Our book has been published

Screen Shot 2017-04-03 at 6.49.30 pm



ISBN: 978-981-10-2076-6 (Print) 978-981-10-2078-0 (Online)
Library of Congress Control Number: 2016946936
© Springer Science+Business Media Singapore 2017
28 chapters


Michael Christie

Brian Devlin

1 A Thematic History of Bilingual Education in the Northern

Territory . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Brian Devlin, Samantha Disbray and Nancy Devlin

2 A Glimmer of Possibility. . . . . . . . . . . . . . . . . . . . .11
Brian Devlin

3 Reflecting on Team Teaching . . . . . . . . . . . . . . . . . . .27
Beth Graham

4  Bilingual Time’  at Willowra: The Beginnings
of a Community-Initiated Program, 19761977 . . . . . . . . . . .  35
Petronella Vaarzon-Morel and Jim Wafer

5 Lessons Learned from Bilingual Education. . . . . . . . . . . . .49
Kathryn Gale

6 Starting Out at Bamyili: Factors Specifi c to the Development
of the Kriol Program . . . . . . . . . . . . . . . . . . . . . . . 61
Dorothy Meehan

7 Boom and then Bust: Lessons Learnt from My Time Teaching
in Three Bilingual Schools in the Northern Territory . . . . . . . 73
Mary-Anne Gale

8 The Policy Framework for Bilingual Education in Australian
Indigenous Languages in the Northern Territory . . . . . . . . . . 85
Graham McKay

9 Consolidation, Power Through Leadership and Pedagogy,
and the Rise of Accountability, 1980 1998 . . . . . . . . . . .  101
Samantha Disbray and Brian Devlin

10 The Development of Successful Bilingual, Biliterate and
Bicultural Pedagogy: Place for Tiwi Teachers
and Tiwi Language in Learning. . . . . . . . . . . . . . . . . . .113
Frances Murray

11 Developing Local Curriculum Materials Learning Metaphors,
Insightful Collaborations, Community Involvement . . . . . . . . .127
Michael Christie

12 The Quest for Community Control at Yirrkala School . . . . . . 141
Trevor Stockley, Banbapuy Ganambarr, Dhuŋgala Munuŋgurr,
Multhara Munuŋgurr, Greg Wearne, W.W. Wunuŋmurra, Leon White
and Yalmay Yunupiŋu

13 Language Revitalisation in a Bilingual Program The Case
of Numbulwar School . . . . . . . . . . . . . . . . . . . . . . . 149
Therese Carr, Melanie Wilkinson and Philippa Stansell

14 Threatened Closure: Resistance and Compromise (1998 2000) . . 165
Brian Devlin

15 Defending Our Program at Wadeye . . . . . . . . . . . . . . . .179
Tobias Ngardinithi Nganbe

16 Sources of Evidence on Student Achievement in Northern
Territory Bilingual Education Programs . . . . . . . . . . . . . .185
Brian Devlin

17 Policy Change in 2008: Evidence-Based or a Knee-Jerk
Response? . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203
Brian Devlin
18 The Areyonga Case: Utulu Kutju Nintiringanyi  Learning
Together. . . . . . . . . . . . . . . . . . . . . . . . . . . .219
Leonard Freeman, Neil Bell, Tarna Andrews and Peggy Gallagher

19 Policy and Practice Now . . . . . . . . . . . . . . . . . . . .237
Samantha Disbray

20 Starting Out at Yuendumu School Teaching in Our Own
Language . . . . . . . . . . . . . . . . . . . . . . . . . . . . .247
Tess Ross and Wendy Baarda

21 Stories from Central Australian Indigenous Community
Schools in the Pintupi-Luritja Region . . . . . . . . . . . . . . 259
Meg Mooney

22 Yipirinya School: That Generation, This Generation . . . . . . 269
Inge Kral

23 The Program at Wadeye, Past and Present. . . . . . . . . . . . 285
Deminhimpuk Francella Bunduck and Teresa Ward

24 We Did It! A Case Study of Bilingual/Bicultural Education
at Ltyentye Apurte Catholic School . . . . . . . . . . . . . . . .293
Ailsa Purdon and Imelda Palmer

25 Forty Years on: Seeking a Way for the FutureDhawalyurr
Yuwalkku Dhukarr. Reflections on Bilingual Education at
Shepherdson College, Galiwin ku. . . . . . . . . . . . . . . . . 307
Noela Hall

26 Reminiscences: Working Together in a Bilingual Classroom. . .. 325
Nancy R.F. Devlin and Dorothy Gapany

27 Reflections on My Years at Elcho and Mä puru (19782015) . .. 331
John Greatorex

28 Digital Futures for Bilingual Books . . . . . . . . . . . . . .347
Catherine Bow, Michael Christie and Brian Devlin

Afterword . . . . . . . . . . . . . . . . . . . . . . . . . . . . 355
Jim Cummins

References . . . . . . . . . . . . . . . . . . . . . . . . . . . .363

Glossary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 365

Places Index. . . . . . . . . . . . . . . . . . . . . . . . . . . 367

NT Languages Index. . . . . . . . . . . . . . . . . . . . . . . . 369

Other Languages Index . . . . . . . . . . . . . . . . . . . . . . 371

Subject Index. . . . . . . . . . . . . . . . . . . . . . . . . . .373

If you would like to order the book or a chapter, here is the link to Springer’s website:



Nutrition and chronic illness

What does the scientific research literature have to say about some of the links between nutrition and chronic illness?

Draft paper dated April 9, 2017

Dr Brian Devlin BA (Hons), Dip.Ed, M.Ed, EdD, FACE

Honorary Professorial Fellow

Charles Darwin University

[Any suggestions for adding to or improving this paper would be appreciated. BCD]


This discussion paper has been written for reasons that are more personal than professional. That is, the goal has been to share some useful scientific findings with a few friends, colleagues and family members. What is presented here does not purport to be a state-of-the-art literature review that would warrant publication in a specialised journal. Rather, it is a brief distillation of what I have been finding out as a result of some reasonably disciplined reading of the research-based literature over the last few years. Quite a few people have helped me in this quest, but I will not acknowledge any of them here, as I would customarily do. The reason is that some of them have been diagnosed with the chronic diseases mentioned here, and I am not at all sure they would want to be identified in that way!

It seems undeniable that, since chronic diseases have a complex aetiology, any program of primary care to manage any one of them is likely to be complex as well. To do justice to the range of interventions that are possible is impossible in a short paper like this, and so no reference is made to the possible benefits associated with surgical procedures, pharmaceuticals, exercise, rest, recreation, and meditation. It is my assumption that, regardless of any primary treatment program, nutrition (and perhaps supplementation) should be a core element in any secondary, preventive approach to chronic disease management.

The term ‘chronic’ is applied to any disease that is long lasting and has persistent effects1; for example, cardiovascular disease, cancer, chronic kidney disease, diabetes, mental health disorders, musculoskeletal conditions (back problems, osteoarthritis, osteoporosis and rheumatoid arthritis), tooth decay, asthma and atopic dermatitis (a chronic type of eczema). Only some of these are referred to in this paper.

It would be fair to argue that “human nutrition science has failed to stem the more recent rise of obesity and associated cardiometabolic disease (OACD)”, as has been claimed by David Raubenheimer and Stephen J. Simpson at the University of Sydney. 2 These researchers introduced the field of nutritional ecology and have shown how their framework, known as nutritional geometry, promises to strengthen human nutrition science and help address its limitations. Their modelling approach, which was borrowed from the field of nutritional ecology, might be a useful way of understanding how chronic diseases might be managed or avoided in the first place.


My starting point was to examine some of the claims that have been made in two best-selling books by Colin Campbell and David Perlmutter 3, 4, then to gauge the strength of evidence on which they have been based by combing through specialist journals such as Alzheimer’s & Dementia, Cancer Causes and Control, Epidemiologic Reviews, European Journal of Clinical Nutrition, Journal of the American Medical Association and Nature. It was not my plan to start with a few favourite conjectures of my own and then to look for supporting evidence. Rather, I have begun with some claims that scientists themselves have made on the basis of available research findings. Then, using the approach that Karl Popper favoured, I have looked for disconfirming evidence as well as findings that appear to corroborate the claims. To keep this paper manageable I have had to limit the number of claims I could assess in this way. In this current version, only 10 claims are investigated, and then only partially. Later, when I have more time, I may seek to broaden the scope and the depth.

Then, in the discussion section of this paper, I have considered some of the claims made by staff at Living Valley Springs (in Kin Kin, Qld.) and evaluated them with respect to relevant findings in the research literature. My purpose in doing that was to gauge whether their guidance aligns with the available research.

