Episode 16 — Chris Masterjohn on cholesterol and heart disease (Part 2)
In this part, we discuss measuring blood lipids:
In this part, we discuss measuring blood lipids:
- What's a "normal" cholesterol level, based on healthy populations with immunity to heart disease? Why should we care?
- What blood lipids should we get tested — cholesterol, triglycerides, lipoprotein particle size — and how reliable are these tests?
- When can we be confident that our blood lipid levels have actually changed? You might be surprised at the answer.
Next time we'll address the question of what we should do if we conclude that important blood lipid measures may in fact have gone out of the "normal" range. The answer, of course, will be "look further," but we'll tackle just how to do that.
And of course, if you missed it, you might want to start with part 1.
And of course, if you missed it, you might want to start with part 1.
Enjoy!
Yet another way of getting the message wanted by the military-industrial complex out I suppose. I hope you can live with yourself.
ReplyDeleteAnonymous, you always have the best insights. I'd write more, but I have to go manufacture some weapons of mass disinformation. :)
ReplyDeleteChris
Hummm I must listen to this radical (?) stuff!!! LOL
ReplyDeleteOh ya, I did! Great stuff Chris! Thanks Karen
From what I've observed, Dr William Davis is having great success with patient testing, most of which you seem to be discrediting in this interview?
ReplyDelete@anonymous: LMAO, I wish this was the stuff promoted by the military=industrial complex. I have recently been activated from the reserves and will be deploying to Afghanistan and I'm honestly dreading it. Wanna know the primary reason why? It's not cause it's a warzone, nor because I got interrupted from my senior year in college, but because military food sucks! Everything is fried/cooked in vegetable oil and grains (specifically the refined kind) base the majority of the diet, so I'm honestly not looking forward to it.
ReplyDeleteIf only Masterjohn had the actual influence to push a more wapf/paleo/whole foods diet in the military, it would make me consider actually making a career out of it. Anyways, just thought your comment was beyond hilarious and I honestly think that you're just really joking and you don't even believe what you write.
You're welcome Karen.
ReplyDeleteBill, I was not addressing anything Dr. Davis does here specifically. If you have a specific question I'll try to answer it.
Chris Rosenfelt -- LOL. Yeah, the military also gets people on Lipitor, as per Duane Graveline's experience.
Chris
Chris,
ReplyDeleteThank you for the excellent podcast! You are a great speaker.
But why did you leave me hanging?? :)
Please don't make me wait too long for part three! I am in the camp with increased cholesterol after starting a paleo/WAPF diet. Well, I only have 2 data points after the diet change, but it is pretty drastic (total cholesteral went from average of about 155 to 260...).
I am especially interested in hearing your perspective on how this relates to the thyroid hormones, because my test revealed slightly low T3.
Thanks again and please keep the great podcasts coming.
When you talk about optimizing thyroid what do you mean? For ex, my FreeT3 was 2.6(range of2.3-4.2) and Free T4 was 1.24( rnage of .89-1.76). TSH was 1.7. My understanding is that thyroid is dynamic and can fluctuate (diet ,stress could affect it) like you have pointed out with cholesterol. Based on my numbers would would optimizing thyroid for me really make much of a difference in LDL receptor activity? What would you recommend for investigation if you think there are things to do with my thyroid that would meaningfully increase the LDL receptor activity? I am searching for answers as i find my cholesterol and particle levels vary substantially with diet, but there is consistency in putting out tons of particles( ie with LDL of 99 i put out 1600 particles; when LDL was 185 i had particles of 2100). If i try a statin and zetia, the LDL falls to 55 and particle count to 640. Family history of heart attack and i am Apo E3/3 which surprised me. Vitmain D has ranged from 40′s to 60′s; weight is 142 and height of 5’6″. I am almost concluding that i may be one of the few who needs a statin since i have CAD via calcium scan, but IMT is normal for my age, 60.
ReplyDeleteVery nice to see a smart guy like you questioning convention and yet maintain open minds. Something clearly missing in dialogue through all parts of our society.
Thanks much
Hi Chris,
ReplyDeleteJust a note about the Masai. My friend lives among them, involved in lion conservation measures. She said that though they are pastoralists, sugar is a major staple for the Masai, especially in the heavily sugared coffee they drink every day. Just a footnote for your discussion with Chris Kresser.
Jill Escher
Hi Jill,
ReplyDeleteThanks. That's true, but traditionally the Masai used honey rather than sugar. I was referring to research back in the 1960s when the Masai were considerably less modernized than they are today.
Chris
I think bill was referring to davis's claim that wheat raises ldl-c substantially.
ReplyDeletepersonally i think wheat belly is just hype
I confess to not having read all of Dr. Davis's posts on this subject, but I didn't find any of the ones I read convincing. I haven't read wheat belly yet. I think what he was saying, though, is that he is reporting clinical experience with particle size. What I said doesn't discredit his clinical success. But insofar as he emphasizes particle size as an important parameter, then what I said about particle size makes that aspect of the evidence for his clinical success questionable. Of course, absence of good evidence isn't good evidence of absence, so I haven't by any means discredited his clinical success, and I don't think his claims to this success are entirely based on lipoprotein particle size.
