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Sugar-Damage & Heart Disease
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Tag Archives: diabetes
Cholesterol & Insulin
diabetes [9]. The underlying mechanisms of the
potential adverse effects of statins on carbohydrate
homeostasis are complex [10] and might be related
to the lipophilicity of the statin [11]. Indeed,
retrospective analysis of the West of Scotland
Coronary Prevention Study (WOSCOPS) revealed
that 5 years of treatment with pravastatin reduced
diabetes incidence by 30% [12]. The authors
suggested that although lowering of trigliceride
levels could have influenced diabetes incidence,
other mechanisms such as anti-inflammatory action
might have been involved; however, in the
multivariate Cox model, baseline total cholesterol
did not predict the development of diabetes [12].
Furthermore, pravastatin did not decrease diabetes
incidence in the LIPID trial which included glucose-
intolerant patients [13]. On the other hand, in the
JUPITER trial (Justification for the Use of Statins in
Prevention: an Intervention Trial Evaluating
Rosuvastatin), which studied apparently healthy
persons without hyperlipidemia but with elevated
high-sensitivity C-reactive protein levels [14], the
risk of diabetes was increased by a factor of 1.25
[95% confidence interval (CI), 1.05 to 1.51] among
individuals receiving rosuvastatin 20 mg daily with
respect to placebo. Strikingly, among persons
assigned to rosuvastatin, the median low density
lipoprotein (LDL) cholesterol level at 12 months was
55 mg per deciliter [interquartile range, 44 to 72
(1.1 to 1.9)].
It is intriguing that salutary lifestyle measures,
which might exert their beneficial action through
an anti-inflammatory mechanism without a strong
cholesterol-lowering effect, beyond reducing
cardiovascular events and total mortality, reduce
also the risk of diabetes and other chronic
degenerative diseases. This fact may represent
a ‘justification’ not to use a drug in low-risk primary
prevention populations: lowering cholesterol at the
expense of increasing diabetes might be counter-
productive over the long-term.
References
9. Sukhija R, Prayaga S, Marashdeh M, et al. Effect of statins
on fasting plasma glucose in diabetic and nondiabetic
patients. J Investig Med 2009; 57: 495-9.
10. Szendroedi J, Anderwald C, Krssak M, et al. Effects of high-
dose simvastatin therapy on glucose metabolism and
ectopic lipid deposition in nonobese type 2 diabetic
patients. Diabetes Care 2009; 32: 209-14.
11. Ishikawa M, Okajima F, Inoue N, et al. Distinct effects of
pravastatin, atorvastatin, and simvastatin on insulin
secretion from a beta-cell line, MIN6 cells. J Atheroscler
Thromb 2006; 13: 329-35.
12. Freeman DJ, Norrie J, Sattar N, et al. Pravastatin and the
development of diabetes mellitus: evidence for
a protective treatment effect in the West of Scotland
Coronary Prevention Study. Circulation 2001; 103: 357-62.
13. K
eech A, Colquhoun D, Best J, et al.; LIPID Study Group.
Secondary prevention of cardiovascular events with long-
term pravastatin in patients with diabetes or impaired
fasting glucose: results from the LIPID trial. Diabetes Care
2003; 26: 2713-21.
14. Ridker PM, Danielson E, Fonseca FA, et al.; JUPITER Study
Group. Rosuvastatin to prevent vascular events in men
and women with elevated C-reactive protein. N Engl J Med
2008; 359: 2195-207.
Link
Cholesterol and insulin
Xia et al. inhibited a late step in the biosynthesis of de-novo cholesterol in murine and human pancreatic β cells [8] and published their findings in 2008. They had previously shown that insulin secretion was sensitive to the acute removal of membrane cholesterol. They now demonstrate that the depletion of membrane cholesterol impairs calcium voltage channels, insulin secretory granule creation, and mobilisation and membrane fusion.
This paper [8] clearly demonstrates that a direct causal link exists between membrane cholesterol depletion and the failure of insulin secretion. Their work is in close accord with data from some statin trials, which also connect cholesterol reduction with increased risk of type 2 diabetes; indeed, statin use has been shown to be associated with a rise of fasting plasma glucose in patients with and without diabetes [9]. The underlying mechanisms of the potential adverse effects of statins on carbohydrate homeostasis are complex [10] and might be related to the lipophilicity of the statin [11]. Indeed, retrospective analysis of the West of Scotland Coronary Prevention Study (WOSCOPS) revealed that 5 years of treatment with pravastatin reduced diabetes incidence by 30% [12]. The authors suggested that although lowering of trigliceride levels could have influenced diabetes incidence, other mechanisms such as anti-inflammatory action might have been involved; however, in the multivariate Cox model, baseline total cholesterol did not predict the development of diabetes [12]. Furthermore, pravastatin did not decrease diabetes incidence in the LIPID trial which included glucose-intolerant patients [13]. On the other hand, in the JUPITER trial (Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin), which studied apparently healthy persons without hyperlipidemia but with elevated high-sensitivity C-reactive protein levels [14], the risk of diabetes was increased by a factor of 1.25 [95% confidence interval (CI), 1.05 to 1.51] among individuals receiving rosuvastatin 20 mg daily with respect to placebo. Strikingly, among persons assigned to rosuvastatin, the median low density lipoprotein (LDL) cholesterol level at 12 months was 55 mg per deciliter [interquartile range, 44 to 72 (1.1 to 1.9)].
