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high glucose accelerates aging?

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#1 eon

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Posted 09 January 2014 - 05:12 AM


How so? Curious if this has something to do with the sweetener "glucose" (aka dextrose)? I've been using glucose as my sweetener instead of table sugar. So taking lots of this leads to accelerated aging or are they implying glucose in the blood or body (and how does it become "bad")? This glucose sweetener is easily utilize by the body, not as sweet, and natural. So it is no worse than table sugar or high fructose corn syrup. Did I misinterpret the article I read? How does glucose become bad when it is also used by the body as energy? I'm not a scientist but glucose is water soluble so if taking it with fats, does it get stored in the liver and body like fat soluble vitamins does? So using glucose for teas is ok since it's water based but using it with tea while eating steak makes glucose bad?

#2 Mind

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Posted 09 January 2014 - 06:34 PM

Excess glucose calories are detrimental to long term health. If you are only consuming the amount that your body uses for immediate or daily energy needs, then you are probably ok. Your body takes excess glucose calories and turns them into fat. Your body LOVES to store fat with those excess calories. Carrying around extra weight (especially white adipose tissue) is strongly correlated with worse health.

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#3 eon

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Posted 10 January 2014 - 09:22 AM

Any idea if phosphatidyl choline is supposed to eliminate fat under the skin? I read that this is being used by way of injections, not oral supplementation. Not sure the effect of oral administration is if it does the same thing. I wish I had no belly fat despite of me being only 150 pounds. So a teaspoon a day of sweetener "glucose" is ok. I might be changing my sweetener once it's done to either stevia or xylitol. Any thoughts on those?

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#4 Mind

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Posted 10 January 2014 - 06:26 PM

Here is a discussion about artificial sweeteners.

#5 misterE

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Posted 08 February 2014 - 06:27 AM

The excessive blood-sugar from diabetes is caused by excessive gluconeogenesis. Eating lots of starch and some simple-sugars (and invoking insulin-secretion) actually regulates proper blood-sugar levels. Beta-cells of the pancreas multiply during high-carb diets and decrease on low-carb diets. With less beta-cells (caused by reduced carbohydrate consumption), you have less insulin-secretion, which increases gluconeogenesis, and that elevates your blood-sugar, which is what is seen in diabetics.
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#6 rwac

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Posted 08 February 2014 - 07:51 AM

Your body takes excess glucose calories and turns them into fat.


"Most experimental data in humans, however, contradict this view of the function of de novo lipogenesis. Initial studies in which indirect calorimetry was used showed little or no net de novo lipogenesis after short-term carbohydrate overfeeding (1). Subsequent isotopic studies confirmed the absence of quantitatively significant flux through hepatic de novo lipogenesis under most conditions of carbohydrate energy surplus (2,3)."

http://ajcn.nutritio...t/74/6/707.full



De novo lipogenesis in humans: metabolic and regulatory aspects.

Abstract


The enzymatic pathway for converting dietary carbohydrate (CHO) into fat, or de novo lipogenesis (DNL), is present in humans, whereas the capacity to convert fats into CHO does not exist. Here, the quantitative importance of DNL in humans is reviewed, focusing on the response to increased intake of dietary CHO. Eucaloric replacement of dietary fat by CHO does not induce hepatic DNL to any substantial degree. Similarly, addition of CHO to a mixed diet does not increase hepatic DNL to quantitatively important levels, as long as CHO energy intake remains less than total energy expenditure (TEE). Instead, dietary CHO replaces fat in the whole-body fuel mixture, even in the post-absorptive state. Body fat is thereby accrued, but the pathway of DNL is not traversed; instead, a coordinated set of metabolic adaptations, including resistance of hepatic glucose production to suppression by insulin, occurs that allows CHO oxidation to increase and match CHO intake. Only when CHO energy intake exceeds TEE does DNL in liver or adipose tissue contribute significantly to the whole-body energy economy. It is concluded that DNL is not the pathway of first resort for added dietary CHO, in humans. Under most dietary conditions, the two major macronutrient energy sources (CHO and fat) are therefore not interconvertible currencies; CHO and fat have independent, though interacting, economies and independent regulation. The metabolic mechanisms and physiologic implications of the functional block between CHO and fat in humans are discussed, but require further investigation.



