Author Archives: Glyn and Liz

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About Glyn and Liz

Writer Liz wainwright and Independent Researcher Glyn Wainwright

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Statins reduce our ability to make vital cholesterol. Cholesterol is used to make memory connections in the brain.  The linked paper is worrying for all statin users.

Synapses

Synaptogenesis and neural cholesterol
Nowhere is the impact of cholesterol depletion more keenly studied than in the neurologic arena.  The work of Pfrieger et al. described the functional role of cholesterol in memory through synapto-genesis [24]. Mauch et al. [25] reported evidence that cholesterol is vital to the formation and correct operation of neurons to such an extent that neurons require additional sources of cholesterol to be secreted by glial cells. A recent mini-review by Jang et al. describes the synaptic vesicle secretion in neurons and its dependence upon cholesterol-rich membrane areas of the synaptic membrane [26]. Furthermore, working on rat brain synaptosomes, Waseem [23] demonstrated that a mere 9.3% decrease in the cholesterol level of the synaptosomal plasma membrane could inhibit exocytosis. These data might be particularly worrisome for lovastatin and simvastatin which are known to cross the blood brain barrier [27].
In fact, the proposed use of statins as a thera-peutic agent in Alzheimer’s disease (AD) [28] counters Pfrieger’s evidence [24]. Indeed, a reduc-tion in cholesterol synthesis leads to depletion of cholesterol in the lipid rafts – i.e. the de-novo cholesterol is required in the neurons for synaptic function and also in the neuronal membrane fusion pores [29].
Cognitive problems are the second most frequent type of adverse events, after muscle complaints, to be reported with statin therapy [30] and this has speculatively been attributed to mitochondrial effects. The central nervous sytem (CNS) cholesterol is synthesised in situ and CNS neurons only produce enough cholesterol to survive. The substantial amounts needed for synaptogenesis have to be supplemented by the glia cells. Having previously shown that in rat retinal ganglion cells without glia cells fewer and less efficient synapses could form, Göritz et al. [31] indicate that limiting cholesterol availability from glia directly affects the ability of CNS neurons to create synapses. They note that synthesis, uptake and transport of cholesterol directly impacts the development and plasticity of the synaptic circuitry. We note their very strong implication that local de-novo cholesterol synthesis in situ is essential in the creation and maintenance of memory.
There should be further consideration of cholesterol depletion on synaptogenesis, behaviours and memory loss for patients undergoing long-term statin therapy. This is particularly important with lipophilic statins which easily cross the blood brain barrier [32].
The effects of statins on cognitive function and the therapeutic potential of statins in Alzheimer’s disease are not clearly understood [28]. Two randomised trials of statins versus placebo in relatively younger healthier samples (lovastatin in one, simvastatin in other) showed significant worsening of cognitive indices relative to placebo [33, 34]. On the other hand, two trials in Alzheimer samples (with atorvastatin and simvastatin respectively) suggested possible trends to cognitive benefit, although these appeared to dissipate at 1 year [35, 36]. A recent Cochrane review concluded that there is good evidence from randomised trials that statins given in late life to individuals at risk of vascular disease have no effect in preventing Alzheimer´s disease or dementia [37]. However, case reports and case series from clinical practice in the real world reported cognitive loss on statins that resolved with discontinuation and recurred with rechallenge [30].

Statin Use Increases Dementia Risk

The ‘statins cure everything’ idea exposed

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Statins are said to be useful against more than heart disease, e.g. cancer, lung disease, heart failure, hip fractures and much more. The way in which researchers have studied these alleged benefits is confounded with a serious error. As an example I shall analyse the allegation that statin treatment prevents Alzheimer’s disease.  The idea goes against common sense. Today we know that not only is the brain the cholesterol-richest organ in the body; cholesterol is also vital for its function, because the creation of nerve impulses demands a steady production of cholesterol.

Uffe Ravnskov

Book Cover

Statin treatment accelerates atherosclerosis – Uffe Ravnskov

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Recently two separate studies showed that people on statin treatment develop atherosclerosis more often than untreated people. One of them was published in Diabetes Care, the other one in Atherosclerosis. You can get more details about this shocking finding in Dr. Mercola´s interview with senior scientist researcher Stephanie Seneff from MIT, who also is a member of THINCS. Read also Dr. Mercola´s comments about statin treatment.

Uffe Ravnskov, MD, PhD,

Independent Investigator
Spokesman of THINCS

The International Network of Cholesterol Skeptics

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If only we could have all the data on ‘Statins’, I have good reasons to suspect that they will become the pharmaceutical industry’s ‘PPI & LIBOR scandal’. In his latest book ‘Bad Pharma’ Ben Goldacre exposes the ways in which the trials of drugs can be used to give us the headline good news whilst toxicity, adverse events and important data about ‘all cause mortality’ is well hidden. Even (especially) the Doctors aren’t told. This book is on my reading list now.  This links to the Guardian review by Luisa Dilner.

