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Hyperinsulinemia (if I'm spelling the word right) is definitely a big word. But, the real question is why am I bothering saying it: Here is the answer---have you ever had a terrible time getting cut on a low-carb cutting cycle? Believe it or not, I know I am not alone here.

Some of you out there have tried the low-carb thing...the fat fast thing...the protein shake diet thing....and still, you have shitty results. Well, that big word I just mentioned might be the problem.

Hyperinsulinemia is the result of cronically high levels of insulin in the blood stream. Those of you who have spent the past decade or so shoveling high carb foods into your mouths and are just now starting to rethink that plan maybe have been suffering from such a high degree of hyperinsulinemia for so long that you have already become very insulin resistant.

A little discussed fact in bodybuilding circles is that ANY type of food, and sometimes even just the smell of food, will release a tiny burst of insulin into the blood stream. For those of us trying to keep our insulin levels low, this can be very disheartening.

Yeah, that's right, even walking past that Cinnabon and getting a whiff can make your body start pumping insulin and storing fat, but before you run out and buy a gasmask to avoid any unwanted smells, it is important to realize that in most normal individuals, the smell of food will not release a detrimental amount of insulin.

But for those of us who have become very insulin insensitive, there is a good chance that even a whiff might cause oceans of insulin to come pouring into our systems, because we have become so insulin resistant that our bodies need to dump tons of insulin out just to get any sort of response from our adipose and muscle tissue.

So what am I getting at with all of this? What I'm trying to say is that a low-carb cutting plan may not be the "quick way" to getting lean that most of us chubby hubbies think it is. If you are very, very insulin insensitive, it could take as long as 6 months or more of strict carbohydrate control just to get your body back to normal.

Now, weight training will, of course, speed this process up. Lifting weights improves insulin sensitivity far more radically than any other form of exercise (in my opinion), and it is that sensitizing factor that causes weight lifting to be such a powerful body comp changing device.

The message here is a simple one. For those of us who have been on a mass phase for the past decade or so, you aren't going to get yourself contest ready in a couple weeks, no matter what training or nutrition program you follow. You'll be lucky to undue the damage you've done to yourself in months, so definitely don't strive for weeks.

A better route is to try patience, get on that low-carb diet and worry about reseting your metabalism. Don't even think of it as a cutting phase....think of it as pre-cutting. Real cutting is still quite a ways down the pipe for you.


and now we wait.....


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Wow, I'm impressed that you rebutted the entire thing. I read the first sentence and dismissed it. OP, you got told.


Thanks BBB, for going through this so I didn't have too lol!

OP if want to learn about REAL diagnosed Hyperinsulinemia buy Harrison's Book on Internal Medicine and read about it there. You will see how laughable your little essay is.

Smelling cinabons CAN regulate voltage gated calcium channels....DUH!


Good reply BBB.

At testup:
So what your saying is that every chef should be fat? I would imagine they cook 5-7 days a week and smell A LOT of foods. The reason the chefs gain weight is that they are surrounded by food to which they eat. So really like BBB said "it doesn't happen".



Actually, the OP is correct. Insulin can be released completely independent from hyperglycemia through the mechanism known as the cephalic phase. The more specific name of this mechanism is cephalic phase insulin release or CPIR. Even saliva is a cephalic reflex to food just as insulin release is although the insulin response isn't as great as when actual glucose hits the blood stream. The purpose of the cephalic phase is to prepare the body for food ingestion which will allow the body to modulate its own influx of ingested nutrients. This will prevent any large deviations in absorption and utilization of the nutrients from occurring. The cephalic reflex can hit the body from the sight, smell, sound, or even the thought of food, but, as I stated previously, the insulin response will generally not be nearly as significant as the response from hyperglcemia itself.

Furthermore, why would a person go into a coma from such amounts of insulin caused by the CPIR? The CPIR COULD cause low blood sugar if no actual carbohydrates are taken in by the body to raise glycemia, but the dangers of hypoglycemia in such conditions where it involves a healthy, non-diabetic individual and having an insulin response natural to the body, especially a CPIR, are very low. Even in the case of a type-II diabetic individual, the amount of insulin produced from CPIR is considered safe because, otherwise, all type-II diabetic individuals would be in for a lot of trouble, more so than in which they already are from being type-II diabetic and, most likely, overweight.

No, the smell of food cannot cause an increase in blood glucose, but, as I have stated before, it can cause secretion of insulin via the CPIR mechanism, a mechanism that is completely independent of the insulin response from hyperglycemia, in anticipation of food ingestion.

Also agreed, but the carb control does help as well.

"Sugary carbs"? I question your use of the term "sugary carbs" because all carbohydrates are made up of glucose, a sugar, so I'm not sure from where you are coming. :wink:

I hope that clears everything up for those who were confused.


I have a man crush on BBB along with Jack Johnson


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Haha yes, "oceans" of insulin could very possibly cause a hypoglycemia-induced coma if the blood glucose levels drop to nil, but the reality is that would of course not happen from levels of insulin excreted via the CPIR and very rarely any cases where only natural levels of endogenous insulin are excreted.

As for the OP's overall "theme of his post," it's pretty all over the place, so it is somewhat hard to tell what at which he's trying to get. He kinda just threw some info in there about insulin being released from smelling it, but he didn't really make any conclusion statement concerning specifically that topic. He just moved right back into talking about insulin sensitivity although he may have been somewhat trying to overshadow the topic of insulin and smelling foods into his essay. Regardless, if his main theme was that smelling foods can dramatically affect body composition, then you would be right.

