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The personal blog of Peter Attia, M.D.

The straight dope on cholesterol – Part I

The straight dope on cholesterol – Part I


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 Dayspring, Dr. Tara Dall, Dr. 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 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 distinction: we 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 formsUC 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.

(To Part II »)


About the Author:

Peter Attia, M.D., is a physician in private practice in NYC and CA. His practice focuses on longevity and healthspan. His clinical interests are nutrition, lipidology, endocrinology, and a few other cool things.


  1. Bradlee Clark  April 25, 2012

    Solid report thus far Dr. Attia. I’m looking forward to Part 2.

    • David Ross  April 26, 2012

      I too love this blog. I understand only about 2/3 of what you write, but I love the passion and verve with which you write it! After 30 years of being mislead by “fat and cholesterol are bad for you”, I’m ready for some good science…..

  2. Perry  April 25, 2012

    Ding! Another brilliant post, Peter. I have to say it was the most difficult to read for me (many words, terms, biological science that I have never even seen).

    But more importantly, how do we break the collective societal “buzz train” about “I have to watch my cholesterol…?”

    I still hear it almost daily in my travels. How in the heck did it get so programmed in everyone’s vernacular?

    Thanks again for all you do.

    • Peter Attia  April 25, 2012

      Good Calories, Bad Calories by Gary Taubes does a good job explaining this mythology and I will give an abridged version in a subsequent post about cholesterol. Probably in Part II or III.

    • lorraine  April 25, 2012

      Hey Hoboken, Exit 9 here

  3. Alexandra M  April 25, 2012

    More! More! More!

    Most people I know still believe those guidelines about limiting cholesterol intake.

    • Peter Attia  April 25, 2012

      Sad, but true. This may end up being a bit of along series. LOTS of damage to undo.

  4. Annika S  April 25, 2012

    Oh wow, I absolutely loved this! Look forward to the continuation on cholesterol – would you mind if I quote and link parts of this (and the continuations) in a future post of my own? I am still learning about the world of nutrition (and psychology) myself, but as I do I like to share with my readers!

  5. Mark Breckenridge  April 25, 2012

    Looking forward to part two – Great post!

  6. Joseph Amit  April 25, 2012

    Great article.I’ve learnt a great deal from it. On a side note do you know how salt affects blood pressure on a low carb diet?


    • Peter Attia  April 25, 2012

      Salt is necessary on a low carb diet to maintain blood pressure. The “salt-blood pressure” story is another complete nutrition “science” debacle.

  7. Mike Hurley  April 25, 2012

    Thanks for starting to tackle this subject. The lipid hypothesis is so intertwined with the insulin hypothesis, and it’s fascinating how the medical establishment is so wrong on both. Despite the fact that I lost a ton of weight on low carb, my cholesterol skyrocketed and freaked out my doctor. It doesn’t worry me, though, but the more I learn about this the better. I’m going to insist on a NMR test when we do a follow up.

  8. Matt  April 25, 2012

    This is one of the most enlightening things I’ve read on this subject. I can’t wait to read the next one.

    One (possibly dumb) question: What measure of certainty do you feel you have that a high-fat diet is the way to go when it comes to cholesterol? Is this Copernicanism circa 1615 or 1915?

    • Peter Attia  April 25, 2012

      I’ll be getting to this question in subsequent posts on this topic. Not a dumb question, at all.

    • Ron  January 24, 2013

      Not sure about the certainty of a high fat diet on cholesterol , but in May of 2011 my lipid panel was- total cholesterol 215, triglycerides 129, HDL 35, and LDL 154. My doctor wanted to put me on a cholesterol medicine, because my totals were high and my LDL was high. I not only don’t like taken pills, I have bad reactions to many of them. Also i am 5′ 8″ tall and weighted 192 lb.So I decided to try and lower them on my own. I started reading every thing I could find about what foods to eat to lower my cholesterol. What I eventually discovered was that I need to quit sugar, Processed foods, Vegetable oils and trans fats. I also took fiber just because of the way it helped my gut. 1 year later my Lipid panel was as follows. total cholesterol 188, triglycerides 72, HDL 62, and LDL 112. Also my weight was down to 149.
      The Dr said my LDL was still to high but was mostly happy. I am not worried at all because I Know because of websites like Dr Attia,s and many more that HDL/ triglycerides is a much better predictor of Heart problems.

  9. vinny sciortino  April 25, 2012

    thanks Peter, this stuff is eye opening.

  10. Larry Daher  April 25, 2012

    Peter, excellent blog for the “non-scientist”. Thank you & this one is getting forwarded to my whole family.

  11. Richard  April 25, 2012

    Thank you for this. I look forward to the rest of the series.

  12. Travis Koger  April 25, 2012

    Another great article Peter. Look forward to Part 2.

  13. lorraine  April 25, 2012

    Very cool of you to take on this topic. And you succeeded in making it very accessible. I can imagine it made your brain hurt deciding how to organize and write it.

    I look forward to future comments about phytosterols, as of course, everyone is supplementing with them to lower cholesterol.

    • Peter Attia  April 25, 2012

      You can bet your last ester side chain I will cover EXACTLY that topic! Here’s the hint: If you’re taking phytosterols…STOP IT!!!!

    • lorraine  April 25, 2012

      Seems like the main thrust for phytosterol suuplementation is coming from MD’s. Kinda blew my mind when I first started hearing it because docs were recommending supps along with drugs…….was the first clue……

    • Peter Attia  April 25, 2012

      Nothing wrong with drugs, per se, but I’ll explain why phytosterols should not be used to combat this problem.

    • lorraine  April 26, 2012

      Yeah, it was more like a couple of years ago it seemed like a memo went out to the effect of prescribing statins with phytosterols.

      Listen, thank you for listing your mentors on this topic in this post. Turns out Dr. Dayspring is local and I see he does work in menopause, my current area of interest. I promise I won’t bum rush his office and tell him you sent me, but I’ll be looking for talks and papers. Very helpful.

  14. Erica  April 25, 2012

    This sh*t is awesome! What a fantastic resource I’ve found (via Ben Greenfield) – I can’t wait for more!

    • Peter Attia  April 25, 2012

      We’ve got a lot more to cover, so I’m glad it’s not too boring.

  15. Colleen  April 25, 2012

    Earlier this week I came across a laudatory article announcing that the percentage of Americans with high cholesterol numbers (maybe 14% – I can’t recall) was below the national target, in part due to so many taking cholesterol lowering medication. Since my discovery of you and Gary Taubes several months ago, I couldn’t help but wonder is this a good thing? Loved the post, looking forward to the rest. I am wondering and will keep reading, should one be concerned with a very low total cholesterol number (naturally occurring, not thru any special diet or medication)?

    • Peter Attia  April 25, 2012

      Great question. You’ll be able to answer this one in about a month. MANY layers to answer this one.

  16. steve  April 25, 2012

    This is great and thank you for what is very hard work by you!
    A question as i may be missing something: You said that we do not absorb the cholesterol we eat. My understanding is that humans absorb about 50% of all sterols eaten(i assume this includes cholesterol) and that hyper-absorbers absorbers a significantly greater amount. What am i not understanding?

    I have to add that the series you are doing is of great public health benefit and all who learn about this, pass the word on, and people get tested will do much to address the cost side of the healthcare problem faced in this country. Much thanks!

    • Peter Attia  April 25, 2012

      Steve, we absorb *some* of the cholesterol we eat, though not 50%. Most of the cholesterol we eat can’t be absorbed because it’s esterified. Needs to be de-esterified to even get absorbed. So at most about 25% of our cholesterol is from our food intake. But the more important part is that other 75% that our body makes, AND the interaction between what we synthesis de novo and what we re-absorb from bile.

  17. David Nelsen  April 25, 2012

    Peter, it’s not boring when for many of us our lives depend on it. Given the amount of misinformation out there on nutrition, you have to take ownership of it yourself. Relying on your GP for health and diet advice could be hazardous to your health. I have a neighbor who is a nutritionist. I was talking to her the other day about low carb and she started rolling her eyes. She said she would only believe certain published authors she believed in. Like your wife, she is very thin and has no insulin resistance. Since she doesn’t personally have to deal with the affects of IR she has everything neatly rolled up in the Calories In/Calories Out box and work out like you’re Jillian Michaels paradigm. On a brighter note, I think I am winning over my GP on advanced lipidology. Keep the great posts coming.

    • Peter Attia  April 25, 2012

      Hopefully this series on lipids, coupled with getting him/her on Lecturepad.org, will help.

  18. Marilyn  April 25, 2012

    Thanks for a very organized and easily understood presentation. Such a beautiful system. It’s tragic that nearly everybody out there is trying to fool — or beat down — Mother Nature.

  19. Cap'n Jan  April 25, 2012

    Great post.

    BTW: I think it is extremely useful to write thoughts down for others to see and criticize – particularly a work in progress. Of course you run the risk of being told ‘But you said……!!!!!!’.

    It is a bloody shame that we can’t, with the use of a clear disclaimer, put down ideas and rearrange/modify/improve/even change them at a later date as we learn more and perhaps have that new knowledge modify what was said. Without, of course, that “Nanny, Nanny, Boo-Boo” stuff. Like you’re never able to alter your views or change your mind. (Only politicians are not allowed to change their mind ;->)

    People get to wrapped around the axle about this kind of intellectual growth, but perhaps a big flashing “This is a Work In Progress!!!!” sign, so as not to be missed would help.

    Again, thanks for your careful and well thought out posts. I’ve been following low-carb discussions now for about 17 years, and other than Peter (it’s all mitochondria) Dobromylskyj and Taubes, I don’t bother with anyone else.

    Speaking of Dobromylskyj – have you read “Power, Sex and Suicide” by Nick Lane? (http://www.amazon.com/Power-Sex-Suicide-Mitochondria-Meaning/dp/0199205647/ref=sr_1_1?ie=UTF8&qid=1335367241&sr=8-1)

    He gets a little off into the dietary weeds with ‘speculation’ toward the end, but can be forgiven. After reading it, I really have to say that it really IS all about mitochondria. I would very much be interested in your opinion. It is a long book, technically involved and very small print, so that’s my disclaimer.

    Fair Winds,

    Cap’n Jan

    • Peter Attia  April 25, 2012

      Have not read it, but I’ll check it out, though pleasure reading (anything other than science papers) is becoming increasingly difficult with time constraints.

  20. Cap'n Jan  April 25, 2012

    Oh, brief modification: 4th paragraph…

    Should read: “Other than Peter (it’s all mitochondria) Dobromylskyj, Taubes and YOU, I don’t bother with anyone else.

    See what I mean? Life is a work in progress.

    Fair Winds, Following Seas,

    Cap’n Jan

  21. Claudia  April 25, 2012

    Absolutely fantastic post, Prof. I especially liked the comparison of steroid hormones synthesis and cholesterol images. So here’s a stupid question: You’re able to get through to lay people like us, we want to learn this stuff, you’re making it possible for us to understand – so why the hell don’t they teach this in med school?!

    • Peter Attia  April 25, 2012

      Great question. I suspect there are several reasons:
      1. Most people teaching in med school don’t actually know this.
      2. Once you start having this discussion (e.g., in a classroom), you find yourself realizing that a lot what is being taught is incorrect. I’ll get to it in a few weeks, but the “cholesterol is evil” story and that “fat is the devil” story crossed paths in the early 80’s and have reinforced each other greatly.
      Very slippery slope…

    • Claudia  April 25, 2012

      Sorry, but that’s letting them off the hook too easily. It’s their job to know this.You yourself said you should have questioned what you were taught. You can’t be alone. There is no excuse for what is going on. How dare they continue to teach what is incorrect. It’s time they were challenged with some facts and real research.
      NuSI can’t come soon enough.

    • Peter Attia  April 25, 2012

      I like your fire, Claudia!

    • Claudia  April 26, 2012

      Look what’s happening to this low-carb blogger:

      “State Threatens to Shut Down Nutrition Blogger –

      Nutrition board says he needs a license to advocate dietary approaches”

      Link here:

    • Peter Attia  April 26, 2012

      I think they’re shutting him down because he’s advocating something in stark contrast to what most doctors say. If he were telling people to eat less fat and/or less red meat I GUARANTEE this would not be happening.

    • Claudia  April 26, 2012

      He’s doing what he thinks is best to beat his risk factors, just like the rest of us.

      We need to get to the tipping point where that is no longer considered “radical”.

      NuSI – faster, please.

    • Alexandra M  April 26, 2012

      I think he should counter-sue the board. They’re the ones not “practicing nutrition!”

    • Peter Attia  April 26, 2012

      I agree, though we need a bit more evidence of the harm of “5-6 servings per day of whole grains” before IJ can launch a counter class action lawsuit.

    • Nicole  April 26, 2012

      Make sure you read this article, Claudia, about the ADA desire to control the industry completely. http://www.forbes.com/sites/michaelellsberg/2012/04/05/american-dietetic-association/

    • Claudia  April 27, 2012

      Thanks, Nicole. I’ll take a look.

