The Truth About Cholesterol

Cholesterol is one of the most feared molecules in the world today.

Yet new research shows it’s one of the most beneficial molecules for your health.

How does everyone have it so backwards?

How Did We Get Here?

Why did cholesterol get put into the penalty box? Three main studies damned cholesterol:

1) 1913 Russian study on rabbits showed that cholesterol caused lesions. 

2) Ancel Keys and his CORRUPT seven countries study showing a correlation b/w saturated fat & heart disease

3) A study in Framingham, MA 60 years ago claimed cholesterol led to heart disease [*].

All three ultimately led to the diet-heart hypothesis and Food Pyramid.

Cholesterol was the critical second link of the diet-heart hypothesis. The hypothesis was that saturated fat increased cholesterol. And based on the studies above, that cholesterol then caused heart disease.

Canola Oil marketed as Heart Healthy

After cholesterol was found to be present in artery walls in patients with heart disease, cholesterol was blamed as the cause of the disease.

But we convicted the wrong enemy.

The Truth About Cholesterol

All three studies used to convict cholesterol would turn out to be flawed and corrupt.

The 1913 study on cholesterol by the russian scientist was on rabbits. Rabbits are herbivores. Of course they react negatively to cholesterol.

Ancel Keys cherry picked seven countries out of 22. After including all the countries there was no correlation.

Percentage of Linoleic Acid Increased in the Last 25 Years

There was not a shred of truth in any of the three studies. 

A 30 year follow up to framingham actually showed a negative correlation between cholesterol and disease.

“There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years (11% overall and 14% CVD death rate increase per 1 mg/dL per year drop in cholesterol levels).” [*]

So of course the USDA and health authorities backtracked on their cholesterol recommendations and saturated fat vilification right…? Of course not. They doubled down and still recommend people limit saturated fat. 

Studies Confirm LDL and Total Cholesterol Are Not Risk Factors

Now that cholesterol has been rigorously tested, more studies continue to emerge that cholesterol is not predictive of heart disease.

In 1987, a thirty year follow up to the Framingham study was conducted — the study that crucified total cholesterol in the first place.

Those aged between 48 and 57 with cholesterol in the mid range (183-222 mg/dL) had a greater risk of heart attack than those with higher cholesterol.

They also found that “for each 1 mg/dL per year drop in serum cholesterol values, there is an 11% increase in both the overall death rate and the CVD death rate.” [*]

In fact, there are zero studies that show that high LDL is a risk factor, independent of triglyceride levels and HDL levels. [*]

What matters is the functioning of your lipid and energy transport system.

And a big reason why there is often a correlation between LDL, HDL and heart disease is because they are potentially indicative of a broken system.

And you know what? New scientific research confirms this.

There’s not a single randomized control trial that shows people with high LDL die younger. David Diamond has done some great work here.

In fact, some studies show that higher LDL-C is associated with equal or greater lifespan [*].

When it comes to total cholesterol, a study in Hawaii found the same. Having low cholesterol for a long time actually increases risk of death:

Study showing gluten increases intestinal permeability

Instead of continuing to dig their heels in, I do appreciate the honesty of the study above: “we have been unable to explain our results”.

Whoops.

This study from UCLA showed that 75% heart disease patients had LDL below 130 mg/dl — the level at which doctors prescribe statins.

List of Food Highest in Lectins

The above data shows that saturated fat can raise cholesterol. But no evidence has shown that, independent of other factors, high  cholesterol is a cause for concern.

New evidence continues to pile up that cholesterol alone is not the culprit when it comes to heart disease. And that lowering it is not necessarily beneficial (in fact in some cases it can cause more damage). 

In 2019, the BMJ reviewed 22 interventional trials and found that “‘The preponderance of evidence indicates that low-fat diets that reduce serum cholesterol do not reduce cardiovascular events or mortality” [*]

In the recently unearthed Minnesota Coronary  experiment researchers lowered cholesterol like they intended by 14%.

But this led to a “22% higher risk of death for each 30 mg/dL reduction in serum cholesterol”

This study was BURIED for 40 years.

2019 Study showing exposure to chemical glyphosate increases risk of cancer

Lastly, remember the seven countries study that blamed saturated fat and cholesterol for heart disease? Well Zoe Harcombe added in 290 more countries and the correlation flipped. Cholesterol actually becomes negatively correlated with heart disease.

2019 Trial Jury found carcinogenic glyphosate in burger

What BioMarkers Are Predictive of Heart Disease?

Yes, cholesterol is present in the artery walls of heart disease patients. 

But it’s because it was there to rescue their artery walls.

It’s like condemning firefighters for starting fires just because they’re present at all fires. The logic is completely backwards.

What matters is how the fire started in the first place.

LDL, the “bad cholesterol”, is not predictive alone. Of course not. Because it is not inherently harmful. It’s only indicative of an atherogenic environment when it’s coupled with inflammation and oxidation.

What is the signature of inflammation and oxidation?

It usually rears its head as high TG / HDL ratios and high fasting insulin.

In a recent study of 103,446 men and women, LDL levels showed very minimal effect on heart disease.

But an increase in triglycerides/HDL ratio doubled the risk of heart disease. [*]

Insulin resistant kool aid

High triglyceride/HDL ratios are indicative of high remnant cholesterol, which is a better indicator for heart disease than LDL alone [*].

Dave Feldman showed below that remnant cholesterol correlated highly with all cause mortality.

Study showing frustose group more insulin resistant and pre-diabetic after 8 weeks

And guess what is significantly associated with remnant cholesterol? Insulin resistance [*].

When it comes to biomarkers, I like to see:

– Total / HDL < 4

– TG / HDL < 1

– HDL > 40

– TG < 100

– Fasting insulin < 10

– Fasting glucose < 5 mmol/L

LDL, the “bad cholesterol”, is nowhere to be found…Why?

Big pharma can’t make money off the REAL predictive biomarkers

Make sure to also keep an eye on fasting insulin levels.

From the great Ivor Cummins: When insulin is low, high LDL particle count and high triglycerides don’t indicate that you’re at higher risk. [*]

But when insulin is high, the risk of high triglycerides and high LDL is magnified.

When fasting insulin is  >15 uU/mL, your risk of heart disease with the same triglyceride levels go up 6.7x. And with the same LDL-P levels, it increases 11x.

High LDL with high insulin is much more concerning than high LDL with low insulin.

