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Flavor-triggered insulin & fat cell capacity . . .

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Author Topic: Flavor-triggered insulin & fat cell capacity . . .  (Read 15705 times)

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bleeding

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #15 on: January 24, 2010, 04:02:36 PM »

Here's a sampling of some views from low-insulin promoters, based on personal experience.  Look especially for Peter (of the Hyperlipid blog) and Lex Rooker's comments, and read Lex's blog - he's kept detailed records of a near-zero carb diet for a couple of years.

http://www.carnivorehealth.com/main/2009/9/7/a-calorie-is-a-calorie-is-a-calorie-is-a-calorie.html

A new protein found a couple of years ago, "Acylation Stimulating Protein" can pack fat into fat cells with no insulin.  If you consistently eat too many calories you will get fat without insulin.

High insulin makes getting fat easier but you don't need high insulin to get fat. 

Low insulin makes losing fat easier. 

And,  I don't see any proof that the primary mechanism of Dr. Roberts' techniques is through an effect on cephalic insulin, also known as preprandial insulin.   And I posted a couple of links hinting (but absolutely NOT proving, I'm the first to admit that) that cephalic insulin is beside the point.   

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

more food for thought ...

My recent low carb diet fat loss (220 pounds to 168) was done using a lot of beef and cottage cheese

Some folks on these boards reported much greater appetite suppression with cottage cheese than with oil - so consider

http://www.cababstractsplus.org/abstracts/Abstract.aspx?AcNo=19920456224

25 grams of cottage cheese insulin response: 309 pmol/litre per h
50 grams of glucose 732 pmol/litre per h

and the cottage cheese insulin response lasts 5 or more hours

High insulin,  tasteless  foods working as Dr. Roberts' theory predicts, just like low insulin foods ...

And beef?   produces more insulin than pasta

http://www.mendosa.com/insulin_index.htm

If I can get the gelatin sheets to work I'll try nose clipped beef,

but the cottage cheese ...

for some people a high insulin food produces better results than low insulin oil/fructose
« Last Edit: January 24, 2010, 08:19:48 PM by bleeding »
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NTB

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #16 on: January 24, 2010, 06:46:32 PM »

...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...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...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.

I don't see any proof that the primary mechanism of Dr. Roberts' techniques is through an effect on cephalic insulin, also known as preprandial insulin.   And I posted a couple of links hinting (but absolutely NOT proving, I'm the first to admit that) that cephalic insulin is beside the point.

bleeding,

You seem to be convinced that AS from SLD derives not from cephalic phase insulin, but from some other mechanism. You suggest that "Something else sets off the chain and insulin joins in later." And you seem to feel that if you consume food without a cephalic phase insulin response (for example by nose-clipping), that somehow this will lead to an elevated post-prandial insulin response (vs. what it would have been with the pre-prandial insulin response) because the liver will not be "prepped" and--paradoxically---more glucose will get into the bloodstream, and this will result in us getting fatter--contrary to what actually happens with SLD. So on that basis, you reject the hypothesis that SLD works because by suppressing flavor, we are suppressing pre-prandial insulin.

I'm trying to understand the logic here, but I must admit I'm struggling. I do not understand why eliminating the cephalic phase insulin would let more glucose "get through to the bloodstream" and thereby elevate the post-prandial phase insulin. I'm missing the logic there. I would assume that cephalic insulin would counteract the rise in blood sugar (vs. what it would be without the cephalic phase insulin) just as post-prandial phase insulin does. What is your evidence that that my assumption on this point is incorrect?  Can you point to any studies that support your supposition that blocking cephalic phase insulin leads to increased blood glucose, relative to permitting cephalic phase insulin?

And now let's suppose for the moment that you are correct--that cephalic phase insulin response does not explain why SLD works? Do you have an alternate explanation?