The theoretical framework adopted for this paper, known as nutritional geometry, encourages a focus on the dynamic interface between nutrition, humans and their environment and how the associated interactions “determine the nutritional properties of foods and how foods in turn combine into meals, diets, and dietary patterns to influence health” 2 This encourages researchers to examine “how mixtures of nutrients (and other dietary components) influence biological outcomes such as health and disease rather than considering any particular nutrient in isolation” 2. I have found this framework to be a helpful aid in critically evaluating some of the claims presented in this paper.  Although some foods and supplements are individually considered on occasion, my preference has been to respect the complex interplay of food, our bodies and the environment and to prefer more integrative approaches.

Conflicting advice

What is immediately apparent to anybody who becomes immersed in the research on nutrition is that some diametrically opposed positions have been put forward by various authors. For example, there are widely differing views on what percentage of protein is appropriate to minimise the risk of chronic disease. Campbell (2015) has no doubt that “10% protein (the RDA) is enough”. He notes that “a whole food plant based (WFPB) diet, with no added oil, can easily provide 10-12% total protein”. On the other hand, Australia’s National Health and Medical Research Council recommends a higher figure (“15–25% from protein” 5. The Keto Diet website recommends 27% protein when higher weight loss is desired. Given my age, height, and a few other statistics this is what its guidance was:

In the United States the Dietary Guidelines Committee has stated that up to 35% protein is acceptable. Campbell’s response to this is unequivocal: “The continued use of an upper ‘safe’ level of 35% protein of total, daily dietary calories in my view is grossly unscientific and completely irresponsible”. 6

Given that divergence, it is not surprising that a moderate-protein high-fat ketogenic diet is favoured by some, whereas we are assured that a whole-foods, plant-based eating plan is the surest way of limiting the risk of chronic illness. 6,7

Claim #1: The gluten hypothesis

It is well known now that, in genetically susceptible individuals, ingestion of gluten (or more specifically, the gluten peptide gliadin) can lead to a chronic autoimmune inflammatory bowel condition known as Coeliac disease. Gluten is found in most cereal grains, including wheat, rye, and barley, whether live grain, multigrain, stone-ground, or whole grain. What is less well known is that atypical symptoms of a gliadin-related problem may include osteoporosis and osteomalacia 7 as well as brain dysfunction 4 even in cases where Coeliac disease has been identified. Non-coeliac gluten hypersensitivity (NCGH) is a recently identified condition in which symptoms resembling those of Coeliac disease are brought on by the ingestion of gluten and need to be resolved with a gluten-free diet, even though “serological tests are negative and the bowel biopsy is normal” 7. Perlmutter (2014, p.6) asks, “is it possible for everyone’s brain to have a negative reaction to this ingredient?” 4

Evidence for Claim #1

A 2015 case–control study found that patients with Coeliac disease had significantly lower bone mineral density (BMD) values and a decrease in bone mechanical strength. 9 This study was the first to demonstrate that “premenopausal women with coeliac disease have lower vBMD, abnormal microarchitecture, and lower strength, measured as stiffness and failure load compared with normal premenopausal women of similar age”. Dos Santosa, & Liote (in press) explain that some studies have shown that, when a gluten-free diet was followed, BMD increased but did not attain normal values, and the fracture risk did not decrease, except in the case of children treated before they were four years of age. 8 However, and much more hopefully, a systematic review of case control and cohort design studies has indicated that BMD values return to normal after five years without gluten: “Gluten-free diet adherence resulted in partial recovery of bone density by one year in all studies, and full recovery by the fifth year”. 10

Failure to gain weight, another potential gluten-related symptom, may be a manifestation of the malabsorption syndrome characterised by micro/normo or macrocytic anaemia (Vitamin B12, folic acid and iron deficiencies). 8

Perlmutter arrived at his conclusions about how what we eat might affect brain function after years as a practising neurologist during which he acquired an in-depth understanding of recent research findings. He reports “countless case studies of epileptic patients whose seizures ended the day they replaced grains with more fats and protein”.4

Claim #2: The sugar hypothesis

“Fruit and other carbohydrates could be health hazards with far-reaching consequences that not only will wreak physical havoc on your brain but will accelerate your body’s aging process from the inside out” (Perlmutter, 2014, p 5). 4 There is a diet-related link between inflammation, which can cause damage to brain tissues, and diseases such as Alzheimer’s (p.52). 4 Consequently, no more than 60 gm of carbs a day is recommended; no more than a serving of fruit (p.12). 4

Evidence for Claim #2

Inflammation lies at the heart of many chronic conditions including brain disease (Perlmutter, 2014, p.12). In recent years researchers have evaluated the association between an anti-inflammatory diet and the incidence of dementia. 11 They used baseline food frequency questionnaire data obtained in another study from 7,109 participants (aged 64 to 80 years). The researchers found that less inflammatory diets were associated with later onset of dementia. 11

Three cellular processes tend to work in tande4m: inflammation, insulin resistance and oxidative stress. 94 “The glucose absorbed from French fries, or from refined carbohydrates (white bread, white rice, pasta), and from sugary candies, sodas, juices and most baked goods, hits your bloodstream fast and hard. That uptick of blood glucose also causes an increase in cytokines, which are inflammatory messengers”. 94 Perlmutter (2014, pp. 114-5) outlines what happens when sugar molecules bind to amino acids, fats and proteins in a process known as glycation. This produces advanced end products (AGEs), also known as glycotoxins, which are linked to diabetic complications and aging.

Campbell & Campbell (2006, p. 306) deplore the fact that wrong dietary guidelines are issued by industry-influenced agencies such as the Food and Nutrition Board (FNB), part of the National Academy of Sciences in the US. The FNB maintains that “adults should get 45% to 65% of their calories from carbohydrates”. More than half this amount (25%) can be “the sugars present in candies, soft drinks and pastries” (Campbell & Campbell, 2006, p. 307). Such a generous nutrient range would allow a disastrous daily meal plan that included a breakfast comprising one cup of fruit loops, one cup of skim milk, one packet of M&M milk chocolate candies, fiber and vitamin supplements, a grilled cheddar cheeseburger for lunch and for dinner three slices of pepperoni pizza, one 16 oz. soft drink and one serving of sugar cookies”. Such a meal plan would fit with the FNB’s guidelines for minimising risk for chronic disease”. Campbell & Campbell add, “when we eat a diet like this day in and day out, we will not just be marching but sprinting into the arms of chronic disease. In sad fact, this is what a large proportion of [the US] population already does” (p. 308). 3

Is the 60 gm-of-carbs-a-day claim warranted?

Perlmutter is a practising board-certified neurologist, and a fellow of the American College of Nutrition. He has devoted more than 35 years of his life to the study of brain diseases (Perlmutter, 2014, p.9). On that basis alone his claims should warrant being taken seriously. Research by Hayden et al. (2016) supports his claim. 11 Other researchers have also concluded that “Microvascular and macrovascular damage, seen in diabetes, is attributed to the accumulation of AGEs in tissues, but it is also associated with atherosclerosis, Alzheimer’s disease, end stage renal disease, rheumatoid arthritis, sarcopenia, cataracts, and other degenerative ophthalmic diseases, Parkinson’s disease, vascular dementia and several other chronic diseases. 12


“Food is a powerful epigenetic modulator—meaning it can change our DNA for better or worse” (Perlmutter, 2014, p.8).  For example, Diabetes and Alzheimer’s are diseases that are “uniquely tied together” and “largely preventable” (Perlmutter, 2014, p.7).  Alzheimer’s is not a heritable disease. 92, 93 What causes it is not so much the genes we inherit from our parents, but the epigenetic expression of those genes and how it is controlled through diet and other factors. “We can naturally prevent, treat and sometimes cure—without drugs—a spectrum of brain-based ailments such as ADHD, depression, anxiety, insomnia, autism, Tourette’s syndrome, headaches and Alzheimer’s disease” (Perlmutter, 2014, p.42).

Claim #3: The animal protein hypothesis

A diet rich in animal protein poses multiple risk factors and is the main dietary cause of heart disease, cancer and related degenerative diseases. 6,7  Sherwell (2010) agrees:  “Plant-based diets dramatically and rapidly reduce heart disease, diabetes, cancer and obesity”. 78

The China Study examines the relationship between the consumption of animal products (including dairy) and various chronic illnesses such as bowel cancer, breast cancer, coronary heart disease, diabetes, and prostate cancer. The authors conclude that people who eat a whole-food, plant-based vegan diet—avoiding all animal products, including beef, cheese, eggs, fish, milk, pork, poultry, and reducing their intake of processed foods and refined carbohydrates—will escape, reduce, or reverse the development of numerous diseases. The authors conclude that there are “multiple health benefits” from “consuming plant-based foods” and “largely unappreciated health dangers” from “consuming animal-based foods, including all types of meat, dairy and eggs” (Campbell & Campbell, 2006, p. 21).

Consequently, people concerned about the risk of chronic disease are advised to limit their intake of animal protein: “The findings from the China Study indicate that the lower the percentage of animal-based foods that are consumed the greater the health benefits….the optimum percentage of animal-based products is zero (Campbell & Campbell, 2006).

