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Peter Attias AboB Straight Dope on Cholesterol post

Commented on March 12, 2014
Created February 26, 2014 at 8:18 AM

I was watching some videos on youtube the other day and I think this guy raised some pretty interesting points.

http://www.youtube.com/watch?v=oWP-JDgAnvg

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?

96440612cf0fcf366bf5ad8f776fca84

(19463)

on March 12, 2014
at 03:56 PM

Very true, and that, in and of itself, is evidence that a vegan diet is unsustainable without technology and evidence that Cordian is right when he says there's no such thing as a vegan civilization/culture in the past. B12 is evidence that humans evolved to eat meat.

But back to this, cholesterol isn't the only issue with CVD.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 12, 2014
at 11:38 AM

B12 is the only issue here. I think any responsible person following a vegan diet knows enough to check their b12 status to see if it is in range, even if they eat fortified foods. Besides that, they can take a b12 supplement a few times a week to keep the levels up.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 08, 2014
at 07:14 AM

Also. LDL does not have to be oxidized to end up as plaque. And the smaller LDL phenotype carries less cholesterol rather than more, which could even make it less atherogenic if anything.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 07, 2014
at 10:15 AM

The sick people I posted about in that study were sick in the fact that they had CHD, most likely from long term elevated LDL. Any human or animal study shows a halt in progression or an actual regression when they get to the level of about 70. You need to understand that healthy active people can develop CVD, this has been shown since the 7CS and even way before then.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 07, 2014
at 08:54 AM

When I talk about saturated fats I'm putting them into food categories for practical reasons. No one eats stearic acid or lauric acid on their own. The foods encouraged around here are Coconut oil, cream, lard, tallow, butter, ghee, palm oil, and cheese (sometimes). These are the foods that effect LDL and Apo-b in a negative way.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 07, 2014
at 08:48 AM

I never said "having LDL is a risk factor". I clearly stated many times that having elevated levels of it, like you see from people following the paleo diet, does indeed increase their risk of heart disease. There's many risk factors but they become more irrelevant when you choose a more sensible dietary approach which keeps LDL in a good range. You say artery damage is required for atherosclerosis but seeming don't understand that high LDL and sometimes other factors actually cause this after damage on their own.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 07, 2014
at 08:38 AM

Since you're big on animal studies. Daniel Steinberg, one of the true experts of cardiovascular disease, notes

"The point is very clearly made: the arteries of virtually every animal species are susceptible to this disease if only the blood cholesterol level can be raised enough and maintained high enough a long enough period of time."

To neglect this fact in a review about humans is to imply that the Darwinian foundation of biomedical research is invalid and/or that there is a body of substantial contrary evidence in humans. Neither is the case."

47cbd166d262925037bc6f9a9265eb20

(55)

on March 06, 2014
at 03:33 PM

Nope, it didn't let me again and again. Maybe because I liked another one of your comments under this answer.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 05, 2014
at 09:32 AM

Some sat fats dont even raise your LDL slightly, some even raise your HDL (lauric acid for example). SCT and MCT reduce obesity, which is a major health risk. So its not just a case of "fat is bad mkay", any more than "carbs are bad". Its about your whole metabolic situation, and the proportion and type of specific foods and how that effects you, as well as your DNA, For general advice however I _will_ say this - you should not eat, IMO, beef and dairy, as if it were a SAD dieter eating bread. A variety of fat sources, plant and animal, in the context of fruit and veg, is more healthful.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 05, 2014
at 09:27 AM

People used to have this silly idea that LDL just "clogged" the artery on its own, which is nonsense. The plaque build up because the LDL has lost the ability to repair properly, due to oxidation, and it just runs away. Because its a dynamic process, of various health misadvertures, heart health isn't all about just LDL. But if someone does have a high LDL, they should consider changing their diet, and also look into the other elements, vascular health, blood pressure, inflammation, nutrient status, quitting smoking etc.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 05, 2014
at 09:24 AM

Basically saying if you have LDL, you have a risk of heart disease is inaccurate, because that alone does not cause it. But hugely elevated LDL doesn't help if you do get it (but also there are various other lipid factors, trigs, LDL density, HDL and so on). Basically the whole situation is complex, and if you look after broader features of health, that just LDL particle count, your better off (but if your LDL particle count goes sky high in connection to milk and beef for example, thats something you should change)

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 05, 2014
at 09:22 AM

Way too much LDL hanging around in the blood is inflammatory and will likely cause oxidization . As I said, the inflammation and probably oxidation that is caused by high LDL will cause the progresssion of plaque. If I was going to blame heart disease on anything it would be high LDL, which is also demonstrated by multilple animal studies as well as human studies.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 05, 2014
at 09:21 AM

Well, this is how I would put it. High LDL, and high apoB transport, in the situation of significant artery wall damage, will put a higher strain on whatever anti-oxidants you have available can contain (increasing the risk of oxidation). That is to say that if you get the conglomoration of atherogenic causes together, higher LDL becomes a contribution, particularly if its very high. Something like a combination of unhealthful features, producing the worst case scenario. But this is also why small dense is worse, because it carries less LDL. So combination of features.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 05, 2014
at 08:04 AM

You have to at least conclude that high LDL can cause inflammation on it's own and lead to oxidation. Which is your main concern apparantly.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 05, 2014
at 07:30 AM

Contribute yes, possibly, especially it its palmitic acid, and the person is apoB mutatation carrying. Cause, no. If you want to be healthy, even heart healthy, its not all about your LDL. I wonder if I am in cordains range. Ill have to check next time.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 05, 2014
at 06:47 AM

How can you say that eating the wrong foods can't contribute to plaque? You're right in the fact that if someone eats a healthy varied diet, exercises, avoids smoking, stress and bad habits they'll probably avoid the last stage heart attack in their lifetime. It helps to have genetics on your side as well.

I want higher standards for myself. I'd rather eat a nutritious whole food diet that keeps my LDL in the optimal range according to Cordain, so I don't even have to think attending the ER from a sudden heart attack. I don't want any plaque I may have progressing.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 05, 2014
at 06:40 AM

The prerequisite, is artery wall damage. Without that, no heart disease. The combination of low anti-oxidant, and high LDL, doesn't improve the picture, if you get that noteable/significant wall damage, but high LDL is not required, only that the level of LDL oxidation, from the artery wall damage, is outranking the bodies ability to anti-oxidize it, and stem the cascade. Very elevated LDL certainly is an important variabe/influence/factor, but its not the cause. The cause is an interactive process, require several elements of poor health.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 05, 2014
at 06:34 AM

Eating does not "cause" plaque. That is established in the above model. I think you may have missed my point. An average person, with non-mutant genes, and a healthy lifestyle, varied diet, doesn't need to eat for a low LDL, to avoid heart attacks. Just look at the picture I described above and think about it. Ongoing artery wall damage, isn't abated by low LDL. Nor is low anti-oxidants, diabetes, smoking etc. You've just reduced one of the contributors, that's all, not changed the whole picture.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 05, 2014
at 06:30 AM

I don't understand how you can say high blood pressure is a cause but high LDL is not. High blood pressure alone has not been shown to cause atherosclerosis when LDL is low. But high LDL without high blood pressure cannot cause the progression. I'm not saying LDL is inflammatory, I'm saying high LDL floating around in the bloodstream can be inflammatory.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 05, 2014
at 06:26 AM

Why, via what mechanism? Whats your biological level proof for that? That last statement does not mean LDL is inflammatory in itself, it merely means that high LDL is contributing to a process (like it might heart disease)

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 05, 2014
at 06:12 AM

I simply can't understand why you would say high blood pressure is a cause but not high LDL. When LDL goes way up, problems arise. There's too much LDL floating around in the blood day after day, month after month, year after year, not for it to cause problems. This can create inflammation and oxidation. Too many particles floating around will cause problems. Lipidoligists like Thomas Dayspring and low carbers like Peter attia will tell you this.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 05, 2014
at 05:58 AM

"In terms of "regression" -those people can then eat normally (not low fat high carb), not take any medications, and not have any increased risk of heart disease?"

Well, if they go back to eating the way that caused their plaque to progress in the first place, then it will once again progress. They would probably be at a bit lower risk than they were before the intervention, but I don't know why they would opt to do that.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 05, 2014
at 05:53 AM

I didn't say LDL in itself is inflammatory, I said HIGH LDL is inflammatory, simply lowering it generally will bring the inflammation in the arteries down. Although general inflammation in the presence of low LDL doesn't seem to be enough to cause heart disease, based on hunter gatherers and animal studies. Daniel Steinberg wrote "it appeared that in the absence of continuing hypercholesterolemia, the inflammatory process was not self-sustaining"

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 05, 2014
at 05:41 AM

How can you say that blood pressure is a direct cause but high LDL isn't. LDL raising can progress heart disease alone, but high blood pressure alone in the presence of low LDL doesn't do the same, in human and animal studies.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 05, 2014
at 05:36 AM

Blood pressure and omega imbalance isn't needed to cause plaque, this has been shown in countless animal studies and people with hypercholestermia.They can die young with no other risk factors besides high cholesterol. You're insistence about the importance of antioxidants to protect from high LDL is like saying you just need enough nitric oxide to prevent the harms of high BS. There is simply no trials showing the establishment or regression of heart diseases through antioxidant status, why not? because it's not a proven strategy or a more useful intervention than LDL lowering.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 05, 2014
at 05:31 AM

Id be interesting to see how and why LDL, the repair molecule, is inflammatory though (specifically the mechanism, and the proof -in healthy people). In terms of "regression" -those people can then eat normally (not low fat high carb), not take any medications, and not have any increased risk of heart disease? Ie they become fully healthy? Or must the very low LDL be maintained, in order to supress the symptoms of a disease that will return the moment the LDL goes within a range tolerable for most people?

