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Flavor-triggered insulin & fat cell capacity . . .

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Author Topic: Flavor-triggered insulin & fat cell capacity . . .  (Read 15531 times)

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lrgiblet

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Flavor-triggered insulin & fat cell capacity . . .
« on: November 08, 2009, 12:52:18 PM »

Hi all.

I don't know if this theory has been posted yet or not.  I haven't read every post in the forum, though I've read quite a few.

I've seen pieces of this theory in places, but not the whole thing.

It does seem to me that insulin should be one of the key parts to the theory.  And user NTB has tried to push this point in another thread.

However, I'm not sure NTB accommodates all of Seth's observations in his report:

www.sethroberts.net/about/whatmakesfoodfattening.pdf

I know NTB has read this, and, by the way, I would encourage everyone to read this document before spinning theories.  It's a good guide to all the things a theory should try to accommodate.

The "perhaps-missed" observation is the appearance of a "set point".

Now, I know that Seth and Gary Taubes had a little exchange about "set point" versus "settling point", and I don't want to put words in Seth's mouth, but it seems to me that this debate, contrary to what Taubes says, might not be that important in this case.

Taubes portrays the two concepts soemthing like this:

Set point: some brain-mediated, thermostat-like thingy.
Settling point: some point at which a homeostatic process, largely mediated by the fat cells, happens to settle at, for who knows what reason.

I'm not sure Seth is really committed to the definition of "set point" as Taubes characterizes it.  When I first read Seth's article, I took him to be describing something of a "black box".  We observe that people who lose weight tend to go back to their original weight, and it's as if there's some sort of "set point" mechanism at play. But who knows if it's mediated in the brain or in the fat cells. 

Anyway, whether Seth is committed to some brain-mediated thermostat-like thingy or not, I'm not sure he needs to be.  I think his theory could work regardless of how the "set point" or "settling point" is mediated.

So, what makes us seem to go back quickly to our original weight, and perhaps overshoot a bit, when we lose our grip on a typical diet?  And what makes us stop putting the weight on so quickly after that point?

One simplistic suggestion would be that our fat cells can only stretch so far.  They have only so much capacity, and when they get full, they begin pushing back, making us less hungry.  They can stretch over time, but it's a relatively slow process.  However, when we take fat out of them, they retain their capacity and, if they shrink over time, it's very slowly.  So our "set point" would be determined by the capacity of our fat cells.  I know I've heard this theory in the past, but I'm not sure where --- maybe it's nothing more than some pseudo-explanation made up by some Cosmo writer rushing to get the latest "top ten reasons you can't lose weight" kind of article :-D   Or maybe there's something to it . . .

Now, on to insulin.

I read somewhere, maybe it was in Taubes, that when we eat a meal there is often more than one insulin spike.  There's often an insulin spike that occurs right as we begin eating, before we even start digesting the calories.  And more insulin is triggered, as needed, as macronutrients begin to make their way into the bloodstream.

And, it could be that the initial insulin spike is a trained response, much as Seth describes.  It's trained by the association of flavor with the calories that repeatedly come a little later.   It could be there are sensors in the nose that trigger this response.  It takes some time to make the association, but once it's there, when we experience a certain insulin-associated flavor, the flavor triggers an initial release of insulin.

So, given all these wild untested assumptions (which seem plausible, but might be wildly wrong), here's why the SLD would work, and why we see the phenomena reported in Seth's PDF:

1.  When we eat flavorless calories, or plug our noses, it prevents the flavor molecules from reaching the sensors in the nose that initiate the preliminary insulin spike.
2.  We wind up producing less insulin in a given day, because we have fewer anticipatory insulin secretion events, and thereby store less fat, and lose weight.  In this way the SLD would work for much the same reason a low carb diet works.  Less insulin = weight loss.
3.  And the set-point type phenomena are produced by the twin factors of insulin always trying to store more fat (once the muscles and liver are full), and fat-cells pushing back once full.

This is a little "off the hip".  If others are interested, I might take a closer look, try to itemize the phenomena in need of explaining from Seth's article, and making a chart comparing how the main live theories in play here accommodate them. (Or if Seth wants to do that . . .   :D )

Jim


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nougat

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #1 on: November 08, 2009, 09:06:56 PM »

this is a very interesting post.

especially the insulin-triggering flavour.  maybe that is why some people still don't lose weight even when they do stick to a diet.  cos the flavour of what they eat triggers insulin anyway - even if it is low in calories  or low carb....

altho i find it very difficult to eat with my nose blocked i'm going to give it a try cos my few hard-lost lbs, despite keeping mostly to a lo-carb diet, are creeping back on.
thanks
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nougat

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #2 on: November 08, 2009, 09:10:02 PM »

about the fat cell size i'm sure i've read this before.   perhaps some of us have more accomodating fat cells that stretch more and faster than others.  the question is will they ever shrink back to a small size....
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lrgiblet

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #3 on: November 10, 2009, 01:20:03 PM »

Actually, I guess my idea wasn't so novel.

