This week we’re glad to welcome Chris Masterjohn back to the show. Chris joined us on Episode 11 to discuss the role of cholesterol in heart disease, and to dispel the many myths associated with those subjects. There was so much to cover, we had to have Chris back for part 2 (and in fact, we still didn’t cover all of the material so he’s going to come back for part 3 in the future!)
In this episode, we discuss (among other things):
- what is a “normal” cholesterol? what can anthropological studies tell us about this?
- are lipoprotein particle size tests accurate? what’s the best way of determining particle size?
- why do some people have high cholesterol (TC & LDL) after adopting a Paleo/WAPF diet? is this something to be concerned about?
Enjoy the show!
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{ 56 comments… read them below or add one }
This was really, really helpful. Chris explained a really plausible scenario for high trigylcerides during weight loss, would love to hear if there’s a similar scenario for higher LDLs (my doc has been stressing out about my LDL level — has been in the 130/140 range while I’ve been losing weight). I convinced her to do a particle test next time, and now I hear that’s not likely to be helpful … oh well
. Good news is that at least she doesn’t want to put me on statins … she’d like to see me ingesting large amounts of oat bran instead.
Hi Beth,
Yes, same issue can raise LDL-C, TGs are just more sensitive to these effects.
Chris
Hi, My question is this: Is it not true that only a certain percentage (fairly low?) of cholesterol comes from diet? If so, what role, if any, do our diets play in raising or lowering cholesterol?
Cheers,
Gordon
Hi Gordon,
Diet plays a role in a number of ways, but I think it is wrong to attempt to modify the concentration of cholesterol in the blood directly through diet as some of the dietary factors that lower cholesterol are not good for you, and others are good for you. We will get to this in the third part, and I’ll cover it in my blog as well.
Chris
Hi, Sorry, one more question: If I had fairly high cholesterol (as tested several times with the right tests, and stable weight, and so on), and if I had an unlimited supply of free Statins, what would be wrong with taking them to lower cholesterol, presuming the drug would also lower the oxidized LDL fraction also. Just to be safe.
Thanks, and no more questions. Promise.
Hi Again Gordon,
Statins have positive effects and negative effects. If your cholesterol is out of whack (i.e. clearly out of the normal range, indicating the possibility of a metabolic issue), I think the first thing that should be done is attempt to identify the metabolic problem, and then the second thing should be to fix it if one is discovered. Since there are no metabolic problems that arise from statin deficiency, I think the better course of action is to address the root cause and use drugs when other approaches have been exhausted.
Chris
Hello Chris. I was curious as to why protein signalling hasn’t been mentioned? It would seem that AGEs would be an issue with lipoproteins as they are with other protein signaling pathways. This leaves us with the main culprits of PUFAs (increasing rate of glycation) and overconsumption of refined sugars. This disruption of protein signalling would seem to increase time spent in circulation and thus increasing oxidation of said lipoproteins.
Hi Gabe,
Well, I did mention protein signaling a little, but I was not discussing the detailed mechanisms in this podcast, but rather the questions, “what are normal blood lipids, does it matter, how do we determine if ours are abnormal? As I’ve said in recent interviews and talks, I consider “cellular miscommunication” to be key part of this. Since proteins are key communicators, this indicates a disruption in protein signaling.
I agree that one cannot discuss the molecular mechanisms of atherosclerosis comprehensively without discussing AGEs, but I’m unsure of why you use the term “protein signaling” to describe them.
I also agree that consumption of refined sugars and PUFAs can increase the aberrant formation of AGEs, but I’m unsure why they would be seen as more specific to this process than to anything else I’ve discussed.
Perhaps you could elaborate.
