Same Calories – Different Results
For many years the common mantra was that ‘a calorie was a calorie’ and that our weight was determined by the simple ‘calories in-calories out’ formula. Conventional thought was that 3,500 extra calories eaten equaled a pound, or 450 grams, of fat on the body regardless of age, gender, race or familial attributes and that therefore being overweight was simply a matter of not enough willpower or being lazy.
As we know, this is not what happens in real life. I can vividly remember my mother and my brother complaining that they seemed to put on weight no matter what they did, while I ate everything in sight and was always slender. It was only when I met my real father in later life and saw that he was quite thin that the mystery was solved and I realized I had inherited what I called my father’s ‘skinny gene’ .
There is no doubt that our modern energy-dense Western diet and increasingly sedentary lifestyles have been the major contributors to the obesity epidemic, however there is now an increasing amount of scientific evidence to show that the picture is far more complex. While the basic premise of calories in-calories out is still at the heart of the issue, how much weight we actually gain is modulated by a complex interplay of genetics, our modern Western diet and differences in our metabolisms and how we process the food that we eat – much of which still remain a puzzle.
A recent headline-grabbing study by a team in Louisiana fed 12 pairs of lean identical twins 1000 calories per day above their usual intake in a highly controlled environment. While the twins in each pair gained the same amount of weight, the amount gained varied threefold among the pairs, leading researchers to conclude with certainty that there are genetic controls for not just how much people want to eat but also how much of what they eat turns to fat. Similar lab rat studies are drawing the same conclusions and it’s now known with certainty that specific random DNA mutations result in widely differing responses to food intake.
Even more importantly for modern humans there may be environmental effects on our genes known as epigenetic changes, that is changes to the stop-go signals stuck on the DNA which affect how the gene expresses itself.
The first evidence for epigenetic changes as a cause of obesity came from the Dutch famine in 1944-45, when the population was limited to 800 calories per day. Women who were pregnant at the time had low birth weight babies, who on the relatively abundant post-war Dutch diet showed a high prevalence of being overweight, meaning the ‘set points’ for hunger and satiety were being programmed by their exposure to maternal calorie restriction.
Since then, there have been a lot of animal studies and some human studies with two other causes of intrauterine programming leading to obesity in humans being identified. One is maternal diabetes, either pre-existing or developing during pregnancy. The offspring have on average higher than normal birth weights and this higher than normal weight status tends to be maintained. Very recently, a protein-deficient maternal diet during pregnancy, as is not uncommon in developing (and some developed) countries, has been shown to produce overweight offspring despite adequate maternal total calorie intake.
In animals, additional maternal interventions (high fat diets, high stress hormones) have been shown to increase offspring weight, although whether this is the case for humans is still not proven.
Added to the subtle but powerful genetic changes our environment is exerting on us, research lately into our high-sugar diets is also revealing some startling information. Insanely cheap but incredibly energy-dense high-fructose corn syrup now finds its way into an ever-increasing number of our daily food items, even those we least expect. Fructose is entirely processed through the liver, which may not be able to metabolize it fully, depleting vital chemicals in the organ and turning into fat. “It’s not about the calories,” says one researcher. “It has nothing to do with the calories. The fructose is a poison by itself.”
What is undeniable is that problems in the liver in turn contaminate and disable other systems, including the insulin production of the pancreas leading to high insulin levels in the blood and a condition known as ‘insulin resistance’. It is now known that in addition to contributing to a number of medical conditions, high insulin levels interfere with the hormone leptin, the signaling device that tells the brain when we’ve consumed enough. So we drink or eat fructose and then we want more – with the inevitable result. The resulting sky-high insulin levels are now thought to be implicated in a wide range of disease entities including the peculiarly modern entity “metabolic syndrome” (a cluster of medical conditions including hypertension, type 2 diabetes, central obesity and dyslipidemia) as well as cardiovascular disease, premature ageing, reduced longevity, and as some recent research may show, Alzheimer’s disease.
Although major food companies hotly contest this information, the inescapable fact is that food additives such as high fructose corn syrup are providing us with massive amounts of energy which we simply don’t need and are making it impossible in subtle metabolic ways for people to do anything other than gain weight.
Today we’ve gone from a society where most people were of ‘normal’ weight and getting enough food was the issue, to a society where the opposite is the problem. This combined with genetic modifications which influence how much we eat and how we process it – modifications which are brought on themselves by changes in our eating habits – and our couch potato lifestyle have had devastating results which affect our society deeply at every level. The end result is a society which is not only increasingly overweight but increasingly unwell, with many people rendered almost incapable of making the required changes, so profound and wide-reaching are the effects of our changed world.
In next month’s article I’ll look at the weight loss industry and various strategies for losing weight – and trying to keep it off.
Dr Sheena Burnell is an Australian-trained doctor currently living and working in Shanghai, China. Her primary training is in anaesthesiology however she is also trained in cosmetic medicine which she has mainly practised since coming to China. Her latest role is Director of Asia Healthcare Consultants, a boutique consultancy specialising in introducing Australian healthcare companies to the China market. She is also a wine educator and a noted specialist on Chinese textiles.