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 05, 2014
at 05:29 AM

High blood pressure is a direct cause of artery damage, so its not so much a contributor, as one of a few possible causes for the cascade. You must first have artery damage, or run away inflammation, for the LDL repair to kick in. Smoking of course is oxiditive, so along with artery damage, can aid the cascade, as is diabetes (but less direct in effect than blood pressure). Inactivity is a major cause of weakened vascular system, or out of wack blood pressure, so it can have quite a direct effect on the artery walls.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 05, 2014
at 05:23 AM

High cholesterol is inflammatory as well. So that could contribute to oxidation. Other factors like high blood pressure, smoking, diabetes, inactivity can all be major contributors with atherosclerosis. And regression is the accurate word for heart disease reversal. It actually regresses and heals itself if LDL goes down for long enough. Dozens of studies on primates and various other animals have shown progression simply through raising LDL and regression simply by lowering LDL for a long enough period of time. Irregardless of what their antioxidant status might may have been

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 05, 2014
at 02:58 AM

If you reload the page, it often allows you to do it. I get the same glitch all the time.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 11:31 PM

And actually regression is inaccurate language. Its not removal of the disease, its suppression of the symptoms only. The word regression is misleading for symptom suppression, and makes it sound like a cure (which it is not). Feeding schizophrenic people anti-psychotics is symptom suppression, for example, and who would call that "regression"? Stop doing the thing, and the disease is still an issue. One would need to actually prevent artery wall damage, and up anti-oxidant status, _as well_ as normalize LDL for a while, to actually "cure" (yet to be tested, but u can bet it will be)

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 11:23 PM

And that brings us back to basic scientific theory. The power of a theory, or model, is the extent to which it explains all the data. In the other incomplete theories, the above countries were regarded as contradictions, outliers. They were ignored, or explained away. The very high level in soviet countries never explained either. All the factors like LDL, trigs, HDL, density, smoking, never fully understood or explained. With this animal model, we can finally bring everything coherently together, and understand the actual influence of every factor. That makes it the better theory.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 11:20 PM

And we know that fruit and veg are protective of cancer already, and that the countries with the absolutely highest rates of heart disease, eat a low amount of produce (like russia, or less so, the US), and those with low rates of heart disease, but very high fat intake eat a lot of nutritionous foods (france and spain), and that even heart disease from smoking seems to be mitagated in japan by omega-3 and high vegetable intake. So absolutely, we should suspect IMO, that nutrition is protective, indeed w/ the model, part of the cause, which fits very much with these example countries.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 11:17 PM

Fruit and veges are an interesting mention. Actually a lot of the "anti-oxidants" in those are very mild carcinogens that act via hormesis, strengthing the bodies response, not actual anti-oxidants. But a variety of foods do contribute to the nutrients for building actual body anti-oxidants, like gluthathione (some animal, and a range of plant ones).

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 11:15 PM

I do not agree, as yet, that the range should be ultra low. I would need to see a lot of strong evidence for that. And I would emphasize that, from what I understand, too much sugar, and beef (and especially for the small number of apoB mutants) are the things that _might_ muck with your blood lipids (better to test your blood, than guess). This is a pet peeve of mine. Theres no need to run around telling people there LDL is elevated, when there is a simple blood test. As far as regression goes, thats not relevant to healthy people, only to the sick.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 11:11 PM

You will not get it, without decent artery wall damage. That stuff doesn't just happen in healthy people. It usually occurs from high blood pressure, chronic cardio, or out of control omega balance (or weak vascular system). It will also not spiral if there is sufficient anti-oxidant for the amount of oxidized LDL in the chain reaction. LDL plays a role, if this process is started, but cannot, alone cause heart disease without the prerequisite factors. I would not advise an out of range LDL though. A healthy lipid is helpful in more than one way anyway.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 11:06 PM

The irony of you calling a newer, updated scientific understanding of heart disease, a model with greater explainatory power in terms of the data, denialism, is not lost on me, and I hope it is not lost on anyone else.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 11:06 PM

Somebody is full of denialism, but it aint me.Your can't talk about a hypothesis without a model. Without a model, you have nothing. Its untestable without a model. You demostratably don't even understand _this_ model (shown by you comparing it to nitric oxide and blood glucose), and you talk and don't listen. You are an example of a human being who cannot engage critical thinking, exists by cogntive dissonance, and indeed lack an understanding of human social interactions.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 10:50 PM

LDL reduction HAS been shown to regress the disease, actually remove plaque build up from arteries, shown by non invasive imagine techniques. Like you said, antioxidant status hasn't accomplished this which is why LDL reduction is reccomended.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 10:16 PM

I think you're missing the point or at least downplaying the importance of LDL. All those other risk factors are indeed contributors, but modulating them from baseline isn't sufficient enough to regress the disease. Atherosclerosis occurs over years and decades, willingly having a high LDL by eating a diet that drives it up isn't a good long term strategy, I'm glad you agree with this.

And if people take from your post that antioxidant status is important and decide to eat more fruits and vegetables, great! As you said these foods and compounds are likely protective.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 09:55 PM

I hope I've at very least given people a glimpse of the stupidity involved in the Cholesterol denialism you see here. I recommended people who are interested in learning and seeing other view points examined check out Plant positives videos. You might be turned off by his tone and want to dismiss it on first glance but if you view enough of his material you'll at the very minimum change your views on some things. He keeps an errata page on his website so if you see any mistakes let him know. Just don't waste his time arguing strawmen & complaining about his voice.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 09:33 PM

Attia and Dayspring both say "a particle is a particle" both are as potentially atherogenic as each other. What matters according to Attia and Dayspring is the number of particles, not size.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 09:29 PM

I'm feeling the same way. I feel your completely ignoring or dismissing studies in favour of your own personal theory of heart disease. At least you have come to agree with me that high Apo-b in people following this diet is problematic and should be addressed.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 09:24 PM

High trigs is a good marker for metabolic health in a lot of people but isn't causal the way LDL can be. You can't change the progression of the disease by lowering trigs alone. Ornish's famous study even showed regression by lowering LDL, even though HDL was lowered and trigs increased slightly. That should at least give you second thoughts on the imporantce of biomarkers in that context.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 12:47 PM

If you ignore every point I make, every question I ask, show a totally miscontrued understanding of the model I am talking about, and expect me to address you points, struggle to understand your non-existant model of heart disease, basically just "talk at me", with next to no attempt to comprehend or listen, you don't understand what motivates people to communicate. Maybe you could read a paper on that?

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 12:41 PM

Ive wasted enough time raising points and questions with you, and having you ignore everything I say.

Medium avatar

(10611)

on March 04, 2014
at 11:51 AM

I'm glad you took the Luddite step here, so I didn't have to. I view dietary cholesterol as a food, and like any food it provides energy for more exercise. Same as protein, carbs and fat. Insofar as bloodstream cholesterol goes, I am able to make more than I need out of any food I eat. Regarding Attia's esoteric tests my health plan doesn't pay for them so I'll never know, and they're irrelevant unless I do so why worry.

47cbd166d262925037bc6f9a9265eb20

(55)

on March 04, 2014
at 10:18 AM

When I try to upvote Drael's answer 6 days ago, it says:

You don't have permission to do this action. Please login as another user

But this is the most revealing one in this page so far.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 09:49 AM

Actually one last comment. I might return to this post at some future, date, but this has wasted enough of my time. I have other priorities. Enough is enough.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 09:36 AM

"However, and this is the important part, when the authors adjusted for the number of LDL particles (in yellow), the same phenomenon was not observed. Now an increase in LDL particle size by 1 standard deviation was associated with an ADDITIONAL 14.5 microns of atherosclerosis, albeit of barely any significance (p=0.05)." He's right, Large fluffy ldl were never better, they appeard in people who had less adverse events. The smaller ldl you get a VAP for doesn't mean anything for non diabetic patients. If anything the larger particles and their increased cholesterol are more problematic..

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 09:29 AM

They were the low 200's. Still enough for athroslcerosis to progress which we have seen in autopsies. Their high omega 3 intake was probably very protective in that regard.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 09:25 AM

What would you want to say about my mental state? I was just posting plant positives comments to this discussion as I thought people would be interested in them. My b12 was really high last time I went to the doctors and I eat a lot of nutrient dense foods.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 09:22 AM

Actually it's rather easy, they count the number of particles, both big and small and come up with a total number. It's a very good proxy for Apo-b as well. LDL-c also tracks closely for most healthy people.

47cbd166d262925037bc6f9a9265eb20

(55)

on March 04, 2014
at 09:13 AM

It's meant that their diet has cholesterol levels off the charts.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 09:07 AM

It's been show in various human and animal studies, with drugs and without drugs. If you want to avoid plaque building up in your arteries, an LDL of 70 seems the best and tested strategy. It has been shown time and time again. Most of us already have some plaque, the question is do you want it to slowly progress and risk having sudden Myocardial infarction in later life or would you take a more prudent approach and actually halt the progression with a better eating approach.I hope you don't take the unfounded antioxidant but high LDL approach, because it will most likely fail you.

543a65b3004bf5a51974fbdd60d666bb

(4493)

on March 04, 2014
at 08:54 AM

could this be a new PH record for comments...56 and counting...

