Sickly Sweet: electronic version.

Sickly Sweet: Sugar, Refined Carbohydrate,
Addiction and
Global Obesity

Simon Thornley and
Hayden McRobbie

ii Simon Thornley and Hayden McRobbie

PREFACE

The thesis of this book offers an alternative view of obesity and weight
loss. We argue that obesity is a disorder of motivation - an addiction. This
distinction is not made just from an academic stand point. The reason we
seek to classify obesity in such a manner is to better understand its nature
and craft improved strategies for those that are trapped by its snare.
Obesity, at a population level, has not always been with us. Nearly 40
years into the global epidemic, we easily forget that not so long ago the
world was not popping its collective buttons. Of all countries, trends in the
United States are perhaps most exaggerated. In 1978, 15% of the
population was defined as obese, then 22 years later, that number had
doubled to 30%, almost one in three adults [1]. Such a rate of change
argues that genetic factors are unlikely to account for this trend. If genetic
factors are not responsible, the only alternative is the environment. So what
is it about our environment that has changed to prompt this global increase
in girth? As a medical doctor, during my training, I had been taught the
scientific consensus which attempts to explain this modern phenomenon.
Succinctly, the World Health Organisation stated that two factors are at
work, first, that food has become cheaper and more energy dense, and
second, that energy expenditure has reduced, due to a reliance on modern
technology, such as motorized transport, which replaces walking or cycling

[2]. When examined more carefully, such a view is based on the law of
conservation of energy in physics which dictates that energy cannot
disappear from a closed system. In an individual, put simply, energy in
must equal energy out. Food intake corresponds to the energy in, and
energy expended by the body, carrying out physiological functions, such as
pumping blood, maintaining a constant temperature and exercise. If this
balance is upset, so that individuals consume more energy than they
expend, the excess is stored as fat and obesity results.
At face value, such an argument appears grounded and compelling,
based on few assumptions. If such a theory is correct, what is the logical
response to reverse this modern epidemic? When nutritional advice is
derived from such a theory, of the three main macronutrients (fat,
carbohydrate and protein), reduction of proportion of energy derived from
fat is the consequence. Why point the finger at fat? When burned, or
metabolized, fat releases just over twice the energy of protein or
carbohydrate. Co-incidentally, from the 1960s, researchers also
recommended reducing intake of saturated fat (mainly derived from animal
fat), to prevent the most common cause of death in Western Countries,
coronary heart disease. End of story; reducing fat seemed to kill two birds
with one stone, potentially reducing obesity and coronary disease in an
easily digestible sliver of nutritional advice. The modern epidemic of
obesity, so it was believed, would be reversed by skimming fat from milk,
trimming the skin off chicken, abstaining from pork crackling and
replacing the fat in dairy products with less energy dense carbohydrate.
Unfortunately, population waistlines have not responded in the way
predicted by this theory. To the contrary, evidence suggests that such
advice has actually increased the prevalence of obesity in most OECD
countries, where regular surveys have been carried out. Asian countries in
the OECD, of which there are only two, South Korea and Japan, stand out
in stark contrast to Western nations, with a stable low prevalence of
obesity. The United States, Australia, New Zealand and the United
Kingdom, all English speaking nations, stand out in contrast, with the

Preface v

greatest rise in obesity between 1980 and 2003 with prevalence doubling
during this period. What is wrong? Two explanations are possible; (1)
either people are ignoring this simple health message, or (2) the message is
incorrect, or even doing harm.
The most surprising aspect of this advice is how widely it has been
taken up, and how spectacularly it has failed. After the Surgeon General's
recommendation in the 1960s that cigarettes cause cancer, many expected
that people would heed this advice and leave their cigarettes as soon as the
message got through. Fifty years later, one in five New Zealand adults
smoke, and although numbers are slowly dropping, progress is
disappointing. As far as public acceptance of the crusade against fat goes,
it has met with surprisingly little resistance. In New Zealand, chicken is
routinely sold, stripped of its fatty flesh, steak is lean, and it's hard to find a
can or packet without a reference to it's purity from the obesigenic, greasy
substance. Almost all products, from sour cream to biscuits are sold in a
“lite” variety, in which fat content is reduced. Where I currently work, in
the University’s, School of Population Health, I have no choice but to
drink skim milk with my tea or coffee - 99.9% fat free.
My own realisation that traditional nutritional theory may be flawed
was initiated by reading Michael Pollan's “In Defense of Food” [3]. Pollan,
who describes himself as a humble journalist rather than a scientist, takes
on the nutrition establishment, and argues that in the United States, the
obsession with healthy eating has paradoxically contributed to obesity. He
identifies that food manufacturers have created confusion in the mind of
consumers by making claims of health benefits for a wide variety of foods.
Also, in the modern food industry's assault on the modern consumer, no
one appears to be stating the obvious, straight forward solution to obesity -
eat less. Pollan goes on to not only attack nutritional science but also the
philosophy of scientific reductionism, arguing that defining food by its
building blocks cannot account for its effects on the body. Importantly,
also he points the finger at nutritional epidemiology, the science from
which nutritional advice springs from, actually suffers from a fundamental
flaw. Simply put, individuals are notoriously error prone when it comes to
recording what they actually eat, so that measuring associations between

vi Simon Thornley and Hayden McRobbie

food intake and health outcomes may not always produce accurate
information on which to base recommendations.
My own experience with food was similar to what I think has been
happening on a grand, population wide, scale. During my time as a medical
student, I was taught the current medical wisdom. Saturated fat was bad for
coronary arteries, and fat in general was obesogenic. I resolved to reduce
the fat content of my meals, shunned the weekly regular servings of fish
and chips, fast food and resolved to drink only the most watery skim milk.
During my time as a clinician, treating people in hospital with heart
attacks, strokes and cancer, my approach was the same; fat was the enemy
- my patients were encouraged to swap full cream milk for the low fat
alternative.
Despite my fat avoidance, belts were loosened and trousers cast aside
until I was roughly fifteen kilograms heavier than I had been in medical
school. By this time, I was now training in public health medicine, and
taking part in research of smokers and how they could be helped to quit.
As a doctor in the hospital, I had an almost arrogant disregard for smokers.
I hated them. They smoked despite decades of research that showed they
were shortening their lives. I'd heard many patients assure me they were
going to quit, and later find evidence that they hadn't either from a spouse
or from laboratory results. In my mind they were lazy and self-centred, and
were responsible for much of the stress I experienced in the over burdened
New Zealand public hospital system. As a junior doctor, often exhausted
from working long hours, smokers were responsible for what came to
them, and that was that.
When I abandoned my career as a hospital doctor, changing instead to
public health research, I discovered how little I knew about addiction. For
the first time, I realized that smokers experience a withdrawal syndrome
when they try to stop, which is unpleasant and lasts for over a month.
Symptoms of craving, irritability, restlessness, depression, difficulty
concentrating, and constipation plague the smoker bent on reform. These
symptoms can get so bad that I've heard of mothers sometimes hitting their
children and husbands abusing their wives. Withdrawal symptoms, such as
irritability are not a justification for this behavior, but do illustrate the

Preface vii

severity of symptoms that some people face. Complete relief is only a
cigarette away. Another revelation was the strength of subconscious drives
and desires created by reward pathways in the midbrain. Most smokers
were completely unaware that the reason they smoked was to avoid
withdrawal discomfort; the smoking was performed almost automatically.
When this was explained to smokers in our studies, instantly the majority
agreed and identified personally with this explanation. The last pearl was
perhaps the most significant. In almost all addictions, time from taking the
substance (such as nicotine from a cigarette) to being absorbed and
stimulating the reward centre in the brain was the critical factor that
determined how effectively a drug could keep you hooked. Cigarettes were
ideal. The nicotine is vaporised by the cigarette's flame, inhaled into the
lungs by the smoker, transported rapidly through the heart to the brain in a
matter of minutes. The nicotine products (gum, patch, lozenge, mouthspray
and pouch) we were testing could not compete. They were absorbed
through the lining of the mouth, an area of the body with much less blood
flow than the lungs, and their time to stimulation of the brain's reward
centres much slower than cigarettes. This time lag had a silver lining,
however. Slowly absorbed nicotine helped relieve some withdrawal
discomfort, but wasn't as stongly rewarding as the cigarettes they replaced.
For many smokers, they are a bridge to freedom.
One day I was working on translating these techniques to help smokers
quit into a palatable, brief education session for family doctors. Across the
road from where I had lunch was a second hand book store. Among the
books that were arranged in a semi-random fashion, I found a couple of
cheap copies of old diet books - the New Glucose Revolution, and The
Atkins Diet. The book by Robert Atkins grabbed my attention
immediately. I knew the diet was based on restricting carbohydrates, out of
favour with most nutrition experts, so I was very skeptical. Through the
pages, however, I noticed that Atkins described patients who experienced
similar feelings to those that smokers reported in cessation clinics. One
was very vivid. He described an overweight executive that was addicted to
sugar:

viii Simon Thornley and Hayden McRobbie

‘‘…often I would shake until I could put some sugar in my mouth’’. I
had an hour’s drive from my office to my home, and I knew very restaurant,
every candy machine and every soft drink dispenser along the whole route.’’

The man experienced tremors that were relieved by a sweet taste, and
described his preoccupation with sources of sugar on his journey home.
The physical symptoms, relieved by sugar, and the cues described were
very similar to the phenomenon of withdrawal described from nicotine. I
was curious. I searched medical journals to find evidence that food was
addictive, like Atkins’ description, but found little. Much had been written
about the theoretical view point, drawing parallels from rat research and
from complicated imaging studies of obese people’s brains, but nothing I
came across considered the implications of such a theory on how
individuals are treated or whether this theory may explain why populations
are expanding their collective girth. Also, the fact that I had made such a
discovery from a book known to be relegated to the medical scrapheap of
pseudoscience increased my cynicism of the established nutritional agenda.
Atkins did not identify that these symptoms may have been part of a
withdrawal syndrome, but did claim that his diet reduced their intensity
and promised recovery.
In the "New Glucose Revolution", I discovered another alternative
theory of nutrition and a different approach to weight loss than that
advocated by the public health establishment. The most important
component was the glycemic index - a physiological measure of how much
a standardised mass of carbohydrate from different foods raises the blood
glucose after eating. The plots of glycemic index and how it was measured
made me think of our nicotine studies and how time-to-‘hit’ was such an
important factor in making products addictive. Why couldn't food be
considered in the same way? Was glycemic index the key to unlocking a
hidden addiction - the obesity epidemic? I was curious to discover more.
Together with tobacco researcher, and colleague, Hayden McRobbie, we
explore the evidence that links sugar and refined carbohydrates with food
addiction and set out an alternative explanation for the burgeoning obesity
epidemic.

