Lee, #170: thanks. That much I can/will do, although here in CT it'll not matter much. (I was surprised, I confess, to see the Dem result here, but if nothing else the Lieberman debacle has energised a progressive base!).
Echoing #17: How? Assume for purposes of argument that one is convinced prevention of a Nader presence on the ballot in NH, or CT where I reside, or elsewhere... what are you requesting/suggesting should be done?
note that comment 63 above was written at a time when this thread had only reached #22... sorry if it took too long to write to appear in the right flowpoint :(
Ye gods. ML actually hits a topic I'm potentially an authority on? :) Woohoo!
[Background/disclaimer: my research is on the impact of metabolic variables on brain function. Specifically, the role(s) of glucose and insulin on cognitive performance, the impact of diabetes on cognitive functions (both acute and long-term) and recently e.g. the links between type 2 (high-insulin, obesity-linked) diabetes and Alzheimer's. For a couple of examples of recent(ish) papers on this kind of stuff, if you care, check e.g. http://www.pnas.org/cgi/content/abstract/97/6/2881 , http://diabetes.diabetesjournals.org/cgi/content/abstract/53/2/418 , or http://bcn.sagepub.com/cgi/content/abstract/1/4/264 ). I’m also a PhD, not an MD; nothing I say here is even close ot being medical advice.]
HFCS: the best comments thus far, I think, were 18 and 21. First, the silly: absent some truly rare genetic enzyme deficiency, we’re perfectly capable of using fructose as fuel. Well, most of us is - the brain runs (in general) exclusively on glucose, and fructose is *not* transported across the blood-brain barrier to the brain. This means among other things that fructose does not activate brain satiety centres; in combination with the noted reduced or absent insulin response (and possibly also reduced or absent release of gut satiety peptides such as leptin), this means that we are potentially* capable of eating far more calories in the form of hfcs than many other sources. But our muscles, lungs, and so on are just fine using energy from fructose, thanks - and as has also been noted, once something is stored as fat, the release of that fat into usable energy is not affacted by the source from which it came.
Then some other stuff. Both glucose and fructose are usable as sources for AcCoA (and hence for e.g. fat synthesis). Fructose is absorbed somewhat differently from the gut (hexose transporters have differing affinities, and fructose is moved primarily through GluT5, for example {that’s Glucose Transporter 5, one of a family; neurons and the brain in general use primarily 1 and 3, both of which work for glucose, and also have some selective expression of 4 which is the same transporter found in the rest of the body to mediate insulin-facilitated glucose uptake}. Sorry this is more than anyone wanted. In non-diabetics, eating food triggers release of insulin (from the pancreas) which signals that energy is available and should be used (specifically, uptake of glucose from the blood). The basis of low-carb diets is that they produce less of an insulin rush, and hence don’t stimulate fat storage; diets based around whole grains are aimed to release glucose more slowly (from starch breakdown) and again minimise insulin release levels.
* Note that while the lower insulin release following fructose intake might (perhaps) allow greater caloric intake without satiety, it may also mean that there’s a lower risk of contributing to development of type 2 diabetes, which is more likely a consequence of (i) obesity and (ii) frequent hyperglycemic/hyperinsulinemic episodes. Indeed, fructose has been suggested as a diabetic-suitable sweetener.
I am not personally a fan of HFCS (and I *am* a fan of The Omnivore’s Dilemma, incidentally); but the lack of convincing evidence as yet for a direct link between e.g. hfcs and obesity leads me to suspect that the problem is rather (as was suggested above) over-consumption of high-energy foods, many of which are these days sweetened using hfcs. The problem is probably the calories, not (mostly) the source.
Finally, Emma’s describing the phenomenon of reactive hypoglycemia: over-release of insulin, in response to food [usually processed sugar, indeed], which then removes so much glucose from the blood that blood glucose gets abnormally and in some cases dangerously low. This, too, is nothing to do with fructose, much more to do with glucose (and is often worse in folks with glucose intolerance, which is generally because of low exercise and/or high weight). The comment that pure fruit juices might be OK is likely because these are high-fructose, low glucose, not the reverse. Obesity because of hyperglycemia? Not enough data to comment on any individual, but I’ve never heard of such; indeed, most type 1 (insulin-deficient) diabetics are skinny exactly because they have little/no insulin to signal fat storage despite having huge levels of insulin in the blood.
Yikes. Sorry; enough, but I live this stuff ;-)
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