The Arguments For Low-Carbing as a Type 1 - Crib Sheet

[Dillinger]

Although I have chosen the name of a famous American depression era gangster for this forum I am actually a lawyer in real life. If I need to go into a contentious meeting about a topic I like to have a crib sheet so that I’ll have any pertinent facts to hand that I can bring up whilst arguing.
I want to do the same thing to have as back up for my next consultant/GP/diabetic nurse appointment and would very much like to get communal input on this.

I’d like to start a draft of the main areas and would really appreciate it if people who have the pertinent information could add it to the document; please feel free to copy and add or delete as appropriate and paste each version as a new quote here (we’ll have earlier ‘drafts’ going back in the pages of this topic so we can go back and forth).

This is from the point of view of Type 1 diabetes and is obviously arguing for a low carbohydrate position. If you do not agree with the low carb view, then that’s fine, but please don’t hijack the document with those opinions; there seems to be a lot of space for your comments in the Low-Carb Diet Forum.

The idea is that at the end of this we’ll all have a short dense fact filled couple of pages to rely on when butting our heads against the wall of the current high carb strategy for managing diabetes. Possibly could also do a Type 2 version when this is in shape?

This could be really interesting and useful or turn into a gigantic bun fight, but let’s see eh?

I would initially propose the following topics, and will add some text as we go along, but don’t have the time to do it all now, but these are what I’d suggest as key points:-

1. The Logic of a Low Carbohydrate Diet and Type 1 Diabetes

Diabetes is a chronic endocrine disease resulting in an absolute failure of the body to metabolise glucose. It cannot make sense to treat the condition on the basis of metabolising high levels of glucose.

Non diabetic people have a very limited spectrum of blood sugar ranges from around [ ] to [ ] mmol/l and corresponding HbA1C’s of 4.5 – 6.0.

The ideal position for a diabetic must be to match non diabetic blood glucose profiles provided that in doing so they are not put under risk of serious problems such as severe or regular hypos.

This can best be achieved by eating a very reduced amount of carbohydrate and reducing your insulin levels. This strategy greatly removes the chances of hypos and means non diabetic blood sugar levels can be achieved.

2. The Lack of Evidence of Adverse Medical Effects from a Low Carbohydrate Diet

No study has show that a low carbohydrate diet causes any adverse medical conditions. [ is there any hard evidence or is this an absence of opposing evidence argument?]

3. The Difference Between Ketosis and Ketoacidosis

Ketosis is not the same as Ketoacidosis and is a normal metabolic response to low carbohydrate content in the diet. It occurs at a mild level with insulin present and low or non diabetic insulin levels. On a low carbohydrate diet we aim to achieve ketosis and it has no harmful side effects.

4. The mechanics of Triglyceride Formation and Reduction


5. The Benefits of Having as Little Insulin As Possible


6. A Response To the Purported Implications of the Accord Study

 

[fergus]

What fun!
Maybe the biggest challenge will be getting all of the supporting arguments condensed into only 2 pages? The more concise option might be a sheet of reasons not to low carb as a type 1? I'm joking by the way.
How do you want to do this Dillinger, shall we do it one point at a time?

fergus

 

[hanadr]

As far as I can understand, the ACCORD study set out with the very best of intentions, on its road to hell.
It starts by postulating that "aggressive" glycaemic control might reduce the risk of Cardiovascular events in Type 2 diabetes.
The problem ,as I see it, Is the means by which that control is to be achieved.
They don't seem to have tried a low carb/low dose medication strategy at all. It all went to high doses of very strong drugs. Unsurprisingly, they actually increased the rate of CVD and deaths.
They proved that high doses of antidiabetic medications are dangerous.
They did not prove, as a large portion of the press said,( after the study was halted) that tight control of T2 diabetes is dangerous.
Other studies, which used reduced cabs in their protocols have shown that tight control, when not achieved soley by medication, is advantageous and improves outcomes.
The ADVANCE study, which was much bigger than ACCORD, found no detrimental efects of tight control. They based their medication protocols on Gliclazide.
More recently, there have been smaller studies , Such as Neilson and the Israeli one, which have investigated lowered carb approaches. In these cases better control has led to better outcomes. I think Neilson is the longest study done, even if it's very small. 44 months and only about 32 people.
None of these studies, used control f the intensity of Bernstein's normal advice to patients.
In Bernstein's filing cabinets, there must be the most valuable data of all. At least 20 years work with patients keeping Bgs at non-diabetic or less.

