Dear Mr American President

 

Hello. We are two girls, aged six and three,
And I know we should still be asleep,
But we’ve been thinking about Grandad’s story.
It was all so new, exciting and deep!

Fire and fury and power and Phut!
The like of which the world has never seen.
On the TV, which we never watch, you put
Carmine lake into the future that’s never yet been.

And you held forth and waved your mighty hand.
Cool! If you want, you can come and see our bonfire
And camp with us here on the quiet white sand.
We can show you our dolls and all our drawings, sire.

Would that be good for you? We wear matching socks.
We help mummy and daddy collect the firewood.
Sometimes we just pick up unusual rocks
Or chase butterflies instead. It’s not what we should

Be doing, we know. By the way, what does ‘fury’ mean?
When you come to see us, could you let us know?
We know what fire is. Bright flames, leaping and keen.
We’d love to hear more about that, but now we must go.

Screen Shot 2017-08-10 at 8.05.03 am

Mr President, the girls have now gone to bed,
So it’s just me talking to you. I’m their grandad.
Um, I’ve been thinking about what you said.
Of course you are worried. Mad and sad!

It is scary to think about Pyongyang’s threat
To strike areas, around the territory of Guam,
With medium-to-long-range missiles. Piles! I bet
it’s a struggle for you to stay serene. Keep calm!

The Andersen Air Force Base appears to be one place,
Now targeted as a serious warning signal to the U.S.
A great concern! Time to breathe deeply, man. If you brace
yourself, and deal we will soon be out of this mess!

You can take the lead on that! And do you know what,
I have an idea that would make you, at any rate,
A historically acclaimed dealmaker. Not
Just any sort of negotiator. One that is truly great!

Kim Jong Un says he might bring fire down on us,
The mother of torments, the apocalyse at the end of time.
Perhaps you will say, “I’m going to stop this particular bus
before it runs all of us over the cliff. If it does, see me climb!”

You’re now in the kingpin negotiator’s seat, firmly aware.
Any fool could press the oblivion button. Obvious red!
A wise leader, as you know, takes time to think, to share,
to get the issues on the table. You are there. At the head!

Now if only you can lay out a plan, so audacious and grand
That Kim Jong Un would just clap his hands and jump with glee,
While in Guam, 2000 odd miles to the southeast of Kim’s land,
they’ll hear such good news from across the sea!

People will salute your leadership, your skill,
Your first-ever, binding, nuclear arms deal,
Only negotiated in the moments before the licence to kill
On a gargantuan scale was almost given your seal!

Like you, I was born after the second world war, in 1946,
After Little Boy and Fat Man had left Hiroshima, Nagasaki,
A total mess, house shells and telegraph poles, bare sticks,
A wasted landscape as far as the eye could see,

Where families, much like ours, had been vaporised.
In those moonscape cities no children were left to play.
That reminds me. Grandchildren! I have surmised
That we have ten between us by the way.

Here’s the thing, Don. You did take command.
You successfully negotiated
UN Security Council sanctions. Their line in the sand!
Such a good deal! Almost consummated!

You have the power to bring work to the workless,
Long-hoped-for peace to the region,
Hope to the hopeless, homes for the homeless,
A brand new purpose for the legion

Of costly weapons at everyone’s disposal.
Excuse me, you ask. What is your plan? I say,
Well, to resolve the conflict you need a winning proposal.
Not fake news! A superb negotiator could suggest a way.

Screen Shot 2017-08-10 at 8.54.04 am

Brian Devlin
August 10, 2017

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An open letter to the Minister for Education and Training

Senator The Hon Simon Birmingham,

Minister for Education and Training,

Parliament House,

Canberra, A.C.T. 2600

August 5, 2017

Dear Minister,

I am writing to request a 15-minute meeting at your convenience sometime in the week after next (August 14-20) to discuss online tertiary education for remote students in Northern Australia. Specifically, I would like to pose the question: “Will the proposed regional study hubs complement or undermine existing regional universities’ online education programs?”. I should add that I have advised on remote rural education in many Asia-Pacific countries as a resource person for UNESCO; for three years I headed up the Education Advisory Council which advised your NT counterpart, and I have been chief investigator on three ARC-funded projects, including one called “Interactive distance e-learning for isolated communities: “Opening our eyes” (2005-9).