Chris
From my understanding, lipoproteins serve at least a duel function (what we may know). One is as a lipid and cholesterol transporter and the other as an immune system modulator. Now, if the surface proteins are not functioning properly (via AGEs), not able to properly be recognized or interact with other cell surface proteins, then one can begin to at least imagine some ill effects resulting from this. Cholesterol “delivery” to cells would be disrupted and the lipoproteins ability to “signal” to immune cells and bind to pathogens and endotoxin would be compromised. I am just trying to make sense of it all. I almost feel like, “Why bother!” Lastly, I believe The Jaminet’s recently blogged about hunter-gatherer populations and concluded that much of the early methods for blood lipid measurements were unreliable and were higher than originally thought to be. Thank you for your response and I really appreciate all of you taking the time to communicate these issues.
Hi Gabe,
I agree there is some support for a role of lipoproteins in the immune system, although I think their role in lipid transport is much more clearly laid out at this point. Either way, if AGEs modify LDL then you get a somewhat similar scenario as you get with oxidation of the lipoprotein. In either case, it is modification of protein that results in the lipoprotein being taken up into an atherosclerotic plaque. In people who are not diabetics, oxidation and nitration seem to be more important. In diabetics, AGE modification seems to be become important.
That said, most AGEs are formed intracellularly, not in plasma. Oxidative stress causes AGE formation, and AGE formation causes oxidative stress. Intracellular AGE modification could well be contributing to oxidation of lipoproteins in plasma. So distinguishing the two reaches a level of detail that is quite beyond the scope of any of the podcasts we’ve done. When I say “degeneration of lipoproteins,” I’m just trying to paint with a broad brush the general picture of deterioration of the lipoprotein that includes oxidation, nitration, or AGE-modification of the phospholipids and protein.
I would say, though, that AGE formation is probably a legitimate form of communication rather than an intrinsic “disruption” of communication. There is evidence for this, and I’ll write about it in future blog posts.
I didn’t talk about any hunter-gatherers. The Masai are pastoralists and the Kitavans are horticulturalists. Neither are hunter-gatherers. When the Masai were studied, the samples were kept on dry ice and analyzed with the support of the Framingham study. So I think those numbers are probably accurate. The Kitavans were studied even more recently than the Masai.
Chris
Excellent presentation: Now i understand why doctors have such a heard time and resort to statin prescriptions for patients. While measurement of Lipoproteins is inexact, i think that what is more meaningful for diagnostic purposes is not so much whether you are Pattern A or B, but what is the total particle level in relationship to the LDL. For example if you LDL is 99, which most consider good and you have particles of 1600 of which 40% are small you may have an issue to address either via diet or some other way of lowering the particle number and changing the mix. Be interested in hearing from each of Chris K and M as to their view on this. Look forward to hearing part three
Hi Steve,
I think this is possible, but again, the importance of particle number and size is in its infancy right now. I think the best evidence is behind promoting rapidly clearance of lipoproteins and preventing oxidation by supporting antioxidant defense, proper endocrine signaling, and minimizing inflammation. Whether particle number or size is an independent contributor to the process rather than just an indicator that these other things have gone wrong is not at all clear to me at this point.
Chris
The reader can look up a study on aging done by Albert Einstein College in the Journal of the American Geriatric Society Aug.2011. In the study 477 people were interviewed who were 94 to 109 years old. Most were Askenazi Jews. They asked them about diet, exercise, smoking, drinking and other factors. They also asked the participants why they thought they lived so long.
I am not going to explain the study but what they found was that diet did not make that much difference but neither did alcohol use, diet, weight etc. Basically, if ones parents lived long, they lived long. The reason given by the participants for their long life varied.
“- why do some people have high cholesterol (TC & LDL) after adopting a Paleo/WAPF diet? is this something to be concerned about?”
It seems like you didn’t actually answer this question – or did I miss it? Anyway, I’m dying to know the answer since this is exactly my predicament. Everything looks great except LDL is super high (~250). Haven’t lost any weight recently and am at ~15%bf. I lift weights regularly, feel fine. I have a large thyroid nodule, but my thyroid levels were normal.