    • Russell Brady  June 16, 2016

      Teaching it in med school would involve flying in the face of big pharma. These are companies (I won’t mention any names) that formulate and test statin medications for lowering LDL (erroneously called cholesterol – it’s actually the transport mechanism for cholesterol). Statins also come with a host of side effects one of which is erectile dysfunction (ED for the PC crowd). The same company then come up with a pill for ED. So they have a cash flow from the cause and one from the treatment of a side effect. Studies have been done which show there is a small number of patients who benefit (don’t die of a heart attack) from statin treatment. I don’t want to go off on a rant against the doctors, but this is why it’s not taught in med school. Also doctors tend to forget their chemistry classes after going into practice. Thankfully there are physicians like Dr. Attia and Dr. Graveline (www.spacedoc.com) who are slowly getting the word out.

  22. D  April 25, 2012

    Peter, iirc, Chris Masterjohn says that cholestrol dietary has ZERO affect on your measured cholestrol levels… for about 80% of us. But something like 20% are affected by it. Does that sound right?

    • Peter Attia  April 25, 2012

      About right. The impact, of course, if even quite variable in that 20%. I’ll get to it.

  23. D  April 25, 2012

    Boy I botched that. I meant to write “dietary cholesterol intake”. Changing words around without reading what you wrote is not a smart thing to do.

  24. jay jay  April 25, 2012

    Excellent work! I really appreciate what you are doing here.

    Will you possibly talk more about low cholesterol levels? I’ve always been around 160-170 total serum, and a few months ago, I came in at 125 (after a year of low carb/high fat).

    My GP dew a little heart with a smiley face in it, and said “Keep doing what you’re doing!”. But based on some reading I have done since then, I’m not so sure she is right.

    • Peter Attia  April 25, 2012

      Almost certainly not, unfortunately. That’s ok. You will soon be able to help.

    • PaulaM  April 29, 2012

      Oh, how cute! A smiley face! My doc ALWAYS draws a line to his comment: “recommend statin. Is at high risk for CVD” (still to this freakin’ day!) when my LDL reports 175 or so. I have been refusing “statins” for a decade from all CW docs.

  25. Nina  April 25, 2012

    Peter, I’m almost speechless with gratitude for all of your work and generosity in sharing this vital information. Thank you.

  26. Gary  April 25, 2012

    This is cool. The suspense is killing me though, I can’t wait to see if the villian Insulin has a role in this diabolical plot too!

  27. DHackam  April 25, 2012

    Hi Peter,
    I agree that VAP or NMR derived LDL-P are far superior to a simple measured LDL cholesterol or even total:HDL ratio. However, change in even the standard lipid profile (SLP) from before to after a low carb/high fat diet can be really illustrative – i.e. the trend over time. For example, my LDL and total cholesterol more than doubled on the low carb, high fat diet. Cardiologists who looked at my SLP thought I had familial hypercholesterolemia, until I told them my baseline. There is a certain proportion of individuals (we guess, what, 10%?) who for some reason may develop dangerous levels of serum hypercholesterolemia (akin to FH levels) from a diet rich in saturated fat and dietary cholesterol. They likely have genetic mutations in intestinal transporters that are unmasked by this diet.

    Bottom line – get your lipids checked when undertaking any diet (both before AND after). The good news is that my CRP, trigs and HDL dramatically improved. The bad news is that I’ve had to take out much of the fat and start on a statin, in order to lower my risk (a meta-analysis of more than a million individuals published in the lancet a few years back suggested that at the present values, my risk of a coronary event was 8.5-fold higher than it was at my pre-diet values).

    • Peter Attia  April 25, 2012

      I dunno, Dan. Now that I’m doing standard cholesterol testing and NMR side-by-side on everyone I bump into (including the UPS guy, if he’s not quick getting off the porch), the amount of discordance between LDL-C and LDL-P is staggering. I would not trust a standard panel or VAP alone ever again, if my life depended it. Wait… it does?!

    • Beth  April 25, 2012

      On the subject of very high serum lipoproteins:

      When I started doing VLC, my TC & LDL went through the roof (e.g. over 400 from about 200 for TC). FWIW, my TG are about 50 & my HDL is about 100 and pretty much all the LDL is the “good” kind (per NMR or whatever fancy test it is).

      Here is my question: What controls the serum lipoprotein level? The body controls the levels of many chemicals via a negative feedback loop. What is the feedback loop that controls the LDL serum levels — or is there one at all?

      Does the body perhaps control the rate of production and removal and the serum level just follow from the relative rates of change of production and removal?

      I can understand that if the feedback loop keeps production and removal in balance, then if one of those things changes suddenly and it takes a while for the other to catch up, then the serum level could change, possibly dramatically.

      I’ve seen discussions of how LDL receptors (and the numbers thereof) control the rate of removal and how statins control the rate of production but never any discussion of how the serum level itself is controlled — hence my wondering if there is actually any direct mechanism at all.

      FWIW, unless I see any good evidence to the contrary, I no longer give a rip if my LDL levels are way over the “recommended” levels. I plan to handle this by not getting it tested anymore. 😉

      BTW — not FH, unless it is a special kind that only appears on VLC.

      Thanks, Beth

    • Ed  May 1, 2012


      Have you checked thyroid levels? I am going to get mine tested after seeing my LDL unexpectedly soar. I just found this post on Paul Jaminet’s website…. Clearly, low T3 levels can dramatically influence LDL clearance by LDL receptors.


    • Magarietha  May 15, 2012

      Hi. Was looking for a site like this all over! Help please! I bought Gary Taubes’ GCBC and have been on low carb diet for more than 4 months solidly. Thing is my GP will not be happy about this. I am a caucasian South African (Afrikaner) and like some Jews (think Ashkenazi? Jews) and our Indian population I have a thing called Frederickson Type IIA hypercholesterolaemia. Sorry about the metric number but it means that without meds my family’s numbers go into double digits like 12 and 13. None of us can tolerate statins due to rhabdomyolisis? so we’re on fibrates and ezetimibes.
      What now with this diet? I was hoping that at least my trigliserides would come down (sorry bout all the bad science spelling). My lovely mother has it and only learned about this in her 60’s. Only took the pills irregularly. Last year we celebrated her 80th birthday. Her staple is lamb – no really. She grew up on a sheep farm. So what now? I do know that a double gene of this stuff is very precarious for bearers.

    • Magarietha  June 10, 2012

      Hi there, so I did have the lipogram done and my doctor was ecstatic. My Lipogram has almost normalised, for the first time in my life. No statins or fibrates (with or without ezetimibe) could get my numbers below 8.8 ever. Now it’s 5.0. I’m in my fifties and my family are opting into a ketogenic diet. Most of my family have the faulty gene. I now know for sure that I can never go off this diet again. I’m going to trash the ezetimibe and have another lipogram done in a month’s time. Must say I cannot find a single person with FH on the internet who has been on a ketogenic diet. I had to do this of my own accord. No doctor would have wanted to touch me with a barge pole. Have done the same experiment once when I went on zero cholesterol diet for 1 month (all I could stand) and my cholesterol numbers soared then – to the chagrin of my doctors. My doctor says “what a pleasure”. He says the numbers don’t lie so there’s no argument. Thanx for placing this. Would love to know if anyone else with FH ever went onto this diet. My family is still afraid for my sake.

    • Peter Attia  June 10, 2012


  28. Bob Johnston  April 25, 2012

    This is shaping up as a great series. Really appreciate your work.

    You mentioned Dr. Dayspring as one of your mentors and that reminded me of a series of youtube videos he appears in with Gary Taubes for Specialty Health. The entire series is good but this video about a case study of a Reno police officer was fascinating.


    • Peter Attia  April 25, 2012

      I was sitting next to them during this video. Gary and I were back in Reno with Dr. Dall and Robb Wolf last week for another round of this series.

    • KevinF  April 26, 2012

      Wow awesome video.

    • lorraine  April 26, 2012

      most excellent vid

    • Alexandra M  April 26, 2012

      Dang! I just spent a good part of the day watching those videos and taking copious notes! I think I’m ready to get back in the game now. 🙂

    • lorraine  April 27, 2012

      What a bonus to have that firefighter/police cohort in Reno. They are keeping wonderful data! A potential study population perhaps?

    • John Dawson  April 28, 2012

      These Specialty Health videos of Dr. Dayspring and Gary Taubes are great. I suggest you provide links on your media page.

    • Peter Attia  April 28, 2012

      I’ll get them up in the next week or so.

  29. Jim  April 25, 2012

    Thanks for tackling this issue for us! Do you plan on addressing FH? With my levels reaching almost 300 on low fat and 500 on high fat diet, those statins are getting harder to resist.

    • Peter Attia  April 25, 2012

      I will talk about FH in time. FH needs medication without any question. Proper diet can reduce the amount, though.

  30. Dan Hackam  April 25, 2012

    I agree there is alot of discordance between LDL-C and LDL-P. But that discordance should be subtracted out by measuring {follow-up minus baseline}. After all, the ratio of LDL-C to LDL-P should not radically change in a given individual from baseline to follow-up – am I right? So while a baseline may be of limited value, if there is a great increase from that baseline (trend over time), you have to wonder what is going on in that individual (if nothing else has changed – e.g. medication, exercise, OTC substances like plant sterols, etc). Put another way, why would the divergence increase so much (LDL-P remain same, while LDL-C increase).

    • Peter Attia  April 25, 2012

      This can, and does, happen all the time, Dan. A drug can easily reduce LDL-C with no change on LDL-P. Think of this way, if we reduce the amount of cholesterol being carried by each particle, but don’t change the number of particles, LDL-C goes down and LDL-P stays the same. Let’s hold off on this thread until everyone else can catch up on these concepts in subsequent posts.

  31. Peter  April 25, 2012

    Please clarify your recommendation for NMR instead of the standard lipid panel(SLP). We read often that an ideal TG/HDL ratio from SLP correlates with mostly ‘large and fluffy’ pattern A in LDL.

    Are you saying that this is not so and that the actual LDL results from NMR may contradict such correlation, as high as 10%?

    You may have an ideal TG/HDL ratio but still have mostly pattern B particles in LDL? If so, what can one do to alter one’s LDL’s composition, within LCHF?

    • Peter Attia  April 25, 2012

      If I had a dollar for every instance in which I saw someone with a great TG/HDL-C ratio who had 90th percentile risk from LDL-P, I’d have a LOT of dollars. Stay tuned for this discussion in coming posts. We need to start with the basics, first, though.

    • PaulaM  April 29, 2012


      Chris Kresser (the researcher/”practitioner”) suggests the TG/HDL-C ratio is one’s guiding light. Just FYI how info can spread around. . . I know you will get to all this. Still don’t get what can be done to alter the LDL-P bad stuff. . . As some of us grow and are older, the inevitable sets in.

    • Peter Attia  April 29, 2012

      I would suggest this is the “poor man’s” quick test for insulin resistance, but little else. If I had a dollar for every patient I’ve seen with a “great” ratio of TG to HDL-C (i.e., 1.0 or better), who also had “great” LDL-C, but had “horrible” LDL-P, I’d have a lot of dollars. Furthermore, every one of these “dollars” I’d collect represents someone who is almost certain to die sooner than they ought to because a simple test was not ordered.

  32. Diane  April 25, 2012

    Phytosterols, is that something like the Benecol butter?

    And I do hope you will talk about super high cholesterol. I’m afraid to get mine tested since changing to low carb. Normal for me was around 265. My mother’s is 400+ when not on a statin. My grandmother’s was similar.

    • Peter Attia  April 26, 2012

      Diane, please get an NMR. Numbers like that do suggest Familial Hypercholesterolemia (FH).

    • PaulaM  April 30, 2012

      Re: Diane’s: Numbers like which? The 256 (hers) or the mother’s (400+)?

      It’s become obvious that we should all know our NMR (LDL-p). A rhetorical question, again: At what point is it . . . the point of no return in terms of age and “damage done”? I am watching the current guiding evidence of Dayspring and Taubes (and you, as I know you were involved with the Specialty Health study) series.

      Thanks for all you do — truly.

  33. Ash Simmonds  April 26, 2012

    Man, fantastic post. Probably a bit sciencey for most but I as a science and medical geek massively appreciate it.

    I seem to constantly get the “watch your cholesterol” thing thrown at me (ketogenic steak fancier) and I ask if they actually know what cholesterol is or does. Almost nobody does, and 100% of people who tell you to be wary of it don’t.

  34. Marilyn  April 26, 2012

    Just wondering. . .At the Mendeley site to which you linked is a statement: “The absorption efficiency of cholesterol is most likely determined by the net effect between influx and efflux of intraluminal cholesterol molecules across the brush border of the enterocyte.” Since, as I understand it, the brush border can be damaged by gluten, and is really damaged by something like Crohn’s, what effects to these conditions have on cholesterol tests, and on cells that depend on cholesterol?

