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. Scompy
    When consuming sugars with fibers, the release of those sugars are slowed--more of a trickling effect into the bloodstream, so the pancreas doesn't need to call upon additional insulin to compensate. Sugar is composed of half glucose and half fructose. The pancreas reacts to the glucose ONLY to release insulin. The fructose component is the poison.

    The only place in the body that fructose can be processed is in the liver. Let me say that again. Fructose can only be broken down in the liver, not muscles, not anywhere else in the body. Glucose on the other hand gets processed throughout the body in comparison. So consuming a lot of sugar at one time stifles the liver's function to work properly for the next X-hours and influences both the pancreas's output of insulin and the liver's ability to function properly. The liver also releases other 'good' compounds into the bloodstream, which are also stifled, such as examples like taurine and carnitine to help deal with what the body needs at a given moment.

    A good goal for consuming of anything sugary after lot of veges and meats before it; think of a 3-course meal where dessert is at the end. The food in the gut acts like a buffer to slow-down the sugar's impact into the bloodstream. People that eat their sugars first are doing it wrong and causing a more rapid uptake of sugar into the bloodstream (this is the glycemic effect).

    This is why pounding the body with excess sugars, especially refined ones with no buffering or fibers present, over the course of months and years leads to continuous inflammation in the body, poor liver health, insulin sensitivity issues, diabetes, and ultimately sets up a wonderful potential for cancer, as cancer also feeds directly upon glucose.

  2. Nigel Kinbrum
    murray said...
    "The hypothesis that LDL concentration is a driving factor is contradicted by data such as from the Framington study that showed no increase in CVD once HDL-C was at 2.2 mmol/L, even when LDL-C when up over 7.0 mmol/L."
    That's not correct. On a linear scale, it looks as though CVD risk isn't increasing, but it is. On a logarithmic scale, it would have been obvious.

    "Other data shows apoB/apoA ratio has strong correlation and the author's hypothesis gives no account of HDL relationship."
    As HDL-c is about reverse *cholesterol* transport, the author's hypothesis takes it into account.

    "There is also no accounting of Dr. Kummerow's findings concerning sphingomyelin and plaque formation."
    Link, please!

    "There is no accounting of the effect of vitamin K2, nor of the success of programs such as Track your plaque which have had success zeroing out CAC scores with LCHF diets that do not have low LDL-C."
    See http://www.modernmedicine.com/modern-medicine/news/modernmedicine/mod...
    Zeroing CAC reduces calcium build-up within the artery wall, but doesn't guarantee no stenosis.

    "Even on the author's hypothesis, there does not appear to be any accounting of the cause of the neovascularization. (Perhaps I missed it while struggling through the clumsy writing.)"
    There is. Read it again. The fact that you have twice mentioned "bad writing" suggests to me that you are a cholesterol denialist and thus you will not believe *anything* bad that's said about LDL-c.

    Reply: #56
  3. Nigel Kinbrum
    Zepp said...
    "Here!

    http://www.dietdoctor.com/lchf-diets-a-threat-to-public-health

    And here!

    http://www.socialstyrelsen.se/publikationer2013/2013-11-8 "
    Thank you. The first link data stops at 2011. The second link data stops at 2012. It is currently the middle of 2014. The Twitter link I posted refers to *recent* increases in CHD cases. It takes time for dietary changes to affect CHD risk.

    Reply: #55
  4. Nigel Kinbrum
    Scompy said...
    "When consuming sugars with fibers, the release of those sugars are slowed--more of a trickling effect into the bloodstream, so the pancreas doesn't need to call upon additional insulin to compensate. Sugar is composed of half glucose and half fructose. The pancreas reacts to the glucose ONLY to release insulin. The fructose component is the poison."
    You've been watching that Lustig video, haven't you? See http://www.alanaragonblog.com/2010/01/29/the-bitter-truth-about-fruct...

    "This is why pounding the body with excess sugars, especially refined ones with no buffering or fibers present, over the course of months and years leads to continuous inflammation in the body, poor liver health, insulin sensitivity issues, diabetes, and ultimately sets up a wonderful potential for cancer, as cancer also feeds directly upon glucose."
    Do dietary guidelines suggest "pounding the body with excess sugars"? No, they do not.

    Why are so many people pounding their bodies with sugar & refined carbs? See http://vimeo.com/67977038 for a few clues.

  5. Zepp
    Yes.. and its the same for your link.. its the same data they have interpreted

    And Andreas did a tread about that in 2013!

    http://www.dietdoctor.com/lchf-diets-a-threat-to-public-health

    Its totaly bogus!

