The Straight Dope on Cholesterol: 10 Things You Need to Know – Part 1
This is a guest post by Peter Attia and is a summary based on a 10-part series of the same name that you can find at The Eating Academy.
To put this summary post and, more importantly, this 10-part series in perspective, let’s examine one of the most pervasive pieces of dietary advice given to people worldwide:
“Eating foods that contain any cholesterol above 0 mg is unhealthy.”
- T. Colin Campbell, PhD, author of The China Study.
No summary of this length can begin to fully address a topic as comprehensive as cholesterol metabolism and the pathogenesis of atherosclerosis. In fact, those of us who challenge conventional wisdom often find ourselves needing to do exactly what Frederic Bastiat suggested:
“We must admit that our opponents in this argument have a marked advantage over us. They need only a few words to set forth a half-truth; whereas, in order to show that it is a half-truth, we have to resort to long and arid dissertations.”
So, at the risk of trying to minimize the “long and arid” part of this process, below are the 10 things you need to know to be the judge – for yourself – if the conventional advice about cholesterol is correct.
1. The sine qua non of atherosclerosis is the presence of a sterol in an artery wall. How it gets there is the only thing we should be worrying about.
Contrary to popular belief, atherosclerosis is not caused by many of things we think of, such as smoking, high blood pressure, diabetes, high LDL (the so-called “bad” cholesterol), or low HDL (the so-called “good” cholesterol). Some of these are certainly markers of risk – low HDL, for example – while others accelerate the process – smoking, for example – but none of these are the direct cause of atherosclerosis.
The sine qua non of atherosclerosis is the presence of sterols (cholesterol or phytosterol) in arterial wall macrophages. Sterols are delivered to the arterial wall by the penetration of the endothelium by an apoB-containing lipoprotein, which transport the sterols. In other words, unless an apoB-containing lipoprotein particle violates the border created by an endothelium cell and the layer it protects, the media layer, there is no way atherogenesis occurs. If this is a bit confusing, don’t worry. It’s all made clear below.
2. Cholesterol is vital for life; no cholesterol = no life.
Cholesterol is a 27-carbon molecule shown in the figure below. Each line in this figure represents a bond between two carbon atoms. 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.
I need to make one 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 below 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.”
One of the biggest misconceptions 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. One 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. 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 imperative for life to exist!
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!
3. The cholesterol we eat has little to do with the cholesterol we measure in our bloodstream.
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. Nearly 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, 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 and regulates cholesterol is really amazing, so I want to spend a bit of time discussing it.
- The blue circle in this figure 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” – for reasons I won’t discuss here) or even too much cholesterol (“too many people”).
- The pink circle in this figure represents a structure called the adenosine triphosphate (ATP)-binding cassette (ABC) transporters ABCG5 and ABCG8. This structure 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., 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).
- 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.
4. The cholesterol in our bloodstream has little to do with the cholesterol in our artery walls (i.e., atherosclerosis).
To understand how cholesterol travels around our body requires some understanding of the distinction between hydrophobic and hydrophilic. A molecule is said to be hydrophobic (also called nonpolar) if it repels water, while a molecule is said to be hydrophilic (also called polar) if it attracts water. Think of your veins, arteries, and capillaries as the “waterways” or rivers of your body. Cholesterol is precious “cargo” that needs to move around, but it needs a “boat” to carry it.
The proteins that traffic collections of lipids are called apoproteins. Once bound to lipids they are called apolipoproteins, and the protein wrapped “vehicle” that transports the lipids are called lipoproteins. Many of you have probably heard this term before, but I’d like to ensure everyone really understands their important features. A crucial concept is that, for the most part, lipids go nowhere in the human body unless they are a passenger inside a protein wrapped vehicle called a lipoprotein. As their name suggests, lipoproteins are part lipid and part protein. They are mostly spherical structures which are held together by a phospholipid membrane (which, of course, contains free cholesterol). The figure below shows a schematic of a lipoprotein.
You will also notice variable-sized proteins on the surface of the lipid membrane that holds the structure together. The most important of these proteins are called apolipoproteins, as I alluded to above. The apolipoproteins on the surface of lipoprotein molecules serve several purposes including:
- Assisting in the structural integrity and solubility of the lipoprotein;
- Serving as co-factors in enzymatic reactions;
- Acting as ligands (i.e., structures that help with binding) for situations when the lipoprotein needs to interact with a receptor on a cell.
Apolipoproteins come in different shapes and sizes which determine their “class.” Without getting into the details of protein structure and folding, let me focus on two important classes: apolipoprotein A-I and apolipoprotein B. ApoA-I is the apolipoprotein that wraps HDL particles. ApoB is the apolipoprotein that wraps VLDL, IDL, and LDL particles.
5. The only way sterols end up in artery walls – the one place we don’t want them to be – is if the sterols are carried there by an apoB-containing lipoprotein particle.
