In the first part of this essay, subtitled ‘Obesity &the Incoherence of Much Current Dietary Advice’, I cited a lecture by Dr Robert
Lustig, Professor of Paediatrics at the University of California in San
Francisco, in which he argues that, despite their widespread currency, the two
most prevalent theories for explaining the increase in obesity, hypertension,
Type 2 diabetes and cardiovascular disease in the second half of the 20th
century are both fundamentally wrong.
The first of these theories – which gained broad acceptance
in the early 1980s – says that one of the most important factors in the
aetiology of all of the above diseases is the level of fat in our diets: a proposition
that is now so well established in our collective belief system that it is not
only generally accepted as a fact, but is the basis upon which much current
dietary advice continues to be given.
According to Professor Lustig, however, not only was the
international study, upon which this
theory was initially grounded, seriously flawed – failing to take into account all
the possible contributory factors – its continued status defies much of the
evidence of the last thirty years. For while our intake of dietary fats has significantly
fallen during this period – by around 25% – the incidence of each of the
diseases with which these fats were believed to be causally related has continued
to rise, reaching near-epidemic proportions.
Over the last ten to fifteen years, as a consequence, a
second theory – one based less on scientific evidence than apparent common
sense – has steadily gained greater currency. Instead of attempting to identify
one particular substance or foodstuff as the principal culprit, it says that
obesity – and all its other attendant diseases – is less the result of what we
eat than simply how much. Based on the first law of thermodynamics, which tells
us that, in a closed system, energy is never lost, it states that if we consume
more in calories than we burn off in exercise and the sheer business of staying
alive then the excess has to go somewhere. And the obvious answer as to where this
might be is in our adipose tissue in the form of fat.
What this physics-based model fails to take into account,
however, is that our bodies not only have different ways of dealing with excess
dietary inputs – some of them hardly entering the closed system of our
metabolism at all – they also have different ways of metabolising the different
substances that do get that far.
In Part I of this essay, I illustrated this by taking the
reader through the biochemistry involved in the metabolism of two common
sugars: glucose and fructose. I shall not rehearse this excursion into the
abstruse and wonderful world of human metabolism again here, not least because
it would involve reproducing most of Part I all over again. The important
point, however, is that it is quite possible for us to ingest identical amounts
of two very similar substances, and for our bodies to treat them in completely
differently ways. In the case of glucose, for instance, our bodies either use
it to produce instantly available energy – in the form of ATP (adenosine triphosphate) – or turn it into the
short-term energy store, glycogen. In contrast, if we ingest any significant
amount of fructose, our bodies turn nearly all of it into fat.
And it is this that Professor Lustig believes to be the real
problem: not the dietary fats which our metabolism largely breaks down into
other (mostly) useful substances; but the non-fats which our bodies turn into
fats, to be stored as such in adipose,
skeletal muscle and cardiac tissue, where, if left unused and allowed to
build up over time, they can do considerable harm. And chief among these
harmful, ‘lipogenic’ non-fats, according to Professor Lustig, is indeed
fructose.
More importantly, I have yet come across a single biochemist
who disagrees with the basic science behind this contention. I can therefore
state with a fair degree of confidence that, even if there are still some
grains of truth in either of the other two theories used to explain the
increase in obesity and heart disease over the last thirty years, if you want
to avoid putting on fat, then the one thing you should certainly do is cut down
on your consumption of fructose.
It is at this point, however, that we run into our first problem.
For even if more people were to become aware of just how lipogenic – or disposed
to fat formation – fructose truly is, it is unlikely that many of us would be
able to tell you just how much of the stuff we are actually eating. This is
because very little of our daily intake comes in a form that is readily
identifiable as such. For most people, for instance, less than 5% of their fructose
consumption comes in the form of fresh fruit – from which, in its broadest
sense, all fructose is ultimately derived. A far greater proportion – the vast
majority, in fact – is added to our food in the form of processed sugar.
Even in this regard, however, it is not always obvious how
much we are consuming. For not all of the sugar we ingest is conspicuously
spooned over strawberries or stirred into our tea or coffee. Most of it, in
fact, is almost entirely hidden, not just in the cakes and biscuits we casually
enjoy as mid-morning snacks, but in the ready-meals and fast-food takeaways –
along with their accompanying soft drinks – that have become such a major part
of our diet over the last thirty years.
