Sickly Sweet: electronic version.

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Sickly Sweet: electronic version.

  1. 1. Sickly Sweet: Sugar, Refined Carbohydrate, Addiction and Global Obesity Simon Thornley and Hayden McRobbie
  2. 2. ii Simon Thornley and Hayden McRobbie
  3. 3. PREFACE The thesis of this book offers an alternative view of obesity and weightloss. We argue that obesity is a disorder of motivation - an addiction. Thisdistinction is not made just from an academic stand point. The reason weseek to classify obesity in such a manner is to better understand its natureand craft improved strategies for those that are trapped by its snare. Obesity, at a population level, has not always been with us. Nearly 40years into the global epidemic, we easily forget that not so long ago theworld was not popping its collective buttons. Of all countries, trends in theUnited States are perhaps most exaggerated. In 1978, 15% of thepopulation was defined as obese, then 22 years later, that number haddoubled to 30%, almost one in three adults [1]. Such a rate of changeargues that genetic factors are unlikely to account for this trend. If geneticfactors are not responsible, the only alternative is the environment. So whatis it about our environment that has changed to prompt this global increasein girth? As a medical doctor, during my training, I had been taught thescientific consensus which attempts to explain this modern phenomenon.Succinctly, the World Health Organisation stated that two factors are atwork, first, that food has become cheaper and more energy dense, andsecond, that energy expenditure has reduced, due to a reliance on moderntechnology, such as motorized transport, which replaces walking or cycling
  4. 4. [2]. When examined more carefully, such a view is based on the law ofconservation of energy in physics which dictates that energy cannotdisappear from a closed system. In an individual, put simply, energy inmust equal energy out. Food intake corresponds to the energy in, andenergy expended by the body, carrying out physiological functions, such aspumping blood, maintaining a constant temperature and exercise. If thisbalance is upset, so that individuals consume more energy than theyexpend, the excess is stored as fat and obesity results. At face value, such an argument appears grounded and compelling,based on few assumptions. If such a theory is correct, what is the logicalresponse to reverse this modern epidemic? When nutritional advice isderived from such a theory, of the three main macronutrients (fat,carbohydrate and protein), reduction of proportion of energy derived fromfat is the consequence. Why point the finger at fat? When burned, ormetabolized, fat releases just over twice the energy of protein orcarbohydrate. Co-incidentally, from the 1960s, researchers alsorecommended reducing intake of saturated fat (mainly derived from animalfat), to prevent the most common cause of death in Western Countries,coronary heart disease. End of story; reducing fat seemed to kill two birdswith one stone, potentially reducing obesity and coronary disease in aneasily digestible sliver of nutritional advice. The modern epidemic ofobesity, so it was believed, would be reversed by skimming fat from milk,trimming the skin off chicken, abstaining from pork crackling andreplacing the fat in dairy products with less energy dense carbohydrate. Unfortunately, population waistlines have not responded in the waypredicted by this theory. To the contrary, evidence suggests that suchadvice has actually increased the prevalence of obesity in most OECDcountries, where regular surveys have been carried out. Asian countries inthe OECD, of which there are only two, South Korea and Japan, stand outin stark contrast to Western nations, with a stable low prevalence ofobesity. The United States, Australia, New Zealand and the UnitedKingdom, all English speaking nations, stand out in contrast, with the
  5. 5. Preface vgreatest rise in obesity between 1980 and 2003 with prevalence doublingduring this period. What is wrong? Two explanations are possible; (1)either people are ignoring this simple health message, or (2) the message isincorrect, or even doing harm. The most surprising aspect of this advice is how widely it has beentaken up, and how spectacularly it has failed. After the Surgeon Generalsrecommendation in the 1960s that cigarettes cause cancer, many expectedthat people would heed this advice and leave their cigarettes as soon as themessage got through. Fifty years later, one in five New Zealand adultssmoke, and although numbers are slowly dropping, progress isdisappointing. As far as public acceptance of the crusade against fat goes,it has met with surprisingly little resistance. In New Zealand, chicken isroutinely sold, stripped of its fatty flesh, steak is lean, and its hard to find acan or packet without a reference to its purity from the obesigenic, greasysubstance. Almost all products, from sour cream to biscuits are sold in a“lite” variety, in which fat content is reduced. Where I currently work, inthe University’s, School of Population Health, I have no choice but todrink skim milk with my tea or coffee - 99.9% fat free. My own realisation that traditional nutritional theory may be flawedwas initiated by reading Michael Pollans “In Defense of Food” [3]. Pollan,who describes himself as a humble journalist rather than a scientist, takeson the nutrition establishment, and argues that in the United States, theobsession with healthy eating has paradoxically contributed to obesity. Heidentifies that food manufacturers have created confusion in the mind ofconsumers by making claims of health benefits for a wide variety of foods.Also, in the modern food industrys assault on the modern consumer, noone appears to be stating the obvious, straight forward solution to obesity -eat less. Pollan goes on to not only attack nutritional science but also thephilosophy of scientific reductionism, arguing that defining food by itsbuilding blocks cannot account for its effects on the body. Importantly,also he points the finger at nutritional epidemiology, the science fromwhich nutritional advice springs from, actually suffers from a fundamentalflaw. Simply put, individuals are notoriously error prone when it comes torecording what they actually eat, so that measuring associations between
  6. 6. vi Simon Thornley and Hayden McRobbiefood intake and health outcomes may not always produce accurateinformation on which to base recommendations. My own experience with food was similar to what I think has beenhappening on a grand, population wide, scale. During my time as a medicalstudent, I was taught the current medical wisdom. Saturated fat was bad forcoronary arteries, and fat in general was obesogenic. I resolved to reducethe fat content of my meals, shunned the weekly regular servings of fishand chips, fast food and resolved to drink only the most watery skim milk.During my time as a clinician, treating people in hospital with heartattacks, strokes and cancer, my approach was the same; fat was the enemy- my patients were encouraged to swap full cream milk for the low fatalternative. Despite my fat avoidance, belts were loosened and trousers cast asideuntil I was roughly fifteen kilograms heavier than I had been in medicalschool. By this time, I was now training in public health medicine, andtaking part in research of smokers and how they could be helped to quit.As a doctor in the hospital, I had an almost arrogant disregard for smokers.I hated them. They smoked despite decades of research that showed theywere shortening their lives. Id heard many patients assure me they weregoing to quit, and later find evidence that they hadnt either from a spouseor from laboratory results. In my mind they were lazy and self-centred, andwere responsible for much of the stress I experienced in the over burdenedNew Zealand public hospital system. As a junior doctor, often exhaustedfrom working long hours, smokers were responsible for what came tothem, and that was that. When I abandoned my career as a hospital doctor, changing instead topublic health research, I discovered how little I knew about addiction. Forthe first time, I realized that smokers experience a withdrawal syndromewhen they try to stop, which is unpleasant and lasts for over a month.Symptoms of craving, irritability, restlessness, depression, difficultyconcentrating, and constipation plague the smoker bent on reform. Thesesymptoms can get so bad that Ive heard of mothers sometimes hitting theirchildren and husbands abusing their wives. Withdrawal symptoms, such asirritability are not a justification for this behavior, but do illustrate the
  7. 7. Preface viiseverity of symptoms that some people face. Complete relief is only acigarette away. Another revelation was the strength of subconscious drivesand desires created by reward pathways in the midbrain. Most smokerswere completely unaware that the reason they smoked was to avoidwithdrawal discomfort; the smoking was performed almost automatically.When this was explained to smokers in our studies, instantly the majorityagreed and identified personally with this explanation. The last pearl wasperhaps the most significant. In almost all addictions, time from taking thesubstance (such as nicotine from a cigarette) to being absorbed andstimulating the reward centre in the brain was the critical factor thatdetermined how effectively a drug could keep you hooked. Cigarettes wereideal. The nicotine is vaporised by the cigarettes flame, inhaled into thelungs by the smoker, transported rapidly through the heart to the brain in amatter of minutes. The nicotine products (gum, patch, lozenge, mouthsprayand pouch) we were testing could not compete. They were absorbedthrough the lining of the mouth, an area of the body with much less bloodflow than the lungs, and their time to stimulation of the brains rewardcentres much slower than cigarettes. This time lag had a silver lining,however. Slowly absorbed nicotine helped relieve some withdrawaldiscomfort, but wasnt as stongly rewarding as the cigarettes they replaced.For many smokers, they are a bridge to freedom. One day I was working on translating these techniques to help smokersquit into a palatable, brief education session for family doctors. Across theroad from where I had lunch was a second hand book store. Among thebooks that were arranged in a semi-random fashion, I found a couple ofcheap copies of old diet books - the New Glucose Revolution, and TheAtkins Diet. The book by Robert Atkins grabbed my attentionimmediately. I knew the diet was based on restricting carbohydrates, out offavour with most nutrition experts, so I was very skeptical. Through thepages, however, I noticed that Atkins described patients who experiencedsimilar feelings to those that smokers reported in cessation clinics. Onewas very vivid. He described an overweight executive that was addicted tosugar:
  8. 8. viii Simon Thornley and Hayden McRobbie ‘‘…often I would shake until I could put some sugar in my mouth’’. I had an hour’s drive from my office to my home, and I knew very restaurant, every candy machine and every soft drink dispenser along the whole route.’’ The man experienced tremors that were relieved by a sweet taste, anddescribed his preoccupation with sources of sugar on his journey home.The physical symptoms, relieved by sugar, and the cues described werevery similar to the phenomenon of withdrawal described from nicotine. Iwas curious. I searched medical journals to find evidence that food wasaddictive, like Atkins’ description, but found little. Much had been writtenabout the theoretical view point, drawing parallels from rat research andfrom complicated imaging studies of obese people’s brains, but nothing Icame across considered the implications of such a theory on howindividuals are treated or whether this theory may explain why populationsare expanding their collective girth. Also, the fact that I had made such adiscovery from a book known to be relegated to the medical scrapheap ofpseudoscience increased my cynicism of the established nutritional agenda.Atkins did not identify that these symptoms may have been part of awithdrawal syndrome, but did claim that his diet reduced their intensityand promised recovery. In the "New Glucose Revolution", I discovered another alternativetheory of nutrition and a different approach to weight loss than thatadvocated by the public health establishment. The most importantcomponent was the glycemic index - a physiological measure of how mucha standardised mass of carbohydrate from different foods raises the bloodglucose after eating. The plots of glycemic index and how it was measuredmade me think of our nicotine studies and how time-to-‘hit’ was such animportant factor in making products addictive. Why couldnt food beconsidered in the same way? Was glycemic index the key to unlocking ahidden addiction - the obesity epidemic? I was curious to discover more.Together with tobacco researcher, and colleague, Hayden McRobbie, weexplore the evidence that links sugar and refined carbohydrates with foodaddiction and set out an alternative explanation for the burgeoning obesityepidemic.
