bs_bs_bannerHiscockReferences                                        4 Widimsky P, Groch L, Zelizko M,                    ...
Sugar intake and cardiovascular riskIntroduction                                                                of non-com...
Thornley et al.   What is sugar? Until recently, this term has encom-        was becoming rapidly accepted and enshrined i...
Sugar intake and cardiovascular risk                                                                              1980 199...
Thornley et al.United States of cardiovascular disease and stroke, com-         liver cells, with the remaining 80% taken ...
Sugar intake and cardiovascular riskTable 1 Positive associations between indicators of exposure to fructose and important...
Thornley et al.                                                                          Table 2 Mean U.S. reported sugar ...
Sugar intake and cardiovascular riskEvidence for competing dietary causes of                                    reporting ...
Thornley et al.   The advice, therefore, from the Australian Heart Foun-         the same 12-month period: (i) taking larg...
Sugar intake and cardiovascular riskWhat are the parallels between food                                         was unable...
Thornley et al.intake and salt to reduce the incidence of cardiovascular                 soft drink, fruit juice, breakfas...
Sugar intake and cardiovascular risk     in obesity. Physiol Rev 2010; 90:                          increased in periodont...
bs_bs_bannerThornley et al.   gender and weight gain on short-term                   56 Grunberg NE. The effects of nicoti...
Upcoming SlideShare
Loading in …5
×

Imj2902

447 views

Published on

A paper written with some Australian colleagues which looks at whether there is any evidence that sugar is related to risk of cardiovascular disease.

Published in: Health & Medicine
0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total views
447
On SlideShare
0
From Embeds
0
Number of Embeds
2
Actions
Shares
0
Downloads
7
Comments
0
Likes
0
Embeds 0
No embeds

No notes for slide

Imj2902

  1. 1. bs_bs_bannerHiscockReferences 4 Widimsky P, Groch L, Zelizko M, infarction: rationale and design of the Aschermann M, Bednár F, Suryapranata DANAMI-2 trial. Am Heart J 2003; 146:1 Assessment of the safety and efficacy of H. Multicentre randomised trial 234–41. anew treatment strategy with comparing transport to primary 7 Dalby M, Bouzamando A, Lechat P, percutaneous coronary intervention angioplasty vs immediate thrombolysis Montalescot G. Transfer for primary (ASSENT-4 PCI) investigators. Primary vs combined strategy for patients with angioplasty versus immediate versus tenecteplase-facilitated acute myocardial infarction presenting thrombolysis in acute myocardial percutaneous coronary intervention in to a community hospital without a infarction. Circulation 2003; 108: patients with ST-segment elevation acute catheterization laboratory. The 809–14. myocardial infarction (ASSENT-4 PCI): PRAGUE study. Eur Heart J 2000; 21: 8 Acute Coronary Syndrome Guidelines randomised trial. Lancet 2006; 367: 823–31. Working Group. Guidelines for the 569–78. 5 Grines CL, Westerhausen DR Jr, Grines management of acute coronary2 Kastrati A, Mehilli J, Schotterbeck K, LL, Hanlon JT, Logemann TL, Niemela M syndromes 2006. Med J Aust 2006; 184 Dotzer F, Dirschinger J, Schmitt C et al. et al. A randomised trial of transfer for (Suppl): S1–S32. Early administration of reteplase plus primary angioplasty versus on-site 9 Bohmer E, Hoffman P, Abdelnoor M, abciximab vs abciximab alone in patients thrombolysis in patients with high-risk Arnesen H, Halvorsen S. Efficacy and with acute myocardial infarction referral myocardial infarction: the air primary safety of immediate angioplasty versus for percutaneous coronary intervention. angioplasty in myocardial infarction ischemia-guided management after JAMA 2004; 291: 947–54. study. J Am Coll Cardiol 2002; 39: thrombolysis in acute myocardial3 Ellis SG, Tendera M, de Belder MA, van 1713–9. infarction in areas with very long transfer Boven AJ, Widimsky P, Janssens L et al. 6 Anderson HR, Nielsen TT, Vesterlund T, distances: results of the NORDISTEMI FINESSE investigators. FAcilitated PCI in Grande P, Abildgaard U, Thayssen P et al. (NORwegian study on District patients with ST- elevation myocardial A comparison of coronary angioplasty treatment of ST-Elevation Myocardial infarction. N Engl J Med 2008; 358: with fibrinolytic therapy versus acute Infarction). J Am Coll Cardiol 2010; 55: 2205–17. coronary angioplasty in acute myocardial 102–10.Sugar restriction: the evidence for a drug-free intervention toreduce cardiovascular disease riskS. Thornley,1 R. Tayler2 and K. Sikaris31Section of Epidemiology and Biostatistics, University of Auckland, Auckland, New Zealand, 2Epworth Hospital, Richmond and 3Melbourne Pathology,Melbourne, Victoria, AustraliaKey words Abstractcarbohydrates, fructose, dietary sucrose,coronary artery disease. Background/Aim: Uncertainty exists about what dietary component is most likely to cause coronary heart disease. Over the last thirty years, attention has focused onCorrespondence saturated fat and salt as guilty parties. More recently, evidence suggests that excess sugarSimon Thornley, Section of Epidemiology and intake is more likely than either traditional factor to lead to atherosclerotic disease.Biostatistics, Level 4, School of Population Some researchers have also speculated that sugar is addictive, in a similar manner toHealth, Tamaki Innovation Campus, The caffeine and established drugs of abuse.University of Auckland, Private Bag 92019, Methods: Here we review the epidemiological, biochemical and psychological evi-Auckland 1142, New Zealand. dence that implicates excess sugar intake as an important cause of ill-health.Email: s.thornley@auckland.ac.nz Results: We found relatively consistent evidence of association between markers of sugar intake and risk factors for cardiovascular disease, or the disease itself. This evi-Received 24 April 2012; accepted 11 May dence contrasted with rather weaker evidence which linked either saturated fat or salt2012. with cardiovascular disease endpoints. We also found some evidence of a sugar addiction syndrome.doi:10.1111/j.1445-5994.2012.02902.x Conclusion: We suggest that advice to restrict sugar intake should be a routine part of clinical care, particularly when patients are being counselled about cardiovas- cular risk. © 2012 The Authors46 Internal Medicine Journal © 2012 Royal Australasian College of Physicians
  2. 2. Sugar intake and cardiovascular riskIntroduction of non-communicable diseases, in his influential work published in 1976.3 If one looks back over a longerAuthorities in the field of nutrition have made contradic- period of time, some experts have drawn attention to thetory statements about the role of sugar in the aetiology of adverse effects of sugar consumption since at least thediabetes, a condition linked to cardiovascular disease: early 1960s.4,5 From this time, nutrition attention shifted It is not yet clear whether any single attribute of the to fat, and interest in sugar was largely abandoned until Western way of life is particularly important in increas- recently. As an example, Professor Jim Mann, an inter- ing the risk of diabetes. Excess sucrose has largely national nutrition expert, describes sugar (sucrose) as been exonerated as an important dietary factor in the ‘exonerated’ in the aetiology of type 2 diabetes when aetiology of type 2 diabetes . . . (2003).J. I. Mann and writing in the prestigious Oxford Textbook of Medicine. The A. S. Truswell1 American Heart Association, which in 2002 had taken a similar view to Mann,2 later changed its mind, reporting Originally proposed as the ideal sweetener for people that fructose (half of the sucrose molecule) was now with diabetes . . . Fructose . . . has been indirectly facing a guilty verdict, whereas it had earlier received a implicated in the epidemics of obesity and type 2 dia- pardon.6 betes (2009).The American Heart Association2 So what can we conclude? Is sugar