  6. murray
    "The fact that you have twice mentioned "bad writing" suggests to me that you are a cholesterol denialist and thus you will not believe *anything* bad that's said about LDL-c."

    Well, since you raise it, the writing in that article is worse than bad, it is terrible. I've read insurance policies and computer code in machine language that have better readability. Bad writing is a touchstone of poor thinking, so that in itself lowers the credibility of the author's hypothesis, which even the author labels as hypothesis, not fact. I don't dismiss the hypothesis, it is interesting, but it has a long ways to go to have enough credibility to base one's own actions on it.

    As to LDL-C, I have no dog in the fight other than my own health. I don't sell statins. I have not sold short the shares of pharmaceutical companies in order to profit from the demise of statins. I don't have to kowtow to the views of health bureaucracies to get research funding or keep my job. I don't profit from writing books on the subject. I just look for credible information and so far I haven't seen any credible empirical evidence that LDL-C is a problem. The evidence I've seen so far implicates oxidized or glycated LDL particles, or perhaps oxidized cholesterol inside LDL particles, or a proliferation of small dense LDL particles (perhaps because they are more prone to oxidation), or the number of LDL particles. Dr. Thomas Dayspring, for example, concludes LDL-C is irrelevant and it is LDL-P that matters.

    Reply: #58
  7. Francois
    It is a shame your physician will not test for HbA1C. it is a relatively cheap test and much, much more sensitive than glycemia to indicate presence of diabetes or not. I recall a policeman in Hawaii that I saw for his annual exam. His blood sugar was normal, he seemed incredibly fit (was muscular and had a six pack) BUT was of Asian ethnicity, ate a SAD diet AND had a HbA1C of 11%, in the diabetic range (was not an error, I rechecked).

    He would have been totally missed should I had not checked his HbA1C.

    As far as LDL particle size analysis, it is not necessary. If your triglycerides are low and your HbA1C is low, you will have the large, flucffy and harmless variety.

  8. Francois
    Murray,

    To further add to your comments, in explaining to the press the (horrible) new cholesterol guidelines, one of the lead authors of the recommendations dropped a bomb that was totally missed for most people. I'll paraphrase: "we dropped the LDL targets because there was never any science behind them: we initially pulled them out of thin air".

    Now, the recommendation of this marvelous committee is to only follow total cholesterol. Which, in my mind, is beyond useless.

    I honestly believe that most people on this forum are not "cholesterol denialists" but rather have a much more nuanced position than the stupid and reductionist argument that "all cholesterol is bad". Extreme low fat diet proponents (the McDougalls and the like) have totally forgotten their basic biochemistry and have no idea of the importance of this molecule. From digestive enzymes, fat digestion and fat soluble vitamin digestion to cell membranes and sex hormones, it is essential for life.

    But increase your carbs to the level of the SAD diet and you<ll dramatically increase triglycerides and insulin, promote systemic and vascular inflammation and bring on intra-vascular lesions that the body will attempt to repair with the small, high- density LDL particles, the ones that can penetrate easily the endothelium. But these particles are in no way responsible for the fire! they are the firefighters!

    Rather than kill the firefighters, why not prevent the fire in the first place by reducing carbs in the diet? It does make a lot more sense.

    If this is being a cholesterol denialist, then I am one. And proud to be, as it proves one can think by himself rather than repeat half-truths and blatant lies pushed by the pharmaceutical industry to increase sales of their statins.

  9. Z.M.
    Nigel Kinbrum, do you have any evidence that lowering cholesterol is beneficial? I'm curious to know what made you think that LDL is so important, because I've looked through the majority of the relevant evidence and came to the conclusion that lowering cholesterol is an utter waste of time.
    Reply: #60
  10. erdoke
    LDL-P is strongly associated with CHD risk, but that does not mean causation. It is also assumed that high HDL-P is able to balance it out to a great extent.
  11. Z.M.
    erdoke, I don't think LDL-P is causal either, and it does not necessarily perform better than other markers in many studies. I think the best case can be made for modified lipoproteins (as a causal factor), but even here the human evidence is very limited.
  12. Nigel Kinbrum
    murray
    Yesterday 18:09
    "Well, since you raise it, the writing in that article is worse than bad, it is terrible. I've read insurance policies and computer code in machine language that have better readability. Bad writing is a touchstone of poor thinking, so that in itself lowers the credibility of the author's hypothesis, which even the author labels as hypothesis, not fact."
    That's an ad-hominem fallacy. The author's writing skills have zero relevance to the validity of his hypothesis. A hypothesis becomes scientific theory when no evidence has come to light to refute it. Do you have any evidence to refute the author's hypothesis?

