Tag Archives: cholesterol

Link

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

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

Link

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

Link

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

Link

More bad news for piles up for statins.

Compared to the individuals not taking statins, those taking statins had higher prevalence of risk factors and obstructive CAD……

Compared to individuals not on statin therapy, individuals who were taking statins were older and had higher body mass index (BMI), risk factors, lower LDL ….& lower HDL….

Statin use was associated with a higher frequency of severe coronary artery stenoses as well as numbers of coronary vessels with obstructive coronary artery disease. Further, statin use was associated with a differentially increased prevalence and extent of mixed-plaque and calcified plaque but not non-calcified plaque.

….the use of statins was associatedwith……..increasing presence and numbers of coronary segments with calcified plaque components.

Many references to contradictions in previous studies and use the word ‘surrogate’ seem to suggest that those who determine medical protocols are going to have problems coming to terms with these disturbing findings.

Statin use is associated with an increased prevalence and extent of coronary plaques possessing calcium.

Statins use and coronary artery plaque composition

Link

Alzheimer’s disease is a devastating disease whose recent increase in incidence rates has broad implications for rising health care costs. Huge amounts of research money are currently being invested in seeking the underlying cause, with corresponding progress in understanding the disease progression. In this paper, we highlight how an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in dietary fats and cholesterol, may lead to the development of Alzheimer’s disease. A first step in the pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins concerned with fat, cholesterol, and oxygen transport. This leads to cholesterol deficiency  in neurons, which significantly impairs their ability to function. Over time, a cascade response leads to impaired glutamate
signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial infection, and, ultimately, apoptosis. Other neurodegenerative diseases share many properties with Alzheimer’s disease, and may also be due in large part to this same underlying cause.

Dr Stephanie Seneff is a senior research scientist at MIT.

Alzheimer’s disease: The detrimental role of a high carbohydrate diet

Link

The diet was hatched in Poland some 40 years ago by Dr. Jan Kwasniewski, who started developing it while working as a dietician for a military sanitarium in Ciechocinek, Poland. There he observed that many of his patients were sick, “not because of any pathogenic factors … but the result of one underlying cause – bad nutrition,” according to his English language “Optimal Nutrition” book. After experimenting on his family and himself, Kwasniewski concluded that the ideal nutritional combo came from eating three grams of fat for every one gram of protein and half a gram of carbohydrates.

Petro Dobromylskyj

Praise the Lard – indeed!

Link

Lech Walesa was diabetic. He was on 52 units of insulin a day, spent 3 days a month in hospital and was under the care of 3 different ‘experts’. He was then treated by Dr Jan Kwasniewski, who has been successfully treating diabetics for 30 years on a low carb/high fat diet. Lech Walesa is no longer diabetic. The body converts carbs straight into glucose.

Petro Dobromylskyj

Diabetes – Lech Walesa