 

[Dillinger]

I think one point at a time, would be good. Doesn't have to be these points exactly (or at all) - this was just my first run at it.

I know that we could lift quite a lot of this from previous threads, i.e. the HbA1C levels for non diabetics and the thread about tryglicerides. Just didn't have time to do that yesterday.

I think the first point I wrote could be condensed as well.

I like the idea of a strict 2 pages of pertinent info...

 

[cugila]

I think if everybody tries to keep it short, sweet and deadly accurate it could end up as a great tool on here.

Ken.

 

[Dillinger]

Ok, I've taken some time out over lunch to update bits of this; please go ahead and add anything you like. I think if we start a bit wordy we can then edit it down to just the facts, ma'am.

1. The Logic of a Low Carbohydrate Diet and Type 1 Diabetes

Type 1 diabetes is a chronic endocrine disease resulting in an absolute failure of the body to metabolise glucose. It cannot make sense to treat the condition on the basis of metabolising high levels of glucose.

Non diabetic people have a very limited spectrum of blood sugar ranges from around [ ] to [ ] mmol/l and corresponding HbA1C’s of 3.5-5.5%.

The ideal position for a diabetic must be to match non diabetic blood glucose profiles provided that in doing so they are not put under risk of serious problems such as severe or regular hypos.

This can best be achieved by eating a very reduced amount of carbohydrate and reducing your insulin levels. This strategy greatly removes the chances of hypos and means non diabetic blood sugar levels can be achieved.

2. The Lack of Evidence of Adverse Medical Effects from a Low Carbohydrate Diet

The Cochrane review (which collated data from 11 randomised trials in 402 patients), confirms a shift in the evidence in recent years, with a number of recent studies suggesting a low-carb diet could offer long-term benefits to diabetics. These benefits include sustained weight loss with no significant effect on glycaemia or lipid levels.

The Cochrane review shows that patients on a diet of foods with a low glycaemic index had an HbA1c level (average blood glucose level) 0.5 per cent lower than controls. There were also significantly fewer episodes of hypoglycaemia in patients on a low-GI diet, with a reduction of 0.8 episodes per patient per month achieved in one trial.


3. The Difference Between Ketosis and Ketoacidosis

Ketosis is not the same as Ketoacidosis and is a normal metabolic response to low carbohydrate content in the diet. It occurs at a mild level with insulin present and low or non diabetic insulin levels. On a low carbohydrate diet we aim to achieve ketosis and it has no harmful side effects.

4. The mechanics of Triglyceride Formation and Reduction

Triglycerides are the key component of LDL (low density lipids) in the blood. The ratio of LDL to HDL (high density lipids) is a key indicator of cardiovascular risk (Source: Circulation (1997;96:2520-2525) Gotto AM Jr. Triglyceride: the forgotten risk factor. Circulation 1998;97(11):1027-8).

Triglycerides in the blood are the direct result of carbohydrates from the diet being metabolised by insulin. These triglycerides do not come directly from dietary fats. They are made in the liver from any excess sugars which have not been used for energy. [ does anyone have a specific study that demonstrates this?]

Elevated glucose levels in the blood have been show in clinical studies to have clear associations with elevated triglyceride levels. (Source : Ostos MA, Recalde D, Baroukh N, Callejo A, Rouis M, Castro G, et al. Fructose intake increases hyperlipidemia and modifies apolipoprotein expression in apolipoprotein AI-CIII-AIV transgenic mice. J Nutr 2002;132(5):918-23).

The easiest way therefore to reduce triglycerides and improve the LDL/HDL ratio is to reduce the carbohydrate content of our diets rather than reduce the fat/protein content.


5. The Benefits of Having as Little Insulin As Possible


6. A Response To the Purported Implications of the Accord Study

The ACCORD study is a large U.S clinical study of adults with established type 2 diabetes who are at especially high risk of cardiovascular disease.

Three treatment approaches were studied: (i) intensive lowering of blood sugar levels compared to a more standard blood sugar treatment;(ii) intensive lowering of blood pressure compared to standard blood pressure treatment; and (iii) treatment of blood lipids by a fibrate plus a statin compared to a statin alone.

Note, that the intensive lowering of blood sugars was not done by a low carbohydrate diet but was done by increased medication. Participants in the intensive group were more likely to be on combinations of drugs than participants in the standard group. For example, 52% of participants in the intensive strategy group were on three oral medications as well as insulin, compared to 16% of those in the standard group.