  9. 9. Preface ix REFERENCES[1] OECD. OECD Health Data 2009: Statistics and Indicators for 30 Countries. Paris: OECD publishing, 2009.[2]World Health Organisation. Obesity: Preventing and Managing the Global Epidemic. Report on a WHO Consultation Technical Report Series, No 894. Geneva: World Health Organisation, 2000.[3]Pollan M. In Defense of Food: An Eater’s Manifesto. First Printing. Penguin Press HC; 2008.
  10. 10. Chapter 1 THE GLOBAL OBESITY EPIDEMIC: EPIDEMIOLOGY, HISTORY AND MILESTONES “It is not yet clear whether any single attribute of the Western way of life is particularly important in increasing the risk of diabetes. Excess sucrose has largely been exonerated as an important dietary factor in the aetiology of type 2 diabetes...” J. I. Mann and A. S. Truswell [1] Diseases of overnourished societies and the need for dietary change: in the Oxford Textbook of Medicine, 4th Edition. “Originally proposed as the ideal sweetener for people with diabetes... Fructose [part of sucrose]... has been indirectly implicated in the epidemics of obesity and type 2 diabetes.” The American Heart Association [2] Sugar and its effect on human health has divided the scientificcommunity over the last ten years. Professor Jim Mann, an internationalnutritional expert describes sugar (sucrose) as “exonerated” in theaetiology of type 2 diabetes in the prestigious Oxford Textbook ofMedicine. The American Heart Association, who, in 2002, had taken asimilar view to Mann [1], later changed their mind, reporting that fructose
  11. 11. (half of the sucrose molecule) was now facing a guilty verdict, from whichit had earlier received a pardon. If one looks back over a longer period oftime, some experts have long scrutinised the adverse effects of sugarconsumption, since at least the early 1960s [3]. Such calls, however, havelargely been ignored until recently. In this book, we examine whatdirection nutritional policy has taken over the last forty years, and in whatnutrition context obesity patterns have developed. We examine overeatingfrom a new paradigm, rather than viewing overeating as a problem ofenergy balance, we instead consider motivation to eat, and what effectsdifferent foods have on hunger. Surely, if eating certain types of food,increases appetite, as alleged for sugar, this has important consequences forthe quantity of food that enters a person’s mouth, ultimately stretching thebelt out a notch, and making difficult work of the juxtaposing of buttons.We will see that such a paradigm, ignoring the powerful biological drivesand learning that occur with eating, has lead to what we believe to be atragic misdirection of nutrition policy in English speaking countries andnow dispersing around the world. When I first started work as a house officer, fresh out of medicalschool, at the dawn of the new millenium, I spent two years working in abusy city hospital. The hospital treated people of a wide variety of ethnicbackgrounds, but Pacific people had a lively community in the area andwere frequently in need of treatment. Migrants from the Pacific islands thatsurround New Zealand are frequently obese, so much so, that during mypublic health training, a colleague advised me that one in four Pacificadults would be eligible for obesity surgery in the jurisdiction in which heworked. Of all the challenges that being a junior doctor entailed, one of themost difficult tasks was the constant need to place intravenous lines inpatients, so that various drugs, and fluids could be administered. What, in athin person, was a trivial task, could provoke severe anxiety when veinswere concealed by layers of fat. If requested to insert a cannula, I wouldfirst take a peek through the curtain to get a rough estimate of how muchfat was likely to impede my progress, and so how many spare lines would
  12. 12. The Global Obesity Epidemic 3be required. In people who tipped the scales, I would load my kidney dishof supplies to overflowing to account for the inevitable event of numerousembarrassing and painful (for both the patient and myself) failures. Onceestablished in the job, I soon realised that the sneak preview wasunnecessary, because the vast majority of people admitted wereoverweight. I might as well overload my kidney dish, the chances were Idhave a battle on my hands. Faced with the relentless demands of caringwith such a load of obese patients, it was difficult to imagine a time whenobesity was a rare sight. For anyone in an English speaking country, obesity has become such acommon occurrence it no longer raises more than a glimmer of curiosity.TV, voyeuristically, still portray the adventures of the super obese, thatcontinue to pull crowds. Only grossly or morbidly obese people attractcomment. Indeed, whilst writing this manuscript, the researcher sittingadjacent to me would easily qualify as obese. Although records are rare,before the 1970s, few Western countries systematically recorded obesityrates in their populations. Why no scientific interest in body size? It seemsthat excess fat simply wasnt a major issue to devote significant time orresource to measuring. This, in itself, suggests that obesity was not a majorconcern - why measure a problem that doesnt exist? Something changed in the 1970s. From the early 1980s, obesitysuddenly appeared on the public health radar, and populations, particularlyin wealthier countries, were measured for height and weight. Theexpanding waistlines of different countries have been thoroughlyresearched, documented up until today, with collective expansion set tocontinue for the foreseeable future. This bleak news hides pockets ofresistance to this trend. Despite this pessimistic outlook, some countriesremain thin. Obesity is strongly patterned by country. Of the thirty wealthycountries contained within the Organisation for Economic Co-operationand Development (OECD), English speaking countries are leading thepack, with the United States way out in front [4]. In sharp relief to thesecountries that are linguistically linked, are the slim societies of Japan andSouth Korea who have maintained low levels of obesity over the sameperiod.
  13. 13. 4 Simon Thornley and Hayden McRobbie To understand what factors underlie the rising tide of global obesity, aphenomenon with a clear temporal pattern, with vastly different impactsbetween countries, we must consider what ideas have been propagated inthese countries, what dietary patterns have emerged and considerdefinitions of obesity. Critical milestones, in terms of nutritional advice,and changes to food processing and content may give clues to what iscausing our collective bursting of buttons. DEFINITIONS Firstly, how do we define someone as overweight or obese? Thissounds simple, but accurate, repeatable, consistent measurements arecritical to our understanding of this disorder. Body mass index (BMI) iscommonly used as a global standard today to define obesity in terms ofweight corrected for height [5]. What is this measure and what does it tellus about an individual? How has this definition changed over time, andwhat does the commonly used term “body mass index” indicate? Obesityhas been labeled a major public health issue because of its association withpremature death and other diseases. If information is to be accuratelyrecorded, a consistent definition must be applied over time to trackpopulation trends. Before 1980, a variety of methods were used to classifypeople as overweight, based on actuarial data derived from life insurancecompanies such as Metropolitan Life, which were labeled “ideal” weightfor height values, or “desirable” body weights [5]. Such standards werederived from a large group of North Americans and Canadian adultspurchasing life insurance policies between 1935 and 1954, with standardsreferring to a group of people that, at the time, had low rates of prematuredeath. From 1980, body mass index (BMI) was more commonly used,which is defined by weight in kilograms, divided by height in meterssquared. This measure is a reasonably good measure of body fat, althoughit is far from perfect. Raised BMI also predicts increased risk of a range ofdiseases such as coronary heart disease, stroke, cancers of the large bowel,womb and breast [6]. A recent study, involving over 900,000 subjects,
  14. 14. The Global Obesity Epidemic 5showed that a body mass index of 22.5 to 25.0 kg/m 2 was linked withoptimal survival. People above this range, with moderate obesity (BMIbetween 30 and 35 kg/m2) would, on average, face in excess of three yearslife lost, and people with extreme obesity (BMI 40-50 kg/m 2) lost morethan 10 years of life. By way of comparison, this latter condition shortensaverage lifespan by about the period as a lifetime of smoking cigarettes [7].Classifications based on body mass index are therefore usually divided intooverweight (BMI ≥ 25.0), and obese (BMI ≥ 30.0). While BMI is a useful measure for characterizing population risk ofobesity, at an individual level it may be less accurate because some,particularly young males, are incorrectly misclassified as overweight dueto increased lean muscle mass rather than excess fat tissue. To avoid thispotential source of error, here, we use a cutoff of BMI ≥ 30.0 kg/m 2 toclassify individuals as obese, and to monitor population trends.
