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I think Kate was shocked by what she was reporting – Fat is actually a good thing to eat!  If only people new how much fat and fat soluble nutrients we need to consume from animal sources, and how alien plant oils are to our biochemical systems. If only the medical profession and population at large could speak and understand the basics of biochemistry.

I was hovering over the nuts display in the supermarket, wondering which to buy. I had just interviewed Oliver Selway, a radical diet-and-fitness coach and proponent of a food regimen that does not fear fats. He had told me macadamias were by far the most nutritious nuts to eat, a nut that any dieter will know is forbidden as it is astonishingly calorific. “They’re the fattiest nuts, you know,” a woman next to me said. “They are so bad.” Cheerily, I repeated Selway’s nutritional proposition: that animal and other natural saturated fats from whole foods are good for us. They are what human bodies have known for millions of years…….All natural fats have functions for health: they are not inherently bad…….margarine ‘the devil’s semen’……..told for decades to cut saturated fat from their diet, they replace have replaced it with what some studies suggest is more harmful: refined carbohydrates. 

Fat lot of good by Kate Spicer – Sunday Times UK

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Lynda Collins is a 1960s teenager who dreams of a better life, and of being loved. Not much to ask, is it? Both wealthy Ellen Heywood and snobbish Sheila Stanworth think that Lynda, brought up in a run-down pub in the poorest part of Milfield, isnt good enough to marry their son. Ellen forces her son, Daniel, to give up Lynda, but Dans best friend, John Stanworth defies his Mother and marries the girl Sheila describes as a cheap imitation Marilyn Monroe with no cooking skills.

The Girl who wasn’t Good Enough (eBook) by Liz Wainwright 9781476479903 | WHSmith.co.uk

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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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quoted from Zoe Harcombe’s Blog on Traffic Light Food Labelling

All real foods in the table above have at least one red/amber traffic light warning and olives and cheese have three. The former being a good source of natural fat – especially the much eulogised mono-unsaturated fat – and the latter being an excellent source of calcium and the other bone nutrients vitamin D and phosphorus.

With one exception, all processed foods in the table above have green lights for fat, saturated fat and sugar. Multi grain bread gets an amber for fat content – because of the highly nutritious seeds that is contains. White bread scores better than multi grain.

Zoe

The law of unintended consequences

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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

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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!

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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