Obesity Pandemic - Infectious, or Personal Responsibility?

reply to post by DevolutionEvolvd


Current evidence indicates that dietary cholesterol accounts for maybe up to 10% of circulating serum cholesterol in hypercholesteremia.

Nonetheless, you keep pushing the idea that diet controls serum cholesterol levels - and that dietary intervention restores cholesterol homeostasis. You are full of it - misinformed, uninformed, decades behind the science - and liable to hurt people with your bs.

Your body, you choose what you do with it.... obviously.
If your fat, its your fault. If you have some bad genetics, its not your fault.

Nobody is forcing people to eat crap.

Originally posted by soficrow
reply to post by DevolutionEvolvd

 

Current evidence indicates that dietary cholesterol accounts for maybe up to 10% of circulating serum cholesterol in hypercholesteremia.

Correct. The liver produces about 90%.

Nonetheless, you keep pushing the idea that diet controls serum cholesterol levels - and that dietary intervention restores cholesterol homeostasis. You are full of it - misinformed, uninformed, decades behind the science - and liable to hurt people with your bs.

Well this I definitely can't agree with you on. There's too much evidence that diet influences serum cholesterol levels. Sometimes it's molecules that change the density of cholesterol particles from vldl, or LDL, to hdl. Sometimes it's molecules that influence the regulation of cholesterol syntheses in the liver. There's probably many more mechanisms than we currently have an explanation for. What I do know is that numerous studies confirm that dietary changes can alter total cholesterol, and the breakdown of it's components into more favorable outcomes. When I'm choosing a dietary plan for my meals of the day, I'm not much thinking of avoiding foods high in cholesterol, rather in getting the correct nutrients so that my body will better manage itself.

If you'd like, I'll come up with at least a dozen references to studies. There's just so many out there! Must get off the iPad first, though..

reply to post by unityemissions

When I'm choosing a dietary plan for my meals of the day, I'm not much thinking of avoiding foods high in cholesterol, rather in getting the correct nutrients so that my body will better manage itself.

There is no doubt that our bodies are designed to be self-healing, or that micro-nutrients have healing power - and the ability to -largely- override the epigenetic effects of underlying disease caused by prions and other misfolded proteins. That's not in question - the question is causation, and whether or not "bad diet" and "irresponsible lifestyle" cause NCDs - or if industrial pollutants and contaminants are responsible for starting the disease processes.

...In fact, there is no doubt that frequent, high-level and/or chronic low-level exposure to industrial contaminants and pollutants results in more misfolded proteins, often hugely overstressed systems, and a far greater burden of chronic disease. These disease consequences are undeniable and help explain why poorer nations and poor people are now bearing the brunt of the NCD Pandemic - they can't counteract their exposures with better food and more micro-nutrients, cleaner water or uncontaminated air.

...In fact, "obesity" is just a side-bar of the NCD Pandemic - but now - the obesity epidemics are overshadowing news about the NCD Pandemic. Suddenly, obesity is getting ALL the attention. Why?

Mainly, because the evidence shows NCDs are being passed on epigenetically, and childhood obesity is the most visible manifestation. But also because obesity is the most visible symptom - and it's so easy to blame the victims -or their parents- for their own plight. In the larger scheme of things though, childhood obesity really is a huge problem - indicating that NCDs are being inherited on a major scale. And 'authorities' have NO idea what to do.

But the focus on obesity to blame the victims is essentially just a distract and deflect strategy, designed to shift the public's attention from the larger issues, and the role industry plays in creating and spreading chronic disease.



Right now, global corporate "persons" are teaming it against real-life humans, blaming the victims - and getting the human victims to blame each other. Hopefully, we can get them to turn on themselves. They already scapegoated the tobacco industry in exchange for protecting the Mad Cow industry and everything else. But they're all culpable.

I'm waiting for the corporate lawsuits claiming:

1. The arsenic in the water from the goldmine is worse than the cadmium in the soil from the cadmium dispersal experiments;

2. The Bisphenol A in food packaging and dental sealants caused more NCDs than the ultra-fine particles from the coal burning plants;

3. The food industry creates more infectious misfolded proteins than Big Pharma; and so on.

Let these games begin - publicly. Because you can bet your Aunt Fanny's big phat butt they've been happening behind closed doors for decades.

Originally posted by soficrow
reply to post by DevolutionEvolvd

 

Current evidence indicates that dietary cholesterol accounts for maybe up to 10% of circulating serum cholesterol in hypercholesteremia.