At our meeting I would like to discuss the purported regional benefits of the Higher Education Reform Package, as itemised  by your government, and the growing concern in the Northern Territory that small regional universities, such as Charles Darwin, will find it very difficult to cope with a 2.8 per cent cut to their budgets. The perception here is that a $63 million hit to CDU would have alarming consequences, not just for the university and its staff, but for the demographic stability of Darwin,  Australia’s premier front-line town.

I speak on my own behalf, not as a paid lobbyist or proxy for some group. As I understand it, $15 million will be committed by the Australian Government over four years to establish and maintain up to eight community-owned, regional study hubs across mainland Australia. It is said that the hubs will improve access to higher education for regional, rural and remote Australia by supporting regional students to study distance education courses locally; i.e., ones delivered by distance from any Australian university. My question to you is: How would these provide “greater access to study support and infrastructure” than is currently offered by regional universities?  Could such an intitiative undermine the excellent online programs that are already being offered? As one of the first staff members at any university in Australia to help put a whole course online (Applied Linguistics in 1988), I would like to discuss this move with you in more detail.

I would like to share a brief story. One day I was in Camberwell, Melbourne, for some meetings at ACER. At that time Professor Peter Karmel was still President of the Australian Council for Educational Research, but those of us who were on ACER’s Council had to vote to extend his tenure by 12 months, because he had reached the customary retirement age.

Several of us met for coffee at ACER this particular morning in 1996. Aware that I was Dean of Education at the time, Peter asked me to share my thoughts about the effect on my university of some financial changes recently introduced by the Howard government. My doubts and concerns led to a more general discussion about whether the Commonwealth would ever allow institutions such as the Northern Territory University (now Charles Darwin, of course) to fail.

Professor Karmel had a more benevolent view than I did. It was his considered opinion that the Commonwealth Government, mindful of the needs of all of its universities, would always make appropriate financial provision for them. Having read Michael Pusey’s book, I asked “Don’t you think that if a Government allowed itself to be driven by a narrow, economic-rationalist approach it would be willing to let a provincial university hang out to dry, and would not care about its fate?”. He was shocked by my question. Professor Karmel could not conceive of that possibility.

Peter Karmel, for me, embodied much of the Australia I cared about then. He was privileged in a sense—having had the opportunity to go to Caulfield Grammar School, whereas you and I were educated in public secondary schools—but he did have a broad, compassionate and enlightened vision of what kind of education was needed for all Australians. As you know, he was a broadly educated economist, as were others of his generation, such as Nugget Coombs, so his view of Australia’s educational future was not focused on short-term expediency nor did it simply mirror the perspectives of the large coastal city populations in Australia.

I know that, as Minister of Education, you have the unenviable task of balancing many seemingly incompatible requests for Commonwealth assistance and support. Even so, it is undeniably true that the achievements of universities servicing remote rural Australia and the tropical north can be overlooked by Canberra’s policy makers.

Throughout my career I have often spoken and written about the challenges of providing adequate support and maintaining high standards in non-mainstream educational contexts. These challenges are never easy for policy-makers, who are always faced with many choices. I do not imagine for a moment that your Higher Education Reform Package was intended to saddle some universities with crippling hardships, but that appears to be the likely effect nonetheless.

This will be the consequence of increasing student contributions, lowering the repayment threshold, decreasing Commonwealth contributions, applying an efficiency dividend to core CGS EFTSL and regional loading, and limiting access to enabling programs, “the try-before-you-buy” opportunity for many who would not otherwise have a chance to set foot on campus.  The pernicious effect of these changes, when combined, could lead to CDU facing a funding shortfall  of up to $63 million over the next four years. The Vice Chancellor has advised that “the University would be hard pressed to absorb a funding shortfall of that magnitude”.

Small regional universities such as Charles Darwin have a geographical, social, moral and strategic responsibility to provide people with pathways into vocational education and higher education, especially those students or potential students in remote areas of Northern Australia, where low SES backgrounds as well as cultural and linguistic differences need to be catered for. It is critical that this work continue, both face to face and online.

All Australians should have a vested interest in the safety, security, education and well being  of Northern Australia. It is imperative that small regional universities such as Charles Darwin should remain strong, responsive and vital so that they can properly fulfil their role. Recently ranked in the top 50 new universities worldwide, CDU deserves better than to fail, because a Canberra-initiated reform package caused it to do so. I am sure you would agree with that.