  15. 15. 6 Simon Thornley and Hayden McRobbieFigure 1. Adult obesity (BMI ≥ 30kg/m 2) prevalence by year for selected OECDcountries (1980 to 2003) [9]. GLOBAL TRENDS IN OBESITY PREVALENCE The start of the global obesity epidemic is difficult to pinpoint.Regular, representative surveys of population obesity were not carried outuntil obesity became a focal point in the medical community andsignificant resource was devoted to its measurement. In the United States,at the turn of the 19th Century, a survey was undertaken, recording heightand weight of Civil War veterans aged 50 to 59 years found that 3.4% hada BMI ≥ 30.0 (obese) [16]. Also, a comparison of the weight of London
  16. 16. The Global Obesity Epidemic 7hospital patients coming to autopsy in 1906 to 1914 and the 1950s showedlittle difference in mean weights between the two periods [8]. Since thistime, until the early 1980s, nationwide, estimates of obesity prevalence aredifficult to find. A summary of obesity prevalence, by country, has beenpublished by the OECD and the prevalence by country between 1980 and2003 are depicted in Figure 1. Several patterns emerge from this figure. First, the country with thehighest prevalence, reported after the year 2000, of obesity is the UnitedStates, with one in three adults meeting the BMI cutoff. Other highprevalence countries are also English speaking, with New Zealand and theUnited Kingdom (one in four) and Australia (one in five) next highest.These within-country trends hide patterns present in some ethnic groups.For example, 43% of Maori and 65% of Pacific adults are obese [10]. Also,the rate of change of obesity (slope of the line) is highest in these Englishspeaking countries (Canada excepted). Further, Japan and South Korea(not displayed) have the lowest prevalence of obesity, of all countries inthe OECD, with fewer than one in twenty adults falling into this category.Other continental European countries, along with Ireland, occupy themiddle ground between English speaking and Asian nations. Whatconclusions can be drawn from this information? First, we observe thatobesity prevalence is slowly rising in all OECD countries presented here,so that an increased burden of obesity is a real global phenomenon. Also,different rates of change in obesity prevalence are observed betweencountries with similar cultural and linguistic traditions. What is it aboutEnglish speaking countries that caused obesity rates to climb so steeply inthe latter part of the twentieth century? To answer this question, we willconsider what changes in nutrition have occurred in these countries. NUTRITIONAL CHANGE BEFORE THE 20TH CENTURY Although record keeping before the 20th century was not ascomprehensive as today, historians of coronary disease have attempted todocument what nutritional changes predated the epidemic of
  17. 17. 8 Simon Thornley and Hayden McRobbiecardiovascular disease observed in the 1950s. Michaels [11] documentsthat sugar consumption only became established in Europe in the 16 thcentury, after mass cultivation of sugar cane got under way in the WestIndies. With the advent of tea and coffee drinking in the 18 th century, sugarbecame more popular. Intake of sugar increased in Great Britain fromabout 2kg/capita/year in 1700, to 9.5 in 1809-13, increasing to 50.6 in1962. In contrast, Michaels identifies that an historic author King, who in1696 provided an account of all aspects of English life, estimated thatconsumption of meat was about 37kg/year. King estimated that half thepopulation (about 2,700,000 people) ate flesh regularly and theirconsumption was about 3.6kg/capita/year higher than people in the UK in1962. Thus total animal fat consumption had probably decreased ratherthan increased over this critical period. In contrast, average sugar intakehas continued to rise [14]. CHANGES IN NUTRITIONAL SCIENCE DURING THE 20TH CENTURY Concern about obesity did not preoccupy nutritionists and the medicalcommunity during the early part of the 20th century. Before obesity everappeared as a public health issue, blocked coronary arteries from fattydeposits, causing an epidemic of heart attacks and premature death werethe primary motivating force behind public health campaigns to changewhat the public consumed [13]. Despite the fact that coronary heartdisease, known more commonly as heart attacks and angina, is the mostcommon cause of premature death in most developed countries, this wasnot always the case. It wasn’t until mid way through the twentieth centurythat coronary artery disease was commonly encountered in clinicalpractice. The first hint of coronary artery disease was recorded in 1768, whenthe famous Physician, William Herbeden described angina pectoris, whichwas the sensation of being strangled in the chest [11]. At the time, he didnot make the connection between these symptoms and the heart. Historicalevidence suggests that although the condition was first described at thistime, it was still extremely rare. Hebeden himself records only
  18. 18. The Global Obesity Epidemic 9encountering 20 cases of angina during his twenty or so years of practice.Records indicate that cases were extremely rare from the late 18 th centuryuntil 1912, when Herrick described a series of six cases with coronarythrombosis, a blood clot in the arteries supplying blood to the heart muscle.This anatomical basis for these symptoms was discovered 32 years earlierby Weigert. Even in the early 20 th century, death from coronary diseasewas a rare event. Michaels reports evidence that deaths from hardening ofthe arteries (arteriosclerosis) were 200 times more numerous in 1962 as1901-10. A common objection to such evidence of a rapid rise in thenumber of cases of coronary artery disease, was that life expectancy wasincreasing, and that latter populations were much older, and thus morelikely to develop disease. Although the number of people aged 50 years orolder did increase in the UK over this period, the magnitude was muchsmaller (threefold; 4,790,000 in 1901 to 14,158,000 in the early 60s) thanthat observed for increasing rates of disease [11]. By the early 1960s, however, the epidemic of coronary artery diseasewas established in Western industrialized nations, and doctors andscientists were seeking explanations. Figure 2 shows the rapid rise inmortality rate from coronary disease and stroke in England and Walesbetween 1921 and 1939 when the epidemic was first identified in medicaljournals, in 1949.
  19. 19. 10 Simon Thornley and Hayden McRobbieFigure 2. Comparative mortality index for different causes of death in males inEngland and Wales between 1921 and 1939 [12]. The medical, public health and epidemiological communities swunginto action to prevent the rapid rise in cases of coronary disease. GaryTaubes, a science writer, has documented the history of nutritionalrecommendations associated with the diet-heart-hypothesis, developed inthe 1930s, and widely accepted in the early 1980s, lead by Dr Ancell Keys[13]. He documents that the American Heart Association released a reportin December 1960, arguing that “the best scientific evidence of the time”strongly suggested that Americans would reduce their risk of heart diseaseif they reduced the fat in their diet and replaced saturated or animal fat withvegetable-derived fat. Initially the advice was aimed only at men at highrisk of heart attacks by virtue of having suffered a previous event, having ahigh cholesterol or being smokers of cigarettes. Such recommendationswere revised annually, so that in 1970 the advice applied to all Americans(including infants, children, adolescents, pregnant and lactating womenand older people). ‘Eat less fat’ was the mantra that we were both taught atmedical school, as the answer to both obesity and coronary heart disease.
  20. 20. The Global Obesity Epidemic 11Keys believed that the ideal heart healthy diet would increase thepercentage of carbohydrates from less than 50% calories to 70%, andreduce saturated fat consumption from 40% to 15%. In contrast, Taubesnotes that Japanese physicians were advising patients to increase their totalcholesterol levels, because low cholesterol levels were associated with riskof haemorrhagic stroke in their home country. Barry Popkin, a Professor of Economics, has described changes in theNorth American diet and contrasted these with changes in Korean andJapanese diets in the latter half of the twentieth century [14]. His analysisis based on population estimates of food consumption derived from UnitedNations Food and Agriculture Organisation Food Balance Sheets. Percapita consumption of a range of food products was estimated bycalculating the national total of food-stuff produced, adding imports andsubtracting exports, then dividing the difference by the total populationestimate at that point in time. The remainder is considered to havedisappeared and so assumed eaten, although a small amount is likely to bewasted. Popkin’s findings showed that, in the United States, the keychanges that occurred between 1977-8 and 1987-8 were a reduction inwhole milk consumption (50 gram/capita/day) with a compensatoryincrease in low fat milk (30 gram/capita/day), along with a decline in highand medium fat red meats (30 gram/capita/day), and an increase in low fatpoultry consumption (10 gram/capita/day). Conversely, soft drinkconsumption increased markedly, with an increase in sugar sweetened softdrinks of 60 gram/capita/day, and diet drinks by 45 gram/capita/day overthis ten year period. In line with the American Heart Association’sguidelines, this analysis, suggests that fat consumption was reduced, with alarge increase in carbohydrate intake, particularly from sugar sweetenedsoft drinks. Like the United States, the National Heart Foundation in NewZealand, Australia and the United Kingdom have consistently advocatedfor reduced consumption of dairy fat, meat fat and reduced fried foodintake. Asian countries, present in the OECD obesity analysis, have undergoneparadoxical changes to those observed in the United States. Althoughoverall fat intake is much lower in these two countries than the US, per
  21. 21. 12 Simon Thornley and Hayden McRobbiecapita fat consumption increased 341 percent between 1946 and 1987. InSouth Korea a similar trend has occurred, with a rising consumption ofanimal products and declining intake of grains during the period between1965 and 1985. Percent of energy derived from fat rose from 8% to 14%,and similarly average grain consumption reduced from 550 to 400grams/capita/day during this twenty year period. Combining such data withthe trends observed in obesity over the last thirty years (Figure 1), weobserve that this increase has not had a substantial impact on theprevalence of obesity in Japan, or South Korea (data not shown), althoughthe prevalence of people who are overweight elsewhere has grownsubstantially in recent decades. So, we have seen a clear difference in the body composition of selectedcountries, in which records of body size, and per capita intake of energyhave been recorded. A clear distinction can be drawn between countrieswho have experienced a rapid increase in the proportion of obesity peopleover the last thirty years – USA, Canada, UK, Australia and New Zealand;and those countries that haven’t – Japan and Korea. SUMMARY What conclusions can we draw from these historical events? First,coronary artery disease is a relatively recent phenomenon, and it was thisepidemic which prompted calls from medical authorities to lower fatintake, particularly in English speaking countries. Second, sugarconsumption has substantially increased over the last three hundred years,and calls to reduce fat intake, by public health authorities, may haveincreased the consumption of carbohydrate and sugar in countries with aBritish colonial heritage. Conversely, in Asian countries, which were risingout of poverty during the 20th century, fat was more commonly consumedthat ever. With two quite different changes in nutrient profile, the changein obesity prevalence between Asian countries and English speakingcountries, recorded from the early 1980s, couldn’t be more different. SouthKorea and Japan have maintained very low levels of obesity in the last
  22. 22. The Global Obesity Epidemic 13thirty years, despite a dramatic increase in the proportion of caloriesobtained from fat. In the remaining chapters we explore the health effectsof carbohydrates, the macronutrient promoted to prevent coronary arterydisease in English speaking countries during the early 1970s, initiated bythe American Heart Association. We also research the effect thatcarbohydrates have on the motivation and reward centres of the brain. Hasthe advice, to reduce fat, and saturated fat, been a case of robbing Peter topay Paul? For us to consider whether the growth in global obesity hasoccurred due to carbohydrate addiction we will have to consider what hasis known about addiction, and carbohydrates. First, we attempt to unpackthe concept of addiction. How do we know something is addictive? Whathas been learned about treating people with addictions? Could thisinformation help us, collectively, beat the obesity epidemic?Figure 2. Changes in consumption of selected food types, 1969 to 1985 [15].