Here's an article that goes into more detail on a very similar proposal. 

http://nielsolson.us/archives/2006/05/ghrelin_leptin.php

It was originally linked to by user NTB in post 34 of this thread:

http://boards.sethroberts.net/index.php?topic=2169.0

I missed that reference when I originally read through the first ten pages or so of that thread.

Jim
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Phoebe

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #4 on: January 21, 2010, 05:31:55 PM »

about the fat cell size i'm sure i've read this before.   perhaps some of us have more accomodating fat cells that stretch more and faster than others.  the question is will they ever shrink back to a small size....

I remember hearing years ago about a theory that when you gain weight, the body creates more fat cells, not just that the fat cells you have get bigger.  Supposedly, one of the reasons that it is hard to keep weight off is that you never lose the extra fat cells.  They just get smaller and wait for their opportunity to stuff up with fat again.  Kind of depressing.  I don't know whether it's true or not.
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bleeding

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #5 on: January 21, 2010, 06:46:24 PM »

the words you're looking for are "cephalic insulin response"
http://www.google.ca/search?hl=en&client=firefox-a&rls=com.ubuntu%3Aen-US%3Aunofficial&q=%22cephalic+insulin%22&btnG=Search&meta=&aq=f&oq=

you're not taking into account the fact that the liver gets
1. first access to insulin, directly from the pancreas, therefore
1a. the liver sees more concentrated insulin than what the rest of the body sees
1b. the liver destroys some insulin before it reaches the rest of the body
1c. more than the rest of the body, the liver gets a "get ready, there's carbs coming" signal

2. first access (mostly) to food

http://www.google.ca/search?hl=en&client=firefox-a&rls=com.ubuntu%3Aen-US%3Aunofficial&q=insulin+%22first+goes+to+the+liver%22&btnG=Search&meta=&aq=f&oq=

because of 1c. the liver usually mops up some carbohydrates, blunting the blood rise in insulin.  The pancreas sees the blood rise and does the "real" insulin release, but because the liver blunted the signal, less insulin is released.  If you know any engineering/physics, the liver plus the pancreas plus the cephalic response makes blood glucose rise  into a ramp function, not a square.

If in fact Seth's diet reduces cephalic insulin response then
1. the liver will not be "pre-prepped" for the incoming carbohydrate - more will get through to the blood, therefore
2. the whole body will get more carbohydrate
3. and faster (because of #1 just above)
4. the pancreatic "real" insulin response will be higher in response to the square instead of the ramp function
5. the body's adipocytes will be exposed to
5a. more glucose (more than if the liver had cleaned some up)
and 5b more insulin (because now the liver will get one huge dump, and less insulin will be destroyed in the liver than if the liver got a small cephalic dose and then later a smaller "real" dose) 

and so on ...

If you follow the chain of events and give the liver the primacy that it has,  then IMHO, if Seth's techniques reduce cephalic insulin response it will make people fatter, if the only thing you're considering is the chemistry.

Hi all.

I don't know if this theory has been posted yet or not.  I haven't read every post in the forum, though I've read quite a few.

I've seen pieces of this theory in places, but not the whole thing.

It does seem to me that insulin should be one of the key parts to the theory.  And user NTB has tried to push this point in another thread.

However, I'm not sure NTB accommodates all of Seth's observations in his report:

www.sethroberts.net/about/whatmakesfoodfattening.pdf

1.  When we eat flavorless calories, or plug our noses, it prevents the flavor molecules from reaching the sensors in the nose that initiate the preliminary insulin spike.
2.  We wind up producing less insulin in a given day, because we have fewer anticipatory insulin secretion events, and thereby store less fat, and lose weight.  In this way the SLD would work for much the same reason a low carb diet works.  Less insulin = weight loss.
3.  And the set-point type phenomena are produced by the twin factors of insulin always trying to store more fat (once the muscles and liver are full), and fat-cells pushing back once full.

