Ketogenic: The Science of Therapeutic Carbohydrate Restriction in Human Health

By Tim Noakes

Ketogenic: The Science of Therapeutic Carbohydrate Restriction in Human Health presents the most up-to-date and evidence-based science and research available in the field of TCR, with the purpose of training medical and allied healthcare professionals on the effective therapeutic use of low-carbohydrate and ketogenic nutrition in clinical practice. This book explores the appropriate, safe, and effective use of TCR to improve patient outcomes in a broad range of chronic metabolic conditions and aims to promote health. 

Focused on lifestyle management, health support and the treatment of diseases rooted in poor nutrition, this book explores the role of food and lifestyle modification as medicine and is a valuable resource for nutritionists, dietitians and medical professionals who provide diet-related counselling, as well as those researching or studying related areas. 

• Presents new best-practice guidelines for using TCR to treat, improve or reverse nutrition-related metabolic conditions and diseases that were previously thought to have a chronic, irreversible progression
• Provides an overview of the most recent evidence outlining the biochemistry and physiology pertaining to human nutrition and health
• Offers evolutionary and historical context to human nutrition
• Contains clinical practice guidelines for the implementation of TCR from medical practitioners who prescribe TCR in their practices, allowing readers to understand real-life concerns in the field
• Features case studies that provide practical examples of how to assess, monitor and intervene with patients that practitioners encounter in their practices
• Explains the physiology and biochemistry of the normal and pathophysiological state for each condition and links these to the application of TCR

• Language: English
• Publisher: Academic Press
• Release date: Jun 22, 2023
• ISBN: 9780128216231

Book preview

Front Cover for Ketogenic - The Science of Therapeutic Carbohydrate Restriction in Human Health - 1st edition - by Timothy David Noakes, Tamzyn Murphy, Neville Wellington, Hassina Kajee, Sarah M. Rice

Ketogenic

The Science of Therapeutic Carbohydrate Restriction in Human Health

Edited by

Timothy David Noakes

Department of Health and Wellness Sciences, Cape Peninsula University of Technology, Cape Town, South Africa

Nutrition Network, Cape Town, South Africa

Tamzyn Murphy

Nutrition Network, Cape Town, South Africa

Neville Wellington

Nutrition Network, Cape Town, South Africa

Hassina Kajee

Nutrition Network, Cape Town, South Africa

Sarah M. Rice

Nutrition Network, Cape Town, South Africa

Table of Contents

Cover image

Title page

Copyright

List of contributors

Preface

Introduction

Part 1: Nutritional fundamentals

Chapter 1. Understanding human diet, disease, and insulin resistance: scientific and evolutionary perspectives

Abstract

1.1 Understanding human diet and disease – the scientific and evolutionary evidence

1.2 Insulin resistance: a unifying feature of chronic disease

1.3 The adoption and evolution of dietary guidelines

References

Chapter 2. Nutritional aspects

Abstract

2.1 Introduction

2.2 Therapeutic carbohydrate restricted dietary intervention

2.3 Physiological ketosis of the Fed State: biochemical and nutritional aspects

2.4 Implications for nutrient needs

2.5 Plant versus animal nutrition

2.6 Conclusion

References

Further reading

Part 2: Medical nutritional therapy

Chapter 3. Endocrine

Abstract

3.1 Introduction

3.2 Liver

3.3 Metabolic syndrome

3.4 Type 2 diabetes

3.5 Adapting medication for type 2 diabetes in the context of therapeutic carbohydrate restriction

3.6 Type 1 diabetes

3.7 Polycystic ovarian syndrome and infertility

3.8 Body weight

3.9 Thyroid health and insulin resistance

3.10 Adrenals and the hypothalamic-pituitary-adrenal (HPA) axis

References

Chapter 4. Cardiovascular disease and its association with insulin resistance and cholesterol

Abstract

4.1 Anatomy and normal physiology of the cardiovascular system

4.2 Cardiovascular pathophysiology

4.3 Cholesterol

4.4 Lipoproteins

4.5 Carbohydrate restricted diets and specific cardiac disorders

4.6 Conclusion

References

Chapter 5. Neurology

Abstract

5.1 A ketogenic diet addresses the pathophysiology underlying diverse neurological disorders

5.2 Neurophysiology and energy metabolism

5.3 Cerebrovascular disease and stroke

5.4 Epilepsy

5.5 Alzheimer’s disease

5.6 The ketogenic diet in mood disorders

5.7 Multiple sclerosis and nutrition

5.8 Parkinson’s disease

5.9 Neurodevelopment and autism spectrum disorder

5.10 Migraine

5.11 Amyotrophic lateral sclerosis

5.12 Traumatic brain injury

Useful websites

References

Chapter 6. Cancer

Abstract

6.1 Cancer as a modern disease

6.2 Cancer as a mitochondrial metabolic disease

6.3 Cancer management using press-pulse ketogenic metabolic therapy

6.4 Implementation of modifiable ketogenic diets in cancer

6.5 Fasting and chemotherapy

References

Further Reading

Chapter 7. Musculoskeletal and immunological considerations

Abstract

7.1 Introduction

7.2 Musculoskeletal conditions

7.3 Gout

7.4 Ageing and therapeutic carbohydrate restriction

7.5 Autoimmunity

7.6 Perspective: autoimmunity in the context of plant and animal nutrition

References

Further reading

Chapter 8. Gastrointestinal health and therapeutic carbohydrate restriction

Abstract

8.1 Introduction

8.2 The human digestive system in health and disease

8.3 Diet and gastrointestinal disorders

8.4 The Microbiome and Therapeutic Carbohydrate Restriction

References

Part 3: Therapeutic carbohydrate restriction for health and fitness

Chapter 9. Exercise and sports performance

Abstract

9.1 Introduction

9.2 The science of low carbohydrate and ketogenic diets for exercise and sports performance

9.3 Practical application of low-carbohydrate high fat diet and ketogenic diets in athletes

9.4 Evidence that the oxidation of liver- (or gut-) derived glucose, but not muscle glycogen, is obligatory for sustained exercise performance in humans

9.5 Nutritional supplementation for athletic performance

9.6 Case study

References

Chapter 10. Therapeutic fasting

Abstract

10.1 Introduction

10.2 Physiology

10.3 Therapeutic fasting

10.4 Conclusion

References

Further reading

Part 4: Managing the patient

Chapter 11. Psychological, behavioural, and ethical considerations

Abstract

11.1 Introduction

11.2 Behaviour change

11.3 Eating control

11.4 Legal and ethical aspects to therapeutic carbohydrate restriction

References

Further reading

Acronyms

Index

Copyright

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Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary.

