My health markers after eight years on LCHF

Scary stuff - or?

Scary stuff – or?

In the summer of 2006, I started eating an LCHF diet and since then I have continued to do so. It has now been eight years and I decided it was time for a thorough checkup.

According to certain fat and meat phobics, I should have been dead a long time ago. Personally, I’m planning to hang in there for about 50 more years. So who’s going to be right?

Here’s the result from my recent blood work:

Background

I’m basically healthy. But as a 42-year old dad to a small child, with some sleep deprivation, and who regularly works 60-hour weeks, this is probably the time when health should start to fail.

If LCFH doesn’t save me.

I’ve eaten an LCHF diet for eight years, at times very strict, at other times less strict. Plenty of butter, eggs, meat and heavy cream – and vegetables. For the last six months I’ve also done intermittent fasting, 16:8, on most weekdays ( I skip breakfast).

Results

Here’s a summary of my results 2007-2014.

Numbers

Click on image to enlarge.

The recent test results are in the colored columns. Numbers converted to US units to the right.

Comment

The wild rumors about how dangerous LCHF is long term, don’t get validated in my blood work. After eight years on LCHF they are excellent, just as when I started. There simply aren’t any big changes during these years.

Many things are typical and the trends are also confirmed in studies on low-carb diets:

  • Low triglycerides (good)
  • Excellent HDL cholesterol levels
  • Nice ApoB/AI ratio
  • A low fasting blood sugar and a low HbA1c (good)
  • Low, but normal, insulin levels, measured as C-peptide (probably excellent)
  • A normal weight and a normal waist circumference
  • A low and good blood pressure

To summarize, all problems associated with the metabolic syndrome and type 2 diabetes usually improve on LCHF. Obesity, high blood pressure, high blood sugar, high insulin levels and dangerously disturbed cholesterol numbers (high triglycerides and low HDL).

My test results also show that the inflammatory level in the body – as measured CRP – is non-detectible on all test occasions.

With these results in mind the fantasy talk about long-term risks with LCHF doesn’t seem to be valid,  at least not in my case. Perhaps you’ll have to put up with me for about 50 more years.

Weight

I’ve kept my weight at a normal weight level effortlessly and without any calorie counting during these years. I’ve gone up and down a few pounds within the normal range.

During my experiment with a strict LCHF diet and ketone measuring, I lost 12 lbs/5 kg. They came back when I returned to liberal LCHF, but disappeared again when I added 16:8.

My experience is that the latter is clearly the easier alternative. At least if you’re like me, and not that sensitive to carbohydrates. So I will continue with liberal LCHF with the addition of 16:8 on weekdays.

What Do You Think?

What has happened to your health markers on LCHF?

Previously

Great Cholesterol Numbers After 4 Years on an Ultra-Strict LCHF Diet

More

LCHF for Beginners

Diabetes – How to Normalize Your Blood Sugar

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159 comments

  1. Nigel Kinbrum
    Any fool can copy & paste text. It takes brains to understand it. Sadly, you will never understand it.

    There's nothing for me to deflect. You're just an empty vessel who likes to makes a lot of noise.

    Reply: #156
  2. Z.M.
    Nigel Kinbrum: " find my blog and look in the Blog Archive for the post I made in December 2008 about Cholesterol And Coronary Heart Disease."

    Found it. I hope you will check out my blog also - http://diettrialclaims.blogspot.com/2013/06/is-cholesterol-really-tha...

  3. murray
    "Nigel Kinbrum: "CA caused by LDL, according to Subbotin's hypothesis."

    Z.M.: Going along with this assumption, I'm curious to know what is the solution to this LDL deposition?"

    Z.M., there is no reason to go along with the assumption as it plainly proves too much. All people have LDL, not all people get coronary disease. Nigel as much as concedes this:

    Nigel: "Now, there's an excellent question. I just wish that I had an excellent answer!

    As CA is a multi-factorial condition, multiple factors need to be addressed."

    Saying "CA caused by LDL" uses an impoverished and faulty definition of "caused." Poor writing is a touchstone of poor thinking. That's not an ad hominem, it's an ad scriptum, hermeneutics.

  4. Nigel Kinbrum
    Z.M. said...
    "Nigel Kinbrum: " find my blog and look in the Blog Archive for the post I made in December 2008 about Cholesterol And Coronary Heart Disease."

