Sugar addiction: The myth re-visited

I have previously blogged on the myth of sugar addiction[1] but I return to that subject today on foot of some recent publications. The first is a chapter in a new book on sugars and health and the section that attracted my attention was an explanation of the rat studies, which first suggested that sugar was addictive[2]. The late Barley G. Hoebel carried out these studies. Rats were given either a 24-hour access to a 10% sugar solution or a 12-hour access to the same solution. Both groups of rats had access to a standard rat diet, perfectly balanced for the nutritional needs of this species. Rats live with a “dark” and “light” cycle of about 12 hours each and it is only during the dark period, when the lights are switched off, that rats eat. In this particular study, the rats in the 12-hour arm of the experiment, only received their sugar, some four hours after the start of the dark cycle. It was well known that if during this dark eating cycle, a rat is deprived of food for the first few hours, then, when presented with the food, the rat will gorge itself on the food and will fully compensate for the period of denial. So when the rats were offered their 10% sugar solution, having spent four hours without access to this highly palatable food, they did precisely as predicted: they gorged.  In fact, during this period of gorging, they amassed 30% of all their daily calories. Thus, without knowing the subtleties of rodent dining protocol, one would happily conclude that when rats were given a sugary solution for a limited period of time, they behaved like alcoholics let into a free bar after a period of booze restraint. Now what about the rats that had access to this sugary solution over a 24-hour period? Well, they consumed exactly the same amount of sugar as their binging, apparently addicted fellow rats that had just 12-hour access. And just to cap it all, neither group of rats went on to become obese as they simply reduced their intake of the standard rat diet. The “addicted” rats showed all the classic neurological signs of addiction including opioid withdrawal when the sugar is removed or when they are treated with opioid blocking drugs. However, the relevance of these studies to humans using this bizarre model is zero.

Which brings me to the second study led by Professor Gary Frost from Imperial College London[3]. This study used the Yale Food Addiction Score  (YFAS). Most criteria to measure addiction are based on clinical models but the Yale version is specifically designed to examine the hypothesis of food (fat and sugar) addiction. The researchers conducted a weight loss intervention study in 178 severely obese subjects (mean BMI of 36.1 kg/m²) taking part in a weight loss programme, which used behavioural therapy to reduce body weight over a 6- month period. They hypotesised that those patients that showed signs of food addiction according to YFAS would be the least successful in weight loss and that significantly more of those with food addiction would drop out. Both hypotheses were shown not to be valid. There was no difference in weight loss between the two groups and there was no difference in attrition. This is by far the largest study to examine food addiction in relation to weight loss.

Consider a study in which alcoholics and social drinkers are compared for their ability to abstain from alcohol or to minimise their alcohol intake. The predicted outcome would be that the alcoholics would fare much worse because their addiction to alcohol is so strong. But that doesn’t happen with this measure of food addiction. In all, some 15% of subjects were declared food addictive at baseline which tallies with the general range seen among the obese population seeking treatment (15-20%). Their “addiction” to food as measured by the Yale scale is so weak that it is simply over-ridden by a behavioural therapy programme.

All in all, while the concept of food addiction might seem attractive, the biology just doesn’t stack up. But, in the area of public health nutrition, why lets the facts spoil a good media story!

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[1] Food and addition blog

[2] Are Sugars addictive? Perspectives for practitioners, by Rebecca LW Corwin and John E Hayes in “Fructose, High fructose corn syrup, sucrose and health, edited by James M. Rippe and published by Humana Press (2014) 

[3] Lent MR et al (2014) Obesity, 22, 52-55

The big fat debate ~ don't blame nutrition: blame epidemiology

Normally, my blogs are built around a recently published scientific paper of relevance to public health nutrition. This week’s blog is a rant. It is a rant against the tsunami of second-rate science that dominates the media and that confuses the consumer allowing all sorts of drivel to be peddled as nutritional science. The truth is that the great majority of these stories are based on nutritional epidemiology, an academic area that gathers vast amounts of data on people and uses statistical models to sort the wheat from the chaff. Their statistical models are bound by the “known knowns” but they necessarily exclude the “known unknowns” and the “unknown unknowns” and thank you, Donald Rumsfeld for this addition to our lexicon. For example, a journalist writing in the Irish times cited a paper, which was built on such epidemiological models relating sugar to cardiovascular disease and ended up by quoting the publication asserting that as the % calories from sugar in the diet rose, the risk of cardiovascular disease rose by some huge figure. The journalist argued that the higher sugar intakes “led” to a rise in cardiovascular disease. It didn’t because there was no intervention that would “lead” anyone anywhere. The statistical model implied so and that implication was limited by the constraints of the “known knowns” of the statistical wizardry. But there was no experiment in which subjects had their diet manipulated and then followed to look for changes in cardiovascular risk factors such as might be measured in blood or detected by imaging or simple monitoring blood pressure. No, this study, like all epidemiological studies does not prove cause and effect. They are merely interesting observations of association awaiting confirmation by the science of experimental nutrition.

