Hyperinsulinemia

Nutrition
21

@ MaximusB

Hahaha…because no thing on this earth is more powerful to break the will of a bodybuilder than a tasty Cinnabon. God, but they are good!

@egnatiosj

I just wanted to make it clear that I’m not suggesting that the obese population is in the same boat as the T2D population. There is clearly a big difference. I think my initial overly dramatic post probably got us down the wrong road here. The pragmatic side of this post was intended to point out the pratical problem of being extremely insulin insensitive. I wanted to point out that even people WHO DO NOT suffer from T2D have differing levels of difficulty with personal insulin sensitivity. Because of this, not all individuals are just going to be able to jump on a reducing diet and expect it to work for them as quickly as for others. A highly insulin sensitive bodybuilder can get on a low carb diet that ranges from 60 to 100 grams of carbs a day and really get satisfying reductions in bodyfat pretty quickly. A highly insensitive person may need to reduce carb intake to as low as 20 to 30 grams a day and still might have to keep up that kind of restriction for 3 months or more, just to restore balance. I mentioned the cephalic reflex in this context because a highly insensitve person MAY additionally suffer from an unusually high release of insulin during the cephalic reflex. I’m not, of course, suggesting we should avoid smelling food. I don’t think you can “fix” your excessive cephalic reflex except by improving your insulin sensitivity generally. Once again, the point was only to show that THERE IS A DIFFERENCE between individuals, even if they haven’t reached the point of T2D.

That being said, for those of you who are no doubt thinking at this point that the fact that there will be differences between individuals is “just obvious”, remember that difference is often the kind of thing that is intellectually recognized by ignored practically. How many articles on reducing diets have we all read that have all put promised to grant eternal life if you just exactly follow the meal plan, but fall short when we try them? Without practically recognizing the difference between individuals and their levels of insulin sensitivity, we can create unnecessary confusion about proper approaches to nutrition because individuals do not gain promised results. A more individualized and open ended approach to nutrition is called for.

22

[quote]egnatiosj wrote:
guitarlifter wrote:

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

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.

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 = )…

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.

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![/quote]

Haha, but I’m sure you’re quite the expert on exogenous insulin. Do you give out scripts for insulin? Anywho.

Actually, I think that the obese population is very comparable and relevant to type-2 diabetics. It’s all matter of measurement standards, and, in this case, it’s insulin resistance. The standards for what levels of systolic and diastolic blood pressure or HDL and LDL are considered to be hypertension and high cholesterol respectively are also standards set by humans.

Rather than measuring the disease by a qualitative method, it is by more of a quantitative method.

57 million Americans in 2009 were considered to be in a pre-diabetic state. Furthermore, about 80% of all type-2 diabetics are obese, after all, and that correlation, in my opinion, is a strong one to try to ignore. It’s not happenstance that this correlation exists.

It’s fairly straightforward in terms of the correlation between obesity and insulin resistance; one is very likely to follow the other. Standard adjustments for all sorts of things like blood pressure, heart rate, cholesterol, etc. have changed over the years where say someone 20 years ago may have been considered to have normal blood pressure, but are now considered to have pre-hypertension.

A simple downward adjustment of standards for what constitutes the conditions for a type-2 diabetic could easily throw all of those 57 million people into the type-2 diabetic category as well. So just because many obese people are not considered type-2 diabetic by a quantitative technicality doesn’t mean that they don’t see similar physiological responses for things like CPIR.

As for the physiological explanation of CPIR, the insulin released in CPIR is caused by from the Autonomic Nervous System, so it could be cholinergic, but I don’t think that incretins or IRS-1 would have a role in CPIR due to its different mechanism of action being different than standard insulin release from hyperglycemia, but they could still affect the amount of insulin released from CPIR.

This isn’t my field of expertise, so don’t quote me on that, haha. The cephalic phase that I learned briefly about in college while studying Exercise Science, then have taken my own time to do a little bit of research. Not even scientists fully understand CPIR let alone the cephalic reflex as a whole yet.

This is why I love T-Nation; we have a lot of members on here that can actually talk about things deeper than which protein to buy and post up articles about how protein builds muscle (among other very readily available information).

23

Just when I think that I have nothing to learn from T-Nation anymore a thread like this pops up. It’s these sparse nuggets of gold that keep me here reading these threads. I swear people like BBB should write some articles on here.