I'm not trying to be difficult. Under the terms in the information you just gave, insulin response is triggered by ALL food. I was asking how broccoli could be as bad as ice cream. In that first few seconds, both foods would cause the same reaction in the body, yes. I feel the facts support the statement that the similarity ENDS there, however.

To CAs, the initial similarity is all that matters. The CAs system knows it is going to receive carbs, it doesn't care about the difference between an ice cream bar and broccoli, it releases insulin to deal with the total carbs. Then because it knows the total carbs, this happens...

In this case, we're not discussing which food is nutritionally better for you, broccoli is of course!, we're discussing the effect both have on a CAs insulin/body mechanisms. So, in this case, there is no difference. That's the point the Heller's were making. It's the point CAs know, have experienced and live with every day!!

I personally think that's a stretch. Using THAT as rationale, why not eat ice cream every meal? If you're going to disregard nutritional value, glycemic LOAD and just focus on the initial release of insulin with ANY food... it proves MY point that it's selective use of a small crumb of truth for shock value. I'm sure it was the marketing division and probably not the Hellers themselves responsible for the advertising.

I'm not calling into question the integrity of the Hellers, OR the effectiveness of CAD. I've used it myself with great success and really don't care HOW it works, just that it DOES work. However, making blanket statements and loose interpretations of fact is irresponsible IMO. Some people have asked me to explain things you're stated as fact and have avoided this forum because you don't accept ANY opinion but your own.

I'm done. Feel free to gloat.

I think you missed the point I was making again. Insulin is only produced in reaction to carb foods. And though some insulin is released with any carb food, more is released in a CA than in a "normal" person due to a faulty insulin mechanism. Therefore, to CAs, only carbs matter, even artificial carbs, even fiber carbs, even perceived sensed/smelled carbs. Remember, CAs' bodies don't work like those of "normal" people, even "normal overweight" people. So no, nutritional value and glycemic load don't matter for controlling our faulty insulin mechanism. Only total carbs or perceived carbs matter.

Saying that doesn't negate that vegetables with fiber are healthy and necessary for good health. So no, I wouldn't select a diet comprised entirely of ice cream. But that isn't what the conversation was about. We aren't talking what the body runs best on. We're talking about how a CAs body reacts and what the ingestion of carbs, even fiber carbs does to a CAs appetite.

I don't think I don't accept any opinion but my own. I'm sorry that's your perception. I read a lot, I research a lot on many subjects. The Heller's have supported their findings in CAD with multiple pages of bibliography as well as original research. I've supported this "opinion" with quotes from both the Heller's books and cited independent research as well as 40+ years of living in a CAs body and experiencing my own reality. I knew the dynamics if not the scientific explanations of carbohydrate addiction before the Hellers even wrote CAD.

Now I'm done too.

Zuleikaa,
You are confusing features of the two insulin phases. Yes there are two phases, however you seem to be under the impression that the 1st phase is in any way influenced by what type of food you eat.

The 1st phase insulin response is initiated in preparation of eating. Tastes, smells, sights, and eating anything at all (whether or not it has calories) will tell your body "meal incoming" and thus start the process of releasing insulin. What you don't seem to realize is this insulin response is a fixed amount completely independent of meal to meal macronutrient or quantity fluctuations. This secretion of insulin is completely independent of blood sugar increases; it is not designed to keep the body out of a hyperinsulinemic state, it exists purely to prepare the individual for meal initiation.

Over a long term trend of time you can increase or decrease the size of this fixed amount (for example, a type 2 diabetic who still has a functioning pancreas will have a larger 1st phase insulin response than someone who has lower resistance to insulin, likewise someone who eats a lot of carbs has trained the body to send out a higher 1st phase insulin response than someone who eats lower carbs). However, meal to meal composition and calorie amounts do not affect how much insulin is released. It's not a plastic thing that corresponds to quantity/type of food like phase 2. It really does not matter at all if you eat broccoli with your meal or if you don't eat broccoli with your meal, as long as you initiate eating you are triggering the insulin release. Eat a chocolate cake, eat a bucket of sugar, it makes no difference the size of the 1st phase insulin response is the same.

Things like drinking diet soda all day or chewing sugarless gum all the time are problematic for some because they trick the body into thinking food is coming and your body releases insulin in preparation for a meal. If you are very sensitive to blood sugar fluctuations, meaning if they tend to give you cravings and set you up for over eating, it's best to avoid these things in absence of a meal. With a meal they can be consumed without a problem, since the 1st phase insulin response is of a fixed amount and is only released in response to anticipation of eating. The problem is when you eat them all day without a proper meal.