    "I don't dismiss the hypothesis, it is interesting, but it has a long ways to go to have enough credibility to base one's own actions on it."
    It currently has credibility because it's supported by current facts, and nobody has provided any evidence to refute it.

    "As to LDL-C, I have no dog in the fight other than my own health. I don't sell statins. I have not sold short the shares of pharmaceutical companies in order to profit from the demise of statins. I don't have to kowtow to the views of health bureaucracies to get research funding or keep my job. I don't profit from writing books on the subject. I just look for credible information and so far I haven't seen any credible empirical evidence that LDL-C is a problem. The evidence I've seen so far implicates oxidized or glycated LDL particles, or perhaps oxidized cholesterol inside LDL particles, or a proliferation of small dense LDL particles (perhaps because they are more prone to oxidation), or the number of LDL particles. Dr. Thomas Dayspring, for example, concludes LDL-C is irrelevant and it is LDL-P that matters."
    Ditto. I also have no dog in the fight other than a desire to debunk pseudoscientific BS which gives low-carb diets a bad name.

    For a given LDL particle size, LDL-P is directly proportional to LDL-C. I am aware that LC diets result in larger LDL particles. However, the Krauss/Dreon studies showing a dramatic change in LDL particle distribution were fatally flawed by the use of a 50/50 complex/simple carbohydrate mixture.

    50% of the carbohydrate was sugars and the other 50% could have been amylopectin or maltodextrin for all we know, which hydrolyses into glucose extremely rapidly.

    I am familiar with Dr. Thomas Dayspring. I've read http://www.lecturepad.org/dayspring/lipidaholics/pdf/LipidaholicsCase... and I follow him on Twitter. I also follow the lipidologist Brian Scott Edwards and he follows me. There is causality between LDL-C and CHD.

    That said, I'm not keen on the use of statins. For moderately raised non-HDL-C, diet & lifestyle modification is a better option. For homozygous FH, statins are probably necessary.

    I am aware of studies where LDL-C appears to make no difference (Lyon Diet Heart Trial). As LDL-P is a better surrogate for CHD, and LDL-P is strongly influenced by LDL-C and LDL particle size, it's possible for someone to have normal LDL-C but elevated LDL-P.

    Replies: #63, #86
  13. FrankG
    Nigel claims, "There is causality between LDL-C and CHD."

    Show your work, by which of course I mean: an RCT of sufficient size and duration where the ONLY variable is the level of LDL-C and the measured outcome is confirmed CHD which had been demonstrated to not exist in the trial participants, prior to the trial.

    And yes I realise that is a big ask but you are making a big claim. Choose your words wisely.

  14. Z.M.
    FrankG: "Show your work, by which of course I mean: an RCT of sufficient size and duration where the ONLY variable in the level of LDL-C and the measured outcome is confirmed CHD that had been demonstrated to not exist in that subject, prior to the trial."

    Damn right. He made a bold claim and is yet to back it up, and all he has done is cite a paper speculating about mechanisms.

  15. Nigel Kinbrum
    FrankG said...
    "Nigel claims, "There is causality between LDL-C and CHD."

    Show your work, by which of course I mean: an RCT of sufficient size and duration where the ONLY variable is the level of LDL-C and the measured outcome is confirmed CHD which had been demonstrated to not exist in that subject, prior to the trial.

    And yes I realise that is a big ask but you are making a big claim. Choose your words wisely."

    I don't think you quite understand how science works. Here's a precis:-

    1) Come up with a hypothesis which explains all of the current known facts and correctly predicts future facts.

    2) If a new fact isn't explained by the hypothesis, the hypothesis is either improved so that it again explains all of the current facts, or it's scrapped. GOTO 1)

    3) When a hypothesis has been around for long enough with no refutation, it's promoted to "scientific theory". E.g. The theory of evolution. Global climate change theory etc.

    Studies provide facts. I don't do studies. It ain't my job!

    I'm not making any claims. Vladimir M Subbotin is! His name sounds Russian, so that explains his poor English. Vladimir M Subbotin has published 92 peer-reviewed articles, which makes him far cleverer than you!

