The science of obesity: what exactly makes us fat?
New research shows that overeating may not be the cause of obesity. It could be due to a metabolic reaction brought on by certain types of sugars, says Jeanette Wang
It's a logical equation: if you earn more money than you spend, you'll have cash in hand. Likewise, if you consume more calories than you expend, you'll be carrying extra calories - and therefore put on weight, right?
Wrong - according to a recent article in the journal BMJ, the obesity equation isn't that straightforward. Gary Taubes, co-founder of the Nutrition Science Initiative in San Diego, says the history of obesity research is one of two competing hypotheses - and that the wrong hypothesis won.
This "energy balance" hypothesis - that overeating is the cause of obesity - along with substandard science, has exacerbated the obesity crisis, and the related chronic diseases, Taubes says. He thinks another look at the causes of obesity is needed, if we are to make any progress with the crisis.
In Hong Kong, as in most countries, obesity is on the rise. About 37 per cent of the population aged 18 to 64 were classified as overweight or obese (a body mass index of 23 and above), including 18.8 per cent as obese, in last year's Behavioural Risk Factor Survey.
A person's beliefs about causes of obesity can affect one's weight, a new study published in the journal Psychological Science has found.
From an initial online survey, researchers Brent McFerran of University of Michigan and Anirban Mukhopadhyay of Hong Kong University of Science and Technology discovered that people seem to subscribe to one of two major beliefs about the primary cause of obesity: poor diet or a lack of exercise. In a series of studies in South Korea, the US and France, the researchers found that people who viewed diet as obesity's primary cause had lower body mass indexes than those who implicated lack of exercise.
They studied Hongkongers and found that participants who were primed to think about the importance of exercise ate more chocolate than those primed to contemplate diet. A Canadian study showed that participants who linked obesity to lack of exercise ate significantly more chocolates than those who linked obesity to diet.
The "energy balance" hypothesis, Taubes says, is largely the product of the influential thinking of two physicians - the German diabetes specialist Carl von Noorden at the beginning of the 20th century, and the American internist and clinical investigator Louis Harry Newburgh, a quarter of a century later.
"Its acceptance as dogma came about largely because its competing hypothesis - that obesity is a hormonal, regulatory disorder - was a German and Austrian hypothesis that was lost with the anti-German sentiment after the second world war, and the subsequent embracing of English, rather than German, as the lingua franca of science."
But does aberrant behaviour really cause obesity? The endocrinological hypothesis rejects this, says Taubes. The hypothesis is based on two distinct ideas, the first dating back to 1923 by Wilhelm Falta, a student of Von Noorden and a pioneer of the science of endocrinology. Falta believed that the hormone insulin was driving obesity.
The second idea, based on the concept of lipophilia, or "love of fat", was proposed in 1908 by Gustav von Bergmann, a German authority on internal medicine, and then taken up by Julius Bauer, who did pioneering work on endocrinology, genetics and chronic disease at the University of Vienna.
Observing that fat deposition was not uniform throughout the body, Von Bergmann proposed that people who are constitutionally predisposed to fatten had adipose tissue that was more lipophilic than that of constitutionally lean individuals.
New research supports this idea of a metabolic link with obesity. In a study published in January in Nature Medicine, an international team of researchers led by the Joslin Diabetes Centre - Harvard Medical School in Boston suggest that obesity is the result of an alteration in the processes that regulate food absorption and energy production. This alteration tips the balance towards excessive storage of fat.
The scientists observed that blocking the expression of a certain gene in mice protects them against obesity and insulin resistance. The gene was found to modulate fat storage by regulating energy expenditure and lipolysis, the process which transforms fat into lipids for the body's energy consumption.
Another study, by University College London published in March in International Journal of Obesity, found a strong genetic component to childhood obesity, supporting the hypothesis that children of obese parents are most at risk of becoming obese. Previous research has shown that obesity runs in families, with heritability estimates at over 50 per cent.
Obesity evolved into an eating disorder in the late 1960s and 1970s, Taubes says. Lab researchers focused - and still do - on identifying why we eat too much, rather than why we store too much fat.
"What makes this transition so jarring in retrospect is that it coincided with the identification of the hormone insulin in the early 1960s as the primary regular of fat accumulation in fat cells," he says. "Had Falta's ideas and the lipophilia hypothesis survived the second world war, this discovery would have served to bring these two hypotheses together.
"Because serum insulin levels are effectively driven by the carbohydrate content of the diet, this hypothesis would implicate refined, high glycaemic grains and sugars as the environmental triggers of obesity. They would be considered uniquely fattening … because they trigger a hormonal response that drives the partitioning of fuel consumed into storage as fat."
Not all calories are created equal. For example, with sugary beverages, the metabolism of fructose in the liver is believed to circumvent leptin signalling, leading to excessive consumption of these drinks. Fructose metabolism may also induce insulin resistance, leading to raised insulin levels and trapping fat in fat cells.
In 2009, the American Heart Association published a paper suggesting that excessive consumption of sugar is linked to several metabolic abnormalities and adverse health conditions.
It stressed a limit of 100 calories a day from added sugar for a woman (six teaspoons) and 150 calories a day for a man (nine teaspoons). Since that publication, several studies have implicated sugar consumption with increasing rates of obesity and type-2 diabetes.
A study by University of Guelph researchers presented in May at the Canadian Neuroscience Meeting showed that high fructose corn syrup, a common sweetener added in processed foods, can cause behavioural reactions in rats similar to those produced by drugs of abuse such as cocaine.
The experts say this suggests that food addiction could explain, at least partly, the obesity epidemic.
Highly processed carbohydrates were also implicated in a study published in the American Journal of Clinical Nutrition last month.
A Boston Children's Hospital research team found that having such foods caused an initial surge in blood sugar levels, followed by a steep crash hours later.
This decrease in blood glucose was associated with excessive hunger and intense activation of the nucleus accumbens, a critical brain region involved in addictive behaviour.