http://www.proteinpower.com/drmike/...tionblog+(The+Blog+of+Michael+R.+Eades,+M.D.)


Part 2 of the Heart of the Matter aired last night in Australia. And not without a lot of courage on the part of ABC and Dr Maryanne Demasi, who conceived of and put the show together. This program, an absolutely devastating expose of the dangers and general uselessness of statin drugs, was fought tooth and toenail by the mainstream statinators. When you watch the show, you’ll know why.

For years I have been harping on this blog about how statins have been grossly oversold to both the doctors and the public. But this should not come as a surprise since statins as a group are the largest selling class of drugs in the world accounting for God only knows how much profit to the pharmaceutical industry. I’m the last person to gripe about someone making money, but in this case, I have a real problem. Why? Because there is so much Big Pharma money out there that it affects everything. It seeps into doctors lives starting with their medical training right through to retirement.

When the pharmaceutical industry first developed cholesterol-lowering drugs, the approach was to sell the patients on them. Scare them to death about their cholesterol levels, and get them to ask their doctors about a prescription. Way back then doctors weren’t taken in by this cholesterol-has-to-be-below 200 mg/dl nonsense, and told their patients not to worry. Then Big Pharma did the sales job on physicians.


MD and I got invited to one of their sales weekends. We, along with about a hundred other docs, were put up in suites at an exclusive resort. Everything was paid for, and, let me tell you, the meal spreads were lavish. We all lounged around over the weekend having multiple receptions of one kind or another – including fabulous food and all the drink one wanted – and a whole lot of laying-by-the-pool time. There was an afternoon of propaganda we all had to attend.

The whole herd of us sat through about three lectures on the evils of elevated cholesterol and how the lipid hypothesis wasn’t really a hypothesis but was the hard truth. They didn’t actually say that in those words, but that was the implication. And they finished off with the now-famous bit about how every percent increase in LDL levels brought about a two percent increase in risk for heart disease. Which, of course, is all hogwash, and was obviously hogwash to anyone paying attention who had a modicum of knowledge about how to interpret a scientific study. Sad to say, most physicians don’t fall into that category. During the farewell reception, where drinks flowed, I could tell that most everyone was sold on the notion of widespread cholesterol checking and aggressive treatment not of a disease but of a lab value. It was truly depressing.

I’ve written about the general uselessness of statins in numerous posts on this blog over the past seven or eight years. The Australian show pretty much confirms everything I’ve written with a few extra dollops of outrage.

I’m almost never surprised when when I learn the lengths to which Big Pharma will go to sell drugs. But some of the revelations in this show stunned even me.

I have had readers write me that their docs were going to fire them as patients if they didn’t take a statin drug for even minor elevations of cholesterol. Having been in practice a many years, I found this almost unbelievable. But now I’ve got a better inkling of what is really going on.

Dr. Beatrice Golomb, an academic physician at the University of California San Diego, is one of the world’s leading researchers on statin drugs. Here is her stunning explanation of why many docs almost force statins on their patients:

Some of them tell us that their doctors fire them as patients if they discontinue their statins, which I really wonder about the ethics of. Some of the people that we hear from also say that their doctor didn’t believe them, that their problem couldn’t be due to statins, and based on how patients perceive it, badger or bully them into resuming or continuing the medication. That’s not an acceptable way for medicine, as a system, to be run.

I think they often intentionally hide those risks because there are often physician incentives that benefit the physician for having more patients on statins. So it pits physician self-interest against patient benefit. This particular woman contacted me, and she had left the practice that she was at because they insisted that at least… I believe it was 80% of her patients be on statins. This has actually been written up in media as something that is actually considered legal and acceptable. I can’t see any way in which that’s acceptable. I’m literally the only researcher I know who studies this class of drugs who has a policy not to take money from industry.

Now you know why those docs were so adamant you take a statin. Many had to meet their quotas to keep getting Big Pharma swag.

