Quote:
Scientists got an unsparing look at what they were up against 50 years ago, when a clinical researcher at Rockefeller University, Dr. Jules Hirsch, did some old-fashioned experiments. He recruited obese people to stay at the hospital and subsist on a 600-calorie a day liquid diet until they reached a normal weight.
The subjects lost 100 pounds on average, and they were thrilled. But as soon as they left the hospital, the pounds piled back on.
Dr. Hirsch and Dr. Rudy Leibel, now at Columbia University, repeated the study again and again, with the same result. Eventually, they found that when a very fat person diets down to a normal weight, he or she physiologically comes to resemble a starving person, craving food with an avidity that is hard to imagine.
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There
is a difference here. Often on a very low calorie diet, after a few days, obese people will report back that they don't experience much in the way of discomfort--in fact they might be less hungry than if they were on a more moderate calorie-restricted plan. Maybe because of the reduction in insulin, fasted and postprandial? Leptin was mentioned--in a weight reduced person, leptin can be much lower. A skinny person inappropriately put on that 600 calorie a day plan will wind up with much lower leptin levels. But look at studies with obese subjects--it goes down much less. This is because leptin is not just about fed status, it's also about body fat status.
Okay, so that's active weight loss, during which calories are very low. Key here I think is that thing where appetite reduces during fasting or the very low calories. Just eating a little bit less than usual would also decrease insulin--but not by as much. There is also data showing that these approaches sort of change the activity of ghrelin and its effect on hunger. Ghrelin has a role in the regulation of glucose, animals on high carb diets suffer reactive hyperglycemia if ghrelin isn't there to stimulate postdigestive secretion of growth hormone, glucagon etc. It also has some more direct roles to play, stimulating hunger in that same part of the brain vaguely alluded to in Gina Kolata's article. Since fasting, very low calorie diets, and ketogenic diets decrease the role of glucose in the metabolism generally, and take people off that glucose roller coaster, there's less of a role for a counterregulatory hormone like ghrelin to prevent the hypoglycemic dips.
Body acting like a starving person's--okay, I get that to some degree. If I eat a diet of pizza and ice cream at my current weight, I'll be hungrier then I was when I ate that way at my top weight, tend to binge more than I did when I was at my fattest. Or make that a wholesome diet of lowish fat banana bread, oat meal and skim milk. Even just eating a more hedonic, typical Atkins diet but with more cheese and nuts, I'll experience this, although years of doing this tells me I won't get as fat as if I'm eating those carbohydrates.
Even on the calorie restricted low fat diet, and my Dad's experience matches for this--I would be hungrier for a few days, but then my appetite would decrease. I think this still fits into the insulin hypothesis. Taubes has suggested in the past that calorie restriction generally means some carb restriction, because that's largely what people eat these days. Well, okay, but with fat intake around 35 percent, there's still room for a fairly substantial decrease in calories on a very low fat diet without dipping much into carbohydrate intake. And decreased fat intake can decrease the insulin response to a carbohydrate load.
I think of it as the lobster trap of weight loss--most approaches to weight loss involve a decrease in insulin, more vigorous approaches might decrease insulin more and make things easier--but some of these vigorous approaches, the non-ketogenic ones, by definition require a higher intake of insulinogenic food (even a ketogenic diet is more insulinogenic than fasting) in maintenance than during the weight loss itself.
Why Are We Still So Fat?
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