I was watching some videos on youtube the other day and I think this guy raised some pretty interesting points.
The paleosphere often links to Peter Attias Straight dope on cholesterol, but did anyone actually read the whole thing and think about what it means.
He says that AboB and LDL-p are the primary drivers of athrosclerosis. Was he unaware of all these studies that show fatty meat, eggs, cream and butter raise AboB and LDL-p?
asked byjames_27 (907)
Get FREE instant access to our Paleo For Beginners Guide & 15 FREE Recipes!
on March 12, 2014
at 10:37 AM
There's also the whole homocysteine thing too, and with the push by CW to feed people egg whites only and discard the yolks for fear of cholesterol, and "a plant based diet", I wonder how many folks are starved of B12, B6, and folate have cardio-vascular damaging homocysteine floating around their arteries, causing all sort of havoc, even above and beyond those with broken genes.
on March 08, 2014
at 12:45 PM
I know this was funded by an apple industry group but look at how just one apple a day can effect cardiovascular health:
And if you can't access the full text, here are 2 articles regarding the study:
on March 04, 2014
at 08:22 AM
I thought I'd re-spell this out in the answer. The model, the process defined in part 1 and 2 of these articles (Ive only linked one above), is that FIRST we have the "call to repair" caused by inflammation, and damage to the artery wall (links to inflammation and blood pressue, and general vascular health). Once we have that call, then the LDL, the repair molecule is carried by the apoB to the damaged site. Now in that process we get some oxidation, and oxidized LDL, continues to cascade the oxidation as it is returned from the site, doing its repair job (from memory by damaging the apoB transport by passing the oxidation on). The point being that the too and from, from the repair site, escalates the oxidation that isn't repaired by the anti-oxidants. Which is why they are central to the process, they prevent the escalation.
Thats where our anti-oxidant comes in. If it repairs the oxLDL, at a suffficient rate, the situation doesn't escalate, crisis averted.
So what can cause this process? Blood pressure issues, too much inflammatory process, not enough anti-oxidant, and mutations in the apoB gene causing overactive transport (probably the reason why _average_ LDL levels go up in studies).
Does naturally raised LDL count, as a factor in this picture? Why yes. So does increased trigs. And HDL also helps. Does smoking hurt? Yes, its an oxidant. Does oxidized food play a role? yes. But all of these things are minor "factors", compared with the central processes that cause the situation to escalate in the first place. Now would lower LDL help? Why yes. But it would also slow the repair of the damaged artery, something that on a more minor, less threatening level, needs doing all the time. A low LDL, combined with high blood pressure for example, could be an equally out of balance situation.
I thought I would explain the model here, in my relatively ignorant way, so that you can see how raised LDL, is NOT a _cause_ of heart disease, but merely a factor, and indeed minor next to say, screwy blood pressure, or not enough anti-oxidant, or wrong o-6 balance. Indeed if anything LDL related has a _major_ impact on that picture, its apoB mutations, which cause huge hyperlipidemia in response to dietary fats. Those are the people for whom their LDL goes sky high when they up their animal fats (and thusly these are also the outliers that skew studies if they aren't controlled for, and indeed most dietary statistics based studies are virtually impossible to control well)
And additonally- sat fats are different. Lauric acid for example, has no negative effect on LDL levels. Indeed it increase HDL from memory. So lumping all sat fats together is wrong minded. If you look at the research on individual sat fats effect on LDL, HDL, trigs etc, you will see each fat varies wildly in its effect. And only a few could be considered truely as raising LDL, in animal models. Probably the best you can say of animal products based on this individual sat fat animal study research is that cow meat might be worth moderating a little (because it contains higher levels of one of those few). Indeed I don't eat steak or mince every day. I eat chicken, eggs, cream, loads of fish, lamb, coconut, olives, avocados. My sources of fats are quite varied, and not at all heavy in cow. Remembering of course, that its the apoB mutants that get the biggest elevation, genetically its probable to me, there are people that can eat cow all week and not get a slight change in LDL. We are all different. Thats why some of us can use plant omegas effeciently and some can't.