    It's not a big ask. it's an impossible ask! Asking for the impossible is a standard tactic used by denialists, known as "Moving the goalposts".

    Replies: #67, #68
  16. Nigel Kinbrum
    Z.M. said...
    "FrankG: "Show your work, by which of course I mean: an RCT of sufficient size and duration where the ONLY variable in the level of LDL-C and the measured outcome is confirmed CHD that had been demonstrated to not exist in that subject, prior to the trial."

    Damn right. He made a bold claim and is yet to back it up, and all he has done is cite a paper speculating about mechanisms."
    I see you're as stupid as FrankG in (not) knowing how science works.

  17. FrankG
    Patronising as ever eh Nigey-poo?

    I'm well aware of how science is supposed to work and your explanation leaves a great deal to be desired.

    It may be an impossible ask but if you want to make the straightforward claim of direct causality for LDL-C, then the straightforward approach I requested is what is required. As soon as only one other variable is included -- such as what each group of partcipants were eating -- then the picture immeditaley becomes a great deal muddier, doesn't it? The "goalposts" are exactly where they should have been in the first place... regulation width.

    And calling people "denialists" and "stupid"... what kind of a tactic is that?

  18. FrankG
    That someone has publsihed far more studies than I, demonstrates nothing about my intelligence... as you yourself just wrote, "I don't do studies. It ain't my job!"
  19. Nigel Kinbrum
    I see your VLCVHF diet has done nothing to improve your intellect, since the last time we "debated".

    You are a cholesterol denialist. Your tactics are so obvious, that even a 5th grader would come to the same conclusion. There's zero point in debating with people like you.

    Your mind is like a steel trap.............................that's been left outside in the rain and rusted shut.

    Goodbye!

  20. Z.M.
    Nigel Kinbrum: "I see you're as stupid as FrankG in (not) knowing how science works."

    Wow, nice to see your true colors. I'm fully aware of how science works, and you have yet to provide any evidence for your bold claims in accordance with science, so you are really in no place to be lecturing anyone about "how science works". It's also sad to see such name calling from a grown man like you.

  21. Nigel Kinbrum
    I nearly forgot....
    FrankG said...
    "That someone has publsihed far more studies than I, demonstrates nothing about my intelligence... as you yourself just wrote, "I don't do studies. It ain't my job!""
    I'm not the one who's trying to refute Vladimir M Subbotin's hypothesis. You are.

    Your writings amply demonstrate your intelligence.

    Reply: #73
  22. Nigel Kinbrum
    Z.M. said...
    "Nigel Kinbrum: "I see you're as stupid as FrankG in (not) knowing how science works."

    Wow, nice to see your true colors. I'm fully aware of how science works, and you have yet to provide any evidence for your bold claims in accordance with science, so you are really in no place to be lecturing anyone about "how science works". It's also sad to see such name calling from a grown man like you."
    Which part of "I'm not making any claims. Vladimir M Subbotin is!" did you not understand?

    If you & FrankG are examples of what VLCVHF diets do to intellect, it's a good enough reason for me to never recommend them to anybody.

    P.S. Nice attempt at deflection - another tactic used by denialists.

  23. FrankG
    I'll leave others to be the judge as to which of us is best demonstrating intelligence here.

    Oh I nearly forgot (LOL)... you are now saying it was some Russian that I am disputing?

    Who wrote this in comment #62 just above..? I've included the whole paragrpah for context. Was it you or Vladimir M Subbotin?

    "I am familiar with Dr. Thomas Dayspring. I've read http://www.lecturepad.org/dayspring/lipidaholics/pdf/LipidaholicsCase... and I follow him on Twitter. I also follow the lipidologist Brian Scott Edwards and he follows me. There is causality between LDL-C and CHD."

    So who was I quoting in regards this claim of direct causality from LDL-C to CHD?

    Like I said, chose your words wisely... ... ... my mistake, you seem inacapable of so doing.

  24. Z.M.
    Nigel Kinbrum: "There is causality between LDL-C and CHD."

    This is a claim.

    If you noticed from my first post, I was curious to know how you came to the conclusion that LDL is important, and so wanted to understand your position. I would certainly never call you stupid or question your intelligence just because you came to a different conclusion.

    BTW I'm not a low-carber.

  25. Nigel Kinbrum
    FrankG said...
    "I'll leave others to be the judge as to which of us is best demonstrating intelligence here.

    Oh I nearly forgot (LOL)... you are now saying it was some Russian that I am disputing?