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List of contributors

Joan Adams,     HPCSA Professional Conduct Commitee, Arcadia, Pretoria, South Africa

Ali Irshad Al Lawati,     Diwan of Royal Court, Muscat, Oman

Nadir Ali,     Webster, TX, United States

Gabriel Arismendi-Morillo,     Instituto de Investigaciones Biológicas, Facultad de Medicina, Universidad del Zulia, Maracaibo, Venezuela

Shawn Baker,     Revero, San Francisco, CA, United States

Miki Ben-Dor,     Department of Archaeology, Tel Aviv University, Tel Aviv, Israel

Miriam Berchuk,     Alberta Health Services, Calgary, Alberta, Canada

Amy Berger,     Nutritionist in Private Practice

Anne-Sophie Brazeau,     McGill University, Montreal, Canada

Natasha Campbell-McBride,     GAPS Science Foundation, Cambridge, United Kingdom

David Cavan,     Independent consultant, London, United Kingdom

Ann M. Childers,     Oregon City, OR, United States

Christos Chinopoulos,     Department of Medical Biochemistry, Semmelweis University, Budapest, Hungary

Catherine Crofts,     School of Interprofessional Health, Auckland University of Technology, Auckland, New Zealand

Mark Cucuzzella,     West Virginia University School of Medicine, Morgantown, WV, United States

Robert Cywes,     JSAPA Metabolic Centre, Jupiter, FL, United States

Trudi Deakin,     X-PERT Health, Hebden Bridge, West Yorkshire, United Kingdom

David M. Diamond,     University of South Florida, Tampa, FL, United States

Dominic P. D’Agostino,     Department of Molecular Pharmacology and Physiology, University of South Florida, Tampa, FL, United States

Georgia Edes,     Psychiatrist in Private Practice

Julienne Fenwick,     Best of both Wellness, Hermanus, Western Cape, South Africa

Gary Fettke,     Launceston, Tasmania, Australia

Mark I. Friedman,     Nutrition Science Initiative, San Diego, CA, United States

Jason Fung,     Scarborough Hospital Network, Scarborough, Ontario, Canada

Elizabeth Gonzalez,     UCF Medical School, Orlando, FL, United States

Cliff Harvey,     Holistic Performance Institute, Auckland, New Zealand

Michael Hoffmann

University of Central Florida, Orlando, FL, United States

Orlando VA Medical Center, Orlando, FL, United States

Joan Ifland,     Food Addiction Reset LLC, Vashon, WA, United States

Diana Isaacs,     Cleveland Clinic, Cleveland, OH, United States

Hassina Kajee,     Nutrition Network, Cape Town, South Africa

Miriam Kalamian,     Dietary Therapies LLC, Hamilton, MT, United States

Bob Kaplan,     Independent researcher, Wayland, MA, United States

Daniel Katambo,     Afyaplanet, Dagoretti Corner, Nairobi, Kenya

Eric H. Kossoff,     Departments of Neurology and Paediatrics, Johns Hopkins Hospital, Baltimore, MD, United States

Meredith M. Kossoff,     Cornell University, Ithaca, NY, United States

Ian Lake

Aspen Medical Practice, Gloucester, United Kingdom

Everyone Health, Cambridge, United Kingdom

The Fasting Method, New York City, NY, United States

Brian Lenzkes,     Internal Medicine, San Diego, CA, United States

Sean McKelvey,     Institute for Personalized Nutrition Therapy, Vancouver, Canada

Nafeeza Hj Mohd Ismail,     School of Medicine, International Medical University, Kuala Lumpur, Federal Territory of Kuala Lumpur, Malaysia

Purna Mukherjee,     Biology Department, Boston College, Boston, MA, United States

Campbell Murdoch,     Millbrook Surgery, Somerset, United Kingdom

Tamzyn Murphy,     Nutrition Network, Cape Town, South Africa

Timothy David Noakes

Department of Health and Wellness Sciences, Cape Peninsula University of Technology, Cape Town, South Africa

Nutrition Network, Cape Town, South Africa

Connor Ostoich,     Scarborough Hospital Network, Scarborough, Ontario, Canada

Amber O’Hearn,     Independent Researcher, Toronto, Canada

Nadia Pataguana,     Public Health Collaboration, United Kingdom

David Perlmutter

American Nutrition Association, Hinsdale, IL, United States

University of Miami Miller School of Medicine, Miami, FL, United States

Graham Phillips,     iHeart Pharmacy Group, Hertfordshire, United Kingdom

Mathew C.L. Phillips,     Waikato Hospital, Hamilton, New Zealand

Laurie Rauch,     Physiological Sciences, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa

Sarah M. Rice,     Nutrition Network, Cape Town, South Africa

Karen Riley,     Institute for Personalized Nutrition Therapy, Vancouver, Canada

Caroline Roberts,     Virta Health, Denver, CO, United States

Elisa Marie Rossi,     UCF Medical School, Orlando, FL, United States

Fabian Rossi

UCF Medical School, Orlando, FL, United States

Clinical Neurophysiology Lab, Orlando VA Medical Center, Orlando, FL, United States

Joshua Rossi,     UCF Medical School, Orlando, FL, United States

Catherine Saenz,     Exercise Science, Ohio State University, Columbus, OH, United States

Thomas N. Seyfried,     Biology Department, Boston College, Boston, MA, United States

James Smith,     Division of Exercise Science and Sports Medicine, University of Cape Town, Cape Town, South Africa

Angela A. Stanton,     Stanton Migraine Protocol, Anaheim, CA, United States

Mateja Stephanovic,     Scarborough Hospital Network, Scarborough, Ontario, Canada

Martha Tettenborn,     Kemble, Ontario, Canada

David Unwin,     Norwood Surgery, Southport, United Kingdom

Jen Unwin,     Norwood Surgery, Southport, United Kingdom

Christopher Webster,     Division of Exercise Science and Sports Medicine, University of Cape Town, Cape Town, South Africa

Neville Wellington

Private Practice, Cape Town, South Africa

Kenilworth Diabetes Medical Centre, Cape Town, South Africa

Nutrition Network, Cape Town, Western Cape, South Africa

Eric C. Westman,     Division of General Internal Medicine, Department of Medicine, Duke University Medical Centre, Durham, NC, United States

Nasha Winters,     Metabolic Terrain Institute of Health, Wilmington, DE, United States

Susan Wolver,     VCU Medical Weight Loss Program, Richmond, VA, United States

William S. Yancy Jr.