Lastly studies that study raised LDL from "sat fats" (as if that were a monolithic entity), that do not control for apoB mutants, cannot be relied apon for generalisable data, because the average is thrown out by the outliers. The link between LDL and heart disease is highly indirect, the link between animal fats and raised LDL, is simplified, and poorly controlled, and thusly likely overstated.
The whole picture is entirely absent the main new co-factor - the anti-oxidant. With too little anti-oxidant, the spiral can occur much more easily. So it should be no suprise that heart disease is highest, globally, in countries with poor nutrition, and that in places with good nutrition, but high fat intake, heart disease rates are far lower than places that eat less fats.
And, worst of all your recommendation to eat more whole food carbs, is subject to the exact same poor science that sat fats are - overall carb consumption is linked with raised trigs, which is more stronlgy linked with heart disease than LDL is. Which carbs? Who knows, who cares, lets mark them all as evil shall we! ;) ;P ?
on March 04, 2014
at 02:27 AM
I go with what Dr Wallach says. Cholesterol is an essential nutrient. You need cholesterol. People in the artic eating whale blubber, whale fat, blubber of all kinds... Cholesterol levels off the charts... no cardiovascular disease. When they come here and eat our food they die. It's not the fat or the cholesterol it's the sugar. You know those big gulps? I guess there's a texas size big gulp in Texas now. That, a snickers bar, and a bag of Doritos all for 99 cents. THAT is the problem.
on March 03, 2014
at 03:20 PM
Plant positive also left another reply to the comment reply's that I'll share here for you all.
""Yes, this discussion is a good example of how the Paleo faithful have responded to my videos. It gives a sense of the religious nature of their beliefs. At the moment three people have replied.
The first one’s thinking is constrained by binary thinking. The oxidized LDL idea is supposed to contradict the lipid hypothesis but he doesn’t support this assumption in any way. I’ve talked about this in my videos like Catalyst 6 and PUFAs Oxidize!. Just to give you something on this, dietary oxidized cholesterol is far more likely to promote oxidized LDLs, as seen here.
And saturated fatty acids promote this more than unsaturated fatty acids.
Of course, if you think oxidized LDL promotes heart disease, you should want no more LDL in circulation than necessary. This doesn’t occur to him.
The next commenter simply didn’t understand the video, name-calling notwithstanding. He says,
“in fact, if you watch that video you'll see an interesting thing 5 minutes in. Attia mentioned LDL-P count, and ApoB, the charlatan who made the video is using misdirection to show a chart clearly labeled LDL-C, not (LDL-P!) as "proof" that eating eggs raises cholesterol levels …Attia has, as part of his discussion, LDL-C vs LDL-P and why LDL-C should not be used as a marker of CVD.”
But my video is a response to Attia’s statement that: "Eating cholesterol has very little impact on the cholesterol levels in your body. This is a fact, not my opinion.” I say this at the beginning of the video and in the video description but he still didn’t get it. I don’t know who he thinks he’s quoting about “proof”.
The third person is having the same problem. He says:
“First of all, this person misuses LDL for LDL cholesterol all the time and this error occurs on at least one paper also.”
Again, I didn’t misuse anything. This person just didn’t understand what the video was about. Again, read the Attia quote. Then he says,
“At 8:11, cholesterol per particle is shown to increase 9% with either increased saturated fat or cholesterol(lard and eggs) and their combination is shown to increase particle size 24%. The commentator skips it.”
But this implies that larger LDLs are less atherogenic and it is Attia who says this is not true. Of course, I say that as well in A Large and Fluffy Distraction. Then he decides he wants to talk about the E4/4 phenotype. He’s referring to my use of this paper.
But he doesn’t understand the paper or the graph in question. All apoE groups experienced increased serum cholesterol from dietary cholesterol. Quoting the paper,
“In the present study, however, the responsiveness of the apoE3/2, E3/3 and E4/3 phenotype groups to cholesterol-rich diet were broadly similar.”
“In summary, a cholesterol rich diet induced statistically significant increases in total cholesterol, LDL cholesterol, and apoB concentrations in all apoE phenotype groups.”