High cholesterol runs in my family while heart disease does not. The vast majority of my relatives have lived to ripe old ages. Doctor wants to put me on statins, of course.
Awesome podcast by the way.
Hi Matt,
Yes, we will get to this in part 3. Establishing how one concludes that one’s cholesterol has gone up enough to care about it took the whole of part 2. If you have abnormal thyroid anatomy, doesn’t this indicate thyroid problems are a likely culprit? I realize they are considered asymptomatic, but am somewhat skeptical. Glad you liked the podcast! Hope the next one and future blog posts of mine can help you.
Sincerely,
Chris
Matt,
I’d second Masterjohn’s thoughts! Consider also testing for apoE status. E4 alleles are associated with higher glycation susceptibility to oxidation as well as higher LDLs
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1684560/?tool=pmcentrez
Your lipoprotein look helluva SUPER to me!
Thyroid nodules are sometimes resultant from mineral discrepancies between utilization and environmental availability and genotypes. All the marine-based minerals are vital to our health (probably those who evolved near the shore more so, than those who evolved in mountainous-steppe areas, I hypothesize, like apo E4 carriers).
How is your selenium status or consumption of mineral rich foods? Low selenium (esp as it relates to iodine sufficiency) may have huge factors in benign thyroid nodule development.
http://www.ncbi.nlm.nih.gov/pubmed/21242171
Great podcast!! My favorite subject…
Hope that helps!
G
That thyroid hormones affect LDL uptake was new information to me. I will definitely be looking into it. Should have seen the endocrinologist instead of the cardiologist in the first place.
Looking forward to part III.
I’m still searching for an answer about my cholesterol numbers… My total cholesterol is about 400, and my LDL is 300… I know that is extremely high, but every other predictor of heart disease is excellent: HDL is 100, triglycerides 52, CRP 0.26, blood pressure 110/70, etc. Should I be worried?
Have you looked into familial hypercholesterolemia?
Chris
I’ve looked into it a little, but I never know who to trust on the subject. My doctor seems convinced that I’ll have a heart attack in my 30′s if I don’t get on statins, but that can’t be true right?
I would try to find genetic testing. You’re interested in the cause — so I would attempt to get the cause tested. Then you can understand better whether you should worry, how much, and what you should do about it.
Chris
What is your view on the value of ApoE testing and the related suggested diets for the variants?
Rob
Hi Rob,
I think it could be useful for explaining blood lipids in some cases, but not so sure about the diets. I’ll try to look into it, think about it, and write about it more in the future. Thanks for the suggestion.
Chris
I agree with Chris. Get the genetic test for FH, then you’ll have a better sense of whether this is a functional or genetic problem.
Awesome, thanks so much Chris and Chris for your help, I really appreciate it. Is this genetic test something I can get from my conventional doctor?
Yes, if he’ll order it for you. It’s called the Familial Hypercholesterolemia Screen, and it’s test #368600 with Labcorp.
Brendan,
Numbers like that can be indicative of heterozygous familial hypercholesterolemia. As Chris mentioned in the last podcast, in the general population there is a higher risk of CVD mortality with FH. This is likely due to increased risk of oxidation of LDL because of poorly functioning LDL receptors. My approach with FH is to optimize thyroid function (because T3 is required to activate the LDL receptor) and reduce risk factors associated with oxidative damage to the greatest extent possible. Unfortunately, we do not have studies of CVD/mortality risk with FH people doing all of this stuff, but I suspect if we did, their risk would be lower than FH people that aren’t. Interesting side note is that one reasons statins work (in the small percentage of the population they do work for) is because they activate the LDL receptor.
Enjoyed the podcast! Looking forward to part 3. I had a major bump in TC & LDL from my historical baselines after adopting a paleo diet.