http://www.ncbi.nlm....pubmed/10365981
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#7 Mind

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Posted 08 February 2014 - 11:02 AM

Excess calories (from whatever source) make people obese. Case closed.
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#8 Mind

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Posted 08 February 2014 - 04:24 PM

Not only does excess sugar (excess carbs as well, since they are near instantly turned to sugar once consumed), lead to accelerated aging, a very large study found it significantly increases heart problems as well.
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#9 niner

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Posted 09 February 2014 - 11:02 PM

One of the seven forms of aging damage cataloged by SENS is glycation. This is the non-enzymatic attachment of sugars to proteins in a fashion that causes them to crosslink and lose functionality. The rate at which glycation occurs is determined mostly by the concentration of sugars in the bloodstream. Eating sugars or other forms of carbohydrate that rapidly break down to sugars tends to raise your blood sugar level, which is a bad thing.
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#10 misterE

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Posted 10 February 2014 - 06:20 AM

Glycation is caused by diabetes and insulin-resistance (excessive blood-sugar levels due to uninhibited gluconeogenesis). Eating starches and simple-sugars won't cause glycation as long as you produce enough insulin (and are sensitive to it) to metabolize the glucose properly.



Basically, if the glucose you eat is being stored as glycogen or converted into fat, then glycation can’t occur. But diabetics, due to insulin-resistance, lose their ability to store glucose away as glycogen and lose their ability to convert glucose into fat (since insulin stimulates DNL). The result of that is a bunch of extracelluar-glucose that is unable to be used as an energy source, so it floats around in the blood-stream for hours and that is when glycation can occur.



With diabetics, the elevated blood-sugar which is commonly seen is a result of sugar being pulled out of cells (and increased gluconeogenesis), due to an elevation in catabolic-hormones like glucagon and cortisol. These hormones also pull BCAA’s and fatty-acids out of cells and into the blood as well, which is why they are also elevated in diabetics. People who are insulin-resistant or diabetic have a hard time storing nutrients (glucose, fatty-acids, BCAA’s) inside their cells, due to an increase in catabolic-hormones and a decrease in insulin-signaling. The solution to this is to eat a highly insulinogenic-diet, which lowers these catabolic-hormones and allows nutrients to be tucked away inside the cells. Low-carb diets further exacerbate diabetes because they simultaneously increase catabolic-hormones and reduce insulin-secretion.

Edited by misterE, 10 February 2014 - 06:32 AM.

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#11 platypus

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Posted 10 February 2014 - 09:37 AM

I think sugar, sweets and simple carbs should be generally avoided. Even transient high blood sugar levels should be avoided so I don't think a "highly insulinogenic diet" is the way to go.
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#12 misterE

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Posted 11 February 2014 - 04:14 AM

I think sugar, sweets and simple carbs should be generally avoided. Even transient high blood sugar levels should be avoided so I don't think a "highly insulinogenic diet" is the way to go.



One of the very first study's conducted with diabetes was done back in the 1920’s by a researcher named Shirley Sweeney. The study he did was very simple and is considered a classic. He got four groups of young adults and fed three of them different diets and starved the fourth group. The first group was a high-carbohydrate diet consisting of both starch and sugar (pancakes/syrup, bananas, potatoes, oatmeal, table-sugar, candy, juice, etc). The second group was a high-protein diet consisting of lean-meat, lean-fish, and egg-whites. The third group was a high-fat diet of egg-yolks, butter, olive-oil and mayonnaise… and the fourth group ate nothing.

What he found was that all the groups had elevated blood-sugar except the high-carbohydrate group. The blood-sugar was so elevated that everyone save the high-carbohydrate group, were technically diabetic. To confirm this, he took a person from the high-carbohydrate group and switched him to the high-fat group and according to his blood-sugars, he became diabetic.

Arch Intern Med (Chic).1927;40(6):818-830. Dietary Factors That Influence The Dextrose Tolerance Test. Sweeney S.


What I think explains this seemingly paradoxical-study is that there is a feedback loop set up in the body that regulates blood-sugar. When you eat lots of carbohydrates, the body is able to produce insulin in response and if need be, the pancreas can even grow extra beta-cells to help out (a process called beta-cell proliferation/differentiation). The insulin produced regulates blood-sugar by two distinct and different ways, the first way is: insulin transports blood-sugar into the muscles and liver to be stored as glycogen, the second way is that insulin shuts off the livers production of glucose (gluconeogenesis). Now when you eat a carbohydrate-deficient diet, you produce very little insulin, which means less blood-sugar partitioning into the muscles and with less insulin, the liver keeps on creating glucose and sending it out into circulation, and without insulin, it is unable to be utilized as energy.

With diabetics, their livers are constantly producing glucose and the beta-cells on their pancreas have all died off (in a process called beta-cell apoptosis).


Edited by misterE, 11 February 2014 - 04:22 AM.

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#13 platypus

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Posted 11 February 2014 - 10:02 AM

Arch Intern Med (Chic).1927;40(6):818-830. Dietary Factors That Influence The Dextrose Tolerance Test. Sweeney S.

What do the current (say post-2000) studies say?
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#14 misterE

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Posted 12 February 2014 - 12:55 AM

What do the current (say post-2000) studies say?




Pretty much the same thing, althou there is a lot more clutter in the data suggesting low-carb diet reduces diabetes risk-factors or biomarkers like body-weight, etc. The evidence being so clear, started with epidemiological observations, followed by the study by Sweeney in the 1920’s, then you had Walter Kempner of Duke University showing complete reversal of metabolic-syndrome with his infamous “rice-diet” in the 1940’s, 50’s and 60’s. Then you had James Anderson showing numerous well designed studies showing high-fiber complex-carbohydrate diets lowering fasting glucose and insulin, then you had the Pritikin research team publishing 30 studies showing reversal of diabetes in the 1980’s and 90’s and now today you have Neal Barnard showing that low-fat vegan diets reduce fasting glucose more than any other available option. Those have been the pioneers; there are tons of other studies showing whole-grains benefit diabetes, while most studies condemn high-fat diets for causing diabetes.



I’m interested in hearing what you think causes elevated blood-sugar or diabetes, you ignored this simple study and dismissed it based on its publication date. Why do you think Sweeney got the results he did?

Edited by misterE, 12 February 2014 - 12:56 AM.

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#15 zorba990

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Posted 12 February 2014 - 02:02 AM

I'd suggest you get a glucose meter and measure the reality of blood sugar to the food you eat. Not just in terms of fasting levels but also post prandial 1,2,3 hours out. The area under the curve is important as well. Resistant starches, lean protein, vegetables, and low glycemic fruits will cause less spike than cooked potatoes, candy, and other junk. Parboiled rice has more resistant starch so it fares better than sticky rice, but measure it youself!
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#16 eon

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Posted 13 February 2014 - 03:25 AM

I was drinking this rootbeer by Virgil's. It has 42 grams of carbs per 12 ounce bottle, which translates to 42 grams of sugars as well. The sugar is made from unbleached cane sugar and caramelized unrefined cane sugar. This rootbeer is sold in organic type supermarket so I figured it's still better compared to other rootbeers you'd see everywhere. Is 42 grams of sugar a bit much? I take 18 grams of inostiol and it is about 4 tablespoons. Just thinking about it that if a 12 ounce bottle of rootbeer would have 42 grams of sugars that's at least 8-10 tablespoons of sugars per 12 ounce bottle. That is if sugar weighed the same as inositol. Inositol powders of course weigh less than sugar powders.

Edited by eon, 13 February 2014 - 03:33 AM.


#17 Adaptogen

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Posted 13 February 2014 - 03:54 AM

i do enjoy a good virgil's rootbeer, but 42 grams of sugar is a ton. You should consider making the switch to kombucha, it is far healthier and just as tasty (i like the "trilogy" w/ ginger, lemon, and raspberry puree, although i've started making my own as of lately).

#18 eon

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Posted 13 February 2014 - 05:36 AM

is "kombucha" sold in supermarkets? Not sure but I think I saw that next to the rootbeers, ginger ales, and cream sodas, etc.

#19 Gerrans

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Posted 18 February 2014 - 04:47 PM

I should think what causes increased aging is being overweight. Glucose is unlikely to play a part unless one is overweight, because it is an essential part of the body's systems. Glucose becomes a problem when there is too much of it, which is the result of overeating. But fat is also a problem in overeating, because elevated levels of fatty acids may also cause insulin resistance, increased fat deposition, etc.

After reading about the glucose-fatty-acid cycle, I find it hard to take seriously the various schools of thought that say either carbohydrates or fats are entirely responsible for health issues such as accelerated aging or diabetes II. If we do not overeat, the cycle works efficiently, first metabolising glucose and then reverting to fatty acids as the chief source of energy. But if we constantly eat too much, particularly of the junk foods that contain mixtures of fat and sugar, the glucose-fatty-acid-sensing mechanisms are overwhelmed and sensitivity lost. The body is designed to sense high glucose levels or high fatty acid levels: how is it supposed to cope when faced with high levels of both, something almost impossible when we were evolving (unless someone feasted on meat and honey at the same time, which would have been rare)?

The body seems to have evolved to process glucose first and then any fats in a meal a couple of hours later. This becomes a challenge for it if one is constantly eating and snacking, with little delay between eating sessions. In that scenario, insulin sensitivity shuts down, fat metabolism is prioritised, and blood sugar gets out of hand.

This is my theory, anyway. There are things it does not explain, such as why some people are or remain insulin resistant when their weight is normal and they do not overeat. But many people do regain insulin sensitivity once their weight is appropriate and they are eating healthily. For most people, therefore, glucose should not accelerate aging, in my opinion, if they do not overeat.

Edited by Gerrans, 18 February 2014 - 04:59 PM.

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#20 eon

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Posted 19 February 2014 - 07:04 AM

Adaptogen, I finally tried some kombucha yesterday. for a 16 ounce bottle is about over $3. It was a GT's Kombucha, which is organic raw. The taste is vinegary, since I bought the "original" to get a real taste of it. I've seen flavored selections as well but for a $3 bottle drink it's not daily that I can drink this stuff. The bottle mentioned "contains trace amount of alcohol" as well. It's got acetic acid, which I think vinegar has as well no wonder it taste like drinking vinegar juice.

#21 JohnD60

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Posted 20 February 2014 - 05:20 PM

I bought a blood glucose and ketone meter, it arrived yesterday. Thought I'd share.
.
My two cents on the original poster question:
Firstly, high glucose levels result in more frequent and prolonged insulin stimulation. Insulin signaling is networked and linked in the human body to a wide range of metabolic processes related to aging. As best as I can tell it is the single most important, and modifiable, variable effecting aging in humans.
Secondly, high glucose levels result in more glycation of proteins within the body. Some of which can not be removed by the body's maintenance resources. The proteins collect over the years in cells and the extra cellular matrix.

#22 misterE

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Posted 20 February 2014 - 11:24 PM

Glucose becomes a problem when there is too much of it, which is the result of overeating. But fat is also a problem in overeating, because elevated levels of fatty acids may also cause insulin resistance, increased fat deposition, etc.




You have this wrong, and understanding what I’m about to say might help you with your theory. Elevated blood glucose and lipids are NOT caused by eating these substances directly, but rather indirectly from excessive gluconeogenesis and lipolysis, due to a lack of insulin. Eating fat and glucose doesn’t cause problems if the body is able to store it as energy. With diabetics, they lose their ability to store glucose and lipids properly and since the energy cannot leave the blood and enter the cells without insulin, glucose and lipids stay elevated until insulin (either internally or externally) is administered into the blood.

Diabetics also have difficulty storing protein properly as well, which is why protein-synthesis is diminished in diabetics.

Edited by misterE, 20 February 2014 - 11:26 PM.

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#23 Gerrans

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Posted 21 February 2014 - 02:28 PM

You have this wrong, and understanding what I’m about to say might help you with your theory. Elevated blood glucose and lipids are NOT caused by eating these substances directly, but rather indirectly from excessive gluconeogenesis and lipolysis, due to a lack of insulin. Eating fat and glucose doesn’t cause problems if the body is able to store it as energy. With diabetics, they lose their ability to store glucose and lipids properly and since the energy cannot leave the blood and enter the cells without insulin, glucose and lipids stay elevated until insulin (either internally or externally) is administered into the blood.