a problem or isn’t it? Definitions What do local authorities have to say? Institutions inAustralasia charged with preventing premature cardio- During the last 20 years, physiological properties of car-vascular death offer advice to reduce a person’s chance bohydrates have attracted little interest due to saturatedof becoming ‘just another statistic’. The Australian Heart fat dominating the nutritional horizon. Present in highestFoundation suggests the following: eat a variety of concentrations in animals, saturated fats are generallyfoods; include vegetables, whole grains, fruit, nuts and solid at room temperature and have all carbon chainsseeds; choose healthier fats and oils; try to limit sugary, (fatty acids) filled (or saturated) with hydrogen. Thefatty and salty takeaway meals; and drink mainly water. warnings of the National Heart Foundations in NewThe New Zealand counterpart solicits several steps to a Zealand and Australia to avoid meat and dairy fat arehealthy heart: eat three meals a day with more plant made on the basis that such sources contain highmaterial, and less dairy fat, meat fat or deep-fried food; concentrations of saturated fat. Fat is also energy-dense,eat low-fat products (lean meat); and avoid excesses of carrying twice the calories of either protein or carbohy-sugar or salt. drate per unit weight. Both the presence of ‘atherogenic’ This advice seems sensible, but does it withstand closer saturated fat and the high density of energy from thisscrutiny? Should a clinician blindly adhere to this advice? source have made it a favourite target of public healthWhat is the evidence for all or part of the guidance? nutritionists seeking to improve population health.Underlying this counsel is the belief that saturated fat, Some properties of carbohydrates have beensugar and salt cause coronary artery disease, or the studied, however. In the early 1980s, the properties ofbroader term ‘cardiovascular disease’ (which encom- glucose-containing foods were classified using the termpasses stroke and peripheral vascular disease events as ‘glycaemic index’ (GI). This measure is the average area-well). A cursory glance at such guidelines suggests that under-the-curve of plasma glucose measurements drawnthe evidence for restricting all components of food is immediately before, and up to 1 h after, the intake of aequal and should be considered on par. If anything, satu- food standardised by the weight of the carbohydrate itrated fat avoidance is prioritised in this advice. Here, we contains. The index discriminates between starchy foods,look closer at the biological and epidemiological evidence made up of high volumes of linked glucose chains.that excess sugar intake causes cardiovascular disease, Refined carbohydrates, such as white bread, white ricebriefly contrast such evidence with that for modifying fat and pasta, are scored high on the GI (>65), while unre-and salt intake, and consider what advice should be given fined carbohydrates, such as whole grain breads andto patients to reduce their risk. lentils, score lower (<55). Foods that are low in carbohy- The varied counsel offered by Australasian heart drate content but high in fat or protein tend to also havehealth agencies glosses over much debate and uncer- low GI due to the effects of the other macronutrients ontainty over nutritional exposures and their effects on gastric emptying. Also, the carbohydrate fructose, foundheart health.The consequences of sugar intake have in highest concentration in sugar, is rated low on a GIdivided the scientific community over the past 30 years. scale (~20), simply because it counts as carbohydrate butCleave first proposed that scientific evidence implicated has a small effect on serum glucose during the first hourexcess sugar and refined carbohydrate intake in a range of the postprandial phase.© 2012 The AuthorsInternal Medicine Journal © 2012 Royal Australasian College of Physicians 47
  3. 3. Thornley et al. What is sugar? Until recently, this term has encom- was becoming rapidly accepted and enshrined in publicpassed all mono and disaccharides that are composed of health nutrition messages, first in the United States. Theeither six- or five-ring sugar molecules. This is a subclass message spread subsequently to other English-speakingof carbohydrates that differentiates ‘sugar’ from small countries, to increase the percentage of daily energychains of carbohydrates (oligosaccharides) and complex eaten from carbohydrate and reduce intake of animal-carbohydrate made up of long chains of sugar molecules derived fat.8,9 In the late 1970s, the U.S. government’s(starch and fibre). In the last 10 years, however, aspiration was to increase carbohydrate consumption toresearchers have focused on the properties of one mol- account for 55–60% of energy and reduce fat intake toecule: fructose. This monosaccharide is most commonly between 30% and 40% of energy.9 While the instigatorfound in disaccharide form in table sugar, also known as of the hypothesis, Professor Ancel Keys and the Ameri-sucrose. Table sugar consists of one glucose joined to one can Heart Association warned the public to forego animalfructose molecule and is commonly added to a variety of fat, a small but vocal minority argued that sugar wasmanufactured foods (yoghurt, breakfast cereals, sauces, much more likely to cause coronary heart disease, andcakes, pastries and soft drinks), and to tea and coffee. that this substance should be the target of public healthFructose is present in a restricted range of foods: fruit, preventative campaigns.3–5honey, refined sugar and high-fructose corn syrup – a We know that since this time (the late 1970s), thesugar-like substance derived from corn – often used as a prevalence of diabetes and obesity has risen considerably,sugar replacement in North America. Nutritionists fre- particularly in English-speaking countries, and that sugarquently distinguish between ‘intrinsic’ sugar, monosac- intake has increased substantially over the same period.charides present in fruit and vegetables, and ‘added’ Professor of economics, Barry Popkin, used food disap-sugar, which is usually sucrose, high-fructose corn syrup pearance data to document a global rise in sugar intake ofor glucose, used as an ingredient in the manufacture of about 30% over the period between 1970 and 2000.10many foods. During the early 1980s, scientific exploration of the health effects of starch began to be summarised in the form of the widely known ‘glycemic index’, coined by DavidA historical perspective Jenkins at the University of Toronto.11 The index discrimi-Before we review the epidemiological and clinical evi- nated between foods, based on their effects on after-mealdence linking food intake with cardiovascular disease, we serum glucose levels. In patients with diabetes, control ofbriefly explore the history of the modern-day ‘diabesity’ blood glucose has been a cornerstone of reducing theepidemic. The recent rising tide of type 2 diabetes, and incidence of complications of the disease. In some nutri-the obesity epidemic, starting in the early 1980s have not tion circles, low-glycaemic diets (restricting diet to low andoccurred in a nutrition vacuum, nor has the epidemic medium GI foods) was recommended to improve glycae-been equally spread over all nations. If we examine the mic control and also for reducing the incidence of compli-evolution of obesity prevalence in a range of deve- cations of diabetes. As a consequence of such a focus onloped countries, using the Organisation for Economic postprandial glycaemia, fructose-containing foods, such asCo-operation and Development (OECD) data from the those that contain high sugar levels, were often classifiedearly 1980s to 2007, we see a stark trend (Fig. 1).7 First, as medium GI and ‘healthy’. Because the GI of sugarthe rate of rise in obesity prevalence has occurred mostly (sucrose) is lower than flour and other refined sources ofin English-speaking countries lead by the United States, starch, sugar became, paradoxically, exonerated from thebut closely followed by the UK, New Zealand, Australia list