Division of General Internal Medicine, Department of Medicine, Duke University Medical Centre, Durham, NC, United States

Center of Innovation to Accelerate Discovery and Practice Transformation, Durham Veterans Affairs Medical Centre, Durham, NC, United States

Duke Diet and Fitness Centre, Duke University Health System, Durham, NC, United States

Caryn Zinn,     Auckland University of Technology, Auckland, New Zealand

Preface

(Robert) Atkins reinvented the nineteenth century Banting diet in 1963, although it took another 30 years to reach prime time in the public consciousness. His regimen closely resembled the ‘Eskimo diet’ that Joslin had inflicted upon his mother in 1898 [1], the actual Inuit diet advocated for health reasons by the explorer Vilhjalmur Stefansson [2] and the diet tested upon overweight DuPont executives by Alfred Pennington in the 1930s. It should by now come as no surprise to the reader that the new diet worked (for some), generated passion, was condemned, vindicated, grudgingly accepted and finally forgotten.

L. Sawyer and A.M. Gale. Diet, delusion and diabetes. Diabetologia 2009, 52, 4.

My dietary Damascene moment occurred on a Saturday morning in December 2010. Probably not by chance, perhaps by divine intervention, I was introduced to the book – The New Atkins for a New You [3] – written by Drs Eric Westman, Steve Phinney and Jeff Volek. At first I was mortified. How, I wondered, could these three associate with the man whose promotion of a diet loaded with ‘artery-clogging’ saturated fats would send all its followers to an early grave?

My instant of doubt occurred as I read the foreword to their book:

In more than 150 articles these three international experts on the use of the low-carbohydrate diets to combat obesity, high cholesterol and Type-2 diabetes mellitus have led the way in repeatedly proving how a low-carbohydrate approach is superior to a low-fat one.

How could this possibly be credible, I wondered. Not once in my academic training had I been introduced to any of these concealed studies. But who was I to believe? These three dissidents? Or my heavily credential academic mentors, all of whom had taught me their shared version of what constitutes a healthy diet during my medical training in Cape Town? And all of whom had convinced me to eat and promote their ‘heart-healthy’, prudent, low-fat, 1977 US Dietary Guidelines diet pyramid, ‘in moderation’, which I did, dutifully, for the next 34 years.

But within 2 hours of opening the three dissidents’ book, the scales of those lost years fell from my eyes. The secreted scientific evidence that they presented appeared overwhelming. Like Saul, I was now on the road to a transformation of holy proportions. That same day I began my personal experiment with the low-carbohydrate high-(healthy) fat (LCHF) diet, also known as therapeutic carbohydrate restriction (TCR). And the rest, as they say, is now history.

Why was this personal experience which I suspect is shared by the majority of, if not all, the authors of this magnum opus, so necessary for us to arrive at a carefully concealed truth?

The likely explanation is that all of us share a common metabolism, present also in most of those now living in the developed and developing world. Our metabolism is simply not designed to cope with foods that raise our blood glucose and insulin concentrations every few hours, daily, 350 days a year for decades; a diet high in carbohydrates that in our ignorance, most of us have promoted since at least 1977. The diet that, we eventually realized, had made us sick and unhealthy and, in my case, caused me also to develop type 2 diabetes (T2D).

But the only way our programmed stupidities would ever admit that revelation was when we finally summoned the courage to ignore everything our education had taught us about ‘healthy’ diets, and, instead, to do the exact opposite. After which we experienced the full range of dramatic health transformations that are described in these pages and which in my case, included putting my T2D into a medically impossible remission.

Without that common experience, there would not have been authors to explain these truths.

The idea of compiling this textbook with the goal of educating healthcare providers of these realities and how best they might assist the world’s neglected metabolic majority was not mine. It came from the team at The Noakes Foundation, most especially Drs Hassina Kajee and Neville Wellington, and our CEO, Jayne Bullen, together with Candice Egnos. They argued that a novel medical discipline often requires the compilation of a textbook to show sceptical healthcare providers that, yes, there is indeed a large body of published scientific evidence backed up by extensive clinical experience, examining TCR. What is more, this published evidence establishes that TCR is entirely safe and highly effective in the management of a wide range of chronic medical conditions.

But without the support of our 62 expert contributors, each of whom provided their expertise without any thoughts of personal remuneration, we could not have amassed this information.

Ultimately, this work reflects the combined contribution of those selfless individuals. But that is just the nature of the professionals involved in promoting TCR and the LCHF lifestyle. The message, not the individual, is what is ultimately important. Thank you all for your generosity, your courage, and your determination to change the future course of healthcare across the globe.

For what their contributions establish once and for all is that the popular opinion that TCR has no evidence-based support is nonsensical. Instead, this textbook definitively establishes that TCR is perhaps the most studied and definitely the most effective dietary intervention known to modern medicine. In these pages, you will find the hardcore scientific evidence to support that judgement.

We invite you to test that opinion by examining what we have jointly contributed.

Perhaps, like us, in these pages you will discover your own Damascene revelation.

Timothy David Noakes

Department of Health and Wellness Sciences, Cape Peninsula University of Technology, Cape Town, South Africa Emeritus Professor, Division of Exercise Science and Sports Medicine, University of Cape Town, Cape Town, South Africa Sports Science Institute of South Africa, Cape Town, South Africa Nutrition Network, Cape Town, South Africa The Noakes Foundation, Cape Town, South Africa Eat Better South Africa, Cape Town, South Africa

References

1. Joslin EP. Treatment of Diabetes Mellitus 2nd ed. Philadelphia: Lea and Ferbiger; 1917;.

2. Lieb CW. The effect of an exclusive, long-continued meat diet Based on the history, experiences and clinical survey of Vilhjalmur Stefansson, Arctic explorer. J Am Med Assoc. 1926;87:25–26.

3. Westman EC, Phinney SD, Volek JS. The New Atkins for the New You The Ultimate Diet for Shedding Weight and Feeling Great New York, NY.: Atria Books; 2010;

Introduction

At the time the low carbohydrate movement exploded into mainstream science, there was a disjointed scientific community of practitioner pioneers dotted around the globe.

Reducing carbohydrate intake a decade ago was considered a fad diet, something that will pass like many other things that have contested the incorrect dietary guidelines. The same guidelines have contributed to an epidemic of diabetes, obesity and most other chronic and metabolic diseases [1,2]. There were a few strong global voices and pillared efforts to do something in the area, flying flags and sharing good research, but it seemed that no one in policy and dietary guidance was listening. As the new science emerged, it was clear that we had to move forward in a more cohesive and evidence-based way.

