The Healthy Skeptic Podcast – Episode 11

June 7, 2011 in Podcasts | 49 comments


ths podcast logoThis week we’re glad to welcome Chris Masterjohn to the show. Chris is currently pursuing a PhD in Nutritional Sciences with a concentration in Biochemical and Molecular Nutrition at the University of Connecticut. He writes a blog called The Daily Lipid and is also a frequent contributor on the Weston A. Price Foundation’s blog.

I consider Chris to be one of the foremost experts on the topic of cholesterol and its relationship to heart disease. In this episode, we discuss (among other things):

  • the history of the cholesterol-heart disease connection
  • misconceptions around diet vs. lipid hypothesis
  • finding middle ground between cholesterol skeptics and proponents of the lipid hypothesis
  • the LDL receptor and familial hypercholesterolemia and what they can tell us about cholesterol and CHD in normal populations

We didn’t get to any questions this time around, but Chris has graciously offered to come back and do an entire episode devoted to Q&A in the future – so look out for that!

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{ 49 comments… read them below or add one }

Wes June 7, 2011 at 10:42 am

Great information! Just a comment about the background noise though, the paper rustling or stuff happening while Masterjohn talked was really distracting.

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Lynn June 30, 2011 at 3:01 pm

I agree about the back ground noise…

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Nikki June 7, 2011 at 1:29 pm

Chris, this has been one of your best podcasts to date. I learned so much! I think the information about the oxidation process and how harmful that is in terms of cholesterol and heart disease was especially eye opening. Masterjohn is incredibly gifted at taking these complex processes and making them more digestible for us non-Phds. Thanks for having him on your show!

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Aaron Blaisdell June 7, 2011 at 2:25 pm

Awesome interview. Now I just need a white-board diagram to detail all of the mechanistic pathways and processes Chris M. described!

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Lorraine June 7, 2011 at 6:37 pm

Just joined your website. I’m a practicing naturopath in Australia, ever struggling against the tide of mainstream, whilst preferring to swim together and be much more integrative. Really enjoyed this podcast. So good to hear voices sharing the info rather than just reading literature. Let’s me multitask. Thank you :)

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Steve June 7, 2011 at 7:30 pm

That was an exceptional interview; i learned a lot from it. If i am to understand Chrs M’s viewpoint, you would conclude that the mix of LDL particles between small and large is not as important as the total amount of LDL particles that carry cholesterol. IF this is correct, then a number of people in the Paleo community may be fooling themselves in to thinking that all is ok when most of their LDL particles are large. It may depend upon how many there are and for those on the high fat diet that might be as many as 2,000 particles floating around and potentially overwhelm the LDL receptors, hang around to long and degrade, get oxidized and cause an inflammatory reaction. Not so good. I guess the question may be what is a good marker- LDL particle number? What are your thoughts?
Thanks for the outstanding podcast!

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Chris Kresser June 8, 2011 at 8:10 am

Maybe Chris M. can chime in, but I’m not sure that’s entirely accurate. From my reading of the research small, dense LDL are more likely to oxidize, and we can’t assume that everyone with high numbers of LDL has ox-LDL. The likelihood rises, but there’s not necessarily a relationship. That would depend on LDL receptor function and overall presence of oxidative factors in their diet and lifestyle.

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gregory barton June 9, 2011 at 6:13 am

I think what CM was saying is that time is of the essence: the longer the LDL particles are in the blood, the more likely the large particles will degenerate into small particles and oxidize. (Something about losing triglycerides – I couldn’t quite hear.) If the LDL receptors are blocked (whether through familial hypercholesterolemia or rT3) and the liver keeps on producing cholesterol then the numbers will rise. Thus high LDL numbers will correlate with cholesterol spending more time in the blood and more opportunity to oxidize. Correct me if I’m wrong.

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Chris Masterjohn June 9, 2011 at 10:09 pm

I’ll write a blog post about LDL particle size, but here’s the gist.

First, LDL particle size can very easily be seen as a marker for time spent in the blood (because this leads to loss of triglycerides to cells and to HDL, and acquisition of cholesterol from HDL, more oxidation and other modifications, all of which make LDL small and dense). Since excess time spent in the blood is primarily a function of poor LDL receptor activity, and since poor LDL receptor activity is by far and away the most definitively established causal risk factor for heart disease, it makes sense to first and foremost consider small dense LDL as a risk factor because it is a marker for poor LDL receptor activity and long time spent in the blood. Thus, there is no reason to assume that treatments that boost LDL particle size through any means other than promoting better LDL receptor activity or preventing oxidation will actually prevent heart disease.

Second, evidence to date suggests that LDL particle size does not add any predictive value to established risk predictors like the total-to-HDL-C ratio. (This, like small dense LDL is, in my view, a marker for poor LDL receptor activity and not a causal risk factor itself.)