Evidence for Claim #3

Early research on animals found that a diet rich in animal protein led to heart disease 13 14, cancer 15, 79  and related degenerative diseases. When intake of protein (specifically, dietary casein) exceeded 10 per cent of diet calories in experiments with animals, tumour formation was dramatically promoted in 100 per cent of cases 79, whereas in no case did hepatic cancer fail to be reversed when animals were switched to low dietary protein diets, i.e., <10% of diet calories). 16 17 “Non-hepatic tumor incidence also was lower in the animals fed the lowest protein diet”. 17

Drawing on data obtained in 1973–75 from 65 counties in China, Campbell & Campbell (2006) reviewed the rates of mortality caused by cancer and other chronic diseases and correlated them with 1983–84 dietary surveys and blood samples from 100 people in each county. The research was conducted in 65 counties where genetically similar populations had tended, for generations, to live in the same locality and to eat similar foods. The study concluded that in counties where a high consumption of animal-based foods was reported in 1983–84 the death rates 1973–75 from “Western” diseases were likely to be higher, whereas the opposite was true in counties where more plant-based foods were eaten.

Ganmaaa & Satoa (2005) investigated associations between breast cancer and diet. They found that the closest correlation was with meat consumption (r = 0.827), closely followed by cow’s milk (r = 0.817) and cheese (r = 0.751). As they put it, meat was “the factor contributing most greatly to the incidence of breast cancer”. 18 While the evidence indicates a connection, it may be stretching the claim too much to treat that association as a cause of breast cancer.

Ganmaaa & Satoa (2005) contend that “increased consumption of animal-derived food may have adverse effects on the development of hormone-dependent cancers”. For example, as their Figure 1 suggests, there appears to be an association between meat consumption and breast cancer.

Ganmaaa & Satoa (2005) also claim that there is a strong association between the consumption of cow’s milk and the incidence of breast cancer. 18, 82 See Figure 2. These researchers also concluded that “milk was most closely correlated with the incidence of ovarian cancer (r = 0.779), followed by animal fats (0.717) and cheese (0.697)”. 18

Is the evidence for Claim #3 robust?

The short answer is yes and no. 22, 89, 90 The China Study was co-authored by Professor Colin Campbell, Jacob Gould Schurman Professor Emeritus of Nutritional Biochemistry at Cornell University, and his son Thomas M. Campbell II, a physician, and Medical Director of the T. Colin Campbell Center for Nutrition Studies. In preparing The China Study Campbell senior drew on his 40 years biomedical research and some 750 references that he and son had consulted. Their book was loosely based on a 20-year study conducted by the Chinese Academy of Preventive Medicine, Cornell University, and the University of Oxford. Professor Campbell was one of the study’s directors. One of the aims of that two-decade study was to test, on large a human population, some hypotheses that had arisen in Campbell’s laboratory work 16 and in other epidemiological studies. On that basis, his nutritional recommendations would seem to be well founded. However, The China Study utilised retrospective analysis to gauge dietary exposure, a technique which is subject to recall bias.

As has been noted earlier, some authorities allow a higher intake of animal protein and fat, as Giavannucci (1998, p.575) explains:

Although specific dietary risk factors have not been firmly established for cancers, the available evidence has been deemed to be sufficient by several scientific bodies to warrant recommendations for a reduction of fat  consumption, particularly animal fat or saturated fat, to 30 percent of total energy or even less, and an increased consumption of fruits, vegetables and whole grain foods.

The above generalisation is based on three reports put out by advisory bodies in the U.S. 19, 20, 21

What the research literature makes clear though is that “high protein intakes” are linked “to accelerated rates of aging and poor latelife cardiometabolic health, especially when coupled with low carbohydrate intakes”.  2, 22 23, 24

Where animal products are completely avoided, as in vegan diets, Campbell & Campbell (2006) recommend regular exposure to sunshine or dietary supplements to maintain adequate levels of vitamin D, as well as supplements of vitamin B12.

Claim #4: The Mediterranean diet may decrease the risk of chronic disease

The Mediterranean diet, which is associated with low protein intake, may lower the risk of some chronic diseases including Alzheimer’s 25 and naso-pharyngeal cancer. 26


The research cited above 26 was a hospital-based case-control study conducted in Italy to assess the association between adherence to a traditional Mediterranean diet and naso-pharyngeal cancer (NPC) risk. The sample included 198 confirmed cases and 594 matched controls. Dietary habits were surveyed using a validated food-frequency questionnaire. The key components of a Mediterranean diet were taken to be “high intake of vegetables, fruits and nuts, cereals, legumes, and fish; low intake of dairy products and meat; high monounsaturated to saturated fatty acid ratio; and moderate alcohol intake” (p. 89). 26 The researchers concluded that the Mediterranean diet played a “a favorable role” in mitigating NPC risk.

Both the traditional Okinawan and Mediterranean diets have been eaten by “exceptionally long-lived human populations”. 2

The Mediterranean diet is quite similar to the dietary protocol advocated by Perlmutter (2014, p. 125). In his view “if you modify the traditional Mediterranean diet by removing all gluten-containing foods and limiting sugary fruits and non-gluten carbs, you have yourself the perfect grain-brain-free diet” (p. 125). 4

In one study 27  three diets are contrasted: (1) The Western diet, which typically includes plenty of animal protein (from eggs, processed meat and red meat) processed foods (desserts, French fries and high-energy drinks; (2) the Prudent diet, which includes fruit, legumes vegetables and whole grains, and therefore has less saturated fat and more fibre, folate, magnesium, potassium, and vitamin B6; and (3) the Mediterranean diet, which is rather like the Prudent diet, but features more plant-based fats, and allows moderate consumption of alcohol (especially red wine).

Claim #5: Certain foods and supplements have been found to promote or inhibit prostate cancer

While prostate cancer growth may be inhibited by certain foods and supplements 28 other foods, such as the fat from red meat, appear to be carconogenic. 29 The consumption of dairy products is also said to be “one of the most consistent, specific links between diet and prostate cancer”. 3, 80

Evidence for Claim #5

Little research attention had been devoted to the relationship between diet and prostate cancer before 1997. 28  Kolenel (1996), for example, reported that “the laboratory literature on diet and prostate cancer is sparse”. 30

However, a few researchers before that time had offered some intriguing speculations about the consequences of dietary change for an individual.  For example, in one study of Japanese men who emigrated to the US, it was found that the rate of prostate cancer increased four to nine times within a generation. 31 The implication was that some factors other than genetics were responsible for their remarkable new susceptibility to chronic illness. Changes in the environment or diet were the most likely explanation.

In another study researchers found evidence to support their hypothesis that “animal fat, especially fat from red meat, is associated with an elevated risk of advanced prostate cancer”. 29

The evidence for some of these claims will now be examined in more detail. However, it should be noted, with reference to a recent report from Britain that health care professionals “did not routinely provide advice on diet and physical activity to men diagnosed with prostate cancer”, but if they did, any information given out by them was usually generic and in keeping with Department of Health guidelines for the general population in the United Kingdom. 32

Red meat

Evidence for the claim above, that total animal fat consumption is directly related to the risk of advanced prostate cancer, was provided by 1986 data from the Health Professionals Follow-up Study in the U.S. In that study a prospective cohort of 51 529 men, 40 to 75 years of age, completed a validated food-frequency questionnaire. After follow-up questionnaires were administered in 1988 and 1990, the researchers focussed on the 300 new cases of prostate cancer that were revealed, including 126 advanced cases. Multiple regression was used to estimate relative dietary risks with a 95% confidence interval. The incidence of cancer was found to be associated with animal fat, but not vegetable fat. The food group which had the strongest positive association with advanced cancer was red meat. However, the risk of advanced prostate cancer was also associated with  alpha-linolenic acid, monounsaturated fat, and saturated fat. 32 Incidentally, it might be worth noting that a 2012 meta-analysis found that “consumption of red and processed meat may be associated with increased risk of esophageal adenocarcinoma”. 33

Comparable findings in the research literature tend to support this claim. 81 For example, researchers in the US studied a cohort of 3,892 men aged 35 and older to assess whether there were any links between the risk of prostate cancer meat and the consumption of meat and dairy foods. 34 They found that “men with a higher intake of processed meat and pork were more likely to be subsequently diagnosed with total and advanced prostate cancer compared to men who consumed lower amounts or did not consume these foods at all”.  This is not surprising, given that the nitrites added to smoked or cured meats to help preserve them, as well as to improve their colour and taste, can be transformed by bacteria in the colon into carcinogenic N-nitroso compounds.