Bad Pharma by Ben Goldacre – book review

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Link to slideshow

Excess exposure to fructose intake determines the liver to metabolize high doses of fructose, producing increased levels of fructose end products, like glyceraldehyde and dihydroxyacetone phosphate, that can converge with the glycolytic pathway. Fructose also leads to increased levels of advanced glycation end products.

The macrophages exposed to advanced glycation end products become  dysfunctional and, on entry into the artery wall, contribute to plaque formation and thrombosis.

Sugar-Damaged Proteins

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In the original study

Among the participants with diabetes, the proportion of glycated haemoglobin at 24 months decreased by 0.4±1.3% in the low-fat group, 0.5±1.1% in the Mediterranean-diet group, and 0.9±0.8% in the low-carbohydrate group. The changes were significant (P<0.05) only in the low-carbohydrate group (P=0.45 for the comparison among groups).

A four year follow up concluded

…a 2-year workplace intervention trial involving healthy dietary changes had long-lasting, favourable post-intervention effects, particularly among participants receiving the Mediterranean and low-carbohydrate diets, despite a partial regain of weight.

Mediterranean and low-carbohydrate diets

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Ever since I read Medical Myths by Joel Kauffman, I have had trouble believing that treating Blood Pressure with one of 5 different chemicals did anything to address the cause of raised blood pressure. Blood pressure is raised by glycation of arterial proteins (Sugar-Damage) how does a pill other than maybe metformin address that?  Lo-Carb Hi-Fat LCHF will address that issue eventually but best not get glycated to start with!

The Independent.ie said today:-

At least 800,000 deaths may have been caused worldwide in the past decade by preventive drugs which are routinely given to patients undergoing surgery to reduce the risk of heart attacks, researchers said yesterday.

And the source of this story is here

“Even if only 10 per cent of doctors followed the guidelines, and that is a conservative estimate, 100 million patients would have been given beta blockers during surgery in the past decade. On the basis of our findings, that means 800,000 would have died prematurely and 500,000 would have suffered a stroke. If our findings are true, that is death on the scale of a world war.” Devereaux P J Associate Professor, Department of Clinical Epidemiology and Biostatistics  Mc Master University

Beta blockers cost more lives than they save!

Immunity & The Complement System

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Neutrophils, Monocytes, Mast Cells, Macrophages, Dendritic Cells, B Cells, T Cells

If germs get through the body’s physical and chemical barriers into he bloodstream, a mixture of liquid proteins called complement is activated and attacks them. The complement system includes a series of proteins. While there are millions of different antibodies in your blood stream, each sensitive to a specific antigen, there are only a handful of proteins in the complement system. They float freely in your blood. Complements are manufactured in the liver. The complement proteins are activated by and work with (complement) the antibodies. They cause lysing (bursting) of cells and signal to phagocytes that a cell needs to be removed.

quoted from My-Immunity follow the link (click here)

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The question I have is: If the questions below are based on real concerns about statins –  Can they possibly be safe to use in the Heart Muscles? The answer right now has to be NO. Not until someone proves statins are beneficial in some way and do not mess with vital cell membrane cholesterol and the huge amounts of neural cholesterol we require to function.This has to be more than a misjudged statistical association. This links to a free article by Parker & Thompson in

Exercise & Sport Sciences Reviews:October 2012 – Volume 40 – Issue 4
p 188–194 doi: 10.1097/JES.0b013e31826c169e

Statins are effective in reducing low-density lipoprotein cholesterol and cardiac events but can produce muscle side effects. We have hypothesized that statin-related muscle complaints are exacerbated by exercise and influenced by factors including mitochondrial dysfunction, membrane disruption, and/or calcium handling. The interaction between statins, exercise, and muscle symptoms may be more effectively diagnosed and treated as rigorous scientific studies accumulate.

Why are researchers forced to make a positive statement about Statins before going on to describe how damaging and dangerous they can be? Notice that this paper limits that to acknowledgement of their ability to block cholesterol production. It is rare now to see any direct claim of benefits. I digress…..

Schematic


Questions about Statins and Skeletal Muscle Damage in Sports

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The authors’ findings suggest that higher levels of cholesterol are associated with a better outcome in the early phase after ischemic stroke.

Neurology. 2000 May 23;54(10):1944-9.
Vauthey C, de Freitas GR, van Melle G, Devuyst G, Bogousslavsky J.

Department of Neurology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.

Better outcome in ischemic stroke with high cholesterol.