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Monday, June 18, 2012

Brain food ~ get it early


The human brain is, pro rata bigger and is far more complex in structure than in any other species. It tends to be a very busy organ and consumes about 25% of the daily caloric intake of an average person. This increases to about 50% of caloric intake in the children aged 1 to 6 years and reaches 55% in 4-6 month olds and a staggering 75% in newborn babies.  Around about the age of 30, the human brain begins to shrink at the rate of 1 milligram per year and if that seems a small rate of decline (a lifetime reduction of 8% volume), the evolution of the human brain to its present size was also 1 milligram per year.  Without question, the biggest fear people have in entering old age is a loss of cognitive function with Alzheimer’s disease the worst-case scenario.  The issue is so important that it attracts all forms of snake-oil merchants promising this or that diet to stave off any decline in cognitive function.

The best place to start the task of ensuring a healthy brain throughout adult life is during pregnancy. During the third trimester of pregnancy, there is a growth spurt in brain development, which continues for 24 months. The human brain is about 60% fat and so when it comes to any discussion of nutrition and brain function, fat is bound to dominate. Specifically, the brain is rich in long chain highly polyunsaturated fatty acids that are abbreviated to EPA (Eicospentaenoic acid) and DHA (Docosahexaenoic acid). These fats cannot be synthesised by the human body and therefore have to be obtained from our diet. Fatty fish are by far the best source of these fatty acids and this raises an interesting question: Why, if the human brain was so important in our evolution, did we not develop the capacity to synthesise these fatty acids ourselves? Stephen Cunnane, author of “Survival of the Fattest” makes the case that man migrated from the Savannah to the shoreline of lakes, rivers and deltas where an abundance of fish, shellfish, eggs, bird and wild life existed. Such a food chain is rich in the brain type fatty acids, EPA and DHA, and there would have been no evolutionary advantage in having the energy demanding metabolic pathways to manufacture these fatty acids ourselves.

The growing foetus is totally dependent on a maternal supply of these fatty acids for brain development and when these enter the mother’s blood supply after a meal, they are preferentially transferred to the foetus. Other types of fats might be shared with the mother’s own fat reserves but not these precious fats. After birth, breast milk should contain adequate levels of these fatty acids and so too should infant formula. The problem begins to arise when post-natal nutrition is inadequate. The first 24 months of life sees a tremendous growth in brain complexity, especially in the frontal cortex through which the new baby acquires the social norms and language of its environment. Inadequate nutrition in this period will greatly diminish intellectual capital for the rest of such an individual’s life.

It goes without saying that an adequate intake of these fatty acids is required throughout adulthood and there are ample studies showing that inadequate intakes of fish oil type fatty acids are associated with a higher risk of loss of cognition in later adulthood.  However, when the putative link between these fatty acids and cognitive decline are tested in dietary intervention studies, the evidence just evaporates. One possible reason for this is in the genetic predisposition to Alzheimer’s disease. There is a protein that is strongly involved in fat transport and distribution, abbreviated to Apo E and it can exist in three different forms of (Apo E2, E3 and E4) and we can inherit any two varieties from either parent. Thus 60% of the population has E3/E3 and they account for 65% of all Alzheimer’s cases. A smaller number (23%) of the population has the E4 variety either alone (E4/E4) or in combination (E4/E3) and this quarter of the population account for nearly half of all cases of Alzheimer’s disease. Thus with such a strong genetic dimension, intervention studies will eventually have to be conducted in which the individuals genetic make-up is taken into account. Moreover, the duration of the studies will have to become much longer if we are to identify a truly protective effect should such an effect actually exist. In addition to fish oil type fatty acids, there has been similar data for some of the B vitamins, most notably, folic acid and vitamin B12. Again, the association data seems very strong but again, when dietary intervention studies are conducted, little supporting evidence emerges. A higher body mass index in middle age is also a risk factor for Alzheimer’s disease and my guess is that this may arise because the more adipose tissue you have the more you will move EPA and DHA to that tissue away from blood which would normally be the route to the brain.

In Celtic mythology, the salmon was referred to as the fish of knowledge and maybe, even as these mythologies evolved, there was anecdotal evidence that fish was good for the brain. In modern Celtic Ireland we have a low intake of EPA and DHA and remarkably, 75% of our intakes of these vital nutrients come from fish oil capsules rather than fish. Some achievement for an island race!


