Food outlets, schools and obesity related outcomes

Understandably, there is a very strong focus in obesity research on the diets of schoolchildren with many schools now attempting to implement healthy eating policies.  Equally, there has been considerable concern about the existence of food retail outlets nearby to schools to which the schoolchildren have access. A group at the University of Oxford has recently published a meta-analysis of all relevant studies, which set out to examine the relationship between obesity outcomes and the proximity of food retail outlets to schools[1].

The authors completed a search of 10 on-line library databases and identified several thousand studies but, as ever, in meta-analyses, many of the initial studies were rejected for a variety of reasons leaving the authors with 30 full studies which met all of the a priori inclusion criteria. Each study had to have defined exactly what was meant by the retail food environment and to have measure quantitatively the relationship between food purchase patterns and obesity-related outcomes. Most of the papers were published between 2011 and 2013 and most were cross-sectional with children ranging in age from five to seventeen years. More than three quarters had sample sizes of over 1,000.

Of the 30 studies, the majority used a defined “buffer zone” around the school but some used route maps between the pupil’s home and school. GIS (Geographic Information Systems) software was the main source of information on retail outlets either within the designated buffer zone or school route. In general the buffer zone applied a distance of between 0.1 to 3.0 miles while the route approach generally used distances of 50 to 100 meters from the road travelled to and from school. The main outcome studied was the child’s BMI (kg/m²). The second most frequent measure of outcome was food intake but this appeared generally to be related to a narrow range of foods: fruit and vegetables, soda drinks or fast food. Some of course used several measures and just three used the overall diet quality index of the schoolchildren which would have included all sources of foods at all times of the day.

One study focused on fast food purchases and found a statistically significant positive association between fast food purchasing and the density of fast food outlets.  Ten studies examined the relationship between food outlets in general  and the consumption of sugar sweetened beverages and of fast food, including crisps, sweets, biscuits, fried food, sugar sweetened beverages and fast foods. Within these 10 papers, a total of 54 associations were examined and only two of these showed a statistically significant association. Four papers examined the association between fruit and vegetable consumption and food retail outlets and within these a total of 32 associations were examined. Only three showed statistically significant associations. Within the 30 studies, only three had data on the overall quality of the pupil’s diet and food retail outlet density. Two of these showed a significant association between diet quality of food outlets. In one case, the data showed a significantly higher diet quality index among pupils attending a school where the nearest retail outlet was greater than 1 km away as compared to those where the distance was less than 1km away. The second study found that the greater the distance to the nearest grocers the better was the overall diet of the pupils.

This is an important paper for several reasons. Firstly, it is a very well conducted study published in a high impact journal. Secondly, it highlights how the existence of evidence is happily ignored by those policy makers who want to place restrictions on the availability of food outlets within the vicinity of schools. Thirdly, it shows that the outcome variables which are easy to measure such as fruit and vegetable intake, soda intake or BMI yield fairly useless conclusions since they do not relate the one aspect of the determinants of food choice (school associated food outlets) to the totality of the effects of all food choice in terms of overall daily nutritional quality. Once again, we see a majority of studies in what is a very important area of public health nutrition, bedevilled by bad design. In the three studies, which did look at the overall quality of the pupil’s diet and density of food retail outlets two showed some significant associations. Now do two swallows make a summer?. No, but they point the way forward for the conduct of scientifically rigorous studies in this very important area of public health nutrition. To discover that the proximity of food outlets influenced specific food intake is of zero importance in public health nutrition. We need to know the full accurate daily nutrient intakes and only then can we judge whether any aspect of the obesigenic environment id truly influencing overall nutritional quality.

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[1] [1] Williams J et al (2014) Obesity reviews Jan 13^th (e pub ahead of print)

Women's health: Cancer, Heart Disease and Misfearing

This blog is based largely on a recent paper in the Perspective series of the prestigious New England Journal of Medicine by US cardiologist Lisa Rosenbaum, entitled:” ‘Misfearing’ – Culture, Identity and Our Perceptions of Health Risks”[1]. First let me explain the term “misfearing”.  It is characterised by two attributes. It describes the widespread human tendency to base fear on emotive reasons and not on fact. It is also characterised by fear of dreadful events, which catch headlines and which are quite often rare (plane crashes, nuclear accidents, severe weather, HIV-AIDS etc.) rather than by fear of the familiar such as heart disease, obesity, smoking which are common and which occupy a great % of the health budget. Rosenbaum discusses this concept of misfear in relation to women’s health and specifically female cancer and female heart disease.

