89 replies to this topic

[misterE]

to say that high glycemic foods don't contribute to elevated blood glucose and hyperinsulinemia is just not accurate.

They do elevate blood-sugar and very quickly too. Potatoes causes a huge spike in both blood-glucose and insulin, however this is very different from elevated insulin and blood-glucose during the fasting state. The rapid rise in blood-sugar that you get from eating high-glycemic foods is handled properly, as long as you remain insulin-sensitive.



Beans are a low-glycemic food, but they spike insulin just as much as potatoes, does that mean beans cause the elevated insulin found in insulin-resistant people? No. Beans are well known to lower fasting blood-sugar and insulin levels.



Whey-protein is extremely insulinogenic (just as much as a potato), but even thou it is highly insulinogenic, giving people whey-protein helps with their diabetes and actually lowers their blood-sugar and fasting insulin.



It seems like a paradox I know, but eating insulinogenic-foods (flour, beans, potatoes, etc.) will actually increase insulin-sensitivity and on the other side… eating foods that don’t stimulate much insulin like fats, oils and fructose CAUSE insulin-resistance and hyperinsulinemia!

Edited by misterE, 12 March 2014 - 03:19 AM.

[misterE]

To the best of my knowledge the liver can not possibly produce enough glucose to overwhelm blood in the long run.

Not true. In fact all the excess glucose in the blood of diabetics is from the liver's overproduction of glucose. Not from high-glycemic foods like Kevnzworld suggests.

I can never understand why can't diabetics simple remove carbohydrates from their diet instead of using insulin?

Cause when you remove carbohydrates from the diet, you have less insulin secretion… And insulin is what keeps you from becoming diabetic. That is why removing carbohydrates from the diet mimics the effects of type-1 diabetes. One of the side-effects of diabetes is rapid weight-loss.

I've also seen it written here that overwhelming FFAs kill insuling producing cells in the final stages of diabetes?



I'd guess that insulin producing cells most probably get overstressed due to extra pressue of generating abnormally high insulin levels via some stress map kinase signalling and die IMO.

Nope. Beta-cells secrete insulin, and insulin in return actually keeps the beta-cells alive, healthy and enables them to keep regenerating. As a person becomes insulin-resistant, the elevation of FFA’s that results causes the beta-cells to become insulin-resistant as well… without insulin interacting with the beta-cells… the begin to undergo apoptosis and die off.

Accumulation of FFAs does cause insulin resistance. The adipose cell is *full*, it can't take any more so it becomes insulin resistant to stop more inflow. But, FFAs don't really accumulate from eating dietary fats alone without carbs because insulin doesnt spike from that. If it did, we would not be able to live off our stored fats either. FFAs accumulate from eating too much carbs which spikes insulin and also forces the liver to churn carbs into fats. Cells that always need glucose to function(retina, nerves, kidneys) can not become insulin resistant so they suffer through the high levels of glucose stuffing caused by high blood sugar and high insulin.
I can't understand why would it benefit a diabetic to repeat this process indefinitely using exogenous insulin until he dies prematurely?

I don’t even know where to begin with this.

Edited by misterE, 12 March 2014 - 04:33 AM.

[Adaptogen]

I stole this excerpt from another website, regarding low carb diets and insulin resistance:

"Physiologic Insulin Resistance

The first thing that needs to be understood is that "physiologic" is doctor speak for "normal". If your doctor performs a blood panel on you, they are hoping that all the readings come back in the "physiological range". This part is actually quite important because the "physiological range" is generally ascertained statistically, by observation. So, a very important question to answer is who have these doctors been observing? Chances are pretty good that it has been patients on the Standard American Diet (SAD).

If your doctor is a conventional one, she will also do a fasting blood glucose test and upon receiving your results, will draw you into her office and with a concerned look on her face tell you that your fasting blood glucose levels are quite high and indicative of a pre-diabetic condition. She will then advise a glucose tolerance test (GTT). If you happen to be on a Very Low Carbohydrate diet (VLC) you will also fail the GTT thereby concerning your conventional doc even further. If your doctor is observant, one thing that will nag at her is the fact that you seem to be quite lean, whereas in general, patients with your test results tend to be quite heavy, with a large amount of subcutaneous body fat. It probably won't bother her enough to make her change her assessment, it's just an interesting anomaly that will soon be forgotten.