Third, LDL particle size testing may not be reliable.

I didn’t go into points 2 and 3 much in this interview, but I’ll blog about them and in the q&a interview I’ll do with Chris K we can talk about those points.

I do not think particle *number* is the issue to look at. Particle number generally increases, in my view, because more particles are synthesized or fewer are cleared. What we want is to promote clearance, but not to stop synthesis, so we don’t want to obsess over particle number per se.

Chris

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gregory barton June 10, 2011 at 2:03 am

Thanks for the clarification. If I understand correctly, you are sayting that “number” is an unreliable marker because it could indicate either increasing synthesis or poor clearance and we cannot distinguish which is which. But in certain cases, would not one be more likely than the other? For example, if cholesterol goes up on a very low carb diet, would it not be fair to presume that the clearance is impeded, rather than synthesis is increasing. You alluded to this issue in a comment to the article Why is My Cholesterol So High on This Diet:

“One thing to look out for is that extended low-carbing can decrease thyroid function, which will cause a *bad* increase in LDL-C, and be bad in itself. So be careful not to go to extremes, or if you do, to monitor thyroid function carefully.”

I look forward to your article on particle size. However, if clearance and promoting receptor activity are the goal of arterial health, I’m sure many of us would welcome an elaboration on this subject too. For example, could you comment on Paul Jaminet’s claim:

“Copper deficiency is, I believe, the single most likely cause of elevated LDL on low-carb Paleo diets. The solution is to eat beef liver or supplement.”
http://perfecthealthdiet.com/?p=2547

Is Paul Jaminet saying that remedying a copper deficiency would promote receptor activity and clearance? What is the connection with thyroid? Does copper deficiency on low carb/paleo lead to decreased thyroid production which leads to decreased LDL receptor activity which leads to elevated LDL?

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Chris Masterjohn June 10, 2011 at 7:37 am

Hi Gregory,

I haven’t reviewed the primary literature on copper and cholesterol metabolism, but this is what the copper chapter of the tenth edition (2006) of Modern Nutrition in Health and Disease has to say:

“Blood cholesterol increases in animals fed copper-deficient diets, but results of studies on the effects of low-copper diets on human blood cholesterol are not consistent. Levels increased in some and declined in others, and copper supplementation increased low-density lipoprotein in a study in men.”

Copper is also pretty widely distributed, though I agree copper status will be better if you eat liver. Overall, I think he has a point, but it should be considered very speculative. I think it is a stretch to conclude that this accounts for most cases of high LDL-C on low-carb diets.

I agree that decrease in thyroid function on low-carb is a possible explanation for increased particle number, although so is increased clearance of VLDL from the liver due to choline or increased cholesterol output due to a lower PUFA-to-SFA ratio. Thus, one should consider the other markers, in particular the total-to-HDL-C ratio. If this is very high in addition to particle number but particle size looks good, the particle size wouldn’t comfort me, especially since low-carb may increase particle size through means that have nothing to do with increases LDL receptor activity and decreasing time spent in plasma. I would look at thyroid function, but the available tests are incomplete. For example, it is very possible that elevated free fatty acids decrease thyroid hormone receptor binding at the nuclear level. So I think you need to be very sophisticated in your approach to evaluating thyroid status.

Chris

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gregory barton June 10, 2011 at 7:43 pm

Thanks Chris. Your comments suggest that the issue is a can of worms for the layman – with the exception of TC to HDL ratio, which you stress over particle size. That’s a very interesting twist on the standard low-carb thesis: large and fluffy is benign.
Further elaboration, at some future date, would be welcome.

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Eric Lepine June 10, 2011 at 7:40 am

That’s awesome Chris. Thanks for clarifying. I was also wondering the same thing…

Great to have you two together on one show. Now, Chris needs to get Kurt Harris, Mat Lalonde, Stephan and you together for 2+-hour marathon!!! That would be the BOMB!!!!

Cheers,
√Čric

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Chris Kresser June 10, 2011 at 8:16 am

Thanks for responding on this, Chris. You say: there is no reason to assume that treatments that boost LDL particle size through any means other than promoting better LDL receptor activity or preventing oxidation will actually prevent heart disease. I see your point, but the “treatments” that I would suggest to increase particle size also happen to be things that prevent oxidation (like reducing intake of PUFA, eating more SFA & MCT, exercising, etc.), so it would seem those treatments would reduce the risk of CVD (though not by altering particle size necessarily). Of course improving thyroid function would have a similar effect, if that were an underlying cause of poor LDL receptor function. I’m looking forward to part 2. I’ve reviewed quite a bit of evidence lately casting doubt on the accuracy of the particle size tests.

