Question:

> I found the thread on saturated fat and cholesterol very interesting, > especially the contributions on insulin resistance from Hua Kul and > Quentin Grady. > When I was first diagnosed T2, about four months ago, I questioned our > diabetic nurse about the dietary recommendations, especially the bit > about keeping dietary fat to a minimum, as I couldn’t see any > relevance to diabetes. (In fact the whole ‘pyramid’ diet advice seemed > to me to be irrelevant to the problems of diabetes, which were to do > with blood sugar, or so I thought at the time, and I haven’t totally > changed that view! The logic of maximising carbohydrate intake whilest > trying to minimise blood glucose concentration, escapes me).

Fat delays the absorption of carbs.  So a little bit of fat with a meal is good.  Too much is bad.  Why?  The carbs you ate might not get into your system when you need them and you would get a hypo.  You would then treat the hypo by eating more carbs.  Then *wham* when you least expect it, those carbs from your meal get into your system on top of what you ate for the hypo.  You then have a spike. > She said that when you eat a meal containing carbohydrate, as well as > getting a surge in blood glucose, you also get a surge in insulin. > With ‘normal’ people, the insulin spike rapidly declines as the > glucose is dealt with, but with T2 diabetics, because they are insulin > resistant, the blood glucose doesn’t fall away as quickly. The > pancreas sees a continuing high level of glucose, so puts out more > insulin and the insulin spike gets bigger. She said it wasn’t the > blood glucose directly that caused many of the problems associated > with diabetes, but the high concentrations of insulin put out by the > pancreas to try and deal with it. Eventually, as a consequence of > these high insulin levels, the pancreas just gives up, and T2’s have > to start injecting.

That may be.  The part about non-diabetics sounds right.  Don’t know enough about the other to comment. > With respect to fat in the diet, she said that diabetics had a greater > tendency to gain weight than normal people (and hence a greater > disposition to coronary disease), so had to be more careful about > their fat intake. This weight gain was as a result of the insulin > spikes. By way of supporting evidence, she said that as soon as > diabetics started to inject insulin, they tended to start putting on > weight, the implication being that insulin injections are themselves > insulin spikes when compared with the normally well regulated output > from the pancreas. (Whether this is true for T1’s as well as T2’s I > don’t know: I had a work colleague who was T1 from a early age and who > was as thin as a bean-pole. Can/do T1’s eventually become insulin > resistant because of these insulin spikes? Do T1’s suffer the same > long term problems of neuropathy etc. as T2’s?).

This sounds a bit garbled.  If a person is watching what they eat and injecting the correct amount of insulin, then weight gain shouldn’t be a problem.  That’s assuming they don’t have other metabolic disorders or are taking some medication that could cause weight gain.  Type 1s certainly CAN become insulin resistant.  And all diabetics can get neuropathy.  Doesn’t matter what type they have. > Although I may not have remembered everything the nurse said quite > correctly, it mostly fits in very well with the points made by Messrs > Kul and Grady, which in turn have greatly increased my understanding > of the whole T2 problem. What surprised me a little was that the nurse > told me all this rather as an aside, as if she wouldn’t normally > confide such information to most of her patients. It’s as if the > medical profession knows a lot more than it’s prepared to let out to > the public. Perhaps they think we wouldn’t understand…..

You are right.  Seems that many people do not want to know about their disease.  They merely want to take a pill and then not worry about it any more. > With respect to fructose, the UK Diabetic association advise against > using fructose as a substitute for sugar, but give no indication why. > This puzzled me, as fructose has one of the lowest glycemic indices of > any carbohydrate (22 IIRC) so shouldn’t be a problem in terms of bg > spikes, although still full of calories of course. But for someone not > needing to lose weight as I don’t, it seemed a good alternative > sweetener. I asked the dietitian about it, and she was also surprised > at the Diabetes UK advice, as she said that fructose was part of the > metabolic pathway and that glucose was converted into it in the body. > I may not have that last bit quite right, but thanks to Messrs Kul and > Grady, I now know that replacing sucrose by fructose wouldn’t be such > a good idea as it promotes insulin resistance directly.

