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THE CASE FOR LOW CARBS.
1. The Logic of a Low Carbohydrate Diet and Diabetes
All forms of diabetes are linked by the inability of the body to process carbohydrate. Type 2 diabetics cover a broad spectrum of impairment from almost normal to almost complete impairment, whilst Type 1 diabetics have no ability to metabolise carbohydrate at all and are dependent upon insulin therapy to survive.
It cannot make sense to treat the condition without addressing the key factor; carbohydrate. Yet that is just what is suggested in the traditional approach to managing this condition. If you are Type 2 you will be told to eat a ‘healthy diet’ which means a low-fat diet. If you are Type 1 you will be told to ‘eat normally’ (the course for Type 1 diabetics is ‘Dose Adjustment For Normal Eating’). What you will not be told to do is to abandon all starchy foods (pasta, rice, flour, potato, bread, fruit and the like). The problem is that is exactly what you need to do if you want to control your blood sugar levels as a diabetic.
All carbohydrate from all sources will eventually be converted into glucose in our bodies; the issue then becomes how do we best manage those blood glucose levels?
Non diabetic people have a very tight control on their blood sugar levels with corresponding HbA1Css (which gives an idea of average blood sugars levels over 3 months) of roughly between 4.6% and 5.4% or between 26.8 mmol/mol and 35.5 mmol/mol in the new units.
We suggest that the ideal position for a diabetic is to match non diabetic blood glucose profiles; if it weren’t important a non-diabetic person would not have such a narrow range of blood sugars. Yet the body is very sensitive to and very aggressive in controlling blood sugar levels in a non-diabetic person.
The best way of achieving non-diabetic levels is by eating a much reduced amount of carbohydrate and thereby reducing your insulin levels (whether produced naturally or injected). This will stop the great blood sugar swings that typically occur if you eat a starchy diet. Additionally, for Type 1’s this strategy greatly removes the chances of hypos and for Type 2’s it drastically cuts out blood glucose spikes which means it is possible to get much closer to non-diabetic levels than can be achieved by eating ‘normally’ and taking drugs to manage the levels.
That does not mean that everyone must stop eating all carbohydrate; it means you need to find out how much carbohydrate you can tolerate and not eat more than that.
2. 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 which means that its levels in our blood largely determine whether fuel is stored or burned. High levels of insulin will mean that fat is not only stored but is specifically not metabolised. Weight gain results. Low levels of insulin allow the body to use fat as fuel and thereby weight loss becomes much more achievable.
As well as the weight point there is some evidence that suggests that elevated insulin levels and elevated IGF-1 (insulin like growth factor) enhance cancerous cell growth. This means that whilst elevated insulin levels are not shown to increase the risk of cancer they will enable cancers to proliferate.
[Source: Integr Cancer Ther. 2003 Dec;2(4):315-29.]
Another recent study has suggested that one of the effects of high insulin levels is the ‘chronic activation’ of the sympathetic nervous system and that this is what induces cardiovascular damage in insulin resistant Type 2 diabetics.
[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]
To add to the above 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 insulin concentrations in their blood, are resistant to insulin-stimulated glucose uptake and often have accompanying lipid disorders.
[Source: American Journal of Nephrology Vol. 16, No. 3, 1996]
2. The Lack of Evidence of Adverse Medical Effects from a Low Carbohydrate Diet
If you are eating a low carbohydrate diet by extension you must be eating more of the other macro-nutrients; fat and protein. This had been considered a problem with traditional nutritionists because of the fear of fat that has informed dietary advice since the 1980’s. However, once you start to look at the studies there is, in reality, very little evidence that fat is a killer (artificial trans-fats being an exception to that general statement).
The Cochrane Collaboration is a body that essentially provides studies of studies; they perform meta-analysis on study results and publish their findings; http://www.cochrane.org/about-us
A Cochrane review is considered the gold standard in study analysis. The Cochrane review on “Reduced or modified dietary fat for preventing cardiovascular disease” found that:
“No significant effect of any dietary fat intervention (and dietary fat subgroups of modified fat diet vs usual, reduced fat vs usual, reduced and modified vs usual) compared to usual or control diet on total mortality (RR 0.98; n=71790, 4292 deaths).”
And;
“No significant effect of any dietary fat intervention (and no effect with the same subgrouping by dietary fat as above) compared to usual or control diet on cardiovascular mortality (RR 0.94; n=65978, 1407 deaths).”
That means that there is no evidence that eating fats or not eating fats causes you to die young or die from a heart attack. In short the fat/heart disease mantra we are all so used to is not supported by the evidence.