Finally, in response to your question regarding evidence that cephalic phase insulin has ever been extinguished.  I have multiple pieces of evidence to support this:
1.  Direct evidence from the great Ivan Pavlov himself.  Do yourself a favor and buy or borrow a copy of "Conditioned Reflexes" by Ivan Pavlov.  It is a masterpiece of physiological psychology.  As I detail on my blog, many people quote summaries of Pavlov's work (including Seth Roberts) but I don't think many have read his original work.  It is a much richer and insightful work than that the simpleminded popular image about "dogs salivating in response to a bell as a conditioned reflex". In fact, Pavlov hardly ever used a bell; he used buzzers, lights, metronomes, hot and cold stimuli, but almost never bells!  One of the best chapeters in the book, Lecture IV, is entitled "Experimental Extinction".  And in fact, Pavlov conditioned his dogs to stop salivating when presented with meat!  Now if you have a dog like my beagle Charlie, you would believe that to be impossible.  But by repeatedly presenting the dogs with meat, and taking it away without allowing them to eat the meat, the salivary secretions (and pancreatic secretions as well) diminished with each repeptition---until they totally extinguished.  Now, the salivation would return the next day, but less; and with further repetitions of "unreinforced exposure" the salivation would die out.
2. Alan Hirsch, in "Scent-sational Weight Loss" developed a method of providing people with "odor inhalers" containing pleasant food aromas.  The participants in his study were directed to sniff the inhaler (a lipstick like device) whenever hungry. Eventually, their cravings diminished significantly, and they lost significant amounts of weight -- more than 100 pounds in several cases.  No explanation is given other than "reprogramming" the aroma-appetite response, but I almost have to believe that this works by extinguishes the secretion of cephalic phase insulin in response to aromatic food cues.
3.  From personal experience, I have been able to fast for up to 48 hours without any hunger or cravings.  A significant part of this was exposing myself to food cues such as aromas and the sight and social context of eating---while not following through on the actual eating. I made sure to expose myself repeatedly and to a variety of aromas.  I even sniffed spices to saturated my sense of smell.  This worked very well, and my appetite is no longer "stoked" by pleasant food aromas.  I just enjoy them for what they are.
4. Others have experienced hunger extinction by means of cue exposure.  Kate (kt) on these forums has written about this, if you check her SLD page, or scan through her many contributions to the "Appetite vs. Setpoint Adjustment" thread that I started.
5. I also have a blog and website that devotes considerable space to the psychology of extinction. There is a lot of evidence that it works, but one has to be patient and use the principles of repetition, frequency, and counter-conditioning. These principles are well known to animal trainers and academic behaviorists, but not very well known to the general public.

bleeding, I think you are right that extinction is often hard.  But it is not impossible.  And if done correctly and systematically it works.  Unfortunately, I think that SLD as advocated by Seth Roberts, does not promote extinction of the flavor-insulin reponse.  But on my blog, I detail a systematic way to to that, aspects of which I have alluded to above.

Todd
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bleeding

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #17 on: January 24, 2010, 07:35:41 PM »

I must have added the cottage cheese and beef examples after you replied.  More suggestive data points suggesting SLD doesn't do its work directly through insulin control

You seem to be convinced that AS from SLD derives not from cephalic phase insulin, but from some other mechanism.

I'm not convinced of anything.  I don't see strong evidence for the proposition. 

I'm trying to understand the logic here, but I must admit I'm struggling. I do not understand why eliminating the cephalic phase insulin would let more glucose "get through to the bloodstream"

The liver sits between the body and the digestive tract.   Glucose doesn't flood the entire body after digestion, with fat cells grabbing what they can and the liver fighting for its scraps.  Food digested in the intestines is collected into the hepatic vein and goes mostly through the liver first then to "the rest of the body".   After the liver there's no more processing before food gets to "the body".