If you do a search on fructose and diabetes, you’ll come up with a ton of information.  Basically, it can lead to heart problems.  But it’s a complicated process and one that I couldn’t explain very well.  The fructose in fruit doesn’t seem to do this.  It is only when it is extracted and used as a sweetener that problems can occur. > So once again gentlemen, thanks for a most interesting and informative > thread. It’s just a pity that this sort of information has to be > dragged out from original papers and reviews in the scientific > literature by dedicated amateurs, rather than being made available in > readable form by the diabetic associations on either side of the > Atlantic. Or have I missed something?

Unfortunately, there is a lot of information out there and it isn’t always so easy to tell if it is accurate or not. — Type 2 http://www.redshift.com/~juliebove/

Response:

I found the thread on saturated fat and cholesterol very interesting, especially the contributions on insulin resistance from Hua Kul and Quentin Grady. When I was first diagnosed T2, about four months ago, I questioned our diabetic nurse about the dietary recommendations, especially the bit about keeping dietary fat to a minimum, as I couldn’t see any relevance to diabetes. (In fact the whole ‘pyramid’ diet advice seemed to me to be irrelevant to the problems of diabetes, which were to do with blood sugar, or so I thought at the time, and I haven’t totally changed that view! The logic of maximising carbohydrate intake whilest trying to minimise blood glucose concentration, escapes me). She said that when you eat a meal containing carbohydrate, as well as getting a surge in blood glucose, you also get a surge in insulin. With ‘normal’ people, the insulin spike rapidly declines as the glucose is dealt with, but with T2 diabetics, because they are insulin resistant, the blood glucose doesn’t fall away as quickly. The pancreas sees a continuing high level of glucose, so puts out more insulin and the insulin spike gets bigger. She said it wasn’t the blood glucose directly that caused many of the problems associated with diabetes, but the high concentrations of insulin put out by the pancreas to try and deal with it. Eventually, as a consequence of these high insulin levels, the pancreas just gives up, and T2’s have to start injecting. With respect to fat in the diet, she said that diabetics had a greater tendency to gain weight than normal people (and hence a greater disposition to coronary disease), so had to be more careful about their fat intake. This weight gain was as a result of the insulin spikes. By way of supporting evidence, she said that as soon as diabetics started to inject insulin, they tended to start putting on weight, the implication being that insulin injections are themselves insulin spikes when compared with the normally well regulated output from the pancreas. (Whether this is true for T1’s as well as T2’s I don’t know: I had a work colleague who was T1 from a early age and who was as thin as a bean-pole. Can/do T1’s eventually become insulin resistant because of these insulin spikes? Do T1’s suffer the same long term problems of neuropathy etc. as T2’s?). Although I may not have remembered everything the nurse said quite correctly, it mostly fits in very well with the points made by Messrs Kul and Grady, which in turn have greatly increased my understanding of the whole T2 problem. What surprised me a little was that the nurse told me all this rather as an aside, as if she wouldn’t normally confide such information to most of her patients. It’s as if the medical profession knows a lot more than it’s prepared to let out to the public. Perhaps they think we wouldn’t understand….. With respect to fructose, the UK Diabetic association advise against using fructose as a substitute for sugar, but give no indication why. This puzzled me, as fructose has one of the lowest glycemic indices of any carbohydrate (22 IIRC) so shouldn’t be a problem in terms of bg spikes, although still full of calories of course. But for someone not needing to lose weight as I don’t, it seemed a good alternative sweetener. I asked the dietitian about it, and she was also surprised at the Diabetes UK advice, as she said that fructose was part of the metabolic pathway and that glucose was converted into it in the body. I may not have that last bit quite right, but thanks to Messrs Kul and Grady, I now know that replacing sucrose by fructose wouldn’t be such a good idea as it promotes insulin resistance directly. So once again gentlemen, thanks for a most interesting and informative thread. It’s just a pity that this sort of information has to be dragged out from original papers and reviews in the scientific literature by dedicated amateurs, rather than being made available in readable form by the diabetic associations on either side of the Atlantic. Or have I missed something? — Chris De-* virgin for e-mail reply

Response:

> I found the thread on saturated fat and cholesterol very interesting, > especially the contributions on insulin resistance from Hua Kul and > Quentin Grady. ><snip> > So once again gentlemen, thanks for a most interesting and informative > thread. It’s just a pity that this sort of information has to be > dragged out from original papers and reviews in the scientific > literature by dedicated amateurs, rather than being made available in > readable form by the diabetic associations on either side of the > Atlantic. Or have I missed something?