In its regular review of the available study data, the ACCORD DSMB noticed an unexpected increase in total deaths from any cause among participants who had been randomly assigned to the intensive blood sugar strategy group compared to those assigned to the standard blood sugar strategy group.

On the whole, the death rates in both blood sugar strategy groups were lower than those seen in similar populations. That is, although the death rate was higher in the intensive treatment group than the standard group, it was still lower than death rates reported in other studies of type 2 diabetes.

The ACCORD participant treatment is scheduled to end in 2009, and researchers plan to report the final results in 2010.

(source :U.S Department of Health & Human Services, National Heart Lung and Blood Institute web site - http://www.nhlbi.nih.gov/health/prof/he ... .htm#trial).

To sum up then; it is an ongoing type 2 study, the increased mortality is related not to tighter control but to the manner in which the tighter control was attempted (i.e. high medication), the intensive blood sugar strategy group still had a better mortality rate than non-control type 2 diabetics.

Therefore, this is not applicable to type 1 diabetics on a low carbohydrate diet and certainly should not be used to equate tight diabetic control with increased CVD risk.

 

[fergus]

Ah, I thought there might be the risk of duplication of effort here....

Here's something for the triglyceride section (4) if you care to use it.

Triglycerides are so called because they are composed of three fatty acids attached to a single glycerol molecule.
They are the form in which the body stores its reserves of fat. They are also typically elevated in the bloodstream of people with a high risk of heart disease, a condition known as atherogenic dyslipidemia.
Some triglycerides in our bodies comes from the fat in the diet, but the majority is manufactured in the liver from its component parts. The glycerol part is a by-product glycerol phosphate and the use of glucose in cellular metabolism so that the more glucose in the bloodstream, the greater the production of triglycerides. As one might expect, triglyceride levels rise significantly following the consumption of large quantities of carbohydrates, not dietary fat.

Ref. - Krauss, R. M. 2005. “Dietary and Genetic Probes of Atherogenic Dyslipidemia.” Arteriosclerosis, Thrombosis, and Vascular Biology. Nov.;25(11):2265-72

fergus

 

[Dillinger]

Thanks Fergus - I've added your stuff below

1. The Logic of a Low Carbohydrate Diet and Type 1 Diabetes

Type 1 diabetes is a chronic endocrine disease resulting in an absolute failure of the body to metabolise glucose. It cannot make sense to treat the condition on the basis of metabolising high levels of glucose.

Non diabetic people have a very limited spectrum of blood sugar ranges from around [ ] to [ ] mmol/l and corresponding HbA1C’s of 3.5-5.5%.

The ideal position for a diabetic must be to match non diabetic blood glucose profiles provided that in doing so they are not put under risk of serious problems such as severe or regular hypos.

This can best be achieved by eating a very reduced amount of carbohydrate and reducing your insulin levels. This strategy greatly removes the chances of hypos and means non diabetic blood sugar levels can be achieved.

2. The Lack of Evidence of Adverse Medical Effects from a Low Carbohydrate Diet

The Cochrane review (which collated data from 11 randomised trials in 402 patients), confirms a shift in the evidence in recent years, with a number of recent studies suggesting a low-carb diet could offer long-term benefits to diabetics. These benefits include sustained weight loss with no significant effect on glycaemia or lipid levels.

The Cochrane review shows that patients on a diet of foods with a low glycaemic index had an HbA1c level (average blood glucose level) 0.5 per cent lower than controls. There were also significantly fewer episodes of hypoglycaemia in patients on a low-GI diet, with a reduction of 0.8 episodes per patient per month achieved in one trial.


3. The Difference Between Ketosis and Ketoacidosis

Ketosis is not the same as Ketoacidosis and is a normal metabolic response to low carbohydrate content in the diet. It occurs at a mild level with insulin present and low or non diabetic insulin levels. On a low carbohydrate diet we aim to achieve ketosis and it has no harmful side effects.

4. The mechanics of Triglyceride Formation and Reduction

Triglycerides are so called because they are composed of three fatty acids attached to a single glycerol molecule.

Triglycerides are the key component of LDL (low density lipids) in the blood. The ratio of LDL to HDL (high density lipids) is a key indicator of cardiovascular risk (Source: Circulation (1997;96:2520-2525) Gotto AM Jr. Triglyceride: the forgotten risk factor. Circulation 1998;97(11):1027-8).

