The Spurlock ‘experiment’

For 30 days Spurlock ate only McDonald’s food and documented the effects on his physical and psychological well-being on film. The effects were dramatic: he gained over 11 kilos in weight; his blood cholesterol went up; fat built up in his liver; and he experienced sexual dysfunction and swings in mood. At last, here was all the proof we needed that eating McDonald’s food makes you fat and sick!

In reality it was nothing of the sort. Proof comes from scientific experiments and Super Size Me bore no resemblance to science. When conducting dietary experiments researchers are careful to control for all the factors that might affect the result. If two things change in a diet, how do you know if an adverse effect is due to one thing or the other?

Spurlock gave his audience the impression that he was testing the QUALITY of McDonald’s food. However, during his 30-day ‘experiment’ he also changed the QUANTITY of food that he ate. In fact, he absolutely stuffed himself, doubling his calorie intake. This binge was why he put on so many kilos and probably why his blood cholesterol and liver fat increased.

The fact that he was eating McDonald’s food actually had nothing to do with his weight gain. Many dietary experiments have shown that diets with widely differing composition have exactly the same effect on body weight if calories are kept constant, and physical activity remains the same. These are the things that determine whether body weight moves up or down. Spurlock actually lowered his level of physical activity during his month-long feast, presumably to ensure the results were as bad as possible.

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Spurlock’s motive

What was Spurlock’s motive? If the intention had been to inform the general public of the facts Spurlock would have teamed up with some nutrition researchers and filmed a real scientific study into the effects of McDonald’s food. I suspect he was aware that the results would hardly have been big news.

At best, Spurlock’s movie may be an extreme case of white hat bias i.e. bias leading to the distortion of information in the service of what may be perceived to be righteous ends. But the predetermined outcome and the misrepresentation of its cause surely pushes ethics to the limit.

Alternatively, maybe Super Size Me was just a stunt designed to generate a lot of publicity and to tarnish McDonald’s name. Irrespective of what we think about the nutritional quality of McDonald’s food, wouldn’t we all be better off if we just heard the facts?

Declaration: Bill Shrapnel has no association with McDonald’s.

About 30% of adult Australians are thought to have non-alcoholic fatty liver disease – fatty liver for short – and its prevalence is increasing. In its early stages fatty liver is of minor concern and there are no symptoms. But it can progress to a stage called NASH where liver cells begin to be damaged and this is associated with inflammation. At the next stage the risk of cirrhosis of the liver increases which may lead to liver failure and even cancer of the liver. Together, fatty liver and NASH are now the number one cause of liver disease in Western countries. However, the major cause of death in people with fatty liver is cardiovascular disease.

What causes fatty liver?

Fatty liver develops when the liver’s normal processes of delivery and removal of fats go awry. Although the exact cause is not known several things could be going wrong:

• Perhaps too much fat is being delivered to the liver
• The liver may have a problem ‘burning’ fats for energy
• Fat (triglyceride) production by the liver may be increased
• The movement of triglycerides from the liver into the bloodstream may be impeded.

But what is the underlying cause?

Fatty liver is now considered to be the liver expression of the metabolic syndrome. This syndrome is a cluster of abnormalities including central obesity (fat around your waist), raised blood glucose, high triglycerides, low HDL-cholesterol and high blood pressure. Usually, not all of these occur in the same person but if you have central obesity and any two of the others then you have the metabolic syndrome. And you are a good candidate for fatty liver too. Not surprisingly, people with type 2 diabetes are twice as likely as the general population to have fatty liver. The association with the metabolic syndrome explains why people with fatty liver are at increased risk for cardiovascular disease.

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The critical link between metabolic syndrome and fatty liver is insulin resistance i.e. the cells of the body have become less sensitive to insulin. When insulin resistance is present more free fats flow from the body’s fatty tissue to the liver which then packages them up into triglycerides and pushes them out into the bloodstream. This high flux of fat through the liver may be the driver of fatty liver.