But yes, the cephalic phase is an interesting topic. The cephalic phase can initiate many of the same digestive functions that activate post-ingestion, so don't research just the CPIR itself, but the cephalic phase as a whole because it is a large topic. I'm glad I could teach something to one as knowledgeable as yourself.

And pedantry is my game, haha. :slight_smile:


@ bushidobadboy:

I seem to have presented myself poorly to you. I'm glad guitarlifter did such a good job at admittedly saving my ass. Yes, I was talking about the cephalic reflex, and yes, if you look into it you will find that it is a well established biological response.

As far as your disgreement with my use of hyperinsulinemia as a chronic disorder, I will grant that I was playing fast and loose with the use of chronic. I identified hyperinsulinemia as chronic because it is recognized as a condition which is often related to metabolic syndrome x. As "conditions" are generally considered chronic, I didn't feel the need to be any more specific. I suppose acute hyperinsulinemia is a real possibility, but not something I find very interesting.

As far as my use of "oceans of insulin", I was being dramatic to make a point. There is a huge difference between even the cephalic response in people who are very insulin resistant and people who have good insulin sensitivity. I didn't mean to suggest that smelling food would send someone into a coma, only that insulin can be a very touchy thing for people who are badly insulin insensitive. For example, a person with good insulin sensitivity maybe able to get away with artificial sweeteners in their diet, because the cephalic reflex isn't so strong in them. A person with poor insulin sensitivity may illicit a cephalic reflex from artificial sweetener use that is so pronounced that he or she may actually fail to improve insulin sensitivity over time as effectively and become frustrated.

As far as guitarlifter's comment on the senselessness of "sugary carbs", he is actually right on this one. Although the complexity of the carb does have an effect on how quickly it is released into the blood stream and thus helps regulate blood sugar more effectively, a carb really is a carb, is a carb, in an important sense.

@ guitarlifter: Thanks again for saying what I said, but in a much better way. I'm really more interested in the discussion than I am in taking credit for coming up with a great post. If I can say it, I'm glad to know there is someone out there who can get across what I'm trying to get a discussion started about.


Oh, I should add, since I would like to become a regular poster here, you'll have to be patient with my style of writing. I honestly wish I could put my ideas together better, but I'm what used to be called a polymath.

I know a lot of shit about a lot of things, and usually that information comes pouring out in a nearly incoherent stream at times. I beg your patience for that, but I tend to get a lot clearer as I argue a point, so it isn't entirely fruitless to argue with me.....it usually helps me, so feel free to bash away on my ideas. It can only help me grow.


Clarification always is helpful. And the OP is right in that the CPIR does vary between regular and type-II diabetic individuals. In a type-II diabetic individual, the body is used to being bombarded with so much glucose that it prepares itself by spewing out fairly decent amounts of insulin in preparation and anticipation of the glucose that would hit the bloodstream. Research suggests that roughly 20% of all insulin production during a meal is actually from the cephalic reflex. Crazy, I know.


Overall, I believe that the OP knew and was already comprehensive everything I stated in this thread, but he just didn't know how to say it. And he used a few terms a little loosely. :slight_smile:


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I was taught, which may or may not be entirely accurate, that the main point of CPIR was to prevent the continued release of hepatic glucose that would be active in a fasting state. Not to cover the, potential, incoming glucose. I think (off the top of my head) I would disagree that T2D would have an increased (pre)insulin release because of elevated somatastatin, which appears to inhibit pre-prandial insulin secretion.


The conversion of liver glycogen to glucose does release insulin when the body calls for glucose when in a fasted state, but this has nothing to do with the cephalic phase insulin response. That is just simply the insulin doing its job. The CPIR is a direct result of any sort of food interaction before actually eating it. Scientists aren't exactly 100% positive as to what the cephalic responses' (including CPIR) functions are, but all of the cephalic phases are, as previously stated, a result of food interaction although a good portion of scientists agree that "cephalic responses may serve as protective reflexes that modulate the influx of nutrients during feeding so as to minimize deviations in regulated substrates and buffer the animal from the stress of the nutrient load." (quoted from an article) Pages 993 and 994 of said article also talk about the possible functions of the cephalic phase.

And I have here a link to a blog that talks about how an article (the same one I cited above) cites several studies that suggest that normal non-obese individuals have little to no CPIR while obese people have a larger CPIR to anticipated food intake. The article suggests that health (being obese or not, etc) has a direct correlation with CPIR which would most definitely include Type-II diabetics who are the most obese and insulin resistant. Of course, there were some non-obese individuals who had a higher response than obese individuals, but the trend was that obese individuals had an overall higher response.

"Analyses with obese humans have obtained comparable or stronger CPIRs."

http://kickincarbclutter.blogspot.com/2009/05/cephalic-phase-insulin-response.html <<< Blog that talks about article
http://www.ajcn.org/cgi/reprint/42/5/991 <<< Actual article

I strongly suggest that anyone and everyone read the article. It's not a short read, but it is extremely informative and packed with information. I read the whole thing It even talks about Pavlov and how he has worked with classical conditioning to induce cephalic phases such as salivating.


Interesting thread. Thank you for the links guitarlifter. I too learned something today! :slight_smile:


Yes, lol, I think my assertion was mis-understood. Nevermind, I was just talking out loud = ).

The response is via a cholinergic stimulus? Do you know if the incretins or IRS complex plays a role? I work exclusively with IDDM, so I am certainly no expert on endo insulin = )...

I will look over the article, tonight, thanks. However, I would disagree with the comparison that the obese population is comparable with T2Ds. Unless the subjects portrayed IGT already, they are not necessary in similar pathological states. But that is a different discussion for a different day...

Good stuff!


OF all things, why was Cinnabon mentioned, damn you.