Tag Archives: statin

The Cholesterol Story – An Essay

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The final edition of Dark Side of Statins by Dr Duane Gravelin MD explains why the drug has been such a huge disappointment and damaging mistake to a large proportion of patients. In it he included my essay “The Wonder of Cholesterol” which is a simplified explanation of why cholesterol is vital to our wellbeing and any attempt to lower it was always doomed to cause ill health. A key point in all this was the failure to recognise that the real cause of lipid dysfunction was sugar-damage (glycosylation) to the lipid receptors in all the organs of the body. We now have huge numbers of patients who are using carbohydrate restriction to reverse age-related diseases like mature-onset diabetes (T2D). Data being recorded by their Health Carers shows that the lipid profile (LDL/HDL) improves as the sugar-damage, as measured by HbA1c, is lowered.

Making Cholesterol in The Body

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In this video extract Glyn explains why it is vital that the body is able to make cholesterol in every cell. A healthy body will make about 3-4 g per day. Cholesterol is required by all the cells in the body and without it they will leak and fail.By blocking this process a statin can damage a large amount of vitality in all organs. Click on this link to watch the explanation on youtube.

Mevalonate Pathway

A video-blog link to Glyn’s explanation

Fats, Sugar, Salt & Cholesterol -the video interview!

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The interest in this video has been amazing and thank you to all who have watched it all. You don’t have to  because those with less time here are the “bite-sized” topic-based links below.

Interview

Video Index – Click on the topics to jump in:-

International Presentation Link

Useful References (linked)

  1. Ravnskov U, McCully KS Ann Clin Lab Sci. 2009 Winter;39(1):3-16.Review and Hypothesis: Vulnerable plaque formation from obstruction of Vasa vasorum by homocysteinylated and oxidized lipoprotein aggregates complexed with microbial remnants and LDL autoantibodies.
  2. Wainwright G, Mascitelli L, Goldstein M. Archives of Medical Science. 2009;5(3):289-295. Review paper Cholesterol-lowering therapy and cell membranes. Stable plaque at the expense of unstable membranes?.
  3. Seneff S, Wainwright G, Mascitelli L. Review paper Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?. Archives of Medical Science. 2011;7(1):8-20. doi:10.5114/aoms.2011.20598
  4. Seneff S, Wainwright G, Mascitelli L. Review Paper Nutrition and Alzheimer’s disease: The detrimental role of a high carbohydrate diet
    Seneff, Stephanie et al. European Journal of Internal Medicine , Volume 22 , Issue 2 , 134 –

Why Statins are Toxic

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Statins are technically defined as HMG Co-enzyme A reductase inhibitors.
Inhibiting HMG Co-enzyme A reductase (mevalonate enzyme) has extremely
toxic implications because our cells rely on the products of this
mevalonate synthesis.  Mevalonate, which is the basic building block for
cholesterol, CoQ10, dolichols and all the regulatory steroid hormones
etc…. (see diagram for more) This assembly line is so important
biochemists named it “The Mevalonate Metabolic Pathway” and teach it in
most basic courses.
The statin gamble – to reduce a symptom (not the
cause) i.e. sugar-damaged lipids. It works in that cholesterol
disappears, the lipids disappear, muscles and neurons start to
disappear. The myth pharma seek to exploit is lower LDL without causing
too much obvious toxic damage.
Sugar control will improve lipid
circulation, function and lipid health – without toxic consequences. It
won’t lower vital cholesterol! and raised LDL without sugar-damage
ensures longevity.  
The cholesterol paradox essay link: http://bit.ly/1fkGYgb

Conflicting Evidence – A Statin Paradox

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We know that all cells (all tissues) cease their exocytosis and endocytosis  activity, if the membrane cholesterol content drops by
around 10%.  This is easily achieved on statin therapy. Everything slows down.

In the case of bone remodelling both osteoclasts (cutters) and osteoblasts (builders) will reduce their repair activity in bone remodelling.
Calcium loss from bones will be reduced but micro-fracture repairs will not be repaired on statin therapy. Bone density is maintained on statin therapy but the developing micro-fractures weaken the skeleton.

It’s all about what is measured and how long you follow through.
Statin trials can be designed to prove both benefit and detriment to bones.
This is why experimental osteoporosis treatment by statins  to maintain bone density ultimately gives way to increased fracture risk.
Two competing bone remodelling processes are failing and conflicting measures can be used to conflict statin safety.

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You will find this pattern repeats in damage and  repair of myelin in MS studies.

To summarise: Short-term gain- long-term pain on statins

Dr Luca Mascitelli and myself went into this in our review paper 2009 at http://bit.ly/Ob9wKM

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The treatment and placebo groups’ mortality lines should be independent: a trend in one should have no consequential influence on the other. However:

  • All 4 lines are essentially identical for 1.6 years.
  • Then there is a departure — by both lines at the same time.

The fact that both lines — treatment and placebo — depart at the same time is important. Why should the treatment suddenly become beneficial at exactly the same time as non-treatment becomes detrimental?

The average line of both treatment and non-treatment groups follows a ‘natural’ mortality curve; any natural survival curve would have its slope increasing downward. (i.e. becoming more negative.)

Both treatment and placebo lines follow this natural curve for 1.6 years. Then both diverge. The placebo group shows this slope change increasing (negative) at a faster rate than all other lines. But, surely, it should follow the natural mortality curve. Why doesn’t it?

The slope of the treatment group is nearly constant from 1.8 years onward. It’s not a curve at all, but an almost straight line — and it shouldn’t be. What it says is that old people die at the same rate as younger ones. And life isn’t like that.

Is this evidence that the data of the 4S trial were not handled in an honest manner? Were deaths occurring in the treatment group assigned to the placebo group? Is this why the two curves, which should be independent, are apparently related? Or is there a mistake somewhere? Is there an error in logic?

Statins: Saviours of Mankind or Expensive Scam?

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Current guidelines encourage ambitious long term cholesterol lowering with statins, in order to decrease cardiovascular disease events. However, by regulating the biosynthesis of cholesterol we potentially change the form and function of every cell membrane from the head to the toe. As research…

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

Cholesterol and insulin