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References                                        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 coronary
2 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 myocardial
3 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 to
reduce cardiovascular disease risk
S. Thornley,1 R. Tayler2 and K. Sikaris3
1
Section of Epidemiology and Biostatistics, University of Auckland, Auckland, New Zealand, 2Epworth Hospital, Richmond and 3Melbourne Pathology,
Melbourne, Victoria, Australia



Key words                                        Abstract
carbohydrates, 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 on
Correspondence                                   saturated fat and salt as guilty parties. More recently, evidence suggests that excess sugar
Simon 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 to
Health, 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 salt
2012.
                                                 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 Authors
46                                                                                 Internal Medicine Journal © 2012 Royal Australasian College of Physicians
Sugar intake and cardiovascular risk



Introduction                                                                of non-communicable diseases, in his influential work
                                                                            published in 1976.3 If one looks back over a longer
Authorities in the field of nutrition have made contradic-                   period of time, some experts have drawn attention to the
tory statements about the role of sugar in the aetiology of                 adverse effects of sugar consumption since at least the
diabetes, 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 in
Australasia 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 saturated
of becoming ‘just another statistic’. The Australian Heart                  fat dominating the nutritional horizon. Present in highest
Foundation suggests the following: eat a variety of                         concentrations in animals, saturated fats are generally
foods; include vegetables, whole grains, fruit, nuts and                    solid at room temperature and have all carbon chains
seeds; choose healthier fats and oils; try to limit sugary,                 (fatty acids) filled (or saturated) with hydrogen. The
fatty and salty takeaway meals; and drink mainly water.                     warnings of the National Heart Foundations in New
The New Zealand counterpart solicits several steps to a                     Zealand and Australia to avoid meat and dairy fat are
healthy heart: eat three meals a day with more plant                        made on the basis that such sources contain high
material, 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 this
scrutiny? Should a clinician blindly adhere to this advice?                 source have made it a favourite target of public health
What 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 been
sugar and salt cause coronary artery disease, or the                        studied, however. In the early 1980s, the properties of
broader term ‘cardiovascular disease’ (which encom-                         glucose-containing foods were classified using the term
passes 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 drawn
the evidence for restricting all components of food is                      immediately before, and up to 1 h after, the intake of a
equal and should be considered on par. If anything, satu-                   food standardised by the weight of the carbohydrate it
rated 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 rice
briefly 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 and
to 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 have
health agencies glosses over much debate and uncer-                         low GI due to the effects of the other macronutrients on
tainty over nutritional exposures and their effects on                      gastric emptying. Also, the carbohydrate fructose, found
heart health.The consequences of sugar intake have                          in highest concentration in sugar, is rated low on a GI
divided the scientific community over the past 30 years.                     scale (~20), simply because it counts as carbohydrate but
Cleave first proposed that scientific evidence implicated                     has a small effect on serum glucose during the first hour
excess sugar and refined carbohydrate intake in a range                      of the postprandial phase.

© 2012 The Authors
Internal Medicine Journal © 2012 Royal Australasian College of Physicians                                                               47
Thornley et al.


   What is sugar? Until recently, this term has encom-        was becoming rapidly accepted and enshrined in public
passed all mono and disaccharides that are composed of        health nutrition messages, first in the United States. The
either six- or five-ring sugar molecules. This is a subclass   message spread subsequently to other English-speaking
of carbohydrates that differentiates ‘sugar’ from small       countries, to increase the percentage of daily energy
chains 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 to
researchers have focused on the properties of one mol-        account for 55–60% of energy and reduce fat intake to
ecule: fructose. This monosaccharide is most commonly         between 30% and 40% of energy.9 While the instigator
found 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 animal
fructose molecule and is commonly added to a variety of       fat, a small but vocal minority argued that sugar was
manufactured foods (yoghurt, breakfast cereals, sauces,       much more likely to cause coronary heart disease, and
cakes, pastries and soft drinks), and to tea and coffee.      that this substance should be the target of public health
Fructose is present in a restricted range of foods: fruit,    preventative campaigns.3–5
honey, refined sugar and high-fructose corn syrup – a             We know that since this time (the late 1970s), the
sugar-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 sugar
quently 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 of
or glucose, used as an ingredient in the manufacture of       about 30% over the period between 1970 and 2000.10
many 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 David
A 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-meal
dence linking food intake with cardiovascular disease, we     serum glucose levels. In patients with diabetes, control of
briefly explore the history of the modern-day ‘diabesity’      blood glucose has been a cornerstone of reducing the
epidemic. 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 and
occurred 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 on
loped countries, using the Organisation for Economic          postprandial glycaemia, fructose-containing foods, such as
Co-operation and Development (OECD) data from the             those that contain high sugar levels, were often classified
early 1980s to 2007, we see a stark trend (Fig. 1).7 First,   as medium GI and ‘healthy’. Because the GI of sugar
the rate of rise in obesity prevalence has occurred mostly    (sucrose) is lower than flour and other refined sources of
in English-speaking countries lead by the United States,      starch, sugar became, paradoxically, exonerated from the
but 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, leading
between a quarter and one-third of all adults are classi-     researchers of GI advocated that people with diabetes
fied as obese. Continental European countries are the          continue to eat and drink high levels of sugar to improve
next lowest prevalence region, with the lowest levels of      their postprandial serum glucose control.12
obesity observed in the only two Asian countries in the          More recently, the tide of evidence and scientific
OECD: Japan and South Korea (<5%). We also note that          opinion is turning in favour of sugar as a significant
the epidemic probably started in the late 1970s and early     vascular disease risk factor, and the substance continues
1980s, for it was in this period that significant efforts      to attract attention as a potential cause of the epidemic of
were made to measure the prevalence of obesity in OECD        non-communicable disease of the 21st century. The
countries.                                                    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 the
occurred 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 Authors
48                                                                   Internal Medicine Journal © 2012 Royal Australasian College of Physicians
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

                                                                                                                                                                          30
Obesity 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

                                                                                                               Year
Figure 1 Adult obesity prevalence (body mass index Ն 30 kg/m2), by year, for selected Organisation for Economic Co-operation and Development
countries (1980–2007).7




© 2012 The Authors
Internal Medicine Journal © 2012 Royal Australasian College of Physicians                                                                                                 49
Thornley et al.