It is intriguing that salutary lifestyle measures, which might exert their beneficial action through an anti-inflammatory mechanism without a strong cholesterol-lowering effect, beyond reducing cardiovascular events and total mortality, reduce also the risk of diabetes and other chronic degenerative diseases. This fact may represent a ‘justification’ not to use a drug in low-risk primary prevention populations: lowering cholesterol at the expense of increasing diabetes might be counter-productive over the long-term.
8. Xia F, Xie L, Mihic A, et al. Inhibition of cholesterol biosynthesis impairs insulin secretion and voltage-gated calcium channel function in pancreatic beta-cells. Endocrinology 2008; 149: 5136-45.
9. Sukhija R, Prayaga S, Marashdeh M, et al. Effect of statins on fasting plasma glucose in diabetic and nondiabetic patients. J Investig Med 2009; 57: 495-9.
10. Szendroedi J, Anderwald C, Krssak M, et al. Effects of high-dose simvastatin therapy on glucose metabolism and ectopic lipid deposition in nonobese type 2 diabetic patients. Diabetes Care 2009; 32: 209-14.
11. Ishikawa M, Okajima F, Inoue N, et al. Distinct effects of pravastatin, atorvastatin, and simvastatin on insulin secretion from a beta-cell line, MIN6 cells. J Atheroscler Thromb 2006; 13: 329-35.
12. Freeman DJ, Norrie J, Sattar N, et
Link
A sample preview of slides for my presentation is linked here.
Publications on which the talk is based are free to download here.
Link
The Bio-chemical Science pages of Glyn Wainwright, Publisher, Independent Reader of Research and Honorary Recording Engineer for Leeds Symphony Orchestra<
Anecdote: A diabetic clinician told me she had noticed that when patients had good control of their hba1c (an indicator of sugar-damage in blood ) their ‘cholesterol’ score also improved.
Every molecule of cholesterol in the body is known to be identical to every other.
The Good/Bad labeling of cholesterol is extremely unscientific and unhelpful, and that is a matter of scientific fact.
How were intelligent, well educated, medical professionals persuaded to popularise this ‘Good ‘ cholesterol versus ’Bad’ cholesterol idea?
The unscientific phrase ‘Bad Cholesterol’ is a misleading description of damage to the ’lipid transport system ‘, whose basic function was described by the Nobel Prize winners James E. Rothman, Randy W. Schekman and Thomas C. Südhof. (Awarded “for their discoveries of machinery regulating vesicle traffic, a major transport system in our cells”.
The lipid transport system is used by the body to deliver essential supplies of fat, cholesterol, and other fat-soluble nutrients.
The lipid transport system is able to repair and recycle, but can be progressively overwhelmed by the damage accumulated over several decades.
This damage to the lipid system is caused by oxidation and glycation: the result of excessive consumption of refined sugars (in particular High Fructose syrups).
It is not ‘bad cholesterol’ but sugar-damage to the proteins that make the lipids available to the organs of our body.
Unconsumed ‘damaged’ ldl in the blood is an indicator of trouble because the organs are being starved of vital fats cholesterol and fat-soluble nutrients.
‘Bad Medicine’ prevents the liver and all other organs from making essential cholesterol indirectly stop the supply of lipids to the blood.
Cholesterol lowering medications have a variety of very broad variety of adverse-effects, all attributable to organs being starved of fat, cholesterol and fat-soluble nutrients.
The ‘bad medicine’s do not tackle the cause of damage to the ldl – lipids supply.
The primary cause of this ldl damage is the oxidation and glycation of the ldl’s components.
The main dietary and lifestyle causes of ldl damage are over-consumption of refined sugars and inactivity.
The reactive sugars like fructose, found in manufactured corn syrups are particularly troublesome, because they directly attach to ldl-protein mechanisms causing a mal-function which starves the organs.
Important protective and anti-oxidant functions rely on Cholesterol and CoQ10 – both of which are reduced anti-cholesterol medications.
The unscientific use of the incorrect description ‘Bad Cholesterol’ has held back medicine for over 40 years and it is time to look at the evidence in more detail:-
Link
Sweden has become the first Western nation to develop national dietary guidelines that reject the popular low-fat diet dogma in favor of low-carb high-fat nutrition advice.
Some quotes from Prof. Nyström translated into English from Dr. Eenfeldt:
Butter, olive oil, heavy cream, and bacon are not harmful foods. Quite the opposite. Fat is the best thing for those who want to lose weight. And there are no connections between a high fat intake and cardiovascular disease.
On Monday, SBU, the Swedish Council on Health Technology Assessment, dropped a bombshell. After a two-year long inquiry, reviewing 16,000 studies, the report “Dietary Treatment for Obesity” upends the conventional dietary guidelines for obese or diabetic people.
For a long time, the health care system has given the public advice to avoid fat, saturated fat in particular, and calories. A low-carb diet (LCHF – Low Carb High Fat, is actually a Swedish “invention”) has been dismissed as harmful, a humbug and as being a fad diet lacking any scientific basis.
Instead, the health care system has urged diabetics to eat a lot of fruit (=sugar) and low-fat products with considerable amounts of sugar or artificial sweeteners, the latter a dangerous trigger for the sugar-addicted person.
This report turns the current concepts upside down and advocates a low-carbohydrate, high-fat diet, as the most effective weapon against obesity.
The expert committee consisted of ten physicians, and several of them were skeptics to low-carbohydrate diets at the beginning of the investigation.
Sugar Damage and Dementia
Link
Link
Thank you Björn Hammarskjöld for the link.
Paper from Sanjay Basu, Paula Yoffe, Nancy Hills, Robert H. Lustig
Link
Fat Chance: Beating the odds against sugar, processed food, obesity, and disease by Robert H. Lustig
Liz & Glyn Wainwright 