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 08:36 AM

If indeed lowered LDL could "reverse" heart disease, ie cure it, a person who lowered their LDL for a while could then go back on a regular diet, with no risks. But lowered LDL doesn't reverse heart disease, it merely supresses the symptoms (heart attacks), and only for those that actually have heart attacks (higher LDL doesn't _cause_ heart disease in healthy people, especially considering the only coherent model we have) . So I do question this "regression" language you use. Thats not more regression than giving anti-psychotics to a schizophrenic.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 08:33 AM

Show me an actually testable _model_, where LDL causes heart disease, like your assuming. Your welcome to be skeptical. Totally. The science does indeed need replicating, and expanding to human trials (where they will surely go next with it). But as a skeptical scientist, you must allow me the same courtesy, to be skeptical of your weakly evidenced, poorly controlled, badly generalizable jumble of primarily correlation and intervention studies, that total lack any coherent testable model (and thus are not even a true hypotheses) and have sieve like missing links in the evidence chain.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 08:29 AM

Read my next answer, you'll see why introducing the anti-oxidants _afterwards_ would not be a complete cure (its one of a few factors). If indeed your reduced inflammation, reduced oxidation, and reduced damage to the artery wall, perhaps then you could reverse it (and such that the person could be considered "cured" rather than illness suppressed) Reduced LDL isn't a cure either though, its a cardiac event suppressor. It doesn't reverse the problem completely.

47cbd166d262925037bc6f9a9265eb20

(55)

on March 04, 2014
at 08:24 AM

No one yet accepts that once one accounts for ldl-p, the relationship of atherosclerosis to particle size is abolished you are repeating. Show the evidence for that. There is also evidence showing that plasma total apo b to ldl-c as estimated by Friedewald formula does not reliably predict ldl-p size:

http://www.sciencedirect.com/science/article/pii/0009898195061316#

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 08:24 AM

About tryclyersices. They are important to keep in range but lowering them isn't enough to stop plaque progession.

Causal Relevance of Blood Lipid Fractions in the Development of Carotid Atherosclerosis: Mendelian Randomization Analysis.

Conclusion: Our findings confirm a causal relationship between LDL-C and CIMT but not with HDL-C and triglycerides. At present, the suitability of CIMT as a surrogate marker in trials of cardiovascular therapies targeting HDL-C and triglycerides is questionable and requires further study"

http://www.ncbi.nlm.nih.gov/pubmed/23275344

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 08:20 AM

"How do you imagine heart disease, mechanically, functionally occurs" From what I understand it's still being worked out, the science in that field is so complex you or I wouldn't be able to understand it.

The simple theory, if there's way too much LDL in the plasma it's likely going to dock somewhere, like in the coronary arteries.It's a linear driven process, (more ldl-P more possible penetration. THis is Attia's stance as well.Oxidation could be a contributor as well.

Therefore I would recommend a diet that has much less of a chance of putting LDL and LDL-p in a higher range.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 08:13 AM

Dude. It's an accepted fact that a diet high in satruated fats raise cholesterol. This has been shown as far back as the 1950's in metabolic wards and countless studies since then. Even most paleo and low carb promoters acknowlege this.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 08:05 AM

If you show me a human that has a high LDL and reverses their plaque build up via antioxidants status let me know. Until then it's speculation and it doesn't seem to have any practicability to it in a larger sense. There has been studies where they increased anti oxidant status and they havn't achieved anywhere near the results of LDL lowering.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 07:57 AM

Well they I guess you would agree with someone that would say that hyperglycemia _does_not_cause nerve, kidney, cardiovascular damage. As you could say It's not a direct mechanism and it can be prevented by nitric oxide, as shown in animal studies.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 07:56 AM

This whole idea of "mitigating" is ass backwards, and shows a lack of comprehension of the model. High LDL doesn't cause heart disease. At all. Your LDL can be sky high, but you get zero heart disease. Its the run away oxidation process, that derives from the artery wall damage, (first inflammation, blood pressure etc, causing the call for repair, then lack of anti-oxidant to mitigate the oxidation - then plaque and heart attack). Only when the process is already engaged/started does the high LDL count for anything, if indeed that even occurs in response 2 dietary fats in the person.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 07:51 AM

I don't remembering arguing that. All I am saying is that the actual process of heart disease is not _caused_ by high LDL at all, but by blood pressure, inflammation and oxidation, the processes that contribute strongly and directly to the model. First one needs a damaged artery wall for a start. Indeed I don't remembering you proving that happens to most people, versus, an on average effect caused by a minority when they eat sat fats (again there are different kinds, they all have different effects on lipids. For example, lauric acid is largely positive on blood lipids)

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 07:48 AM

But do trigs go up? Science can't yet answer that, my friend. its only studied total carbs (just like its only studied total sat fats, both not a complete picture). At least you have finally but one of your cards on the table, and answered just ONE of my damn questions. Even if your ideal is model-less, spurious, disconnected and ignored that different sat fats have different effects on LDL (and trigs are raised by total carb consumption), at least I have an answer to ONE of my many questions!

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 07:00 AM

What diet do I think is optimal? I think one that at the very least emphasis's whole foods that lower LDL/LDL-p. You don't even see that advice to cut back on saturated fat been offered in paleo forums though, even when people report their LDL increasing dramatically.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 06:35 AM

Metabolic ward studies as far back as the 1950's show that saturated fats raise LDL. This isn't even debatable, even low carb and paleo promoters acknowledge this, they justify it by noting that HDL increases or that by claiming that the LDL phenotype that increases is non-atherogenic, (which is has been proven false).

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 06:27 AM

Paleo followers show high LDL and high LDL-p all the time, they are told that isn't a problem and they should continue eating the foods they are eating. Even studies from Phinney and Volek have shown cholesterol increase quite dramatically. Studies show Apo-b is raised by eating more saturated fat and cholesterol so this shouldn't be a surprise. The general advice for people to eat more saturated fat and cholesterol is ill advised, I'm thinking you can at least agree with this much.

141c6b3d5e9506dd93881e3f9737f297

(55)

on March 04, 2014
at 06:24 AM

life's too short for regrets

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 06:07 AM

You're argument that higher LDL levels are fine if you have enough anti-oxidants to mitigate damage done is like saying that Hyperglycemia is fine if you have enough nitric oxide to prevent the complications it causes. Research in mice has shown that it can stop the problems high blood sugar can cause. Even if it is true, I think everyone can agree the logical and sensible conclusion is to reverse the high blood glucose levels that make the problems possible in the first place.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 05:48 AM

"IMO, the real question is why would your LDL be 2x as high as normal, not what drugs can I take to lower it."

I'm not suggesting drugs. When people cut back on their saturated fat intake and replace it with healthy whole food carb sources, LDL goes down. This has been shown in countless studies, many of which Plant positive showed in his video. We live in a sanitized environment unlike Hunter gatherers which have parasitic infections that keep their cholesterol down.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 05:40 AM

I'm not defining anything. Did you read Cordains paper? He makes the argument that the optimal LDL is between 50-70. He is basing that on the normal levels observed in animals as well Hunter gatherer's that have been examined.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 05:26 AM

You're saying that plasma oxidized LDL is the problem but ignoring that oxidized dietary cholesterol can be a contributor to this.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 05:15 AM

continued - "considerable evidence that patients with predominantly small dense low-density lipoprotein adverse clinical outcomes than do those with large buoyant LDL."

Attia correctly says this is true, smaller LDL are correlated with less adverse events and appear to be protective. But, " Once you account for LDL-P, the relationship of atherosclerosis to particle size is abolished (and even trends towards moving in the “wrong” direction – i.e., bigger particles, more atherosclerosis).

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 05:14 AM

The first two sentences clearly say that I was sharing Plant positives comment.

Anyway, you're not understanding why smaller LDL are correleated with more adverse events. That study doesn't contradict anything. The abstract states --

0ba891d22837788c4d5ccf3f33f60329

(30)

on March 04, 2014
at 05:13 AM

Yeah, you're right. Not an essential nutrient, same as cholesterol. We can synthesize both glucose and cholesterol endogenously so they don't need to be consumed, though both are essential at a biological level.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 04:59 AM

Id like to ask again - what diet do you consider optimal? What is your physical model for HOW heart disease occcurs (not stats, or links, but an actual model) And additionally seeing as you brought it up, what is your proof that eating animal products (which all have different lipid profiles, btw, and should actually be studied seperately), leads to higher LDL in _most people_. Not on average. Not in general. Specific proportions of people, individuals, in a study. Thanks. I grow a bit tired of asking basic questions and having them dodged.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 04:56 AM

"Which saturated fats?"

The ones that raise Apo-b. The same foods that are encouraged to be eaten liberally around here.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 04:54 AM

Glucose essential? I believe you can survive entirely by ketosis, and don't need to consume glucose. Which makes it technically non-essentially. Fats can be somewhat interconvertered, but with relatively poor effeciency most of the time. So it would probably be technically a semi-essential nutrient. Certainly we need LDL, and we need apoB, and we need phosolipidcholine, saturated fat, and omega fats.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 04:53 AM

I'm well aware of cholesterol's critically important functions in the body. The question is what is the right amount. Blood glucose serves critically important functions as well yet I'm sure you're aware that having elevated levels of it isn't a good idea.

0ba891d22837788c4d5ccf3f33f60329

(30)

on March 04, 2014
at 04:08 AM

Bah, couldn't remember the password after the site change. Tried getting it back, but whatever, it's all good. If i get around I'll at least make my avatar a banana person again haha.

543a65b3004bf5a51974fbdd60d666bb

(4493)

on March 04, 2014
at 03:56 AM

what happened to your old @Mscott account...?