In its final report the Higher Education Infrastructure Working Group noted (p.51) that “Charles Darwin University may obtain advances from the Treasurer, an overdraft from an Authorised Deposit-taking Institution or from any other person”. Is it the intention, Minister, to encourage small universities such as CDU to go into debt? That seems to fit with the terms of reference of the small working group you set up in May 2014; e.g., “to examine…opportunities for better employment of internal reserves and all available financing mechanisms, including capital markets, to support development of infrastructure”.

I submit to you, Minister, that while public-private partnerships for the development and management of infrastructure might make sound financial sense, significantly pegging back the level of Commonwealth support for smaller universities’ programs creates considerable financial risk for them. I would love to have the opportunity to meet you so that I could try to persuade you not to go down that path.

Out of courtesy I advise that this letter will be shared by e-mail and social media with a few individuals, including the Vice-chancellor Professor Simon Maddocks, several politicians, and some colleagues.

Yours sincerely,

Brian

Brian Devlin
Honorary Professorial Fellow
 
Education/LEBA
M: +61 4 1782 9496
E: brian.devlin@cdu.edu.au
W: cdu.edu.au

CHARLES DARWIN UNIVERSITY
Darwin, Northern Territory 0909 Australia
CRICOS Provider No. 00300K (NT/VIC) I 03286A (NSW) | RTO Provider No. 0373

Postscript: Fuhrman and Mosley

After I had sent out an earlier draft of my nutrition paper, several friends and relatives sent back some really useful comments. One of my nieces, Shona, suggested that I should investigate Dr Joel Furhman’s work.  Another niece, Linda, referred me to Dr Michael Mosley’s videos. It is thanks to their suggestions that I can add these concluding comments.

In sum, after figuring out my own eating plan based on a lot of extensive reading, I have discovered that Fuhrman and Mosley are advocating very similar healthy eating strategies.

Fuhrman’s website is a good starting point, if you are interested in reading about his Nutritarian Diet. As far as I can judge, his recommendations all accord with the scientific evidence I have reviewed.

To access what Mosley has to say, one can either access his books (e.g., Mosley, 2014, 2015), or view one of his videoed presentations such as this one in Sydney. Although trained as a medical practitioner himself, he points out that, apart from specialists, or those who make a concerted effort to keep up with the latest science, many doctors are not well informed about nutrition or weight loss. Mosley, a former sugar-addict, is one MD who has kept abreast of the latest research.

References

Fuhrman, J. (1998). Fasting–and eating–for health: A medical doctor’s program for conquering disease. St Martins Press.

Fuhrman, J. (2011). Eat to live: The amazing nutrient-rich program for fast and sustained weight loss. New York: Little, Brown & Company.

Fuhrman, J. (2013). Eat to live cookbook: 200 delicious nutrient-rich recipes for fast and sustained weight loss, reversing disease, and lifelong health. HarperOne

Mosley, M.& Spencer, M. (2014). The fast diet: Lose weight, stay healthy, and live longer with the simple secret of intermittent fasting. London: Short Books.

Mosley, M. (2015). The 8-Week blood sugar diet. London: Short Books.

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

Contents

Foreward
Michael Christie

Preface
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:

goo.gl/DlMNm8

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]

Introduction

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.

Method

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

Implications

“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

Evidence

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.

Dairy

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

Selenium

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

Soy

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

Discussion

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

Discussion

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.

Discussion

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.

References

  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

In search of that beautiful calm

Fancy that. Leonard Cohen’s song “Suzanne” was not even owned by him.

He had brought forth much dark poetry and song,

Whittled each word using the hard edge of life,

Portioned out love, by loving often,

And survived the haze of raucous nights with friends when not

Hunched over a guitar or mic,

Dressed from head to toe in black

On stage.

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He managed somehow to fight through the gloom,

The loss of fortune, the sad clutch of despondency,

And turn the page.

Straight as a shabbat candle,

Poor as a Buddhist monk,

Helped by his stays in Mumbai,

He eventually broke clear, came into the light,

Saw that love was service,

And realised that his songs could be given over

To other women to sing.

No longer songs of seduction, or pathways to fame,

His later songs for Adjani, his muse,

Written under pressure of time,

Almost granted her custody of his genius,

But did not.