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Chris Masterjohn June 10, 2011 at 10:12 am

Chris, I agree that those are things that should reduce CVD risk. I meant the comment targeted at treatments designed specifically to alter LDL particle size. By the way, I do think it is plausible that small dense LDL is in fact more atherogenic because it is smaller, but I think it’s just a hypothesis at this point, so I’m not ruling it out or ruling it in. The stuff you sent me was my first introduction to the technical problems with particle size assays, so thank you.

Chris

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Resurgent June 8, 2011 at 6:25 am

That was absolutely outstanding – Cant wait to hear him again in Part 2

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Jeremy June 8, 2011 at 8:40 am

WOW! great podcast, this should be on everyones list of things to be interested in.

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steve June 8, 2011 at 11:19 am

Chirs: What you say is correct, but i am unsure/ unclear that just because you have lots of large LDL paticles and only a small amount of small LDL particles that it is clear sailing. In numbers, let’s say that you have Large LDL particle count of 2500 and small of only 150. Does this mean you have little chance of suffering with Oxidation risk no matter how pristine the diet via minimization of Omega 6, eating sat fats, and low starch and no sugar? If you look at the NMR report they would categorize this level of LDL particles as being dangerous, or very high risk. Granted the population selected is one that has been on the SAD diet, but the question remains.

Thanks again for the very informative podcast!

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engineering-health.org June 8, 2011 at 2:00 pm

Amazing podcast! I had trouble sleeping last night since the ideas were so interesting I couldn’t stop thinking about it, especially the idea that leptin resistance could be responsible for down-regulating the hepatic LDL receptor.

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Unleash the Kraken! June 8, 2011 at 7:16 pm

Great podcast, gents. CM’s explanations are very clear.

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michele bird June 9, 2011 at 1:53 am

Thank you for the informative lecture- my question is : with hypothyroidism and familial hypercholestrolomia and a dr. prescribing eltroxin and statins and not knowing how much my m.d . really knows, how safe is my health – when is the second lecture scheduled for please

NOT LIKING STATINS – SOUNDS REALLY SCARY

wishing us all the best of good health

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Diane @ Balanced Bites June 9, 2011 at 10:24 pm

Once again I’m thrilled to hear some really smart people get together and have frank, analytical discussions of scientific literature on a controversial and confusing topic in a way that’s easy enough for the public to comprehend. I appreciate that the level of the discussion is high enough that practitioners can get some take-aways that are descriptive of mechanisms but also elementary enough that we can use our common sense to glean some great take-aways.

Thanks for doing this. Looking forward to more, as always.

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Chollie June 9, 2011 at 10:44 pm

The podcast was great, lots of great info. I want Chris M, if he has the time, to consider this ‘real world’ example:

Person A has an LDL of 100 and a total cholesterol <200. He happens to be on a standard high-carb diet deficient in many micronutrients, among other things. Of course, his doctor would be very pleased with these levels but an NMR test shows that his LDL is predominantly Pattern B.

Person B on the other hand has an LDL of 180 and total cholesterol of 280. His HDL and Trigs are good and he happens to be on a low-carb diet taking a lot of pains to see he gets all his micros from either food or supplementation. Of course, his doctor will be quick to prescribe a statin and completely ignore the fact that the NMR shows his LDL to be Pattern A.

Does Person A have anything to worry about? More importantly, does Person B have anything to worry about?

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Chris Masterjohn June 10, 2011 at 10:22 am

Chollie, they both may have something to worry about. The thing to remember is that *no* lipid tests have any diagnostic value. They have risk prediction value, and they have value as metabolic clues. This hypothetical doctor is trying to treat cholesterol levels as if they are a disease, but they are neither a disease nor diagnostic for a disease.

In both cases, there should be further evaluation. What are person A’s triglycerides? What are person A’s fasting glucose and insulin? A diet high in carbs and low in cholesterol is likely to reduce LDL particle size directly, but this may not be a problem, perhaps, unless it is associated with insulin resistance. In any case, person A should obviously eat a more nutritious diet that does not contain micronutrient deficiencies.

Person B should get free fatty acids, a full thyroid panel including reverse T3, and various markers of oxidative stress.

Hepatic triglycerides wouldn’t be a bad idea in either of them, nor would adding any of person A’s tests to person B and vice versa. Also, total-to-HDL-C ratio rather than total and LDL-C separately should be used. The point though is that these are clues, not diagnostics.

Chris

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Jack Goldmaker June 10, 2011 at 1:16 am

I’m a bit confused again Chris M. From what I understand, arteries harden from calcification as calcium is used from the body to plug any exposed muscle tissue as the arterial walls get eroded from free radicals.