Men with the highest intake of dairy products are four times more likely to die of prostate cancer compared to those who consume less. 3, 35 Many researchers have identified a link between higher dairy intake, particularly high-fat dairy, and aggressive or lethal prostate cancer. 36 As Vieth (2002) puts it, “anything beyond just one glass of milk daily seems to increase the risk of prostate cancer”. 37  Giovannucci (1998) contends that higher prostate cancer risk is more consistently associated with dairy products rather than with total fat. 38

Newmark  &  Heaney (2010) theorise that it is high dietary phosphate content in dairy products rather than the calcium content that is the risk factor for prostate cancer. 39  For some scientists it is casein, the main protein in dairy foods, that is of particular concern, because in experiments it “has been shown to promote cancer and increase blood cholesterol and atherosclerotic plaque” (Campbell & Campbell, 2006, p. 294).  Others consider that dairy intake may promote prostate cancer progression in other ways. “Calcium and phosphorous, both abundant in dairy products, may lower levels of 1,25(OH)2D, a form of vitamin D that has been shown to inhibit prostate carcinogenesis and promote apoptosis”.  40

Campbell & Campbell (2006, p. 179) identify the serum insulin-like growth hormone IGF-1 as the factor linking cancer with the consumption of animal-based foods such as meat and dairy products. That is, IGF-1 can be regulated by animal protein intake. “Conventionally produced” milk has been found to contain 14% higher levels of IGF-1 than organic milk does. 41

Those with higher than normal levels of IGF-1, according to Campbell & Campbell (2006), have “5.1 times the risk of advanced-stage prostate cancer”. Support for this claim is provided by other researchers who have shown that IGF-1 is suppressed by a low-protein diet. 42

One group of researchers investigated the proliferation of prostate cancer cells treated with casein. 43 They found that casein “promotes the proliferation of prostate cancer cells such as PC3 and LNCaP”.

‘Dairy’ is a broad term. A compounding factor is that the majority of studies fail to “distinguish between low and high-fat dairy products” . Downer et al (2017) criticise this oversight on the grounds that “ there is wide variation in nutritional composition across dairy products, and these components may influence disease progression differently. For example, whole milk has an approximately 40-fold greater saturated fat content compared to skim milk”. In one study low-fat dairy products were associated with a better overall dietary nutritional profile. 44 Nonetheless Downer and colleagues (2017) found that “low-fat milk consumption may elevate the risk of overall mortality among men with advanced prostate cancer”. A study of several thousand Finnish and Swedish patients a decade earlier found that “only the consumption of low-fat milk was found to be associated with increased risk of prostate cancer”. 44

Although researchers often refer to ‘milk’ and ‘dairy’ without specifying the source it can be assumed that they mean milk, butter and cheese from cows. If so, this raises the question: Would milk and other dairy products from goats afford better cancer protection. We know that circulating concentrations IGF-I are higher (P < 0.01) in cows than goats 46, but this is a question that requires some more investigation.

It should be noted that some researchers have reported no association between the dairy intake and prostate cancer. 47

One group of researchers found that “the data from observational studies do not support an association between dairy product use and an increased risk of prostate cancer”.  47 A study of US men did not find “a statistically significant association between the consumption of dairy foods and prostate cancer”. 34

Vitamin D

Giovannucci (1998) set out to test a Vitamin D hypothesis; namely, that high dairy and meat consumption increased risk of prostate cancer by lowering the biologically active form of vitamin D known as 1,25(OH)2D. One reason for this is that “consumption of diets rich in meats, fish, and eggs, as a result of their high content of sulfur-containing amino acids, induces a chronic, low-grade metabolic acidosis, which a reduces 1-a-hydroxylase activity and 1,25(OH)2D levels” (Giovannucci,1998, 574). This suggests that it would be beneficial to take Vitamin D3 as a supplement. Perlmutter (2014, p. 224) advocates a daily dose of 5 000 IU of D3.

However, two cautions should be noted. The first is that it is not yet known whether increasing Vitamin D levels would have any mitigating effect on advanced prostate cancer (Giovannucci,1998, p. 574). 38, 83 The second is that promising laboratory results cannot necessarily be extrapolated to the outside world. As Begley & Ellis (2012) point out, “An enduring challenge in cancer-drug development lies in the erroneous use and misinterpretation of preclinical data from cell lines and animal models”. Chan & Giovannucci (2001) confidently assert that “The anticarcinogenic properties of vitamin D have been studied in the laboratory for many years, and 1,25 dihydroxyvitamin D3 (1,25 D), the most potent vitamin D metabolite, has consistently been shown to inhibit prostate cancer cell growth and development” (p. 87). However, they also have to acknowledge that “despite the compelling results from laboratory studies, the potential protective effect of vitamin D has been much more difficult to assess in human populations” (Chan & Giovannucci, 2001, p. 88).

Vitamin A

This vitamin may elevate the risk of prostate cancer in men who are 75 or younger. 28


A 63% decrease in the incidence of prostate cancer has been reported for men receiving supplemental selenium. 28


Arnott (2000, p.40) summarises the role of genistein, which is secreted in the roots of the soybean to attract bacteria that fix nitrogen in the soil, noting that “it acts in nearly half a dozen different ways as an anticancer agent”, such as inhibiting angiogenesis (i.e., stopping new blood vessel growth in cancer cells), increasing P-27 expression (thereby slowing down the prostate cancer cell cycle), blocking epidermal cell receptors and acting as an anti-oxidant (pp. 40-42). The recommended daily dose of soy protein is 40 gm (p. 46). 49

Claim #6: Many cardiometabolic deaths are attributable to a small set of dietary factors

Almost half of all cardiometabolic deaths can be linked to just a few key dietary factors such as too much salt, too many processed meats and not enough fruit, vegetables, nuts or seeds. 50

Evidence for Claim #6

The term ‘cardiometabolic risk’ refers to the chance of developing diabetes, heart disease or stroke. A recent study found that 10 dietary factors were linked to many cardiometabolic deaths. 50 Most of the deaths due to heart disease, stroke, or type 2 diabetes were caused by excess sodium intake (too much salt), an insufficient quantity of nuts or seeds, the consumption of too many processed meats, and not enough seafood omega-3 fats. These, which were all variously referred to as ‘suboptimal intake’, contributed to 45.4% of cardiometabolic deaths.

In order of severity most of the diet-related cardiometabolic deaths were related to high sodium intake (9.5%), low consumption of nuts/seeds (8.5%), high intake of processed meats (8.2%), low consumption of seafood omega-3 fats (7.8%), low intake of vegetables (7.6%) and fruits (7.5%), and high consumption of sugar-sweetened beverages (7.4%). It is generally true that “Excess intakes of energy, sodium, saturated fat, and trans fat are associated with increased risk for cardiometabolic syndrome”. 51


If 7.5% of cardio-vascular deaths were caused by not enough fruit in the diet, what constitutes the right amount? Clearly, it is not appropriate to conclude that the more fruit one eats the better off one would be, especially given the cautions expressed by Perlmutter (2014). What he recommends is “one piece or serving of low-sugar fruit (e.g., grapefruit, orange, apple, berries, melon, pear, cherries, grapes, kiwi, plum, peach, nectarine)” (Perlmutter, 2014, p. 247). Note that this is lower than the minimum two serves of fruit specified in official Australian dietary guidelines.

After a Roy Morgan Poll had been conducted in 2015 the investigators summarised what they had found in this way:

Ask any Australian aged 14+ if they eat two serves of fruit and five serves of vegetables each day, and chances are the answer will be no. According to the latest findings from Roy Morgan Research, only 2% of the population does — despite this being the minimum daily fruit-and-veg intake recommended by the National Health and Medical Research Council 52

This, of course, raises the question: What is a serve of fruit or vegetables and how many would be appropriate each day? 77 A study led by the Imperial College London concluded that while five daily portions of fruit and vegetables was good, 10 a day was even better. 53 One portion is defined as 80g; for example, one banana, one tomato or three tablespoons of peas. 53

Claim #7: There is a link between insufficient ‘Vitamin’ D intake and chronic illness

Vitamin D deficiency is said to be linked to several chronic neurodegenerative diseases, including Alzheimer’s, Parkinsons, and multiple sclerosis (Perlmutter, 2014, p. 92). This is claimed to be true of osteoporosis as well. Even though calcium has been long known to be an important micronutrient in promoting bone mass, Vitamin D intake that is higher than the current recommendation (600 IU in the US) may be needed for optimal bone health (Nieves, 2005). Professor Jelinek, a leader in the field of Multiple sclerosis research, has pointed out that “opinion leaders in neurology have publicly stated that if they themselves were diagnosed with early demyelination, they would take high dose vitamin D supplements”. 54

Evidence for Claim #7

Vitamin D is a critically important micronutrient (Perlmutter, 2014, p.18 and like vitamins A, E and K, can only be absorbed from the small intestine in combination with fat, not being soluble in water (Perlmutter, 2014, p. 89). Actually, it is not really a vitamin, but more a secosteroid or hormone.