of suspects as a cause of the epidemics of diabetes,and Canada. In each of these countries (except Canada), obesity or coronary heart disease.1 In fact, leadingbetween a quarter and one-third of all adults are classi- researchers of GI advocated that people with diabetesfied as obese. Continental European countries are the continue to eat and drink high levels of sugar to improvenext lowest prevalence region, with the lowest levels of their postprandial serum glucose control.12obesity observed in the only two Asian countries in the More recently, the tide of evidence and scientificOECD: Japan and South Korea (<5%). We also note that opinion is turning in favour of sugar as a significantthe epidemic probably started in the late 1970s and early vascular disease risk factor, and the substance continues1980s, for it was in this period that significant efforts to attract attention as a potential cause of the epidemic ofwere made to measure the prevalence of obesity in OECD non-communicable disease of the 21st century. Thecountries. changing attitude of large scientific bodies is perhaps best What was the dominant change in nutrition policy that highlighted in the change of opinion expressed by theoccurred in the 1960s and 1970s that predated the American Heart Association between 2002 and 2009.obesity epidemic? In the 1960s, the diet-heart hypothesis The organisation, charged with a mission to rid the © 2012 The Authors48 Internal Medicine Journal © 2012 Royal Australasian College of Physicians
  4. 4. Sugar intake and cardiovascular risk 1980 1990 2000 1980 1990 2000 1980 1990 2000 Spain Sweden Switzerland Turkey United Kingdom United States 30 20 10 Netherlands New Zealand Norway Poland Portugal Slovak Republic 30Obesity prevalence (% >= body mass index 30 kg / m2 ) 20 10 Ireland Italy Japan Korea Luxembourg Mexico 30 20 10 Finland France Germany Greece Hungary Iceland 30 20 10 Australia Austria Belgium Canada Czech Republic Denmark 30 20 10 1980 1990 2000 1980 1990 2000 1980 1990 2000 YearFigure 1 Adult obesity prevalence (body mass index Ն 30 kg/m2), by year, for selected Organisation for Economic Co-operation and Developmentcountries (1980–2007).7© 2012 The AuthorsInternal Medicine Journal © 2012 Royal Australasian College of Physicians 49
  5. 5. Thornley et al.United States of cardiovascular disease and stroke, com- liver cells, with the remaining 80% taken up by skeletalpiled a summary statement in 2002 for health profession- and smooth muscle, and other organs in the presence ofals about the effects of sugar on cardiovascular and insulin. Only about 5% of starch is converted to fatty acidsmetabolic health. The article concluded that there was ‘no by liver cells, compared with almost 50% of fructose.definitive evidence’ to limit sugar intake, and that individual After continued ingestion of high doses of fructose, thephysicians should ‘rely on professional judgement’. The presence of high levels of triglycerides within liver cellsstance of the authors of the report was best summed up results in insulin resistance, non-alcoholic fatty liverby the following statement: disease and long-term deterioration in glycaemic control. Consuming fructose either free or in the form of sucrose has neither beneficial or adverse effects.2 Epidemiological associations between fructose intake and risk factors for By 2009, however, opinions had changed. The organi- cardiovascular diseasesation concluded that the weight of scientific evidencehad turned against sugar, concluding that men should With our biochemical understanding of fructose, weconsume no more than nine teaspoons per day, with six might expect that fructose intake is associated with arecommended for women.6 Risk of weight gain and range of conditions, such as weight gain, high levels ofdeveloping diabetes were the main concerns associated serum urate (and gout), diabetes, dyslipidaemia andwith excess sugar intake, summarised in the following possibly cardiovascular disease. Do the epidemiologicalstatement: studies support such assertions? Several exposure– disease (or risk factor for disease) associations have con- Originally proposed as the ideal sweetener for people sistently emerged from such studies. Before we consider with diabetes . . . Fructose . . . has been indirectly the evidence, however, we reflect on possible barriers implicated in the epidemics of obesity and type 2 that distort nutrition-related exposure–disease relation- diabetes.6 ships. The first is the measurement error associated with In the remainder of this paper, we consider the accu- recording what individuals actually eat. A 24-h dietarymulating evidence that the fructose component of sugar recall, considered by some to be the most accurate of allis responsible for risk factors for cardiovascular disease; nutrition exposure assessments (although resource-what factors may make sugar intake difficult to limit; and intensive), in one examination underestimated sugarcontrast this evidence with more established nutrition intake by about 20%.15 Put simply, people have badexposures, such as to saturated fat and salt. memories for what they eat and drink. Part of this may be explained, as we discuss in later sections, by the subcon- scious drives to eat so that much intake is not consciouslyPhysiology of fructose recorded.Although fructose is a carbohydrate-like glucose, it has a What effect does this inaccuracy have on exposure–completely different metabolic profile. From the work disease effect estimates? Measurement error, if random,done on GI, researchers have observed that fructose has tends to lower the magnitude of these relationships andalmost no effect, in the short term, on postprandial gly- bias towards a null (or ‘no effect’) value. If the error iscaemia in contrast to glucose-rich foods, such as breads, systematic, the effect estimate may be biased in eitherrice and pasta. If fructose intake does not result in con- direction.version to glucose, what is its metabolic fate? From small Another major impediment to accurate estimation ofclinical and animal studies, after ingestion, fructose is risk of nutrition exposures is the cost, complexity andabsorbed from the small intestine, almost completely ethical restrictions placed on randomising exposure totaken up by the liver from the portal circulation, in an varying diets. For this reason, most nutritional studiesinsulin-independent manner. Fructose is then slowly have been observational, and lack the necessary com-converted to both glucose (~50%)13 and fatty acids, which ponent (randomisation) to balance unmeasured con-are then released into the peripheral circulation as a founders between the experimental and control groups.combination of triglycerides and very low-density lipo- The presence of unmeasured residual confounding is anproteins. During the metabolism of fructose to fructose- ever-present threat to the conclusion of observational1-phosphate, intracellular energy is depleted (adenosine epidemiological studies (cross-sectional, cohort or casetriphosphate converted to adenosine diphosphate) and control).uric acid is produced.14 This contrasts with the metabolic With such limitations in mind, we approach the epide-fate of glucose and starch-containing foods in which only miological literature to evaluate the strength of evidenceabout 20% of the absorbed carbohydrate is taken into of adverse health outcomes, linked to high intakes of © 2012 The Authors50 Internal Medicine Journal © 2012 Royal Australasian College of Physicians