You state that small dense LDL phospholipid layers will be attracted into what? I had thought that the role of LDL in the arteries was totally different than its usual role of delivery. Much like a truck on a milk run, it has to go back and forth on a highway before it does its work in its local area. However, once in the arteries, any calcification or ischemia would be kamikazed by the LDL to coat the calcification and prevent platelet damage in the high speed tube. How does the oxidized LDL cause the calcification?

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Chris Masterjohn June 10, 2011 at 10:26 am

Calcification of the media occurs in diabetes, kidney disease, aging, and vitamin K deficiency. This is very bad for blood vessel function, statistically associated with CVD mortality, and is not a protective factor.

Calcification of the intima occurs in very advanced atherosclerosis in association with cell death. It is almost certainly disadvantageous, but it is not a major cause of heart attacks, as most of these occur due to plaque rupture or erosion secondary to inflammation, and only a minority occur in response to calcified nodules or protrusion of the plaque into the lumen. Calcification does not drive atherosclerosis, it occurs very late, probably in response to the cell death that accompanies advanced oxidative and inflammatory scenarios. Oxidation of LDL causes the initiation of atherosclerosis long before any calcification occurs.

Chris

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Jack Goldmaker June 10, 2011 at 3:05 pm

Chris M. I am still confused because I learned from Mary Enig’s book as well as Sally Fallon Morrell that what they were saying was that cholesterol deposition is the LAST process in the damaging of the arterial walls. The example was “You cannot blame the ambulance for showing up at an accident as the cause of the accident”. Hence Calcium deposition took place before LDL ever showed up.

Allow me then to use my own example based upon your podcast in laymens terms. You are saying, basically, that LDL is like a Ziploc bag and it contains all kinds of stuff like fat soluble vitamins, triglycerides and varioius fluffy and unfluffy particles of cholesterol.

Various things in the blood cause these bags to shrivel up. So, lets say for a moment the artery is a small creek and if one dumps crude oil into the river, it simply dissipates. However, if one puts the oil in a zipper bag, it catches along the side of banks of the river. Then the bags begin to shrivel up and get sticky and make tar on the sides of the creek. Then something comes along and covers the tar with powder such as calcium to contain the spill.

This powder then crystallizes and turns hard making the river bank more like a rocky outcropping. Then if any shiny new zipper bags full of oil come down the river, they smash into the rocks and spill cholesterol on them to polish it and make it so that platelets don’t get damaged?

This is what I thought plaque was, and that if a large surge came down river the ‘current’ which wears down the older LDL zipper bags, (sort of like shrivelling up a bag with a hot air gun) snaps off the rocky outcropping and then a clog occurs, damming the river somewhere downstream.

But the current is, really, not the problem it is the pollution in the river that is destroying the LDL bags, and this is somehow causing the bags to want to head to the shoreline because they are all now shrivelled up? That eating cream makes them healthy and shiny again, that the shrivelled bags are now quite easy to catch on the shoreline versus the shiny new ones. That they purposely migrate to the shoreline and infuse with it? That this is the ‘bad particles’ in the phospholipid layer (ie the plastic in the bag decomposes) that drives the older LDLs into the riverbank?

And this is where I get confused. For I understand that calcium, if removed by chelation, will be automatically replaced by the body as it will rob calcium from the bones to replace the clog, as it does to STENTS. and stents are not made up of biological materials. Yet they are always clogging up. Does this mean that there is some sort of electrolytic action going on because even stainless steel is attracting the phospholipid layers of the zipper bags (LDL)?

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Chris Masterjohn June 10, 2011 at 4:10 pm

Hi Jack,

I’m not responsible for other people’s views of heart disease regardless of how much respect I give them and how much they deserve.

Oxidized LDL is not an ambulance. It’s a toxic factor that causes atherosclerosis. Ambulances and police cars aren’t very good analogies because they imply something is either perpetrator or victim. LDL is a victim here, but once victimized it perpetrates damage. A better analogy would be infectious disease. The person who gets sick is a victim, and though they make others sick, you don’t call them a criminal or a perpetrator. If anything is an ambulance here, it would be the monocyte that forms a plaque to protect the endothelial cell from the toxicity of all the oxidation products within the oxidized LDL particle. However, quarantine is a better analogy than ambulance.

I disagree with your analogy because you cite calcification as a protective factor. Calcification, to my knowledge, does not play a protective role. The immune cell plays a protective role by securing the lipid oxidation products within an atherosclerotic plaque, which protects the cells that line the blood vessel from their toxic effects. However, the “protective” plaque looks like this: relatively poor in lipid, rich in collagen, covered by a stable fibrous cap, without protruding much into the lumen and without calcium deposits.

I’ve never claimed that cholesterol accumulation in plaque is a protective factor. To the extent I’ve claimed anything about it, I’ve said it’s not all that relevant.