So what drives a LDL particle to do something as sinister as to leave the waterway (i.e., the bloodstream) and “illegally” try to park at a dock (i.e., behind an endothelial cell)? Well, it is a gradient driven process which is why particle number is the key driving parameter.
As it turns out, this is probably a slightly less important question than the next one: what causes the LDL particle to stay there? In the parlance of our metaphor, not only do we want to know why the boat leaves the waterway to illegally park in the dock with its precious cargo, but why does it stay parked there? This phenomenon is called “retention” in lipidology-speak.
Finally, if there was some way a LDL particle could violate the endothelium, AND be retained in the space behind the cell (away from the lumen on the side aptly called the sub-endothelial space) BUT not elicit an inflammatory (i.e., immune) response, would it matter?
I don’t know. But it seems that not long after a LDL particle gets into the sub-endothelial space and takes up “illegal” residence (i.e., binds to arterial wall proteoglycans), it is subject to oxidative forces, and as one would expect an inflammatory response is initiated. The result is full blown mayhem. Immunologic gang warfare breaks out and cells called monocytes and macrophages and mast cells show up to investigate. When they arrive and find the LDL particle, they do all they can to remove it. In some cases, when there are few LDL particles, the normal immune response is successful. But, it’s a numbers game. When LDL particle invasion becomes incessant, even if the immune cells can remove some of them, it becomes a losing proposition and the actual immune response to the initial problem becomes chronic and maladaptive and expands into the space between the endothelium and the media.
The multiple-sterol-laden macrophages or foam cells coalesce, recruit smooth muscle cells, induce microvascularization, and before you know it complex, inflamed plaque occurs. Microhemorrhages and microthrombus formations occur within the plaque. Ultimately the growing plaque invades the arterial lumen or ruptures into the lumen inducing luminal thrombosis. Direct luminal encroachment by plaque expansion or thrombus formation causes the lumen of the artery to narrow, which may or may not cause ischemia.
Check back tomorrow for Part 2 of The Straight Dope on Cholesterol: 10 Things You Need to Know
Posted By: Mark Sisson
Great post. Ive always wondered about the cholesterol in our bloodstream vs the cholesterol we eat. I had a pretty solid idea that they were not the same. I guess this post just confirms that for me. Love the eating academy also. It gets a little bit more into the science than MDA, but still gotta love them both.
Well done for making a subject that probably needs a Phd to understand accesible to us!
Something else to show my doctor who still cannot believe my cholesterol levels in view of what I eat!
I agree. This is a great post. As someone whose blood cholesterol was super high and yet a heart scan showed absolutely no signs of a problem, I have read a huge amount of data including Peter’s site on this problem. Statins are the result of people not understanding and handing over their heart health to someone else so this kind of information is priceless.
My doc can’t believe my cholesterol either… went from 204 pre-diet to 138 post… in 8 months! She actually demanded a diet recall, haha. Then had the nerve to ask me where the wheat and sugar were in my diet. It would be helpful if they had more than a 1/2 day of nutrition education in medical school.
Actually, I can refute T. Colin Campbell’s half-lie in a few words- “Cholesterol rich foods are some of the healthiest foods you can eat.” It just might take long, arid dissertations to back that up.
Amen to that John. I’ve eaten two eggs almost every day for the last 12 years. Cholesterol level between 155 and 157. It has reached that number primarily because of my love of fast food. Wendy’s, Burger King, etc. I lived on an island with no fast food places and my cholesterol was 127 despite the egg routine.
I’ve been thinking I should do a cholesterol test just to see where I’m at but articles like this and the ones by Chris Masterjohn kind of confuse me on what to do with the information. If I just did a test at Walgreens would that give me any useful info?
The original 10 part series had a pretty good rundown on what to do with the testing data & what it actually means. I’m guessing that Dr. Attia will touch on that in the next part of this summary.
If T. Colin Campbell was even half the doctor he claims to be, why did he make such an erroneous statement that clearly can be defined by seemingly simple science?
Additionally, how to we keep the boat from illegally parking in the first place? Perhaps this will be cleared up in a future post or maybe I missed it?
To answer the first part of your question, refer to the old axiom, “Fifty percent of all doctors graduated in the lower half of their class, so they didn’t know much to begin with. The other half never bother to update their antiquated data base. They’re too busy making money.”
A couple more things to remember (actually told to me by a doctor): “You don’t have to be smart to be a doctor; you just have to have a good memory.” And: “The only really healthy people are the ones who have never gone for a medical exam; if they had done so, the doctor would have surely found something ‘wrong’ with them.”
These things aren’t true of all doctors, of course, but most of us have at least a few horror stories regarding visits to an MD.
+1
Coincidentally I had a chat with a Japanese friend yesterday (I live in Japan)who sounded concerned why I don’t go for regular medical check ups.
.
I told him I am doing daily exercise and eating healthily. I am losing weight at the rate of average .15 kilos a day I am now 218 targeting 156. What can a doctor tell me ? only to lose weight and take pills for BP and Cholesterol.