Some triglycerides in our bodies come from the fat in our diet, but the majority are manufactured in the liver from fatty acids and glycerol. The glycerol part is a by-product glycerol phosphate and the use of glucose in cellular metabolism so that the more glucose in the bloodstream, the greater the production of triglycerides. (Source: Ref. - Krauss, R. M. 2005. “Dietary and Genetic Probes of Atherogenic Dyslipidemia.” Arteriosclerosis, Thrombosis, and Vascular Biology. Nov.;25(11):2265-72)

As one might expect, triglyceride levels rise significantly following the consumption of large quantities of carbohydrates, not dietary fat and this link between glucose and triglyceride levels has been clearly demonstrated in clinical studies. (Source : Ostos MA, Recalde D, Baroukh N, Callejo A, Rouis M, Castro G, et al. Fructose intake increases hyperlipidemia and modifies apolipoprotein expression in apolipoprotein AI-CIII-AIV transgenic mice. J Nutr 2002;132(5):918-23).

The easiest way therefore to reduce triglycerides and improve the LDL/HDL ratio is to reduce the carbohydrate content of our diets rather than reduce the fat/protein content.


5. The Benefits of Having as Little Insulin As Possible


6. A Response To the Purported Implications of the Accord Study

The ACCORD study is a large U.S clinical study of adults with established type 2 diabetes who are at especially high risk of cardiovascular disease.

Three treatment approaches were studied: (i) intensive lowering of blood sugar levels compared to a more standard blood sugar treatment;(ii) intensive lowering of blood pressure compared to standard blood pressure treatment; and (iii) treatment of blood lipids by a fibrate plus a statin compared to a statin alone.

Note, that the intensive lowering of blood sugars was not done by a low carbohydrate diet but was done by increased medication. Participants in the intensive group were more likely to be on combinations of drugs than participants in the standard group. For example, 52% of participants in the intensive strategy group were on three oral medications as well as insulin, compared to 16% of those in the standard group.

In its regular review of the available study data, the ACCORD DSMB noticed an unexpected increase in total deaths from any cause among participants who had been randomly assigned to the intensive blood sugar strategy group compared to those assigned to the standard blood sugar strategy group.

On the whole, the death rates in both blood sugar strategy groups were lower than those seen in similar populations. That is, although the death rate was higher in the intensive treatment group than the standard group, it was still lower than death rates reported in other studies of type 2 diabetes.

The ACCORD participant treatment is scheduled to end in 2009, and researchers plan to report the final results in 2010.

(source :U.S Department of Health & Human Services, National Heart Lung and Blood Institute web site - http://www.nhlbi.nih.gov/health/prof/he ... .htm#trial).

To sum up then; it is an ongoing type 2 study, the increased mortality is related not to tighter control but to the manner in which the tighter control was attempted (i.e. high medication), the intensive blood sugar strategy group still had a better mortality rate than non-control type 2 diabetics.

Therefore, this is not applicable to type 1 diabetics on a low carbohydrate diet and certainly should not be used to equate tight diabetic control with increased CVD risk.

 

[fergus]

Item 5's looking a bit thin, so here's some meat on the bones:

Insulin is an anabolic hormone which has many metabolic effects besides simply lowering blood sugar. It is the principal regulator of dietary metabolism such that its serum levels largely determine whether fuel is stored or burned. Elevated insulin levels effectively displace fatty acid metabolism in the Krebs cycle and preferentially burn glucose while storing excess as triglycerides. Weight gain results.

Recent evidence supports the role of insulin and IGF-1 as important growth factors, acting through the tyrosine kinase growth factor cascade in enhancing tumor cell proliferation.
Integr Cancer Ther. 2003 Dec;2(4):315-29.

Chronic activation of the sympathetic nervous system may be a pathogenetic mechanism by which hyperinsulinemia induces cardiovascular damage in insulin-resistant NIDDM patients. Effects of insulin on vascular tone and sympathetic nervous system in NIDDM.
C J Tack, P Smits, J J Willemsen, J W Lenders, T Thien and J A Lutterman

Individuals with abnormal glucose and insulin metabolism have a higher incidence of hypertension, and recent interest has focused on the fact that patients with untreated essential hypertension have higher than normal plasma insulin concentrations, are resistant to insulin-stimulated glucose uptake and often have accompanying lipid disorders.
American Journal of Nephrology
Vol. 16, No. 3, 1996

Cheers,

fergus

 

[Dillinger]

Just back from a week away so thanks Fergus your additional stuff has been added, I've added a new section and may tinker with this a bit. Thanks for the input!

1. The Logic of a Low Carbohydrate Diet and Type 1 Diabetes

Type 1 diabetes is a chronic endocrine disease resulting in an absolute failure of the body to metabolise glucose. It cannot make sense to treat the condition on the basis of metabolising high levels of glucose.