    • Peter Attia  April 26, 2012

      That’s a great question. To be honest with you, I don’t know the answer to this question. We do know that folks with intestinal disorders, which can impact ABCG5,G8, have problems with bile reabsorption, which can lead to gallstones…so it seems plausible that this, too, can impact sterol absorption/secretion. The real question, of course, is whether or not this is clinically relevant given the body’s ability to up- or down-regulate synthesis, if necessary, to compensate for changes in gut absorption. If anyone knows the answer, please do share.

  35. Alexandra M  April 26, 2012

    I was going to put this where I asked about Pattern A and Pattern B, but maybe it’s more appropriate here:

    Have you told Gary and Tom Naughton? Because they’ve been exhibiting their “pattern A” LDL as a diploma from the low carb school. Though I must say that saying that LDL doesn’t matter and then saying that it does if it’s large and fluffy doesn’t make sense to me.

    But, this particle size thing does seem to matter: What if somebody goes low carb, their TGs go down, their HDL goes up, but their LDL(-C) remains the same? Doesn’t that mean they’ve improved their lipid profile? Because high HDL and low TGs strongly correlate* with large LDL, which would suggest that even though the quantity of cholesterol has remained the same, the number of particles must have gone down?

    *I found a paper – from the Netherlands, I think, though I haven’t been able to find it again – that said NMR was an unnecessary waste of money because of this strong correlation.

    So, now I have to go tell the troll who said low carb was bad because of elevated LDL, that what I told him about different types of LDL was wrong? (Not that it will really matter, because I buried him so deep that he never came back.)

    • Peter Attia  April 26, 2012

      I’ll get to this in detail. 30-40% discordance is far to large to rely on a correlation. Furthermore, the cost of NMR is not nearly as great as people make it out to be. Is it really worth pinching pennies if you’re in the 30-40% of the population where LDL-P is higher than predicted by LDL-C?

  36. Ellen  April 26, 2012

    I love this.. every time the truth about cholesterol is shared, we take the Diet Heart Hypothesis down another peg. I think the “cholesterol is bad” lie is at the root of much of the medical and pharmaceutical deviance in our healthcare system, and yet it continues to thrive, like some kind of mythical zombie.

    I devoted a whole page on the importance of cholesterol and all the stuff it does in the body here. I’m going to link to this series just to drive home that message with the weight of your medical credentials. Thanks for writing this!

  37. Jim Bowron  April 26, 2012

    This post reminded me of an article in our local paper last week. (I know, a bad source for comments on science) The article referenced media release which suggested that cholesterol may inhibit cancer growth. The researchers at SFU comment on this research, and the published paper, at http://www.sfu.ca/pamr/media-releases/2012/study-finds-cancer-fighting-goodness-in-cholesterol.html
    Clearly not the final word on this subject, but adds to the ‘good’ cholesterol comments made here.
    Thanks for the education.

  38. Paul  April 26, 2012

    Thanks Peter, great stuff. I keep hoping that with bloggers like you, my father and brother (both doctors) may one day awake from their dis-interest in this topic and get healthy. I still can’t find the right words to make them think they can learn about health from me (just a Naval officer and aviator and CrossFitter, what do I know about health, eh?).

  39. Marilyn  April 26, 2012

    Thank you, Peter! Another question has been rattling around in my head: Through the years, I’ve read a lot of discussion about the various cholesterol measurements being “associated with” or a “risk factor for” or “predictive of” heart attack, stroke, whatever. I hope you’re planning to discuss whether cholesterol has ever been proven to cause any of the things it’s accused of, and if so, how it does so.

  40. Alex Carvalho  April 26, 2012

    I have my standard colesterol test scheduled for tomorrow… I wonder if I shouldI even bother…

  41. maXXX poWer  April 26, 2012

    I look forward to every new post on your blog, keep up this great work, u are a dynamo, how do u find the time?

  42. John Dawson  April 26, 2012

    Thank you so much for this great blog!

    You said “Certainly possible with the right nutrient mix, but requires more attention.”

    I am interested in some detail on the right nutrient mix for adding muscle mass. I hope you plan to address this in a post.

  43. Allan  April 26, 2012

    First, thank you for this incredible service. Really helpful.

    Request: A major punchline here is the proportion of circulating cholesterol derived from the diet. You’ve got the numbers but it’s left to the reader to stitch them together (for example, 25% of cholesterol is exogenous, but then >50% of that is esterified and not absorbed, thus <12.5% of the cholesterol used by the body is derived from diet, which is similar to, perhaps the same number as, the 15% exogenous UC which is the complement of the 85% endogenous you cite…). A picture would be helpful; I'm imagining arrows of various thicknesses going from diet, liver, etc. into the gut and then into circulation, cells, etc.

    On a related note: it would be nice, if the data are known, to know the relationship between change in cholesterol intake and change in circulating cholesterol. That is, if one quadruples the amount of cholesterol one eats, what is the effect on cholesterol in the body? The naive notion would be "it quadruples"; the prediction from cholesterol being tightly regulated would be "it does not change". Has such a study been done?

    • Dan  April 28, 2012

      Allan, for some people, LDL cholesterol and LDL-P can go up markedly on a high fat low carb diet, particularly with consumption of large amounts of saturated fat and dietary cholesterol. This effect is unpredictable and could be limited to people who have genetic mutations in intestinal transporter genes – we really don’t know. Some people think it is related to ApoE status. The only way to know is to draw measurements before and after diet. This was true of my case, in which low carb / high fat normalized by triglyercides, HDL and hs CRP, but radically increased my total and LDL cholesterol (I am still waiting for the LDL-P to come back from the lab). The result is that I had to cut down on my dietary fat consumption, switching more to lean proteins, and start taking a statin. Even to begin with, my LDL was a bit on the high side, but nothing like it was after the diet. So to say there is no relationship between the cholesterol or fat in the diet and the cholesterol (or fat) in the blood is really a stretch….

      Note I’ve seen this phenomenon in others too, and it has been amply documented in the literature since the 1940’s.

  44. Maryann  April 26, 2012

    Thank you so much for all of your hard work Peter! For the first time ever, I will miss not having my computer on vacation! I will be reading for hours when I get back.

    Thank you to all who post comments, too. It is nice to have a thoughtful, enthusiastic, eager-to-learn community of like-minded people to exchange ideas with, and such a one-of-a-kind teacher in charge of it all.

    We have taken Red Yeast Rice, phytosterols and sytrinol to lower our cholesterol. Are these things harmful?

    Great post Peter, I look forward to the continuation of the series, thank you! Maryann

    • Peter Attia  April 26, 2012

      No role for phytosterols whatsoever. I’ll address this at a later time.

  45. Michael  April 26, 2012

    Can you add a print button to your blog so I could print this post and read it on the bus? I spend too much time in front of a computer screen already. IMO all blogs should be printer friendly.

    • Peter Attia  April 26, 2012

      Why not just copy it into WORD and print from there?

  46. lorraine  April 26, 2012

    Tara Dall’s video series on Lecturepad was beyond impressive. Thanks for the lead.

  47. steve  April 26, 2012

    If it is LDL particles being lodged in the artery wall and the cholesterol in the LDL particle that then causes a plaque( along with other things) would having less cholesterol in the LDL particle be beneficial? Seems to me not from the info you have provided above, and yet many Lipidologists continue to stress avoidance of saturated fat(raises cholesterol in their view)and emphasize mono and poly fats.
    Where do your mentors Dayspring, Dall, Cromwell, etc stand on the diet recommendations? They may all agree with less carbs, but on the type of fat?
    Also, what is the best strategy for reversing coronary plaque, with diet and what resulting NMR profile- How low must particles be? Thanks.

    • Peter Attia  April 26, 2012

      Patience, Steve…. If I answer every (great) question being asked that is beyond the scope of THIS post, I’ll have to quit my job, divorce my wife, and take up a nasty cocaine habit. And I still won’t have enough time.

    • steve  April 26, 2012

      wouldn’t want you to do any of that; nor would i want you to neglect your kids,if you have them! Thanks.

    • Peter Attia  April 26, 2012

      Thanks for understanding.

    • Maryann  April 26, 2012


    • Lex  August 10, 2012

      RE the question of where do Drs. Dayspring, Dall, et al, stand on dietary recommendations; I was surprised to find on Tara Dall’s site a testimonial from a patient stating that Dr. Dall advised removal of red meat from the diet. Can you comment on this subject yet?

    • Peter Attia  August 10, 2012

      I can’t really speak for her. It’s quite likely that just as my understanding of lipoproteins is evolving, so too is Dr. Dall’s understanding of nutrition. They may not represent her current views.

  48. Anna  April 26, 2012

    Hi Peter,

    I’m curious about statins. It seems bizarre how popular they are, given the information above.


    • Peter Attia  April 26, 2012

      Statins are great drugs, IF they are used to treat the right problem. I’ll get into this later in the series. Think of statins like a hammer — great for hammering nails; lousy for cleaning your window.

    • Claudia  April 27, 2012

      “Think of statins like a hammer — great for hammering nails; lousy for cleaning your window.”
      Just keep it up, you’ll have us all understanding this in no time.

  49. Victoria  April 26, 2012

    Peter, thank you so much for this website. Like many women, I have dieted since my first child ( yes, a long time ago!). My husband found Gary Taubes and it lead me to your website. I am on my 31st day of ketosis and very energetic and happy!! I feel amazing and ummmm…according to me, starting to look good as well! I have devoured this website and think I am caught up on my reading and the rest of the gang! Thank you! Thank you!

    • Peter Attia  April 26, 2012

      Thank you. Glad you’re finding it helpful.

  50. James  April 26, 2012

    A little off-topic, but I was wondering if you had an opinion on the necessity (or lack thereof) of taking a CoQ10 supplement along with statins. I’ve read that statins can deplete CoQ10 and that supplementation might help with potential side effects but haven’t seen a whole lot written about it by people who seem to really understand lipidology.

    • Peter Attia  April 27, 2012

      James, sorry to do this, but I need to quote, directly from the post, not just because of your question, but because so many others have missed my request: “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.”
      I will address this in the future.

    • James  April 27, 2012

      Completely fair. I had searched for any other posts where you might have mentioned it to see if there was somewhere more appropriate to ask that question. Knowing that it’s on your radar is sufficient for me at this point.

    • Peter Attia  April 27, 2012

      No problem. Thanks for your patience.

  51. Stephen Brand, CPT, SFN, SSF  April 27, 2012

    Interesting. Keep up the good work!

  52. Maryann  April 27, 2012

    Hi Peter,

    Does the NMR reflect just a snapsot of what is happening in the body at the time? Or is it the picture of years of the body’s state of health? And can lipid testing be affected by exercise? Should exercising be avoided the morning of blood work to ensure accurate results? Thanks, Maryann

    • Peter Attia  April 27, 2012

      NMR, per se, reflects what’s going at a moment in time, but of course it’s highly dependent on what’s BEEN going on up to that point. Nothing is really static.

  53. Denise  April 27, 2012

    Coincidentally, reading this chapter in “Good Calories Bad Calories” right now. I just finished reading “Real Food” by Nina Planck where she draws this picture: Where you see a fire, you’ll probably see firemen. Blaming cholesterol for Atherosclerosis is like blaming the firemen for starting the fire.

    I believe the internet will be the new tool for mass re-indoctrination on the health front. Unfortunately, I couldn’t get most of my friends and family to read and digest this article without a fantastic infographic.

  54. Bob Kaplan  April 27, 2012

    “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).”

    Really good point and might be analogous to the idea that there’s always an “excess” of nutrients sitting outside cells (something Craig Thompson at Sloan-Kettering pointed out in a paper in Science), but cells won’t take them up unless they are told to (like insulin and glucose). The mere presence of “too much” of a substance in the blood stream isn’t really the issue. There is almost always an “excess” of fat, cholesterol, and nutrients in the body.

    You are not what you eat; you are what you do with what you eat. The same can be applied to the different molecules and compounds inside and outside of cells.

    • Peter Attia  April 28, 2012

      Exactly. Worth re-stating: You are not WHAT you eat…You are what your body DOES with what you eat.

  55. Mike  April 28, 2012

    Absolutely FANTASTIC explanation! Most useful blog on ketosis and general health I’m following so far, keep up the good work!

  56. Suzy  April 29, 2012

    It begins…
    Everyone who cares about the freedom of people like Peter to continue to do what they do needs to read this.

    • Mark Jacobs  April 30, 2012

      Very scary, this guy lives close by me here in NC.

  57. Mark Jacobs  April 30, 2012

    Thank you so much Peter for your work and sharing with us. I like so many others are eternally greatful that you are taking the time to supply this information. I am learning much more about the human body than I ever thought I would.

    It truly is disappointing that cholesterol has been made out as a bad actor in our minds. I like so many others, before I discovered low carb thought it (cholesterol) was something to be scared of. So refreshing to actually learn.