Monday, June 11, 2012

Sugar taxes re-visited: An economic and nutritional analysis


Following an extremely successful Policy Workshop of the UCD Institute of Food and Health last Friday, I return to the issue of fat and sugar taxes. We had two economists and two nutritionists from UCD.  The main focus was a tax on sugar-sweetened beverages, which interests the Irish government, such that they have created a Health Impact Assessment exercise to explore this option.  Just under half or Irish adult males are overweight while the comparable figure for females in just under one third. The respective figures for obesity levels are one quarter and one fifth. So, we have a problem as has most developed countries. Anne Nugent presented data from the National Adult Nutrition Survey and used these data to examine various parameters across quartiles of calories from sugars (non-milk sugars). From the lowest to the highest quartiles, there were no differences in any measure of obesity or of fat distribution.  It could be argued that total non-milk sugars is a poor tracker of the intake of sugar-sweetened beverages so Anne made a comparison of obesity indicators cross thirds of intakes in sugary beverages and only among consumers of these products. Going from the lowest third to the highest third of intakes of sugar-sweetened beverages, there were absolutely no differences in any measure of obesity or fat distribution. One very important statistic is that only 40% of Irish individuals actually consume sugar-sweetened beverages on a regular basis. It is this 40% alone who would pay a tax on sugary beverages.  Moreover, a tax on sugar-sweetened beverages would ignore the obesity issues in the 60% of the population that doesn’t consume these products. The total contribution of sugar-sweetened beverages to caloric intake is 1.2% for the populations as a whole (consumers plus non-consumers) and this rises to 3.6% among consumers only. Even if a tax were to reduce intakes of these products by 50%, it would have reduced their contribution to caloric intake by 1.8%. It’s hard to see how that would have an effect since quite some of that would be compensated by the intake of other foods. Moreover, there is 60% of the population who are mere spectators in this charade since they don’t consume sugar-sweetened beverages.
The question also arises of alternatives to sugar-sweetened carbonated beverages – what could or should people consume instead?  Fruit juices represent the most commonly consumed beverage in Ireland after teas, coffees and waters and could be suggested as a ‘healthier’ alternative. If the 40% of Irish consumers of carbonated beverages were to switch to drinking fruit juice at the same volumes which they currently consume sugar sweetened carbonated beverages, the difference in calorie intakes between the two beverage types works out at a mere 10 kcal/d!
My own contribution ranged across the epidemiology of obesity, physical activity and the genetics of obesity but the most important points relevant to this blog are the policy issues presented. . Most of the studies linking sugar-sweetened beverages and obesity are based on observational studies, an example of which are the data presented by Anne Nugent. These data do not prove cause and effect. To do so, we need to construct very large multi-centre studies of sufficient duration to see any true effect. The Women’s Health Initiative on dietary fat, The DASH study on diet and hypertension, The DART and GISSI studies on fish oil, the MRC trial on folic acid are all examples of these large internationally approved intervention studies specifically design to test the true cause and effect hypothesis. As regards reducing or increasing intakes of sugar-sweetened beverages, no such study exists. In the EU, we demand multiple human intervention trials to sustain health claims on foods and clearly that bar is too high for public health nutrition policy.
Dr Kevin Denny of the UCD Geary Institute gave on over-view of some of the wider issues that economists would take into account with regard to taxes on foods or nutrients. Kevin pointed out that economists start with the view that the individual knows what is best for them personally. However, for some groups and in certain instances, this may not be the case. The information upon which a decision is to be made may be poorly available, too complex or because time and emotion defer an informed decision. Policy decisions in such instances therefore start with education and then move to regulation of some form, which might include taxes. Taxes that are designed to introduce enhanced social behaviour are referred to as Pigouvian taxes and it could be argued that food taxes fall into this category if we think that people’s consumption of food is not socially optimal for some reason.  But one needs to be clear about why people’s food consumption imposes a burden on society. The standard argument is that eating too much (& hence causing obesity) imposes a burden as the tax-payer will pick up most of the additional health costs (estimated at about €400 million p.a. in Ireland). In that context however, taxing nutrients such as calories should only apply to those calories that are consumed in “excess . If for example, people don’t consume many calories or they burn-off what they consume through exercise, there is no reason to tax such calories. Taxing calories for individuals in energy balance would be unfair. The taxing of nutrients is made more complex by the fact that foods contain multiple nutrients. Taxing the fat in cheese ignores the important contribution cheese makes to calcium intake among consumers of cheese. A key point made by Kevin is the sequence of steps the economist would look at always assuming the nutritionists really did have genuine target for taxation in the first instance: How much to tax? How does that affect price given that taxes are often not passed on in full to consumers? In turn, how does that influence consumption of the foods concerned? How the does that influence BMI and, of course eventually health costs? He went on to cite the work of Powell & Chaloupka who conclude that: “The limited existing evidence suggests that small taxes or subsidies are not likely to produce significant changes in BMI or obesity prevalence but that nontrivial pricing interventions may have some measurable effects on Americans' weight outcomes, particularly for children and adolescents, low-SES populations, and those most at risk for overweight. Additional research is needed to be able to draw strong policy conclusions regarding the effectiveness of fiscal-pricing interventions aimed at reducing obesity”. In other words minor taxes will have little effect and that effect would only be seen with quite considerable taxes.
This leads nicely into the paper by Professor David Madden of the School of Economics.  He used data from the nationally representative Household Budget Survey to examine the impact of possible fat taxes on poor households.  His results showed that pretty much any food-based fat-tax will have a disproportionate effect on poor households, reflecting the general tendency across all countries for poor households to devote a higher fraction of their budget to food.  However, a revenue neutral tax/subsidy package, with higher taxes on some foods combined with lower taxes on other foods would be neutral in its poverty impact, and could even be mildly beneficial to poor households.  In terms of a tax on sugar-sweetened beverages, the impact of a 10% tax on poor households would be relatively modest, given that sugar-sweetened beverages are a relatively small fraction of the budgets of poor households.  Depending upon the ability of government to accurately target poor households to compensate them for such a tax, the cost of compensation in 2005 prices would most likely be less than €10m.  However, this takes no account of the loss in welfare borne by non-poor households from such a tax.

So, in summary we have a proposal to tax sugar-sweetened beverages, which contribute 0% of daily calories among the 60% of the population who don’t consume them and which contribute a mere 3.6% to the caloric intake among consumers of these products. In doing so, we ignore the obesity issues of the 60% of non-consumers and, among consumers, we tax those who are lean and those with excess body fat. And we do all this with zero data from internationally acceptable randomised controlled intervention studies on the effects of sugar-sweetened beverages on medium term body weight regulation.  Whereas we insist that such studies govern health claims as regulated by the European Food Safety Authority, that doesn’t seem to apply to public health nutrition policy. Moreover, we do so knowing that food taxes that are small will be ineffective and to be successful they must be significant. And of course we do this knowing that it will hit the poorest in society with the greatest financial burden  unless we find some way to subsidize a healthy food eaten in significant quantities by poorer households. Simple, isn’t it?

Monday, May 28, 2012

My popular book on food and health:"Something to chew on: Challenging controversies in food & health"


Today’s blog is something of a cheat. It simply lays out the content of the individual chapters of my new book:’Something to chew on – Challenging controversies in food and health’. I wrote this book to help the average person to gain some understanding of the mainstream science of food & health and in so doing to de-bunk many common myths and misperceptions. The book is available at www.ucdpress.ie, at www.amazon.co.uk and http://www.bookdepository.com. If you are so inclined, you can “like” the Facebook page of the book here.