In addition to that there are numerous studies showing that compared to a higher carbohydrate diet a high fat diet has positive benefits; the following link provides details on numerous such studies:
http://authoritynutrition.com/23-studies-on-low-carb-and-low-fat-diets/
The following study shows that there is no evidence of a risk to heart health by removing carbohydrate from the diet (i.e. there is no evidence that carbohydrate is ‘heart healthy’);
http://www.sciencedaily.com/releases/2006/11/061109095850.htm
Lastly, here is a compilation of studies that challenge the traditional high carb low fat diet recommended by so many nutritionists and dieticians;
http://authoritynutrition.com/how-to-win-an-argument-with-a-nutritionist/
3. The Difference Between Ketosis and Ketoacidosis
If you follow a low carbohydrate diet you can go into ketosis with ketones being removed from your body in urine. Often this will cause great alarm amongst other diabetics and health care providers (who really should know better).
Type 1 diabetics can if they fail to take insulin enter into a life threatening condition known as diabetic ketoacidosis and no-one is suggesting that that is something to be aspired to or not to be immediately and urgently treated.
Ketoacidosis is an extreme and uncontrolled form of ketosis. In ketoacidosis, the liver breaks down fat and proteins in response to a perceived lack of available glucose in the blood (i.e. where no insulin is present to metabolise glucose even though high levels of glucose are present – so the body behaves as if you are starving as it cannot access the glucose) causing such a severe accumulation of keto acids that the pH of the blood is substantially decreased; thereby becoming more acidic.
Ketosis, though, 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.
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.
This is one of the wonderful things about the human body; we are dual fuel. We can run on fats and protein very easily and can swap to running on carbohydrate/glucose as well.
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 our health whatsoever. Low-carbing and ketosis are linked but it is not essential that you go into ketosis whilst low-carbing, however if you do then you can be sure that your blood sugar levels are running as close to non-diabetic levels as possible.
Whilst there are no problems with being in ketosis there are some very interesting studies suggesting that ketosis is beneficial for a wide range of conditions form certain types of cancer (breast cancer in particular) to epilepsy and even Alzheimer’s disease and other forms of dementia.
4. Is Fat The Real Enemy?
Of the blood lipids that are tested a lot of weight is given to our cholesterol levels yet we know that there is not a clear link between cholesterol levels and death from heart disease and/or all-cause mortality at all.
This is a very short explanation of that by Dr Malcolm Kendrick: https://www.youtube.com/watch?v=i8SSCNaaDcE
However, one element of the lipid results we get could well be more significant than the general cholesterol level and that is our triglyceride scores.
Triglycerides are so called because they are composed of three fatty acids attached to a single glycerol molecule and they are the key component of LDL (low density lipids) in the blood. The ratio of LDL to HDL (high density lipids) is held to be a key indicator of cardiovascular risk (rather than your total cholesterol level which is in reality pretty meaningless).
(Source: Circulation (1997;96:2520-2525) Gotto AM Jr. Triglyceride: the forgotten risk factor. Circulation 1998;97(11):10278).
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 comes from 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 (which are all broken down into glucose), and not in response to dietary fat. 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.
6. A Response To the Purported Implications of the ACCORD Study
This point seems to come up less than it did, but the ACCORD study was often cited as evidence that reducing blood sugar levels posed some sort of risk in and of itself. This is something that needs to be clarified and it may still be useful to have the background on this if your HCP’s come up with this old and flawed point of view; the key point to take away is how the blood sugars were reduced rather than the reduction itself.
The ACCORD study was 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 people carrying out the ACCORD study 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 and decided to stop the intensive blood sugar strategy group element of the trial.
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.
One of the conclusions from this was that intensive lowering of blood sugar levels raised the risk of coronary disease and caused the higher death rate. What wasn’t taken into account was that one of the drugs used to reduce blood sugar levels was rosiglitazone (trade name Avandia). Despite rosiglitazone's effectiveness at decreasing blood sugar in type 2 diabetics, studies showed a clear association with increased risk of heart attacks and death; the very thing that the ACCORD study showed.
What many health care professionals took away from the ACCORD study was not ‘don’t take Avandia’ but ‘don’t lower your blood sugar levels’. A bizarre and incredibly damaging view by any stretch of the imagination.
Due to the ACCORD study and the general high failure rate of Type 2 diabetics to normalise their blood sugar levels with the tools and information given them under current treatment protocols meant that the advice was to avoid ‘dangerously low HbA1cs’ by which they mean less than 6.4% even though exactly the opposite is shown by the DCCT trial and EDIC trials for Type 1 diabetics (see below).
