Thursday 10 May 2012

Fat tissue growth drives over-eating

NOT the other way around.

This is why Taubes is smarter than those who ridicule him. He understands the logic, and has the cause and affect the correct way around. Unlike people such as Guyenet, who think that the obesity epidemic is caused by our average increase in calorie consumption of ~400 per day. What makes Guyenet so sure he has his cause and affect the right way around? Maybe our average calorie intake has increased BECAUSE we are fatter, and maybe we are fatter BECAUSE our food is more insulinogenic than it has ever been.

Does an increase in salary ( income ) of $4000 encourage you to go to the bank and take out a loan? That doesnt make any sense does it? If were getting paid more money, why would we need a loan from the bank?

Alternatively

What does taking out a loan from the bank do? It encourages us to ask our boss for a $4000 increase in salary to help us make the monthly payments on said loan.

The increase in debt ( fat tissue ) causes us to seek increased income ( food intake )

This gets all the more serious when you realise that taking on a loan as debt creates an obligation, you are obligated to repay it. Fat tissue is the same, when new fat tissue grows, you are obligated to maintain it, fat cells do not like to be atrophied.

The monkey study also offers very good evidence for my argument. They administered drugs to obese monkeys that caused apoptosis in their fat tissue, the result was a DECREASE in food intake and probably also an INCREASE in energy expenditure. ( as spoken of in the rodent study )

If gluttony and sloth was the driver of obesity, you would of expected these monkeys to continue their old eating habits. Right? Afterall, they were fat because they were gluttons, right??, and surely melting off some of their fat tissue shouldn't change their lack of "will power" to stop themselves over-eating, should it?

BTW, the researchers in that study appear to have violated the first law of thermodynamics and made some calories vanish. If you destroy a bunch of fat cells by apoptosis, all that fat they are carrying has to go somewhere, right?

Given the rapid loss of adipose tissue over a short period of time, one might have expected an abnormal increase in serum-free fatty acids and possibly dyslipidemia because of rapid fat mobilization. Surprisingly, free fatty acid concentrations showed a decreasing trend throughout the treatment interval
Damn, where the fuck did those calories go??!?

With the rapid reduction in white adipose tissue observed, the possibility of abnormal fecal elimination of lipids was considered.
Maybe the monkeys shit them out?! Usually when you take orlistat the side affects are quite apparent, they include
oily stools, flatulence, fecal incontinence, and diarrhea.
OK, I got a plan, lets see what kind of mess the monkeys leave when they go to bog room.....

the absence of these side effects was considered inconsistent with increased fecal elimination of lipids
Damn! (In other words, the researchers have no idea where the calories went. They lost em. Lesson learnt, Never trust a medical researcher with your calories!)

2 comments:

  1. If ASPLODING the fat cells resulted in monkies being adverse to their insulinogenic monkeychow, the drop in FFA may be reflected in their oral food intake decreasing more than their fat release from fat tissue. A fasting monkey eating no sugar makes no fat, and is insulin hypersensitive. This is also to be expected, at least temporarily, until leptin gets involved and long term body weight regulation has its say.

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  2. It doesn't make any more sense that somebody would one day just randomly consciously decide to eat too much for no biochemical reason any more than it makes sense that they would decide to breathe, drink, urinate, defecate etc. more for no reason. There has to be a plausible biological mechanism underpinning any drastic change in such basic physiologic processes. It's called DISEASE.

    Taubes gets it (and this is his crucial insight, not the carb thing), whereas the research community does not.

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