See. That's your problem. The truth, in fact, is that the effect of dietary cholesterol on serum cholesterol is modest at best, except in those few with sensitivities.

Nonetheless, you keep pushing the idea that diet controls serum cholesterol levels - and that dietary intervention restores cholesterol homeostasis. You are full of it - misinformed, uninformed, decades behind the science - and liable to hurt people with your bs.

I'm afraid you just lack any true understanding of lipid metabolism and the difference between exogenous and endogenous/local and periphery in regards to physiological effects. That's ok, however, because I'm here to point you in the right direction.

I mean...I've already repeated this multiple times, but I guess I have to give you external links for you to take it as fact..so:

Hypercholesterolemia, or high cholesterol, is defined as: en.wikipedia.org...

Elevated cholesterol in the blood is due to abnormalities in the levels of lipoproteins

It's also described as dyslipidemia (abnormal lipid levels), Hyperlipidemia (high serum lipid levels) and Hyperlipoproteinemia (high serum lipoprotein).

We can learn a lot from genetic conditions such as familial hypercholesterolemia(FHC). Most cases of FHC occur when an individual inherits one abnormal copy of a certain gene that controls LDL receptor activity causing LDL cholesterol build up in the blood because receptor activity is significantly to severely (depending on the individual) diminished.

Drugs have been developed that increase cellular LDL receptor activity as a result of the above observation. Statin drugs, for example, inhibit the production of the enzyme responsible for cholesterol biosynthesis.

Statins act by competitively inhibiting HMG-CoA reductase, the first committed enzyme of the HMG-CoA reductase pathway.

en.wikipedia.org...

Because of this, the cell's natural compensatory response is to increase LDL receptor activity which effectively lowers serum levels of LDL.

Liver cells sense the reduced levels of liver cholesterol and seek to compensate by synthesizing LDL receptors to draw cholesterol out of the circulation.

Why is this important? Insulin resistance, and hyperinsulinemia, increases HMG-CoA reductase activity. This, in turn, effectively shuts down LDL receptor activity and leaves LDL to circulate and build-up in the blood.

HMG-CoA reductase is active when blood glucose is high. The basic functions of insulin and glucagon are to maintain glucose homeostasis.

en.wikipedia.org...

in a nutshell, this means that, in most cases, high-cholesterol can be reversed by restoring insulin sensitivity in the liver and lowering fasting insulin levels through the same molecular pathways that Statins do, but without the side-effects.

Of course, we also know that high carbohydrate diets, especially those high in sugar, lead to increased triglycerides. And anyone who's studied biochemistry knows that triglycerides are packaged in the blood in VLDL and that VLDL eventually becomes LDL. So, there are TWO main processes by which dietary interventions, mainly lowe-carb, effectively lower LDL levels establishing cholesterol homeostasis and reversing hypercholesterolemia.

And if you really, really want me to, I'll get you ALL the studies you want proving what I wrote above (i just don't think it's necessary right now.

reply to post by DevolutionEvolvd


You are to medicine what computer salespeople are to the communications industry - trained to parrot key phrases and razzle-dazzle ignorant consumers, but essentially ignorant and in the end, dangerous.


Once again, in case you missed it:

Right now, global corporate industries are teaming it against real-life humans, blaming the victims - and getting the victims to blame each other. Hopefully, we can get them to turn on themselves. They already scapegoated the tobacco industry in exchange for protecting the Mad Cow industry and everything else. But they're all culpable.

I'm waiting for the corporate lawsuits claiming:

1. The arsenic in the water from the goldmine is worse than the cadmium in the soil from the cadmium dispersal experiments;

2. The Bisphenol A in food packaging and dental sealants caused more NCDs than the ultra-fine particles from the coal burning plants;

3. The food industry creates more infectious misfolded proteins than Big Pharma; and on and on.

Let these games begin - publicly. Because you can bet your Aunt Fanny's big phat butt they've been happening behind closed doors for decades.

Originally posted by soficrow
reply to post by DevolutionEvolvd

 

You are to medicine what computer salespeople are to the communications industry - trained to parrot key phrases and razzle-dazzle ignorant consumers, but essentially ignorant and in the end, dangerous.

You're really making yourself look bad when you ignore the content of my posts and proceed attack me for questioning your "theory". It's becoming ever so clear that you're lack of understanding of even the most basic physiological processes is driving this.

Right now, global corporate industries are teaming it against real-life humans, blaming the victims - and getting the victims to blame each other.