People like this won’t make these criticisms in my comments sections. They aren’t interested in learning anything. I’ll admit, I was naïve enough to think that these people could be reasoned with when I started this project. But as Paleo dieters, they are self-selected for their lack of critical thinking abilities. I’ve wondered in the past if I should type up a response like this to discussion threads but it feels like a waste of my time. I probably won’t respond again unless someone says something interesting."
on March 03, 2014
at 05:34 AM
Plant positive commented on your 2 studies that you linked. I thought I'd share them here with you as it won't fit into your comment reply section and you won't read them elsewhere.
"The latest commenter says, "Check these simple studies also and think back on whether it is necessary to check this guy called plant positive's videos."
This is a characteristic response. Links are posted but no explanation is given how they relate to what you asked, so there is no evidence this person has critically assessed them. It doesn't directly or honestly respond to the video of mine in question. The first link in no way addresses the fact that controlled trials have demonstrated that eggs raise serum cholesterol – contradicting Attia – or that they raise apoB levels.
Apparently these are just references this person finds reassuring. He (?) posts two links. One is a study of 235 women who self-reported their dietary intake. Two thirds of them were on hormone replacement therapy. All had established coronary heart disease. For practical purposes we can say they were obese as well. We know that obese individuals are especially likely to misreport their dietary intake. They say their food assessment was trustworthy, but they said "saturated fat intake was not associated with LDL concentrations in our study," but we know from metabolic ward trials and ecological studies that saturated fat does raise cholesterol, so this should have raised questions.
Read this study and see how it is discussed in later publications and you'll see that to some it raises questions about risk factors in insulin resistant, obese, older women. They'll point out that most studies relating diet to heart disease have been conducted with men. So is this commenter citing this an older obese woman with established heart disease? If not, why is he citing this? I'm a younger, relatively fit man. My blood tests look perfect. So this one doesn't seem so relevant to me. Maybe these "Paleo" individuals aren't like me that way.
Look further at the study and you'll see that the women in the lowest-saturated fat were more likely to come into the study having had a prior heart attack, which means their heart disease was already more likely to progress due to increased inflammation, and they were more likely to have had angioplasty.
Chances are these were the women most motivated to change their diets. They also had higher LDL and apoB, so this study can be said to reinforce the connection between LDL and heart disease. As I've said in my videos, heart disease develops over many decades. People often try to change after the horse has left the barn. This study only covered three years. It provides no insight into how these women came to be obese heart disease patients in the first place. And what sort of carbs would you think they were consuming? The authors say they adjusted for a multitude of confounders, but at this point we must say that this study is the weakest sort of evidence – a short-term statistical analysis of a sick, fat, free-living population that self-reported their behavior.
I'd have to go to the library to pull the other study but for now I can point out that the author has received funding from the American Egg Board. She says eggs don't raise cholesterol for most people, but you can watch my video to see that she's wrong. She also asserts that HDL-raising through saturated fat is protective, a belief without any support from clinical trials. As I've pointed out, even Dayspring and Attia say HDL-raising has never been shown to accomplish anything. They also disagree with the author's claim that larger LDLs are less atherogenic. Of course, I've made a video about this, too."
on March 02, 2014
at 11:00 AM
And about epoxy cholesterols and diet derived oxidized fatty acids in the study you posted, that's the reason I eat my egg yolks raw and limit PUFAs to mainly raw seeds and nuts, freshly ground when needed ground, and soaked in salted water when convenient which is actually about phytates and minerals, and use extra virgin/virgin olive oil raw when I do, and cook animal meats and seafood to just above the minimum safe cooking temperatures.
on March 02, 2014
at 10:48 AM
The reason LDL-cholesterol is associated with cardiovascular risk is that depending on the LDL receptor sensitivity, LDL particles stay and become susceptible to oxidation longer.
Check these simple studies also and think back on whether it is necessary to check this guy called plant positive's videos.
on February 28, 2014
at 11:40 AM
First of all, this person misuses LDL for LDL cholesterol all the time and this error occurs on at least one paper also.