Non diabetic people have a very limited spectrum of blood sugar ranges from around [ ] to [ ] mmol/l and corresponding HbA1C’s of 3.5-5.5%.

The ideal position for a diabetic must be to match non diabetic blood glucose profiles provided that in doing so they are not put under risk of serious problems such as severe or regular hypos.

This can best be achieved by eating a very reduced amount of carbohydrate and reducing your insulin levels. This strategy greatly removes the chances of hypos and means non diabetic blood sugar levels can be achieved.

2. The Lack of Evidence of Adverse Medical Effects from a Low Carbohydrate Diet

The Cochrane review (which collated data from 11 randomised trials in 402 patients), confirms a shift in the evidence in recent years, with a number of recent studies suggesting a low-carb diet could offer long-term benefits to diabetics. These benefits include sustained weight loss with no significant effect on glycaemia or lipid levels.

The Cochrane review shows that patients on a diet of foods with a low glycaemic index had an HbA1c level (average blood glucose level) 0.5 per cent lower than controls. There were also significantly fewer episodes of hypoglycaemia in patients on a low-GI diet, with a reduction of 0.8 episodes per patient per month achieved in one trial.


3. The Difference Between Ketosis and Ketoacidosis

Ketosis is not the same as Ketoacidosis and is a normal metabolic response to low carbohydrate content in the diet. It occurs at a mild level with insulin present and low or non diabetic insulin levels. On a low carbohydrate diet we aim to achieve ketosis and it has no harmful side effects.

4. The mechanics of Triglyceride Formation and Reduction

Triglycerides are so called because they are composed of three fatty acids attached to a single glycerol molecule.

Triglycerides are the key component of LDL (low density lipids) in the blood. The ratio of LDL to HDL (high density lipids) is a key indicator of cardiovascular risk (Source: Circulation (1997;96:2520-2525) Gotto AM Jr. Triglyceride: the forgotten risk factor. Circulation 1998;97(11):1027-8).

Some triglycerides in our bodies come from the fat in our diet, but the majority are manufactured in the liver from fatty acids and glycerol. The glycerol part is a by-product glycerol phosphate and the use of glucose in cellular metabolism so that the more glucose in the bloodstream, the greater the production of triglycerides. (Source: Ref. - Krauss, R. M. 2005. “Dietary and Genetic Probes of Atherogenic Dyslipidemia.” Arteriosclerosis, Thrombosis, and Vascular Biology. Nov.;25(11):2265-72)

As one might expect, triglyceride levels rise significantly following the consumption of large quantities of carbohydrates, not dietary fat and this link between glucose and triglyceride levels has been clearly demonstrated in clinical studies. (Source : Ostos MA, Recalde D, Baroukh N, Callejo A, Rouis M, Castro G, et al. Fructose intake increases hyperlipidemia and modifies apolipoprotein expression in apolipoprotein AI-CIII-AIV transgenic mice. J Nutr 2002;132(5):918-23).

The easiest way therefore to reduce triglycerides and improve the LDL/HDL ratio is to reduce the carbohydrate content of our diets rather than reduce the fat/protein content.


5. The Benefits of Having as Little Insulin As Possible

Insulin is an anabolic hormone which has many metabolic effects besides simply lowering blood sugar. It is the principal regulator of dietary metabolism such that its serum levels largely determine whether fuel is stored or burned. Elevated insulin levels effectively displace fatty acid metabolism in the Krebs cycle and preferentially burn glucose while storing excess as triglycerides. Weight gain results.

Recent evidence supports the role of insulin and IGF-1 as important growth factors, acting through the tyrosine kinase growth factor cascade in enhancing tumor cell proliferation. [Source: Integr Cancer Ther. 2003 Dec;2(4):315-29.]

Chronic activation of the sympathetic nervous system may be a pathogenetic mechanism by which hyperinsulinemia induces cardiovascular damage in insulin-resistant NIDDM patients. [Source: Effects of insulin on vascular tone and sympathetic nervous system in NIDDM. C J Tack, P Smits, J J Willemsen, J W Lenders, T Thien and J A Lutterman]

Individuals with abnormal glucose and insulin metabolism have a higher incidence of hypertension, and recent interest has focused on the fact that patients with untreated essential hypertension have higher than normal plasma insulin concentrations, are resistant to insulin-stimulated glucose uptake and often have accompanying lipid disorders.
[Source: American Journal of Nephrology Vol. 16, No. 3, 1996]


6. A Response To the Purported Implications of the Accord Study

The ACCORD study is a large U.S clinical study of adults with established type 2 diabetes who are at especially high risk of cardiovascular disease.