 

Nevertheless, something, somewhere, lit the fuse

Of transformation. He became an old man philosophising

Through a young woman’s voice,

As if allowing himself to step free of body and desire

To become a poet of this age. A mere shadow on the stage,

Even less of who he was than before,

He took to the long road and found his way home.

Brian Devlin

January 7, 2017

Sunrise Beach

At the close of day, December 31, 1970

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Photos by John Lucy, Carlton, 1970

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Picture if you will a white-washed room

Where seagrass matting covered the floor.

A few friends and I sat smoking, expecting no more,

Our evening unplanned, more bust than boom.

One of two wooden doors open to the east.

Two parties declined. No chance of a feast.

 

Two pairs of shoes clattered up the stairs

And two young women came into my loft

Seeking my friend Di Ruby, who was there,

For they had failed to find her anywhere.

First entered Margaret: hair curly, eyes soft,

Followed by Nancy. That caught me unawares.

“This reminds me of my parents’ place,” Nancy announced

After clambering up the steps. Then she stood, tall,

Quite regal, with striking long hair, but that was not all.

Waving her nut brown arms, she held us in thrall

With a rapidly told story about the Champs Elysees

And being stopped by some gendarmes from proceeding that way.

 

“Let’s find some parties,” they challenged, so I rose to go.

Crammed into an old Morris Minor, green and slow,

Lent by Margaret’s aunt, we reached two houses, almost empty,

Their kitchens short of food. I brushed her hair,

We talked without end then, just before first light,

We parted for the night.

I’d have to check with Nancy, but I’m fairly certain that’s right.

 

The next three days were full of truthful sharing:

Soul talk that is a little like poetry.

Lying side by side on coloured lengths of cloth outside, we

Conjured up the lives we’d lead and offered them for inspection,

Then more bright talk, silence, and soon introspection.

“What would you say if I asked you to marry me?” I ventured.

“I’d say yes,” she said, her ticket to Bali still on the sideboard.

“Should you ever wish to leave, remember it’s there,” I said.

“No need,” she replied. “From this moment forward

We can travel together and be of use to others.”

I, who would write and ceaselessly learn alone, agreed.

 

Betrothed so soon after three days. What a dope!

Let’s face it, everyone. This was a match unlikely to last

Though no-one would ever know until the years had passed.

As it turned out, although seemingly insubstantial,

There’s nothing quite as solid as trust and hope,

And the awesome power of kindness-in-togetherness.

It is enough to temper a man’s unsatisfying wildness!

Brian Devlin
Sunrise Beach

December 31, 2016

Photo by anonymous photographer, Mexico City, January 1972

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A chess player’s analysis of the new world order

Brian Devlin

November 17, 2016

What a wealth of analysis we have been offered by journalists, politicians, scholars, writers and other concerned citizens in the last few months! Just for the sake of a different perspective, here is one from a chess player.

The conservative playbook is well known. Take command of the centre, as if it is your right to rule. Keep your hands on the levers of power (so that you can check and eventually checkmate the enemy king when you can). Set up clusters of pieces that work seamlessly together (such as fabulously endowed think tanks). Queen your pawns whenever you can (get your key people elected to high office).

Also quite familiar are the progressive strategies of influencing the media, the entertainment industry, academia and the government through ideas and critiques–whether these frameworks are based on socialism, the Frankfurt School, or some deconstructive, postmodernist strain associated with a favourite French philosopher (take over the flanks and exert influence on the board from there).

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This photo was taken in Bali on January 17, 2014, before I could finish (and, I think, win) this game. Unfortunately, my chess partner was not around when I returned the following year to continue it. White to move.

At the grandmaster level of play a consistent strategy may be followed from start to finish. One can see this in the great games of Akida Rubinstein, Alexander Alekhine, Magnus Carlsen, Mikhail Botvinnik, Anatoly Karpov, Garry Kasparov, Bobby Fischer, José Raúl Capablanca, Emanuel Lasker and other wonderful exponents of the game. ‘Immortal’ games have long been celebrated in books and newspapers. At my level of play the bold ideas do not always come off. Nonetheless, the game is played by rules, which specify what moves are allowed.