If the liver processes some glucose, the processed glucose does not get to "the body".   It's an either/or situation- either the liver gets it or "the rest of the body" gets it.    If one gets more, the other gets less.  And the liver gets first call.  And if there's cephalic insulin, the liver gets first call on that too, because insulin's dumped directly, right into the liver (into the hepatic vein, right before it enters the liver).   Insulin has a much greater effect on the liver than on any other organ, any muscle, any fat cell, any skin cell ... because the liver gets whacked with the concentrated dose, directly, PLUS the liver destroys insulin - reducing "the rest of the body" 's exposure. 

http://www.medbio.info/Horn/Time%203-4/homeostasis_2.htm
>>> Insulin is destroyed in the liver, the half-life being approximately 5 minutes.  The rate of secretion of insulin is, therefore, difficult to measure.

If the liver has been prepped by insulin it will grab more glucose (for liver glycogen, for the liver's own energy purposes, also for a couple of enzyme systems - I think the mixed function oxidases use a little) than if the liver has had no insulin.

Basic energy balance.  "in minus out = (accumulated or destroyed)"

Without the cephalic response, lots of glucose gets through the liver before significant insulin is delivered to the liver. 

I've run hundreds of simulations like this in my (unfortunately long deceased) engineering career.  Just laying out the flow and order of nutrients gave me a feel for who (which organ/tissue, or translated to industrial simulation, which tank or plate or bed)  would end up with what.

Finally, in response to your question regarding evidence that cephalic phase insulin has ever been extinguished.  I have multiple pieces of evidence to support this:

1.  Direct evidence from the great Ivan Pavlov himself. 

Good for salivation,  what about insulin?   

and yes, salivation ... so a reflex conditioned over a couple of months took several weeks to die out.

And the insulin reflex, conditioned and reinforced over say 30 years, will die out in 2 days?

And I posted a (weak-evidence) review article that showed that blocking cephalic responses did not alter learned eating behaviors. 

There are some learned behaviors that never go away ... I posted some examples above.   Moshe Feldenkrais, who studied Pavlov and his contemporaries deeply, I think in the 70s had lists of learned behaviors that, once developed, never go away.   I've forgotten most of the list unfortunately. 

And now let's suppose for the moment that you are correct--that cephalic phase insulin response does not explain why SLD works? Do you have an alternate explanation?

The fact that the phenomenon was predicted by a different theory lends heavy support to that theory.   But I see deficiencies for Dr. Roberts' proposed Leptin mechanism.

later addition: actually it wasn't one phenomenon, but several different phenomena/techniques predicted by the theory.  That did impress me.  Let's see if it actually works for me.

I'm searching for an explanation, something that will keep it off this time.    I'd rather have a correct answer and have my fat problem solved than accept an incorrect answer that temporarily satisfies me and have to solve it again 2 or 3 years from now, for the 10th time. 

I've been through this cycle too many times, from Pritikin (yes, you read that right) on down to today, to let myself pat myself on the back, again,  at having succeeded,  and let my guard down and let the whole thing repeat itself AGAIN.

Low carb plus counting calories plus resistance training is working, and I'd like to keep on top of developments so I can nip the problem in the bud if it starts again.  Insulin control looks like an important ingredient but it's not the holy grail.

Next time I get a block of time I'll go through some of the literature Dr. Roberts used to develop the theory and see where I can go from there.  That's a different world to me.

We should agree to end this amicably soon and resume in a couple of months as more old papers are found and the science moves on.   Maybe there is an old paper showing extinction of the cephalic insulin response/reflex.   That would go a way toward establishing this as a good mechanism for the effect.

I really DO NOT have an answer.  I am seeking one.
« Last Edit: January 24, 2010, 08:48:57 PM by bleeding »
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kt

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #18 on: January 24, 2010, 08:15:53 PM »

Hi, bleeding,

from your previous post:

blockade of cephalic-phase
responses (with atropine) does not disrupt the initiation of
eating in response to learned cues (Weingarten, 1984)


True, if you have no interest in avoiding eating...I, of intentionally low self-discipline in many things, am motivated enough, when feeling no hunger in my stomach and no desire to feel food in my mouth (chewing/munching desire) to not bother with eating things during the time that I fast (until 4 or 5 pm).  I don't even want gum or mints, just clean liquids, like tea.