I’m not sure what your “current” is supposed to be analogous to. Plaque rupture is caused by inflammation and perhaps diminished capacity to synthesize collagen because of micronutrient deficiencies.

Your analogy, in my opinion, makes things more confusing rather than clarifying anything. LDL particles aren’t anything like ziplock bags at all. Shriveling isn’t very analogous to oxidation. The LDL particle is supposed to get to the shoreline to transfer its contents there. However, it is not supposed to have all its contents destroyed when it does so. The shoreline shouldn’t be analogous to a plaque.

Try this: the LDL particle is a cargo ship. It is supposed to land at various docks to deliver over the goods. However, it is also supposed to protect the goods so that they are in good shape when the ship gets to the dock. However, there are often pirates at sea, and they may attack both the people at shore as well as the cargo ships. If they block entry to the dock, the ship cannot refuel or purchase more ammunition for defense. If the ship is thus left at sea, it runs out of ammunition and the pirates are then able to effectively sabotage it, ruin its goods, and purposefully plant explosives and release infectious diseases on the boat. Then, when it does get near shoreline, the folks at the dock catch illnesses and are caught in terrorist explosions. Thus, the immune system, like a navy and national guard, rescues the cargo ships that have been attacked (oxidized LDL), and quarantines them and any toxic factors released from them in something like a superfund site, where the surrounding community is protected as best as possible.

I’m not entirely sure what you mean in your last paragraph, but calcification is not caused by calcium, so of course chelating it isn’t going to do anything. As I said before, calcification of the intima during atherosclerosis is a very late event of advanced plaques that is precipitated by the process of cell death. Calcification of the media is a harmful factor associated with CVD but with quite different causes, and vitamin K deficiency might be a major part of it. Technically, it’s not really part of the atherosclerotic process.

Chris

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Jack Goldmaker June 10, 2011 at 6:11 pm

Perhaps I have not elaborated on my perception of the Lipoproteins and how they work in the body in laymans terms. I understand the concept of the delivery vehicle much like I understand that insulin is also a transporter of sugar. However, I failed to explain that in my perception of it, LDL is indeed a delivery of its contents when in the vascular system. However, it is my understanding that nature herself has more than one purpose at times for various body systems. It is a necessity to have multi tasking, so while I have neglected to mention that I understand all of what you are stating about the delivery mechanism as well as the other Lipids when it comes to transporting their contents to the cells, I have also come to the conclusion that when the LDL and perhaps other lipids are in the high speed arteries, they have a different function, that of being suicide bombers when it comes to particles of calcium and other garbage in the blood that have been trapped by the fibrin used to repair the exposed arterial muscle that is growing inwards signalling the artery to close down to prevent a high pressure leak into the body cavity.

Sorry, I neglected to mention that to me, there are two different functions for LDL, one in a static mode such as when on delivery like your cargo ship analogy. But in a high speed highway it collides with any accidents covering up the damage to prevent platelets from being ripped to shreds in a high speed tube. This is why I mentioned ‘current’ because I am under the perception that when one cuts into an artery blood spews everywhere like in an old Kung Fu movie. To me, LDL simply cannot do anything but travel when inside an artery due to the speed of the blood. It is like white water rafting.

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Jack Goldmaker June 10, 2011 at 6:34 pm

Yeesh! I just read what I posted. It sounds quite confusing. Let me simplify this.

I AM ONLY REFERRING TO EVENTS WITHIN THE ARTERIES.

I am suggesting that due to the DUALITY of IDL, that if one applies a voltage to the outer shell of IDL it changes from looking like a coin to looking like a soap bubble. A biochemical voltage that is, to the phospholipid layer. That it makes sense that LDL does something like that as well. Depending on the CHARGE of the phospholipids (ie. the outer layer of the lipoprotein) it has a different function. I am postulating that the electrical charge of the LDL in the arteries is a different charge than when it is on delivery.

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Chris Masterjohn June 10, 2011 at 7:06 pm

Hi Jack,

I think we’ll have to agree to disagree on the mechanisms of atherosclerosis. I do not think it has anything to do with patching up a leak, and I think calcifying an artery is a horrible way of repairing anything.

LDL does some delivery in the artery too. I agree it has more than one function, and glomming some stuff up could theoretically be one function, as in the case of mopping up bacteria or endotoxin. But I don’t think patching up holes in arteries is one.

Chris

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Garry June 10, 2011 at 6:42 pm

Excellent info! This podcast goes on the All-Time list for sure, and I look forward to Part 2 (and 3 and 4 if we’re lucky!).

Chris M, can you clarify what can be done clinically to improve LDL receptor function (and thus avoid LDL oxidation etc.)?