I really don't know why you keep claiming I'm on the corporate industry's side. I don't blame victims for being misinformed and being given nutrition advice that's not only extremely incorrect but also extremely dangerous. Your argument is nothing more than a figurative red herring. You're ignoring most of the content I'm posting, diverting the attention away from the true conflict, creating an entirely different conflict, arguing against it and then claiming I'm wrong based on your argument against...something to which I'm not even subscribing.

1. The arsenic in the water from the goldmine is worse than the cadmium in the soil from the cadmium dispersal experiments;

2. The Bisphenol A in food packaging and dental sealants caused more NCDs than the ultra-fine particles from the coal burning plants;

3. The food industry creates more infectious misfolded proteins than Big Pharma; and on and on.

Even though I'm not sure why you posted this in response to me...I'll respond.

If arsenic and cadmium, BPA in food packing and Prions caused by big Food is are the reasons we see the current explosions in rates of chronic disease, then why do we see these diseases in nations and people without exposure to BPA, highly-processed foods and arsenic/cadmium?

Just a friendly interjection:

It seems you two have reached an impasse..

I would suggest focusing on the topic at hand, instead of dogging each other.

We know all of us mean well, so perhaps it would be best to let the links, and data presented speak for itself at this point.

Members viewing the thread are free to come to their own conclusions.

Peace!

reply to post by DevolutionEvolvd

If (industrial pollutants and contaminants) are the reasons we see the current explosions in rates of chronic disease, then why do we see these diseases in nations and people without exposure to (industrial pollutants and contaminants) ?

Duh. Where do think all our jobs went? And all the pollution that went along with those jobs? ….Ever heard of atmospheric winds? Global trade? Travel? ….Infectious proteins are nasty little suckers - forget sterilization and sanitation; not much works to get rid of them, not even autoclaving.

We're seeing more of these diseases in poorer nations and poor people because they don't have the resources to counteract the effects of pollution and industrial contamination.

There is no doubt that frequent, high-level and/or chronic low-level exposure to industrial contaminants and pollutants results in more misfolded proteins, often hugely overstressed systems, and a far greater burden of chronic disease. These disease consequences are undeniable and help explain why poorer nations and poor people are now bearing the brunt of the NCD Pandemic - they can't counteract their exposures with better food and more micro-nutrients, cleaner water or uncontaminated air.

……..While China’s factories crank out consumer goods for the planet, workers in these plants – who often toil in horrible conditions – are seeing their rates of respiratory illness and cancer soar.

The causes of deaths in an industry-dense area: example of Dilovasi

It is known that being exposed to air pollution for a long time increases the risk of respiratory illnesses and respiratory system cancers (20). It has also been observed that the mortality rate related to lung cancer has increased due to air pollution caused by industry (21,22). According to the World Health Report 2004, 12.5% of the deaths in the world are caused by cancer (12).

……Approximately 30,000 chemicals are commonly used today in industry and less than 1% of these have been subjected to a detailed assessment in terms of their toxicity and health risks (24). Some pollutants, such as suspended particular matter, sulphur dioxide, nitrogen dioxide, ozone, and carbon monoxide, are used for routine air quality monitoring.

…….It may be possible for the chemical pollutants to enter the human body via the food chain and by the pollutants in both air and water. ….
…………………………

Also see: Air quality and health

As far as your big focus on the liver - the liver is the body's "first responder" - and takes the first -and most major- hit from industrial contaminants and pollution; it also builds proteins, and is the location where many proteins first misfold.

The main functions of the liver is to process nutrients from food, make bile, remove toxins from the body and build proteins.
..........

The liver is a vital organ present in vertebrates and some other animals. It has a wide range of functions, including detoxification, protein synthesis, and production of biochemicals necessary for digestion. ……The liver is thought to be responsible for up to 500 separate functions, usually in combination with other systems and organs.

One of the myths propagated by eugenicists masquerading as "experts-in-genetics" is that all mutant proteins result from mutant genes. The rationale is that proteins are gene products, therefor, diseases involving mutant proteins are ipso facto genetic diseases. Wrong.

One key research area involves "pharmacoperones" - drugs used to target and treat misfolded proteins rather than the genes that produce the proteins. This research helps explain that the problems lie with the proteins NOT the DNA.