Disregarding the learned cues is probably as simple as having enough information (were Weingarten's subjects people who knew they could eat as much as they wanted later on?) to decide to NOT eat right then, and wait until I want to eat.  If I was afraid that I couldn't have that slice of pizza later, and I wanted it, I'd probably eat two - just because it was lunch time.  That's not the case, for those of us who fast, then eat freely (and have wide-open access to food). I simply wait, hunger-free, until the end of my working day, when the pace slows down enough for me to enjoy and savor my food.  Lots of days I don't eat until I've had a chance to make something I really like.  I eat whatever I feel like, no worries, and continue to lose!

The statement about a lack of preprandial insulin not overriding initiation of learned eating (above) is true, as I've demonstrated this F-Sun, eating all day although never feeling hungry nor desiring food or drink, starting late morning, and going as late as 10 tonight, intentionally eating in order to disrupt my fasting schedule.  I literally had to internally tell myself to find something to eat/drink with calories, at the required mealtimes for a normal American.  As soon as I began eating or drinking, I felt fine doing it.  It felt like being on Mars, although I was simply eating a typical set of 2-3 meals and coffee/soda each day. 

Contrast this with my impulsive trips to the store/fast food to satisfy cravings, even when I was on SLD and losing weight (thank you, McD's dollar menu hot fudge sundae), and my lifelong battle with in-between meal hunger and munchie urges.

I'm not sure what your situation is, but sometimes, as all mothers know, anecdotal knowledge leads to solutions while scientists work to explain the exact "why" of it.  Do what works for you, trust it, and STAY with it until it stops working.  As a scientist and a mother, I find that a definitive body of research often takes too long to benefit us right now.

Good luck-if you are still trying to lose, and if not, don't panic - these boards have lots of creative solutions that may work for you should you start gaining again.

Kate
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bleeding

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #19 on: January 24, 2010, 08:53:09 PM »


from your previous post:
blockade of cephalic-phase
responses (with atropine) does not disrupt the initiation of
eating in response to learned cues (Weingarten, 1984)

 (were Weingarten's subjects people who knew they could eat as much as they wanted later on?)

Study's not publicly available, that I can find.  Next time I'm near one of the universities I may go & see if they have a copy.

Even in the 80s I don't think Western universities let profs poison undergrads (much as the profs may want to) 

probably rats/mice  (which is why I always label this as weak evidence for humans)

Good luck-if you are still trying to lose, and if not, don't panic - these boards have lots of creative solutions that may work for you should you start gaining again.

Lost most of what I wanted to before I found out about this.  Now I just need to know how to maintain, maybe build some muscle, and definitely how to control the random disastrous once per month binges.
« Last Edit: January 25, 2010, 01:50:00 PM by bleeding »
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shovelqueen

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #20 on: January 25, 2010, 05:00:49 AM »


I'm not sure what your situation is, but sometimes, as all mothers know, anecdotal knowledge leads to solutions while scientists work to explain the exact "why" of it.  Do what works for you, trust it, and STAY with it until it stops working.  As a scientist and a mother, I find that a definitive body of research often takes too long to benefit us right now.

Kate

What she said!!  I'm all for scientific validation and finding the WHY, but does that mean that we have to wait, continuing to do the wrong thing until some "authority" tells us it's now OK to do what was working all along? 