Realistically then what do you think really caused the higher death rates in the ACCORD study? Normalised blood sugar levels or intensive use of multiple medications including the known risk of Avandia?
[summary of the ACCORD trial http://diabetes.diabetesjournals.org/content/57/5/1163.full ]
If anything this demonstrates that increased medication is the problem rather than tighter control and how do you get tighter control without increased medication? Low-carbing, of course.
7. Why tight control is essential, and the NICE guidelines are too high
NICE currently suggest that diabetics should aim for HbA1c targets of less than 7.5% for the prevention of microvascular disease and less than or equal to 6.5% for those at increased risk of arterial disease of levels.
[ 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 (by which they meant the group achieved an 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 compared to the control group of diabetics with an HbA1c of about 9.0%
[Source: DCCT/EDIC, reported in December 22, 2005, issue of the New England Journal of Medicine.]
It is well worth reading this summary of the DCCT and its follow up observational study the EDIC;
http://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/GetPdf.cgi?id=phd000390
Whilst this was a study on Type 1 diabetics by extension the benefits of reducing blood sugar levels must extend to Type 2 diabetics; the disease mechanism may be different between Type 1 and Type 2 but the complications arise from the same thing; elevated blood glucose levels.
What is particularly striking is that the results achieved on ‘intensive treatment’ are pretty laughable compared to what is readily achievable on a low-carb diet.
The intent of the ‘intensive treatment (IT)’ limb of the study was to achieve blood glucose levels of 70-120 mg/dL in the morning and before meals, <180 mg/dL after meals, and an HbA1c in the non-diabetic range which they set at an HbA1c of less than 6.05% (by way of comparison my current blood tests results flag an HbA1c of above 5.9% as diabetic).
During the study they found that it was not feasible to achieve those glycaemic targets consistently in the majority of the subjects assigned to the IT group (fewer than 5% maintained an average HbA1c below 6.05%),but there was a substantial difference in glycaemic control between the IT and the conventional treatment (CT) groups.
The CT group maintained an average HbA1c of about 9.0% (similar to their values when they joined the study) throughout the 3-9 (mean 6.5) years of follow-up. Those in the IT group lowered their HbA1c to about 7.0% and maintained this for the duration of the study.
So, that is where the current recommendations come from for targets, and why most Type 1 diabetics are put on multiple daily injections (i.e. ‘intense control’) but we know we can do much better.
I can see no logical reason to suppose that the marked improvement across all outcomes cannot be improved upon by further reducing the HbA1c to real non-diabetic ranges.
These are the benefits of ‘intense control’ presented by the DCCT:
• Intensive therapy aimed at achieving glycaemic levels as close to the non-diabetic range as safely possible reduces the development and progression of all diabetes-specific complications by up to as much as 76%.
• Intensive therapy reduces measures of atherosclerosis over time, and probably reduces CVD events as well.
• Intensive intervention is most effective when implemented early in the course of diabetes; if intensive intervention is delayed, the momentum of complications is harder to slow, as shown by the results of the secondary intervention group.
We know that looking at blood sugar levels from the other direction that high blood sugars damage almost everything in our bodies. The following link (from the excellent Blood Sugar 101 site) provides a large number of studies attesting to those risks:
http://www.phlaunt.com/diabetes/14045678.php
Lastly there is a clear link between elevated HbA1c and cardiovascular disease and all cause mortality:
“Persons with HbA1c concentrations less than 5% had the lowest rates of cardiovascular disease and mortality. An increase in HbA1c of 1 percentage point was associated with a relative risk for death from any cause of 1.24” which means a 24% increase.
[ Source: Association of Haemoglobin A1c with Cardiovascular Disease and Mortality in Adults: The European Prospective Investigation into Cancer in Norfolk. Kay-Tee Khaw, MBBChir FRCP; Nicholas Wareham, MBBS, FRCP; Sheila Bingham, PhD; Robert Luben, BSc; Ailsa Welch, BSc; and Nicholas Day, PhD. Annals of Internal Medicine, 9/21/2004, Vol 141, no 6, 413-420 ]
Conclusion
So, we know we need to normalise our blood sugar levels, we know we need to do that with as little drug intervention as possible and we know that the major disrupting factor for blood sugar levels is the carbohydrate that we eat. So what to do?
Low carb!