While this is not the place to explain Vitamin D synthesis in any detail, it is worth pointing out that in order for vitamin D as a secosteroid to become biologically active, in two enzymatic transformations or hydroxylations are required.  The first process occurs in the liver creates calcidiol, a prohormone and the major circulating form of vitamin D; the second occurs in the kidneys, creating calcitriol or 1,25(OH) 2 D, the hormonal form of vitamin D. Calcitriol achieves its biological effects by interacting with specific hormone receptors known as vitamin D receptors, or VDRs, which exist in both normal cells and malignant ones. The anticancer effects of calcitriol have now been noted by researchers. 55

There is no agreement in the literature about what the optimum doses should be if D3 is to be obtained by means of supplementation (rather than from oily fish, such as sockeye salmon, or sunlight alone). Nieves (2005) recommends 800–1000 IU for the elderly (age ≥ 65 y) to ensure optimal bone health, and to reduce fracture risk. 56 As noted earlier, others recommend a daily dose of 5 000 IU of D3 (Perlmutter, 2014, p. 224).

With reference to Vitamin D-deficient children it has been pointed out that, when supplementing vitamin D, simultaneous calcium supplementation is needed “because of the risk of hypocalcemia from decreased demineralization of bone and increased remineralization as parathyroid hormone levels normalize. Therefore, vitamin D-3 should be given in conjunction with adequate calcium until parathyroid hormone and vitamin D levels normalize”. 57

Claim #8: There is an association between lactose intolerance and asthma

Asthma may be linked to lactose intolerance. This claim was made by an American naturopath in May 1981 when an Australian woman happened to mention that her young son had contracted severe asthma. Once a lactose-free diet was implemented the symptoms decreased. Some five years later the mother passed this useful information on to the presenter of a talk in Darwin on asthma, but he was not interested, asserting that the link was ‘not proven’.

Evidence for Claim #8

‘Lactose intolerance’ is a term used by paediatricians to refer to non-immunological hypersensitivity. 58, 91 This disease is quite distinct from cow milk allergy as “the first is due to a congenital or acquired lactase deficiency and the second is due to an immunologic disorder” according to several researchers 58, who reported that “a woman allergic to milk presented several atopic dermatitis and asthma exacerbations after respiratory exposure to CM proteins traces. The symptoms began when bronchodilator (formoterol) was delivered with a dry powder inhaler, instead of a spray”.

Yet, even as late as 2015, it could be reported in a specialist journal that not much was known about “available on the prevalence of food hypersensitivity among adults with asthma”. 59

Claim #9: It is not yet known, for sure, what diet is best for tackling obesity

Obesity is not classified as a disease by the World Health Organization, but it is associated with cardiovascular disease, diabetes mellitus, musculoskeletal disorders, and several forms of cancer. 61, 62 Some discussion of this topic is therefore deemed to be relevant to this paper.

Those who have researched links between obesity and cancer offer some hopeful findings, including the claim that “obesity has emerged as a major preventable cause of cancer”. 63 A decision to lose weight intentionally “may well lead to meaningful reductions in cancer risk”. 63

The scientific research literature indicates that many factors contribute to obesity. For example, sleep deprivation can cause a drop in the levels of leptin, triggering hunger pangs and a tendency to indulge in high carbohydrate foods, especially sweets (Perlmutter, 2014, p. 212). Exercise, sleep, diet, stress are all relevant considerations, and a fuller study would take account of all of them, but it is nutrition specifically that I want to target here, even though “an optimal diet for the treatment and prevention of obesity has not yet been determined”. 63, 64 Although weight reduction can be achieved by means of  a protein-rich diet with high meat intake 64 a possible link has also been established between the risk of obesity and the consumption of both red meat and processed meat.  61 In that regard the researchers concerned are careful to point out that while “red and processed meat intake was directly associated with risk of obesity” it might be overstating the case to argue that this is a causal link. 61

A group of Australian health science researchers conducted a systematic review of 16 randomised controlled trials involving adults in 2009 and 2011. They concluded that “there is some evidence that a healthy diet higher in vegetables may be conducive to weight loss in overweight adults”. 66 This, of course, begs the question: What is a healthy diet?  Four of the studies used the DASH diet framework (which “stipulates the number of serves of staple food groups in a total diet, including five serves of vegetables/day”. 66 In the end, they concluded, “In the end, it is not vegetable consumption per se that affects weight loss, but total dietary energy”. 66

Claim #10: The dietary acid load hypothesis

It is claimed that the typical Western diet creates a dietary acid load that may adversely impact bone formation and mass by disrupting calcium metabolism. 67 Acidosis is also associated with loss of muscle mass and strength (sarcopenia) and diminished renal function. 68

Older diets, which once included more fruits and vegetables, were a rich source of alkaline potassium salts. A characteristic of many modern diets is that they induce low-grade metabolic acidosis. This is because they feature higher protein and cereal grain intake and a reduced consumption of fruits and vegetables. In fact, “acidifying constituents such as animal proteins may negatively affect calcium metabolism and accelerate bone resorption, thus representing an aggravating factor for osteoporosis”. 69

Alkaline diets are therefore promoted based on the basis that many modern Western diets acidify the body causing chronic diseases, including cancer, cardiovascular disease and osteoporosis.  70, 71, 88  My question is whether this approach to diet is scientifically justified.

Evidence for Claim #10

It does seem clear that a limited fruit and vegetable intake does result in chronic consequences that only worsen as we grow older. These include diminishing bone density and declining renal function. 72

A positive correlation has been discovered between a higher alkaline diet load and improved skeletal muscle mass in women. 68  While acknowledging that protein is important for maintaining muscle mass, some researchers conclude that eating fruits and vegetables which supply adequate amounts of potassium and magnesium is also essential. One benefit is that such a diet can help  prevent muscle loss. 68 For older men and women, potassium citrate supplementation has been found to achieve a sustained improvement in calcium balance. 67

In relation to osteoporosis, Bonjour (2013) argues that “systemic acidosis of pure dietary origin remains a hypothesis that has not been scientifically  demonstrated”. He criticises those who considered  it to  be  a  proven pathophysiological mechanism leading to osteoporosis and rejects the hypothesis that “foods associated with an increased urinary acid excretion are deleterious for the skeleton” because they lead “to osteoporosis and enhanced fragility fracture risk”. 73 Nor does he support the notion that foods which generate neutral or alkaline urine favour bone growth and calcium balance and thereby prevent bone loss and reduce osteoporotic fracture risk. 73

In connection to cancer, Fenton & Huang (2016) systematically reviewed both the published and the grey literature in search of randomised intervention and observational studies which investigated varying acidbase dietary intakes and/or the use of alkaline water. They concluded that “the literature revealed a lack of evidence for or against diet acid load and/or alkaline water for the initiation or treatment of cancer”. 74


Recently, my wife and I booked ourselves into Living Valley Springs for a week-long health retreat. It was a generally excellent stay. My aim in this section of the paper is to assess some of my experiences there in the light of the research findings I have briefly summarised.

On rising early in the morning we would have a glass of water then teaspoonfuls of Vitamin C powder, lemon juice and apple cider vinegar, also mixed into water. We were told that this combination was excellent for the liver. Jessica Gaunt, the LVS naturopath, also suggested that I have Basica Vital E-1 each day as it is “rich in alkalising minerals and citrates and helps to maintain healthy pH levels”.

One of the paradoxes we encounter when we start reading in the field of nutrition is that the acid or alkaline-forming tendency of food, once it has been ingested into the body, is said to have nothing to do with its potential of hydrogen (pH) levels. These claims can be broadly summarised in this way. If we test the pH of meat it will be alkaline before digestion, but later it will leave acidic residue in the body. In common with all animal products, meat can therefore be regarded as acid-forming. Similarly, lemons are acidic, but the end-products they are said to produce after digestion and assimilation are alkaline. In that sense, lemons are alkaline-forming in the body, and so too is apple cider vinegar, which is regarded as a wonderful alkaliser which can be used in salad dressings. Is Living Valley Springs practice in this regard supported by scientific research?

A literature review focussing on 21 animal and 24 human studies “evaluated the effects of vinegar on glucose and lipid metabolism or body weight”. 75 The reviewers found that in most of the clinical studies they reviewed vinegar/acetic acid was shown to have a beneficial effect on glucose metabolism in healthy people, as well as those with insulin resistance or diabetes mellitus. Some studies found no beneficial effect on glucose metabolism though.

