Total Pageviews

Monday, July 9, 2012

Calorie counting on menus ~ The US experience


The Minister for Health here in Ireland wants to introduce calorie counts on menus and has given the industry 6 months to implement the proposal or, if they fail to  do so, legislation will be introduced. All packaged food requires full nutrition labeling, so it would seem quite reasonable to require the food service sector to follow suit. Calorie counts on menus were first introduced into New York in 2008 and, in 2010, the US Congress passed an act which required menu labeling for all restaurants with 20 or more locations. Researchers at the University of North Carolina conducted a systematic review of the impact of this legislation on actual average caloric intake in the US food service sector. A systematic review sets out very clearly, the criteria that a published paper must meet in order to be considered by the reviewers. In this case the studies had to have an experimental or quasi-experimental design comparing a calorie labeled menu with a menu without any caloric data. The review only considered studies with data on either consumption or purchase and, of course, only English language publications.[1]
They identified 164 titles, of which only 32 appeared from the title to meet the entry criteria. Having read the abstracts of these 32, a total of 18 papers were read in full and of these, 7 were included in the review. Two reported reductions in calorie intake with calorie labeling, 3 reported no change, 1 reported an increase and 1 found that of the 11 largest fast food chains, 3 reported a decrease (McDonald’s -44, Au Bon Pain -80 and KFC -59), 1 reported an increase (Subway +133) while 7 reported no change (Burger King, Wendy’s, Popeye’s, Domino’s, Pizza Hut, Papa John’s and Taco Bel)[2].

This might sound like music to the ears of the food service sector but before the rapture begins lets just ask ourselves if the data should surprise us. Research shows that consumers do not rate obesity and overweight as an important risk for them personally but they do see it as a risk to society as a whole. That is explained by the fact that although a consumer may be fat, they are themselves in control of the situation and if and when they decide to lose weight, they can manage that without any doubt. However, they are not convinced that the rest of society has such marvelous self control and hence, weight is a societal issue but not a personal issue. So if they are asked for their opinion on the listing of calories on menus, they will see the value. Now when consumers go out to dine in a cafeteria, fast food outlet or a restaurant, those that are in the mode of counting calories will be able to benefit from menu labeling. Since this is a minority, we should not be surprised that on average, there was no impact of caloric labeling. If the research was to include those who wanted to lose weight, then almost certainly, the outcome would be positive.

One useful and informative paper comes from Tacoma-Pierce County in Washington and was written by those members of the County Health department that set out to promote menu labeling in a program called SmartMenu[3]... This programme targeted locally  owned restaurants, not the food chain restaurants and this was done specifically to see how such local restaurants with less resources than the chains, could cope with the challenge. Of the 600 restaurants contacted, only 24 agreed to participate and of these, only 18 finally posted the data on their menus. By far the biggest barrier was the preparation of the menu items into a standardized format that could be entered into a nutritional analysis software programme. In the words of the authors: “The challenge for locally owned restaurant owners who are not using standardized recipes to participate in this programme cannot be overstated”. The average time from a signed agreement to participate to the posting of the menus was 8 months. The costs for the restaurants ranged from $1,500 to $8,400. Besides the time, complexity and costs issues, other barriers included the perceived business risk of labeling (the “I got fat eating in your restaurant which mislabeled the caloric value of my favourite dish” law suit) and the low perceived demand for such calorie labeling.

As ever, things are not as straight forward as first imagined. That does not mean that we shouldn’t try to label menus if indeed we believe that it will help those who are dieting and who are generally weight conscious. A few further observations can be made. We must also be aware that there are consumers who rate monetary value higher than health aspects when purchasing foods and who in fact might opt for the best value in terms of calories per euro. Based on the experience of Tacoma-Pierce County, someone is going to have to invest in this if it is going to work. If it is the restaurant owners, then guess who’s ultimately going to pay for the service. Then again, when you go out for dinner, cost is not really an issue.  Finally, last night we ate in a delightful Thai restaurant and nobody ate everything served. How many calories were left on the plate?