0ba891d22837788c4d5ccf3f33f60329

(30)

on March 04, 2014
at 03:14 AM

Also, Inuit generally have cholesterol in the low 200's, not exactly "off the charts": http://perfecthealthdiet.com/2011/07/serum-cholesterol-among-the-eskimos-and-inuit/

0ba891d22837788c4d5ccf3f33f60329

(30)

on March 04, 2014
at 03:10 AM

Glucose is an essential nutrient, but elevated levels in the blood seem to bad.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 02:36 AM

c) clearly there is genetic variation, which effects LDL, as in my case. Neither of us can cite studies on the actual proportions of people effected by diet re LDL so far (because I think they don't exist). Even if that were a minority, as such, you cannot advise this to all people, even if your theory were true, because that could be terrible for those who have lower LDL from eating animal meats - the best you could do would be to advise LDL tests in heavy animal eaters, and advise a range you think is ideal, based on your sick people studies (which to me is spurious evidence)

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 02:34 AM

Even if what you said was true, it wouldn't be true for all sat fats, nor are all meats just sat fat. If what you said was true (which I know it isn't, heart disease requires more factors than diet), then a) sugar would be worse - its statistically a higher risk to have elevated trigs b) all meats would be different, some good some bad & the only way to truely study it would be to look at micros, in a controlled way

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 02:30 AM

For you to be able to say, qualified, "most people" you would need to be able to cite a study which either focuses on individuals, or on proportions, in terms of raised LDL. You would also need to have those same studies control for types of saturated fats, not saturated fat as a monolithic nutrient (because animal studies show, individual sat fats behave very differently). We are on such different pages, its not even funny. Unless you understand the animal model, and why an animal model is needed, and the other evidence is too weak, too hard to control, it will stay that way.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 02:27 AM

Atherogenic particles are oxLDL. Nothing else is, they are merely co-factors. So, in fact, you are missing the point. And your also missing the second point, raise "on average", not in the majority of individuals, because those studies never deal in either individuals, or proportions of individuals, only on the stastical significance (which is an average). Averages can be thrown out by common outliers, such as the common apoB mutations.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 02:25 AM

Raised LDL isn't a "driver" either. Indeed raised trigs is considered more of a "risk factor" than raised LDL in statistical studies. See the animal model regarding what is actually a driver, which is actually a combination of about 3 or 4 prerequisite "drivers", Then with more minor influence by all the numerous "risk factors". Stats without a tested/testable model, is almost like superstition, as others might be able to see, its largely the subjective interpretation of correlation (which is actually the technical definition of superstition btw)

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 12:51 AM

And this is why the animal model, summarized in the part 1 and 2 (I only posted part 2), is so powerful. Because it is a tested full model of how this all works. And while compatible with the data of all the prior studies, its not compatible with the conclusions, which is what makes it ground breaking. Should it be replicated, examined further? yes, absolutely. But because it is a specific, single factor, controlled, biological, tested, full model, it is miles away from correlation studies, and streaks ahead of intervention studies. You could never control any of those well enough anyway.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 12:44 AM

If carbs are a risk factor, we need deeper studies on trig risks, and which carbs cause this risk. And of course, the lipid hypothesis itself needs to be tethered to a model that has evidence, for without that, its not a real hypothesis to be tested (and typically that would either be a cell study, organ study or animal study, as opposed to a statistics one)

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 12:42 AM

With no model to fit all these seperated assumptive ideas, coming out with a strong conclusion is scientifically inappropriate IMO. If different SFA's for example have different effects, and meats have different levels of MUFA, then we cannot give blanket advice for "meat" and instead need studies that examine different lipid profiles in different types of meat. If some individuals respond more neutrally to increased fat intake, then we need proportional figures on what numbers of people do what, and genetic studies on the differences.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 12:39 AM

In reality each different saturated fat has a different effect on LDL. In reality there is more monounsaturated fat in most meats, which is linked with raised HDL, and considered heart healthy. And in addition, this is an averaging effect. We are not talking about, or controlling for the common apoB mutations, that cause hyperlipidemia. And in this case we are ignoring also raised tryglycerides from carbs, which are a stronger risk factor than raised LDL. Finally, the lipid hypothesis has no actual model of how its supposed to work. This is several breaks in the theories evidential chain.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 12:35 AM

Because elevated LDL is not a cause in the model. It can be a factor, but it is not a cause (which is what the lipid hypothesis states it is). Of course the second spurious link that the lipid hypothesis makes is that because _average_ LDL goes up, across populations, this means that most people get increased LDL from eating sat fats (which ones, there are different kinds with different animal lipid profiles). This is an oversimplification issue.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 12:33 AM

He clearly doesn't understand the animal model. We are not talking about incidental ingested oxLDL, this is a process which involves escalating oxLDL from artery wall repair, and insufficient anti-oxidant. Incidental oxLDL might not be good for you (you can always slow cook your meats, as I do), but will not, in itself _cause_ the process, in the model. The process is _caused_ by a combination of factors, which the statistically established risk factors can feed into, but do not cause. This is why it contradicts the lipid hypothesis.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 12:28 AM

You said "most people", so you should be able to produce a study that examines the proportion of people for whom that occurs, especially if the video mentions it. If its averages, that cannot be extrapolated to "most people".

47cbd166d262925037bc6f9a9265eb20

(55)

on March 03, 2014
at 05:57 PM

james 27, I'm hardly holding myself not to comment on your mental state. Have you been lacking some nutrients like vitamin b12, methyl folate, other active B vitamins, cholesterol that come with cholesterol and saturated fat ?

47cbd166d262925037bc6f9a9265eb20

(55)

on March 03, 2014
at 02:48 PM

and we know what increases particle sizes and we know who are more likely to consume them. To accurately measure the extent particle sizes are relevant when ldl-p adjustment is done in a study like that there are so many factors that it can never be done. Which mainly has to do with what diet and lifestyle those people had and it never can be adjusted good enough.

47cbd166d262925037bc6f9a9265eb20

(55)

on March 03, 2014
at 02:46 PM

That perimenopausal women study looked at the changes. If the people in the lowest saturated fat group were more likely to modify their diet health consciously, this adds to the conclusion that saturated fat was good.

The statement that "particle sizes are irrelevant when ldl-p adjustment is done" is not good enough because it seems to be raised with this kind of studies:

http://www.ncbi.nlm.nih.gov/pubmed/16563891

47cbd166d262925037bc6f9a9265eb20

(55)

on March 03, 2014
at 02:26 PM

I was thinking about NMR lipoprofile but now I see apo-b is accurate in ldl-p also.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 03, 2014
at 12:03 PM

Hey james. A) what diet do you endorse as healthy, given you question the consumption of animal fats b) what is your actual model for heart disease? (not stats, not studies of sick people, your actual physical mechanism for how heart disease takes place). For part a) -please put your cards on the table, I tire of this disingenious dance. For part b) if you have a whole bunch of data, but can't explain how it works, or how it fits together, especially if the data is weak on some level, your just not there yet in terms of understanding.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 03, 2014
at 11:58 AM

I thought you were fond of studies of sick abnormal people.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 03, 2014
at 11:56 AM

Well the drugs don't work. But your right, within a very broad range of naturalistic lifestyles and diets, the human body should be able to cope. If it doesn't, its gone vastly off track.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 03, 2014
at 11:54 AM

What works for sick people, isn't automatically applicable to healthy people. In fact generally we would assume the opposite. Especially with no proposed model or mechanism.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 03, 2014
at 11:54 AM

Okay, so you are talking about some kind of stastical correlation. Well that might or might not be interesting (I wouldn't know I haven't read any such studies, just the one for sick people you posted, which does not apply to healthy people), but its useless without a mechanism.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 03, 2014
at 11:51 AM

apob is the transport for LDL. LDL is the repair molecule, for artery wall damage. When the wall is damaged, apo-b carries the LDL to do its repairman job. I think you'll find if you keep referring to natural body compounds as if they were the devil and had no function, it will get you confused (such as calling them "atherogenic particles" when you have yet to even describe a model which would make them such)

96440612cf0fcf366bf5ad8f776fca84

(19463)

on March 03, 2014
at 10:57 AM

And anyway, as Attia said, exogenous unesterified cholesterol does not raise endogenous cholesterol except at max by 0.5g - at those levels, food sources are completely meaningless. So I'm not worried that the author of the study you mention received funding from the egg board. The same would be true of any food cholesterol source.

96440612cf0fcf366bf5ad8f776fca84

(19463)

on March 03, 2014
at 10:55 AM

"She says eggs don't raise cholesterol for most people, but you can watch my video to see that she's wrong."

Wait, your video, or Plant Positive's video? Are you saying you're "Plant Positive"?

96440612cf0fcf366bf5ad8f776fca84

(19463)

on March 03, 2014
at 10:51 AM

IMO, the real question is why would your LDL be 2x as high as normal, not what drugs can I take to lower it. If it's 2x what it should be, either you're eating things that cause it to be high (usually carbs), or you have an infection that your body is trying to attempt to fix, or your LDL receptors are broken. The mechanism that raises the level is there for a reason and it should be able to reach homeostatis on its own, without drugs.

96440612cf0fcf366bf5ad8f776fca84

(19463)

on March 03, 2014
at 10:48 AM

Who is us, or you, or better yet, reference ranges from lab results? Are these generic SAD eaters? Are these hunter gatherers? Are these long lived or short lived populations? Or just what the lab has seen in its references? Are the values of what is "normal" influenced by big pharma's attempt to say "Statins are so wonderful they should be put in the water"?

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 03, 2014
at 09:10 AM

Which saturated fats? There's a load of different ones, all with different effects on lipid metabolism. They are highly varied. Compare say palmitic acid with lauric acid. So which ones? And most meats are more monounsaturated than saturated. Which is associated with lowered heart disease risk, higher HDL. Only dairy really is primarily sat fat, although studies also show that's associated with lower BMI, which itself lowers health risks. Human dietary studies are so very hard to control properly, its very sad that people draw such strong conclusions from such weak evidence really.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 03, 2014
at 09:04 AM

What do you think the ideal diet is? How do you imagine heart disease, mechanically, functionally occurs (like what is your actual model of how it occurs)?