Three reviewers explored the link between insulin resistance in humans and the role of dietary acid load and mild metabolic acidosis.  76 They found that

There is mounting evidence to suggest that a diet with high acid load increases body acidity and predicts insulin resistance and type 2 diabetes. It remains unknown however, whether a low dietary acid load (or alkaline diet) can buffer mild metabolic acidosis, improve insulin sensitivity and reduce diabetes risk. 76

In their review of the literature these scholars explain that

The pH of arterial blood is close to 7.40, with a normal range considered to be approximately 7.35–7.45. An arterial pH less than 7.35 is classified as acidaemia, whilst the underlying condition characterised by hydrogen ion retention or loss of bicarbonate or other bases, is referred to as acidosis 76

On the fourth day at Living Valley Springs a late afternoon talk was given by John (Toby) Tobin, who manages the team of naturopaths there. These were some of the points he made. Blood pH is 7.4. Any minor changes to it would have profound consequences. For example, a pH of 7.2 would lead to a coma. Tap water generally has a pH of 6 to 6.5. It is worth noting that a can of Coke has a pH of 2.6 and so do other phosphoric beverages.

Acidity deletes oxygen. At times metabolism can revert to anaerobic processes. The more we operate in an anaerobic state the more lactic acid is produced. Many organisms (like candida) thrive in low-oxygen environments.

He presented a disease model which showed how acid stress leads to free calcium, to chronic inflammation, as well as to anaerobic metabolism, which leads to oxidative stress, 93 and then again to chronic inflammation. Free calcium excess was explained in this way. Calcium has to be bound to albumen, so the rest is in free form. It will tend to calcify, or harden, and the result may be kidney stones, gall; stones and so on. Calcified pineal glands have even been found in autopsies of young children. Free calcium contributes to chronic inflammation in forms such as arthritis, nephritis, colitis, pancreatitis.

Kidneys, he pointed out, are the primary pH regulators. Anything compromising the kidneys will affect the pH balance. By the time people reach the age of 70 about 40 per cent of kidney function has been lost. Water intake is crucial to maintain kidney function. Diuretics such as tea, coffee and alcohol cause the kidneys to work harder. Moderating sugar intake is also helpful in this regard.

Foods containing animal protein such as meat and dairy products are generally acid-forming. What Living Valley Springs advocates is ‘adequate’ protein intake. For someone 175 cm tall that would be 75 gm. Little bits of protein distributed across meals would be better than one large, protein-rich meal. Other acidic foods are sugar, eggs, alcohol, fried foods, soft drinks and grains, especially white flour products. Transfats are particularly damaging, which is a good reason to avoid margarine, vegetable shortening and fast food.

The alkaline foods tend to be plant based—fruits and vegetables—however vegetables are the ones to concentrate on, particularly the dark, leafy green varieties 94.  Just to cite one benefit, “epidemiologic studies have linked diets rich in cruciferous vegetables, such as broccoli, Brussels sprouts, and cauli-flower, with a marked reduction” in prostate cancer risk”.  94

More specifically, epidemiologic studies have linked diets rich in cruciferous vegetables, such as broccoli, Brussels sprouts, and cauli- flower, with a marked reduction in PCa risk (Hebert et al. 1998; Giovannucci et al. 2003).

Twelve serves a day would be needed to offset the typical Western diet. Five to six cups would be optimal. This is doable if the day is started with a savoury breakfast. A great tip for busy people is to prepare Mason Jar salads for the week. I am indebted to my sister Helen for that tip.

A typical meal at Living Valley.

Litmus paper obtained from a chemist was said to be the best way to measure ph in our bodies. It is better to measure the pH in urine rather than in saliva. The level we are aiming for is 6.5-6.7 in urine. Toby’s advice was to measure for four days, calculate the mean then, take measurements on a weekly basis thereafter.

To correct pH these prescriptions were offered: (1) Measure and record; (2) Correct lifestyle violations; (3) Encourage friendly bacteria; (4) Remember that lemons and limes convert to citrate; (5) Mineralise; (6) Be happy; Forgive others; (7) Share knowledge. Make a difference. Implement the changes yourself.


This draft paper has briskly touched on dietary topics as diverse as gluten, sugar, animal protein, acid-forming foods, the Mediterranean diet and carcinogenic foods. In doing so my aim has been to avoid proposing easy solutions to complex problems or asserting any straightforward cause-and-effect relationships. 84 Chronic illnesses arise for complex reasons. 85, 86 There are associations between the food and supplements we take, on the one hand, and our health on the other, but these are not likely to be simple, one-to-one, easily isolatable connections. There are webs, synergies, and subtle perturbations at work that are far beyond my understanding. 2, 87 So much so that I would love to see, for example, a supercomputer simulation of a stochastic model to help us visualise autoreactive lymphocytes and their role in the development of autoimmune disease. In time, such simulations will be available, I expect. In the meantime, I welcome the contributions that biochemists, neurologists, and new nutritional ecologists are making available in the published research literature. I have shared some of their insights in the hope that the information offered here might be of use.