United States of cardiovascular disease and stroke, com-         liver cells, with the remaining 80% taken up by skeletal
piled a summary statement in 2002 for health profession-         and smooth muscle, and other organs in the presence of
als about the effects of sugar on cardiovascular and             insulin. Only about 5% of starch is converted to fatty acids
metabolic 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, the
physicians should ‘rely on professional judgement’. The          presence of high levels of triglycerides within liver cells
stance of the authors of the report was best summed up           results in insulin resistance, non-alcoholic fatty liver
by 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 disease
sation concluded that the weight of scientific evidence
had turned against sugar, concluding that men should             With our biochemical understanding of fructose, we
consume no more than nine teaspoons per day, with six            might expect that fructose intake is associated with a
recommended for women.6 Risk of weight gain and                  range of conditions, such as weight gain, high levels of
developing diabetes were the main concerns associated            serum urate (and gout), diabetes, dyslipidaemia and
with excess sugar intake, summarised in the following            possibly cardiovascular disease. Do the epidemiological
statement:                                                       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 dietary
mulating evidence that the fructose component of sugar           recall, considered by some to be the most accurate of all
is 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 sugar
contrast this evidence with more established nutrition           intake by about 20%.15 Put simply, people have bad
exposures, 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 consciously
Physiology 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 and
almost no effect, in the short term, on postprandial gly-        bias towards a null (or ‘no effect’) value. If the error is
caemia in contrast to glucose-rich foods, such as breads,        systematic, the effect estimate may be biased in either
rice 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 of
clinical and animal studies, after ingestion, fructose is        risk of nutrition exposures is the cost, complexity and
absorbed from the small intestine, almost completely             ethical restrictions placed on randomising exposure to
taken up by the liver from the portal circulation, in an         varying diets. For this reason, most nutritional studies
insulin-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 an
proteins. During the metabolism of fructose to fructose-         ever-present threat to the conclusion of observational
1-phosphate, intracellular energy is depleted (adenosine         epidemiological studies (cross-sectional, cohort or case
triphosphate 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 evidence
about 20% of the absorbed carbohydrate is taken into             of adverse health outcomes, linked to high intakes of

                                                                                                                           © 2012 The Authors
50                                                                     Internal Medicine Journal © 2012 Royal Australasian College of Physicians
Sugar intake and cardiovascular risk


Table 1 Positive associations between indicators of exposure to fructose and important risk factors for cardiovascular disease or the disease itself

Exposure                           Disease or risk factor                        Nature of evidence                    Strength of effect and comparison
                                        for disease

Soft 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 trial18
Soft 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 glucose
Fructose                       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/L
Sugar 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 1.19–1.49
Sweetened 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)29

CHD, coronary heart disease; CI, confidence interval; HDL, high-density lipoprotein; LDL, low-density lipoprotein; RR, relative risk; SSB, sugar-sweetened
beverages.




fructose. Because fructose does not enter the diet in pure                                Although individual observational studies support no
form, and has only recently been identified as a nutri-                                 association between fructose intake and weight gain or
tional exposure likely to cause disease, many publications                             other indices associated with cardiovascular disease,30,31
point the finger at exposures, which are likely indicators                              the majority of systematic reviews support a positive
of high levels of fructose exposure, such as soft drink or                             association. If consistent associations are found among
sugar 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 of
instead, we focus on summary studies, such as system-                                  observational studies that found evidence of positive
atic reviews and meta-analyses. Such studies enable us                                 associations between sugar intake and outcomes, such as
to assess where the weight of the scientific evidence                                   weight gain, hyperuricaemia and gout, high levels of
stands, 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 variable
tigators. 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 intake
absent, single study results have been reported), and we                               of sugar-sweetened beverages. One systematic review is
refer the reader to the original articles to explore further                           revealing about the nature of the study and reported
the nature and strength of the relationship reported                                   effect: it showed that sugar and beverage industry-funded
between 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 Authors
Internal Medicine Journal © 2012 Royal Australasian College of Physicians                                                                                    51
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 routine
Figure 2 A plausible causal diagram that may explain the nature of the
association between dental caries and coronary artery disease.33 Solid    clinical measures of cardiovascular disease risk (except
arrows indicate proposed direction of causal relationship between vari-   cigarette smoking) are assessing, indirectly, indicators of
ables, 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.16
Cross-sectional studies are more open to error, such as
                                                                          Sources of fructose in the diet
from survivor bias and the lack of a temporal separation
between exposure and disease. Case control studies suffer                 How much sugar do we consume on average, and where
from the uncertainty that comes from the need to select                   does most of it come from? Data from the United Nations
and recruit a suitable control group. Therefore, cohort                   Food and Agriculture Organisation which estimate
studies, which incorporate a time component, are gener-                   average food disappearance (annual production + import
ally considered more reliable than either cross-sectional                 – export/the number of people in the population) suggest
or case control designs, and were more likely to show                     that we eat and drink, on average, between 30 and 40
positive 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 the
note with interest the consistent positive association                    corresponding figures, 38 for New Zealand and 46 for
observed between dental caries and cardiovascular                         the United States. Survey estimates of daily sugar intake
disease 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).36
the association involving pathogenic bacteria present                     Men generally consume more than women, with a
in the mouth, we argue that the association observed                      pattern of declining intake in older age groups. Soft
between 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. Fruit
in the manner depicted in Figure 2.34 At the time of                      juice, confectionary and breakfast cereals are other major
writing, a cohort study appeared which reported a direct                  sources (Table 3).
association between sugar sweetened beverage intake
and 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. diet34
tiles of intake. The study included 42 883 men with 3 683
outcomes and over 22 years of follow up.35 Such a finding                  Category                                              Proportion (%) of added
                                                                                                                                     sugar intake
supports our idea presented in Figure 2.
   In a similar way, as proposed for dental caries, we                    Regular soft drinks                                              33.0
speculate from the evidence in Table 1 that dyslipidaemia,                Sugars and candy                                                 16.1
hyperuricaemia, a diagnosis of type 2 diabetes, hyperten-                 Cakes, cookies, pies                                             12.9
                                                                          Fruit drinks                                                      9.7
sion and obesity – all of which are themselves associated
                                                                          Other grains (toast and waffles)                                   5.8
with incident cardiovascular disease – all have evidence of