Then there is the 2nd phase insulin response. This starts shortly after eating in response to an increase in blood sugar. This is the part where we get mondo sized swings in blood sugar which result in hard core cravings, and over eat all the time. This insulin response is entirely, 100% dependent upon the rate and amount of glucose entering the blood stream. Again, eating broccoli as part of your meal can only help mitigate and blunt the insulin effect, since the fiber in broccoli works to slow down the rate of glucose entering the blood. Fiber can never ever be absorbed and metabolized as sugar by the body since we don't have the cellulose enzymes to do so.

So, fiber from broccoli can't adversely affect insulin response. It doesn't have sugar so it doesn't increase phase 2 response, and it is consumed with a meal anyway so it is neutral in regards to phase 1 (since the meal itself is going to trigger the response). Unless you are sitting around eating broccoli all day out of boredom (like people do w/ DC and chewing gum), it is highly unlikely that broccoli is interfering with your weight loss or giving you cravings because of any insulin issue. If you think it is, it's probably more to do with the dressings that people put on broccoli. The little "nodes" of the tree branches are reallygood about absorbing sauce, salt, fat, and other things which stimulate appetite and can lead to over eating. If you ate just the stems, I doubt you would consider broccoli a problem.

As to whether or not icecream or broccoli is better at controling weight and blood sugar... well that's just beyond ridiculous. Ice cream has the same potential for initiating the phase 1 insulin response as the broccoli, so they are equal in this respect. However, ice cream has a whole bunch more "net carbs" and thus a higher phase 2 response so in this respect it is way worse than the broccoli. Plus, ice cream has like 20 times the calories of broccoli as well which can make weight loss difficult. Then there is the nutritional factor. Ice cream has sugar, fat (which we can get from more nutritious sources i.e. nuts and meat), very little protein and some scant calcium/vitamin a/vitamin d. Broccoli though low in energy (protien/fat/carbs) is replete with minerals vitamins and antioxidants.THere is absolutely no comparison between ice cream and broccoli, I don't care if a test told you you were a "carbohydrate addict". There is no justification for eating ice cream over broccoli and actually believing it is better. You're only hurting yourself.

This is incorrect. It's simply not true.

Insulin is released in response to meal initiation. It doesn't matter if you eat pure olive oil, pure protein, or fiber, or plastic. All the various physiological changes that occur when food is being consumed (the smell of food, the salivation, taste bud stimulation, chewing, the swallowing, the entry of nutrients in the gut, etc) trigger phase 1 insulin response. This is a very small amount of insulin which will produce a very minor change in blood sugar.

I myself notice when I chew sugarless chewing gum (my bad habit), I can literally anticipate feeling shaky and crappy soon there after (oh and my stomach will hurt too, but I think thats more to do with the SAs than the blood sugar mess up). I'm very sensitive to the adrenal hormone release that comes from insulin secretion and the blood sugar fluctuations, so I can always tell when there's been a sudden change. It's a very very very minor thing (like a "blip" I call it... it's not enough to drive me to be hungry or anything, just minor discomfort), but I have verified it. Plus, there is a whole body of research which shows that the perception of eating (this includes diet sodas) - not blood sugar itself - is what triggers phase 1 insulin release.

I can appreciate that some people might be more sensitive to the phase 1 insulin response, and would therefore be well served by limiting how frequent they eat and definitely not take to chewing gum and drinking dc all day. Perhaps this is what a carbohydrate addict is... someone who is very sensitive to the p1 response and it can give them cravings driving them to over eat. This, I think, is the real value of CAD. It helps people who tend to eat more when their drive to eat is being over-stimulated by drinking DC and chewing gum.

However, eating broccoli as part of a proper structured meal isn't going to adversely affect anything. You're going to eat anyway, phase 1 insulin release is going to happen, what difference does the broccoli's fiber make now? Remember, phase 1 is a fixed amount of hormone release, it is not dependent on blood sugar or type of matter being ingested (that's where phase 2 comes on). So what will fiber do then? Oh that's right, it will slow the rate of glucose entrance into the blood thus minimizing the phase 2 response. The net result of fiber is positive effect on satiety and blood sugar control.

Is the medical status of being a "carbohydrate addict" able to be assessed via any sort of blood test or screening procedure? Just how do you know if you are a "CA"? Is it scoring high on that test? Cool, before Atkins I scored like a 7 I think. I would have gotten higher but salt/fat has always been my junkfood weakness, whereas the test is biased in favor of fat/sweet eaters.