So what is going on here? Well, the standard SAD patient is periodically ( continually? ) dousing their system in "healthy" carbs and "healthy" low fat, guaranteeing a strong insulin response and ensuring a blood sugar level that whipsaws throughout the day. When blood sugar levels crash, they crash hard, and the poor individual eating this way becomes ravenous and starts hunting around for the next hit of easily assimilated carbohydrate. A metabolism adapted to this kind of eating relies on glucose as an energy substrate because there are periodic large exogenous (from the outside) infusions of glucose administered. Consequently, when the anticipated glucose infusion fails to materialize due to fasting for a blood test, blood sugar drops fairly low because tissues have been consuming blood glucose for energy. The real tragedy here is that this state in conventional medicine has come to be defined as "normal" due to its prevalence.

For the VLC eater, because carbohydrates are not a significant part of the diet, the metabolism shifts towards fat burning, in order to spare glucose for those tissues that are incapable of meeting their energy needs from fat oxidation ( the brain, red blood cells ). So what happens when you fast prior to a blood test? Well, not much, really. Your tissues are adapted to deriving their metabolic needs from fat oxidation, and unless you are insanely lean, your body has plenty of adipose tissue around to feed itself during the 12 hour fast mandated prior to a blood panel. As a result, your blood sugar levels are higher relative to the pathology of the SAD eater. Unlike the SAD eater, though, the VLC eater has a much narrower band of blood sugar, that is, the blood sugar never strays much above fasting levels even after eating, thereby explaining their leanness to a large extent.

So how does this all relate to insulin resistance? Well, tissues express insulin receptors when they are energy deficient. If your system is constantly bathed in insulin, you need proportionally fewer receptors to achieve the same effect than if you had lower insulin levels, so, in the interest of efficiency, tissues express fewer receptors. But that means that over time for a given glucose load, your pancreas needs to secrete ever increasing amounts of insulin to have tissues respond. The pancreas secretes increasing amounts of insulin, tissue express fewer and fewer insulin receptors, and we have ourselves a nice metabolic arms race. Welcome to hyperinsulinemia and insulin resistence.

If you are VLC, your tissues rely on fat as an energy substrate, and if their energy needs are being met that way, they will also not express insulin receptors. The net effect of this is that those cells that cannot oxidize fat as an energy substrate will still express insulin receptors, and still rely on the relatively meager amounts of blood glucose for their energy. The bulk of your tissues, however, will be insulin resistant and that is precisely what you want. The last thing you need is to have large masses of tissue that really don't need glucose for survival competing with those relatively few tissues that absolutely require the glucose. Welcome to physiologic insulin resistance!

The above also explains why you will fail a GTT on a VLC diet. This test basically consists of administering 50g ( I think ) of glucose to a 12h fasted subject and monitoring blood sugar levels to see how quickly the glucose is assimilated. In the SAD, the entire body serves as a sink for glucose, and this amount of glucose is roughly equivalent to one Dunkin Donuts Coffee roll. So, for the SAD eater this is a trivial amount of energy to dispose of or assimilate. For the VLC eater, however, most of the body is satiated due to fat oxidation, not dependent on glucose, and therefore does not serve as a sink for glucose assimilation. Accordingly, it will take longer to dispose of this glucose, leading our earnest doctor to conclude that we have a pre-diabetic condition presenting."

[misterE]

Med Sci (Paris). 2003 Aug-Sep;19(8-9):827-33.

Contribution of free fatty acids to impairment of insulin secretion and action: mechanism of beta-cell lipotoxicity.

Girard J.


Abstract

Type 2 diabetes is characterized by two major defects: a dysregulation of pancreatic hormone secretion (decrease of insulin secretion, increase in glucagon secretion), and a decrease in insulin action on target tissues (insulin resistance). The defects in insulin action on target tissues are characterized by a decreased in muscle glucose uptake and by an increased hepatic glucose production. These abnomalities are linked to several defects in insulin signaling mechanisms and in several steps regulating glucose metabolism. These post receptor defects are amplified by the presence of high circulating concentrations of free fatty acids. Indeed, elevated plasma free fatty acids contribute to decrease muscle glucose uptake (mainly by reducing insulin signaling) and to increase hepatic glucose production (stimulation of gluconeogenesis). Chronic exposure to high levels of plasma free fatty acids induces accumulation of long-chain fatty-acids into pancreatic beta-cells and to the death of 50 % of beta-cell by apoptosis (lipotoxicity).

Edited by misterE, 12 March 2014 - 04:29 AM.

[misterE]

You can see that glucose stays elevated above the baseline for much longer with the low GI food.

Great point! This just goes to show that the glycemic-index is dumb. OK, it’s not dumb but it shouldn’t be used to base your diet off of. If you were to eat a low-glycemic diet, you would be better off eating a stick of butter than a carrot. You would be better off drinking corn-oil than eating a baked-potato… surely no one in their right mind would see this as a solution for diabetes, except for maybe addx.