Something to chew on
Challenging controversies in food and health
Mike Gibney
Chapter summaries

Chapter 1: With regard to food

This chapter sets the scene for the book. It describes the evolution of the modern food supply beginning with the era of widespread malnutrition in the most developed economies from the turn of the 20th century.  The extent of this malnutrition was exacerbated by two world wars either side of a great economic depression.  Following the end of World War II, a remarkable period of investment in science and technology emerged as the global economy expanded. Agricultural output and efficiency soared and as more women entered the work force, the demand for more convenience food and the necessary kitchen technology to use these new products was developed. Food companies grew by mergers and acquisition and the great retail giants emerged. The era of cheap and abundant food had arrived. During this post war period the science of human nutrition also evolved from a century of researching what was essential to sustain life to an era of researching what was necessary for optimal health. Nutrition had arrived on the political agenda. And then the Vietnam War started an era of challenge of the military industrial complex and the concept of people power emerged from the hippy and civil rights movements in the US to the student riots of Europe. Now an era of mistrust in science and technology evolved and the green movement began to shape the political agenda. And food now came under the microscope. The public got scared of high tech food with an increasing mistrust of the food industry which was blamed for food scares and an epidemic of obesity. That led to the development of a rapid expansion of interest in organic and ethical food. The advent of the BSE crisis obliterated the reassurances of the government in the safety of the food chain and the arrival of genetically modified foods heightened this mistrust. This book looks at all these challenges to the human food chain and attempts to give a scientific dimension to what are often emotional issues surrounding concerns about food.


Chapter 2: Sugar and spice and all things nasty

Plants abound in natural chemicals which exist for normal plant function including germination, growth, reproduction, repelling pests and attracting the birds and bees. It is these that give plant food their beautiful colours and their delicious tastes and flavours. They also give rise to a wide array of natural plant compounds from pure poisons (hemlock), to the downright dangerous (cocaine, nicotine) and onwards to natural plant compounds which have healthy properties (which lower blood cholesterol or which lower blood pressure). Irrespective of their effects on man, these natural compounds are not regulated. They are after all natural. Man-made chemicals are very strictly regulated and this chapter deals with food additives, pesticides and contaminants as examples of man-made chemicals all of which must prove they are safe to enter the food chain. The toxicity of the natural and man made compounds are compared showing an equal if not a greater burden of risks from natural compounds. It also deals with the practice of adding nutrients to foods through food fortification. Finally, this chapter challenges the myth that organic food is more nutritious, more tasty, more flavoursome and more environmentally friendly than conventionally grown crops.    

Chapter 3: Modified foods: genetic or atomic?

The human food chain has been genetically manipulated from the dawn of agriculture and this chapter examines the present scare about genetically modified foods. It first describes conventional plant breeding which is preferred by the environmental groups in their vigorous opposition to GM crops. The common belief is that conventional crop breeding is a loving task of nature carried out by a devoted plant breeder out in the field.  This is not so. Conventional plant breeding involves hitting thousands of plants with levels of atomic radiation 100 times stronger than that used in the application of radiation to cancer therapy. The plants genome is rattled to bits and the vast majority of the mutants die. But some survive and go on to exhibit new properties which can then be crossed back with the normal variety in the hope of transmitting the new desirable trait. The UN International Atomic Energy Agency champions the use of atomics radiation to induce mutations and boasts over 2000 crop varieties in existence today developed using this totally unregulated technology. In contrast, for GM technology, the genes to be inserted are known in advance to be linked to some desirable characteristic and only these genes are inserted. The chapter challenges the claims of environmental groups that GM foods are a danger to human health and to the environment.



Chapter 4: The metrics of food and health

We are constantly learning from reports in the media about new findings linking some food or other with this or that disease. How is this done? This chapter looks at the tools available to measure food and nutrient intake and makes the point that they are all fundamentally flawed. All dietary surveys will encounter very significant levels of the under-reporting of the true intake of food. In simple language, it is the norm in large dietary surveys for a very significant proportion of the study population to fail to report (a) ever eating some food, (b) reporting the consumption of the food but under-reporting the frequency of consumption and/or(c) under-reporting the quantity consumed at a given eating occasion. This phenonomen might be explained on the basis that most people have one approach to food intakes on Mondays which reflects a desire to have a truly healthy week ahead and which quite often falls by the wayside later in the week. When asked to record their usual dietary patterns, survey participants frequently report the restrictive Monday type for the whole week. Thus a major problem is that in the measurement of patterns of food consumption, we simply cannot be accurate. Notwithstanding these limitations, we now seek to link dietary patterns with those of various diseases, which is the science of epidemiology. when a positive or negative association is found, it means just that, an association. It cannot prove cause and effect. To do that we need to construct an experiment in which two groups are compared where everything is identical except the test food or nutrient. We examine two contrasting cases of dietary intervention.



Chapter 5: Personalized nutrition – fitting into your genes
When you general practitioner tells you that your cholesterol is high, by high, he or she means above a reference point established in large population studies. Such studies show that on average, individuals with cholesterol values above that point have a higher than average likelihood of going on to develop heart disease. In that last sentence, the word average was used twice. Suppose now the GP could establish in this regard that you were in reality above or below average in the likelihood of developing a heart attack with your level of cholesterol. Then your advice might be a little more personalised than simply average. The mapping of the human genome in 2003 was a major step in making that possible. This chapter explores the concept of personalised nutrition by which is meant a set of nutritional advice which is targeted specifically to you on the basis of our knowledge of your genetic make up and of our developing understanding of how the human responses to changes in nutrient intakes are very mush influenced by known genetic variability. Many companies will sell you a genetic analysis and personalised dietary advice over the internet for about US $500. This chapter casts serious doubt on the reliability of this advice and explains also the great difficulty that the human food chain would have in matching true genetic requirements for nutrients with our present day retail system. However, it does try to foster the hope that in the course of time, we will reach a point where simple dietary advice on diet and conditions such as blood pressure, weight gain, cholesterol or allergy will all have some robust element of genetic analysis to sharpen the tools of preventative nutrition. 