How is it a 10 question test is sophisticated enough to isolate a minority within a minority who has a profound metabolic abnormality? Heck, a disease where you can't eat broccoli w/o later binging sure sounds to me like a rather profound disease.

Zuleikaa I'm not trying to give you a hard time. I'm trying to get you and everyone else to think critically about this. You are using circular logic. YOu have identified yourself as a "carbohydrate addict", but the criteria which defines being a "carbohydrate addict" is identifying yourself as such after taking a cosmo-magazine like quiz. Every time you are asked to prove why you believe something is the way it is, you go back and say "oh only for those who are carbohydrate addicts is this true" as if the term "carbohydrate addict" was predefined and the answer therefore obvious. It's illogical. It's sort of how if I asked "cats use a litterbox, so why can't you" and then you said "humans can't use a litterbox". Seeing as the term human is predefined to all of us, your explanation has an obvious logical reasoning (humans use toilets, not a litterbox, so your explanation to my question makes sense).

However, there is no such thing as a CA. This is a made up term that one is labeled with if they so choose. There is no medical test by which you can test positive for being a carbohydrate addict. There is no defect in the endocrine system identified by which a certain subset of the population has a phase 1 insulin response that is made stronger/more pronounced than the average person if they eat certain things on a meal to meal basis.
SO when you say "carbohydrates can't eat broccoli" as if that solved the issue, it really solves nothing. As far as I know, carbohydrate addict is a meaningless label. You still have to prove that carbohydrate addicts, as defined by you and the Hellers, even exist.

Its the Woo
Actually, there is a medical test for it. The Hellers use it all the time. There is a time-reaction test that the Hellers use to confirm the status, severity of case and particular level of sensitivity.

Additionally, the identification of being a CA isn't based on just a 10 question survey. That test is sort of a lead in for people to investigate further. The survey that is used in the clinical environment is an in depth, multipage one. You can see part of the longer test in their book. So being classified as a CA is not as simplistic as the 10 questions make it sound. I agree with that.

Indeed, I am arguing that the initial insulin response is the only important one for carbohydrate addicts. The first phase is based upon both anticipatory release (this in fact is based upon your body's knowledge of prior meals...therefore if they were perceived to be high carb, this release is in proportion to the perceived carb count of the prior meal). So yes, it's in response to any food but in anticipation of the amount of carbs you consumed in a prior meal (insulin is released to deal with only carbs. Insulin sweeps sugar out of your blood, sugar only comes from carbs)...and when you put the food in your mouth. So if your sensory/olfactury sensors feel it's carbs, the release amount is adjusted upward and remember my argument and the Drs. Hellers is that this release is exaggerated in carbohydrate addicts. That last paragraph certainly sounds like a description of increased appetite and cravings to me!!

Therefore, it further doesn't matter that the carbs are fiber and won't be digested. At this point, all the body knows is that carbs are coming and not only is anticipitory insulin released but anticipatory glucose as well which incurs a further release of insulin in the gastric phase. Again exaggerated in CAs. This is why it is so important for a CA and those on CAD that the meals before the reward meal are very low carb. It's not about calorie restriction. And while it's true that the early phase insulin release is small relative to the later release during the gastric phase, it's more powerful than the later, greater release.

My reading of this is that fiber, which slows the release of carbohydrates and resulting glucose/insulin release in the second phase, actually increases the initial release of insulin. Again, this initial release is all that matters to CAs. And the initial release, though smaller, is more powerful than the second.

Note: It's starting to irritate me that you (not you in particular, but people who want to argue and dispute with me about CAD) can quote tired, erroneous scientific arguments as truth but I have to find studies and research to support my point. Nor am I allowed to quote the Hellers, the founders of the diet as backup, because no one believes what they wrote or their research anyway. I can imagine how the founders of this board felt when people wanted to argue Atkins with them by quoting dietary "truisms' that became the truth by people constantly repeating them and quoting the people that quoted the people that repeated them.

You mean like a glucose tolerance test? That tests insulin resistance and can identify diabetes, not "carbohydrate addiction".

If not, what is the test called? Do scientists recognize this test as diagnostic of having an abnormal cephalic insulin response?

So basically another survey is used to identify people who have this severe metabolic abnormality. This makes sense to you?