Dr. John Abramson, a Harvard physician who often testifies as an expert witness in litigation agains drug companies, makes the following case against statins, which is the same case I’ve made over the years in the pages of this blog. Statins don’t do anything for overall health and longevity. All they really do is trade one set of risk factors for another;

People are more than their cardiovascular system, and what we really want to do is improve people’s overall health, longevity and the risk of serious illness. If you look at overall health, we haven’t done anything for them. Now, do people want to take a statin to trade one cardiovascular event for some other very serious illness – in other words, no net benefit – and expose themself to the risk of harm from the statins? Do you want to do that? I think it’s a bad deal. If somebody has a particular fear of heart disease and says, ‘Look, I don’t care if I get diabetes, I don’t care if I have muscle symptoms, I don’t care if I can’t exercise the way I want to exercise, I do not want to have heart disease,’ fine, take a statin. But understand that that’s why you’re taking a statin, not because it’s going to improve your overall health.

If, after watching the show below, you want more info on not just statins, but other overprescribed drugs that have been shown to be useless or even harmful, take a look at Dr. Abramson’s book Overdosed America: The Broken Promise of American Medicine. If you are on any number of worthless prescription drugs, the info in this book can save you vast multiples of its modest cost.The book goes into much greater depth on the statin issue along with other commonly prescribed drugs in to a much greater extent than can be done in a half hour show. You will be as outraged after reading it as you will be after watching the show below.

Here is the take home message on statins:

Statins do not decrease all-cause mortality in the vast majority of people. Long-term studies have never been able to demonstrate that women of any age or with any degree of heart disease live longer by taking statins. The same long-term studies show that men over the age of 65 live no longer by taking statins. Men under 65 who have never had heart disease – and were talking actual heart disease here, not just an elevated cholesterol level – gain no longevity benefit from taking statins. The only small group of people who have been shown to benefit from statins are men under 65 who have had a heart attack. But unfortunately that benefit is small.

Multiple studies have shown that taking statins does reduce both the incidence and severity of heart attacks. But these same studies don’t show any increase in longevity for those taking statins (other than the small benefit for men under 65 who have had heart attacks). Why. Statins simply trade one risk for another. Take them and you reduce the risk of a heart attack but increase your risk for cancer, diabetes, kidney failure, and side effects related to the drugs themselves. Many people die each year from statin-induced side effects. Despite what anyone may tell you, statins are not benign drugs.

http://vimeo.com/78259209

Dr. Ernest Curtis, who is prominently featured in the show, wrote a terrific book on the world’s obsession with cholesterol titled The Cholesterol Delusion. Whenever I see statistics about the number of people taking statins, I’m haunted by a paragraph in this book considering the future that perhaps may await these individuals:

As severe as some of these short-term side effects can be [Dr. Curtis had been discussing statin side effects], they pale into relative insignificance when compared to the potential long-term problems. The chief difficulty here is that no one knows what the long-term effects may be from altering the basic biochemistry of the human body over a period of time. Because cholesterol is the key element in the formation of cell membranes, which are the protective coat for the cells, it may be that blocking cholesterol’s production will weaken the protective barrier and allow the entry of toxins or carcinogens that were previously excluded. There are disturbing reports of increased cancer in some cholesterol-lowering studies, but, in fact, this process make take many years to play out. It’s enough at this point to acknowledge that the long-term effects are completely unknown. This is a risk that should receive serious attention before half the population is placed on these drugs that, in effect, accomplish nothing more than low-dose aspirin or an extra glass or two of water each day.

A sobering thought.

Let me know of any stories you might have of doctors trying to force statins on you. Or of side effects you’ve experienced.

 

First of all, I am surprised there are not dozens of replies on this thread already. When more and more people of the world come to realize the impacts of statins, big pharma will have a lot of explaining to do. I personally never will take a statin drug, ever. I have a brother and sister who are dealing with polymyalgia as a result of statin drugs for two years. My sisters muscle pain and weakness started almost immediately. She was on the drug for three weeks before I convinced her to stop taking them. Unfortunately muscle wasting had already started and continued to get worse over the next year. She can hardly perform normal daily tasks to this day. They put her through a battery of tests, prednisone, methotrexate...same thing with my brother. He was on this new statin drug for almost 3 months before quitting.
People still wonder why I say absolutely no to statins so I try to explain the best I can what these drugs are doing, and practically beg them to at least take co q10 if they won't stop the statin. They don't know what to say when I tell them that cholesterol is fuel for the brain. And what about the fact that Merc has the patent on a drug that is a combo of a statin and co q10 - but won't exercise the patent as that would be an admission that statins deplete co q10?