Lifestyle management of fatty liver

In the absence of any evidence-based drug treatment of fatty liver the best option is lifestyle intervention but it has to be said that there is little in the scientific literature to go on. With the general acceptance that insulin resistance is the core of the problem strategies that are known to improve insulin sensitivity, such as increased physical activity and weight loss, are generally supported.

There were encouraging findings from a recent meta-analysis that showed a benefit of exercise on liver fat, even when weight loss was minimal or absent. However, the quality of the available trials included in this study was only fair.

Weight loss of 5% or more lessens fatty liver and weight loss of 7% or more lowers inflammation of the liver, according to a recent meta-analysis by Musso and colleagues. Again, there are only a handful of good studies. The American Association for the Study of Liver Diseases recommends weight loss of 5-10% for overweight people with fatty liver.

Diet composition

There is no established diet for fatty liver and no evidence-based clinical guidelines. There are simply too few published randomised controlled trials to provide the data necessary to create such guidelines.

A review by Conlon and colleagues draws on the American Diabetes Association guidelines for the prevention and management of diabetes and cardiovascular disease for inspiration for the dietary management of fatty liver. A dietary intake pattern that emphasises whole grains, fruits, vegetables, legumes and low-fat dairy is recommended, together with a limit on calories, less saturated fat and less refined carbohydrates. No limit on total carbohydrate is recommended. Glycaemic Index is discussed but there are no firm guidelines. It’s all quite general and all extrapolated from recommendations for other conditions.

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Mediterranean diet

Recently, an Australian randomised controlled trial into the effects of a Mediterranean diet on people with insulin resistance and fatty liver was published. Compared to the control low fat/high carbohydrate diet the Mediterranean diet improved insulin sensitivity and reduced liver fat, even though body weight was not affected. Whether the effect was due to the monounsaturated fats in the Mediterranean diet or the carbohydrates they effectively displaced is unclear. The higher polyphenol content of the Mediterranean diet may also be relevant.

Fructose

It has been hypothesised that fructose intake may affect the risk for fatty liver. To test this hypothesis Chiu and colleagues recently conducted a meta-analysis of controlled feeding trials to determine the effect of fructose on two markers of fatty liver. They considered two types of trials – one where fructose was exchanged for other carbohydrates without affecting calorie intake, and the other where diets were supplemented with fructose thereby increasing the energy intake.

The researchers found that when calorie intake was constant fructose had no effect on markers of fatty liver. But overfeeding with fructose was associated with increases in both markers of fatty liver. They concluded that the adverse effects observed in the latter trials may be due to excess calorie intake rather than fructose per se.

The authors noted that the small number of trials available for inclusion in their meta-analysis was a limitation. They identified a need for larger, longer, high-quality trials of the effect of ‘real-world’ intake patterns of fructose on markers of fatty liver in at-risk populations.

Summary

For people with fatty liver, regular physical activity and 5-10% weight loss in those who are overweight are the best ways of managing the problem. Because these lifestyle measures also improve insulin sensitivity they will have beneficial effects on other elements of the metabolic syndrome and lower the risk for cardiovascular disease.

The CensusAtSchool survey

CensusAtSchool is an annual nationwide survey of students’ everyday lives, experiences, opinions and interests conducted by the Australian Bureau of Statistics. Participation is voluntary so the data produced are not necessarily representative of the whole school population, just those who completed questionnaires. Nevertheless, the findings provide insight into the trends, habits, attitudes and lifestyles of Australian students.

According to the latest survey of nearly 24,000 children, about 15 percent do not consume breakfast and the figure has been rising in recent years. There is considerable variation in breakfast skipping across Australia, from 12 percent of Victorian school children to over 22 percent in the Northern Territory.

Earlier reports from the same survey have highlighted how breakfast consumption declines as children get older. Typically about 7-8 percent of primary school children skip breakfast but the figure rises to about 20 percent for children at secondary school.

An international trend

The downward trend in breakfast consumption is not just limited to children or limited to this country. About 20 percent of European adults skip breakfast. Consumer surveys in the United Kingdom also show that home breakfast occasions are declining as people opt to eat breakfast on-the-move and at work. Those who do eat breakfast at home are wolfing it down, spending just eight minutes on breakfast on weekdays compared to 15 minutes 20 years ago. It seems that everyone is just very, very busy.

