Our Food Industry & How It’s Killing Us (Part II): The Rise of the High Sugar Diet

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 20^th 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).

Figure 2: US Per Capita Sweetener Consumption 1965-2010

(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.

Our Food Industry & How It’s Killing Us (Part I): Obesity & the Incoherence of Much Current Dietary Advice

In 1980, a large-scale study by the epidemiologist Ancel Keys was featured on the cover of Time magazine. Called The Seven Countries Study, it compared per capita fat intake in the USA, Canada, Australia, England, Wales, Italy and Japan, and appeared to demonstrate a simple and direct correlation between dietary fat and the relative incidence of cardiovascular disease (CVD) in each of the countries concerned. It also marked something of a turning point in history. For over the next decade or so, it fundamentally changed our attitudes to what we eat.

For those brought up in a world in which this change had already taken place, this may be somewhat difficult to appreciate; but prior to the 1980s, the prevailing attitude was largely one of innocence. Mealtimes were still mostly family affairs, comprising regular family favourites, which most of us, I suspect, simply took for granted, enjoying the odd treat now and again as one of life’s simple pleasures, but never really giving our diet, as such, that much thought. It was The Seven Countries Study – or, perhaps more accurately, the flurry of media attention and paternalistic government action that followed in its wake – that lifted the scales from our eyes. For as departments of health throughout the western world responded to the growing political imperative by issuing dietary guidelines and mounting ‘healthy eating’ campaigns, we were all ineluctably made aware of the hazards inherent in our previously incontinent lifestyles, and were thereby forced, as much by social pressure as any concern for our hearts, to start ‘watching’ what we ate.

Indeed, it was as much their appeal to our vanity as their play upon our fears, that in the end, I suspect, made all those government campaigns to have us eat more healthily so successful. For successful, they certainly were. Over the next thirty years, the amount of fat in our diet, as a percentage of total calorific intake, fell from around 40% in the late 70s, to just over 30% today. Indeed, it’s hard to think of another campaign to change our behaviour on such a scale that has had anywhere near this level of success. The only problem was, of course, that it didn’t actually have the desired effect. For despite getting us to do all the things we were supposed to do, it didn’t bring about the changes in our health that it was believed would follow. In fact, during that same thirty year period in which we managed to reduce our fat intake by 25%, not only did our average weight increase – by as much as 25 pounds (12 kg) in the USA – but the incidence of obesity, hypertension, Type 2 diabetes, and coronary heart disease all continued to rise.

So what went wrong? Was dietary fat not to blame after all? Not if you count the number of articles on this subject still being submitted to major medical journals. If one listens carefully, however, there has been a subtle change in the way many healthcare professionals now seem to approach the subject. If you ask most dieticians, for instance, they are far more likely to tell you that it is not what we are eating that is the problem but how much. For although a ‘low-fat diet’ is still what is ‘officially’ recommended, this once simple message is now being combined with what is arguably an entirely different and diametrically opposed explanation as to why we’re all getting so fat. This is the view that it doesn’t actually matter whether our calorific intake is in the form of carbohydrates, proteins or fats, in that, in energy terms, the value of every calorie is the same. What is important, therefore, is the simple maths: that if we ingest n calories and only burn off n-1 calories in exercise, then the remaining calorie has to be put into storage, almost certainly in the form of fat.

Apart from sending out a mixed and therefore somewhat confusing message, the real problem with this new ‘quantitative’ approach to the problem, of course, is that it is simply wrong – a matter to which I shall return shortly. What makes it all the more damaging, however, is the effect it is having on our already dysfunctional relationship with food. For if being told to cut down on fat made us that much more self-conscious with respect to what we were eating, being told that a healthy diet is simply a matter of inputs and outputs, which can be counted and controlled, has made us positively obsessive – assuming, that is, that we haven’t already given up altogether and fallen into that slough of self-loathing, despair and depression, which is so often the psychological correlate of our physical malaise. 