And to really get them thinking, I add in the fact that I eat BUTTER, eggs, bacon, red meat, fish, avocado, foods high in good fats, I don't count calories or eat processed foods, flours, grains, and my cholesterol numbers from tests a couple weeks ago are the best results I have ever had. My LDL/HDL ratio is 2.1:1. My TC/HDL ratio is 3.5:1. My BP is 110/70. My trigs are 125 and my glucose is 87 ( which actually was higher than it was 2 yrs ago). So I choose to spend my $ on salmon and steak instead of useless drugs!

 

dietary cholesterol has nada to do with your serum level........another fallacy

 

For followers of Dr. Eades blog, it is old news. He has been writing eloquently against statins for years and years.

 

http://www.cnn.com/2013/11/12/health/cholesterol-guidelines/index.html

Why even bother to look at the numbers is apparently the new attitude. As a physician, this makes me ill.

 

I cringed today when I heard this news

New heart guidelines could put more Americans on statins

 

Yup, I get that but I do use my diet and serum levels to get others to begin to question what they believe to be true.

 

The Myositis Assn forum has a number of members whose polymyositis and dermatomyositis were triggered after they were prescribed statins. We used to laugh wryly, sadly, at that ad where the guy fell off the diving board because he wasn't on Lipitor. It took years for the pharm companies to put warnings about muscle weakness and wasting on their webpages. Patients were ridiculed for insisting that their symptoms had never occurred until after they began taking statins.

The other issue of cognitive effects was also denied. My elderly father, after years on lovastatin complained that he was always "confused." When the doc agreed to take him off, his confused faded (though he still had mild dementia). When another doc put him on simvastatin the confusion returned, then faded when we took him off again.

It's pathetic when these kinds of side effects don't come to light until enough sufferers complain loudly about them.

 

Heart of the Matter Part 2 - Cholesterol Drug War can be viewed at

 

I am a man under 65 (53) who had a heart attack 4 months ago resulting in a stent. I have been on Atorvastatin 40mg/day for the last 4 months.

From the research I can see that , at best, if I stay on this drug for 4.5 years it may extend my lifespan, not my health-span, by 5.3 days. WTF??

I really don't like how the drug works by blocking HMGCoA reductase - which many people know also affects CoQ10 and hence lowers ATP.

What many people - (including my GP) - do not know is that another effect of blocking that pathway is that it also blocks Mevalonate. This is the rate limiter for PCSK9 so PCSK9 and NARC1 are upregulated. This blocks the LDL receptors on the hepatocyte, thus defeating the increased expression of the LDL receptors associated with the statin.
https://www.ahajournals.org/doi/10.1161/01.atv.0000134621.14315.43

So why am I still taking it? There are other pleiotropic effects of the drug - some beneficial, some not. I'm doing my own research in order to make an informed choice rather than panic either way.#skininthegame

On the subject of trading one set of risks for another, here's something about how lipophyllic versus hydrophyllic statins double dementia risk.
https://jnm.snmjournals.org/content/62/supplement_1/102

 

oh BTW, Marianne Demasi started speaking on this subject again in 2018 after a long silence after the Catalyst show was shutdown due to pressure from the mainstream.

 

Sorry to hear about your heart attack.
I wish you the best.

For a long time, I have not seen your posts.
Wonder if you could keep posting your findings but especially the actions you will take.
That may be highly beneficial to some readers of this board.

On offhand I am thinking of using lumbrokinase.

...........

 

Hi JanSz,

Indeed I have not posted since 2018. Great to see you are still here.

Yes, my intention is to document my n=1 somewhere here for the benefit of myself and others. It will be a long story. At the moment I'm still compiling the history and the things I've learned so far. It will also highlight how n=1 becomes even more important when you are an outlier but get treated as if you are within the 1st or 2nd standard deviations of the medical bell curves. I'll also document and take responsibility for my own actions contributing to my heart attack. It will be quite the story.