This is a little "off the hip".  If others are interested, I might take a closer look, try to itemize the phenomena in need of explaining from Seth's article, and making a chart comparing how the main live theories in play here accommodate them. (Or if Seth wants to do that . . .   :D )

My reckoning is that overall more insulin will be produced, and it will have more effect on adipocytes without the cephalic response.      It's as if the liver tries to protect the rest of the body from insulin and glucose (we'll leave fructose out for now) and the cephalic insulin is part of this protective mechanism
« Last Edit: January 21, 2010, 10:44:11 PM by bleeding »
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Pinkmug

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #6 on: January 22, 2010, 02:47:30 AM »

Jim, a lot you say makes sense with my observation that chewing gum makes me hungry.
(just chewed one to confirm... as if I didn't know it)
My brain is very foggy right now but I'd like to add the vomeronasal organ in the equation. I posted about it some time ago. Wouldn't that explain why even noseclipping and eating non flavored foods doesn't work for some of us. (me! me! me!)
Maybe only those who don't have a vomeronasal organ lose weight.
I thought of covering my VNO but couldn't find an effective way. (damn the mouth is always wet).

and Phoebe, i sort of recall your fat cells are the same number all your life after adolescence, expect in very specific cases - lipomas (me! me! me!)
now I'm not sure what happens to peeps who undergo liposuction and get fat again - is it new cells or the remaining ones that get bigger?  :?
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Phoebe

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #7 on: January 22, 2010, 09:09:09 AM »

Phoebe, i sort of recall your fat cells are the same number all your life after adolescence, expect in very specific cases - lipomas (me! me! me!)
now I'm not sure what happens to peeps who undergo liposuction and get fat again - is it new cells or the remaining ones that get bigger?  :?

Good to know.  Although if someone had told me this when I was an adolescent, I would've eaten fewer HoHo's. :(   BTW, I have also heard that people who get liposuction and gain weight again wind up with strangely assymetrical fat pockets.  For example, instead of going to your thighs where it was before, it winds up around your knees or some such thing.  However, I'd take that with a grain of salt.  I suppose it could be an urban legend.
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NTB

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #8 on: January 22, 2010, 09:54:25 AM »

If in fact Seth's diet reduces cephalic insulin response then
1. the liver will not be "pre-prepped" for the incoming carbohydrate - more will get through to the blood, therefore
2. the whole body will get more carbohydrate
3. and faster (because of #1 just above)
4. the pancreatic "real" insulin response will be higher in response to the square instead of the ramp function
5. the body's adipocytes will be exposed to
5a. more glucose (more than if the liver had cleaned some up)
and 5b more insulin (because now the liver will get one huge dump, and less insulin will be destroyed in the liver than if the liver got a small cephalic dose and then later a smaller "real" dose) 

and so on ...

If you follow the chain of events and give the liver the primacy that it has,  then IMHO, if Seth's techniques reduce cephalic insulin response it will make people fatter, if the only thing you're considering is the chemistry. ...  My reckoning is that overall more insulin will be produced, and it will have more effect on adipocytes without the cephalic response.  It's as if the liver tries to protect the rest of the body from insulin and glucose (we'll leave fructose out for now) and the cephalic insulin is part of this protective mechanism

Bleeding, it is a pleasure to have you on these forums. I find that the most productive way to approach diet is to probe the underlying physiological and psychological mechanisms. There are so many people out there who base their dietary theories on evolutionary arguments, but the trouble is that you can argue almost anything based on evolutionary considerations, and these arguments are typically not easy to put to the test because not many of us were around in the cave man days.

Regarding your specific argument above about cephalic phase insulin, you raise an interesting paradox.  If your logic is correct, then SLD would not work as advertised.  Well, in fact SLD does work quite well for many or most people, so something must be wrong with the argument -- either the assumptions, or the logic, right?  My contention would be that your initial premise is correct (that SLD reduces or eliminates cephalic phase insulin response), and that point (1) is also correct (that with SLD the liver will not be "prepped" and so blood glucose will elevate more than it would have with insulin in the system). However, point (2) does not follow, that "the whole body" will get more carbohydrate.  What I think will happen is that the faster and higher blood glucose peak (due to less insulin available to store it) will bring on satiety earlier, and the person will stop eating earlier than otherwise.  This is the nature of appetite suppression.  Then postprandial insulin secretion will gradually bring blood glucose back down to its basal level.  Because less total insulin will have been secreted, the opportunity for insulin "overshoot" is reduced, and the overall rise and fall of glucose is more gradual than otherwise, so the chances of recurrent hunger are reduced.  By contrast, a strong cephalic phase insulin response tends to encourage more ravenous eating, a sharper post-prandial insulin response, and some potential for overshooting, a drop in blood sugar, and additional cycles of appetite-eating, appetite-eating etc.  In fact, the whole point of "appetizers" and multi-course meals is to encourage people to eat more than they otherwise would.  Restaurants are savvy to this sort of thing, and they know quite well how to string you along with recurrent waves of appetite stoking. 