To complicate matters further, different types of sugar
contain different amounts of fructose: a fact which has led to the fairly
widespread belief that there is one type of sugar – used exclusively in the
industrial manufacture of food products – that is worse than all the others. The
believed culprit is High Fructose Corn Syrup, or HFCS, which first made its
appearance in the mid-1970s, after President Nixon asked his then Secretary of
State for Agriculture, Earl Butz, to find a way of stabilising food prices so
as to prevent them from becoming a political issue. Butz did this by
subsidising the large scale production of HFCS made from maize grown in
America’s Mid-West. 40% cheaper than sucrose – which is made from either
sugarcane or sugar beet – it very quickly caught on with the food industry,
especially with manufacturers of soft drinks such as Coca-Cola and Pepsi, which
has further led to its demonization among certain campaigners, the view being
that if Coca-Cola is using it, then it’s got to be evil.
This, however, is a very distorted view of what is actually
going on here. For while it may not be entirely coincidental that the
introduction of HFCS occurred more or less at the same time as the start of the
period of rapid growth in obesity and CVD, to assume that this correlation is
either simple or direct would be to make the same kind of mistake researchers
in the 1970s made with respect to dietary fats. They saw a correlation and
immediately assumed a cause.
One can see this more clearly if one steps back from the US
context – where most of this debate is taking place – and takes a more global
perspective. For despite what many campaigners seem to think, the production
and consumption of HFCS is still very much a US phenomenon. In 2010, for
instance, HFCS accounted for around 38% of the sugar – or ‘sweetener’ – consumed
by the average American. In Europe, in contrast, it accounted for less than 5%.
Yet Europe too – and the UK in particular – is experiencing a similar trend
with respect to obesity and CVD. It may not be as pronounced as in the USA,
where it started earlier, but it is following a very similar path.
Even more significantly, HFCS and sucrose are very similar
in terms of their biochemistry. As can be seen in Figure 1,
sucrose comprises a bonded pair of fructose and glucose molecules, which almost
immediately breaks apart on digestion, producing one fructose molecule and one
glucose molecule. One can therefore say that sucrose is more or less 50%
fructose and 50% glucose. HFCS, in comparison, is 55% fructose and 42% glucose,
with the other 3% being mostly water. The difference in the amount of fructose
in each of these forms of sweetener may not be entirely trivial, but it is not
enough, therefore, to blame one and not the other. In fact, singling out HFCS
for attack, as many people seem to want to do, merely allows the food industry
to counter by arguing that it is no more harmful than sucrose, which is more or
less correct.
Figure 1: Molecular Structure of Sucrose
The real problem, therefore, is not the type of processed
sugar we are consuming, but the total amount. Here, however, we have another
problem. For obtaining reliable data on sugar consumption is not easy.
The first difficulty one encounters is in determining what
counts as ‘sugar’ in the various datasets that are out there, and what is meant
by ‘consumption’. A recent report by the Indian Council of Agricultural
Research (ICAR), for instance, states that Brazil has the highest per capita
consumption of sugar of any country in the world, with each Brazilian consuming
58 kg (128lbs) of the stuff per year. The USA, in contrast, comes in in seventh
place, with each American only consuming half this amount, 29 kg (64lbs). It is
only when one looks at the data in more detail that one starts to realise that
this claim isn’t quite what it seems.
The first clue comes in the attribution of authorship on the
title page. For while the report may have been published by ICAR, it was
actually written by the Sugarcane Breeding Institute in Coimbatore. It will
not, therefore, come as much of a surprise to discover that, under the heading
‘sugar’, the report only actually includes sucrose produced from sugarcane,
which is a major agricultural crop in both India and Brazil. In Brazil,
however, the sugar produced is not only sold in granulated form and used to
sweeten manufactured foods and drinks; it is also used to produce Cachaça, one
of Brazil’s most popular alcoholic beverages. This means that a large part of
Brazil’s so-called ‘sugar consumption’ is not ingested as sugar at all – but as
ethanol – and while it may make sense, from an economic and agricultural
perspective, to include it as one of the more important raw materials consumed
by the Brazilian economy, to include it as part of the country’s official per capita sugar intake gives one a
totally distorted impression.