ReplyDeleteChris
Chris,
ReplyDeleteWheat Belly is definitely an interesting read. When I listened to part 1 of your podcast with Chris Kressler I also noticed some small differences between what you were saying and what he is suggesting.
Some of it also gels a bit as well, which is great.
He does suggest that LDL particle size, in his experience, has some relation to atherosclerosis. At one point he does seem to agree with you in that it is the oxidation (also glycation) of LDL that may be the issue. As far as I can tell he attributes this to poor uptake of small LDL by liver LDL receptors. The longer LDL remains the greater the chance of oxidation? Appears to more or less gel with what you say? No?
How LDL becomes "small" he describes in a bit of detail, but the gist seems to be blamed on high triglyceride levels causing increased VLDL production which in turn contribute to creating small LDL (swap of cholesterol and triglyercides by way of interaction, and then LDL losing triglyceride via hepatic lipase).
The other interesting part of his chapter on particle size is his claim that intake of triglycerides via fat has only a transient effect (and to a small degree) on triglyceride levels. He mentions that the body creates its own triglycerides and the chief factor in this is carbohydrate intake (via wheat). He sites this paper when referencing that fat intake doesn't play a large part. Thoughts?
"Carbohydrate-induced hypertriacylglycerolemia: historical
perspective and review of biological mechanisms"
I actually messaged Dr. Davis via Facebook asking about this same thing since I am reading his book and he does say that small dense LDL is a causative factor in heart disease. He said he wasn't directly familiar with your work (why the heck not?!) but maybe my message will motivate him to check it out? We shall see.
ReplyDeleteI don't think "Wheat Belly" is hype. I think he did a good job at marketing the title and it's information that people NEED. Wheat today is not the same as it was historically, that can't be denied.
Hi Andrew and Diane,
ReplyDeleteI haven't read Wheat Belly yet, but I never got the impression that it was all hype. All correct, probably not. I'm sure it contains a lot of good stuff and I look forward to reading it.
I am not arguing that small, dense LDL is *not* a causal factor in heart disease, but there is as yet no clear evidence that it is and there are multiple hypotheses to explain its correlation with CVD risk.
It is apparently true that large relatively TG-rich and relatively cholesterol-poor VLDL particles are more likely to be metabolized to small dense LDL because they are more likely to be metabolized by lipases in the plasma than taken up by the LDL receptor. However, there numerous other mechanisms by which LDL particles become small and dense, including the following:
-- high enzymatic activity of CETP or various extracellular lipases
-- oxidation
-- poor LDL receptor activity.
Since we have the most definitive evidence that poor LDL receptor activity is a casual factor in heart disease, I'm inclined to give that explanation the most weight. In this explanation, particle size merely correlates with CVD risk but isn't a cause.
That said, there are numerous ways particle size *could* be a cause, and these include greater likelihood of slipping behind the endothelium, greater likelihood to get stuck there, and greater vulnerability to oxidize. These are hypotheses that need to be further investigated.
As of yet, there is no evidence whatsoever that specific interventions to change particle size change a person's CVD risk.
The principle cause of high TG, apart from certain genetic defects, is almost certainly insulin resistance, and not dietary intake of anything except insofar as a bad diet eventually leads to insulin resistance.
Sincerely,
Chris
Thanks for that, Chris.
ReplyDeleteThanks Chris, great podcast and I look forward to #3.
ReplyDeleteAny thoughts as to whether small dense LDL have a harder time getting picked up the LDL receptor vs larger puffy LDL? That is what Dr Davis seems to infer. Just curious if there is some merit to this or is he just seeing poor receptor activity in his patients and making the correlation between the two
i.e. his unhealthy patients had small dense LDL (if the tests are even accurate I suppose), and poor liver receptor activity, then there may be a correlation (this is what I assume he is putting forward).
Chris wrote: "The principle cause of high TG, apart from certain genetic defects, is almost certainly insulin resistance, and not dietary intake of anything except insofar as a bad diet eventually leads to insulin resistance."
ReplyDeleteHow would you explain the observations that in studies of low-carbohydrate ad libitum (most of the time, anyway) compared to low-fat, calorie-restricted diets, that subjects on the low-carb diets reduce their TGs significantly more than baseline and the low-fat, calorie-restricted group?
https://lh3.googleusercontent.com/mS1sAjE_j-WqBhqOQB_GSPQv6p7wAAZBLArQ3OtWtt39mcOb_AwLhaoiC7CQis3ISwooWDL8TwTh4oNf0YnH39m82G6Ti2iq-axmW1Gyi1SaggsaN54
Have they reversed, or attenuated their insulin resistance? More so than the low-fat, CR group?
Chris wrote: "As of yet, there is no evidence whatsoever that specific interventions to change particle size change a person's CVD risk."
ReplyDeleteIn that case, how should we think about Dr. Davis' clinical experience? After years of trial and error with an at-risk population, he has established a set of diet and health interventions that slow if not stop the increase of his patient's calcium scores. (Admittedly, a calcium score is not a direct measure of CVD risk.) One of his interventions is a low-carb diet, especially a gluten-free diet, to reduce small LDL particles in his patients. Doesn't Dr. Davis' tinkering count as some type of evidence?