Fri, Sep-18-09, 11:09
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Here is a quote from GCBC (p. 349).
Please note that the defect he talks about here does not have to be genetic, but could be caused by anything. It's our job to disprove this hypothesis. No one has been able to at this point. So it is still valid.
Quote:
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.
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The quoted hypothesis above is not necessarily about carbs. It's about how our metabolism works. How our homeostasis is maintained, etc... Until dis-proven it stands. Personally, I think it's future proof. Whatever is causing the effects described in it.
It's bigger than insulin alone or whatever stimulates its secretion.
Patrick |
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