  23. 23. 14 Simon Thornley and Hayden McRobbie REFERENCES[1] Mann, JI, Trusswell, A. S. Diseases of overnourished societies and the need for dietary change. USA: Oxford University Press; 2003.[2] Johnson RK, Appel LJ, Brands M, Howard BV, Lefevre M, Lustig RH, et al. Dietary Sugars Intake and Cardiovascular Health: A Scientific Statement From the American Heart Association. Circulation. 2009;120(11):1011-1020.[3] Yudkin J. Dietary fat and dietary sugar in relation to ischaemic heart- disease and diabetes. Lancet. 1964 Jul 4;2(7349):4-5.[4] OECD. OECD Health Data 2009: Statistics and Indicators for 30 Countries. OECD publishing; 2009.[5] Kuczmarski RJ, Flegal KM. Criteria for definition of overweight in transition: background and recommendations for the United States. Am J Clin Nutr. 2000;72(5):1074-1081.[6] Prospective Studies C, Whitlock G, Lewington S, Sherliker P, Clarke R, Emberson J, et al. Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies. Lancet. 2009;373(9669):1083-96.[7] Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to smoking: 50 years observations on male British doctors. BMJ. 2004 Jun 26;328(7455):1519.[8] Morris JN. Recent history of coronary disease. Lancet. 1951;1:1.[9] OECD. OECD Health Data 2009: Statistics and Indicators for 30 Countries. OECD publishing; 2009.[10] Ministry of Health. A Portrait of Health: Key Results of the 2006/07 New Zealand Health Survey. Ministry of Health; 2008.[11] Michaels L. Aetiology of coronary heart disease: an historical approach. British Heart Journal. 1966;28:258-64.[12] Ryle JA, Russell WT. The natural history of coronary disease a clinical and epidemiological study. British Heart Journal. 1949;11(4):370-389.[13] Taubes G. The Diet Delusion. New York: Vermilion; 2007.
  24. 24. The Global Obesity Epidemic 15[14] Popkin BM. Nutritional Patterns and Transitions. Population and Development Review. 1993;19(1):138-157.[15] Kim SH. Changing nutritional status affected by rapid economic growth of Korea. In: International Symposium on Food Nutrition and Social Economic Development. Beijing: Chinese Academy of Preventive Medicine; 1991. p. 472-478.[16] Helmchen LA, Henderson RM. Changes in the distribution of body mass index of white US men, 1890-2000. Annals of Human Biology. 2004;31(2):174-181.
  25. 25. Chapter 2 ADDICTION: CLINICAL FEATURES AND BIOLOGY After first reporting global trends in food and nutrient intake, thenrecent trends in obesity, you may wonder why we are now venturing intoseemingly unrelated territory. To the contrary, we believe that recentglobal food trends may only be understood by considering the rewardingproperties of food, and the similarities between these everyday items andother products commonly accorded ‘addictive’ status. Of course many ofthe substances we frequently refer to as addictive are often illicit, or theirsupply is controlled in some way. Cigarettes and alcohol are commonsuspects, leading to addiction, but food, surely not - we retain consciouscontrol of what we eat for breakfast, lunch, dinner and in between, dontwe? Does eating share characteristics of addictions more commonly seenwith drugs? Before we can answer this question, we must consider whatfeatures make a drug (or food) addictive? How is addiction recognised?Which techniques can help people beat addictions? We discuss the generalfeatures of addiction, so that we can make sense of eating behavior andobesity – do they fit the same mould? Many medical professionals would strongly refute the hypothesis thatsome foods (such as sugar) have ‘addictive’ properties. What we proposehere goes against the grain. This is, however, often how the medical field
  26. 26. develops. Take nicotine for example. Today, people generally agree thatnicotine, present in a cigarette, is responsible for hooking people ontobacco. However this was not always the accepted mantra. Not until the1970s was nicotine first recognised as a drug of dependence. Before this,most scientific bodies viewed smoking as a habit, not an addiction. Therationale of this thinking, at this time, was that a well-defined withdrawalsyndrome after stopping smoking was not well described and methodsavailable were equally effective, or ineffective for helping people stop forgood. Sound familiar? In 1971, Russell, a pioneer in the study of tobacco,published an argument that nicotine was a dependence-producing(addictive) substance [1]. This was the beginning of a change in attitudestowards smoking. Soon after, the Royal College of Physicians decreed thattobacco smoking was due to nicotine addiction and in 1980 the AmericanPsychiatric Association (APA) recognised that smoking met most of thecriteria for drug dependence, so that this condition was then included intheir diagnostic “bible”, the DSM-III. It was not until the late 1980s thatthe US Surgeon General issued a report entitled ‘Nicotine Addiction’,which concluded that tobacco was addictive, nicotine was responsible, andthat the effects of nicotine on the brain share features of other major drugsof addiction such as heroin and cocaine [2]. WHAT IS ADDICTION? To lay people, the word addiction conjures an image of a sadalcoholic or cocaine addict, lost in their own world, often dishevelled,caring for nothing else but another fix from their drug of choice. Other lessintense preferences for substances are more commonly referred to ashabits, implying that they are easier to give up. The chances are, whether,working as a health care professional or not, most of us can picture aperson who roughly fits the addiction stereotype. Although, at first glance,this may sound simplistic, it reveals two key components of addiction, the
  27. 27. Addiction: Clinical Features and Biology 19substance and the individual’s relationship with it. In the familiar case ofsubstance abuse to cocaine, or alcohol, the primary place in the personslife that the substance takes, distinguishes the addict from those aroundthem. While others may place no value on acquiring or consuming thesubstance, to the addict, their object of desire dominates their priorities andthey have difficulty controlling their use of it. Time is spent ensuring thatthe addict has sufficient supplies, usually to avoid the unpleasant feelingsof withdrawal that might accompany prolonged abstinence. Time spentobtaining the substance often takes precedence over other priorities, whichmight be thought, on considered reflection, to be more important: such asfamily, work and the wider community. Medics are generally well versedin these consequences, with a mnemonic summarising the most commonlyharmed areas of a persons life: health (liver), family (lover), work(livelihood), and society (law). Such extremes allow us to falsely assume that addiction, and theprocesses that underlie it, only occur in a small subset of the population.Addiction can, however, be more subtle and resist these stereotypes. Forexample, perhaps the most common daily addiction is caffeine. Although,coffee and tea drinkers’ lives are usually not ruled by their caffeine intake,some characteristics of more severe addiction syndromes are shared. Forexample, the presence of a withdrawal syndrome is closely tied toaddiction and substance abuse. Caffeine withdrawal is a subtle discomfortthat starts soon after abstinence. Although the symptoms would be unlikelyto ever prompt a visit to the doctor, they are nonetheless real. Cravings andurges for a source of caffeine, headaches, reduced concentration, irritabilityand restlessness are an attempt to more accurately label the feeling of “notquite feeling right”. Regular tea and coffee drinkers rarely, if ever, have toremind themselves of their need for a cup. Often the smell or sight of thesubstance will initiate the caffeine addict to reach for the tea bag orplunger. Although we may not realize it, our brains are hard-wired for reward.We need to eat, drink and reproduce to survive so that behavioursassociated with such necessities are rewarded. The ‘machinery’ that isresponsibly for subconscious reward lies in a part of our brain that governs
  28. 28. 20 Simon Thornley and Hayden McRobbieautomatic survival functions. It’s known as the mesolimbic dopaminergicpathway and consists of a number of structures in the midbrain andprefrontal cortex. Activation of this brain pathway leads to reward,subconscious learning and the feeling of pleasure. Food, for example,stimulates this pathway which ultimately leads to release of the chemicalmessenger, dopamine, and a sense of pleasure. However the ‘amount’ ofpleasure depends on how enjoyable the food is and how hungry you are atthe time of eating [3]. It just so happens that drugs such as nicotine andcocaine hijack this reward system and, depending on our genetic makeup,the environment in which we live, and our backgrounds, some people aremore susceptible than others. The mechanics of what motivates an addict are often glossed overunless one pays careful attention to the subtle symptoms that precedesubstance use, and observe what effect use has on such symptoms. Let’s goback to our example of nicotine. Unlike cocaine and heroin, a puff on acigarette does not give you much of a ‘positive hit’. For those who haveever tried smoking, you will, no doubt, remember your first few puffs. Idoubt that it left you feeling high and wanting more. In fact you probablyfelt a bit sick. With persistence, however, smokers develop tolerance tothese unpleasant effects. One might think then that because nicotine is onlya mild stimulant, it might be easier to give up than other drugs ofdependence, such as alcohol, cocaine or heroin. This, however, is not thecase. Early studies that investigated the ‘addictiveness’ of nicotine askedpeople who used tobacco, cocaine, heroin and alcohol to rate how muchthey liked each drug (on a 5-point scale: 1=dislike; 5=like a lot) and howmuch they needed to use each drug (on a 4-point scale: 1=no need; 5=needa lot). Tobacco rated second for ‘liking’, after heroin, and in terms of‘needing’, tobacco came out on top, followed by heroin, cocaine andalcohol [4]. These results showed that most smokers do not smoke tobaccofor the positive effects but instead to keep themselves from withdrawal.The onset of subtle withdrawal symptoms that follow abstinence becomeincreasingly unpleasant until relief is sought. Drinking a cup of coffee,injecting or snorting cocaine, or smoking a cigarette deliver variableamounts of euphoria, but they all consistently relieve negative withdrawal
  29. 29. Addiction: Clinical Features and Biology 21symptoms in their respective addicts. This sense of relief becomes a subtlebut powerful motivator – more so than the ‘hit’. Familiar learningmechanisms consist of the reward that accompanies good behavior, orpositive re-inforcement. For example, children receive praise from theirparents for good behavior to increase the chance that the child continues tobehave in the future. More subtle is the converse when feelings ofdiscomfort or pain are relieved. For example, the relief one gets fromremoving tight shoes, or a heavy load. Such relief is often experienced aspleasure, and can be indistinguishable from positive reward whenunpleasant effects are regular and sustained. This mechanism, called“negative reinforcement” is a powerful motivator. We have glossed oversome of the important features of addiction, but how has addiction beentraditionally defined within medical and psychiatric circles? DEFINITIONS Various authors or professional bodies have attempted to defineaddiction, although wide variation exists and agreement about the precisemeaning of the term lacks consensus. Perhaps the best known definition ofaddiction, often used in clinical practice, is the Diagnostic and StatisticalManual (IV), published by the American Psychiatric Association [5]. Tofulfill the criteria, the patient must recount at least three or more of thefollowing over a twelve month period: 1. Taking larger amounts and over a longer period of time than was intended 2. Unsuccessful efforts to cut down or control substance use 3. Overinvestment of time spent in activities to both obtain and use the substance, or recover from its effects 4. Giving up important social activities to use the substance 5. Continued use despite negative consequences, such as health risks 6. Tolerance - having to use more of the substance to achieve the desired effect