                                                                                                                                      © 2012 The Authors
52                                                                                Internal Medicine Journal © 2012 Royal Australasian College of Physicians
Sugar intake and cardiovascular risk



Evidence 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 part
Although we do not focus on this issue, we draw atten-                      of some researchers to ‘prove a hypothesis’ in the face
tion to the relative paucity of evidence which indicates                    of generally unsupportive statistical evidence. We are
statistical associations between other potential causes of                  unclear as to why this one positive association is so widely
cardiovascular 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.37,41
than limiting sugar intake in dietary guidelines and                           Similarly, a recent Cochrane review of randomised
public health campaigns, such as those prepared by                          trials that studied the effects of salt restriction showed
national heart health organisations.                                        that, in normotensive and hypertensive cohorts, no sig-
   Briefly, systematic reviews and quantitative meta-                        nificant decline occurred in incidence of cardiovascular
analyses 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 trial
of modified or reduced fat on total and cardiovascular                       of salt restriction that enrolled subjects with congestive
mortality reported no effect in the pooled analysis of                      heart failure (RR 2.59, 95% 1.04–6.44).42 Despite such
randomised studies (pooled relative risk (RR): 0.98, 95%                    negative statistical evidence, salt restriction remains an
confidence 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 cardiovascular
is 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 disease
benefit, and the benefit from the overall reduction in                        risk, and a physiological index of absorption of these
total cardiovascular disease (CVD) events was small (14%                    nutrients is embodied in the GI. Diets that restrict intake
reduction). 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 a
between fat-modifying diets and indices of cardiovascular                   range of nutritional exposures, reported best evidence for
risk, such as adverse lipid profiles. Others focus on the                    a Mediterranean diet, a ‘high quality diet’, increased
outcome of reports which report subgroup analyses. One                      intake of vegetables, nuts and diets that restrict high GI
study, for example, which pooled a limited selection of                     foods or reduce a participant’s glycaemic load.41 The first
cohort data for which individual-level data were available,                 two exposures are complex, so they make it difficult to
showed a positive association between replacing saturated                   establish a causal exposure. Nuts and vegetables tend to
fat 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 CVD
and cardiovascular mortality (pooled hazard ratio 0.57;                     risk profile. One other meta-analyses (of observational
95% CI 0.42–0.77).39,40 The findings were, however,                          studies) has similarly reported a reduction in risk of a
inconsistent 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 of
with a similar null result reported for replacing saturated                 risk (RR) between highest and lowest quintile groups
fat 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 controlled
saturated fat is truly the causal exposure because the                      trials, is unavailable for assessing the effect of such diets
nature 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 on
on 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 loss
viduals from developing disease. The fact that researchers                  at follow-up in short-term studies (from 5 weeks to
are investigating such exposure subgroups rather than                       6 months).44