A New Understanding of Protein Mutation Unfolds

Most diseases with a genetic basis involve a mutation in some gene that affects how much of its protein is made or how well that protein works. However, a growing body of research indicates that this scenario may not be universally true. .....

reply to post by soficrow


I'm not denying that pollutants, contaminants and radiation exposure cause cancer. This thread was intended to address the obesity pandemic, and associated diseases (most of which are heart disease and diabetes) and whether they're caused by environment and infectious agents, such as prions, or by personal decisions, such as diet and lifestyle choices.

So, back to my question... If obesity (heart disease, diabetes) is caused by environmental factors driven by industrialization, then why do we observe such maladies in NON-INDUSTRIALIZED people? I'm talking about people that aren't exposed to pollutants and contaminants at the level you're suggesting.

Of course, the obvious answer is... These are multi-factorial diseases, especially cancer.

The thing about science is... Your theory must explain the the known observations rationally, independently from other theories and, most importantly, very specifically. Here's the problems I see...

Your theories are so shrouded in ambiguity... It's hard to distinguish between yours and others. In fact, I've repeatedly tried to solicit specific mechanisms from you as to how such metabolic/physiologic pathways specifically and directly cause obesity. To which your response has been...

You are to medicine what computer salespeople are to the communications industry - trained to parrot key phrases and razzle-dazzle ignorant consumers, but essentially ignorant and in the end, dangerous.

and...

You are full of it - misinformed, uninformed, decades behind the science - and liable to hurt people with your bs.

and..

Wotta guy. 3 posts of narrative bs, not one single link to back up your claims - yet you have the gall to lay out a HUGE list of demands, expecting me to drop my own priorities to play your silly games. Get a grip. I'm not here to do your research for you. Oh yeah, you did post an inaccessible 2005 op-ed piece for another member. ..........BLEEP.............Educate yourself! ...Here, let me help you get started. ..............BLEEP............

and...

.I confess I do not understand your agenda, although you clearly have one. Are you simply arguing to support the legitimacy of 'alternative health' solutions, or are you trying to defend corporate industry from liability charges?

Your strawman tactics are OBVIOUS attempts to avoid my direct questions...such as these posted in this thread by myself..

can you please describe the biochemical processes associated with Prion Disease and Obesity?

...and

So how do misfolded proteins affect the biochemical pathways that drive fat deposition and obesity?

and...

dietary intervention absolutely corrects most cases of dyslipidemia. So...if diet isn't causing [hypercholesterolemia], in most cases, why does dietary intervention correct the problem?

and..

[in response to an association you've so gladly pointed out] ..but how does this describe the methods by which Prions cause obesity?

If anybody is wasting their time, it's me. I've consistently asked you, from my first post, to describe the mechanisms that would account for the observed association between obesity (and high cholesterol) and Prion disease. Instead of admitting that you don't have an answer, you go out and find more links that provide more associations and correlations but don't describe specific causal pathways.

In fact, you completely blew your immediate association and the reason for posting the OP. Somehow, you took papers detailing elevated intracellular cholesterol and prions and decided to connect that with hypercholesterolemia. IT's not even a valid association to be posting.

So, until you can get your stuff together and at least make an attempt to have a real discussion here, I will be discontinuing any further posts in the thread directed towards you.

reply to post by DevolutionEvolvd

......I've consistently asked you, from my first post, to describe the mechanisms that would account for the observed association between obesity (and high cholesterol) and Prion disease.

Right - you've consistently asked for a highly academic, dry and inaccessible dissertation focusing on mechanisms and processes in a manner guaranteed to totally alienate any readers who might be interested in the topic.

You on the other hand, spout the corporate drivel designed to blame the victims, and take the heat off corporate industry. You provide NO references - but want me to present a fully articulated and properly sourced thesis that you can rip to pieces point by point. Or perhaps, sell as your own work. Dream on.

You want a professional thesis - pay me. Otherwise, I'm glad to see you go.

For anyone here who didn't catch the real problem with childhood obesity - it seems to be playing out that obesity is one of the main symptoms of epigenetically inherited chronic disease (NCDs). Obesity is common in pandemic NCDs, but everyone with NCDs is not obese - so we know obesity is not inherent to acquired and sporadic cases. The four main pandemic NCDs are cancer, heart disease, diabetes and lung disease - NCD-related obesity seems to appear only after the disease agent infects victims' neurons. The current epidemics of NCDs with obesity in children suggest epigenetically inherited NCDs involve the nervous systems from the get-go.

Fortunately, unlike diseases caused by genetic mutations in the DNA, disease that is inherited epigenetically tends to reverse after a few generations if the environmental triggers are removed.