    Found it. I hope you will check out my blog also - http://diettrialclaims.blogspot.com/2013/06/is-cholesterol-really-tha... "
    Excellent! Will do. I wonder why I can't post links to my blog on here..... :-(

  5. Nigel Kinbrum
    murray said...
    "Saying "CA caused by LDL" uses an impoverished and faulty definition of "caused." Poor writing is a touchstone of poor thinking. That's not an ad hominem, it's an ad scriptum, hermeneutics."
    Do you know the difference between the following two sentences?:-

    1) LDL is a cause of CA.

    2) LDL is the cause of CA.

    I'm claiming 1). Have you got it, now? Please tell me that you have.

    Replies: #108, #109, #110
  6. Nigel Kinbrum
    Meanwhile, FrankG posts another pointless YouTube video, using his one last surviving working brain cell.

    FrankG is like one of those yappy little dogs. He makes a lot of noise, humps people's legs and tries to nip their ankles.

    A swift kick in the nuts usually stops such silliness, but FrankG is a stubborn little tyke. Or a masochist. :-D

  7. FrankG
    Is this what you meant when you wrote in comment #62 above, "There is causality between LDL-C and CHD."

    LDL-C has something to do with CHD or CA ..?

    The coronary arteries probably have something to do with CA as well.

    Being human is a cause of CA ...or CHD

    Got it now..?!?

    I could have sworn the earlier discussion was about CHD... oh right, the old bait 'n switch routine :-P

  8. FrankG
    Not only taking liberties with the plain truth, also with the definition of the scientific method but now with the English language itself... all just to win the internet! How pathetic...

    If I wrote, "the bruising and swelling around your eye was caused by my fist hitting your face" what meaning would you apply to the "caused by"..? Is it just one of potentially many factors to be considered, or does it imply that my fist making contact had the most significance in the outcome?

    Sure we could nit-pick and say that maybe your rude and arrogant attitude, your childlike behaviour was causal in the overall picture but really when it comes down to it, you and we all know, exactly what you meant when you wrote "CA caused by LDL"

  9. murray
    "CA is caused by LDL deposition" is your sentence, not mine.

    The sentence does not say "LDL is a cause of CA." If you meant that, then that is a trivial observation. No one doubts LDL particles play a role.

    I generally have a lot of time to consider the viewpoints of engineers, who typically bring a problem-solving perspective in multi-cause phenomena that is generally lacking among scientists and physicians. Scanning your website, which I encourage other readers here to view, the engineering approach is not readily apparent to me.
    http://nigeepoo.blogspot.ca/

    For purposes of comparison, one might review the analysis of Ivor Cummins, a process control chemical engineer, who has also delved into the issue of cholesterol and coronary disease.
    http://www.thefatemperor.com/
    His presentation The Cholesterol Conundrum Seminar Video offers a different perspective.

    Another useful comparison is Peter Attia, who was educated as a mechanical engineer and offers a different analytic approach and perspective.
    http://eatingacademy.com/

    Reply: #112
  10. BluntF
    Nigel's out of his depth...

    Deflecting perfectly valid arguments.

    This focus on LDL is just too much, and all this observational poppy-cock doesn't belong in the discussion of CVD. Fact remains that correlation is not causation. Until we get an RCT, which will never happen, LDL remains an innocent bystander because we know it all so well. It has nothing, for an absolute fact, to do with anything other than metabolic improvement after the last 50 years of conspiratorial abuse that we have suffered at the hands of the establishment.

    In fact, we'll strive for even more LDL than what is physiologically seen in most pre-industrial populations... because they weren't slammed so many times on the head with a hammer. And we'll have more hammers as well! We'll only talk about LDL as an issue when we're selectively citing Taubes, or babbling on like an OCD patient about fluffy or dense particles, because cholesterol only matters when we're engaged in the mighty and righteous crusade against the status quo. Otherwise, it doesn't matter, especially when low carbing -- then everything is certifiably good and we don't need RCT evidence for that claim.

    Us? Deluded?! Pshaw! It's these cholesterol apologists who're deluded. Heathens must produce RCTs to be taken seriously in this sacred circle(-jerk), or we shall have nothing of such unworthy discussions engineered to sully the sacred LDL cholesterol. LIFE!

    Praise be to the Almighty Uffe Ravnskov and his Holy Prophet, Gary Taubes.

    We stand vindicated and proud!

  11. FrankG
    Even if we accept "CA is caused by LDL deposition" as valid -- which I'm not clear that Subbotin is saying in his hypothesis -- Subbotin does seem clear that LDL deposition is a result of a pathological neovscularisation "...of the normally avascular coronary DIT by permeable vasculature from the adventitial vasa vasorum..."