Currently, since returning to a LCHF diet with intermittent fasting ranging between 18:6 and OMAD (one meal a day) I feel absolutely fantastic despite the myriad medications. Mental acuity has also been a byproduct of the increased autophagy IF brings, so that is helping immensely with researching.

It was while researching familial hypocholesterolaemia and PCSK9 inhibitors that I found out about statins up-regulating PCSK9 by blocking mevalonate. My GP used to work for the Heart Foundation and he was unaware of this. He said they had tested the PCSK9 inhibitors and found little benefit so they aren't available in New Zealand - but as it turns out, they only tested them combined with statins - not separately. Interstingly, the research I linked above shows that this upregulating of PCSK9 is very dose dependent.


4 months of Atorvastatin has had absolutely no impact on my lipid panel. Of course, my cardiac support nurse first suspected I wasn't taking them, then her suggestion was to double the dose Turns out it might work better at a lower dose, not a higher one - not that Im concerned about LDL absolute levels. I'm more interested in LDL particle size distribution.

 

My last Spectracell test (Feb 12/2021) shows some excessive LDL, most of which is large.

 

Nice profile!! Exactly what I'm aiming for.

At the risk of deviating from the thread subject . . . .

They don't test that deeply in New Zealand. Fortunately I found some info that can give an idea using information from a standard lipid panel.
https://drive.google.com/file/d/1BkwVMhAxsUL68rVvu3bX-9E5NhCB9Pgf/view?usp=sharing

Those charts are screenshots from this presentation by Dr. Paul Mason. Go to time 9:35 and then 16:12 of the video.


. . and the research the charts are based on is here . . .
https://www.ahajournals.org/doi/pdf/10.1161/01.CIR.82.2.495
https://care.diabetesjournals.org/content/diacare/23/11/1679.full.pdf

 

I will have to tell my doctor about this golden nugget
time 24:24 on the video in your post above:
fasting increases LDL because it lowers insulin
my fasting insulin is rather low at the time blood was drawn for the test.

 

Anyhow,
I got the impression that possibly except for triglyceride,
any discussion about (high) cholesterol always leads to the use of a variety of statins.
We as patients are looking for health, in this instance for clean or cleaner arteries.
A doctor is looking for an excuse to sell statins.

The status of arteries can be checked using the Agatston Calcium score.
Lumbokinase is the only thing that I have seen about having tests being mentioned where arteries clearance was somewhat reversed.
That was somewhere at Jeffrey Dach MD website where he talks about
====================================================================================


https://forum.jackkruse.com/index.php?threads/pg-e2-ratio.6427/page-7#post-247017

This thing dissolves plaque.

https://jeffreydachmd.com/2018/06/fibrinolytic-proteolytic-enzymes-medical-use/

Lumbrokinase was useful in treatment of Ischemic Stroke, angina, myocardial ischemia, deep venous thrombosis, hypertension, vascular dementia and hypercoagulation-associated complications.

Nutricology Lumbrokinase, Capsules, 60-Count (synthetic)
https://smile.amazon.com/Nutricolog...8&qid=1534083552&sr=8-3&keywords=Lumbrokinase

Boluoke 120 Count (natural)
https://smile.amazon.com/Canada-RNA...oluoke+120+capsules&psc=1&smid=A2H5B2ZO5OI7LQ

-----
“serrapeptase is not considered a strong fibrinolytic enzyme and should primarily be used for inflammation and pain association with oral/facial surgeries, sinus infection, arthritis, or chronic airway diseases. Respectively, nattokinase and lumbrokinase would be more suited for patients with mild and severe hypercoagulation or for patients with low and high cardiovascular risks.” Quote from (27)

-------
Proteolytic Enzymes Dissolve Biofilms – Assist Antibiotics

A number of studies show that proteolytic enzymes enhance antibiotic effects by breaking up biofilms. The enzymes are useful add-ons for antibiotic treatment of infectious micro-organisms known to produce bio-films.