I was a university Nutrition student during the 80's, thoroughly indoctrinated into the emerging low-fat dogma.  It was "breaking science" then.  I don't believe that any more, but I'm part of a profession that still has to "toe the party line" when it comes to what we can say in public.  And all the "best practice" guidelines are years behind what we are experimenting with here.  I personally wish I could put some of my obese anti-psychotically medicated residents on SLD, or pump omega-3 fats into my frail elderly residents, but I have to work within the establishment.  I have got most of my docs onto the probiotics bandwagon, and I'm working on other stuff, but it's slow. As a mom, however, I can try other "out there" interventions to see what helps him. 
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NTB

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #21 on: January 31, 2010, 01:15:57 PM »

You seem to be convinced that AS from SLD derives not from cephalic phase insulin, but from some other mechanism....I do not understand why eliminating the cephalic phase insulin would let more glucose "get through to the bloodstream"
The liver sits between the body and the digestive tract.  Glucose doesn't flood the entire body after digestion, with fat cells grabbing what they can and the liver fighting for its scraps.  Food digested in the intestines is collected into the hepatic vein and goes mostly through the liver first then to "the rest of the body".  After the liver there's no more processing before food gets to "the body"... If the liver has been prepped by insulin it will grab more glucose...Without the cephalic response, lots of glucose gets through the liver before significant insulin is delivered to the liver. 

bleeding,

Re-reading our dialogue above, I realize that I got mixed up with what I first wrote about glucose and the liver. In fact you are absolutely correct that suppressing cephalic phase (sometimes also called a Phase I response) will result in blood glucose rising more quickly than it would had there first been a cephalic phase response.  The result is that by suppressing the cephalic phase response (for example using SLD, noseclipping, or avoiding sensory cues), not only will "pre-meal" hunger be reduced (because there is less circulating insulin prior to eating, but also blood glucose will rise faster after eating, and satiety will kick in more quickly (assuming one is not insulin resistant and has healthy glucose transporter function to the cells).

But this fact actually supports my main point...that SLD works because it suppresses cephalic phase insulin, keeping blood glucose from dipping before eating (staving off hunger longer) and allowing blood glucose to rise faster after eating (suppressing futher appetite during the meal and inducing one to eat a smaller meal  than otherwise).

Finally, in response to your question regarding evidence that cephalic phase insulin has ever been extinguished.  I have...evidence to support this...from the great Ivan Pavlov himself. 
Good for salivation,  what about insulin? ... and yes, salivation ... so a reflex conditioned over a couple of months took several weeks to die out. And the insulin reflex, conditioned and reinforced over say 30 years, will die out in 2 days? And I posted a (weak-evidence) review article that showed that blocking cephalic responses did not alter learned eating behaviors.  There are some learned behaviors that never go away ... I posted some examples above.   Moshe Feldenkrais, who studied Pavlov and his contemporaries deeply, I think in the 70s had lists of learned behaviors that, once developed, never go away.   I've forgotten most of the list unfortunately. 
These reflexes took hours, or in some cases days, to die out--not weeks. And this applied to unconditioned (natural) responses to direct presentation of food, not just recently conditioned responses.  Furthermore, Pavlov was not just measuring external salivation. He also surgically inserted collection tubes directly into the dogs' digestive tract (stomach, instestines, pancreas) so that he could collect internal secretions.  And these digestive secretions extinguished as well as the salivary secretions.  Pavlov himself was unaware of the existence of insulin until later in his career, but other labs were quick to show that the insulin response was just as subject to classical conditioning as the salivary response. Here is one recent study showing this effect:
http://ajpendo.physiology.org/cgi/content/abstract/249/6/E639
Karen Teff, in her article "The Physiology of Flavour Perception" details how this response is mediated by the tractus soliarus in the brain's appetite center. This is a conditioned response by which appetite cues become associated or dissociated from an autonomic response of the vagus nerve, which controls preprandial secretions of insulin and other hormones in the digestive organs.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6VHY-3WJNMDT-81&_user=10&_coverDate=12%2F31%2F1996&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1187668406&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=215aaebcd461762c424df88a05484c55

Regarding the claim that "there are learned behaviors that, once developed, never go away", I can understand that it may be difficult (e.g. for strong addictions), but I would not say it is impossible, and would be hesitant to use the word "never".  There are many examples of the use of successful extinction of unwanted behaviors, and where extinction per se is not enough, counterconditioning and even aversive conditioning can override and reverse learned behaviors. In recent years, psychologists and neurologists are learning that neuroplasticity is far greater than once realized.  The key insight is that changing neural pathways is often slow and arduous, requiring extensive repetition and reinforcement.