[misterE]

Adaptogen, my suggestion to you, would be to look at insulin-resistance from the lipotoxicity standpoint. Once you understand lipotoxicity, your entire view on insulin-resistance will become clear.

[Kevnzworld]

Certainly elevated free fatty acids and triglycerides are implicated in insulin resistance, as is a diet high in carbs and sugar. Sugars, from carbs , desserts and drinks contribute to triglyceride/ free fatty acid elevation. It's negative feedback loop.
" Elevated levels of free fatty acids and triglycerides in the blood stream and tissues have been found in many studies to contribute to diminished insulin sensitivity.[10][20][21][22] Triglyceride levels are driven by a variety of dietary factors. They are correlated with excess body weight.[23] They tend to rise due to overeating and fall during fat loss.[24] At constant energy intake, triglyceride levels are positively correlated with trans fat intake and strongly inversely correlated with omega-3 intake. High-carbohydrate, low-fat diets were found by many studies to result in elevated triglycerides,[25] in part due to higher production of VLDL from fructose and sucrose, and in part because increased carbohydrate intake tends to displace some omega-3 from the diet.
Several recent authors suggested that the intake of simple sugars, and particularly fructose, is also a factor that contributes to insulin resistance.[26][27] Fructose is metabolized by the liver into triglycerides, and, as mentioned above, tends to raise their levels in the blood stream. Therefore, it may contribute to insulin resistance through the same mechanisms as the dietary fat. Just like fat, high levels of fructose and/or sucrose induce insulin resistance in rats,[28][29] and, just like with fat, this insulin resistance is ameliorated by fish oil supplementation.[30] One study observed that a low-fat diet high in simple sugars (but not in complex carbohydrates and starches) significantly stimulates fatty acid synthesis, primarily of the saturated fatty acid palmitate, therefore, paradoxically, resulting in the plasma fatty acid pattern that is similar to that produced by a high-saturated-fat diet.[3 "
http://en.wikipedia....ulin_resistance

[addx]

To the best of my knowledge the liver can not possibly produce enough glucose to overwhelm blood in the long run.

Not true. In fact all the excess glucose in the blood of diabetics is from the liver's overproduction of glucose. Not from high-glycemic foods like Kevnzworld suggests.

It is true. That's why there is ketosis, to make up for the lack of energy due to the liver not being able to deliver enough glucose at times of fasting.

I believe glucose pools up in the blood because of lack of cellular uptake leaving the cells hungry for glucose(and stuffed with fats) and the blood loaded with glucose that cant get into the cells. The only cells taking up glucose are the ones that can't resist insulin. So the diabetic feels weak even though his blood is pooled with energy.

There's no point in resuming to feed him insulin. The sugar in blood should be controlled but I can only advocate drugs that supress gluconeogenesis during the time the patient can't control his blood sugar in spite of eating only fats. I do believe this situation would change over time, the body would restore its ability to keep levels of sugar in check during ketosis. After a while of this diet, one would then have to slowly, gradualy introduce carbs because his insulin cells might be overreacting from being accumstomed to body-wide insulin resistance.

I can never understand why can't diabetics simple remove carbohydrates from their diet instead of using insulin?

Cause when you remove carbohydrates from the diet, you have less insulin secretion… And insulin is what keeps you from becoming diabetic. That is why removing carbohydrates from the diet mimics the effects of type-1 diabetes. One of the side-effects of diabetes is rapid weight-loss.

No, insulin is what made you diabetic. In combination with lack of growth hormone action resulting from lack of cells soaked with beta-endorphins(mu-opioid) after excercise and an inability of the cell to put nutrients to use since it hasn't been given the instruction to proliferate. The cells becomes overwhelmed with insulin imported nutrients and defend by becoming resistant.

I've also seen it written here that overwhelming FFAs kill insuling producing cells in the final stages of diabetes?



I'd guess that insulin producing cells most probably get overstressed due to extra pressue of generating abnormally high insulin levels via some stress map kinase signalling and die IMO.

Nope. Beta-cells secrete insulin, and insulin in return actually keeps the beta-cells alive, healthy and enables them to keep regenerating. As a person becomes insulin-resistant, the elevation of FFA’s that results causes the beta-cells to become insulin-resistant as well… without insulin interacting with the beta-cells… the begin to undergo apoptosis and die off.

That makes sense, thank you.

Accumulation of FFAs does cause insulin resistance. The adipose cell is *full*, it can't take any more so it becomes insulin resistant to stop more inflow. But, FFAs don't really accumulate from eating dietary fats alone without carbs because insulin doesnt spike from that. If it did, we would not be able to live off our stored fats either. FFAs accumulate from eating too much carbs which spikes insulin and also forces the liver to churn carbs into fats. Cells that always need glucose to function(retina, nerves, kidneys) can not become insulin resistant so they suffer through the high levels of glucose stuffing caused by high blood sugar and high insulin.
I can't understand why would it benefit a diabetic to repeat this process indefinitely using exogenous insulin until he dies prematurely?