-----------
https://amzn.to/2MWTffU
Lumbrokinase

https://amzn.to/2MStkWQ
Nattokinase

https://amzn.to/2MUpKeJ
Serrapeptidase

-----------------
================================================================
https://forum.jackkruse.com/index.php?threads/pg-e2-ratio.6427/page-7#post-248600

 

Bringing this back on topic, I'll attempt to show below how and why a statin can be ineffective in lowering LDL when on a low carbohydrate diet . . . .

Here is my lipid panel taken in Feb 2021 immediately post myocardial infarction.
Total 5.3 mmol/L
Triglyceride 1.2 mmol/L
HDL Cholesterol 1.18 mmol/L
LDL Cholesterol - calculated 3.6 mmol/L

Here is my lipid panel 4 months later in June 2021 after 4 months on Atorvastatin at 40 mg/day
Total 5.8 mmol/L
Triglyceride 1.6 mmol/L
HDL Cholesterol 0.98 mmol/L
LDL Cholesterol - calculated 4.1 mmol/L

Note that every aspect got worse!!!

In the few days before the June blood test I switched to LCHF. The Feldman protocol shows how this can cause a high LDL result.


@JanSz A lot to go through in your post. Thank you.

Reducing/reversing arterial plaque can be done by elevating HDL (reverse cholesterol transport) and by up-regulating autophagy (recycling of damaged/broken/unnecessary tissue). I'm using intermittent fasting to up-regulate autophagy.


Rapamycin can also up-regulate autophagy.

https://www.nature.com/articles/cdd2008110

However, I would rather use an endogenous process to accomplish that than an exogenous one because there is a risk of making the plaques unstable if it happens too rapidly. Apparently plaque stabilization is one of the pleiotropic effects of statins. Another pleiotropic effect is as an anti-inflammatory which still happens at very low doses.

 

Cholesterol – what is it, what does it do and why has it been demonized over the last 160 years by medicine and now functional, integrated medicine and naturopathic communities?

From the very small interactions within human cells to gross human biological functions, cholesterol is vital in every step. Cholesterol is a component of the phospholipid bilayer and is vital in the construction healthy cellular structure and all membrane functions. So, what is it? -> Cholesterol is a steroid hormone lipid-protein. It is the basic building block for all our hormones. https://www.ncbi.nlm.nih.gov/books/NBK513326/

When investigating any human biological function, what is important to understand is the mechanism of action. Since cholesterol is a fundamental biologically molecule for all steroid hormones, let’s take a look into how cholesterol is used for some of them.

“Vitamin” D is a human hormone - https://courses.lumenlearning.com/wm-biology2/chapter/vitamin-d-synthesis/#:~:text=In the presence of sunlight,the vitamin) in the kidneys.

https://vdmeta.com -> real-time analysis in 84 studies -> Sunlight is an effective treatment for COVID-19.

When UVB solar light penetrates our derma, the free cholesterol under the skin begins its first transformation to cholecalciferol. Cholecalciferol is shuttled from the lymph to the blood; however, it must be converted in the liver and kidneys into 25-hydroxyvitamin D. This does not always work so well. We know “vitamin” D is vital for immune function. However, so many people are “vitamin” D deficient. There are three main reasons. 1) Their free cholesterol is too low 2) They do not get proper UVB solar exposure 3) They have liver &/or kidney dysfunction. There are now thousands of articles on this subject. Here is one to start with: “Sunlight & Vitamin D” - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3897598/

Since cholesterol is the precursor for all endogenous human sex steroid biosynthesis, its deficiency may be obvious.


http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/basics/steroidogenesis.html

Let’s start with testosterone. Free cholesterol must be converted into pregnenolone and progesterone, which are sequentially converted to DHEA. DHEA must then be converted by the 5α-androstanedione pathway into the sex hormone testosterone. The metabolism of these biofluids is greatly influenced and hindered by cholesterol-lowering herbs (such as red yeast extract) or statins which destroy this pathway.

Let’s step through this: Within our mitochondria’s inner membrane, a cytochrome enzyme called P450scc oxidoreductase (CYP11A1), cholesterol is converted into pregnenolone by the electron-donated redox in the ATP synthesis.