I can appreciate and understand you doing what you thinks works for you. But come on, when you say things like "carbohydrate addicts shouldn't eat broccoli" when there is in reality no validity for such a claim, or even the status of "carbohydrate addiction", you have to feel a little awkward about it. Being a carbohydrate addict is in essence defined by the hellers as someone with a 1st phase insulin release that is "smart", whereas for everyone else it is a fixed amount that is blind to the nature of the ingested matter. So, for a supposed "carbohydrate addict", if they ingest material that is similar to carbs in any way, it starts the individual on a blood-sugar cycle which leads to cravings/hunger and finally a binge. If you ate a piece of meat and cheese but NO broccoli, the cephalic stage insulin response would be smaller than if you ate the same meal with broccoli. This would start a chain of events that is not conducive to thinness.

You don't seem to appreciate that this belief flies in the face of what we understand about biology. As I said numerous times, the cephalic stage insulin response is a fixed amount that is independent of meal-to-meal macronutrient variations or amounts. THe size of this amount is dependent on things like biology, insulin resistance (raises it), and a long term history of dietary patterns (high carb & high calorie raises it). It is triggered only by the perception of an initiation of a meal (which may not necessarily include calorie or sugar uptake). Furthermore, it is so very small that it is really not enough to cause any significant grief to most people even if it is a "false start". Again let me refer back to my chewing gum example... it produces uncomforting feelings, but they are not what I would call a strong factor which affects food intake and weight.

If you are to prove carbohydrate addiction exists, you have to prove the following:
a) that in a minority of people the 1st phase insulin response IS dependent upon meal-to-meal nutrient composition...
b) that this minority, if it exists, sees the problem made worse when those meals are in any way comprised of foods that remind the body of carbohydrate. This causes the cephalic phase to be larger, triggering glycogen dumping, which triggers the phase 2 response which is where trouble begins and you get on a blood sugar cycle.


It's not that I can't relate to having "faith" in something and really believing it. I have my own crazy beliefs. For one, I believe in astrology. I believe the signs and placements upon my birth symbolically represent traits I have. I believe being someone predominantly libra ruled probably gives me my annoying love of debate and playing devil's advocate. I believe having the moon in pisces makes me sensitive and prone to engaging in nutty things like astrology. I really could argue in depth about the signs and planets having researched the topic. I do think astrology has helped me sort out feelings, problems, and my outlook on life.

Despite my love of astrology, I am capable of separating what is real and proven and logical from what is feeling and fantasy. Astrology is fantasy. It has a place, that place is relegated to the status of "fun"... Ouija boards and fortune tellers and other things which purport to be guidance tools but really have no basis in reality for doing what they purport do. Even though in my personal life or among other like minded individuals I would speak of astrology as if it were proven and scientific, I am capable of setting boundaries and drawing limits on my imagination. I would never walk into a gathering where people were discussing psychiatry or psychological help, and start blathering about astrology as if they were the same thing. Know what I'm saying?

Your insistence upon recognizing "carbohydrate addiction" (defined above) as a real state, when this has never been proven in reality, is similar to me saying you must hold the beliefs you do because you have a lot of neptune aspects. I'm sorry Zuleikaa but you have to admit it's simply not real. Fantasy. Never been proven. Zero evidence to support it, other than personal testimony.

You are absolutely free to believe what you want to believe... just as I am free to believe that I am a double libra with a pisces moon, and just as I am free to believe in aliens and ufos and ghosts etc. However, when you give erroneous advice to others because of your fantasy inclinations, when you take something that was originated in the fantasy-realm and speak about it like it's fact (that broccoli can cause blood sugar disturbances in this minority of people and that even ice cream is a better choice), that's just irresponsible. Come on, you have to be aware that this belief is at heart foolish. Even if you don't totally believe that people should disregard nutrition, you have believe that no one ever got fat on broccoli, nor did broccoli ever drive anyone to eat too much. That's just silly.


Again this hearkens back to my original point of contention. You seem to be under the impression that cephalic insulin release is contingent upon a meal-to meal basis when this is entirely false. You seem to think that if you eat broccoli, your body will "think carbs are coming" and produce a larger cephalic response in anticipation. This is not true and it is physiologically impossible since the cephalic phase insulin response is, as I have said numerous times, a fixed amount which is not dependent on type or quantity of matter consumed.

It is solely the amount of insulin your body has learned it should produce after a very long term trend. Furthermore, it is an extremely tiny amount of insulin, not enough to cause major blood sugar upsets. If you are sensitive to blood sugar fluctuations it might be a problem for you though.