I had on two occasions ages 26 and 38 (in Australia) had duodenal ulcers which I was advised to take medications and avoid certain foods. I did neither and have never had an ulcer problem since. I am now a young 66 yo. I also was diagnosed (in UK) with having holes in my colon when I was 42 and was required to take medication for the rest of my life. I didn’t even pick up the prescription. 22 years later I had a colonoscopy and results were normal. Just goes to prove the healing powers inside each of us providing we have a healthy outlook and a positive mindset
(Grok style of course
Can I use your post above on my Facebook page? I can reference your blog or not say anything at all of where I got it! This is exactly what I have been trying to say to my fellow friends and family.
Sure.
In case you’ve not yet come across these good sources of info on cholesterol, check out the following:
The Cholesterol Myth by Prof Uffe Ravnskov MD PhD
The Great Cholesterol Con by Anthony Colpo (1497 medical references, examines major cholesterol studies, foreward by Dr Ravnskov)
The Great Cholesterol Con by Dr Malcolm Kendrick MD
Cholesterol and the French Paradox by Frank Cooper (naturopath and who has the genetic condition familial hypercholesterolaemia – permanently high cholesterol level)
and http://www.thincs.org – The International Network of Cholesterol Sceptics (all members are medically qualified in some discipline or other)
Google for articles using the terms cholesterol site:westonaprice.org
and the Cholesterol & health site by Chris Masterjohn (PhD student specialising in Biochemical and Molecular Nutrition):
http://www.cholesterol-and-health.com/
It might just be due to a greater level of irresponsiblity, which according the Hippocratic ethic, is simply incompetence but I think it’s more likely, given the amount of effort and scholarship that is required in order to put together a study as exhaustive as Campbell’s “China Study,” that he is guilty of another indiscretion..and that is of the idea of putting his own personal politics ahead of medical truth.
I believe that Campbell is simply an animal lover to the extreme and the “China Study” is simply his part in the ongoing war on animal cruelty, meat consumption and any other similarly alignned political belief that he adheres to. “Forks Over Knives” obviously expounds upon that platform.
cause (and anyone please correct me) Dr Campbell is not and has never been a “practising” doctor with regular patients to cure etc etc. he is the head of a science research doctor-kind of operation and has massive investment in exactly the twisty little con he has played with the china data.
he “sells” ongoing education and “plant-based nutrition” certification training and certificates so you can go on to con others in his esteemed name.
so, half a doctor would be a generous estimation…
more like 1 1/2 a shill… ;-0
Not sure what part II will bring, but I have heard that the endothelium can be “nicked” by high blood-sugar levels caused by excess starch/sugar consumption and/or diabetes. Here’s a link to several studies linking the 2: http://scholar.google.com/scholar?q=endothelial+inflammation+and+diabetes&hl=en&as_sdt=0&as_vis=1&oi=scholart&sa=X&ei=K3Q-UK6pI-KEjALJu4E4&ved=0CBwQgQMwAA
This causes the gaps that allow the sterols to enter the lumen and get lodged there. So I’m pretty sure this series of articles will wind up saying that as long as you avoid processed carbs/sugars, you won’t have to worry much about atherosclerosis…
Correct…factors that “harm” the endothelium make this problem worse. Smoking and high blood pressure are two examples of forces that challenge the integrity of the endothelium and increase the probability of an apoB containing particle violating it.
I seem to remember in Dr Mary Enig’s book “Know Your Fats” that she mentions the TYPE of fat consumed eventually comes to affect the quality of cell membranes throughout the body. More PUFAs and particularly trans fats make cells less pliable and more friable (my rewording btw! Dr Enig uses excellent scientific terminology) and so more likely to become damaged. This may be a part contributor to the “car crashing into the artery wall”.
Peter,
Does the parking of sterols inside endothelial walls initiate inflammation or is it the result of it? Or are both possible?
Why do they only lodge themselves in the coronary and carotid arteries? Why not throughout the entire body? Why only are humans and the few animals that don’t make their own vitamin C affected?
They can lodge in any artery; the author says they “most famously” lodge in the coronary and carotid arteries. Big difference.\
OK, so “most famously” sounds like a cop out to me, like they don’t know or won’t address it. Never heard of anyone having a “leg attack” or “kidney attack”. Even if they do lodge in other places, my question remains, WHY do they “most famously” lodge in the coronary and carodid arteries??
My mother has a stent in each femoral artery. She was experiencing numbness in her legs, got it checked out and found they were blocked.
When blood flow is blocked to your legs they stop working. When blood flow is blocked to the heart, it stops working.
You can live with legs that aren’t working.
Do a search on “Peripheral Vascular Disease” or PVD. It’s poor circulation/infarction in your extremeties due to atherosclerosis.
I recall hearing that it had to do with the fact that arteries have higher pressure and oxygenated blood. Perhaps the heart and neck arteries being especially high traffic, high pressure, high oxygen compared to the arteries that lie farther away from the lungs and heart. What do you think?