The ATP electrons are transported to microsomal forms (i.e. cytochrome P450). It begins by the acceptance of electrons from NADPH. These negatively charged electrons (from NADPH) to the ferredoxin (Fedx) reductase (FeRed) which are used by P450 to convert cholesterol to pregnenolone. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3365799/

So, what could go wrong with that? -> Cytochrome enzyme P450 deficiency. It turns out P450 is dependent on DHEA which facilitates the flow of electrons to P450. This translates to an inability of P450 to convert progesterone, resulting in hyponatremia, hyperkalemia, acidosis, hypertension, and high concentrations of cortisol.

What is interesting is our mitochondria’s cytochrome enzyme P450 is also used in the process to convert 17α-hydroxypregnenolone to DHEA. This process also uses the NADPH pathway as described above. https://www.researchgate.net/public...released_intermediate_17a-hydroxypregnenolone

And wonders of wonders DHEA conversion by the 5α-androstanedione pathway into the sex hormone testosterone is also metabolized within the cytochrome enzyme P450. https://sci-hub.se/10.1023/a:1007124417566

Once the cholesterol molecule has been “rebirthed”, the now testosterone molecule is bathed in cholesterol, adding rich cholesterol receptors onto the testosterone molecule. If this process “fails” or is diminished, the testosterone molecule will not have the cholesterol’s protective mechanism and will fall subject to DHT degradation. https://academic.oup.com/jcem/article/84/9/3217/2864438, https://itestosterone.com/dht-hormone-benefits/ & why you shouldn’t block it.

So, what is interesting is -> the conversion of NADPH to NADP+ within the ferredoxin reductase “process” is very important, because it is where we get the “energy” electron transport to step the biosynthesis of the cholesterol molecule. And what is this primary energy conversion? -> it comes from sunlight into biomass oxygenic photosynthesis. https://earth.callutheran.edu/Academic_Programs/Departments/BioDev/omm/jsmolnew/fnr_fd/fnr_fd.html

But, but, wait a minute, photosynthesis is a plant “thing” right? We now know it’s a fundamental human thing too. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4125832/

For a nice overview: “Functional Characterization of Cytochrome P450 17A1 (CYP17A1) Gene Variants for their Steroidogenic Enzymatic Activities” - https://deepblue.lib.umich.edu/bitstream/handle/2027.42/120831/ccapper_1.pdf?sequence=1

Let’s take a look into this NADPH to NAD+ mitochondria process. NADPH oxidases (Nox) enzymes comprise around 500 amino acids. These lipid proteins are activated by – drum roll please – cholesterol & arachidonic acid (AA). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4221629/ It is well known that Nox2 is not only expressed in macrophages and neutrophils, but also in somatic tissues like epithelial cells through the COX pathway. https://link.springer.com/article/10.1007/s10354-018-0640-4 We know NAD+ is the central role of energy transduction within the mitochondria.

The problem with most of these studies, however, is the basic belief that glycation is fundamental. This creates presupposition that carbohydrates are the primary biological fuel for all living forms – (insects to humans). Let’s just start with this figure above, watch the arrows, it all begins with Glucose which makes its way up to NAD+ then to Pyruvate, which is used to make NAD+ again, which is used in the TSA Cycle beginning with Acetyl-CoA. The next great cycle of glucose is through the Glutamate & Citrate process to NAD+. Ok, so what? -> reactive oxygen species (ROS). It is reactive α,β-dicarbonyl species such as methylglyoxal and glyoxal, which are up to 50,000-fold more reactive than glucose. Glycation takes place in the extracellular environment, in our cells, in the cytosol, in organelles, starting from our mitochondria. As total available glucose availability increase this “little mitochondrial motor” will rev up, producing advanced glycation species (AGS) https://www.hindawi.com/journals/ijcb/2012/843505/

Of course, cell damage occurs from advanced glycation species as it oxidizes everything in its path. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3556769/, https://www.nature.com/articles/s41598-017-04214-6 This proinflammatory chemistry takes its toll. There are no chronic diseases which do not have its roots in “inflammation”. C-Reactive Protein (CRP) is one of our liver’s responses to glycation.

