Who’s the cholesterol expert now?

My new chemical engineer friend and colleague, Ivor Cummins, has turned biochemistry into his hobby. Although I can think of many more entertaining hobbies it is fascinating to watch Ivor use his engineering skills, calculating his way through piles of evidence to solve the nutrition, cholesterol and health equation. Listen and watch his technical but fascinating presentation, The Cholesterol Conundrum – and Root Cause Solution:

My favorite slide and discussion starts at around 45 minutes into the presentation, looking at LDL-C relative to HDL-C. Direct observation from the Framingham heart study data: LDL-C does NOT predict cardiovascular risk as HDL-C rises (see the image below using international units mmol/l).

In other words, LDL-C becomes mostly irrelevant as HDL-C improves! To date ONLY a nutritional approach, specifically a well formulated low carb high fat (LCHF) diet reduces risk by raising HDL-C, and lowering triglyceride, consistent with the favorable markers observed in the original Framingham study. We also now know that LCHF diets favorably improve cholesterol size and quality regardless of LDL particle count/concentration (a surrogate measurement to LDL-C), based on modern advanced NMR lipid testing.

Good luck Big Pharma finding a blockbuster drug for this one. BTW, Mother Nature figured this out long ago!

ivor cummins ldl hdl predictors

It’s unfortunate that decades of research, based on mostly weak evidence and unproven hypotheses, leaves mainstream to believe that lowering LDL-C via low fat, low calorie diets or cholesterol medication is the only way to reduce risk. Mainstream needs to better understand nutrition including whole foods diets and how to critically look at the evidence (or lack of it).

I hope to collaborate with Ivor and applaud his well done effort.

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  • rami

    hi ivpr, great video. only one thind please. thr reference “diagram adapted from article in Journal of Cardiovascular medicine 2011,Vol 00,No 00″ is wrong. can you please give me the link for the original article?

    • http://www.thefatemperor.com ivor cummins

      Hi Rami
      Ooops – here’s the raw data I converted to mmol/L and tried to make easier for audience by using my multiple line graph format rather than the stacked bars – not sure where that other ref came from – think I have a few sources of this graph (it’s that good, right?) Anyway, reference in below pic should work – I also have another ref for same essential data if req’d :)
      cheers & thanks for comments
      Ivor

  • http://nigeepoo.blogspot.com/ Nigel Kinbrum

    I spotted this on Twitter:- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492120/ Emphasis, mine.
    “Neovascularization of the normally avascular coronary DIT by permeable vasculature from the adventitial vasa vasorum is the cause of LDL deposition and CA. DIT enlargement, seen in early
    CA and aging, causes hypoxia of the outer DIT and induces neovascularization. According to this alternative proposal, coronary atherosclerosis is not related to inflammation and can occur in individuals with normal circulating levels of LDL, consistent with research findings.”
    Sounds like a pretty good hypothesis, to me.

    • http://denversdietdoctor.com Jeffry Gerber, MD

      The neovascularization mechanism sounds similar to that what causes age related macular degeneration. I wonder if there is a connection?

  • http://nigeepoo.blogspot.com/ Nigel Kinbrum

    “Krauss has produced some stellar data…”
    Krauss repeatedly conflates “sugars” with “carbohydrates” in his studies. Increasing sugars % (also possibly amylopectin & maltodextrin %) increases the % of pattern B LDL which, by implication, increases the risk factor for coronary heart disease.

    Carbohydrates from Basmati Rice (especially if refrigerated before eating), Corn, New Potatoes (especially if refrigerated before eating), Sweet potatoes, Beans, Whole fruits etc do not increase the risk factor for coronary heart disease.

  • http://nigeepoo.blogspot.com/ Nigel Kinbrum

    I’m not happy (surprise, surprise!) with the above graph of Heart Disease Risk Vs LDL & HDL. The vertical axis should be logarithmic, not linear. On a linear scale, an increase in risk from 0.2 to 0.4 (doubling) looks tiny compared to an increase in risk from 1 to 2 (also doubling). On a logarithmic scale, it would look the same.