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What are the nutritional consequences?

According to the latest CensusAtSchool report the most popular breakfast foods in Australia are bread, breakfast cereal, milk and juice. Forgoing nutrient-rich foods and drinks like these would be expected to have adverse nutritional consequences and this turns out to be the case. An Australian study showed that children and adolescents who skipped breakfast were much more likely to have inadequate intakes of thiamin, riboflavin, calcium, magnesium and iron. There were similar findings in a United States study, which also found 20 percent of children and nearly 32 percent of adolescents skipped breakfast. A portent of things to come?

The lost milk opportunity is important. The Children’s Nutrition and Physical Activity Survey (2007) highlighted the decline in milk consumption in girls as they moved into adolescence. Not surprisingly older girls were the most at risk of not meeting their dietary requirements for calcium. The decline in breakfast has probably contributed to this problem and can be expected to exacerbate it in the future.

The CensusAtSchool  report also found that about one percent of children drank soft drink at breakfast and another one percent ate lollies or potato chips, so obviously some parents have interesting ideas about nourishing their kids.

Could missing breakfast be a good idea?

Nutritionists are always saying that breakfast is the most important meal of the day and encouraging its regular consumption. But then again, we are in the middle of an obesity epidemic and the question arises whether skipping one of the main meals, such as breakfast, might actually help to lower daily energy intakes.

In fact, the reverse seems to be true, at least according to evidence from the United States. Two studies – one considering breakfast consumption in children and adolescents and the other considering breakfast cereal consumption in primary school children, have found inverse associations with body weight. It would appear that children who skip breakfast more than compensate for their missing breakfast calories later in the day, with relatively nutrient-poor foods.

Another US study confirmed that breakfast cereal consumption by children and adolescents was associated with lower body weight, though this study had an interesting twist – the researchers considered the sugar content of the breakfast cereals. But it wasn’t relevant. They found that kids eating sugary cereals for breakfast had lower body weights than those who skipped breakfast altogether, and they had higher nutrient intakes.

Now there’s food for thought. If a sugary cereal encourages kids to eat breakfast, facilitates the consumption of milk, increases nutrient intakes and is associated with lower body weight, is it a bad thing?

What should we do?

The decline in breakfast consumption is a problem that’s plain to see but what should nutritionists’ response be? Should we push back against the societal trend and just implore people to take the time to eat traditional breakfast foods at home? Or should we go with the trend and accept that for many people breakfast may be a milk-based drink sipped through a straw on the train or in a car?

I tend to be pragmatic on these issues. Just have a decent breakfast. And if the least worst option is a milk-based drink on the train that would be better than nothing at all, especially for those adolescent girls with low calcium intakes.

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Coeliac disease

All dietitians and nutritionists are familiar with coeliac disease – the gastrointestinal disorder suffered by about one percent of the population. It’s due to an inflammatory response to gluten, a protein found in wheat, rye and barley, which damages the gut wall resulting in malabsorption of nutrients leading to gas, distension, diarrhoea and weight loss. Adopting a gluten-free diet provides great benefits to those with coeliac disease but it has long been thought that such a diet offers no benefit to people without the condition.

What about gluten sensitivity?

More recently, a hypothesis has emerged that there is a spectrum of reactions to gluten with full-blown coeliac disease at one end and mildly irritable bowel at the other. The term gluten sensitivity has been coined to describe the “no man’s land” in the middle. If it’s true, millions of people could be affected. But gluten sensitivity is almost impossible to diagnose as the gut wall is not damaged and there is no diagnostic biomarker. So, if you have tummy troubles and they seem improve when you go on a gluten free diet, well, maybe, perhaps you have gluten sensitivity.

However, there is hardly any scientific evidence that gluten sensitivity actually exists. The scant scientific literature uses terms such as ‘emerging concept’ or ‘evolving paradigm’ or ‘hypothesis’.