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 03, 2014
at 09:03 AM

Your defining your own healthy range. On spurious data. Good for you, but don't expect us to buy it, unless you sell it much better than you have (ie, with healthy people, not with heart attack victims). Although probably LDL does go down with exercise. *shrugs*, and if you have basically no LDL, yes conventional heart disease would be less likely, but what about the efficacy of artery wall repair? LDL does actually have a job, and an important one.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 03, 2014
at 09:00 AM

On average, or "most people" individually? I don't generally waste my bandwidth on youtube, especially not for some fella talking. If you have an actual study that shows "most people" individually, have raised LDL from eating sat fats, even just an abstract.summary, please share it. Everything ive see so far is statistics, which creates averages, averages that would be thrown out by the common apoB mutations, essentially by outliers. Ive seen loads of averaging studies, but that actually tells us nothing about how we expect an individual or "most people" to react to dietary changes.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 03, 2014
at 08:12 AM

Adding to that. The videos cite several studies that show these foods raise Abo-p, which is the amount of atherogenic particles.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 03, 2014
at 07:40 AM

Again, you might not get elevated LDL from a diet. You're on one end of the bell curve, so to speak. When it comes to general paleo reccomendations they don't make these disctintions, they see high LDL and claim it as a positive, mainly because a false and untrue belief that their LDL is "large and fluffy".

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 03, 2014
at 07:36 AM

"Normal" LDL by the standards of the overweight American public. If your talking normal and optimal by Cordains standards based of hunter gatherers then that is so much less likely.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 03, 2014
at 07:34 AM

It didn't happen to you and I'm glad for that. But I would still like to know what your LDL is. If it dropped I'm assuming it would of been in the presenence of weight loss and/or increased activity.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 03, 2014
at 07:30 AM

They are in the video's i linked. Raised LDL and Apo-b from those foods. Refined sugar can be a problem down the line if it induces insulin resistance. You could consider that A factor but it's far from one of the primary drivers.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 03, 2014
at 05:35 AM

I posted Plant Positives comments on your 2 links in the comment section.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 03, 2014
at 05:28 AM

Did you miss the various studies that that show Apo-b is raised from saturated fat and cholesterol?

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 03, 2014
at 05:20 AM

I'll quote Attia again.

"The most frequently used and guideline-recommended test that can count the number of LDL particles is either apolipoprotein B or LDL-P NMR, which is part of the NMR LipoProfile"

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 03, 2014
at 05:18 AM

@Drael

"why do you assume most people who eat sat fats get high LDL (individually because averages dont show that) & whats your evidence for that"

Did you watch the video? It shows lots of controlled studies that these foods raise LDL and apo-b.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 03, 2014
at 05:16 AM

What regresses heart disease shows us what it takes to halt it.

http://circ.ahajournals.org/content/108/22/2757.full.pdf

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 03, 2014
at 05:02 AM

You're missing the point that the the Apo-b test is the most accurate measure of atherogenic particles along with LDL-p NMR. You're also missing that the video cites various studies that show saturated fat and cholesterol raise apo-b along with LDL-c.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 10:54 AM

Yeah probably the main things that pop into mind about our communication is a) if you read both articles, both part 1 & 2 (I only linked part 2), you may understand my perspective better b) what do you think an ideal diet should be, if you said that we might communicate better c) try and actually imagine the process, the model, of how heart disease is actually occuring. LDL is a repair molecule. How does that all go wrong? d) why do you assume most people who eat sat fats get high LDL (individually because averages dont show that) & whats your evidence for that.

47cbd166d262925037bc6f9a9265eb20

(55)

on March 02, 2014
at 10:48 AM

What's the source of palmitic acid ? Palm oils are the biggest sources and it's known that processed palm oil causes endotoxemia, but I don't think red palm oil does that. If it's isolated palmitic acid it's probably even worse.

Has there been any studies that show increased LDL-p from saturated fat or cholesterol on any kind of population ? Don't forget that LDL is misused for LDL cholesterol and post them if you know of any.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 10:39 AM

It is physically less particles. The larger the particle, the more LDL it carries with less particles, and less transports. There you go again with "most people". Show me a study that shows most of the individuals eating higher fat have a out of conventional range LDL particle count (indeed that these are the only people that get high particle counts), rather than an averaging metric that could be spoiled by apoB mutant outliers. I mean, visualize this stuff. In your mind, how is the mechanism actually occuring? How is a high LDL, by itself, a substance used for repair, causing damage?

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 10:35 AM

Indeed I can see no sense in low fat at all. Too low fat is just as linked with heart disease risk. There is also lots of other science to make one question the high omega-6, low fat, high carb old fashioned heart diet. Such as the link the omega balance in heart disease, and carbs with trigs and heart disease. there isn't even a 1 to 1 relationship between diet and blood lipids anyway, nor do the lipid levels themselves nessasarily help. The pills lower levels, but have questionable effects on preventing attacks. The response of the body to diet seems to be heavily genetic.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 10:32 AM

Its also perfectly obvious from the model, that for those with hyperlipidemia, or pre-existing heart disease, fat moderation (not low fat per se, but a balance of sorts), could very well be wise. Once the process starts it spirals hard. And high ldl isn't a cause but it IS a factor, if your someone who gets it.. However, in someone with low bodily inflammation, who exercises, no disease, no apoB mutation, eats omega-3, has good aerobic fitness, healthy blood pressure, lots of nutrients, doesn't smoke (ie is healthy)- there is no sense to me in restricting nutrients the body needs.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 10:27 AM

BTW If you read part 1 and part 2 of the article, I linked (I linked only part 1), it explains the full model, and how anti-oxidants protect so powerfully against the ultra hyperlipidemic GM animals, why oxLDL causes heart disease etc. When you understand the animal model, the way it works, you'll see why elevated LDL is only a factor in a process that has more important elements, on a functional level. Also why ldl-p matters. You'll see why the pipid hypothesis studies showed the results they did, and why all that was a little misleading as it was interpreted.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 10:26 AM

Please explain the relevance of regression, in the context of normal healthy human beings without heart disease?

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 10:22 AM

Look into for example triglycerides and carbs. Or omega 3-6 balance and disease generally. Fructose and vegetable oil and the link to fatty liver. I could go on and on. Indeed the body makes heavy use of fats, and if you eat vege oil heavy, and carb heavy, as traditionally recommended, that comes with body lipid changes and those things are equally implicated in numerous diseases. Im happy to admit that if someone has an apoB mutation, or pre-existing heart disease, depending on their bloods, it could be wise to moderate fat intake. But even then I would not recommend low fat/high carb

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 10:17 AM

I don't know if your arguing for a vegan or low fat diet or something, but its worth considering if you are, that your brain is mostly made of fats, also uses fats, that your liver and heart run better on fats, that your liver uses lipids to mobilize adipose etc. Also that a diet that is higher in carbs is also statistically considered a health risk in stats studies, and linked to risk factors. And that a lack of bioavailable omega-3 (ie animal fat) is linked to numerous inflammatory diseases such as stroke, and heart disease.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 10:14 AM

I do however appreciate you posting a full research paper, although I think you'd be hard pressed to draw anything conclusive from it, because its about trends not cause or direct links, and it doesn't relate to diet either. Either way, theres nothing in there I didn't expect. It might be possible to have a super low LDL, and thus avoid the oxLDL run away effect entirely (doubtful with a normal ldl), but your body would be starved of lipids most likely, and if you did get artery damage, you'd be less able to repair it (thats what ldl does, that's why we have it).

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 10:09 AM

When did I talk about regressing existing heart disease? The animal study prevents it from occuring, where genetically it is certainty. It doesn't deal with treatment of the disease after it occurs. As for your claim that damage to the artery wall is not sufficient to cause heart disease in normal LDL ranges, I would like proof of that claim. Perferrably large scale proof. And for low LDL, thats kinda wrong right there- the pills lower LDL, but they have been severely questioned by the scientific community.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 10:02 AM

Lol. No problem.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 10:02 AM

As for "most people" getting raised LDL from eating sat fats. Proof please? Most of those studies are stastical, and deal with averages, not numbers of individuals. A single outlier can ruin the ability to generalize such trends to "most people". If you understand stats. And apoB mutations are oddly common, and cause hyperlipidemia, particularly with fatty diets. They are not however "most people". Irregardless, my LDL level came down eating animal fats. Ive heard plenty of others say the same. Id venture than all this is probably understudied, which individuals, or what number of them.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 09:58 AM

Athrogenic? Nah. oxLDL is the cause. As far as fluffy ldl -you'd expect them to be safer, because more LDL is carried on less particles, lowering the particle number. Less particle number, less transport to and from the artery wall, less run away oxidation process. I do believe that sugar is associated with small dense ldl, and that even organisations like the heart foundation are compelled to believe that they are a higher risk factor on the evidence (in fact I corresponded to them about their researchers about just that)

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 02, 2014
at 08:29 AM

I read the animal study you posted. It doesn't show anything that contradicts the lipid hypothesis. Yes, antioxidants are protective against high LDL. But how protective? they haven't been shown to regress plaque in humans in trails. On the other hand LDL, Lowering has been shown to regress plaque when it gets to around 75.

http://www.ncbi.nlm.nih.gov/pubmed/14623804

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 02, 2014
at 08:05 AM

Although it doesn't lead to a lower particle count. Most people eating a lot of saturated fat have mainly pattern A LDL sizes and also have high LDL-p. Because once again, in Plant positive's videos he shows you countless studies that shows people mostly have an increase in ApoB from eating saturated fat and dietary cholesterol.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 02, 2014
at 07:53 AM

You're looking at it backwards. Inflammation (which I assume you think is one of the causes of oxidized LDL) in the presences of low LDL is not sufficient to cause atherosclerosis in humans. LDL antixoidant status hasn't been shown to regress heart disease. Basically the only thing that has been shown to regress coronary plaque is low LDL

http://circ.ahajournals.org/content/108/22/2757.full.pdf

"physiologically normal LDL"