    Who wrote this in comment #62 just above..? I've included the whole paragrpah for context. Was it you or Vladimir M Subbotin?

    "I am familiar with Dr. Thomas Dayspring. I've read http://www.lecturepad.org/dayspring/lipidaholics/pdf/LipidaholicsCase... and I follow him on Twitter. I also follow the lipidologist Brian Scott Edwards and he follows me. There is causality between LDL-C and CHD."

    So who was I quoting in regards this claim of direct causality from LDL-C to CHD?

    Like I said, chose your words wisely... ... ... my mistake, you seem inacapable of so doing."

    You blithering idiot, Frank!
    "There is causality between LDL-C and CHD" comes from Vladimir M Subbotin's hypothesis. SMH.

    Reply: #77
  26. Nigel Kinbrum
    @Z.M.
    Sorry if I've been excessively snarky, but this tends to happen every time I "debate" with FrankG. It's been a while since our last "debate", and I'd forgotten just how infuriating he can be. I should have stood by the old motto:-

    "Never argue with idiots. They drag you down to their level, then beat you with experience!" :-D

    I'm outta here!

    Cheers, Nige

    P.S. We're having a heat-wave here. A temperature of 34°C is not exactly helping my mood!

  27. FrankG
    So that whole paragraph which I quoted, was from Vladimir M Subbotin's hypothesis? Unbelieveable!

    Yeah "blithering idlot" is right :-P

    Don't let the door hit your arse on the way out!

  28. Nigel Kinbrum
    FrankG rambled incoherently...
    "So that whole paragraph which I quoted, was from Vladimir M Subbotin's hypothesis? Unbelieveable!"
    NO! Try actually using your brain, for once in your miserable life.

    Vladimir M Subbotin's hypothesis made it clear that coronary atherosclerosis is an LDL-C-mediated phenomenon, not an inflammation-mediated one.

    The fact that LDL-C level doesn't correlate with coronary atherosclerosis risk has been explained.

    Reply: #79
  29. FrankG
    What did you call this tactic earlier... "deflection"..?

    You sure know a great deal about tactics eh? Use them often?

    I quoted YOU Nigel. It is clear from the context that these were your own words. That you don't have the backbone to defend them but are desperately trying this weasely-mouth approach of saying these were not your own words, is pathetic and ridiculous.

    That I am using my own brain, is self-evident from the fact that I see so readily through your tissue of lies.. as do, I expect, the majority of readers here.

    Even if (IF) you were quoting Vladimir M Subbotin's hypothesis, which you and the conext of your comment in no way make clear, are you now saying that you don't agree with, nor stand by those words? That I should take it up with him and leave you, an innocent bystander, alone?

    Go take a cold shower and maybe (just maybe) your few surviving brain-cells might see it through the heatwave :-P

    You see, this is how it is when you bring people down to your level.

  30. Nigel Kinbrum
    I've had it with your strawman fallacies. Go **** yourself, you ****ing troll.
    Reply: #81
  31. FrankG
    Right back at you :-P
  32. Z.M.
    Nigel, to be accurate it does not seem that Subbotin thinks LDL to be a major factor judging by some of his statements (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492120/):

    "However, the statement that high levels of LDL are the main cause of coronary atherosclerosis is inconsistent with established medical concepts."

    Even citing Stehbens and Ravnskov at one point, both very critical of the lipid hypothesis:

    "The lack of association between total or LDL cholesterol and degree of atherosclerosis in unselected individuals was demonstrated by a study during the 1930s [47] and has since been noted by many others, notably by W. E. Stehbens [48-54] and U. Ravnskov [55-59], and others, e.g. [60]. Therefore, the hypothesis that elevated blood cholesterol constitutes a major cause of coronary arteriosclerosis is questionable. Undoubtedly, high LDL levels are an important risk factor and a vital tool in CA prevention, but logically, it must be concluded that high LDL levels are not "a major cause" of coronary atherosclerosis."

    "High LDL levels are not a fundamental cause of coronary atherosclerosis, as lowering such levels protects only 30-40% of those at risk. Furthermore, humans and animals with normal LDL levels can suffer from coronary atherosclerosis."

  33. FrankG
    Risk factor is not necessarily causative.. which comes first... chicken or egg? Does the almost 100% association of firefighters and house-fires lead to the conclusion that firefighters cause house-fires? I hear sirens and see a big red truck in my rear-view mirror.. oh there is probably a fire nearby... there's your "risk factor" association.

