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Monday, May 28, 2012

My popular book on food and health:"Something to chew on: Challenging controversies in food & health"

Today’s blog is something of a cheat. It simply lays out the content of the individual chapters of my new book:’Something to chew on – Challenging controversies in food and health’. I wrote this book to help the average person to gain some understanding of the mainstream science of food & health and in so doing to de-bunk many common myths and misperceptions. The book is available at, at and If you are so inclined, you can “like” the Facebook page of the book here.

Something to chew on
Challenging controversies in food and health
Mike Gibney
Chapter summaries

Chapter 1: With regard to food

This chapter sets the scene for the book. It describes the evolution of the modern food supply beginning with the era of widespread malnutrition in the most developed economies from the turn of the 20th century.  The extent of this malnutrition was exacerbated by two world wars either side of a great economic depression.  Following the end of World War II, a remarkable period of investment in science and technology emerged as the global economy expanded. Agricultural output and efficiency soared and as more women entered the work force, the demand for more convenience food and the necessary kitchen technology to use these new products was developed. Food companies grew by mergers and acquisition and the great retail giants emerged. The era of cheap and abundant food had arrived. During this post war period the science of human nutrition also evolved from a century of researching what was essential to sustain life to an era of researching what was necessary for optimal health. Nutrition had arrived on the political agenda. And then the Vietnam War started an era of challenge of the military industrial complex and the concept of people power emerged from the hippy and civil rights movements in the US to the student riots of Europe. Now an era of mistrust in science and technology evolved and the green movement began to shape the political agenda. And food now came under the microscope. The public got scared of high tech food with an increasing mistrust of the food industry which was blamed for food scares and an epidemic of obesity. That led to the development of a rapid expansion of interest in organic and ethical food. The advent of the BSE crisis obliterated the reassurances of the government in the safety of the food chain and the arrival of genetically modified foods heightened this mistrust. This book looks at all these challenges to the human food chain and attempts to give a scientific dimension to what are often emotional issues surrounding concerns about food.

Chapter 2: Sugar and spice and all things nasty

Plants abound in natural chemicals which exist for normal plant function including germination, growth, reproduction, repelling pests and attracting the birds and bees. It is these that give plant food their beautiful colours and their delicious tastes and flavours. They also give rise to a wide array of natural plant compounds from pure poisons (hemlock), to the downright dangerous (cocaine, nicotine) and onwards to natural plant compounds which have healthy properties (which lower blood cholesterol or which lower blood pressure). Irrespective of their effects on man, these natural compounds are not regulated. They are after all natural. Man-made chemicals are very strictly regulated and this chapter deals with food additives, pesticides and contaminants as examples of man-made chemicals all of which must prove they are safe to enter the food chain. The toxicity of the natural and man made compounds are compared showing an equal if not a greater burden of risks from natural compounds. It also deals with the practice of adding nutrients to foods through food fortification. Finally, this chapter challenges the myth that organic food is more nutritious, more tasty, more flavoursome and more environmentally friendly than conventionally grown crops.    

Chapter 3: Modified foods: genetic or atomic?

The human food chain has been genetically manipulated from the dawn of agriculture and this chapter examines the present scare about genetically modified foods. It first describes conventional plant breeding which is preferred by the environmental groups in their vigorous opposition to GM crops. The common belief is that conventional crop breeding is a loving task of nature carried out by a devoted plant breeder out in the field.  This is not so. Conventional plant breeding involves hitting thousands of plants with levels of atomic radiation 100 times stronger than that used in the application of radiation to cancer therapy. The plants genome is rattled to bits and the vast majority of the mutants die. But some survive and go on to exhibit new properties which can then be crossed back with the normal variety in the hope of transmitting the new desirable trait. The UN International Atomic Energy Agency champions the use of atomics radiation to induce mutations and boasts over 2000 crop varieties in existence today developed using this totally unregulated technology. In contrast, for GM technology, the genes to be inserted are known in advance to be linked to some desirable characteristic and only these genes are inserted. The chapter challenges the claims of environmental groups that GM foods are a danger to human health and to the environment.