I did lose some weight, not a crazy amount, when I started eating paleo lowish carb. This has got me thinking though, about the other changes that occurred when I changed from my SAD diet to a paleo diet. I started taking a table spoon or two of carlson’s fish oil every day for the first month then titrated down to a teaspoon a day. I also stopped taking citrucel/metmuscil which I had taken daily for about the last 5 years. I wonder if those things could also be factors?
Citrucel maybe but likely not if it’s all cellulose, as it is mostly soluble fibers that lower cholesterol. Metamucil, quite certainly, as psyllium has been demonstrated to lower cholesterol, probably by a mechanism similar to cholestyramine — binding bile acids and sterols in the intestine and increasing liver LDL receptor as the liver attempt to make up for the lost cholesterol and bile acids.
Chris
I realize I’m several months late and Chris may not be checking comments on this page any longer, but hopefully.
In regards to psyllium – my husband had his cholesterol checked for the first time since adopting a paleo diet. The LDL number is 182, which doctor was very concerned about. (HDL 62, TG 76). Doctor advised he take psyllium to lower the number. Is there any point in taking psyllium or would this actually do more harm? I’m not so worried about his numbers, but he would like to get the doctor “off his back” so to speak.
Hi Pam,
I don’t check the comments but I’m subscribed my email. Ah the wonders of the internet.
Psyillium will lower his cholesterol, assuming he behaves according to the group means of previous studies. The mechanism is not totally worked out. I suspect that it acts similarly to cholestyramine, by binding bile acids and diverting cholesterol into the bile acid synthesis pathway. In all likelihood, it probably promotes the excretion of various toxins, so that is another benefit. If it is fermented to short-chain fatty acids it might also lower cholesterol by some other means when these are absorbed. On the whole, I think if it doesn’t seem to cause gastrointestinal discomfort, it’s likely to be somewhere between harmless and beneficial, and it will probably help get the doctor off his back.
Hope that helps,
Chris
@41min in “There’s no good research on … fasting … on blood lipids” What do you think of?:
http://www.marksdailyapple.com/statins-do-not-decrease-smalld-dense-ldl-cholesterol/
‘Do Statins Reduce Small, Dense LDL? Fasting Sure Does ‘
That’s a great example of what I was talking about. There was no control group and the order of the three phases were not randomized. The study is essentially a large-sized anecdote.
Chris
Just a quick comment. If it’s the Varady study you are both referring to, then the study subjects acted as their own control in the initial two weeks of the study. This is quite legitimate in clinical research. And the use of control groups is not always necessary to draw hard conclusions if the effects you are testing are well-known (if it is an extension trial, for example). Plus, the fact that the study phases were not randomized, which is a very, very minor point, does not invalidate the study. This is actually an informative study. Not observational or anecdotal. I don’t understand why you dismiss it so offhandedly, Chris.
Hi Stipetic,
I disagree with you. It is of course quite possible to publish a paper like this and indeed it is done quite often, but randomization is the key element that allows legitimate causal inferences whether subjects act as their own controls or whether some subjects act as controls for others. That you consider this a “very minor point” indicates we have very different philosophical approaches to experimental design. I’d be happy to discuss them further if you’d like.
Chris
Randomisation of subjects is crucial–we do it in every study we conduct. That’s not the issue here. The Varady study had only one group of subjects (as far as I can tell from the abstract), so randomization was not possible. Now that I’ve reread your original comment, I’m not sure what type of randomisation you were talking about. Stage order randomisation? Study designs are usually not randomised (they are typically templates, ie. 2-period, 2-sequence, crossover, etc). Study stages are not randomised, subjects are. So, I don’t believe it’s philosophical at all and there really is no need to discuss this further. I was just making a point about how I find some people are misinterpreting the the presence or absence of a control group since I design study trials for a living (and the Varady study did not fail my whiff test). Everyone is free to accept or reject what I say for whatever reasons.