Thank you for the compliment, Mr. Hogg.  Any contributions I make come from those much more knowledgable and/or experienced than I.  I’m continually amazed at the detailed and deep knowledge of the unassuming Mr. Grady.  As Ben Stein says on his show "Win Ben Stein’s Money" after someone actually does, "I bow to your superior intellect." I too am puzzled by the lack publicity for recent research.  Much of it could be life-extending information.  I’m distressed about the (US) FDA and it’s illicit love affair with big business, as well as some of it’s harmful policies.  For example, glucophage was first put on the market in 1959 in France.  Despite decades of safe use by millions of diabetics it wasn’t put on the market in the US until the 1990’s.  How many millions of people could have avoided early death or disability if we had a more reasonable process for approving non-patentable drugs?  For these reasons and others I have a great desire to understand those things that affect my life, and especialy those truths that fly in the face of "common knowledge" and "popular wisdom."  The internet is a fantastic tool for finding information. With some diligence (and preferably a high speed connection) it’s possible uncover those truths. –Hua Kul

Response:

You are a pretty dab hand at explaining these things, also, Quentin. You have blessed more people than you will ever know. Annette A really good person doesn’t know he is.

– Hide quoted text — Show quoted text -> This post not CC’d by email >A lot of good information is nthis dialog.  As to fructose, lactose, >sorbital and many of the other sugars.  17 years ago, after diagnosis of the >disease, I had heavy sugar cravings.  I ate these other sweets. >The result – Blindness. > Oh … s**t.   <Traditional Kiwi empathetic expression> > Sometimes the consequences of bad advice are so horrible. >The liver and body are not capable of handling >large quantities of these other "sugars".  So it deposits these sticky >substances in the eyes.  When this happens, the eye is not able to focus.  I >was led around by my wife for 8 months until my body flushed out most of >these phony sugars. > I am so glad you are not having to use text to voice software to use > your computer.  It is a horrifying thought. > For those who haven’t heard, the tissue in the eye does not have > insulin receptors to control the flow of glucose into the eye. The > glucose flows in and out very much like the tide.  If blood glucose is > elevated then the blood glucose in the eye is similarly elevated. > Inside the eye the glucose must either be used or converted to > sorbitol.  The conversion to sorbitol is regulated by an enzyme. If I > recall correctly it is aldose reductase.  Whatever.  The essential > tidbit for diabetics is that certain bioflavanoids can inhibit this > enzyme and so protect the eye.  One of the better known ones is > quercetin, a pale yellow bioflavanoid widely distributed in various > foods, eg onions, citrus. > In the movies one often knows something bad is about to happen when > certain actors appear.  Well in this little drama, sorbitol wears the > bad hat. When sorbitol is allowed to form in the eye all manner of bad > things can happen eg cataracts, loss of fine vision in the centre of > the eye. Other useful bioflavanoids for eye protections are lutein and > zeaxanthin present in yellow and orange capsicums, dark green and > yellow green leaf vegetables, free range egg yolks etc.  These protect > the eyes from UV and blue light damage. The short wavelength light > triggers free radical reactions which basically scramble proteins. > As an aside for newbies,  temporary blurriness of eyesight is a common > symptom after treatment commences.  Fluctuation in the osmotic > pressure as the blood glucose levels fall causes the eyeballs to go > temporarily out of focus.  It is largely a nuisance and temporary. > Paradoxically it is a sign of improvement in the handling of blood > glucose. > Best wishes and thank you. > — > Quentin Grady       ^  ^  / > New Zealand,       >#,#< [ >                     / / > "... and the blind dog was leading." > http://homepages.paradise.net.nz/quentin

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This post not CC'd by email >You are a pretty dab hand at explaining these things, also, Quentin.

Thanks Annette,  I've had thirty five years of practice.  When I look at my career it has been one long series of explanations making the complex seem simple. Come December I have to figure out how to make that a marketable item. >You have blessed more people than you will ever know.

Thank you, >Annette >A really good person doesn't know he is.

What if she is a woman?  <grin> -- Quentin Grady       ^  ^  / New Zealand,       >#,#< [                     / /     "... and the blind dog was leading." http://homepages.paradise.net.nz/quentin

Response:

This post not CC'd by email >A lot of good information is nthis dialog.  As to fructose, lactose, >sorbital and many of the other sugars.  17 years ago, after diagnosis of the >disease, I had heavy sugar cravings.  I ate these other sweets. >The result - Blindness.  