Because it’s pretty noticeable when you die abruptly.
So – lemme get this straight – you’re complaining that you’re not getting spoon-fed information in a digestible enough manner? This guy writes a freakishly long series about cholesterol and then, because he’s crazy passionate about sharing his knowledge with others, tries to condense it into 2 brief posts & you can’t be bothered to google “plaque in kidneys”? And then to top it off, you accuse him of ignorance and avoidance?
People do have “strokes” in other parts of their bodies… I believe it’s called an infarction. IF it’s in your brain it’s called a stroke, if it’s your heart, it’s a heart attack, (myocardial infarction?) and if it’s somewhere else it’s an infarction… wasn’t Dr House from “House” a fictional eg of this?
Yes, both leg attacks (peripheral vascular disease) and kidney attacks (renal artery stenosis) are very common. Atherosclerosis can affect vascular beds anywhere, though the worst disease tends to occur in the areas of highest turbulence (which is why the carotid bifurcation is a common locus)
JimB, I had the EXACT question! You’re right. Why don’t they get stuck in the femoral artery? Maybe they do and it’s easier for the body to deal with that? I hope we get an answer.
This post help me understand something that happened to my grand father, almost 15 years ago. He had a ‘tongue stroke’ (infarctus de la langue) and trust me it made more than a few ‘chuckle’ but it’s true. At the time the doctors reported he was a very rare case, as in maybe 1 in 8 they had ever heard of.
My understanding is that they do lodge in all arteries in the body. The coronary and carotid arteries are particularly important because blockage in the coronary artery results in a myocardial infarction (heart attack), while blockage of the carotid can result in a cerebrovascular accident (stroke).
In some cases, they do lodge themselves in other vessels, hence peripheral vascular disease (PVD). They get “claudication” symptoms in their calves or thighs/buttocks usually, similar to angina in the chest. The vessels are larger, though, so symptoms generally show up later. It’s a BAAAAD thing.
“Why only are humans and the few animals that don’t make their own vitamin C affected?”
As I understand it:
Not enough Vit C = ‘leaky blood vessels’
Body makes cholesterol plaques to block the leaks.
This causes blood vessels to stiffen and narrow – ‘atherosclerosis’.
Enough vit C = healthy blood vessels = no leaks for body to plug.
Check out the ‘Optimum Nutrition Bible’ by Patrick Holford for a more in-depth look at this phenomenon (‘m just reciting from what I remember reading).
Oh! Also this is a good explanation:
http://www.natural-health-information-centre.com/cholesterol-and-heart-disease.html
Great reading, all 5 times. But after 5 times, I think I have a layman’s understanding of the point. However, what seems to be missing is an instructive piece that would direct indicate what measures a person can take against having their sterols carried to their artery wall by an apoB-containing lipoprotein particle. How does one prevent that “illegal residence” from happening? Awaiting part II in the hope of an answer.
Me too.
3
4
John,
The more LDL-P (LDL Particles) you have, the more tickets you have bought to the ‘apoB int he artery wall’ lottery.
So you want to keep LDL-P low.
LDL-C (LDL Cholesterol) is typically what is measured (or estimated) on a standard cholesterol test.
If your LDL-P is big, then each one can carry lots of LDL-C, and a high LDL-C reading means nothing.
If your LDL-P is small, then a high LDL-C means a high LDL-P, and that is frown town.
What can you do about it? Eating low carb will decrease your Triglycerides and increase your LDL-P size.
Based on the best available evidence, it seems there are 2 major steps to take:
1. Reduce the number of boats. Fewer boats = lower probability of boats sneaking past the gate.
2. Reduce factors that damage the endothelium (e.g., smoking, high blood pressure)
While it is also highly likely that reducing inflammation plays a role, it’s not exactly clear this is sufficient in the absence of the other points. It might be — but it’s not demonstrated by the data.
That lost me a bit. Any chance of a lay mans version.
I LOVE The Eating Academy, but I have to have Wikipedia open to research words and terms I don’t understand when I read Peter’s posts. I really enjoy the science behind it all. Great stuff.
Just read the headings, that is the layman’s version:
1. The sine qua non of atherosclerosis is the presence of a sterol in an artery wall. How it gets there is the only thing we should be worrying about.
2. Cholesterol is vital for life; no cholesterol = no life.
3. The cholesterol we eat has little to do with the cholesterol we measure in our bloodstream.
4. The cholesterol in our bloodstream has little to do with the cholesterol in our artery walls (i.e., atherosclerosis).
5. The only way sterols end up in artery walls – the one place we don’t want them to be – is if the sterols are carried there by an apoB-containing lipoprotein particle.
I can see 1. and 5. maybe needing a bit of translation:
1. Hardening of the arteries is caused when sterols (including cholestorol) go where they are not supposed to, their mere presence in other places does not indicate any problems.
5. We don’t know why they illegally park where they shouldn’t go. But it’s only an issue when too many people illegally park AND there aren’t enough tow trucks to remove them.