    What say you, Ivor?

    • http://denversdietdoctor.com Jeffry Gerber, MD

      Nigel, should risk always be reported in orders of magnitude?

    • http://denversdietdoctor.com Jeffry Gerber, MD

      Nigel, should risk always be reported in orders of magnitude? Makes sense, but still risk increased 4 1/2 fold comparing the lowest HDL to the highest HDL (0.4-2.4 risk). This would still be apparent using a log scale. Glad to have all the engineers (Nigel and Ivor) commenting, just to verify the statistical trickery.

      • http://nigeepoo.blogspot.com/ Nigel Kinbrum

        I believe that it should. It’s impossible to tell on the above graph, but I think that the risk of heart disease after 4 years increases by the same proportion with increasing LDL, whatever the HDL level. Obviously, as HDL increases, the risk decreases.

        It’s also impossible to extrapolate the plots beyond 5.68mmol/L, as there’s insufficient data to fit curves to them.

        • http://www.thefatemperor.com ivor cummins

          …I’ll be honest in that I’m trying to not get really too caught up in LDL > 6mmol/L, for guys who ask me about that I refer them to a published specialist in the local area – for example I sent a >9mmol/L guy to him, HDL 1.8 I think…. Still I believe the Tot/HDL largely holds, and noted in passing a while back that a FH specific study showed average HDL of 0.8 across the cohort, with LDL generally >6 I think, so again the ratios are crazy high, and no doubt these guys contribute to the relationship seen above, as their mortality incidence drags the RHS of the curves upward…………

    • http://www.thefatemperor.com ivor cummins

      Wow Nigel, you’re like an argumentative gopher, popping up all over the place, I have to be alert to attend to all your queries – but I do enjoy them immensely! This one is interesting as it’s kind of a philosophical point in addition to being a mathematical one – what really matters to our dear readers in their quest for clarity? I might politely suggest that if I was on the lowest end of population risk (say 0.2), then doubling my risk, although sounding quite horrid, would not really mean too much to me personally – I’m already doing soooooo well compared to the guys well above me, who are the real problem – should I get exercised about this “relative risk”? I would suggest not unduly so – in fairness I practice what I preach here, in that I am not obsessed with lowering my current risk further from this particular matrix perspective (I’m around 0.45 above btw). I would rather move on from this part of the puzzle, and focus on driving down my Insulin remorselessly, a la Ron Rosedale! If someone threatened to double my risk of being eaten by an escaped lion in the next 10 years, would I lie awake at night?
      Interestingly, the drug boys use the converse of this in a genuinely knavish way – taking a low absolute endpoint likelihood, and screaming the relative risk ratios, to excite the potential purveyors of the profitable product; again this revs up the relative, and sneakily avoids the absolute. Let’s just say I’m an absolute kinda guy really, who keeps an appropriate watch on the relative!
      Note also that there is not really a mathematical precision on this – no study is perfect, the error bars are really stretchy, so I’d suggest chill on the exact placement in any risk spectrum, and rather navigate your personal metrics towards the best “zone”, triangulated across many studies and many factors – again absolute risk is a very practical way of viewing your overall “placement” in the mortality leagues.
      Yet another interesting example of obfuscation was from your favourite researcher Krauss – he used log scales to show changes in Triglyceride in one study, but not so for the other metrics – I noticed this and said hold on a minute – that almost disappears a very important response in the experiment; sure enough when backed out you could see the massive reduction in Trigs for the high fat diet, neatly disguised by the log scale (shenanigans as you would say yourself!). Jeff Volek plotted all the data sans logs and it was very informative in this format, and communicable to the moderately technical audience – and indeed I borrowed his summary for the talk. So in short after such disgraceful verbosity, I’d say logarithmic is not appropriate in this instance – we’re talking about people’s lives here man – let’s not confuse the (absolute) message! cheers Ivor

      • http://nigeepoo.blogspot.com/ Nigel Kinbrum

        I’m retired, so I’m everywhere, most of the time! Argumentative? moi? ;-)

        O.K. I agree that, for practical (mortality) reasons, a linear scale is more appropriate. It just makes the lower plots look too “flat”. As the lower plots are actually rising at a similar rate to the upper plots, the risk of heart disease after 4 years would become significant at higher LDL values. But anyway…

        If fasting insulin level is a major causative factor for atherosclerosis, the best plan of action is to reduce it, amirite? Which leads to the next question…

        What are good ways to reduce fasting insulin? I know what you prefer to do. I think you know what I prefer to do. Would anyone else like to comment with their preferred method?

