Since Greenwood proposed this LPL gatekeeper hypothesis, researchers have reported that obese humans have increased LPL activity in their fat tissue. They’ve also reported that LPL activity in fat tissue increases with weight loss on a calorie-restricted diet and it decreases in muscle tissue; both reactions will work to maintain fat in the fat tissue, regardless of any negative energy balance that may be induced by the semi-starvation diet. During exercise, LPL activity increases in muscle tissue, enhancing the absorption of fatty acids into the muscles to be burned as fuel. But when the workout is over, LPL activity in the fat tissue increases. The sensitivity of fat cells to insulin will also be “sufficiently altered,” as the University of Colorado physiologist Robert Eckel has described it, so as to restock the fat tissue with whatever fat it might have surrendered.

The open question, as Eckel wrote, is whether the particular hormonal environment that leads us to regain weight once we’ve lost it—elevated LPL activity on the fat cells and decreased LPL activity in the skeletal muscle—is the same as the one that leads us to grow fat to begin with. If insulin drives obesity, then this is an obvious hypothesis. There is no evidence to refute it, so it must be taken seriously. It has to be noted, too, that carbohydrate-rich meals increase LPL activity in the fat tissue, which would be expected, because they increase insulin secretion as well. Fat-rich meals do not. And so, as Eckel, a recent president of the American Heart Association, has put it, “habitual dietary carbohydrate intake may have a stronger effect on subcutaneous fat storage than does dietary fat intake.”

Since none of this research is particularly controversial, it’s hard to imagine why obesity researchers would not take seriously the hypothesis that carbohydrates have a unique ability to fatten humans—or, as Thomas Hawkes Tanner put it in The Practice of Medicine almost 140 years ago, that “farinaceous and vegetable foods are fattening, and saccharine matters are especially so.” Researchers who study carbohydrate metabolism have found this science compelling. In 1991, the Belgian physiologist Henri-Géry Hers, an authority on what are known as glycogen-storage diseases, one of which is named after him, put it this way: “Eating carbohydrates will stimulate insulin secretion and cause obesity. That looks obvious to me….” But this simple chain of cause and effect has nonetheless been rejected out of hand by authority figures in the field of human obesity, who believe that the cause of the condition is manifestly obvious and beyond dispute, that the law of energy conservation dictates that obesity has to be caused by eating too much or moving too little.