1. The Logic of a Low Carbohydrate Diet and Diabetes
All forms of diabetes are linked by the inability of the body to process carbohydrate. Type 2 diabetics cover a broad spectrum of impairment from almost normal to almost complete impairment, whilst Type 1 diabetics have no ability to metabolise carbohydrate at all and are dependent upon insulin therapy to survive.
It cannot make sense to treat the condition without addressing the key factor; carbohydrate. Yet that is just what is suggested in the traditional approach to managing this condition. If you are Type 2 you will be told to eat a ‘healthy diet’ which means a low-fat diet. If you are Type 1 you will be told to ‘eat normally’ (the course for Type 1 diabetics is ‘Dose Adjustment For Normal Eating’). What you will not be told to do is to abandon all starchy foods (pasta, rice, flour, potato, bread, fruit and the like). The problem is that is exactly what you need to do if you want to control your blood sugar levels as a diabetic.
All carbohydrate from all sources will eventually be converted into glucose in our bodies; the issue then becomes how do we best manage those blood glucose levels?
Non diabetic people have a very tight control on their blood sugar levels with corresponding HbA1Css (which gives an idea of average blood sugars levels over 3 months) of roughly between 4.6% and 5.4% or between 26.8 mmol/mol and 35.5 mmol/mol in the new units.
We suggest that the ideal position for a diabetic is to match non diabetic blood glucose profiles; if it weren’t important a non-diabetic person would not have such a narrow range of blood sugars. Yet the body is very sensitive to and very aggressive in controlling blood sugar levels in a non-diabetic person.
The best way of achieving non-diabetic levels is by eating a much reduced amount of carbohydrate and thereby reducing your insulin levels (whether produced naturally or injected). This will stop the great blood sugar swings that typically occur if you eat a starchy diet. Additionally, for Type 1’s this strategy greatly removes the chances of hypos and for Type 2’s it drastically cuts out blood glucose spikes which means it is possible to get much closer to non-diabetic levels than can be achieved by eating ‘normally’ and taking drugs to manage the levels.
That does not mean that everyone must stop eating all carbohydrate; it means you need to find out how much carbohydrate you can tolerate and not eat more than that.
2. 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 which means that its levels in our blood largely determine whether fuel is stored or burned. High levels of insulin will mean that fat is not only stored but is specifically not metabolised. Weight gain results. Low levels of insulin allow the body to use fat as fuel and thereby weight loss becomes much more achievable.
As well as the weight point there is some evidence that suggests that elevated insulin levels and elevated IGF-1 (insulin like growth factor) enhance cancerous cell growth. This means that whilst elevated insulin levels are not shown to increase the risk of cancer they will enable cancers to proliferate.
[Source: Integr Cancer Ther. 2003 Dec;2(4):315-29.]
Another recent study has suggested that one of the effects of high insulin levels is the ‘chronic activation’ of the sympathetic nervous system and that this is what induces cardiovascular damage in insulin resistant Type 2 diabetics.
[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]
To add to the above 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 insulin concentrations in their blood, are resistant to insulin-stimulated glucose uptake and often have accompanying lipid disorders.
[Source: American Journal of Nephrology Vol. 16, No. 3, 1996]
2. The Lack of Evidence of Adverse Medical Effects from a Low Carbohydrate Diet
If you are eating a low carbohydrate diet by extension you must be eating more of the other macro-nutrients; fat and protein. This had been considered a problem with traditional nutritionists because of the fear of fat that has informed dietary advice since the 1980’s. However, once you start to look at the studies there is, in reality, very little evidence that fat is a killer (artificial trans-fats being an exception to that general statement).
The Cochrane Collaboration is a body that essentially provides studies of studies; they perform meta-analysis on study results and publish their findings; http://www.cochrane.org/about-us
A Cochrane review is considered the gold standard in study analysis. The Cochrane review on “Reduced or modified dietary fat for preventing cardiovascular disease” found that:
“No significant effect of any dietary fat intervention (and dietary fat subgroups of modified fat diet vs usual, reduced fat vs usual, reduced and modified vs usual) compared to usual or control diet on total mortality (RR 0.98; n=71790, 4292 deaths).”
And;
“No significant effect of any dietary fat intervention (and no effect with the same subgrouping by dietary fat as above) compared to usual or control diet on cardiovascular mortality (RR 0.94; n=65978, 1407 deaths).”
That means that there is no evidence that eating fats or not eating fats causes you to die young or die from a heart attack. In short the fat/heart disease mantra we are all so used to is not supported by the evidence.