(50-70 if you're listening to Loren Cordain and the Hunter gatherers studied)

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 02, 2014
at 07:42 AM

Again, it's the number of particles. The large fluffy ones aren't not that much bigger than the small dense ones and they are both athrogenic. There's no evidence that the larger ones reduce oxidation at all. Eating saturated fat and cholesterol, for most people raises LDL-p. Alot of the time, frighteningly so.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 07:38 AM

Actually on the topic of hyperlipidemia, and too low, I used to eat an insane 90% carbs. Mostly plants, mainly wheat, rice. Suprised I am still alive, but one of the effects was raised LDL. My GP was talking about pills. Since I went high fat, low carb, my numbers are normal. So I have personal experience a) with how I respond to high fat eating and b) how hyperlipidemia and other imbalances can be caused by too little fat

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 07:35 AM

Yes, your right it makes no sense, lol.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 07:35 AM

As for the overwhelming majority of people - they don't have increased particle counts. Its a minority of people that have hyperlipidemia. BTW Im sure for those that have screwed up genes (ie apo-b gene mutations), diet probably does matter, and moderating fat intake could be wise, even if its not a direct cause, its a factor. If you already have heart disease, similar story. Of course low fat isn't the solution there either, because thats also a risk factor, going too low, and your body compensating by hording LDL.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 07:32 AM

Ah. But ldl-p is lower if the LDL is light and fluffy, because each "particle" carries more LDL. Which is why removing particle count from particle size makes no sense to me. When we consider the animal model, we can see _why_ particle count matters, and why bigger particles, making for lower count, reduces oxidation in the run away process (because it reduces the amount of transport).

543a65b3004bf5a51974fbdd60d666bb

(4493)

on March 02, 2014
at 07:31 AM

thx for the edit Drael...i can go back to chillin'

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 07:25 AM

The particle count is the whole reason why larger LDL is better in the first place, because it leads to a smaller particle count. Sounds like this attia guy has a screw lose!

543a65b3004bf5a51974fbdd60d666bb

(4493)

on March 02, 2014
at 07:24 AM

"I could care less"...

pet gripe of mine...how the English phrase of 'could Not care less' got Americanised to 'could care less'...end of gripe :)

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 07:23 AM

Really man, read the article. Part one and two. its not just a little incidental oxidation. Its a run away/escalating process of oxidation from the repair of the artery wall.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 02, 2014
at 07:21 AM

You misunderstood my friend. There's pattern A which is large and pattern b which is small, both are LDL- phenotypes. What matters According to Attia and Thomas Dayspring is not the size of the particles in the LDL, but the amount of them combined. High LDL-p he says is the main driver of atherosclerosis because once the particle number has been accounted for sizes don't matter. The high LDL-p and Abop is usually concordant with a high LDL-c in the overwhelming majority of people.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 07:19 AM

And for the record, the study actually shows a reduction in oxLDL, and heart disease, with administration of the anti-oxidant - and this is in severely lipid screwed genetically altered mice, that get heart disease without any particular prompting. It's also not analogous to smoking. Tobacco is a direct cause genotoxin. The oxidation in the animal model comes from a specific process, with no direct relationship to sat fats or similar. It's more like a "spiral out of control" situation anyway, rather than any gradual exposure. Not remotely similar.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 07:15 AM

Well, actually it is in opposition. Lipid hypothesis says raised LDL is a _cause_ of heart disease. The smoking gun-ish animal model, shows that you can have not only raised LDL, and not even have the oxLDL run away situation, let alone heart disease. That the specific mechanism is the cause, in which, raised LDL, for those who get that, is only a minor factor, not a cause - and people with normal LDL, can indeed have the heart disease via this mechanism. Which is a million miles from raised LDL being the cause of heart disease, even where that is occuring.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 07:10 AM

Although I can say that your oxidation link isn't really relevant to the animal model. Its a run away process leading from LDL artery repair - its the repair process that causes the chain of even increasing oxLDL. A little pre-oxidized fat isn't the cause, even if you ate that kind of fat, already oxidized before consumption, it would contribute basically nothing to the mechanics of the animal model. I keep getting the impression, you havent read part 1 or 2, of the link I posted. If you want to argue against it, you may wish to read it.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 07:08 AM

I don't know how higher LDL is relevant to the mechanic but regardless, thats not an individual effect, thats the average of statistics. IMO, probably caused by apoB gene mutations. My LDL is normal. I eat loads of sat fats. I adore them. If your going to keep falling back on raised LDL, you'll need to speak more directly to someone who actually gets that from a high fat diet. I really can't examine abstracts in terms of methodology, unless you at least give me a more detailled secondary write up btw.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 02, 2014
at 07:00 AM

Attias clearly has theories. Me? Not so much. What you just said though, doesn't make any sense. Larger particles carry more ldl, with a small particle number. Thats why they are less prone to oxidation, because of the reduced particle number (which again would make sense if you read the model, the oxidation increases from transport to and from the damaged artery). If you take out the number, then of course the effect is abolished. Thats like saying once you remove rain, from the rain, you no longer get wet. Unless I misunderstood.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 02, 2014
at 05:37 AM

Also. If you're really worried about LDL oxidation, dietary cholesterol can be a major contributor.

http://www.ncbi.nlm.nih.gov/pubmed/16270280

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 02, 2014
at 05:12 AM

Also. Unsaturated fats seem to be more protective against LDL oxidation if that's what you're interested in.

http://www.ncbi.nlm.nih.gov/pubmed/21078775

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 02, 2014
at 05:08 AM

@Moors. You are still tied up in thinking that the larger "fluffy" LDL particle size are less atherogenic than the smaller LDL. I'll repeat Attia's conclusion from his blog post.

"Let me repeat this point: Once you account for LDL-P, the relationship of atherosclerosis to particle size is abolished (and even trends towards moving in the “wrong” direction – i.e., bigger particles, more atherosclerosis)"

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 02, 2014
at 04:57 AM

Again, there's no evidence that the oxidation theory is in opposition to the lipid hypothesis. You seem to be thinking that people can get away with twice as much LDL floating around in the blood if they have enough antioxidants to protect them. It's like saying you can get away with smoking a pack of cigarettes a day if you have enough circulating antioxidants to protect you from cancer. It's non nonsensical. Since I'm posting this reply at paleohacks and all I think link might at least give you something to think about.

http://www.ncbi.nlm.nih.gov/pubmed/15172426

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 02, 2014
at 04:35 AM

You're completely ignoring Attia's blog posts. That's made obvious by your belief in the "small LDL is bad, large LDL is good" theory. It's not correct, it never was correct. It was a biomarker low carbers got way too excited about in a subset of people with metabolic syndrome. As Attia states "Let me repeat this point: Once you account for LDL-P, the relationship of atherosclerosis to particle size is abolished (and even trends towards moving in the “wrong” direction – i.e., bigger particles, more atherosclerosis)"

3ce6a0d24be025e2f2af534545bdd1d7

(26217)

on February 28, 2014
at 02:55 PM

well then good. congrats. I just saw the diamond and didn't hear the announcement. The site certainly needs active moderators.

96440612cf0fcf366bf5ad8f776fca84

(19463)

on February 28, 2014
at 02:35 PM

Others sneak in urls pointing back to their website as fake answers to old questions. They usually say generic CW stuff like "eat a low fat diet, avoid saturated fat, see this article." after watching several of these posts you see they point to the same website, so they're obviously farming for clicks.

96440612cf0fcf366bf5ad8f776fca84

(19463)

on February 28, 2014
at 02:33 PM

Sure, I hunt trolls and spammers down for sport. Sometimes, you have people who may behave the similarly to trolls but actually aren't - I don't censor those. Typically you see new users who "ask" questions and use Markov chains of text to point to their spam site, presumably for SEO - those I delete outright. Others have a leading question from one account, with an answer from another (i.e. "where can I find weight loss pills with no effects?" - usually both q and a have very bad grammar/English.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 02:09 PM

Prior studies regarding merely raising LDL or lowering bear no resemblance. This study reveals a direct mechanism, combined with everything else we know, creates a complete model, as the articles outline. Everything prior is speculation by comparison.The "animal model" represents the missing piece, in heart disease research. Indeed the closest thing to a "smoking gun" than such research has acheived to date. This type of research, the animal model, is much stronger than intervention studies, or epidemiology.

3ce6a0d24be025e2f2af534545bdd1d7

(26217)

on February 28, 2014
at 02:07 PM

Off topic. Are you are moderator now?

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 02:05 PM

That's the study that the article is talking about with regard to the full animal model/mechanism discussed. Blocking heart disease is an impressive newer step forward, especially when the mechanism is understood, because it means now we can see a whole picture, a full model of the mechanism, and how all these elements come together. We have a initial reaction of the LDL repair, due to damage/inflammation on the artery wall, leading to spiraling oxLDL, when insufficient anti-oxidant is available, and everything else feeds into that, as explained by both this article, and part 1.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 02:02 PM

That's the study that the article (the one I posted a link to) are talking about with regard to the full animal model discussed. Blocking heart disease is an impressive newer step forward, especially when the mechanism is understood, because it means now we can see a whole picture, and how all these elements come together. We have a initial reaction of the LDL repair, due to damage/inflammation on the artery wall, leading to spiraling oxLDL, when insufficient anti-oxidant is available, and everything else feeds into that, as explained by both this article, and part 1.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 01:56 PM

http://www.sciencedirect.com/science/article/pii/S0021915007003413

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 01:52 PM

Well true. That's the only one studied, but the body has other common anti-oxidants, that would be present in the arteries.