Preface ix

REFERENCES

[1] OECD. OECD Health Data 2009: Statistics and Indicators for 30
Countries. Paris: OECD publishing, 2009.
[2]World Health Organisation. Obesity: Preventing and Managing the
Global Epidemic. Report on a WHO Consultation Technical Report
Series, No 894. Geneva: World Health Organisation, 2000.
[3]Pollan M. In Defense of Food: An Eater’s Manifesto. First Printing.
Penguin Press HC; 2008.

Chapter 1

THE GLOBAL OBESITY EPIDEMIC:
EPIDEMIOLOGY, HISTORY AND
MILESTONES

“It is not yet clear whether any single attribute of the Western way of
life is particularly important in increasing the risk of diabetes. Excess
sucrose has largely been exonerated as an important dietary factor in the
aetiology of type 2 diabetes...”
J. I. Mann and A. S. Truswell [1]
Diseases of overnourished societies and the need for dietary change: in
the Oxford Textbook of Medicine, 4th Edition.

“Originally proposed as the ideal sweetener for people with diabetes...
Fructose [part of sucrose]... has been indirectly implicated in the epidemics
of obesity and type 2 diabetes.”
The American Heart Association [2]

Sugar and its effect on human health has divided the scientific
community over the last ten years. Professor Jim Mann, an international
nutritional expert describes sugar (sucrose) as “exonerated” in the
aetiology of type 2 diabetes in the prestigious Oxford Textbook of
Medicine. The American Heart Association, who, in 2002, had taken a
similar view to Mann [1], later changed their mind, reporting that fructose

(half of the sucrose molecule) was now facing a guilty verdict, from which
it had earlier received a pardon. If one looks back over a longer period of
time, some experts have long scrutinised the adverse effects of sugar
consumption, since at least the early 1960s [3]. Such calls, however, have
largely been ignored until recently. In this book, we examine what
direction nutritional policy has taken over the last forty years, and in what
nutrition context obesity patterns have developed. We examine overeating
from a new paradigm, rather than viewing overeating as a problem of
energy balance, we instead consider motivation to eat, and what effects
different foods have on hunger. Surely, if eating certain types of food,
increases appetite, as alleged for sugar, this has important consequences for
the quantity of food that enters a person’s mouth, ultimately stretching the
belt out a notch, and making difficult work of the juxtaposing of buttons.
We will see that such a paradigm, ignoring the powerful biological drives
and learning that occur with eating, has lead to what we believe to be a
tragic misdirection of nutrition policy in English speaking countries and
now dispersing around the world.
When I first started work as a house officer, fresh out of medical
school, at the dawn of the new millenium, I spent two years working in a
busy city hospital. The hospital treated people of a wide variety of ethnic
backgrounds, but Pacific people had a lively community in the area and
were frequently in need of treatment. Migrants from the Pacific islands that
surround New Zealand are frequently obese, so much so, that during my
public health training, a colleague advised me that one in four Pacific
adults would be eligible for obesity surgery in the jurisdiction in which he
worked. Of all the challenges that being a junior doctor entailed, one of the
most difficult tasks was the constant need to place intravenous lines in
patients, so that various drugs, and fluids could be administered. What, in a
thin person, was a trivial task, could provoke severe anxiety when veins
were concealed by layers of fat. If requested to insert a cannula, I would
first take a peek through the curtain to get a rough estimate of how much
fat was likely to impede my progress, and so how many spare lines would

The Global Obesity Epidemic 3

be required. In people who tipped the scales, I would load my kidney dish
of supplies to overflowing to account for the inevitable event of numerous
embarrassing and painful (for both the patient and myself) failures. Once
established in the job, I soon realised that the sneak preview was
unnecessary, because the vast majority of people admitted were
overweight. I might as well overload my kidney dish, the chances were I'd
have a battle on my hands. Faced with the relentless demands of caring
with such a load of obese patients, it was difficult to imagine a time when
obesity was a rare sight.
For anyone in an English speaking country, obesity has become such a
common occurrence it no longer raises more than a glimmer of curiosity.
TV, voyeuristically, still portray the adventures of the super obese, that
continue to pull crowds. Only grossly or morbidly obese people attract
comment. Indeed, whilst writing this manuscript, the researcher sitting
adjacent to me would easily qualify as obese. Although records are rare,
before the 1970s, few Western countries systematically recorded obesity
rates in their populations. Why no scientific interest in body size? It seems
that excess fat simply wasn't a major issue to devote significant time or
resource to measuring. This, in itself, suggests that obesity was not a major
concern - why measure a problem that doesn't exist?
Something changed in the 1970s. From the early 1980s, obesity
suddenly appeared on the public health radar, and populations, particularly
in wealthier countries, were measured for height and weight. The
expanding waistlines of different countries have been thoroughly
researched, documented up until today, with collective expansion set to
continue for the foreseeable future. This bleak news hides pockets of
resistance to this trend. Despite this pessimistic outlook, some countries
remain thin. Obesity is strongly patterned by country. Of the thirty wealthy
countries contained within the Organisation for Economic Co-operation
and Development (OECD), English speaking countries are leading the
pack, with the United States way out in front [4]. In sharp relief to these
countries that are linguistically linked, are the slim societies of Japan and
South Korea who have maintained low levels of obesity over the same
period.

4 Simon Thornley and Hayden McRobbie

To understand what factors underlie the rising tide of global obesity, a
phenomenon with a clear temporal pattern, with vastly different impacts
between countries, we must consider what ideas have been propagated in
these countries, what dietary patterns have emerged and consider
definitions of obesity. Critical milestones, in terms of nutritional advice,
and changes to food processing and content may give clues to what is
causing our collective bursting of buttons.

DEFINITIONS

Firstly, how do we define someone as overweight or obese? This
sounds simple, but accurate, repeatable, consistent measurements are
critical to our understanding of this disorder. Body mass index (BMI) is
commonly used as a global standard today to define obesity in terms of
weight corrected for height [5]. What is this measure and what does it tell
us about an individual? How has this definition changed over time, and
what does the commonly used term “body mass index” indicate? Obesity
has been labeled a major public health issue because of its association with
premature death and other diseases. If information is to be accurately
recorded, a consistent definition must be applied over time to track
population trends. Before 1980, a variety of methods were used to classify
people as overweight, based on actuarial data derived from life insurance
companies such as Metropolitan Life, which were labeled “ideal” weight
for height values, or “desirable” body weights [5]. Such standards were
derived from a large group of North Americans and Canadian adults
purchasing life insurance policies between 1935 and 1954, with standards
referring to a group of people that, at the time, had low rates of premature
death. From 1980, body mass index (BMI) was more commonly used,
which is defined by weight in kilograms, divided by height in meters
squared. This measure is a reasonably good measure of body fat, although
it is far from perfect. Raised BMI also predicts increased risk of a range of
diseases such as coronary heart disease, stroke, cancers of the large bowel,
womb and breast [6]. A recent study, involving over 900,000 subjects,


showed that a body mass index of 22.5 to 25.0 kg/m 2 was linked with
optimal survival. People above this range, with moderate obesity (BMI
between 30 and 35 kg/m2) would, on average, face in excess of three years
life lost, and people with extreme obesity (BMI 40-50 kg/m 2) lost more
than 10 years of life. By way of comparison, this latter condition shortens
average lifespan by about the period as a lifetime of smoking cigarettes [7].
Classifications based on body mass index are therefore usually divided into
overweight (BMI ≥ 25.0), and obese (BMI ≥ 30.0).
While BMI is a useful measure for characterizing population risk of
obesity, at an individual level it may be less accurate because some,
particularly young males, are incorrectly misclassified as overweight due
to increased lean muscle mass rather than excess fat tissue. To avoid this
potential source of error, here, we use a cutoff of BMI ≥ 30.0 kg/m 2 to
classify individuals as obese, and to monitor population trends.


Figure 1. Adult obesity (BMI ≥ 30kg/m 2) prevalence by year for selected OECD
countries (1980 to 2003) [9].

GLOBAL TRENDS IN OBESITY PREVALENCE

The start of the global obesity epidemic is difficult to pinpoint.
Regular, representative surveys of population obesity were not carried out
until obesity became a focal point in the medical community and
significant resource was devoted to its measurement. In the United States,
at the turn of the 19th Century, a survey was undertaken, recording height
and weight of Civil War veterans aged 50 to 59 years found that 3.4% had
a BMI ≥ 30.0 (obese) [16]. Also, a comparison of the weight of London


hospital patients coming to autopsy in 1906 to 1914 and the 1950s showed
little difference in mean weights between the two periods [8]. Since this
time, until the early 1980s, nationwide, estimates of obesity prevalence are
difficult to find. A summary of obesity prevalence, by country, has been
published by the OECD and the prevalence by country between 1980 and
2003 are depicted in Figure 1.
Several patterns emerge from this figure. First, the country with the
highest prevalence, reported after the year 2000, of obesity is the United
States, with one in three adults meeting the BMI cutoff. Other high
prevalence countries are also English speaking, with New Zealand and the
United Kingdom (one in four) and Australia (one in five) next highest.
These within-country trends hide patterns present in some ethnic groups.
For example, 43% of Maori and 65% of Pacific adults are obese [10]. Also,
the rate of change of obesity (slope of the line) is highest in these English
speaking countries (Canada excepted). Further, Japan and South Korea
(not displayed) have the lowest prevalence of obesity, of all countries in
the OECD, with fewer than one in twenty adults falling into this category.
Other continental European countries, along with Ireland, occupy the
middle ground between English speaking and Asian nations. What
conclusions can be drawn from this information? First, we observe that
obesity prevalence is slowly rising in all OECD countries presented here,
so that an increased burden of obesity is a real global phenomenon. Also,
different rates of change in obesity prevalence are observed between
countries with similar cultural and linguistic traditions. What is it about
English speaking countries that caused obesity rates to climb so steeply in
the latter part of the twentieth century? To answer this question, we will
consider what changes in nutrition have occurred in these countries.