Three treatment approaches were studied: (i) intensive lowering of blood sugar levels compared to a more standard blood sugar treatment;(ii) intensive lowering of blood pressure compared to standard blood pressure treatment; and (iii) treatment of blood lipids by a fibrate plus a statin compared to a statin alone.

Note, that the intensive lowering of blood sugars was not done by a low carbohydrate diet but was done by increased medication. Participants in the intensive group were more likely to be on combinations of drugs than participants in the standard group. For example, 52% of participants in the intensive strategy group were on three oral medications as well as insulin, compared to 16% of those in the standard group.

In its regular review of the available study data, the ACCORD DSMB noticed an unexpected increase in total deaths from any cause among participants who had been randomly assigned to the intensive blood sugar strategy group compared to those assigned to the standard blood sugar strategy group.

On the whole, the death rates in both blood sugar strategy groups were lower than those seen in similar populations. That is, although the death rate was higher in the intensive treatment group than the standard group, it was still lower than death rates reported in other studies of type 2 diabetes.

The ACCORD participant treatment is scheduled to end in 2009, and researchers plan to report the final results in 2010.

[Source :U.S Department of Health & Human Services, National Heart Lung and Blood Institute web site - http://www.nhlbi.nih.gov/health/prof/he ... .htm#trial].

To sum up then; it is an ongoing type 2 study, the increased mortality is related not to tighter control but to the manner in which the tighter control was attempted (i.e. high medication), the intensive blood sugar strategy group still had a better mortality rate than non-control type 2 diabetics.

Therefore, this is not applicable to type 1 diabetics on a low carbohydrate diet and certainly should not be used to equate tight diabetic control with increased CVD risk.

7. Why tight control is essential, and the NICE guidelines are too high

NICE currently suggest that blood glucose control should be optimised towards attaining HbA1c targets for prevention of microvascular disease (less than 7.5%) and, in those at increased risk, for prevention of arterial disease (less than or equal to 6.5%) as appropriate. [ Source: NICE AND DIABETES: A summary of relevant guidelines July 2006 ]

However, for every percentage point drop in HbA1c blood test results (from 8.0 percent to 7.0 percent, for example), the risk of diabetic eye, nerve, and kidney disease is reduced by 40 percent. Lowering blood sugar reduces these microvascular complications in both type 1 and type 2 diabetes.

Intensive blood sugar control in people with type 1 diabetes (average HbA1c of 7.4%) reduces the risk of any CVD event by 42 percent and the risk of heart attack, stroke, or death from CVD by 57 percent. [Source: DCCT/EDIC, reported in December 22, 2005, issue of the New England Journal of Medicine.]

Furthermore a recent study conducted at Cambridge University analysing results from 33,000 Type 2 diabetics found getting HbA1c levels closer to the level of non diabetics could cut the risk of heart attacks by 17%.

[ Source: BBC News website Friday 22nd May 2009]

 

[increasingly cynical]

Hi Dillinger (and others..)

This is a superb idea...

A couple of quesries/suggestions whatever:

1). I'm guessing that what is really going on with the suggestion of medics/diabetes nurses that we stay 'high carb' is that they are 'treating' the insulin rather than the patient's basic problem. If 'Type 1's' (including LADA) are virtually all on insulin (which they are, judging by this forum alone) then the medics' main problem is keeping them alive/unharmed given the well-established risks attached to low blood sugar/ ketoacidosis. The latter two risk in this 'medicated' scenario are most easily avoided by a high carb diet (for obvious reasons). So, no litigation risks to the medic if a high-carb diet is recommended. So, in your crib sheet we should encourage medics to explicitly make the distinction between what they would recommend for an "untreated" diabetic and for someone they have "treated" but who is consequently at risk due to the impact of the medications..


2) It would also help if we could provide proof of what we are asserting here... do any of you keep note of your ketones? Do you have data of what carbs you were taking on as these ketones were expressed? Similarly blood glucose readings; blood pressure etc. ??

