January is a grey month, a burnt-out shell between streamingly festive December and "back in the pink" February, when we all feel just about OK and our bank balances skip back into the black. It is a time of navel gazing – quite literally – when the ghost of Christmas dinner past comes back to visit. A time when we look down at our much grown waistlines in despair and think: "I'd better do something about this."
But what to do? Some of us pledge to take exercise, get on that bike and find a waistline. Others promise to give up red meat, cut out the butter and learn to say "no" to that extra slice of chocolate cake.
In short, most of us will do what we always have done when we wanted to drop some weight. We'll follow the guidelines drilled into us by successive health tsars, chief medical officers and ministers of health down the years: we'll cut our intake of fat. It is the standard course – but it simply isn't working.
According to the International Federation of the Red Cross, there are now more obese people (1.5 billion) than hungry people (925 million). The figures for diabetes are equally arresting: 5 per cent of the world's population now have the disease. In 1980 the figure was 2.5 per cent. Little wonder the Secretary-General of the UN recently said that the biggest threat to the world, developed and developing, is not from communicable diseases such as HIV or malaria but the non-communicable: obesity, heart disease, cancer, Alzheimer's and of course diabetes. The death rate from those conditions alone is 35 million each year.
As no one can claim with any degree of realism that they are unaware of the dangers of unhealthy eating – this raises a question. Do these figures represent an almost universal collapse of will? Are they down to bad choices on the part of the individual?
"That is the easy and pejorative answer," says Dr Robert Lustig, professor of clinical paediatrics at the University of California and a noted endocrinologist. "But that does not explain the epidemic of toddler obesity. We have an epidemic of obese six-year-olds. They don't make bad choices. Something else is going on. It is easy to say obesity is due to gluttony and sloth.
"Our research, however, shows that these behaviours are the result of biochemical alterations, which are the result of changes in our environment. Bottom line: biochemistry drives behaviour, not the other way around."
So what is the explanation? According to Dr Lustig, whose new book Fat Chance: The Bitter Truth about Sugar, it comes down to a change in diets in the 1970s; a change most of us probably didn't even notice. The Seventies saw the development of foods with manipulated low-fat contents. And low-fat food, according to Dr Lustig, is making us fat.
"When you remove fat from food, it tastes like cardboard, The food industry knows that. So when they took fat out, they had to add the carbohydrate in; and in particular fructose sugar," says Dr Lustig. So as the low-fat dogma took hold, we cut out the fat and started taking on vastly more fructose. In America fructose intake (mostly in the form of high-fructose corn syrup) has increased 100-fold since 1970.
In the UK, the quantity of stand-alone bags of sugar sold – stuff lingering in granny's baking cupboard – has decreased. Yet in the period from 1990 to 2000 consumption of sugar went up by around a third – and a significant quantity of that is sucrose, which is 50 per cent made up of fructose. This is what researchers mean when they refer to the rise of "invisible sugar".
It is invisible in the sense that few of us notice it but it very much exists. Take, for instance, a Volvic Touch of Fruit Lemon and Lime (1.5 litres) – how much sugar would you guess was in that? You'd be hard pressed to guess: 16 sugar cubes. Or barbecue flavour Pringles? They have 1.5 cubes. A plain bagel? 1 cube.
How have we become accustomed to sugar in just about everything that passes our lips in such a relatively short period of time? According to Charles Spence, professor of experimental psychology at the University of Oxford, we are used to it because we eat more – and we eat more because we need more. "We experience it in increasing amounts and grow accustomed to it. Think of it like eating chillies – the more you eat, the more you need to eat to feel the level of heat."
This goes some way to explaining what the writer Felicity Lawrence found when she studied fruit and vegetable production in 2007. She discovered that farmers are increasingly concentrating on producing super-sweet varieties of fruit that hitherto had been thought sweet enough. Why? Because our whole diet has an ambient quantity of sugar in it – so a sweet apple suddenly seems bland.
The effects of this are, unsurprisingly, not exactly favourable. Because although sugar – as we know it – is made up of glucose, which is essential for life, it also has a fructose component. It is this that causes the problems, says Dr Lustig: "The mitochondria (the energy-burning factories in our cells) in our liver have a fixed capacity for burning the fructose. When you overload them with extra fructose, they will burn some, but they have no choice but to turn the excess into liver fat.
"That starts the cascade of insulin resistance, which then promotes chronic metabolic disease, including diabetes and heart disease."
Dr Lustig also contends – and this is not an undisputed position to take – that there is further co-occurring effect for obese people. When fat cells have sufficient energy, they release a hormone called leptin, which is supposed to give feedback to the brain to tell it you have enough fuel on board and to now eat less and move more in order to keep a stable weight. Dr Lustig suggests that this cycle has broken down.
"We've learnt from two decades of study that leptin levels are high in obese people, but it's not shutting down their appetites, and they continue to gain weight anyway. Clearly, leptin is there, but it's not working. That's leptin resistance. Obesity is leptin resistance. The question is why is this happending? Because if we could fix leptin resistance, we could solve obesity.
"Our research (along with others) has shown that insulin is a cause (although not the only one) of leptin resistance. So high insulin levels cause you to store energy in fat cells (obesity), and then prevent leptin from signalling (starvation) so that you eat more (gluttony) and burn less (sloth). And what's the fastest way to high insulin levels? Sugar," says Dr Lustig.
If his thesis is correct not only does it mean that obesity can no longer be seen as a product of recklessness on the part of the individual, it also means as a society we have an urgent problem.
So what do we do? There is a simple solution: curb availability. Go for the environment, rather than the behaviour . But as we know, simple solutions are often the hardest to implement. Is it likely that we'll see the imposition of a soft drinks and biscuit tax any time soon? Probably not. And so are we likely to see even more people dying of those non-communicable diseases? Sadly, it's something of a certainty.
Fat Chance: The Bitter Truth about Sugar by Dr Robert Lustig, priced £13.99, is published by Fourth EstateReuse content