NUTRITIONAL CHANGE BEFORE THE 20TH CENTURY

Although record keeping before the 20th century was not as
comprehensive as today, historians of coronary disease have attempted to
document what nutritional changes predated the epidemic of


cardiovascular disease observed in the 1950s. Michaels [11] documents
that sugar consumption only became established in Europe in the 16 th
century, after mass cultivation of sugar cane got under way in the West
Indies. With the advent of tea and coffee drinking in the 18 th century, sugar
became more popular. Intake of sugar increased in Great Britain from
about 2kg/capita/year in 1700, to 9.5 in 1809-13, increasing to 50.6 in
1962. In contrast, Michaels identifies that an historic author King, who in
1696 provided an account of all aspects of English life, estimated that
consumption of meat was about 37kg/year. King estimated that half the
population (about 2,700,000 people) ate flesh regularly and their
consumption was about 3.6kg/capita/year higher than people in the UK in
1962. Thus total animal fat consumption had probably decreased rather
than increased over this critical period. In contrast, average sugar intake
has continued to rise [14].

CHANGES IN NUTRITIONAL SCIENCE
DURING THE 20TH CENTURY

Concern about obesity did not preoccupy nutritionists and the medical
community during the early part of the 20th century. Before obesity ever
appeared as a public health issue, blocked coronary arteries from fatty
deposits, causing an epidemic of heart attacks and premature death were
the primary motivating force behind public health campaigns to change
what the public consumed [13]. Despite the fact that coronary heart
disease, known more commonly as heart attacks and angina, is the most
common cause of premature death in most developed countries, this was
not always the case. It wasn’t until mid way through the twentieth century
that coronary artery disease was commonly encountered in clinical
practice.
The first hint of coronary artery disease was recorded in 1768, when
the famous Physician, William Herbeden described angina pectoris, which
was the sensation of being strangled in the chest [11]. At the time, he did
not make the connection between these symptoms and the heart. Historical
evidence suggests that although the condition was first described at this
time, it was still extremely rare. Hebeden himself records only


encountering 20 cases of angina during his twenty or so years of practice.
Records indicate that cases were extremely rare from the late 18 th century
until 1912, when Herrick described a series of six cases with coronary
thrombosis, a blood clot in the arteries supplying blood to the heart muscle.
This anatomical basis for these symptoms was discovered 32 years earlier
by Weigert. Even in the early 20 th century, death from coronary disease
was a rare event. Michaels reports evidence that deaths from hardening of
the arteries (arteriosclerosis) were 200 times more numerous in 1962 as
1901-10. A common objection to such evidence of a rapid rise in the
number of cases of coronary artery disease, was that life expectancy was
increasing, and that latter populations were much older, and thus more
likely to develop disease. Although the number of people aged 50 years or
older did increase in the UK over this period, the magnitude was much
smaller (threefold; 4,790,000 in 1901 to 14,158,000 in the early 60s) than
that observed for increasing rates of disease [11].
By the early 1960s, however, the epidemic of coronary artery disease
was established in Western industrialized nations, and doctors and
scientists were seeking explanations. Figure 2 shows the rapid rise in
mortality rate from coronary disease and stroke in England and Wales
between 1921 and 1939 when the epidemic was first identified in medical
journals, in 1949.


Figure 2. Comparative mortality index for different causes of death in males in
England and Wales between 1921 and 1939 [12].

The medical, public health and epidemiological communities swung
into action to prevent the rapid rise in cases of coronary disease. Gary
Taubes, a science writer, has documented the history of nutritional
recommendations associated with the diet-heart-hypothesis, developed in
the 1930s, and widely accepted in the early 1980s, lead by Dr Ancell Keys
[13]. He documents that the American Heart Association released a report
in December 1960, arguing that “the best scientific evidence of the time”
strongly suggested that Americans would reduce their risk of heart disease
if they reduced the fat in their diet and replaced saturated or animal fat with
vegetable-derived fat. Initially the advice was aimed only at men at high
risk of heart attacks by virtue of having suffered a previous event, having a
high cholesterol or being smokers of cigarettes. Such recommendations
were revised annually, so that in 1970 the advice applied to all Americans
(including infants, children, adolescents, pregnant and lactating women
and older people). ‘Eat less fat’ was the mantra that we were both taught at
medical school, as the answer to both obesity and coronary heart disease.


Keys believed that the ideal heart healthy diet would increase the
percentage of carbohydrates from less than 50% calories to 70%, and
reduce saturated fat consumption from 40% to 15%. In contrast, Taubes
notes that Japanese physicians were advising patients to increase their total
cholesterol levels, because low cholesterol levels were associated with risk
of haemorrhagic stroke in their home country.
Barry Popkin, a Professor of Economics, has described changes in the
North American diet and contrasted these with changes in Korean and
Japanese diets in the latter half of the twentieth century [14]. His analysis
is based on population estimates of food consumption derived from United
Nations Food and Agriculture Organisation Food Balance Sheets. Per
capita consumption of a range of food products was estimated by
calculating the national total of food-stuff produced, adding imports and
subtracting exports, then dividing the difference by the total population
estimate at that point in time. The remainder is considered to have
disappeared and so assumed eaten, although a small amount is likely to be
wasted. Popkin’s findings showed that, in the United States, the key
changes that occurred between 1977-8 and 1987-8 were a reduction in
whole milk consumption (50 gram/capita/day) with a compensatory
increase in low fat milk (30 gram/capita/day), along with a decline in high
and medium fat red meats (30 gram/capita/day), and an increase in low fat
poultry consumption (10 gram/capita/day). Conversely, soft drink
consumption increased markedly, with an increase in sugar sweetened soft
drinks of 60 gram/capita/day, and diet drinks by 45 gram/capita/day over
this ten year period. In line with the American Heart Association’s
guidelines, this analysis, suggests that fat consumption was reduced, with a
large increase in carbohydrate intake, particularly from sugar sweetened
soft drinks. Like the United States, the National Heart Foundation in New
Zealand, Australia and the United Kingdom have consistently advocated
for reduced consumption of dairy fat, meat fat and reduced fried food
intake.
Asian countries, present in the OECD obesity analysis, have undergone
paradoxical changes to those observed in the United States. Although
overall fat intake is much lower in these two countries than the US, per


capita fat consumption increased 341 percent between 1946 and 1987. In
South Korea a similar trend has occurred, with a rising consumption of
animal products and declining intake of grains during the period between
1965 and 1985. Percent of energy derived from fat rose from 8% to 14%,
and similarly average grain consumption reduced from 550 to 400
grams/capita/day during this twenty year period. Combining such data with
the trends observed in obesity over the last thirty years (Figure 1), we
observe that this increase has not had a substantial impact on the
prevalence of obesity in Japan, or South Korea (data not shown), although
the prevalence of people who are overweight elsewhere has grown
substantially in recent decades.
So, we have seen a clear difference in the body composition of selected
countries, in which records of body size, and per capita intake of energy
have been recorded. A clear distinction can be drawn between countries
who have experienced a rapid increase in the proportion of obesity people
over the last thirty years – USA, Canada, UK, Australia and New Zealand;
and those countries that haven’t – Japan and Korea.

SUMMARY

What conclusions can we draw from these historical events? First,
coronary artery disease is a relatively recent phenomenon, and it was this
epidemic which prompted calls from medical authorities to lower fat
intake, particularly in English speaking countries. Second, sugar
consumption has substantially increased over the last three hundred years,
and calls to reduce fat intake, by public health authorities, may have
increased the consumption of carbohydrate and sugar in countries with a
British colonial heritage. Conversely, in Asian countries, which were rising
out of poverty during the 20th century, fat was more commonly consumed
that ever. With two quite different changes in nutrient profile, the change
in obesity prevalence between Asian countries and English speaking
countries, recorded from the early 1980s, couldn’t be more different. South
Korea and Japan have maintained very low levels of obesity in the last


thirty years, despite a dramatic increase in the proportion of calories
obtained from fat. In the remaining chapters we explore the health effects
of carbohydrates, the macronutrient promoted to prevent coronary artery
disease in English speaking countries during the early 1970s, initiated by
the American Heart Association. We also research the effect that
carbohydrates have on the motivation and reward centres of the brain. Has
the advice, to reduce fat, and saturated fat, been a case of robbing Peter to
pay Paul? For us to consider whether the growth in global obesity has
occurred due to carbohydrate addiction we will have to consider what has
is known about addiction, and carbohydrates. First, we attempt to unpack
the concept of addiction. How do we know something is addictive? What
has been learned about treating people with addictions? Could this
information help us, collectively, beat the obesity epidemic?

Figure 2. Changes in consumption of selected food types, 1969 to 1985 [15].


