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Tuesday, July 22, 2014

Super-foods, super-diets and pseudo science

From time to time, certain  “super-foods” and “super-diets” emerge to dominate the menus of fashionable restaurants and chique delicatessens. The most recent super-food has been quinoa (pronounced KEEN-wah). Apparently, it will treat hypertension, diabetes is a natural appetite suppressor and is anti ageing[1]. In fact, the UN Food and Agricultural Organization deemed 2013 to be “The Year of Quinoa”[2]. The Director General of FAO stated that “…quinoa can play an important role in eradicating hunger, malnutrition and poverty”. The facts are however somewhat at variance with this view of quinoa as a super-food. Firstly, it is stated that its protein quality is unique in the plant world in that it is complete in all the 8 essential amino acids. This leaves the non-expert think that some plant foods therefore lack one or more essential amino acids. Not so. All plant proteins contain all amino acids but they vary in the relative amount of each. To rank the quality of a protein, its “protein digestibility corrected amino acid” (PDCAA) score is calculated. Three proteins gain a perfect score of 1.0: two of animal source, egg and whey protein and one of plant origin, soy protein. According to an entry in Wikipedia (most Internet listings for quinoa are from advocacy groups), quinoa, along with amaranth, buckwheat, hempseed, and spirulina fall below 1.0 but they are still called complete proteins because they contain sufficient of all the nine essential amino acids to meet the dietary needs of man[3]. So, quinoa is hardly unique despite its hype. If we turn to protein levels, we find that the following are the levels of protein in average servings of some plant food: amaranth, 3.8; rice, 4.0; beans, 15.0; lentils, 18.0 and soybeans 29.0[4]. Again, this hardly qualifies quinoa as a super-food. Quinoa is putatively “packed” with dietary fibre. An average serving of quinoa has the same amount of fibre as amaranth (5g) which does not compare well with other plant foods: lentils with 16g per serving and both beans and soybeans with 30g. Quinoa is also a truly marvelous source of antioxidants but most of these are simply natural bioactives and not nutrients and there is no serious data linking such plant bioactives to the incidence of chronic disease or risk factors for chronic disease. The hype on quinoa has caught the interest of researchers. Thus in the 20 year period from 1991 to 2011, PubMed lists 20 studies published on quinoa. In the last 2.5 years, a further 20 were added to the literature. According to the Wall Street Journal, there was a 9-fold increase in quinoa imports to the US between 2000 and 2007 and the price per pound almost doubled. This is all good news for the Andean farmers who grow it but not for the Andean people who rely on this crop as a staple food. Quinoa is more likely to grace the shelves of niche food stores in Manhattan to feed the worried well than it is to feed the billion people who go to bed hungry every night.
Besides super-foods we have super-diets and to illustrate the nonsense of super-diets, I will draw heavily on the writings of Harvey Levenstein in his book: “Fear of Food[5]” and specifically the chapter on “Natural Foods in Shangri-La”.
Sir Robert McCarrison (1878-1960), a medical doctor with the British Army in India, toured a remote valley at the foot of the Himalayas, now in Kashmir, Pakistan, which was the home of the Hunza people, the Hunzakut. He attributed their longevity and their physical and sexual fitness to their diet of unprocessed natural foods of milk, eggs, grain, fruit and vegetables. In the late 1940’s a former employee of the US Inland Revenue Service, wrote a book on the Hunzakut, never having visited the region. His book began to attract some attention and by 1957, the New York Times chief foreign correspondent visited the Hunza valley and confirmed that indeed the inhabitants lived to a very old age on a diet of dried apricots and powdered milk. Films were made featuring the Hunzakut and more books were written on their great health, physique, longevity and sexual prowess which persisted well into their 90s. In 1959, President Eisenhower’s cardiologist had an air-force doctor fly to the Hunza valley to check out there cardiac function and sure enough, a perfect bill of health came back. He added: “ A man in really good shape can eat up to 3,000 apricots in one sitting”! If it takes say 20 seconds to eat an apricot, then an apricot feast would last over 16 hours!!! The Hunza fever in the US reached the dizzy heights of an editorial in the Journal of the American Medical Association[6]. Then in 1956, a US geologist set up a small clinic in the Hunza Valley and was instantly inundated with cases of malaria, dysentery, parasitic infestations and symptoms of vitamin deficiency. He noted that in Spring, the entire valley ran out of food and starved until the barley harvest arrived. The Mir who ruled the valley, owned 25% of the land and of course was well fed as were his lackeys. He did visit the clinic to be treated for dyspepsia, requiring an ant-acid for relief. Subsequent visits by British, Japanese and French physicians confirmed widespread deficiency diseases such as goiter, a deficiency of iodine. Malnutrition was found to be rampant. Hunzamania is still rampant. You can buy on Amazon “Crystal Energy Hunza Water” and if you buy 2 you get 1 free[7]. How much? US $99.99!!

The fashion for super-foods and super-diets isn’t new and we will see quinoa slip in favour of the next fad. Its mainly pseudo-science.

[5] Fear of Food is published by Chicago University Press (2012)
[6] JAMA (1961) February25th. “Longevity in Hunza land”

Friday, July 4, 2014

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!

[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

Monday, June 16, 2014

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 (

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.

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

Thursday, April 24, 2014

US Salt intake ~ No change in 40 years

In 1977, The US Senate Select Committee on Nutrition and Human Needs issued the 1st 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.

[1] Bernstein AM & Willett WC (2010) AJCN 92, 1172
[2] Pfeiffer CM et al (2014) J Nutr 144, 698