At 8:11, cholesterol per particle is shown to increase 9% with either increased saturated fat or cholesterol(lard and eggs) and their combination is shown to increase particle size 24%. The commentator skips it.
Increased cholesterol numbers from dietary cholesterol covers lipoproteins and decreases the chance of their oxidation and forms the better pattern. Increasing cholesterol per particle and particle sizes decreases cardiovascular risk.
The graph shown at 11:55 shows the highest increases for E4/4 phenotype which is a homozygosity of E4 polymorphism and E4 polymorphism exists in about 14% of the people and that means the frequency of the E4/4 phenotype is probably less than 1.96% becuase it's a polymorphism that can be associated with lower reproductivity.
"E4 is found in approximately 14 percent of the population. E4 has been implicated in atherosclerosis, Alzheimer's disease, impaired cognitive function, reduced hippocampal volume, HIV, faster disease progression in multiple sclerosis, unfavorable outcome after traumatic brain injury, ischemic cerebrovascular disease, sleep apnea, accelerated telomere shortening  and reduced neurite outgrowth."
At 14:24 HDL-C and apo A-1 decreased 10% and 3% respectively and apo-II(which is actually apo A-II) increased 4% all of which are associated with higher cardiovascular risk and the commentator skips them.
The only point that may be important for us willing to decrease cardiovascular risk is that high monounsaturated fat diet achived a better ApoB/ApoA1 ratio than high saturated fat diet, but this alone doesn't translate into monounsaturated fats being better than saturated fats easily.
Saturated fats are better when it comes to oxidation and particle sizes, both of which is directly related with less cardiovascular risk.
on February 26, 2014
at 12:12 PM
James, why would you link to a Vegan Propaganda youtube series by an obvious troll by the name of "Plant Positive"? Or are you one of the trolls that was spamming here a week ago attempting to "expose" Dr. Attia as a "fraud"?
And yes, I've read his entire thing, no it's not changing how I eat very much, if anything, full steam ahead.
I see some other gems from you like calling WAPF "A Bunch of Cranks" and that paleolithic humans ate grains, and worst advice you ever got was "eat more fat", and you gave someone advice to "eat oats" and how you told a mother trying to remove gluten from her kid's diet ridiculous and she'd give him food sensitivities.
So yeah, I'm calling you out, are you last week's troll?
Edit: in fact, if you watch that video you'll see an interesting thing 5 minutes in. Attia mentioned LDL-P count, and ApoB, the charlatan who made the video is using misdirection to show a chart clearly labeled LDL-C, not (LDL-P!) as "proof" that eating eggs raises cholesterol levels. The slide is titled "Effects of Dietary Cholesterol and Fatty Acid on Plasma Lipoproteins." Figure 1 clearly shows on the left, the legend LDL-C.
Same happens at 6:10 on a slide titled "Effects of Insulin Resistance and Obesity on Lipoproteins and Sensitivity to Egg Feeding" I see LDL-C, not LDL-P.
Attia has, as part of his discussion, LDL-C vs LDL-P and why LDL-C should not be used as a marker of CVD: http://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-part-iv
Mr. "Plant Positive" is clearly a fraud.
on February 26, 2014
at 09:00 AM
There's the actual smoking gun for atherosclerosis:
Interesting irony really.
If your eating for example, eggs, they are rich in cysteine (as are animal proteins more broadly), which are part of what liposomal glutathione, along with glutamine (also found in animal proteins), is made of. Thats what protects your body from oxidized LDL, in fact its a downright powerful anti-oxidant all around.
Whereas the heart foundation has been telling us to avoid nutrition essentially, and focus on empty foods. Now there is an actual (god bless those scientists) animal model, we can stop just talking about wild speculations, and start talking about the actual mechanism.
Interesting if you look at the absolutely highest countries in terms of heart disease and their diet (russia being an example, US being another), you'll find that the average diet is severely nutrient low.
If you look at the countries that are low in heart disease (france included, and spain, both heavy fat eaters), they all eat very nutritious diets, full of variety. They also tend to eat lower sugar (which is implicated in smaller LDL, as are carbs generally, smaller LDL is more likely to get oxidized)