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Nutrition Past and Future

The Drivers of the Herd, Part 19

The NuSI Guys, Part 9  (ApoB at the Eating Academy)

Slide 3         

Dr. Peter Attia wrote a long blog series about cholesterol called “The straight dope on cholesterol” that was mostly focused on the subtleties of clinical biomarkers. Why did he do that? How many of his readers found it useful? As I read it, I imagined his readers wading through it all, hoping for a big payoff with each new post that would affirm their low-carb lifestyle, and then feeling let down when that payoff never came. I hesitated to make a video about his discussion of these biomarkers but here it is. Stick with me in this one. You might find all this interesting.


Slide 4         

First I want to point out something Dr. Attia got very right. At the top of this slide you can see that he correctly argues that LDL size is of little consequence. If you saw video 7 of this playlist then you know that Aseem Malhotra doesn’t understand this. Malhotra thinks that large LDLs are not atherogenic but he is wrong. As for Dr. Attia, I draw your attention to a passage from the paper he selected to explain this important idea. It states that the reason larger LDLs can be dangerous is because they are so loaded with cholesterol. It says this is what happens when people eat too much saturated fat. The authors said they found that larger LDLs correlated with the progression of atherosclerosis. This is the study Attia chose. Based on that passage, it wasn’t the best choice for a low carb promoter. More on this later.


Slide 5         

Dr. Attia’s main message in these blog posts is that LDL particle number is the best indicator of what he calls your “risk of atherosclerosis.”


Slide 6         

p.244. Leeson, Paul. Cardiovascular Imaging. Oxford: Oxford University Press, 2011. Google Books.

Think about this slide. At the top Dr. Attia says that if your LDL particle count is high you are at risk of atherosclerosis. But right after that he says atherosclerosis is “unfortunately-ubiquitous.” You can see in the bottom half of this slide that atherosclerosis is indeed considered universal at midlife. Despite its common usage, this is why I don’t think the phrase “risk of atherosclerosis”. Just because you didn’t fail a stress test or some other diagnostic procedure doesn’t mean you don’t have atherosclerosis. By the time someone is diagnosed for this their cardiovascular health is seriously compromised, with plaques built up over many years.


Slide 7         

Attia believes that LDL particle concentration is the biomarker that represents the development of atherosclerosis in the most fundamental way. Does this matter to you? Do you like to argue about the clinical utility of LDL-C versus apoB or LDL-P or non-HDL-C? Why would you care? Well, here’s why Peter Attia’s audience would care: their LDL-C, which represents LDL cholesterol, is likely to be terrible. They are low carbers after all. Rather than entertain second thoughts about whether they are hurting themselves and confront the possibility they were wrong about low carb all along, they split hairs about biomarkers. Maybe one could say, “My LDL-C looks bad but my LDL-P is in range so I must be OK.” Because he’s deeply invested in the low-carb fantasy, Dr. Attia is in the same boat. I explain the problem with this sort of thinking in my video, “The Map Is Not the Territory”.  You don’t see vegans arguing about these things.


Slide 8                   Carpenter, Keri LH, et al. "Lipids and oxidised lipids in human atheroma and normal aorta." Biochimica et Biophysica Acta (BBA)-Lipids and Lipid Metabolism 1167.2 (1993): 121-130.

The basic problem with his particle number argument is obvious.  Diseased plaques are engorged with cholesterol. Each low density lipoprotein carries nearly 2000 lipid molecules but just one apoB protein molecule. From where is he getting this idea?


Slide 9         

Graph from: Cromwell, William C., et al. "LDL particle number and risk of future cardiovascular disease in the Framingham Offspring Study—implications for LDL management." Journal of clinical lipidology 1.6 (2007): 583-592.

Attia presents this graph based on Framingham data. It represents the probability of avoiding a heart disease event against time. The steeper the slope of the curve, the worse the risk. The bottom line with the steepest slope represents the people who did the worst – those with low LDL cholesterol but high LDL particle number. We are supposed to find it surprising that people with low LDL cholesterol did so poorly. Attia is saying that this graph tells us that excessive LDL particle concentration is therefore the cause of heart disease, not high cholesterol. If ever there were an appropriate moment to say “correlation isn’t causation,” this is it.


Slide 10                 Attia says this tells us that LDL-P is a great predictor of adverse events. Oh, so he’s in the adverse event prediction game now. Are you? This is interesting stuff for a cardiologist who is trying to decide exactly how sick the sick patient in front of her is. But there is a huge difference between a predictor of who is going to have a heart attack and a biomarker representing a multi-decade disease process.


Slide 11                 Look at this graph again. The folks who were doing the best were the ones who had the lowest LDL particle number and the lowest LDL cholesterol. Attia tells us that when LDL-P and LDL-C are considered discordant a doctor should focus on LDL-P. Maybe so, but that’s beside the point. That doesn’t mean particle numbers drive atherosclerosis, as he says.


Slide 12       

Here is a statement he makes that I don’t think he can back up. He says that atherosclerosis is not about cholesterol molecules. Again, this is obviously wrong.