No matter what the nutritional challenge is, there are normally, with some few exceptions, the means to experimentally test the observed associations of epidemiology. As the Nobel Laureate in Immunology, Sir Peter Medawar wrote: “If politics is the art of the possible, then science is the art of the soluble.”

This rant is written in the heart of the Chianti region of Tuscany where village shops abound in beautiful fresh fruit, vegetables and legumes, fresh fish, lean meat, nuts, breads and of course beautiful red wine.  This is the Mediterranean diet and unless you’ve been a hermit here in Europe for the last 30 years, you will know that the Mediterranean diet is the most healthful on the planet.  Or so the epidemiologists told us. But it took a consortium of Spanish scientists and their funders to put in place the critical test of the hypothesis that the Mediterranean diet was all it was cooked up to be. The Predimed[1] study, as it is called, had the following design as outlined in the abstract: “In a multicenter trial in Spain, we randomly assigned participants who were at high cardiovascular risk, but with no cardiovascular disease at enrollment, to one of three diets: a Mediterranean diet supplemented with extra-virgin olive oil, a Mediterranean diet supplemented with mixed nuts, or a control diet (advice to reduce dietary fat). Participants received quarterly individual and group educational sessions and, depending on group assignment, free provision of extra-virgin olive oil, mixed nuts, or small nonfood gifts. The primary end point was the rate of major cardiovascular events (myocardial infarction, stroke, or death from cardiovascular causes). On the basis of the results of an interim analysis, the trial was stopped after a median follow-up of 4.8 years”.

The outcome was clear. Both the intervention diets reduced cardiovascular disease by about 30%. Now we have experimental data to search, analyse and interpret, knowing that the data is the outcome of a dietary intervention study. Some may not like the outcome and some may criticise the design or query its policy implications. But in as far as is humanly possible, this consortium of Spanish scientists has adhered to the correct scientific rigour and has not stopped at epidemiological observations.

The media simply do not get this vitally important difference of an association between two factors and a proven effect of the causative factor (the Mediterranean diet) on the effect under study (cardiovascular disease). Consider for example the major feature article, which recently appeared in Time magazine by Brian Walsh. The work of the epidemiologist Ancel Keys, who first presented evidence of a link between saturated fats and heart disease, is rubbished in this article. But Walsh never once refers to the follow up to that epidemiological observation. Both Keys and his colleague Pepe Grande subsequently conducted multiple dietary intervention studies in psychiatric hospitals in which the major part of protein, carbohydrate and fat were provided as milks with the subjects allowed a small selection of vegetables. The results were conclusive. As the % calories from saturated fats rose, blood cholesterol levels also rose while when polyunsaturated fats were increased, blood cholesterol levels fell. In fact the effects was so consistent that a set of predictive equations were established which can still operate today. Decades later, Martijn Katan at Wageningen University in the Netherlands, also concluded several dietary intervention studies which showed a role of olive oil type fats (monounsaturated) and an undesirable effect of trans fats. Once again, a rich stream of experimental data could inform policy. Indeed, Katan still operates a web-based tool for calculating how blood lipids change in response to changes in the composition of dietary fats (http://www.katancalculator.nl).

None of these dietary intervention studies appears in Walsh’s article. He relies solely on epidemiological studies. He argues that nutritionists were wrong to advocate a low fat diet. We didn’t. Going back as far as the first set of dietary guidelines issued in the mid 1970s by Senator George McGovern, nutritionists asked for a modest reduction in fat intake (from 40% to 35 % of energy) but with major reductions in saturated fat intakes (based on experimental evidence). To this day, that advice still persists within national and international bodies that are charged with issuing dietary advice. It was the media, the food industry and the “pop nutritionists” which sold an ever-decreasing fat intake as the holy grail of diet. We in nutrition knew back then that a low fat diet would raise blood triglycerides and re-shape that structure of the so-called bad cholesterol LDL, into a higher quantity of very small and dense LDL particles. We in nutrition also knew that studies on fasting subjects, which epidemiologists insisted on using, bore no relation to the manner in which the body metabolised fats after a meal, an area, which is today’s new “hot topic” in nutrition.