        Cheers, Nige

        • http://www.thefatemperor.com ivor cummins

          you reminded me of a little joke – a friend of mine used to say (with raised eyebrows) “Pretentious? – Moi?”….!
          Good question though, and very topical – what’s the ideal way to get your Insulin down and bouncing along the floor – and then how do you get it………………….lower still!
          Let’s see what people have to say on this learned forum

          • http://nigeepoo.blogspot.com/ Nigel Kinbrum

            I saw it on TV!

            So, good ways to reduce fasting insulin level?

        • http://nigeepoo.blogspot.com/ Nigel Kinbrum

          I’m just going to leave this here and run… ;-)

          See http://www.ncbi.nlm.nih.gov/pubmed/10535381
          For example, the mean insulin concentration in 50- to 74-year-old Kitavans was only 50% of that in Swedish subjects.

          How did the Kitavans achieve this?

          See http://www.staffanlindeberg.com/TheKitavaStudy.html
          “The residents of Kitava lived exclusively on root vegetables (yam, sweet
          potato, taro, tapioca), fruit (banana, papaya, pineapple, mango, guava,
          water melon, pumpkin), vegetables, fish and coconuts. Less than 0.2% of
          the caloric intake came from Western food, such as edible fats, dairy
          products, sugar, cereals, and alcohol, compared with roughly 75% in
          Sweden. The intake of vitamins, minerals and soluble fibre was therefore
          very high, while the total fat consumption was low, about 20%, as was
          the intake of salt (40-50 mmol Na/10 MJ compared with 100-250 in
          Sweden). Due to the high level of coconut consumption, saturated fat
          made up an equally large portion of the overall caloric intake as is the
          case in Sweden. However, lauric acid was the dominant dietary saturated
          fatty acid as opposed to palmitic acid in Sweden. Malnutrition and
          famine did not seem to occur.”

          It was a high-carb (about 70%), low-fat (about 20%) diet, but not Western junk. Food for thought, eh?

  • http://www.thefatemperor.com ivor cummins

    Jeff….Just another excerpt from a well run analysis that we touched on briefly last week – even LDLp gets knocked off its lofty perch depending on the study quality and analysis approach….will discuss details further, need to collate quite a lot in coming period, as Insulin gets wrestled to the ground….
    ivor

    • http://denversdietdoctor.com Jeffry Gerber, MD

      Ivor, Insulin looks like the better metric here and what you posted below.

      BTW I was looking at some of Dr. Ravnskov’s research. He says that there is a discordant relationship between inflammation (use of NSAIDS) and atherosclerosis. He is exploring infection as another possible area to look at. NSAIDS do increase the risk for cardiovascular events, but then maybe all inflammatory pathways are not the same. More homework for me!

      • http://www.thefatemperor.com ivor cummins

        Yep – he had a look at my content and pointed out this hypothesis – I’ll send you the papers on it in case you don’t have them all – very interesting but came too late for me to incorporate (also my content conflicts with the orthodox view quite enough already, so I thought I’d leave the leading edge stuff for later!)

  • http://denversdietdoctor.com Jeffry Gerber, MD

    I wanted to re-post one of Ivor’s favorite slides. Higher ApoB concentrations >119 do signify risk as insulin levels rise >12. If insulin remains low <12 then ApoB concentrations again become mostly irrelevant, quite similar to the relationship between LDL and HDL.