Slide 13                 Of course, it’s about cholesterol molecules.


Slide 14                 Otvos, James D., et al. "Clinical implications of discordance between low-density lipoprotein cholesterol and particle number." Journal of clinical lipidology 5.2 (2011): 105-113.

Here’s another graph he presented. Now the top line represents the people who did the worst. They had low LDL cholesterol but not a low particle count. The point is the same. You can still get into trouble with low LDL cholesterol.


Slide 15       

Attia says he thinks this one is significant because the lowest risk was found among those with high LDL-C and low LDL-P. As a low-carber, you are supposed to then assure yourself that your high LDL cholesterol is no problem. You’ll probably assume that your LDL-P is looking good because what other point could he be making with all this?


Slide 16                 Otvos, James D., et al. "Clinical implications of discordance between low-density lipoprotein cholesterol and particle number." Journal of clinical lipidology 5.2 (2011): 105-113.

But understand the context of this article. Read those quotes from it. This information pertains to people who have been treated with drugs to lower their LDL cholesterol. The point is that once someone’s LDL cholesterol is looking better after treatment, there still might remain what is called “residual risk.” Does this apply to the readers of Attia’s blog? Does he assume that his readers are already on statins? They probably should be. But I think he wants his readers to think that their LDL cholesterol score is not important. That’s not a good health message, Dr. Attia.


Slide 17                 Just to wrap up on this particular study, they did measure how plaque progressed and found LDL-P to be a better predictor than LDL-C. Again, the message is that when LDL-P and LDL-C are discordant, a cardiologist should focus on LDL-P. Does this finding back up his claim that atherosclerosis isn’t about cholesterol molecules?


Slide 18                 I don’t think so. Look at the sort of people in whom this discordance occurred. They had more diabetes. They had more metabolic syndrome. So how can someone say this was a story about LDL-P rather than insulin resistance?


Slide 19                 Kornerup, Karen, et al. "Transvascular Low-Density Lipoprotein Transport in Patients With Diabetes Mellitus (Type 2) A Noninvasive In Vivo Isotope Technique." Arteriosclerosis, thrombosis, and vascular biology 22.7 (2002): 1168-1174.

As I’ve said before, the arteries of diabetics are more vulnerable to infiltration. LDL-P and LDL-C are discordant when the individual is diabetic or insulin resistant. They have other problems. High LDL-P is just a part of that package. I don’t think it’s clear that we can generalize aspects of their condition to everyone else.


Slide 20                 Weingärtner, Oliver, et al. "The relationships of markers of cholesterol homeostasis with carotid intima-media thickness." PloS one 5.10 (2010): e13467.

It’s rather typical of medical research that the focus is placed on the sick with the overriding objective of improving drug treatment. Why not focus a bit on how the healthy can stay healthy without drugs? I really tried to find a study that gave that same measure they used for the degree of atherosclerosis in that study, carotid intima-media thickness, but in vegetarians. Here you see what I found. Strict vegetarians were excluded from this study. Why bother with the healthy people, right?


Slide 21                 Jarauta, Estíbaliz, et al. "Carotid intima-media thickness in subjects with no cardiovascular risk factors." Revista Española de Cardiología (English Edition)63.1 (2010): 97-102.

The best I could do in my search was this one. There was nothing special about these subjects. They just happened to be students and staff at the University of Zaragoza in Spain where this study took place. Their LDL cholesterol was actually way too high. Compare their IMT thickness with those in the MESA study that Attia selected. The MESA cohort on average had nearly 30% more thickness than these healthy-ish people. In Attia’s MESA study, they were not studying a healthy population.


Slide 22                 Attia signals his wrong-headedness about this by bringing up the inapt example of Tim Russert. Attia warns us that he had a heart attack even though his LDL cholesterol was low. Therefore, LDL cholesterol doesn’t tell you much.  Read this and notice that Attia is now focusing on people showing up at the hospital in dire straits. Again, this is looking at the less-relevant end of the spectrum of heart disease for those of us who are younger and healthier and trying to do a little better than simply avoiding the emergency room.


Slide 23                 Wood, Shelley. "Media Mulls Russert's Death as Cardiologists Weigh In." Medscape. Heartwire, 19 June 2008. Web.

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Tim Russert does not make for a good example for people not on medication for high cholesterol. Russert already had coronary artery disease. He was being treated with drugs to get his LDL that low. That means he had much higher LDL at one time. Why is Attia writing about his case at “The Eating Academy” if not to confuse and mislead low-carbers?


Slide 24                 He gives away what I think is his true purpose in all this when he complains that he doesn’t understand why doctors are still measuring LDL-C. Understand that low carbers are often confronted with frightful LDL cholesterol numbers. Attia would rather they just didn’t see them. Why? Because he so passionately believes that LDL-C isn’t as good as LDL-P at predicting heart attacks in overweight, insulin resistant people? This is ridiculous! He just wants them to ignore their LDL-C scores. This whole discussion is a disservice to the typical reader at his site.