  6. 6. Sugar intake and cardiovascular riskTable 1 Positive associations between indicators of exposure to fructose and important risk factors for cardiovascular disease or the disease itselfExposure Disease or risk factor Nature of evidence Strength of effect and comparison for diseaseSoft drinks (SSB) Weight gain Systematic review and meta-analysis of SSB: correlation coefficient: r = 0.08; observational studies.16,17 P < 0.001 Randomised controlled trial18Soft drinks Gout and hyperuricaemia Cohort studies19 Comparing highest and lowest quintile Multivariate RR for gout: 2.02 (1.49–2.75; P for trend <0.001)Fructose Rise in blood pressure Single randomised crossover study20 6.2 mmHg increase 30 min after administration of 60 g of fructose, compared with no change after 60 g of glucoseFructose High levels of triglycerides Meta-analysis of small randomised Compared with starch; standardised crossover studies in patients with mean difference 0.24 mmol/L (95% CI diabetes.21 0.05–0.44)Sugar-sweetened Type 2 diabetes (and Meta-analysis of observational studies22 1–2 SSB/day versus <1 serving/month; beverages weight gain) relative risk 1.26 (95% CI 1.12–1.41)Caloric sweetener Dyslipidaemia (high LDL, low Cross-sectional study23 Comparing daily intakes of <5% energy HDL, high triglycerides) with >25% energy; mean difference in HDL was 0.3 mmol/LSugar intake Dental caries Systematic review of literature24–26 Pooled effect not carried out.Dental caries Cardiovascular disease Meta-analysis of observational studies27 Compared adults with periodontal disease to those without: relative risk 1.14, 95% CI 1.07–1.21)Serum urate CHD and all cause mortality Meta-analysis of observational studies28,29 Compared adults with hyperuricaemia to those without: pooled RR for CHD 1.34, 95% CI 1.19–1.49Sweetened beverages Coronary heart disease Cohort study Compared upper quartile of consumption to lower quartile (adjusted RR 1.20; 95% CI: 1.09 to 1.33)29CHD, coronary heart disease; CI, confidence interval; HDL, high-density lipoprotein; LDL, low-density lipoprotein; RR, relative risk; SSB, sugar-sweetenedbeverages.fructose. Because fructose does not enter the diet in pure Although individual observational studies support noform, and has only recently been identified as a nutri- association between fructose intake and weight gain ortional exposure likely to cause disease, many publications other indices associated with cardiovascular disease,30,31point the finger at exposures, which are likely indicators the majority of systematic reviews support a positiveof high levels of fructose exposure, such as soft drink or association. If consistent associations are found amongsugar intake. many studies, which use different methods, then this We will not attempt to fully describe the epidemiologi- strengthens the evidence for causal claims.32 We identi-cal evidence for disease from excess fructose intake; fied several systematic reviews and meta-analyses ofinstead, we focus on summary studies, such as system- observational studies that found evidence of positiveatic reviews and meta-analyses. Such studies enable us associations between sugar intake and outcomes, such asto assess where the weight of the scientific evidence weight gain, hyperuricaemia and gout, high levels ofstands, and help us avoid possible biases created by triglycerides, and dental caries. Dyslipidaemia, a recog-distorted results that may emerge from individual inves- nised association with coronary disease and a variabletigators. Table 1 outlines the patterns that emerge con- used to help predict disease from popular Framingham-sistently from the summary studies (where these are derived equations, was positively associated with intakeabsent, single study results have been reported), and we of sugar-sweetened beverages. One systematic review isrefer the reader to the original articles to explore further revealing about the nature of the study and reportedthe nature and strength of the relationship reported effect: it showed that sugar and beverage industry-fundedbetween markers of fructose intake and outcome and cross-sectional studies were less likely to show posi-measures.16–29 tive associations with weight gain than longitudinal-© 2012 The AuthorsInternal Medicine Journal © 2012 Royal Australasian College of Physicians 51
  7. 7. Thornley et al. Table 2 Mean U.S. reported sugar intake (teaspoons/day)34 Age group (years) Males Females 9–13 29.2 23.2 14–18 34.3 25.2 Ն19 25.4 18.3 a statistical association with excess intake of fructose. Evidence of association is usually considered a prerequi- site for making a case that an exposure causes disease, although other considerations should be taken into account.32 Indeed, this information suggests that routineFigure 2 A plausible causal diagram that may explain the nature of theassociation between dental caries and coronary artery disease.33 Solid clinical measures of cardiovascular disease risk (exceptarrows indicate proposed direction of causal relationship between vari- cigarette smoking) are assessing, indirectly, indicators ofables, while dashed arrow shows apparent (epidemiological) association. dietary fructose intake. If the major risk factors for cardio- vascular disease are associated with fructose intake, this supports the hypothesis that the disease itself is caused by this upstream exposure.designed studies which were independently resourced.16Cross-sectional studies are more open to error, such as Sources of fructose in the dietfrom survivor bias and the lack of a temporal separationbetween exposure and disease. Case control studies suffer How much sugar do we consume on average, and wherefrom the uncertainty that comes from the need to select does most of it come from? Data from the United Nationsand recruit a suitable control group. Therefore, cohort Food and Agriculture Organisation which estimatestudies, which incorporate a time component, are gener- average food disappearance (annual production + importally considered more reliable than either cross-sectional – export/the number of people in the population) suggestor case control designs, and were more likely to show that we eat and drink, on average, between 30 and 40positive associations in our review. teaspoons of ‘added’ sugar per day. In 2007, the amount Sugar intake is probably best known for causing dental of sugar and sweeteners, on average, consumed in Aus-caries, and this effect is relatively uncontroversial.26 We tralia was estimated at 33 teaspoons per day, with thenote with interest the consistent positive association corresponding figures, 38 for New Zealand and 46 forobserved between dental caries and cardiovascular the United States. Survey estimates of daily sugar intakedisease incidence.27,32 While most authors argue that an are generally lower, which may reflect underreporting,immunological mechanism is likely to be responsible for common in nutritional survey instruments (Table 2).36the association involving pathogenic bacteria present Men generally consume more than women, with ain the mouth, we argue that the association observed pattern of declining intake in older age groups. Softbetween rotten teeth and incident cardiovascular disease drinks are a major source of added sugar in the US. diet,is more likely to be due to a third (or confounding) variable accounting for about one-third of reported intake. Fruitin the manner depicted in Figure 2.34 At the time of juice, confectionary and breakfast cereals are other majorwriting, a cohort study appeared which reported a direct sources (Table 3).association between sugar sweetened beverage intakeand incident cardiovascular disease (adjusted RR 1.20;95% CI: 1.09 to 1.33), comparing upper with lower quar- Table 3 Major sources of added sugars in the U.S. diet34tiles of intake. The study included 42 883 men with 3 683outcomes and over 22 years of follow up.35 Such a finding Category Proportion (%) of added sugar intakesupports our idea presented in Figure 2. In a similar way, as proposed for dental caries, we Regular soft drinks 33.0speculate from the evidence in Table 1 that dyslipidaemia, Sugars and candy 16.1hyperuricaemia, a diagnosis of type 2 diabetes, hyperten- Cakes, cookies, pies 12.9 Fruit drinks 9.7sion and obesity – all of which are themselves associated Other grains (toast and waffles) 5.8with incident cardiovascular disease – all have evidence of © 2012 The Authors52 Internal Medicine Journal © 2012 Royal Australasian College of Physicians