47cbd166d262925037bc6f9a9265eb20

(55)

on February 28, 2014
at 01:25 PM

I agree. And other antioxidants must also be relevant to a degree.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 01:04 PM

Very nice response. There's more mono's in most meats than saturated fats. Very few foods are mainly sat fats (indeed most likely each individual fat has an entirely different profile). And I believe oxidation isn't just the risk, its the part of the mechanism itself (artery wall inflammation = increased LDL oxidation. Minus glutathione = heart disease).

.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 12:43 PM

As for inflammation being secondary, clearly you didn't read the study. Without increased inflammation and/or artery wall damage, the whole oxLDL thing doesn't get out of hand. Repairing the damage, or responding to inflammation is how the LDL gets oxidized. And then it getting out of hand depends on the oxLDL swamping the glutathione. You can get a load of oxLDL with normal LDL, or high LDL. You can get heart disease with completely normal LDL. You can have high LDL, and no inflammation, and decent glutathione, and no issues with oxLDL. Read the study, you'll see.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 12:35 PM

It would be fairer to talk about only those for whom, animal products do in fact increase LDL (usually those with mutations in their apoB gene IMO), even if you did consider increased LDL, alone, a cause of heart disease (with neither inflammation/damage leading to oxidation, nor a lack of the anti-oxidant - which it isn't), rather than a mere factor.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 12:23 PM

I could say what is your evidence that the anti-oxidant is not sufficient to prevent (when indeed the study shows that the anti-oxidant prevents the whole show). But lets instead focus on your first assumption. Higher LDL. I have a normal LDL, according to now outdated heart medicine. I eat loads of animal fats. I eat 100-150 grams carbs. Animal products for breakfast and dinner, in abundance. Why should I care about your claim that animals fats increase heart disease, if its dependant on a step that clearly doesn't happen for me? Why should anyone else that doesn't have a high LDL?

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 12:16 PM

So attia is wrong. When did he write his blog? Over two years ago? More LDL neither causes oxidation, nor more inflammation (LDL fixes the damage, it doesn't cause it), nor a lack of ability to produce glutathione. Higher LDL, if your one of those people who gets hyperlipidemia from higher fat consumption (which I for example am not), is merely a factor, not a driver, from the point of veiw of the mechanism. You need to have the other ingredients for it to mean anything.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 12:10 PM

Oh, thats not what most people mean when they say apoB. They mean the gene usually not the protein. I believe its mentioned in the animal model study above (the LDL carrier, not the gene)

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 12:09 PM

Its a gene, that codes a protein.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 12:07 PM

As for attias, I could give a rats arse what someones theory is. If it doesn't match the evidence, its wrong. Same with the framington crowd. The cause of heart disease is oxLDL and inflammation. End of story.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 12:06 PM

This is not simply "a animal study", its "an animal model". When dealing with such things, an animal model is the smoking gun of the actual mechanism (or as close as science can get yet). It's what all the heart disease research has been missing until this point. If you have something that can switch off, fully prevent the occurance of heart disease, and you know why, your miles ahead of "factors" and guesswork.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 12:02 PM

If you have the anti-oxidant in abundance, the ox-LDL isn't an issue. LDL itself fixes the damage from inflammation. Inflammation is required for the LDL oxidation. High LDL doesn't track well to high fat intake either, even if it was a predictor, _on its own_, of heart disease, which to me is silly. It might for some, but for many it doesn't.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 11:59 AM

Who's "theory"? I think you lost me. For me, ldl-p, is not a cause of heart disease. Its only a potential factor, given a lack of anti-oxidants, and an excess of oxidation - which is propelled more by small dense LDL, if anything (and thusly ldl-c is better). Genetically determined in part to boot and effected by a lack (My ldl went down when I lowerd carbs and ate much more fats). Because I am familiar with the animal model study, in terms of heart disease, I am not really dealing with theories.

96440612cf0fcf366bf5ad8f776fca84

(19463)

on February 28, 2014
at 11:38 AM

I don't know about any infighting in the WAPF, I do know of his work and I find it mostly compatible with paleo. Eating oats is terrible advice, it's a grain, and as such has gluten analogues, though not as bad as gluten, also most oats are contaminated with gluten from processing on the same equipment as wheat. Perhaps you're not aware, but fat isn't bad for us, at least, not saturated or MUFA, and for the most part not fresh unoxidized n3. There was a troll here a week ago trying to "disprove" Attia by spamming.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on February 28, 2014
at 08:28 AM

BTW. I wasn't posting here last week. This is my only account. The other posts about receiving bad dietary advice by being told to "Add more fat" was legitimate and justified. It received several up-votes. Eating oats? that's good advice. As for the WAFP cranks, I take that information from someone who used to be a president chapter. Which she later abandoned due to her belief they were agenda driven and didn't represent Weston Price's work accurately.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on February 27, 2014
at 10:58 AM

@Drael. LDL-p should matter to you because it contradicts your theory that Pattern A is atherogenic whilst pattern B is not. They are both equally atherogenic and what matters according to Attia is the actual number of particles, which generally tracks very closely to LDL-C exepct in the case of people with metabolic syndrome or Type III dyslipoproteinemia patients.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on February 27, 2014
at 10:11 AM

Attias correct assertion in his blog post that clearly says that Small dense Pattern B are just as anthropogenic as Pattern A. What matters is the complete particle count and ApoB that determine risk of atherosclerosis progression. And LDL and LDL-p are concordant and track each other closely in healthy people. There may be discordance between LDL and LDL-p when people have metabolic syndrome or diabetes

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on February 27, 2014
at 07:44 AM

And did you read Attias blog post? He correctly stated that pattern B LDL phenotype is no more atherogenic than the larger Pattern A LDL

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on February 27, 2014
at 07:43 AM

Inflammation is secondary to high LDL. Less LDL hanging around in the plasma = less chance it becomes oxidised. Yes, dietary antioxidants can protect from atherosclerosis but they're not self sufficient enough to regress atherosclerosis in the presence of high LDL. I'm not sure why you're citing animal studies when referring to the mechanisms behind atherosclerosis, as tonnes of different animals studies have shown progression and regression of plaque simply raising and lowering LDL through various methods.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on February 27, 2014
at 07:33 AM

...

Then he shows you studies that eggs and saturated fat clearly effect ApoB for the worse, which is why I linked the video. Did you miss them all or did you put your hands over your eyes and ears because you don't want to acknowledge this?

@Drael. You seem confused. Please google Apolipoprotein B.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on February 27, 2014
at 07:32 AM

I'm not sure if you're intentionally misinterpreting what he states in this video but it seems like it. PP clearly states that this video is about Attias assertions that dietary cholesterol has insignificant effects on serum cholesterol, he then shows you evidence to the contrary.

Then he states "We’re going to be seeing a lot more about apoB in this video. If we see that something increases apoB, we should infer from Attia’s statement that that food increases the primary driver of atherosclerosis",

continued next post..

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on February 27, 2014
at 07:27 AM

"Have you tried asking him" Yes, he hasn't replied yet. Maybe he wasn't aware of this research and regrets giving contradictory advice? That's my best guess.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 26, 2014
at 01:35 PM

Oh, low density? That's the good stuff. Its the dense stuff thats more concerning (in the absence of the anti-oxidant). I don't think this person is very literate in the area. Apo-b (mispelled in his post), is a gene that everyone possesses. Mutations can cause increased LDL. He mentions eggs and meat increasing the gene! (or the mutation, either way, it makes zero sense). Good spot BTW. What a charlatan to make a video about particle count, and then use graphs showing increases in the more healthy cholesterol as your "proof". What a lol.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 26, 2014
at 09:37 AM

Why is ldl-p supposed to matter btw? I thought it was small dense LDL that was more prone to oxidation (which is associated with carbs in studies). And whats the gene apolipoprotein B have to do with eating meat? Meat does not "raise" a gene, nor mutations in that gene, as far as I am aware.

141c6b3d5e9506dd93881e3f9737f297

(55)

on February 26, 2014
at 08:35 AM

"Was he unaware of all these studies that show fatty meat, eggs, cream and butter raise AboB and LDL-p?"

I would guess Peter is the only one that can answer that.

have you tried asking him

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11 Answers

0
96440612cf0fcf366bf5ad8f776fca84

(19463)

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.

https://en.wikipedia.org/wiki/Homocysteine

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 12, 2014
at 11:38 AM

B12 is the only issue here. I think any responsible person following a vegan diet knows enough to check their b12 status to see if it is in range, even if they eat fortified foods. Besides that, they can take a b12 supplement a few times a week to keep the levels up.

0
47cbd166d262925037bc6f9a9265eb20

(55)

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:

http://www.sciencedirect.com/science/article/pii/S1756464612001363

And if you can't access the full text, here are 2 articles regarding the study:

http://www.greenmedinfo.com/blog/apple-day-helps-prevent-heart-disease-just-one-month

http://www.sciencedaily.com/releases/2012/10/121002143220.htm

0
8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

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 ?

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 09:49 AM

Actually one last comment. I might return to this post at some future, date, but this has wasted enough of my time. I have other priorities. Enough is enough.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 04, 2014
at 10:16 PM

I think you're missing the point or at least downplaying the importance of LDL. All those other risk factors are indeed contributors, but modulating them from baseline isn't sufficient enough to regress the disease. Atherosclerosis occurs over years and decades, willingly having a high LDL by eating a diet that drives it up isn't a good long term strategy, I'm glad you agree with this.

And if people take from your post that antioxidant status is important and decide to eat more fruits and vegetables, great! As you said these foods and compounds are likely protective.

0
54eb85f12ef6e51dd9705a4a01cb0f84

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.