    Sounds to me like the LDL-C is being found guilty by association only (firefighters and house-fires) and we need to focus on why the pathological neovascularisation is occurring...

    Potentially the cause for the pathological neovascularisation may also not be the initial stage in this process... so we go back further.. all the way to the hammer blows on the head.

  12. FrankG
    But never fear... I see this from Nigey-poo on a comment at ZM's blog

    "If you can show using evidence that I've got something wrong, I admit to my cock-up and correct the error."

    It's rare to meet a man of such integrity these days... scout's honour! LOL

    Uhh Nigey... actions speak louder than words :-P

  13. BluntF
    Nige, Nige, Nige...

    Don't you understand? The LDL is innocent--and revered--until proven guilty through RCT and only RCT (even then we'll have mountains of questions, so hah!). This is the court of democratic law! Get yourself checked.

    How dare you insult our firemen? The audacity! Coming in here. Addressing inconvenient associations. Bringing up troubling questions. Annoying us with facts and enquiries rather than the talk-points that we enjoy between ourselves. Shattering the delicate fabric of innocence until guilt that is the legal syste--scientific method... with your dissent!

    For shame!

  14. Nigel Kinbrum
    murray said
    "The sentence does not say "LDL is a cause of CA." If you meant that, then that is a trivial observation. No one doubts LDL particles play a role."
    Hurrah! Consensus at last!

    "I generally have a lot of time to consider the viewpoints of engineers, who typically bring a problem-solving perspective in multi-cause phenomena that is generally lacking among scientists and physicians. Scanning your website, which I encourage other readers here to view, the engineering approach is not readily apparent to me."
    You like sites that say what you want to hear.

    You don't like inconvenient facts that contradict your dietary beliefs. Any facts that confirm your beliefs, you cherry-pick. Any facts that contradict your beliefs, you deny using any old excuse.

    I'm friends with Ivor Cummins. I'm also friends with Jeffry Gerber, the LC diet doctor in Denver, Colorado. I support LC diets, in case you hadn't noticed!

    What I don't support is pseudoscientific BS. There's an awful lot of that on the internet.

  15. Nigel Kinbrum
    FrankG yodelled...
    "But never fear... I see this from Nigey-poo on a comment at ZM's blog

    "If you can show using evidence that I've got something wrong, I admit to my cock-up and correct the error."

    It's rare to meet a man of such integrity these days... scout's honour! LOL

    Uhh Nigey... actions speak louder than words :-P "

    You've learned how to read? SWEET! :-D
    I see you selectively quoted from ZM's blog to leave out the bit where I said "I did this just the other day on the Bray et al post."

    As I've already said, you are intellectually dishonest. I don't know why you even bother to leave comments, you worthless individual.

  16. Nigel Kinbrum
    RE Bray et al shows that a calorie *is* a calorie (where weight change is concerned):

    It now starts with:-

    "EDIT: I made an error in stating that all of the extra calories came from fat, in the fat overfeeding phase. Thanks to commenter CynicalEng for pointing this out. It doesn't change the conclusion."

  17. FrankG
    Fortunately for me I am confident in my own intelligence, my ability to think critically and reason for myself; so I'm not looking for any kind of validation, or even acceptance from the likes of you, Nigel (what an appropriate moniker! LOL)

    On the other hand, you have convincingly demonstrated yourself to be an untrustworthy, arrogant, blowhard; who apparently has to "win the internet" at any cost.. truth be damned.

    Your opinion means nothing to me and your nutritional advice even less... you have zero credibility.

    And now over to you, as we all know how you love to have the last word...

  18. Nigel Kinbrum
    FrankG blathered incoherently...
    "Fortunately for me I am confident in my own intelligence, my ability to think critically and reason for myself; so I'm not looking for any kind of validation, or even acceptance from the likes of you, Nigel (what an appropriate moniker! LOL)"
    You are the epitome of http://en.wikipedia.org/wiki/Dunning%E2%80%93Kruger_effect
    You really are too stupid to know that you're stupid.

    "On the other hand, you have convincingly demonstrated yourself to be an untrustworthy, arrogant, blowhard; who apparently has to "win the internet" at any cost.. truth be damned."
    You're too stupid to realise that there is no truth, in the world of diet & nutrition. There's evidence for & against things. I provide quality peer-reviewed evidence to support what I'm saying. What do you rely on? Anecdotes, stupid metaphors and your opinion, which is worth absolutely zero.