  30. 30. 22 Simon Thornley and Hayden McRobbie 7. A withdrawal syndrome that occurs after periods of abstinence; or the substance is used to avoid such symptoms. This definition embodies the three most important elements ofaddiction - the failure of resolve to reduce consumption in the face ofnegative consequences, along with the physical dependence elements ofsymptoms of withdrawal and tolerance. The International Classification of Disease was developed by theWorld Health Organisation in the late 1800s to systematically classifydisease [6]. The most current version (ICD-10) defines substancedependence similarly to the DSM. The ICD-10 requires a minimum ofthree criteria to be met for a person to be considered dependent. Theseinclude: (1) a strong desire or compulsion to take the substance; (2)difficulties controlling substance-taking behaviour; (3) a withdrawalsyndrome that becomes evident when substance use is stopped; (4)tolerance; (5) neglect of other pleasures or interests in life; (6) continuedsubstance use despite knowledge of harm; and (7) the person should eitheruse, or have a desire to use the substance. The DSM IV criteria for substance abuse only apply to illicitsubstances such as opiates (cocaine or heroine), or amphetamines, andhave some limitations. Let’s compare heroin and nicotine use. Heroinfulfills all criteria with ease. Nicotine use fits with the withdrawal criteria,difficulty controlling use or compulsive use, and use despite the occurrenceof related harm. The remaining four criteria, however: tolerance, usingmore than intended, spending a great deal of time using the drug andgiving up activities to use the drug, don’t as easily apply. These differencesare not solely due to the nature of the addiction to these substances, butalso relate to the social context. If use of these substances results inbreaking the law, and isolated social circles; then the deterioration in socialfunction as a result of these disorders can vary widely. For example, beforeopiates were criminalised, several famous authors, such as Thomas deQuincey and Samuel Taylor Coleridge used heroin daily, yet still publishedinfluential works of prose during this time, and participated in societywithout scorn or isolation. Caffeine use also does not, as far as we know,
  31. 31. Addiction: Clinical Features and Biology 23cause harm to health, however, a withdrawal syndrome and tolerance to thesubstance is commonly reported. Caffeine addicts (us included) can carryout normal social and work functions, even with frequent need for druguse. If caffeine were suddenly criminalized we would be in trouble!Caffeine illustrates one important feature of addiction – that addictivesubstances are not necessarily harmful to health. The same is true fornicotine. If smokers didn’t inhale the tar present in cigarettes, theywouldn’t suffer any adverse effects, as far as we know. Nicotine, taken inisolation, such as through patches or gum, has little or no adverse effectson health. Although addiction is most commonly described in association withsubstance use, other addictions have been described for behaviors that donot involve substances at all. Examples include gambling, sex, and internetuse. Delving deeper into the machinery of addiction, an important element,not captured in official definitions, is the value the addict places onimmediate over delayed rewards. Ainsley [7] noted that a pervasiveelement of the learning in animal and human subjects is the high valueplaced on small, but immediate rewards over delayed, larger ones.Although such preferences are observed in normal people, people withaddictions have an even stronger preference for rapid gratification. Such apreference is reflected in the rate of absorption of drugs of abuse. Drugs orsubstances with the greatest addictive potential tend to be quicklyabsorbed, so that time to relief of withdrawal symptoms is short. Thesecharacteristics may be manipulated to help people with addiction recover.Perhaps some of the best known drugs which assist recovery are nicotinereplacement therapy, in the form of gum, transdermal patch, or lozenge.Cigarette smoke is inhaled, and absorbed across the small air sacks(alveoli) in the lung. The high rate of blood flow through the lungs,coupled with the vast surface area of the alveoli, result in rapid absorptionof the nicotine and rapid relief of tobacco withdrawal. What seems, onpaper, to be a favourable effect of the drug, also gives the product itsaddictive sting. Cigarette companies manipulate the pH of tobacco smoke,by adding ammonia to increase its rate of absorption and thus the addictive
  32. 32. 24 Simon Thornley and Hayden McRobbiepotential of their products. In contrast, nicotine gum, for example, releasesnicotine slowly after chewing, across the lining of the mouth. The lowerblood flow and lower surface area of this body region, slow the absorptionof nicotine. As a result, nicotine gum more slowly relieves tobaccowithdrawal discomfort, but is much less likely than cigarettes to be usedlong term. In a similar manner, methadone is often used as a bridge torecovery for users of intravenous opiates, such as heroin. We will considerin later chapters how this important concept may be applied to food. Ifobese people are addicted to some foods, giving the food version of thenicotine patch, may provide a path to recovery. CLINICAL FEATURES OF WITHDRAWAL SYNDROMES Although we have briefly discussed the salient features of addiction,we will discuss further the nature and time course of common withdrawalsymptoms in more detail. A wide variety of symptoms are described afterabstinence from different substances, and some are better known thanothers (Table 1). The presence of withdrawal symptoms is often considereda pathognomonic, or unique, sign that a substance should be consideredaddictive [8]. Of commonly encountered withdrawal syndromes, perhaps thatassociated with alcohol withdrawal is best known. Classic symptoms havebeen described since antiquity, and are best known as delirium tremens.The symptoms are often so severe, that patients abstaining from alcoholafter a heavy drinking career are frequently treated in a specialised unit torecover. In the first three days after stopping alcohol, patients oftendevelop psychiatric symptoms in which they percieve their skin to becrawling with ants or other insects. They also have dramatic fluctuations ofphysiological measures such as heart rate, blood pressure or temperature.These symptoms are often treated with drugs such as benzodiazepines, ifavailable. After about ten days, such dramatic symptoms subside, but urgesand cravings to drink continue. The most severe symptoms last for aboutthree months, then slowly resolve. Despite the resolution of these
  33. 33. Addiction: Clinical Features and Biology 25withdrawal symptoms, recovered alcoholics are often aware that no morethan a single drink of alcohol can undo months of recovery, and send themback down a destructive path. Table 1. Signs and symptoms of nicotine and other substance withdrawal Alcohol Opioids Sedatives Cocaine Nicotine Stimulants Sweating Yes Yes Nausea Yes Yes Yes Change in heart Increase Increase Decrease rate Sleep Yes Yes Yes Yes Yes Yes Disturbance Anxiety Yes Yes Dysphoric Yes Yes mood Fever Yes Increased Yes Yes appetite Irritability Yes Yes Difficulty Yes concentrating Time course Onset 6-12 4-6 1 week 2-12 hours hours hours Peak 3-7 2-3 days 2-3 days days Duration 1-2 2 weeks Up to 3-4 weeks 10 weeks weeksAdapted from: American Psychiatric Association 2000; Hughes et al. 1994.
  34. 34. 26 Simon Thornley and Hayden McRobbie Tobacco withdrawal symptoms are more subtle than those observed foralcohol, but retain considerable hold over recovering smokers. Symptomsinclude: 1. Craving and urge to smoke 2. Increased appetite 3. Reduced concentration 4. Restlessness 5. Depressed mood 6. Constipation 7. Mouth ulcers (less common) [9]. The severity of tobacco withdrawal is generally less than thatassociated with opioid or alcohol withdrawal and may have a lesser effecton the ability of an addict to undertake normal daily activities. Just becausethe tobacco withdrawal syndrome may be less severe it does not mean thatit is easier to quit than other substances. For example Kozlowski [10]surveyed 1000 people seeking treatment for drug or alcohol dependenceand asked them how difficult quitting smoking cigarettes would becompared to stopping other substances. Over half said that cigaretteswould be harder to quit, even though they rated cigarettes as lesspleasurable to use. Although the nature and severity of these symptoms variessubstantially between patients and different substances, the time courseover which the withdrawal symptoms occur is relatively constant. If thesmoker is able to hold their resolve and abstain continuously, the severityof symptoms generally peaks in the first three days, then wanes over one tothree months. A similar time course is observed with opiate, alcohol, andmetamphetamine addiction. Abstinence is tenuous in people withaddictions, partly from the knowledge, often subconscious and deeplyingrained, that relief from these unpleasant symptoms is only one smoke,snort or drink away. The sight of other users acts as a cue, amplifyingurges, cravings and desires to consume the addict’s substance of choice.While these withdrawal symptoms may respond to the effects of slow
  35. 35. Addiction: Clinical Features and Biology 27release forms of the addictive substance, this treatment often only partiallyrelieves such unpleasant symptoms, often not giving the same hit as theaddictive substance. BIOLOGICAL BASIS OF ADDICTION SYMPTOMS Although we don’t delve too deeply into the technical detail, we willbriefly touch on how neuroscience has added a further dimension to ourunderstanding of addiction, outside the clinical picture, previouslydescribed. The identification of the part of the brain activated by drugs ofabuse has contributed to our understanding of what makes some substancesaddictive over others. The origin of addiction has been linked to a part ofthe human brain responsible for subconscious control of behaviour andmotivation, associated with survival functions, such as eating, drinking andsexual reproduction. One can readily appreciate that drug addiction may beviewed as a ‘hunger’ for drugs, such that some substances become asimportant, or even more important than eating food and consuming waterand other drinks. This anatomic site, the dopaminergic mesocorticolimbicprojection or reward centre, present in the midbrain, is most oftenimplicated in the biology of addiction. In human and animal studies,administration of substances of abuse increases concentrations of thechemical messenger or neurotransmitter, dopamine, in this centre,considered the main component of the brain reward system [11]. Forexample, an intravenous dose of cocaine results in increased release ofdopamine by blocking re-uptake by nerve terminals in a part of the braincalled the nucleus accumbens. Other substances, such as opioids, nicotineand alcohol act in a different area of the reward pathway, stimulating nervecells in other regions, which ultimately influence the nucleus accumbens,increasing dopamine concentrations in this area. This common anatomicsite, along with the linked chemical, dopamine, has therefore, progressedour understanding of the biology of drug addiction, and their commonfeatures [12].