Reply to 5 about cholesterol “parking” where it is not supposed to. It’s one one the nature’s jokes, I call it.
I study inflammation (which is the ROOT of so many diseases and it seems it’s part of aging) and in Wikipedia there is an article about it and the arachidonic acid (ARA):
http://en.wikipedia.org/wiki/Arachidonic_acid
ARA can be metabolized to both pro-inflammatory and anti-inflammatory molecules…
In people who have some inflammation
“it is being more readily converted to inflammatory compounds” while “does not appear to have proinflammatory effects in healthy individuals”….
Another nature’s joke!!!
I have condensed comic book versions of cholesterol that lays it down in in a more layman’s manner if you’re interested.
LDL cholesterol comic:http://thefatnurse.wordpress.com/2012/06/06/cholesterol-for-all-ages/
How HDL works comic:http://thefatnurse.wordpress.com/2012/07/05/hdl-for-all-ages/
Cardiovascular markers comic: http://thefatnurse.wordpress.com/2012/06/18/cardiovascular-markers-for-all-ages/
Even tho the material is presented in comic form they are still semi long reads tho!
I read part 1-9 last week. He did a terrific job. Can’t wait for part 10 to be released. Haven’t found that on his site yet.
More info can be found on lecturepad.org as well from the lipid gurus.
Does the cholesterol content on food labels take into account esterified/unesterified cholesterol?
Great question. I don’t know the answer, but I would shocked if it explicitly did. Most cholesterol we eat is, in fact, esterified (hence, most cholesterol we eat is not absorbed, since the esterification prevents absorption).
I’m looking forward to reading this series – great way to break it down. I just had a conversation with a friend who told me that he gave up eggs for breakfast because his cholesterol was too high. Now I’ll have something to point him to that will back up my claims!
Well, I’ve been following the Primal Blueprint for about a month and my total cholesterol has gone from 261 mg/dL to 208 mg/dL!! No statins and farm fresh eggs everday! Take that conventional wisdom!!
High Five! Chest Bump!
Hi Laura,
Those values are LDL-C. That’s how much cholesterol you have in each LDL particle (average value). This value is almost meaningless for predicting heart disease risk (it’s more a marker of insulin resistance and you have obviously improved along those lines). For heart disease, it’s the LDL-P particle number that’s important (i.e. how may particles you have). I’m sure Peter will clarify this, and dip into discordance, tomorrow. But if you want to jump the gun, check out his website. Kudos to you.
I could fist pound you for mentioning Frederic Bastiat…brilliant Looking forward to the follow-ups.
+1 for Frederic Bastiat!
Freddy B!
I hope to see an email from marks daily apple inviting paleoers to participate in detailed study- one that includes a questionnaire on diet history, exercise history and tests for artery build up. Please chime in if you’d volunteer or not. I would.
Im new to this, so please forgive me and inform me if I’ve missed the extensive data comparing modern paleoers risk for heart disease to the general western population.
Unfortunately, such a self-selected study would have little value. If it came out poorly, paleo advocates could (rightly) claim that the population was searching out an alternative because they were sick in the first place, and paleo critics could (possibly rightly) claim that the people who volunteered for the study are the ones who are most likely to already be healthy.
Fortunately, Attia is working with Taubes on a non-profit called NuSci that will advocate the study of diet in detail in randomized, controlled conditions. The ancestral weight loss registry at http://www.awlr.org/ is the closest thing I know of to the data you’re talking about in the last paragraph.
I would totally volunteer for that research!
Does anybody know if certain foods have higher proportions of esterified cholesterol?
The majority of cholesterol in foods are esterified. That’s why we don’t absorb much of it. And that’s one of the reasons it doesn’t make much of a difference to cut down on cholesterol-rich foods. The other reason is cholesterol homeostasis–if you cut down in the amount of cholesterol you eat (it does contain some unesterified/free cholesterol), the body will produce more to compensate.
Why bother worrying about it?
Is there an animation to explain this? Or perhaps something like “eggs don’t cause this, your body will make cholesterol if you don’t eat it, do this to keep cholesterol from being an issue.” All I’m getting is some weird cellular malfunction making our immune system go all keystone cop berserk.
I don’t know of an animation, but there’s a comic: http://thefatnurse.wordpress.com/2012/06/06/cholesterol-for-all-ages/
ACH! still too hard! I’m sorry for deriding everyone who found the food pyramid too confusing!
I guess it boils down to “what simple statement should I use as a guideline.” I know that’s what made people start blindly throwing out eggyolks, but I just hopped on the “eggyolks aren’t bad” wagon because they’re the point of eating eggs.
The thing is – there are no shortcuts. There are no easy answers. The science on this stuff is REALLY hard. Nobody KNOWS much of anything with regard to the optimum human diet, and if they claim to they’re either lying or unwise, especially given human diversity.