Public health nutrition has benefited greatly from the theories that nutritional epidemiology has generated. But public health nutrition that eschews experimental evidence where it exists, will ruin the public’s confidence in nutrition. So to those readers who influence policy in whatever way, might I ask that henceforth, any story you come across, which claims to link some nutritional pattern with some health outcome, should ask the following question: “Is the study based on a dietary intervention that allows cause and effect to be established?” If it isn’t, tread carefully until the evidence emerges from the true scientific tradition of experimentation.

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[1] R Estruch et al (2013) N Engl J Med 368 1279-1290

US Salt intake ~ No change in 40 years

In 1977, The US Senate Select Committee on Nutrition and Human Needs issued the 1^st edition of Dietary Goals for the United States. One of the recommendations was to: “Reduce salt consumption by about 50 to 85 percent to approximately 3 grams per day”. This equated to 1,200 milligrams of sodium, which is the element of salt (sodium chloride) implicated as a contributory factor for the development of hypertension. This is slightly below the current sodium recommendations of the American Heart Association of <1,500 milligrams per day but is half what the Institute of Medicine set out as a target for the US population in its most recent report on dietary guidelines (2,300 milligrams per day). Whatever the figure, which the public is blissfully ignorant of, a campaign to lower salt intake has been in operation now for almost 50 years. Two recent papers have looked at the pattern of salt intake in the US over that period.

Measuring salt intake in our diet is very difficult because, over the short periods that dietary surveys are completed (1-4 days) salt intake can fluctuate dramatically. An equally important limitation in this area is the accuracy of food composition tables as to salt levels in foods. It should be noted that over 80% of salt intake comes from foods and not the saltcellar. Thus an alternative to measuring salt intake is to measure salt excretion, specifically sodium excretion, since the body does not normally accumulate sodium and thus the quantity excreted over 24 hours should roughly equal the amount ingested over the same period.

Collecting all ones urine over a 24-hour period is very difficult. The subjects have to carry a 5 liter plastic container with them throughout the day and everywhere they go and they have to bring the container to the bathroom to collect all of the urine excreted at each urinary event. Thus, not surprisingly, such studies tend to have relatively small numbers. Researchers at the Harvard School of Public Health searched the literature for all studies that involved a 24-hour urinary sodium excretion measure among US citizens over the period 1957 to 2003[1]. They found 38 studies. Of these, 5 were large with an average of 2,900 subjects but the remaining 33 were relatively small with an average of <400 subjects per study. The average daily output of sodium in milligrams per 24 hours was 3,526 prior to 1980, 3,418 across the ‘80s, 3,499 across the ‘90s and 3,849 post-2000. Thus over the 40 years from the 1970’s, there was no significant change in daily sodium excretion and the estimated average daily intake of sodium was 3,526 milligrams per day, well above any of the dietary guidelines issued.

Recently, another study on trends in sodium excretion was published in which a single urine sample (“spot” urine sample) was used to extrapolate to a 24-hour sodium excretion using adjustment equations set about by an international research consortium called INTERSALT. In this study, they used random samples from the US National Dietary Surveys[2].  Overall, they also found no change in sodium excretion over the period 1988 to 2010 (3,160 mg/d for 1988-1994, 3,290mg/d for 2003-2006 and 3,290 for 2010). This equated to a daily sodium intake of 3,317 milligrams per day, which is very close to what the Harvard researchers found.

What do we take from these findings of a complete resistance to change in sodium intakes? Reducing sodium in the human food chain is quite different to reducing the levels of fat or sugar (the other two so-called  “evils” of modern food). There are techniques and technological solutions, which allow sugar intake to be reduced without a loss of sweetness and also for fat reduction without the loss of the mouth feel of fat. That is not the case for salt. If the level of salt intake is reduced in breads it needs to be done over a long period so that consumers slowly adapt their palate to lower salt levels.  There is no adequate sodium alternative.

There is a second way to look at these data. According to the Darth Vaders of public health nutrition who would protect us all from the inferior aspects of the  modern diet, the food industry has dramatically manipulated salt, fat and sugar levels in foods over the last 40 years to manipulate our palate and their sales. As Michael Pollan put it in his book “In Defense of Food”:

“Today foods are processed in ways specifically designed to sell us more food by pushing our evolutionary buttons-our inborn preferences for sweetness and fat and salt”.

If salt intake hasn’t changed between the early 70’s and today, a 40-year period, then, has the food industry failed in their attempts to push our evolutionary button for salt preference? To me, the most likely explanation is very simple. Those who promulgate a food conspiracy, do so without addressing the available evidence on food and nutrient intake patterns, which should guide their thinking. But regrettably, when individuals set our their stance on some issue of science, it is rarely for changing, whatever the data might say.