REFERENCES

[1] Mann, JI, Trusswell, A. S. Diseases of overnourished societies and the
need for dietary change. USA: Oxford University Press; 2003.
[2] Johnson RK, Appel LJ, Brands M, Howard BV, Lefevre M, Lustig
RH, et al. Dietary Sugars Intake and Cardiovascular Health: A
Scientific Statement From the American Heart Association.
Circulation. 2009;120(11):1011-1020.
[3] Yudkin J. Dietary fat and dietary sugar in relation to ischaemic heart-
disease and diabetes. Lancet. 1964 Jul 4;2(7349):4-5.
Countries. OECD publishing; 2009.
[5] Kuczmarski RJ, Flegal KM. Criteria for definition of overweight in
transition: background and recommendations for the United States. Am
J Clin Nutr. 2000;72(5):1074-1081.
[6] Prospective Studies C, Whitlock G, Lewington S, Sherliker P, Clarke
R, Emberson J, et al. Body-mass index and cause-specific mortality in
900 000 adults: collaborative analyses of 57 prospective studies.
Lancet. 2009;373(9669):1083-96.
[7] Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to
smoking: 50 years' observations on male British doctors. BMJ. 2004
Jun 26;328(7455):1519.
[8] Morris JN. Recent history of coronary disease. Lancet. 1951;1:1.
Countries. OECD publishing; 2009.
[10] Ministry of Health. A Portrait of Health: Key Results of the 2006/07
New Zealand Health Survey. Ministry of Health; 2008.
[11] Michaels L. Aetiology of coronary heart disease: an historical
approach. British Heart Journal. 1966;28:258-64.
[12] Ryle JA, Russell WT. The natural history of coronary disease a
clinical and epidemiological study. British Heart Journal.
1949;11(4):370-389.
[13] Taubes G. The Diet Delusion. New York: Vermilion; 2007.


[14] Popkin BM. Nutritional Patterns and Transitions. Population and
Development Review. 1993;19(1):138-157.
[15] Kim SH. Changing nutritional status affected by rapid economic
growth of Korea. In: International Symposium on Food Nutrition and
Social Economic Development. Beijing: Chinese Academy of
Preventive Medicine; 1991. p. 472-478.
[16] Helmchen LA, Henderson RM. Changes in the distribution of body
mass index of white US men, 1890-2000. Annals of Human Biology.
2004;31(2):174-181.

Chapter 2

ADDICTION: CLINICAL FEATURES
AND BIOLOGY

After first reporting global trends in food and nutrient intake, then
recent trends in obesity, you may wonder why we are now venturing into
seemingly unrelated territory. To the contrary, we believe that recent
global food trends may only be understood by considering the rewarding
properties of food, and the similarities between these everyday items and
other products commonly accorded ‘addictive’ status. Of course many of
the substances we frequently refer to as addictive are often illicit, or their
supply is controlled in some way. Cigarettes and alcohol are common
suspects, leading to addiction, but food, surely not - we retain conscious
control of what we eat for breakfast, lunch, dinner and in between, don't
we? Does eating share characteristics of addictions more commonly seen
with drugs? Before we can answer this question, we must consider what
features make a drug (or food) addictive? How is addiction recognised?
Which techniques can help people beat addictions? We discuss the general
features of addiction, so that we can make sense of eating behavior and
obesity – do they fit the same mould?
Many medical professionals would strongly refute the hypothesis that
some foods (such as sugar) have ‘addictive’ properties. What we propose
here goes against the grain. This is, however, often how the medical field

develops. Take nicotine for example. Today, people generally agree that
nicotine, present in a cigarette, is responsible for hooking people on
tobacco. However this was not always the accepted mantra. Not until the
1970s was nicotine first recognised as a drug of dependence. Before this,
most scientific bodies viewed smoking as a habit, not an addiction. The
rationale of this thinking, at this time, was that a well-defined withdrawal
syndrome after stopping smoking was not well described and methods
available were equally effective, or ineffective for helping people stop for
good. Sound familiar? In 1971, Russell, a pioneer in the study of tobacco,
published an argument that nicotine was a dependence-producing
(addictive) substance [1]. This was the beginning of a change in attitudes
towards smoking. Soon after, the Royal College of Physicians decreed that
tobacco smoking was due to nicotine addiction and in 1980 the American
Psychiatric Association (APA) recognised that smoking met most of the
criteria for drug dependence, so that this condition was then included in
their diagnostic “bible”, the DSM-III. It was not until the late 1980s that
the US Surgeon General issued a report entitled ‘Nicotine Addiction’,
which concluded that tobacco was addictive, nicotine was responsible, and
that the effects of nicotine on the brain share features of other major drugs
of addiction such as heroin and cocaine [2].

WHAT IS ADDICTION?

To lay people, the word 'addiction' conjures an image of a sad
alcoholic or cocaine addict, lost in their own world, often dishevelled,
caring for nothing else but another fix from their drug of choice. Other less
intense preferences for substances are more commonly referred to as
habits, implying that they are easier to give up. The chances are, whether,
working as a health care professional or not, most of us can picture a
person who roughly fits the addiction stereotype. Although, at first glance,
this may sound simplistic, it reveals two key components of addiction, the

Addiction: Clinical Features and Biology 19

substance and the individual’s relationship with it. In the familiar case of
substance abuse to cocaine, or alcohol, the primary place in the person's
life that the substance takes, distinguishes the addict from those around
them. While others may place no value on acquiring or consuming the
substance, to the addict, their object of desire dominates their priorities and
they have difficulty controlling their use of it. Time is spent ensuring that
the addict has sufficient supplies, usually to avoid the unpleasant feelings
of withdrawal that might accompany prolonged abstinence. Time spent
obtaining the substance often takes precedence over other priorities, which
might be thought, on considered reflection, to be more important: such as
family, work and the wider community. Medics are generally well versed
in these consequences, with a mnemonic summarising the most commonly
harmed areas of a person's life: health (liver), family (lover), work
(livelihood), and society (law).
Such extremes allow us to falsely assume that addiction, and the
processes that underlie it, only occur in a small subset of the population.
Addiction can, however, be more subtle and resist these stereotypes. For
example, perhaps the most common daily addiction is caffeine. Although,
coffee and tea drinkers’ lives are usually not ruled by their caffeine intake,
some characteristics of more severe addiction syndromes are shared. For
example, the presence of a withdrawal syndrome is closely tied to
addiction and substance abuse. Caffeine withdrawal is a subtle discomfort
that starts soon after abstinence. Although the symptoms would be unlikely
to ever prompt a visit to the doctor, they are nonetheless real. Cravings and
urges for a source of caffeine, headaches, reduced concentration, irritability
and restlessness are an attempt to more accurately label the feeling of “not
quite feeling right”. Regular tea and coffee drinkers rarely, if ever, have to
remind themselves of their need for a cup. Often the smell or sight of the
substance will initiate the caffeine addict to reach for the tea bag or
plunger.
Although we may not realize it, our brains are hard-wired for reward.
We need to eat, drink and reproduce to survive so that behaviours
associated with such necessities are rewarded. The ‘machinery’ that is
responsibly for subconscious reward lies in a part of our brain that governs


automatic survival functions. It’s known as the mesolimbic dopaminergic
pathway and consists of a number of structures in the midbrain and
prefrontal cortex. Activation of this brain pathway leads to reward,
subconscious learning and the feeling of pleasure. Food, for example,
stimulates this pathway which ultimately leads to release of the chemical
messenger, dopamine, and a sense of pleasure. However the ‘amount’ of
pleasure depends on how enjoyable the food is and how hungry you are at
the time of eating [3]. It just so happens that drugs such as nicotine and
cocaine hijack this reward system and, depending on our genetic makeup,
the environment in which we live, and our backgrounds, some people are
more susceptible than others.
The mechanics of what motivates an addict are often glossed over
unless one pays careful attention to the subtle symptoms that precede
substance use, and observe what effect use has on such symptoms. Let’s go
back to our example of nicotine. Unlike cocaine and heroin, a puff on a
cigarette does not give you much of a ‘positive hit’. For those who have
ever tried smoking, you will, no doubt, remember your first few puffs. I
doubt that it left you feeling high and wanting more. In fact you probably
felt a bit sick. With persistence, however, smokers develop tolerance to
these unpleasant effects. One might think then that because nicotine is only
a mild stimulant, it might be easier to give up than other drugs of
dependence, such as alcohol, cocaine or heroin. This, however, is not the
case. Early studies that investigated the ‘addictiveness’ of nicotine asked
people who used tobacco, cocaine, heroin and alcohol to rate how much
they liked each drug (on a 5-point scale: 1=dislike; 5=like a lot) and how
much they needed to use each drug (on a 4-point scale: 1=no need; 5=need
a lot). Tobacco rated second for ‘liking’, after heroin, and in terms of
‘needing’, tobacco came out on top, followed by heroin, cocaine and
alcohol [4]. These results showed that most smokers do not smoke tobacco
for the positive effects but instead to keep themselves from withdrawal.
The onset of subtle withdrawal symptoms that follow abstinence become
increasingly unpleasant until relief is sought. Drinking a cup of coffee,
injecting or snorting cocaine, or smoking a cigarette deliver variable
amounts of euphoria, but they all consistently relieve negative withdrawal


symptoms in their respective addicts. This sense of relief becomes a subtle
but powerful motivator – more so than the ‘hit’. Familiar learning
mechanisms consist of the reward that accompanies good behavior, or
positive re-inforcement. For example, children receive praise from their
parents for good behavior to increase the chance that the child continues to
behave in the future. More subtle is the converse when feelings of
discomfort or pain are relieved. For example, the relief one gets from
removing tight shoes, or a heavy load. Such relief is often experienced as
pleasure, and can be indistinguishable from positive reward when
unpleasant effects are regular and sustained. This mechanism, called
“negative reinforcement” is a powerful motivator. We have glossed over
some of the important features of addiction, but how has addiction been
traditionally defined within medical and psychiatric circles?