Yes, the cephalic release is more powerful in some people (type 2 diabetics and high calorie / high carb eaters primarily), and yes over time you can train your body to anticipate a need for more insulin upon eating and thus increase the amount of that fixed amount.
However, the size of the cephalic phase insulin reaction is not contingent upon the nutrient make up of the current meal you are eating. I can't say this enough since this is the major justification for carbohydrate addiction but it is at odds with biological reality. THe first stage insulin response is determined by things like genetics, insulin resistance, and a long term past history of eating a high carb/high calorie diet... but eating broccoli with dinner is not one of them. One thing is certain. Eat broccoli or do not eat broccoli, it really doesn't matter. The cephalic insulin response in that moment will be the same, since it is the same for all matter - sweet or not, carbohydrate containing or not, fiber or not. It is dependent only upon long term past history, genetics, and physical state.

While calorie restriction alone might not be the sole reason that people lose weight, all weight loss is caused by you burning more calories than you take in. Low carb diets, including CAD, make it easier to take in less calories and they tend to increase the rate that you burn calories (in some people this is a very large difference). It's not magic, it's reality, the laws of energy conservation and thermodynamics and what not.

With that said, do you honestly believe the rigid restrictions and frequency of the CMs have nothing to do with tricking people into reducing caloric intake throughout the day so that the RM can be justified? Come on Zuleikaa . If I have 2 CM comprising of a chicken drumstick and a salad (under 300 calories each), even if I eat a big chinese dinner for my RM (700 calories) I've only consumed 1300 calories. Furthermore, most of those calories come from foods which tend to have a low efficiency and more of a thermic effect. If I am very overweight, 1300 calories of mostly LC food would produce very fast weight loss (heck even at my weight it would produce slow but sure weight loss).

I think the real magic behind CAD is that it allows a person to eat whatever they want without over-eating. If you are someone who hates restricting what you eat (I do not have this problem, my gripe is with the exercise part grumble grumble), if you tend to "fall off the wagon" all the time because you loathe dietary restriction, and if you have an especially troublesome problem with fat/sweets/starches, then CAD might be the plan for you. I don't have a problem with atkins or any low carb diet because I've always been a fat/salt/starch eater. I've never been inclined toward over eating sweets and can very much do without them. Even though I miss my starch, I have no problem eating only meat for the rest of my life, not that I do this or anything (I'm just trying to illustrate that Atkins doesn't make me feel deprived).

If you are the sort who really loves sweets simply because you like their taste and mouth feel, or you can't be without starch or whatever your low carb diet issue is, you will eventually fall off the wagon. Again and again. CAD is a great way for you to low carb and not let yourself feel so deprived that you get to the point where you abandon everything. So I do support a cad-like diet in principle (if you restrict a lot earlier then you can justify indulgences later). CAD works for primarily emotional and behavioral reasons and it offers limited physiological advantages over the other LC plans as far as I can tell. The scientific justification for the broccoli claim is very, very weak.

The initial release of insulin is a fixed amount and it is very, very small. It responds only to perception of the eating act, not anything in particular that you eat. Furthermore, it is so infinitesimally small that it isn't enough to cause major swings in blood sugar. It might make you a little hungrier and uncomfortable (I am sensitive to the adrenal hormone release associated with blood sugar fluctuations, so this "false start" to dcs and chewing gum makes me feel jittery and icky). It likely will not start you on a blood sugar roller coaster, unless you are extremely sensitive to blood sugar fluctuations. I would liken it to eating a very tiny piece of candy.


That's not the same thing Zuleikaa. If low carb pioneers wanted to debate the merits of carbohydrate restriction, they had numerous studies to support them. A study was just done that showed when all other variables are controlled for, mice on a high glycemic diet develop more signs of syndrome x than those on a low glycemic diet.

There is no scientific evidence to support this "abnormal cephalic stage insulin response" theory. THere is anecdotal and observational evidence, but so is there observational evidence that people behave like their rising, sun and/or moon sign. That's not good enough. Some observations that the processes even exist might be a start.

Okay
It seems you don't like the word carbohydrate addict and say there is no definition. Here is the definition:

Car-bo-hy-drate Ad-dic-tion:
• A compelling hunger, craving, or desire for carbohydrate-rich foods;
an escalating, recurring need or drive for starches, snack foods, junk food, or sweets.
• Carbohydrate-rich foods include, but are not limited to: breads, bagels, cakes, cereal, chocolate, cookies, crackers, danish, fruit and fruit juice, ice cream, potato chips, pasta, potatoes, pretzels, rice, pie, popcorn, and sugar-sweetened beverages.
• In addition, carbohydrate act-alikes (sugar substitutes, alcoholic beverages, and monosodium glutamate) may trigger intense or recurring carbohydrate cravings and/or weight gain.