For those who still buy the corporate spin that obesity epidemics are occurring in countries without pollution - guess what! There are NO countries without pollution and environmental contamination. ...Africa is lagging behind, but it's definitely catching up now.

reply to post by soficrow


...no. I want you to just answer a few questions, sofi. This is a DISCUSSION forum.

When you take an association, find papers through a google search and then claim they are proof that their is cause...without even knowing the difference between intracellular high cholesterol and hypercholesterolemia and citing the former as proof that prions are causing the latter, I think there's cause for alarm and questioning.

It'd be like if someone came onto ATS saying they invented an anti-gravity device but couldn't provide proof or even describe the most basic of concepts of physics.

Originally posted by soficrow
For those who still buy the corporate spin that obesity epidemics are occurring in countries without pollution - guess what! There are NO countries without pollution and environmental contamination.

...but there are isolated populations that have extremely minimal exposure to radiation, contamination and pollution, if any at all.

And low exposure can actually be beneficial.

In toxicology, hormesis is a dose response phenomenon characterized by a low dose stimulation, high dose inhibition, resulting in either a J-shaped or an inverted U-shaped dose response. Such environmental factors that would seem to produce positive responses have also been termed “eustress”

en.wikipedia.org...

reply to post by DevolutionEvolvd


Isolated populations are still exposed via atmospheric winds as well as other avenues. Global trade and travel are also factors in the absence of local industry. .......However, in general, isolated populations with minimal exposures to pollution and other industrial contaminants tend to have far lower incidence of chronic disease.

reply to post by DevolutionEvolvd

without even knowing the difference between intracellular high cholesterol and hypercholesterolemia

Please feel free to provide references proving that cholesterol cannot and does not ever leave the cell to enter serum, blood stream or other body system.

reply to post by soficrow


Yes. Isolated populations do have less "chronic" disease incidence, generally. But, typically, chronic disease incidence increases proportionately with an increase in "western" food consumption in said populations (examples would be the Alaskin Inuit as described and documented by Vilhjalmur Stefansson to today, The Pima of New Mexico prior/post gold rush, numerous African tribes, etc.).

And we know that this isn't a phenomenon of increased contaminant exposure from pollution, etc. because once this specific type of diet is cessated, disease incidence begins to decrease (with cancer incidence being the most controversial), regardless of industrialization.

reply to post by DevolutionEvolvd


Your whole argument is premised on the idea that cholesterol inside cells cannot / does not leave the cellular environment. So okay. :sigh: Here are a couple of old papers that describe how cholesterol moves/is moved out of cells.

1971 - Previous studies have described the exchange of free cholesterol molecules of macrophage membranes with those of serum lipoproteins (1). Exchangeable cholesterol was found in two compartments. The rapidly exchanging compartment was identified as the plasma membrane, and the slowly exchanging compartment was associated with intracellular membranes (2). …..Under physiological and pathological conditions macrophages are exposed to other forms of both free cholesterol and CE's. Effete erythrocytes, tissue cells, and chylo-microns are taken up by phagocytosis (4-6), and subsequently are localized within cytoplasmic phagolysosomes. Many of their constituents are then degraded by acid hydrolases (7-9).

Similar events take place under in vitro culture conditions and may lead to the formation of an intralysosomal compartment of free and esterified cholesterol, clearly distinct from the membrane-associated intracellular pool. The processing and fate of cholesterol and CE's within the digestive vacuole is poorly understood.

In this paper we describe the formation of intralysosomal pools of particulate-free and esterified cholesterol, their intracellular processing and excretion from the macrophage, and their influence on the kinetics of exchange. In addition, a lysosomal cholesterol esterase has been characterized and its function evaluated in cell lysates and in the intact macrophage.

1996 - Like cholesterol, 250HC was removed from cells by an extracellular acceptor such as high density lipoprotein. Unlike cholesterol,250HC was also rapidly and extensively removed from cells by serum albumin, but not by ovalbumin.The differential removal of oxysterols and cholesterol from cells by albumin allows separation of cellular effects due to oxysterols and cholesterol.

reply to post by DevolutionEvolvd

And we know that this isn't a phenomenon of increased contaminant exposure from pollution, etc. because once this specific type of diet is cessated, disease incidence begins to decrease (with cancer incidence being the most controversial), regardless of industrialization.

Real food has healing power - I'm walking proof of that, and also of the fact that lifestyle choices can mitigate underlying disease (delay progression, etc.). I should be dead - or at the very least, really really sick. I'm not - but I'm not "cured" either.