[1] 1 English is the language of scientific publication and papers published in other languages are always excluded from systematic reviews. To use them would require a full translation with the help of the author to retain accuracy and that is not feasible. Moreover, journals in non-english language have a local focus and are always of  a very low impact factor.
[2] 2 JJ Swartz et al (2011) International Journal of Behavioral Nutrition and Physical Activity 8, 135
[3] 3 JW Britt et al (2011) Health Promotion Practice 12, 18-24

Tuesday, July 3, 2012

Fructose - challenging the myths


In the past, the sugar component of most sweetened beverages was obtained either from sugar beet or cane sugar. For both sugar cane and sugar beet, the sugar found is called sucrose and it is one molecule of glucose linked to one molecule of fructose. In the late 1960s, an alternative to sugar was developed which was cheaper to use and less prone to the volatility of the global sugar market in terms of price and volume. This alternative is known as High Fructose Corn Syrup (HFCS) and it is produced in two stages. Ordinary cornstarch is first broken down to its basic constituent glucose and the glucose is then treated with a natural enzyme that converts it to fructose. The two sugars, glucose and fructose can now be blended yielding mixes with varying ratios. For the soft drinks industry, the ratio is 55% fructose and 45% glucose.

For some time now, various “experts” have come down heavily on fructose for its deleterious effects on health. Google the word ‘fructose and within the top three sites you find “Fructose-Sweet but dangerous” and “Sugar may be bad but fructose is far more deadly”. The latter has a link to a You Tube video by Robert Lustig, a professor of pediatrics at the University of California, San Francisco. The video is entitled “Sugar – the bitter truth”. In his video, he outlines his belief that our modern food supply is  “adulterated, contaminated, poisons and tainted” and the culprit is fructose. It really is difficult to understand the use of these terms by a medical professional. These are intended to get people scared and to grab their attention so that the learned doctor can give you the diagnosis and the cure. He goes on to ask the audience: ”What is in coke”. First he tells us that there is caffeine there, which, being a mild diuretic will make us thirsty and he then goes on to say that a can of coke has 55mg of sodium, which he says “is like drinking liquid pizza”. As far as I can tell from a 30 second search of the USDA food composition on-line database, an average serving of pizza from a fast food chain would contain about 800 mg of sodium. Why does the good doctor choose to distort the facts? He argues that the sodium and the caffeine diuretic are designed to make you thirsty. He then goes on to ask his audience why sugar is added to Coke. Why, of course, it’s to mask the salt content!

The good doctor goes on to explain that what fructose does to your blood proteins is what happens to your steak when it goes brown. Wrong again doc. When red meat is cooked, the iron containing protein in muscle, myoglobin, begins to lose its iron and as the temperature rises, the myoglobin loses more and more iron, thus turning brown. White meat such as chicken and pork do not brown in cooking because they contain much less myoglobin. What Prof Lustig probably meant was that the effect of fructose on blood proteins is, at a considerable stretch of the imagination, similar to the browning of toast where sugars react with proteins under the effect of strong heat.  Of course you don’t toast your blood so the analogy is a bit far fetched.
From the scientific point of view, a very recent systematic review of the literature of controlled human feeding studies, shows that among diabetics, where high sugar levels can react with proteins, causing undesirable clinical consequences, substituting fructose for other forms of carbohydrates actually lowers this process known as glycation[1]. This work was funded by the Canadian Institute of Health Research and completed by Professor David Jenkins, a world authority on diet and blood glucose. In a previous set of correspondence in the Journal of the American Dietetic Association, Jenkin’s challenges Lustig’s hypothesis that fructose promotes the accumulation of fat in the liver and adipose tissue in an article entitled “Is fructose a story of mice but not men?” The authors point out that studies in animals need to very carefully interpreted before the findings of such studies are extrapolated to man. Thus in mice and rats, the conversion of carbohydrates to fats can reach 70%. However, in man, the efficiency of conversion of carbohydrates to fat is much lower at about 5%. They point out that in studies with very high intakes of fructose in humans, this effect can double the rate of conversion of carbohydrate to fat, but the levels remain at 10%, a fraction of what is seen in experimental animals. Moreover, animal models often use very high levels of fructose well above (upwards of 6 times) that normally associated with human diets.

The idea that in man, carbohydrate conversion to fat is low is often greeted with surprise if not disbelief; so a little explanation is worthwhile. Many animals have the capacity to convert carbohydrate to fat but when physiologists started to look at this in humans using live-in calorimeters to study precise changes in the oxidation of fat and carbohydrate, they found that when excess calories were consumed as carbohydrate, the oxidation of body fat stores fell dramatically and that the excess carbohydrate calories were used for fuel thus sparing the fat. Thus if you require 2,500 calories a day from a typical mixed diet (fat 35%, carbohydrate 50% and protein 15%) and you consume an additional 200 calories of carbohydrate, instead of using all the ingested fat (35% of calories would be about 875 calories or 97 grams), you would only use 675 calories from fat, allowing 22 grams of fat to be spared. So, carbohydrate spares the burning of fat in man but it is poorly converted to fat in humans, even if it is as fructose and with high doses of fructose.

