Fat Metabolism and Obesity: What the Regulation of Our Fat Tissue Implies about Why We Gain Weight and How We Can Lose It
The science of fat metabolism is, oddly, not very controversial. As science writer Gary Taubes points out in an eloquent video lecture, by 1965, researchers had essentially worked out the biochemistry of our fat tissue. Since that time -- more than four decades ago -- the story hasn't changed significantly.
Taubes also points out the tremendous disconnect between the science of adipose tissue regulation -- which deals with the biochemistry of what goes on at the level of our fat cells and hormones -- and the science of nutrition and public health.
The Caloric Balance Hypothesis says that we get fat when we overeat and don't do enough activity, and we lose weight when we restrict calories and increase our activity.
The Lipophilia Hypothesis says that fat metabolism derangement causes excess calorie consumption. Something drives our fat tissue to be out of whack, if you will, and then the fat tissue acts to preserve itself at its inflated level -- even at great cost to the rest of you.
Which of these hypotheses makes the most sense in terms of describing how we accumulate fat?
The Caloric Balance Hypothesis tells us that fat accumulation and mobilization is a matter of simple accounting. Fat is like a piggybank. When we eat 500 calories more than we should -- when we indulge in a 500 calorie slice of chocolate cake, for instance -- those 500 "extra" calories get deposited right into our bellies or our thighs or wherever. When we go to the gym the next day and hop on the Stairmaster, we burn off those 500 calories and thus keep from getting fat.
The Lipophilia Hypothesis tells us that fat accumulation and mobilization involve complex biochemical interactions at the level of our fat tissue. Glucose, insulin, the enzyme lipoprotein lipase, and a molecule called alpha glycerol phosphate all play key roles. Calorie counting is irrelevant.
So can Lipophilia be validated. Do insulin and glucose, for instance, actually affect fat metabolism?
In fact -- and this is the bizarre part -- evidence abounds to show that they do. And it's not even controversial evidence.
1. Insulin is lipogenic. In other words, it causes us to store fat. Here is a randomly selected article which confirms this idea: "Insulin action on adipocytes. Evidence that the antilipolytic and lipogenic effects of insulin are mediated by the same receptor."
That may sound like nonsense "science-speak." So let's translate. What that says is that the hormone insulin drives the creation of new fat and prevents fat from being broken down.
2. Here's another article from the National Institute of Health archives -- The Journal of Biochemistry from 1972. "The immediate effects of insulin and fructose on the metabolism of the perfused liver. Changes in lipoprotein secretion, fatty acid oxidation and esterification, lipogenesis, and carbohydrate metabolism."
3. Here's another one, "Opposite effects of insulin and glucagon in acute hormonal control of hepatic lipogenesis."
These articles drive home the point that insulin is a lipogenic agent. It makes us fat. It controls fat metabolism.
But how can insulin make us fat if excess calories make us fat? This is a disconnect, a contradiction, a paradox.
Caloric Balance tells us explicitly that "Calories In" and "Calories Out" regulate fat tissue accumulation. So how can insulin play any role -- let alone the role prescribed precisely by the competitor hypothesis, Lipophilia?
The answer is, it can't. Caloric Balance tells us nothing about fat metabolism. It tells us nothing about the hormonal regulation of the adipose tissue. It says nothing about why and how and where we accumulate fat and why some of us accumulate fat while others don't.
How can one conclude that this hypothesis is anything other than untenable, preposterous, and possibly even dangerous?
And yet this hypothesis serves as the foundation for all our dietary wisdom.