Chapter 4: The metrics of food and health

We are constantly learning from reports in the media about new findings linking some food or other with this or that disease. How is this done? This chapter looks at the tools available to measure food and nutrient intake and makes the point that they are all fundamentally flawed. All dietary surveys will encounter very significant levels of the under-reporting of the true intake of food. In simple language, it is the norm in large dietary surveys for a very significant proportion of the study population to fail to report (a) ever eating some food, (b) reporting the consumption of the food but under-reporting the frequency of consumption and/or(c) under-reporting the quantity consumed at a given eating occasion. This phenonomen might be explained on the basis that most people have one approach to food intakes on Mondays which reflects a desire to have a truly healthy week ahead and which quite often falls by the wayside later in the week. When asked to record their usual dietary patterns, survey participants frequently report the restrictive Monday type for the whole week. Thus a major problem is that in the measurement of patterns of food consumption, we simply cannot be accurate. Notwithstanding these limitations, we now seek to link dietary patterns with those of various diseases, which is the science of epidemiology. when a positive or negative association is found, it means just that, an association. It cannot prove cause and effect. To do that we need to construct an experiment in which two groups are compared where everything is identical except the test food or nutrient. We examine two contrasting cases of dietary intervention.

Chapter 5: Personalized nutrition – fitting into your genes
When you general practitioner tells you that your cholesterol is high, by high, he or she means above a reference point established in large population studies. Such studies show that on average, individuals with cholesterol values above that point have a higher than average likelihood of going on to develop heart disease. In that last sentence, the word average was used twice. Suppose now the GP could establish in this regard that you were in reality above or below average in the likelihood of developing a heart attack with your level of cholesterol. Then your advice might be a little more personalised than simply average. The mapping of the human genome in 2003 was a major step in making that possible. This chapter explores the concept of personalised nutrition by which is meant a set of nutritional advice which is targeted specifically to you on the basis of our knowledge of your genetic make up and of our developing understanding of how the human responses to changes in nutrient intakes are very mush influenced by known genetic variability. Many companies will sell you a genetic analysis and personalised dietary advice over the internet for about US $500. This chapter casts serious doubt on the reliability of this advice and explains also the great difficulty that the human food chain would have in matching true genetic requirements for nutrients with our present day retail system. However, it does try to foster the hope that in the course of time, we will reach a point where simple dietary advice on diet and conditions such as blood pressure, weight gain, cholesterol or allergy will all have some robust element of genetic analysis to sharpen the tools of preventative nutrition. 

Chapter 6: Plastic babies – the phenonomen of epigenetics and nutrition
When a foal is born, it knows immediately to stand up on all fours, to recognise its mother, to run with the herd and to interpret the sight sound and smell of danger. Its brain is hardwired and all switches in the nervous system are fully operational. In contrast, a human baby is born with quite an immature brain and for good reason. Babies born in Belfast, Burundi, Beijing and Baghdad will all have to recognise speech but speech in quite different languages. They will have to learn to behave within a society into which they are born and the social norms vary greatly across cultures around the globe. We inherit DNA from our parents and the sequence we end up with is a random mix of both - Dad’s hair, mum’s eyes. But the sequence once made is never changed. What distinguishes the foal from the human baby is the extent to which the genetic sequence is managed. Imagine the genetic sequence to be like a complex electronic code to manage a sophisticate lighting system. All the codes and their sequences for the lighting system remain unchanged. But the settings of the switches can be changed - more of this and less of that. From the pre-natal period in the womb through to the first few years  of post-natal life, we slowly and methodically make adjustments to the genetic code, not to its sequence but to the extent to which each gene in the sequence is switched up or down. Once finally adjusted, that is it for life. This chapter looks at this phenonomen and the very important role that diet plays in this tweaking of the human genome and in turn how that tweaking made in the early days of life can greatly influence our health four to five decades later. It looks at the uniqueness of human pregnancy which is necessitated by our larger brains and at the need for our genetic development and our brain development to be highly flexible at the onset of life. That is what gives us our evolutionary advantage and we will look at that in the context of man’s probable aquatic origin.

