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Chapter 1. The Problem. Cascading Impairment Driving Multimorbidity.

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


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

From 2015 Onwards – Escalating Evidence.

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

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

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

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

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

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

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

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

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

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

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

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

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

The January 2026 U.S. Dietary Guideline Shift.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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


Chapter 2. The Total Carbohydrate Burden & Individual Vulnerability


REFERENCES

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Information

  • NEWS NOW: RECLAIMING HEALTH
  • SCIENCE FOR PUBLIC GOOD
  • PSGR REPORTS & PAPERS
  • RESPONSES/SUBMISSIONS TO PUBLIC CONSULTATIONS
    • GENERAL GOVERNMENT
    • MINISTRY OF HEALTH (MoH)
    • MINISTRY FOR THE ENVIRONMENT (MfE)
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