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Chris Masterjohn June 10, 2011 at 7:06 pm

Thanks! Yes, in future blogs and when I come back on the show.

Chris

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HPTNS June 11, 2011 at 12:56 am

Chris,

I think I understand your views re- CVD causation, in which inflammation plays a key role in impacting upon LDL receptor mobilization. Thus, serum lipid levels and composition are only markers for potential problems.

I am less sure regarding your views about the role of infection in causing or combining with inflammation and lipids, to lead to CVD. Some cholesterol skeptics argue that the reason that vascular disease is localized at particular points in the heart (or elsewhere), for instance, is that it is the combination of infection, inflammation and lipids, that leads to eventual MIs at specific locations.

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Chris Masterjohn June 11, 2011 at 1:02 pm

Hi HPTNS,

I’m not sure what you’re referring to by my views on the role of infection, but the localization of plaques is clearly related to hemodynamic factors. In any species, to my knowledge, including humans and rabbits, plaques occur in areas of disturbed blood flow. Shear stress, caused by uninterrupted parallel blood flow, increases synthesis of nitric oxide which is a protective factor in the optimal range, and, probably more importantly, upregulates tight junction proteins which decrease the permeability of the vessel. It has been experimentally demonstrated for near 100 years that plaques occur where the blood vessels are most permeable, and that anything affecting the permeability causes a proportional affect in the degree of atherosclerosis. Inflammation, for example, causes a general increase in permeability and thus enhances atherosclerosis. Exercise should theoretically have the opposite effect, since it increases blood flow and thus shear stress.

Chris

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Jack Goldmaker June 11, 2011 at 4:36 pm

Hi Chris M.

I am not stating that calcification of the arteries is a repair process. It is a permanent fix. Once the artery is fully clogged, arteriogenesis takes place in the nearby areas as the body grows its own bypass by creating new micro vessels that cannot be seen by conventional X ray technology.

Chest pain is necessary for these microvessels to grow as it triggers the immune response. One can run a sharp knife along one arm and it will hurt and bleed, while a butter knife on the other arm will do nothing, and there will be no immune response. Thus CVD is a silent killer unless one exercises regularly and tolerates chest pain. After the artery is clogged solid, the body rejects any chance for a bypass to be man made by constantly filling Stents and clogging up the new bypassed arteries. We all saw how Dick Cheney was always going in for ‘maintenance’ work on his heart. How Bill Clinton was up on stage after his bypass surgery as a poster boy for the Heart Association. However these two fellows had a team of 20 surgeons who had hedged their bets on doing more bypasses for the average American.

It would be nice if some sort of natural artery cleaning took place such as lipolysis, although I would not think it would be healthy to clean out an artery be it by catheterization or stent or other means. I would welcome a method to do this but from experience in technology the story of “If it ain’t broke, don’t fix it” comes to mind with a fully plugged artery. I would not be happy if a fully plugged artery was being unplugged slowly leaving dangerous bits of plaque able to break off at any sign of a sudden increase in blood pressure.

According to the late Dr. Howard Wayne of the San Diego Non Invasive heart center, the difficulties today with the concepts of bypass surgery were all due to the fact that NO imaging technology existed, nor does exist that can measure the amount of micro vessels that are grown by the immune system around a clogged artery naturally. This can only be done after autopsy under a microscope.

Thus, LDL has no part in the repair process of a fully calcified artery as it has been abandoned permanently by the body and a detour has been made by the blood being detoured into the collateral arteries which then stretch open slowly with much pain. However this pain is necessary because it signals the immune system to begin the repair process and grow new microvessels.

Pain is from the collaterals under new pressure to expand much like those sausage balloons the clown at the birthday party is trying to inflate so that he can twist it into a sausage dog.

One cardiologist once told me “But it IS broken” and offered to ream me out for 15 minutes so that he could collect approx $30,000.00 for the treatment according to US charges. He threatened me that I I would die if he was not allowed to do this. I also noticed at the time that the Ontario (Canada) association of Cardiologists at that time were lobbying the government demanding that each cardiologist in the province be allowed to do a minimum of 260 catheterizations (angioplasties) a year so that they could have an American like lifestyle.

One does not need a surgery license to do angioplasties and this became a great income source for Cardiologists. Dr Wayne however, thought to manage plugged arteries with medications only and was quite successful during his years in practice.

He had found this ‘natural’ bypass, and just like transplant rejections thought that cleaning clogged arteries was a waste of time because they just grew back clogged even more than ever. So LDL does clog and calcium does clog them up for good. Fully repaired by being fully clogged.