The majority of women would say that breast cancer is a bigger threat to women’s health than heart disease. However, the facts are the reverse, hence the concept of misfearing. In the US, over the period 2006 to 2010, the number of cases of all cancers in women was 2.8 million. The comparable figure for heart disease was 12.7 million, 4.5 times greater. The data skeptics will immediately argue that the heart disease data are flooded by statistics on high blood pressure, high blood cholesterol as well as actual cases of heart attack.  So let us consider deaths from cancer and heart disease in women. During this same period, 40,000 US women died from all forms of cancer. The comparable figure for deaths from heart disease was 410,000. Now, as regards mortality, the difference between all causes of female cancer and female heart disease is 10 fold.  Ten times as many graves of women who died of heart disease compared to all forms of cancer combined.

Why therefore is female health to a considerable health dominated by cancer, specifically breast cancer? The answer is largely sociological. But first consider the power and emotion behind the misfear of breast cancer. Rosenbaum points out that in 2009, the US Preventative Services Task Force recommended that the frequency of mammography in younger women should be reduced noting “…the potential harms outweighed the benefits”. The reaction among women was powerful. USA today conducted a poll of women aged 35 to 49 years and 84% intended to ignore the recommendations. So powerful was the backlash that the Affordable Care Act ignored the task force’s recommendations requiring insurers to base coverage on previous screenings. This perpetuated in law, a policy that the experts deemed did more harm than good. Rosenbaum writes: “Have pink ribbons and Races for the Cure so permeated our culture that the resulting female solidarity lends mammography a scared status? Is it the issue that breast cancer attacks a part of the body that is so fundamental to female identity that, to be a woman, one must join the war on this disease?”

I Googled the term “Famous women who have had breast cancer” and from the 20 listed, here are the ones whose names I recognise: Singers Kylie Minogue, Olivia Newton John, Sheryl Crow, and Carly Simon, actresses Cynthia Dixon of Sex and the City, Dame Maggie Smith, and Angelina Jolie. I did the same for “Famous women who have had heart disease” which oddly was dominated by men but I found one female name I recognised, Nancy Reagan. To me, it is understandable why women care more about breast cancer than heart disease. It is a disease that is unique to women and to womanhood. It is thus an extremely emotional thing. Heart disease is for all humanity. However emotional the issue of breast cancer may be, the census of the dead shows that female heart disease is ten times that of all female cancers combined. Men also have their emotional links with a cancer that has an incidence rate way below that of heart disease, namely prostate and testicular cancer. Indeed it’s a man thing to grow a moustache for a man’s cancer charity in “Mowvember”.

Rosenbaum explores her explanation in our commitment to cultural groups. It is a distinctive mark of human society that we alone cooperate beyond families and into groups and societies. What we lose as individual or selfish rights, we gain as communal rights[2]. Group identity is central to human society. For a group to thrive, it needs to support and reinforce the very reasons why it is a group. Misfearing is based not on fact but on emotions. It is what keeps opponents of pylons, fracking, intensive agriculture, fast food and the like together. She ends her article thus: ”Certainly, understanding of one’s risk for any disease must be anchored in facts. But if we want to translate into better health, we may need to start talking more about our feelings”.

Years ago during my two decades as a member of the EU Scientific Committee for Food, I learned the difference between fear based on facts and fear based on emotions. The social groups opposed to food additives and pesticides share this common misfear theme and pouring facts into this group is a waste of time. However I might see their “facts” as nonsense or unfounded or disproved, they see them as central and moreover, they see mine as threatening to the central belief of their group.

So how does public health and in my case, public health nutrition, tackle the misfearing among women who wrongly, if facts are the basis of truth, put breast cancer well ahead of heart disease as a threat to their health. Imagine if a mammography test required a prior blood lipid profile test and an ambulatory test? Would that not capture the problems of heart disease in women? Maybe so but the majority of cases of heart disease in women are among the poorer and the more socially disadvantaged. And thus the answer is not so obvious. Diet and lifestyle changes have a far greater link to the reduction in risk of heart disease than they do of most cancers. We need to advertise the fact that for every female death that arises from any cancer, ten times more women will die of heart disease. Simple measures such as blood lipid screening and blood pressure monitoring must be promoted among women.  And the promotion of healthy eating for heart disease prevention needs to gain as much print and social media as that which links diet and cancer, where, like it or not, the strength of evidence is much weaker.

