Tag Archives: dementia

Cholesterol  – under attack again – by vaccine!

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With yet another misguided attempt to remove cholesterol from humans let me explain their stupidity:

The lipid nutrition cycle has large low-density lipids (LDL)
out-bound from the liver, taking fatty nutrition to all organs in the body.
Smaller high-density lipoproteins (HDL) form on the return side, taking excess
or damaged lipids back to the liver. In a healthy person there is a ratio of
about 5:1 (LDL/HDL) when the cycle is working correctly.

The unscientific characterisation this lipid nutrition cycle
ratio as ‘good cholesterol’ and ‘bad cholesterol’ has created an extremely poor
understanding, and consequently inappropriate treatment, of total serum
cholesterol.

The bitly link to my conference presentation (notes &
references) gives the detailed explanation.

In summary it is the failure of the lipid receptor mechanism that allows LDL to build up and that damage is often glycation (AGE) caused by reactive blood sugars (glucose and more recently fructose).

Professionals who talk about good cholesterol and bad cholesterol are simply displaying total ignorance of their field.

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Link

The impact of statin drugs goes far beyond those declared by the advisory leaflet in the packet. It is really time that the professions got to grips with the fundamental biochemistry of mevalonate inhibitions. More about the book ‘The Dark Side of Statins’ later in the year!

I hope this video will encourage people to consider the wider implications of the biochemical action of statins as they target the important pathway affecting much more than cardiovascular outcomes.

Statin drugs will continue to devastate the quality of life of its users. ‘All cause mortality data’ is not fully released. Failure to appreciate mevalonate pathway effects is allowing this devastating avalanche of adverse impacts to continue, with the blessing of professionals who should know better.

Dark Effects of statins are listed on in adverts and on the leaflet supplied with the medication. more info at: http://www.spacedoc.net .

Statins – The Dark Side – Video Link

Sugar Damage and Dementia

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A normal brain requires reliable supplies of fatty nutrients supplied by the liver as LDL. LDLs are fatty packets of nutrients travelling in the blood to feed the brain and other organs.  LDL receptors on the organs recognise the LDL packets and absorb them. The ‘empty packets’ (HDL), carrying waste for recycling, return to the liver via the blood stream.
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Over time sugars damage the LDL labels, and thus stop the nutrients from being recognised by the brain’s LDL receptors. Consequently LDL stays in the blood and less HDL packets are produced.  This raised LDL. and lower HDL. is associated with poor health. The cause is sugar-damage. image

Sugar damage causes the brain to be starved of vital fat and cholesterol.

Treatments which lower ‘LDL cholesterol’ do not help. They further deprive the brain of LDL, The brain and other organs become starved of fatty nutrients. Meanwhile, any excess dietary sugars (fructose & glucose) become the cause many ‘diabetes associated’ illnesses.

Fructose, which is increasingly being added to food products, is the new problem sugar. It is more reactive and 10 times more damaging than glucose.

The vital fatty nutrients in LDL are falsely called ‘Bad Cholesterol’.

Raised blood lipids (LDL) are a symptom, and again the cause is sugar-damage.

Is it any wonder that years of the dogmatic policy of ‘Cholesterol Reduction’ have failed to deliver health benefits, and is fraught with problems such as muscle wastage, diabetes and dementia?

The above is a very simplified overview of our paper. If you click on this link you can read our full paper, as published in the Archives of Medical Science.

Click here for our Dementia Paper

(These are ‘free access’ publications)

Link

Key points in our paper are:-

The amyloid-β present in Alzheimer’s plaque may not be causal,
since drug-induced suppression of its synthesis led to further
cognitive decline in the controlled studies performed so far.

• Researchers have identified mitochondrial dysfunction and brain
insulin resistance as early indicators of Alzheimer’s disease.
• ApoE-4 is a risk factor for Alzheimer’s disease, and ApoE is involved
in the transport of cholesterol and fats, which are essential for signal
transduction and protection from oxidative damage.
• The cerebrospinal fluid of Alzheimer’s brains is deficient in fats and
cholesterol.
• Advanced glycation end-products (AGEs) are present in significant
amounts in Alzheimer’s brains.
• Fructose, an increasingly pervasive sweetening agent, is ten times as
reactive as glucose in inducing AGEs.
• Astrocytes play an important role in providing fat and cholesterol to
neurons.
• Glycation damage interferes with the LDL-mediated delivery of fats
and cholesterol to astrocytes, and therefore, indirectly, to neurons.
• ApoE induces synthesis of Aβ when lipid supply is deficient.
• Aβ redirects neuron metabolism towards other substrates besides
glucose, by interferingwith glucose and oxygen supply and increasing
bioavailability of lactate and ketone bodies.
• Synthesis of the neurotransmitter, glutamate, is increased when
cholesterol is deficient, and glutamate is a potent oxidizing agent.
• Over time, neurons become severely damaged due to chronic exposure
to glucose and oxidizing agents, and are programmed for apoptosis
due to highly impaired function.
• Once sufficiently many neurons are destroyed, cognitive decline is
manifested.
• Simple dietary modification, towards fewer highly-processed
carbohydrates and relatively more fats and cholesterol, is likely a
protective measure against Alzheimer’s disease.

Fructose and Dementias

Link

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

Link

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

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The world’s big pharmaceutical companies are cutting back their research into treatment for Alzheimer’s, after being hit by the failure of a number of high profile, and expensive, drugs trials. Sir John Bell, Life Sciences Champion for the government, and Stephen Whitehead, head of the Association of the British Pharmaceutical Industry discuss why it is proving so hard to find something that works.

BBC Radio4 Today: Thursday 20th September 07:50 BSTOur Paper on Alzheimers Disease
Source: lizscript.co.uk