    "Your opinion means nothing to me and your nutritional advice even less... you have zero credibility."
    Ditto for you. What articles have you ever written? Where's your blog? Where's your evidence?

    "And now over to you, as we all know how you love to have the last word..."
    Thank you.

    I use the "SCIENCE" side of the following chart:-
    http://31.media.tumblr.com/b546aaabaedeac5224996c52a8def01d/tumblr_n9...

    You use the "PSEUDOSCIENCE" side.
    Q.E.D.
    Have an ice day! :-D

  19. Dharma
    Have been on strict LCHF for 5 months.

    Weight loss, waist circumference loss, leaning out of my body. Good.

    Just got my first LCHF blood results. Weird:

    Total Cholesterol from 5.0 to 6.9
    LDL from 3.2 to 4.9
    Trig 1.3 to 0.9
    HDL 1.2 to 1.6
    VLDL 0.6 to 0.4

    Here's the interesting bit -
    ALT 26 to 47 U/L
    AST 20 to 28 U/L

    So does this mean LCHF stresses the liver seeing that the AST and ALT are elevated (ALT is over the top limit)?

    Is the liver being hammered processing so much fat and protein?

    In which case is the downside of LCHF liver issues?

    Reply: #121
  20. Zepp
    It quite comon that total cholesterole goes up at least in the first 6 months.. often by higher HDL.. but altso by lower triglycerids.. ie, its often a counting failure!

    http://www.docsopinion.com/2013/12/15/10-pitfalls-of-using-ldl-choles...

    Your VLDL is lower.. it means that you produce less APOb.. so its almoste sure its less LDL and bigger fluffier LDL.. thats good!

    Mayby its a stress to your whole body.. (and mind), to do such diet change.. but ALAT/ASAT do change over hours!

    "Significantly elevated levels of ALT (SGPT) often suggest the existence of other medical problems such as viral hepatitis, diabetes, congestive heart failure, liver damage, bile duct problems, infectious mononucleosis, or myopathy, so ALT is commonly used as a way of screening for liver problems. Elevated ALT may also be caused by dietary choline deficiency. However, elevated levels of ALT do not automatically mean that medical problems exist. Fluctuation of ALT levels is normal over the course of the day, and they can also increase in response to strenuous physical exercise."

    http://en.wikipedia.org/wiki/Alanine_transaminase

  21. Dharma
    Thanks Z. So what do you think of "However, long-term maintenance on a ketogenic diet stimulates the development of NAFLD and systemic glucose intolerance in mice"

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3679496/

    Reply: #123
  22. Zepp
    Well, mice are not small fury humans.. they are not adapted to a high fat diet!

    And often they have to ad sugar to those diets, for making them eating it!

    But.. studies on humans.. how not is mice.. says the oposite!

    "Curbing carbohydrates is more effective than cutting calories for individuals who want to quickly reduce the amount of fat in their liver...."

    http://www.diabetesincontrol.com/index.php?option=com_content&vi...

    Reply: #154
  23. Dharma
    Thanks Z. Helpful feedback mate. Cheers.
    Reply: #125
  24. Zepp
    Here you can listen to a seminar about blood lipids, cholesterole, cardiovaskular healt and all that complex things!!

    http://www.youtube.com/watch?v=fuj6nxCDBZ0

    If you make it 1 and ½ hour.. you know more about that topic then your GP!

    And ofcourse.. keep monotoring your blood values.. I think they gonna improve?

  25. NS
    Not exactly related, but this will conceivably help many with their blood sugars:

    http://koreajoongangdaily.joins.com/news/article/article.aspx?aid=299...|home|newslist2

  26. Nigel Kinbrum
    Dharma said...
    "Have been on strict LCHF for 5 months.

    Weight loss, waist circumference loss, leaning out of my body. Good.

    Just got my first LCHF blood results. Weird:

    Total Cholesterol from 5.0 to 6.9
    LDL from 3.2 to 4.9
    Trig 1.3 to 0.9
    HDL 1.2 to 1.6
    VLDL 0.6 to 0.4"
    See http://bit.ly/WGVVnk

    "Here's the interesting bit -
    ALT 26 to 47 U/L
    AST 20 to 28 U/L

    So does this mean LCHF stresses the liver seeing that the AST and ALT are elevated (ALT is over the top limit)?

    Is the liver being hammered processing so much fat and protein?

    In which case is the downside of LCHF liver issues?"
    Yes. Dietary fat can be stored as ectopic liver fat. See http://bit.ly/1rR0G85

  27. Nigel Kinbrum
    Zepp said...
    "It quite comon that total cholesterole goes up at least in the first 6 months.. often by higher HDL.. but altso by lower triglycerids.. ie, its often a counting failure!

    http://www.docsopinion.com/2013/12/15/10-pitfalls-of-using-ldl-choles...

