Tuesday, 14 May 2013

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:

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: