74 replies to this topic

[pone11]

 

Am J Clin Nutr. 1980 Jan;33(1):81-5.

 

A mathematical relationship between the fatty acid composition of the diet and that of the adipose tissue in man.

 

Beynen AC, Hermus RJ, Hautvast JG.

 

Abstract

 

Based on literature data, the hypothesis is advanced that in human subjects a direct mathematical relationship exists between the average fatty acid composition of the habitual diet and that of the lipid stores of subcutaneous adipose tissue. Since the half-life of adipose tissue fatty acids in man is in the order of 600 days, the fatty acid pattern of depot fat provides a qualitative measure of the fat intake over a period of 2 to 3 years. It is concluded that in long-term experimental and epidemiological nutritional surveys the adipose tissue fatty acid pattern of the subjects is a useful index of the average composition of their habitual dietary fat.

 

 

This is exactly what I said.   I believe one's O3 and O6 tissue saturation depends on what fats you eat.  I don't believe it depends on whether you eat high or low carbohydrates.   It's not clear why you quoted this study, because it says nothing in support of your thesis, and it does support mine.

 

 

 

The way I see it: During lipolysis free-fatty-acids (FFAs) are being released as energy. Once energy demands are met, any excess FFA is repackaged inside VLDL and sent back to storage inside the adipocyte. Eating carbohydrates and stimulating insulin lowers lipolysis and FFAs and stimulates lipoprotein-lipase, which removes the fatty-acids from VLDL back into the adipocyte for safe-keeping.

 

If you are insulin-resistant, you either lack insulin production or your insulin is insufficient enough to stimulate lipoprotein-lipase and are unable to store fat inside the adipocyte, thus you accumulate it outside of  the adipocytes, which is unhealthy, it that case your adipose-tissue turnover rate is accelerated, like what is seen in diabetes.

 

Also since fatty-acids are mobilized and released from the adipocytes by their degree of unsaturation, too much lipolysis would release a huge outpour of free-AA into the circulation, which would be harmful.

 

 

Even if someone agreed with your mechanisms, how does that provide advice to the more than 80 million Americans who are prediabetic and insulin resistant?    Your advice to load up on carbs would be great for most 25 year olds and a death sentence for those 80 million people.

 

An insulin resistant person who loads up on carbs ends up with dangerous glucose levels, tissue damage from glycation, and very importantly they get very very fat.  Insulin levels always being high signal the body to always remain in fat storage mode.  That only makes the insulin resistance worse.  For those 80 million people, your advice to load up on carbs is just bad advice.

 

You are practicing one-size-fits-all nutrition advice, and this is an area where one size does not fit all.   There are many possible causes for insulin resistance.   In my case, I became mercury toxic.  It turns out that the insulin receptor is a di-thiol and mercury binds to it, disabling it!   And it turns out that the insulin molecule that fits into that receptor is a single-thiol, so it can also be disabled by high blood mercury levels.   Advising the person with that sort of insulin defect to "load up on carbs" would not be good.

 

Rather than trying to come up with universal theories that simply do not work with large numbers of people, the better advice would be to test, test, test and learn how your body reacts to specific types of food.   This is an area where you can solve real problems empirically and with some simple application of the scientific method much better than you can by reading a textbook on fatty acid metabolism.

[misterE]

 

{1} how does that provide advice to the more than 80 million Americans who are prediabetic and insulin resistant?   

 

 

 

{2} An insulin resistant person who loads up on carbs ends up with dangerous glucose levels, tissue damage from glycation, and very importantly they get very very fat.  Insulin levels always being high signal the body to always remain in fat storage mode.  That only makes the insulin resistance worse. 

 

{3} You are practicing one-size-fits-all nutrition advice, and this is an area where one size does not fit all.   There are many possible causes for insulin resistance.  

 

 {4}  Advising the person with that sort of insulin defect to "load up on carbs" would not be good.

 

 

 

{1} Americans ate much more grains, beans, potatoes and flour in 1909. And the total percentage of calories from carbohydrate was also higher back then. Americans do NOT eat a high-carb high-fiber low-fat diet. French-fries are high-fat, meat is high-fat, fried-food is high-fat, cheese is high-fat, ice-cream is high-fat. Oil is high-fat. These are all staple foods in America. How many Americans do you see eating meals that contain just vegetables and grains?

 

{2} No. In diabetes, the person loses their ability to store not only fat, but also glucose and protein, this is why diabetics have high blood levels of fat (triglycerides, FFAs), sugar (glucose) and amino-acids (BCAAs). Diabetics are not in "fat-storing" mode as you claim... but rather diabetics are undergoing unrestrained lipolysis and are actually burning fatty-acids (at the expense of glucose).

 

{3} Sure, there are multiple-causes, but for the majority of people, the main cause of insulin-resistance is an elevation of FFAs, caused by an elevation of glucocorticoids, caused by an increased demand for glucose (carbs).

 

{4} I disagree. Eating a low-carb diet increases your glucocorticoids and actually raises blood-sugar, even starvation will increase blood-sugar long-term due to a lack of insulin.

Edited by misterE, 29 December 2014 - 12:55 AM.

[misterE]

 

 

Am J Clin Nutr. 1980 Jan;33(1):81-5.

 

A mathematical relationship between the fatty acid composition of the diet and that of the adipose tissue in man.

 

Beynen AC, Hermus RJ, Hautvast JG.

 

Abstract

 

Based on literature data, the hypothesis is advanced that in human subjects a direct mathematical relationship exists between the average fatty acid composition of the habitual diet and that of the lipid stores of subcutaneous adipose tissue. Since the half-life of adipose tissue fatty acids in man is in the order of 600 days, the fatty acid pattern of depot fat provides a qualitative measure of the fat intake over a period of 2 to 3 years. It is concluded that in long-term experimental and epidemiological nutritional surveys the adipose tissue fatty acid pattern of the subjects is a useful index of the average composition of their habitual dietary fat.

 

 

This is exactly what I said.   I believe one's O3 and O6 tissue saturation depends on what fats you eat.  I don't believe it depends on whether you eat high or low carbohydrates.   It's not clear why you quoted this study, because it says nothing in support of your thesis, and it does support mine.

 

 

 

I was citing the reference for Drew_ab. He asked about the half-life of fatty-acids. Obviously we are going to agree that the only way omega-6 and omega-3 get inside the body is through consumption. I was making the point, that since it is nearly impossible to completely avoid omega-6, the lower the total omega-6 content of our diet, the easier it is for us to manage our ratio with an overall lower total amount of polyunsaturates. And carbohydrate consumption is then a non-issue because once our carbohydrate needs are met and surpassed, the body will synthesize fats that don't affect the delicate omega-ratio. Carbohydrates will also suppress the release of polyunsaturated FFAs.

Edited by misterE, 29 December 2014 - 02:34 AM.

[pone11]

 

 

{1} how does that provide advice to the more than 80 million Americans who are prediabetic and insulin resistant?   

 

 

 

{2} An insulin resistant person who loads up on carbs ends up with dangerous glucose levels, tissue damage from glycation, and very importantly they get very very fat.  Insulin levels always being high signal the body to always remain in fat storage mode.  That only makes the insulin resistance worse. 

 

{3} You are practicing one-size-fits-all nutrition advice, and this is an area where one size does not fit all.   There are many possible causes for insulin resistance.  

 

 {4}  Advising the person with that sort of insulin defect to "load up on carbs" would not be good.

 

 

 

{1} Americans ate much more grains, beans, potatoes and flour in 1909. And the total percentage of calories from carbohydrate was also higher back then. Americans do NOT eat a high-carb high-fiber low-fat diet. French-fries are high-fat, meat is high-fat, fried-food is high-fat, cheese is high-fat, ice-cream is high-fat. Oil is high-fat. These are all staple foods in America. How many Americans do you see eating meals that contain just vegetables and grains?

 

{2} No. In diabetes, the person loses their ability to store not only fat, but also glucose and protein, this is why diabetics have high blood levels of fat (triglycerides, FFAs), sugar (glucose) and amino-acids (BCAAs). Diabetics are not in "fat-storing" mode as you claim... but rather diabetics are undergoing unrestrained lipolysis and are actually burning fatty-acids (at the expense of glucose).

 

{3} Sure, there are multiple-causes, but for the majority of people, the main cause of insulin-resistance is an elevation of FFAs, caused by an elevation of glucocorticoids, caused by an increased demand for glucose (carbs).

 

{4} I disagree. Eating a low-carb diet increases your glucocorticoids and actually raises blood-sugar, even starvation will increase blood-sugar long-term due to a lack of insulin.

 

 

(1) Modern diets are loaded with omega-6 fats.   Those are all industrial seed oils, all polyunsaturated.  There is no comparison to be made against diets from 1909.   The beneficial high fat diets have mostly saturated fats from non-dairy sources and monounsaturated fats.   I work extremely hard to keep O3 and O6 below about 5% of my calories ingested.  No modern American is eating that little polyunsaturated fat.

 

(2) and (3)  You completely misunderstand the actions of insulin in type 2 diabetes.  The myth about diabetes is that the tissues fail to store glucose because of insulin resistance.  Actual research measurements show that type 2 diabetics uptake of glucose into muscle is INCREASED over normoglycemic people, not decreased.

 

This is the single best article in the research literature that I have ever found on insulin resistance.  Your posts fall into every stereotype and misconception about the disease that the author calls out:

http://bja.oxfordjou...nt/85/1/69.long

 

As the author says in this article:  "...the fasting hyperglycaemia of diabetes results from hepatic over‐production of glucose alone, since peripheral glucose utilization is increased despite the lack of insulin."   Any person with a loved one who is affected by this disease should read that article.  It will completely alter your understanding of what happens in this disease.   The tissues do not fail to uptake glucose.   The tissues actually uptake glucose faster than non diabetics.   The key to beating diabetes is finding a diet that will shut down the liver's overproduction of glucose.  Period.

 

The author of the above review has a very interesting section near the beginning:

"The key question is: is the fasting hyperglycaemia of diabetes due to overproduction of glucose by the liver or underutilization of glucose by peripheral tissues?

When this question was posed to participants of the Royal College of Anaesthetists’ Basic Science Course in 1998 and 1999, a show of hands revealed virtually unanimous support for the second alternative, with only one or two hands in favour of the correct answer (overproduction of glucose by the liver). This is a typical response, seen from the overwhelming majority of both undergraduate and postgraduate audiences in the UK and the rest of the world. It is important to have the right understanding if insulin is to be used appropriately and to maximum benefit. This may perhaps seem a trivial or pedantic point but it is not. Correct understanding of what goes wrong with metabolism in the face of insulin deficiency is essential in the understanding and execution of logical and safe forms of treatment."

 

(4)  I have yet to find a single study in the research literature where they feed high carbs to diabetics and have *BOTH* the fasting glucose and the insulin levels go down.  What usually happens is fasting glucose comes down and insulin levels stay high.  This is important because many of the health risks of diabetes actually attach to the insulin levels, not the glucose levels.  If you can find a free copy, this guy's discussion of insulin levels and disease is phenomenal:

http://www.sciandmed...072&article=844

 

One of the things you learn from that review is that many people have *normal* glucose levels but elevated insulin, and that condition often goes completely undetected.   Those individuals end up coming down with heart disease and many of the secondary diseases that full on type 2 diabetics get.

 

On the other hand, I have found many studies where they feed low carbs, and both fasting glucose AND insulin crash.  I have personally observed this effect as well in dozens of people, and that is with me pushing them to get insulin measurements before and after meals, not just taking blood glucose readings.   About 30% of the people I have tried to help with this never get that effect.   It's a very difficult disease, particularly once an insulin resistant person gets a lot of body fat.   Low carb does not mean NO carb, and I think you are right that going too low on carbs (below about 50 grams of starchy carbs a day) can produce very erratic results.    But feed someone healthy fats, moderate protein, lots of non-starchy vegetables (which have nutrition not carbs), and then challenge them with very modest and small starchy carbs, and their glucose and insulin both usually normalize quickly.   

Edited by pone11, 29 December 2014 - 05:58 AM.

[ikon2]

 

 

(1) Modern diets are loaded with omega-6 fats.   Those are all industrial seed oils, all polyunsaturated.  There is no comparison to be made against diets from 1909.   The beneficial high fat diets have mostly saturated fats from non-dairy sources and monounsaturated fats.   I work extremely hard to keep O3 and O6 below about 5% of my calories ingested.  No modern American is eating that little polyunsaturated fat.

 

 

Prone, please expand on why you keep your overall fat intake so low or am I misunderstanding you?  When you say "O3", do you mean all O3 or just polyO3?  Or all fats in general i.e. saturated fats and/or including MCT's (coconut oil), etc?

 

Two glaringly opposing trends in this (great) thread is that there seems to be very knowledgeable people here who keep their overall fat intake low (despite the fats consumed being the agreed upon healthier/non-DHA/polyunsaturated types) and then other very knowledgeable people here seem to have a healthy type fat intake of up to 50% of their totals daily calories consumed.

 

I guess this could be discussed as a separate topic entirely but maybe we could touch on it here as it is so relevant to the conversation at hand.

 

So if you are indeed keeping your overall fats so low, why?  Can anyone on the extremes of the fat-intake spectrum here please weigh in with their reasoning as well?

 

Forgive my idiocy, but what is the net/net here (assuming one subscribes to this theory,which I for one am becoming increasingly convinced of given the continued studies supporting it)?

 

Would a good approach be to make 30% of one's diet fats and within that percentage make:

 

33% LA (coconut oil, macadamia nuts)

 

33% ALA (Flax)

 

33% MUFA (olive oil, avocado)

 

Would this approach satisfy realizing the benefits of MUFA's, realize the benefits of keeping n-3 to n-6 at approx 1:1 and also keep the DHA intake to a minimum and let the body convert what it needs?  And am I correct to assume that Flax, although a PUFA is the type one would want?

 

Am I missing anything here or are any of my foods/fat sources or ratios off?  Is Olive oil considered a HUFA?

 

Also, how does one know if a PUFA (when reading a nutrition label) know if it is a short chain or long chain?

 

And not too much talk about MUFA's in this thread.  Are these good or bad in terms of this theory?

 

Bump (for answer)

 

 

Again, forgive my idiocy but still bumping

 

I realize my post falls under the "just tell me what to eat" category, but there is a ton of info on this great thread, and some of it conflicting.  Is there not a consensus of what, at least from a general perspective, foods one should derive their fats from and generally what percentage?

 

 

Edited by ikon2, 29 December 2014 - 02:01 PM.

[pone11]

 

 

(1) Modern diets are loaded with omega-6 fats.   Those are all industrial seed oils, all polyunsaturated.  There is no comparison to be made against diets from 1909.   The beneficial high fat diets have mostly saturated fats from non-dairy sources and monounsaturated fats.   I work extremely hard to keep O3 and O6 below about 5% of my calories ingested.  No modern American is eating that little polyunsaturated fat.

 

 

Prone, please expand on why you keep your overall fat intake so low or am I misunderstanding you?  When you say "O3", do you mean all O3 or just polyO3?  Or all fats in general i.e. saturated fats and/or including MCT's (coconut oil), etc?

 

Two glaringly opposing trends in this (great) thread is that there seems to be very knowledgeable people here who keep their overall fat intake low (despite the fats consumed being the agreed upon healthier/non-DHA/polyunsaturated types) and then other very knowledgeable people here seem to have a healthy type fat intake of up to 50% of their totals daily calories consumed.

 

I guess this could be discussed as a separate topic entirely but maybe we could touch on it here as it is so relevant to the conversation at hand.

 

So if you are indeed keeping your overall fats so low, why?  Can anyone on the extremes of the fat-intake spectrum here please weigh in with their reasoning as well?

 

 

I don't want to take for granted that you understood the original post here, so just to repeat his thesis:

 

* saturated and monounsaturated fats are stable when incorporated into cell membranes

* polyunsaturated fats are extremely unstable lipids and subject to damage during oxidative stress

 

I eat a high fat diet, mostly saturated and monounsaturated fats.   I get about 55% of my calories from fat, 15% from protein, and the rest from veggies and a very small amount of starchy carbs.  I eat HUGE amounts of veggies, but it is all low carb stuff.   At breakfast I often have three CUPS of shredded celery in coconut milk.  At lunch I have a HUGE salad with mixed greens.  I want the veggies for nutrition, and I avoid the types of carbs that deliver pure huge doses of sugar (e.g., breads, pastas, potatoes, etc).

 

I get about 5% of calories from polyunsaturated fats (used to be much less).   O3 and O6 are the two broad families of polyunsaturated fats.  O3=Omega-3 and O6=Omega-6.

 

I have to say that the poster who started to talk about eating starchy carbs took this thread off topic.   The original poster had a focused and very good topic.   The question this thread was posing was NEVER about how much calories you should get from saturated or monounsaturated fat versus carbs!!  The original question was about the value of avoiding polyunsaturated fats.    I agree with 90% of the original poster's comments, and he made me aware of things I had not known on this topic.   My only real disagreement was that he is taking a form of Omega-3 called ALA that very inefficiently converts to another Omega-3 called DHA.   DHA is the fat that is most commonly found in your brain tissue, in neurons.   I just argued to take the minimum amount of DHA needed to support brain function and don't expose yourself to even more polyunsaturated fat by taking high doses of ALA.   I think he and I don't disagree about very much.

 

 

 

Forgive my idiocy, but what is the net/net here (assuming one subscribes to this theory,which I for one am becoming increasingly convinced of given the continued studies supporting it)?

 

Would a good approach be to make 30% of one's diet fats and within that percentage make:

 

33% LA (coconut oil, macadamia nuts)

 

33% ALA (Flax)

 

33% MUFA (olive oil, avocado)

 

Would this approach satisfy realizing the benefits of MUFA's, realize the benefits of keeping n-3 to n-6 at approx 1:1 and also keep the DHA intake to a minimum and let the body convert what it needs?  And am I correct to assume that Flax, although a PUFA is the type one would want?

 

Am I missing anything here or are any of my foods/fat sources or ratios off?  Is Olive oil considered a HUFA?

 

Also, how does one know if a PUFA (when reading a nutrition label) know if it is a short chain or long chain?

 

And not too much talk about MUFA's in this thread.  Are these good or bad in terms of this theory?

 

 

Honestly I would like to suggest you make that a new thread and then send me a private message to reply there.   This has much broader scope than the original question, and you are just encouraging the other poster to talk about high carb diets.   This thread should have been about how much poly fat should you eat.

 

For the question how much O3 and O6 should you eat:

 

1) Many biochemists would say you should eat only 1% to 2% of your total calories consumed as Omega-3 and Omega-6!!  Seriously.   And almost no one can do that now because the US food chain is so polluted.  The chicken you eat is loaded with Omega-6 because they feed the chicken industrial seeds.   The beef you buy is fed grain and has Omega-6.  You really have to be a very dedicated and knowledgeable person to arrange a diet that is low in these polyunsaturated fats.

 

2) Many doctors would recommend you get about 10% to 20% of calories from Omega-3 and Omega-6 because of studies on heart disease.

 

3) The people who run our government apparently think we should get 25% to 30% of calories from Omega-3 to Omega-6.

 

I lean towards the biochemists, and I definitely believe these fats should make up less than 6% of total calories ingested.   The lower the better as long as you measure your fatty acids in cell membranes every year and make sure you are not running some huge deficiencies.

 

 

Edited by pone11, 29 December 2014 - 02:32 PM.

[misterE]

 

 

 

 

 

 

{1} Modern diets are loaded with omega-6 fats.

 

{2} There is no comparison to be made against diets from 1909.  

 

{3} The beneficial high fat diets have mostly saturated fats from non-dairy sources and monounsaturated fats.

 

{4} I work extremely hard to keep O3 and O6 below about 5% of my calories ingested.

 

{5} No modern American is eating that little polyunsaturated fat.

 

{6} You completely misunderstand the actions of insulin in type 2 diabetes.  The myth about diabetes is that the tissues fail to store glucose because of insulin resistance.  Actual research measurements show that type 2 diabetics uptake of glucose into muscle is INCREASED over normoglycemic people, not decreased.

 

{7} The tissues actually uptake glucose faster than non diabetics.  

 

{8} The key to beating diabetes is finding a diet that will shut down the liver's overproduction of glucose.  Period.

 

{9} The author of the above review has a very interesting section near the beginning:

"The key question is: is the fasting hyperglycaemia of diabetes due to overproduction of glucose by the liver or underutilization of glucose by peripheral tissues?

 

{10}  I have yet to find a single study in the research literature where they feed high carbs to diabetics and have *BOTH* the fasting glucose and the insulin levels go down.

 

 

 

 

{1} Agreed.

 

{2} Sure there is. The difference is huge.

 

{3} Sure, plant-fats are usually considered healthier than animal-fats (probably due to the absence of arachidonic-acid in plant-fat).

 

{4} So do I. But my food choices are high-carbohydrate instead of high-fat like yours, which is an inferior "last-resort" type of fuel, especially for exercise.

 

{5} Agreed.

 

{6} That is false. Diabetics have reduced ability to store glucose as glycogen, this is well established.

 

{7} Nope, the opposite.

 

{8} Agreed, and the only way to shut off the livers production of glucose... is to eat glucose. The body has a negative-feedback loop installed in the body, a counter regulatory process if you will. If you restrict glucose intake, the liver will make more to supply the brain.

 

{9} The Answer to the question: is both. Reduced uptake of glucose into the muscles combined with excessive glucose production by the liver, causes the elevated blood-sugar found in diabetes.

 

{10} You haven't looked very hard:

 

 

Diabetes Care. 1983 May-Jun;6(3):268-73.

 

Long-term use of a high-complex-carbohydrate, high-fiber, low-fat diet and exercise in the treatment of NIDDM patients.

 

Barnard RJ, Massey MR, Cherny S.

 

Abstract

 

The purpose of this study was to assess the long-term effects of a high-complex-carbohydrate, high-fiber, low-fat diet and exercise on 69 NIDDM patients. During the initial 26-day program, fasting glucose was reduced from 179.5 +/- 10.6 to 133.5 +/- 4.0 mg/dl. This decrease in fasting glucose was achieved along with the discontinuation of oral hypoglycemic agents in 24 of 31 patients and of insulin in 13 of 18 patients; one patient was placed on insulin. Serum cholesterol and triglycerides were reduced by 25% and 27%, respectively. At 2-3 yr of follow-up, fasting glucose was not significantly different from the value observed at the end of the 26-day program. Compared with the end of the 26-day program, seven more patients were taking oral agents and four more were on insulin. Exercise and diet inventories obtained at follow-up indicated good compliance to the program and also indicated that the main difference between those patients who went back on medication at follow-up compared with those remaining off medication was the percent of calories derived from fat.

 

 

 

Am J Clin Nutr. 1977 Mar;30(3):402-8.

 

Effect of carbohydrate restriction and high carbohydrates diets on men with chemical diabetes.

 

Anderson JW.

 

Abstract

 

The influence of low carbohydrate (CHO) diets, starvation, and high CHO diets on glucose tolerance tests (GTT) and plasma insulin response of men with chemical diabetes was studied. The GTT and insulin responses of these seven lean diabetic men were unchanged when the carbohydrate content of the diet was reduced from 44 to 20% of calories. After a 48-hr fast a significant deterioration of the GTT was observed in these diabetic men but the percentage change was identical to that reported previously for normal men. Thus these studies indicate that changes in glucose mtes are quite similar to those reported previously for normal men. The fasting plasma glucose values of seven lean and four obese men with chemical diabetes were significantly lower after one week on a 75% CHO diet than values on a 44% CHO diet. The 75% CHO diet also was accompanied by slight improvements in the oral and intravenous GTT and by slightly lower plasma insulin responses. The improvement in glucose metabolism on high CHO diets appears to results from increased insulin sensitivity. Serum triglyceride values were approximately 55% higher on the 75% CHO diet than values on the 44% CHO diet for the 11 men but these differences were not statistically significant. These studies support previous observations and suggest that high CHO diets may be beneficial in the management of certain diabetic patients. However, further studies are required to determine the long-term effects of high CHO diets containing natural foods on the glucose and lipid metabolism of diabetic patients.

 

 

 

 

 

 

Edited by misterE, 29 December 2014 - 03:40 PM.

[misterE]

I will agree with pone11 that this has gotten off topic. But since we are on the topic of diabetes I wanted to show some information I gathered on diabetes in regards to polyunsaturated-fat intake.

 

The storage of triglycerides inside the adipocytes doesn't pose harm or reduce peripheral insulin-resistance. It is actually the release of triglycerides in the form of FFAs that causes peripheral insulin-resistance (in organs like the blood-vessels, liver, muscles, pancreas, etc.). The adipocytes mobilize and release fatty-acids by their degree of unsaturation [1]. Meaning that all of the polyunsaturated-fat is first released, followed by monounsaturated-fat and then saturated-fats. The adipocytes retain saturated-fats, while easily releasing polyunsaturated-fats. Since polyunsaturated-fats are so highly oxidized, they will compete with oxidation of glucose. The Randle-cycle only allows for one primary type of fuel to be burned, and since unsaturated-fats are easily oxidized, high levels of unsaturated FFAs will interfere with glucose metabolism, agitating diabetes.

 

Also of importance is that the release of polyunsaturated FFAs also inhibits insulin-secretion from the pancreas [2-3], leading to more lipolysis, leading to more polyunsaturated FFAs being released into circulation. Saturated FFAs like palmitic, lauric or steric-acid actually stimulates the secretion of insulin from the beta-cells and helps prevent insulin-resistance. In fact hyperinsulinemia, which is often thought of as a bad thing, actually is your body's way of trying to fend off diabetes. The hyperinsulinemia is caused by increased circulation of saturated FFAs, which is stimulating your pancreas to release insulin. However excessive chronic levels of circulating FFAs will start to accumulate on the pancreas and actually damage your beta-cells, thus reducing the amount of insulin you are able to make. Fortunately eating carbohydrates and making insulin will help regenerate these beta-cells, most of this is accomplished with the incretin hormones; GLP-1 and GIP. After a carbohydrate-rich meal you increase incretin secretion, which not only helps assist in insulin-secretion, but also promotes beta-cell mass and proliferation.

 

 

 

 

 

[1] Biochem J. 1997 Jun 15;324 ( Pt 3):911-5. Selective release of human adipocyte fatty acids according to molecular structure. Raclot T, Langin D, Lafontan M.

 

 

 

[2] J Clin Invest. 1997 Jul 15;100(2):398-403. The insulinotropic potency of fatty acids is influenced profoundly by their chain length and degree of saturation. Stein DT, Stevenson BE, Chester MW.

 

 

[3] Diabetes. 2002 Jun;51(6):1825-33. The composition of dietary fat directly influences glucose-stimulated insulin secretion in rats. Dobbins RL, Szczepaniak LS, Myhill J.

 

 

 

 

 

Edited by misterE, 29 December 2014 - 04:45 PM.

[Ark]

Has a person's age been factored into the equation?

Edited by Ark, 29 December 2014 - 05:42 PM.

[HaloTeK]

Pone11, low fat diets are not a death sentence.  I wouldn't go totally vegan, but look at this study.

 

Ma-Pi 2 macrobiotic diet and type 2 diabetes mellitus: pooled analysis of short-term intervention studies.

Porrata-Maury C¹, Hernández-Triana M, Ruiz-Álvarez V, Díaz-Sánchez ME, Fallucca F, Bin W, Baba-Abubakari B, Pianesi M.

Author information

Abstract

The macrobiotic, Ma-Pi 2 diet (12% protein, 18% fat and 70% carbohydrate), has shown benefit in adults with type 2 diabetes mellitus (T2DM). This pooled analysis aims to confirm results from four, 21-day intervention studies with the Ma-Pi 2 diet, carried out in Cuba, China, Ghana and Italy. Baseline and end of study biochemical, body composition and blood pressure data, were compared using multivariate statistical methods and assessment of the Cohen effect size (d). Results showed that all measured indicators demonstrated significant changes (p < 0.001); most of them with a very high (d ≥ 1.30), or high (d = 0.80-1.29) effect size. The global effect size of the diet was Italy (1.96), China (1.79), Cuba (1.38) and Ghana (0.98). The magnitude of the individual effect on each variable by country, and the global effect by country, was independent of the sample size (p > 0.05). Similarly, glycemia and glycemic profiles in all four studies were independent of the sample size (p = 0.237). The Ma-Pi diet 2 significantly reduced glycemia, serum lipids, uremia and cardiovascular risk in adults with T2DM. These results suggest that the Ma-Pi 2 diet could be a valid alternative treatment for patients with T2DM and point to the need for further clinical studies. Mechanisms related to its benefits as a functional diet are discussed.

[misterE]

Has a person's age been factored into the equation?

 

Well as a person ages, not only have they accumulated more polyunsaturated-fat in their tissues (compared to a younger person), but the more polyunsaturated-fat inside the adipocytes makes them very susceptible to lipolysis, which is one of the main underlying causes of the diabetes. Diabetes causes a release of stored polyunsaturated-fats into the peripheral circulation.

 

Think of a baby or a child. Most of their storage-fats are either saturated or monounsaturated-fats obtained directly from the fats in mothers-milk or through de-novo-lipogenesis of sugars. They have not had much exposure to polyunsaturated-fats, and are usually free of diabetes. Unfortunately today many children are fed high polyunsaturated-fat diets (chicken strips, French-fries, etc.) and even the amount of linoleic-acid has increased in the breast-milk of American and European mothers. Perhaps this is an overlooked explanation for the childhood-obesity and diabetes epidemics today.