© 2012 The Authors
Internal Medicine Journal © 2012 Royal Australasian College of Physicians                                                                53
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 of
have 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) tolerance
slowed 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 of
advice to lower fat intake on a GI-restricted diet, the           control, tolerance and a withdrawal syndrome when the
overall 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 often
implicitly makes: that the health properties of a food may        associated with a reward perceived as ‘a hit’ or ‘feeling
be determined from its short-term effect on serum                 high’. As well as the positive symptoms, drug use
glucose. As discussed, high-fructose intake, which has            alleviates negative withdrawal symptoms, which are
little acute effect on serum glucose, in epidemiological          thought to lead to subconscious learning and deeply
studies showed statistical associations with deterioration        entrenched behaviour. Neurophysiological studies shed
of long-term glycaemic control and increased risk of              light on how this behaviour occurs. The loss of control
weight 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 the
Evidence for a sugar addiction                                    nucleus accumbens with the ventral tegmental area in
syndrome                                                          the midbrain. Learning by positive reinforcement
Evidence from a completely different line of enquiry may          involves linking an association between a behaviour
shed light on what effect the campaign against fat intake         and a positive reward. That then leads to the behaviour
has 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 reinforcement
Western 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 negative
position in the modern diet? Most lay people are familiar         stimuli is reinforced (such as the unpleasant withdrawal
with the term ‘sugar hit’ and find sugar especially palat-         symptoms that accompany tobacco abstinence in
able. Addiction theory, which has been developed to               dependent smokers). This reward is likened to the
explain the obsessive use of various substances (such as          pleasure that comes from taking off tight shoes. The
tobacco 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 temporarily
Curiously, the best evidence for an addictive component           relieve these symptoms. The latter mechanism is
of 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. Balfour
What is addiction?
                                                                  describes nicotine effects on two parts of the nucleus: the
Addiction, as an entity, is often poorly understood. Nick         core and medial shell which have distinct effects on
Heather defines the syndrome as ‘repeated failures to refrain      behaviour.48 Increases in dopamine concentration in the
from 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). The
substance, (ii) craving for the drug and (iii) ‘akrasia’ –        shell, in contrast, is thought to mediate stimulus response
failures 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 the
that is taken to prevent the onset or relieve established         smell of tobacco) can lead to subconscious urges to take
withdrawal symptoms. The Diagnostic and Statistical               the drug.
Manual-IV47 criteria for substance use are commonly used             We have introduced the biological basis and clinical
to adjudicate addiction in the individual. These criteria,        observations associated with established addictions. Does
summarised, are a maladaptive pattern of substance use            eating behaviour show similarities that suggest it too can
manifest by three or more of the following, present over          be considered in the same light?

                                                                                                                            © 2012 The Authors
54                                                                      Internal Medicine Journal © 2012 Royal Australasian College of Physicians
Sugar intake and cardiovascular risk



What are the parallels between food                                         was unable to lose weight despite use of emetics and
consumption and addiction?                                                  laxatives, or even undergoing obesity surgery:

                                                                              The executive recalls ‘often I would shake until I could
First, the same neural circuits linked to reward from
                                                                              put some sugar in my mouth’. Cues are also described
addictive 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 and
phy studies, eating stimulates neural activity in the
                                                                              every soft drink dispenser along the whole route’.
mesolimbic-dopaminergic pathway known to mediate
cocaine and nicotine addiction.49 Reduced dopamine (D2)                        This may be an extreme case, but the patient described
receptor availability is strongly correlated with increased                 tremor linked to short-term restriction from sugar. Such
body mass index (Pearson correlation coefficient 0.71),                      symptoms mirror some of those experienced after acute
indicating that increased dopamine levels are likely to be                  opiate abstinence.59 The executive recounted relief from
found 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 attention
addicted 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 report
levels of mesolimbic free D2 receptors have similarly been                  has been published. The features of the syndrome were
reported in individuals addicted to cocaine, opiates and                    tremors, headaches and abdominal pains that lasted about
alcohol.                                                                    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 intense
addictions, 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 in
trying to stop smoking is linked to an increased risk of                    modern western diets, obese people may not experience
relapse.51,52 Smoking acutely reduces hunger,53–55 and in                   withdrawal symptoms unless prolonged abstinence
some 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 concentration
after 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 case
and cocaine, abstain from their use, they experience a                      in addictions such as tobacco, where often the threat of
cluster of symptoms known as withdrawal. When obese                         such symptoms prompts subconscious drives to perform
people abstain from sugary or high GI food, do they                         the addictive behaviour.48
experience such symptoms? Opiate withdrawal is char-                           Some researchers advocated that obesity be considered
acterised by nausea, stomach cramps, muscular spasm                         a type of addiction. Volkow,63 for example, analysed the
and twitching, feelings of coldness, and heart pounding.                    similarities between the neural mechanisms underlying
What is common to many forms of withdrawal is the                           obesity and drug addiction, and argued that obesity be
time-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.64
evaporate after 30 days if abstinence is maintained.59 For                     The main determinants of an addictive substance are
nicotine, 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 have
include urges, craving, reduced concentration, irritability,                higher concentrations of fructose than natural sources,
increased appetite and depressed mood. Symptoms                             we speculate that manufactured sugary foods and
usually peak in the first few days after quitting and                        drinks (which take less time to consume) are most
largely subside after a month of continuous abstinence.                     addictive.
We know relatively little about whether an equivalent
withdrawal syndrome exists for food. Although carbohy-                      Conclusion
drate craving has been defined,60 a withdrawal syndrome
has 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 a
example, Atkins61 described a real estate executive who                     nutritional backdrop that has focused on reducing fat

© 2012 The Authors
Internal Medicine Journal © 2012 Royal Australasian College of Physicians                                                               55
Thornley et al.


intake and salt to reduce the incidence of cardiovascular                 soft drink, fruit juice, breakfast cereals and seemingly
disease. Second, excess intake of fructose, due to the                    healthy sweetened yogurts is revealed. For the clinician
accumulating, consistent epidemiological evidence of                      advising people to cut down their intake of sugar, we
links with risk factors for cardiovascular disease, suggests              recommend first advice about how to reduce intake of
that 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 the
overeating 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 that
that 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 are
lines 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 the
From food disappearance data, average daily sugar con-                    house, such as the presence of available sugary foods, are
sumption is between 30 and 40 teaspoons per day in                        likely to prompt consumption especially in the early
English-speaking countries, such as the UK, United                        phases (<1 month) of restriction. We, therefore, suggest
States, 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 resolve
reduce 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 accepted
source of added sugar in the United States comes in liquid                practice for many cardiologists, general physicians and
form, either from soft drinks and fruit juice which may be                family doctors concerned with reducing the CVD risk of
overlooked 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 on
the nutrition panels on manufactured foods, into tea-
                                                                          Conflicts of interest
spoons. Four grams of sugar is about 1 teaspoon. When
patients 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 this
Many people are taken aback when the sugar content of                     manuscript.