Two recent trials

Just a handful of randomised controlled trials have been conducted to assess whether gluten sensitivity is real, two of them by the same research group in Melbourne. In the first trial subjects thought to have gluten sensitivity ate bread and muffins containing gluten or similar control foods without gluten. Their bowel symptoms got worse on the gluten-containing foods so it appeared that gluten sensitivity could be real.

However, in the second study the same researchers were careful to limit confounding dietary factors. Importantly, the 2-week run-in diet was low in FODMAPS – fermentable, oligo-, di- and monosaccharides and polyols known to produce gas and distension. Although subjects for the trial were presumed to have gluten sensitivity, their symptoms improved on the run-in diet low in FODMAPs. But when they were challenged with gluten no adverse effect was observed. The researchers concluded:

These … studies showed no evidence of specific or dose-dependent effects of gluten in patients with [non-coeliac gluten sensitivity] placed on a low FODMAP diet… These data suggest that [non-coeliac gluten sensitivity] … might not be a discrete entity or that this entity might be confounded by FODMAP restriction, and that … gluten might be not be a specific trigger of functional gut symptoms once dietary FODMAPs are reduced.

The current diet craze

That’s the science but let’s face it, all the scientific facts in the world are never going to get in the way of a good diet craze like the current gluten-free mania. TIME labelled the gluten-free movement as Number 2 on its top 10 list of food trends for 2012. Gluten-free options are popping up on menus all over the United States. Earlier this year the NDP Group, a leading information company, reported that one in every three American adults claimed to be cutting down on gluten or avoiding it altogether… and it’s growing. According to NDP “This is the health issue of the day”.

Health issue? What’s the health issue exactly?

To get a deep understanding of the benefits of going gluten-free one has to rely on insights from a long line of celebrities. Gwyneth Paltrow apparently found that going gluten free has made her feel lighter and more relaxed. Prior to going gluten-free, Gwynnie says she had “a lot of unexpressed anger. I made everyone else’s feelings more important than my own. I’d suck it up and then be alone in my car yelling at traffic or fighting with hangers in my closet when they got stuck together.”

Miley Cyrus told her fans that “Everyone should try no gluten for a week. The change in your skin, physical and mental health is amazing.” Elisabeth Hasselbeck has apparently discovered myriad benefits of a gluten-free diet, including the alleviation of autism. Victoria Beckham, Miranda Kerr and the appropriately named Lady Gaga have reportedly embraced a gluten-free diet as a means of losing weight.

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Who’s spreading all this bulldust?

OK, it’s time to put your Sceptical Nutritionist hat on. Given that there is negligible evidence that a gluten-free diet will provide any health benefit to 99% of the population, what’s driving this diet craze? How do celebrities in the United States, Britain and Australia simultaneously come to a collective belief that a gluten-free diet is amazingly good for you? Why are two of them – Paltrow and Hasselbeck – so convinced of the benefits that they have written books on the topic? Coincidence?

Celebrities earn a living from being famous which provides opportunities for endorsements. But why the sudden collective endorsement of the gluten-free diet? This has got ‘public relations campaign’ written all over it.

But who is writing the cheques? Who stands to benefit from a jihad against wheat and other grains?

Brave new world

Welcome to the brave new world of global food marketing. If conventional nutrition science gets in the way of business the way forward for your industry is clear: Firstly, concoct a baseless health campaign. Then recruit a gaggle of celebrities to carry the message directly to the general public. It’s important to bypass nutrition experts altogether. After all, who needs an informed voice of reason when you have testimonials from celebrities? And then you roll the campaign out globally.

The idea is not to promote your own food category but to damage a competitor category, changing the paradigm of what comprises a healthy diet in the process, at least in the minds of the star-struck public.

It’s issues management on a global scale. Very cynical but very effective.

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Targeted taxation of foods

The rationale for targeted taxation of foods to improve health draws on the fundamental economic principle that the demand for any good is related to its price. If the price goes up, the demand goes down, and vice versa. Hence the demand for goods is said to be ‘elastic’. Viewed through this prism, addressing diet-related chronic disease becomes straightforward – use the tax system to increase the price of junk foods and lower the price of healthier foods. Too easy.