  1. Australian Institute of Health and Welfare (2015). Chronic diseases. Retrieved March 15 from http://www.aihw.gov.au/chronic-diseases/
  2. Raubenheimer, D. & Simpson, S. (2016). Nutritional ecology and human health. Annual Review of Nutrition, 36, 603-626. Retrieved on March 18, 2016 from goo.gl/3D8Ycl
  3. Campbell, C., & Campbell, T. (2006). The China study: Startling implications for diet, weight loss and long-term health. Dallas, TX: Benbella Books.
  4. Perlmutter, D. with Loberg, K. (2014). Grain brain: The surprising truth about wheat, carbs and sugar—Your brain’s silent killers. London: Hodder & Stoughton.
  5. National Health and Medical Research Council (2013). Australian Dietary Guidelines. Canberra: National Health and Medical Research Council.
  6. Campbell, C. (2015a). Dr. Campbell’s recommendations for Dietary Guidelines. Retrieved on March 31, 2017 from http://nutritionstudies.org/2015-dietary-guidelines-commentary/
  7. Campbell, C. (2015b, December 2). Personal interview with Carol Grieve. Retrieved on March 31, 2017 from goo.gl/ET7QMI
  8. Dos Santosa, S., & Lioté, F. (in press). Osteoarticular manifestations of celiac disease and non-celiac gluten hypersensitivity. To be published in Joint Bone Spine. Retrieved March 16, 2017 from goo.gl/w2kl1y
  9. Stein, E., Rogers, H., Leib, A., McMahon, D., & Young, P. (2015). Abnormal skeletal strength and microarchitecture in women with celiac disease. The Journal of Clinical Endocrinology and Metabolism,100, 2347–53.
  10. Grace-Farfaglia, P. (2015). Bones of contention: bone mineral density recovery in celiac disease—a systematic review. Nutrients, 7, 3347–69.
  11. Hayden, K., Beavers, D., Steck, S., Hebert, J., Tabung, F., Casanova, R., Manson, J., Padula, C., Salmirago-Blotcher, E., Snetselaar, L., Zaslavsky, O., & Rapp, S. (2016). Impact of inflammatory diet on global cognitive function and incident dementia in older women. Alzheimer’s & Dementia, 12(7), Supplement, 579-80.
  12. Luevano-Contreras, C., & Chapman-Novakofski, K. (2010). Dietary advanced glycation end products and aging. Nutrients, 2(12), 1247–1265. Retrieved March 13 from http://www.pnas.org/content/111/13/4743.full.pdf
  13. Clarkson, S., & Newburgh, L. (1926). The relation between atherosclerosis and ingested cholesterol in the rabbit. Journal of Experimental Medicine, 43, 595-612
  14. Kritchevsky, D. (1995). Dietary protein, cholesterol and atherosclerosis: A review of the early history. Journal of Nutrition, 125, 589-593.
  15. Campbell, C. (2014). Untold Nutrition. Nutrition and Cancer, 66(6), 1077-1082.
  16. Appleton, B. & Campbell, C. (1983). Effect of high and low dietary protein on the dosing and postdosing periods of aflatoxin B1-induced hepatic pre-neoplastic lesion development in the rat. Cancer Research, 43(5), 2150–2154.
  17. Youngman, L., & Campbell, C. (1992). Inhibition of aflatoxin B1-induced gamma-glutamyl transpeptidase positive (GGTC) hepatic preneo- plastic foci and tumors by low protein diets: evidence that altered GGTC foci indicate neoplastic potential. Carcinogenesis 13(9), 1607–1613.
  18. Ganmaaa, D., & Satoa, A. (2005). The possible role of female sex hormones in milk from pregnant cows in the development of breast, ovarian and corpus uteri cancers. Medical Hypotheses, 65(6), 1028–1037.
  19. Committee on Diet Nutrition and Cancer, Assembly of Life Sciences, National Research Council (1982). Diet, nutrition, and cancer. Washington, DC: National Academy Press.
  20. National Research Council, Committee on Diet and Health. (1989). Diet and health: Implications for reducing chronic disease risk. Washington, DC: National Academy Press.
  21. National Cancer Institute. (1987). Diet, nutrition, and cancer prevention: A guide to food choices. NIH Pub. No. 87-28-78. (Ed.) PHS National Institutes of Health, U.S. Dept. Health and Human Services. Washington, DC: U.S. Government Printing Office.
  22. Simpson S., Le Couteur, D., & Raubenheimer, D. (2015). Putting the balance back in diet. Cell, 161(1), 18–23.
  23. Solon-Biet, S., McMahon, A., Ballard, J., Ruohonen, K., Wu, L, et al. (2014). The ratio of macronutrients, not caloric intake, dictates cardiometabolic health, aging, and longevity in ad libitum-fed mice. Cell Metabolism, 19(3), 418–30.
  24. Solon-Biet, S., Mitchell, S., de Cabo, R., Raubenheimer, D., Le Couteur, D., & Simpson, S. (2015). Macronutrients and caloric intake in health and longevity. Journal of Endocrinology, 226(1), R17–28
  25. Lourida, I., Soni, M., Thompson-Coon, J., Purandare, N., Lang, I., Ukoumunne, C., & Llewellyn, D. (2013). Mediterranean diet, cognitive function, and dementia: A systematic review. Epidemiology 24(4), 479–489.
  26. Turati, F., Bravi, F., Polesel, J., Bosetti, C.,  Negri, E., Garavello, W., Taborelli, M., Serraino, D., Libra, M., Montella, M.,  Decarli, A., Ferraroni, M.,  & La Vecchia, C. (2017). Adherence to the Mediterranean diet and nasopharyngeal cancer risk in Italy. Cancer Causes and Control, 28, 89–95.
  27. Williams, R., Kozan, P., & Samocha-Bonet, D. (2016). The role of dietary acid load and mild metabolic acidosis in insulin resistance in humans. Biochimie, 124, 171-177.
  28. Fair, W., Fleshner, N., & Heston, W. (1997). Cancer of the prostate: a nutritional disease? Urology, 50(6), 840-8.
  29. Giovannucci, E., Rimm, E., Colditz, G., Stamfer, M., Ascherio, A., Chute, C., & Willett, W. (1993). A prospective study of dietary fat and risk of prostate cancer. Journal of the National Cancer Institute, 85, 1571-1579.
  30. Kolonel, L. (1996). Nutrition and prostate cancer. Cancer Causes & Control, 7(1), 83–94.
  31. Shimizu, H., Ross, R., Bernstein, L., Yatani, R., Henderson, B., & Mack, T. (1991). Cancers of the prostate and breast among Japanese and white immigrants in Los Angeles County. British Journal of Cancer, 63, 963-966.
  32. Sutton, E., Hackshaw-McGeagh, L., Aning, J., Bahl, A., Koupparis, A., Persad, R., Martin, R., & Lane, J. (2017). The provision of dietary and physical activity advice for men diagnosed with prostate cancer: A qualitative study of the experiences and views of health care professionals, patients and partners. Cancer Causes & Control, 28(4), 319–329.
  33. Huang, W., Han, Y., Xu, J., Zhu, W., & Li, Z. (2012). Red and processed meat intake and risk of esophageal adenocarcinoma: A meta-analysis of observational studies. Cancer Causes & Control, 24(1), 193–201.
  34. Rohrmann, S.,Platz, E.,Kavanaugh, C., Thuita, L., Hoffman, S., & Helzlsouer, K. (2007). Meat and dairy consumption and subsequent risk of prostate cancer in a US cohort study. Cancer Causes Control, 18, 41–50.
  35. Chan, J., & Giovannucci, E. (2001). Dairy products, calcium, and Vitamin D and risk of prostate cancer. Epidemiologic Reviews, 23(1), 87-92.
  36. Giovannucci, E.,Liu, Y., Stampfer, M., & Willett, W. (2006). A prospective study of calcium intake and incident and fatal prostate cancer. Cancer epidemiology, biomarkers & prevention,15(2),203–10.
  37. Vieth, R. (2002). Dairy products, calcium, and prostate cancer risk in the Physicians’ Health Study. American Journal of Clinical Nutrition, 76(2), 490-491.
  38. Giovannucci, E. (1998). Dietary influences of 1,25(OH)2 vitamin D in relation to prostate cancer: A hypothesis. Cancer Causes and Control, 9, 567-582.
  39. Newmark, H., & Heaney, R. (2010). Dairy products and prostate cancer risk. Nutrition and Cancer, 62(3), 297-299.
  40. Downer, M., Batista, J. Mucci, L., Stampfer, M., Epstein, M., Håkansson, N., Wolk, A., Johansson, J. Andrén, O., Fall, K, & Andersson, S. (2017). Dairy intake in relation to prostate cancer survival. International Journal of Cancer, 140(9), 2060–2069.
  41. Um, C., Fedirko, V., Flanders, W., Judd, S., & Bostick, R. (2017). Associations of calcium and milk product intakes with incident, sporadic colorectal adenomas. Nutrition and Cancer, 69(3), 416-427.
  42. Doi, S., Rasaiah, S., Tack, I., Mysore, J., Kopchick, J, Moore, J., Hirszel, P., Striker, L., & Striker, G. (2001). Low-protein diet suppresses serum insulin-like growth factor-1 and decelerates the progression of growth hormone-induced glomerulosclerosis. American Journal of Nephrology, 21(4), 331-9.
  43. Park, S., Kim, J., Kim, Y., Lee, S., Lee, S., & Chung, M. (2014). A milk protein, casein, as a proliferation promoting factor in prostate cancer cells. World Journal of Men’s Health, 32(2), 76–82.
  44. Vidal-Casariego, A., Pintor-de la Maza, B., Calleja-Fernández, A., Villar-Taibo, R., Cano-Rodríguez, I. & Ballesteros-Pomar, M. (2014). Consumption of low-fat dairy products and energy and protein intake in cancer patients at risk of malnutrition. Journal Nutrition and Cancer, 67(1), 191-195.
  45. Torniainen, S., Hedelin, M., Autio, V., Rasinperä,H., Bälter,K., Klint, A., Bellocco, R., Wiklund, F., Stattin, P., Ikonen, T., Tammela, T., Schleutker, Grönberg H., & Järvelä, I. (2007). Lactase persistence, dietary intake of milk, and the risk for prostate cancer in Sweden and Finland. Cancer epidemiology, biomarkers & prevention, 16, 956–61.
  46. Toral, P., Chilliard, Y., Rouel, J., Leskinen, H., Shingfield, K., & Bernard, L. (2015). Comparison of the nutritional regulation of milk fat secretion and composition in cows and goats. Journal of Dairy Science, 98, 7277–7297. Retrieved March 21 from goo.gl/Dc1CPf
  47. Rodriguez, C., McCullough, M., Mondul, A., Jacobs, E., Fakhrabadi-Shokoohi, D., Giovannucci, E., Thun, M., & Calle, E. (2003). Calcium, dairy products, and risk of prostate cancer in a prospective cohort of United States men. Cancer epidemiology, biomarkers & prevention, 12(7), 597-603.
  48. Huncharek, M., Muscat, J., & Kupelnick, B. (2008). Dairy products, dietary calcium and vitamin D intake as risk factors for prostate cancer: A meta-analysis of 26,769 cases from 45 observational studies. Nutrition and Cancer, 60(4), 421-441.