Diabetics also have difficulty storing protein properly as well, which is why protein-synthesis is diminished in diabetics.

Eating too much causes the body trouble with its regulatory mechanisms, which are of course all linked, in the liver, the pancreas, or other systems. Whether overeating causes problems directly or indirectly, immediately or gradually, the concentration of fatty acids and glucose in the bloodstream can be directly increased by eating too much.

I follow Keith Frayn, Professor of Human Metabolism at Oxford University, who wrote:

The glucose-fatty acid cycle may lead to adverse consequences in unusual situations where both non-esterified fatty acids and glucose are elevated. (These include stress and diabetes.) The effect can also occur after a particularly large meal of fat and carbohydrate. The muscle cannot oxidise non-esterified fatty acids and glucose at the rate expected from their concentrations in plasma. Then the operation of the glucose-fatty acid cycle leads to an impairment of glucose uptake and metabolism, with the net effect that glucose uptake by muscles is reduced compared to that expected at given concentrations of glucose and insulin in the plasma. It appears that glucose does not stimulate glucose uptake as normal, and this is known as insulin resistance, perhaps better termed as reduction to sensitivity to insulin. (Metabolic Regulation, 2003)

But all I am saying is that glucose might contribute to aging only as a result of overconsumption. The culprit might be overconsumption of foods that mix fat and sugar: things like chocolate, cakes, biscuits, ice cream, and desserts. These also seem to reduce the satiety signals that occur through sensors in many different parts of the system. An experiment with rats, for example, seemed to show that they overate such foods, whereas they did not overeat when fed high-sugar or high-fat foods separately. Then there was the famous "cafeteria diet" experiment, in which they overate junk foods and got fat.

#24 misterE

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Posted 21 February 2014 - 04:38 PM

What I was trying to clarify was that many people think the elevated blood-glucose in diabetics is caused by the carbohydrates they are eating… which is wrong. It is actually caused by excessive gluconeogenesis and glycerol release from lipolysis.

Now overfeeding for long periods causes adipocytes to enlarge and become insulin-resistant. These adipocytes, when resistant to the antilipolytic effects of insulin, release FFA into the circulation and are unable to store triglycerides. This is why blood-lipids are elevated in diabetes. Overfeeding of saturated-fats (which are much more attracted to adipocytes than unsaturated-fats) and simple-sugars (which are both insulinogenic and lipogenic) are much more effective at overstuffing your adipocytes than starch and protein (which have a hard time converting into fatty-acids and stimulate satiety hormones). But short-term saturated-fats and simple-sugars can’t really cause much damage if you have enough insulin and insulin-sensitivity to handle these nutrients. And the transportation of fatty-acids into adipocytes is actually beneficial and desirable, because it means less ectopic accumulation.

But starvation or underfeeding has the same effect (as insulin-resistance). This is one of the major flaws with long-term CR and why many people who are starving show the same symptoms as diabetes, like muscle wasting, decreased testosterone and sex-drive, bone-loss, elevated FFA’s, increased liver-fat, etc. With underfeeding or especially on low-carbohydrate diets, you have less insulin-secretion in general, and that allows gluconeogenesis and lipolysis to occur, leading to elevated blood glucose and lipids.

A good way to describe this is: with insulin—nutrients* are being stored out of the blood and inside the cells. Without insulin—nutrients are coming out of the cells and into the blood. It is the latter that leads to metabolic-syndrome.



*Nutrients meaning glucose, fatty-acids, amino-acids, minerals, etc.

Edited by misterE, 21 February 2014 - 04:47 PM.

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#25 Gerrans

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Posted 21 February 2014 - 05:28 PM

What I was trying to clarify was that many people think the elevated blood-glucose in diabetics is caused by the carbohydrates they are eating… which is wrong. It is actually caused by excessive gluconeogenesis and glycerol release from lipolysis.