Industry was running rife with diabetes and obesity, along with the many other syndromes that we now know are connected to the broader, complex condition known as insulin resistance; they were slowly building momentum and becoming the dire health tsunami we now face and are stuck with as a planet. Healthcare is now doing the tireless, unrewarding work of mopping them up, with little success.

Healthcare workers at the time were getting their continued professional development notches from fancy pharmaceuticals-funded events that came with sweet treats and sweet handshakes [3]. These meetings between doctors and big pharma led, and sadly still lead today, to the branded prescription book for patients [3].

One could call it industry-driven science and learning. We were in a situation where a patient would go to a doctor for medical advice for a chronic condition that was just rearing its head and leave with advice and/or medication that would be guaranteed, for the most part, to make them ill and possibly do more harm than good over time.

When we look back on the past 50 years of global treatment of disease, we see a scary evolving picture. The food industry, and big food in particular, influences consumer choice and shapes demand. Highly processed, addictive foods influence consumer taste and choices [4]. Along with processing and flavour additives, the demand for sugar has escalated at an unimaginable rate, which has fueled the demand for more [4]! Sugar addiction and the addiction to highly processed, often high fat carbohydrate laden foods, fueled by the low fat generation, lay the foundations for a silent health tsunami on a scale no one in the 60s could ever have foreseen or predicted. But here we are today, dealing with a massively obese, diabetic, hypertensive population. Children are having early onset diabetes and fatty liver disease [5] and paediatric bariatric surgery presents ethical dilemmas [6,7] such that alternative approaches demand consideration [8,9].

The simple truth is that we need a full societal change in the way that diet and lifestyle are treated. They need to be brought back into the core principles and ethical tenets of medicine. Doctors and healthcare have to start refocussing on the somehow forgotten link between a patient’s landscape, what they eat and their health. By landscape, I mean the trauma they may face, their stress levels, sleep, exercise patterns and the quality of their lives. We need a full change in the way that we eat and understand diet and its role in our health.

Unable to find answers from their doctors, patients would write to us at The Noakes Foundation, asking Prof Noakes why their doctors would not support their successes on the then called Banting diet.

I have lost 32 kgs, am off all my medications and my diabetes/hypertension have reversed, but my doctor will not agree that I am on the right path was the kind of email we were getting regularly, far too often to ignore.

We started to look for doctors who understood how to help these patients, for referral reasons, and apart from those who are now our medical directors, they were few and far between.

We knew that we had to build a practising community of some kind to support patients, via their doctors, to make them better and improve their lives. And clearly, we had no time to waste!

Fast track several years and we have now taken over 20 trainings to the medical community and trained thousands of medical professionals around the world in how to apply this simple dietary advice to patient care responsibly, meaningfully, robustly and confidently. We have a huge and growing body of evidence alongside global partners and hubs of excellence in all areas of life.

This textbook was developed as a reference guide to support our medical community adjacent to their training. This essential approach to the treatment of the plethora of medical conditions with metabolic underpinnings (not least among these, type 2 diabetes, hypertension and obesity) has to be clearly included in medicine in the future, in significant mainstream ways.

What we know now is the following:

• Changing the way dietary medicine is approached will require a huge, systemic societal shift

• This implies that all areas of society are impacted: what we eat, how we eat and how we get food to people around the world is a multifactorial and complex story that is associated with our climate, ecology, community, history, beliefs, ancestry and also our genetics and beliefs.

When looking at the physiological impact of insulin resistance and its ability to affect most or all systems of the body, the complexity of this particular project is immense. It requires a massive scope of specialisations, broad and different areas of medicine and pathophysiology and a deep, complex understanding of disease pathways and progression. I would like to thank and take a deep bow to the extraordinary professionals from so many fields and places in the world who agreed to write, contribute, edit and co-create this essential piece of literature.

We are honoured to have been able to publish this volume of knowledge in this way and with this degree of expertise, knowledge, care, precision, depth and, also, love and are deeply grateful to our incredible, committed team of researchers, editors, scientists and doctors who hold this space and know beyond any doubt that:

Integratively applied, this knowledge is already changing and will change the face of health for our planet.

The science is now overwhelming, and it is essential to put this evidence in the public domain in a way that can make a real difference to people's lives, alongside old medical textbooks. It can no longer be ignored or set aside or passed off for a medication manual. Diabetes, alongside its related metabolic diseases, can and will no longer be considered a terminal disease because in light of the evidence presented in this textbook, its patients and treating practitioners will no longer accept or allow that to happen, when appropriate dietary intervention can change lives.

Our immense gratitude goes to Prof Tim Noakes for his tireless work in Challenging Beliefs and uncovering the errors in science, to Elsevier for taking on this big idea with and for us, and then to each of our 62 contributors, 7 editors and 5 reviewers for their tireless hard work in taking this book to print. Huge congratulations to the team at Nutrition Network for the years of tirelessly working on this book and its content and in particular to Tamzyn Murphy for her exceptional editing.

Really, when it comes to this body of work, manifest into this profound and important book, only two words apply:

Sorry to the millions that have succumbed to diseases that they should not have due to false dietary information and incorrect nutritional science that they listened to, and

Thank you to the thousands who are part of this massive change that is manifesting, helping to secure future healthy outcomes for humanity.

We have a lot of work to do.

Jayne Bullen

Nutrition Network, Cape Town, South Africa The Noakes Foundation, Cape Town, South Africa Eat Better South Africa, Cape Town, South Africa

References

1. Harcombe Z, Baker JS, Cooper SM, et al. Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis. Open Heart. 2015;2(1):e000196.

2. O’Keefe J. Problems with the 2015 Dietary Guidelines for Americans: an alternative. Missouri medicine. 2016;113:74–78.

3. Amazon.com: Bad Pharma: How Drug Companies Mislead Doctors and Harm Patients. Goldacre, Ben: Books [Internet]. [cited 2022 Aug 15]. 9780865478008. Available from: https://www.amazon.com/Bad-Pharma-Companies-Mislead-Patients/dp/0865478007.

4. Schiestl ET, Rios JM, Parnarouskis L, Cummings JR, Gearhardt AN. A narrative review of highly processed food addiction across the lifespan. Prog Neuropsychopharmacol Biol Psychiatry. 2021;106:110152.

5. Schwarz JM, Noworolski SM, Erkin-Cakmak A, et al. Effects of dietary fructose restriction on liver fat, de novo lipogenesis, and insulin kinetics in children with obesity. Gastroenterology. 2017;153(3):743–752.

6. Hofmann B. Bariatric surgery for obese children and adolescents: a review of the moral challenges. BMC Med Ethics. 2013;14:18.