 

[Dillinger]

Updated the ketosis bit again. Thanks for the input! Hello IC - I use Ketostix to test for ketones and get either trace or at the highest mild levels of ketones. High levels would be worrying and would imply ketoacidosis and not enough insulin but by carefully managing basal/bosul insulin you can happily maintain a mild level of ketosis. I would prefer to refer to studies or more weighty sources than pure anecdote here though so I haven't added that here. Your other point is very true; I feel the population of diabetics is being treated not the individuals, and if you are treating a population you are aiming at reducing the chronic risks and assuming the worst control from that population. A consultant said to me he thought blood glucose control was irrelevant compared to blood pressure control in diabetes...! That is a prime example of that population vs individual view point.

1. The Logic of a Low Carbohydrate Diet and Type 1 Diabetes

Type 1 diabetes is a chronic endocrine disease resulting in an absolute failure of the body to metabolise glucose. It cannot make sense to treat the condition on the basis of metabolising high levels of glucose.

Non diabetic people have a very limited spectrum of blood sugar ranges from around [ ] to [ ] mmol/l and corresponding HbA1C’s of 3.5-5.5%.

The ideal position for a diabetic must be to match non diabetic blood glucose profiles provided that in doing so they are not put under risk of serious problems such as severe or regular hypos.

This can best be achieved by eating a very reduced amount of carbohydrate and reducing your insulin levels. This strategy greatly removes the chances of hypos and means non diabetic blood sugar levels can be achieved.

2. The Lack of Evidence of Adverse Medical Effects from a Low Carbohydrate Diet

The Cochrane review (which collated data from 11 randomised trials in 402 patients), confirms a shift in the evidence in recent years, with a number of recent studies suggesting a low-carb diet could offer long-term benefits to diabetics. These benefits include sustained weight loss with no significant effect on glycaemia or lipid levels.

The Cochrane review shows that patients on a diet of foods with a low glycaemic index had an HbA1c level (average blood glucose level) 0.5 per cent lower than controls. There were also significantly fewer episodes of hypoglycaemia in patients on a low-GI diet, with a reduction of 0.8 episodes per patient per month achieved in one trial.


3. The Difference Between Ketosis and Ketoacidosis

Ketosis is not the same as Ketoacidosis and is a normal metabolic response to low carbohydrate content in the diet and/or fasting where insulin is present. It occurs at a mild level with insulin present at low or non diabetic insulin levels.

Ketoacidosis is a type of metabolic acidosis which is caused by high concentrations of ketone bodies formed by the breakdown of fatty acids and the deamination of amino acids. The two common ketones produced are acetoacetic acid and β-hydroxybutyrate.

Ketoacidosis is an extreme and uncontrolled form of ketosis. In ketoacidosis, the liver breaks down fat and proteins in response to a perceived need for respiratory substrate (i.e. where no insulin is present to metabolise glucose even though high levels of glucose are present) causing such a severe accumulation of keto acids that the pH of the blood is substantially decreased.

Insulin inhibits ketosis and therefore a diabetic on a low carbohydrate diet (with an appropriate insulin regime) will not develop ketoacidosis but will merely display trace or low levels of ketones produced via normal metabolic ketosis.

On a low carbohydrate diet we aim to achieve low level ketosis and there are no studies to suggest that ketosis has any detrimental effect on liver function or other negative health implications.

4. The mechanics of Triglyceride Formation and Reduction

Triglycerides are so called because they are composed of three fatty acids attached to a single glycerol molecule.

Triglycerides are the key component of LDL (low density lipids) in the blood. The ratio of LDL to HDL (high density lipids) is a key indicator of cardiovascular risk (Source: Circulation (1997;96:2520-2525) Gotto AM Jr. Triglyceride: the forgotten risk factor. Circulation 1998;97(11):1027-8).

Some triglycerides in our bodies come from the fat in our diet, but the majority are manufactured in the liver from fatty acids and glycerol. The glycerol part is a by-product glycerol phosphate and the use of glucose in cellular metabolism so that the more glucose in the bloodstream, the greater the production of triglycerides. (Source: Ref. - Krauss, R. M. 2005. “Dietary and Genetic Probes of Atherogenic Dyslipidemia.” Arteriosclerosis, Thrombosis, and Vascular Biology. Nov.;25(11):2265-72)

As one might expect, triglyceride levels rise significantly following the consumption of large quantities of carbohydrates, not dietary fat and this link between glucose and triglyceride levels has been clearly demonstrated in clinical studies. (Source : Ostos MA, Recalde D, Baroukh N, Callejo A, Rouis M, Castro G, et al. Fructose intake increases hyperlipidemia and modifies apolipoprotein expression in apolipoprotein AI-CIII-AIV transgenic mice. J Nutr 2002;132(5):918-23).