So no - I do not question the benefits of good food, clean air, uncontaminated water, 'natural' products and stress-free living.

But I am saying we're fighting a losing battle - most evident in the fact that chronic disease is being epigenetically inherited by our children, and most visibly manifested by the childhood obesity pandemics.

.....All the "responsible choices" in the world will not turn back this tide unless and until we clean up our planet.

Originally posted by soficrow

Please feel free to provide references proving that cholesterol cannot and does not ever leave the cell to enter serum, blood stream or other body system.

I never once said that intracellular cholesterol is stuck in the cell. Please don't put words in my mouth...err...posts. Before I begin posting the sources, let me preface. Even though intracellular biosynthesis of cholesterol is increased by prions (at least according to your sources), there is a clear, definitive reason for this: Because prions are USING cholesterol to propagate. Also, the studies you referenced were speaking specifically about Neuronal Cells and cholesterol buildup within those specific brain cells. That being said...

You were talking as if celllular increase in cholesterol production causes an overflow into the bloodstream causing hypercholesterolemia. However, in the vast majority of cases, hypercholesterolemia is not because of an increase in choleserol per se, but rather a problem with lipoprotein metabolism and LDL receptor activity.

Elevated cholesterol in the blood is due to abnormalities in the levels of lipoproteins

en.wikipedia.org...

Once again, hypercholesterolemia is commonly described more accurately as hyperlipoproteinemia, since it's the lipoproteins transporting the cholesterol that is causing the real metabolic abnormalities.

Familial hypercholesterolaemia (FH) is the most thoroughly studied lipoprotein disorder.

[snip]

The diagnosis is based on elevated plasma LDL cholesterol, the presence of a family history of premature CAD and the presence of xanthomas. A molecular diagnosis is sometimes required. Defects at the LDL-R gene that alter the function of the LDL-R protein and its function are the cause of FH(Figure 2 (7)); this causes accumulation of LDL particles in plasma.

www.springerlink.com...

The reason why high-cholesterol or hypercholesterolemia has such large implications is primarily because of it's propensity to cause heart disease. Now, people with heterozygous FH develop premature heart disease by 30 and those with homozygous FH, receiving a copy of the defective gene from each parent, don't normally live past 30 because it's so aggressive. Although it's not a common form of Hypercholesterolemia, it is the most studied form because it so accurately describes the mechanisms involved with the pre-development of atherosclersosis.

Typical "high-cholesterol" or hypercholesterolemia found in the vast majority of the population closely mimics that of FH, only to a lesser extent. In fact, as I've stated in a previous post, statin drugs were developed as a result of studies conducted on FH. They work by inhibiting an enzyme in the pathway that produces intracellular cholesterol, which, in turn, upregulates the LDL receptor.

And just as there is a small cohort of the population that has a defective LDL receptor gene, so is there a small cohort that has genetically increased LDL receptor activity.

mice lacking Pcsk9 have increased levels of hepatic LDL receptors, and they remove LDL from the plasma at an accelerated rate.11 Thus, high levels of PCSK9 lead to high plasma levels of LDL cholesterol, whereas low levels of PCSK9 lead to low LDL cholesterol levels.

www.nejm.org...=articleBackground

A genetic propensity to have low PCSK9 leads to increased LDL activity which decreases serum LDL levels...and as a result...

3.2 percent had a sequence variation in PCSK9 that was associated with a 15 percent reduction in LDL cholesterol and a 47 percent reduction in the risk of CHD

These data indicate that moderate lifelong reduction in the plasma level of LDL cholesterol is associated with a substantial reduction in the incidence of coronary events, even in populations with a high prevalence of non–lipid-related cardiovascular risk factors.

www.nejm.org...

Despite other factors that are considered high-risk for cardiovascular disease development, those with increased LDL receptor activity had a "substantial reduction" in coronary events.

Why does this matter? Getting back to what you were saying...

You were associating hypercholesterolemia with increased cellular biosynthesis of cholesterol in brain cells due to prion presence. The reasoning, then, was that Prion Diseases and misfolded proteins were leading to increased cholesterol and hypercholesterolemia. Well, unfortunately, based on the above, this just isn't the case in most cases of hypercholesterolemia, as it's not a CHOLESTEROL issue...it's a Lipoprotein and LDL receptor issue.

So to answer this question...

Please feel free to provide references proving that cholesterol cannot and does not ever leave the cell to enter serum, blood stream or other body system.

I say it's irrelevant.