Too Little Cholesterol is Worse Than Too Much

Cholesterol is an organic molecule found in cell membranes and most tissues. It’s in the food we eat and is naturally occurring within our bodies.

Of the cholesterol present, around 75% is created in our bodies, and 25% is ingested.

Cholesterol is one of the most vital compounds in our bodies. So vital that our bodies make around 3000 mg of it every single day. [*] We can’t leave it to chance to get it externally – it’s that important.

Without cholesterol, we would literally be dead.

Cells would disintegrate. We’d have no hormones, no brain function, and no muscles. Every cell membrane is constructed out of cholesterol.

All of the following critical body components are made from cholesterol: [*][*]

  • Estrogen
  • Testosterone
  • Cortisol (anti-inflammatory stress hormone)
  • Aldosterone (regulates salt balance)
  • Vitamin D
  • Bile (required for fat and vitamin absorption)
  • Brain synapses (neurotransmitter exchange)
  • Myelin sheath (insulates nerve cells)

Not having any cholesterol is MUCH worse than having too much of it.

Conclusion

Cholesterol is one of the most important molecules in your body. It is not a direct etiological agent in heart disease — it is merely correlative because it can indicate fundamental damage. 

Source: https://carnivoreaurelius.com/the-truth-about-cholesterol/

Video

Carbohydrates Are Major Cause Of High Triglycerides

Cause Of High Triglycerides E1421970213372

Triglycerides are fats that are found in the blood and they are normally healthy and contribute to important physiological processes. They are used by the body for energy and are used for the storage of it as well. They are also essential to the transport of cholesterol, necessary for brain and nerve health, throughout the body. However, sometimes the triglycerides levels in the blood can become too high, and this can lead to long term health complications like heart attacks and strokes. One major cause of high triglycerides comes in the form of foods that we eat every day.

Foods that are high in saturated fat are a big contributor to the buildup of excess triglycerides in the blood. And, foods high in triglycerides to begin with like oils and butters are also responsible for increasing triglyceride levels. But, there is another food source of these elevated levels in the form of carbohydrates, particularly simple carbohydrates. The body takes in carbohydrates and converts them into body fuel producing glucose. Extra glucose that the body does not use for energy purposes is stored in the form of fat. And therefore an excess of calories from simple sugar sources can lead to an excess of triglycerides in the body.

Essentially, the way in which simple sugars are a major cause of high triglycerides has to do with the way in which the body processes these so differently from complex carbohydrates. When foods rich in simple carbs are ingested, the body uses them for energy very quickly, and the result is a rapid rise in glucose levels in the bloodstream. The pancreas responds by upping its production of insulin. An overload of carbs that the body simply can not use all at once combined with a maximum capacity of the storage of glycogen can lead to the conversion of the excess glucose into triglycerides by the liver. These manufactured triglycerides are sent to fat cells. This relationship between triglycerides and sugar intake indicates the extreme connection between diet and maintaining healthy levels of blood fats, and shows how simple carbohydrates can be a key cause of high triglycerides.

High triglycerides can negatively impact the body in many different ways. And, the presence of higher than acceptable ranges can also indicate other issues with the blood fat levels within the body. Persons with elevated triglycerides also often have lower than desirable levels of HDL or “good” cholesterol, which can protect against heart disease. The cholesterol HDL ratio in these individuals can also be elevated. It is acceptable for the ratio of triglycerides to HDL cholesterol to be 2 or less (this number can be calculated by dividing the level of triglycerides by the total HDL). Higher ratios can often coincide with the presence of blood clotting disorders as well.

Higher than normal levels of bad cholesterol and triglycerides are associated with a significantly increased risk of both heart attacks and strokes. In fact, high triglycerides have been linked to a nearly thrice as likely chance of having a heart attack. It has been suggested that evaluating the levels of cholesterol and triglycerides within the body can be the best way to predict heart disease, furthering the importance of identifying these levels early and eliminating any known cause of high triglycerides and cholesterol.

High sugar foods should be avoided like a plague to eliminate the risk of elevated levels of triglycerides. Sweets like donuts and cakes as well as candies should be avoided by persons who have higher than desirable levels of the blood fats. Another often forgotten simple sugar based cause of high triglycerides is sugary beverages like soda and many fruit juices. Even diets that reduce or eliminate some food sources can be stymied by the incorporation of these sugary drinks. But, it is not just the tasty sweets that can be considered a cause of high triglycerides. Many foods that aren’t often thought of as necessarily bad for the body can be culprits too. White flour and white rice, for example, contain simple sugars that the body uses the same way it does the simple sugars from a candy bar. Complex carbohydrate choices are better substitutes for these such as brown rice and whole wheat flour.

The management of high triglycerides is typically a complex assortment of varied treatment methods including medical management and monitoring, lifestyle and dietary changes as well as sometimes the use of medications like fibrates and statins if necessary. Many people happily find however that reducing the dietary cause of high triglycerides has a dramatic impact on returning the levels of these blood fats to healthy levels, therefore dramatically decreasing the risk for serious and long term health complications.

References:
https://healthyeating.sfgate.com/conversion-carbohydrates-triglycerides-2218.html
http://www.yourmedicaldetective.com/

Source: https://triglycerideslevels.org/carbohydrates-are-major-cause-of-high-triglycerides/

The Straight Dope On Cholesterol

Welcome to a topic near and dear.

I’ve been planning to write at length about this topic for a few months, but I’ve been hesitant to do so for several reasons:

  1. To discuss it properly requires great care and attention (mine and yours, respectively).
  2. My own education on this topic only really began about 9 months ago, and I’m still learning from my mentors at a geometric pace.
  3. This topic can’t be covered in one post, even a Peter-Attia-who-can’t-seem-to-say-anything-under-2,000-word post.
  4. I feel a bit like an imposter writing about lipidology because my mentors on this topic (below) have already addressed this topic so well, I’m not sure I have anything to add.

But here’s the thing.  I am absolutely – perhaps pathologically – obsessed with lipidology, the science and study of lipids.  Furthermore, I’m getting countless questions from you on this topic.  Hence, despite my reservations above, I’m going to give this a shot.

A few thoughts before we begin.

