The ‘High Cholesterol’ Paradox

For some people, being told they have ‘high cholesterol’ suggests a decline, for others it is a sign of healthy longevity. What is really going on?

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The real story is the way in which high dietary levels of refined sugars such as Fructose can adversely modify our lipid-protein-labels and break the fatty nutrition cycle supplying all our organs.

Normally high lipid levels with good ratios of LDL (larger nutrient packages) and HDL (returning ’empty’ packages for recycling) are seen in people with healthy long life prospects. 

When the LDL package address (protein marker) is sugar-damaged (glycated) LDL backs up in the blood and less HDL is recycled. The blood lipids are up but the organs can’t use it. e.g The brain is starved of vital fat-soluble nutrients. Taking medication to block cholesterol production will lower blood lipids BUT…. the brain, muscles etc. are  still starved of vital fat-soluble nutrition and the outcome worsens.

The HbA1c test for sugar-damage in the blood protein hemoglobin looks likely to be a great indicator for sugar damage in general so..

‘High Cholesterol’ with good HbA1c levels is a healthy sign.

‘High Cholesterol’ with poor HbA1c levels is a very unhealthy sign.

THE REAL STORY IS SUGAR-DAMAGE

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A small increase in a small risk is still a slightly bigger but small risk and we are relieved to note there is no association of cancer with red meat consumption.

Why do we allow the abuse of statistics to create a scare story about food and health, because the figures quoted are meaningless due to confounders not discussed. 

How to make a scare out of very little with statistics:

Suppose a 1% risk is a 1.3% risk…lets use the 0.3% increase in (absolute) risk or use the ratio (0.3 to 1) to get an impressive 33% increase in (relative) risk – Same risk increase but more journalistic scare power!

Enjoy the bacon with eggs – as with all traditional foods.

CBN News has a much more important story to tell!.

BBC News – Processed meat ‘early death’ link

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The brain is only 2% of your body mass but it contains 25% of your cholesterol.  The cholesterol is vital to memory formation (synapses)  and nerve protection (myelin).  Our livers make 2.5g of fresh cholesterol every day to replace the losses.  The liver delivers the brains fresh daily supply of cholesterol to the brain in small lipid droplets known as LDL.  The empties return to the liver known as HDL with various waste products for recycling and disposal.

To get these vital supplies into the brain the LDL droplets have to cross the blood-brain barrier. The particles carry a protein label which is recognised by the receptors.  The brains receptors lock onto the LDL and allow the particles to pass though into the brains astrocyte cells. These astrocytes use the cholesterol  and fats in the care and feeding of the neurons and all is well with our thoughts and memories.

If we consume a lot of sugary products, especially fructose, the receptors become damaged by sugary attachments and fail to work.  The LDL then builds up in the blood and the brain is starved of fat and cholesterol.  All is now not well with our thoughts and memories.

This is a simplification of our biochemical papers on this matter. Other organs like the heart are also affected this way. How is it possible for an educated professionals to go on misleading us by referring to LDL as “Bad Cholesterol”?   

Fructose is getting away with murder and the blame is being laid upon the good guys  – fat and cholesterol.  

Please click on and read our free peer reviewed medical journal publications and ask your medical advisors some tough questions about this low cholesterol ‘madness’.

“Cholesterol Lowering Therapies and Membrane Cholesterol”

Wainwright G   Mascitelli L  &  Goldstein M R

Archives of Medical Science Vol. 5 Issue 3 p289-295 2009

“Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?”

 Seneff S, Wainwright G, and Mascitelli L

Archives of Medical Science  Vol. 7 Issue 1 p8-20 2011 doi: 10.5114/aoms.2011.20598

“Nutrition and Alzheimer’s disease: the detrimental role of a high carbohydrate diet”

Seneff S., Wainwright G., and Mascitelli L.

European Journal of Internal Medicine 2011  doi:10.1016/j.ejim.2010.12.0172011

Low Cholesterol – Madness

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Duane Graveline MD MPH (Author), Glyn Wainwright MSc (Introduction)

Try to imagine a drug possessing the ability to cause DNA mutations using the same mechanisms that have evolved for natural aging. When confronted with a patient experiencing weakness and unsteadiness, muscle aches and pains, memory loss and depression, the quite natural response from most doctors is, “You have to expect this kind of thing now; you are over 50”. Most doctors do not have a clue as to the truth. It is not natural aging that has depleted you so. This is premature aging – aging in months according to many statin victims – and this entire complex of symptoms from a drug so safe that many doctors feel it should be put in the drinking water. The class of drugs is called statins, simple reductase inhibitors capable not only of lowering cholesterol but also CoQ10 and dolichols as well, leading directly to mitochondrial damage and mutation. No, this is not impossible. It is happening today to thousands of us.

The Dark Side of Statins

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Over the 40 years from 1969 to 2009, I had a forty year anecdotal adventure in biochemistry leading to the publication of a seminal paper on cell-membranes and an invitation to contribute more biochemical thoughts in new hypotheses about modern medicine.  12 years involved in teaching chemistry followed by 28 years in Information technology.

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The anecdotal adventures in biochemistry started in the 1970s. Working as a chemistry teacher I found myself increasingly troubled by contact dermatitis and eczema.   This career trauma led to my retraining as a computer scientist and information technologist, a cleaner environment in which to survive and explore modern science.

The Anecdotal Biochemist

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There is NO evidence that in an otherwise healthy person measuring blood cholesterol and taking a statin to lower blood cholesterol will live any longer than not doing so. Even the Canadian Government in allowing the publication of these ads swallowed the big lie.

All primary prevention trials to date of cholesterol lowering with drugs (LRC-CPPT, WOSCOPS, ASCOT-LLA) have shown NO total mortality benefit.  But they keep trying to sell the red rice yeast toxins etc…

Don’t believe the claims of the manufacturers!

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Quoting from Saudi Gazette Report from King of Organs Heart Conference in Hofuf:

The overall impression that evolved from the presentations was summed up in the words of Dr. Malcom Kendrik, “The whole cholesterol thing is bunk”.

King of Organs Conference - Saudi Arabia

Brothers in arms in the assault on the shibboleths of commercial medicine exchange views during a break in proceedings at the King of Organs conference in Hofuf on Tuesday. (L-R) David Diamond, Malcom Kendrick, Carlos Monterio and Paul Rosch. — SG photo

“Dark chocolate is a far better drug to take than statins” David Diamond.

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MILLIONS who take statins to ward off heart attacks and strokes must cut their dose over fears they are at risk of serious side-effects.

The fact that the raised blood lipids (LDL) associated with CVD is caused by sugar-damaged to the LDL   (Fructose & Glucose) is still a big secret. Cholesterol was never the guilty party but everyone (including many in the medical profession) still hold this myth about cholesterol and completely miss the cause being dietary sugars!

Statins are bad for you!

STATINS IN NEW HEALTH ALERT

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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