In addition to that there are numerous studies showing that compared to a higher carbohydrate diet a high fat diet has positive benefits; the following link provides details on numerous such studies:
http://authoritynutrition.com/23-studies-on-low-carb-and-low-fat-diets/
The following study shows that there is no evidence of a risk to heart health by removing carbohydrate from the diet (i.e. there is no evidence that carbohydrate is ‘heart healthy’);
http://www.sciencedaily.com/releases/2006/11/061109095850.htm
Lastly, here is a compilation of studies that challenge the traditional high carb low fat diet recommended by so many nutritionists and dieticians;
http://authoritynutrition.com/how-to-win-an-argument-with-a-nutritionist/
3. The Difference Between Ketosis and Ketoacidosis
If you follow a low carbohydrate diet you can go into ketosis with ketones being removed from your body in urine. Often this will cause great alarm amongst other diabetics and health care providers (who really should know better).
Type 1 diabetics can if they fail to take insulin enter into a life threatening condition known as diabetic ketoacidosis and no-one is suggesting that that is something to be aspired to or not to be immediately and urgently treated.
Ketoacidosis is an extreme and uncontrolled form of ketosis. In ketoacidosis, the liver breaks down fat and proteins in response to a perceived lack of available glucose in the blood (i.e. where no insulin is present to metabolise glucose even though high levels of glucose are present – so the body behaves as if you are starving as it cannot access the glucose) causing such a severe accumulation of keto acids that the pH of the blood is substantially decreased; thereby becoming more acidic.
Ketosis, though, 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.
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.
This is one of the wonderful things about the human body; we are dual fuel. We can run on fats and protein very easily and can swap to running on carbohydrate/glucose as well.
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 our health whatsoever. Low-carbing and ketosis are linked but it is not essential that you go into ketosis whilst low-carbing, however if you do then you can be sure that your blood sugar levels are running as close to non-diabetic levels as possible.
Whilst there are no problems with being in ketosis there are some very interesting studies suggesting that ketosis is beneficial for a wide range of conditions form certain types of cancer (breast cancer in particular) to epilepsy and even Alzheimer’s disease and other forms of dementia.
4. Is Fat The Real Enemy?
Of the blood lipids that are tested a lot of weight is given to our cholesterol levels yet we know that there is not a clear link between cholesterol levels and death from heart disease and/or all-cause mortality at all.
This is a very short explanation of that by Dr Malcolm Kendrick: https://www.youtube.com/watch?v=i8SSCNaaDcE
However, one element of the lipid results we get could well be more significant than the general cholesterol level and that is our triglyceride scores.
Triglycerides are so called because they are composed of three fatty acids attached to a single glycerol molecule and they are the key component of LDL (low density lipids) in the blood. The ratio of LDL to HDL (high density lipids) is held to be a key indicator of cardiovascular risk (rather than your total cholesterol level which is in reality pretty meaningless).
(Source: Circulation (1997;96:2520-2525) Gotto AM Jr. Triglyceride: the forgotten risk factor. Circulation 1998;97(11):10278).
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 comes from 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 (which are all broken down into glucose), and not in response to dietary fat. 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.
6. A Response To the Purported Implications of the ACCORD Study
This point seems to come up less than it did, but the ACCORD study was often cited as evidence that reducing blood sugar levels posed some sort of risk in and of itself. This is something that needs to be clarified and it may still be useful to have the background on this if your HCP’s come up with this old and flawed point of view; the key point to take away is how the blood sugars were reduced rather than the reduction itself.
The ACCORD study was 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 people carrying out the ACCORD study 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 and decided to stop the intensive blood sugar strategy group element of the trial.
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.
One of the conclusions from this was that intensive lowering of blood sugar levels raised the risk of coronary disease and caused the higher death rate. What wasn’t taken into account was that one of the drugs used to reduce blood sugar levels was rosiglitazone (trade name Avandia). Despite rosiglitazone's effectiveness at decreasing blood sugar in type 2 diabetics, studies showed a clear association with increased risk of heart attacks and death; the very thing that the ACCORD study showed.
What many health care professionals took away from the ACCORD study was not ‘don’t take Avandia’ but ‘don’t lower your blood sugar levels’. A bizarre and incredibly damaging view by any stretch of the imagination.
Due to the ACCORD study and the general high failure rate of Type 2 diabetics to normalise their blood sugar levels with the tools and information given them under current treatment protocols meant that the advice was to avoid ‘dangerously low HbA1cs’ by which they mean less than 6.4% even though exactly the opposite is shown by the DCCT trial and EDIC trials for Type 1 diabetics (see below).