Of course, my selection of this rather extreme example to illustrate
what is a fairly general point means that it is not entirely typical of most of
the data on sugar consumption one finds on the internet. Statistically, it is a
bit of an outlier. In many ways, however, it is actually far less misleading
than quite a few reports I could have cited. For the vast majority of websites
providing statistical information of this kind not only fail to reference their
data’s provenance or define what it includes, in many cases they are produced
on behalf of clearly vested interests, of which more trusting readers need to
be aware.
There are, of course, plenty of scientific studies available,
which, given peer-review, one can assume to be without intentional bias. But most
of the ones at which I’ve so far looked are primarily concerned with
correlating sugar consumption with the incidence of various specific diseases,
and tend to be based on fairly small sample populations taken from a single
geographical region, comprising a single sex in a fairly narrow age-range. In
terms of helping us quantify per capita
sugar consumption, they are therefore of little use. If we are looking for
reliable data, as a consequence, all we really have to go on are official
national statistics. And in the UK, even these are not very helpful.
The ONS, for instance – the Office of National Statistics – has
absolutely nothing on the subject. DEFRA – the Department for Environment, Food
and Rural Affairs – has figures for UK sugar production; but nothing on
consumption. And while, for the purposes of ‘Health Education’, the Department
of Health has published one or two papers on the dangers of high sugar diets, it
appears not to have commissioned any real scientific work on the subject since
1999.
Part of the problem is that, in the UK, sugar consumption has
not yet become a political issue. This, however, is certainly not something you
can say about the USA, where the problem, if anything, is one of
over-politicisation. Last year, for instance, it was announced that per capita sugar consumption in the USA had
exceeded 100lbs (45kg) the first time ever – though, again, what was included under
the heading ‘sugar’ is not absolutely clear. In October, however, the US Department
of Agriculture, ever-mindful of the need to keep Midwest farming interests
onside, announced that it was changing the way in which sugar intake would be
calculated in future and duly revised the 2012 figure down to 76.7lbs (34.8kg).
(Source:
US Department of Agriculture)
The irony is that, if one looks at the official figures which
the Department of Agriculture published in September 2010 – before this change
in methodology took place – they actually reveal a marked decline in per capita sugar consumption over the
last decade, very possibly as a result of the growing campaign against HFCS
which began in the early 2000s. Changing the method of calculation is therefore
likely to obscure this.
What Figure 2
most strikingly reveals, however, is not only how rapidly HFCS substantially replaced
sucrose (here designated as ‘Refined Sugar’) during the 1970s and early 80s,
but how its per capita consumption still
continued to grow even after the consumption of sucrose more or less levelled
off, thereby leading to a marked increase in total sugar intake during a period
in which the USA coincidentally experienced its most significant increase in the
incidence of obesity and CVD.
To attribute this increase solely to the extra 5% fructose
in HFCS, however, simply beggars belief, as does the argument that following
the US consumer’s rejection of HFCS – and the subsequent decline in overall
sugar consumption – the problem has now been resolved. For although some
American consumers – having watched Professor Lustig’s lecture on YouTube perhaps
– may be voting with their wallets and refusing to buy products containing HFCS,
this does not mean that they have fundamentally changed their diet, or that the
American food industry is now gearing itself up to produce food with a
significantly lower sugar content. Indeed, it is questionable whether this
latter is even possible. For having already reduced the amount of fat in foods
they are producing – largely by replacing it with sugar – the question now
facing all food manufacturers is with what – if they were forced to it – would
they replace the sugar.
Not that they are in any imminent danger of being forced to
make this decision, of course. For not only is the US Food & Drug
Administration (FDA) still a long way from accepting that HFCS – or any other form
of sugar – is harmful, but politicians and industry-insiders alike know full well
that were they required to reduce the sugar content of their products, not only
would many manufacturers go out of business, the effect on the overall US
economy would be devastating.
This is because, as Earl Butz recognised, sugar is the key
to cheap, mass-produced food. Without it, many manufactured foods would either be
too lacking in flavour to be saleable, or too expensive for them to actually have
a mass market.
To understand this, however, one needs to understand the
economics of our food industry in the way that it is currently structured. And it
is this that will be the subject of my third and last essay in this series,
subtitled ‘Paying the Price.’
In it I shall not only describe how our food industry got
itself – and us – into this extremely dire and possibly intractable predicament,
I shall also attempt to outline the even more dire consequences that may follow
if no solution can be found.
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