    What roles does cholesterol have in healing the body? Why is the body producing it? Why is it only a problem in recent years..? So much so that there is serious talk of testing and statinating children!? Why was cholesterol not a problem for our ancestors? What has changed in recent years that somehow we are all statin deficient?

    Like I said earlier... there is a way to show a direct casual link if such a link existed... why has no such study been done in all these decades? Perhaps because it is not so easy to do.. but it is easy to make grandiose claims and pass those off as "science".. especially when that help sell drugs.

  34. Nigel Kinbrum
    Z.M. said...
    "Nigel, to be accurate it does not seem that Subbotin thinks LDL to be a major factor judging by some of his statements (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492120/):

    "However, the statement that high levels of LDL are the main cause of coronary atherosclerosis is inconsistent with established medical concepts.""

    The fact that LDL level is inconsistent with coronary atherosclerosis doesn't rule out LDL as a causative factor, because it's LDL particle number that counts. Let me explain...

    LDL level is directly proportional to LDL amount

    LDL amount = LDL per particle * LDL particle number

    LDL per particle = (4/3)*π*r^3 , where r = LDL particle radius

    Note: A 10% decrease in particle radius results in a 27% decrease in particle volume

    For a given LDL per particle:-
    LDL particle number is directly proportional to LDL amount, and
    LDL particle number is directly proportional to LDL level

    Therefore, even though LDL particle number counts, rather than LDL level, coronary atherosclerosis is still an LDL-mediated phenomenon. The relationship between LDL level, LDL per particle and LDL particle number causes confusion.

    I hope that clarified things!

  35. Z.M.
    Nigel, no confusion here as I'm fully aware that particles are said to be causal as seen in the popular "response to retention" hypothesis. However, I don't see how claiming that LDL particle counts changes anything, since this claim also lacks evidence of causality.
  36. Murray
    "That's an ad-hominem fallacy. The author's writing skills have zero relevance to the validity of his hypothesis. A hypothesis becomes scientific theory when no evidence has come to light to refute it. Do you have any evidence to refute the author's hypothesis?"

    It's not an ad hominen. I know nothing about the person other than the writing. Inability to organize and express one's ideas well undermines the credibility of the ideas, as poorly presented writing casts doubt on the reliability of the hypothesis, doubt that the hypothesis is well constructed from available evidence. In one of my philosophy of science courses the professor had us write our paper as a letter to a friend who had never taken philosophy. It was a good exercise, not just in writing, but in learning to think through one's ideas from perspectives outside of the baroque architecture of technical jargon. Logical edifices are enchanting (I was a math and computation theory major), but in the real world, as Nietzsche observed, every syllogism is a slander against reality.

    Whether or not an hypothesis is valid is irrelevant because we do not know whether or not it is valid. Talking about validity begs the question. One looks for indicators of reliability.

    You present an interesting philosophy of science. So if several people come up with hypotheses, all consistent with the data but inconsistent with one another, you have several valid yet inconsistent theories. Okay. But such theories have no particular appeal to me as a decision maker. Unlike pure science, in law, for example, one must make difficult decisions, act, on incomplete information. As Oliver Wendell Holmes Jr. observed, the life of law has been experience, not logic.

    So in life, the burden of proof is on change and departure from what in experience appears to be working well. There is embedded knowledge in tradition and experience counts more than logic from necessarily incomplete logical models.

    So I begin from my experience. My experience was that after doing a considerable amount of investigation and ruminating on the implications of various findings, and then as a result changing from low-fat, no processed food diet with lots of exercise and low LDL cholesterol, to high-fat, low-carb diet with higher LDL cholesterol, I significantly improved my health and sense of wellbeing in numerous ways. When I eat coconut oil, for example, which elevates my LDL, my skin is much much better and I don't get colds or flus at all (a bonus living in Canada, which is winter six months of the year). I could go on. My cohorts of my age all have greying hair and belly paunches-- even the low-fat low-cholesterol ones who work out 3 weekdays a week and do endurance sports on the weekend (a few of whom developed heart arrhythmia from that). My hair started greying six years ago, until I went LCHF and upped my LDL and then the greying reversed and I have not greyed at all since. (I don't think LDL had a causal role in that. I think it was related to improved mitochondrial health.) Joint pain eliminated, tinnitus gone, better endurance, etc. My executive health clinic (which conducts innumerable tests it seems, sheets of results on blood work and urinalysis) fusses about LDL, although they have seen i can easily manipulate LDL through diet (what number do you want me to have on the follow-up, doctor, if it makes your file look better). Since every other marker I have is stellar, they conclude I seem to be thriving. The cognitive dissonance they endure is palpable. The bliss of being n=1 with no pressure to create n=2.