Realistically then what do you think really caused the higher death rates in the ACCORD study? Normalised blood sugar levels or intensive use of multiple medications including the known risk of Avandia?
[summary of the ACCORD trial http://diabetes.diabetesjournals.org/content/57/5/1163.full ]
If anything this demonstrates that increased medication is the problem rather than tighter control and how do you get tighter control without increased medication? Low-carbing, of course.
7. Why tight control is essential, and the NICE guidelines are too high
NICE currently suggest that diabetics should aim for HbA1c targets of less than 7.5% for the prevention of microvascular disease and less than or equal to 6.5% for those at increased risk of arterial disease of levels.
[ 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 (by which they meant the group achieved an 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 compared to the control group of diabetics with an HbA1c of about 9.0%
[Source: DCCT/EDIC, reported in December 22, 2005, issue of the New England Journal of Medicine.]
It is well worth reading this summary of the DCCT and its follow up observational study the EDIC;
http://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/GetPdf.cgi?id=phd000390
Whilst this was a study on Type 1 diabetics by extension the benefits of reducing blood sugar levels must extend to Type 2 diabetics; the disease mechanism may be different between Type 1 and Type 2 but the complications arise from the same thing; elevated blood glucose levels.
What is particularly striking is that the results achieved on ‘intensive treatment’ are pretty laughable compared to what is readily achievable on a low-carb diet.
The intent of the ‘intensive treatment (IT)’ limb of the study was to achieve blood glucose levels of 70-120 mg/dL in the morning and before meals, <180 mg/dL after meals, and an HbA1c in the non-diabetic range which they set at an HbA1c of less than 6.05% (by way of comparison my current blood tests results flag an HbA1c of above 5.9% as diabetic).
During the study they found that it was not feasible to achieve those glycaemic targets consistently in the majority of the subjects assigned to the IT group (fewer than 5% maintained an average HbA1c below 6.05%),but there was a substantial difference in glycaemic control between the IT and the conventional treatment (CT) groups.
The CT group maintained an average HbA1c of about 9.0% (similar to their values when they joined the study) throughout the 3-9 (mean 6.5) years of follow-up. Those in the IT group lowered their HbA1c to about 7.0% and maintained this for the duration of the study.
So, that is where the current recommendations come from for targets, and why most Type 1 diabetics are put on multiple daily injections (i.e. ‘intense control’) but we know we can do much better.
I can see no logical reason to suppose that the marked improvement across all outcomes cannot be improved upon by further reducing the HbA1c to real non-diabetic ranges.
These are the benefits of ‘intense control’ presented by the DCCT:
• Intensive therapy aimed at achieving glycaemic levels as close to the non-diabetic range as safely possible reduces the development and progression of all diabetes-specific complications by up to as much as 76%.
• Intensive therapy reduces measures of atherosclerosis over time, and probably reduces CVD events as well.
• Intensive intervention is most effective when implemented early in the course of diabetes; if intensive intervention is delayed, the momentum of complications is harder to slow, as shown by the results of the secondary intervention group.
We know that looking at blood sugar levels from the other direction that high blood sugars damage almost everything in our bodies. The following link (from the excellent Blood Sugar 101 site) provides a large number of studies attesting to those risks:
http://www.phlaunt.com/diabetes/14045678.php
Lastly there is a clear link between elevated HbA1c and cardiovascular disease and all cause mortality:
“Persons with HbA1c concentrations less than 5% had the lowest rates of cardiovascular disease and mortality. An increase in HbA1c of 1 percentage point was associated with a relative risk for death from any cause of 1.24” which means a 24% increase.
[ Source: Association of Haemoglobin A1c with Cardiovascular Disease and Mortality in Adults: The European Prospective Investigation into Cancer in Norfolk. Kay-Tee Khaw, MBBChir FRCP; Nicholas Wareham, MBBS, FRCP; Sheila Bingham, PhD; Robert Luben, BSc; Ailsa Welch, BSc; and Nicholas Day, PhD. Annals of Internal Medicine, 9/21/2004, Vol 141, no 6, 413-420 ]
Conclusion
So, we know we need to normalise our blood sugar levels, we know we need to do that with as little drug intervention as possible and we know that the major disrupting factor for blood sugar levels is the carbohydrate that we eat. So what to do?
Low carb!
Last edited by Paul on Fri Oct 03 2014, 14:34; edited 5 times in total (Reason for editing : Edited to update at the request of the author)
Low carbing is for all of us? This might surprise a few people! 