Hi Stipetic,
I agree that it is subjects we randomize and not study designs. A study design, however, needs to have an element of randomization in order to draw causal inferences. If it doesn’t have one, it’s not illegitimate, but it is observational and the inferences one can make are different. In a crossover design, one would randomize the subjects to undergo one of two or more orders for the trial periods. I would call that randomized order for simplicity, but technically it is the subjects who are randomized.
Chris
When you guys 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.
Very nice to see smart people like the both of questioning convention and yet maintain open minds. Something clearly missing in dialogue through all parts of our society.
Thanks much
Excellent podcast, gents. I’ve always enjoyed Chris Masterjohn’s work; in both his writing and public speaking he excels at clearly explaining complex mechanisms. Definitely bring him back for part 3.
Seems everything comes in cycles..
First it was Ancel Keys on why saturated fat and dietary cholesterol is bad for you.. but then the Atkins Low Carbers, strike back…
Then Denise Minger goes at it with the China Syndrome book and documentaries
(Even fructose got into the mix when Alan Aragon and Robert Lustig got into a heated debate!)
And now of course the battle continues with…
The Gary Taubes / Tom Naughton / Paleo / Primal / Diet de-jour vs Stephen Guyenet , James Krieger, Chris MasterJohn , etc
It seems obesity, like gravity, even after decades+ of research, we understand the effects, but have little understanding on what makes it work.
At heart of the (current) controversy, seems to be whether or not a carb-rich diet causes obesity and that increase in fat storage is directly attributed to an elevated insulin response…
Chris: An interview with bloggers like CarbSane (NEFA fame) or Ned Kock would be great! They seem to be have balanced thinking!
Great podcast, wondering if one of you could post the references mentioned, particularly the ones describing different results on nmr vs vap?
Hi Greg,
Here are the ones for particle size accuracy:
http://www.ncbi.nlm.nih.gov/pubmed/19162266
http://www.clinchem.org/cgi/content/full/52/9/1643#_jmp0_
http://circ.ahajournals.org/cgi/content/full/119/17/2396#_jmp0_
http://www.clinchem.org/cgi/content/full/52/9/1722#_jmp0_
Chris
Steve,
Optimal thyroid would be in the upper half of the range. Your free T3 is low.
You would get more assistance from the yahoo rT3 group.
Chris^2 – great podcast. Looking forward to Part 3. I have a friend that recently called me very concerned about her increased lipid levels after adopting a Paleo diet and so these podcasts are timely for her. Thanks so much!!!
Cheers,
Aravind
Hey Aravind,
Thanks, and you’re welcome!
Chris
Thanks for this podcast. Very clear and hit a number of important nails on the head. In particular, it was good to hear Chris M discuss the fallibility of testing for lipids. What we usually find, with the annual cholesterol check, is a mere snapshot in time. What we want to know is whether the number is trending or moving in a range. In most cases lipid numbers will move in a range. It would be more meaningful to represent lipids as a range over a period of time, such as Chris K’s testing over a week or two, rather than a single snapshot in time.
Further confusing the issue is the margin of error in measurement. During a recent weekly lipid testing mania, my lab technician performed two (and occasionally three) tests on the same sample. Variations were as much as 10% between the test results, sometimes greater.
Tendency to form wide ranges and margins of error in testing limit the value of pinning a single cholesterol number on a person. The broad range of optimal lipid values in the O Primitivo study of 164 countries, as cited on Paul Jaminet’s site, reflects the fact that normal cholesterol moves in a much wider range than conventional medicine would allow.
Looking forward to Part 3!
Hi Gregory,
Excellent point. Population variation in this sense, is a fallacy. Not because there isn’t any, but because estimating it based on a single measurement incorporates the intraindividual variation.
I’m looking forward to it too!
Chris
Excellent podcast guys.