That said, some implementations of some theories seem to be working for some people. i.e. I think this is what you are looking for http://www.marksdailyapple.com/primal-blueprint-101/#axzz24xrcNJHg
For me it boils down to
a) stop eating refined foods, esp sugar
b) minimize grains of any kind (less than 1 serving per day)
c) maximize low intensity and some high intensity exercise
d) eat the stuff that you (probably) thought was icky when you were 9 years old – vegetables, exotic cuts of meat, etc.
Egg yolks are the best part of the egg! So sweet, smooth, and tasty!
Ha, great comic! Thanks!
This is such a fantastic article. The subject of cholesterol is close to my heart (literally!) after being told to go on statins at the age of 48 as a result of super-high blood cholesterol. A heart scan showed zero signs of calcification but if I hadn’t done my research (thank you Dr Attia!) and left it at the blood test, I’d have been a lifelong drug-taker.
This post is encouraging to me after reading yesterday the recommendation at a conference in Germany that statins should be given to all over-50s, regardless of their health history. Ugh.
I think that’s all these companies want, a market for their pills. Doctors, unfortunately, buy into the scam.
That’s because 85% of doctors get their “continuing education” from Big Pharma. Once they begin to practice, they are taught the latest “standard of care” from drug representatives. I should know, I work for Big Pharma and we have a huge team of reps that get extensive training on teaching doctors the latest in drug research, etc.
Sad, but true. And that part is not going to change anytime soon. It works.
RE: Pharma’s education to docs
Have you seen well dressed people with bags in their hands walking to the doctor’s office? They are Pharma’s salespeople with samples of RXs to give away for free to patients.
I heard that docs get kick-backs for prescribing RXs…
I found a doc (functional medicine) that first tells you to take supplements, not RXs! I love that!
I think, here is the order of “fixing” what’s wrong (and preventing)
- diet
- supplements
- tests (this science is good)
- RXs if nothing works and it’s serious
The problem with diet is that our food is bad!!! Not everybody knows it. People trust the FDA and stores.
Dr. Mercola (my mentor for over 10 years) writes about it often. Today he sent a HOPEFUL article:
http://articles.mercola.com/sites/articles/archive/2012/09/01/growing-change-documentary-investigates-food-system.aspx?e_cid=20120901_DNL_artNew_1
Eva
The guy who recommended statins for all over-50′s has some links to the pharmaceutical industry.
If I remember correctly from reading Chris Masterjohn’s posts, and others, “sheer pressure” (the pressure exerted on the artery wall as the blood pulses throuth them) makes the endothelium cells produce nitric oxide which helps to bind the endothelium cells together tighter. However, at a branch in the artery or a curve, the sheer pressure drops and, I belive, this is where plague is found most often. This is also why getting your heart rate up, intense exercise, helps, because it creates more sheer pressure, ergo, more nitric oxide.
Chris Materjohn has also suggested that the LDL, which has a PUFA sheath, so to speak, can get oxidized if the LDL receptor sites are full or not functioning correctly and the LDL has to circulate in the blood too long. It’s the PUFA that gets oxidized and it causes a shrinkage in the size of the LDL, which may be a factor in slipping behind the endothelium cells.
I haven’t gone back to verify this. I’m just pulling it out of my memory, but I pretty sure that’s correct.
Excellent summary explanation and pretty sure your memory is bang on!
It would be nice if Peter could comment on Chris’ interpretation. Chris seems to believe oxidation happens prior to entry into the endothelium, while Peter appears to believe it happens after. I’ve always been a “before” guy and that’s the only aspect of Peter’s theory I’m still having a difficult time wrapping my head around.
However, if the strategy to decrease the oxidation is the same, then, for me, this is a rather moot point.
I think that would be “shear” pressure, like in wind shear. Fluid mechanics lingo.
I’m four months post bypass surgery at age 62. Active (4 to 6 triathlons / year)non smoker with LDL numbers a little above 100. ie no risk factors other than perhaps genetics. More than anyone I’d like to know the why as well. I have calcification up the wazoo and would like to understand why and do something about it.
long duration aerobics have been found in recent studies to damage the right ventricle and create numerous inflammatory oxidative processes. Do short burst aerobics and resistance training, take curcumin & omega 3′s for inflammation and certainly the ubiquinol form of COQ10 (100 mg twice a day). If you take calcium supplements or ingest a fair amount of dairy you MUST take K1 & K2 to keep it out of your arteries.
Read this;
http://www.ourhealthcoop.com/pdf/MikeCiell_unified_theory.pdf
…and you might want to think twice about those triathalons, they’ll kill you!
LOVE THE EATING ACADEMY – it is on my bookmark menu right next to MDA
I’m still not convinced 100% I am still on the boat that its inflammation caused by oxidation or (whatever). THEN the cholesterol builds up to try and heal the inflammation… NO inflammation – no problems.
I have a hard time believing Apo-B or small LDL “just happen” to get under the layer and start havoc.
I’d like to read the rest of this series to see if this is clarified also. My understanding has been that there was damage to the endothelium prior to the ApoB lipos getting lodged there, and that damage could come from toxins like cigarette smoke, or even from viruses (hence some correlation between heart attacks and recent flu symptoms).