    Your VLDL is lower.. it means that you produce less APOb.. so its almoste sure its less LDL and bigger fluffier LDL.. thats good!"
    That's bad! LDL particle size isn't important. LDL particle count (LDL-P) is important.

    As LDL-P ∝ LDL-C, Dharma's sky-high LDL-C is likely to give him high LDL-P, despite having larger LDL, which tends to lower LDL-P.

    See http://www.lecturepad.org/dayspring/lipidaholics/pdf/LipidaholicsCase... for more information. Check out the Kaplan-Meier Event-free survival plots on Page 11.

    Reply: #129
  28. Zepp
    Well.. if one have less VLDL.. then one typical produce less APOb.. then one typical produce less LDL-P!

    But if one only measure cholesterole.. one measure Tot and HDL-C.. and in this case they have measuered VLD-C too!

    In this context.. one dont count the apolipoprotein particels.. one can only do some estimations!

    Soo.. its not about cholesterole.. its about Apolipoproteins as a prediction for future cardio vascular healt!

    And its about how average people do react on lower carb and higher fat!

    The misconception is that cholesterole is the evile.. its not.. its APO-b.. or if you like.. LDL-P!

    Or rather.. its the high levels of APO-b (LDL-P) thats tell you if there are some malfunctions.. dietary or geneticaly.. or both!

    Soo.. again.. APO-B/APOA1 is the new golden standard to predict future atherosklerosis!

    "Lipids, lipoproteins, and apolipoproteins as risk markers of myocardial infarction in 52 countries (the INTERHEART study): a case-control study."

    http://www.ncbi.nlm.nih.gov/pubmed/18640459

    "Low-density-lipoprotein subclasses and response to a low-fat diet in healthy men."

    http://www.ncbi.nlm.nih.gov/pubmed/7625363

    "Change in LDL particle size is associated with change in plasma triglyceride concentration."

    http://atvb.ahajournals.org/content/12/11/1284.abstract

    And soo on!

    You know.. it seems that you are trying to brake in open doors.. those of us that you are debating whit that often wrights here is aware of different subclasses and Apolipoproteins.. and even of genetical dysfunctions of fatmetabolisme!

    The thing still is.. metabolic syndrome/hyperinsulinemia is the major cause for elevated APO-B, small more atherogenic LDL and high LDL-P!

    http://www.youtube.com/watch?v=fuj6nxCDBZ0

  29. Nigel Kinbrum
    So you're saying that the lipidologist Dr. Thomas Dayspring doesn't know what he's talking about?

    You're also focusing on fasting triglycerides. You're forgetting that postprandial triglycerides are elevated for long periods, on VLCVHF diets.

    ""Low-density-lipoprotein subclasses and response to a low-fat diet in healthy men."

    http://www.ncbi.nlm.nih.gov/pubmed/7625363

    "Change in LDL particle size is associated with change in plasma triglyceride concentration.""

    Maybe you're not aware of the fact that all of the Krauss et al studies used a 50/50 mixture of complex & simple carbohydrates.

    50% of the carbohydrates were sugars.

    The other 50% could have been anything. Amylopectin & maltodextrin are both complex carbohydrates that have GI ~100, where glucose =100.

    Those studies are worthless.

    Finally, take a look at Page 10 of https://www.drmcdougall.com/misc/2013nl/feb/pritikinpdf3.pdf

    Oh, dear!

    Replies: #131, #132
  30. erdoke
    I looked at the introduction and the start of the fifth paragraph actually prevented me from reading on.
    When you start a speech with trying to persuade the audince with a shameless big lie, than anything that follows is simply not credible.
    I'm talking about this:
    "The low incidence of atherosclerosis in populations on low fat diets has been observed by many investigators"
    THIS IS NOT TRUE! Anybody starting up this way is completely ridiculed and I'm not ready to listen to what else he tries to convince me about. Considering the huge number of trials actually trying to prove this and also the much lower number of not biased trials, this is simply a blatant lie.
    Check Denise Minger's blog about how to read statistical analyses. She is very good at making it simple for those not being experienced or at least familiar with working with huge amount of data.
    Coming back to lipoproteins, it is very likely that if HDL is high (around or above 2) and triglycerides are low, LDL does not really matter. In any cases where LDL-P is very high, HDL and triglycerides are not in the green zone either.
    It is also clear that we should talk about lipoprotein values vs. CHD risk for men and women separately.
  31. Zepp
    Well Im not sure of what you are trying to tell us at all.. its rather seems to be a mish mash of anything!