Oh ... s**t.   <Traditional Kiwi empathetic expression> Sometimes the consequences of bad advice are so horrible. >The liver and body are not capable of handling >large quantities of these other "sugars".  So it deposits these sticky >substances in the eyes.  When this happens, the eye is not able to focus.  I >was led around by my wife for 8 months until my body flushed out most of >these phony sugars.

I am so glad you are not having to use text to voice software to use your computer.  It is a horrifying thought. For those who haven't heard, the tissue in the eye does not have insulin receptors to control the flow of glucose into the eye.  The glucose flows in and out very much like the tide.  If blood glucose is elevated then the blood glucose in the eye is similarly elevated. Inside the eye the glucose must either be used or converted to sorbitol.  The conversion to sorbitol is regulated by an enzyme. If I recall correctly it is aldose reductase.  Whatever.  The essential tidbit for diabetics is that certain bioflavanoids can inhibit this enzyme and so protect the eye.  One of the better known ones is quercetin, a pale yellow bioflavanoid widely distributed in various foods, eg onions, citrus.   In the movies one often knows something bad is about to happen when certain actors appear.  Well in this little drama, sorbitol wears the bad hat. When sorbitol is allowed to form in the eye all manner of bad things can happen eg cataracts, loss of fine vision in the centre of the eye. Other useful bioflavanoids for eye protections are lutein and zeaxanthin present in yellow and orange capsicums, dark green and yellow green leaf vegetables, free range egg yolks etc.  These protect the eyes from UV and blue light damage. The short wavelength light triggers free radical reactions which basically scramble proteins.   As an aside for newbies,  temporary blurriness of eyesight is a common symptom after treatment commences.  Fluctuation in the osmotic pressure as the blood glucose levels fall causes the eyeballs to go temporarily out of focus.  It is largely a nuisance and temporary. Paradoxically it is a sign of improvement in the handling of blood glucose. Best wishes and thank you. -- Quentin Grady       ^  ^  / New Zealand,       >#,#< [                     / /     "... and the blind dog was leading." http://homepages.paradise.net.nz/quentin

Response:

the following words into the void: - Hide quoted text -- Show quoted text - >(Whether this is true for T1's as well as T2's I >don't know: I had a work colleague who was T1 from a early age and who >was as thin as a bean-pole. Can/do T1's eventually become insulin >resistant because of these insulin spikes? Do T1's suffer the same >long term problems of neuropathy etc. as T2's?). >many type 1s are thin because they don't have an excess of insulin in >the system.  Some people are just naturally thin, some of them are >diabetics too.  One warning we get though when first starting to pump >is not to go crazy eating everything in sight thinking we can simply >cover it with a few button clicks to bolus some extra insulin.  While >on injections I never went above 155 lb in my life.  Shortly after >starting on the pump I went up to 208 lbs.  I've lost some and am now >down to 105 lbs.

sorry typo that should be 205. >Some type 1s will develop resistance to injected insulin.  All of us >are susceptible to neuropathy and all the other complications.

Mack Type 1 since 1975 Minimed 508 Insulin Pump http://www.alt-support-diabetes.org http://sweetblood.org http://www.insulin-pumpers.org http://www.diabetesinterview.com http://www.zerolimit.net (irc server webpage for our chat room) #diabeticnet is the name of our IRC chat on zerolimit.net http://www.zerolimit.net/files/zl-mirc.exe  http://www.irchelp.org/irchelp/misc/webtv.html http://www.xs4all.nl/~ircle/  <--Ircle Mac IRC software http://www.ftc.gov/opa/2001/06/cureall.htm

Response:

(Whether this is true for T1's as well as T2's I >don't know: I had a work colleague who was T1 from a early age and who >was as thin as a bean-pole. Can/do T1's eventually become insulin >resistant because of these insulin spikes? Do T1's suffer the same >long term problems of neuropathy etc. as T2's?).