I never imagined that there might be a new revolutionary version of chess, one that corresponds to international e-populism. We all know who the international populists are, for recently we have seen evidence of their activity in events such as Brexit, building the Hungarian wall, and the election of Donald Trump. But  international e-populism? What’s that? Well, you are forgiven for not having heard of it, for I have only just made up the phrase. It refers to a movement which uses social media brilliantly to achieve stunning influence, and so surprise those who trust polls, or read books and broadsheets made from paper. The heroes in this space have been people such as Andrew Breitbart and Stephen Bannon, skilled drivers of new ‘rage machines’ (Rebecca Mead, New Yorker, May 24, 2010).

Mr Bannon brings phenomenal social media mastery to his new role as chief White House strategist. As I am only a social chess player, I can only dimly intuit the rules of the new, revolutionary version of chess, but let me share with you what I have figured out so far.

The starting point is to forget about the game as a pleasant activity. It is an epochal, high-stakes, face-off. Your pieces are not just quaint medieval symbols: castle, king, queen, bishops, knights, peasants. The aim is not to work in feudal harmony while jousting chivalrously with the other side. Not at all. The forces at your disposal actually comprise the church militant, arrayed in all its ferocious might, true crusaders and forgotten people alike, pitted against Jihadist Islamic fascism and other forms of terrorism, crony capitalist Republicans, Ayn Rand libertarians and other enemies of those enlightened, commonsense,  Judeo-Christian working men and women whose jobs have been stolen from them.

In conventional chess the moves may be daring and brilliant, but they must be allowable. For example, the bishop can only move in a straight line in his own colour.  That familiar rule book has its corollary in real life, where peacetime virtues such as truthfulness, diplomacy, decency, tact and politeness are normally respected, and wartime activities are constrained by agreements such as the Geneva Convention through the procedures to be followed when handling prisoners of war.  In revolutionary chess new rules have been devised because of totally new thefts or threats. Two simple examples will suffice. Trillions of dollars have been diverted, as a result of the Global Financial Crisis, since 2008. Not only have those responsible not been held accountable, the resulting losses have often been covered by governments which can ill-afford to pay. The Panama papers give us a just a glimpse of new system that allows the ultra-wealthy ‘one percent’ to opt out of the old taxation systems in which only the losers pay for schools, hospitals and roads. Then there is the rise of Islamic State, which  calls for new rules of engagement. Its fighters have to be tracked down the rabbit hole with Leninist zeal. And so the revolutionary chess game seems to work in this way: You create your own post-factual marquee online. You devise avatars such as Joe (the Plumber) Wurzelbacher to be your mouthpieces. You assemble your audience, and entertain them in your own expanding echo chamber with a dizzying display of acrobatics, clowning and performing with tigers. Who knows? The virtual power you amass on the internet could even turn into real power in the physical world.

Let me hasten to add that I was only able to spare a few moments to write this piece, because I want to return to a game of traditional chess, which has begun to look very drawish. I look forward to playing in this old style way with my six-year-old grand daughter, Amy, in a few weeks time. She is learning to move her pieces very thoughtfully, and so we are now able to play some great games together. Meanwhile, I will await with interest the moves that will be played next in the revolutionary chess competition that is now being staged by international e-populists for all the world to see.

Evidence-based policymaking, extreme events, humanitarian crises, and the new US presidency