As many as seventy-five percent of those who are overweight, and many normal-weight individuals as well, are carbohydrate addicted. Though many people may suspect there is a physical imbalance that makes them crave carbohydrates and put weight on easily, the underlying cause of their cravings and weight struggles often goes undiagnosed and untreated.
Carbohydrate addiction is caused by an imbalance - an over release of the hormone, insulin, when carbohydrate-rich foods are eaten. Among its many jobs, insulin signals the body to take in food (it has been called the "hunger hormone") and, once the food is consumed, signals the body to store the food energy in the form of fat.
Too much insulin results in too strong an impulse to eat, too often, and a body that too readily stores food in the form of fat.
The scientific term for this condition is post-prandial reactive hyperinsulinemia which means too much insulin is released after eating. Over time, people who are hyperinsulinemic become insulin resistant, that is, the cells in their muscles, nervous systems, and organs start to close down to the high levels of insulin in their blood. Insulin is no longer able to open the doors to these cells and allow food energy (blood sugar or glucose) to enter. At this point, one may experience symptoms of low-blood sugar levels (hypoglycemia) including irritability, shakiness, tiredness, intense cravings, confusion, and headaches. Since the blood sugar cannot easily enter the muscles, nervous system, or organs, much of the food energy gets channeled into the fat cells and weight gain comes easily. Over time, however, as high insulin levels continue, even the fat cells can shut down and the blood glucose gets trapped in the blood stream bringing on the condition known as adult-onset diabetes.

Now post-prandial reactive hyperinsulinemia is definitely recognized, tested and studied.

Hyperinsulinism (hyperinsulinemia): Increased levels of insulin in the plasma due to increased secretion of insulin by the beta cells of the pancreatic islets and decreased liver removal of insulin or insulin resistance. This condition is most commonly found in obese persons with hyperglycemia.

And since you're assuming that I and other adults are self-identifying and assuming our symptoms, perhaps you'll take this as testimony that it does exist. After all infants can't read yet:
http://www.homestead.com/emguidemap...oglycemia.html-

hyperinsulinemic infants commonly present with increased appetite and demand for feedings, jitteriness, wilting spells, and seizures; hypoglycemia develops 4 - 8 hours after feedings and high doses of glucose (10 - 15 mg/kg/min) may be required to maintain a blood glucose > 100mg/dl; acidosis and ketosis are usually absent and elevated levels of serum proinsulin and C-peptide are present
- persistent hyperinsulinism in infants can be due to familial and non-familial hyperinsulinism, beta-cell adenoma (insulinoma), beta cell hyperplasia and factitious hyperinsulinism (sulfonylurea use)

then
http://www.endotext.org/diabetes/di.../diabetes16.htm
FFA) (3,71,157). Initially, hyperinsulinemia compensates for insulin resistance, thus preserving normal glucose tolerance. However, over time, hepatic insulin resistance worsens and b-cell compensation deteriorates, culminating in fasting hyperglycemia. Pharmacological therapies that inhibit carbohydrate breakdown in the gut (a-glucosidase inhibitors), stimulate insulin secretion (sulfonylureas, meglitinides), suppress hepatic glucose production (metformin, thiazolidinediones), or increase skeletal muscle glucose metabolism (metformin, thiazolidinediones) exhibit a beneficial effect on fasting and/or post-prandial plasma glucose and overall metabolic control in patients with type 2 diabetes. There is a growing realization by physicians and other caregivers that successful glycemic control, for most patients, will eventually require combination therapy.

More reading you can do:

http://www.findarticles.com/p/artic..._25/ai_87128753

http://www.findarticles.com/p/artic...i_19652423/pg_3

http://diabetes.diabetesjournals.or...nt/47/5/788.pdf

http://www.findarticles.com/p/artic...v47/ai_20318179

http://www.rense.com/general53/ob.htm

http://www.joplink.net/prev/200201/01.html

As I said in an earlier post, when the Hellers wrote CAD they had pages of bibliography on studies that were done proving the existence of carbohydrate addiction or post pradial hyperinsulieminia but you don't seem to want to accept that.

I'm done.

We'll just have to agree to disagree.

Sigh.