many type 1s are thin because they don't have an excess of insulin in the system.  Some people are just naturally thin, some of them are diabetics too.  One warning we get though when first starting to pump is not to go crazy eating everything in sight thinking we can simply cover it with a few button clicks to bolus some extra insulin.  While on injections I never went above 155 lb in my life.  Shortly after starting on the pump I went up to 208 lbs.  I've lost some and am now down to 105 lbs. Some type 1s will develop resistance to injected insulin.  All of us are susceptible to neuropathy and all the other complications. Mack Type 1 since 1975 Minimed 508 Insulin Pump http://www.alt-support-diabetes.org http://sweetblood.org http://www.insulin-pumpers.org http://www.diabetesinterview.com http://www.zerolimit.net (irc server webpage for our chat room) #diabeticnet is the name of our IRC chat on zerolimit.net http://www.zerolimit.net/files/zl-mirc.exe  http://www.irchelp.org/irchelp/misc/webtv.html http://www.xs4all.nl/~ircle/  <--Ircle Mac IRC software http://www.ftc.gov/opa/2001/06/cureall.htm

Response:

- Hide quoted text -- Show quoted text - > (Whether this is true for T1's as well as T2's I >don't know: I had a work colleague who was T1 from a early age and who >was as thin as a bean-pole. Can/do T1's eventually become insulin >resistant because of these insulin spikes? Do T1's suffer the same >long term problems of neuropathy etc. as T2's?). > many type 1s are thin because they don't have an excess of insulin in > the system.  Some people are just naturally thin, some of them are > diabetics too.  One warning we get though when first starting to pump > is not to go crazy eating everything in sight thinking we can simply > cover it with a few button clicks to bolus some extra insulin.  While > on injections I never went above 155 lb in my life.  Shortly after > starting on the pump I went up to 208 lbs.  I've lost some and am now > down to 105 lbs.

Please tell me that 105 is a typo... Please?  That would make you much skinnier than I am, and I'm not overweight. Damn body image issues. A. -- From last year: "This is the last class before the exam. If you don't let me go to class, I won't pass the exam. If I don't pass the exam, I won't pass the class. If I don't pass the class, I won't get my degree." "I think you put too much pressure on yourself."

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This post not CC'd by email > In any case, fat is calorie-dense, 9 kcal/gram as opposed to > the 4 kcal/gram of carbo.  One of the easiest ways of gaining >weight is to eat a diet rich in fat.  One of the worst things >for a diabetic to do is to gain weight.  Hence, the dieticians > push the high carb diets.

G'day G'day Al,   Thanks for an excellent exposition on insulin and eating.  As a teacher of too many years experience, I can but admire the clarity with which you have presented the concepts.  IMHO it is easy to forget the lurkers who haven't yet come forward to ask a question.  Providing clear general explanations supports them and refreshes the ideas for all of us.  Thank you.   With respect to the cut and paste from your post, it always amazes me that dieticians don't eventually stumble upon the obvious.  If the key to losing weight is lower calorific density foods eg carbs rather than fat then the logical extension is to go for food with a lot of 0 kcal/gram nutrients.   The most obvious choice is high water content foods.  Put simply make low carb vegetables a staple part of ones diet.   Another nutrient choice with virtually zero calories is fibre. Darn ...  some things are so simple.  Which foods have high fibre in relationship to calories.  Your guessed it.  Low carb vegetables. This of course have nothing to do with becoming a vegetarian.   We all need Vit 12 and diabetics benefit from taurine, an amino acid combination found only in non-vegetable sources. It is rather a plea for people to consider viewing vegetables in preference to grains as sources of minerals, vitamins, carbs etc. Best wishes, And special thanks for an excellent summary. -- Quentin Grady       ^  ^  / New Zealand,       >#,#< [                     / /     "... and the blind dog was leading." http://homepages.paradise.net.nz/quentin

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other useful and provocative information):  >   6.  Putting information out in readable form.  >   When you read the diabetic info pushed at the general  > public, it is frightening.  They simplify, and simplify, and  > in general try to coerce folks into half-way measures  > because they know if they tell them too much and ask too  > much, they will completely lose their audience.  They figure  > a little bit of good is a whole lot better than nothing. I could accept simplification.  When I was in the hospital, however, the booklet I was given on diet had at least ten times as much stuff on fat as on sugar.  And it had NOTHING on any other carbohydrates. Now, this was published by an insulin company.  But I don't think that they were saying to themselves, "We aren't going to mention carbohydrates because the more carbohydrates they eat the more insulin they will buy." I think that somebody asked a nutritionist for advice, and the nutritionist wrote what he knew. -- Frank Palmer

Response:

A lot of good information is nthis dialog.  As to fructose, lactose, sorbital and many of the other sugars.  17 years ago, after diagnosis of the disease, I had heavy sugar cravings.  I ate these other sweets. The result - Blindness.  The liver and body are not capable of handling large quantities of these other "sugars".  So it deposits these sticky substances in the eyes.  When this happens, the eye is not able to focus.  I was led around by my wife for 8 months until my body flushed out most of these phony sugars.