    I made a comment that I started VLC eating in March and have dropped 23 pounds since then, your reply was to keep up the work, Peter eating VLC is NOT work. It’s a joy to finally eat what I have always enjoyed eating and it’s a joy to stop eating so much sugar and grain. I feel fantastic. The only work is getting over my anger at the medical community and US government for not looking into this “alternative” way of eating.

    Thank you again

    • Peter Attia  April 30, 2012

      Really glad to hear, Mark. Keep up the “pleasure!”

  58. Lesley  April 30, 2012

    Thanks for the clear and informative post and for all your hard work in ths area, you are delivering an amazing public service as these posts are shared on many other sites. Look forward to the rest of the series.

  59. Ed  April 30, 2012

    SKYROCKETING LDL-P(as measured by Apo-B) on a VLC diet:

    Your post is extremely timely for me because I just learned last week that my LDL and Apo-B (my particles are large) has SKYROCKETED on a LC diet (not ketogenic, prob 100g day in non starchy vegetables), and from the comments here I am probably in the very small minority but certainly not alone. PLEASE if you share this same experience, contact me and let’s share notes. I will attempt to contact Dan who also posted on this. 2 months into my LC diet, I had my best numbers ever… 200 TC, 120 LDL, good HDL and TG (which was 60 points less than before the LC diet, as way of reference). My LDL-C is now 300, and TC is 400. ApoB of 200 suggests I have 2x the number of particles that they use as a cutoff. This is way higher than when I was fat!

    The interesting thing is that low carbing clearly has helped me in almost all measures except my Apo-B/ LDL-C. My weight, blood pressure, energy levels, HDL, Triglycerides… all improved. My CRP after 3 months of LC was barely measurable. My LDL levels initially responded the way that is predicted by most Low Carb diet trials. HDL up significantly, TG way down, and LDL flattish… in fact, my LDL improved a bit at one point. All this news came at the same time with Gary Taubes life changing book, so it was self reinforcing.

    I’ve been low carb for almost exactly 1 year… completely transformed my body in a positive way, but this LDL phenomenon is a MAJOR wakeup call that maybe I shouldn’t be as zealous as I have been advocating low carb.

    My 3 avenues for follow up (as of now) are:
    1) Thyroid hormone. There has been some chatter in LC circles that LC can reduce Thyroid, or specificially TSH to T3 conversion and increase in reverse T3. I havent explored this in depth, but a first pass google search reveals that T3 is related to LDL receptor activity. Since Familial Hyperchosteremia is a result of poor LDL receptor function, clearly, a down-regulation in LDL receptor activity would increase plasma levels of LDL-C and presumably LDL-P. But can changes in thyroid hormone explain that much a change in LDL? I wish there was some clinical data accessible about that. Peter- I hope you address this in your next post.

    I also recall from somewhere that LDL receptor activity may be influenced by insulin levels. There is also the potential and paradoxical issue of INCREASED INSULIN RESISTANCE on a low carb diet, as your body becomes more insulin resistant in an attempt to conserve glucose levels for the brain. I thought one extremely interesting clinical application from Dr Dall’s lecture was the use of Metformin to cut LDL-P by almost 50% in one case. Peter, if you get a moment to comment on what mechanism might be at work there, it would be helpful, but I’m guessing it would have something to do with insulin signaling and probably related to LDL receptor activity.

    So I had my first sweet potato last night, and a little bit of rice… I didn’t like the fact that my glucose level shot up from 95 to 140 in the first hour but perhaps that’s another sign that my insulin sensitivity has gotten worse since going on LC. Perhaps it’s just a little TOO LC.

    2) Gut absorption. Perhaps I’m an over absorber. I hate to go into this level of detail but one downside of LC has been changes in bowel movement patterns. Maybe something has changed the efflux/influx ratio of cholesterol from bile since I went low carb. One thing that Dr Dayspring mentioned was to check lathosterol/desmosterol because that gives some indication whether you are producing too much or absorbing too much.

    3) Dietary fat. This seems less likely, but there are classes of saturated fats that seem to raise blood cholesterol levels differently, and dairy is high in palmitate. Seems unlikely but I didn’t eat a lot of dairy a year ago and my cholesterol was a lot lower so I’ll give that a try.


    Yes, there is a clear association between LDL-C, LDL-P and atherogenesis. And LDL-P appears to be a stronger association than LDP-C. But if there is no inflammatory cascade, is it a problem to have high LDL-P? How does this risk factor stack up against other risk factors such as high Blood Pressure, Increased adiposity, etc? One thing that doesn’t seem to make a lot of sense to me is that if you have 1000 particles its OK, but somehow at 2000 you are going to get atherosclerosis? One particle is ok but 2 isnt? Plus, even with these risk associations, it seems as if there are plenty of people with high LDL-P that don’t get CVD and some people with Low LDL-P that do. Maybe I’m wrong… maybe everyone with high LDL-P has atherosclerosis but no measured CVD event. Peter can you elaborate?

    Any other patients out there with a similar experience? Lets share data. mail.edward.lee@gmail.com. One frustration I have from reading studies is that the numbers are always shown in averages. We are not averages.

    • Ed  April 30, 2012

      NMR vs VAP vs Standard Lipid PaneI:
      I totally understand your bias for getting particle counts which is much better than knowing the amount of serum cholesterol. You are measuring smoke, not the fire. But why would you consider the VAP panel inferior to NMR? You get an Apo-B stat out of a VAP Panel, and as I understand it, LDL particles only have 1 Apo-B molecule, so that essentially gives you a particle count. I know that Chylomicrons, VLDL, IDL also have 1 Apo-B per particle as well, so there could be some discrepancies if the ratio of those other Apo-B particles to LDL changes (as Dr Dall alluded to in her clinical application talk on LecturePad). I know VAP provides an estimated Apo-B, and perhaps the estimation correlations are poor, but assuming their Apo-B numbers are good, one would think this would be just as useful as an LDL-P stat. From what I have read, all Apo-B particles could have some atherogenic qualities, so wouldn’t you want to know stats for these other classes of lipoproteins? Plus, wouldn’t you want to see the various levels of Lipoprotein subclasses to give a window into how these lipoproteins are being metabolized/catabolized in your body? When I see an NMR panel, it doesn’t seem to show anything about these other subclasses or particles.

    • Peter Attia  May 1, 2012

      VAP estimates apoB, which is known to have mistakes. Furthermore, there are examples of apoB – LDL-P discordance. The NMR test is so simple. There is little need to avoid it.

    • Peter Attia  May 1, 2012

      Completely agree with your point. We are not averages!

    • Anu  May 1, 2012

      I thought from reading Taubes’ Good Calories Bad Calories, that LDL-C was only very weakly correlated with atherosclerosis and heart disease risk — so I’m not sure why you’re saying that there is a clear association between LDL-C and atherosclerosis. Your triglycerides, HDL, and VAP/NMR are much more important measures. If everything else is going well, why get hung up over a number? I don’t this is an indication that you’re going too low carb at all!

    • lorraine  May 1, 2012

      Ed, On your low carb and thyroid issue, this has come up for me again just yesterday, after listening to a podcast at Jimmy Moore’s featuring Chris Kresser who spoke on this very issue. Here’s a copy of my comment on that podcast posted below.

      “As a thyroid patient, struggling with all the issues that thyroid patients struggle with, I had been aware of, and concerned by, the reduced T3/increased rT3 levels associated with carbohydrate restricted and calorie restricted diets. I read a lot of the literature, including the old stuff from way back in the 50’s and a couple of textbooks, and while it confirms the changes in the levels of the hormones with carb/calorie restriction, generally it appears that resting energy expenditure only decreases on severely restricted caloric diets. So, are the changes in T3 and rT3 levels really clinically significant; ie, do the changes in the levels mean that thyroid function itself is harmed by carbohydrate restriction? A discussion of this question appears in a 2004 paper by Wolfgang Kopp in the journal Medical Hypotheses in which the author reviews the literature on the topic and indicates that, “The sharp decline in T3 levels as a result of very low carbohydrate diets is not associated with a reduction in the resting oxygen uptake, or symptoms of functional hypothyroidism (cold intolerance, dry skin, increased need for sleep). Despite decreased T3 concentrations, basal TSH levels are normal or even mildly decreased. The lack of clinical symptoms, together with normal or mildly decreased TSH levels suggest that the organism does not suffer from a deprivation in thyroid hormone in association with carbohydrate restriction.” His rationale is that our modern “normal” levels of T3 may be quite higher than our paleo ancestors exactly because of the carbohydrate load of modern diets. He concludes that “the metabolism of dietary carbohydrate is a thyroid hormone consuming process.” I really liked this guest and felt he had a great command of the thyroid and how it works. However, I felt he implied that carb restricted diets decrease thyroid function (not just thyroid hormone levels), sort of like you should watch out that if you carb restrict and lower your insulin levels that you won’t be able to convert T4 to T3, and you’ll go down this metabolic dead end with production of rT3. It appears there is a reasonable argument to be made that in the carb restricted state, you don’t need as much T3, and that this lower level of thyroid hormone is more aligned with that of our paleo ancestors.”

      I see that there is another interview that Chris Kresser does on his website with Chris Masterjohn that gets into some of this, which I have not yet listened to, so who knows if there’s a wider perspective that I lack.

    • Ed  May 1, 2012


      Thanks for your comment! The internet is a great community and helps provide better suggestions or ideas than my own doctor.

      Thanks to the power of google, and my sudden fascination on the subject, I managed to find that very same interview and listened to it on my commute to work. So my Thyroid testing panel is definitely on my “TO DO LIST”.

      Another post I found which very topical to the SOARING LDL-C/LDL-P/Apo-B vs Thyroid discussion is here on Paul Jaminet’s website. http://perfecthealthdiet.com/?p=4457

      Anyone worried with soaring LDL as a result of low carb should take a look at that one, too. Now what’s great about this is that it has a personal story chronicled by someone with this exact issue, that has kept clinical records of his “self-experimentation”. His TC went from 250 to 360 back to 200 very quickly with T3 supplementation. Now I know his data doesnt include the NMR or VAP results, but I think it gives a good ideas of the magnitudes of changes that can be involved if this is the root cause.

      There obviously is a much broader question here, and perhaps Peter is going to address this in his next post. Should we care about LDL-C, LDL-P at all? For example, if T3 is causing LDL receptor activity to diminish, and LDL-P and LDL-C rise dramatically as a result, does this imply more CVD risk, if all other biomarkers associated as risk factors such as HDL, TG, Blood Pressure, HbA1C, weight are improved?

    • Peter Attia  May 1, 2012

      I will be addressing this, but not this week. LOTS to learn before we can have that discussion. This week will cover cholesterol transport.

    • Ed  May 1, 2012


      I agree that LDL-C is probably a weaker association with atherosclerosis than those other measures. In fact, I thought a very funny study recently came out that surveyed hospitals and CVD events over the last 5 years and showed that average LDL-C for those patients were BELOW national averages. But I have seen enough epidemiological data (including those in Asia, as I am of asian descent) that suggest that CVD is more common in those with higher levels of LDL-C. Should we fixate on LDL-C, LDL-P? No, I doubt it, and perhaps Peter will shed more light on this in his next post, but I think a very elevated level (above 95th percentile according to Dr Dall’s lecture) should at least cause one to “think it through”.

      But it is a good question. What should one do if you have 1 very elevated risk factor, but have reduced risk factors for everything else? Thats something I cant seem to find good information on. You cant live your life trying to manage every single number that might be deemed a risk factor.

    • Dan  May 1, 2012

      Ed, like you my LDL soared on low carb high fat diet. According to a meta-analysis of >900,000 patients published in The Lancet in 2007, I increased my risk of dying from coronary disease by somewhere between 8 and 16-fold (the exact number is about 8 x sqrt(2) – I have not yet done the math). All other parameters that you mention including BP, triglycerides, CRP, glucose, insulin, A1c have fabulously improved. I am still waiting for my LDL-P to come back but I am scared enough from the epidemiological data to cut my intake of red meat, cheese, whipping cream and the like, and pursue lean protein sources instead. I have not increased my carbohydrate intake and my TSH/fT4/T3 levels were all within normal range. I have also started a statin, which we know from 15-year follow-up of hyperlipidemic individuals does reduce mortality. In our case, there is no need to abandon low carb, but I would recommend abandoning high fat, or at least replacing high fat with healthier fat sources and protein. I realize this will be very controversial here but I don’t know of another way to proceed (and I’m not waiting for my LDL-P to take action). Like you, I am probably very sensitive to the effects of saturated fat and dietary cholesterol.

    • Ed  May 2, 2012


      I guess you already investigated the thyroid connection and didn’t find any issues. That in itself is another datapoint.

      I was on a statin at one point, but after improving all my other risk factors on an LC diet (except for LDL-C and LDL-P), i decided to ditch them for a while… especially after thinking through how they work. I started to question how I should weigh the well-documented potential improvements in heart health against the anectodal body of evidence that statins might impair brain health long term. So for now I am taking my chances… but this latest test result might swing me in the other direction.