Chapter 6: Plastic babies – the phenonomen of epigenetics and nutrition
When a foal is born, it knows immediately to stand up on all fours, to recognise its mother, to run with the herd and to interpret the sight sound and smell of danger. Its brain is hardwired and all switches in the nervous system are fully operational. In contrast, a human baby is born with quite an immature brain and for good reason. Babies born in Belfast, Burundi, Beijing and Baghdad will all have to recognise speech but speech in quite different languages. They will have to learn to behave within a society into which they are born and the social norms vary greatly across cultures around the globe. We inherit DNA from our parents and the sequence we end up with is a random mix of both - Dad’s hair, mum’s eyes. But the sequence once made is never changed. What distinguishes the foal from the human baby is the extent to which the genetic sequence is managed. Imagine the genetic sequence to be like a complex electronic code to manage a sophisticate lighting system. All the codes and their sequences for the lighting system remain unchanged. But the settings of the switches can be changed - more of this and less of that. From the pre-natal period in the womb through to the first few years  of post-natal life, we slowly and methodically make adjustments to the genetic code, not to its sequence but to the extent to which each gene in the sequence is switched up or down. Once finally adjusted, that is it for life. This chapter looks at this phenonomen and the very important role that diet plays in this tweaking of the human genome and in turn how that tweaking made in the early days of life can greatly influence our health four to five decades later. It looks at the uniqueness of human pregnancy which is necessitated by our larger brains and at the need for our genetic development and our brain development to be highly flexible at the onset of life. That is what gives us our evolutionary advantage and we will look at that in the context of man’s probable aquatic origin.

Chapter 7: Your insides out:  food - the gut and health

In recent years we have begun to appreciate that the gut is an organ which plays a central role in food and health, not just in digestion and absorption of the food we eat but in our immune system, in obesity and in our reflex actions in times of stress. The present chapter explores some of the very exciting science that is emerging from this research with far reaching consequences for food and health. The stress element of our gut  is governed by a major nervous system which has evolved quite independently from the brain. It is required to prepare us for “fight-or-flight” circumstances and is responsible for a host of common phrases such as “butterflies in your stomach” or “not having the guts” for some challenge. The bacteria in our gut weigh 1.5 kg and have 100 times more DNA than the human body which hosts them. The two have established a “treaty” in which one gives to the other in a symbiotic way. We gain energy from the fibrous foods they alone can digest and they gain access to fuels we can’t use. They actually can cause our genes to be up or down regulated to suit them and they work with us to make sure that rogue bacteria don’t break the treaty leading to sickness. In recent times, these bacteria have been shown to play a pivotal role in obesity. Rats raised in totally sterile conditions don’t get obese on diets that would normally cause obesity in a non-sterile environment. The gut will be a major focus of food and health in the future


Chapter 8: A tsunami of lard: the global epidemic of obesity

Obesity is seen as a simple problem: people get overweight because they eat more calories than they expand. That’s a bit like saying “cancer is simply a cell gone wrong”. This chapter begins by briefly explaining the biology of the diabetes associated with obesity and then moves to the biology of the control of food intake. It makes the point that rodent studies of the regulation of food intake are of interest but we have a large part of our brain, the neo-cortex, responsible for higher human functions, which overrides simple biology signals such as hunger. We refuse to eat cat food when hungry whereas a rat will readily do so. We then move to genetics and specifically to twin studies and show how powerful the heritability element of obesity is. A strong case is made in this chapter that much of the research in this area focusing on foods responsible for obesity (fast food, soft drinks, processed foods) is going nowhere largely because of the reasons outlined in chapter 4 on our poor ability to accurately quantify food intakes. The case for a greater focus on linking genetics to food related behaviour is made. Dieting is dealt with as is physical activity and the stigmatization of the obese. Finally this chapter looks at little known data on the rise in obesity pointing out that obesity has been rising in the US in waves dating back to the early 20th century. The conventional wisdom that it is simply junk food is challenged and data on inter-generational augmentation of obesity through epigenetics, discussed in chapter 6 is discussed.


Chapter 9: Greying matters – food and the elderly

This chapter outlines the dramatic demographic changes that will occur in the developed countries in the next 30 years. In some countries such as Japan and Sweden, over 1% of the population will be over 100 years by 2050. The chapter outlines the areas of aging which can be influenced by diet. The decline in the regulation of food intake and an obesigenic environment mean that we now have the phenonomen of the frail obese elderly; not enough muscle and too much fat. We look at bone health and its decline from the early part of mid life and deal with the conflicting advice on sunshine from two different camps, those concerned with skin cancer and those concerned with exposure to sunlight to get adequate vitamin D. The chapter deals with sarcopenia, the loss of muscle in the elderly and also the role of diet in declining eye sight. Finally, the chapter deals at length with memory and its decline with aging and reviews the relevant data linking diet and Alzheimer’s disease. The link between obesity in mid life and the risk of Alzheimer’s disease in the elderly is explored.


Chapter 10: Food and Health – The science, policy and politics

The role of four players in the drama of food politics is explored. First the practice of linking major multinational food companies with the problems of over-nutrition is explored and challenged.  Potatoes account for 12% of caloric intake in Ireland and have a zero advertising budget. All chocolate combined accounts for 2% of caloric intake and has a massive advertising budget. Most likely, potatoes are more important in over-nutrition in Ireland than chocolate. We look at 4 classes of scientists which range from the one wired to the laboratory and never gets involved in the regulatory side if things to the “issue advocate scientists” who get involved everywhere and push an a priori agenda. Next we look at the UN agencies and an independent analysis of their style of risk assessment and risk communication and show large shortfalls in proper procedures in the analysis of particular problems. We also look at how they can pre-empt scientific publications they don’t like with their own gloss on events. Finally we turn to NGOs who play a powerful role in our participatory democracy and the chapter accuses some NGOs of being dogmatic and anti-science.