    You could also direct treatment to lower ApoB specifically with a low fat diet or a statin while ignoring the high insulin level. Unfortunately this is what most of my doctor colleagues frequently do because insulin is usually not in their radar zone unless a sky high blood sugar is staring in their face. However, addressing lower insulin levels yields a much greater global benefit including CV risk reduction, improving diabetes, obesity, etc…

  • charles grashow
  • charles grashow
  • bill

    Excellent video by Ivor.

  • charles grashow

    http://www.lipidcenter.com/pdf/lipidaholics/Lipid_Cases_2009.pdf

    “Why does the Dean Ornish extreme low fat diet so effectively reduce all cholesterol levels? Well the initial substrate from which cholesterol is synthesized is acylCoA (acetoCoA, acetylacetyl CoA) which is derived from fatty acid breakdown (oxidation). So eliminating fat from the diet will drastically reduce endogenous cholesterol synthesis and all cellular cholesterol levels will lessen. As cellular cholesterol synthesis reduces, less is effluxed via ABC family transporters into HDL particles: HDL-C will lessen. Also in people significantly restricting fat intake, the liver will have less cholesterol (less chylomicron delivery of fat, less production, less being brought back to the liver in HDLs: the results is when the liver makes VLDLs and IDLs, they carry a lot less cholesterol (less VLDL-C, less IDL-C and this will ultimately result in less LDL-C. Of course Ornish showed that by drastically reducing TC levels (as well as LDL-C) via fat restriction angiographic improvement occurs in persons with CHD. It mattered little that because of reduced cellular cholesterol, HDLs were no longer being fully lipidated (thus reducing HDL-C).”

    Your thoughts

    • http://www.thefatemperor.com ivor cummins

      Hi Charles – very busy right now but in fairness I’ll glance at Ornish’s Opus again (when I did before, some time ago, my memory is that it was severely lacking in substance and control, and not really worth considering from an engineering perspective).
      Best of luck with your ultra-low fat diet
      Ivor

      • charles grashow

        I’m definitely NO on an ultra low fat Ornish type diet. I eat full fat raw goat milk, full fat goat milk kefir, grass fed meat, eggs, nuts, seeds, etc.

      • http://nigeepoo.blogspot.com/ Nigel Kinbrum

        It’s Dr. Thomas Dayspring’s Opus, actually!

        • http://www.thefatemperor.com ivor cummins

          I’m only replying to the Ornish angiographic antics Nigel, not Mr. Dayspring’s learned theory (Ornish’s low-fat prescription makes me feel ill!)

        • http://denversdietdoctor.com Jeffry Gerber, MD

          Nigel, I have found it curious that although Dr. Dayspring promotes low carb in some, he recommends cholesterol lowering therapy if the LDL-P goes way up. Dr. Daysping believes that too much cholesterol is dangerous regardless of diet, including LCHF.

          A bit of cognitive dissonance going on here, when a low carb high fat diet will raise LDL-P, yet giving a stain to counter the rising LDL-P certainly confuses the brain (at least mine). I agree that statins have been show to reduce risk (mild at best for primary prevention) so could it be that low carb high fat diets and statins operate via mechanisms independent of cholesterol?

          • http://nigeepoo.blogspot.com/ Nigel Kinbrum

            Low-carb diets are not necessarily high-fat. The PSMF is a high-protein (~1g/lb bodyweight), low-carb, low-fat diet that’s very effective in depleting overfilled tissues.

            I don’t approve of very-low-carb, very-high-fat “nutritional ketosis” diets and have blogged extensively on the reasons why (backed-up with evidence). Dr, Dayspring has posted about such diets at http://www.lecturepad.org/dayspring/lipidaholics/pdf/LipidaholicsCase291.pdf

          • http://denversdietdoctor.com Jeffry Gerber, MD

            Nigel, thanks for the link and I also had a look at your Blog. I must admit, the ‘Summertime Love’ video caught my attention. Sabrina rocks! It so 80′s and reminds me of my youth.

            It is obvious that we all share in the passion here. I am familiar with the work of Dr. Daysrping and Peter Attia. I have even heard Peter speak at our physician obesity conference last year and the offspring cohort chart was in his PowerPoint. Indeed, LDL-P looks like it is more predictive of risk relative to LDL-C.