I don’t even know where to begin with this.

Begin somewhere because there are communities of people devoted to this truth and they're alive and kicking and handling their diabetes.

There's a nice blog with a guy explaining most of this through study anlaysis and what not. I've read most of his blog and spent some time looking at studies myself.

http://high-fat-nutr...raise-lard.html

The diet he follows, kwasniewskis diet - the optimal diet was crafter for elderly people, it consists of high fat and returns life to old people. They become energized, their blood sugar levels stabilize and mentally they become sharper. So, science should not turn a blind eye to this.

-----

If anything, I am 100% sure that during the prediabetic stage one can reduce carbs to almost zero, induce ketosis and restore his insulin sensitivity. I'm not sure if the pancreas of long time diabetics can come back to life but it's worth a try. They dont even consider it.


The essential issue with diabetes is not fats or sugars, it's the combination that is unnatural. And along with no excercise(no mu-opioid proliferation instructions erk 1/2 mapk) and too much stress (too much kappa opioid stress activation p38 mapk) keeping the cells in a "death wish state" that doesnt consume nutrients stuffed in by insulin.

Animals eat carbs during a season. They turn them into fat. They use up fat during the winter(fasting).

The animal never uses them both at the same time. It's seasonal and as "seasonal depression", high fat diet actually can induce hypomania(it did in me) which links diet to seasons to seasonal mood changes which humans tend to ignore and override.

Animals that eat meat/fats normally always eat them. They dont eat carbs.

So, maybe we should stop being narcissistc assholes and look at what animals to understand where we went wrong.

Edited by addx, 12 March 2014 - 08:27 AM.

[zorba990]

High glycemic foods increase blood sugar more than low glycemic foods. I know this because I test my blood 2 hours after eating various foods. My fasting glucose level is 82-86.

The total exposure to increased glucose levels is similar between high and low glycemic foods. The difference is that high glycemic foods result in a short duration exposure to a high intensity "spike" of glucose, whilst low glycemic foods result in a long duration exposure to a low intensity "wave" of glucose. Here is an idealized example of the phenomena:



You can see that glucose stays elevated above the baseline for much longer with the low GI food.

If your baseline is 100 then you are IMO already headed for trouble. Lets see what the curve is for people with
a baseline 75-80...

[eon]

what determines a sweetener as "glucose"? I only know of one sweetener with the same name "glucose" (aka dextrose). So xylitol is "sugar free", why is it sweet? What determines a sugar, glucose, or simply sweetener? Xylitol must fall under the "sweetener" category, whereas "glucose" a sugar or simply "glucose"? I'm confused. What would be the sugars be in an apple? It certainly has plenty for a tiny piece of fruit. An 8 ounce green apple has about 25g of sugars, and 34g of carbs. I'm confused.

[Kevnzworld]

what determines a sweetener as "glucose"? I only know of one sweetener with the same name "glucose" (aka dextrose). So xylitol is "sugar free", why is it sweet? What determines a sugar, glucose, or simply sweetener? Xylitol must fall under the "sweetener" category, whereas "glucose" a sugar or simply "glucose"? I'm confused. What would be the sugars be in an apple? It certainly has plenty for a tiny piece of fruit. An 8 ounce green apple has about 25g of sugars, and 34g of carbs. I'm confused.

Sugar ( sucrose ) is made up of glucose and fructose. An apple is fructose. Xylitol is a sugar alcohol, and one of the better ones IMO ( vs mannitol ). Sugar free is only technically sucrose free. Sugar alcohols have varying glycemic indexes.
http://en.wikipedia....i/Sugar_alcohol
I find the " sugar free " labeling misleading and dangerous, at least for diabetics. Some carbs like white flour in sugar free products are sugar like from your body's point of view. I test my blood sugar often, and I can tell you that " sugar free " mannitol products give me a 20-30 pt blood glucose spike. I sometimes bake with a truvia blend, which is a mixture of a stevia derived product, sugar and erythritol. Erythritol is one of the better sugar alcohols.
I am not diabetic, and my fasting blood sugar is in the 85 range. My goal is to find foods that I like that don't spike my blood sugar, or triglyceride levels.
The final arbiter of success or failure in an endeavor like this is your Hba1C , fasting blood glucose , insulin, and triglycerides levels. ( lower being better ).

Edited by Kevnzworld, 12 March 2014 - 08:42 PM.