This short essay has been written for anyone who would care to join me on a short journey of reading and thinking. I would welcome dialogue on this issue. The title of this piece is a bit unwieldy, but I wanted to yoke together those particular ideas right at the beginning.
By way of introduction, I will just say that over the last few decades I have guided postgraduate students in weighing up all kinds of research findings and evaluating them critically.
What I would like to do in this short piece is to link seven online statements, ranging from a tweet to a PhD thesis. It is almost intuitively obvious that a tweet leads itself to expressing an opinion, briefly, and that a PhD is a perfect vehicle for laying out an argument in detail, and defending it at length.
Here are the seven pieces:
Now the challenge in starting to talk about any of them is we need to avoid a few traps, such as (1) assuming that a certain phrase such as ‘global warming’ has the same meaning for you and me, (2) deciding that an issue is hopelessly polarised that it is impossible to progress the debate and (3) convincing ourselves that we are right before we even start talking.
So protect myself against those traps, let me declare at the outset, as modestly as I can, and as impartially as I can, that I am simply venturing to express a viewpoint that might be helpful. I just ask the reader to accept that my motivation is to contribute, not to persuade, criticise or defame anybody.
I should add, as I began this foray, that it might be valuable to recall the wonderful advice expressed in The argument culture by Deborah Tannen and Etzioni’s, The new golden rule. For example: Don’t demonise those with whom you disagree. I have tried not to do that in this piece. Don’t affront the deepest moral commitments of your opponents. One way to do that is to avoid taking the high moral ground, being sanctimonious or holier than thou. Talk less of rights, which are non-negotiable, and more of needs, interests and wants. This is highly pertinent, for in a previous professional role I had thought that human rights were, front and centre, one of the key issues to be resolved. As I transition to a different role now, I can perhaps begin thinking more deeply and clearly about the needs, interests and wants of a whole range of people. Leave some issues out. Yes, it helps to travel lightly, to focus on one or two things clearly, before turning one’s attention to something else. Engage in a dialogue of convictions. Don’t be so reasonable and conciliatory that you lose touch with a core of beliefs you feel passionately about. Again, this is sound advice. My conviction is that the planet earth is being transformed and challenged by mega-urbanisation, careless destruction of natural environments, and pollution. As a grandparent I would love for these trends to be moderated–or better, reversed– so that my two wonderful grand daughters will have a world they can love and appreciate as they grow up. At the same time I appreciate that there are hardworking people in extractive industries (coal, oil and gas) helping to supply an energy-hungry world. Their immediate needs and interests have to be considered.
Amy & Liora, Nov 2015.png
My two grand daughters talking while drinking babicinos, November 2015
It is not my purpose now to provide a short cut and summarise all of the items I listed above. If you are interested, you can read them yourself. Nor am I going to tell you the conclusion I came to, for that would be giving you the punchline without you doing your own reading and thinking!
All I will venture to do for the moment is to offer these three reflections: (1) Australia is fortunate to have a Bureau of Meteorology that includes climate scientists such as Dr Blair Trewin, who writes often for The Conversation. The subject of his doctoral research was Extreme temperature events in Australia. (2) Since scientists are inclined to labour over long reports, and politicians to dash off quick tweets, it can be difficult to see any middle ground, where actions and events can be intelligently and dispassionately discussed, but that doesn’t mean that the effort to locate some space in which such dialogue is possible is a waste of time. (3) Professor Paul Cairney reminds us of the choice we have: we can bemoan policy makers’ quick decisions, or adapt to them by working out why they say and do certain things so that we, in turn, can understand the results of their fast thinking in context, and deal with that, regardlesss of whether we see it as denialism in a ‘post-truth’ society. It is harder to try to see the whole picture than it is to cling to the elephant’s leg and swear, hand on heart, that the animal does not have a tail. To evaluate and compare ideas, it helps to value practitioner experience, but there is a strategic choice to be made. We need to be clear about whether we want to be honest brokers, who present some evidence and leave it that. Or are we seeking influence? To seek influence is to get our hands dirty by beginning to issue emotional appeals, and manipulating people in an effort to persuade, in the knowledge that people do make emotional decisions.
Choosing the most effective technique in a difficult debate can be the beginning of a slippery slope. We may end up being as manipulative as those we criticise. I accept the legitimacy of democratically elected leaders saying and doing unpopular things. Yet, as a citizen, I think it is reasonable to try to encourage others to frame a contentious issue in a more constructive way so that we all benefit, now and into the future.
“This is what is likely to work in your context. This is the kind of evidence that seems relevant”. To what extent is this a reasonable starting point when dealing with politicians who deny that planet earth has a problem, and that all that counts is the economy, protecting jobs and all of that?

A reflection on Cohen and Trump

When I look back on this last week in years to come, it may be that I will feel more hopeful. Maybe I will have a broader, wiser perspective. By then I might have much greater capacity to laugh at the irony and the comic ridiculousness of some aspects of human life. Right now though, I am filled with sadness.

My daughter and her wonderful family remind me of the importance of naming what we feel grateful for each evening, and sharing that. My son impresses me with his courage, his courtesy, his appetite for life, and his ability to include others. My wife is gracious, caring and giving, and is loved by many. My mother is alive, and keeping up her spirits in the face of adversity. So I should be happy, right?