I think this phenomenon also underlies the principle of "sensory specific satiety" which is exploited by the Flavor Point Diet and the Sensa tastants.  The idea is that you will only secrete so much insulin in response to a single flavor category.  Once the taste and flavor receptors for that flavor are saturated, pre-prandial insulin drops off.  And you have only the post-prandial insulin, so you will get no insulin overshoot, and you'll remain sated.  However, if you are then exposed to Flavor #2, and Flavor #3, etc., you are exposing a new set of flavor receptors that have not yet been saturated, setting off new waves of cephalic phase insulin, and new rounds of appetite and eating.  That's why many of us can always find a "second stomach" for dessert after being absolutely stuffed with the main course.  But in the Flavor Point Diet, by confining yourself two one or two flavor categories at a meal, you limit your total cephalic phase response and fill up on less food than otherwise.
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bleeding

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #9 on: January 22, 2010, 06:41:43 PM »

>>> If your logic is correct, then SLD would not work as advertised.

Or if the logic is correct plus SLD works, then SLD does not work via a direct effect on cephalic insulin.  It has to have an effect on insulin but the insulin effect is downstream from the way SLD works.   It's a common math proofs technique: take the premises/postulates/axioms/(rules of deriving from all of these) and follow them out.  If the end conclusion is unreasonable, either the (rules of derivation) or the (premises/postulates/axioms) the rules apply to were incorrect.

have you come across research showing cephalic insulin has been extinguished by non drug means?   I've studied it off and on as an amateur looking for personal solutions for 20 years and haven't seen it. 

Some learned behaviors are staggeringly hard to change, or cannot be unlearned for decades.   Accents and some motor skills are famously proof of this.    If something as simple as not playing the guitar correctly - a bad habit learned after just a dozen repetitions can persist after years of trying to stamp it out, how much harder must it be to change a reflex of chemicals?

Bulimia, anorexia are other (perhaps learned / reinforce behaviors/reflexes) more relevant to this area.

As an indicative example, Bulimics don't get the full blood sugar effect of a meal, but they have "normal"  cephalic responses (abstract only)

http://www3.interscience.wiley.com/journal/112413637/abstract?CRETRY=1&SRETRY=0

______________
From the last time I looked not a lot has happened in the field, or at least not much more has become freely accessible.  There is some but they're all mouse/rat models, so I don't want to apply it to humans. 

http://www.google.ca/search?hl=en&q=block+%22cephalic+phase+insulin%22&btnG=Search&meta=&aq=f&oq=

It's just a hint, but the hint is there ...

http://journals.cambridge.org/action/displayFulltext?type=1&fid=2843372&jid=PNS&volumeId=58&issueId=01&aid=2843360
(my emphasis below)
>>>
 insulin release and gastric acid
secretion (the so-called cephalic phase of digestion), the
consequences of which feed back to the brain where they are
interpreted as an internal signal for hunger. Against this,
however, is the finding that blockade of cephalic-phase
responses (with atropine) does not disrupt the initiation of
eating in response to learned cues
(Weingarten, 1984)
<<<<<<<<<<<

Insulin will be involved, cephalic and post-prandial.  Must be.  The question is whether its involvement is adjunct or primary- associated or causative to the techniques on this site.   

It doesn't seem to be the primary in rats/mice.   I don't like applying rat/mice models to humans, so many of them have been incorrect,  so I cannot rule out that in humans Insulin is in some way the primary mover making Seth's techniques effective.   but I seriously doubt Insulin is the primary in humans.   Something else sets off the chain and insulin joins in later. 
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kt

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #10 on: January 23, 2010, 08:19:06 PM »

Ok, bleeding and ntb,

You are losing me a bit here, but hopefully due to my general laziness reading multiple posts and cited articles carefully enough.  Bleeding, your 1. seems to leave out the obvious lack of carbs/insulin-release causing carbs in the SLD dose.  It is this that leads to AS for almost everyone, not some alteration of cephalic insulin response vis a vis SLD dose contents.  The SLD doses are described by Seth as NOT recognized in the same way as other flavors - in our terms, chasing the insulin response, the doses don't cause the response at all, because they are fats, or the seemingly non-insulin-stimulating fructose or sucrose water. 

Or I'm up too late, and not reading you nerds (meant as a compliment) carefully enough/with enough brain power. 

Kate



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bleeding

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #11 on: January 23, 2010, 08:55:41 PM »

 

 Bleeding, your 1. seems to leave out the obvious lack of carbs/insulin-release causing carbs in the SLD dose.  It is this that leads to AS for almost everyone, not some alteration of cephalic insulin response vis a vis SLD dose contents. 