DEFINITIONS

Various authors or professional bodies have attempted to define
addiction, although wide variation exists and agreement about the precise
meaning of the term lacks consensus. Perhaps the best known definition of
addiction, often used in clinical practice, is the Diagnostic and Statistical
Manual (IV), published by the American Psychiatric Association [5]. To
fulfill the criteria, the patient must recount at least three or more of the
following over a twelve month period:

1. Taking larger amounts and over a longer period of time than was
intended
2. Unsuccessful efforts to cut down or control substance use
3. Overinvestment of time spent in activities to both obtain and use
the substance, or recover from its effects
4. Giving up important social activities to use the substance
5. Continued use despite negative consequences, such as health risks
6. Tolerance - having to use more of the substance to achieve the
desired effect


7. A withdrawal syndrome that occurs after periods of abstinence; or
the substance is used to avoid such symptoms.

This definition embodies the three most important elements of
addiction - the failure of resolve to reduce consumption in the face of
negative consequences, along with the physical dependence elements of
symptoms of withdrawal and tolerance.
The International Classification of Disease was developed by the
World Health Organisation in the late 1800s to systematically classify
disease [6]. The most current version (ICD-10) defines substance
dependence similarly to the DSM. The ICD-10 requires a minimum of
three criteria to be met for a person to be considered dependent. These
include: (1) a strong desire or compulsion to take the substance; (2)
difficulties controlling substance-taking behaviour; (3) a withdrawal
syndrome that becomes evident when substance use is stopped; (4)
tolerance; (5) neglect of other pleasures or interests in life; (6) continued
substance use despite knowledge of harm; and (7) the person should either
use, or have a desire to use the substance.
The DSM IV criteria for substance abuse only apply to illicit
substances such as opiates (cocaine or heroine), or amphetamines, and
have some limitations. Let’s compare heroin and nicotine use. Heroin
fulfills all criteria with ease. Nicotine use fits with the withdrawal criteria,
difficulty controlling use or compulsive use, and use despite the occurrence
of related harm. The remaining four criteria, however: tolerance, using
more than intended, spending a great deal of time using the drug and
giving up activities to use the drug, don’t as easily apply. These differences
are not solely due to the nature of the addiction to these substances, but
also relate to the social context. If use of these substances results in
breaking the law, and isolated social circles; then the deterioration in social
function as a result of these disorders can vary widely. For example, before
opiates were criminalised, several famous authors, such as Thomas de
Quincey and Samuel Taylor Coleridge used heroin daily, yet still published
influential works of prose during this time, and participated in society
without scorn or isolation. Caffeine use also does not, as far as we know,


cause harm to health, however, a withdrawal syndrome and tolerance to the
substance is commonly reported. Caffeine addicts (us included) can carry
out normal social and work functions, even with frequent need for drug
use. If caffeine were suddenly criminalized we would be in trouble!
Caffeine illustrates one important feature of addiction – that addictive
substances are not necessarily harmful to health. The same is true for
nicotine. If smokers didn’t inhale the tar present in cigarettes, they
wouldn’t suffer any adverse effects, as far as we know. Nicotine, taken in
isolation, such as through patches or gum, has little or no adverse effects
on health.
Although addiction is most commonly described in association with
substance use, other addictions have been described for behaviors that do
not involve substances at all. Examples include gambling, sex, and internet
use.
Delving deeper into the machinery of addiction, an important element,
not captured in official definitions, is the value the addict places on
immediate over delayed rewards. Ainsley [7] noted that a pervasive
element of the learning in animal and human subjects is the high value
placed on small, but immediate rewards over delayed, larger ones.
Although such preferences are observed in normal people, people with
addictions have an even stronger preference for rapid gratification. Such a
preference is reflected in the rate of absorption of drugs of abuse. Drugs or
substances with the greatest addictive potential tend to be quickly
absorbed, so that time to relief of withdrawal symptoms is short. These
characteristics may be manipulated to help people with addiction recover.
Perhaps some of the best known drugs which assist recovery are nicotine
replacement therapy, in the form of gum, transdermal patch, or lozenge.
Cigarette smoke is inhaled, and absorbed across the small air sacks
(alveoli) in the lung. The high rate of blood flow through the lungs,
coupled with the vast surface area of the alveoli, result in rapid absorption
of the nicotine and rapid relief of tobacco withdrawal. What seems, on
paper, to be a favourable effect of the drug, also gives the product its
addictive sting. Cigarette companies manipulate the pH of tobacco smoke,
by adding ammonia to increase its rate of absorption and thus the addictive


potential of their products. In contrast, nicotine gum, for example, releases
nicotine slowly after chewing, across the lining of the mouth. The lower
blood flow and lower surface area of this body region, slow the absorption
of nicotine. As a result, nicotine gum more slowly relieves tobacco
withdrawal discomfort, but is much less likely than cigarettes to be used
long term. In a similar manner, methadone is often used as a bridge to
recovery for users of intravenous opiates, such as heroin. We will consider
in later chapters how this important concept may be applied to food. If
obese people are addicted to some foods, giving the food version of the
nicotine patch, may provide a path to recovery.

CLINICAL FEATURES OF WITHDRAWAL SYNDROMES

Although we have briefly discussed the salient features of addiction,
we will discuss further the nature and time course of common withdrawal
symptoms in more detail. A wide variety of symptoms are described after
abstinence from different substances, and some are better known than
others (Table 1). The presence of withdrawal symptoms is often considered
a pathognomonic, or unique, sign that a substance should be considered
addictive [8].
Of commonly encountered withdrawal syndromes, perhaps that
associated with alcohol withdrawal is best known. Classic symptoms have
been described since antiquity, and are best known as delirium tremens.
The symptoms are often so severe, that patients abstaining from alcohol
after a heavy drinking career are frequently treated in a specialised unit to
recover. In the first three days after stopping alcohol, patients often
develop psychiatric symptoms in which they percieve their skin to be
crawling with ants or other insects. They also have dramatic fluctuations of
physiological measures such as heart rate, blood pressure or temperature.
These symptoms are often treated with drugs such as benzodiazepines, if
available. After about ten days, such dramatic symptoms subside, but urges
and cravings to drink continue. The most severe symptoms last for about
three months, then slowly resolve. Despite the resolution of these


withdrawal symptoms, recovered alcoholics are often aware that no more
than a single drink of alcohol can undo months of recovery, and send them
back down a destructive path.

Table 1. Signs and symptoms of nicotine and other substance
withdrawal

Alcohol Opioids Sedatives Cocaine Nicotine Stimulants
Sweating Yes Yes
Nausea Yes Yes Yes
Change in heart Increase Increase Decrease
rate
Sleep Yes Yes Yes Yes Yes Yes
Disturbance
Anxiety Yes Yes
Dysphoric Yes Yes
mood
Fever Yes
Increased Yes Yes
appetite
Irritability Yes Yes
Difficulty Yes
concentrating
Time course
Onset 6-12 4-6 1 week 2-12
hours hours hours
Peak 3-7 2-3 days 2-3 days
days
Duration 1-2 2 weeks Up to 3-4
weeks 10 weeks
weeks
Adapted from: American Psychiatric Association 2000; Hughes et al. 1994.


Tobacco withdrawal symptoms are more subtle than those observed for
alcohol, but retain considerable hold over recovering smokers. Symptoms
include:

1. Craving and urge to smoke
2. Increased appetite
3. Reduced concentration
4. Restlessness
5. Depressed mood
6. Constipation
7. Mouth ulcers (less common) [9].

The severity of tobacco withdrawal is generally less than that
associated with opioid or alcohol withdrawal and may have a lesser effect
on the ability of an addict to undertake normal daily activities. Just because
the tobacco withdrawal syndrome may be less severe it does not mean that
it is easier to quit than other substances. For example Kozlowski [10]
surveyed 1000 people seeking treatment for drug or alcohol dependence
and asked them how difficult quitting smoking cigarettes would be
compared to stopping other substances. Over half said that cigarettes
would be harder to quit, even though they rated cigarettes as less
pleasurable to use.
Although the nature and severity of these symptoms varies
substantially between patients and different substances, the time course
over which the withdrawal symptoms occur is relatively constant. If the
smoker is able to hold their resolve and abstain continuously, the severity
of symptoms generally peaks in the first three days, then wanes over one to
three months. A similar time course is observed with opiate, alcohol, and
metamphetamine addiction. Abstinence is tenuous in people with
addictions, partly from the knowledge, often subconscious and deeply
ingrained, that relief from these unpleasant symptoms is only one smoke,
snort or drink away. The sight of other users acts as a cue, amplifying
urges, cravings and desires to consume the addict’s substance of choice.
While these withdrawal symptoms may respond to the effects of slow


release forms of the addictive substance, this treatment often only partially
relieves such unpleasant symptoms, often not giving the same 'hit' as the
addictive substance.

BIOLOGICAL BASIS OF ADDICTION SYMPTOMS

Although we don’t delve too deeply into the technical detail, we will
briefly touch on how neuroscience has added a further dimension to our
understanding of addiction, outside the clinical picture, previously
described. The identification of the part of the brain activated by drugs of
abuse has contributed to our understanding of what makes some substances
addictive over others. The origin of addiction has been linked to a part of
the human brain responsible for subconscious control of behaviour and
motivation, associated with survival functions, such as eating, drinking and
sexual reproduction. One can readily appreciate that drug addiction may be
viewed as a ‘hunger’ for drugs, such that some substances become as
important, or even more important than eating food and consuming water
and other drinks. This anatomic site, the dopaminergic mesocorticolimbic
projection or reward centre, present in the midbrain, is most often
implicated in the biology of addiction. In human and animal studies,
administration of substances of abuse increases concentrations of the
chemical messenger or neurotransmitter, dopamine, in this centre,
considered the main component of the brain reward system [11]. For
example, an intravenous dose of cocaine results in increased release of
dopamine by blocking re-uptake by nerve terminals in a part of the brain
called the nucleus accumbens. Other substances, such as opioids, nicotine
and alcohol act in a different area of the reward pathway, stimulating nerve
cells in other regions, which ultimately influence the nucleus accumbens,
increasing dopamine concentrations in this area. This common anatomic
site, along with the linked chemical, dopamine, has therefore, progressed
our understanding of the biology of drug addiction, and their common
features [12].