Everything you just quoted on hyperinsulinemia and hypoglycemia has to do with an abnormally exaggerated phase 2 insulin response. You are completely changing the topic of discussion here. I never disagreed that the phase 2 response if exaggerated can cause all those problems listed. I never disagreed that the phase 2 response was dependent on dietary composition and blood sugar and individual resistance, and is therefore very much capable of being exaggerated and causing the wild swings in sugar which produce physical addictive symptoms. I would never do that since I would be saying something completely unscientific.

We were talking about phase 1 insulin response originally. You seem to believe that this is a fluid, fluctuating thing and can be influenced by meal composition like phase 2 can. Meaning, if you eat broccoli with your dinner, you will cause your body to produce too much insulin immediately due to the fiber, which will push your sugar too low, which will trigger glycogen dumping, which will trigger the phase 2 response. This is entirely untrue and will not happen. The 1st phase insulin response is, for the final time, a fixed very small amount of insulin. If you are eating a meal you will release the same amount of insulin in the 1st stage as you would have, whether you eat broccoli or meat or a bucket of sugar or plastic. It makes no difference, since it is contingent only upon the initiation of eating and is blind to actual nutrients. That's where the phase 2 comes in, to actually mop up the sugar. Phase 1 is just "prep" for eating.

Even if you are one of those people who has a larger phase 1 response due to your diet or genetics or insulin resistance, it is STILL far too small to produce the wild swings in blood sugar like the 2nd insulin response can. That's why the overwhelming majority of people can do things like drink dc and chew gum constantly without being made to feel ravenous by it at the end of the day. If the phase 1 response was of any magnitude to even a normal phase 2 response, just smelling food could trigger clinical hypoglycemia. People would have to hurry by pizza parlors to avoid passing out. LOL.

Furthermore, the definition of a carbohydrate addict that you're using now is basically someone who likes to eat fat/sweet or fat/starch combination foods (no one eats a bagel w/o cream cheese or a fat free cookie of their own volition, right ?). What does this definition have to do with the relevant aspect of supposed "carbohydrate addiction" that we are discussing in this moment? Though you never directly said it, if we are to be logically consistent what truly defines a carbohydrate addict from normal people, even normal people who have an abnormal insulin mechanism, is that they have an abnormal cephalic stage insulin response. For a carb addict, eating broccoli will trip the wire for the phase 2 response indirectly because their phase 1 response can magically tell what kind of food you are eating and is capable of changing in magnitude and potency based on that. Broccoli leads to body thinking carbs are coming which leads to a very large insulin response, which leads to too low sugar which leads to glycogen dumping which leads too too large of a phase 2 response which starts the cycle.
For everyone else, the phase 1 insulin response is a fixed very small amount.

What does this definition do to prove any of your/their theory regarding the abnormal 1st stage response? Yes, so some people really like cakes and cookies or pizza and hoagies. How does this prove that they like it because of the condition you claim they have? Maybe they have an emotional eating problem. Maybe they simply are eating too many carbs because of the former and screwing up the 2nd phase response as a response. I do not deny that hyperinsulinemia from insulin resistance coupled with a too high carb diet can cause addictive type behaviors/feelings for sugar. So again don't give me research which deals with the 2nd phase since I wasn't debating that.

What we were debating is whether or not the 1st phase insulin response can do the following:
a) in some people it is capable of changing meal-to-meal, type of substance to type of substance.
b) in some people, if they eat the "wrong" things like fiber and artificial sweeteners, the response can be very powerful and result in a hypo, which results shortly after in glycogen dumping, which then triggers the phase 2 response, thus opening the floodgates of problems.

You have yet to prove any of that. All evidence shows the first phase insulin response is a small fixed amount. It doesn't care if you're eating plastic bits or a box of sugar, it's the same. Furthermore, it is a small amount, too small to ever produce the profound lows that you think can result in glycogen dumping (at least in normal people... however in diabetics this might be different... some diabetics have reported that drinking dc and eating a large volume low calorie meal can trigger glycogen dumping for them, but is important to remember most people are NOT diabetics). Even if it could do this, you are eating a meal anyway so the effect is mitigated.

I'm still talking about phase 1. It's post ingestion, not post digestion.

And again we're talking only about carbohydrate addicts (there's those two hateful words again), excuse me pphs, so it doesn't matter how long "other" people can chew gum or drink diet soda without an insulin reaction, does it? They don't have the condition.

Actually I posted an article that said the first phase though smaller is more powerful than the second.