I just got out if the hospital today. one artery was 99. something closed with atherosclerosis. had a stent put in, now I am on the plavix, this stent requires the plavix to stop clots from forming.
now , I am not sure how to proceed, now how do I convince myself , my family , doctor that my lifestyle is ok? ( plus mos, primal and have not lost any weight , now have a stent? anyone else had this happen?
I, too, have two stents since a year ago. Age 67, no “risk factors” other than genetic. Was told by family doctor and cardiologist that people with lipid profiles like mine don’t get these problems, but I did. Low carb diet for years. I’m taking a lot of vit-C now and arginine for vasodilation. Yes, also taking a statin now and the newest blood thinner.
I’m not a doctor, so take this free musing for what it’s worth, but the first thing to note is that atherosclerosis, like cancer, is not an overnight thing. It’s a slow process over many years of inflammatory conditions. 9 months of living primal could not cure your heart disease any more than 9 months of stopping smoking could cure the lung cancer of a pack-a-day smoker. Once it’s gotten that bad, it’s going to take a long time and some drastic medical interventions to begin to heal. Primal living is a piece of that puzzle as you try to work toward restoring and healing your body as much as you can.
You don’t elaborate on exactly what “9 months primal” means to you, either. Are you a quality-sleeping, sun-getting, organ-chowing, veggie packing, slow-moving, heavy-lifting, occasionally sprinting diehard? Or are you the guy trying to figure out how to “paleo” up his pancakes and muffins, who just replaced all those bread carbs with fruit carbs? If you’ve made all the right changes and have been dialed in for a long time, how have you been feeling independent of the (lack of) weight loss?
Especially since you have these complicating medical issues, I think you could probably benefit from some more structured and hands-on expert help, such as engaging Robb Wolf’s team of consultants. We used them as a resource when trying to get a specific plan to manage my wife’s autoimmune disease. Their prices are pretty reasonable, especially compared to some of the expenses you’ll be facing on the hamster wheel of pharmaceutical heart maintenance.
Good luck.
Organ chowing? can you say more about that? was never big on liver since reading years ago that livers catch all the crap that an animal gets in its diet and other environmental exposures (as they are farmed). I do like a nice chicken liver marinated in curry spices and grilled, though.
should read 9 plus months on primal eating. I have been read the riot act and have been prescribed statins,
Uhhh… soooo…. can we get a more simple layman’s version of #5 which is the most crucial part to this series please! The paragraph that starts with “I don’t know” is very hard to understand, at least to me. What is he saying? The very last paragraph is ridiculous.
Agreed that the very last paragraph is ludicrous.
Can you be more specific about what you don’t understand? It’s saying that your body doesn’t like having (chole)sterol particles in the arterial walls. The last paragraph is what your body does when this happens:
Oversimplification: Basically, clean-up cells (kinda like white blood cells) are eating up the sterols, but they get stuck in the artery walls & pretty quickly, your body starts to build specialized tissue (inflammation/plaque) to protect the surrounding cells from the unwanted sterols. This plaque gets bigger and bigger until it starts to block the inside of the artery, and I think you know what happens from there.
Thanks, I appreciate the “oversimplification” — what causes the sterols to get stuck there in the first place? If it’s NOT from eating cholesterol, which is what I’m gathering, then what causes it?
Thanks again.
I think the answer is nobody knows for sure. The leading theory is that the size and number of the LDL particles is more important than the amount of LDL stuff in your blood. The more saturated (high number of paticles) your blood is with LDL particles, the more it wants to leave your blood. Kind of like a damp sponge doesn’t leak much water, but a completely soaked sponge does.
Something causes your body to make more cholesterol particles, rather than just bigger ones. Genetics obviously play a huge role here, but I think diet is as important – sugar and starch seem to encourage more cholesterol particles, whereas a fat based diet seems to encourage bigger particles.
I think I stole this metaphor, but it’s like the cholesterol is people & the vehicles are the particles. If you can get everybody to ride the bus (big particles), you have less overall traffic than if everybody takes their own car (high number of particles).
Please note that this all applies only to LDL particles. HDL particles is a whole ‘nother shebang.
Hopefully part 2 will address this but I think inflammation is the answer.
Great article I am excited for the follow ups. It does take a tremendous amount of information to change paradigms. As Mark Twain said: “a lie can travel around the world while the truth is still putting on its shoes.”
I always thought that was a Churchill quote but after a quick bit of googling – From politicsdaily :-
>>>>
The chestnut that “a lie can travel halfway around the world before the truth can get its boots on” sounds like Mark Twain, and he’s often cited (by politicians, no less) as the source. But British pastor Charles Haddon Spurgeon really deserves the credit, and he appropriated it from a proverb in 1855 — when Sam Clemens was 20, well before he was Mark Twain.<<<
Alright I give. I am either baffled by science or BS. The LC Primal way is definitely improving every thing I can measure, feel and understand so I’m going to bet (my life) that this is my best course of action. I certainly don’t trust the medical profession to know best. I had that much figured out when I was five.