    So given my experience, which is in full accord with the apparent metabolic advantages of a ketogenic LCHF diet, the burden of proof is on the LDL-cholesterol-is-necessarily-bad-at-any-dose hypothesis to establish its case convincingly enough to displace the wisdom of experience. The methods and prejudices of chalkboard science and publication pressures are one thing, the realm of real-world action is another. As I noted earlier, the hypothesis is interesting and I will follow with interest its development from hypothesis potentially to operational reality. Thank you for the reference, I am genuinely grateful for it. Nonetheless, it is hypothesis, and in the world of action one can't be slaying one's mate every time some Iago whispers a hypothesis in one's ear simply because it sounds logical and has not yet been definitively disproven.

    I find the cholesterol mania amusing sometimes. I recall reading reports on research investigating the action of cholesterol ester transfer protein, moving cholesterol from HDL particles into LDL particles. Of course the LDL-cholesterol-is-necessarily-bad-at-any-dose scientists speculated that this created new drug potential, to impede CETP activity to lower LDL cholesterol and therefore be good good good. And of course the drug worked and lowered LDL, but "counterintuitively" the reduced CETP activity increased incidence of CVD. Of course, after hearing the whispers of Iago in the first report, I declined to act until the impede-CETP activity hypothesis (not yet refuted) was tested by experience. So yes, I allow the possibility hypotheses bear fruit, and so I wait to see how the hypothesis bears out in experience before acting on it. At least I can take comfort in knowing that by maintaining my status quo keto-LCHF diet pending evidence to warrant change, that my hair will not turn grey worrying about LDL. Nor do I need to get riled up and use dramatic punctuation and abusive elisions. Failure to convince others should be cause to reflect on why the communication was unpersuasive, not to insult the person unconvinced.

    In any event, people come here to learn and share, not to convince.

    Reply: #87
  37. bill
    Well said, Murray. Thanks for that.
  38. Sara K
    Diet Doc, question about THYROID.

    I was curious about your opinion on the theory that ketogenic diets are harmful to thyroid function. You're TSH & other thyroid markers look rather good, although I'm not sure that you are in ketosis the majority of the time since you stated that you aren't always on a "strict" LCHF diet.

    This ketogenic experimenter goes into some detail about his experience with altered thyroid function: http://bjjcaveman.com/2013/04/28/the-effect-of-a-ketogenic-diet-on-th...

    Thoughts?

  39. Nigel Kinbrum
    Murray said...
    "It's not an ad hominen. I know nothing about the person other than the writing."
    Irrelevant, m'lud! Ad hominem means that you attack the person instead of their argument. That's exactly what you did.

    RE The rest of your long, rambling comment: Get a life. Please!

    Reply: #96
  40. Nigel Kinbrum
    FrankG waffled...
    "Risk factor is not necessarily causative.. which comes first... chicken or egg? Does the almost 100% association of firefighters and house-fires lead to the conclusion that firefighters cause house-fires? I hear sirens and see a big red truck in my rear-view mirror.. oh there is probably a fire nearby... there's your "risk factor" association."
    Oh, Frank. The 1980's called. They want their metaphors back!

    That's all you're capable of - mindless drivel sound-bites. You contribute nothing worthwhile to any conversation, other than fallacies.

    Your favourite fallacy is the Straw man. You deliberately mis-quote & mis-represent your opponent's argument and attack the mis-representation. That's intellectual dishonesty. You're as bent as a nine-bob note. Ciao!

    Reply: #97
  41. Nigel Kinbrum
    Z.M. said...
    "Nigel, no confusion here as I'm fully aware that particles are said to be causal as seen in the popular "response to retention" hypothesis. However, I don't see how claiming that LDL particle counts changes anything, since this claim also lacks evidence of causality."
    From http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492120/
    "Neovascularization of the normally avascular coronary DIT by permeable vasculature from the adventitial vasa vasorum is the cause of LDL deposition and CA."
    CA is caused by LDL deposition.
    ∴ CA caused by LDL, according to Subbotin's hypothesis.
    Reply: #95
  42. Z.M.
    Nigel Kinbrum: "CA caused by LDL, according to Subbotin's hypothesis."

    Going along with this assumption, I'm curious to know what is the solution to this LDL deposition?

