Wednesday, 16 July 2014

Leptin and Gherlin

The Leptin, Ghrelin duo are a watershed for me. They're the only things I had no grasp or understanding about coming into FA. Not even sure whether I'd heard of them before. Leptin possibly.

My response to them has been monumental indifference. I simply cannot make myself give much of a fig about either. Despite someone winning a prize for the discovery of one of them. They've been described as hormones.

Leptin; "is a mediator of long-term regulation of energy balance," okay.  "...suppressing food intake and thereby inducing weight loss." Don't see why. "Suppressing intake" presumably, equals a dampening / switch off of hunger/appetite signalling. Why would that necessarily lead to weight loss, even over time?

Gherlin "... is a fast-acting hormone," fast? Okay.  "....seemingly playing a role in meal initiation."

Meal initiation? Seems oddly specific. Does that mean you proceed from hunger to actually "initiate" that's a meal or no? Anorexics can be agonized with hunger, but eating action fails between that and their "eat button."

My sketchy take on this lack of engagement is the 'obesity' crew have come up with very little of any use to any person fat or otherwise, apart from mainly the unethical and the unspeakable. I believe they're unlikely to do better anytime soon, if  many of them are even trying-more than for show.

Ob as a field of endeavour is doa-the arrival point being basic critical scrutiny or even, consciousness. It makes no sense to compartmentalize the study of metabolic function across size. Weight needs to be viewed as a (whole) spectrum. Defining fat people as disease is stupid. Studying biology in them to pathologize and justify that pre-decided branding, leads to obscuring of everyone's metabolic, that is biological function.

An obvious example is the assumption many have that weight rebound-after calorie restriction diet induced loss is specific to fat people. That its part of our purported failings as human beings (despite us already being robbed of that definition). When this can be observed in all people from thinner to fatter. Hence the former always losing the same 5, 10, 15, 30 etc., pounds.

Obviously if you rebound all the time whilst always being thin that isn't going to show. How can this confusion be a good thing? Seems like wasting the efforts of those who are putting the work in.

Hardly my idea of science.

Anyway. I happen to have clicked on the above link on some article or post and it lead to that paper.You can tell exactly what line it takes. "As a growing number of people suffer from obesity...." oh please. Studying mechanisms that have "influence on energy balance has been a subject of intensive research." That has amounted to what practical applications exactly?

Perhaps its shortness drew my eye. "In obese subjects the circulating level of the anorexigenic hormone leptin is increased, whereas surprisingly, the level of the orexigenic hormone ghrelin is decreased." Yeah, whatev's.
"It is now established that obese patients are leptin-resistant."

That was like a cattle prod. It's been "established" has it? On what basis? Immediate thought. Any chance its this? Yes, it seems thus. Because you expect a high amount of leptin in the blood to =less eats and fat people by (your) definition=too much eats. Ergo, ob must be resistant to leptin.

Naughty old obeses. Not only don't they listen to physics/their docs/everybody knows. Their blood is naughty too-it doesn't listen to its leptin.

It's leptin non-complaint.

Well, that's what happens when you turn people into biochemistry to make the ridiculous idea that they are disease look as if it makes sense. Well it does-to an army of self deluding bigots.

Let's just check the circulating leptin of people suffering from underweighcity, bet its as low as fatz is high, eh? Seems so; "Plasma leptin levels were significantly lower in underweight patients than those in normal weight patients and in healthy controls."

So, the action of the body regulating itself is bad on one end, because that's the bad end.

These papers are from 2007. Though the latter came after the former and there's nothing wrong with being wrong in pursuit of knowledge. This still indicates the underlying problem with framing, interpretation and presentation.

Rather than studying human metabolic function, through the weight to map out how it works overall. Discovering any pathology through digging that out, rather than seeking only to confirm your desired moribund hypothesis.

The former, gives all sorts of flexibility. It helps us to understand ourselves better and helps facilitate greater understanding of where and when things go awry.

Corrected or not though, why bother to create this unnecessary hurdle? What's the point of it? To police behaviour? To keep fat phobes nervous systems on high alert so they can keep thought on lockdown? You think science can take such and retain its integrity?

I still don't know exactly what leptin or ghrelin are for. I can't even buy completely into  the interpretation of insulin resistance.....yet.

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