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[1] Rosenbaum, L (2014) New Eng J Med, 370, 595-597

[2] Wired for Culture – the natural history of human cooperation” Mark Pagel, 2012, Allen Lane, London

Sorry Dr Lustig: A calorie is still a calorie

In his book: “Fat chance: The bitter truth about sugar”, Dr Robert Lustig argues that a calorie is not a calorie or basically, not all calories from different foods are equal. He makes three arguments to support his idea. This part of his argument is central to the subsequent claim he makes that sugar and in particular fructose is the villain of obesity.

He begins by pointing out that weight loss frequently reaches a plateau because as we lose weight our resting energy expenditure falls. This resting energy expenditure is the energy required to keep our heart beating, our kidney’s filtering, our lungs breathing, our brain thinking and so on. It’s the calories you burn when you are asleep. The fall in resting energy expenditure is one of several adaptions the body makes when energy intake is restricted. Another adaptation is that the brain agrees to reduce its insistence on glucose as its sole fuel and agrees to start burning fats for fuel. If it did not do this, then the body would have to make glucose from amino acids, which would deplete body protein stores. So, several adaptations are made when energy is restricted but this has absolutely nothing to do with the calorific value of the fuels used by the body. The calorific value of amino acids, glucose, fats and ethanol are determined by metabolic pathways that allow energy to be extracted from these metabolites and these pathways are not amenable to change. Adaptations do occur but the calorific value of nutrients remains absolutely constant. A major US trial of diet composition on diet-induced reduction in resting energy expenditure found no evidence that this drop in resting energy expenditure was related to variation in dietary composition[1]

The second argument made is that within the categories of nutrients (carbohydrate, fat and protein) there is considerable variation. Thus Lustig points out that there are good fats and bad fats, that proteins vary in their quality or nutritional value and that carbohydrates range from complex molecules such as starch to simple molecules such as sugar. So lets consider fats. A typical dietary fat is made up of one molecule of glycerol (a sugar alcohol) and three fatty acids. Each fatty acid can vary in length typically from12 to 22 carbons long and the amount of hydrogen attached to each carbon can vary between 1 and 2. So, of course there is a wide variety of fats but that has no bearing on their calorific value. Since hydrogen is the atom that is central to the extraction of biological energy, we can predict exactly what the energy value of a fat can be based on its hydrogen count. A gram of fat can be made up of a lot of small chain fats or a a lesser amount of long chain fats. The calorific content will not change. Some fats are primarily designed to contribute to the structure of the body and their energy potential is not their primary function. Thus the fatty acid arachidonic acid (which the body synthesizes from fats found in vegetable oils) plays a major role in cell wall architecture and in the regulation of blood clotting and inflammation. The fatty acid eicospentaenoic acid (EPA derived from fatty fish) plays a role in the structure of nerves and in the transmission of nerve signals. Sure, fats vary in their structure and function but this has nothing to do with the theory that not all calories are the same.

The third argument he makes is that that our diet quality has changed and that we have reduced our fat intake and increased our sugar intake. However, the calorific value of fats and sugars remain constant. A calorie is still a calorie. Indeed in a major dietary intervention study of weight-reducing diets involving 811 obese subjects using the following 4 radically diets found no significant difference in weight loss.

Diet	% calories from
	Fat	Protein	Carbohydrate
1	20	15	65
2	20	25	55
3	40	15	45
4	40	25	35

 So its calories that count and a calorie really is just that irrespective of the nutrient or food it comes from.[2]

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[1] De Jonge L et al (2012) Obesity,20(12):2384-9. Effect of diet composition and weight loss on resting energy expenditure in the POUNDS LOST study

[2] de Souza RJ et al (2012) Am J Clin Nutr. (2012) 95(3):614-25 Effects of 4 weight-loss diets differing in fat, protein, and carbohydrate on fat mass, lean mass, visceral adipose tissue, and hepatic fat: results from the POUNDS LOST trial.