For the implication of this new  quantitative approach, of course, is that, if we are overweight, it is entirely our own fault. We eat too much and exercise too little. We are, in short, guilty of two deadly sins: gluttony and sloth. And how our media love to rub our noses in it! On UK television at present, there is a programme called ‘Big Body Squad’. It is about members of the emergency services who are tasked with the problem of getting grossly obese patients out of their homes in order to take them to hospital: a task which almost invariably involves taking out windows, knocking down walls and the use of a crane. 

In fact, watching morbidly obese people being ritually humiliated for our derision and delight has become something of a new spectator sport. Importantly, however, the deep vein of inhumanity and cruelty to which this kind of reality programming panders is not the only form of sickness it exploits. For while the gross and unlovely flesh of our fallen brethren may initially reinforce our sense of moral superiority – that wholly unsought, if not entirely unpleasant by-product of the hours we spend each week in the gym, turning our bodies into temples to the god Narcissus – it also serves as a cautionary tale as to what could so easily happen should we allow our iron discipline to falter, thus adding further impetus to our own obsessive-compulsive behaviour. 

What is really troubling, however, is the fact that, for those who are overweight, it is not just the state of their own bodies over which they are made to feel guilty and ashamed. As parents, they also have to take responsibility for the obesity epidemic that is now sweeping through our children. For the sad fact is that today’s overweight ten-year-olds are very probably members of the first generation for over a century to have a lower life expectancy than that of their progenitors. So bad are we at feeding our children and ensuring that they have enough healthy exercise, in fact, that we are now even producing obese babies. For the first time in history, infants as young as six months old are experiencing problems requiring medical intervention purely as a result of their weight. It’s no wonder, therefore, that we, their parents, feel guilty. The question, however, is whether the shame and anger we rightly feel, ought, more appropriately, be directed at someone other than ourselves.

For think about it: how do six-month-old babies become obese? Do we really believe that it is because they are gluttonous and slothful? After all, at that age, they have no psychological or behavioural triggers that would cause them to eat more than they need. Might it not be the case, therefore, that just as the healthcare profession may have got it wrong over the role of dietary fats in the aetiology of heart disease, so too they may have been slightly over-quick to judgement over the role of sin.

One endocrinologist who certainly thinks so is Dr Robert Lustig, Professor of Paediatrics at the University of California in San Francisco. In July 2009, a video of one of his lectures was posted on YouTube, in which he argues that both of the current views on the causes of obesity and cardiovascular disease are wrong.

With respect to the view that it is dietary fat that is to blame, not only does he point out that reducing fat intake hasn’t had the desired effect, he also questions the scientific rigour of the study which raised this whole question in the first place, arguing that, despite being based on a multivariate regression analysis – one designed to identify and weight all the contributory factors in a complex causal matrix – The Seven Countries Study completely failed to take into account the contribution of another common foodstuff: one which, at the time, represented a very similar relative proportion of each of the diets studied, and which could therefore be shown to have the exact same simple and direct correlation with cardiovascular disease as dietary fat. What this ‘other common foodstuff’ is, I shall return to shortly.

Just as importantly, he also argues that the view that all calories are the same, and that it doesn’t matter what we eat as long as our calorific inputs and outputs are balanced, is equally misguided. This is because it fails to take into account the very different ways in which our bodies metabolise different foods. 

We can demonstrate this quite simply if we compare the biochemistry involved in the metabolism of two common carbohydrates:

1. fructose, which is the sugar that is found in fruit; and
2. glucose, which most of us obtain from starchy staples such as bread, pasta, rice and root vegetables.

If we start with the latter, the first and most important thing to know about glucose is that it is one of the few substances we ingest that can be directly absorbed and metabolised by more or less every cell in the body. This is because when glucose enters the bloodstream it triggers the pancreas to release insulin. The insulin molecules then attach themselves to the outer membranes of our  cells, and attract to them – from within the cells – a protein called GLUT4 (Glucose transporter type 4), which, together with the insulin, forms a physical conduit through the cell membrane – a bit like a valve – through which individual glucose molecules are able pass. Once inside, the cell’s mitochondria then
use the energy produced by glucose breakdown to produce adenosine triphosphate (ATP) – the ‘molecular unit of currency of intracellular energy transfer’, as it is sometimes called – which then combines with different enzymes and different structural proteins to be consumed by or to facilitate other cellular processes.