- Hide quoted text -- Show quoted text -> I found the thread on saturated fat and cholesterol very interesting, > especially the contributions on insulin resistance from Hua Kul and > Quentin Grady. > When I was first diagnosed T2, about four months ago, I questioned our > diabetic nurse about the dietary recommendations, especially the bit > about keeping dietary fat to a minimum, as I couldn't see any > relevance to diabetes. (In fact the whole 'pyramid' diet advice seemed > to me to be irrelevant to the problems of diabetes, which were to do > with blood sugar, or so I thought at the time, and I haven't totally > changed that view! The logic of maximising carbohydrate intake whilest > trying to minimise blood glucose concentration, escapes me). > She said that when you eat a meal containing carbohydrate, as well as > getting a surge in blood glucose, you also get a surge in insulin. > With 'normal' people, the insulin spike rapidly declines as the > glucose is dealt with, but with T2 diabetics, because they are insulin > resistant, the blood glucose doesn't fall away as quickly. The > pancreas sees a continuing high level of glucose, so puts out more > insulin and the insulin spike gets bigger. She said it wasn't the > blood glucose directly that caused many of the problems associated > with diabetes, but the high concentrations of insulin put out by the > pancreas to try and deal with it. Eventually, as a consequence of > these high insulin levels, the pancreas just gives up, and T2's have > to start injecting. > With respect to fat in the diet, she said that diabetics had a greater > tendency to gain weight than normal people (and hence a greater > disposition to coronary disease), so had to be more careful about > their fat intake. This weight gain was as a result of the insulin > spikes. By way of supporting evidence, she said that as soon as > diabetics started to inject insulin, they tended to start putting on > weight, the implication being that insulin injections are themselves > insulin spikes when compared with the normally well regulated output > from the pancreas. (Whether this is true for T1's as well as T2's I > don't know: I had a work colleague who was T1 from a early age and who > was as thin as a bean-pole. Can/do T1's eventually become insulin > resistant because of these insulin spikes? Do T1's suffer the same > long term problems of neuropathy etc. as T2's?). > Although I may not have remembered everything the nurse said quite > correctly, it mostly fits in very well with the points made by Messrs > Kul and Grady, which in turn have greatly increased my understanding > of the whole T2 problem. What surprised me a little was that the nurse > told me all this rather as an aside, as if she wouldn't normally > confide such information to most of her patients. It's as if the > medical profession knows a lot more than it's prepared to let out to > the public. Perhaps they think we wouldn't understand..... > With respect to fructose, the UK Diabetic association advise against > using fructose as a substitute for sugar, but give no indication why. > This puzzled me, as fructose has one of the lowest glycemic indices of > any carbohydrate (22 IIRC) so shouldn't be a problem in terms of bg > spikes, although still full of calories of course. But for someone not > needing to lose weight as I don't, it seemed a good alternative > sweetener. I asked the dietitian about it, and she was also surprised > at the Diabetes UK advice, as she said that fructose was part of the > metabolic pathway and that glucose was converted into it in the body. > I may not have that last bit quite right, but thanks to Messrs Kul and > Grady, I now know that replacing sucrose by fructose wouldn't be such > a good idea as it promotes insulin resistance directly. > So once again gentlemen, thanks for a most interesting and informative > thread. It's just a pity that this sort of information has to be > dragged out from original papers and reviews in the scientific > literature by dedicated amateurs, rather than being made available in > readable form by the diabetic associations on either side of the > Atlantic. Or have I missed something? > -- > Chris > De-* virgin for e-mail reply