    • Dan  May 2, 2012

      Ed, I checked TSH, fT4, fT3. I did not check rT3. However, I also checked am cortisol and insulin.

      If you are convinced you are hyper-absorbing, there are drugs which block intestinal cholesterol absorption such as ezetimibe, colesevelam, cholestipol and cholestyramine. For myself, I prefer a statin, as my LDL at trough on a high carb low fat diet was quite high (and even worse on low carb high fat). Also, statins are much more evidence-based (of those 4 medications, only cholestyramine has a positive clinical trial but this dates to >30 years ago, and it’s a real hassle to take).

      To be honest, I am not sure what to make of the “rT3” story. Looking to first principles, it is pretty clear from the literature that adding sat. fat and dietary cholesterol can alone boost LDL to tremendous levels (when I showed 2 cardiologists my lipid panel, they thought I had genetic familial hypercholesterolemia).

    • JohnJ  May 4, 2012

      Apparently you don’t necessarily need high fat for a ketogenic diet. But probably has to be calorie restricted. It can lower LDL.

      The Effects of a High-protein, Low-fat, Ketogenic Diet on Adolescents


    • KevinF  May 4, 2012

      @JohnJ: well yeah, at an unsustainable “650 to 725 calories” a day for 8 weeks, these kids had to be in ketosis to keep from dropping dead. But I’m guessing they couldn’t have added much more protein than what they ate and still be ketotic … the “high fat” diet comes into play on the assumption that you don’t want to be starving. A more interesting question is whether these kids could have still lost a lot of weight if they’d been allowed a few more hundred cals of fat per day.

    • JohnJ  May 5, 2012

      It is not about a fixed ratio there are just general suggestions for people wanting to become keto adapted. You don’t have to stuff yourself with fat to get to a certain ratio, if you are losing weight the amount of fat you lose will contribute to your fat ratio. How sensitive you are to carbohydrates and protein with your insulin response will also have to be taken into account. If you have very high insulin resistance leaving insulin around longer it will also influence how hard it will be to become keto adapted. Each individual has to experiment see what works for him according to his goals, the meter testing can be expensive, but the Ketosis urine test strip even not the best are cheap.

  60. George Henderson  May 1, 2012

    I’m thinking, if you pushed up your cholesterol by eating lots of sugar, that would be harmful high cholesterol.
    If you elevated it by eating lots of healthy animal fats, that would be healthy high cholesterol.
    Cholesterol testing doesn’t really distinguish between the very different scenarios that the lipids are one symptom of.

    It’s like weight: you can weigh a certain amount sitting at home because of the gravitational effect of the Earth on your mass;
    or you can weigh the exact same amount in zero gravity because you’re in a rocket accelerating away into empty space.

    The exact same phenomenon, weight, and the same weight, as far as you’re concerned, but the consequences for you over time will be very different…

  61. greensleeves  May 1, 2012

    Should we just abandon LDL as a treatment target? One Yale medical professor says yes:


  62. David Nelsen  May 1, 2012

    Greensleeves, If you mean LPL-C – then yes it has little value. LPL-P is another story. I found out today that both blood draws I have had to get the NMR lipid profile were screwed up and I have to get it done yet again.

    Looking at the NMR lipid profile website http://www.theparticletest.com I found that they are pretty clueless in how to lower LPL-P. The following is cut and pasted from their website:

    Eat more whole grains, fruits and vegetables. Eating more of these foods, like whole-wheat pasta, beans, nuts, berries, spinach and broccoli, are good for your heart. Limit your red meat — like steak and hamburgers — eat fish at least once a week and lean turkey or chicken without the skin. Use olive oil or canola oil in place of butter. Avoid fried foods or those meals served with heavy sauces.

    In my case, hopefully the 3rd time will be the charm.

    • PaulaM  May 2, 2012

      David — I am on that website now. I am not done snooping around, but so far I cannot find any such dietary recommendation; however, is this not counter to everything we (you know the ‘we’ I am referencing) are aiming for!?

      Wait . . . it’s a joke, right?!

  63. David Ma  May 1, 2012

    I stumbled upon this article from JAMA in 2003 which found higher levels of APO-B in patients undergoing the ketogenic diet. From what I understand APO-B is more closely related to cardiac disease than other lipid profile measures: http://jama.ama-assn.org/content/290/7/912.full

    What do you think of the conclusions? JAMA is fairly reputable and not many crappy studies slip through the cracks.

    • Peter Attia  May 1, 2012

      I’ll give it a read when I get some time, but please don’t assume something is “good” because it’s in JAMA or NEJM. Lots of good AND bad stuff in all journals, including the most prestigious.

  64. Kypros  May 2, 2012

    Hi Peter,

    I would be interested to know what you think about looking at lp(a) to measure heart disease risk. Is research showing that there is a high concentration of lp(a)in atherosclerotic plaques reliable? Finally if levels of lp(a) are determined by genes what can you do to lower it? Niacin?

    Thanks again for your great work!

    • Kelly  August 6, 2014

      All — I just discovered Peter’s wonderful work and your many excellent comments, and, while I am 3 months late to this thread, I’ll add two questions here and hope for the best while trying to get caught up!

      Kypros — Thank you for your question about lp(a) – particularly important when one has both alleles for this gene (as I do) — as I am on both Lipitor (generic) and heavy daily doses of Niacin.

      Peter — Maybe I have missed it, but is there a reason why you have not recommended the Berkeley Lab test for at least some individuals when it provides such detailed info about the many different types & sizes of both HDL and LDL particles as well crucial genetic profile data?

      Thank you, and best to all!

    • Peter Attia  August 6, 2014

      I’m not convinced (yet–but I’m open to changing my mind) that particle size is as important as particle number. I prefer NMR by HDL, Inc. (using Liposcience) than BL, but BL is fine, too.

  65. Thom  May 2, 2012


    Great post as always. I entered ketosis about a month ago and have felt great while dropping some unnecessary fat stores. Through this process I have developed a few questions that I would value your insight into:

    1. Is there a way to back into the rate of fat loss using a fasted blood ketone level?
    2. How significantly does caffeine affect insulin levels when eating primarily fat and protein (I noticed that Australian ketogenic diet recommendation include the elimination of caffeine from the diet)?


    • Peter Attia  May 2, 2012

      1. Not in a reliable manner. People are wondering if a fat-secreted hormone, adiponectin, might play a role there, but not B-OHB.
      2. I’ll cover this in the future, but it does appear that caffeine does impact insulin in some people.

  66. Rakesh Patel MD  May 3, 2012

    You can now get direct Apo B thru Atherotech when ordering VAP, has been available now for about a year

  67. Katrina Bourne  May 5, 2012

    I Too am a supporter of our chloresterol!! Having been told by my Dr here in the UK that despite my being at the right weight (BMI 24) my chloresterol figures, were in her opinion, too high, (the “Good” and “bad” were almost the same figures and as we measure ours differently to the USA I won’t quote them here) and I had to lose at least 14lbs I more or less told her thanks but no thanks and left. I have had to change my diet anyway because of milk and yeast intolerances which have had the side effects of altering my chloresterol figures anyway so I don’t need the hassle. I feel marvellous because I no longer have IBS and am not so tired and at nearly 60 feel fitter than i did at 30!!

    My guru on the subject of Choleresterol is Dr Malcolm Kendrick. He wrote a book called “The Chloresterol Con” here in the UK and it has become my bible. It debunks the statin debate and shows that the only way to keep healthy is to follow a sensible lifestyle. I think the only reason that statins have become the panaceas they have is that they are seen as a “fix all” without anyone having to change their lifestyle. They can continue to be overweight, eat crap and sit on their bums, the pills will keep them going!!!!

    I do think that the 21st Century diet is the killer. The chemicals we spray on and add to our food, the muck that is in the air, and the god knows what that is in our water all lead to a cocktail of sludge that gets into our bodies. I am not a “lentil cruncher” I like a good steak, but an organic one that has come from a bullock that has been in a field eating good grass with the sun on his back and has led a happy life! Too much to ask for?

    We reap what we sow. We must not only question our DRs but also they way we eat and what we eat. The air we breathe and the water we drink. It is encumbant on us to think of our grandchildren and what we are leaving behind for them.

  68. Sam  May 10, 2012

    I’m not a physician or otherwise knowledgeable about the hard sciences so I’ve had to read these articles a few times to understand a good portion of what you’re saying – please excuse this if it is a dumb question: Can you explain more about why we don’t need to worry about ingested/exogenous cholesterol? If our body makes all it needs we don’t need any from our food, right? Even though >50% of dietary cholesterol is CE, doesn’t that still leave a significant amount (<50% of total)of exogenous UC for the body to absorb? It seems to me that if you have a cholesterol-rich diet these numbers could really add up over what the body needs.

    • Peter Attia  May 10, 2012

      The body is smarter than us. If you give it too much, it’s probably going to respond by changing esterification and/or absorption. Ultimately, the data get the final say: when this is studied, there is not link between ingested cholesterol and atherogenic particles.

    • Sam  May 10, 2012

      Is there a breaking point? The pancreas secretes insulin when we eat too much sugar, but we can break that mechanism through overuse and wind up with diabetes. Have any studies shown if we can similarly break the mechanism that clears excess exogenous UC cholesterol?

    • Peter Attia  May 10, 2012

      I don’t know.

  69. Gary Althiser  May 24, 2012

    Been away from the blog for a couple weeks Pete, and the first post I catch up on blows my mind! Especially this:

    Eating cholesterol has very little impact on the cholesterol levels in your body. This is a fact, not my opinion.

    Can’t wait to read the rest. And if eating cholesterol does next to nothing harmful, there’s no reason to not keep eating it. Can’t wait for lunch!

    • Peter Attia  May 24, 2012

      My man! You’ve got some serious work ahead of you! Hope you’ve got some free time in the next few days…

  70. Paul Van Hoesen  May 27, 2012

    Hi Peter,
    I have just begun your series and I like the science side of it and the analogies.
    I will keep this Q to the subject of this post:

    Homogenized milk, which is ubiquitous in the U.S. since the early 70’s, is made so by pushing pasteurized milk through a very fine sieve at very high pressures ( super homogenizers work at over 1000 times atmospheric pressure- 14,500psi+). Before homogenization, fat globules range in size from 1-10 microns (a micron = ~0.00004 inch). After, the size range is reduced to 0.2-2 microns.

    I have read a few scientific articles stating that this process has two negative effects:
    1. It makes many more (5x) fat molecules to be presented to the NCP1N1 receptor (the “Ticket Taker”) than would normally happen if the milk fat had been left at the larger size. The larger size molecules of fat would simply pass right through the gut to the large intestine and be broken down by other processes but not absorbed into the bloodstream.

    2. The homogenization process causes xanthine oxidase (XO) from cow’s milk to be absorbed in the gut at a far higher rate which causes a host of health issues. (we could get into a debate about steroidal animal enhancements ending up in humans but I won’t digress).

    Is the small fat molecule theory plausible?
    Q. How exactly are Cholesterol molecules presented at the NCP1N1 receptor?
    Q. If the surface area of the fat is increased, isn’t it logical to assume that these receptors will see potentially more cholesterol?

    Here’s my experience: I have stopped drinking 2% milk or putting Half & Half in my coffee since both are homogenized.
    I started drinking drinking whole organic pasteurized milk (not homogenized) and kept my carb intakes limited at any snack or meal to 9g or less. (I cut Vitamin Water (32g in a 20oz bottle) or cranberry juice with water to 5:1 ratio if I want an “energy” drink). This keeps insulin at a minimum.
    I might eat 5 times a day but it doesn’t seem to matter. I am losing 2-3lbs a week. The whole milk has had a wonderful effect on my digestion.

    Before I added the real milk, I was still losing weight with the low carb routine but my digestive system was not anywhere near as healthy as it is now.
    There is something unique about milk and the lipids and other nice things in it.

    Thanks for your great work,


    • Peter Attia  May 27, 2012

      Paul, welcome to the series. I can’t say I definitively know the answer to your questions. My strong hypothesis is that there is enormous variation. We know, for example, that a non-trivial section of the population don’t “properly” regulate the interaction between the NCP1L1 receptor the ABCG5,G8 receptor, so right away some folks may in fact have more difficultly with certain fats or cholesterol esters. However, the NCP1L1 receptor is specific to cholesterol. Triglycerides enter circulation via enterocytes, but through a combination of simple diffusion and different protein transporters. I do not know the relationship between these, however.
      I don’t doubt that your experience at least suggests that less dairy is helping you. Many people experience this. I guess I’m just saying I can’t tell you exactly why.

  71. Paul Van Hoesen  May 28, 2012

    Thanks for the response. I just read your Part II and now realize how little I know about any of this.
    I didn’t actually reduce my milk intake, just changed what type of milk I drink – nothing homogenized.