What are the clinical features of drug-induced dopamine release in
human subjects? Two principal effects are commonly described [12].
Firstly, release is accompanied by pleasure, or the feeling of a ‘hit’ and
behaviours that produce this are reinforced. A vicious cycle results in deep
seated learning to take the substance. The increase in dopamine
concentration focuses the individual on sensory elements (‘cues’, such as
the smell of tobacco among smokers) associated with drug taking. The
sensation of such elements often initiates automatic, subconscious,
Pavlovian stimulus-response drug taking when an individual is
subsequently exposed to these cues. This is commonly observed in people
that smoke, so that the sight of cigarettes, other people smoking, ash trays,
or lighters, can ‘switch-on’ the automatic lighting of a cigarette, in people
addicted to tobacco [13, 14].
Although dopamine has been closely linked to addiction, the
neurotransmitter also plays a role in people with psychosis – seeing or
hearing things that are not there. Indeed, dopamine has been referred to as
the “wind of the psychotic fire”, when describing its pivotal role in the
symptoms and treatment of psychotic disorders such as schizophrenia [15].
Evidence for dopamine's importance emerges from clinical practice - for
example, treatment of patients with Parkinson’s disease using therapeutic
doses of levo-dopa, a dopamine like substance, can result in a drug-
induced psychosis in a small proportion of these patients. Conversely,
drugs used to treat psychoses such as schizophrenia interfere with
dopamine pathways, and may result in unwanted Parkinsonism, manifested
by expressionless, blank faces and a characteristic pill-rolling tremor.
If addiction and psychosis share the same biological pathway and
neurotransmitter (dopamine), then we might expect that such mental
disorders and addiction commonly coexist in individuals. For workers in
the mental health field, such disorders are all too frequently associated,
with the term “dual-diagnosis” used to summarise the occurrence of the
two disorders in the same patient. In one summary, the prevalence of
smoking was between 80 and 90% in people treated in hospital with
schizophrenia [16]. Numerous epidemiological studies describe the co-
occurrence of schizophrenia and other forms of addiction, such as to


alcohol, metamphetamine and opiates [16]. Further, the presence of illicit
drug use in people with schizophrenia predicts relapse, treatment resistance
and need for further hospital treatment.
Logically, we might expect that if obesity and weight gain are also
related to this pleasure chemical, dopamine, then when the effects of
dopamine are blocked in some way, for example by drugs that exert such
effects in the brain, then people that take these drugs may put on weight.
Such observations do, in fact, commonly occur in clinical practice. Drugs
used to treat psychosis, all, to a greater or lesser extent, block the action of
dopamine, and all are known to cause weight gain, with some drugs having
more potent side effects than others [17]. Even in people with psychosis,
many are overweight before they start treatment, compared to the
frequency in the general population, increasing speculation that overeating
may play a role in the development of psychotic disorders [18]. We will
explore the implications of food addiction later in the book. For the
meantime, we simply draw attention to such theories, showing how both
the biology and clinical manifestations of these disorders show similar
features.

SUMMARY

In this chapter we have reviewed the nature and context of addiction,
noting that it shares some features similar to hunger. In fact, one could
observe that drug dependence could be described as a ‘hunger’ for drugs.
Other common features of drug addiction include difficulty stopping the
behaviour, due to the presence of a withdrawal syndrome that manifests
when an individual stops. The addict who attempts abstinence knows,
either consciously or subconsciously, that taking the substance they have
become fond of can relieve these symptoms rapidly. If they do continue to
abstain, most of the unpleasant discomfort begins to tail off after about
three months. The biology of addiction is also beginning to be understood,
such that the chemical dopamine, present in the part of the brain
responsible for motivation, is stimulated by addictive drugs, and this
chemical plays an important part in severe mental disorders, characterised


by psychosis. With this information in mind, we move on to consider
whether eating behaviour and various foods show similar characteristics to
drugs of addiction? Could this information help us find the key to unlock
the modern obesity epidemic?

REFERENCES

[1] Russell MA. Cigarette dependence. I. Nature and classification.
BMJ. 1971 5;2(5757):330-331.
[2] Center for Health Promotion and Education. Office on Smoking and
Health, United States. Public Health Service. Office of the Surgeon
General. The Health Consequences of Smoking: Nicotine Addiction: A
Report of the Surgeon General [Internet]. 1988 [cited 2011 Mar
24];Available from: http://profiles.nlm.nih.gov/NN/B/B/Z/D/
[3] Balfour DJK. The neurobiology of tobacco dependence: A
preclinical perspective on the role of the dopamine projections to the
nucleus. Nicotine and Tobacco Research. 2004;6(6): 899-912.
[4] Blumberg H., Cohen D, et al. British Opiate Users: I. People
Approaching London Drug Treatment Centres. Substance Use and
Misuse. 1974;9(1): 1-23.
[5] APA. Diagnostic and Statistical Manual of Mental Disorders.
Washington DC: American Psychiatric Association; 1995.
[6] WHO| International Classification of Diseases (ICD) [Internet]. [cited
2011 Mar 24];Available from: http://www.who.int/
classifications/icd/en/
[7] Ainslie G. Breakdown of Will. 1st ed. Cambridge University Press;
2001.
[8] Heather N. A conceptual framework for explaining drug addiction.
Journal of Psychopharmacology. 1998;12(1):3-7.
[9] West R, Schiffman S. Smoking Cessation. Fast Facts: Indespensible
Guides to Clinical Practice. Oxford: Oxford Health Press Limited;
2004.
[10] Kozlowski LT, Wilkinson DA, Skinner W, Kent C, Franklin T, Pope
M. Comparing Tobacco Cigarette Dependence With Other Drug


Dependencies. JAMA: The Journal of the American Medical
Association. 1989 Feb 10;261(6):898 -901.
[11] Tzschentke TM. The medial prefrontal cortex as a part of the brain
reward system. Amino Acids. 2000;19(1):211-9.
[12] Drevets WC, Gautier C, Price JC, Kupfer DJ, Kinahan PE, Grace
AA, et al. Amphetamine-induced dopamine release in human ventral
striatum correlates with euphoria. Biological Psychiatry. 2001;49:81-
96.
[13] West R. Theory of addiction. Oxford: Blackwell Publishing; 2006. p.
10.
[14] Munafo M, Albery I. Cognition and Addiction. Oxford: Oxford
University Press; 2006.
[15] Laruelle M, Abi-Dargham A. Dopamine as the wind of the psychotic
fire: new evidence from brain imaging studies. J Psychopharmacol.
1999;13(4):358-371.
[16] Batel P. Addiction and schizophrenia. European Psychiatry.
2000;15(2):115-122.
[17] Baptista T. Body weight gain induced by antipsychotic drugs:
mechanisms and management. Acta Psychiatrica Scandinavica.
1999;100(1):3-16.
[18] Peet M. Diet, diabetes and schizophrenia: review and hypothesis.
The British Journal of Psychiatry. 2004;184(47):s102-105.

Chapter 3

CARBOHYDRATES, SUGARS AND HUMAN
HEALTH: A SUMMARY OF THE EVIDENCE

INTRODUCTION

In the first chapter, we explored recent trends in food intake during the
th
20 century, preceding the modern day obesity epidemic, starting from the
1970s to present. Two different national or cultural dietary changes
preceded the English speaking, collective popping of buttons in the early
1980s to the present day. Anglophones, driven by a desire to reduce the
burden of cardiovascular disease, initially in the United States, strove to
reduce the fat intake of the populace. Although the macronutrient target
changed from all fat, to animal derived, saturated fat; the message was
often confused, with “99% fat free” a common health claim, adorning
labels everywhere on manufactured food products. Once, when shopping
with my son, I (ST) was shocked to see that marshmallows were
proclaiming their nutritious properties, with large type “99% fat free”
smeared over their plastic wrapper!
Contrary to this anti-fat trend, Asian countries have followed an
opposite trajectory, increasing the proportion of fat in their diets, as their
economies have strengthened and more expensive animal fat has been

more widely affordable. Similarly, obesity statistics in these countries
couldn’t be more different: in the OECD, English speaking countries have
lead the stakes, with obesity barely raising a murmur in either Japan or
South Korea. In this chapter, we consider, more carefully at an individual
and clinical level, what effect modifying carbohydrate intake has on health,
and contrast these effects with other diets. From chapter 2, we have
reviewed the subject of addiction, concluding that the concept of
withdrawal shares some similarities with hunger, usually applied to food.
From our medical training we were once firm believers in the supposed
adverse health effects of eating calorie rich fat, but what about
carbohydrates that have filled the void created by fat in the last thirty
years? Are carbohydrates potentially harmful or healthy when consumed in
large amounts? Do they contribute to weight gain, and are there any
potential properties of carbohydrates that can help us understand the
modern epidemic of obesity?
In our medical training, we received little information about the effects
of carbohydrates on health. With the benefit of hindsight, we now attribute
this to the dominant theory of the time, which emphasised energy density
as the most important aspect of food by which one could adjudicate food as
good, bad or otherwise. Because fat has twice the energy density of other
macronutrients, protein or carbohydrate, the finger of nutritional blame
was always pointed at greasy targets. Basic biochemical pathways were,
however, taught. I soon realized that the brain, perhaps the most critical
organ, on which human survival depends, runs almost entirely on an
uninterrupted supply of the single sugar, glucose. The body possesses a
neat mechanism by which alternative fuels can be mobilised in the event of
a prolonged carbohydrate drought; however, this was presented as a quirk
of nature rather than being of much relevance to health or weight loss.
Carbohydrates were also relevant to the metabolism of individuals who
suffered from another disorder, diabetes. People with this condition have
poor regulation of glucose, through either immune destruction or
exhaustion from overwork of the visceral organ, the pancreas, which

Carbohydrates, Sugars and Human Health 35

secretes insulin, the primary regulator of glucose levels in the body.
Interestingly, the alternative brain fuel, ketones, produced in the starving
state, are also switched on in one form of diabetes (type I), characterised
by a complete lack of insulin.
First, what are carbohydrates? Most people are familiar with the
concept now with the popular diets that we will explore. Some
misconceptions and confusing terminology abound, however. The most
common types of carbohydrate are starches, which form the backbone of
most diets around the globe. Starch consists of long chains of glucose
molecules, linked to form long chains. Starchy products include anything
made up of white flour, such as bread, baked goods, pasta, semolina; root
vegetables such as potatoes and taro, and other staples such as rice and
maize. Glucose exists as a simple sugar, with a sweeter taste and is often
added to sports drinks to provide instant energy. Glucose is familiar
territory for most doctors. After glucose enters the body, the gut organ, the
pancreas, secretes insulin into the blood, so that the body can take up the
glucose into the liver and muscle. The body possesses complex machinery
for keeping the levels of glucose reasonably stable in the body, so that the
precious grey matter within the brain is constantly supplied with enough
fuel to keep us going. If the level of glucose drops below a certain
threshold, people with low blood glucose levels experience ravenous
hunger, become sweaty and faint, and eventually drop unconscious. People
with diabetes are not able to regulate the levels of this sugar in the blood,
usually due to either a lack of insulin, or insensitivity to this hormone and
high levels of glucose can be measured in the veins of people diagnosed
with the disorder, before they are treated. Treatment of diabetes, at present,
is based on reducing the levels of glucose in the blood by increasing the
levels of insulin either by taking drugs that stimulate insulin release or by
injecting the substance directly under the skin. Manipulation of the diet of
people with diabetes is another way of improving blood sugar, although
this has been more controversial. Monitoring blood glucose levels, hence,
becomes the obsession of people with diabetes, and the doctors charged
with their care.


