Balaji Ravichandran: Sugar is the new tobacco

balajiSugar is the new tobacco. It is dangerous, addictive, and toxic, and it cannot be controlled by education or legislation alone. This is a war, between public health and private industry, and one that is best waged through the courts.

These were some of the more dramatic pronouncements heard at what was ostensibly an academic symposium on sugar, obesity, and metabolic syndrome. But then the keynote speaker of the event was Professor Robert Lustig, a paediatric endocrinologist from University of California, San Francisco, known as much for his forthright manner and the theatricality of his presentations as for his academic research. He was the star of the entire conference, the uneasy knowledge of which permeated the words of every other academic on the stage.

The two-day symposium was organised by Food and Behaviour (FAB) Research, a charity that furthers research into the link between nutrition and human behaviour.[1] It was extremely well-attended, especially by people who described themselves as “nutritionists” or “nutritional therapists,” but also by general practitioners, cardiologists and, interestingly, members of the public. Dr Alex Richardson, a founder of FAB, was in no doubt as to who drew the crowds and attracted such media attention. All credit to Dr Lustig, she told me, who achieved fame after his lecture on the health effects of sugar went viral on YouTube.[2]

The opening speaker, Professor Jason Halford of Liverpool, set out the problem. Almost two-thirds of the adult population in the UK was overweight or obese in 2010, and, if this continued, the NHS would soon become overwhelmed, he said. Obesity is traditionally thought of as a problem of energy balance, the difference between what we consume and what we expend. But this equation is at once deceptive and simplistic, he argued. He drew attention to the Foresight Report of 2007,[3] which posited the existence of a constellation of variables that influence our feeding habits and our levels of activity, most of which are outside our control. So, to blame individuals, or to implicate one macro- or micronutrient at the expense of another, was problematic.

In a way, Professor Halford established the dominant theme of the conference. Obesity and metabolic syndrome are not questions of individual responsibility. That is a myth propagated by the food industry and the politicians, who, through their unholy alliance, maintained a toxic environment conducive to the spectrum of disorders that constitute metabolic syndrome. What does it mean to have a choice, every researcher asked, when good, healthy food was out of the hands of most of the general public, especially the poor and the vulnerable, and the available food is designed to trick the hormonal systems of the body into overeating and becoming addicted to sugary, fattening foods?

We already know how powerful the sugar and beverage industries are. Professor Michael Yudkin, son of John Yudkin, recalled how his father’s book Pure, White and Deadly, which argued for a strong link between sugar consumption and metabolic syndrome, was quickly rubbished by the sugar industry, and subsequently forgotten by academic researchers. It was a concerted effort, and the industry spent millions of pounds in recruiting doctors and academics to combat the message of the book. Ancel Keys, the man behind the low-fat diets, and who wanted to blame saturated fats, not sugar, went so far as to describe John Yudkin’s work as “a mountain of nonsense.” It was therefore a matter of great pride to the younger Yudkin that his father’s work has, at the hands of researchers like Professor Lustig, achieved a measure of vindication.

Professor Lustig was greeted on to the stage with rapturous applause from the audience, punctuated with whistles and shouts of approbation. One could see why his manner provoked resentment among some of his academic colleagues. He began by quoting Gandhi: “First they ignore you, then they laugh at you, then they fight you, then you win.” Now, he said, “we’re at the fighting stage.”

Metabolic syndrome, not obesity, is the problem

“I don’t care about obesity,” he then declaimed. “Obesity is not the problem. Metabolic syndrome is.” Why? Nearly 20% of clinically obese were completely healthy, with no health problems. But almost 40% of the population with normal weight had metabolic syndrome, and they presented the greatest threat to public health, he said. The issue of weight was a distraction, one used by the food industry and the politicians to blame the individual rather than the toxic environment to which they in collusion gave birth. It was not surprising, therefore, that we had no uniform definition of metabolic syndrome, as we had used the idea of weight to drive research. Had we defined metabolic syndrome mechanistically, as engendered by insulin resistance, we would have rightly seen obesity as a symptom, not as a disease.

Another declamation soon followed. What caused metabolic syndrome and insulin resistance? A clip from the film Men in Black provided the answer. Tommy Lee-Jones asks Will Smith over the telephone: “Do you know what’s the most destructive force in the world?” Smith responds: “Sugar?”