Sugar bashing is popular and fructose bashing is even more fun but basically built on very bad science. But, why let bad science get in the way of a good story or a nice video with 2.6 million viewings?




[1] Effect of fructose on glycemic control in diabetes. A systematic review and meta-analysis of controlled feeding trials. Diabetes Care Volume 35, July 2012

Monday, June 25, 2012

Obesity and social disadvantage


Frequently, when chatting with my middle class friends on nutrition and health, I have to argue long and hard against some preconceived notion of the truth behind the topic of discussion. Of all of these issues, the one I encounter most frequently and the one that meets most resistance to change is the view that the problem of obesity is really a problem of the lower socio-economic groups.  A frequent argument put forward is that  “if you look at their shopping trolleys in supermarkets, they are laden with all sorts of junk foods”.  So let me give you the facts. Taking the Irish population as a whole and using the IUNA database, body mass index (BMI kg/m2) is 26.8 among the professional workers, 27.4 among non-manual workers, 28.4 among skilled workers and 26.0 among the unskilled workforce. An acceptable level of BMI is 25 and I should add that the variance (standard deviations) of these figures is broadly similar. Now you can look at this and say: ”See I told you so. There is a graded rise in BMI from professional to skilled workers” and this goes nicely with the social class stereotype. The socio-economically disadvantaged are seen as lacking money to buy healthy food, and so poorly health aware as to not know good food choices from bad food choices and, in some cases, they are deemed to lack the literary skills to read labels correctly. This leads the debate on public health nutrition to shift into policy decisions in which actions toward social issues begin to dominate. In case you think that this Irish data is unique, please consult the Report of the Health and Social Care Information Centre’s report: Statistics on obesity, physical activity and diet: England, 2011.  To directly quote the report: “Table 7.3 on page 128 of the HSE 2009 report shows that there are very little differences in mean BMI by equivalised household income for men with the exception of those in the lowest income quintile who had slightly lower BMI; in contrast for women, those in the lower income quintiles had a higher mean BMI than women in the highest quintile. Among women, the proportions who were obese were higher in the lowest three income quintiles (ranging from 27%-33%) than women in the highest two quintiles (ranging from 17%-21%). The relationships between BMI and income for men were less clear”. Canadian data is quite similar but US data[1] does show quite a different pattern with obesity rising more rapidly among the socially disadvantaged. However, these data when carefully examined reveal some intriguing facts.  Among white men and women, the rate of rise in the % obese has grown equally across socio-economic status (SES) over the 30 years from 1970 to 2000. The lowest SES in 2000 had an obesity rate of 28.3% in men compared with 23.9% among those in the highest SES. For women, the figures were 36.3% and 26.6% respectively. However, when we look at black males, the % obese jumped from 4% to 33% in that 30-year period among the highest SES. The middle and lowest SES groups started off with a figure of 15%, which grew to 24%. For black women, the total reverse was seen. How does on e begin to make sense of that?


I should add that if you look at dietary patterns across socio-economic status in the Irish IUNA data, you see no biologically meaningful change in the % energy from fat or sugar and this is borne out by data from the Household Budget Survey which tracks expenditure on foods. That data shows no difference in food purchasing patterns across socio-economic status.


There is a bottom line here and that is that obesity is everywhere. To argue over one unit of BMI between the haves and the have-nots is to quite simply miss the point. Statisticians can construct models, which show that controlling for age, gender, smoking and so on, the relative risk of obesity rises with lower socio-economic status. They are welcome to that but if it begins to drive public health nutrition policies toward some social solutions, then they are being unhelpful. Of course, social disadvantage needs to be a factor we consider in all aspects of public health. But what is driving the increased adiposity of judges, teachers, doctors and so forth. It is not a lack of knowledge, not due to literacy or lack of income. The do-gooders of public health nutrition need to read the real population statistics and make appropriate recommendations.


[1] The Obesity Epidemic in the United States—Gender, Age, Socioeconomic, Racial/Ethnic, and Geographic Characteristics: A Systematic Review and Meta-Regression Analysis Youfa Wang and May A. Beydoun Epidemiologic Rev 2007;29:6–28

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.