[sensei]

 

 

{1} how does that provide advice to the more than 80 million Americans who are prediabetic and insulin resistant?   

 

 

 

{2} An insulin resistant person who loads up on carbs ends up with dangerous glucose levels, tissue damage from glycation, and very importantly they get very very fat.  Insulin levels always being high signal the body to always remain in fat storage mode.  That only makes the insulin resistance worse. 

 

{3} You are practicing one-size-fits-all nutrition advice, and this is an area where one size does not fit all.   There are many possible causes for insulin resistance.  

 

 {4}  Advising the person with that sort of insulin defect to "load up on carbs" would not be good.

 

 

 

{1} Americans ate much more grains, beans, potatoes and flour in 1909. And the total percentage of calories from carbohydrate was also higher back then. Americans do NOT eat a high-carb high-fiber low-fat diet. French-fries are high-fat, meat is high-fat, fried-food is high-fat, cheese is high-fat, ice-cream is high-fat. Oil is high-fat. These are all staple foods in America. How many Americans do you see eating meals that contain just vegetables and grains?

 

{2} No. In diabetes, the person loses their ability to store not only fat, but also glucose and protein, this is why diabetics have high blood levels of fat (triglycerides, FFAs), sugar (glucose) and amino-acids (BCAAs). Diabetics are not in "fat-storing" mode as you claim... but rather diabetics are undergoing unrestrained lipolysis and are actually burning fatty-acids (at the expense of glucose).

 

{3} Sure, there are multiple-causes, but for the majority of people, the main cause of insulin-resistance is an elevation of FFAs, caused by an elevation of glucocorticoids, caused by an increased demand for glucose (carbs).

 

{4} I disagree. Eating a low-carb diet increases your glucocorticoids and actually raises blood-sugar, even starvation will increase blood-sugar long-term due to a lack of insulin.

 

I'm living proof that your hypothesis is rubbish.

 

Oh, and American consume waaaay more carbs today then 100 years ago. 1 20oz soda = 10% of your daily caloric intake at 240 calories. A bowl of breakfast cereal -- Apple Jacks for instance is 90% carbs -- per serving.

 

And don't forget that rubbish food pyramid 5-6 servings of grains/starch a day.

 

Most juice is HFCS plus water and a little bit of real juice -- again sugars -- oh and BTW carbs and sugars prematurely age you.

 

My diet is 50% fat, 35-40% protein, and 10-15% carbs. I am extremely active and need approximately 170-180 grams of protein a day to maintain muscle mass. Has been for 2 years

 

I have a blood glucose level of 104-109 consistently for 2 years and an A1C of 5.1.

 

 

Edited by sensei, 30 December 2014 - 01:08 AM.

[HaloTeK]

Wow, u are prepared to say a fasting glucose of 104-109 is good?

[Logic]

he   addition     of  thesynthetic     antioxidant      BHT   (0.02%,   wt/wt    oil)  to  thefish  oil  diet   significantly     reduced   lipid  peroxidation     ascompared     with    the   control    fish   oil   diet.   The   higherconcentration      of  BHT  (2.0%)  was  more   effective    than the   0.02%   level.

 

The   addition    of  high   levels   of  antioxidantsto  the   fish   oil  diet   reduced    TEARS   concentrations      inall    organs    and    in   whole     body

 

http://www.2ndchance...onzalez1992.pdf

[aribadabar]

I'm living proof that your hypothesis is rubbish.

 

 

Oh, and American consume waaaay more carbs today then 100 years ago. 1 20oz soda = 10% of your daily caloric intake at 240 calories. A bowl of breakfast cereal -- Apple Jacks for instance is 90% carbs -- per serving.

 

And don't forget that rubbish food pyramid 5-6 servings of grains/starch a day.

 

Most juice is HFCS plus water and a little bit of real juice -- again sugars -- oh and BTW carbs and sugars prematurely age you.

 

My diet is 50% fat, 35-40% protein, and 10-15% carbs. I am extremely active and need approximately 170-180 grams of protein a day to maintain muscle mass. Has been for 2 years

 

I have a blood glucose level of 104-109 consistently for 2 years and an A1C of 5.1.

 

 

You are living proof that quasi-keto diet is not working for your health, perhaps due to your ApoE profile.

I would have expected much lower than 104 fasting glucose and A1C sub 5.0 at such a low % of carbs.