[misterE]

Certainly elevated free fatty acids and triglycerides are implicated in insulin resistance, as is a diet high in carbs and sugar. Sugars, from carbs , desserts and drinks contribute to triglyceride/ free fatty acid elevation.

Triglycerides are raised by dietary-fats and simple-sugar (fructose). Starchy foods have a difficult time converting into triglycerides thou, so understand that high-fiber complex-carbohydrates don’t raise triglycerides. However with that said, I personally don’t believe that triglycerides themselves are a problem as long as they are being shuttled into the adipocytes and not accumulating in organs.

[misterE]

It is true. That's why there is ketosis, to make up for the lack of energy due to the liver not being able to deliver enough glucose at times of fasting.

addx, you do understand that uncontrolled diabetes will eventually lead to ketosis don’t you? And prolonged ketosis leads to ketoacidosis? How is this supposed to help treat or cure diabetes? It seems obvious to me that if you want to avoid diabetes, you would want to take your metabolism away from entering ketosis.

I believe glucose pools up in the blood because of lack of cellular uptake leaving the cells hungry for glucose(and stuffed with fats) and the blood loaded with glucose that cant get into the cells.

I would agree completely, but you are leaving out the other major part; uninhibited gluconeogenesis.

The only cells taking up glucose are the ones that can't resist insulin.

Yes, like the brain and blood-cells. All other organs start burning fat for fuel during insulin-resistant states.

So the diabetic feels weak even though his blood is pooled with energy.

Right, because insulin either isn’t there, or is unable, to transport and store nutrients within our cells.

the patient can't control his blood sugar in spite of eating only fats.

Agreed, because fat doesn’t stimulate insulin… and without insulin, gluconeogenesis stays uninhibited (which increases blood-sugar).

No, insulin is what made you diabetic.

Insulin is what is given to diabetics to keep them from dying. All drugs used to treat type-2 diabetes are centered on making insulin more potent; amplifying the effects of insulin.

In combination with lack of growth hormone action

Growth-hormone is actually elevated in diabetics and their IGF-1 concentration is low.

That makes sense, thank you.

No problem, just trying to clean up the confusion

Begin somewhere

I would suggest reading the thread from the beginning …



But I’ll give you the short version: Excessive lipolysis and FFA’s and the root cause of diabetes. Eating carbohydrates stimulates insulin, which inhibits lipolysis and lowers FFA’s, thus increasing insulin-sensitivity and preventing diabetes.

The essential issue with diabetes is not fats or sugars, it's the combination that is unnatural.

I would agree here. Eating sugar (which is highly insulinogenic) would make the adipocyte absorb the triglycerides from the fatty-meal, now this is actually healthy fat metabolism believe it or not, but doing this constantly like Americans do, will cause insulin to shove all that fat into the adipocyte until a point is reached where the adipocyte becomes overstuffed and purposely becomes insulin-resistant (causing excessive lipolysis).



The adipocyte becomes insulin-resistant as an attempt to prevent anymore fat-gain, the release of FFA’s from the adipocyte restores the adipocyte’s insulin-sensitivity… but the exported FFA’s cause insulin-resistance in other parts of the body.



With that said, since fat and sugar are obviously poor fuel sources for the body. I would suggest starch as the main fuel source. Starch stimulates insulin and inhibits lipolysis, but is unable to convert readily into triglycerides and overstuff your adipocytes.

So, maybe we should stop being narcissistc assholes

“We” or me? I’m not trying to come off narcissistic; I’m just trying to clear the confusion. To make the statement that “insulin makes you diabetic” indicates major confusion on your part (no offense).

Edited by misterE, 12 March 2014 - 11:57 PM.

[misterE]

what determines a sweetener as "glucose"? I only know of one sweetener with the same name "glucose" (aka dextrose). So xylitol is "sugar free", why is it sweet? What determines a sugar, glucose, or simply sweetener? Xylitol must fall under the "sweetener" category, whereas "glucose" a sugar or simply "glucose"? I'm confused. What would be the sugars be in an apple? It certainly has plenty for a tiny piece of fruit. An 8 ounce green apple has about 25g of sugars, and 34g of carbs. I'm confused.

Good question. Usually sugar is a single molecule of either glucose combined to something other than another glucose molecule (like sucrose for example: with a glucose molecule bound not to another glucose molecule, but a fructose molecule). Maltose which is a glucose molecule combined with another glucose molecule is sweet, but is not considered a “simple-sugar”. Corn-syrup (not high-fructose-corn-syrup) but plain ol’ corn-syrup is mostly pure maltose. Starch is hundreds or thousands of glucose molecules bound together.