  49. Arnott, B. (2000). The prostate cancer protection plan. The foods, supplements, and drugs that could save your life. Boston: Little, Brown and Company.
  50. Micha, R., Peñalvo, J., Cudhea, F., Imamura, F., Rehm, C., & Mozaffarian, D. (2017). Association between dietary factors and mortality from heart disease, stroke, association between dietary factors and mortality from heart disease, stroke, and type 2 diabetes in the United States. JAMA, 317(9), 912-924. doi:10.1001/jama.2017.0947
  51. Urban, L., Roberts, S., Fierstein, J., Gary, C., & Lichtenstein, A. (2014). Temporal trends in fast-food restaurant energy, sodium, saturated fat, and trans fat content, United States, 1996-2013. Preventing Chronic Disease, 11.
  52. Roy Morgan Research (2015, January 15). Research shows only 2% of Australians are eating the recommended daily intake of fruit and vegetables. Retrieved March 18 from goo.gl/CL0MV3
  53. Boseley, S. (2017). Forget five a day, eat 10 portions of fruit and veg to cut risk of early death. The Guardian. Retrieved March 31, 2017 from goo.gl/8gMZhC
  54. Jelinek, G., Marck, C., Weiland, T., Pereira, N., van der Meer, D., & Hadgkiss, E. (2015). Latitude, sun exposure and vitamin D supplementation: Associations with quality of life and disease outcomes in a large international cohort of people with multiple sclerosis. BMC Neurology, 15. Retrieved March 15, 2017 from goo.gl/hSUz1L
  55. Schwartz, G., & Blot, W. (2006). Vitamin D status and cancer Incidence and mortality: Something new under the sun. Journal of the National Cancer Institute, 98(7). Retrieved March 15 from goo.gl/u1T2Qs
  56. Nieves, J. (2005). Osteoporosis: The role of micronutrients. The American Journal of Clinical Nutrition, 81(5): 1232S–9S. PMID 15883457. Retrieved March 15, 2017 from http://ajcn.nutrition.org/content/81/5/1232S.long
  57. McCloud, E., & Papoutsakis, C. (2011). A medical nutrition therapy primer for childhood asthma: Current and emerging perspectives. Journal of the American Dietetic Association, 111, 1052-1064.
  58. Morisset, M., Moneret-Vautrin, D., Commun, N., Schuller, A., & Kanny, G. (2006). Allergy to cow milk proteins contaminating lactose, common excipient of dry powder inhalers for asthma. Journal of Allergy and Clinical Immunology, 117(2), Supplement, 95.
  59. Rentzos, G., Johanson, L., Sjölander, S., Telemo, E. & Ekerljung, L. (2015). Self-reported adverse reactions and IgE sensitization to common foods in adults with asthma. Clinical and Translational Allergy, 5. Retrieved March 16, 2017 from http://ctajournal.biomedcentral.com/articles/10.1186/s13601-015-0067-6
  60. Rouhani, M., Salehi-Abargouei, A., Surkan, P. and Azadbakht, L. (2014). Is there a relationship between red or processed meat intake and obesity? A systematic review and meta-analysis of observational studies. Obesity Reviews, 15, 740–748
  61. Visscher, T., Lakerveld, J., Olsen, N., Küpers, L., Ramalho, S., Keaver, L., Brei, C., Bjune, J., Ezquerro, S., Yumuk, V. (2017). Perceived health status: Is obesity perceived as a risk factor and disease? Obesity Facts, 10, 52­–60.
  62. Byers, T., & Sedjo, R. (2011). Does intentional weight loss reduce cancer risk? Diabetes, Obesity and Metabolism, 13(12), 1063–1072.
  63. Shay, C., Van Horn, L., Stamler, J., Dyer, A., Brown, I., Chan, Q., Miura, K., Zhao, L., Okuda, N., Daviglus, M., Elliott, P., INTERMAP Research Group. (2012). Food and nutrient intakes and their associations with lower BMI in middle-aged US adults: The International Study of Macro-/Micronutrients and Blood Pressure (INTERMAP). American Journal of Clinical Nutrition, 96, 483–491.
  64. Clifton P. (2012). Effects of a high protein diet on body weight and comorbidities associated with obesity. British Journal of Nutrition, 108, 122–129.
  65. Tapsell, L., Dunning, A., Warensjo, E., Lyons-Wall, P., & Dehlsen, K. (2014). Effects of vegetable consumption on weight loss: A review of the evidence with implications for design of randomized controlled trials. Critical Reviews in Food Science and Nutrition, 54(12), 1529-1538.
  66. Moseley, K., Weaver, C., Appel, L., Sebastian, A., & Sellmeyer, D. (2013). Potassium citrate supplementation results in sustained improvement in calcium balance in older men and women. Journal of Bone and Mineral Research, 28(3), 497–504.
  67. Welch, A., MacGregor, A., Skinner, J., Spector, T., Moayyeri, A., Cassidy, A. (2012). A higher alkaline dietary load is associated with greater indexes of skeletal muscle mass in women. Osteoporosis International, 24(6), 1899-908.
  68. Buclin, T., Cosma M., & Appenzeller, M., Jacquet, A., De ́costerd, L., Biollaz, J., & Burckhardt, P. (2001). Diet acids and alkalis influence calcium retention in bone. Osteoporos International, 12, 493–9.
  69. Jackson G. (2014). Alkaline foods for the alkaline diet: Feel the pH miracle of a healthy pH diet. Createspace Independent Publishing Platform.
  70. Marra, J. (2014). Cause, cure, and cancer free: How I became a cancer free escapee. Pennsylvania: Sakura Publishing and Technologies.
  71. Frassetto, L., Morris, R., & Sebastian, A. (1996). Effect of age on blood acid-base composition in adult humans: Role of age-related renal functional decline. The American Journal of Physiology, 271(6 Pt 2), 1114-22.
  72. Bonjour, J-P (2013). Nutritional disturbance in acid–base balance and osteoporosis: a hypothesis that disregards the essential homeostatic role of the kidney. The British Journal of Nutrition, 110(7), 1168–1177.
  73. Fenton T., & Huang, T. (2016). Systematic review of the association between dietary acid load, alkaline water and cancer. BMJ Open, 6. Retrieved March 15, 2017 from http://bmjopen.bmj.com/content/bmjopen/6/6/e010438.full.pdf doi:10.1136/bmjopen-2015-010438
  74. Petsiou, E., Mitrou, P., Raptis, S., & Dimitriadis, G. (2014). Effect and mechanisms of action of vinegar on glucose metabolism, lipid profile, and body weight. Nutrition Reviews, 72(10), 651–661.
  75. Williams, R., Kozan, P., & Samocha-Bonet, D. (2015). The role of dietary acid load and mild metabolic acidosis in insulin resistance in humans. Biochimie, 124, 171-7.
  76. Agudo, A. (2004). Measuring intake of fruit and vegetables. Background paper for the Joint FAO/WHO Workshop on fruit and vegetables for health, September 1-3, 2004, Kobe, Japan. Retrieved on March 20 from http://www.who.int/dietphysicalactivity/publications/f&v_intake_measurement.pdf
  77. Sherwell, P. (2010, October 3). Bill Clinton’s new diet: Nothing but beans, vegetables and fruit to combat heart disease. The Daily Telegraph.
  78. Madhavan, T., & Gopalan C. (1968). The effect of dietary protein on carcino-genesis of aflatoxin. Archives of pathology, 85, 133–137.
  79. Barnard, N. (n.d.). Milk consumption and prostate cancer. Retrieved on March 20, 2017 from http://www.pcrm.org/health/health-topics/milk-consumption-and-prostate-cancer
  80. Fogelholm, N., Kanerva, N., & Männistö, S. (2015). Association between red and processed meat consumption and chronic diseases: The confounding role of other dietary factors. European Journal of Clinical Nutrition, 69, 1060–1065.
  81. Maliou, D., & Bitam, A. (2015). Implication of milk and dairy products consumption through insulin-like growth factor-I in induction of breast cancer risk factors in women. Nutrition Clinique et Métabolisme, 29, 219–225.
  82. Schwartz, G., & Hulka, B. S. (1990). Is vitamin D deficiency a risk factor for prostate cancer? Anticancer Research,10, 1307-1311.
  83. Armstrong, B., & Doll, R. (1975). Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices. International Journal of Cancer, 15(4), 617–631.
  84. Begley, C., & Ellis, L. (2012, 29 March). Drug development: Raise standards for preclinical cancer research. Nature, 483, 531–533. doi:10.1038/483531a
  85. Campbell, C., Junshi, C., Brun, T., Parpia, B., Yinsheng, Q., Chumming, C. & Geissler, C. (1992). China: From diseases of poverty to diseases of affluence. Policy implications of the epidemiological transition. Ecology of Food and Nutrition, 27, 133-­144. Retrieved March 12, 2017 from goo.gl/fB0BTM
  86. Hackshaw-McGeagh, L., Perry, R., Leach, V., Qandil, S., Jeffreys, M., Martin, R., & Lane, J. (2015). A systematic review of dietary, nutritional, and physical activity interventions for the prevention of prostate cancer progression and mortality. Cancer Causes Control, 26, 1521–1550.
  87. Young, R. (2002). The pH miracle—balance your diet, reclaim your health. New York: Warner Books.
  88. Irving, D. (2011). The protein myth. Alresford, UK: John Hunt.
  89. Howell M. (1974). Factor analysis of international cancer mortality data and per capita food consumption. British Journal of Cancer, 29, 328-336. Retrieved July 20, 2017 from goo.gl/qPZkWE
  90. Dreborg, S. (2015). Debates in allergy medicine: Food intolerance does not exist. World Allergy Organization Journal, 8. Retrieved March 16 from goo.gl/3zXghx
  91. Mercola, J. (2017, March 12). How to boost brain performance and prevent dementia using no- or low-cost strategies. Retrieved March 13, 2017 from goo.gl/qdCMLe
  92. Mercola, J. (2017). The grain brain whole life plan: Boost brain performance, lose weight, and achieve optimal health: A special interview with Dr. David Perlmutter. Retrieved March 12, 2017 from http://mercola.fileburst.com/PDF/ExpertInterviewTranscripts/Interview-Perlmutter-TheGrainBrainWholeLifePlan.pdf
  93. Blackburn, E., & Epel, E. (2017). The telomere effect. London: Orion Spring.
  94. Abbas, A.,  Hall, J.,  Patterson, W., Ho, E., Hsu, A.,  Al-Mulla, F., & Georgel, P. (2016).
    Sulforaphane modulates telomerase activity via epigenetic regulation in prostate cancer cell lines. Biochemistry and Cell Biology, 94, 71–81 dx.doi.org/10.1139/bcb-2015-0038