Chapter 11: The hazards of food
This chapter explains how society assesses risk in respect of our food supply and explains the detailed process of testing for safety. It introduces the reader to the concept of risk management and looks at the EU’s precautionary principle which is being used to block innovation such as GM technology. We then look at risk communication and we show how consumers presented with the same data expressed in different ways (% who will die during treatment or % who will survive) adopt different stances. We explore the concept of “world views”, how these are acquired and how these shape the emotional response to perceived danger. The chapter argues that throwing “knowledge” at consumers will not allay their fears since these fears are frequently emotional and thus not readily open to rational argument. It contrasts how regulators (mostly scientists) see risk and how consumers see the same risk. For the consumer the fear increases as they lose control over the avoidance of the risk and as the risk gives rise to effects which are both dreaded unfamiliar (BSE). In contrast, real public health risks such as obesity are seen as controllable (“I can lose weight whenever I want”) and are both familiar and not dreaded

Chapter 12: How the other half dies

This chapter looks at the problems of global malnutrition. “Wasting” is the condition of malnutrition seen on TV, gaunt corpse-like children with zero fat beneath their skins. “Stunting “ is the condition of malnutrition where a child is too short for their age. The final form of malnutrition is that of “hidden hunger”, the blindness of vitamin A deficiency, the anaemia of iron deficiency and the goitre of iodine deficiency. The chapter argues that the global aid agencies, the IMF and the World Bank in the Thatcher-Regan era, adopted a policy in development aid of getting the fiscal system working and leaving it all to the markets. This is only slowly now being abandoned and investment in agriculture and nutrition is now back on the agenda. The chapter looks at recent books which argue that Africa is being starved of science by anti-GM and organic farming NGOs and which look at the basic geo-political reasons for the existence of the world’s “bottom billion”. The chapter looks at how malaria and HIV/AIDS is wrecking Sub Sahara Africa. The chapter ends with the Alliance for a Green Revolution for Africa led by Kofi Annan which is seeking to sink billions into improving African agriculture. This requires an investment in scientific agriculture including GM crops.




Chapter 13: Mankind and Mother Earth
Previous predictions of doom and gloom (Club of Rome, Y2K and the Ozone layer) are examined in relation to the lingering scepticism on global warming and climate change. We then look at leading climate scientists who believe they have to “sex up” the data to get attention. Thereafter the focus is on scientific facts on two vistas of the environment and the human food chain – how agriculture influences the environment and how environmental changes influences agriculture. We begin by looking at the global population and with a focus on the developing world where the main growth of population will occur. The 50% increase by 2050 in global population (6 to 9 billion) will be mostly in developing countries. Agriculture affects the environment in two ways. It produces large amounts of greenhouse gases primarily through energy demanding livestock production and through deforestation and desertification. Secondly agriculture absorbs over 70% of global water, presently at a rate where extraction from aquifers is 2-5 times the rate of re-charge with rainfall. All of the various solutions mooted are mentioned from no-till farming to drip irrigation. We also look at and refute the importance of “food miles” as quantitatively important in climate change and make the case that this is just part of the repertoire of the anti globalisation, anti-capitalism movement. Finally, we look at how changing temperatures and rainfalls will affect global agriculture. The developing world will fare worst. They will get hotter to the point where crop yields will fall; they will get longer periods of drought and heavier but more intense rainfall. In the developed world with the exception of Australia, there will be higher crop yields from higher levels of atmospheric carbon dioxide and from higher temperatures.

Chapter 14: Reflections and projections
A final chapter with a focus on the two great food tragedies of modern times: obesity and malnutrition


Monday, May 21, 2012

Food Choice: Disgust, pain and preferences


Food choice is a complex issue. At one level, we share the same biology as all animals as regards hunger, appetite and satiety. Rat studies can thus explain some of the mechanisms but they fall far short of the bigger picture because humans have a large and very complex frontal cortex, which governs all the things that make us human and not rats. It is through the cortex that we think, learn, speak and assimilate and disseminate complex ideas. More than anything else, these attributes allow us to divide labour and live in a sophisticated society and that society itself plays a major role in food choice.

In lecturing my students on food intake, I ask them to close their eyes and to think of some occasion when they were really hungry. I then tell them that when they open their eyes, the PowerPoint slide will show a food and I want to know would they eat it.  Invariably, they indicate their refusal to consume the food, which is a very nice bowl of highly nourishing and succulent cat food. They do agree that if the choice was between staying alive and eating the cat food, then they would eat it and just hope not to gag. Having recently read “How Pleasure Works” by the Yale professor of psychology, Paul Bloom, I now know that the reaction of my students is one of disgust. I also learned from Bloom that disgust is not a property of the cat food but a socially conditioned belief. Quite simply, I know of nobody and, dear reader, I would bet you know of nobody, who eats cat food. The cat food is nutritious, safe, made from high quality ingredients by branded companies for highly fussy pet owners. So there is nothing inherently disgusting in cat food. It’s simply a disgusting thing to eat by our social norms. Rats would have no qualms in eating cat food. Eating insects is disgusting to us but not to many nomadic tribes and eating pork is disgusting to a devout Muslim but not to the majority of Irish people. Paul Bloom goes on to point out that whereas society decrees what is acceptable to eat, within that framework, individuals can show disgust or more correctly, aversion to specific foods and, in general, such aversions can be related to some life experience. Thus I like fish but if given a choice, I would not eat mackerel. I still recall the stink in our kitchen at home when my father would head, tail, gut and fillet a bucket of mackerel for grilling, which he and his mates had caught in Dublin bay.