  8. 8. Sugar intake and cardiovascular riskEvidence for competing dietary causes of reporting overall pooled results consistent with the origi-cardiovascular disease nal hypothesis (that saturated fat causes coronary disease) suggests post hoc analysis and enthusiasm on the partAlthough we do not focus on this issue, we draw atten- of some researchers to ‘prove a hypothesis’ in the facetion to the relative paucity of evidence which indicates of generally unsupportive statistical evidence. We arestatistical associations between other potential causes of unclear as to why this one positive association is so widelycardiovascular disease, such as excess saturated fat and reported when the overall picture from a range of system-salt intake. This is important because these exposures atic reviewers shows little support for such a statistical(saturated fat and salt) are usually accorded higher status association, let alone a causal effect.37,41than limiting sugar intake in dietary guidelines and Similarly, a recent Cochrane review of randomisedpublic health campaigns, such as those prepared by trials that studied the effects of salt restriction showednational heart health organisations. that, in normotensive and hypertensive cohorts, no sig- Briefly, systematic reviews and quantitative meta- nificant decline occurred in incidence of cardiovascularanalyses have been disappointing when assessing the link disease (RR among normotensive groups: 0.71, 95% CI:between modifying saturated fat intake and incidence of 0.42–1.20; RR among hypertensive groups 0.84, 95% CI:cardiovascular disease.37 A ‘Cochrane review’ of the effect 0.57–1.23), with an increase in mortality risk in one trialof modified or reduced fat on total and cardiovascular of salt restriction that enrolled subjects with congestivemortality reported no effect in the pooled analysis of heart failure (RR 2.59, 95% 1.04–6.44).42 Despite suchrandomised studies (pooled relative risk (RR): 0.98, 95% negative statistical evidence, salt restriction remains anconfidence interval (CI) 0.93–1.04), no reduction in established part of nutritional wisdom, frequently dis-cardiovascular mortality (pooled RR: 0.94, 95% CI 0.85– seminated from public health authorities.1.04), but an overall reduction in total cardiovascular If replacing saturated fat with other nutrients or dis-events (pooled RR: 0.86, 95% CI 0.77–0.96).38 Of interest carding salt is a tenuous strategy to reduce cardiovascularis that the most objectively recorded outcomes (cardio- disease risk, is there any evidence for other dietary expo-vascular mortality and total mortality) showed no sures? Intake of starch and glucose may confer diseasebenefit, and the benefit from the overall reduction in risk, and a physiological index of absorption of thesetotal cardiovascular disease (CVD) events was small (14% nutrients is embodied in the GI. Diets that restrict intakereduction). The inconsistency of effect for the three of high GI foods show relatively consistent positive asso-similar outcomes was also noted.39 ciations with reduced risk of cardiovascular disease. A Some people in the scientific community discount these comparative meta-analysis, which evaluated the evi-results and focus on positive associations observed dence for effects on cardiovascular disease risk from abetween fat-modifying diets and indices of cardiovascular range of nutritional exposures, reported best evidence forrisk, such as adverse lipid profiles. Others focus on the a Mediterranean diet, a ‘high quality diet’, increasedoutcome of reports which report subgroup analyses. One intake of vegetables, nuts and diets that restrict high GIstudy, for example, which pooled a limited selection of foods or reduce a participant’s glycaemic load.41 The firstcohort data for which individual-level data were available, two exposures are complex, so they make it difficult toshowed a positive association between replacing saturated establish a causal exposure. Nuts and vegetables tend tofat with polyunsaturated fat in reducing total cardiovas- have low GI so their effect is consistent with the hypoth-cular events (pooled hazard ratio 0.69; 95% CI 0.59, 0.81) esis that reducing refined carbohydrates improves CVDand cardiovascular mortality (pooled hazard ratio 0.57; risk profile. One other meta-analyses (of observational95% CI 0.42–0.77).39,40 The findings were, however, studies) has similarly reported a reduction in risk of ainconsistent in that replacing saturated with monounsatu- range of chronic diseases when different levels of glycae-rated fat resulted in no association with coronary death, mic food intake are compared, with the pooled ratio ofwith a similar null result reported for replacing saturated risk (RR) between highest and lowest quintile groupsfat with carbohydrate. If we limit our discussion to this for incidence of CVD calculated at 1.25 (95% CI: 1.00,single study, the findings raise the question of whether 1.56).43 High-level evidence, from randomised controlledsaturated fat is truly the causal exposure because the trials, is unavailable for assessing the effect of such dietsnature of the replacing nutrient (carbohydrate, monoun- on CVD disease incidence. A Cochrane review of ran-saturated or polyunsaturated fat) should have little effect domised studies indicated, however, that diets based onon the risk of cardiovascular disease. The results, to us, are glycaemic load or index were more effective than stand-more consistent with polyunsaturated fat protecting indi- ard (often low-energy) diets at achieving weight lossviduals from developing disease. The fact that researchers at follow-up in short-term studies (from 5 weeks toare investigating such exposure subgroups rather than 6 months).44© 2012 The AuthorsInternal Medicine Journal © 2012 Royal Australasian College of Physicians 53
  9. 9. Thornley et al. The advice, therefore, from the Australian Heart Foun- the same 12-month period: (i) taking larger amounts, (ii)dation, to eat vegetables, nuts and whole grains does unsuccessful efforts to cut down, (iii) overinvestment ofhave some empiric support. However, a little-known fact time, (iv) giving up important social activities, (v) con-is that intake of fat (and protein) reduces GI (due to tinued use despite negative consequences, (vi) toleranceslowed gastric emptying), and so the advice to eat unre- (greater need) and (vii) use to avoid unpleasant with-fined food but also reduce fat intake is somewhat contra- drawal symptoms. The essential features of addiction are,dictory when viewed from a GI perspective. If one adds therefore, a combination of clinical impairment, loss ofadvice to lower fat intake on a GI-restricted diet, the control, tolerance and a withdrawal syndrome when theoverall effect will increase GI. We have also mentioned substance is discontinued.the assumption that the ‘glycemic-index philosophy’ Substance use, in people with addictions, is oftenimplicitly makes: that the health properties of a food may associated with a reward perceived as ‘a hit’ or ‘feelingbe determined from its short-term effect on serum high’. As well as the positive symptoms, drug useglucose. As discussed, high-fructose intake, which has alleviates negative withdrawal symptoms, which arelittle acute effect on serum glucose, in epidemiological thought to lead to subconscious learning and deeplystudies showed statistical associations with deterioration entrenched behaviour. Neurophysiological studies shedof long-term glycaemic control and increased risk of light on how this behaviour occurs. The loss of controlweight gain and being diagnosed with type 2 diabetes. that accompanies addiction is mediated, in part, by operant conditioning or instrumental learning in the mesolimbic dopaminergic pathway, which connects theEvidence for a sugar addiction nucleus accumbens with the ventral tegmental area insyndrome the midbrain. Learning by positive reinforcementEvidence from a completely different line of enquiry may involves linking an association between a behaviourshed light on what effect the campaign against fat intake and a positive reward. That then leads to the behaviourhas had on population and individual metabolic health. becoming subconscious (such as smoking and experi-With evidence that sugar harms health, why do people in encing a ‘hit’ from nicotine). Negative reinforcementWestern