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- Hide quoted text -- Show quoted text - >I found the thread on saturated fat and cholesterol very interesting, >especially the contributions on insulin resistance from Hua Kul and >Quentin Grady. >When I was first diagnosed T2, about four months ago, I questioned our >diabetic nurse about the dietary recommendations, especially the bit >about keeping dietary fat to a minimum, as I couldn't see any >relevance to diabetes. (In fact the whole 'pyramid' diet advice seemed >to me to be irrelevant to the problems of diabetes, which were to do >with blood sugar, or so I thought at the time, and I haven't totally >changed that view! The logic of maximising carbohydrate intake whilest >trying to minimise blood glucose concentration, escapes me). >She said that when you eat a meal containing carbohydrate, as well as >getting a surge in blood glucose, you also get a surge in insulin. >With 'normal' people, the insulin spike rapidly declines as the >glucose is dealt with, but with T2 diabetics, because they are insulin >resistant, the blood glucose doesn't fall away as quickly. The >pancreas sees a continuing high level of glucose, so puts out more >insulin and the insulin spike gets bigger. She said it wasn't the >blood glucose directly that caused many of the problems associated >with diabetes, but the high concentrations of insulin put out by the >pancreas to try and deal with it. Eventually, as a consequence of >these high insulin levels, the pancreas just gives up, and T2's have >to start injecting. >With respect to fat in the diet, she said that diabetics had a greater >tendency to gain weight than normal people (and hence a greater >disposition to coronary disease), so had to be more careful about >their fat intake. This weight gain was as a result of the insulin >spikes. By way of supporting evidence, she said that as soon as >diabetics started to inject insulin, they tended to start putting on >weight, the implication being that insulin injections are themselves >insulin spikes when compared with the normally well regulated output >from the pancreas. (Whether this is true for T1's as well as T2's I >don't know: I had a work colleague who was T1 from a early age and who >was as thin as a bean-pole. Can/do T1's eventually become insulin >resistant because of these insulin spikes? Do T1's suffer the same >long term problems of neuropathy etc. as T2's?). >Although I may not have remembered everything the nurse said quite >correctly, it mostly fits in very well with the points made by Messrs >Kul and Grady, which in turn have greatly increased my understanding >of the whole T2 problem. What surprised me a little was that the nurse >told me all this rather as an aside, as if she wouldn't normally >confide such information to most of her patients. It's as if the >medical profession knows a lot more than it's prepared to let out to >the public. Perhaps they think we wouldn't understand.....  . .[snip]. . . >So once again gentlemen, thanks for a most interesting and informative >thread. It’s just a pity that this sort of information has to be >dragged out from original papers and reviews in the scientific >literature by dedicated amateurs, rather than being made available in >readable form by the diabetic associations on either side of the >Atlantic. Or have I missed something? >– >Chris