Chapter 7: Your insides out:  food - the gut and health

In recent years we have begun to appreciate that the gut is an organ which plays a central role in food and health, not just in digestion and absorption of the food we eat but in our immune system, in obesity and in our reflex actions in times of stress. The present chapter explores some of the very exciting science that is emerging from this research with far reaching consequences for food and health. The stress element of our gut  is governed by a major nervous system which has evolved quite independently from the brain. It is required to prepare us for “fight-or-flight” circumstances and is responsible for a host of common phrases such as “butterflies in your stomach” or “not having the guts” for some challenge. The bacteria in our gut weigh 1.5 kg and have 100 times more DNA than the human body which hosts them. The two have established a “treaty” in which one gives to the other in a symbiotic way. We gain energy from the fibrous foods they alone can digest and they gain access to fuels we can’t use. They actually can cause our genes to be up or down regulated to suit them and they work with us to make sure that rogue bacteria don’t break the treaty leading to sickness. In recent times, these bacteria have been shown to play a pivotal role in obesity. Rats raised in totally sterile conditions don’t get obese on diets that would normally cause obesity in a non-sterile environment. The gut will be a major focus of food and health in the future

Chapter 8: A tsunami of lard: the global epidemic of obesity

Obesity is seen as a simple problem: people get overweight because they eat more calories than they expand. That’s a bit like saying “cancer is simply a cell gone wrong”. This chapter begins by briefly explaining the biology of the diabetes associated with obesity and then moves to the biology of the control of food intake. It makes the point that rodent studies of the regulation of food intake are of interest but we have a large part of our brain, the neo-cortex, responsible for higher human functions, which overrides simple biology signals such as hunger. We refuse to eat cat food when hungry whereas a rat will readily do so. We then move to genetics and specifically to twin studies and show how powerful the heritability element of obesity is. A strong case is made in this chapter that much of the research in this area focusing on foods responsible for obesity (fast food, soft drinks, processed foods) is going nowhere largely because of the reasons outlined in chapter 4 on our poor ability to accurately quantify food intakes. The case for a greater focus on linking genetics to food related behaviour is made. Dieting is dealt with as is physical activity and the stigmatization of the obese. Finally this chapter looks at little known data on the rise in obesity pointing out that obesity has been rising in the US in waves dating back to the early 20th century. The conventional wisdom that it is simply junk food is challenged and data on inter-generational augmentation of obesity through epigenetics, discussed in chapter 6 is discussed.

Chapter 9: Greying matters – food and the elderly

This chapter outlines the dramatic demographic changes that will occur in the developed countries in the next 30 years. In some countries such as Japan and Sweden, over 1% of the population will be over 100 years by 2050. The chapter outlines the areas of aging which can be influenced by diet. The decline in the regulation of food intake and an obesigenic environment mean that we now have the phenonomen of the frail obese elderly; not enough muscle and too much fat. We look at bone health and its decline from the early part of mid life and deal with the conflicting advice on sunshine from two different camps, those concerned with skin cancer and those concerned with exposure to sunlight to get adequate vitamin D. The chapter deals with sarcopenia, the loss of muscle in the elderly and also the role of diet in declining eye sight. Finally, the chapter deals at length with memory and its decline with aging and reviews the relevant data linking diet and Alzheimer’s disease. The link between obesity in mid life and the risk of Alzheimer’s disease in the elderly is explored.

Chapter 10: Food and Health – The science, policy and politics

The role of four players in the drama of food politics is explored. First the practice of linking major multinational food companies with the problems of over-nutrition is explored and challenged.  Potatoes account for 12% of caloric intake in Ireland and have a zero advertising budget. All chocolate combined accounts for 2% of caloric intake and has a massive advertising budget. Most likely, potatoes are more important in over-nutrition in Ireland than chocolate. We look at 4 classes of scientists which range from the one wired to the laboratory and never gets involved in the regulatory side if things to the “issue advocate scientists” who get involved everywhere and push an a priori agenda. Next we look at the UN agencies and an independent analysis of their style of risk assessment and risk communication and show large shortfalls in proper procedures in the analysis of particular problems. We also look at how they can pre-empt scientific publications they don’t like with their own gloss on events. Finally we turn to NGOs who play a powerful role in our participatory democracy and the chapter accuses some NGOs of being dogmatic and anti-science.