The easiest way therefore to reduce triglycerides and improve the LDL/HDL ratio is to reduce the carbohydrate content of our diets rather than reduce the fat/protein content.


5. The Benefits of Having as Little Insulin As Possible

Insulin is an anabolic hormone which has many metabolic effects besides simply lowering blood sugar. It is the principal regulator of dietary metabolism such that its serum levels largely determine whether fuel is stored or burned. Elevated insulin levels effectively displace fatty acid metabolism in the Krebs cycle and preferentially burn glucose while storing excess as triglycerides. Weight gain results.

Recent evidence supports the role of insulin and IGF-1 as important growth factors, acting through the tyrosine kinase growth factor cascade in enhancing tumor cell proliferation. [Source: Integr Cancer Ther. 2003 Dec;2(4):315-29.]

Chronic activation of the sympathetic nervous system may be a pathogenetic mechanism by which hyperinsulinemia induces cardiovascular damage in insulin-resistant NIDDM patients. [Source: Effects of insulin on vascular tone and sympathetic nervous system in NIDDM. C J Tack, P Smits, J J Willemsen, J W Lenders, T Thien and J A Lutterman]

Individuals with abnormal glucose and insulin metabolism have a higher incidence of hypertension, and recent interest has focused on the fact that patients with untreated essential hypertension have higher than normal plasma insulin concentrations, are resistant to insulin-stimulated glucose uptake and often have accompanying lipid disorders.
[Source: American Journal of Nephrology Vol. 16, No. 3, 1996]


6. A Response To the Purported Implications of the Accord Study

The ACCORD study is a large U.S clinical study of adults with established type 2 diabetes who are at especially high risk of cardiovascular disease.

Three treatment approaches were studied: (i) intensive lowering of blood sugar levels compared to a more standard blood sugar treatment;(ii) intensive lowering of blood pressure compared to standard blood pressure treatment; and (iii) treatment of blood lipids by a fibrate plus a statin compared to a statin alone.

Note, that the intensive lowering of blood sugars was not done by a low carbohydrate diet but was done by increased medication. Participants in the intensive group were more likely to be on combinations of drugs than participants in the standard group. For example, 52% of participants in the intensive strategy group were on three oral medications as well as insulin, compared to 16% of those in the standard group.

In its regular review of the available study data, the ACCORD DSMB noticed an unexpected increase in total deaths from any cause among participants who had been randomly assigned to the intensive blood sugar strategy group compared to those assigned to the standard blood sugar strategy group.

On the whole, the death rates in both blood sugar strategy groups were lower than those seen in similar populations. That is, although the death rate was higher in the intensive treatment group than the standard group, it was still lower than death rates reported in other studies of type 2 diabetes.

The ACCORD participant treatment is scheduled to end in 2009, and researchers plan to report the final results in 2010.

[Source :U.S Department of Health & Human Services, National Heart Lung and Blood Institute web site - http://www.nhlbi.nih.gov/health/prof/he ... .htm#trial].

To sum up then; it is an ongoing type 2 study, the increased mortality is related not to tighter control but to the manner in which the tighter control was attempted (i.e. high medication), the intensive blood sugar strategy group still had a better mortality rate than non-control type 2 diabetics.

Therefore, this is not applicable to type 1 diabetics on a low carbohydrate diet and certainly should not be used to equate tight diabetic control with increased CVD risk.

7. Why tight control is essential, and the NICE guidelines are too high

NICE currently suggest that blood glucose control should be optimised towards attaining HbA1c targets for prevention of microvascular disease of less than 7.5% and in those at increased risk of arterial disease of levels less than or equal to 6.5% as appropriate [ Source: NICE AND DIABETES: A summary of relevant guidelines July 2006 ]

However, for every percentage point drop in HbA1c blood test results (from 8.0 percent to 7.0 percent, for example), the risk of diabetic eye, nerve, and kidney disease is reduced by 40 percent. Lowering blood sugar reduces these microvascular complications in both type 1 and type 2 diabetes.

Intensive blood sugar control in people with type 1 diabetes (average HbA1c of 7.4%) reduces the risk of any CVD event by 42 percent and the risk of heart attack, stroke, or death from CVD by 57 percent. [Source: DCCT/EDIC, reported in December 22, 2005, issue of the New England Journal of Medicine.]

Furthermore a recent study conducted at Cambridge University analysing results from 33,000 Type 2 diabetics found getting HbA1c levels closer to the level of non diabetics could cut the risk of heart attacks by 17%.

[ Source: BBC News website Friday 22nd May 2009]

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