Your nurse had some opinions not shared by all medical folks, or all diabetics.   1.  Gaining weight on insulin:  It’s much more complicated  than that.  Folks who shoot insulin are making guesses as to how much they need.  If they guess wrong, and shoot too much, two things happen:     a.  They go slightly low and have a fierce craving for food         for hours and hours.     b.  They go much too low (hypo) and must eat unnecessary food         immediately or suffer grave consequences.  In most cases, they end up eating too much unnecessary food and  thus gain weight.  This is called "feeding the insulin".     If they guess low, and shoot too little insulin, they go  high.  The smart ones immediately shoot more insulin and knock  down the high.  This buys them relief from ugly diabetic complications due to high blood sugar at the cost of again needing to eat unnecessary food unless they guess exactly right when they knock down the high. It is very difficult to lose weight while on insulin because of  these effects.  Possible, but difficult.  2.  Fat in the diet:  Type 2 diabetics suffer from damage to their arteries due to the effects of high Insulin Resistance.   Fat in the diet traditionally has been thought to make this situation worse.  There are a lot of opinions on proper choice of fats which don’t make the situation worse, but that is another thread.   In any case, fat is calorie-dense, 9 kcal/gram as opposed to  the 4 kcal/gram of carbo.  One of the easiest ways of gaining weight is to eat a diet rich in fat.  One of the worst things for a diabetic to do is to gain weight.  Hence, the dieticians  push the high carb diets.   Note that you can follow the high-carb type pyramid diet if  you exercise enough and take enough meds.  However, many folks  hate the thought of a high-med life style so we have this division between the dieticians and many in the diabetic world. I follow the high-carb diet and favor the high med route (I have  to take insulin, the maximum med, since I am T1).  On Tues, I  exercised quite a bit and my highest bG of the day was 74.  3.  T1 Insulin spikes:  I am a T1.  At lunch, I shot 4 units of  the fastest insulin on the market.  It took more than 3 hours to enter my blood stream.  That is not much of a spike.  Almost  any newly diagnosed T2 had more insulin in his/her blood than I did this afternoon.  4.  Pancreas which "just gives up".  Actually, when I read the  medical sites, I get the impression that the beta cells are sorta poisoned rather than worn out.  The loss of self-generated  insulin capacity is accompanied by the deposition of Amyloid  Polypeptoid bodies in the beta cells (whatever that means).   The loss of self-generated T2 insulin capacity is caused by insulin resistance.  About half of a T2’s capacity is lost by the time they are first diagnosed.  5.  T1’s and complications/insulin resistance  T1’s will become insulin resistant if they gain too much weight  and live too sedentary a lifestyle.  Insulin spikes have nothing to do with it.  Insulin resistance is directly related to fat and exercise levels.  T1’s traditionally have had a bad time with complications because their bG’s are more difficult to control.  We don’t have  an automatic control system anymore, it’s all up to us.  Also,  we haven’t even had good insulins or meters until the last 30 years or so.  However, we now have the good meters and better insulins.  A T1  willing to test and shoot and test and shoot and test, etc  (i.e. turn himself into a pin cushion) can match or beat the control of many T2’s not-on-insulin.   Perhaps we actually beat most of the T2’s.  A T1 who doesn’t  work at it dies quick.  A T2 who doesn’t work at it can linger  in great distress for years and years.   6.  Putting information out in readable form.  The people who find their way to his newsgroup (like you for  instance) represent the odd folks who are willing to do  difficult things to beat this disease.  The bulk of the  diabetic population doesn’t care, doesn’t understand what they  read, and in general have few clues as to what is really going  on.  Actually, a lot of the nurses and many docs are really  obsolete and can get us into trouble.   When you read the diabetic info pushed at the general public,  it is frightening.  They simplify, and simplify, and in general  try to coerce folks into half-way measures because they know if  they tell them too much and ask too much, they will completely  lose their audience.  They figure a little bit of good is a  whole lot better than nothing. Regards  Old Al (T2 since. . .Oops!  Surprise!  He’s an adult-onset T1)   A retired engineer who read all the T2 stuff then had to go back two years later and read the T1 stuff when they changed the  diagnosis.

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This post not CC’d by email >With respect to fructose, the UK Diabetic association advise against >using fructose as a substitute for sugar, but give no indication why. >This puzzled me, as fructose has one of the lowest glycemic indices of >any carbohydrate (22 IIRC) so shouldn’t be a problem in terms of bg >spikes

G’day G’day Chris,   Thank you for a most complimentary post.  Like you I am most impressed by Hua’s posts. Fructose is rather like one of those trilogies that somehow spawns a fourth saga. Fructose does have a low conversion into blood glucose. That is how it delivers its sucker punch.  Since most people here loosely equate blood sugar with blood glucose it comes as a surprise to many to learn that fructose can glycate various proteins we have become quite fond of and make them non-functional.  Even galactose from lactose can glycate.  The bottom line is any simple sugar that gets loose in the blood stream can do a bit of glycation.  Fructose slides beneath the radar screen of blood GLUCOSE testing because it isn’t glucose yet still does damage.   This is why diet surveys often fail to find any improvement in health from eating low GI foods.  Lower GI in the general untamed population equates with increased sucrose intake instead of starch.  Many people fantasize that low GI means eating lots of healthy low GI foods like pearl barley etc.  Feral people aren’t so discriminating as to make that a reality.  <grin> The liver preferentially processes fructose over glucose.  Since the liver cleans up most chemical messes like a big waste disposal recycling factory this would seem like a good thing.  The downside is if the fructose intake is excessive then the control room in the liver takes a direct hit.  It is meant to shut down production of saturated fats when a meal contains fats.  When it is totally fructosed it gets its signals wrong and continues to pour out fat.  With a lot of blokes the fat doesn’t get very far as the rise in the incidence of middle-age male pregnancy would indicate. There is probably more that could be said but I’d have to go and think about it.  There is a post summarizing an article from New Scientist somewhere in the archives.  Someone is probably up to date with which sites currently provide the best user group archives and how to access them. Best wishes, — Quentin Grady       ^  ^  / New Zealand,       >#,#< [                     / /     "… and the blind dog was leading." http://homepages.paradise.net.nz/quentin

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