Chapter 11: The hazards of food
This chapter explains how society assesses risk in respect of our food supply and explains the detailed process of testing for safety. It introduces the reader to the concept of risk management and looks at the EU’s precautionary principle which is being used to block innovation such as GM technology. We then look at risk communication and we show how consumers presented with the same data expressed in different ways (% who will die during treatment or % who will survive) adopt different stances. We explore the concept of “world views”, how these are acquired and how these shape the emotional response to perceived danger. The chapter argues that throwing “knowledge” at consumers will not allay their fears since these fears are frequently emotional and thus not readily open to rational argument. It contrasts how regulators (mostly scientists) see risk and how consumers see the same risk. For the consumer the fear increases as they lose control over the avoidance of the risk and as the risk gives rise to effects which are both dreaded unfamiliar (BSE). In contrast, real public health risks such as obesity are seen as controllable (“I can lose weight whenever I want”) and are both familiar and not dreaded

Chapter 12: How the other half dies

This chapter looks at the problems of global malnutrition. “Wasting” is the condition of malnutrition seen on TV, gaunt corpse-like children with zero fat beneath their skins. “Stunting “ is the condition of malnutrition where a child is too short for their age. The final form of malnutrition is that of “hidden hunger”, the blindness of vitamin A deficiency, the anaemia of iron deficiency and the goitre of iodine deficiency. The chapter argues that the global aid agencies, the IMF and the World Bank in the Thatcher-Regan era, adopted a policy in development aid of getting the fiscal system working and leaving it all to the markets. This is only slowly now being abandoned and investment in agriculture and nutrition is now back on the agenda. The chapter looks at recent books which argue that Africa is being starved of science by anti-GM and organic farming NGOs and which look at the basic geo-political reasons for the existence of the world’s “bottom billion”. The chapter looks at how malaria and HIV/AIDS is wrecking Sub Sahara Africa. The chapter ends with the Alliance for a Green Revolution for Africa led by Kofi Annan which is seeking to sink billions into improving African agriculture. This requires an investment in scientific agriculture including GM crops.

Chapter 13: Mankind and Mother Earth
Previous predictions of doom and gloom (Club of Rome, Y2K and the Ozone layer) are examined in relation to the lingering scepticism on global warming and climate change. We then look at leading climate scientists who believe they have to “sex up” the data to get attention. Thereafter the focus is on scientific facts on two vistas of the environment and the human food chain – how agriculture influences the environment and how environmental changes influences agriculture. We begin by looking at the global population and with a focus on the developing world where the main growth of population will occur. The 50% increase by 2050 in global population (6 to 9 billion) will be mostly in developing countries. Agriculture affects the environment in two ways. It produces large amounts of greenhouse gases primarily through energy demanding livestock production and through deforestation and desertification. Secondly agriculture absorbs over 70% of global water, presently at a rate where extraction from aquifers is 2-5 times the rate of re-charge with rainfall. All of the various solutions mooted are mentioned from no-till farming to drip irrigation. We also look at and refute the importance of “food miles” as quantitatively important in climate change and make the case that this is just part of the repertoire of the anti globalisation, anti-capitalism movement. Finally, we look at how changing temperatures and rainfalls will affect global agriculture. The developing world will fare worst. They will get hotter to the point where crop yields will fall; they will get longer periods of drought and heavier but more intense rainfall. In the developed world with the exception of Australia, there will be higher crop yields from higher levels of atmospheric carbon dioxide and from higher temperatures.

Chapter 14: Reflections and projections
A final chapter with a focus on the two great food tragedies of modern times: obesity and malnutrition

Monday, May 21, 2012

Food Choice: Disgust, pain and preferences

Food choice is a complex issue. At one level, we share the same biology as all animals as regards hunger, appetite and satiety. Rat studies can thus explain some of the mechanisms but they fall far short of the bigger picture because humans have a large and very complex frontal cortex, which governs all the things that make us human and not rats. It is through the cortex that we think, learn, speak and assimilate and disseminate complex ideas. More than anything else, these attributes allow us to divide labour and live in a sophisticated society and that society itself plays a major role in food choice.

In lecturing my students on food intake, I ask them to close their eyes and to think of some occasion when they were really hungry. I then tell them that when they open their eyes, the PowerPoint slide will show a food and I want to know would they eat it.  Invariably, they indicate their refusal to consume the food, which is a very nice bowl of highly nourishing and succulent cat food. They do agree that if the choice was between staying alive and eating the cat food, then they would eat it and just hope not to gag. Having recently read “How Pleasure Works” by the Yale professor of psychology, Paul Bloom, I now know that the reaction of my students is one of disgust. I also learned from Bloom that disgust is not a property of the cat food but a socially conditioned belief. Quite simply, I know of nobody and, dear reader, I would bet you know of nobody, who eats cat food. The cat food is nutritious, safe, made from high quality ingredients by branded companies for highly fussy pet owners. So there is nothing inherently disgusting in cat food. It’s simply a disgusting thing to eat by our social norms. Rats would have no qualms in eating cat food. Eating insects is disgusting to us but not to many nomadic tribes and eating pork is disgusting to a devout Muslim but not to the majority of Irish people. Paul Bloom goes on to point out that whereas society decrees what is acceptable to eat, within that framework, individuals can show disgust or more correctly, aversion to specific foods and, in general, such aversions can be related to some life experience. Thus I like fish but if given a choice, I would not eat mackerel. I still recall the stink in our kitchen at home when my father would head, tail, gut and fillet a bucket of mackerel for grilling, which he and his mates had caught in Dublin bay.