Why then should I be bothering myself, right now, with questions about language, honesty and deceit. Well, it is because I have been thinking about two well-known figures, Leonard Cohen and Donald Trump: What they represent and the legacy they might leave.

Screen Shot 2016-11-13 at 2.23.27 pm.png
(Source: The Leonard Cohen files)

Cohen’s recent death from cancer has been a jolt. Over the last few days I have been recalling his poems, his novels, the first album of songs he released in 1967. At that time, it seemed to me, he wrote and sang as if composing from an inner space, in an almost sacramental way. I saw Cohen as a seeker, an enchanter, who could take you down to a place where  Suzanne, “wearing rags and feathers from Salvation Army counters”, lived by the river.  Not a strange unnamed woman, but Suzanne.

And just when you mean to tell her that you have no love to give her

Then he gets you on her wavelength

And she lets the river answer that you've always been her lover

And you want to travel with her, and you want to travel blind

Born into an affluent Montreal family, Cohen would often dress in sharp suits, but he could lead us as he sang, and we would consent to travel blind with him , even although he would confess to his audiences  that “I don’t know the answers to anything”.  For me this was the badge of his authenticity. Like Boris Pasternak though, he wondered if his work was invalid and irrelevant.

Cohen returned from a retreat at a Zen Buddhist monastery one day to find that his manager had fleeced him, leaving nothing for him and his family. It was this crisis that forced him back on the road, even though performing on stage was so excuciating for him that he sometimes drank lots of wine (Chateau Margaut) to get back up there and work for our smiles. We were the beneficiaries of that manager’s theft, for it meant that Cohen could never retire; that is, until death claimed him in the end.

Where Cohen’s death has taken me back, Trump’s election victory, on the other hand, causes me to wonder about the future, particularly as it might affect my grand daughters and their generation as they come of age.

During the week I have spoken to many people, including a leading public figure, and I have been surprised by their eagerness to assure me that Trump will be fine as President, because of the checks and balances that are in place. Haven’t they heard? Don’t they know their history? I will return to that theme in a moment.

I thought I might begin my reflection on Trump by saying something about his speeches. First, because I am a sociolinguist with a strong interest in languages and their roles in framing what people do, but I am also a historian, so it interests me to analyse the election of Trump as President in the light of what we know about some European leaders who came to power in the early 1930s.

The day before the election Trump spoke at a campaign rally in Scranton, Pennsylvania. The stage was decked with flags in front of a partisan audience holding placards. All the journalists were corralled together in an enclosure at the back of the hangar like sheep, an arrangement that was the brainchild of Hope Hicks, Trump’s young press secretary. After the national anthem had been playing for a while, Trump denigrated “the corrupt political class” and “the failed political elite that has bled this country dry”, and promised “to put the factory workers, miners and the steelworkers back to work”. Then he looked up from the teleprompt and shaded his eyes histrionically: “See the dishonest people back there, the media, the totally dishonest people….They are so dishonest”. He then paused, to let the crowd boo, and continue booing, at the media representatives roped in behind them. Then he continued,  “The New York Times is a total lie. It is so false….The Times is going out of business soon. That’s the good news”.

The speech at Scranton was,  of course, carefully scripted and stage managed. The words, the symbols, the flags, and the music were all carefully designed to swell listeners’ breasts with pride, to stir their anger, to encourage hope, and to make them angry. The journalists huddled at the back were just doing their job, but they were hissed and booed for playing that role, as if they were reviled outcasts, with encouragement from Trump. They were the scapegoats that day. Who is next? The audience was then told that Trump’s first step would be “immediately repealing and replacing the disaster known as Obamacare”.

Two insights are helping me to make sense of Trump’s electoral victory. The first is that he is a brand. ‘Trump’ stands for affluence and brashness. It is a brand that has financial value,  and so it is bought and sold. For example, a 70-story condominium in Panama pays one of Trump’s companies $5 million annually for use of his name, including the right to display it in enormous letters all over its hotel, marina and the sails of its casino. The second insight is that his campaign relied on naming and shaming groups of people, and that his partisan supporters shared his scorn for them. Adam Gopnik has written about the ‘weird free form nastiness’ that now passes for political oratory and debate.

So the angry, alienated voters of Scranton had a lot to be grateful for. There, in their very own depressed town, half the size of what it had been in 1940, they could come before a famous rich guy who knew other influential rich guys, and hear about a dream to make America great again.

