If the excerpts below seem interesting, read even more at the full original article HERE
(Main conclusions of research are highlighted at the bottom)
…”‘Population-wide’ explosions in the prevalence of obesity along with increases in the occurrence of diabetes that frankly strain the imagination: a disease that leads to blindness, kidney failure, amputation, heart disease and premature death, and that was virtually non-existent in hospital inpatient records from the mid-19th century, now afflicts one in 11 Americans; in some populations, as many as one in two adults are diabetic.
In the midst of such a public health crisis, the obvious question to ask is why. Many reasons can be imagined for any public health failure, but we have no precedents for a failure of this magnitude. As such, the simplest explanation is that we’re not targeting the right agent of disease; that our understanding of the aetiology of both obesity and diabetes is somehow flawed, perhaps tragically so.”
“…it’s quite possible that the causes are misunderstood.
The history of obesity and nutrition research suggests that this is indeed what has happened. In the decades leading up to the Second World War, German and Austrian clinical investigators had concluded that common obesity was clearly caused by a hormonal disturbance; starting in the1960s, other research would link that disturbance to the sugar in our diets. But the German and Austrian thinking evaporated with the war, and the possibility that sugar was to blame never took hold, dismissed by a nutrition community who, by the 1970s, became fixated on dietary fat as the trigger of our chronic diseases. Now, with an explosion of the epidemic and compelling new research, it’s time to reconsider both our causal thinking on obesity and diabetes, and the possibility that sugar is playing the critical role.”
“…The WHO and other health organisations have recently taken to arguing that sugar and particularly sugary beverages should be taxed heavily or regulated. But they do so not because they say sugar causes disease – using the same definition of causality that we use when we say cigarettes cause lung cancer – but, rather, because, from their perspective, sugar represents ‘empty calories’ that we eat in excess. By this thinking, we still get fatter because we eat too much or exercise too little. The solution is to eat in moderation, and consume sugar in moderation or balance it with more physical activity.
The energy balance paradigm implies that the only way in which foods influence our body fat is through their energy content, or calories – that is, through the energy that we absorb without excreting, and so make available to be oxidised or stored. This is the only variable that matters. It’s the implication of the phrase ‘a calorie is a calorie’, which, by the 1960s, had become a mantra of nutrition and obesity researchers, evoked invariably to support the dogma that only calories count when it comes to understanding and treating human obesity.
This logic has been the lifeblood of the sugar industry. If sugar was uniquely toxic, in that it possessed some special property that made us respond to it by accumulating fat or becoming diabetic, then government health agencies would have to regulate it. If all sugar does is add calories to the diet, just as any other food does, then it is, in effect, benign. When the sugar industry embarked in 1956 on a nationwide advertising offensive to knock down reports that sugar is ‘fattening’, it did so on the seemingly sound scientific basis that ‘[s]ugar is neither a “reducing food” nor a “fattening food”’, as the industry advertisements explained. ‘There are no such things. All foods supply calories and there is no difference between the calories that come from sugar or steak or grapefruit or ice cream.’
Thinking of obesity as an energy-balance disorder is as meaningless as calling poverty a money-balance problem
Even 60 years later, in 2015, when The New York Times reported that academic researchers were doing the bidding of Coca-Cola by taking its money to fund a Global Energy Balance Network and ‘shift blame for obesity away from bad diets’, this was still the logic invoked in sugar’s defence: if you believe that obesity is caused by a mere caloric surplus, then the solution to the epidemic is not necessarily to avoid Coca-Cola, but to either consume it (and everything else) in moderation or to burn off the excess calories with physical activity. For the sugar industry and the purveyors, such as Coca-Cola, of sugar-rich foods and beverages, this remarkably resilient, century-old conception of why some of us get fat (or are born fat) and others don’t (or aren’t) has been the gift that keeps on giving.
So here’s another way to frame what is now the imperative question: is the energy-balance hypothesis of obesity correct? Is it the right paradigm to understand the disorder? The competing hypothesis has existed for over a century: in this paradigm, obesity is not an energy-balance disorder but a disorder of excess fat accumulation and so, clearly, a hormonal and metabolic disorder – the result of an ‘endocrine disturbance’, as it was phrased in the 1930s by Eugene Du Bois, then the leading American authority on metabolism. By this logic, the foods we eat influence fat accumulation not because of their caloric content but because of their macronutrient content, the proteins, fats and carbohydrates they contain. This paradigm attends to how organisms (humans, of course, in particular) orchestrate the careful ‘partitioning’ of the macronutrient fuels they consume, determining whether they will be burned for energy or stored or used to rebuild tissues and organs. It proposes that dysregulation of this exquisitely-evolved, finely-tuned homeostatic system (a system that is biologically balanced) is the necessary component to explain both the excessive storage of calories of fat – obesity – and the diabetes that accompanies it.