Bloom also raises another aspect of social influence on food choice: pain. Now it might seem strange to write about pain in a book on pleasure but so long as the recipient is in control of the situation, mankind likes a little bit of pain. We go to horror movies, which can be terrifying and we take amazing risks on crazy rides in amusement parks. In foods, we eat chilies and although our taste buds tell us not to do so, we overcome these because society decrees some consumption of chilies to be worthwhile. Thus in Mexico, where chili consumption is high, children are gradually weaned on to a high chili diet. Such a diet in earlier times helped give an identity to a group in much the same way as their language, music or dance did. You can imagine the fun these people had when a stranger was given their hospitality only to scream for water to cool their burning palates!

Let us now return to the physiology of taste and flavour and see how that competes with social pressure. Paul Bloom draws on a joint study carried out by the business schools at MIT and Columbia. Subjects were asked to taste two beers: a regular Boston brand or a “new” MIT beer. The latter was no more than the regular Boston beer with a dash of balsamic vinegar. The first group (the control group) were not given any information at all and simply asked which brand they preferred. They voted 60:40 for the “new” MIT beer The second group were told that the regular Boston beer was to be compared to a “new” MIT brew and they were told that this beer was just the regular beer plus balsamic vinegar. Now the vote was only 20% for the MIT brew. A third group was treated like the control group but immediately after they had drunk it and before they expressed their preference, they were told the truth: that the “new” MIT beer was just ordinary beer with balsamic vinegar added. They voted like the control – 60% preferring the MIT brew. Clearly, the latter group, like the controls, formed an opinion that if a beer came out of MIT it must be good. Having now made their minds up, the third group stuck to this assumption even though they knew that it was just a stupid concoction. The values we give to foods in making food choice are very complex. The idea that a beer from MIT had to be good goes hand in hand with our preferences for brands. Indeed, Bloom points out that studies show that Coca Cola drinkers enjoy Coke more when the glass is a Coke branded glass. Status is very important in food choice because, like the peacock’s tail, it is a symbol of ones power and status.
Rat studies are thus of limited use in understanding food choice. They might explain the mechanisms, which determine the desire to eat but not food preferences. They are socially determined to a great extent. The simpletons of public health nutrition reduce the obesity issue to a higher probability of choosing some food such a sugar sweetened beverages or fast food because that’s the simpleton’s fashion – simple and stupid. Some people make the conscious decision to take up smoking or alcohol intake. But nobody wakes up and says:” Guess what. I’m going to get fat”. It happens and we know so little about how that passive accumulation of energy occurs and how our food preferences promote this weight gain. We need less research money spent on studying why rats chose to eat or not and more money spent on human behavioural sciences, particularly food choices and preferences. 

Monday, May 14, 2012

Dietary advice with a grain of salt


Salt is one of the most ancient ingredients used as a food preservative, particularly for the preservation of meat. Roman soldiers pay was named “salarium” from which the word salary is derived because it was expected that salt would be one of their main items of expenditure. Cities such as Salzburg were associated with salt and Mahatma Gandhi marched with many thousands of Indians on the "Dandi March" or "Salt Satyagraha", where they made their own salt from sea water in a protest against the tax levied on salt by their British rulers. Today, however, salt is seen as an food ingredient which is associated with high blood pressure and drives to lower the salt levels of processed foods are operational in many countries, Processed foods provide about 90% of salt intake while the salt cellar accounts for a mere 10%.
In 1949, an MD from Durham, North Carolina by the name of Walter Kempner published a paper in Annals of Internal Medicine in which he showed a dramatic effect of a diet based on rice on a number of cardiovascular risk factors, among which was hypertension. This was a very low salt diet and thus the association between salt and hypertension had gained momentum. In 1964, Lewis Dahl, working at the Brookhaven National Laboratory in New York found that about 25% of his rat colonies were resistant to increased blood pressure when given a high salt diet. Thus he genetically bred two strains of Dahl rats, an R-strain that was resistant to salt-induced hypertension and an S-strain that was sensitive in this respect. These rats were widely used to see how salt interacted with other nutrients such as potassium, in moderating blood pressure and thus the salt-blood pressure story grew. It is important to note that by my calculations (others have done like wise and agree), the quantity of sodium ingested by these rats would translate into about 400g per day for a 70kg human. Bearing in mind that a high salt intake in free-living humans might be 15g per day, the relevance of these rat studies (as is generally the case for animal models) to human physiology is laughable.  However, a spate of poorly designed human intervention studies followed putatively confirming the rat work and so salt was served up on the first ever set of dietary guidelines published by the US Senate Select Committee in the mid 1970’s. That a reduction in sodium intake would reduce blood pressure became accepted wisdom and in the world of nutrition guidelines that is as sacred and immutable as the dogmas of the Vatican or the Kremlin.

Professor Roger McCarron of the Department of Medicine at the University of Oregon published studies, which began to criticise these data. Of course he was generally regarded as a heretic by the high priests of healthy eating. But he stuck to his guns and began to provide data that other nutrients were more important such as calcium and that obesity was a significant factor. Slowly, evidence began to emerge which suggested that a broad modification of diet might be better than  a single nutrient-based approach and so the DASH (Dietary Approaches to Stop Hypertension) trial was initiated, funded by the US National Institute of Health. This was a very large randomly controlled intervention study involving 459 adults who were put on a control diet for the initial 3 weeks. This was a typical US diet high in fat and low in fruit and vegetables. Half the subjects were then put on the same diet but with increased fruit and vegetable intake for 8 weeks and the other half also had this diet but, additionally, had high intakes of low fat dairy products together with a low fat, low saturated fat diet, again for 8 weeks. Very importantly, no changes were made to salt intake, either as table salt or salt in normal foods. The results showed that the diet high in fruits, vegetables and dairy products and low in total and saturated fat significantly reduced blood pressure to a clinically significant level in subjects whose blood pressure was normal or elevated.