So, what does all that have to do with cholesterol?
mCRP selectively binds to low density lipoprotein (LDL), specifically, very low-density lipoproteins (VLDL). It is in this form that cholesterol becomes the “coolant” anti-inflammatory agent. This form of cholesterol chemically reduces the reactive oxygen species through the process we understand to be the redox potential. However, the cholesterol is damaged in the process when it takes on oxidation and it is converted into oxidized LDL (ox-LDL). To restate it a little more “scientifically” -> The microenvironmental pH at the inflammation site plays a key role in the binding of CRP to lipoproteins, as the binding site for ox-LDL is only revealed after modifications in the structure of CRP triggered by acidic milieus. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4897210/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3315351/ Take a read of “Oxidized LDL might actually be 'good guy'” - https://www.sciencedaily.com/releases/2014/09/140904121247.htm

Ox-LDL attracts white blood cells (monocytes-derived macrophage) and immune cells which engulf ox-LDL and shuttle them through the lymph and blood to the liver for processing and excretion. https://www.mdpi.com/2227-9059/8/8/262/pdf

Ok, so cholesterol is the first at the scene of an inflammatory event. It is our innate anti-inflammatory molecule. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5986484/ For example:

Plasma PAF-AH (Lp-PLA2) mainly plays an anti-inflammatory role in leukocyte/platelet/endothelium activation and seems to suppress atherogenic changes in plasma lipoproteins (such as LDL) by promoting the catabolism of PAF and by removing oxidised phospholipids present in Ox-LDL, including oxidized phospholipids that mimic PAF, which are generated by oxidative modifications of lipoproteins such as LDL during pro-atherogenic and atherosclerotic events.

Let’s look at glucocorticoids - they are cholesterol-derived steroid hormones synthesised and secreted by the adrenal gland. Glucocorticoids are anti-inflammatory in all tissues, and control metabolism in muscle, fat, liver and bone. They also affect vascular tone, and in the brain influence mood, behaviour and sleep‒wakefulness cycles. https://www.endocrinology.org/endoc...cocorticoids-restoring-balance-during-stress/ Glucocorticoids bind DNA and recruit coactivate and/or corepressor proteins to increase and/or decrease DNA-bound transcription factor expression and regulation.

For example, liver-specific transcription factors such as HNF4 (hepatocyte nuclear factor 4) facilitate GR binding to (and regulation of) metabolic genes, whereas macrophage-specific transcription factors such as PU.1 recruit GR to genes important in immunity.

Glucocorticoid responses are therefore fine-tuned to consider context. This is how glucocorticoids can control metabolism in livmer, activation of macrophages, and promote death of T-cells.

Glucocorticoids modulates the mTOR pathway in the Hippocampus - https://academic.oup.com/endo/article/153/9/4317/2424070
Glucocorticoids plays an important role in BDNF-induced neurotransmitter and neuron survival. – https://www.ncnp.go.jp/nin/guide/r3/staff/numakawa_files/bmc-2012-0012.pdf

Cholesterol behaves more like an antioxidant - https://sci-hub.se/10.1016/0891-5849(91)90187-8

Cholesterol antioxidant mechanism is a bio-chemical redox interaction intracellular and exocellular. Cholesterol enhances antioxidant activity of alpha-tocopherol in liposomes. Cholesterol decreases lipid peroxidation and echinocyte formation. https://www.revespcardiol.org/en-the-antioxidant-function-high-density-articulo-13062946 HDL's function as an LDL antioxidant. Cholesterol is a brain antioxidant – protecting brain cells against the ravages of free radicals. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2900496/ The list maybe endless, however, just as all antioxidants whether it is vitamin E or other antioxidant molecule, they give up their negative electrons (-e) “trying” to fix the inflammatory issue through the bio-chemical redox process; they too become damaged and must be removed through autophagy.