    For example.. postprandial triglycerides is one thing.. its the way its supose to be after eating fat.. but you dont recon high high triglycerid long time after a high carb diet.. thats bad.. its abnormal!

    Yes Im aware of Krauss et al diet.. its about the SAD diet.. thats the point!

    More sugars and more refined carbs, the worse outcome.. didnt you understand that?

    I rather think that you dont understand what you are reading?

    Reread this paper again!

    http://www.lecturepad.org/dayspring/lipidaholics/pdf/LipidaholicsCase...

    Or rather read up on the topic!

    Heres one that done the job for us!

    What we’ve learned so far

    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 forms – unesterified or “free” (UC) and esterified (CE) – and the form determines if we can absorb it or not, or store it or not (among other things).

    4. Much of the cholesterol we eat is in the form of CE. It is not absorbed and is excreted by our gut (i.e., leaves our body in stool). The reason this occurs is that CE 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 (i.e., endogenous produced cholesterol) 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 see an important reference on this topic, please look here.

    8.Cholesterol and triglycerides are not soluble in plasma (i.e., they can’t dissolve in water) and are therefore said to be hydrophobic.

    9.To be carried anywhere in our body, say from your liver to your coronary artery, they need to be carried by a special protein-wrapped transport vessel called a lipoprotein.

    10.As these “ships” called lipoproteins leave the liver they undergo a process of maturation where they shed much of their triglyceride “cargo” in the form of free fatty acid, and doing so makes them smaller and richer in cholesterol.

    11.Special proteins, apoproteins, play an important role in moving lipoproteins around the body and facilitating their interactions with other cells. The most important of these are the apoB class, residing on VLDL, IDL, and LDL particles, and the apoA-I class, residing for the most part on the HDL particles.

    12.Cholesterol transport in plasma occurs in both directions, from the liver and small intestine towards the periphery and back to the liver and small intestine (the “gut”).

    13.The major function of the apoB-containing particles is to traffic energy (triglycerides) to muscles and phospholipids to all cells. Their cholesterol is trafficked back to the liver. The apoA-I containing particles traffic cholesterol to steroidogenic tissues, adipocytes (a storage organ for cholesterol ester) and ultimately back to the liver, gut, or steroidogenic tissue.

    14.All lipoproteins are part of the human lipid transportation system and work harmoniously together to efficiently traffic lipids. As you are probably starting to appreciate, the trafficking pattern is highly complex and the lipoproteins constantly exchange their core and surface lipids.

    15.The measurement of cholesterol has undergone a dramatic evolution over the past 70 years with technology at the heart of the advance.

    16.Currently, most people in the United States (and the world for that matter) undergo a “standard” lipid panel, which only directly measures TC, TG, and HDL-C. LDL-C is measured or most often estimated.

    17.More advanced cholesterol measuring tests do exist to directly measure LDL-C (though none are standardized), along with the cholesterol content of other lipoproteins (e.g., VLDL, IDL) or lipoprotein subparticles.

    18.The most frequently used and guideline-recommended test that can count the number of LDL particles is either apolipoprotein B or LDL-P NMR, which is part of the NMR LipoProfile. NMR can also measure the size of LDL and other lipoprotein particles, which is valuable for predicting insulin resistance in drug naïve patients, before changes are noted in glucose or insulin levels.

    19.The progression from a completely normal artery to a “clogged” or atherosclerotic one follows a very clear path: an apoB containing particle gets past the endothelial layer into the subendothelial space, the particle and its cholesterol content is retained, immune cells arrive, an inflammatory response ensues “fixing” the apoB containing particles in place AND making more space for more of them.

    20.While inflammation plays a key role in this process, it’s the penetration of the endothelium and retention within the endothelium that drive the process.

    21.The most common apoB containing lipoprotein in this process is certainly the LDL particle. However, Lp(a) and apoB containing lipoproteins play a role also, especially in the insulin resistant person.

    22.If you want to stop atherosclerosis, you must lower the LDL particle number. Period.

    23.At first glance it would seem that patients with smaller LDL particles are at greater risk for atherosclerosis than patients with large LDL particles, all things equal.

    24.“A particle is a particle is a particle.” If you don’t know the number, you don’t know the risk.