I'm searching for an explanation, something that will keep [the weight] off this time.    I'd rather have a correct answer and have my fat problem solved than accept an incorrect answer that temporarily satisfies me and have to solve it again 2 or 3 years from now, for the 10th time. I've been through this cycle too many times, from Pritikin (yes, you read that right) on down to today, to let myself pat myself on the back, again,  at having succeeded,  and let my guard down and let the whole thing repeat itself AGAIN. Low carb plus counting calories plus resistance training is working, and I'd like to keep on top of developments so I can nip the problem in the bud if it starts again.  Insulin control looks like an important ingredient but it's not the holy grail.
We are all on a long journey of self-improvement.  It seems that you have a lot to share with us, and I especially appreciate the physiological insights you've picked up, not only from the literature, but from your own experience.  Both of us are in agreement that low carb is important, but may not be sufficient, for weight control (not to mention the many other health benefits of controlling blood sugar and insulin).  I am also a big believer in resistance training, particularly high intensity resistance training that pushes you to the limit, for that is what really builds muscles and improves insulin sensitivity.  I am a follower of Doug McGuffs's "Body by Science" and the more practical books on "slow cadence" resistance training like "Slow Burn" and "Power of Ten". This high intensityy method has also helped my wife to significantly improve her ability to get around, having had multiple sclerosis for 20 years. She can now walk more or less unassisted by canes.

I think the main limitation of low carb is that it doesn't go far enough.  I think one may also need to limit protein and increase fat in order to really allow fat loss to occur.  You can say that those of us with "stubborn metabolisms" need to do more to lose weight.  But another way to look at it is that we are very efficient, and as long as our appetites are satisfied and we are getting adequate vitamins, minerals, and essential fatty acids, we are "cheap keeps" and we can lower our grocery bills more than those who eat more liberally.
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NTB

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #22 on: January 31, 2010, 07:34:45 PM »

Here is an interesting article that uses cephalic phase (pre-prandial) insulin response to explain why sugar water suppresses appetite, but apple pie doesn't (at least in men!) This may answer the age old question about why "sugar" (and other pure sweet tastes) is not a "flavor" in the SLD diet. The boldface is my addition:

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T0P-3YYTHR8-D&_user=10&_origUdi=B6VHY-3WJNMDT-81&_fmt=high&_coverDate=06%2F30%2F1995&_rdoc=1&_orig=article&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=b8ba8be2680a3aa75923bd2a1150a9a3

Teff et al, "Sweet taste: Effect on cephalic phase insulin release in men",
Physiology & Behavior, Volume 57, Issue 6, June 1995, Pages 1089-1095

Abstract
To determine whether sweet-tasting solutions are effective elicitors of cephalic phase insulin release (CPIR) in humans, two studies were conducted using nutritive and nonnutritive sweeteners as stimuli. Normal weight men sipped and spit four different solutions: water, aspartame, saccharin, and sucrose. A fifth condition involved a modified sham-feed with apple pie. The five stimuli were administered in counterbalanced order, each on a separate day. In study l, subjects tasted the stimuli for 1 min (n = 15) and in study 2 (n = 16), they tasted the stimuli for 3 min. Arterialized venous blood was drawn to establish a baseline and then at 1 min poststimulus, followed by every 2 min for 15 min and then every 5 min for 15 min. In both study 1 and stud) 2, no significant increases in plasma insulin were observed after subjects tasted the sweetened solutions. In contrast, significant increases in plasma insulin occurred after the modified sham-feed with both the 1 min and 3 min exposure. These results suggest that nutritive and nonnutritive sweeteners in solution are not adequate stimuli for the elicitation of CPIR.
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kt

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #23 on: February 01, 2010, 07:12:32 AM »

...which makes me wonder if our bodies know that sugars are not the best source of fuel for us...