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   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 coronary
intervention in centres without on-site cardiac surgery
E. Oqueli
Ballarat Health Services, Ballarat, Victoria, Australia



Key words                                                 Abstract
percutaneous 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 last
Ernesto Oqueli, Internal Medicine Department,             decade, have significantly decreased the rates of complications requiring emergency
Ballarat Base Hospital, Drummond Street                   cardiac surgery, from approximately 4% to 6% in the balloon angioplasty era to as low
North, 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 at
Received 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 Author
58                                                                                          Internal Medicine Journal © 2012 Royal Australasian College of Physicians

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Imj2902

  • 1. bs_bs_banner Hiscock References 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 coronary 2 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 myocardial 3 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 to reduce cardiovascular disease risk S. Thornley,1 R. Tayler2 and K. Sikaris3 1 Section of Epidemiology and Biostatistics, University of Auckland, Auckland, New Zealand, 2Epworth Hospital, Richmond and 3Melbourne Pathology, Melbourne, Victoria, Australia Key words Abstract carbohydrates, 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 on Correspondence saturated fat and salt as guilty parties. More recently, evidence suggests that excess sugar Simon 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 to Health, 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 salt 2012. 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 Authors 46 Internal Medicine Journal © 2012 Royal Australasian College of Physicians
  • 2. Sugar intake and cardiovascular risk Introduction of non-communicable diseases, in his influential work published in 1976.3 If one looks back over a longer Authorities in the field of nutrition have made contradic- period of time, some experts have drawn attention to the tory statements about the role of sugar in the aetiology of adverse effects of sugar consumption since at least the diabetes, 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 in Australasia 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 saturated of becoming ‘just another statistic’. The Australian Heart fat dominating the nutritional horizon. Present in highest Foundation suggests the following: eat a variety of concentrations in animals, saturated fats are generally foods; include vegetables, whole grains, fruit, nuts and solid at room temperature and have all carbon chains seeds; choose healthier fats and oils; try to limit sugary, (fatty acids) filled (or saturated) with hydrogen. The fatty and salty takeaway meals; and drink mainly water. warnings of the National Heart Foundations in New The New Zealand counterpart solicits several steps to a Zealand and Australia to avoid meat and dairy fat are healthy heart: eat three meals a day with more plant made on the basis that such sources contain high material, 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 this scrutiny? Should a clinician blindly adhere to this advice? source have made it a favourite target of public health What 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 been sugar and salt cause coronary artery disease, or the studied, however. In the early 1980s, the properties of broader term ‘cardiovascular disease’ (which encom- glucose-containing foods were classified using the term passes 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 drawn the evidence for restricting all components of food is immediately before, and up to 1 h after, the intake of a equal and should be considered on par. If anything, satu- food standardised by the weight of the carbohydrate it rated 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 rice briefly 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 and to 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 have health agencies glosses over much debate and uncer- low GI due to the effects of the other macronutrients on tainty over nutritional exposures and their effects on gastric emptying. Also, the carbohydrate fructose, found heart health.The consequences of sugar intake have in highest concentration in sugar, is rated low on a GI divided the scientific community over the past 30 years. scale (~20), simply because it counts as carbohydrate but Cleave first proposed that scientific evidence implicated has a small effect on serum glucose during the first hour excess sugar and refined carbohydrate intake in a range of the postprandial phase. © 2012 The Authors Internal Medicine Journal © 2012 Royal Australasian College of Physicians 47
  • 3. Thornley et al. What is sugar? Until recently, this term has encom- was becoming rapidly accepted and enshrined in public passed all mono and disaccharides that are composed of health nutrition messages, first in the United States. The either six- or five-ring sugar molecules. This is a subclass message spread subsequently to other English-speaking of carbohydrates that differentiates ‘sugar’ from small countries, to increase the percentage of daily energy chains 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 to researchers have focused on the properties of one mol- account for 55–60% of energy and reduce fat intake to ecule: fructose. This monosaccharide is most commonly between 30% and 40% of energy.9 While the instigator found 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 animal fructose molecule and is commonly added to a variety of fat, a small but vocal minority argued that sugar was manufactured foods (yoghurt, breakfast cereals, sauces, much more likely to cause coronary heart disease, and cakes, pastries and soft drinks), and to tea and coffee. that this substance should be the target of public health Fructose is present in a restricted range of foods: fruit, preventative campaigns.3–5 honey, refined sugar and high-fructose corn syrup – a We know that since this time (the late 1970s), the sugar-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 sugar quently 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 of or glucose, used as an ingredient in the manufacture of about 30% over the period between 1970 and 2000.10 many 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 David A 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-meal dence linking food intake with cardiovascular disease, we serum glucose levels. In patients with diabetes, control of briefly explore the history of the modern-day ‘diabesity’ blood glucose has been a cornerstone of reducing the epidemic. 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 and occurred 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 on loped countries, using the Organisation for Economic postprandial glycaemia, fructose-containing foods, such as Co-operation and Development (OECD) data from the those that contain high sugar levels, were often classified early 1980s to 2007, we see a stark trend (Fig. 1).7 First, as medium GI and ‘healthy’. Because the GI of sugar the rate of rise in obesity prevalence has occurred mostly (sucrose) is lower than flour and other refined sources of in English-speaking countries lead by the United States, starch, sugar became, paradoxically, exonerated from the but 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, leading between a quarter and one-third of all adults are classi- researchers of GI advocated that people with diabetes fied as obese. Continental European countries are the continue to eat and drink high levels of sugar to improve next lowest prevalence region, with the lowest levels of their postprandial serum glucose control.12 obesity observed in the only two Asian countries in the More recently, the tide of evidence and scientific OECD: Japan and South Korea (<5%). We also note that opinion is turning in favour of sugar as a significant the epidemic probably started in the late 1970s and early vascular disease risk factor, and the substance continues 1980s, for it was in this period that significant efforts to attract attention as a potential cause of the epidemic of were made to measure the prevalence of obesity in OECD non-communicable disease of the 21st century. The countries. 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 the occurred 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 Authors 48 Internal Medicine Journal © 2012 Royal Australasian College of Physicians