Sucrose= glucose+fructose (considered a simple-sugar, very sweet)

Maltose= glucose+glucose (not considered a simple-sugar despite being sweet)

Starch = glucose+glucose+glucose+glucose etc… (not considered a sugar, not sweet)

My personal opinion is that maltose (corn-syrup) is the healthiest sweetener. But starch is the healthiest carbohydrate.

Edited by misterE, 12 March 2014 - 11:54 PM.

[addx]

It is true. That's why there is ketosis, to make up for the lack of energy due to the liver not being able to deliver enough glucose at times of fasting.

addx, you do understand that uncontrolled diabetes will eventually lead to ketosis don’t you? And prolonged ketosis leads to ketoacidosis? How is this supposed to help treat or cure diabetes? It seems obvious to me that if you want to avoid diabetes, you would want to take your metabolism away from entering ketosis.

I would agree completely, but you are leaving out the other major part; uninhibited gluconeogenesis.

Gluconeogenesis as most systems in the body is modulated by opposite control of glucagon and insulin. While insulin does inhibit gluconeogenesis, for uninhibited gluconeogenesis one would require overactivity of glucagon secreting cells would one not?

So, maybe we should stop being narcissistc assholes

“We” or me? I’m not trying to come off narcissistic; I’m just trying to clear the confusion. To make the statement that “insulin makes you diabetic” indicates major confusion on your part (no offense).

Sorry, we as a civilization.

Why is it major confusion? Hypothesise it

I've seen a number of studies all proving the same thing.

Diabetes is reversible with a high fat diet up to a point when too much damage occurs.

My main point is, the pre diabetes stage is easily detected by tests, but not just average sugar levels but also reactive.

People with pre diabetes should be put on a low carb diet to emulate winter fasting to restore proper insulin sensitivity. After it is restored one should start introducing carbs again and start to exercise.

Insulin resistance is a physiological process, not a pathological. What is pathological is our lack of fasting periods and exercise to allow the body to cycle metabolic stages as animals inevitably seasonally have to due to not owning fridges or being able to buy food in supermarkets.

Oh yea, and while there might be plenty GH (it is stimulated by insulin is it not?), this plentiful GH has nothing much to do unless beta-endorphins soak mu opioid receptors of muscle cells and such and this doesn't happen from sitting on a chair.

Edited by addx, 13 March 2014 - 12:48 AM.

[misterE]

Gluconeogenesis as most systems in the body is modulated by opposite control of glucagon and insulin. While insulin does inhibit gluconeogenesis, for uninhibited gluconeogenesis one would require overactivity of glucagon secreting cells would one not?

Yes indeed, and if you were familiar with the research, you would see that diabetics have increased glucagon secretion from the pancreas and a decrease in insulin-secretion. Glucagon is one of the main hormones that causes elevated blood-sugar in diabetics, along with cortisol, GH and other glucocorticoids.

Why is it major confusion? Hypothesise it

The major confusion is that carbohydrates and the insulin they induce causes insulin-resistance and diabetes.

Diabetes is reversible with a high fat diet up to a point when too much damage occurs.

Diabetes induces weight-loss as an attempt to restore insulin-sensitivity… but excessive lipolysis, while great for weight-loss, can cause serious damage.

People with pre diabetes should be put on a low carb diet to emulate winter fasting to restore proper insulin sensitivity.

This would only makes diabetes worse because putting them on a low-carb diet would only increase lipolysis more and elevate the same hormones that cause diabetes (like cortisol, GH, glucagon, and glucocorticoids).

Insulin resistance is a physiological process, not a pathological. What is pathological is our lack of fasting periods and exercise.

Fasting and exercise do increase insulin-sensitivity, but prolonged fasting and exercise also causes insulin-resistance also by increasing lipolysis too much and once again elevating catabolic-hormones.

Oh yea, and while there might be plenty GH (it is stimulated by insulin is it not?)

No. Insulin lowers GH. Actually, insulin converts GH into IGF-1. This process doesn’t occur with diabetics because their insulin in is unable to make this conversion process due to insulin-resistance. Without insulin converting GH into IGF-1, you see an increase in GH and a decrease in IGF-1 in diabetic patients.

[eon]

Mr. E, if insulin lowers GH, why is it that insulin and GH are used together by bodybuilders? I never understood this. Is the use of insulin to counter GH's what? I thought the whole point is to have as much GH in the system?

Anyway...

D-ribose and inositol are sweet, are they considered sugar alcohol? These are sweet so I don't know what it will do to the body, if anything regarding becoming diabetic. I've been using 18g of inositol daily for weeks now. I know studies showed no negative changes in the body. D-ribose is sweeter. I only take it on workout days anywhere from 5-10g daily.