    Physics would suggest that if I increase the number of milk fat molecules significantly via homogenization, I am going to present orders of magnitude more opportunities for fat molecules to dock with ANY receptors in the digestive tract. Consequences unknown and probably multiple.

    The TicketTaker is going to be obviously busier because alot more people are showing up to the Enterocyte Club. Those pesky phytosterols are also going show up somewhat oxidated already before the show even begins because far more of them have been exposed to water molecules via homogenization. They might be illegally dispensing free radicals at the bar before the Bouncer gets to them – who knows.

    Khan Academy’s series on Organic Chemistry is a good 101 foundation to understand what a lipid molecule really is. Once you grasp the basic Chemistry principles this discussion becomes far more “digestible”. http://www.khanacademy.org/science/organic-chemistry

    In all these analogies is a new, sane way to teach real health to K-12 kids…that’s who really needs to get it.


  72. Scott C. Irwin  August 14, 2012

    Hi Peter,

    Did you see this article?

    “Because egg yolks are high in cholesterol, eating whole eggs increases cholesterol, a known risk factor for coronary artery disease (CAD) and heart attacks. ”

    I see a lot of C.W. here. I am learning to relearn everything about food and health. Relatively new to this/your/Sisson’s/Taubes/paleo/primal approach. Would love your thoughts on this study.


    • Peter Attia  August 14, 2012

      You’re right to disregard this, Scott. This is complete and utter bad science.

  73. Brian  August 20, 2012

    I’m very late to this party as I just found your site through Chris Kresser complimenting your work at the AHS. Great info you have here, Peter. The hardest part: discussing it with the lay person. Try telling a friend that eating cholesterol has little impact on the cholesterol levels in your body. Most people think you’re a crackpot. A conspiracy theorist. The government is wrong, Brian? They’ve been lying to us all these years? Let me guess…they also synthesized AIDS in a lab, didn’t they? These notions are so engrained in the American psyche that I have little hope of new information being accepted widely.

    • Peter Attia  August 20, 2012

      The government has a track record for being wrong. Didn’t the government (in a profoundly bipartisan way) say that if every American owned a home, the world would be a better place? This led to the lending policies of circa 1996-2008. They said financial derivatives would reduced risk in the market place. That didn’t turn out so well. They said turning corn into ethanol would be good energy policy. Hard to find one scientist who agrees with that today. Want more? Don’t confuse a conspiracy — which I do not believe this to be — with a mistake.

    • Brian  August 20, 2012

      Thank you, Peter!

    • Kat  March 29, 2014

      Actually, Peter, finance is my wheelhouse.. Financial derivatves do spread risk and do it very well. You just don’t really understand the relatively complex product and the mental lightweights in the media are deeply confused by the most plain vanilla derivative. But your pont that government is amlmost always wrong is an excellent one. What other outcome can we expect when decisions in government are made by political fiat? None of us should ever take a single government guideline seriously. Only a fool would.

  74. Stikwoman  September 12, 2012

    I’ve been low-carb for a year (<20g/day) but I did not limit protein. I'm 43, female, 5'3", down to 140 from 158 Aug 11. I adjusted my carbs to <15 and limited my protein to 60g/day on 8/19, started ketone testing my blood on 8/22 and ranged from 1.1 to 3.1 so i've been in constant ketosis since i started testing. I had routine bloodwork and urinalysis done 9/7. Physician's assistant, of course, flags my "bad" cholesteral at 152 but she also says I have ketones in my urine and that long-term ketones in your urine will cause kidney disease. I explained my current dietary approach and she said low-carb/high protein diets are harmful. I corrected her that I am low carb, ADEQUATE protein but she still insisted that a "balanced diet is better." I've read Gary Taubes, you and Volek/Phinney so I "get it." My question – I assume my ketone spilling is a product of my recent jump into ketosis and that it will go away shortly but is there evidence that long-term urine ketones can cause kidney disease? Also, does ketosis affect bullirubin? I have elevated levels, as of this test, though my mother always has, also.

  75. Nick  October 21, 2012

    What happens to exogenous oxidised cholesterol? It that absorbed or not? Sounds like it is not by your description.

    • Peter Attia  October 21, 2012

      Most exogenous cholesterol is actually not oxidized and in fact is esterified so, you are right, it is not even absorbed.

  76. Ray  November 3, 2012

    Since CE cannot be absorbed by the enterocytes, I’m confused because in this post we’re going from the GI tract to a cell in the quadriceps, but we’re going there with both UC and CE. What’s the pathway for the CE for getting into the bloodstream like this?

    • Peter Attia  November 5, 2012

      UC can only be absorbed, but it can get esterified once in the body.

  77. Taylor George  December 17, 2012

    What is the very best test available to determine cardiovascular health? NMR? Is there something even better than NMR? Been LCHF for a couple weeks now.

    • Peter Attia  December 18, 2012

      No single test. Would take a few hours to explain the nuance. Need to differentiate between imagine (anatomical) tests, function tests, biomarkers (which can indicated either).

  78. Adam  December 18, 2012

    I have been doing LCHF for several months now (6-7months), and I had my cholesterol checked today. My work checks us for free every 6 month’s, but it is the standard test, no NMR.
    My results were:
    total: 182
    HDL-C: 61
    LDL-C: 116
    Trig: 75
    Of course my ldl was flagged as high, but my trig/hdl is still over 1. Am I doing something wrong? What can I do to improve the ratio? This was my first time getting my cholesterol tested, so I don’t have any other values to compare to unfortunately.

  79. Samantha  February 9, 2013

    I have a question, can you use HPLC (high performance liquid chromatography) to identify different cholesterols and lipids? I use HPLC and GCMS (and many other instruments) to identify plant and algal lipids that were from rocks or mud, so I was just wondering if you knew of any studies that used this technique.

  80. Brigit Laberge  April 2, 2013

    Hello Peter, my husband and I have been following your blog, and we have been consuming a high fat, moderate protein, low carb diet since October 2012.
    We would like to have blood work done,, so hypathetically, If you were getting blood work done, what would you specifically have tested? ie. cholesterol, triglycerides…
    Thanks for all of your time and hard work.

    • Peter Attia  April 3, 2013

      Later in the cholesterol series, can’t remember which part, I outline most of the tests.

  81. Zack  April 6, 2013

    This description is a bit to technical for some. I this guy does a better job simplifying the whole idea.

    Cholesterol: What’s up with that? http://anameyoucantrust.blogspot.com/2013/03/cholesterol-whats-up-with-that.html

  82. David  May 1, 2013

    Lowering cholesterol, sugar and stress by Yoga and Acupuncture

    —by Paramjit S Tappia and Yan Jun Xu, Winnipeg, Canada, CV network 2013

    Elevations in LDL-cholesterol, obesity and stress are major cardiovascular disease risk factors (1). Due to the side effects of a number of pharmacological agents, the potential of Yoga and acupuncture on cholesterol levels as alternative therapies has been explored, particularly in the Western world. Yoga is an ancient type of mental and physical exercise originating in India, and has been reported to reduce oxidative stress, body weight and blood cholesterol. Acupuncture has been used in China to treat a variety of diseases since about two thousands years ago. In ancient times, people used a sharp stone to pressure some points for pain relief. Subsequently, acupuncture has been found to be effective in the reversal of coma and stroke as well as for the treatment of chest pain, irregular heart beat, hypertension and other conditions including asthma and insomnia.

    Recently it has been found that acupuncture is also effective for the control of blood lipids, glucose and oxidative stress. A literature review of 220 publications conducted by Peplow and Bater (2) has revealed that acupuncture with electrical stimulation (electro-acupuncture) can control elevations in blood sugar in obese women. In animal studies, electrical stimulation (15Hz) for 30-60 minutes is required for positive results. From the literature available on Traditional Chinese Medicine books, Zhongwan, Zusanli, Yishu and Geshu acupuncture points appear to be most frequently used for diabetic patients. Liang and Koya (3) reviewed acupuncture literature between 1979 and 2009; it was evidenced that acupuncture can reduce insulin resistance, hypertension, metabolic disorder, obesity and improve blood lipid profile. Furthermore, frequently used acupuncture points were Zusanli, Fenglong, Tianshu, Neiting, Sanyinjiao, Quchi, Qihai, Zhongwan, Guanyuan, Yinlingquan and Pishu.

    Siu et al (4) have reported that electro-acupuncture is able to lower oxidative stress by stimulation of the Zusanli point. It appears that electrical stimulation at low frequency (2 Hertz), 30 min/day for 4 weeks yields beneficial effects. It is pointed out that different frequencies of stimulation can exert different effects. The underlying mechanism of acupuncture is that stimulation of different points release different neuropeptides and hormones. In addition, it has also been suggested that resistance of nerve fibres and electrical signals are altered in different disease that can be re-balanced by acupuncture. Acupuncture and yoga promote well-being and health and have the potential to be used as a complimentary therapeutic regimen to improve blood lipid and glucose profiles as well as attenuate oxidative stress.


    1. Adameova A, Xu YJ, Duhamel TA, Tappia PS, Shan L and Dhalla NS. Anti-atherosclerotic molecules targeting oxidative stress and inflammation. 2009; 15: 3094-3107.

    2. Peplow PV and Baxter GD. Electro-acupuncture for control of blood glucose in diabetes: Literature revies. J Acupunct Meridian Stud 2012; 5:1-10.

    3. Liang F and Koya D. Acupuncture: is it effective for the treatment of insulin resistance? Diabetes, Obesity and Metabolism. 2010; 12:555-569.

    4. Siu FKW, Lo SCL, and Leung MCP. Effectiveness of multiple pre-ischemia electro-acupuncture on attenuating lipid peroxidation induced by cerebral ischemia in adults rats. Life Sciences. 2004; 75:1323-1332.

  83. Christina  August 20, 2013

    I lost 26 pounds 154 to 128 lbs and my cholesterol went from 190 to 274 and my ldl went up as well. It occurred during menopause. I am not a fan of statins. Both my father and grandmother developed diabetes about a year after taking statins. Can you give me any advise?

  84. maria silva  September 28, 2013

    In view of the 10 to 1 gradient between concentrations of LDL in plasma and interstitial fluid, a level of LDL-cholesterol in plasma of 25 mg/dl would be sufficient to nourish body cells with cholesterol. This is roughly one-fifth of the level usually seen in Western societies. Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl. In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels. Second, the LDL level in newborn humans is approximately 30 mg/dl, well within the range that seems to be appropriate for receptor binding. Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl.

  85. Monica  February 26, 2014

    Although I know the main issue is high chlesterol, is there any chance all this could be be used to study how to increase cholesterol levels on children with learning delays, autism, etc, and very low cholesterol levels?

  86. Magarietha Zondagh  March 5, 2014

    Hi Dr. Attia, (I have sent this same letter to some lipid specialists but I think I should rather hve sent it to you. Here goes. just know in my knower that even with these specialists we will be given a lowfat diet regimen and statins. I have the disease, so do my 2 sons. My eldest son just had quintuple bypass at 34. My heart is broken. My mother has it and she’ll turn 83 this year. I also don’t have CVD. BUT, I went onto KETOGENIC diet in 2012 and for the first time in my life my total cholesterol came down to 6. Even on lots of lipid lowering drugs (NO, we cannot tolerate statins – we certainly WILL die on them – we get rhabdomyolises on it) my numbers never went lower than 8.8. NEVER. THUS I feel that our ilk have been left out with true research. They’re thinking like Ancyl Keys that eating fat is deadly for us, whereas my own GP told me that the blood can’t lie! AND, when my son tell them he can’t tolerate statins, they shrug their shoulders and say, “well now that’s a great pity”. I am quite cross and I need some diet science aimed at us! I do believe it lies with keto dieting. AND, very quickly too my cholesterol plunged on this diet! But my boys! I need them to live and not get sick on the only thing on offer and that horrible low fat diet. Sorry to be so abrasive, but I’m sick to death of this disease. I don’t care any longer if I die or not, but my sons OMG!
    ps I daresay too, that the motherload of these people are here in South Africa. They count among white Afrikaners, Ashkenazi Jews and strangely enough, our Indian population. I doubt very much whether we count as 1 in 500 – over here I wouldn’t be surprised if it’s 1 in every 40 or 50 people. My mother is surrounded by 4 other old ladies (strangers) in her retirement village who also have it. Of course, the men are not in that village, since they never MADE it!

  87. Stephen Johnson  March 19, 2014

    Very interesting! I have just come from a wellness checkup and was told that my “bad” cholesterol (triglyceride levels) was too high and pravastatin was prescribed to me. So, I came directly to do a little more research – before buying the drug! Just from the side-effects of the drug, make me question using it, now I see I need more research/education to learn the real issue of my cholesterol.
    Thank you.

    • Stephen Johnson  April 2, 2014

      Actually it is my “calculated LDL” is too high, which apparently means my HDL and triglycerides are too low. Will keep reading to learn if the provastatin (pravastatin?) is warrantied as prescribed.