7. Moreira LAC. Ética e aspectos psicossociais em crianças e adolescentes candidatos a cirurgia bariátrica. Rev Bioét. 2017;25(1):101–110.

8. Cakmak HM, Ilknur Arslanoglu, Sungur MA, Bolu S. Clinical picture at attendance and response to flexible family based low-carb life style change in children with obesity. Int J Child Health Nutr. 2021;10(1):9–16.

9. Zinn C, Lenferna De La Motte KA, Rush A, Johnson R. Assessing the nutrient status of low carbohydrate, high-fat (LCHF) meal plans in children: a hypothetical case study design. Nutrients. 2022;14(8):1598.

Part 1

Nutritional fundamentals

Outline

Chapter 1 Understanding human diet, disease, and insulin resistance: scientific and evolutionary perspectives

Chapter 2 Nutritional aspects

Chapter 1

Understanding human diet, disease, and insulin resistance: scientific and evolutionary perspectives

Timothy David Noakes¹,², Catherine Crofts³ and Miki Ben-Dor⁴,    ¹Department of Health and Wellness Sciences, Cape Peninsula University of Technology, Cape Town, South Africa,    ²Nutrition Network, Cape Town, South Africa,    ³School of Interprofessional Health, Auckland University of Technology, Auckland, New Zealand,    ⁴Department of Archaeology, Tel Aviv University, Tel Aviv, Israel

Abstract

Nutritional authorities promote high-carbohydrate, low-fat diets to combat modern diseases such as obesity, type 2 diabetes and heart disease. However, the science behind this ideology is flawed. Virtually everything the public knows about diet can be challenged. The foods that cause harm are the very food groups the public believes are healthy: carbohydrates and polyunsaturated vegetable oils. Conversely, human physiology, from brain size to gastrointestinal morphology appears to support a carnivorous design. While low amounts of certain carbohydrates are tolerable, chronic consumption of processed carbohydrates promotes non-communicable diseases (NCDs). Indigenous cultures adopting modern agriculture develop diseases practically absent beforehand. Processed foods have been linked to systemic inflammation, mitochondrial dysfunction, and more. Their mechanism is insulin resistance, which is crucially involved in most NCDs. The chronic disease pandemic only worsens despite the billions of dollars invested to treat them. A new perspective is needed.

Keywords

Diet; (therapeutic) carbohydrate restriction; (therapeutic) carbohydrate reduction; low-carbohydrate high-fat (LCHF); low carbohydrate; ketogenic; lifestyle modification; metabolism; metabolic syndrome; type 2 diabetes; obesity; inflammation; insulin; insulin resistance; cardiovascular disease (CVD); evolution; dietary guidelines

1.1 Understanding human diet and disease – the scientific and evolutionary evidence

Miki Ben-Dor and Timothy David Noakes

1.1.1 Evolutionary evidence: the species-specific natural human diet

1.1.1.1 Defining a species specific diet

The success of a species is determined by its ability to survive and to procreate. The primary condition for survival is the ability to acquire and assimilate a sufficient quantity of appropriate food, daily. This food must be secured in competition with other animals and then eaten, digested, and absorbed to serve either as energy or as nutrients for other bioprocesses.

Thus, in competition with other species, all living creatures are under constant evolutionary pressure to optimise their bodily structures efficiently to acquire, eat, digest, and metabolise specific foods in an environment that is as favourable to those needs as is possible. But no animal can adapt to eating all the foods that are available in any particular environment.

Evolution is a process of selection between alternative solutions to these challenges, under the constant pressure of trade-offs. ‘The concept of trade-offs underpins much of the research in evolutionary organismal biology, physiology, behavioural ecology, and functional morphology’ [1].

With regard to food choices, this means that every adaptation to the consumption of one type of food may make an animal less able to obtain, digest, or metabolise another type of food. When hominins descended from the trees, some six million years ago, and began to exploit more terrestrial resources, the shape of their bodies changed to favour bipedal locomotion. This in turn allowed hominins to cover long distances on land and to view the landscape from a greater height.

However, bipedal locomotion meant hominins became less effective than other competing primates at acquiring high-hanging fruits [2]. Having their noses at a higher level, far from the ground, also impaired their ability to track other animals by smell and to locate underground food sources. But by developing a larger brain, they were better able to obtain meat without the need for speed or other key physical features of other predators with whom they were in competition [3]. However, to offset the greatly increased energy demand of the larger brain, hominins had to reduce the size of their energetically expensive gut by as much as 40% [4]. This decrease in gut size caused a substantial reduction in the ability to ferment highly fibrous plant-based food sources in a much shortened large bowel (colon).

Thus, this newly acquired ability to obtain meat from animal sources came with a significant trade-off – a diminished capacity to extract nutrients from lower quality, fibrous plants and fruits. The internal structure of the gut also had to change substantially, further limiting humans’ future food choices.

In summary, evolution is very much a process of trade-offs, surrendering one ability in order to obtain another. In nutritional terms, evolution leads to optimal but different diets for all the different species on the planet. We now refer to each of these different diets as the natural (species-specific) diet for that species.

1.1.1.2 The herbivorous gut

With the adoption of agriculture approximately 11,500 years ago, humans, specifically adapted for animal food consumption, needed to bypass some of these physiological evolutionary constraints by adopting plant-sourced foods as a primary food type. This involved a critical switch from what is the species-specific natural human diet. As will be shown later in the chapter, the more recent introduction of novel industrially produced, highly addictive foods made predominantly from grains, seed oils, and sugar or high fructose corn syrup has been associated with profoundly deleterious physiological consequences for all humans.

We begin by reconstructing how humans’ species-specific natural diet came about. Although humans are the descendants of primates, we evolved to eat differently.

Chimpanzees, our closest phylogenetic relatives, have eaten the same diet for the past six million years comprising, for the most part, fibre-laden fruits, plant stems, and leaves, with a small additional contribution from meat [5].

The challenge posed for all mammals eating a plant-based diet is that none has the capacity to digest the cellulose (fibre) that forms the cell lining of all plants. To overcome this deficiency, mammals eating plant materials have developed a symbiotic relationship with anaerobic gut bacteria. Billions of anaerobic bacteria are given safe residence in specially adapted intestinal organs, where they busily ferment ingested cellulose into usable mammalian food. In chimpanzees, this special organ is a voluminous large bowel (colon), making chimpanzees ‘hindgut fermenters’ [6], a feature they share with horses, pigs, zebras, elephants, warthogs, rhinoceroses, rabbits and other rodents. In other grass-eating ruminants, including cattle, sheep, antelope, and gazelles, the special fermenting organ is a four-chambered stomach in the foregut. Hence they are referred to as ‘foregut fermenters’.