  36. 36. 28 Simon Thornley and Hayden McRobbie What are the clinical features of drug-induced dopamine release inhuman subjects? Two principal effects are commonly described [12].Firstly, release is accompanied by pleasure, or the feeling of a ‘hit’ andbehaviours that produce this are reinforced. A vicious cycle results in deepseated learning to take the substance. The increase in dopamineconcentration focuses the individual on sensory elements (‘cues’, such asthe smell of tobacco among smokers) associated with drug taking. Thesensation of such elements often initiates automatic, subconscious,Pavlovian stimulus-response drug taking when an individual issubsequently exposed to these cues. This is commonly observed in peoplethat smoke, so that the sight of cigarettes, other people smoking, ash trays,or lighters, can ‘switch-on’ the automatic lighting of a cigarette, in peopleaddicted to tobacco [13, 14]. Although dopamine has been closely linked to addiction, theneurotransmitter also plays a role in people with psychosis – seeing orhearing things that are not there. Indeed, dopamine has been referred to asthe “wind of the psychotic fire”, when describing its pivotal role in thesymptoms and treatment of psychotic disorders such as schizophrenia [15].Evidence for dopamines importance emerges from clinical practice - forexample, treatment of patients with Parkinson’s disease using therapeuticdoses of levo-dopa, a dopamine like substance, can result in a drug-induced psychosis in a small proportion of these patients. Conversely,drugs used to treat psychoses such as schizophrenia interfere withdopamine pathways, and may result in unwanted Parkinsonism, manifestedby expressionless, blank faces and a characteristic pill-rolling tremor. If addiction and psychosis share the same biological pathway andneurotransmitter (dopamine), then we might expect that such mentaldisorders and addiction commonly coexist in individuals. For workers inthe mental health field, such disorders are all too frequently associated,with the term “dual-diagnosis” used to summarise the occurrence of thetwo disorders in the same patient. In one summary, the prevalence ofsmoking was between 80 and 90% in people treated in hospital withschizophrenia [16]. Numerous epidemiological studies describe the co-occurrence of schizophrenia and other forms of addiction, such as to
  37. 37. Addiction: Clinical Features and Biology 29alcohol, metamphetamine and opiates [16]. Further, the presence of illicitdrug use in people with schizophrenia predicts relapse, treatment resistanceand need for further hospital treatment. Logically, we might expect that if obesity and weight gain are alsorelated to this pleasure chemical, dopamine, then when the effects ofdopamine are blocked in some way, for example by drugs that exert sucheffects in the brain, then people that take these drugs may put on weight.Such observations do, in fact, commonly occur in clinical practice. Drugsused to treat psychosis, all, to a greater or lesser extent, block the action ofdopamine, and all are known to cause weight gain, with some drugs havingmore potent side effects than others [17]. Even in people with psychosis,many are overweight before they start treatment, compared to thefrequency in the general population, increasing speculation that overeatingmay play a role in the development of psychotic disorders [18]. We willexplore the implications of food addiction later in the book. For themeantime, we simply draw attention to such theories, showing how boththe biology and clinical manifestations of these disorders show similarfeatures. SUMMARY In this chapter we have reviewed the nature and context of addiction,noting that it shares some features similar to hunger. In fact, one couldobserve that drug dependence could be described as a ‘hunger’ for drugs.Other common features of drug addiction include difficulty stopping thebehaviour, due to the presence of a withdrawal syndrome that manifestswhen an individual stops. The addict who attempts abstinence knows,either consciously or subconsciously, that taking the substance they havebecome fond of can relieve these symptoms rapidly. If they do continue toabstain, most of the unpleasant discomfort begins to tail off after aboutthree months. The biology of addiction is also beginning to be understood,such that the chemical dopamine, present in the part of the brainresponsible for motivation, is stimulated by addictive drugs, and thischemical plays an important part in severe mental disorders, characterised
  38. 38. 30 Simon Thornley and Hayden McRobbieby psychosis. With this information in mind, we move on to considerwhether eating behaviour and various foods show similar characteristics todrugs of addiction? Could this information help us find the key to unlockthe modern obesity epidemic? REFERENCES[1] Russell MA. Cigarette dependence. I. Nature and classification. BMJ. 1971 5;2(5757):330-331.[2] Center for Health Promotion and Education. Office on Smoking and Health, United States. Public Health Service. Office of the Surgeon General. The Health Consequences of Smoking: Nicotine Addiction: A Report of the Surgeon General [Internet]. 1988 [cited 2011 Mar 24];Available from: http://profiles.nlm.nih.gov/NN/B/B/Z/D/[3] Balfour DJK. The neurobiology of tobacco dependence: A preclinical perspective on the role of the dopamine projections to the nucleus. Nicotine and Tobacco Research. 2004;6(6): 899-912.[4] Blumberg H., Cohen D, et al. British Opiate Users: I. People Approaching London Drug Treatment Centres. Substance Use and Misuse. 1974;9(1): 1-23.[5] APA. Diagnostic and Statistical Manual of Mental Disorders. Washington DC: American Psychiatric Association; 1995.[6] WHO| International Classification of Diseases (ICD) [Internet]. [cited 2011 Mar 24];Available from: http://www.who.int/ classifications/icd/en/[7] Ainslie G. Breakdown of Will. 1st ed. Cambridge University Press; 2001.[8] Heather N. A conceptual framework for explaining drug addiction. Journal of Psychopharmacology. 1998;12(1):3-7.[9] West R, Schiffman S. Smoking Cessation. Fast Facts: Indespensible Guides to Clinical Practice. Oxford: Oxford Health Press Limited; 2004.[10] Kozlowski LT, Wilkinson DA, Skinner W, Kent C, Franklin T, Pope M. Comparing Tobacco Cigarette Dependence With Other Drug
  39. 39. Addiction: Clinical Features and Biology 31 Dependencies. JAMA: The Journal of the American Medical Association. 1989 Feb 10;261(6):898 -901.[11] Tzschentke TM. The medial prefrontal cortex as a part of the brain reward system. Amino Acids. 2000;19(1):211-9.[12] Drevets WC, Gautier C, Price JC, Kupfer DJ, Kinahan PE, Grace AA, et al. Amphetamine-induced dopamine release in human ventral striatum correlates with euphoria. Biological Psychiatry. 2001;49:81- 96.[13] West R. Theory of addiction. Oxford: Blackwell Publishing; 2006. p. 10.[14] Munafo M, Albery I. Cognition and Addiction. Oxford: Oxford University Press; 2006.[15] Laruelle M, Abi-Dargham A. Dopamine as the wind of the psychotic fire: new evidence from brain imaging studies. J Psychopharmacol. 1999;13(4):358-371.[16] Batel P. Addiction and schizophrenia. European Psychiatry. 2000;15(2):115-122.[17] Baptista T. Body weight gain induced by antipsychotic drugs: mechanisms and management. Acta Psychiatrica Scandinavica. 1999;100(1):3-16.[18] Peet M. Diet, diabetes and schizophrenia: review and hypothesis. The British Journal of Psychiatry. 2004;184(47):s102-105.