            I think that we are all heading in the right direction here, but online, most feel the need to draw lines in the sand. Maybe it is the nature of the beast, however I do not have this luxury when it comes to seeing patients. I see vegans, carnivores and everything in between. Some take medications including statins and some do not. Everyone is different and we track progress using the tools available today in clinical medicine. I don’t try to force the issues, but try to keep all well informed and make decisions together.

            Thanks for your input.

          • http://nigeepoo.blogspot.com/ Nigel Kinbrum

            You’re welcome!

            I’m concerned about people (I know of two) eating humongous amounts of butter and encouraging others to do so, glossing-over any adverse effects. I hope that you could tell from my writings that I am fine with low-carb diets in general.

          • http://denversdietdoctor.com Jeffry Gerber, MD

            Nigel, I too express the same concern. Most will just see the cover of Time magazine ‘Eat Butter’ and not even read the article. There is much more to it as you know!

            I enjoy your analysis and humor and plan to follow your Blog.

          • http://nigeepoo.blogspot.com/ Nigel Kinbrum

            Thanks! Diet & Nutrition is considered “boring” by a lot of people, so I try to present information in an accurate but more interesting way. I’ve just written a new blog post that has a link at the bottom which refers to the Time magazine ‘Eat Butter’ article.

  • charles grashow

    http://www.lecturepad.org/dayspring/lipidaholics/pdf/LipidaholicsCase291.pdf

    My goodness! If a new healthy looking, normal weight patient showed up with an LDL-C ~ 230 mg/dL, we are all presuming that familial hypercholesterolemia is present. At the age of 54 we would be searching for arcus senilis, a sternotomy scar or xanthomata. Although there is no premature CHD, there are certainly cholesterol issues in her family. Although we do not have a baseline LDL-P or apoB, how can one go from a perfect lipid profile to a seeming very high risk one in a very short period of time? Can CV lipid/lipoprotein-related risk be worsened by the weight loss? Or perhaps the question is – does it matter what one consumes to lose weight? Is there a danger too low carbs/high fat in some people? Or how about this absurd question – can an LDL-P of ~2600 nmol/L not be associated with atherothrombotic risk? It has been reported for years that diets high in saturated fat raise TC and LDL-C and diets with reduced saturated fat lowers them (Evidence Level IA in NCEP ATP-III). MUFA and PUFA can be neutral or lower LDL-C. MUFA may raise HDL-C. Of course we now know what any therapy does to CV outcomes likely has little if any relationship to what that therapy does to HDL-C but the story that raising LDL-C is associated with or causal of atherosclerosis is widely accepted. I, other lipidologists, and many patients themselves, are starting to see that the above lipid response to a high fat diet as not being very rare response in people who abandon carbs and replace it with saturated fat, especially in those doing extreme carb restriction to achieve nutritional ketosis.”

    “Let’s get rid of the nonsense seen all over the internet that atherosclerosis is an inflammatory disease, not a cholesterol disease. That is baloney-with the reality being that it is both. One cannot have atherosclerosis without sterols, predominantly cholesterol being in the artery wall: No cholesterol in arteries – no atherosclerosis. Plenty of folks have no systemic vascular inflammation and have atherosclerotic plaque. However clinicians have no test that measures cholesterol within the plaque – it is measured in the plasma. It is assumed, that if total or LDL-C or non-HDL-C levels are elevated the odds are good that some of that cholesterol will find its way into the arteries, and for sure there, are many studies correlating those measurements with CHD risk. Yet, we have lots of patients with very low TC and LDL-C who get horrific atherosclerosis. We now recognize that the cholesterol usually gains arterial entry as a passenger inside of an apoB-containing lipoprotein (the vast majority of which are LDLs) and the primary factor driving LDL entry into the artery is particle number (LDL-P), not particle cholesterol content (LDL-C). Because the core lipid content of each and every LDL differs (how many cholesterol molecules it traffics) it takes different numbers of LDLs to traffic a given number of cholesterol molecules: the more depleted an LDL is of cholesterol, the more particles (LDL-P) it will take to carry a given cholesterol mass (LDL-C). The usual causes of cholesterol depleted particles are that the particles are small or they are TG-rich and thus have less room to carry cholesterol molecules. Who has small LDLs or TG-rich LDL’s? – insulin resistant patients! After particle number endothelial integrity is certainly related to atherogenic particle entry: inflamed endothelia have inter-cellular gaps and express receptors that facilitate apoB-particle entry. So the worse scenario is to have both high apoB andan inflamed dysfunctional endothelium. Is it better to have no inflammation in the endothelium – of course! But make no mistake the driving force of atherogenesis is entry of apoB particles and that force is driven primarily by particle number not arterial wall inflammation.”