The basis for this mammal-bacteria symbiosis is that, in exchange for an environment where they can safely reproduce, the bacteria convert the cellulose into a form of saturated fat called volatile short-chain fatty acids, on which the host mammal bases its existence [7]. The important point is this: grass-eating ruminants convert 100% nutrient-poor carbohydrate food (grass) into the energy-dense saturated fatty acids that are essential for mammalian survival. When humans eat those ruminants, that process also ensures our survival.

To summarise, the specifically adapted fore- and hind- guts of herbivores can rightly be labelled super-specialised organs for manufacturing saturated fats from cellulose. All plant-eating mammals use that cellulose as the growth medium for the bacteria in their intestines. These bacteria then produce the fatty acids that are missing in the nutrient-poor grass, roots, fruits, and shoots on which these mammals must survive. What is more, when absorbed by the herbivores’ intestines, the cell bodies of these dead bacteria provide the protein needed for their own tissue growth.

1.1.1.3 Specialised omnivores

In the pre-agricultural era, humans were the only primates able to source and to survive on a completely carnivorous diet. Omnivory is defined as the ability to obtain energy from two or more trophic levels of food sources, in the case of humans, from both animals and plants. A common belief is that humans are omnivores and thus have substantial flexibility in their food choices. However, this human potential for omnivory means that humans can, at least acutely, replace animal-based foods with plant-sourced foods should that choice be imposed by constraints in their natural environment. It does not indicate that omnivory is the sole dietary choice for humans.

When living in their natural environments, omnivorous species are seldom fully adapted to obtain their nutrition equally from more than one trophic level of food. Chimpanzees, for example, are omnivores since they consume meat on occasion. However chimpanzees are unable to compensate for the dietary deficiencies caused by a lack of fruit, by simply switching to eating more meat as the dominant component of their diet. Chimpanzees simply do not have the biological capabilities to obtain enough meat to avoid starvation if fruits and plants suddenly became unavailable. Designed by a specific evolutionary history, their morphology and physiology have adapted chimpanzees to live in trees where they are best able to obtain and digest fruits and shoots. Alternatively, wolves can gorge on berries during the summer and autumn. But they are far better equipped to hunt animals; making them specialised carnivores but, at the same time, facultative omnivores.

The energetic returns for modern hunter-gatherers from hunting animals are tens of times greater than the returns from gathering plants (tables 3 and 4 in Ref. [8]). In the past, this difference would have been even greater due to the relatively greater abundance of large animals compared to edible plants [9]. To obtain the equivalent amount of energy from the environment, a human who had to ‘shop in nature’s supermarket’ in the pre-agricultural era, would have had to ‘pay’ tenfold more in energetic terms to gather and consume plants than to hunt animals.

This means that early humans could not easily have switched from animals to plants as a food source. Thus it is perhaps not surprising that among mammals, most omnivores are specialised, consuming over 70% of their food from either plant or animal sources.

1.1.1.4 Did all early humans eating their species-specific natural diet have a shortened life-expectancy?

A common misconception is that all humans eating the pre-industrial species-specific human diet died at a young age. This would indicate that modern humans would be ill-advised to adopt that specific diet.

This misconception is based on the finding that modern human life expectancy at birth is twice that of humans living in the pre-industrial era. However, this is potentially misleading because the rate of death at birth or shortly thereafter was 100 times greater in the past than it is today (fig. 7 in Ref. [10]). So to compensate for the large number of infants dying before the age of one in the pre-industrial era, an equal number of adults would have had to live to age 70 to produce an overall average life expectancy of 35 years.

Moreover, recent studies of modern hunter-gatherers find that most adult hunter-gatherers who reach maturity survive to become grandparents, despite an absence of protection from predators and without access to the medical and sanitary services that modern societies provide [10].

We can now turn to a more complete reconstruction of the natural, species-specific evolutionary human diet.

1.1.1.5 Reconstructing the natural, species-specific, evolutionary human diet

The natural diets of most living species can be determined by observing what those species eat in their natural environments. However, humans have progressed far from the state in which they and their ancestors lived for millions of years; first by domesticating their food sources during the last 10,000 years, and more recently by industrialising the production of the foods we now eat.

In an attempt to reconstruct our ancestors’ diet, intuitively we turn to archaeologists who dig Homo’s base camps that are millions of years old. But if we rely only on the pre-historical archaeological record, with its thousands of sites containing fossilised animal bones including just a few sites with plant residues, we might conclude that humans are specialised hypercarnivores. However this archaeological view of the natural human diet is biased by the different preservation potentials of plant and animal remains over millions of years. Therefore, while archaeology can reveal a great deal about what animal foods we ate, it tells us very little about the relative contribution of animals or plants to the diet eaten by early hominins.

Consequently, most scientists attempting to reconstruct the natural human diet have focused on the food choices of modern hunter-gatherer groups in remote corners of the world [11–18]. But more recent research shows that modern ecological conditions are so different from those that prevailed during the long history of human evolution that this information does not provide a valid measure of the natural species-specific human diet [9,19–21].

So, if we cannot rely on the archaeological record and recent ethnographic observations, where do we find the best evidence for what constitutes the natural, species-specific human diet?

The growth of paleobiology as a vibrant scientific discipline provides the basis for a different approach to re-discover the natural human diet [22]. This approach assumes that the shape of the human body, the structure of our organs, our genetic composition, and our metabolism are largely the result of adaptations to our species-specific diet during our evolution as the genus Homo. Paleobiology enables a review of unique features in human morphology and physiology which can only have developed in humans that eat a species-specific diet [20,21].

Table 1.1. lists 14 biological human features which indicate that a specialised carnivorous diet drove human evolution, with plants as a fall-back food. Additional evidence from archaeology, palaeontology, and zoology support the conclusion that humans evolved as hypercarnivores, obtaining at least 70% of their calories from animal-sourced foods [19,21]. Increased consumption of plant-sourced foods becomes evident only toward the end of the Pleistocene, 80,000–15,000 years ago. By which time Homo sapiens had been established as a distinct species for more than 200,000 years.

Table 1.1

1.1.1.6 The critical role of animal fat in human evolution

The evidence that humans were carnivorous during the Palaeolithic period has important implications for our understanding of the biology of fat and protein consumption and metabolism in humans. Carnivores have a large capacity to consume protein for energy. Cats, for example, can obtain over 70% of their energy from the metabolism of protein [55]. Consumption of protein for energy requires the removal of the toxic nitrogen element from the protein molecule. However, humans have a limited capacity to perform this removal. It is estimated that nitrogen removal becomes limiting when protein intake exceeds 35%–45% of the total caloric intake [56]. This limitation means that 55%–65% of calories in the human diet must come from animal fat or from fat and carbohydrates in plant materials. Since humans were hunters of large animals and large animals store over 50% of their calories as fat [19], it may be deduced that fat provided a very high percentage of the ingested calories of early humans.