  • 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 30 Obesity 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 Year Figure 1 Adult obesity prevalence (body mass index Ն 30 kg/m2), by year, for selected Organisation for Economic Co-operation and Development countries (1980–2007).7 © 2012 The Authors Internal Medicine Journal © 2012 Royal Australasian College of Physicians 49
  • 5. Thornley et al. United States of cardiovascular disease and stroke, com- liver cells, with the remaining 80% taken up by skeletal piled a summary statement in 2002 for health profession- and smooth muscle, and other organs in the presence of als about the effects of sugar on cardiovascular and insulin. Only about 5% of starch is converted to fatty acids metabolic 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, the physicians should ‘rely on professional judgement’. The presence of high levels of triglycerides within liver cells stance of the authors of the report was best summed up results in insulin resistance, non-alcoholic fatty liver by 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 disease sation concluded that the weight of scientific evidence had turned against sugar, concluding that men should With our biochemical understanding of fructose, we consume no more than nine teaspoons per day, with six might expect that fructose intake is associated with a recommended for women.6 Risk of weight gain and range of conditions, such as weight gain, high levels of developing diabetes were the main concerns associated serum urate (and gout), diabetes, dyslipidaemia and with excess sugar intake, summarised in the following possibly cardiovascular disease. Do the epidemiological statement: 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 dietary mulating evidence that the fructose component of sugar recall, considered by some to be the most accurate of all is 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 sugar contrast this evidence with more established nutrition intake by about 20%.15 Put simply, people have bad exposures, 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 consciously Physiology 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 and almost no effect, in the short term, on postprandial gly- bias towards a null (or ‘no effect’) value. If the error is caemia in contrast to glucose-rich foods, such as breads, systematic, the effect estimate may be biased in either rice 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 of clinical and animal studies, after ingestion, fructose is risk of nutrition exposures is the cost, complexity and absorbed from the small intestine, almost completely ethical restrictions placed on randomising exposure to taken up by the liver from the portal circulation, in an varying diets. For this reason, most nutritional studies insulin-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 an proteins. During the metabolism of fructose to fructose- ever-present threat to the conclusion of observational 1-phosphate, intracellular energy is depleted (adenosine epidemiological studies (cross-sectional, cohort or case triphosphate 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 evidence about 20% of the absorbed carbohydrate is taken into of adverse health outcomes, linked to high intakes of © 2012 The Authors 50 Internal Medicine Journal © 2012 Royal Australasian College of Physicians
  • 6. Sugar intake and cardiovascular risk Table 1 Positive associations between indicators of exposure to fructose and important risk factors for cardiovascular disease or the disease itself Exposure Disease or risk factor Nature of evidence Strength of effect and comparison for disease Soft 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 trial18 Soft 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 glucose Fructose 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/L Sugar 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 1.19–1.49 Sweetened 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)29 CHD, coronary heart disease; CI, confidence interval; HDL, high-density lipoprotein; LDL, low-density lipoprotein; RR, relative risk; SSB, sugar-sweetened beverages. fructose. Because fructose does not enter the diet in pure Although individual observational studies support no form, and has only recently been identified as a nutri- association between fructose intake and weight gain or tional exposure likely to cause disease, many publications other indices associated with cardiovascular disease,30,31 point the finger at exposures, which are likely indicators the majority of systematic reviews support a positive of high levels of fructose exposure, such as soft drink or association. If consistent associations are found among sugar 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 of instead, we focus on summary studies, such as system- observational studies that found evidence of positive atic reviews and meta-analyses. Such studies enable us associations between sugar intake and outcomes, such as to assess where the weight of the scientific evidence weight gain, hyperuricaemia and gout, high levels of stands, 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 variable tigators. 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 intake absent, single study results have been reported), and we of sugar-sweetened beverages. One systematic review is refer the reader to the original articles to explore further revealing about the nature of the study and reported the nature and strength of the relationship reported effect: it showed that sugar and beverage industry-funded between 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 Authors Internal Medicine Journal © 2012 Royal Australasian College of Physicians 51