societies consume the substance in such large also results in subconscious learning but with the stimu-quantities, and why has it assumed such a dominant lus and reward reversed: behaviour that avoids negativeposition in the modern diet? Most lay people are familiar stimuli is reinforced (such as the unpleasant withdrawalwith the term ‘sugar hit’ and find sugar especially palat- symptoms that accompany tobacco abstinence inable. Addiction theory, which has been developed to dependent smokers). This reward is likened to theexplain the obsessive use of various substances (such as pleasure that comes from taking off tight shoes. Thetobacco and opiates), may also partially explain the global onset of withdrawal (such as irritability or craving)rise in sugar intakes observed over the last 30 years.10,45 prompts the smoker to light a cigarette to temporarilyCuriously, the best evidence for an addictive component relieve these symptoms. The latter mechanism isof food includes the simple sugars, both fructose (as thought to be the dominant cause of automatic,sucrose) and glucose. learned, smoking behaviour. Drugs that produce dependence influence dopamine concentrations in the nucleus accumbens. BalfourWhat is addiction? describes nicotine effects on two parts of the nucleus: theAddiction, as an entity, is often poorly understood. Nick core and medial shell which have distinct effects onHeather defines the syndrome as ‘repeated failures to refrain behaviour.48 Increases in dopamine concentration in thefrom drug use despite prior resolutions to do so’. He describes core result in physiological reward, making the behav-three features of addiction: (i) neuroadaptation to the iour more likely (such as puffing on a cigarette). Thesubstance, (ii) craving for the drug and (iii) ‘akrasia’ – shell, in contrast, is thought to mediate stimulus responsefailures of resolve to stop using the substance.46 Such a (‘Pavlovian’) action, so that both the behaviour and asso-definition suggests that physical dependence is a related ciated sensory stimuli are linked by reward. Such path-phenomenon – associated with adaptation to a drug ways help explain why environmental cues (such as thethat is taken to prevent the onset or relieve established smell of tobacco) can lead to subconscious urges to takewithdrawal symptoms. The Diagnostic and Statistical the drug.Manual-IV47 criteria for substance use are commonly used We have introduced the biological basis and clinicalto adjudicate addiction in the individual. These criteria, observations associated with established addictions. Doessummarised, are a maladaptive pattern of substance use eating behaviour show similarities that suggest it too canmanifest by three or more of the following, present over be considered in the same light? © 2012 The Authors54 Internal Medicine Journal © 2012 Royal Australasian College of Physicians
  10. 10. Sugar intake and cardiovascular riskWhat are the parallels between food was unable to lose weight despite use of emetics andconsumption and addiction? laxatives, or even undergoing obesity surgery: The executive recalls ‘often I would shake until I couldFirst, the same neural circuits linked to reward from put some sugar in my mouth’. Cues are also describedaddictive drugs are also implicated in the physiology of – ‘I had an hour’s drive from my office to my home,appetite and hunger. In slow positron emission tomogra- and I knew every restaurant, every candy machine andphy studies, eating stimulates neural activity in the every soft drink dispenser along the whole route’.mesolimbic-dopaminergic pathway known to mediatecocaine and nicotine addiction.49 Reduced dopamine (D2) This may be an extreme case, but the patient describedreceptor availability is strongly correlated with increased tremor linked to short-term restriction from sugar. Suchbody mass index (Pearson correlation coefficient 0.71), symptoms mirror some of those experienced after acuteindicating that increased dopamine levels are likely to be opiate abstinence.59 The executive recounted relief fromfound in these regions of the brain. This paucity of recep- eating or drinking sugar, along with cues to eat encoun-tors is likely to reflect the drug tolerance observed in tered on his way home from work. The increased attentionaddicted individuals. That is, increasing quantities of paid to such cues is typical of addiction and abstinence.the substance are required to achieve a similar reward Although formal definition of sugar or carbohydrate with-response due to the presence of fewer receptors. Low drawal, to our knowledge, does not exist, a case reportlevels of mesolimbic free D2 receptors have similarly been has been published. The features of the syndrome werereported in individuals addicted to cocaine, opiates and tremors, headaches and abdominal pains that lasted aboutalcohol. 1 month after abstinence from ‘processed sugar and flour’, Observation of people experiencing drug withdrawal which were voluntarily removed from the correspond-has suggested a link between hunger and established ent’s diet.62 Symptoms were reported to be most intenseaddictions, such as smoking. Restricting food intake during the third day after abstinence.increases cigarette smoking,50 and restricting intake while Given the ubiquity of sugar and carbohydrates intrying to stop smoking is linked to an increased risk of modern western diets, obese people may not experiencerelapse.51,52 Smoking acutely reduces hunger,53–55 and in withdrawal symptoms unless prolonged abstinencesome studies, decreased desire for and consumption of (>48 h) is tried. Instead, the experience of obese indi-sweet-tasting foods.56 Hunger is also a symptom of nico- viduals may be subtle symptoms similar to those of caf-tine withdrawal, and people may gain an average of 7 kg feine withdrawal, such as irritability, poor concentrationafter stopping smoking.57,58 and urges that accompany short-term abstinence from When frequent users of drugs, such as alcohol, tobacco sugary food. These may be underrecognised, as is the caseand cocaine, abstain from their use, they experience a in addictions such as tobacco, where often the threat ofcluster of symptoms known as withdrawal. When obese such symptoms prompts subconscious drives to performpeople abstain from sugary or high GI food, do they the addictive behaviour.48experience such symptoms? Opiate withdrawal is char- Some researchers advocated that obesity be consideredacterised by nausea, stomach cramps, muscular spasm a type of addiction. Volkow,63 for example, analysed theand twitching, feelings of coldness, and heart pounding. similarities between the neural mechanisms underlyingWhat is common to many forms of withdrawal is the obesity and drug addiction, and argued that obesity betime-course. In the case of unassisted or cold-turkey included as a specific subtype of the psychiatric disease:withdrawal, the symptoms peak in 48–72 h and largely substance abuse.64evaporate after 30 days if abstinence is maintained.59 For The main determinants of an addictive substance arenicotine, the withdrawal syndrome that accompanies its concentration and speed of absorption (time-to-hit).abstinence is well described.58 Common symptoms Given that foods with added sugar are likely to haveinclude urges, craving, reduced concentration, irritability, higher concentrations of fructose than natural sources,increased appetite and depressed mood. Symptoms we speculate that manufactured sugary foods andusually peak in the first few days after quitting and drinks (which take less time to consume) are mostlargely subside after a month of continuous abstinence. addictive.We know relatively little about whether an equivalentwithdrawal syndrome exists for food. Although carbohy- Conclusiondrate craving has been defined,60 a withdrawal syndromehas not been similarly described. However, some brief What do we conclude from this survey of the evidence?case reports exist, often present in the lay literature. For First, sugar intakes have increased substantially against aexample, Atkins61 described a real estate executive who nutritional backdrop that has focused on reducing fat© 2012 The AuthorsInternal Medicine Journal © 2012 Royal Australasian College of Physicians 55