 :P

Kate
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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #24 on: February 04, 2010, 12:23:41 AM »

Thanks for keeping me updated, I appreciate it.

I think much of the research on cephalic response has not made it into electronic format yet.   I researched it as best I could, being a layman,  last time I had free access to a medical school's libraries. 

Not being a researcher I'm sure I missed a lot.

And where is your blog - maybe I can check there occasionally,  instead of you having to do extra work typing your information twice.

Here is an interesting article that uses cephalic phase (pre-prandial) insulin response to explain why sugar water suppresses appetite, but apple pie doesn't (at least in men!) This may answer the age old question about why "sugar" (and other pure sweet tastes) is not a "flavor" in the SLD diet. The boldface is my addition:

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #25 on: March 04, 2010, 09:03:09 PM »

Thanks for keeping me updated, I appreciate it.

I think much of the research on cephalic response has not made it into electronic format yet.   I researched it as best I could, being a layman,  last time I had free access to a medical school's libraries. 

Not being a researcher I'm sure I missed a lot.

And where is your blog - maybe I can check there occasionally,  instead of you having to do extra work typing your information twice.

Here is an interesting article that uses cephalic phase (pre-prandial) insulin response to explain why sugar water suppresses appetite, but apple pie doesn't (at least in men!) This may answer the age old question about why "sugar" (and other pure sweet tastes) is not a "flavor" in the SLD diet. The boldface is my addition:

bleeding, if you are interested in more background on the preprandial (or cephalic phase) insulin response and flavor, there are two posts on my new blog that go into this:

1. The Deconditioning Diet (www.gettingstronger.org/diet) summarizes the science behind conditioning and deconditioning of appetite, and lays out a three stage diet plan

2. Flavor Control Diets (http://gettingstronger.org/2010/02/flavor-control-diets/) tries to provide a coherent explanation for something that always mystified me: How can it be that Seth's SLD (which advocates flavorless calories) and the Flavor Point Diet and Alan Hirsch's Sensa tastants (which advocate increasing the intensity of flavors) can paradoxically BOTH lead to effective weight loss and appetite suppression?  What's interesting is that after researching the details, I believe they actually use a common mechanism -- but in different ways! This post also examines some clues in Hirsch's other weight loss approach -- odor inhalers, which work by a deconditioning principle that shares many of the elements of the Deconditioning Diet.

I'd be very interested in your thoughts and feedback on these posts, bleeding.  And that goes for anyone else on this forum.

I do have a special request to anyone else who is interested in this topic. It's not easy to launch a new blog from scratch. So in addition to leaving feedback here, please help me get my new blog forum started by leaving some comments and even starting some new threads on the "Getting Stronger" forum page:
http://forum.gettingstronger.org/index.php

It doesn't have to be lengthy or profound - even a few simple insights or personal experiences are often enough to get a good discussion going.  And by being an early contributor, you can really help shape the conversations that take place. A few SLDers have already posted there, and I thank them for helping to get things started.

Thanks!
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Click HERE to check out the Deconditioning Diet and other self-improvement ideas on my blog "Getting Stronger"

abs999

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Re: Flavor-triggered insulin & fat cell capacity . . .
« Reply #26 on: July 26, 2012, 02:12:18 AM »

It is impossible to have high levels of insulin in your system while burning fat at the same time. Think about that. If you eat a meal that has too high of a Glycemic Index, your blood sugar will spike, causing a large release in insulin. During this period of time your body cannot use fat for fuel (even if you are operating under a calorie deficit and even if you workout like crazy). You can get everything else right and not make good progress if you allow your insulin levels to get out of whack.
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