Pure, White and Deadly is a 1972 book by John Yudkin, a British nutritionist and former Chair of Nutrition at Queen Elizabeth College, London. Published in New York, it was the first publication by a scientist to anticipate the adverse health effects, especially in relation to obesity and heart disease, of the public's increased sugar consumption. At the time of publication, Yudkin sat on the advisory panel of the British Department of Health's Committee on the Medical Aspects of Food and Nutrition Policy (COMA). He stated his intention in writing the book in the last paragraph of the first chapter: "I hope that when you have read this book I shall have convinced you that sugar is really dangerous."
The book and author suffered a barrage of criticism at the time, particularly from the sugar industry, processed-food manufacturers, and Ancel Keys, an American physiologist who argued in favour of restricting dietary fat, not sugar, and who sought to ridicule Yudkin's work. In later years, Yudkin's observations came to be accepted. A 2002 cover story about sugar by Gary Taubes in The New York Times Magazine, "What if It's All Been a Big Fat Lie?", attracted attention,Taubes, Gary (7 July 2002). "What if It's All Been a Big Fat Lie?". The New York Times. and the following year a World Health Organization report recommended that added sugars provide no more than 6–10% of total dietary intake. In 2009 a lecture on the health effects of sugar by Robert Lustig, an American pediatric endocrinologist, went viral.Lustig, Robert (26 May 2009). "Sugar: The Bitter Truth", University of California Television (uploaded to YouTube on 20 July 2009). The subsequent interest led to the rediscovery of Yudkin's book and the rehabilitation of his reputation.
Two further editions of the book were published, the second after Yudkin's death in 1995. An expanded version appeared in 1986, revised by Yudkin himself, to include much additional research evidence. In 2012 the book was re-published by Penguin Books with a new introduction by Robert Lustig to reflect the changed nutritional context that the book had helped to create.
Synopsis 1972 edition
The book was first published in 1972 in New York by the publisher Peter H. Wyden under the title Sweet and Dangerous, and a few weeks later in London by Davis-Poynter as Pure, White and Deadly: The Problem of Sugar. Pure, White and Deadly was used for subsequent editions and is the title by which the book became known.
At the time of publication, it was generally accepted that the alarming recent increase in the incidence of coronary heart disease (CHD) was due to the excessive consumption of animal fat. Yudkin believed that this view was wrong and that, instead, an important cause of CHD was the excessive consumption of sugar (i.e. sucrose). More generally, he argued, excessive sucrose consumption provokes a metabolic disturbance that has several undesirable results.
The author makes the initial case that sucrose is a dangerous food by emphasising the contrast between starch and sucrose. Both of these are carbohydrates, but starch occurs as a bulk constituent of cereals (such as rice, wheat and maize), legumes and a few root crops like potatoes, while sucrose is present in large quantities in sugar cane, sugar beet and ripe fruits. It used to be thought that sucrose and starch are metabolised in similar ways, and so are interchangeable from the nutritional point of view, but more recent evidence had shown that their metabolism is significantly different. The need for carbohydrate as a component of the diet can be entirely satisfied by starch (often in the form of bread or pasta), which is broken down in the body to glucose. On the other hand sucrose, which is broken down to equal quantities of glucose and fructose, is not an essential dietary component even in small amounts.For there being "no physiological requirement for sugar", see . Evolutionary history suggests that our pre-Neolithic ancestors ate a diet that consisted largely of meat, with some nuts, berries, leaves and root vegetables, and we can presume that a taste for sweet fruit developed because it directed people to a rich source of vitamin C, an essential nutrient.
The development of agriculture during the Neolithic Revolution (from c. 10,000 BCE) led to a large increase in the consumption of starch, to which humanity adapted well. By contrast, it is only since the early 19th century that greatly improved methods of cultivation of sugar cane and sugar beet, and improved technology of refining, led to sucrose becoming readily available and remarkably cheap. Yudkin refers to these developments as the separation of palatability from nutritional value. As a result the quantity consumed has increased about 50-fold in the past 150 years, with sucrose increasingly used not only in the home and in cafés but also by the manufacturers of soft drinks and as a sweetening agent for many pre-prepared foods. The human species has not had time to adapt to this extremely rapid change. Three problems result. First, unlike glucose, which is metabolised throughout the body, the fructose produced from the breakdown of sucrose is metabolised almost exclusively in the liver, where much of it is converted to fat. Secondly, since it is not uncommon for people to take as much as 30% of their daily caloric intake as sucrose, this consumption crowds out more desirable foods and can sometimes lead to deficiencies of certain nutrients. Thirdly, since many people find sucrose appetising, it is often taken in excess of caloric requirements, thus leading to obesity.