A comprehensive review led Jochim [57] to formulate the Fat Hypothesis, which proposes that a hunted prey’s fat content was an essential criterion that directed early humans’ hunting decisions. He writes [[57], p. 87]: ‘The most efficient procurement of fatty meat is given priority over that of lean meat in the decision-making process, as is that of big meat package over small’. At times, the hunted prey was abandoned once it was deemed fatless [58,59]. Humans preferentially hunted large animals as they contained a higher body fat content [19,47,60]. They specifically exploited those animal body parts that contain greater amounts of fat [61,62]. They also selectively hunted adult prey in their physical prime because this group of animals contains more fat than do the easier-to-catch younger and older animals [19,63]. Finally, at great energetic expense, they extracted fat by boiling bones [46,64].

In summary, the physiological and archaeological evidence supports the conclusion that the natural species-specific human diet involved the daily consumption of significant amounts of animal fat and protein.

1.1.1.7 Summary of evidence for the species-specific natural human diet

The evidence presented here and elsewhere [20,21] strongly supports the hypothesis that humans evolved to become specialised carnivores. This dietary pattern lasted until very late into the Pleistocene period, approximately 15,000 years ago. A slight modification towards a greater inclusion of plants may have started in Africa some 85,000 years ago. This is suggested by changes in the FADS group of genes. That trend has increased in intensity towards the arrival of the Neolithic culture and the beginning of agriculture, starting between 11,000 and 5000 years ago, depending on the geographic region.

It is clear from the evidence presented in Table 1.1 that the evolutionary adaptations to the consumption of large quantities of meat and fat remain deeply embedded in human biology.

1.1.1.8 The appearance of agriculture causes the first changes to the species-specific natural human diet

The next stage in the evolution of the human diet began with the domestication of plants, starting about 10,000 years ago in The Fertile Crescent in Asia [65].

The addition of cereals and grains to the human diet reduced human reliance on hunting, fishing, and gathering. A secure source of storable, year-round food allowed the growth of stable communities living together in towns and villages. Jared Diamond suggests that, for the future of the earth and the human species, agriculture was ‘the worst mistake in the history of the human race’ [66]. According to Diamond, the adoption of farming produced a number of serious disadvantages, including starvation, epidemic diseases and malnutrition. By 3000 BC humans living on cereals and grains had lost at least 13 cm in height.

Since then, agriculture has coexisted in different communities with either hunting and gathering or exclusively with the herding of domesticated and semi-domesticated animals.

Never in our pre-history has there been a group of humans that existed solely on the exclusive cultivation or gathering of plants or on a purely vegetarian/vegan diet.

1.1.1.8.1 The health and diets of farmers compared to hunter-gatherers

During most of the Holocene, the period of improved (warmer) climate that started approximately 11,650 years ago, the human diet became more varied than it had ever been. We find societies living side by side but eating diets that range from almost exclusively animal-based to predominantly agricultural- and plant-based. But it is clear that the health of those societies that continued to eat an animal-based diet was superior.

In 1877, Lieutenant Scott, a US cavalry scout, wrote about the Cheyenne scouts, whose actions led to the defeat of General Custer at the Battle of the Little Bighorn in 1876 [67]: ‘… they were all keen, athletic young men, tall and lean and brave, and I admired them as real specimens of manhood more than anybody of men I have ever seen before or since. They were perfectly adapted to their environment, and knew just what to do in every emergency and when to do it, without any confusion or lost motion. Their poise and dignity were superb; no royal person ever had more assured manners. I watched their every movement and learned lessons from them that later saved my life many times on the prairie’. Scott also noted that the Crow, the enemies of the Cheyenne, hunted bison once a week from large herds and that their camp, ‘was full of meat drying everywhere. Everybody was carefree and joyous’.

Others reported that the American Plains Indians were free of the diseases that afflicted European settlers, including diabetes, cancer, heart disease, and most infectious diseases: ‘It is rare to see a sick body amongst them’ and that they are ‘unacquainted with a great many diseases that afflict the Europeans such as gout, gravel and dropsy, etc’. [68]. Plains Indians were also amongst the tallest peoples then living on earth [69]. Today type 2 diabetes mellitus (T2D) and obesity are rampant among their descendants [70].

Another group of hunter-gatherers, the Inuit of the Arctic, consumed diets based on meat and animal fat, as did the Masai herders living close to the Equator, as well as the herders of the high plateau of Central Asia. Other hunter-gatherers living in warmer climates subsisted on a diet with a higher component of plants [18], whereas coastal societies lived on fish and other aquatic foods.

In the same historical period, peoples who lived close to the large rivers - such as the Nile, the Euphrates, the Indus and the Yangtze - relied on an agricultural diet high in plant-based foods, supplemented with dairy and meat from domesticated animals. Besides the change in food acquisition methods, the post-Palaeolithic period is also characterised by the more intensive use of food processing methods [71].

However this change to the agricultural diet was clearly associated with worsening human health.

In their seminal book, Paleopathology at the Origins of Agriculture, Cohen et al. [72] show that the transition to agriculture was forced rather than voluntary; a change born of a shortage of natural foods and not the result of sudden, marvellous inventions in plant and animal domestication. Based mainly on studies of bone pathology, these authors show that humans suffered many novel chronic diseases after switching from a diet based on hunting to one grounded on the consumption of domesticated foods. North America, where agricultural groups lived side by side with hunter-gatherers, provides pathological evidence that the hunter-gatherers were healthier than the agriculturalists. Steckel et al. [73] have written: ‘Diet was also closely related to change in the health index, with performance being nearly 12 points lower under the triad of corn, beans, and squash than with the more diverse diet of hunter-gatherer groups’.

Africa also includes ethnic groupings that chose to eat different diets either predominantly carnivorous or mainly plant-based. In 1931, Orr and Gilks [74] compared the health and physical attributes of the Kikuyu, a ‘vegetarian tribe’ eating predominantly cereals supplemented with roots and fruits, with the ‘largely carnivorous’ Masai, whose diet comprised milk, meat and raw blood. Compared to adult Kikuyu, adult Masai were about 5 inches (13 cm) taller, 23 pounds (10 kg) heavier, and 50% stronger when tested with a hand dynamometer. In addition, bony deformities, dental caries, anaemia, pulmonary conditions, and tropical ulcers were more prevalent in the Kikuyu, whereas rheumatoid arthritis and ‘intestinal stasis’ were more common in the Masai [74].