  40. 40. Chapter 3 CARBOHYDRATES, SUGARS AND HUMAN HEALTH: A SUMMARY OF THE EVIDENCE INTRODUCTION In the first chapter, we explored recent trends in food intake during the th20 century, preceding the modern day obesity epidemic, starting from the1970s to present. Two different national or cultural dietary changespreceded the English speaking, collective popping of buttons in the early1980s to the present day. Anglophones, driven by a desire to reduce theburden of cardiovascular disease, initially in the United States, strove toreduce the fat intake of the populace. Although the macronutrient targetchanged from all fat, to animal derived, saturated fat; the message wasoften confused, with “99% fat free” a common health claim, adorninglabels everywhere on manufactured food products. Once, when shoppingwith my son, I (ST) was shocked to see that marshmallows wereproclaiming their nutritious properties, with large type “99% fat free”smeared over their plastic wrapper! Contrary to this anti-fat trend, Asian countries have followed anopposite trajectory, increasing the proportion of fat in their diets, as theireconomies have strengthened and more expensive animal fat has been
  41. 41. more widely affordable. Similarly, obesity statistics in these countriescouldn’t be more different: in the OECD, English speaking countries havelead the stakes, with obesity barely raising a murmur in either Japan orSouth Korea. In this chapter, we consider, more carefully at an individualand clinical level, what effect modifying carbohydrate intake has on health,and contrast these effects with other diets. From chapter 2, we havereviewed the subject of addiction, concluding that the concept ofwithdrawal shares some similarities with hunger, usually applied to food.From our medical training we were once firm believers in the supposedadverse health effects of eating calorie rich fat, but what aboutcarbohydrates that have filled the void created by fat in the last thirtyyears? Are carbohydrates potentially harmful or healthy when consumed inlarge amounts? Do they contribute to weight gain, and are there anypotential properties of carbohydrates that can help us understand themodern epidemic of obesity? In our medical training, we received little information about the effectsof carbohydrates on health. With the benefit of hindsight, we now attributethis to the dominant theory of the time, which emphasised energy densityas the most important aspect of food by which one could adjudicate food asgood, bad or otherwise. Because fat has twice the energy density of othermacronutrients, protein or carbohydrate, the finger of nutritional blamewas always pointed at greasy targets. Basic biochemical pathways were,however, taught. I soon realized that the brain, perhaps the most criticalorgan, on which human survival depends, runs almost entirely on anuninterrupted supply of the single sugar, glucose. The body possesses aneat mechanism by which alternative fuels can be mobilised in the event ofa prolonged carbohydrate drought; however, this was presented as a quirkof nature rather than being of much relevance to health or weight loss.Carbohydrates were also relevant to the metabolism of individuals whosuffered from another disorder, diabetes. People with this condition havepoor regulation of glucose, through either immune destruction orexhaustion from overwork of the visceral organ, the pancreas, which
  42. 42. Carbohydrates, Sugars and Human Health 35secretes insulin, the primary regulator of glucose levels in the body.Interestingly, the alternative brain fuel, ketones, produced in the starvingstate, are also switched on in one form of diabetes (type I), characterisedby a complete lack of insulin. First, what are carbohydrates? Most people are familiar with theconcept now with the popular diets that we will explore. Somemisconceptions and confusing terminology abound, however. The mostcommon types of carbohydrate are starches, which form the backbone ofmost diets around the globe. Starch consists of long chains of glucosemolecules, linked to form long chains. Starchy products include anythingmade up of white flour, such as bread, baked goods, pasta, semolina; rootvegetables such as potatoes and taro, and other staples such as rice andmaize. Glucose exists as a simple sugar, with a sweeter taste and is oftenadded to sports drinks to provide instant energy. Glucose is familiarterritory for most doctors. After glucose enters the body, the gut organ, thepancreas, secretes insulin into the blood, so that the body can take up theglucose into the liver and muscle. The body possesses complex machineryfor keeping the levels of glucose reasonably stable in the body, so that theprecious grey matter within the brain is constantly supplied with enoughfuel to keep us going. If the level of glucose drops below a certainthreshold, people with low blood glucose levels experience ravenoushunger, become sweaty and faint, and eventually drop unconscious. Peoplewith diabetes are not able to regulate the levels of this sugar in the blood,usually due to either a lack of insulin, or insensitivity to this hormone andhigh levels of glucose can be measured in the veins of people diagnosedwith the disorder, before they are treated. Treatment of diabetes, at present,is based on reducing the levels of glucose in the blood by increasing thelevels of insulin either by taking drugs that stimulate insulin release or byinjecting the substance directly under the skin. Manipulation of the diet ofpeople with diabetes is another way of improving blood sugar, althoughthis has been more controversial. Monitoring blood glucose levels, hence,becomes the obsession of people with diabetes, and the doctors chargedwith their care.
  43. 43. 36 Simon Thornley and Hayden McRobbie With the treatment of diabetes centered squarely on glucose, anothermonosaccharide found in table sugar has received much less attention inthe research world until relatively recently. I (ST) confirmed this fact,when I began to read about the health effects of fructose, I wondered why Ihadn’t heard anything about this sugar during my training. I scouted in theuniversity library for a text book of clinical nutrition, flicked to the indexand looked under ‘f’ for fructose. Nothing. I couldn’t believe it, so I pickedup another, then another. The same result. Until the last five years or so,fructose has been off the nutrition radar for all but a small handful ofresearchers. Sugar is slightly different to glucose. It consists of two sugarsjoined together to form a disaccharide: one is the familiar building block ofstarch, glucose, while the second is the enigmatic monosaccharide,fructose. As the name suggests, fructose is found mainly in fruit. Fructoseis most concentrated in table sugar, and to a lesser extent, in honey. Insugar, fructose makes up about 50% of the weight of the crystallinesubstance, joined to glucose as the disaccharide, sucrose. High fructosecorn syrup, as the name suggests, is a synthetic derivative of the starchderived from corn. When corn starch is boiled down to break the chemicalbonds, free glucose is left. To make something like sugar, an enzyme isadded, which converts some of the free glucose to fructose. High fructosecorn syrup is the sweetener most commonly added to manufactured foodsin the United States and Canada. Due to governmental subsidies for corngrowers, high fructose corn syrup has become the most economicallyfavorable sweetener for the North American food industry. The onlydifference between this product and sugar is that the glucose and fructoseexist in free, single sugar, monosaccharide form in high fructose cornsyrup, whereas table sugar consists of the two single sugars joined by achemical bond as the double sugar sucrose (figure 1). With glucose beingeasy to measure in patient’s blood, and defining the diagnosis of diabetes,it is easy to understand why fructose has been largely ignored as a focus ofnutrition research. What is more, fructose is found in fruit, what couldpossibly wrong with eating fruit? We return to fructose later in the chapter,as a relatively late development in the carbohydrate story. We first
  44. 44. Carbohydrates, Sugars and Human Health 37consider whether diets based on modifying carbohydrates, either in total, orbased on glucose have shown any benefits to human health.Figure 1. The constituents of table sugar, glucose and fructose, free as present in highfructose corn syrup, and joined at the hip, as sucrose, found in table sugar. PHYSIOLOGY OF GLUCOSE AND INSULIN The first clue that I had that carbohydrates may be important in theregulation of weight was observed in people with type 1 diabetes, morecommon in children, who produce little or no insulin. The lack of thispancreatic hormone occurs because their own antibodies have, for anunknown reason, destroyed their cells that produce the protein. Diabetesspecialists know that young women with this disorder, who are often
  45. 45. 38 Simon Thornley and Hayden McRobbieobsessed with their weight, will reduce their insulin dose, from prescribedlevels, to shed a few pounds. Although these patients may be admonishedby their doctors about the long term adverse consequences of suchbehaviour, living with precariously high levels of glucose coarsing throughtheir veins - causing rotten eyes, limbs and heart muscle - the immediatedesire to control weight may be too strong. The first lecture that I receivedon the subject of this type of diabetes at medical school acknowledged thisseeming paradox, that diabetes was “starvation in the face of plenty”.Before effective treatment to reduce blood glucose was available, sufferersof diabetes could seemingly eat to excess and lose weight simultaneously,all because of the lack of a crucial hormone that was critical for processingglucose into stored energy or body fat. Despite the apparent centrality of insulin to weight regulation inpatients, beliefs handed down from academics for the apparent excessweight and skyrocketing rates of diabetes was generally attributed toenergy density. People with diabetes acquired the disease from fat and notsugar. From the observation that fat contains twice the energy per unitweight (energy density) than either of the two other macronutrients, proteinor carbohydrate, this rather simplistic, but seemingly elegant principle,enshrined the basis of public health and nutritional strategies to treat thegrowing tide of people with diabetes that were beginning to swamp healthservices.HEALTH EFFECTS OF CARBOHYDRATE MODIFIED DIETS Which diets are commonly used that are based principally onmodifying carbohydrates? The Atkins’ diet [1] consists of almost abandoning carbohydratealtogether, no more than 20g per day or less than one slice of bread isallowed in the early phases. On the other hand, Atkins lets dieters eat asmuch fat and protein as their heart desires, a polar opposite to usualnutritional approaches of limiting fat and total energy.