Much like a pipe in the basement full of lime, rather than reaming it out and having chunks fly out of the taps upstairs, he patched in a small network of tiny plastic pipes rather than a large copper bypass. He did this by DOING NOTHING but allowing the body the time to let the immune system stimulate new growth. Like the example with the butter knife, nothing happens because nothing is damaged. However if an arm is cut open by a knife, there is much pain and soon, fibrin arrives and the repair process begins.

This is quite similar to the ‘Non oxidized LDL’ arriving at a site where there is damage is it not? I can only surmise that the possibility exists that there are outer voltages on the outside of the LDL that work like docking stations depending on their values when they arrive at the liver etc. Your theory of the outer layer of the lipids seems to align with this concept as well. Has anyone charted the values of the various sites of the body where these events take place on an electrical level? Potential differences etc?

It appears that if Intermediate density Lipoprotein does this then why does it do this. Why does it go flat like a coin? Is it due to the fact that it is empty, this would mean that there would be sensors inside the lipoprotein indicating that it is empty. Suddenly it looks to me more like an email delivery system than a chemical one, where there is a link layer as you are describing, like chemicals, wheras there is also a transport layer that signals the various Lipoproteins with voltage values.

No wonder this is not well known should the electronics industry get an hand on it.

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Peter June 11, 2011 at 5:23 pm

Chris,
I’ve got an off-topic question. I heard you say once that you eat a 24-hour soured sourdough bread. I’ve googled for it but can’t find it. What’s it called? Thanks – Peter

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taylor June 12, 2011 at 7:43 pm

Hi Chris
I know your busy so I will try and make this brief. I am 22 years old weigh 141 pounds and am just shy of 5 feet 8 inches. I am writing to you because I have gotten some troubling blood test results and have also have a few associated problems. To be brief, I have been having trouble putting on weight despite upping my calorie intake to about 4000 calories a day. My diet is paleo with a focus on whole natural foods with the exception that I do eat dairy as I am trying to put on weight. I am approximately 8% body fat. I work out between 3-5 times a week focusing on strength training and my training is what I would call smart as my girlfriend is a personal trainer and I am an avid listener of Robb Wolf. My issues are that I have been unable to put on muscle mass and my lifts have not been increasing despite being fairly new to working out (7) months. I went to the doctor and got my testosterone and thyroid checked out. My results were the following:
TSH- 4.82
T3- 1.5
Thyroxine 8.0
Testosterone 307!!
Free Testosterone 50
Testosterone, LC-MS-MS 315

These results are troubling because I appear to have slight hypothyroidism and my testosterone is way to low for my liking. My doctor wants to put me on synthetic thyroid but after doing a lot of research I know this isn’t a cure for the issue only the symptoms. Even though I am 22 I do not grow alot of body hair especially on my face. I am writing to you because 1) I need to know what to have my doctor check for because he thinks to think that my results are fine and 2) what could be causing my symptoms. Also, just a side note I have been having a reoccuring pain in my left testicle and after seeing a specialist was told that it was an inflamed epididymis. I am concerned that this inflamation might have a connection with my hypothyroidism and low testoserone. I got an ultra sound (of my testicle) and everything was reported to me as being fine. Finally, to give full disclosure I do smoke weed about once a day and I know that could have an affect on testosterone. It is very frusterating to me to find out that I have a 300 level testosterone and it is frightening to learn that my thyroid might not be working. Just some more detail I have been smoking weed for about 5 years and In my “younger” days I would smoke what I would say would be a heavy amount. I use to drink alot to but since turning to paleo I have quit beer for the most part now only drinking at the most 2-3 times a month and not heavily (5-8 beers when i do). I did smoke cigarettes from the age of 17.5 until June of 2010. I have been cigarette free for a year now. Please point me in the right direction as far as what tests I should have my doctor run and what possible reasons could be causing my thyroid and testosterone levels. Also, I do not think that it is genetic because my younger and older brother have no problem growing hair and both of them were sprouting beards at very young ages. Also my dad said he had a beard at a very young age as well.

Thanks you for everything you do and I hope you get the time to respond

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Matthew June 12, 2011 at 11:04 pm

Clarification on Greenpastures Fermented Cod Liver Oil: you said that this oil will oxidize when left out at room temperature, but this traditionally fermented oil is supposedly safe to store at room temperature. Is this actual fact or were you simply trying to say that Fermented CLO might oxidize when left at room temperature? Thanks for the quick clarification.

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Chris Kresser June 14, 2011 at 9:03 am

What I meant was that most cod liver oils are processed with heat, which can oxidize the fragile fatty acids. Fermented cod liver oil is cold-processed via fermentation, which doesn’t have the same effect. It should still be stored in the fridge.