  1. I’m not even going to attempt to cover this topic entirely in this post, so please hold off on asking questions beyond the scope of this post.
  2. Please resist the urge to send me your cholesterol numbers.  I get about 30 such requests per day, and I cannot practice medicine over the internet.  By all means, share your story with me and others, but understand that I can’t really comment other than to say what I pretty much say to everyone: standard cholesterol testing (including VAP) is largely irrelevant and you should have a lipoprotein analysis using NMR spectroscopy (if you don’t know what I mean by this, that’s ok… you will soon).
  3. This topic bears an upsettingly parallel reality to that of nutrition “science” in that virtually all health care providers have no understanding of it and seem to only reiterate conventional wisdom (e.g., “LDL is bad,” “HDL is good”).  We’ll be blowing the doors off this fallacious logic.

By the end of this series, should you choose to internalize this content (and pick up a few homework assignments along the way), you will understand the field of lipidology and advanced lipid testing better than 95% of physicians in the United States.  I am not being hyperbolic.

One last thing before jumping in:  Everything I have learned and continue to learn on this topic has been patiently taught to me by the words and writings of my mentors on this subject: Dr. Tom DayspringDr. Tara DallDr. Bill Cromwell, and Dr. James Otvos. I am eternally in their debt and see it as my duty to pass this information on to everyone interested.

Are you ready to start an exciting journey?

Concept #1 – What is cholesterol?

Cholesterol is a 27-carbon molecule shown in the figure below. Each line in this figure represents a bond between two carbon atoms.  Sorry, I’ve got to get it out there.  That’s it.  Mystery over.

All this talk about “cholesterol” and most people don’t actually know what it is.  So there you have it.  Cholesterol is “just” another organic molecule in our body.

Cholesterol molecule

I need to make one important distinction that will be very important later.  Cholesterol, a steroid alcohol, can be “free” or “unesterified” (“UC” as we say, which stands for unesterified cholesterol) which is its active form, or it can exist in its “esterified” or storage form which we call a cholesterol ester (“CE”).  The diagram above shows a free (i.e., UC) molecule of cholesterol.  An esterified variant (i.e., CE) would have an “attachment” where the arrow is pointing to the hydroxyl group on carbon #3, aptly named the “esterification site.”

Since cholesterol can only be produced by organisms in the Animal Kingdom it is termed a zoosterol. In a subsequent post I will write about a cousin of cholesterol called phytosterol, but at this time I think the introduction would only confuse matters.  So, if you have a question about phytosterols, please hang on.

Concept #2 – What is the relationship between the cholesterol we eat and the cholesterol in our body?

We ingest (i.e., take in) cholesterol in many of the foods we eat and our body produces (“synthesizes”) cholesterol de novo from various precursors.   About 25% of our daily “intake” of cholesterol – roughly 300 to 500 mg — comes from what we eat (called exogenous cholesterol), and the remaining 75% of our “intake” of cholesterol — roughly 800 to 1,200 mg – is made by our body (called endogenous production).  To put these amounts in context, consider that total body stores of cholesterol are about 30 to 40 gm (i.e., 30,000 to 40,000 mg) and most of this resides within our cell membranes.  Every cell in the body can produce cholesterol and thus very few cells actually require a delivery of cholesterol. Cholesterol is required by all cell membranes and to produce steroid hormones and bile acids.

Of this “made” or “synthesized” cholesterol, our liver synthesizes about 20% of it and the remaining 80% is synthesized by other cells in our bodies.  The synthesis of cholesterol is a complex four-step process (with 37 individual steps) that I will not cover here (though I will revisit), but I want to point out how tightly regulated this process is, with multiple feedback loops.  In other words, the body works very hard (and very “smart”) to ensure cellular cholesterol levels are within a pretty narrow band (the overall process is called cholesterol homeostasis).  Excess cellular cholesterol will crystalize and cause cellular apoptosis (programmed cell death). Plasma cholesterol levels (which is what clinicians measure with standard cholesterol tests) often have little to do with cellular cholesterol, especially artery cholesterol, which is what we really care about. For example, when cholesterol intake is decreased, the body will synthesize more cholesterol and/or absorb (i.e., recycle) more cholesterol from our gut. The way our body absorbs cholesterol is so amazing, so I want to spend a bit of time discussing it.

In medical school, whenever we had to study physiology or pathology I always had a tendency to want to anthropomorphize everything. It’s just how my brain works, I guess, and understanding cholesterol absorption is a great example of this sort of thinking.  The figure below, from the Gastroenterology Journal, shows a cross-section of a cell in our small intestine (i.e., our “gut”) called an enterocyte that governs how stuff in our gut actually gets absorbed.  The left side with the fuzzy border is the side facing the “lumen” (the inside of the “tube” that makes up our gut).  You’ll notice two circles on that side of the cell, a blue one and a pink one.

[What follows is a bit more technical than I would have liked, but I think it’s very important to understand how this process of cholesterol absorption works.  It’s certainly worth reading this a few times to make sure it sinks in.]

Enterocyte cell
  • The blue circle represents something called a Niemann-Pick C1-like 1 protein (NPC1L1).  It sits at the apical surface of enterocytes and it promotes active influx(i.e., bringing in) of gut luminal unesterified cholesterol (UC) as well as unesterified phytosterols into the enterocyte.  Think of this NPC1L1 as the ticket-taker at the door of the bar (where the enterocyte is the “bar”); he lets most cholesterol (“people”) in.  However, NPC1L1 cannot distinguish between cholesterol (“good people”) and phytosterol (“bad people” – I will discuss these guys later, so no need to worry about it now) or even too much cholesterol (“too many people”). [I can’t take any credit for this anthropomorphization – this is how Tom Dayspring explained it to me!]
  • The pink circle represents an adenosine triphosphate (ATP)-binding cassette(ABC) transporters ABCG5 and ABCG8.  This complex promotes active efflux (i.e., kicking out) of unesterified sterols (cholesterol and plant sterols – of which over 40 exist) from enterocytes back into the intestinal lumen for excretion.  Think of ABCG5,G8 as the bouncer at the bar; he gets rid of the really bad people (e.g., phytosterols as they serve no purpose in humans) you don’t want in the bar who snuck past the ticket-taker (NPC1L1).  Of course in cases of hyperabsorption (i.e., in cases where the gut absorbs too much of a good thing) they can also efflux out un-needed cholesterol.  Along this analogy, once too many “good people” get in the bar, fire laws are violated and some have to go. The enterocyte has “sterol-excess sensors” (a nuclear transcription factor called LXR) that do the monitoring and these sensors activate the genes that regulate NPC1L1 and ABCG5,G8).