With the treatment of diabetes centered squarely on glucose, another
monosaccharide found in table sugar has received much less attention in
the research world until relatively recently. I (ST) confirmed this fact,
when I began to read about the health effects of fructose, I wondered why I
hadn’t heard anything about this sugar during my training. I scouted in the
university library for a text book of clinical nutrition, flicked to the index
and looked under ‘f’ for fructose. Nothing. I couldn’t believe it, so I picked
up another, then another. The same result. Until the last five years or so,
fructose has been off the nutrition radar for all but a small handful of
researchers. Sugar is slightly different to glucose. It consists of two sugars
joined together to form a disaccharide: one is the familiar building block of
starch, glucose, while the second is the enigmatic monosaccharide,
fructose. As the name suggests, fructose is found mainly in fruit. Fructose
is most concentrated in table sugar, and to a lesser extent, in honey. In
sugar, fructose makes up about 50% of the weight of the crystalline
substance, joined to glucose as the disaccharide, sucrose. High fructose
corn syrup, as the name suggests, is a synthetic derivative of the starch
derived from corn. When corn starch is boiled down to break the chemical
bonds, free glucose is left. To make something like sugar, an enzyme is
added, which converts some of the free glucose to fructose. High fructose
corn syrup is the sweetener most commonly added to manufactured foods
in the United States and Canada. Due to governmental subsidies for corn
growers, high fructose corn syrup has become the most economically
favorable sweetener for the North American food industry. The only
difference between this product and sugar is that the glucose and fructose
exist in free, single sugar, monosaccharide form in high fructose corn
syrup, whereas table sugar consists of the two single sugars joined by a
chemical bond as the double sugar sucrose (figure 1). With glucose being
easy to measure in patient’s blood, and defining the diagnosis of diabetes,
it is easy to understand why fructose has been largely ignored as a focus of
nutrition research. What is more, fructose is found in fruit, what could
possibly wrong with eating fruit? We return to fructose later in the chapter,
as a relatively late development in the carbohydrate story. We first


consider whether diets based on modifying carbohydrates, either in total, or
based on glucose have shown any benefits to human health.

Figure 1. The constituents of table sugar, glucose and fructose, free as present in high
fructose corn syrup, and joined at the hip, as sucrose, found in table sugar.

PHYSIOLOGY OF GLUCOSE AND INSULIN

The first clue that I had that carbohydrates may be important in the
regulation of weight was observed in people with type 1 diabetes, more
common in children, who produce little or no insulin. The lack of this
pancreatic hormone occurs because their own antibodies have, for an
unknown reason, destroyed their cells that produce the protein. Diabetes
specialists know that young women with this disorder, who are often


obsessed with their weight, will reduce their insulin dose, from prescribed
levels, to shed a few pounds. Although these patients may be admonished
by their doctors about the long term adverse consequences of such
behaviour, living with precariously high levels of glucose coarsing through
their veins - causing rotten eyes, limbs and heart muscle - the immediate
desire to control weight may be too strong. The first lecture that I received
on the subject of this type of diabetes at medical school acknowledged this
seeming paradox, that diabetes was “starvation in the face of plenty”.
Before effective treatment to reduce blood glucose was available, sufferers
of diabetes could seemingly eat to excess and lose weight simultaneously,
all because of the lack of a crucial hormone that was critical for processing
glucose into stored energy or body fat.
Despite the apparent centrality of insulin to weight regulation in
patients, beliefs handed down from academics for the apparent excess
weight and skyrocketing rates of diabetes was generally attributed to
energy density. People with diabetes acquired the disease from fat and not
sugar. From the observation that fat contains twice the energy per unit
weight (energy density) than either of the two other macronutrients, protein
or carbohydrate, this rather simplistic, but seemingly elegant principle,
enshrined the basis of public health and nutritional strategies to treat the
growing tide of people with diabetes that were beginning to swamp health
services.

HEALTH EFFECTS OF CARBOHYDRATE MODIFIED DIETS

Which diets are commonly used that are based principally on
modifying carbohydrates?
The Atkins’ diet [1] consists of almost abandoning carbohydrate
altogether, no more than 20g per day or less than one slice of bread is
allowed in the early phases. On the other hand, Atkins lets dieters eat as
much fat and protein as their heart desires, a polar opposite to usual
nutritional approaches of limiting fat and total energy.


Although the Atkins diet has been lampooned in nutrition circles for
almost half a century as antithetical to interventions grounded on energy
density, another carbohydrate based-diet, which measures the intensity of
the blood glucose response from a standardised portion of food has become
more accepted into the mainstream of nutritional thought. First developed
in the 1980s, glycemic index (GI) is a measure of what effect a food,
altered in size to include 50g of carbohydrate, has on the area under the
curve of a blood glucose (an indicator of the average glucose level) vs time
graph [3]. Pure glucose is the reference standard, designated 100, by which
all other foods are compared. Starchy foods are highest, for example, white
bread is about 70, with whole grains, such as lentils, and fruit and
vegetables generally lower - in the 30s and 40s.
The so called “low glycemic index” diet consists of eliminating
consumption of foods whose glycemic index is greater than an arbitrary
figure of about 55. The diet was initially considered most useful in
lowering blood glucose in people with diabetes, which is thought to reduce
the onset of complications from the disease [4]. In such people, blood
glucose becomes elevated, and higher average levels correlate with
increased adverse effects. Indeed, much of the treatment of diabetes is
focused on reducing blood glucose through the use of both medicines and
insulin, and limiting the intake of starchy foods. As long chains of glucose,
starch is broken down and, following absorption, results in a spike of
glucose in the bloodstream. If glucose levels could be controlled through
diet, lowering dependence on drugs, then surely this strategy might
improve the health of people with diabetes. Given that this condition is a
relatively arbitrary cut-off at one end of an extreme end of the spectrum of
glucose control, maybe everyone would be better off eating low GI food?
Also, insulin is an important hormone which promotes the laying down of
fat, encouraging the liver to convert a digested glucose meal to cholesterol
which is then transported in the blood stream to the periphery and stored as
excess flab. Insulin release follows a glucose meal, so that choosing foods
that do not produce such a large bolus of glucose would theoretically
improve average glucose levels, help people lose weight and reduce the
chance of them developing life threatening complications of diabetes such


as heart attacks or strokes. Because less insulin is produced, then
theoretically, such a diet would also help people lose weight.
So much for the theory, what has been born out in reality? Although
very skeptical about the adverse effects of carbohydrates, the medical
literature continues to fill with evidence that diets based on eating low
glycemic index foods result in greater weight loss and better health
outcomes than traditional diet methods (reducing energy density or fat).
Such is the volume of studies on glycemic index that some researchers
have pooled many studies to look at the overall effect of the diet on weight
loss and risk of developing chronic disease, using a technique called meta-
analysis. Such studies are often accorded the highest level of evidence,
among the hierarchy of scientific evidence. Two influential so called
“meta-analyses” have been published, one demonstrating that people
following glycemic index diets reduce their weight [5] with another
showing reduced risk of a range of important and common chronic
diseases from such a diet [6]. One study, which used a similar technique to
compare a range of dietary techniques at reducing risk of heart attack
showed that glycemic index was in the top four methods to lower one’s
chances of such an outcome [7]. According to the study, the best means of
reducing risk of a heart attack was the Mediterranean diet, which again,
emphasises the intake of unrefined, low-glycemic-index, carbohydrate
food.
In patients with diabetes, an American endocinologist, Eric Westman,
compared a low glycemic index diet with the Atkins diet to assess their
effects on glycemic control, weight loss, blood pressure and other indices
of cardiovascular risk [8]. The results were astonishing. Although many
subjects dropped out of the study (41%), the Atkins diet group had most
weight loss at 6 months (-11 vs -7kg) and almost all no longer needed drug
treatment for diabetes (95% compared to 62%). Such results strongly
indicate that both diets help reverse the metabolic effects of type 2
diabetes, but reducing all carbohydrate seems to confer additional benefit,
over only limiting high glycemic index, or starchy foods. Later we
speculate that glycemic index overlooks the effects of an important sugar –