  • 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 routine Figure 2 A plausible causal diagram that may explain the nature of the association between dental caries and coronary artery disease.33 Solid clinical measures of cardiovascular disease risk (except arrows indicate proposed direction of causal relationship between vari- cigarette smoking) are assessing, indirectly, indicators of ables, 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.16 Cross-sectional studies are more open to error, such as Sources of fructose in the diet from survivor bias and the lack of a temporal separation between exposure and disease. Case control studies suffer How much sugar do we consume on average, and where from the uncertainty that comes from the need to select does most of it come from? Data from the United Nations and recruit a suitable control group. Therefore, cohort Food and Agriculture Organisation which estimate studies, which incorporate a time component, are gener- average food disappearance (annual production + import ally considered more reliable than either cross-sectional – export/the number of people in the population) suggest or case control designs, and were more likely to show that we eat and drink, on average, between 30 and 40 positive 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 the note with interest the consistent positive association corresponding figures, 38 for New Zealand and 46 for observed between dental caries and cardiovascular the United States. Survey estimates of daily sugar intake disease 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).36 the association involving pathogenic bacteria present Men generally consume more than women, with a in the mouth, we argue that the association observed pattern of declining intake in older age groups. Soft between 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. Fruit in the manner depicted in Figure 2.34 At the time of juice, confectionary and breakfast cereals are other major writing, a cohort study appeared which reported a direct sources (Table 3). association between sugar sweetened beverage intake and 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. diet34 tiles of intake. The study included 42 883 men with 3 683 outcomes and over 22 years of follow up.35 Such a finding Category Proportion (%) of added sugar intake supports our idea presented in Figure 2. In a similar way, as proposed for dental caries, we Regular soft drinks 33.0 speculate from the evidence in Table 1 that dyslipidaemia, Sugars and candy 16.1 hyperuricaemia, a diagnosis of type 2 diabetes, hyperten- Cakes, cookies, pies 12.9 Fruit drinks 9.7 sion and obesity – all of which are themselves associated Other grains (toast and waffles) 5.8 with incident cardiovascular disease – all have evidence of © 2012 The Authors 52 Internal Medicine Journal © 2012 Royal Australasian College of Physicians
  • 8. Sugar intake and cardiovascular risk Evidence 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 part Although we do not focus on this issue, we draw atten- of some researchers to ‘prove a hypothesis’ in the face tion to the relative paucity of evidence which indicates of generally unsupportive statistical evidence. We are statistical associations between other potential causes of unclear as to why this one positive association is so widely cardiovascular 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.37,41 than limiting sugar intake in dietary guidelines and Similarly, a recent Cochrane review of randomised public health campaigns, such as those prepared by trials that studied the effects of salt restriction showed national heart health organisations. that, in normotensive and hypertensive cohorts, no sig- Briefly, systematic reviews and quantitative meta- nificant decline occurred in incidence of cardiovascular analyses 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 trial of modified or reduced fat on total and cardiovascular of salt restriction that enrolled subjects with congestive mortality reported no effect in the pooled analysis of heart failure (RR 2.59, 95% 1.04–6.44).42 Despite such randomised studies (pooled relative risk (RR): 0.98, 95% negative statistical evidence, salt restriction remains an confidence 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 cardiovascular is 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 disease benefit, and the benefit from the overall reduction in risk, and a physiological index of absorption of these total cardiovascular disease (CVD) events was small (14% nutrients is embodied in the GI. Diets that restrict intake reduction). 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 a between fat-modifying diets and indices of cardiovascular range of nutritional exposures, reported best evidence for risk, such as adverse lipid profiles. Others focus on the a Mediterranean diet, a ‘high quality diet’, increased outcome of reports which report subgroup analyses. One intake of vegetables, nuts and diets that restrict high GI study, for example, which pooled a limited selection of foods or reduce a participant’s glycaemic load.41 The first cohort data for which individual-level data were available, two exposures are complex, so they make it difficult to showed a positive association between replacing saturated establish a causal exposure. Nuts and vegetables tend to fat 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 CVD and cardiovascular mortality (pooled hazard ratio 0.57; risk profile. One other meta-analyses (of observational 95% CI 0.42–0.77).39,40 The findings were, however, studies) has similarly reported a reduction in risk of a inconsistent 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 of with a similar null result reported for replacing saturated risk (RR) between highest and lowest quintile groups fat 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 controlled saturated fat is truly the causal exposure because the trials, is unavailable for assessing the effect of such diets nature 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 on on 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 loss viduals from developing disease. The fact that researchers at follow-up in short-term studies (from 5 weeks to are investigating such exposure subgroups rather than 6 months).44 © 2012 The Authors Internal Medicine Journal © 2012 Royal Australasian College of Physicians 53
  • 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 of have 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) tolerance slowed 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 of advice to lower fat intake on a GI-restricted diet, the control, tolerance and a withdrawal syndrome when the overall 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 often implicitly makes: that the health properties of a food may associated with a reward perceived as ‘a hit’ or ‘feeling be determined from its short-term effect on serum high’. As well as the positive symptoms, drug use glucose. As discussed, high-fructose intake, which has alleviates negative withdrawal symptoms, which are little acute effect on serum glucose, in epidemiological thought to lead to subconscious learning and deeply studies showed statistical associations with deterioration entrenched behaviour. Neurophysiological studies shed of long-term glycaemic control and increased risk of light on how this behaviour occurs. The loss of control weight 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 the Evidence for a sugar addiction nucleus accumbens with the ventral tegmental area in syndrome the midbrain. Learning by positive reinforcement Evidence from a completely different line of enquiry may involves linking an association between a behaviour shed light on what effect the campaign against fat intake and a positive reward. That then leads to the behaviour has 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 reinforcement Western 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 negative position in the modern diet? Most lay people are familiar stimuli is reinforced (such as the unpleasant withdrawal with the term ‘sugar hit’ and find sugar especially palat- symptoms that accompany tobacco abstinence in able. Addiction theory, which has been developed to dependent smokers). This reward is likened to the explain the obsessive use of various substances (such as pleasure that comes from taking off