Edited by eon, 13 March 2014 - 04:11 AM.

[misterE]

Mr. E, if insulin lowers GH, why is it that insulin and GH are used together by bodybuilders? I never understood this. Is the use of insulin to counter GH's what? I thought the whole point is to have as much GH in the system?

The reason why is because when you have high levels of GH and insulin simultaneously together, they synergize and create IGF-1. And it is IGF-1 that really stimulates protein-synthesis and allows for muscle-growth. IGF-1 has both growth promoting and insulin like effects.

Edited by misterE, 13 March 2014 - 05:07 AM.

[Brett Black]

High glycemic foods increase blood sugar more than low glycemic foods. I know this because I test my blood 2 hours after eating various foods. My fasting glucose level is 82-86.

The total exposure to increased glucose levels is similar between high and low glycemic foods. The difference is that high glycemic foods result in a short duration exposure to a high intensity "spike" of glucose, whilst low glycemic foods result in a long duration exposure to a low intensity "wave" of glucose. Here is an idealized example of the phenomena:



You can see that glucose stays elevated above the baseline for much longer with the low GI food.

If your baseline is 100 then you are IMO already headed for trouble. Lets see what the curve is for people with
a baseline 75-80...

The same glucose response is seen in those with fasting glucose in the 75-80 range.

[addx]

It's more probably the area under the curve and above baseline that describes the integrated effects of high glucose over time.

In that sense, the areas look to me to be pretty much the same but the the sharp rise and decline of the high glycemic index probably results in an inability of downstream metabolic effects to engage and activate properly.

Edited by addx, 13 March 2014 - 09:20 AM.

[DukeNukem]

So, someone explain to me please: Why do doctors tell diabetics to eat carbs instead of a high fat diet? They're worried about their mucosal linings thining from lack of glucose and increasing cancer risk? Seriously?

This is an easy one.

Most diabetics are fat, and therefore most doctors believe that being fat is the cause of diabetes, and these same misinformed doctors think that the leading cause of being fat is easting fat. So, it just goes against every fiber in their body to recommend a high-fat (aka low-carb) diet.

Five years ago, I came up with the term, carb-ass, which I still use to this day:
http://www.longecity...he-new-fat-ass/

Edited by DukeNukem, 14 March 2014 - 03:18 PM.

[misterE]

So, someone explain to me please: Why do doctors tell diabetics to eat carbs instead of a high fat diet? They're worried about their mucosal linings thining from lack of glucose and increasing cancer risk? Seriously?

The reason why diabetics are instructed to eat less fat is because fat is calorie-dense, easy to overeat and easily stored in body-fat (contributing to obesity, insulin-resistance and lipotoxicity). Starch contains 55% less energy than fat, is hard to overeat and is not easily stored as body-fat.
Also carbohydrates induce insulin (which helps prevent diabetes in numerous ways), while fat does not. See here:



Am J Clin Nutr. 1995 Jul;62(1):19-29.

Fat and carbohydrate overfeeding in humans: different effects on energy storage.

Horton TJ, Drougas H, Brachey A, Reed GW, Peters JC, Hill JO.

Abstract

Both the amount and composition of food eaten influence body-weight regulation. The purpose of this study was to determine whether and by what mechanism excess dietary fat leads to greater fat accumulation than does excess dietary carbohydrate. We overfed isoenergetic amounts (50% above energy requirements) of fat and carbohydrate (for 14 d each) to nine lean and seven obese men. A whole-room calorimeter was used to measure energy expenditure and nutrient oxidation on days 0, 1, 7, and 14 of each overfeeding period. From energy and nutrient balances (intake-expenditure) we estimated the amount and composition of energy stored. Carbohydrate overfeeding produced progressive increases in carbohydrate oxidation and total energy expenditure resulting in 75-85% of excess energy being stored. Alternatively, fat overfeeding had minimal effects on fat oxidation and total energy expenditure, leading to storage of 90-95% of excess energy. Excess dietary fat leads to greater fat accumulation than does excess dietary carbohydrate, and the difference was greatest early in the overfeeding period.


&

Nutr Metab (Lond). 2009 Sep 28;6:37.

Early responses of insulin signaling to high-carbohydrate and high-fat overfeeding.

Adochio RL, Leitner JW, Gray K, Draznin B, Cornier MA.

Abstract

BACKGROUND: Early molecular changes of nutritionally-induced insulin resistance are still enigmatic. It is also unclear if acute overnutrition alone can alter insulin signaling in humans or if the macronutrient composition of the diet can modulate such effects.