The effects on human health of the transition to farming are also revealed in the mummified bodies in South America and Egypt. The mummies from groups eating the agricultural diet exhibit a wide range of diseases, including tuberculosis and cancer [75–80].

It seems that, with time, humans learned how to overcome some but perhaps not all of the unhealthy effects of eating the agricultural diet.

1.1.2 Food as a source of health and disease: the evidence

1.1.2.1 The health-promoting diet of the Mid-Victorians (1850–80)

Victorian England, between 1850 and 1880, provides an excellent example of the state of health before the change to the human diet caused by the introduction of industrially mass-produced food. This mid-Victorian period is now recognised as the golden era of British health. It is explained by the high quality of the mid-Victorians’ diet [81–84].

Farm-produced real foods were available in such abundance that even the working-class poor ate highly nutritious foods. As a result, life expectancy in Britain in 1875 was equal to, or even surpassed that of modern Britons. This was especially true for men (whose life expectancy was higher by about three years). In addition, the profile of diseases was quite different from those prevalent in Britain today. The authors concluded:

[This] shows that medical advances allied to the pharmaceutical industry’s output have done little more than change the manner of our dying. The Victorians died rapidly of infection and/or trauma, whereas we die slowly of degenerative disease. It reveals that with the exception of family planning, the vast edifice of twentieth century healthcare has not enabled us to live longer but has in the main merely supplied methods of suppressing the symptoms of degenerative disease which have emerged due to our failure to maintain mid-Victorian nutritional standards [84].

This mid-Victorians’ healthy diet included freely available and cheap vegetables such as onions, carrots, turnips, cabbage, broccoli, peas, and beans; fresh and dried fruit, including apples; legumes and nuts, especially chestnuts, walnuts, and hazelnuts; fish, including herring, haddock, and John Dory; other seafood, including oysters, mussels and whelks; meat, which was considered ‘a mark of a good diet’, so much so that ‘its complete absence was rare’, was sourced from free-range animals, especially pork, and also included offal such as brain, heart, pancreas (sweetbreads), liver, kidneys, lungs, and intestine; eggs from hens that were kept by most urban households; and hard cheeses [84].

Their healthy diet was therefore low in cereals, grains, sugar, trans-fats, and refined flour, and high in fibre, phytonutrients, and omega-3 polyunsaturated fatty acids, entirely compatible with the modern Paleo or low-carbohydrate high-fat (LCHF) diets [84].

But this period of nutritional ‘paradise’ changed drastically after 1875, when cheap imports of white flour, tinned meat, sugar, canned fruits and condensed milk became more readily available [84]. The result was immediately noticeable. By 1883, the British infantry was forced to lower by three inches, its minimum height for recruits; by 1900, 50% of British volunteers for the Anglo-Boer War were rejected because of undernutrition [82]. The changes were associated with an alteration in disease patterns in these populations, as clearly described by Yellowlees [85] (see later) in the patients in his rural medical practice in the Scottish Highlands.

The remarkable health of other pre-industrial societies eating their traditional diets and conversely its immediate destruction with the adoption of the industrial (colonial) diet, has been captured in the unique and remarkable writings of Dr. Weston Price.

1.1.2.2 Weston Price investigates the health and diet of traditional societies

In the 1930s, Weston Price, a dentist in Cleveland, Ohio, USA, noticed that dental caries were becoming more prevalent in his young patients. At the time he had observed that the teeth of children with type I diabetes prescribed high-fat diet in the pre-insulin era, were free of caries [86]. The diet comprised milk, cream, butter, eggs, meat, cod liver oil, bulky vegetables, and fruit. His own experiments had also shown that one meal a day high in fat-soluble vitamins could prevent the progression of dental decay in children with active dental caries [87]. He also knew that the teeth of ancient South African fossils did not have dental caries [88]. He wondered whether perhaps a recent dietary change could explain the increase in dental caries among the children in his dental practice. He knew that to answer that question, he would need to travel the world in search of peoples who were still eating the ‘control’ diet that they had eaten before the spread of the modern industrial diet. If they were healthy, he would know that the adoption of that novel diet is a key driver of the ill-health of modern humans.

1.1.2.2.1 The healthy populations

With his wife in support, over the next decade, Price examined the teeth and general health of the Swiss inhabitants of the Lötschental Valley; of Scottish families living on the Outer and Inner Hebrides; of the Inuit (Eskimos) of Alaska; of the Indians of north, west and central Canada, the western United States and Florida; of the Melanesians and Polynesians inhabiting eight archipelagos of the Southern Pacific; of six tribes in eastern and central Africa, including the Masai; of the Aborigines of Australia; of Malay tribes living on islands north of Australia; of the Maori of New Zealand; and of South Americans in Peru and the Amazon Basin. Wherever possible, the health of those continuing to eat traditional foods was compared with that of others in the area who had begun to eat imported diet of processed foods. Prices travelled with a mobile laboratory as well as photographic equipment to collect food samples and to photograph the teeth and faces of the people they examined, as well as recording their general state of health. They also analysed these traditional foods for the presence of vitamins and minerals. The results of this six-year project are described in the remarkable book ‘Nutrition and Physical Degeneration’ [89].

The Prices discovered that those farmers and herders who adhered to their traditional diets were, in general, very healthy. Specifically, those who continued to eat the foods of their ancestors showed:

• an almost total absence of tooth decay;

• broad faces, wide nostrils and perfect dental arches;

• superior immunity, demonstrated by an absence of tuberculosis in some communities (such as the Swiss of the Lötschental Valley); and

• an absence of most of the modern ‘chronic diseases of lifestyle’, including cancer, rheumatic diseases, and other autoimmune diseases.

For example, they described the Inuit of Alaska as ‘an example of physical excellence and dental perfection such as has seldom been excelled by any race in the past or present’ and as ‘robust, muscular and active, inclining rather to sparseness than corpulence, presenting a markedly healthy appearance. The expression of the countenance is one of habitual good humor. The physical constitution of both sexes is strong’.

His findings of the generally good health of the Inuit matched those of Harvard biologist Vilhjalmur Stefansson who wrote several books describing his multi-year experience of living with the Inuit and eating their very low carbohydrate animal-based diet [90]. Stefansson also observed that the Innuit appeared to be free of cancer [91].

In Australia, Weston Price reserved special praise for the health and physical abilities of those Aborigines