Sugar was not the only enemy, Professor Lustig was quick to add. Trans-fats, branched-chain amino acids (BCAA), ethanol, and fructose all had a part to blame. But the latter were not subject to regulation by insulin. Yet in being composed of glucose and fructose, sucrose, he said, involved both insulin and fructose at the same time, which is what made sugar particularly unique and problematic. He brushed aside suggestions that fructose and glucose were metabolised in the same way by the liver. The five-member furan ring of fructose was inherently unstable, and at equilibrium, existed in the linear form. When they bound to amino acids, it could result in protein misfolding, which in turn could make insulin receptors scarce in liver cells, thus generating insulin resistance. In addition, while the liver shunted glucose towards the generation of glycogen, fructose was preferentially metabolised to fat droplets, and at high concentrations this resulted in fatty liver.

Worse, he said, fructose was more likely to bind to protein than glucose, and in doing so released reactive-oxygen species (ROS), implicated in ageing and all aspects of metabolic syndrome. He also drew attention to a study in methionine-choline deficient mice, a model for non-alcoholic fatty liver, which showed that sucrose was necessary for steatosis.[4] Most important of all, he said, the downstream effects of fructose in liver cells were such that there were no available drug targets which could stop metabolic syndrome. In other words, we could not design drugs to stop fructose and sucrose from inducing insulin resistance and de novo lipogenesis in the liver.

Sugar as a toxin
Finally, he drew attention to the study he published in PLoS One two weeks ago,[5] which suggested that a quarter of the prevalence of diabetes around the world could be explained by sugar alone, after controlling for other confounding factors. The econometric analysis, he said, in being a repeated cross-sectional study across a decade amounted to a “causal medical inference,” the same level of proof that was used to implicate tobacco as being responsible for lung cancer. Sugar, therefore, was a toxin in its own right. Given that, of the 600,000 items in the American food supply chain, 80% had added sugars, the sugar industry would do everything in its power to fight these findings, he said. “This is a war,” he concluded, in his typical dramatic manner, “and you didn’t even know you were fighting it… This is a war, and I throw down my gauntlet.”

There was not a single reaction in the body, Professor Lustig said, that required fructose. But surely fruits are healthy, and they have fructose, someone asked. Lustig responded by saying that there wasn’t a single sweet substance in nature that was poisonous to us, and that was no coincidence. It was evolution’s way of guiding us to essential nutrients and antioxidants. But nor was there a single substance in nature rich in fructose and devoid of fibre. Indeed, the level of fructose was roughly proportional to the amount of fibre in the fruit, he said. Fibre kept the insulin response and fructose absorption down. The problem, he said, was that food processing removed both the fibre and micronutrients, and left the sugar fully intact.

In his final statement, Professor Lustig said that neither education nor governmental regulation worked on their own in combating obesity, and certainly not fast enough. But, he said, at least in the United States, there was another way: the courts. It worked in the battle against cigarettes, and he was certain it would work just as well against the sugar industry. This, to him, was the best way forward.

Balaji Ravichandran is a freelance writer, DPhil candidate at The Queen’s College, Oxford, and former editor, Student BMJ


1. See
2., 13 March, 2013) Dr Lustig has also published a book on the same topic, called Fat Chance, which he was in part promoting at the symposium.
3. (Accessed 13 March, 2013)
4. Pickens, MK, Yan, JS, Ng RK et al. Dietary sucrose is essential to the development of liver injury in the methionine-choline-deficient model of steatohepatitis. J Lipid Res. October; 50(10): 2072–2082, 2009.
5. Basu S, Yoffe P, Hills N, Lustig RH (2013) The Relationship of Sugar to Population-Level Diabetes Prevalence: An Econometric Analysis of Repeated Cross-Sectional Data. PLoS ONE 8(2): e57873. doi:10.1371/journal.pone.0057873
6. Livesey, G and Taylor, R. Fructose consumption and consequences for glycation, plasma triacylglycerol, and body weight: meta-analyses and meta-regression models of intervention studies. Am J Clin Nutr. 2008 Nov;88(5):1419-37.
7. (Accessed 13 March 2013)
8. (Accessed 13 March, 2013)