  88. Mark Lewis  March 28, 2014

    Question: what percentage of cholesterol in eggs is esterified?

    I have read that “the vast majority” and “the majority” of cholesterol we eat is esterified (and hence we excrete it unless our body decides we need more and un-esterifies it. But does that mean 51% or 90%? Specifically with eggs – which I have taken to eating several of each day, what percentage of cholesterol in eggs is esterified?

  89. Billy  April 9, 2014

    I eat on average 6 raw egg yolks a day, so this won’t effect my cholesterol?

  90. Tim Harrison  May 6, 2014

    Can you tell me where I could find documented proof that Canada removed the limitations of dietary cholesterol. My dad has had high cholesterol for years, had bypass surgery done on both his legs and his heart and has been on statins for as long as I can remember. He blindly follows the advice of his cardiologist and if he even sees butter in my house, he starts to lecture me and since my last blood test showed that I had high cholesterol, it won’t get any better. Great article by the way! It really confirms a lot of the research that I’ve been checking out, like Framington, Massachusetts and others. I really do believe that if you do some research and follow the money trail, you really find the truth.

  91. Gerry  May 12, 2014

    Hi Peter,
    You may know everything about cholesterol but your mastery of Roman Numerals is a bit off, check your chapter numbering above….

  92. Stan  August 5, 2014

    Everywhere I read that the quantity of dietary cholesterol does not affect the level in the blood. But in all discussion sites people say that after going paleo their cholesterol shoots up – mine did (TC), from 150 in 2010 to 220-240 and the last 260 in 2014. So maybe more than 20% experience this. Of course all other things improve but people are still contemplating limiting high cholesterol foods like eggs, liver, butter, red meat, cheese – all good things.

    • Peter Attia  August 6, 2014

      It’s probably more related to the dietary fat, than dietary cholesterol. I’m hoping to write about this at some point.

    • Will  August 9, 2014

      Two years ago I was diagnosed with Hashimotos disease and high cholesterol. I didn’t take the statins because of side effects, but did start thyroid med. To address cholesterol I began a low carb diet. Three weeks later my lipid panel was normal and three weeks after that I was diagnosed with Guillian Barre Syndrome. I recovered about 90% of muscle strength and have some residual tingling in hands and feet. I followed no particular diet during recovery, but ate more meat than usual. After GBS I fell back into a high carbo diet and felt awful. I’m back on a low carb diet, feel MUCH better, but have some lingering concern that my GBS was somehow related to the low carb diet. My doctors say it’s not possible and I find nothing “in the literature” relating GBS to diet. Have you ever heard of any such relationship?

  93. Sara  October 2, 2014

    What about those with the apoe4/3 or apoe4/4 variant following a high-fat ketogenic diet? My understanding is that LDL levels rise to compensate for the lack of uptake in the brain.

    I can foresee two outcomes: brain has enough, total LDL drops or brain never has enough, LDL always goes up. Considering LDL particulate size matters, would the diet be a net benefit regardless?

    • Peter Attia  October 2, 2014

      ApoE 3/4 and 4/4 are complicated, and their management deserves its own post at some point. The clinical implications are clear. The optimal dietary strategy is less clear, though I have my very strong bias.

  94. Mark Littlewood  December 15, 2014

    Dietary cholesterol does not effect blood level cholesterol – not true. Chris Masterjohn reckons 80% of people are not effected by dietary cholesterol and based on my personal experience I would say he is correct. When I eat eggs and or lambs liver my cholesterol shoots up, when I cut them out it returns to normal

    • Peter Attia  December 15, 2014

      How do you know it’s the cholesterol and not, say, the fat?

  95. Brian Kenward  February 24, 2015

    If cholesterol enters the system mainly via the liver, then how do I enhance that to end up with optimal cholesterol levels? How do I keep cholesterol out of places it does bot belong?
    Can I achieve these goals without statins and/or other drugs?

  96. Silentima  March 19, 2015

    Hello Peter,
    My mother has just made her blood test done, and she was very depressed by the level of cholesterol she had. I told her not to stress out. She doesn’t speak English, so I want to translate your posts on this topic into Russian, so she will be able to get this knowledge.

    There is also a very good site about Low-Carb-High-Fat (LCHF) diet, which tries to debunks the myths about lipids, carbs, cholesterol etc. Is it possible to post the translation of your posts on this website? With all references, of course.


    • Peter Attia  March 19, 2015

      By all means. Translate away.

    • Rudy  March 21, 2015

      Don’t worry about it, my mother was 90 years old and her doctor had her on statins!! The human body does not produce toxins, only metabolized byproducts which are excreted. Chol and all of it’s derivatives are produced for a reason. THE BODY NEEDS THEM. 40-60% of chol is used by the brain. That’s why cognitive disorders (memory loss, dementia) are listed as one of several side effects! Just remember that in spite of all of the rhetoric, genetics are the source of the problem not Lipids (chol, LDL, HDL, etc). See my lengthy response on this subject with todays date on the blog site. Just so you’ll know. I’m a medical biochemist.

  97. Fidel  May 27, 2015

    Shouldn’t you edit your statement that cholesterol is only produced by organisms in the animal kingdom? Cholesterol is found in much smaller amounts in various plants.

    Maybe you should also clarify the statement that 25% of our cholesterol comes from what we eat, considering that those who choose not to eat animal products are getting only a miniscule percentage of their cholesterol from what is eaten.

  98. Vernon McVety Jr.  June 9, 2015

    I love this latest (and completely legit) knowledge about cholesterol. It’s high time someone gave us the truth for our high tails. Thanks Dr. Loop.

    Statin therapy, and the institutionalization for it is a very grotesque conspiracy involving the drug companies, the FDA and other medical institutions, including those who don’t know the truth. Some involved are not directly involved in the conspiracy.The FDA and the drug companies are manipulating science and physiology with incomplete and false research, passing it off as legitimate. And main-stream Doctors have to accept it as something real. But it is fraudulent and lacks a scientific foundation. If you look up the right kind of researchers they will prove this to you. Our modern day Cholesterol/Heart disease research paranoia is bogus. This is happening because it was discovered in the late 80’s (I don’t have documented proof, but rather hearsay, from a reliable source) it was discovered that artificially induced “free radicals” caused by toxins found in drugs and medications are also triggering off heart attacks and strokes. And if the general public knew this it would put the drug companies out of business, or at least in their proper place. (See Craig Bowman’s “Cholesterol Miscast As Villain In Fight Against Heart Disease” & google Dr. Matthew Loop).

    Statin therapy is actually being used as a diversion for the drug companies to create the appearance that heart disease is entirely “natural causes”, so they use a natural substance in the body to blame it on – “cholesterol.” When in truth the drug companies themselves are largely responsible for heart attacks and strokes. Cholesterol is nothing but a scapegoat. It has also been recently discovered that large amounts of “Homocysteine” in the body causes the inflammatory stage of heart dis-ease, “inflammation.” And we are not hearing any of the legitimate studies, such as this, in the main-stream media. It all centers around the myth on national TV. And the FDA refuses to dislodge the fallacies because of the money involved.

    Certain pre-med and other medical students are actually being taught, in some schools, that coronary and arterial plaque build-up is almost 100% cholesterol. An absolute lie. Even the teachers believe it. But nothing could be further from the truth. Read Craig Bowman’s article. American people who have plaque removed from their bodies are not allowed to see it. But Craig is a Canadian. He knows better. He explains it. The cholesterol/heart disease paranoia is the biggest medical fraud in the history of mankind. It’s a multi-billion dollar cover-up. The drug companies and FDA have several legislators in their pockets.

    Spiritually speaking, that one element of grace left in Pandora’s box will suffice for us all. Let’s trust in our own higher powers. That’s all the hope we need. In the book of Revelation it tells us that the adversary is allowed to rule and control this world. God allows it all to happen. Our collective societal karma must be able to unfold by itself, on its own, so mankind can realize his mistakes and see his lack of conscious light. Mankind is asleep. But some day all will be well.- Vernon

  99. Vernon McVety Jr.  June 9, 2015

    Sorry Peter. I thought Dr. Loop was the author until I got a look at the top caption. The credit is yours. Very instructive. Thank you. – Vernon

  100. Garry Smith  June 16, 2015

    Dan is right – the ratio LDL-C and HDL-C provide better indication for health problms

  101. James  July 16, 2015

    Cholesterol is a compound of the sterol type found in most body tissues, including the blood and the nerves. Cholesterol and its derivatives are important constituents of cell membranes and precursors of other steroid compounds, but high concentrations in the blood (mainly derived from animal fats in the diet) are thought to promote atherosclerosis.

    • Vernon McVety Jr.  July 27, 2015

      James, the contention that so-called LDL cholesterol produces plaque build-up and/or inflammation is a subversive (false) research tactic, as well as an illogical red herring used by the drug industry and the FDA to divert professional attention away from the reality of “Free Radicals,” and to maintain the treatment of the symptom. The LDL/heart disease connection has no true scientific foundation. It’s promoted as a “straw man” to keep attention off the truth; all for commercial interests. Why do you think they have Legislators who speculate on the stock commodities of the statin drug products using “inside trader information?” It’s a conventional fraud!!!!!!!!!!!!!!!!!!!!!!!!!!!! Do you think they’re going to turn two-faced and blow the whistle? BE REAL.

  102. Paul  August 6, 2015


    I realize this is an older article but it was one of the most thorough I have read in my search! Thank you for that. I do have one question and I hope you are still answering.

    I am 67 years old and have recently had two strokes. My doctor prescribed my Crestor, but since I haven’t been able to afford it (thanks to a fixed income) I buy generic crestor online. Is this enough to help lower my cholesterol? Is there any problem with generic medications? This is where I buy it, if it helps: http://canadapharmacyrx.com/generic-crestor.html

    I just want to eat my eggs in peace! My wife keeps hiding them from me!


    • Peter Attia  August 11, 2015

      The eggs aren’t the problem…

  103. Dan  November 5, 2015

    In the Framingham study does anyone know if LDL is reported as an estimate via the Friewald equation or was it directly measured? My measured is 30 pts lower than calculated.

    • Peter Attia  November 7, 2015

      Probably calculated in the original. Possibly measured in the offspring. In fact, the only reason an assay for measuring HDL-C was developed was to calculate LDL-C.

  104. Simone  November 18, 2015

    Thank you so much for this series on what cholesterol really is and the science behind how it works in the body. It is so refreshing to hear the topic discussed in terms I can better understand and the real science that makes sense! My son (5 years old) actually has a mild version of Smith-Lemli-Opitz syndrome. His cholesterol levels (based on the standard cholesterol tests) are at the low end of normal range across the board, but his 7-DHC levels are much higher than a typical person (52 micrograms/mL vs. normal range ~ 0.16 micrograms/mL) so they can clearly identify that there is an error in cholesterol synthesis and can diagnose SLOS. If cholesterol tests only tell us the blood concentration of cholesterol, is there a way to find out if actual cells might/might not have enough cholesterol? How do we know how “depleted” cells might be of cholesterol even if blood concentration is typical? Or can we assume cholesterol levels in the cells are pretty good based on the blood concentration? My running theory is that he might be on the very “mild” end of the SLOS spectrum because his body is actually producing enough (close to enough) cholesterol, but the pesty 7-DHC left behind due to the slightly defected cholesterol synthesis might be the bigger reason for his developmental delays. 7-DHC oxidizes so easily (200x more easily than cholesterol) and can aggregate to interfere with cell signalling, etc. Anyway, my questions really are: 1.) Do you know if there are tests that can be run to check out cellular health and cholesterol content at the cell level? 2.) We are currently advised to try to increase whole body cholesterol through dietary intake — primarily through egg yolk — since SLOS typically means the body is having trouble producing it on its own (though I question just how depleted my son’s body is of cholesterol). If only “free” cholesterol can be absorbed in the body are there certain foods that contain more “free” cholesterol than others? Is egg yolk recommended because it has less esterified cholesterol? In a typical body it makes sense that most cholesterol consumed through diet doesn’t effect blood concentration of cholesterol since the body is so well regulated and only certain types of cholesterol can even be considered for absorbtion, but if the body does need cholesterol are there better ways than others to get cholesterol through diet? Thanks for any info you might have to help me on this journey!

  105. ben  February 10, 2016

    I didn’t see it mentioned in this post, but there’s a great video where this material is presented!

    There’s also good videos by Chris Masterjohn (and Chris Kresser) that also are worth a watch!

    BTW, in the video, at the 5m12s mark, he says corn has more phytosterols than all but one other plant.. WHAT’S THE OTHER PLANT?!

    Also, not exactly cholesterol related, but what are your thoughts on the the insulin model of obesity popularized by Gary Taubes? i.e. eating carbs, leads to chronic elevated insulin in the blood, which leads fat gain and insulin resistance? I know many researchers say the evidence doesn’t support the model (ex. http://wholehealthsource.blogspot.com/2016/01/testing-insulin-model-response-to-dr.html ) but would love to hear your take!