tight shoes. The tobacco 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 temporarily Curiously, the best evidence for an addictive component relieve these symptoms. The latter mechanism is of 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. Balfour What is addiction? describes nicotine effects on two parts of the nucleus: the Addiction, as an entity, is often poorly understood. Nick core and medial shell which have distinct effects on Heather defines the syndrome as ‘repeated failures to refrain behaviour.48 Increases in dopamine concentration in the from 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). The substance, (ii) craving for the drug and (iii) ‘akrasia’ – shell, in contrast, is thought to mediate stimulus response failures 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 the that is taken to prevent the onset or relieve established smell of tobacco) can lead to subconscious urges to take withdrawal symptoms. The Diagnostic and Statistical the drug. Manual-IV47 criteria for substance use are commonly used We have introduced the biological basis and clinical to adjudicate addiction in the individual. These criteria, observations associated with established addictions. Does summarised, are a maladaptive pattern of substance use eating behaviour show similarities that suggest it too can manifest by three or more of the following, present over be considered in the same light? © 2012 The Authors 54 Internal Medicine Journal © 2012 Royal Australasian College of Physicians
  • 10. Sugar intake and cardiovascular risk What are the parallels between food was unable to lose weight despite use of emetics and consumption and addiction? laxatives, or even undergoing obesity surgery: The executive recalls ‘often I would shake until I could First, the same neural circuits linked to reward from put some sugar in my mouth’. Cues are also described addictive 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 and phy studies, eating stimulates neural activity in the every soft drink dispenser along the whole route’. mesolimbic-dopaminergic pathway known to mediate cocaine and nicotine addiction.49 Reduced dopamine (D2) This may be an extreme case, but the patient described receptor availability is strongly correlated with increased tremor linked to short-term restriction from sugar. Such body mass index (Pearson correlation coefficient 0.71), symptoms mirror some of those experienced after acute indicating that increased dopamine levels are likely to be opiate abstinence.59 The executive recounted relief from found 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 attention addicted 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 report levels of mesolimbic free D2 receptors have similarly been has been published. The features of the syndrome were reported in individuals addicted to cocaine, opiates and tremors, headaches and abdominal pains that lasted about alcohol. 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 intense addictions, 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 in trying to stop smoking is linked to an increased risk of modern western diets, obese people may not experience relapse.51,52 Smoking acutely reduces hunger,53–55 and in withdrawal symptoms unless prolonged abstinence some 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 concentration after 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 case and cocaine, abstain from their use, they experience a in addictions such as tobacco, where often the threat of cluster of symptoms known as withdrawal. When obese such symptoms prompts subconscious drives to perform people abstain from sugary or high GI food, do they the addictive behaviour.48 experience such symptoms? Opiate withdrawal is char- Some researchers advocated that obesity be considered acterised by nausea, stomach cramps, muscular spasm a type of addiction. Volkow,63 for example, analysed the and twitching, feelings of coldness, and heart pounding. similarities between the neural mechanisms underlying What is common to many forms of withdrawal is the obesity and drug addiction, and argued that obesity be time-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.64 evaporate after 30 days if abstinence is maintained.59 For The main determinants of an addictive substance are nicotine, 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 have include urges, craving, reduced concentration, irritability, higher concentrations of fructose than natural sources, increased appetite and depressed mood. Symptoms we speculate that manufactured sugary foods and usually peak in the first few days after quitting and drinks (which take less time to consume) are most largely subside after a month of continuous abstinence. addictive. We know relatively little about whether an equivalent withdrawal syndrome exists for food. Although carbohy- Conclusion drate craving has been defined,60 a withdrawal syndrome has 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 a example, Atkins61 described a real estate executive who nutritional backdrop that has focused on reducing fat © 2012 The Authors Internal Medicine Journal © 2012 Royal Australasian College of Physicians 55
  • 11. Thornley et al. intake and salt to reduce the incidence of cardiovascular soft drink, fruit juice, breakfast cereals and seemingly disease. Second, excess intake of fructose, due to the healthy sweetened yogurts is revealed. For the clinician accumulating, consistent epidemiological evidence of advising people to cut down their intake of sugar, we links with risk factors for cardiovascular disease, suggests recommend first advice about how to reduce intake of that 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 the overeating 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 that that 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 are lines 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 the From food disappearance data, average daily sugar con- house, such as the presence of available sugary foods, are sumption is between 30 and 40 teaspoons per day in likely to prompt consumption especially in the early English-speaking countries, such as the UK, United phases (<1 month) of restriction. We, therefore, suggest States, 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 resolve reduce 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 accepted source of added sugar in the United States comes in liquid practice for many cardiologists, general physicians and form, either from soft drinks and fruit juice which may be family doctors concerned with reducing the CVD risk of overlooked 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 on the nutrition panels on manufactured foods, into tea- Conflicts of interest spoons. Four grams of sugar is about 1 teaspoon. 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  • 13. bs_bs_banner Thornley 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 coronary intervention in centres without on-site cardiac surgery E. Oqueli Ballarat Health Services, Ballarat, Victoria, Australia Key words Abstract percutaneous 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 last Ernesto Oqueli, Internal Medicine Department, decade, have significantly decreased the rates of complications requiring emergency Ballarat Base Hospital, Drummond Street cardiac surgery, from approximately 4% to 6% in the balloon angioplasty era to as low North, 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 at Received 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 Author 58 Internal Medicine Journal © 2012 Royal Australasian College of Physicians