There is another nuance to this, which is where the CE versus UC distinction comes in:

  • Only free or unesterified cholesterol (UC) can be absorbed through gut enterocytes.  In other words, cholesterol esters (CE) cannot be absorbed because of the bulky side chains they carry.
  • Much (> 50%) of the cholesterol we ingest from food is esterified (CE), hence we don’t actually absorb much, if any, exogenous cholesterol (i.e., cholesterol in food).  CE can be de-esterified by pancreatic lipases and esterolases – enzymes that break off the side branches and render CE back to UC — so some ingested CE can be converted to UC.
  • Furthermore, most of the unesterified cholesterol (UC) in our gut (on the order of about 85%) is actually of endogenous origin (meaning it was synthesized in bodily cells and returned to the liver), which ends up in the gut via biliary secretion and ultimately gets re-absorbed by the gut enterocyte.  The liver is only able to efflux (send out via bile into the gut) UC, but not CE, from hepatocytes (liver cells) to the biliary system.  Liver CE cannot be excreted into bile. So, if the liver is going to excrete CE into bile and ultimately the gut, it needs to de-esterify it using enzymes called cholesterol esterolases which can convert liver CE to UC.
  • Also realize that the number one way for the liver to rid itself of cholesterol is to convert the cholesterol into a bile acid, efflux that to the bile (via a transporter called ABCB11) and excrete the bile acids in the stool (typically most bile acids are reabsorbed at the ileum).

Concept #3 – Is cholesterol bad?

One of the biggest misconceptions out there (maybe second only to the idea that eating fat makes you fat) is that cholesterol is “bad.”  This could not be further from the truth.  Cholesterol is very good!  In fact, there are (fortunately rare) genetic disorders in which people cannot properly synthesize cholesterol.  Once such disease is Smith-Lemli-Opitz syndrome (also called “SLOS,” or 7-dehydrocholesterol reductase deficiency) which is a metabolic and congenital disorder leading to a number of problems including autism, mental retardation, lack of muscle, and many others.

Cholesterol is absolutely vital for our existence.  Let me repeat: Cholesterol is absolutely vital for our existence. Every cell in our body is surrounded by a membrane.  These membranes are largely responsible for fluidity and permeability, which essentially control how a cell moves, how it interacts with other cells, and how it transports “important” things in and out. Cholesterol is one of the main building blocks used to make cell membranes (in particular, the ever-important “lipid bilayer” of the cell membrane).

Beyond cholesterol’s role in allowing cells to even exist, it also serves an important role in the synthesis of vitamins and steroid hormones, including sex hormones and bile acids.  Make sure you take a look at the picture of steroid hormones synthesis and compare it to that of cholesterol (above). If this comparison doesn’t convince you of the vital importance of cholesterol, nothing I say will.

One of the unfortunate results of the eternal need to simplify everything is that we (i.e., the medical establishment) have done the public a disservice by failing to communicate that there is no such thing as “bad” cholesterol or “good” cholesterol.  All cholesterol is good!

The only “bad” outcome is when cholesterol ends up inside of the wall of an artery, most famously the inside of a coronary artery or a carotid artery, AND leads to an inflammatory cascade which results in the obstruction of that artery (make sure you check out the pictures in the links, above). When one measures cholesterol in the blood – we really do not know the final destination of those cholesterol molecules!

And that’s where we’ll pick it up next time – how does “good” cholesterol end up in places it doesn’t belong and cause “bad” problems?  If anyone is looking for a little extra understanding on this topic, please, please, please check out my absolute favorite reference for all of my cholesterol needs, LecturePad. It’s designed primarily for physicians, but I suspect many of you out there will find it helpful, if not now, certainly once we’re done with this series.

To summarize this somewhat complex issue

  1. Cholesterol is “just” another fancy organic molecule in our body, but with an interesting distinctionwe eat it, we make it, we store it, and we excrete it – all in different amounts.
  2. The pool of cholesterol in our body is essential for life.  No cholesterol = no life.
  3. Cholesterol exists in 2 forms – UC and CE – and the form determines if we can absorb it or not, or store it or not (among other things).
  4. Most of the cholesterol we eat is not absorbed and is excreted by our gut (i.e., leaves our body in stool). The reason is it not only has to be de-esterified, but it competes for absorption with the vastly larger amounts of UC supplied by the biliary route.
  5. Re-absorption of the cholesterol we synthesize in our body is the dominant source of the cholesterol in our body. That is, most of the cholesterol in our body was made by our body.
  6. The process of regulating cholesterol is very complex and multifaceted with multiple layers of control.  I’ve only touched on the absorption side, but the synthesis side is also complex and highly regulated. You will discover that synthesis and absorption are very interrelated.
  7. Eating cholesterol has very little impact on the cholesterol levels in your body. This is a fact, not my opinion.  Anyone who tells you different is, at best, ignorant of this topic.  At worst, they are a deliberate charlatan. Years ago the Canadian Guidelines removed the limitation of dietary cholesterol. The rest of the world, especially the United States, needs to catch up.

Source: https://peterattiamd.com/the-straight-dope-on-cholesterol-part-i/

Video

Should You Be Worried About Cholesterol?

Cholesterol tends to spike on a carnivore diet. Should you be worried?

It’s permanently etched in most people’s brains that meat will spike cholesterol and cause heart disease. 

Since the 1950s, cholesterol, like saturated fat, has been feared. 

The first Google search for “steak and cholesterol” suggests we avoid steak because it raises cholesterol. 

Blood glucose and insulin

How did this happen? And should you really be worried?

How Did We Get Here?

Why did cholesterol get put into the penalty box? Three main studies damned cholesterol: 

1) 1913 Russian study on rabbits showed that cholesterol caused lesions. But rabbits are herbivores

2) Ancel Keys and his CORRUPT seven countries study showing a correlation b/w saturated fat & heart disease

3) A study in Framingham, MA 60 years ago claimed cholesterol led to heart disease [*].

All three ultimately led to the diet-heart hypothesis and Food Pyramid. 

Cholesterol was the critical second link of the diet-heart hypothesis. Ancel Keys came to the conclusion that heart disease tended to be related to cholesterol. And saturated fat tended to increase cholesterol. Therefore saturated fat and cholesterol caused heart disease. 

After cholesterol was found to be present in artery walls in patients with heart disease, cholesterol was blamed as the cause of the disease. 

But we convicted the wrong enemy.