  106. Nirmala  April 12, 2016

    Hi, I love eating oilly foods. If a Product’s Package Reads “Low Cholesterol,” Does That Mean It’s Low in Fat?

  107. Frances Katrishen  September 7, 2016

    Dear Peter,

    You said you would discuss phytosterols (plant sterols) in later posts but I can’t find them mentioned again. You said in this thread that people should STOP taking them. Why? The current evidence is that supplementation with phytosterols can lower LDL significant, almost as much as with Statins. It seems like an easier and “natural” way to lower LDL. What am I missing?



    • Peter Attia  September 7, 2016

      Complicated, but a person has a defective ATPBC G5,G8 (which about 15% of folks do), they retain phytosterols which are more atherogenic than cholesterol.

  108. John Anderson  October 6, 2016

    “Eating cholesterol has very little impact on the cholesterol levels in your body. This is a fact, not my opinion. ”

    Just wondering, how come the data by many people who post their cholesterol levels before and after a bulletproof diet contradict this claim? The other aspects in the bulletproof diet, (outside of adding butter/ghee) are such that one wouldn’t expect higher cholesterol levels (?) I’ve noticed that in Dave’s podcasts this is acknowledged to happen in ~30% of people, but it’s dismissed. If the primary conclusion of dietary cholesterol not affecting cholesterol levels isn’t accurate, what can we then say about the follow on conclusion that it’s not a problem? questionable at best? Just trying to understand.

    • Peter Attia  October 9, 2016

      I’ve addressed this in other posts and comments, but short answer is likely fatty acid composition. Not cholesterol content.

  109. Karen  October 12, 2017

    Is anyone who is looking to do a low-carb high fat diet a vegan and if so how do you manage the protein


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  81. Anyone share the same problem with me? - www.hardwarezone.com.sg  December 9, 2013
  82. An Open Letter To Jay-Z On Plant Based Diets » Ancestral Nutrition  December 13, 2013
  83. Myth: Eating Fat is Bad | Brain to Body  December 20, 2013
  84. Cholesterol 101 | Lean Protocol  December 28, 2013
  85. 9 Lies About Fat That Destroyed The World’s Health | BaciNews  December 29, 2013
  86. 10 Reasons Green Tea Is The Healthiest Drink In The World | BaciNews  December 29, 2013
  87. 9 Lies About Fat That Destroyed The World’s Health | Britt Weber Fitness  December 30, 2013
  88. Keto-Adaptation: Health, Performance, and Beyond | Grumpy Old Low Carber  December 31, 2013
  89. 9 Lies About Fat That Destroyed The World’s Health | The Minority Report Blog  December 31, 2013
  90. 9 Lies About Fat That Destroyed The World’s Health #sirnaturalhealthinfo | Sirnatural's Blog  January 3, 2014
  91. Should We Believe Anything We Read? | Against The Grain  January 8, 2014
  92. Liptoprotien(a) ... Lp(a) what is this ? | Mark's Daily Apple Health and Fitness Forum page  January 9, 2014
  93. Cholesterol Mythology | towards an optimal field  January 21, 2014
  94. The official ATB healthy living and weight loss thread  January 29, 2014
  95. Top 9 Biggest Lies About Dietary Fat and Cholesterol | Healthy Holistic LivingHealthy Holistic Living  January 29, 2014
  96. 9 Lies About Fat That Destroyed The World's Health | Chauvet - The Dream Unlocked  January 29, 2014
  97. Dietary Cholesterol - Page 3 | Mark's Daily Apple Health and Fitness Forum page 3  February 2, 2014
  98. Conventional meats effects on cholesterol/CVD? | Mark's Daily Apple Health and Fitness Forum page  February 8, 2014
  99. 9 Lies About Fat That Destroyed The World’s Health | Wholefood KidsWholefood Kids  February 21, 2014
  100. What's Wrong With Our Modern Diet?  February 24, 2014
  101. 10 Reasons You Need Cholesterol : Cooking Inspired By Love  February 26, 2014
  102. 9 Lies About Fat That Destroyed The World’s Health | Welcome to Mike's Kitchen  February 26, 2014
  103. 10 Health Benefits of Green Tea | Care2 Healthy Living  February 26, 2014
  104. 10 Health Benefits of Green Tea | Health Senses by AllureSenses.com  February 27, 2014
  105. Fat | metadoxa  March 10, 2014
  106. Health Benefits of Green Tea (lets go green) | emahealthy  April 17, 2014
  107. Why Dietary Cholesterol is Important - IDM 4  April 18, 2014
  108. Over- en ondergewicht - deel 3 - Pagina 124  April 29, 2014
  109. How Increasing Your Fat Intake Can Actually Make You Healthier | Jacked Dad Blog  May 17, 2014
  110. Cholesterol Confusion | Depasi Fitness Solutions  May 29, 2014
  111. What determines blood cholesterol level? | Mark's Daily Apple Health and Fitness Forum page  June 24, 2014
  112. Diet, Cholesterol and Lipoproteins Explained in Human Terms  June 29, 2014
  113. Colesterol | No vuelvo a engordar  July 19, 2014
  114. 9 Lies About Fat That Destroyed The World's Health | Physical Solution  July 24, 2014
  115. Blood Lipid Panel - Help! | Mark's Daily Apple Health and Fitness Forum page  July 28, 2014
  116. (Question) Hope you all can help - www.hardwarezone.com.sg  July 30, 2014
  117. ¿Eleva el colesterol el consumo de grasa? | No vuelvo a engordar  July 31, 2014
  118. Si como grasa, ¿me subirá el colesterol? | No vuelvo a engordar  July 31, 2014
  119. Over-Fed and Under-Nourished: The Western Way | mrchiro blog  August 6, 2014
  120. Is this bull$#*t? | Mark's Daily Apple Health and Fitness Forum page  August 10, 2014
  121. The straight dope on cholesterol – Part I...  August 25, 2014
  122. That Forty-Something Weight Gain: Pass the Green Tea Please | Properly Improper  September 4, 2014
  123. Why the World Has Gone Bananas for Lipitor and Other Statins  November 6, 2014
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  127. | “WE DON’T NEED NO [NUTRITIONAL] EDUCATION” | | retromush  December 6, 2014
  128. Great New Story – Top 9 Biggest Lies About Dietary Fat and Cholesterol  December 8, 2014
  129. I Love Tea! - La Buona VitaLa Buona Vita  December 9, 2014
  130. What's the Deal with Cholesterol: Part 2 - Mad Wellness  December 15, 2014
  131. Cholesterol Is Not "Bad": It Is Vital for Human Existence - Davis and Crump  December 17, 2014
  132. 10 – The Straight Dope on Cholesterol (2012) – On Advertise.com Blog  December 19, 2014
  133. Green Tea Helps Support Healthy Brain Function and Much More | BrainHealth.net  December 24, 2014
  134. 9.4% Body Fat – Final Body Composition – December 27, 2014  December 29, 2014
  135. One Last Thought to Ponder about Statins and Lipitor - Davis and Crump  January 10, 2015
  136. My n=1 nutritional ketosis study criteria | Ironman or Bust  January 20, 2015
  137. My (Failed) High Fat Low Carb Diet Experiment | Laye-ing it down  January 22, 2015
  138. Eggs: The Ultimate Nutrition  February 27, 2015
  139. Paleo Egg Cups - (healthy) Vittles and Bits  March 10, 2015
  140. 9 Lies About Fat the Made The Nation’s Health Worse | My Healing Tips  March 12, 2015
  141. LDL and vascular damage theory question | Mark's Daily Apple Health and Fitness Forum page  March 13, 2015
  142. SNR #59: Danny’s Recommended Nutrition Reading (That Are Free!) | Sigma Nutrition  March 27, 2015
  143. A Changing View of Cholesterol as Bad - Return2Health  April 16, 2015
  144. Keto Krate | 10 Myth Busting Arguments for the Safety of Ketosis  May 10, 2015
  145. 1 year on and still piecing together the puzzle | Ashish's Heart Surgery  May 12, 2015
  146. The Cholesterol Conundrum | livecookeat.com  May 18, 2015
  147. 10 Proven benefits of Of Green Tea 9 (No3 Very Important) | Slim 2B Healthy...  June 24, 2015
  148. Slim 2B Healthy...  June 25, 2015
  149. .:: 9 Lies About Fat That Destroyed The World’s Health | Desert CrossFit ::.  July 10, 2015
  150. Is Fructose Bad For You? A Summary of the Research - Diagnosis: Diet  July 20, 2015
  151. 10 Proven Benefits of Green Tea | Platinum Labs  July 21, 2015
  152. » Cholesterol Is Not "Bad": It Is Vital for Human Existence  July 28, 2015
  153. Cholesterol References | MESSFIT  August 2, 2015
  154. Is there a Bipolar Diet? | Bipolar First Bipolar Together  August 12, 2015
  155. 10 dôkazmi-podložených zdravotných výhod zeleného ?aju - Fitnessa  August 21, 2015
  156. Why Cholesterol Is Not Bad  September 6, 2015
  157. Cholesterol na lavici obžalovaných, ?ást I. | RuFee  October 14, 2015
  158. A biochemical Argument For The Safety of Saturated Fats | benmahalik  October 23, 2015
  159. Diane Sanfilippo | New York Times bestselling author of "Practical Paleo" and "The 21-Day Sugar Detox" | Home of the Balanced Bites Podcast  December 1, 2015
  160. Taking on Cholesterol Part 1 - Food Move Collective  December 9, 2015
  161. Proven Benefits of Green Tea. why it is Very Impressive ? – Ulta Din  December 10, 2015
  162. Green Tea and its Benefits: | engineerahmedblog  December 12, 2015
  163. 10 Proven Benefits of Green Tea | Greentea Vietnam  December 16, 2015
  164. If Not Cholesterol, What? | Rob Arthur  December 31, 2015
  165. 9 lies about fat that destroyed the world’s health | What's Up Doc?  January 10, 2016
  166. 10 Proven Benefits of Green Tea (No. 3 is Very Impressive) - Hungry Rabbit  January 29, 2016
  167. 10 Proven Benefits of Green Tea – Nowchild Blog  February 5, 2016
  168. Best Green Tea For Weight Loss... - My Weight Loss Guy  February 8, 2016
  169. Green Tea | conceptech  February 11, 2016
  170. Peter Attia Resources | MESSFIT  February 13, 2016
  171. 10 Proven Benefits of Green Tea (No. 3 is Very Impressive) – BASELOOK  March 15, 2016
  172. 10 Proven Benefits of Green Tea – teacoffeeandhotchocolate  March 23, 2016
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  174. 5 Nutrition Blogs You Should Follow – Rational Cook Blog  April 22, 2016
  175. Crestor Lawsuit Rhabdomyolisis | Lawyer - How To Claim Injuries  May 12, 2016
  176. 10 Proven Benefits of Green Tea  June 24, 2016
  177. 10 Proven Benefits of Green Tea – Aspe Fitness  July 3, 2016
  178. 10 Benefits Of Green Tea – the uk loose leaf tea company  July 19, 2016
  179. All About CholesterolZero Carb Health | Zero Carb Health  July 27, 2016
  180. How to Get 2,000 Calories for Under $2.00/Day | Upstart Blog  July 27, 2016
  181. Why Cholesterol Isn’t Bad – KevMD  August 2, 2016
  182. Healthy Alternative to Help You Kick Your Soda Habit Out The Door…Forever! – Halestorm Fitness Personal Training  August 8, 2016
  183. Is the Keto diet Safe? 10 Myth-Busting Arguments for the Safety of Ketosis | Keto Krate  November 6, 2016
  184. What’s the Deal with Cholesterol: Part 2 | Maddie Berky  November 9, 2016
  185. LDL Particle Number Possibly Accurate Predictor of Heart Disease Risk  November 30, 2016
  186. LDL Particle Number: Possibly an Accurate Predictor of Heart Disease Risk – EveryoneHealthy.XYZ  November 30, 2016
  187. Is Keto Dangerous While Pregnant, Breastfeeding, or for Children? - Ketogains  December 15, 2016
  188. Backyard Chickens, Honey, Endogenous Cholesterol, etc. | Q&A - Raising Backyard Chickens  February 23, 2017
  189. How I was able to increase my focus tenfold with the ketogenic diet - BULLET FOCUS  March 5, 2017
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  194. Does a Ketogenic Diet Change Your Lipid Profile - Perfect Keto Exogenous Ketones  June 23, 2017
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  196. Rafale 35 : Prévention du cancer des intestins, l'hyperglycémie c'est le mal - Paléo Québec  July 26, 2017
  197. Resident Wellness Support Group Weeks 5 & 6 – Darcy Trenkle, M.D.  August 8, 2017
  198. Beyond the Lipid Hypothesis: Plaque Development » Cholesterol Code  November 1, 2017
  199. High Cholesterol on a Keto Diet - Should You Be Concerned? - Practical Daddy  November 8, 2017