Bloom also raises another aspect of social influence on food choice: pain. Now it might seem strange to write about pain in a book on pleasure but so long as the recipient is in control of the situation, mankind likes a little bit of pain. We go to horror movies, which can be terrifying and we take amazing risks on crazy rides in amusement parks. In foods, we eat chilies and although our taste buds tell us not to do so, we overcome these because society decrees some consumption of chilies to be worthwhile. Thus in Mexico, where chili consumption is high, children are gradually weaned on to a high chili diet. Such a diet in earlier times helped give an identity to a group in much the same way as their language, music or dance did. You can imagine the fun these people had when a stranger was given their hospitality only to scream for water to cool their burning palates!

Let us now return to the physiology of taste and flavour and see how that competes with social pressure. Paul Bloom draws on a joint study carried out by the business schools at MIT and Columbia. Subjects were asked to taste two beers: a regular Boston brand or a “new” MIT beer. The latter was no more than the regular Boston beer with a dash of balsamic vinegar. The first group (the control group) were not given any information at all and simply asked which brand they preferred. They voted 60:40 for the “new” MIT beer The second group were told that the regular Boston beer was to be compared to a “new” MIT brew and they were told that this beer was just the regular beer plus balsamic vinegar. Now the vote was only 20% for the MIT brew. A third group was treated like the control group but immediately after they had drunk it and before they expressed their preference, they were told the truth: that the “new” MIT beer was just ordinary beer with balsamic vinegar added. They voted like the control – 60% preferring the MIT brew. Clearly, the latter group, like the controls, formed an opinion that if a beer came out of MIT it must be good. Having now made their minds up, the third group stuck to this assumption even though they knew that it was just a stupid concoction. The values we give to foods in making food choice are very complex. The idea that a beer from MIT had to be good goes hand in hand with our preferences for brands. Indeed, Bloom points out that studies show that Coca Cola drinkers enjoy Coke more when the glass is a Coke branded glass. Status is very important in food choice because, like the peacock’s tail, it is a symbol of ones power and status.
Rat studies are thus of limited use in understanding food choice. They might explain the mechanisms, which determine the desire to eat but not food preferences. They are socially determined to a great extent. The simpletons of public health nutrition reduce the obesity issue to a higher probability of choosing some food such a sugar sweetened beverages or fast food because that’s the simpleton’s fashion – simple and stupid. Some people make the conscious decision to take up smoking or alcohol intake. But nobody wakes up and says:” Guess what. I’m going to get fat”. It happens and we know so little about how that passive accumulation of energy occurs and how our food preferences promote this weight gain. We need less research money spent on studying why rats chose to eat or not and more money spent on human behavioural sciences, particularly food choices and preferences. 