Cholesterol was present in all heart disease patients because it was there to rescue their artery walls

It’s like condemning firefighters for starting fires just because they’re present at all fires. The logic is completely backwards. 

What matters is how the fire started in the first place. 

What is Cholesterol? We Can’t Survive Without It

Cholesterol is an organic molecule found in cell membranes and most tissues. It’s in the food we eat and is naturally occurring within our bodies. 

Of the cholesterol present, around 75% is created in our bodies, and 25% is ingested. 

Cholesterol is one of the most vital compounds in our bodies. So vital that our bodies make around 3000 mg of it every single day. [*] We can’t leave it to chance to get it externally – it’s that important. 

Without cholesterol, we would literally be dead. 

Cells would disintegrate. We’d have no hormones, no brain function, and no muscles. Every cell membrane is constructed out of cholesterol. 

All of the following critical body components are made from cholesterol: [*][*]

  • Estrogen
  • Testosterone
  • Cortisol (anti-inflammatory stress hormone)
  • Aldosterone (regulates salt balance)
  • Vitamin D
  • Bile (required for fat and vitamin absorption)
  • Brain synapses (neurotransmitter exchange)
  • Myelin sheath (insulates nerve cells)

Not having any cholesterol is MUCH worse than having too much of it. 

Insulin blocks fat burning

Studies Confirm Total Cholesterol Is Not an Issue

In 1987, a thirty year follow up to the Framingham study was conducted — the study that crucified total cholesterol in the first place. 

Those aged between 48 and 57 with cholesterol in the mid range (183-222 mg/dL) had a greater risk of heart attack than those with higher cholesterol. 

They also found that “for each 1 mg/dL per year drop in serum cholesterol values, there is an 11% increase in both the overall death rate and the CVD death rate.” [*]

Talk about shooting yourself in the foot. Not only was total cholesterol not predictive, it actually had a negative correlation. Low cholesterol increased risk. 

The last supporting thread of Keys’ diet-heart hypothesis should have been broken. 

But not so fast…

Scientists Shift Focus to Good and Bad Cholesterol

We’ve had a breakthrough in lipidology in recent years, and nutritionists have shifted their focus from total cholesterol to its constituent parts.

You’ve probably heard of LDL and HDL – often referred to by doctors as “good” and “bad” cholesterol. LDL was dubbed “bad” and HDL has been dubbed “good” because of a number of associational studies (i.e. studies closer to astrology than real science.)

In 1984 it was deemed an “irrefutable fact” that LDL (LDL-C for those following along) causes heart disease. 

Michael Brown and Joseph L. Goldstein, who won a Nobel Prize for their work, cemented this “fact”, declaring that the research “demonstrates unequivocally the causal relation between an elevated circulating LDL and atherosclerosis” [*]. 

Instead of focusing on total cholesterol, Brown and Goldstein convinced the medical establishment that LDL was the real cause of heart disease. 

Maybe the third time was the charm? 

Epidemiological studies around this same time also showed that low HDL levels were associated with higher heart disease risk [*], which forced some to acknowledge that maybe cholesterol wasn’t completely a villain after all.

But the segmentation into “good and bad” cholesterol is inaccurate. HDL and LDL both play important roles. Neither LDL or HDL are inherently good or bad. 

Dr. Peter Attia puts it best: 

“What’s bad is when good cholesterol ends up in places it’s not supposed to be.” [*]

Or said another way, good cholesterol becomes “bad” when it gets damaged by bad foods. 

What are HDL and LDL Anyway? 

Part of the confusion stems from what LDL and HDL actually are.

LDL and HDL aren’t even cholesterol, but energy transport vehicles that are partially composed of cholesterol [*].

A fat molecule repels water, and thus cannot travel through our largely water-based blood on its own. Cholesterol, along with other proteins, forms a floatie for fat to cling onto. 

These floaties are called lipoproteins. Think of them like cars that each fat molecule and nutrient can use to get to cells. All in all, they make up what is often referred to as the lipid transport system. 

Standard american diet causes weight gain

The ratio of lipid-to-protein determines its density. HDL is the most dense. And VLDL the least.

Despite the mixed results of studies, LDL has become the target of doctors who rush to prescribe drugs if LDL is over 190 mg/dL. 

Today, LDL, the notoriously “bad” cholesterol, is the target of the MASSIVE cholesterol suppressing statin industryLipitor has made Pfizer $125bn since 1997 [*]. 

This is a huge part of the reason why the world has been so slow to shift. $125bn is on the line. Of course they don’t want change. Sorry Pfizer.

But merely evaluating LDL levels distracts from the real story of what is biochemically occuring behind the scenes.

The Cholesterol Response To A High Fat Diet

This brings us to the carnivore diet. 

Like many nutritionists fear, people on the high-fat ketogenic diet often see their LDL cholesterol and total cholesterol rise.

Should you be concerned that the supposedly bad cholesterol is rising? What does the rising cholesterol really mean? 

Why Cholesterol Tends to Rise on a High Fat Diet

The Lipid Transport System

Dave Feldman has done a remarkable job breaking down the lipid energy transport system and cholesterol’s + lipoprotein’s crucial role. 

Going back to the car analogy, LDL is like a car, and the passengers are like the fat and nutrients.

LDL-P, in this case, are vessels that take fat (energy) to cells. 

HDL are the clean up crew. Sort of like draino for your blood vessels. 

High LDL levels is similar to having lots of cars on the street making lots of deliveries. Not necessarily a problem, and evident of a thriving ecosystem.

One reason why LDL tends to rise for healthy, active, low-carb-high-fat dieters is because more cars are simply needed to make more deliveries. 

Your body is both secreting and using more fat as energy. [*]

Remember: you either use fat or carbohydrates for energy. When you cut out carbohydrates, you need to deliver fat to your cells to survive. 

Think of it like a cab during New Year’s Eve. 

A lot of cabs are around, because there are more customers to use them. This doesn’t mean that the city is broken – it just means that more people need to get around.

In fact, as many of you have experienced, Dave Feldman also found that when metabolically healthy people switch to low carb, their cholesterol levels tend to rise. 

As you can see below from Dave Feldman, an improvement in body fat and metabolic health, actually led to an increase in cholesterol.

Insulin resistance is related to all chronic disease

What’s happening is that your body is secreting and using more of these LDL delivery boats. 