The author then turns to the evidence that the consumption of sucrose is associated with certain specific disorders other than obesity. Some of this evidence is epidemiological and some experimental. Both types have limitations, which the author discusses in a chapter called Can you prove it?, but both are strongly indicative of an involvement of sucrose in the aetiology both of CHD and of what used to be called maturity-onset diabetes (type 2 diabetes).
The epidemiological evidence that sucrose contributes to CHD had started to accumulate in 1957; in that year Yudkin showed that a comparison of data from several countries indicated an association between coronary mortality and the consumption of sucrose, and that the association with sucrose consumption was stronger than with fat consumption. Subsequent studies from South Africa and Israel found that sub-populations that had historically consumed only small quantities of sucrose had much less CHD than those who consumed large quantities, but that as their sucrose consumption increased so too did their incidence of CHD. Experimental evidence from animal studies showed that consumption of a sugar-rich diet leads to biochemical changes that are associated with CHD, such as an increase in blood triglyceride, an increase in platelet stickiness, and an accumulation of fat in the liver. Results similar to some of these were found in human subjects.
Epidemiological evidence similarly pointed to excess sugar consumption as a contributory factor in the development of type 2 diabetes. As before, the evidence relied on a comparison between different countries in the incidence of type 2 diabetes and the consumption of sucrose, and also on within-country differences between sub-populations that consumed less or more sucrose. Moreover, in developed countries, the increase in sucrose consumption that had occurred over the past several decades appeared to run parallel to the increase in the incidence of type 2 diabetes. Experiments with rats showed that the feeding of sucrose led to impaired glucose tolerance (results with human subjects were more equivocal). The author mentions several other conditions that he believed were caused by or exacerbated by the consumption of sucrose: dyspepsia (indigestion), dental caries, seborrhoeic dermatitis, changes in the refractive index of the eye, and various forms of cancer. With the exception of dental caries, none of these conditions showed as strong a link with sucrose consumption as CHD and type 2 diabetes did.
How does the consumption of sucrose lead to these deleterious effects? For dental caries the answer is clear: it is converted to dextran, which is extremely adhesive and promotes the growth of acid-producing bacteria. For the general metabolic effects that lead to CHD and/or to type 2 diabetes, the author suggests that alterations either in the rate of production of insulin or in the body’s sensitivity to it may be one of the early effects of excessive sucrose consumption. This suggestion foreshadows the subsequent widespread recognition of insulin resistance and the metabolic syndrome, and the condition known as non-alcoholic fatty liver disease (NAFLD). NAFLD is believed to result from the accumulation of fat in the liver—often as a consequence of excess dietary sucrose.
A chapter called Sugar should be banned suggests that sooner or later legislation will be needed to prevent people from consuming so much sucrose (this time foreshadowing the UK’s Soft Drinks Industry Levy or "sugar tax"). Yudkin concludes his book with some examples of the ways in which organisations connected with the sugar industry, and with the manufacturers of processed foods that use sugar, sought to interfere with his research or with its publication.
1986 edition Fourteen years after the first publication of Pure, White and Deadly, Yudkin decided that the book was out of date in important respects, and in 1986 he published a new edition to incorporate more recent experimental results. The 1986 edition has many more references, and a much fuller index. In Chapter 12 of the new edition (Can you prove it?) he wrote about several experiments with human subjects in which fat intake had been manipulated by the reduction of animal fat; the results had not supported the fat hypothesis. Chapter 14 (Eat sugar and see what happens) described further experiments from Yudkin’s department at Queen Elizabeth College, both with experimental animals and with human volunteers fed on diets rich in sugar. Chapter 17 (A host of diseases) introduced a new section on disease of the liver.
The inclusion of these additional results is one reason why the new edition (published by Viking in 1986 and by Penguin in 1988) is substantially longer than its predecessor. In addition, the author rearranged and expanded a good deal of the material in chapters 3, 4 and 5 of the 1972 edition, so that these three chapters (which largely concerned the chemistry of sucrose, methods for its production, and the difference between white and brown sugar) now became seven. In the last chapter, Yudkin gave many additional examples of the ways in which his research and the publication of his results had been impeded by the sugar industry and by organisations influenced by it.
2012 edition The 2012 edition was published by Penguin under the title Pure, White and Deadly: How Sugar Is Killing Us and What We Can Do to Stop It. Yudkin's text is identical to that of the 1986 edition. In addition the new edition has an introduction by Robert Lustig, who had, independently of Yudkin, discovered some of the deleterious effects of sucrose, particularly in the aetiology of obesity in childhood. This edition of Pure, White and Deadly has been translated into German and Korean.
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