Chris M – I have a curvy question – Is there any method you know of, to temporarily reduce LDL? swing it towards the lower end of the 2 S.D that you mention? It’s not that I am worried myself perse, but just to get some “desirable” numbers on my test and to get others off my back! (mainly work, as it’s on annual medical thing) LDL has been creeping up from 130 to 140, which I am not so worried about in the general scheme of things.
HDL is 60-ish, Trig mid 60′s.
Thanks!
Hi Dean,
Maybe you could try a soluble fiber like psyllium. You could, of course, take a natural statin like red yeast rice, if you feel it’s really worth it. I’d take a formula that has CoQ10 in it though if you’re going to go that route.
Chris
Heh, is oxLDL collapsing the economy or are you that musician guy? Chris Martenson, Chris Masterson…Matterson? Googling you is hard!
Funny thing is, I like Chris Martenson a lot too. He might be the Chris Masterjohn of energy, environmental and economic analysis.
Hi Chris and Chris. Thanks so much for putting this together. There is so much confusion out there on this topic and it’s nice to have people digging into the nitty gritty.
As you both know, I’ve been around for a bit. I’m all up in the Paleo Blogosphere and understand what it really means to eat whole healthy nutrient dense foods. It’s what I do.
Chris Masterjohn, you chimed in on my VAP results from July with some great insight that was much appreciated by many. Given my situation, I’ve become somewhat of a poster boy for a person who has gone all in with adopted a Paleo/WAPF style diet and seen some concerning changes to my blood lipids.
Well.. I just got tested again for a host of markers last Friday. Much of the panel came back with what I would consider pretty positive results, which was encouraging to me. But this morning, I received the VAP results back from my Doc, and I gotta say, it was tough to see.
I posted my labs on PaleoHacks and they are ‘hacking’ away to try to make sense of this.
http://paleohacks.com/questions/64890/hack-jack-kronks-latest-lab-results-sept-2011
Also, I was glad to hear you mention in the end of this podcast about people losing weight not getting wrapped up in lipid numbers until their desired weight is reached. I posted this other question on PH earlier today before hearing your podcast tonight. If you want a prime example question related to exactly what you addressed there, have a look at this:
http://paleohacks.com/questions/65030/an-intrinsically-tricky-dilemma-how-should-i-proceed-with-my-brothers-and-sisters
Here’s the deal. I love this community. I think you all are some of the brightest folks in the health world. I’m all about it. I just don’t want to be irresponsible or flippant with my personal situation, and coupling what I’ve learned about how to eat well with my results leaves me quite confused.
My question for you is… if you were me… would you be concerned to see that VAP come back with your name on it? and if yes, what would you do?
As always, any insight into this is much appreciated, by me of course, by I think at this point, by many others as well.
Thanks.
-JK
I was excited to see that there would be a discussion about raised TC from paleo or HF diets. However, I was quite stunned to hear that a 17mg/dl changed is called “huge”! I have my lipid profiles for six years now, dating from when I ate a conventional diet, through strict paleo, then into high-fat so a good baseline. During that time my trigs fell (300 to 100) while my LDL rose (200 to 300). In spite of trying to keep up with all the latest knowledge on this subject, I’m still at a loss as to whether I should do anything about this. It looks like I have either high TGs or high LDL, depending on what I eat. (HDL has always been good, >70).
It can be frustrating and scary to think that you’ve changed your nutrition for the better only to have your lab tests put your doctors into freak-out mode…
Hi Chris,
My husband recently had blood work done which shows his blood cholesterol at 310, triglycerides at 154, Hdl at 40 and Ldl at 239. We are not concerned about the cholesterol number but I gather from some of what you’ve said that some of his ratios could show he’s at risk for heart disease. Would that be accurate?
Thanks, Anita
If I might add:
How do we know if he has oxidized Ldl? Does the blood work show that?
My husband is 56 years old – if that is a factor here.
There aren’t any commercial tests for ox-LDL right now. If he’s eating a lot of polyunsaturated fats and isn’t eating antioxidant rich foods, he probably ox-LDL.