It is hard to know whether Trump’s contempt for journalists was real or simply confected for the benefit of his reality television show, sorry his campaign, but I cannot help wondering whether those who work for newspapers, magazines and televsion stations are now feeling nervous, having been labelled collectively as ‘totally dishonest’. Since I am a writer too, like the journalists who were the butt of Trump’s anger, I find this attitude quite disconcerting.

Trump’s lie were preposterous and daring. He maintained that Obama founded ISIS. He claimed that Obama had not been born in America. These were lies masquerading as history of course, but as outrageous as they were, they helped get him get to the White House. This is why so many young people I know are upset. They keep asking “What does Trump’s election mean? Will it just encourage people to turn on one another? Does his success mean that it is unimportant to distinguish between lies and the truth? Does it tell us that what really counts now is money (lots of it) and success, especially huge, swaggering, in-your-face, name-plastered-over-lots-of-buildings success?

All of which leads me to the question of checks and balances. It just is not true that the American system of balancing the legislature, executive and judiciary is working well, and that the pendulum will easily swing back to whatever great and imagined state American democracy was in before. The net effect of the Patriot Act in 2002 and the Military Commissions Act of 2006 was to grant the President the power to declare any person, US citizen or not, an enemy combatant. Anyone thus designated can be immediately deprived of any rights, including the right to legal representation. Someone deemed to be an enemy combatant can be handed over to an alternative system of justice and detention, where torture is permitted. Naomi Wolf’s Letters to a young patriot spells out these worrying developments. She points to some uncomfortable parallels between ‘the fascist turn’ in America and those changes in Germany that allowed a fundamentally undemocratic new leader, but one  offering hope, to come to power in Germany on January 30, 1933. What he brought instead was incalculable grief and destruction.

For several months in the summer of 1964 I shared a work hut in the Grampians with a Holocaust denier. His outlandish belief that the Holocaust was a fabrication never wavered, no matter how much evidence I tried to piece together to show him that he was wrong, factually and historically.

I have no doubt that the ex-miners, ex-factory workers, ex-steelworkers of Scranton have really welcomed the attention paid to their situation, and deservedly so, since so much of the once-productive heartland of American manufacturing has been hollowed out, shuttering buildings, blanketing hope.

I would love to believe that, when Trump railed against corrupt elites, what he had in mind was a fairer arrangement which would limit the ability of ultrawealthy individuals and corporations to secret their holdings outside the normal tax environment in which ordinary workers and the government struggle hard to build and maintain public schools, hospitals, railways and roads. Somehow, I don’t think so.

After the Treaty of Versailles (June 18, 1919) democracy came to be synonymous with humilation and defeat, and so in time Germany preferred to put its trust in a strong leader, even though America had shown that it was possible to flourish socially and economically as a constitutional democracy, protected by a framework of law.

President Woodrow Wilson planned to end destructive wars by setting up a League of Nations that would allow potential conflicts to be handled through dispute resolution procedures rather than through the use of force. However, he was never able to persuade his own country to join this new collective security arrangement. As a result, the League was weakened as a cooperative system, and war-weary nations re-armed. By the 1930s the world had become a haven for aggressors once again. We all know what that lead to.

My father served in Bougainville and elsewhere in New Guinea during the Second World War, yet apart from a few interesting anecdotes, he never talked about the hellfire that he and others went through. Partly as a consequence, I was brought up believing in democracy, the importance of truthfulness, honesty and prudence and the possibility of lasting peace. When only the strong seem to prosper,  these are values to treasure

As the day caves in

And the night is all wrong

(Cohen, Ballad of the Absent Mare)

If it seems that truth is no defence against the outrageous lie, is it enough to say “don’t dwell on it”?

The birds they sang

At the break of day

Start again

I heard them say

Don't dwell on what

Has passed away

Or what is yet to be.

(Cohen, Anthem Lyrics)

If it seems that the peacemaker always loses out to the bully, just remember:

Ah the wars they will

Be fought again

The holy dove

She will be caught again

Bought and sold

And bought again

The dove is never free.

Ring the bells that still can ring

Forget your perfect offering

There is a crack in everything

That's how the light gets in.

(Cohen, Anthem Lyrics)