    Your thoughts

    • http://www.thefatemperor.com ivor cummins

      We’re mulling over a hypothesis that may very well encompass all of your points and more Charles – watch this space!
      Best Regards
      Ivor

      • George

        Is it relevant that cholesterol is a major product of linoleic and alpha-linoleic acids?

        http://www.ncbi.nlm.nih.gov/pubmed/14559071

        Palmitic acid does not increase cholesterol synthesis, PUFAs do. You may have less in your serum (at about 7%E PUFA, once LDL-R increases) but you will have more in your body. Do we want a high tissue cholesterol level, to get a low serum level?
        Or do we assume the low serum level is better, because we have no way of testing the tissue level?

        • billy the k

          George–I’ve just discovered your website and what a great find it is. Your current posting [lipid hypothesis=bunk] is just one of many of yours that are now bookmarked in my iPad for quick reference. In addition to the current postings, your previous analyses of what dietary saturated fat does and does not do are superb.

          Having gone through your past postings, I’ve not seen your take on the claims (often made) that dietary saturated fat is, if not a CVD culprit, an especially bad actor with respect to increasing one’s insulin resistance.

          Do you think this is the case? If so, would this be a problem if one maintained a carb intake at ~50 to 100g/day?

          • George

            Thanks Billy! I guess everyone has an optimal carb intake that they need to work out for themselves, using TG-HDL ratio as a proxy for IR seems useful, but most people with IR will have other symptoms to judge by.
            For example, there’s a fascinating use, in the works of Dr Joseph Kraft, of tinnitus as a sign of hyperinsulinaemia.
            http://profgrant.com/2013/08/16/joseph-kraft-why-hyperinsulinemia-matters/
            I don’t see SFA promoting IR at low-carb intakes (below 150g) but anecdotally some people gain weight with hgher SFA/PUFA ratio.
            Probably more likely with high-palmitate vegetable fats like palm oil.
            Also, past generations eating dripping and flour had lower rates of metabolic disease than today, with oil and more sugar, but some individuals were susceptible to the starch plus fat combo.
            But at low-carb levels, you would have to try hard to combine SFA badly.
            It is possible – this is research that tests the limits. 31%E carb, 31%E protein, 10%E of that beef protein, and 15%E SFA mostly from dairy didn’t look good,
            but 15%E SFA from dairy was fine with more mixed protein (less beef), and 31%E protein with beef was fine with olive oil.
            http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3491165/

            What would happen at 10%E carbs?

            Indians eating ghee at 20%E SFA had low rates of DM2 and CVD, but they didn’t eat beef.

          • http://denversdietdoctor.com Jeffry Gerber, MD
          • George

            Thanks Jeffry.
            You might be interested in the posts labelled NASH 1-5 where I started (from a position of some scepticism) to see a role for dietary cholesterol in disease. This might have been discounted too readily in the past. It may be that factors producing MetSyn create a scenario in which dietary cholesterol is mismanaged, and the results are seen in amounts and behaviours of tissue cholesterol, not necessarily serum lipids.
            http://hopefulgeranium.blogspot.co.nz/search/label/NASH%20part%201%20cholesterol%20pork%20and%20cirrhosis

          • http://denversdietdoctor.com Jeffry Gerber, MD

            George, I like your interest in tissue cholesterol. As you point out measuring tissue levels are difficult especially in clinical medicine. Do you think blood lipoprotien measurement can provide clues as to what is going on in the cells?