But that did not detract from the salt reduction zealots who have protected their dogma with great passion. However, in 2011, a series of papers published in prestigious journals have shown that all is not rosy in the salt garden.   In 2011, an international consortium reported on an 8-year study of 3681 subjects based on 24-hour urinary sodium data, collected at the outset of the study[1]. The reason for using a 24-hour urine collection to measure sodium output is that dietary data on salt intake is utterly unreliable. In contrast the urinary data doesn’t lie and give an accurate measure of sodium intake. They divided the subjects according to their level of sodium excretion: The lowest, middle and highest thirds of excretion. The 8-year incidence of cardiovascular disease went as follows: 4.1% in those with the lowest sodium excretion, 1.9% at the middle and a mere 0.8% among those with the highest intake. No, I didn’t type it wrongly. That’s how it stood. Low salt intakes had a higher risk of hear disease that the low salt group. Higher salt intakes increased diastolic blood pressure but not systolic blood pressure and overall, increasing sodium excretion did not increase the levels of clinical hypertension. A second study published in 2011 explored baseline urinary sodium with cardiovascular events over a 56 month period and they found that the relationship was “J-shaped”[2]. In other words, heart disease was higher at low levels of sodium excretion (by about 30%), which fell to a minimum at about the average for sodium excretion and then rose again at the higher level of sodium excretion (by about 70%). Finally, we had a major review of existing literature where 167 studies, covering high and low sodium diets were examined[3]. Salt reduction reduced blood pressure by 1% in those with normal blood pressure and by 3.5% in those with high blood pressure. However, plasma lipids rose by 7%, which may explain the adverse effects of low sodium diets on cardiovascular risk, observed in the other two papers

One might imagine that the salt-hypertension debate might take a major turn in fortune in light of these papers but as I have pointed out before, scientific dogmas are like oil tankers – hard to turn around. The WHO has issued a call for public comments as part of its forthcoming review of its current recommendations on salt and hypertension. It will be interesting to see the outcome.



[1] JAMA. 2011;305 (17):1777-1785
[2] JAMA.2011; 306 (20):2229-2238
[3] Am J Hyper (2012), 1, 1-15

Monday, April 30, 2012

Organic food and agricultural romanticism


A seed has three main parts: an outer husk to protect it until germination (bran), a reserve of energy (endosperm) and the cells that have the DNA to kick start growth (germ). After planting into the earth with sufficient moisture to break down the bran, the process of growth starts. The germ cells use the nutrient reserve in the endosperm to get started in making fledgling leaves and roots and eventually, the seedling breaks through to the infinite energy of photosynthesis from sunlight. The roots develop and start to move water from the soil through the plant to be evaporated from the leaves and in so doing, the water brings the minerals the plant needs to grow, of which one is nitrogen. 
Nitrogen is absorbed from the soil as either ammonium (NH4+) or as nitrate (NO2-). Both are released from commercial fertilizers and both are released from farmyard manure. The ammonium and the nitrate ions of both commercial fertilizers and manure are absolutely identical and there is simply no way a plant can differentiate between the two. The same is true of all the other minerals which plants absorb from soil such as sulphates and phosphates. The minerals absorbed are used for all sorts of functions but most of the nitrogen and sulphur ends up in plant amino acids and proteins. Some will end up in the vitamins that the plant makes and also the phytochemicals which give plants their colour, texture, smell, taste and so forth. The plant assemble all of these compounds according to its DNA. Unlike animals, plants do not have any nervous system and thus cannot make choices. Thus they are hardwired to do exactly what their genes tell them to do. Thus a carrot seed becomes a carrot and not a parsnip and vice-versa. Those who espouse organic farming harbour the view that the plant grows differently in the presence of organically derived minerals as compared to those that are industrially derived. This is utter nonsense. Michael Pollan, for example, argues that synthetic fertilizers force plants to grow at a faster than average rate and that in so doing, the plants get things wrong. Rubbish!!!
Plant growth, like animal growth, is determined by growth hormones which are genetically controlled but which also respond to climate. These hormones determine the rate of growth and thus the demand for minerals from soil and it doesn’t matter one iota if the minerals are from manure or “chemical” fertilizers. This has an analogy in human growth. Athletes can eat as much protein as they like but that will not drive muscle growth. Hormones drive muscle growth and athletes can take hormones illegally or they can increase their natural levels by training and conditioning. 
Let us now turn to the idea promoted by organic enthusiasts that organic food is tastier and more nutritious. Firstly, theory would say that that is not possible as explained above but the proof of the pudding is in the eating. Research published in the American Journal of Clinical Nutrition and FUNDED by the Danish organic farming movement, categorically failed to find any difference in the nutritional value of plants grown under organic or conventional farming conditions. Equally, researchers at the University of Kansas found that consumer panels could not distinguish between the taste of organically grown fruit and vegetables and those grown using industrially produced fertilizers. Endless reviews by eminent scientists and funded by governmental bodies reach similar conclusions. For example, the UK Food Standards Agency commissioned a review of all the literature relating to the nutritional quality of organic food. The review concluded: ‘On the basis of a systematic review of studies of satisfactory quality, there is no evidence of a difference in nutrient quality between organic and conventionally produced foodstuffs’. The taste and flavour of plants are determined to some extent by microclimate and the variation in these qualities between growing seasons or between different parts of the same field exceeds any variation between crops grown under either conditions.
The organic movement also suggest that foods grown under organic conditions are better for the environment. A report commissioned by the UK Department of Food, Environment and Rural Affairs
 concluded: “There is insufficient evidence available to state that organic agriculture overall would have less of an environmental impact than conventional agriculture. In particular, from the data we have identified, organic agriculture poses its own environmental problems in the production of some foods, either in terms of nutrient release to water or in terms of climate-change burdens. There is no clear-cut answer to the question: which ‘trolley’ has a lower environmental impact - the organic one or the conventional one?”. 
Finally, we turn to pesticide residues. By definition, organic food should not contain residues of synthetic pesticides. However, studies repeatedly show that about 15% of organic crops will contain some minute level of pesticide residues which is explained by “drift” ~ farmers upstream from the wind direction spraying their crops with downward drift of some spray. By definition, conventional crops will contain pesticide residues and as with organic crops, the levels are minute. In neither case do these residues contain a shred of threat to health since they are present at  ultra-low levels, and well below the agreed residue levels in legislation. Of course there have been cases of neglect or accident where pesticide levels above this threshold have been found and even some very rare cases of sickness arising from these high levels. But these are accidents or neglect and they can also occur in organic agriculture where contamination with E. Coli on organic food has led to food poisoning.
As I pointed out in a previous blog, all the scientific arguments in the world will not change the views of the agricultural romanticists. Theirs is a view based on emotion and not science, or a distorted view of science. But if such arguments help the very many who haven’t the resources to pay for organic food to feel better about conventionally produced foods, then it is very worthwhile making the case. 