Slide 25       

Attia says we should be focused on dietary interventions that lower LDL-P. Remember this. It’s a statement that totally undercuts his advocacy for saturated fat. I’ll tell you more about that in the next video. But after all his multiple meandering blog posts – look at Part VIII and you’ll see why I say that – what is the final payoff for his readers? What does he want to tell us about eating for heart health at The Eating Academy?



Slide 26       

Here’s one study he finds instructive. Naturally, it’s one that promotes saturated fat and low carb. Predictably, the subjects were obese – it is a low-carb study after all. Unsurprisingly, it’s an obscure study you can’t readily access.


Slide 27                 Hays, James H., et al. "Effect of a high saturated fat and no-starch diet on serum lipid subfractions in patients with documented atherosclerotic cardiovascular disease." Mayo Clinic Proceedings. Vol. 78. No. 11. Elsevier, 2003.

There you see it. It’s some study. No control group. Everyone was on statins.


Slide 28                 The starting point in this one was obese people keeping their own food logs. They said they were eating only one to three servings of red meat and no more than two eggs per week [before the study period]. We’re supposed to believe that.


Slide 29                 These people experienced reductions in their insulin and blood sugar [while] eating all that saturated fat [during the study period] and that’s what Attia wants you to care about. But notice what Attia doesn’t mention. First, their LDL cholesterol went up, as you can see at the bottom. Well, of course it did, they were eating a bunch of saturated fat! Notice also that these people happened to lose weight. Attia leaves that part out. A diet is really bad when LDL goes up even as weight is lost.


Slide 30                 Fontana, Luigi, et al. "Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans." Proceedings of the National Academy of Sciences of the United States of America 101.17 (2004): 6659-6663.

Look at how weight loss affected LDL in this other study. Granted, this was over a longer period of time but the point is, as I’ve said many times, LDL cholesterol is supposed to drop during weight loss in overweight people. Lower LDL would be just one sign that they are getting healthier. But on low carb, weight loss hardly ever brings with it this benefit.


Slide 31                 If we look at Dr. Attia’s chosen study a bit closer we see something interesting. On the bottom you can see that yes, LDL particle number dropped. But you can also see that LDL cholesterol increased, as I just pointed out. This resulted in an increased size of the average LDL particle. This is what you get with saturated fat. The funny thing here is that the title says the diet was high in saturated fat but it had no starch, as if starch is a bad thing.


Slide 32                 Davy, Brenda M., et al. "High-fiber oat cereal compared with wheat cereal consumption favorably alters LDL-cholesterol subclass and particle numbers in middle-aged and older men." The American journal of clinical nutrition 76.2 (2002): 351-358.

But if you look at what oats, a very healthy starch, does to the lipid profile, you’ll see that it will drop LDL cholesterol and drop LDL particle concentration at the same time, even though there is no weight loss! All these people in this study did was add an oat cereal to their diets. This shows you that by eating better you can improve your LDL-C and your LDL-P at the same time. There were no low carb tricks in this study, like confusing the picture with the confounding of weight loss.


Slide 33                 Saturated fats increase LDL cholesterol and they increase LDL diameter. But Dr. Attia has told us that larger LDLs aren’t any less of a danger than small ones, so this is not an advantage. When Attia argued this very point, he used a study that warned that saturated fats increase LDL diameter. He doesn’t seem to have understood this message.


Slide 34                 Siri-Tarino, Patty W., et al. "Saturated fatty acids and risk of coronary heart disease: modulation by replacement nutrients." Current atherosclerosis reports12.6 (2010): 384-390.

This is why low carbers have been so invested in the idea that large LDLs aren’t atherogenic. For example, Ronald Krauss has been the most prominent promoter of the LDL phenotype hypothesis. Every paper on the subject references him. And he says he likes low-carb diets. He has taken money from the dairy industry, the beef industry, and the Atkins Foundation. You see he also has patents based on the LDL phenotype hypothesis.


Slide 35                 Here’s an application for one of them. Ronald Krauss is definitely invested in the LDL phenotype hypothesis. Krauss understands that saturated fats increase particle size. If you start out with the position that saturated fats have to be good, then you have to believe that larger LDLs are A-OK. But that belief is completely unsupportable. Attia knows that. How will Attia resolve this contradiction and retain his membership in good standing with the low-carb community? Keep checking his blog for the latest in hair-splitting.


Slide 36                 Stanhope, Kimber L., et al. "Consumption of fructose and high fructose corn syrup increase postprandial triglycerides, LDL-cholesterol, and apolipoprotein-B in young men and women." Journal of Clinical Endocrinology & Metabolism96.10 (2011): E1596-E1605.

His other big payoff study for this set of blog posts was this one. People consumed 25% of their calories in the form of refined sugars. Mass quantities of high-fructose corn syrup and pure fructose raised their apoB levels. So there’s your lesson from The Eating Academy, folks. It’s bad to guzzle nutrient-free synthetic simple sugars. Therefore, low-carb, Q.E.D.

Do you think Dr. Peter Attia is really trying to help you reduce your apoB? If you do, you’re in for a rude awakening in the next video.