Oh Sugar! Wrong about fructose

Of late, the words “toxic”, “sugar” and “fructose” have been widely used together, implying a most dangerous aspect of sugar on human metabolism. The irony is that in Greek mythology, Cronus, the Titan leader was fed so much honey that he fell into a deep sleep during which time his son Zeus killed him. The original words of the Greek legend refer to the “intoxicating effect” of the large intake of honey on Cronus. Just as we are amused but not troubled by the language or beliefs of Greek mythology, we should not be so troubled by the same nonsense reformulated in modern Californian mythology.  Honey was always held as a truly prized food: hard to harvest, made by bees through some mysterious process foreign to all other plant and animal foods, golden in colour and above all, sweet as nothing else ever known to man. The sweetness of honey was down to a combination of two simple sugars, fructose and glucose present at 55% and 45% respectively. Sugar, as we know it today, is also an ancient food but newer, relatively speaking, than honey. It is plant-derived and the very first commercial facility for the extraction of sugar in crystalline form from sugar cane or sugar beet was located on the Island of Crete.  The Arabian merchants who funded this production facility had another name for Crete, which they called Qandi. Hence the term “candy”, used today mainly in the US for sugar confectionary products. The main component of this sugar derived from cane or beet is the sugar “sucrose” which is a couplet of two sugars joined together, fructose and glucose.

Honey and particularly sugar, dominated the sweetness aspect of the human diet. That was to change in the 1980’s with the advent of high fructose corn syrup (HFCS) production, driven by simple economics. In the period up to the early 1980’s, US and global sugar prices were pretty identical and highly subject to wild fluctuations in market supply. Thus, in 1974 and 1979-1980, US and global sugar prices soared 5 fold in two separate market peaks. The advent of a new technology that could replace sugar with an identical alternative at a stable low price became a simple no-brainer. Sugar was priced out of the US markets with strict import quotas introduced in the early 1980s to maintain very high domestic sugar prices, double the global price.  HFCS was to almost completely replace sugar in the US diet. The manufacture of HFCS is technically simple. Starch, which is a polymer of glucose units, is extracted from corn and enzymes are used to first break down the starch to glucose. Half the glucose is converted to fructose, again using a simple enzyme system.  The glucose and fructose can now be blended together and the most popular blend with consumers was 55% fructose and 45% glucose, an identical blend to that found in honey.  HFCS intakes soared 8-fold in the US from 1975 to the 80s-90s. However, in recent years HFCS intake has fallen in the US and is now back to values in 1980. During the surge in the use of HFCS, that of sugar fell pro rata.

In 2004, some leading US obesity researchers published data to show that the epidemic of obesity in the US coincided with the surge in HFCS use in the food chain. Whilst most scientific commentators have dismissed this putative link, the debate rages on with thousands of doom-laden Internet postings fuelled by a handful of media-friendly scientists. The term “high fructose corn syrup” was in hindsight a foolish name to introduce since HFCS is quite simply not high in fructose, equal in fact to the level found in honey and almost equal to the level found in sugar. Fructose is the element of HFCS that has been singled out as the bad part and the research in this area leaves a lot to be desired. To begin with, humans don’t and never have consumed fructose in isolation. It is always consumed with glucose and thus experiments in humans or animals using diets with high fructose levels with no accompanying glucose are basically unrealistic. They may show what is possible but they have no bearing on what is probable. In a paper presented to the US Experimental Biology conference in 2012[1], the levels of fructose used in these diets was compared to the average daily intake of fructose by US adults. In every one of the 37 human studies and every one of the 21 animal studies, the level of fructose used exceeded the US average intake value (9% of calories). Of course the average hides high consumers so this paper also looked at the fructose intake of the top 5% of fructose consumption (15% of calories). Only 3 human and 1 animal study were at or below this very high level of intake. The majority of animal studies used as much as 55% of calories from fructose, a situation, which is impossible to envisage in the human diet except maybe in the make-believe land of milk and honey.

None of these studies needed to be funded since a natural experiment was being acted out on both sides of the Atlantic. Just as the US jacked up sugar prices to promote HFCS usage, in the EU sugar beet farmers were protected under the CAP limiting the use of HFCS to 5% of total supply. Thus beverages in the US contain HFCS whilst beverages in the EU do not. Nonetheless, obesity levels have grown dramatically either side of the ocean.  While the debate on HFCS rages on the Internet, two key organisations have pinned their colours to the mast. Both the American Medical Association[2] and the American Dietetic Association[3] have issued position statements dismissing any claim that HFCS use contributes to obesity or associated biochemical abnormalities of blood lipids or blood glucose.

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[1] White JS (2013) Adv Nutr, 4, 246-256

[2] http://www.ama-assn.org/resources/doc/csaph/csaph3a08-summary.pdf

[3] Journal of the American Dietetic Association, (2004) 104, 255-275