Because you’re metabolically healthy and not eating carbohydrates, your body needs to mobilize more fat as energy. And this is a big reason why these people are getting leaner. They should be celebrating their higher LDL numbers because it means they’re actually burning body fat for energy unlike their carb-ridden counterparts. 

LDL and HDL Aren’t Inherently Good or Bad

It’s a massive oversimplification to say that LDL is harmful because it puts cholesterol into the cell walls and thus should be feared. 

High LDL alone is not “bad”. Nor is high HDL “good”. 

Why would our bodies make any particles that inherently cause heart disease? If the particles were inherently bad, we should remove our brains because they’re signaling to make 3000mg+ a day. 

The particles on their own don’t cause heart disease. 

As Dave Feldman says, what causes plaques in arteries is not the particles themselves, but a broken energy delivery system.

This isn’t to say you shouldn’t be concerned about high LDL levels. Technically, in Peter Attia’s terms, heart disease occurs when LDL-P gets into your arteries, becomes inflamed, and plaques up [*]. 

But this doesn’t mean that LDL independently causes it. 

Studies Confirm LDL Alone Is Not an Issue

In fact, there are zero studies that show that high LDL is a risk factor, independent of triglyceride levels and HDL levels. [*]

What matters is the functioning of your lipid and energy transport system. 

And a big reason why there is often a correlation between LDL, HDL and heart disease is because they are potentially indicative of a broken system.

And you know what? New scientific research confirms this.

There’s not a single randomized control trial that shows people with high LDL die younger. David Diamond has done some great work here. 

In fact, some studies show that higher LDL-C is associated with equal or greater lifespan [*]. 

Low insulin speeds up metabolism

When it comes to total cholesterol, a study in Hawaii found the same. Having low cholesterol for a long time actually increases risk of death:

Fructose causes insulin resistance

Instead of continuing to dig their heels in, I do appreciate the honesty of the study above: “we have been unable to explain our results”. 

Whoops.

This study from UCLA showed that 75% heart disease patients had LDL below 130 mg/dl — the level at which doctors prescribe statins. 

Vegetable antinutrients cause insulin resistance

The above data shows that saturated fat can raise cholesterol. But no evidence has shown that, independent of other factors, high cholesterol is a cause for concern.

Lastly, remember the seven countries study that blamed saturated fat and cholesterol for heart disease? Well Zoe Harcombe added in 290 more countries and the correlation flipped. Cholesterol actually becomes negatively correlated with heart disease. 

Vegetable oils cause insulin resistance

It’s time to stop worrying about LDL, the “bad cholesterol”. 

So What Really Causes Heart Disease? 

As we’ve seen, high LDL levels on their own don’t cause heart disease. They’re not shooting into your artery walls for no reason. This is why LDL independently is not a good predictor for heart disease. 

Our bodies have been producing LDL cholesterol forever. But heart disease really only appeared in the last 100 years. It can’t be the LDL independently causing issues. 

With that being said, it doesn’t mean you should ignore LDL levels, Because high LDL can be indicative of a broken system. It’s seen in both high and low risk patients.  

And a broken system is what causes heart disease. 

Atherosclerosis is the disease caused by this lipid delivery cycle being broken. It’s when plaques start forming in your arteries.

When the cycle is broken, LDL cholesterol is usually high. But this doesn’t necessarily mean that high LDL is the sole cause.

Let me explain with the analogy. 

What’s bad is not if there are a lot of cabs around. It’s bad if the passengers – the energy – aren’t getting delivered to the proper places. Or if the vehicles themselves are damaged (oxidized), yet still driving.

When this happens, there is an underlying problem. Your immune system reacts and causes inflammation, which leads to plaquing. 

Damaged LDL is The Problem

There’s no such thing as “good and bad” cholesterol. What’s bad is when your cholesterol gets damaged (or oxidized). When it’s damaged, your immune system traps the damaged cholesterol in your artery walls to prevent it from doing even more damage elsewhere. 

High protein diet reverses insulin resistance

How do you damage your cholesterol particles? Sugar and vegetable oils. Two of the first things you cut out on the carnivore diet. 

Sugar does a couple of things to your cholesterol particles that cause problems: 

  1. Sugar tends to stick to your LDL lipoproteins, causing them to lose their motor functionality. [*] This is often referred to as oxidation or glycation.
  2. Sugar damages HDL, causing it to be rapidly cleared from the blood. [*]
  3. Triglycerides cannot be delivered to the cell because the fat cells are already full because of sugar, and are likely insulin resistant. 

Vegetable oils do something similar. LDL is more prone to oxidation when it contains unstable linoleic acid from seed oils. LA is the most common fatty acid from LDL. 

Once LDL is oxidized, LDL receptors no longer recognize it. Instead, the immune system takes over. When LDL is oxidized your body actually intentionally pulls it into your artery walls to prevent them from causing damage elsewhere [*

These damaged lipoproteins will then cause an inflammatory response, foam cells and plaquing. Macrophages basically ingest the modified LDL and turn into foam cells. Over time, multiple of these foam cells form fatty streaks together. 

If this damage continues long enough, muscle cells are attracted to the area to health the foam cells. This good faith attempt by the immune system ends up becoming atherosclerotic plaque. 

High fat diet reverses insulin resistance

Well, on the carnivore diet, you tend to have big fluffy and healthy cholesterol. It’s only when you damage LDL particles with sugar and vegetable oils, do they cause issues.

LDL Also Increases Because of Inflammation

Another reason LDL is often high when people have heart disease is because it’s indicative of an inflammatory environment. 

LDL plays an indispensable protective role. There’s a reason why we produce it. LDL is protecting you from disease, not causing it.

High intensity exercise reverses insulin resistance

Because of its protective role, LDL actually increases when there’s inflammation. LDL can bind to pathogens so that the immune system can expel them. 

So, the reason it’s high in those with heart disease is because LDL binds to pathogens. It’s getting rid of damage so that it doesn’t spread. 

LDL is protecting you from disease, not causing it. 

Siobhan Huggins does a great job dissecting this process here.

BMI and insulin resistance

What the mainstream thinks: LDL shoots into your artery and causes disease.

What really happens: LDL is recruited to heal inflammation and can be a sign of an atherogenic, inflammatory environment. It’s there to help, NOT cause disease.

Again, the causation here is backwards. LDL tends to be high in environments that are atherogenic. It’s not causing the inflammation. 

It’s your crappy diet causing disease.

What BioMarkers Are Predictive of Heart Disease? 