This alternate hypothesis implies that sugar has unique effects in the human body leading directly to both diabetes and obesity, independent of the calories consumed. By this way of thinking, refined sugars are indeed toxic, albeit over the course of years or decades. We get fat and diabetic not because we eat too much of them – although that is implied tautologically merely by the terms ‘overconsumption’ and ‘overeating’ – but because they have unique physiological, metabolic and hormonal effects that directly trigger these disorders. If all this is right, then thinking of obesity as an energy-balance disorder is as meaningless as calling poverty a money-balance problem (caused, of course, by earning too little or spending too much, or both). By conceiving of obesity as a problem caused by the behaviours of excessive consumption and physical inactivity, researchers not only took a physiological defect – the excess accumulation of fat, often to a massive extent – and turned it into a behavioural problem. But they made a critical error, one that has grown over the course of decades into an idea that seems too big to fail.”
“…obesity was clearly not a problem of energy balance, but of fat trapping (just as global warming is not an energy-balance problem, but an energy-trapping one). The question that had to be answered is why this trapping occurs. Any viable hypothesis of obesity had to explain why the fat tissue of the obese is so avid in hoarding calories as fat, rather than allowing that fat to be metabolised and provide energy for the body.
By 1930, Julius Bauer of the University of Vienna – the ‘noted Vienna authority on internal diseases’, as The New York Times called him – had taken up von Bergmann’s ideas, arguing that obesity had to result from a dysregulation of the biological factors that normally work to keep fat accumulation under check. Bauer argued that fat cells are clearly being driven by these factors to hoard excessive calories as fat, and this in turn would deprive the rest of the body of the energy it needed to thrive. In this hormonal/regulatory conception, excessive fat-accumulation causes hunger and physical inactivity, not the other way around.
Bauer likened the fat tissue of an obese person to that of ‘a malignant tumour or … the foetus, the uterus or the breasts of a pregnant woman’, all with independent agendas, causing them to take up calories of fuel from the circulation and hoard them or put them to localised use, regardless of how much the person might be eating or exercising. With obesity, wrote Bauer, ‘a sort of anarchy exists, the adipose tissue lives for itself and does not fit into the precisely regulated management of the whole organism’.”
“…Obese animals would frequently manifest what Newburgh might have described as a perverted appetite (technically, hyperphagia): as they grew fatter they would be exceedingly hungry and consume great amounts of food. But they would invariably get obese, or at least significantly fatter, even when they didn’t eat any more, or weren’t allowed to eat any more than control animals, often littermates, that remained lean. Some of these animals would remain excessively fat even as they were being starved.
Insulin partitions how we use the fuels we consume: it directs fat cells to store fat
Whatever the defect or fundamental fault that caused these animals to accumulate excessive fat, a perverted appetite (ie, overeating) could be ruled out. The defect had to be working either to cause the fat cells to hoard calories as fat, or to suppress the animals’ ability to burn fatty acids for fuel. Or both.
Not until the 1960s, though, would researchers elucidate the basic mechanisms of fat accumulation. To do so required invention of a technology that allowed researchers to accurately measure the level of hormones circulating in the bloodstream. This was the work of Rosalyn Yalow, a medical physicist, and Solomon Berson, a physician. When Yalow was awarded the Nobel Prize for the work in 1977 (by then, Berson was not alive to share it), the Nobel Foundation described it aptly as bringing about ‘a revolution in biological and medical research’. Those interested in obesity could now finally answer the questions on which the pre-war European clinicians could only speculate: what hormones regulate the storage of fat in fat cells and its use for fuel by the rest of the body?
Answers began coming with the very first publications out of Yalow and Berson’s laboratory and were swiftly confirmed. As it turns out, virtually all hormones work to mobilise fatty acids from fat cells so that they can then be used for fuel. The one dominant exception to this fuel-mobilisation signalling is insulin, which partitions how we use the fuels we consume: in particular, it directs fat cells to store fat, while facilitating the uptake and oxidation of glucose (blood sugar) by muscle and organ cells. In other words, when insulin is secreted – primarily in response to the carbohydrates in our diet – it directs our cells to burn carbohydrate as fuel and store fat. And so, the one biological factor necessary to mobilise fat from storage and have it used for fuel, as Yalow and Berson suggested in 1965, is ‘the negative stimulus of insulin deficiency’. Put simply, when insulin levels in circulation are elevated, we store fat and use glucose for fuel; as insulin levels drop, fat is mobilized and we burn it instead.”
Put more simply, when we eat carbs, especially sugar, it raises insulin levels and tells out body to STORE FAT. Carbs are BAD, Sugar is TOXIC level bad.
If interested, read even more at the full original article HERE or read Gary Taubes book:
The Case Against Sugar