This doesn’t mean, of course, that all ingested glucose is instantly absorbed in this way. How much of it is depends on the rate of ingestion. If drip fed intravenously, for instance, at a slow but steady rate – as happens to patients in hospitals – non-hepatic metabolism can get fairly close to 100%. Normal ingestion, however, accomplished through eating, is a little more erratic, leading to peaks and troughs in blood/sugar levels. To use an example from Professor Lustig’s lecture, if you were to eat a sandwich comprising two slices of bread containing 120g of glucose – ignoring the sandwich’s other contents, and assuming that you are hungry, and that your blood isn’t already glucose saturated – then it is likely that about 80% of the glucose (96g) would be taken up and metabolised as described above. The rest would end up in your liver, the body’s more general metabolic factory, where most of it would then be turned into glycogen – as shown in Figure 1 – a highly accessible, medium term energy store, of which our livers can actually hold an almost limitless amount without experiencing dysfunction or damage.

This is what happens, in fact, when marathon runners ‘carb up’ the night before a race, usually by eating vast amounts of pasta. Most of the excess glucose is stored in the liver as glycogen, which is then released back into bloodstream as glucose as the runner’s blood/sugar starts to fall. This goes on until, eventually, all the glycogen is used up and the runner hits ‘the wall’.

Figure 1: Metabolism of Glucose in the Liver

If we now compare this with what happens to fructose, the story is very different. To begin with, the presence of fructose in the bloodstream does not trigger the release of insulin. Nor can it use any insulin/GLUT4 conduits that may already exist. For although it is a slightly smaller molecule than glucose, like a key with the wrong number of notches, with one extra carbon atom it is physically the wrong shape. In fact, to enter our cells at all, it needs another transporter, GLUT5. Apart from in our intestines, however, GLUT 5 is only produced in our livers. And it is in the liver, therefore, that all ingested fructose is metabolised.

Even in the liver, the metabolism of fructose still has to follow a different course from that of glucose. For just as fructose molecules are the wrong shape to use insulin/GLUT4 conduits, so too they have the wrong chemical composition to be turned into glycogen. The result is that, depending upon the rate at which the fructose is absorbed by the liver, it then follows one of four different metabolic pathways, as shown in Figure 2.

1.  The most benign of these is the one shown towards the top of the diagram in which the fructose is first used to produce ATP by the mitochondria of the hepatic cells, in the same way as happen to glucose in other cells of the body. It then follows one of two pathways – again depending upon the rate of absorption – the most benign of which results in its eventual transformation into glucose. This only happens, however, to a very small proportion of the ingested fructose, or when the absorption rate is very low.
2. If the absorption rate is faster than the rate at which ATP can be turned into glucose, this results in a depletion of the available phosphate within the cell, which then triggers the activation of the scavenger enzyme adenosine monophosphate deaminase-1, which recoups intracellular phosphate by converting the ATP breakdown products – adenosine diphosphate (ADP), adenosine monophosphate (AMP), and inosine monophosphate (IMP) – back into ATP, leaving a residual waste product in the form of uric acid.
3. The real problem occurs, however, when the rate of absorption exceeds the rate at which the mitochondria can turn the fructose into ATP in the first place. It then enters a process known as de novo lipogenesis (DNL) or the creation of new fat, in which the majority of it is first turned into pyruvate, before entering what is known as the citrate shuttle – a sequence of biochemical transformations, including feedback loops – from which most of it finally emerges as VLDL (Very Low Density Lipoprotein), a transporter protein containing, among other by-products of this process, cholesterol and triglycerides (fats), which are then eventually deposited in adipose, cardiac and skeletal muscle tissue throughout the body.
4. Alternatively, the various lipids created in DNL can also form fatty droplets which are actually deposited within the liver, itself, producing an effect on the liver very similar to that of alcohol.