LDL, the “bad cholesterol”, is not predictive alone. Of course not. Because it is not inherently harmful. It’s only indicative of an atherogenic environment when it’s coupled with inflammation and oxidation. 

What is the signature of inflammation and oxidation? 

It usually rears its head as high TG / HDL ratios and high fasting insulin. 

In a recent study of 103,446 men and women, LDL levels showed very minimal effect on heart disease.

But an increase in triglycerides/HDL ratio doubled the risk of heart disease. [*]

Fed and fasted states controlled by insulin

High triglyceride/HDL ratios are indicative of high remnant cholesterol, which is a better indicator for heart disease than LDL alone [*]. 

Dave Feldman showed below that remnant cholesterol correlated highly with all cause mortality. 

Intermittent fasting and insulin

And guess what is significantly associated with remnant cholesterol? Insulin resistance [*].

When it comes to biomarkers, I like to see: 

– Total / HDL < 4

– TG / HDL < 1 

– HDL > 40

– TG < 100

– Fasting insulin < 10

– Fasting glucose < 5 mmol/L

LDL, the “bad cholesterol”, is nowhere to be found…Why? 

Big pharma can’t make money off the REAL predictive biomarkers

Make sure to also keep an eye on fasting insulin levels. 

From the great Ivor Cummins: When insulin is low, high LDL particle count and high triglycerides don’t indicate that you’re at higher risk. [*]

Intermittent fasting benefits

But when insulin is high, the risk of high triglycerides and high LDL is magnified. 

When fasting insulin is  >15 uU/mL, your risk of heart disease with the same triglyceride levels go up 6.7x. And with the same LDL-P levels, it increases 11x. 

High LDL with high insulin is much more concerning than high LDL with low insulin. 

Carbohydrates Also Damage the Arterial Defense Layer

What else causes heart disease? A damaged endothelial layer. 

Not only do carbohydrates lead to insulin resistance and high remnant cholesterol, they also damage your arterial defense system.

The image from Ivor Cummins below shows your glycocalyx, your first line of defense,before and after eating carbohydrates.

Carbohydrates destroy the arterial defenses. 

How You Can Start Getting Healthier Now

All in all, heart disease is much more complicated than “high LDL” shooting into arteries. It’s a complex interplay between inflammation, lipoprotein health,and overall metabolism. Be wary of people who simplify this. 

So how do you cut your heart disease risk? The three most important first steps are:  

  1. Lowering inflammation
  2. Ensuring the health of your lipoproteins 
  3. Increasing nutrient intake that heal blood vessels

The Carnivore diet is the best way to do so. 

Lowering Inflammation

The carnivore diet switches your body to fat based metabolism which is less oxidatively stressful and has been shown to lower inflammation. 

Glucose is oxidatively stressful, causes inflammation and can produce reactive oxygen species [*]. 

A study of 29 people found that those consuming just 40 grams of added sugar had an increase in inflammation, insulin resistance and weight gain [*].

The carnivore diet can also reverse leaky gut. Leaky gut increases inflammation because it allows foreign toxins into your bloodstream. Your immune system is mobilized to expel it, which creates inflammation. The carnivore diet cuts out antinutrients like Lectin and Gluten that pry the gut open. And it is also high in nutrients that reinforce the gut lining. 

Lipoprotein Health

As discussed above, LDL is only bad when it is oxidized. It only becomes oxidized when your diet is high in  polyunsatured seed oils and sugar. 

Unlike natural saturated fats, these oils are unsaturated and have more double bonds. The double bonds allow oxygen to sneak in and oxidize the fatty acids, particularly when heated. When “oxidized” they produce free radicals. Free radicals are electrons that play a role in every known disease.

They are unpaired electrons looking to find a match. In the process of doing so, they restructure every single cell they come into contact with. Think of them like a drunk person in a singles bar.

Cooking foods in vegetable oils blasts them with these free radicals which can destroy every cell in your body. It’s these oxidized lipoproteins and free radicals that cause your immune system to trap them in your artery wall. 

If you’re not convinced yet, here’s a revealing study.

The Sydney Heart Health study which was a randomized control trial that was supposed to support the AHA’s hypothesis ended up showing the disastrous consequences of vegetable oils. The group that replaced saturated fat with vegetable oils had a 62% higher death rate [*]. Of course this was buried.

Sugar also sticks to and glycates LDL. Glycation is the process by which glucose binds to a protein on the lipoprotein and damages the receptors your body uses to identify it [*].

Sugar and seed oils are the real enemy. NOT saturated fat, even though it increases your cholesterol. 

Increased Nutrient Intake

The carnivore diet is very high in nutrients that heal your artery wall and lipoproteins. 

One of the most risk factors for heart disease is artery wall calcification [*]. Vitamin K2 can reverse the calcification process. 

Vitamin K2 has the ability to scavenge calcium that’s deposited in your arteries and shuttle it back to where it’s supposed to be — your bones. But most people are deficient in this critical vitamin. 

One study showed that 360mcg of Vitamin K2 per day (taken as MKT) significantly improved artery health (reduced stiffness) [*].  

Vitamin K2 is only found in animal source foods. You can get it in high doses in beef liver and fermented dairy products like cheese. 

Additionally, the carnivore diet is high in antioxidants like Vitamin E, that can help lipoproteins resist oxidative damage. This study showed that Vitamin E significantly decreased LDL  and HDL susceptibility to damage [*]. Vitamin E is only found in animal source foods. 

Starting  to notice a pattern here…The Standard American Diet both damages your arteries and is low in nutrients that can help to heal them. 

Conclusion

You’ve been brainwashed into believing made up causes of heart disease:

– Steak

– Cholesterol

– Saturated Fat

But the real causes have nothing to do with these three. They are:

– Refined carbs

– Seed oils

– Oxidized LDL particles

– Inflammation damaging the glycocalyx

– High blood pressure

Too little cholesterol is WAY worse than too much. Lowering LDL too far is the fastest way to die.

Meat’s effect of raising cholesterol should be touted as a benefit, not a drawback. 

We’ve talked about a lot here, and I really hope that you get a lot out of this article. It wasn’t easy for me to learn all this information – it took me years to learn about these things and improve my own health.

It’s time to take back control.

Source: https://carnivoreaurelius.com/cholesterol-on-carnivore-diet/

Video

Cholesterol In Food

Cholesterol in food only has a small effect on the level of cholesterol in your blood.

