Pennington proposed that a metabolic defect is what causes obesity in humans. The adipose tissue amasses fat calories in a normal manner after meals, but it doesn’t release those calories fast enough, for whatever reason, to satisfy the needs of the cells between meals.

By hypothesizing the existence of such a defect, Pennington was able to explain the entire spectrum of observations about obesity in humans and animals simply by applying the same law of energy conservation that other obesity researchers had misinterpreted. The law applies to the fat tissue, Pennington noted, just as it does to the entire human body. If energy goes into the fat tissue faster than it comes out, the energy stored in the fat tissue has to increase. Any metabolic phenomenon that slows down the release of fat from the fat tissue—that retards the “energy out” variable of the equation—will have this effect, as long as the rate at which fat enters the adipose tissue (the energy in) remains unchanged, or at least does not decrease by an equal or greater amount. Fat calories accumulating in the adipose tissue wouldn’t be available to the cells for fuel. We would have to eat more to compensate, or expend less energy, or both. We’d be hungrier or more lethargic than individuals without such a defect.

Pennington suggested that as the adipose tissue accumulates fat its expansion will increase the rate at which fat calories are released back into the bloodstream (just as inflating a balloon will increase the air pressure inside the balloon and the rate at which air is expelled out of the balloon if the air is allowed to escape), and this could eventually compensate for the initial defect itself. We will continue to accumulate fat—and so continue to be in positive energy balance—until we reach a new equilibrium and the flow of fat calories out of the adipose tissue once again matches the flow of calories in. At this point, Pennington said, “the size of the adipose deposits, though larger than formerly, remains constant: the weight curve strikes a plateau, and the food intake is, again, balanced to the caloric output.”

By Pennington’s logic obesity is simply the body’s way of compensating for a defect in the storage and metabolism of fat. The compensation, he said, occurs homeostatically, without any conscious intervention. It works by a negative feedback loop. By expanding with fat, the adipose tissue “provides for a more effective release of fat for the energy needs of the body.” Meanwhile, the conditions at the cellular level remain constant; the cells and tissues continue to function normally, and they do so even if we have to become obese to make this happen.

This notion of obesity as a compensatory expansion of the fat tissue came as a revelation to Pennington: “It dawned on me with such clarity that I felt stupid for not having seen it before.” By working through the further consequences of this compensatory process, Pennington said, all the seemingly contradictory findings in the field suddenly fit together “like clockwork.”

This defect in fat metabolism would explain the sedentary behavior typically associated with obesity, and why all of us, fat and lean, will become easily fatigued when we restrict calories for any length of time. Rather than drawing on the fat stores for more energy, the body would compensate by expending less energy. Any attempt to create a negative energy balance, even by exercise, would be expected to have the same effect.

This was the metabolic defect that causes obesity, he said, and it could apparently be corrected or minimized by removing carbohydrates from the diet.

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Quoted from Good Calories, Bad Calories by Gary Taubes.

Patrick

Which page is that?

Hardcover edition, page 349 near the bottom and page 350.

Patrick

Thanks. It does explain everything, doesn't it? Fat tissue grows bigger when its ability to release fat is compromised or limited. As it grows bigger, its ability to release fat also increases proportionately. This goes on until it reaches a size/ability that matches the rate at which it takes in fat. This implies that the rate at which it takes in fat is limited by something else, probably the gut. The reverse is true for diabetics type 1.

It allows us to speculate on the fat tissue's other functions like retarding aging due to its ability to continue to take in glucose when all other tissues are insulin resistant thereby preventing them from suffering the aging effects of hyperglycemia. Or serving as a toxic buffer where toxins are stored temporarily.

Yep, it's my favorite quote from the entire book !

And like you said, it leaves space for researchers to work in their own hypothesis of the details.

Patrick

This makes way more sense than the simplistic insulin model. I remember an expert on obesity like Michael Schwartz explaining technically why insulin resistance is a mechanism to prevent further weight gain, so it couldn't possible lead to overweight or obesity. Reduced insulin secretion is a predictor of the tendency to gain weight. Besides insulin is secreted in huge amount when meat or whatever other protein is consumed (I know people with diabetes who have to bolus more for proteins than carbs) and fat storage is even then independent of insulin.

Like I said before Dorian, Taubes explains it all better than me. It's a great book, but don't take my word for it, everyone with a taste for science needs to read it all by themselves to understand the complete hypothesis.

Anyway, it still comes down to the fact that the calories we intake do not matter by themselves. My girlfriend is really thin but with an athletic body (5' 7" and 112 pounds) and she eats a lot more than me and all the carbs she wants. Her father is exactly the same way too, very thin and athletic, and he can eat a whole pecan pie by himself for dessert. It really pisses me off sometimes.

Patrick

OMG -- pecan pie? I can barely remember what it tastes like, but I'm drooling, LOL -- I would love to have that type of metabolism, and I wish they knew whether one could achieve that type of metabolism through special dietary means.

There is no distinction between the simplistic insulin model and this one. They are one and the same. The difference lies in the depth of explanation, i.e. "carbohydrate drives insulin drives fat accumulation" is the simplest form of the two.

Indeed, the simplistic insulin model comes from the same book, Good Calories Bad Calories by Gary Taubes. If you haven't read it yet, you should. I think that it will also prompt you to rethink a few of your statements about insulin just now.

It's a completely different model. Insulin doesn't drive anything arbitrarily unless there's an excess to stock. Several studies have shown that people with hyperinsulinemia don't store more fat of an isocaloric diet than people with normal insulin levels, in fact even injecting insulin directly didn't increased fat storage. Proteins drives insulin often more than carbs, which is why diabetics individuals must often bolus more for proteins rich foods than carbohydrates. Pennington model explains a defect where lipogenesis is faster than lipolysis and because of this an adaptation is required to prevent a total (maybe deadly) lack of energy for the invidial where adopicites becomes bigger and hence the instruction for the body becomes to store fat (regardless of insulin levels) Your model just claim that a transporter hormone arbitrarily makes everyone's body store fat for everyone just by being released, which of course is not even remotely true.

I had never heard of the so-called "honeymoon period" mentioned below - perhaps that is precisely why so many people have such difficulty reversing obesity - maybe their entire immune system has become deranged.



Technology Review: Immune Overhaul for Diabetes

http://www.technologyreview.com/biomedicine/22465/

That's why I like Pennington's explanation. It's future proof. We can augment the minutia details with time to explain the exact way it all happens. But in the end his hypothesis still says that we do not become obese just by eating too much, it takes a defect, whatever causes it. The causes becomes important when we want to correct the defect. That's were low-carbing might come into play.

Patrick

Dorian, seriously, read the book. Otherwise we'll just be spending our time correcting your misinterpretation of something you didn't read. Further, it ain't my model, it's a model.

Hmm. Well not to flog a dead horse some MORE, why is it that some people can finally lose weight by lowering protein intake and increasing fat (and possibly carbs shock horror)? If 'excess' protein did not induce insulin release, this wouldn't happen - in fact the opposite should happen.

How do you explain that Martin? I know Taubes doesn't touch on this subject - or if he does he refutes it, but I've seen this happen in a lot of people. I don't think you can ignore that. Don't you think there is the slightest possibility that GCBC is not the Holy Bible of low-carbing on ALL aspects?

I'm curious why you are extremely stubborn on this one point, which could be very important for people who are flat-out stalled in their fat-loss on a low-carb diet.

Not trying to pick a fight by the way.

I think Martin already knows that an excess of protein can stimulate insulin secretion. I mean, we all know that an excess of protein is converted to glucose. Anyway, I don't want to reply in your stead Martin of course.

Patrick