So, we’ve started off with cholesterol converting to “vitamin” D, then we went to one of the sex hormones. What’s next:

Oxytocin receptors are rich in cholesterol protective molecules - https://pubmed.ncbi.nlm.nih.gov/10785367/

o Because they are strongly steroid dependent - https://pubmed.ncbi.nlm.nih.gov/12436925/

o http://www.allnaturaladvantage.com.au/home/wp-content/uploads/2014/11/Oxytocin-and-Cholesterol

• This cholesterol steroid is found throughout the body including the brain facilitating the electrical activity neurons.
• Cholesterol is used by the body as communication messengers throughout all neurotransmitters.
• Cholesterol is synthesized in large amounts to form the myelin that surrounds the axons.
• Cholesterol is transported to neurons in the form of Apo E complexes in discoidal HDL-like particles, for which seven main receptors have been identified in brain cells that take up cholesterol from these lipoproteins. Apo E is synthesized in the brain, and its transcription is regulated by 24-hydroxy-cholesterol concentrations.
• In the brain and central nervous system, cholesterol synthesis is regulated independently of that in peripheral tissues, mainly by forms of the liver X receptor (LXR).
• Cholesterol and oxysterols are involved in providing neuroprotective effects and lowering neuroinflammation, dysregulation of their concentrations has been noted in many neurodegenerative disorders.
• Most of the lipoproteins in cerebrospinal fluid differ from the nascent poorly-lipidated HDL secreted by astrocytes, suggesting that the latter are modified during maturation.
• Cholesterol esters are major constituents for the adrenal glands.
• Cholesterol is a component of the phospholipid bilayer and is vital in the construction healthy cellular structure and membrane function.

o Cholesterol diffuses across the lipid bilayer of the plasma membrane of all cells and adhere to intracellular receptors within the cytoplasm, organelles and nucleus. It signals pathways for regulation of gene expression and synthesis of mRNA.

From the very small interactions within human cells to gross human biological functions, cholesterol is vital in every step. It is very anti-inflammatory. Nature uses it to “calm” the fire of inflammation in our body. It is often “the first responder at the scene of the crime”. Whether, it’s a cardiovascular issue, metabolic issue, digestive issue, brain or cognitive issue, muscle tissue injury, cholesterol is there in its various forms to mediate and facilitate healing.

Ok, so cholesterol is needed. How did it get villainized?
Over 160 years ago, a hypothesis arose that cholesterol was blamed as the primary reason for cardiovascular disease. It was affirmed, in 1856, by Rudolf Virchow who described atherosclerotic plaque as fundamentally comprised of the molecule cholesterol (C27H460). Then the home-run for this hypothesis was headed up by Dr. Ancel Keys with the “China Study” also known as the Seven Countries Study. Dr. Keys “cherry picked” the data and with a little “statistical license”, he “proved” cardiovascular disease was associated with cholesterol.

In the 1950s, the pathway for cholesterol synthesis in the body had four stages: 1) condensation of three acetate units to form a six-carbon intermediate, mevalonate; (2) conversion of mevalonate to activated isoprene units; (3) polymerization of six 5-carbon isoprene units to form the 30-carbon linear squalene; (4) cyclization of squalene to form the steroid nucleus, with a further series of changes to produce cholesterol.

In the 1960s, many drug companies pursued R&D money for identify molecules which could inhibit the synthesis of cholesterol from acetyl-coenzyme A (CoA). In 1979, Merck isolated a statin first called mevinolin (then lovastatin), which had a structure similar to compactin from the fungus Aspergillus terreus. Since then, statin drugs have become one of the largest profitable medical products.

But let’s step back a moment in time to Dr. Ancel Keys and let’s look at one of his disciples - Dr. Ivan Frantz. He developed and conducted a study called the Minnesota Coronary Experiment. In this study, he controlled for “saturated fat” and “vegetable oil”. He recruited seven institutions (hospitals). Patients were separated into matched groups and given either the “saturated fat” diet or the “polyunsaturated fat” diet. The only food the patients got was delivered on trays by the hospital staff, and Frantz arranged the meals to look identical. The study was truly a randomized double-blind design. It went from 1968 to 1973. However, Frantz never published the results. It turns out that after Frantz’s death, the raw data was reviewed and published by Dr. Ransden in the British Medical Journal: “Available evidence from randomized controlled trials shows that replacement of saturated fat with linoleic acid effectively lowers serum cholesterol – but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease”.

Every study since Keys’ monumental success has had rich pharmaceutical support and wonder of wonders they all say cholesterol is associated with cardiovascular disease.