In what I consider the pinnacle of Ouroboros logic, today's CEDNEC award goes to a group of scientists who have declared that being fat is what makes people fat.
Proving that stupid news races around the world much faster than the beleaguered Olympic Torch, the story comes from Popular Science, The BBC, and CTV British Columbia. Each features the requisite scare-pic that have become almost stock; a headless fat caucasian belly in as unflattering a pose as possible. At least Popular science shows some originality here; their picture is a closeup of frying bacon that will turn any vegetarian an interesting shade of green. Even the fat ones :-)
The Canadian researchers claim that abdominal fat cells produce a hormone (Neuropeptide Y, dubbed NPY). They claim that "NPY increases fat cell number by stimulating the replication of fat cell precursor cells, which then change into fat cells."
Their theory is that this appetite-stimulating hormone is released by the belly fat, triggering excess hunger, causing the fat person to overeat, creating more fat from the precursor cells created by the NPY.
The researchers are, apparently, all ways of giggly over the "possible therapeutic applications" of this discovery (i.e. drugs that block NPY production or uptake, i.e. appetite suppressants).
I don't even know where to begin with this one. Maybe the entire underlying premise that fat people eat more than thin people? Maybe. That's a good start at any rate. Many studies have actually started out with the determined intention to prove that fat people eat more (on average) than thin people, but could not do so. Of course we all know (either personally or anecdotal) a fat person who does eat a lot. We also know a thin person who can pack away four-square plus snacks and never put on an extra pound. That's what "on average means." But, of course, these researches must have some secret hidden (unreferenced) knowledge that shows every fat person secretly binges hourly on cartons of baby-flavored donuts cooked in bacon fat and topped with double cream...all in the thralls of overactive appetite hormones. My goodness, all this time and what we really needed was another unproven, theoretical new appetite suppressant. Because anorectics are such an innovative and never-before-tried method of losing weight. And oh-so effective. Evidenced, of course, by the fact that they've been around for over a century and look at how fewer fat people there are.
Oh, and I love how they assume actual binge-disorder eating has anything to do with physical hunger. What are these, high-school biology students?
But effectiveness has rarely stopped the pharmaceutical diet industry, and when the research institute behind the study (Lawson Health Research Institute) lists it's "Worldwide Business and Industry Partners" as: "including large corporations such as Bayer, Eli Lilly, Fujisawa, GE Medical, GlaxoSmithKline Inc, Medtronic, Merck Frosst Canada, Novartis, Pfizer, Schering...." You really have to wonder whether the science behind this was ever actually intended to be disinterested.
9 comments:
I agree, the science as reported is dumb. But it makes sense that the body would want to conserve fat (because 250,000 years of evolution, give or take, knows that FAT = LIFE when food is scarce.) What's dumb is trying to do an end-run around a perfectly sensible, functional evolutionary advantage.
The biggest problem I see with this is that everyone, even anorexics, have some abdominal fat. Therefore, if this were, in fact, the cause of obesity, EVERYONE should be getting hungrier, put on a little more weight, eat more, put on more weight and never stabilize. EVERYONE would have to develop intense self control and rigid portion control, even in the face of increased hunger not to get fat.
It would be barely possible that anorexic MEN would be able to circumvent this endless loop, but even anorexic men have SOME abdominal fat. Even anorexic women would have a problem staving off the hunger created by their abdominal fat because women have a higher body fat percentage than men.
One wonders how belly fat is different from breast fat, ass fat, thigh fat and brain fat that these parts don't also contribute to the never ending loop.
So we have X number of fat cells as adults, and they either enlarge or shrink, depending on whether energy is being stored or burned in excess. Why would the cell becoming larger by storing more globules make it behave completely differently? How do they know they're going up to the brain at all? What's the mechanism for fat communicating with the brain?
Right off the bat they're saying that fat comes from eating too much, whatever that means, and since fat and thin people have been shown to eat pretty much alike, there's a flaw right on the surface.
Karen, I'm just wondering if you usually refer to obesity as opposed to referring to fat. Sorry, that word gives me a nasty jolt anymore when it isn't coming out of the pens and mouths of asshat reporters and other talking heads.
Have you actually read the paper under discussion, or are you getting all your information from secondary news sources? Because those secondary news sources are notorious for screwing up the reporting of primary scientific research, and it is incredibly foolish to rely solely on them when discussing the research and attempting to be critical of it.
If you read even just the abstract, you'd see that this is an animal study, not a human study. The researchers don't just "claim" what you say. NPY is increased in visceral fat. And it does increase proliferation of adipose progenitor cells. These are facts. Saying that it is what they "claim" implies that you do not believe them.
You can disagree with what it might mean on a macro scale, and whether or not it might apply to humans, but you cannot dispute the actual evidence they obtained.
Not if you want any credibility, anyway.
Evelyn:
1) The third article linked to has the entire abstract posted. I'm sure JoGeek read it. The second article references the paper well enough to get the point of the study.
2) This research hasn't proven a damn thing of use for humans. Therefore, you cannot claim it's a "fact."
3) Science isn't the be-all, end-all of knowledge. Treating it so lacks credibility.
This research hasn't proven a damn thing of use for humans. Therefore, you cannot claim it's a "fact."
Huh? Did you miss the part where I pointed out that this was an animal study, and where I said "You can disagree with what it might mean on a macro scale, and whether or not it might apply to humans"?
What I said was fact was the data. In animals. (Sorry, I didn't say the latter part explicitly, but I would have thought that would have been obvious from the earlier statement about how it was an animal study. Apparently I was mistaken.)
The original post appears to have doubt about the legitimacy of the data, which is what I have a problem with. Unless you are suggesting that the data is fabricated, which would be a pretty serious accusation to make, the data is what it is. It is fact.
If you have a dispute here, it's only with the conclusions based on the data. I'm sorry, but I have no patience for people who don't understand the difference.
And I don't really know what "Science isn't the be-all, end-all of knowledge" even means. All I'm asking is that when people attempt to discuss science, they actually know what they are talking about.
Evelyn: My language is indeed specifically geared to express doubt; not because I outright deny their findings (as applied to rats, although the study conclusion exceeds the reach of the actual study) but because I do not automatically accept it as fact and therefore do not use absolute language in describing it. By the way? while I don't necessarily accept the data of any single study as absolute, my dispute is indeed mainly with the conclusion and application of the data, which is where most research goes wrong. A popular classroom exercise for grad students is to give each the same data and ask them to draw a conclusion. Nearly every student comes up with something different, and they often contradict that of their classmates.
If you read the abstract, it only once mentions that the study uses a rat model , using subsequent language in the conclusion to imply that they believe the findings to apply to all visceral adipose tissue, regardless of species, and that increased visceral adipose tissue (regardless of species) can be attributed to an increased expression of NPY. By not specifying, they imply generality in their conclusions (which is what leads to bad interpretation by journalists, who further confuse things by mixing up subcutaneous and visceral fat and their causes).
"Their picture is a closeup of frying bacon that will turn any vegetarian an interesting shade of green."
I believe the shade you are referring to is "barf green." :P
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