Kate

where I run a scenario, I'm not writing about the SLD calories themselves.

I'm talking  about meals you eat after the effect (set point reduction or appetite suppression or whatever) has kicked in.  What I'm saying is:

>>>
if SLD works by getting rid of your cephalic insulin response

let's say it has happened - you did SLD and it IS WORKING because: you do not have a cephalic response to your next meal (this is the assumption).  If this is true, THEN,

this is what will happen when you eat that next regular meal


1. no cephalic insulin
2. no insulin for the liver before the food hits the liver
3. the liver doesn't do some of its regular prepratory activities 
...
...
and so on
...
<<<<<<<

and if you follow the events to the end,  in the end I have you getting FATTER from a regular meal

Since you don't get fatter from your regular meals, something between the <<< and >>> marks above is incorrect.  It could be the steps I lay out, but I think it's that first assumption under the <<<<< "If SLD works by ...."
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kt

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #12 on: January 24, 2010, 05:56:52 AM »

Got it...

thanks!
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kt

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #13 on: January 24, 2010, 06:07:58 AM »

Oh, I agree with your last line. 

The SLD dose probably worked to reduce my appetite through the mechanism Todd delineated earlier - by getting "stealth" nutrients (fat) into the bloodstream and inducing satiety without causing an insulin spike.  This dovetailed, for me, by causing me to naturally stop desiring food later in the day, often just munching on raw veggies out of a fear of not getting enough nutrients.  In other words, the SLD dose helped me begin fasting, and limiting my calorie consumption to only a few hours of the day.  I further pushed things to reduce insulin response when not eating...using Todd's recs regarding controlling pre-prandial response by smelling foods but not eating anything until hunger passes.  This is intermittent fasting, fast-5 and SLD comingled, I know, but it really works.  I was a size eight/ten in August, and am now wearing fours/sixes, down about 13 pounds...

I'll try to dig up the thread and post it here...

Kate
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kt

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #14 on: January 24, 2010, 06:12:27 AM »

See NTB's post on p. 2 of Appetite Suppression v. Setpoint Adjustment thread, excerpt below:

In short: The net outcome of the SLD is to reduce insulin levels, inducing satiety and allowing the release and oxidation of fatty acids stored in fat cells -- thereby resulting in weight loss.  It is particularly powerful because it gets the satiety inducing nutrients -- fatty acids and glucose -- into to the bloodstream in a "stealth" manner -- with no or little insulin secretion, so instead of being whisked away to storage in the cells, these satiety inducing nutrients are allowed to remain there, shut down appetite and provide a supply of energy!  Even better, the body is now in a mode where it can pull additional fatty acid and gluose energy from storage to provide further energy.  Great deal!

The insulin hypothesis is also attractive because it explains much, much more than just the SLD diet.  For example, it explains why it is so hard for obese individuals, or people with certain genetic backgrounds, e.g. the Puma indians,  to lose weight -- it is because their genes in combination with their diets have caused them to become hyperinsulimic -- their basal level of insulin is so high that even the tiniest amount of food is scavenged by their cells.   These high insulin levels are REAL -- unlike a "setpoint" they can be measured from blood samples!  And it takes a lot to quiet this insulin response, but it can be done -- by a very low carb diet, by the SLD diet, or even by meditation and stress reduction as proven by Jon Gabriel (See his amazing diet, The Gabriel Method which, I believe, facilitates weight loss by using visualization and mediation to quiet the insulin response).   This also explains why dieting and excercise so often fail, because elevated insulin levels leave the blood depleted of glucose and fatty acids, and cause intense cravings even when calories are cut back.   On the other hand, it should be encouraging to those who have the patience and persistence to know that, as they lose weight and reduce insulin levels, their basal insulin levels will slowly decrease, and maintaining their low weight will become easier with time.   Setpoint theories, by themselves., would not predict this fact.

(Another interesting aside relevant to the SLD:  fructose, the sugar in Kool-Aid and other flavored sodas mentioned in SLD, has no ability by itself to induce an insulin response.  So that could explain the appetite suppressing effect of some of Seth's French sodas.  However, if any glucose is combined with fructose, as is the case with sucrose (table sugar) or high fructose corn syrup, the insulin response is induced and in fact fructose is more easily converted to triglycerides in the liver as long as there is insulin around).

To summarize:  The key to weight loss is ingesting calories without inducing insulin.  Flavorless calories just happen to be one cleverly stealth way of doing this, but it is certainly not the only technique available.
(NTB)
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