  46. 46. Carbohydrates, Sugars and Human Health 39 Although the Atkins diet has been lampooned in nutrition circles foralmost half a century as antithetical to interventions grounded on energydensity, another carbohydrate based-diet, which measures the intensity ofthe blood glucose response from a standardised portion of food has becomemore accepted into the mainstream of nutritional thought. First developedin the 1980s, glycemic index (GI) is a measure of what effect a food,altered in size to include 50g of carbohydrate, has on the area under thecurve of a blood glucose (an indicator of the average glucose level) vs timegraph [3]. Pure glucose is the reference standard, designated 100, by whichall other foods are compared. Starchy foods are highest, for example, whitebread is about 70, with whole grains, such as lentils, and fruit andvegetables generally lower - in the 30s and 40s. The so called “low glycemic index” diet consists of eliminatingconsumption of foods whose glycemic index is greater than an arbitraryfigure of about 55. The diet was initially considered most useful inlowering blood glucose in people with diabetes, which is thought to reducethe onset of complications from the disease [4]. In such people, bloodglucose becomes elevated, and higher average levels correlate withincreased adverse effects. Indeed, much of the treatment of diabetes isfocused on reducing blood glucose through the use of both medicines andinsulin, and limiting the intake of starchy foods. As long chains of glucose,starch is broken down and, following absorption, results in a spike ofglucose in the bloodstream. If glucose levels could be controlled throughdiet, lowering dependence on drugs, then surely this strategy mightimprove the health of people with diabetes. Given that this condition is arelatively arbitrary cut-off at one end of an extreme end of the spectrum ofglucose control, maybe everyone would be better off eating low GI food?Also, insulin is an important hormone which promotes the laying down offat, encouraging the liver to convert a digested glucose meal to cholesterolwhich is then transported in the blood stream to the periphery and stored asexcess flab. Insulin release follows a glucose meal, so that choosing foodsthat do not produce such a large bolus of glucose would theoreticallyimprove average glucose levels, help people lose weight and reduce thechance of them developing life threatening complications of diabetes such
  47. 47. 40 Simon Thornley and Hayden McRobbieas heart attacks or strokes. Because less insulin is produced, thentheoretically, such a diet would also help people lose weight. So much for the theory, what has been born out in reality? Althoughvery skeptical about the adverse effects of carbohydrates, the medicalliterature continues to fill with evidence that diets based on eating lowglycemic index foods result in greater weight loss and better healthoutcomes than traditional diet methods (reducing energy density or fat).Such is the volume of studies on glycemic index that some researchershave pooled many studies to look at the overall effect of the diet on weightloss and risk of developing chronic disease, using a technique called meta-analysis. Such studies are often accorded the highest level of evidence,among the hierarchy of scientific evidence. Two influential so called“meta-analyses” have been published, one demonstrating that peoplefollowing glycemic index diets reduce their weight [5] with anothershowing reduced risk of a range of important and common chronicdiseases from such a diet [6]. One study, which used a similar technique tocompare a range of dietary techniques at reducing risk of heart attackshowed that glycemic index was in the top four methods to lower one’schances of such an outcome [7]. According to the study, the best means ofreducing risk of a heart attack was the Mediterranean diet, which again,emphasises the intake of unrefined, low-glycemic-index, carbohydratefood. In patients with diabetes, an American endocinologist, Eric Westman,compared a low glycemic index diet with the Atkins diet to assess theireffects on glycemic control, weight loss, blood pressure and other indicesof cardiovascular risk [8]. The results were astonishing. Although manysubjects dropped out of the study (41%), the Atkins diet group had mostweight loss at 6 months (-11 vs -7kg) and almost all no longer needed drugtreatment for diabetes (95% compared to 62%). Such results stronglyindicate that both diets help reverse the metabolic effects of type 2diabetes, but reducing all carbohydrate seems to confer additional benefit,over only limiting high glycemic index, or starchy foods. Later wespeculate that glycemic index overlooks the effects of an important sugar –
  48. 48. Carbohydrates, Sugars and Human Health 41fructose. Perhaps the main difference between the two groups, in this trial,was fructose intake? With such glowing evidence, has use of the glycemic index or Atkins(low carbohydrate diet) become common place in medical practice to helppeople control their weight? The answer is that it has and it hasnt.Nutrition ideas are slow to change, and as we have discussed in chapter 1,the public health and medical community, lead by the American HeartAssociation, has campaigned against the intake of fat and saturated fat tolower heart disease risk. One of the side effects of this advice, althoughoften not acknowledged, was to increase the amount of carbohydrateconsumed. Also, public health professionals are fond of simple messagesto convey to the public. The message to reduce fat is easy. Most peoplerecognise fat on meat and know the greasy feel of fried food. Such amessage is easily communicated and understood. Glycemic index, incontrast, is complicated, and takes more effort to convey to the public.Also, when the low fat message is combined with the low glycemic indexone, they may appear contradictory and confusing. If you are admonishedto reduce fat, your only recourse is to eat either protein or carbohydrate.Protein supply is often limited due to expense (animals are costly tocultivate), so carbohydrate naturally floods the void created by the low fatdiet. What is not often stated is the contradictions between the low fat andlow (or modified) carbohydrate approaches. Fat, taken with carbohydrate,actually delays the emptying of the stomach and so, in a purely mechanicalfashion, lowers the GI of a carbohydrate meal. Protein and acid have asimilar effect, slowing down the rate at which the stomach, the body’s foodstorage bag, empties, allowing the nutrients to be absorbed by the smallintestine. Glycemic index and low fat diets are uncomfortable bed fellows. Has the glycemic index diet been popular? In contrast to the reticenceshown by the medical profession, the glycemic index range of books,published by an Australian group from the University of Sydney, havecertainly been successful in marketing their ideas. The continually iteratingversions of the “New Glucose Revolution” consistently hits the best sellerlists on Amazon, and the penetration of glycemic index into the Australianpsyche has been dramatic. The “GI” symbol, signifying a low glycemic
  49. 49. 42 Simon Thornley and Hayden McRobbieindex food is commonly found on products displayed on Australiansupermarket shelves. No more than 1,000 kilometres away in NewZealand, a country that shares similar cultural traditions with Australia, haslittle recognition of glycemic index, and the “GI” symbol is not widelydisplayed. For example, a new refined, low-GI table sugar, recentlymarketed in Australia, rapidly claimed 4% of the supermarket sugarmarket, however, the same product, on sale in New Zealand, struggles toreach supermarket shelves. Initially, we were taken with glycemic index. When seeking to identifya property of food that may predict its addictive potential as well as havingproven effects on human health, glycemic index appeared to fit the bill.What we found puzzling was that, in general, glycemic index ranks somerefined carbohydrate laden foods higher (more dramatic glucose response)and whole foods lower. Sugar, however, is an important exception. Weknow from global records of food production, import and export that sugarintake has risen substantially, and is one of the most dominant nutritionchanges in the latter half of the twentieth century [9]. The country with themost dramatic sweetening of their food supply, the United States, also hasthe highest proportion of obese adults of all industrialized nations.However, if you believe the glycemic index is the most important predictorof the health value of food, sugar appears relatively benign. Pure sucrosehas a GI of 68 [3], and many sugar containing products have lower GIs,due to either their fat content. The most popular book written on the effectsof the glycemic index actually encourages its readers to enjoy eating sugar[3]. What is it about sugar that gives it such a low GI, despite it being ahighly refined substance? Does sugar have any special properties whichmay cause weight gain or other diseases to occur in people with a sweettooth? SUGAR Fructose holds the key to understanding the effect sugar has on health.Sugar, the variety you buy in the supermarket, is derived from sugar cane,
  50. 50. Carbohydrates, Sugars and Human Health 43with only one substance left after all the other parts of the plant arestripped away in the refining process: sucrose, a molecule consisting of onepart glucose and one part fructose, chemically linked. Molasses, a black,tarry, licorice tasting goo is made early in the process of making sugarfrom sugar cane. In the United States, as we mentioned earlier, sugarcontained in manufactured foods is slightly different, usually derived fromcorn (high fructose corn syrup). What is unique about sugar (or HFCS) is its concentration of fructose-roughly 1:1, or 50% by weight, which is much higher than naturallyoccurring sources. Fructose is also found in fruit, honey and somevegetables, however, the sugar in these items is far less concentrated(bananas contain about 10% fructose). Fructose has often been ignored innutritional circles, because, it is assumed that since it is found in fruit,which have been a key part of low fat diets, so it must be harmless... or isit? Can something that nature provides be bad for us? Studies of human risk perception show that naturally occurring hazardsare thought to be much less dangerous than those that are man made [10].For example, radioactive waste is likely to engender more fear than saytobacco, even though the latter causes far more deaths. Also, riskyexposures we come across every day are perceived as much less importantas rarely encountered ones. Sugar is often considered a “natural”sweetener, particularly when contrasted to low calorie counterparts such asaspartame and sucralose. However, the briefest glance into themanufacturing process, by which sugar cane is turned into table sugar,indicates that this process is far from “natural”. Sugar cane is crushed,mixed with lime, and then mixed with a number of chemicals, such asphosphoric acid and calcium hydroxide, to produce white sugar. Sucrose,in high (99%) concentration is left, with all other plant material strippedaway. If we leave the argument over whether sugar is “natural” to one sidefor a moment, we now consider whether sugar affects health, and if so,how? Interestingly, in the late 1990s and early new millenium, theAmerican Diabetes Association advocated increasing fructose consumptionin people with diabetes [11]. It seems counter-intuitive to most people
  51. 51. 44 Simon Thornley and Hayden McRobbiewithout nutritional training to advise people with diabetes to eat sugar, butthat was a policy, and I even came across a jar of jam recently that claimedto be healthy due to its high fructose content. This policy was derivedmainly as a result of fructoses modest short term effect on the glucoselevel in the blood, after a sugary or fruity meal. Much of the damage fromdiabetes is thought to accrue from high levels of glucose circulating in theblood vessels of patients with diabetes, and if fructose intake may improvesuch a measure, then surely it must be safe, right?Figure 2. The different metabolic paths of glucose and fructose. The theory behind this advice was that fructose did not increase bloodglucose levels, because it is broken down by the liver, after being absorbedin the gut, and before it enters the blood stream, where it can be easilymeasured. Because treatment for diabetes is based on measurement of, andcontrol of blood glucose, diabetes experts initially considered fructoseharmless. Fructose, unlike glucose, does not stimulate insulin release andbecause it is commonly found in fruit, it was thought to be a healthy
  52. 52. Carbohydrates, Sugars and Human Health 45alternative for people whose bodies suffered from a lack of insulin, orsensitivity to the hormone, and couldnt process glucose properly. Fructoseis taken up by the liver independent of insulin (Figure 2), and could sparethe body from potentially harmful exposure to glucose. However, it wassoon found that fructose had adverse effects on fat levels in the blood,being readily converted to this form of energy storage, in contrast toglucose that is mostly used for energy. High fructose intakes unequivocallyraise serum triglycerides levels [2]. Although debate continues about whichsubgroup of fats found in the blood cause heart attacks (high densitylipoprotein is probably the strongest contender), high triglyceride levelshave been linked to heart attacks in several observational studies [12].Although these downsides of fructose have been largely conceeded, andadvocates for fructose have withdrawn advice to consume sugar as a healthfood, a rising tide of evidence indicates that fructose not only contributesto high triglyceride levels, but also give rise to a range of other commonand devastating diseases. Animal studies have documented adverse metabolic effects of refinedfructose intake. Rodents fed on high fructose and sucrose diets, but nothigh glucose diets, develop features of the metabolic syndrome, such ashyperinsulinemia, hyperuricemia and hypertriglyceridemia [13]. To explore the effect fructose may be having on our health, weconsider in more detail the physiological effects of fructose, beforereviewing possible health effects of excess consumption. A full discussionof the metabolism of fructose is beyond the scope of this chapter, but isdiscussed elsewhere [13]. After eating, fructose is absorbed from the smallbowel and enthusiastically broken down by the liver, independent ofinsulin. Unlike glucose, fructose does not stimulate insulin release, whichsignals fullness or satiety. Metabolism of fructose depletes cellular energystores (ATP), and induces uric acid production (which causes a particulartype of arthritis - gout). The principal products of liver fructose break-down are triglycerides, which are then released into the blood. Whilefructose is processed, conversion of glucose to glycogen (glycogenesis) inthe liver is blocked. The reduction in glucose processing by the liver, inturn, causes insulin levels to rise so that glucose is taken up in alternative

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