Taxing saturated fat

The Danish approach was to apply a tax to all foods with a saturated fat content above 2.3%. Dear oh dear – flawed science from the very beginning. Readers of this blog will know that ‘Limit saturated fat’ is no longer evidence-based advice. Lowering dietary saturated fat only lowers the risk for heart disease when it is replaced with unsaturated fats. Replacing saturated fat with carbohydrate has no effect on coronary risk, yet this is precisely what the Danish fat tax encouraged.

As the saturated fat level was set low at 2.3% the tax effectively became a tax on all fatty foods – it applied equally to both butter and unsaturated vegetable oils. So rather than encouraging the replacement of saturated fat (butter) with unsaturated fat (oils), the tax encouraged the replacement of both fats with carbohydrate. The carbohydrate-for-saturated fat exchange has no effect on the risk for coronary heart disease but the carbohydrate-for-unsaturated fat exchange actually increases risk. As this has been known since 2009 there was really no excuse for introducing a flawed policy initiative two years later.

Even earlier in 2007, in a thoughtful paper titled ‘Could targeted food taxes improve health?’ academics from the University of Oxford highlighted ‘unintended potentially detrimental effects’ of taxation applied to saturated fat. Here are some extracts from their paper:

When designing the best outcome taxation strategy, we found it hard to achieve a reduction in serum cholesterol: when taxing broad categories of foods, if the intake of saturated fat is reduced the intake of other fats such as polyunsaturates and monounsaturates is also reduced. The reduction in intake of polyunsaturates and monounsaturates causes a rise in serum cholesterol that counters the fall achieved from the reduction in saturated fat.

… we observed that reducing saturated fat consumption tended to increase salt consumption and that fruit consumption tended to fall as a result of taxation on milk and cream … [and that this might] … result in more deaths than it averts.

With both nutrition science and specific studies into the effects of taxing saturated fat clearly indicating it was a flawed concept you have to wonder why it was agreed to proceed.

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The public response

Predictably the fat tax was disliked by food producers and retailers but it was the response from consumers that brought the tax unstuck. When the price of cheese went up following the introduction of the tax the expectation was that demand for cheese would go down. Instead, many well-to-do Danes jumped in their cars and crossed over into Germany to stock up with their favourite cheeses at lower prices. Less well off people just bought cheaper cheese. So the price signal from the tax affected human behaviour but not in the intended way. The rationalism of economics only goes so far when it rubs up against the deep engagement that people have with their food.

Butter consumption actually went up after the introduction of the tax, the result of a popular cooking show extolling the virtues of butter – a temporary win for the dairy industry and the taxman but not the result that public health advocates were looking for.

Better health or better revenue?

When announcing the repeal of the tax Mette Gjerskov, the Danish Minister for Food, Agriculture and Fisheries, stated “The fat tax is one of the most maligned we [have] had in a long time … Now we have to try improving the public health by other means.”

In a frank moment she might have conceded that this exercise wasn’t really about public health at all. Had the fat tax been a genuine public health initiative the Danish government would have deployed all of the revenue from the tax towards lowering the price of healthier foods, but this did not occur. Like most governments in Europe the Danish government is strapped for cash and the fat tax was just a revenue-raising exercise dressed up as a health policy.

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Furthermore, the fat tax was regressive. As low income earners spend a greater proportion of their income on food than high income earners, the fat tax had a greater financial impact on the less well off. Also, without an associated fall in the price of healthier foods one effect of the fat tax was to force those in the poorer sections of society seek out cheaper products, with potentially adverse nutritional implications.

Opportunity lost

The experiment with the fat tax in Denmark has been a failure, the death knell for such taxes around the world. Should any future initiatives for such a tax be suggested the critics will point to the Danish example and say “It has been trialled and it failed”. In a related decision to the repeal of the fat tax the Danish tax ministry cancelled plans for a sugar tax. Just days before, plans to impose a tax on sugary drinks in California were canned.

The opportunity for improved public health nutrition through targeted taxation of foods has been squandered by a combination of poor science and ulterior motives.