    Reply: #104
  43. Nigel Kinbrum
    Z.M. said...
    "Nigel Kinbrum: "CA caused by LDL, according to Subbotin's hypothesis."

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

    As I'm not allowed to post links to my blog (I just tried and the comment didn't appear), you're going to have to google my username, find my blog and look in the Blog Archive for the post I made in December 2008 about Cholesterol And Coronary Heart Disease.

    Reply: #94
  44. FrankG
    In Comment #62 Nigel wrote (in his own words, to punctutae a paragraph about how widley read he claims to be on the subject) "There is causality between LDL-C and CHD." whcih he later tried to pass off as an (unnattributed and out of context) quote from Subbotin's hypothesis.

    In Comment #67 I wrote "...if you want to make the straightforward claim of direct causality for LDL-C, then the straightforward approach I requested is what is required. As soon as only one other variable is included -- such as what each group of partcipants were eating -- then the picture immeditaley becomes a great deal muddier, doesn't it?"

    ...and now we are told that "As CA is a multi-factorial condition, multiple factors need to be addressed."

    So now it is not just as straightforward as LDL-C... we have more variables to consider... other potential causes... the picture is muddier!

    To spell it out: you are now saying that LDL-C by itself is not causative of CHD but just part of that wonderful, all encompassing phrase of "multi-factorial"... double-speak for "we don't really have a clue but want to appear smart all the same"

    ---

    As a side note I find it interesting how those like Nigey-poo, who act as if they have superior understanding often use the tactic of bait and switch... one minute discussing CHD then substiturting in CA, as if the two were the identical... if they were the same thing there woud be no need for the two terms, now would there?

    ---

    You're an arrogant jacka$$ Nigel, glad to see that others here and have seen your true colours.

    Did you leave yet? You keep saying goodbye. How trustworthy is anything you say?

  45. FrankG
    From http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492120/
    "Neovascularization of the normally avascular coronary DIT by permeable vasculature from the adventitial vasa vasorum is the cause of LDL deposition and CA."
    CA is caused by LDL deposition.
    ∴ CA caused by LDL, according to Subbotin's hypothesis.

    I read "Neovascularization ... is the cause of LDL deposition and CA"

    Why twist that to see LDL as the cause of CA? If anything, your quote states "Neovascularization ... is the cause of ... CA"

    If I hit you over the head with an hammer, no doubt a complex pathway of chemical and electrical signals could be followed that ultimately lead to your perception of pain.

    Do we now isolate just one of those chemical/electrial signals as the cause of your discomfort? Or should we ultimately look to the hammer?

    This is about as old as your 2008 blog post...
    http://www.youtube.com/watch?v=otCpCn0l4Wo

  46. FrankG
    Nigel whined, "Ad hominem means that you attack the person instead of their argument. That's exactly what you did.

    RE The rest of your long, rambling comment: Get a life. Please!"

    I'm sure I'm not the only one who sees the complete hypocrisy in that comment :-P

  47. FrankG
    As you are such an avid enthusiast of my metaphors Nigey here's another...

    A man working in a scissor factory, goes to the company Doctor complaining about the number of unsightly scabs and scars on his body... a consequence of his frequent, work-related, sharp-edge implement-interactions.

    The Doctor takes a look at his blood-work and decides that: in order to avoid the scabs forming in the first place, the very best course of action would be to reduce the number of platelets, the amount of fibrin and various other clotting factors... that should do the trick!

  48. Nigel Kinbrum
    FrankG wittered...
    "As you are such an avid enthusiast of my metaphors Nigey here's another..."
    If you believe that, that's conclusive proof for everyone posting here to see, that you don't have even two working brain cells to rub together!

    Thank you, Frank. You make ridiculing you too easy for me, 'cos you do a sterling job ridiculing yourself!

  49. Nigel Kinbrum
    FrankG blustered...
    "Did you leave yet? You keep saying goodbye. How trustworthy is anything you say?"
    Who appointed you as guardian of Andreas Eenfeldt's blog?

    You did, I expect. The Dunning-Kruger effect strikes again!

    https://theiceblog.files.wordpress.com/2009/09/i-see-dumb-people.jpg

    Poor, poor FrankG. Too dumb to know he's dumb!

    Reply: #100
  50. FrankG
    I'm glad you're sticking around... the more you post, the more you reveal of your delusional state. It was you who offered the goodbyes (or maybe you were quoting some (Russian?) :-P

    But there you go deflecting again... rather that than face the incoherence of your argument, eh?

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