Love the Eating Academy & Dr. Attia’s posts. Since finding MDA in Feb this year and EA (under a different name) in May, I’ve been transitioning to LC/Primal and have lowered by total cholesterol by 25 points, my Triglycerides by 250pts and raised my HDLs by 40! Reading these posts makes me wish I had stuck it out with biology/chemistry in undergrad…
Great post Mark , my mom is another great testimony of High Cholesterol and has a perfect heart .
So, what’s wrong with eating 2-3 free-range eggs every day cooked with lard and coconut oil?
I read that also Paleo/Primal gurus believe that eating eggs every day is not a smart decision.
Why???
Thanks,
Michael
Not sure if this is what the “Paleo/Primal Gurus” are referring to, but my husband and son have some food sensitivities, and the allergist we went to warned us against eating anything day after day, especially something like eggs which is a known allergen for many people. We recently went on vacation and had a whey shake with raw eggs for breakfast every day, but I try to keep them to every other day usually. My husband, who tested positive for egg sensitivity at one time, tries to limit them to every third or fourth day to try and avoid reactivating the sensitivity. Hope this helps, Michael.
Egg whites contain lysozyme which is an enzyme that breaks down intestinal mucosa. It probably is the driver for the egg allergy people have. Although there are paleo folks that eat MANY eggs (I did 20/week at some opin in time) the availability of such large quantities in real paleolitic diet is disputed.
In England today they have said on the news that everyone over 50 should be prescribed Statins regardless of whether they need them or not and that this would cut out 10,000 heart attacks a year. Wonder how many they would cut if everyone went primal.
Yes, and they’d have a much larger market for their pills.
Absolutely! We should be taught to start with what we put into our bodies — our diet!! So many people have no clue that they hurt themselves and their children (who cannot know any better) by sugar-grain diet! I try to tell but get mixed results, some think I am crazy! “No bread? No potatoes? No ice cream? No soft drinks! The TV commercials say otherwise…”
BTW: If FDA would declare sugar as “poison” which it it, the food industry and the whole economy would collapse… it is so sugar oriented…
Great stuff Dr. Attia.
Thank you Mark for featuring Dr. Peter Attia! He has one of the best blogs out there.
This post was a great example of a very scientific approach to a controversial topic with the right mix of analogies for the lay person to get the idea.
AS a trainer, I battle the egg yolk phobics every day. I think Peter’s work can chip away at the status quo and start the paradigm shift that we need. I just want to eat my steak and eggs in peace!
Everyone has opinions so thanks for taking on the good fight with scientific facts and intelligence.
Looking forward to part two!
I wonder if these medical reports that suggest eating no fat and only 4 eggs per week are based on factory farmed produce.
ie. caged hens and cattle. Which are fed grain and injected with antibiotics and steroids causing the animals to become sick. Grok only ever ate free range and ate as much as he liked. I am eating my grass fed and free range steak and eggs in peace !
Yes, yes yes!! This, absolutely. There is a world of difference between factory farmed and free range animal produce, and I’d bet anything that the free range stuff is many, many times healthier due to the way that the animals have been allowed to live their lives.
Keep a creature in a tiny cage, bred and fed specifically to put on as much weight as possible in as short a time span as possible, while feeding it antibiotics etc. and you’re going to get a fat, stressed, unhealty animal with no natural immune system (not so different from the human cubicle farmers/office workers then!)
Give animals space to behave naturally, breed and feed them for natural health without drugs and allow them to grow slowly until they’re big enough and old enough to slaughter and you’ve got much, much healthier creatures, producing much healthier meat.
Slaughter itself should also be looked into, as right now far too many animals are killed badly and suffer greatly in the last few minutes of their lives, thus causing even more stress hormones to flood through their bodies and thus into the meat that we eat. It’s poison, essentially and nothing at all like what Grok would have been eating. I do concede that the chase and kill of the hunt would cause the same sort of stress response in the animals being hunted, but they wouldn’t have had a lifetime of suffering before the final kill…
See also ‘Eating Animals’ by Johnathan Safran Foer. I think it should be compulsory reading for everyone (especiall Americans) who eats meat, as it gives you the facts on the horrors of the factory farming industry while allowing you to make up your own mind as to how to source your meat (if you continue to eat it – and I do).
When I catch ants and bite their heads off quick, they taste alright. If I hold onto them like they aren’t food as they wriggle around then eat them, they usually don’t taste as good. Less like a little mineral pill in shell form that spits lemon juice and more like urine. It’s best not to hesitate and play with your food when you’ve got to kill it like cats that aren’t hungry and batter a creature into a broken toy. Remember when hunting you’re committing murder for nutrition. Better be respectful about it.
A couple theories to explain why cats play with their catch is to tire it out to make the kill safe and easy or to get the animal full of adrenaline to tenderize its meat.