  11. 11. Thornley et al.intake and salt to reduce the incidence of cardiovascular soft drink, fruit juice, breakfast cereals and seeminglydisease. Second, excess intake of fructose, due to the healthy sweetened yogurts is revealed. For the clinicianaccumulating, consistent epidemiological evidence of advising people to cut down their intake of sugar, welinks with risk factors for cardiovascular disease, suggests recommend first advice about how to reduce intake ofthat substantial health gains will result from limiting added sugar. This includes fruit juice, soft drink, cordials,intakes. Third, from the parallels among drugs of abuse, sweetened yoghurts and breakfast cereals, as well as theovereating and carbohydrate addiction, we speculate that better understood sources in chocolate, sweets, desserts,many patients will find it difficult to limit their intake of cakes and biscuits.sugar due to stimulation of reward pathways in the brain, From the published evidence of a likely sugar with-and the experience of unpleasant withdrawal symptoms drawal syndrome, we also suggest warning patients thatthat accompany attempts to restrict intake. they are likely to suffer withdrawal symptoms when they The American Heart Association has published guide- attempt to restrict their sugar intake. Such symptoms arelines that suggested limiting intake of sugar to no more likely to include irritability, loss of concentration, hunger,than six teaspoons per day for women and nine for men.6 craving for sugar and restlessness. Cues left around theFrom food disappearance data, average daily sugar con- house, such as the presence of available sugary foods, aresumption is between 30 and 40 teaspoons per day in likely to prompt consumption especially in the earlyEnglish-speaking countries, such as the UK, United phases (<1 month) of restriction. We, therefore, suggestStates, Canada, Australia and New Zealand. The implica- removing sugary foods from the house and work envi-tions of the advice are enormous: most adults should ronment, reducing the chance that the patient’s resolvereduce their intake by between 1/6 and 1/3 of their to forego sugar will be broken.current consumption. As we have shown, the largest This paper suggests a deviation from widely acceptedsource of added sugar in the United States comes in liquid practice for many cardiologists, general physicians andform, either from soft drinks and fruit juice which may be family doctors concerned with reducing the CVD risk ofoverlooked by patients. the patient that they have before them. Rather than One of the authors (RT) has considerable experience of reaching for the prescription pad, we suggest a brief con-advising patients how to cut down their intake of sugar. versation about the perils of a high-sugar diet and prac-He suggests making patients aware of their intake by tical advice about how to cut down.translating weight (grams), which is often reported onthe nutrition panels on manufactured foods, into tea- Conflicts of interestspoons. Four grams of sugar is about 1 teaspoon. Whenpatients understand how many teaspoons are in com- The authors have declared no potential conflicts of inter-monly consumed food portions, they are often surprised. est. No funding was received for the preparation of thisMany people are taken aback when the sugar content of manuscript.References disease and diabetes. Lancet 1964; Goals for the United States. Washington 2: 4–5. DC: United States Senate; 1977. 1 Mann JI, Trusswell AS. Diseases of 5 Morris J. Recent history of coronary 10 Popkin BM, Nielsen SJ. The sweetening overnourished societies and the need for disease. Lancet 1951; 1: 1–7. of the world’s diet. Obes Res 2003; 11: dietary change. In: D. A. Warnell, T. M. 6 Johnson RK, Appel LJ, Brands M, 1325–32. Cox, J. D. Firth, eds. The Oxford Textbook Howard BV, Lefevre M, Lustig RH et al. 11 Jenkins D, Wolever T, Taylor RH, of Medicine. Oxford: Oxford University Dietary sugars intake and cardiovascular Barker H, Fielden H, Baldwin JM et al. Press; 2003; 1027–36. health: a scientific statement from the Glycemic index of foods: a physiological 2 Howard BV, Wylie-Rosett J. Sugar and american heart association. Circulation basis for carbohydrate exchange. Am J cardiovascular disease: a statement for 2009; 120: 1011–20. Clin Nutr 1981; 34: 362–6. healthcare professionals from the 7 Organisation for Economic Co-operation 12 Wolever T, Miller J. Sugars and blood committee on nutrition of the council and Development (OECD). OECD Health glucose control. Am J Clin Nutr 1995; 62: on nutrition, physical activity, and Data 2009: Statistics and Indicators for 30 212S–21S. metabolism of the american heart Countries. Paris: OECD Publishing; 2009. 13 Delarue J, Normand S, Pachiaudi C, association. Circulation 2002; 106: 523–7. 8 Page IH, Allen EV, Chamberlain FL, Beylot M, Lamisse F, Riou JP. The 3 Cleave TL. Saccharine Disease: The Master Keys A, Stamler J, Stare FJ. Dietary fat contribution of naturally labeled C-13 Disease of Our Time. New Canaan, CT: and its relation to heart attacks and fructose to glucose appearance in Keats Publishing; 1993. strokes. Circ J 1961; 23: 133–6. humans. Diabetologia 1993; 36: 338–45. 4 Yudkin J. Dietary fat and dietary 9 The Staff on the Select Committee on 14 Tappy L, Le KA. Metabolic effects of sugar in relation to ischaemic-heart Nutrition and Human Needs. Dietary fructose and the worldwide increase © 2012 The Authors56 Internal Medicine Journal © 2012 Royal Australasian College of Physicians
  12. 12. Sugar intake and cardiovascular risk in obesity. Physiol Rev 2010; 90: increased in periodontitis: a saturated fat in the prevention of 23–46. meta-analysis. Am Heart J 2007; 154: cardiovascular disease: where does the15 Karvetti RL, Knuts LR. Validity of the 830–7. evidence stand in 2010? Am J Clin Nutr 24-hour dietary recall. J Am Diet Assoc 28 Kim SY, Guevara JP, Kim KM, Choi HK, 2011; 93: 684–8. 1985; 85: 1437–42. Heitjan DF, Albert DA. Hyperuricemia 40 Jakobsen MU, O’Reilly EJ, Heitmann16 Malik VS, Schulze MB, Hu FB. Intake of and coronary heart disease: a systematic BL, Pereira MA, Bälter K, Fraser GE sugar-sweetened beverages and weight review and meta-analysis. Arthritis Care et al. Major types of dietary fat and risk gain: a systematic review. Am J Clin Nutr Res (Hoboken) 2010; 62: 170–80. of coronary heart disease: a pooled 2006; 84: 274–88. 29 de Koning L, Malik VS, Kellogg MD, analysis of 11 cohort studies. Am J Clin17 Vartanian LR, Schwartz MB, Brownell Rimm EB, Willett WC, Hu FB. Nutr 2009; 89: 1425–32. KD. Effects of soft drink consumption on Sweetened beverage consumption, 41 Mente A, de Koning L, Shannon HS, nutrition and health: a systematic incident coronary heart disease, and Anand SS. A systematic review of the review and meta-analysis. Am J Public biomarkers of risk in men. Circulation evidence supporting a causal link Health 2007; 97: 667–75. 2012; 125: 1735–41. between dietary factors and coronary18 Ebbeling CB, Feldman HA, Osganian SK, 30 Parnell W, Wilson N, Alexander D, heart disease. Arch Intern Med 2009; 169: Chomitz VR, Ellenbogen SJ, Ludwig DS. Wohlers M, Williden M, Mann J et al. 659–69. Effects of decreasing sugar-sweetened Exploring the relationship between 42 Taylor RS, Ashton KE, Moxham T, beverage consumption on body weight sugars and obesity. Public Health Nutr Hooper L, Ebrahim S. Reduced dietary in adolescents: a randomized, controlled 2008; 11: 860–6. salt for the prevention of cardiovascular pilot study. Pediatrics 2006; 117: 673–80. 31 Janket S-J, Manson JE, Sesso H, Buring disease. Cochrane Database Syst Rev 201119 Choi HK, Curhan G. Soft drinks, JE, Liu S. A prospective study of sugar Jul 6; 7: CD009217. fructose consumption, and the risk of intake and risk of type 2 diabetes in 43 Barclay AW, Petocz P, McMillan-Price J, gout in men: prospective cohort study. women. Diabetes Care 2003; 26: 1008–15. Flood VM, Prvan T, Mitchell P et al. BMJ 2008; 336: 309–12. 