0ba891d22837788c4d5ccf3f33f60329

(30)

on March 04, 2014
at 03:14 AM

Also, Inuit generally have cholesterol in the low 200's, not exactly "off the charts": http://perfecthealthdiet.com/2011/07/serum-cholesterol-among-the-eskimos-and-inuit/

0ba891d22837788c4d5ccf3f33f60329

(30)

on March 04, 2014
at 03:10 AM

Glucose is an essential nutrient, but elevated levels in the blood seem to bad.

Medium avatar

(10611)

on March 04, 2014
at 11:51 AM

I'm glad you took the Luddite step here, so I didn't have to. I view dietary cholesterol as a food, and like any food it provides energy for more exercise. Same as protein, carbs and fat. Insofar as bloodstream cholesterol goes, I am able to make more than I need out of any food I eat. Regarding Attia's esoteric tests my health plan doesn't pay for them so I'll never know, and they're irrelevant unless I do so why worry.

0
5dd50f78f47b8848d93724d6eb38d4c1

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.

http://www.ncbi.nlm.nih.gov/pubmed/16270280

And saturated fatty acids promote this more than unsaturated fatty acids.

http://www.ncbi.nlm.nih.gov/pubmed/21078775

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.

http://www.ncbi.nlm.nih.gov/pubmed/1575961

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.”

And later:

“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."

47cbd166d262925037bc6f9a9265eb20

(55)

on March 03, 2014
at 05:57 PM

james 27, I'm hardly holding myself not to comment on your mental state. Have you been lacking some nutrients like vitamin b12, methyl folate, other active B vitamins, cholesterol that come with cholesterol and saturated fat ?

0
5dd50f78f47b8848d93724d6eb38d4c1

on March 03, 2014
at 05:34 AM

@Moors

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."

47cbd166d262925037bc6f9a9265eb20

(55)

on March 03, 2014
at 02:48 PM

and we know what increases particle sizes and we know who are more likely to consume them. To accurately measure the extent particle sizes are relevant when ldl-p adjustment is done in a study like that there are so many factors that it can never be done. Which mainly has to do with what diet and lifestyle those people had and it never can be adjusted good enough.

47cbd166d262925037bc6f9a9265eb20

(55)

on March 03, 2014
at 02:46 PM

That perimenopausal women study looked at the changes. If the people in the lowest saturated fat group were more likely to modify their diet health consciously, this adds to the conclusion that saturated fat was good.

The statement that "particle sizes are irrelevant when ldl-p adjustment is done" is not good enough because it seems to be raised with this kind of studies:

http://www.ncbi.nlm.nih.gov/pubmed/16563891

96440612cf0fcf366bf5ad8f776fca84

(19463)

on March 03, 2014
at 10:55 AM

"She says eggs don't raise cholesterol for most people, but you can watch my video to see that she's wrong."

Wait, your video, or Plant Positive's video? Are you saying you're "Plant Positive"?

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 03, 2014
at 11:58 AM

I thought you were fond of studies of sick abnormal people.

96440612cf0fcf366bf5ad8f776fca84

(19463)

on March 03, 2014
at 10:57 AM

And anyway, as Attia said, exogenous unesterified cholesterol does not raise endogenous cholesterol except at max by 0.5g - at those levels, food sources are completely meaningless. So I'm not worried that the author of the study you mention received funding from the egg board. The same would be true of any food cholesterol source.

0
47cbd166d262925037bc6f9a9265eb20

(55)

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.

0
47cbd166d262925037bc6f9a9265eb20

(55)

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.

http://www.ncbi.nlm.nih.gov/pubmed/15531663

http://www.ncbi.nlm.nih.gov/pubmed/16340654

47cbd166d262925037bc6f9a9265eb20

(55)

on March 02, 2014
at 10:48 AM

What's the source of palmitic acid ? Palm oils are the biggest sources and it's known that processed palm oil causes endotoxemia, but I don't think red palm oil does that. If it's isolated palmitic acid it's probably even worse.

Has there been any studies that show increased LDL-p from saturated fat or cholesterol on any kind of population ? Don't forget that LDL is misused for LDL cholesterol and post them if you know of any.

0
47cbd166d262925037bc6f9a9265eb20

(55)

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.[13] E4 has been implicated in atherosclerosis,[19] Alzheimer's disease,[20][21] impaired cognitive function,[22][23] reduced hippocampal volume,[23] HIV,[24] faster disease progression in multiple sclerosis,[25][26] unfavorable outcome after traumatic brain injury,[27] ischemic cerebrovascular disease,[28] sleep apnea,[29][30] accelerated telomere shortening [31] and reduced neurite outgrowth.[32]"

http://en.wikipedia.org/wiki/Apolipoprotein_E

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.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on March 02, 2014
at 05:08 AM

@Moors. You are still tied up in thinking that the larger "fluffy" LDL particle size are less atherogenic than the smaller LDL. I'll repeat Attia's conclusion from his blog post.

"Let me repeat this point: Once you account for LDL-P, the relationship of atherosclerosis to particle size is abolished (and even trends towards moving in the “wrong” direction – i.e., bigger particles, more atherosclerosis)"

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 28, 2014
at 01:04 PM

Very nice response. There's more mono's in most meats than saturated fats. Very few foods are mainly sat fats (indeed most likely each individual fat has an entirely different profile). And I believe oxidation isn't just the risk, its the part of the mechanism itself (artery wall inflammation = increased LDL oxidation. Minus glutathione = heart disease).

.

0
96440612cf0fcf366bf5ad8f776fca84

(19463)

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.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on February 27, 2014
at 07:33 AM

...

Then he shows you studies that eggs and saturated fat clearly effect ApoB for the worse, which is why I linked the video. Did you miss them all or did you put your hands over your eyes and ears because you don't want to acknowledge this?

@Drael. You seem confused. Please google Apolipoprotein B.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on February 27, 2014
at 07:32 AM

I'm not sure if you're intentionally misinterpreting what he states in this video but it seems like it. PP clearly states that this video is about Attias assertions that dietary cholesterol has insignificant effects on serum cholesterol, he then shows you evidence to the contrary.

Then he states "We’re going to be seeing a lot more about apoB in this video. If we see that something increases apoB, we should infer from Attia’s statement that that food increases the primary driver of atherosclerosis",

continued next post..

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on February 28, 2014
at 08:28 AM

BTW. I wasn't posting here last week. This is my only account. The other posts about receiving bad dietary advice by being told to "Add more fat" was legitimate and justified. It received several up-votes. Eating oats? that's good advice. As for the WAFP cranks, I take that information from someone who used to be a president chapter. Which she later abandoned due to her belief they were agenda driven and didn't represent Weston Price's work accurately.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 26, 2014
at 01:35 PM

Oh, low density? That's the good stuff. Its the dense stuff thats more concerning (in the absence of the anti-oxidant). I don't think this person is very literate in the area. Apo-b (mispelled in his post), is a gene that everyone possesses. Mutations can cause increased LDL. He mentions eggs and meat increasing the gene! (or the mutation, either way, it makes zero sense). Good spot BTW. What a charlatan to make a video about particle count, and then use graphs showing increases in the more healthy cholesterol as your "proof". What a lol.

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 04, 2014
at 04:59 AM

Id like to ask again - what diet do you consider optimal? What is your physical model for HOW heart disease occcurs (not stats, or links, but an actual model) And additionally seeing as you brought it up, what is your proof that eating animal products (which all have different lipid profiles, btw, and should actually be studied seperately), leads to higher LDL in _most people_. Not on average. Not in general. Specific proportions of people, individuals, in a study. Thanks. I grow a bit tired of asking basic questions and having them dodged.

0
8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on February 26, 2014
at 09:00 AM

There's the actual smoking gun for atherosclerosis:

http://lwtinternational.com/blog/ldl-oxidation-the-smoking-gun-behind-heart-disease-2/

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)

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on February 27, 2014
at 07:43 AM

Inflammation is secondary to high LDL. Less LDL hanging around in the plasma = less chance it becomes oxidised. Yes, dietary antioxidants can protect from atherosclerosis but they're not self sufficient enough to regress atherosclerosis in the presence of high LDL. I'm not sure why you're citing animal studies when referring to the mechanisms behind atherosclerosis, as tonnes of different animals studies have shown progression and regression of plaque simply raising and lowering LDL through various methods.

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on February 27, 2014
at 07:44 AM

And did you read Attias blog post? He correctly stated that pattern B LDL phenotype is no more atherogenic than the larger Pattern A LDL

5dd50f78f47b8848d93724d6eb38d4c1

(907)

on February 27, 2014
at 10:11 AM

Attias correct assertion in his blog post that clearly says that Small dense Pattern B are just as anthropogenic as Pattern A. What matters is the complete particle count and ApoB that determine risk of atherosclerosis progression. And LDL and LDL-p are concordant and track each other closely in healthy people. There may be discordance between LDL and LDL-p when people have metabolic syndrome or diabetes

47cbd166d262925037bc6f9a9265eb20

(55)

on March 04, 2014
at 10:18 AM

When I try to upvote Drael's answer 6 days ago, it says:

You don't have permission to do this action. Please login as another user

But this is the most revealing one in this page so far.

543a65b3004bf5a51974fbdd60d666bb

(4493)

on March 04, 2014
at 08:54 AM

could this be a new PH record for comments...56 and counting...

8b9c2dcd3dfc929a0428d3d6dac4918e

(70)

on March 03, 2014
at 12:03 PM

Hey james. A) what diet do you endorse as healthy, given you question the consumption of animal fats b) what is your actual model for heart disease? (not stats, not studies of sick people, your actual physical mechanism for how heart disease takes place). For part a) -please put your cards on the table, I tire of this disingenious dance. For part b) if you have a whole bunch of data, but can't explain how it works, or how it fits together, especially if the data is weak on some level, your just not there yet in terms of understanding.

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