Figure 2: Metabolism of Fructose in the Liver

To summarise, therefore:

• If you ingest glucose, your body turns it into instantly available energy, and/or the short-term energy store, glycogen.
• If you ingest any significant amount of fructose, your body turns it into the long-term energy store, fat.

Anyone who tells you that a calorie is a calorie is a calorie, therefore, just doesn’t understand the biochemistry. 

There is also another way in which the metabolism of glucose differs from that of fructose. Ordinarily, an increase in lipoproteins and triglycerides in the bloodstream triggers the release of a hormone called leptin, which makes us feel full and uncomfortable whenever we eat too much. It is our bodies’ way of sending a message to our brains to say that we’ve had enough. As can be seen in Figure 1, this is what happens when we consume large amounts of glucose. If the rate of ingestion is too rapid for all of it to be turned into glycogen, then glucose, too, can end up entering the citrate shuttle, to be turned into fat, thus releasing leptin and making us feel as if we couldn’t eat another bite. It’s why marathon runners, in carbing up, have to eat very slowly. In the case of fructose, however, one of the free fatty acids created as a by-product of its breakdown (FFA in Figure 2) causes insulin to act as a leptin inhibiter. It actually stops the brain from getting the message.

Combined with our bodies’ overall disposition to turn fructose into fat, this suggests, in fact, that at some point during our history, our bodies’ way of dealing with fructose had an evolutionary value. A hundred thousand years ago, when we were still hunter gatherers, but had left the all-year-round bounty of Africa behind, our ancestors would only have eaten fruit during a few months of the year, in late summer and early autumn. Individuals who were able to gorge themselves on this harvest without feeling bloated, and whose bodies were naturally disposed to lay all this abundant energy down as fat, would therefore have had a far greater chance of surviving the lean months of winter than individuals who either couldn’t force themselves to eat that much fruit, or whose bodies didn’t metabolise fructose in this way. As a result of natural selection, therefore, these are the bodies we have inherited. The problem is that although our consumption of fructose is no longer confined to two or three months of the year, our prehistoric bodies still treats it as if it were.

‘But fruit!’ I hear you say. ‘I thought it was good for us.’ And so it is. In addition to fructose, it contains a whole raft of other beneficial and necessary nutrients. Moreover, if you eat it as whole fruit – rather than as fruit juice, for instance – it also comes packaged in a large amount of fibre, which slows down its digestion and the rate at which it enters the liver. If one were to eat just two or three pieces of whole fruit a day, therefore, not only would this be enough to provide one with all the additional nutrients one needs, but most of the fructose would follow the first of the metabolic pathways described above and be turned into glucose. The problem for most of us, however, is that most of the fructose we ingest no longer comes in the form of whole fruit. Most of it, indeed, has so little connection with any fruit we would recognise as such, that its fruit-based origin is purely nominal. For most of the fructose that now arrives on our plates or in our glasses is actually in the form of processed sugar, not conspicuously spooned into cups of tea or coffee, on which we could choose to cut down, but hidden in the industrially manufactured food and drink upon which most of our diets are now based. And it is this hidden sugar that Professor Lustig argues is the real cause of the obesity and CVD epidemics that are slowly killing us.

In the second part of this essay – ‘Our Food Industry and How it is Killing Us (Part II): The Rise of the High Sugar Diet’ – I shall therefore be looking at the rate at which our sugar consumption has increased over the last thirty years, and at the role of one type of sugar, in particular, High fructose Corn Syrup or HFCS.

In Part III, subtitled ‘Paying the Price’, I shall then examine how this change in what our food industry is feeding us came about, and consider the consequences of what may follow if nothing is done about it.

For those more interested in the health aspects of this issue, however, you might like to watch the 2009 lecture by Professor Lustig I mentioned earlier, which can be found at:

http://www.youtube.com/watch?v=dBnniua6-oM&feature=youtu.be

While for those who would like to take a closer look at the biochemistry involved in the metabolism of fructose, there is also a published scientific paper by Professor Lustig available at:

http://podcast.uctv.tv/webdocuments/fructose-and-ethanol.pdf