Originally posted by ItsTheWoo
Oh that's great...now infants with the condition who exhibit increased appetite have emotional eating problems and like hoagies. I don't think they start that young, lol!!!

Originally posted by ItsTheWoo
As I said insulin is also adjusted by the carbohyrate taste/content of what you put in your mouth. This is also part of the cephalic phase. There are enzymes in the mouth that are only activated in the presence of carbs/carb likes and these send a further signal to produce insulin
phttp://diabetes.diabetesjournals.org/cgi/content/full/50/5/1030
The reabsorptive or cephalic phase insulin response, which lasts for 10 min, is initiated by meal ingestion, as has been demonstrated in humans and rats (123456789). It is abolished by vagotomy in rats (1) and by atropine in rats (1) and humans (10), suggesting mediation by cholinergic mechanisms. However, the mechanism is probably more complex than that executed solely by cholinergic actions on islet ß-cells; noncholinergic mechanisms might also contribute to the response. For example, islet parasympathetic nerves harbor several neuropeptides in addition to acetylcholine, such as vasoactive intestinal polypeptide (VIP), pituitary adenylate cyclase-activating polypeptide (PACAP), and gastrin-releasing polypeptide (GRP) (2). These neuropeptides are released after vagal nerve activation of the pancreas (111213) and stimulate insulin secretion (2,14). Prevention of their effects inhibits the insulin response to oral administration of glucose in mice (151617). It is also possible that the gut hormones, gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1), contribute to the cephalic phase insulin response to meal intake, as both these hormones are potent insulin secretory hormones released during meal ingestion (18) and their secretion is under neural control (192021).
It has recently been established that the early insulin response to meal ingestion is of great importance for subsequent glucose tolerance. This was first suggested by results demonstrating a negative correlation between the 30-min insulin response to oral glucose, as a marker for early insulin secretion, and the 120-min glucose value, as a marker of glucose tolerance (22). Furthermore, prevention of the early insulin response by somatostatin results in glucose intolerance (23), and sham feeding, which increases circulating insulin, improves glucose tolerance after intragastric glucose (9). The importance of the early insulin response for postprandial glucose tolerance is also illustrated by studies reporting that brief administration of a minute amount of insulin during the first 15 min after food intake markedly improves glucose tolerance in obese (10) and type 2 diabetic subjects (24). Whether specifically the neurally mediated cephalic insulin response to meal ingestion is of importance for postprandial glucose homeostasis has, however, not been established

I stand by my position.

The bantering between Zul and Woo is fascinating. I've skimmed some but will read more later. I do have a question though..

Let's say I accept the theory that insulin is released as a small fixed amount at the start of a meal/snack. What happens if instead of finishing up a snack or meal within, say, an hour? What if you don't overeat, but say you keep sipping on a sugary drink (like fruit punch) or munch on something sweet for HOURS but take in "normal" calories within that period (like 400 cals all together). How does insulin play a role when you keep on munching on carbs for that long?

Will there be an overload of insulin?

TrinityX
I don't agree with ItsTheWoo that insulin is released in a small fixed amount. I believe and I think I've proved that insulin is released in variable amounts depending on the total carbs anticipated, sensed, ingested and digested. Insulin response is variable. 1. By the smell of carbs/food or anticipacipation of carbs 2. By the amount of carbs that go into your mouth. 3. The amount of carbs that are digested. Further there is a loop back system that check back to see to see if all glucose is cleared out of the system with the insulin already released or more needs to be released. Additionally, ingestion/digestion can be a continuing cycle out side that hour...so if you continue eating/drinking the process starts again and again, i.e you can be almost continually cycle releasing insulin. This, in fact is what can cause hypoglycemia, insulin resistance, and diabetes, the body continually releases insulin until the cells stop accepting it and the pancreas beta cells stop producing it.

I need to add a caveat to this though. In a normal person, one who does not have hyperinsulimia or insulin resistance, the body releases insulin appropriate to the carb load. So the release cycle could still be constant but the insulin released is in smaller amounts. In fact, the rise in frequent ingestion of sugary drinks, an the concurring frequency of insulin release accounts for a great part of the reason insulin resistance develops and has become so common.

So, Grylygrl......


How are you getting on, hon?

Don't get bogged down by all this...just do what it says in the book you're reading regarding what foods you can eat for CMs and keep your RMs balanced and eaten within 60 minutes.

It DOES work! (WHO CARES WHY?!!! - LET'S JUST LOSE SOME POUNDS!)


Sue