Monday, May 14, 2012

Dietary advice with a grain of salt

Salt is one of the most ancient ingredients used as a food preservative, particularly for the preservation of meat. Roman soldiers pay was named “salarium” from which the word salary is derived because it was expected that salt would be one of their main items of expenditure. Cities such as Salzburg were associated with salt and Mahatma Gandhi marched with many thousands of Indians on the "Dandi March" or "Salt Satyagraha", where they made their own salt from sea water in a protest against the tax levied on salt by their British rulers. Today, however, salt is seen as an food ingredient which is associated with high blood pressure and drives to lower the salt levels of processed foods are operational in many countries, Processed foods provide about 90% of salt intake while the salt cellar accounts for a mere 10%.
In 1949, an MD from Durham, North Carolina by the name of Walter Kempner published a paper in Annals of Internal Medicine in which he showed a dramatic effect of a diet based on rice on a number of cardiovascular risk factors, among which was hypertension. This was a very low salt diet and thus the association between salt and hypertension had gained momentum. In 1964, Lewis Dahl, working at the Brookhaven National Laboratory in New York found that about 25% of his rat colonies were resistant to increased blood pressure when given a high salt diet. Thus he genetically bred two strains of Dahl rats, an R-strain that was resistant to salt-induced hypertension and an S-strain that was sensitive in this respect. These rats were widely used to see how salt interacted with other nutrients such as potassium, in moderating blood pressure and thus the salt-blood pressure story grew. It is important to note that by my calculations (others have done like wise and agree), the quantity of sodium ingested by these rats would translate into about 400g per day for a 70kg human. Bearing in mind that a high salt intake in free-living humans might be 15g per day, the relevance of these rat studies (as is generally the case for animal models) to human physiology is laughable.  However, a spate of poorly designed human intervention studies followed putatively confirming the rat work and so salt was served up on the first ever set of dietary guidelines published by the US Senate Select Committee in the mid 1970’s. That a reduction in sodium intake would reduce blood pressure became accepted wisdom and in the world of nutrition guidelines that is as sacred and immutable as the dogmas of the Vatican or the Kremlin.

Professor Roger McCarron of the Department of Medicine at the University of Oregon published studies, which began to criticise these data. Of course he was generally regarded as a heretic by the high priests of healthy eating. But he stuck to his guns and began to provide data that other nutrients were more important such as calcium and that obesity was a significant factor. Slowly, evidence began to emerge which suggested that a broad modification of diet might be better than  a single nutrient-based approach and so the DASH (Dietary Approaches to Stop Hypertension) trial was initiated, funded by the US National Institute of Health. This was a very large randomly controlled intervention study involving 459 adults who were put on a control diet for the initial 3 weeks. This was a typical US diet high in fat and low in fruit and vegetables. Half the subjects were then put on the same diet but with increased fruit and vegetable intake for 8 weeks and the other half also had this diet but, additionally, had high intakes of low fat dairy products together with a low fat, low saturated fat diet, again for 8 weeks. Very importantly, no changes were made to salt intake, either as table salt or salt in normal foods. The results showed that the diet high in fruits, vegetables and dairy products and low in total and saturated fat significantly reduced blood pressure to a clinically significant level in subjects whose blood pressure was normal or elevated.

But that did not detract from the salt reduction zealots who have protected their dogma with great passion. However, in 2011, a series of papers published in prestigious journals have shown that all is not rosy in the salt garden.   In 2011, an international consortium reported on an 8-year study of 3681 subjects based on 24-hour urinary sodium data, collected at the outset of the study[1]. The reason for using a 24-hour urine collection to measure sodium output is that dietary data on salt intake is utterly unreliable. In contrast the urinary data doesn’t lie and give an accurate measure of sodium intake. They divided the subjects according to their level of sodium excretion: The lowest, middle and highest thirds of excretion. The 8-year incidence of cardiovascular disease went as follows: 4.1% in those with the lowest sodium excretion, 1.9% at the middle and a mere 0.8% among those with the highest intake. No, I didn’t type it wrongly. That’s how it stood. Low salt intakes had a higher risk of hear disease that the low salt group. Higher salt intakes increased diastolic blood pressure but not systolic blood pressure and overall, increasing sodium excretion did not increase the levels of clinical hypertension. A second study published in 2011 explored baseline urinary sodium with cardiovascular events over a 56 month period and they found that the relationship was “J-shaped”[2]. In other words, heart disease was higher at low levels of sodium excretion (by about 30%), which fell to a minimum at about the average for sodium excretion and then rose again at the higher level of sodium excretion (by about 70%). Finally, we had a major review of existing literature where 167 studies, covering high and low sodium diets were examined[3]. Salt reduction reduced blood pressure by 1% in those with normal blood pressure and by 3.5% in those with high blood pressure. However, plasma lipids rose by 7%, which may explain the adverse effects of low sodium diets on cardiovascular risk, observed in the other two papers

One might imagine that the salt-hypertension debate might take a major turn in fortune in light of these papers but as I have pointed out before, scientific dogmas are like oil tankers – hard to turn around. The WHO has issued a call for public comments as part of its forthcoming review of its current recommendations on salt and hypertension. It will be interesting to see the outcome.

[1] JAMA. 2011;305 (17):1777-1785
[2] JAMA.2011; 306 (20):2229-2238
[3] Am J Hyper (2012), 1, 1-15