Let me guess. You're going to lose weight. Let me guess again. You won't succeed for long. The standard approach, the one that almost always fails, is to treat weight as an exercise in accounting.
I call it the ''federal budget'' approach. If only the Treasurer spent a little less money each month or took in a little more tax, the deficit would shrink. If only you or I took in a little less food each month or did a bit more exercise, our tummies would shrink.
It ought to be true because it's a truism: energy in equals energy out plus weight gained. But the equation tells us nothing about the mechanism. Cutting your energy going in (by eating less) might just as easily cut your energy going out (by making you lethargic) as it would cut your weight. And even if it did cut your weight, a few weeks later you might find yourself getting ravenously hungry and getting your weight back. It's what usually happens. It is why we keep making the same resolution each December 31.
What if there is something else - something not in the equation - which is driving all three parts of it, just as the broader economy drives the budget? It's not exactly a far-fetched idea. We used to think that stomach ulcers were caused by stress, until in 2005 two Australian researchers were awarded a Nobel prize for discovering the real cause - a bacterial infection.
We know that hormones trigger growth in children. During growth spurts they eat more and exercise less, but only in the trivial sense is it true that eating causes their growth. It would be just as true to say that growth causes their eating, more true to say that both are caused by something else.
Hormones drive the development of breast and buttock fat in women at puberty. They drive hunger during pregnancy.
Is it really so unlikely that they could also drive how much we eat, how much we exercise, and how much we store as fat?
We don't need to look far to find the hormones involved. Insulin, and its partner leptin, drive the packing and unpacking of fat cells and the signals that tell our brain it has had enough and is no longer hungry. Each responds to sugar.
And please don't tell me sugar is ''a natural part of life'', as the ads used to say. In his massively viewed YouTube lecture Sugar: The Bitter Truth, childhood obesity expert Robert Lustig makes the point that until relatively recently pure sugar was inaccessible, protected by either fibre (sugar cane is extraordinarily tough) or bees.
Ordinary sugar is half glucose and half fructose. There are about 16 teaspoons in a 600 millilitre drink. The glucose triggers a surge of insulin that packs fatty acids into fat cells and temporarily prevents them getting out. It also directs glucose to muscles where it is stored as glycogen. The fructose helps build insulin resistance and also resistance to leptin, the chemical messenger that turns off the feeling of hunger. The greater our exposure to fructose, the longer we feel hungry and the more insulin we produce, directing fat to our fat cells (fructose itself is turned into fat).
Lustig says Americans are producing twice the insulin they were 25 years ago.
None of this would matter much if it was merely making us big, but it is also driving high blood pressure, strokes and heart attacks. It's helping kill us.
In September the international investment bank Credit Suisse wrote to clients comparing sugar to tobacco. ''There is not a single study showing that added sugar is good for you,'' it said.
Credit Suisse says what worked for tobacco will work for sugar. Extra taxes on full-calorie soft drinks should quickly cut consumption; all the more so because unlike cigarette manufacturers, soft drink makers already provide healthier alternatives.
We are likely to be told repeatedly that the science isn't settled, that we need more research. And we are likely to keep remaking the same new year's resolution.
~Thanks to Peter Martin
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