwally, A.A. et al. (2025) Individual variations in glycemic responses to carbohydrates and underlying metabolic physiology. Nat Med 31:2232–2243. DOI: 10.1038/s41591-025-03719-2

[66] Song J, Oh TJ, Song Y. (2023) Individual Postprandial Glycemic Responses to Meal Types by Different Carbohydrate Levels and Their Associations with Glycemic Variability Using Continuous Glucose Monitoring. Nutrients, 15:3571. DOI:10.3390/nu15163571

[67] Barber TM, Kabisch S, Pfeiffer AFH, Weickert MO. (2020) The Health Benefits of Dietary Fibre. Nutrients. 12(10):3209. DOI: 10.3390/nu12103209

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[69] Gill SK, Rossi M, Bajka B. et al. (2021) Dietary fibre in gastrointestinal health and disease. Nat Rev Gastroenterol Hepatol 18:101–116. DOI:10.1038/s41575-020-00375-4

[70] Gearhardt et al. (2023). Social, clinical, and policy implications of ultra-processed food addiction.

[71] Zinn C, Campbell JL, Fraser L. 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.

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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. Prediabetes 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 regularly 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.

Chapter 6. New Zealand's Carbohydrate-Rich Guidelines.

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[27] Esquivel Zuniga R, & DeBoer MD. (2021). Prediabetes in Adolescents: Prevalence, Management and Diabetes Prevention Strategies. Diabetes, Metabolic Syndrome and Obesity, 14, 4609–4619. DOI: 10.2147/DMSO.S284401

[28] CDC Spotlight on Diabetes Data. Prediabetes in U.S. adolescents. https://gis.cdc.gov/grasp/diabetes/diabetesatlas-spotlight.html

[29] Prediabetes: A fasting plasma glucose (FPG) 100–<126 mg/dL or hemoglobin A1c (A1c) 5.7–<6.5% and the lack of a diabetes diagnosis. In ElSayed NA, Aleppo G, Aroda VR, Bannuru RR, Brown FM, Bruemmer D, et al. (2023) Classification and Diagnosis of Diabetes: Standards of Care in Diabetes-2023. Diabetes Care. 46(Suppl 1):S19-S40.

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[34] Prediabetes diagnostic criterion is having a haemoglobin A1C (HbA1c) between 41 and 49 mmol/mol (5.8%–6.7%)

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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

RETURN TO CONTENTS PAGE.

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[97] Fixsen, A. (2024). The Construction of Eating Disorders: Psychiatry, Politics and Cultural Representations of Disordered Eating (The Politics of Mental Health and Illness). Palgrave Macmillan.

[98] Dietch DM, Kerr-Gaffney J, Hockey M, et al. (2023). Efficacy of low carbohydrate and ketogenic diets in treating mood and anxiety disorders: systematic review and implications for clinical practice. BJPsych Open. 9(3):e70. DOI:10.1192/bjo.2023.36

[99] Boltri M, Scalia A, Brusa F et al. (2025). Keto therapy–unveiling the potential of ketogenic diet in psychiatric care: A scoping review. Nutrition, 134:112710, DOI: 10.1016/j.nut.2025.112710

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For over 20 years the Physicians and Scientists for Global Responsibility New Zealand Charitable Trust (PSGR) has produced reports and submitted to government Bills and Inquiries.

We’ve been extraordinarily busy over the past 2 years with our work.

This Update aims to inform members and colleagues – and act as a go-to summary of our recent work.

2022 UPDATE - PDF

As well as our recent work All PSGR’s submissions are available to the public on our Submissions pages. In addition, we are now on LinkedIn, Twitter, Odysee & Instagram.

MEMBERSHIP

Please – without your support and membership PSGR cannot do this work. We’ve kept our fees deliberately low because your membership is important to us.

MOVING FORWARD 2022+

The PSGR recognise that the perspectives that have been expressed by the PSGR from 2020 onwards will not necessarily reflect the perspectives of all trustees and all members.

However, we sincerely hope that PSGR’s perspectives are more likely to reflect the perspectives of the majority of our membership and of collegial organisations – which represents a diverse quorum of inquiring minds.

We hope that we have demonstrated a consistency to our work, that reflects and upholds the principles reflected in 20 years of research, information communications and submissions to policy

Reports and Papers

Royal Commission

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