Monday, April 23, 2012

Michael Pollan's "In defense of food" - a critique


Michael Pollan’s book “In Defense of Food’ has been a global best seller within the genre of books on food and health. It appears to be extremely popular among journalists since it bashes conventional wisdom on food. Twice, correspondents for the Irish Times chose to feature this book and marvel at its wisdom. Pollan’s book is peppered with half-truths, circular arguments and highly selective supporting material. His fundamental point is that we should focus our dietary choice on foods and not bother too much, if at all, with all of this nutritional advice that abounds today.


Pollen’s belief that health is the driver of food choice in the modern era is a cornerstone of his argument. Take for example the statement he makes: “That eating should be foremost about bodily health is a relatively new, and I think, destructive idea”.  As I pointed out in my blog of April 2nd, the interest in healthy eating is as old as civilisation and this obsession is the pursuit of a relatively minor section of society[1]. The vast majority chooses food that they plan to enjoy and, in making those choices, take care to get some level of balance as regards to their personal health. Every study that has examined the drivers of food choice have come away with the conclusion that the “go – no go” part of food choice is whether the consumer likes the food.  Pollan’s assumption that it is the pursuit of health that drives food choice is an opinion based his personal reflections and observations. However, our own research, published in peer-reviewed journals shows the opposite. In a survey of over 14,000 consumers across the EU, some 71% either ‘agreed strongly’ or ‘agreed’ with the statement: “I do not need to make changes to my diet as my diet is already healthy enough”.  Figure that Mr Pollan!

The putative obsession with food and health of modern consumers that Pollan puts forward arises from the dogmatism and doctrine, which he calls “nutritionism”. He argues that nutrition has reduced the food and health issue to nutrients. In his view, nutritionists see foods solely as purveyors of nutrients and summarises their view thus: “Foods are essentially the sum of their nutrient parts”.  He quotes his fellow food saviour and author Marion Nestle who says of nutrition: “…it takes the nutrient out of the food, the food out of the diet and the diet out of the lifestyle”. Eloquent, but utter baloney! This needs to rebutted along several lines. In 1996, I chaired a joint WHO-FAO committee that issued a report entitled “Preparation and use of food-based dietary guidelines”. The notion behind this was that many developing countries did not have detailed data on the nutrient content of their food supply, that they didn’t have nutritional surveys and that we should encourage the development of healthy eating advice in terms that consumers can understand. Indeed, statistical techniques such as cluster analysis are widely used to study food intake patterns and moreover, there are many examples of systems that score food choice for their nutritional quality. To write a book based on the impression that nutritionist see foods solely in terms of nutrients is simply daft.
Let me go a little further with this. Take the disease spina bifida, which is one of several forms of neural tube defects (NTD) that occur early in pregnancy. Extensive human intervention studies have shown that an increased intake of the B vitamin, folic acid, will significantly reduce the re-occurrence of an NTD birth in women who have previously had a child with this condition. This research has led to a threshold value of folic acid in blood above which this reduction occurs and the research shows that in human intervention studies, it is not possible to attain this threshold with normal foods, naturally rich in folate. Such folate has a rather low bioavailability and the threshold can only be reached if the volunteers consumed foods fortified with synthetic folic acid. This has led to the mandatory fortification of flour in the US with folic acid leading to a dramatic reduction in the incidence of new cases of spina bifida.
What is laughable about Pollan’s approach is that he himself engages in his so-called reductionism because he devotes at least almost 11 pages to the argument for and against the polyunsaturated fats from plants (omega-6 variety) and the polyunsaturated fats from fish (omega-3 variety), ultimately favouring the latter and then ends up with the statement: ”Could it be that the problem with the Western diet is a gross deficiency in this nutrient?” Now Michael you can’t have it both ways. You can’t decry nutritionists for studying individual nutrients in relation to health and then proceed to do so yourself! And remarkably, this champion of foods over nutrients goes on to argue that older persons should take multivitamins. Don’t take a bow Michael. Just stop doing summersaults.

The final piece in his jigsaw is to dismiss the modern processed food as though bread, cheese, yogurt, pasta, wine, chocolate, coffee and the like are not processed. Their processing details were worked out long ago and so they don’t qualify for the derogatory tag of “processed”. As I pointed out in a recent blog, the first sugar refinery was built in Crete in 1000 AD and that the Arabic name for Crete, Qandi, gave rise to what we today call “candy”. This process requires the sugar can to be pulped in water, the water filtered through muslin and the water evaporated in the searing heat of the Crete sunshine, which is why Crete was chosen and not Cork. And he makes the inevitable mistake of the agricultural romanticist that organic food is nutritionally superior to conventionally farmed food, which is palpably untrue but let that be next week’s blog.




[1] Sex, obesity and the seven deadly sins