    25.With respect to laboratory medicine, two markers that have a high correlation with a given outcome are concordant – they equally predict the same outcome. However, when the two tests do not correlate with each other they are said to be discordant.

    26.LDL-P (or apoB) is the best predictor of adverse cardiac events, which has been documented repeatedly in every major cardiovascular risk study.

    27.LDL-C is only a good predictor of adverse cardiac events when it is concordant with LDL-P; otherwise it is a poor predictor of risk.

    28.There is no way of determining which individual patient may have discordant LDL-C and LDL-P without measuring both markers.

    29.Discordance between LDL-C and LDL-P is even greater in populations with metabolic syndrome, including patients with diabetes. Given the ubiquity of these conditions in the U.S. population, and the special risk such patients carry for cardiovascular disease, it is difficult to justify use of LDL-C, HDL-C, and TG alone for risk stratification in all but the most select patients.

    30.To address this question, however, one must look at changes in cardiovascular events or direct markers of atherosclerosis (e.g., IMT) while holding LDL-P constant and then again holding LDL size constant. Only when you do this can you see that the relationship between size and event vanishes. The only thing that matters is the number of LDL particles – large, small, or mixed.

    31.HDL-C and HDL-P are not measuring the same thing, just as LDL-C and LDL-P are not.

    32.Secondary to the total HDL-P, all things equal it seems smaller HDL particles are more protective than large ones.

    33.As HDL-C levels rise, most often it is driven by a disproportionate rise in HDL size, not HDL-P.

    34.In the trials which were designed to prove that a drug that raised HDL-C would provide a reduction in cardiovascular events, no benefit occurred: estrogen studies (HERS, WHI), fibrate studies (FIELD, ACCORD), niacin studies, and CETP inhibition studies (dalcetrapib and torcetrapib). But, this says nothing of what happens when you raise HDL-P.

    35.Don’t believe the hype: HDL is important, and more HDL particles are better than few. But, raising HDL-C with a drug isn’t going to fix the problem. Making this even more complex is that HDL functionality is likely as important, or even more important, than HDL-P, but no such tests exist to “measure” this.

    http://eatingacademy.com/cholesterol-2/the-straight-dope-on-cholester...

    And he has listen a lot of Dayspring!

  32. Z.M.
    Nigel Kinbrum: "So you're saying that the lipidologist Dr. Thomas Dayspring doesn't know what he's talking about?"

    I'd say so, just look at his statements. He says to reduce saturated fat intake when reducing and/or modifying fat intake have been shown to be an utter failure. He says to take statin/ezetimibe when ezetimibe has never shown benefits and their combination was an utter failure in the only two trials done. He claims statins to be effective drugs when they have failed to reduce mortality in almost every trial ever done and have failed to provide benefits in just about every population.

    This is what happens when one puts so much faith on surrogate markers and pretend to know about causes when you're actually speculating.

    Reply: #134
  33. Zepp
    Then you and I read Dayspring whit different eys!

    He point on.. in that article, on those on low carb high fat, that got a bad outcome of the diet!

    Perticaly high LDL-P, (ApoB)!

    And provide some explanation for that.. moste of them well knowed.. even in Low carb comunities!

    And then.. one can like NK make this to be the major outcome of a low carb high fat diet.. but thats not true.. its less then 1 percentage that got those problems in the population!

    Im beeing along that many years that I have stumble on a few of those people.. and its then contraproductive to be a denyalist.

    But its about a few people that dont handle saturated fat, fats and cholesterole in diet properly!

  34. Z.M.
    Zepp, I don't think anyone denies that different people react differently. However, this means nothing if you're just going by a surrogate markers. I'm not sure how you define a "bad outcome" here.
    Reply: #136
  35. Zepp
    I mean that high APOb/LDL-P.. is a bad marker in 80% of the cases!

    Its not what one want.. not what one aim at.. its a higher risk!

    And sciens and Dayspring provide some cures.. lower saturated fat and eat more monosaturated fat.. IE, eat more beef and its lard!

    Im all in whit you that surrogate markers dont tell us the whole picture.. but there are a big differens of denying that a few could have problems.

    And this discution is more of if surogate markers improve or get worse for general populations on a high carb diet or on a low carb high fat diet!

  36. Nigel Kinbrum
    I'm not engaging with you Cholesterol denialists.

    Goodbye!

    Reply: #139
  37. Z.M.
    Nigel Kinbrum: "I'm not engaging with you Cholesterol denialists."

    Depends what you mean by "cholesterol denailist". Until you define it, it is meaningless and no one could defend against such a claim.