fructose. Perhaps the main difference between the two groups, in this trial,
was fructose intake?
With such glowing evidence, has use of the glycemic index or Atkins
(low carbohydrate diet) become common place in medical practice to help
people control their weight? The answer is that it has and it hasn't.
Nutrition ideas are slow to change, and as we have discussed in chapter 1,
the public health and medical community, lead by the American Heart
Association, has campaigned against the intake of fat and saturated fat to
lower heart disease risk. One of the side effects of this advice, although
often not acknowledged, was to increase the amount of carbohydrate
consumed. Also, public health professionals are fond of simple messages
to convey to the public. The message to reduce fat is easy. Most people
recognise fat on meat and know the greasy feel of fried food. Such a
message is easily communicated and understood. Glycemic index, in
contrast, is complicated, and takes more effort to convey to the public.
Also, when the low fat message is combined with the low glycemic index
one, they may appear contradictory and confusing. If you are admonished
to reduce fat, your only recourse is to eat either protein or carbohydrate.
Protein supply is often limited due to expense (animals are costly to
cultivate), so carbohydrate naturally floods the void created by the low fat
diet. What is not often stated is the contradictions between the low fat and
low (or modified) carbohydrate approaches. Fat, taken with carbohydrate,
actually delays the emptying of the stomach and so, in a purely mechanical
fashion, lowers the GI of a carbohydrate meal. Protein and acid have a
similar effect, slowing down the rate at which the stomach, the body’s food
storage bag, empties, allowing the nutrients to be absorbed by the small
intestine. Glycemic index and low fat diets are uncomfortable bed fellows.
Has the glycemic index diet been popular? In contrast to the reticence
shown by the medical profession, the glycemic index range of books,
published by an Australian group from the University of Sydney, have
certainly been successful in marketing their ideas. The continually iterating
versions of the “New Glucose Revolution” consistently hits the best seller
lists on Amazon, and the penetration of glycemic index into the Australian
psyche has been dramatic. The “GI” symbol, signifying a low glycemic


index food is commonly found on products displayed on Australian
supermarket shelves. No more than 1,000 kilometres away in New
Zealand, a country that shares similar cultural traditions with Australia, has
little recognition of glycemic index, and the “GI” symbol is not widely
displayed. For example, a new refined, low-GI table sugar, recently
marketed in Australia, rapidly claimed 4% of the supermarket sugar
market, however, the same product, on sale in New Zealand, struggles to
reach supermarket shelves.
Initially, we were taken with glycemic index. When seeking to identify
a property of food that may predict its addictive potential as well as having
proven effects on human health, glycemic index appeared to fit the bill.
What we found puzzling was that, in general, glycemic index ranks some
refined carbohydrate laden foods higher (more dramatic glucose response)
and whole foods lower. Sugar, however, is an important exception. We
know from global records of food production, import and export that sugar
intake has risen substantially, and is one of the most dominant nutrition
changes in the latter half of the twentieth century [9]. The country with the
most dramatic sweetening of their food supply, the United States, also has
the highest proportion of obese adults of all industrialized nations.
However, if you believe the glycemic index is the most important predictor
of the health value of food, sugar appears relatively benign. Pure sucrose
has a GI of 68 [3], and many sugar containing products have lower GIs,
due to either their fat content. The most popular book written on the effects
of the glycemic index actually encourages its readers to enjoy eating sugar
[3]. What is it about sugar that gives it such a low GI, despite it being a
highly refined substance? Does sugar have any special properties which
may cause weight gain or other diseases to occur in people with a sweet
tooth?

SUGAR

Fructose holds the key to understanding the effect sugar has on health.
Sugar, the variety you buy in the supermarket, is derived from sugar cane,


with only one substance left after all the other parts of the plant are
stripped away in the refining process: sucrose, a molecule consisting of one
part glucose and one part fructose, chemically linked. Molasses, a black,
tarry, licorice tasting goo is made early in the process of making sugar
from sugar cane. In the United States, as we mentioned earlier, sugar
contained in manufactured foods is slightly different, usually derived from
corn (high fructose corn syrup).
What is unique about sugar (or HFCS) is its concentration of fructose-
roughly 1:1, or 50% by weight, which is much higher than naturally
occurring sources. Fructose is also found in fruit, honey and some
vegetables, however, the sugar in these items is far less concentrated
(bananas contain about 10% fructose). Fructose has often been ignored in
nutritional circles, because, it is assumed that since it is found in fruit,
which have been a key part of low fat diets, so it must be harmless... or is
it? Can something that nature provides be bad for us?
Studies of human risk perception show that naturally occurring hazards
are thought to be much less dangerous than those that are man made [10].
For example, radioactive waste is likely to engender more fear than say
tobacco, even though the latter causes far more deaths. Also, risky
exposures we come across every day are perceived as much less important
as rarely encountered ones. Sugar is often considered a “natural”
sweetener, particularly when contrasted to low calorie counterparts such as
aspartame and sucralose. However, the briefest glance into the
manufacturing process, by which sugar cane is turned into table sugar,
indicates that this process is far from “natural”. Sugar cane is crushed,
mixed with lime, and then mixed with a number of chemicals, such as
phosphoric acid and calcium hydroxide, to produce white sugar. Sucrose,
in high (99%) concentration is left, with all other plant material stripped
away.
If we leave the argument over whether sugar is “natural” to one side
for a moment, we now consider whether sugar affects health, and if so,
how? Interestingly, in the late 1990s and early new millenium, the
American Diabetes Association advocated increasing fructose consumption
in people with diabetes [11]. It seems counter-intuitive to most people


without nutritional training to advise people with diabetes to eat sugar, but
that was a policy, and I even came across a jar of jam recently that claimed
to be healthy due to its high fructose content. This policy was derived
mainly as a result of fructose's modest short term effect on the glucose
level in the blood, after a sugary or fruity meal. Much of the damage from
diabetes is thought to accrue from high levels of glucose circulating in the
blood vessels of patients with diabetes, and if fructose intake may improve
such a measure, then surely it must be safe, right?

Figure 2. The different metabolic paths of glucose and fructose.

The theory behind this advice was that fructose did not increase blood
glucose levels, because it is broken down by the liver, after being absorbed
in the gut, and before it enters the blood stream, where it can be easily
measured. Because treatment for diabetes is based on measurement of, and
control of blood glucose, diabetes experts initially considered fructose
harmless. Fructose, unlike glucose, does not stimulate insulin release and
because it is commonly found in fruit, it was thought to be a healthy


alternative for people whose bodies suffered from a lack of insulin, or
sensitivity to the hormone, and couldn't process glucose properly. Fructose
is taken up by the liver independent of insulin (Figure 2), and could spare
the body from potentially harmful exposure to glucose. However, it was
soon found that fructose had adverse effects on fat levels in the blood,
being readily converted to this form of energy storage, in contrast to
glucose that is mostly used for energy. High fructose intakes unequivocally
raise serum triglycerides levels [2]. Although debate continues about which
subgroup of fats found in the blood cause heart attacks (high density
lipoprotein is probably the strongest contender), high triglyceride levels
have been linked to heart attacks in several observational studies [12].
Although these downsides of fructose have been largely conceeded, and
advocates for fructose have withdrawn advice to consume sugar as a health
food, a rising tide of evidence indicates that fructose not only contributes
to high triglyceride levels, but also give rise to a range of other common
and devastating diseases.
Animal studies have documented adverse metabolic effects of refined
fructose intake. Rodents fed on high fructose and sucrose diets, but not
high glucose diets, develop features of the metabolic syndrome, such as
hyperinsulinemia, hyperuricemia and hypertriglyceridemia [13].
To explore the effect fructose may be having on our health, we
consider in more detail the physiological effects of fructose, before
reviewing possible health effects of excess consumption. A full discussion
of the metabolism of fructose is beyond the scope of this chapter, but is
discussed elsewhere [13]. After eating, fructose is absorbed from the small
bowel and enthusiastically broken down by the liver, independent of
insulin. Unlike glucose, fructose does not stimulate insulin release, which
signals fullness or satiety. Metabolism of fructose depletes cellular energy
stores (ATP), and induces uric acid production (which causes a particular
type of arthritis - gout). The principal products of liver fructose break-
down are triglycerides, which are then released into the blood. While
fructose is processed, conversion of glucose to glycogen (glycogenesis) in
the liver is blocked. The reduction in glucose processing by the liver, in
turn, causes insulin levels to rise so that glucose is taken up in alternative


sites, such as muscle tissue. As a result of high insulin levels, muscles
compensate by becoming insulin resistant. Such a mechanism may explain
how fructose has little acute effect on serum glucose levels, but
importantly, impairs blood glucose control after long term exposure to high
doses.
In contrast to animal studies, links between fructose intake and disease
outcomes have not been so conclusively demonstrated in humans, although
regimens with longer follow up periods and higher doses of fructose
(>200g/day or the equivalent of two cups of sugar/day) tend to produce
clearer links with risk factors for disease. For example, small intervention
studies have shown that high doses of fructose provoke insulin resistance
within one week [14], whereas smaller doses (<100g/day or the equivalent
of one cup per day) do not provoke insulin resistance and may conversely
improve the ability of the body to regulate blood glucose [13]. Fructose
consumption acutely raises blood pressure after short term exposure in
normal young men compared to water and glucose controls (mean change
in systolic blood pressure from baseline 4mmHg, 2 hours after 60g meal,
compared to a 1 mmHg change in both control groups) in a cross-over
design [15]. A rise in systolic blood pressure of 7 mmHg was observed
after two weeks treatment with 200g of fructose per day in a randomised
trial (74 individuals took part in the study) [15]. This trial also found
adverse effects on triglycerides, fasting insulin and the number of people
that met the criteria for metabolic syndrome (a cluster of metabolic
indicators which indicate high risk of cardiovascular disease). Other effects
of fructose consumption include modest weight gain in some short term
intervention studies [16]. The health effects of long term, high dose
exposure of fructose have not been rigorously studied in randomised
controlled trials. Given the consistent evidence of adverse effects of high
dose fructose in short term studies, giving the carbohydrate long term at
such a level is likely to be hampered by ethical stumbling blocks to
conducting such a study.
Perhaps the most investigated effect of fructose intake, in humans, is
the deterioration in blood fat profiles. A meta-analysis indicated a
consistent effect of fructose worsening serum triglyceride concentrations in

Sickly Sweet: electronic version.

Sickly Sweet: electronic version.

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Sickly Sweet: electronic version.