Tuesday, 7 June 2016


There's a programme on tonight called "Horizon: Why Are We Getting So Fat?" Some guy in the guardian commented thus,
Dr Giles Yeo is the charming host of a fun but flabby grab-bag of theories on obesity......Yeo investigates the genes that make excess fat more likely, and looks at whether hormonal appetite suppressants might be the future. It’s meant to deflate demands to eat less and exercise more, but that often does prove to be the answer. Meanwhile, our emotional relationship with food is touched on too lightly.
Oh is it really you "flabby"-minded knobend? Well, that's tremendously in its favour. The mere prospect of this flatulent idiocy of emeaushuns being parked in a ditch of irreverence fills my heart with glee [that's an emo right?]

Yeo's article in the DM [don't click if you hate them] goes into more detail. The headline's instructive, "The jab that's almost as effective as a gastric bypass: Hormone injection 'tricks the body into thinking it's full'" I asked again to butch impersonating scientists, why go all Loki with physiology? Are you tricking it, or are you switching features up/down? Hunger is on a scale that must register anything from normal daily energy needs to environmental famine level ravaging. That's range.

According to himself, cutting out numerous stomachs has yielded,
.....that while gastric bypass reduces the absorption of some nutrients, the key reason for patients’ change in appetite is hormonal; because food is delivered farther down the gut in a form not normally seen, the gut responds by releasing a different mix of hormones, which then trick your brain into thinking you are full.
Sounds like Dr. Francesco Rubino,
Dr. Rubino's prior research has shown that the primary mechanisms by which gastrointestinal bypass procedures control diabetes specifically rely on the bypass of the upper small intestine — the duodenum and jejunum. This is a key finding that may point to the origins of diabetes. "When we bypass the duodenum and jejunum, we are bypassing what may be the source of the problem," says Dr. Rubino, who is heading up NewYork-Presbyterian/Weill Cornell's Diabetes Surgery Center.
Interesting, [genuinely!] It doesn't explain though, why both the loss and the effect can go into reverse in some who've had GBS. I wonder as I have for yonks whether this is part of a larger process-instigated by metabolic function, which works by altering the tissues, as a primary device or as a side effect.

And does this restoration mean where the food hits (the ilium?) also becomes changed like the bypassed parts of the gastrointestinal tract? And why would that change have stopped before that point pre-operation? Is that because that tissue also alters similarly as part of the body's inherent drive to restore CRIWL?

And what about the virtually missing stomach? It has also been stated that cells/tissue that most communicate with the brain are cut out (unsurprisingly) and that this is responsible for the loss of hunger. Is either or both responsible for the dampening of hunger?

Yeo's take that fatness is genetically mediated will please a lot of people. I wouldn't get too excited though, the key underlying question has always been that of biological mechanics. The emphasis on genes seems more about cementing the strange determinism underlying 'obesity' despite its much touted insistence that fatness is a temporary state.

He even says himself as they often do as a qualifier that genes don't matter when it comes to the law of slim and I agree in the sense that this doesn't answer the question of why the mechanics of the body-which produce all these chemicals can't produce them to alter metabolic function.

To put it another way, why must people be injected when there's no explanation as to why the body cannot be made to up or reduce its production of whatever hormones are required to prompt a change of outcome.

And don't bother to tell me it's genes, it isn't.

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