          • George

            Definitely in the case of liver diseases, because of the livers central role in everything to do with cholesterol, high serum LDL is associated with better prognosis, as we would expect if LDL-R uptake was contributing to excess cholesterol in that organ. For other organs, it might be possible to triangulate from what is known about dietary and other factors, taken together with lipids.
            For example, statins might be most protective in patients with high linoleic acid intakes causing over-active cholesterol synthesis. This would be ironic if it turned out to be true.
            It may be possible to find some marker for unesterified tissue cholesterol in HDL, assuming that some of it ends up in reverse transport, and that it has a different character in HDL or forms adducts with lipoprotein.
            Taurine (and glycine), EPA and DHA are compounds needed to neutralise unesterified cholesterol, so response to these is another factor to consider.
            All generally connected to heart health.

          • http://denversdietdoctor.com Jeffry Gerber, MD

            George, I wonder what Chris Masterjohn would say about tissue cholesterol? Also, it would be interesting to look at rare individuals with FH, looking at tissue cholesterol and LDL-R activity.

          • http://www.thefatemperor.com ivor cummins

            hi George – echo the comments on the quality of your material; your mention of beef triggered a memory actually; Krauss has produced some stellar data, some of which I referred to in the vid, but I also caught something from him a while back where they explored high fat / low carb but specifically dominated by beef in the diet, and didn’t see quite such positive results – at the time he attributed the outcome to the high iron content of the beef, but without elaborating. Will explore this further, have no backup info right now, but you might have some thoughts on it….
            Thanks
            ivor

          • George

            Yes, that’s the paper I linked above. I can’t think of mechanism for heme iron to affect lipids with SFA – more likely with LA one would think – but iron undoubtedly major player in pathology. Rabbithole starts here: http://www.biomedcentral.com/1755-8794/2/2

    • http://www.thefatemperor.com ivor cummins

      Just
      another quick thought Charles as an interim reply – I think that the LDLp question is indeed a fascinating one, and I have some reservations about its globally assumed causal nature (in spite of your “absurd question ” sarcasm above!). Couple of items for your further thought:

      1.
      If LDLp risk is primarily a matter of mathematics and probability of deleterious endothelial ingress (Dayspring and others have implied this for example), then the increase in LDLp should translate into a linearly increasing incidence of atherosclerotic burden and hard end-points – but my understanding is that there appears to be a threshold level of LDLp above which your risk accelerates disproportionately. To an engineer, this generates significant questions around the validity of the causal chain assumptions, and thus is ignored at one’s peril. For example, an LDLp of <1000 would be perceived as nice, while one of 2000 would be scary stuff, right? But with the mathematical probability" hypothesis, it should be only double the risk……..no major deal, considering the other risk ratios that I believe I've spoken on at some length (Tot chol/HDL, Trig/HDL, HbA1c, F. Gluc,F. Insulin etc etc)

      2.
      Have a look at the attached graph from Quebec Cardio Study (one of my favorite studies btw, these guys did it properly!); my expertise is in complex interactions and synergy decoding – so you can imagine how my interest was piqued by this and other intriguing snippits of data, which I believe hint at the ultimate goal for all of us in this arena: the pursuit and mastery of broad root cause for this decades long conundrum!
      In short I believe Dr. Ron Rosedale, Gary Taubes and countless other insightful problem solvers have the Tiger by the tail – the incessant implication of Insulin in the Root Cause roundup….unsurprisingly, my target was <10uU/ml, before I got this particular data below, and it's where the human population SHOULD generally reside (in my humble engineering opinion).
      Very best regards
      Ivor

      • http://www.thefatemperor.com ivor cummins

        oops – some uploading glitches here – see http://www.thefatemperor.com/slideshows/ , the Cholesterol Conundrum pack is there, slide 87 for the graph in question……..and again apologies for not answering all of your points; sadly, time is the fire in which I burn!