32 Hofler M. The Bradford Hill Glycemic index, glycemic load, and20 Brown CM, Dulloo AG, Yepuri G, considerations on causality: a chronic disease risk – a metaanalysis of Montani J-P. Fructose ingestion acutely counterfactual perspective. Emerg Themes observational studies. Am J Clin Nutr elevates blood pressure in healthy young Epidemiol 2005; 2: 11. 2008; 87: 627–37. humans. Am J Physiol Regul Integr Comp 33 Janket S-J, Qvarnstrom M, Meurman 44 Thomas D, Elliott E, Baur L. Low Physiol 2008; 294: R730–7. JH, Baird AE, Nuutinen P, Jones JA. glycaemic index or low glycaemic load21 Sievenpiper JL, de Souza RJ, Mirrahimi Asymptotic dental score and prevalent diets for overweight and obesity. A, Yu ME, Carleton AJ, Beyene J et al. coronary heart disease. Circulation 2004; Cochrane Database Syst Rev 2007 Jul 18; 3: Heterogeneous effects of fructose on 109: 1095–100. CD005105. doi:10.1002/14651858. blood lipids in individuals with type 2 34 Thornley S, McRobbie H, Jackson G. 45 Thornley S, McRobbie H, Eyles H, diabetes systematic review and The New Zealand sugar (fructose) Walker N, Simmons G. The obesity meta-analysis of experimental trials in fountain: time to turn the tide? N Z Med epidemic: is glycemic index the key to humans. Diabetes Care 2009; 32: 1930–7. J 2010; 123: 58–64. unlocking a hidden addiction? Med22 Malik VS, Popkin BM, Bray GA, Després 35 de Koning L., V. S. Malik, Shannon H. Hypotheses 2008; 71: 709–14. J-P, Willett WC, Hu FB. Sugar- H., and Anand S. S. (2012) Sweetened 46 Heather N. A conceptual framework sweetened beverages and risk of beverage consumption, incident for explaining drug addiction. metabolic syndrome and type 2 diabetes. coronary heart disease, and biomarkers J Psychopharmacol (Oxf) 1998; 12: 3–7. Diabetes Care 2010; 33: 2477–83. of risk in men. Circulation 125(14): 47 APA. Diagnostic and Statistical Manual of23 Welsh JA, Sharma A, Abramson JL, 1735–1741, S1731. Mental Disorders. Washington DC: Vaccarino V, Gillespie C, Vos MB. 36 National Cancer Institute. Usual Dietary American Psychiatric Association; 1995. Caloric sweetener consumption and Intakes: Food Intakes, US Population 48 West R. Theory of Addiction. Oxford: dyslipidemia among US adults. JAMA 2001–04. Bethesda, MD: National Cancer Blackwell Publishing; 2006; 10. 2010; 303: 1490–7. Institute; 2008. 49 Wang GJ, Volkow ND, Logan J, Pappas24 Burt BA, Pai S. Sugar consumption and 37 Siri-Tarino PW, Sun Q, Hu FB, Krauss NR, Wong CT, Zhu W et al. Brain caries risk: a systematic review. J Dent RM. Meta-analysis of prospective cohort dopamine and obesity. Lancet 2001; 357: Educ 2001; 65: 1017–23. studies evaluating the association of 354–7.25 Gussy MG, Waters EG, Walsh O, saturated fat with cardiovascular 50 Cheskin LJ, Hess JM, Henningfield J, Kilpatrick NM. Early childhood caries: disease. Am J Clin Nutr 2010; 91: Gorelick DA. Calorie restriction current evidence for aetiology and 535–46. increases cigarette use in adult smokers. prevention. J Paediatr Child Health 2006; 38 Hooper L, Summerbell Carolyn D, Psychopharmacology (Berl) 2005; 179: 42: 37–43. Thompson R et al. Reduced or modified 430–6.26 Sheiham A. Dietary effects on dental dietary fat for preventing cardiovascular 51 Hall SM, Tunstall CD, Vila KL, Duffy J. diseases. Public Health Nutr 2001; 4: disease. Cochrane Database Syst Rev 2011 Weight gain prevention and smoking 569–91. Jul 6; 7: CD002137. cessation: cautionary findings. Am J27 Bahekar AA, Singh S, Saha S, Molnar J, 39 Astrup A, Dyerberg J, Elwood P, Public Health 1992; 82: 799–803. Arora R. The prevalence and incidence Hermansen K, Hu FB, Jakobsen MU 52 Borrelli B, Spring B, Niaura R, Hitsman of coronary heart disease is significantly et al. The role of reducing intakes of B, Papandonatos G. Influences of© 2012 The AuthorsInternal Medicine Journal © 2012 Royal Australasian College of Physicians 57
  13. 13. bs_bs_bannerThornley et al. gender and weight gain on short-term 56 Grunberg NE. The effects of nicotine and et al. Abuse potential of carbohydrates relapse to smoking in a cessation trial. cigarette smoking on food consumption for overweight carbohydrate cravers. J Consult Clin Psychol 2001; 69: and taste preferences. Addict Behav 1982; Psychopharmacology (Berl) 2008; 197: 511–15. 7: 317–31. 637–47.53 Perkins KA, Epstein LH, Stiller RI, 57 Parsons AC, Shraim M, Inglis J, Aveyard 61 Atkins R. Dr Atkins New Diet Revolution. Sexton JE, Jacob RG. Chronic tolerance P, Hajek P. Interventions for preventing London: Vermillion; 2003. to nicotine’s effects on suppressing weight gain after smoking cessation. 62 Thornley S, McRobbie H. Carbohydrate hunger and caloric intake. NIDA Res Cochrane Database Syst Rev 2009 Jan 21; withdrawal: is recognition the first step Monogr 1991; 105: 563–4. 1: CD006219. to recovery? N Z Med J 2009; 122:54 Jo YH, Talmage DA, Role LW. Nicotinic 58 West R, Schiffman S. Smoking Cessation. 133–4. receptor-mediated effects on appetite Fast Facts: Indespensible Guides to Clinical 63 Volkow ND, Wise RA. How can drug and food intake. J Neurobiol 2002; 53: Practice. Oxford: Oxford Health Press addiction help us understand 618–32. Limited; 2004. obesity? Nat Neurosci 2005; 8: 555–60.55 Li MD, Kane JK, Konu O. Nicotine, 59 Farrell M. Opiate withdrawal. Addiction 64 Volkow ND, O’Brien CP. Issues for body weight and potential implications 1994; 89: 1471–5. DSM-V: should obesity be included as a in the treatment of obesity. Curr Top Med 60 Spring B, Schneider K, Smith M, brain disorder? Am J Psychiatry 2007; Chem 2003; 3: 899–919. Kendzor D, Appelhans B, Hedeker D 164: 708–10.Current state of the performance of percutaneous coronaryintervention in centres without on-site cardiac surgeryE. OqueliBallarat Health Services, Ballarat, Victoria, AustraliaKey words Abstractpercutaneous coronary intervention,angioplasty, myocardial infarction. Before the routine use of coronary stents, potential complications of percutaneous coronary interventions required the presence of backup cardiac surgery on-site.Correspondence Advances in pharmacotherapy and interventional techniques, particularly in the lastErnesto Oqueli, Internal Medicine Department, decade, have significantly decreased the rates of complications requiring emergencyBallarat Base Hospital, Drummond Street cardiac surgery, from approximately 4% to 6% in the balloon angioplasty era to as lowNorth, Ballarat, Vic. 3350, Australia. as 0.3% to 0.6% in the contemporary era of routine intracoronary stent implantation.Email: oquelie@yahoo.com.au An early invasive approach has been shown to improve outcomes among patients with non-ST elevation acute coronary syndromes (NSTEACS), particularly in those atReceived 10 July 2012; accepted 16 July 2012. the highest risk, emphasising the importance of early access to revascularisation premises in such patients.doi:10.1111/j.1445-5994.2012.02898.x Patients with ST-segment elevation myocardial infarction require immediate and sustained recanalisation of the culprit vessel to obtain rapid reperfusion of the threat- ened myocardium, in order to reduce infarct size and improve outcomes. Primary percutaneous coronary intervention at hospitals without on-site cardiac surgery improves clinical outcomes and reduces length of stay when compared with fibrinolytic therapy. It also significantly reduces door-to-balloon times when compared with transfer for percutaneous coronary interventions at hospitals with on-site surgery. It has been published that risk-adjusted mortality rates for patients undergoing percutaneous coronary interventions in centres without on-site surgical backup are comparable with those of percutaneous coronary intervention facilities that have cardiac surgery on-site, regardless of whether percutaneous coronary intervention was per- formed as primary therapy for ST-segment elevation myocardial infarction or in a non-primary setting. To achieve these results however, an adequate percutaneous coronary intervention programme is required, including proper hospital infrastructure and appropriately trained interventional cardiologists. © 2012 The Author58 Internal Medicine Journal © 2012 Royal Australasian College of Physicians

×