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Aron June 14, 2011 at 9:17 am

Incredible podcast. This one and Kurt Harris’ episode are classics. Can’t wait for part 2! Small complaint: the paper rustling and background noises are pretty distracting in some of your podcasts. Thanks for the amazing amount of info.
Aron

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Chris Kresser June 14, 2011 at 9:29 am

Thanks for the feedback. I don’t have paper around me when I record them, so I can only assume it must be a guest. We’ll try to pay more attention to that.

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Daniel F. June 14, 2011 at 12:02 pm

Loved the podcast. I have sort of a simple question.

Kresser states “The name of the game according to our current understanding is to support healthy LDL receptor site function and Iessen the amount of time LDL is floating around in the blood and to reduce the chance that LDL will oxidize which is related to that first goal. So you mention in one of your articles that there are no specific antioxidant’s we can take to specifically prevent that.”

Two questions, and the second question will kind of lead us into the next topic I want to talk about. Is there a way for people to improve their LDL receptor function and what are some of the main things outside of diet and what we’ve been talking about that regulate receptor function?”

Chris Masterjohn goes onto to explain the big picture and focuses on leptin resistance and say it plays a major role in LDL receptor activity.

What are the best ways for your typical, healthy (no overt disease or symptoms) person to increase their LDL receptor site activity to promote quicker clearance of LDL particles? Is the best way for your typical person to increase LDL receptor activity/function is to focus on increasing leptin sensitive?

The answer is usually eat a paleo type diet, but I was wondering if there were other steps/actions a typical person (not someone suffering from hypercholesterolemia) could take fairly easily to improve their LDL receptor site activity?

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Chris Kresser June 14, 2011 at 3:14 pm

The main thing would be to improve thyroid function. For the average person, the first step would probably be determining iodine and selenium status and supplementing with both if necessary.

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Paleo Beginner June 14, 2011 at 2:22 pm

Hi Chris,
I have been following the Paleo diet for a month or so and loving it.
The thing is that i am muslim and our month of fasting (Ramadhan) is starting in August. The fasting starts an hour or so before sun rise and end with sun down.
I used to load up on slow digesting carbs in the morning so that i have energy till late afternoon at least. Do you have any suggestions regarding what i can have in the morning that is slowly digested and can provide energy for a long time.
I was thinking of drinking Casein Protein shakes but i have heard of its potential of causing GI irritation/Leaky gut.
I dont have any medical conditions (that i know of).
Thanks for your response.

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Paleo Beginner June 14, 2011 at 3:57 pm

Also love the podcast and looking forward to Part two. Like many of the commentators above i am curious about finding out ways to improve LDL receptor activity.

Also wanted to ask what your opinion is regarding hormone therapy in increasing LDL particle size or even improving LDL receptor activity. Dr Davis likes to use them alot in his Track Your Plaque program.

Thanks

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Matt Stone June 22, 2011 at 12:10 pm

And I’m going to go ahead and say that leptin resistance is caused by, primarily, excess of glucocorticoids. The master, master, master general.

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Roger Fisher June 29, 2011 at 12:41 pm

I’ve been on a Paleo diet for about 18 months and my LDL has risen from about 100 to 176 (I guess LDL receptors are doing a poor job?) while my HDL/Total C has increased from 2.4 to 2.7. My Lp(a) is 25. My doc tells me that the Lp(a) and LDL values both indicate high risk of CVD, and that together the risk goes up “exponentially”. How would you view these numbers; and any guide on bringing LDL down (doc wants me to eliminate sat fats and eggs). Thanks.

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Chollie June 30, 2011 at 1:43 pm

I’d kill for your numbers. My total Cholesterol went up as high as 376, now ‘down’ to 308. Total/HDL-C ratio was 4.6, now 4.9. I never had myself tested before going low-carb/paleo. In between these readings, I got my TC down to 274 but with a Total/HDL-C ratio of 5.3. This I achieved while cutting my fat intake during a phase where I was trying to lose most of my excess bodyfat. Now down to about 7-8%, so very lean and very fit and no health issues at all.

I’ve been supplementing with Iodine, Magnesium, Fish oil/Cod liver oil, Vitamin C, Vitamin D, Calcium, while Selenium and Copper I get plenty from my multivitamin. Also, I switched from eating mostly chicken to mainly eating beef, added coconut oil (2 tbsps a day), eat lots of salad veggies and occasionally cauliflower, okra, spinach, etc. Recently added back some starch in the form of a baked potato post-workout. Also, I eat a serving of sardines everyday for some natural omega-3. The last test was before I added the potato and sardines, but I’d already been doing everything else for at least a couple of weeks, yet my TC rose from 274 to 308.

The lipid profile doesn’t make sense, or if it does, I’m going to die in the prime of my life (I’m 27). LDL has not been measured, but the calculated value was as high as 286, now down to 215. Lowest it got was 202.

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