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[1] Bernstein AM & Willett WC (2010) AJCN 92, 1172

[2] Pfeiffer CM et al (2014) J Nutr 144, 698

Organic food does not protect against cancer

The Soil Association[1] was founded in 1946 and today is the main body for the certification of organic farms in the UK. It’s website has a section on pesticides, which states the following: “Around 31,000 tonnes of chemicals are used in farming in the UK each year to kill weeds, insects and other pests that attack crops. There is surprisingly little control over how these chemicals are used in the non-organic sector and in what quantities or combinations. What we do know is that 150 of the available 311 pesticides commonly used have been identified as potentially causing cancer and many of us would have been exposed to these pesticides before we were born”. It then goes on to state: ”Even food that we think is healthy, such as non-organic Cox's apples, can be sprayed 18 times. The most dangerous chemicals used in farming, such as organophosphates, have been linked with a range of problems including cancer, decreasing male fertility, foetal abnormalities, chronic fatigue syndrome in children and Parkinson's disease”. This linking of organic food with a reduced exposure to so-called cancer-causing pesticides is a widely held belief among organic food advocates.

That view within the organic movement is unlikely to be changed by a recent study refuting this belief but the majority of people who are made to worry about this alleged pesticide-cancer link will take solace from its findings. The paper, published in the British Journal of Cancer[2] was based on data from The Million Women study, which was based on a million women screened for breast cancer, followed these women over a 12 year period with questionnaires on lifestyle completed at baseline and at years 3, 8 and 12. In the year 3 questionnaire, women were asked about their consumption of organic food within categories, “never”, “sometimes”, “usually” or “always”. A total of 751,975 provided data on their organic food intake in year 3. In this particular study part of the study, women were excluded if they had changed their diet in the previous 5 years because of an illness. That then left the researchers with data on 623,080 women.

At the outset of the study, 30% of women reported never consuming organic food, 63% sometimes consumed organic food and 7% reported always or usually eating organic food. During the follow up period of almost 9 years, a total of 53,769 women were diagnosed with some form of cancer. The authors looked at the relative risk of 16 cancers across the frequency of use of organic food. They controlled for age, area of residence, body mass index, smoking, physical activity, alcohol intake, age at first birth, fibre intake and type of meat intake. Compared to women who never consumed organic food, there was a 9% greater incidence of cancer among women who usually or always consumed organic food. The one exception was Non-Hodgkin Lymphoma (NHL) where those who usually or always consumed organic food had a 21% lower risk of NHL than women who never consumed organic food.

Already the organic movement is claiming that the 21% reduction in NHL is proof that pesticides are a causative factor in cancer. However, NHL in the UK accounts for just 4% of all cancers. Thus there were 161,215 cases of cancer among UK women in 2011 of which 155,358 or 96% of all cases did not involve NHL with cancer of the breast, bowel, lung, uterus and ovaries accounting for 62% of all cancers[3]. No matter what way the organic advocates dredge the data, the simple fact remains that the consumption of organic food had no overall protective effect against cancer (indeed it was 9% higher in the organic food consumers).

Plants maintain a natural defence system against pests and thus the overall load of exposure to natural pesticide is enormous concerned to our exposure to pesticides used in agriculture whether for commercial or organic agriculture. Data shows that using the rodent carcinogenic model, of the plants natural pesticides, 55% were positive carcinogens and 45% were not[4]. All available data show that about half of all naturally derived chemicals are positive in the rat carcinogenic model. The figure for all synthetic chemicals is also about 50%. Natural doesn’t equate with safety. Think of hemlock, magic mushrooms, opium, caffeine and nicotine to name a few.

People make all sorts of decisions about their lifestyle including diet. Some opt to be vegetarian. Some prefer to eat organic food. Some choose food based on a perceived allergy. The reasons are endless. So live and let live but please don’t preach about the health virtues of organic food to consumers who are not so inclined for whatever reason. Enjoy your food whatever your choice and let others enjoy theirs. There are many great challenges facing us in terms of public health nutrition. This paper, the first of its kind, has binned the claim of the organic food movement that consuming conventionally farmed foods can lead to exposure to cancer causing pesticides.

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[1] https://www.soilassociation.org

[2] Bradbury KE et al 2014 March 24 (e print ahead of publication)

[3] http://www.cancerresearchuk.org

[4] Ames BN & Gold LS (1997) FASEB J. 1Nov;11(13):1041-52