METHODS: To investigate the molecular correlates of metabolic adaptation to either high-carbohydrate (HC) or high-fat (HF) overfeeding, we conducted overfeeding studies in 21 healthy lean (BMI < 25) individuals (10 women, 11 men), age 20-45, with normal glucose metabolism and no family history of diabetes. Subjects were studied first following a 5-day eucaloric (EC) diet (30% fat, 50% CHO, 20% protein) and then in a counter balanced manner after 5 days of 40% overfeeding of both a HC (20% fat, 60% CHO) diet and a HF (50% fat, 30% CHO) diet. At the end of each diet phase, in vivo insulin sensitivity was assessed using the hyperinsulinemic-euglycemic clamp technique. Ex vivo insulin action was measured from skeletal muscle tissue samples obtained 15 minutes after insulin infusion was initiated.

RESULTS: Overall there was no change in whole-body insulin sensitivity as measured by glucose disposal rate (GDR, EC: 12.1 ± 4.7; HC: 10.9 ± 2.7; HF: 10.8 ± 3.4). Assessment of skeletal muscle insulin signaling demonstrated increased tyrosine phosphorylation of IRS-1 (p < 0.001) and increased IRS-1-associated phosphatidylinositol 3 (PI 3)-kinase activity (p < 0.001) following HC overfeeding. In contrast, HF overfeeding increased skeletal muscle serine phosophorylation of IRS-1 (p < 0.001) and increased total expression of p85α (P < 0.001).

CONCLUSION: We conclude that acute bouts of overnutrition lead to changes at the cellular level before whole-body insulin sensitivity is altered. On a signaling level, HC overfeeding resulted in changes compatible with increased insulin sensitivity. In contrast, molecular changes in HF overfeeding were compatible with a reduced insulin sensitivity.

Edited by misterE, 15 March 2014 - 12:09 AM.

[misterE]

It's not the hamburger or hot-dog buns that are causing diabetes, but rather the hunk of grease that sits between. Hot-dogs are 55% fat. Ground-beef is 70% fat!



Many junk-foods that people think are high-carb are actually high-fat… for instance:



Potato-chips: 60% fat

Cheese-cake: 60% fat

Frosted-doughnut: 50% fat

French-fries: 45% fat

Chocolate-chip cookie: 40% fat

Cheese-pizza: 40% fat





Compare that to natural starches:





Oats: 15% fat

Corn: 10% fat

Brown-rice: 7% fat

Wheat: 5% fat

Barley: 3% fat

Pinto-beans: 3%fat

Potato: 1% fat

Edited by misterE, 15 March 2014 - 12:41 AM.

[eon]

Mr E, would plantain chips be better off than potato chips? I see the ingredients are usually just plantain, oil and salt. Both plantain and potatoes are fried when made into chips so I don't know why potatoes seem higher with fats and carbs.

Edited by eon, 15 March 2014 - 04:57 AM.

[Vardarac]

Mr E, would plantain chips be better off than potato chips? I see the ingredients are usually just plantain, oil and salt. Both plantain and potatoes are fried when made into chips so I don't know why potatoes seem higher with fats and carbs.

I don't know if this is an option for you, but once a week making (emphasis: homemade, not premade) an enormous batch of kale chips for your week might be an even better choice. A head makes 2+ servings, so you'll probably need to chop quite a bit of kale and have a good oven/olive oil.

[APBT]

I fully stand with you with the sad difference I cannot get access to metformin I would like to try.

You could try ordering Metformin from IAS http://www.antiaging...formin-metforal

[albedo]

Great discussion. I went back to my numbers. Averaging over 10 years (ref):

• FG 89.6 (70-104)
• A1C 5.4 (4-6)
• Insulin 6.0 (2-20)
• HOMA 1.3 (<2.4)
• Ins./FG 0.07 (<0.3)

[eon]

has anyone here looked into inosine supplement as it "suppresses the increase of glucose and insulin in the blood". I've seen these as workout supplements but might need it in bulk powder for higher dosage and cheap price. It has nootropic potential as well something to do with nerve growth factor inducing.

Edited by eon, 16 March 2014 - 07:40 AM.

[eon]

why is xylitol 100% sugar free yet it is a "sugar alcohol"?

 

where does D-ribose fall under? I don't see it as a sugar alcohol. 

[eon]

I notice some gray on my beard (at least 3 gray hairs). Not sure if this had anything to do with me using glucose as my "sweetener" and or my stack with creatine pre/post workout. I don't take excessive amount of it just 1 serving (1 teaspoon/4 grams daily). Maybe there's other factors involved here.

 

I do take a chromium supplement so I'm sure it could counter whatever glucose "spike" there is. Would using a blood glucose monitoring system tell me what's going on here? Could this product ever determine if a person is diabetic? What could the reading be?