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 with 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 much 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. High levels of insulin will mean that fat is not only stored but is specifically not metabolised. Weight gain results.
Recent evidence supports the role of insulin and IGF-1 (insulin like growth factor) 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.] This means that whilst elevated insulin levels are not shown to increase the risk of cancer they will enable cancers to proliferate.
A 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]
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]
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 and stopped 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.
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 cardiovascular risk. If anything this demonstrates that increased medication is the problem rather than tighter control.
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 (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]