  38. Zepp
    Didnt you know that Dayspring and Taubes are buddies?

    Here they do a hearing togheter about obesety, food, lipidology, cholesterole and all that difficult things!

    Listen and learn.. then come back and discus different matters!

    http://www.youtube.com/watch?v=hRoxvI1p1Bc&index=1&list=PLk...

  39. Nigel Kinbrum
    Z.M said...
    ""Nigel Kinbrum: "I'm not engaging with you Cholesterol denialists.""

    Depends what you mean by "cholesterol denailist". Until you define it, it is meaningless and no one could defend against such a claim."
    It's not meaningless. http://en.wiktionary.org/wiki/denialist#Noun
    I knew you'd slime your way out of refuting my argument.

  40. Nigel Kinbrum
    Zepp said...
    "Didnt you know that Dayspring and Taubes are buddies?

    Here they do a hearing togheter about obesety, food, lipidology, cholesterole and all that difficult things!

    Listen and learn.. then come back and discus different matters!

    https://www.youtube.com/watch?v=hRoxvI1p1Bc "
    From the comments to your video:-
    "luisrd said...
    7 months ago

    Ad Hominems, the tools of discourse of the un-educated.
    http://en.wikipedia.org/wiki/Ad_hominem "
    You sir, are uneducated. You are dismissed!

  41. Z.M.
    Nigel Kinbrum: "It's not meaningless. http://en.wiktionary.org/wiki/denialist#Noun
    I knew you'd slime your way out of refuting my argument."

    Strange, why take so long to reply. I thought you were done.

    I didn't say define denialist, I said define "cholesterol denialist". There are many different hypotheses as to how cholesterol is involved, so be precise.

  42. Christian
    Hi!

    had some recent bloodwork and was astounished by my LDL-C
    it is 150mg/dl
    my HDL-C is 42
    how can I change this?
    could that be because of fasting the day the blood test was done?

    I was strictly low carb except on friday the week before (min 1 week difference to bood test) where was the refeed....

    is it ok to go more protein? like paleo?
    or should I raise fat?
    the stall continues.. but I guess its the sweeteners.. lets see what happens if I cut them...

    experiences?

    Reply: #144
  43. Zepp
    Its not your LDL thats to high.. its your HDL thats very low.. its as low as mine!

    No.. its probably not the sweteners, its more probably metabolic syndrome.. but sweteners is no help, it just make you use to eat sweet food!

    Did you watch this?

    https://www.youtube.com/watch?v=fuj6nxCDBZ0

  44. Christian
    yeah metabolic is but quite reversed only the weight lingers... rest of the blood profile is really good :)

    is it possible to raise HDL? I have no clue about that...
    workout? or eat other things?

    hmm not sweeteners? odd.. always thought they inhibit ketosis?

  45. Darag
    Andreas, I've met two people recently whose TG's were below 1 before starting LCHF and raised to above 2 with LCHF.

    Have you looked at this TG issue and what would you recommend?

    Reply: #147
  46. Zepp
    Im not Andreas, but its more common whit high triglycerides at start and they get lower after blood sugar is going down.

    Could it be that fat frome the liver is released?

    Some report they dont lose any weight but there waist is shrinking, it must have gone some other place?

  47. Charles Grashow
    Your health markers were all BETTER in 2007. What was your diet like then?
    Reply: #149
  48. erdoke
    I don't see a big difference in the overall picture.
    Also, I guess you are aware that these values fluctuate throughout the day and depend on meals consumed prior the blood sampling among other things. This way many of the variances are not statistics ally significant,me specially not based on 1 yearly measurement.
  49. BryanD
    After reading this article I'm wondering why my numbers don't look like those in the article. I have been on an LCHF diet for 6 months, after my doctor told me my cholesterol was a little high and I wanted to lose a few pounds. I had a blood workup done when I started and 6 months later. After 6 months I have lost 32 Lbs. but my cholesterol has gotten worse. My total Chol. went from 218mg/dL to 286mg/dL. Hdl from 35mg/dL to 49mg/dL, ldl from 148mg/dL to 205mg/dL, triglycerides from 174mg/dL to 161mg/dL, and my total chol/hdl ratio went from 6.2 to 5.8. Now my doc wants me to go on statins to lower my cholesterol, which I don't want to do. I have been very strict with my LCHF livestyle. I don't understand these results, am I eating to much fat? I am 50 yrs. old, now weigh 178 lbs., 6'-1" tall. Any help from Doc, Zepp or anyone would be appreciated.
    Reply: #151
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