Cholesterol is a fat found in your blood. It’s produced naturally in your body, and you can also get cholesterol from some foods.

High total blood cholesterol is a risk factor for heart disease. Find out more about blood cholesterol.

Worried about your cholesterol levels?

When it comes to your blood cholesterol levels, cholesterol in food is less important than eating less saturated and trans fats, and more healthy fats.

Cholesterol in food has only a small effect on the bad (LDL) cholesterol in your blood. Saturated and trans fats in food cause a much greater increase in LDL cholesterol. Eating healthy fats helps the cholesterol balance by decreasing LDL and increasing the good (HDL) cholesterol.

You can include some cholesterol-rich foods as part of a healthy balanced diet low in saturated fat. Cholesterol-rich foods include offal (e.g. liver, pâté and kidney) and prawns.

What about eggs?

Most people don’t need to worry about eggs and cholesterol. Eggs are very nutritious. They contain good quality protein, lots of vitamins and minerals, and healthier polyunsaturated fat. The dietary cholesterol in eggs has only a small effect on blood LDL cholesterol, so you can enjoy up to six eggs each week as part of a healthy balanced diet.

Read more about eggs

Learn more about blood cholesterol.

Source: https://www.heartfoundation.org.au/healthy-eating/food-and-nutrition/fats-and-cholesterol/cholesterol-in-food

Video

Does Stress Affect Your Cholesterol?

Introduction

High cholesterol can increase your chance of heart attack and stroke. Stress can do that as well. Some research shows a possible link between stress and cholesterol. 

Cholesterol is a fatty substance found in some foods and also produced by your body. The cholesterol content of food is not as noteworthy as the trans fats and saturated fats in our diets. These fats are what can cause the body to make more cholesterol.

There are so-called “good” (HDL) and “bad” (LDL) cholesterols. Your ideal levels are:

  • LDL cholesterol: less than 100 mg/dL
  • HDL cholesterol: more than 60 mg/dL
  • total cholesterol: less than 200 mg/dL

When bad cholesterol is too high, it can build up in your arteries. This affects how blood flows to your brain and your heart, which could cause stroke or heart attack.

Risk factors for high cholesterol

Risk factors for high cholesterol include:

  • family history of high cholesterol, heart problems, or strokes
  • obesity
  • diabetes
  • smoking tobacco

You might be at risk for high cholesterol because you have a family history of it, or you might have a family history of heart problems or strokes. Lifestyle habits can also have a big impact on your cholesterol levels. Obesity, defined as a body mass index (BMI) of 30 or higher, puts you at risk for high cholesterol. Diabetes can also damage the inside of your arteries and allow cholesterol to build up. Smoking tobacco can have the same effect.

If you’re 20 years old or older, and have not had a heart problem, the American Heart Association recommends that you have your cholesterol checked every four to six years. If you’ve already had a heart attack, have a family history of heart problems, or have high cholesterol, ask your doctor how often you should have a cholesterol test.

Stress and cholesterol link

There is compelling evidence that your level of stress can cause an increase in bad cholesterol indirectly. For example, one study found that stress is positively linked to having less healthy dietary habits, a higher body weight, and a less healthy diet, all of which are known risk factors for high cholesterol. This was found to be especially true in men.

Another study that focused on over 90,000 people found that those who self-reported being more stressed at work had a greater chance of being diagnosed with high cholesterol. This may be because the body releases a hormone called cortisol in response to stress. High levels of cortisol from long-term stress may be the mechanism behind how stress can increase cholesterol. Adrenaline may also be released, and these hormones can trigger a “fight or flight” response to deal with the stress. This response will then trigger triglycerides, which can boost “bad” cholesterol. 

Regardless of the physical reasons why stress can impact cholesterol, multiple studies show a positive correlation between high stress and high cholesterol. While there are other factors that can contribute to high cholesterol, it seems that stress can be one, too. 

Treatment and prevention

Coping with stress

Since there is a correlation between stress and cholesterol, preventing stress may help to prevent high cholesterol caused by it. 

Long-term chronic stress is more damaging to your health and cholesterol than brief, short-term periods of stress. Lowering stress over time can help to prevent cholesterol problems. Even if you can’t cut any stress from your life, there’s options available to help manage it. 

Coping with stress, whether brief or ongoing, can be difficult for many people. Coping with stress can be as simple as cutting out a few responsibilities or exercising more. Therapy with a trained psychologist can also provide new techniques to help patients manage stress. 

Exercise

One of the best things you can do for both stress and cholesterol is to get regular exercise. The American Heart Association recommends walking for about 30 minutes a day, but they also point out that you can get a similar level of exercise just by cleaning your house!

Of course, going to the gym is also recommended, but don’t put too much pressure on yourself to get in Olympic shape overnight. Start with simple goals, even short workouts, and increase activity over time.

Know what kind of exercise routine suits your personality. If you’re more motivated to do the same exercise at a regular time, stick with a schedule. If you get bored easily, then challenge yourself with new activities.

Healthy eating

You can also significantly affect your cholesterol levels by eating more healthfully.

Start by reducing the saturated and trans fats in your grocery cart. Instead of red meats and processed lunch meats, choose leaner proteins like skinless poultry and fish. Replace full-fat dairy products with low- or nonfat versions. Eat plenty of whole grains and fresh produce, and avoid simple carbohydrates (sugar and white flour-based foods).

Avoid dieting and focus on simple, incremental changes. One study showed that diets and severely reduced calorie intake were actually associated with increased cortisol production, which raises your cholesterol.

Medications and alternative supplements 

If reducing stress hasn’t sufficiently reduced high cholesterol, there are medications and alternative remedies that you can try.

These medications and remedies include:

  • statins
  • niacin
  • fibrates
  • omega-3 fatty acids

Whether using prescription medications or alternative supplements, always consult your doctor before making any changes to your treatment plan. Even if they’re natural, small changes in a treatment plan can interfere with medications or supplements you’re already taking.

Takeaway

There’s a correlation between high stress and high cholesterol, so whether your cholesterol levels are great or need lowering, maintaining a low stress level can be helpful. 

If stress is affecting your overall health, consult your doctor. They can advise you on an exercise program, a healthy diet, and medications if necessary. They may also refer you to a therapist to learn stress management techniques, which can be extremely beneficial.

Source: https://www.healthline.com/health/high-cholesterol/does-stress-affect-cholesterol