Now overfeeding for long periods causes adipocytes to enlarge and become insulin-resistant. These adipocytes, when resistant to the antilipolytic effects of insulin, release FFA into the circulation and are unable to store triglycerides. This is why blood-lipids are elevated in diabetes. Overfeeding of saturated-fats (which are much more attracted to adipocytes than unsaturated-fats) and simple-sugars (which are both insulinogenic and lipogenic) are much more effective at overstuffing your adipocytes than starch and protein (which have a hard time converting into fatty-acids and stimulate satiety hormones). But short-term saturated-fats and simple-sugars can’t really cause much damage if you have enough insulin and insulin-sensitivity to handle these nutrients. And the transportation of fatty-acids into adipocytes is actually beneficial and desirable, because it means less ectopic accumulation.

But starvation or underfeeding has the same effect (as insulin-resistance). This is one of the major flaws with long-term CR and why many people who are starving show the same symptoms as diabetes, like muscle wasting, decreased testosterone and sex-drive, bone-loss, elevated FFA’s, increased liver-fat, etc. With underfeeding or especially on low-carbohydrate diets, you have less insulin-secretion in general, and that allows gluconeogenesis and lipolysis to occur, leading to elevated blood glucose and lipids.

A good way to describe this is: with insulin—nutrients* are being stored out of the blood and inside the cells. Without insulin—nutrients are coming out of the cells and into the blood. It is the latter that leads to metabolic-syndrome.



*Nutrients meaning glucose, fatty-acids, amino-acids, minerals, etc.


I agree with all this. There are also other causes of insulin resistance, which might explain cases that do not fit overfeeding or underfeeding scenarios. For example, sodium imbalance can cause insulin resistance, by screwing up blood pressure, etc.

My general view is that insulin resistance is a phenomenon caused by pressures of our modern way of eating that did not apply at the time our systems were evolving. It was impossible, for example, for apes and early man to consume the amount of sodium that many people do these days.

#26 eon

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Posted 22 February 2014 - 05:45 AM

All these explanations are great theories. But what would make the stuff we eat put to good use then? Exercise after eating?

Since the stuff we eat have to come out of the body, what makes it the cause of making people sick then? Is it over consumption to a point the body can't handle too much of it? If you look at how dogs eat, they eat everything until they are full, how come they aren't affected by diabetes?The people I know with liver issues comes from over-drinking for years. Same goes with smokers.

Edited by eon, 22 February 2014 - 05:49 AM.


#27 misterE

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Posted 23 February 2014 - 02:11 AM

But what would make the stuff we eat put to good use then?





Insulin and insulin-sensitivity. With proper insulin metabolism, nutrients are partitioned and metaboliozed properly. Without insulin or insulin-sensitivity, your body has difficulty using those nutrients properely.


Since the stuff we eat have to come out of the body, what makes it the cause of making people sick then?



Without insulin-signaling, glucose and fatty-acids elevate in the blood and can damage organs like the endothelium, pancreas, heart, thyroid, liver, kidneys, muscles, etc. My view is that people have metabolic-syndrome due to a lack of eating insulinogenic starches like flour, potatoes and pinto-beans.



Is it over consumption to a point the body can't handle too much of it?



Yes, but the basic condition is diminished insulin-signaling. Prolonged overfeeding (especially with saturated-fats and simple-sugars) causes adipocyte expansion and insulin-resistance within the adipocytes. This reduces your ability to properly store fat, so the fat ends up accumulating ectopically, and the increase in FFAs as a result of adipocyte insulin-resistance causes both insulin-resistance within the entire body and also forces the liver to convert muscle into glucose. However, in starvation or with low-carb diets, the exact same phenomenon occurs, due once again to decreased insulin secretion and subsequent signaling.



If you look at how dogs eat, they eat everything until they are full, how come they aren't affected by diabetes?



Normally, when you eat insulinogenic-foods, you activate satiety mechanisms. When energy is transported by insulin into the cells, the body releases a hormone called leptin, which regulates satiety and energy expenditure. Insulin-signaling is needed for leptin to cross the blood-brain-barrier, where it can promote its effects. Fats, oils and fructose do not trigger insulin signaling nor leptin signaling.

Edited by misterE, 23 February 2014 - 02:18 AM.

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#28 APBT

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Posted 24 February 2014 - 10:21 PM

If you look at how dogs eat, they eat everything until they are full, how come they aren't affected by diabetes?

Not to stray off-topic but, dogs can develop diabetes.
http://en.wikipedia....iabetes_in_dogs
http://www.aspca.org...g-care/diabetes

#29 eon

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Posted 25 February 2014 - 04:16 AM

of course the diabetes council just had to have a diabetes division for dogs, much like a hotel for dogs. Always had to be the #1 beloved animal. Why not cats or ferrets? There's just more money in the dog loving business I suppose.

If you look at how dogs eat, they eat everything until they are full, how come they aren't affected by diabetes?

Not to stray off-topic but, dogs can develop diabetes.
http://en.wikipedia....iabetes_in_dogs
http://www.aspca.org...g-care/diabetes


sounds like you're saying that diabetes is genetics, had to be? Like if a person have the wrong liver, immune system, insulin whatever, then the person is easily affected by it.

But what would make the stuff we eat put to good use then?





Insulin and insulin-sensitivity. With proper insulin metabolism, nutrients are partitioned and metaboliozed properly. Without insulin or insulin-sensitivity, your body has difficulty using those nutrients properely.


Since the stuff we eat have to come out of the body, what makes it the cause of making people sick then?



Without insulin-signaling, glucose and fatty-acids elevate in the blood and can damage organs like the endothelium, pancreas, heart, thyroid, liver, kidneys, muscles, etc. My view is that people have metabolic-syndrome due to a lack of eating insulinogenic starches like flour, potatoes and pinto-beans.



Is it over consumption to a point the body can't handle too much of it?



Yes, but the basic condition is diminished insulin-signaling. Prolonged overfeeding (especially with saturated-fats and simple-sugars) causes adipocyte expansion and insulin-resistance within the adipocytes. This reduces your ability to properly store fat, so the fat ends up accumulating ectopically, and the increase in FFAs as a result of adipocyte insulin-resistance causes both insulin-resistance within the entire body and also forces the liver to convert muscle into glucose. However, in starvation or with low-carb diets, the exact same phenomenon occurs, due once again to decreased insulin secretion and subsequent signaling.



If you look at how dogs eat, they eat everything until they are full, how come they aren't affected by diabetes?



Normally, when you eat insulinogenic-foods, you activate satiety mechanisms. When energy is transported by insulin into the cells, the body releases a hormone called leptin, which regulates satiety and energy expenditure. Insulin-signaling is needed for leptin to cross the blood-brain-barrier, where it can promote its effects. Fats, oils and fructose do not trigger insulin signaling nor leptin signaling.


Edited by eon, 25 February 2014 - 04:18 AM.


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#30 Kevnzworld

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Posted 26 February 2014 - 12:52 AM

My thoughts:
I believe that the science definitely shows that people with higher blood sugar levels have higher levels of glycation as is easily measured by an A1C test.. I also believe that elevated glycation leads to accelerated aging as we obviously see in diabetics. I test my blood regularly, fasting, post prandial and A1C to see how various foods and supplements effect the numbers. Mister E is at least partially correct as uncontrolled gluconeogenesis does elevate blood sugar levels. Supplements like green coffee bean extract limit glucoeogenesis and reduce blood sugar levels. I know this because I test often. I also know that high simple high carb foods and starches spike blood sugar levels, the key I guess is how long does it take for insulin to reduce those levels. The variability in each of us individually in terms of insulin sensitivity determines that. I don't need to read a study, my sore fingers have clearly shown me how various foods effect my numbers.
I take Metformin and various gluconeogenesis inhibiting supplements to suppress my glucose levels and hence my levels of glycation. I also take supplements that have been shown to reduce glycation....carnosine, p5p, benfotiamine, ALA, vitamin C etc.
I've been able to reduce my A1C levels from as high as 5.6 to currently 5.0. I'm hoping to break 5.0 the next test. I've begun also taking / testing LEF 's " tri sugar shield " product.
Re: green coffee bean. http://www.lef.org/m...een coffee bean

Edited by Kevnzworld, 26 February 2014 - 01:28 AM.






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