The Drivers of the Herd, Part 4
Catalyst Corrected 4, The Preset Mindset
Slide 3 Catalyst’s message number 2 says that nothing in your diet has much effect on your cholesterol levels. Does anyone really believe this? Well, yes, and Dr. Maryanne Demasi thought he deserved more attention. Let’s listen to what cardiologist Ernest Curtis has to say about diet and cholesterol.
Slide 4 Curtis: “The reason for that is that your body manufactures 80 to 90% of your cholesterol. Really, very little of it comes from the diet. Most people seem to have a genetically preset level for the cholesterol in their body, and maybe in a range. But they're generally going to seek to stay within that range. So, if somebody cuts all the cholesterol out of their diet, their body will simply start making a little bit more to bring it back up into the range.”
This is a very ignorant opinion. He is conflating the wrong but common belief that dietary cholesterol doesn’t affect serum cholesterol with the notion that individuals have “genetically preset” levels of cholesterol. He is combining two wrong beliefs to form one very wrong belief.
Slide 5 p.19. Curtis, Ernest. The Cholesterol Delusion. Dog Ear Publishing, 2010. Google Books.
This isn’t just a case of someone not having his thoughts together while speaking extemporaneously. He’s also written a substandard book about cholesterol in which he conflates these wrong beliefs the same way. Please read this excerpt. At first he is talking about “excess cholesterol” being consumed. Then he says “diet has only a trivial effect on cholesterol levels.” He says “nobody disputes any of these facts.” Well, I’m sorry, sir, but the real facts disagree with your made-up “facts.”
I have a video later in this playlist, video number 20, in which I deal directly with the way dietary cholesterol raises blood cholesterol. For now, let’s just think about his claim at the bottom, that diet doesn’t affect cholesterol levels much. It’s a crazy belief, but it’s one that Dr. Maryanne Demasi shares.
Slide 6 Demasi: “An extensive review of the literature showed that the data was highly inconsistent. In fact, there were many long-term studies that refute the idea that saturated fat raises cholesterol.”
She thinks studies are out there that refute the idea that saturated fat raises cholesterol. Again, this is an exceptionally ignorant claim.
Slide 7 Lee, Kyu Taik, J. N. Davies, and R. A. Florentin. "Geographic studies of atherosclerosis." Geriatrics 21.1 (1966): 166.
After all, the diet-heart idea was in part the result of observations that different populations with different diets and lifestyles had dramatically different mean cholesterol values. Korean farmers and vegetarian Buddhist monks had cholesterol below 140 while American soldiers averaged 222. When Korean soldiers ate American foods their cholesterol was higher than their counterparts eating Korean foods. Now unless Dr. Curtis is willing to argue that these four different groups of Koreans – Korean farmers, Korean monks, and two groups of Korean soldiers – all had different genetics somehow, it’s going to be tough for him to maintain that we have genetically preset cholesterol concentrations.
Slide 8 Note that the populations with the lowest cholesterol numbers were eating high-carbohydrate, low-fat diets which were very low in animal products.
Slide 9 The famous Seven Countries Study of Ancel Keys made explicit the contrasting cholesterol levels in different populations around the world. He found that the more saturated fat people ate, the higher their cholesterol was and the younger they died of heart disease.
Slide 10 Mann, George V., et al. "Cardiovascular disease in African Pygmies: a survey of the health status, serum lipids and diet of Pygmies in Congo." Journal of Chronic Diseases 15.4 (1962): 341-371.
Diet-heart critic George Mann, whom I mentioned in the first video of this set, found that hunter-gatherer populations had remarkably low cholesterol levels. I have argued that our ancient ancestors likely had much lower cholesterol levels than ours, and that this gives us a good reason try to bring ours down as much as we can. If you think evolution can tell us anything about what the normal cholesterol homeostasis for our species looks like, then you’ll have to conclude that very low cholesterol is actually normal cholesterol.
Slide 11 http://www.plantpositive.com/27-ancestral-cholesterol-1/
I’ve covered this topic in depth in these two videos called “Ancestral Cholesterol.” Watch them and you’ll learn why hunter-gatherers had such low cholesterol.
Slide 12 Thorogood, M., et al. "Plasma lipids and lipoprotein cholesterol concentrations in people with different diets in Britain." British medical journal (Clinical research ed.) 295.6594 (1987): 351.
Notice that cholesterol numbers tend to go up as meat consumption increases. Would Dr. Curtis argue that vegans have different genetics than vegetarians, who have different genetics than fish eaters, and they all have different genetics than meat eaters? As I said, he’s adopted a deeply ignorant opinion about this. Consider this table when you hear this comforting fiction from the Catalyst broadcast …
Slide 13 Demasi: “Dr. Sinatra says blaming cholesterol for causing plaques is like blaming firemen for causing fires, just because they're always at the scene.”
Sinatra: “Cholesterol is really not the villain. I mean, we need it to live. The problem is cholesterol is involved in a repair process. Look, cholesterol is found at the scene of the crime. It's not the perpetrator.”
Dr. Sinatra would make a very bad lawyer. Let’s think about his metaphor. Would you buy it if a defense attorney said, “Members of the jury, it’s true that my client is somehow always present at the scenes of these crimes. But he’s not the perpetrator! He’s just trying so damn hard to be helpful at crimes, he always ends up leaving his fingerprints at crime scenes!” Sorry, Dr. Sinatra, but the glove fits.
Slide 14 Thorogood, M., et al. "Plasma lipids and lipoprotein cholesterol concentrations in people with different diets in Britain." British medical journal (Clinical research ed.) 295.6594 (1987): 351.
Dr. Demasi, if you really believe that cholesterol is like a fireman putting out fires, then why do vegans have so much less of a problem with fires than meat eaters? What are these meat eaters doing besides eating meat that’s causing them to need so much repair, day after day, decade after decade? Cholesterol must do a pretty lousy job of repairing things if the problem never seems to get fixed!
Slide 15 http://www.nhlbi.nih.gov/health/health-topics/topics/atherosclerosis/
Plaques are filled with cholesterol. Which artery would you say is working better? Is the bottom picture your idea of good repair work?
Slide 16 Yudkin, John. "Sucrose and heart disease." Nutrition Today 4.1 (1969): 16-20.
Even top thought leaders of the low-carb and high-cholesterol world didn’t buy this crazy belief that there are no fats that raise cholesterol. John Yudkin, the guy Dr. Demasi portrayed as a hero for his belief in sugar’s effect on heart disease risk, knew that the quality of dietary fat affected cholesterol levels.
Slide 17 Taubes, Gary. Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health. New York: Anchor Books, 2008. Print.
One of her favorite cranks, Gary Taubes, has even written that saturated fats raise cholesterol. Here he said it in Good Calories, Bad Calories.
Slide 18 p.186. Taubes, Gary. Why We Get Fat and What to Do About It. New York: Alfred A. Knopf, 2011. Print.
Here he said it in Why We Get Fat. “Saturated fat raises total cholesterol and LDL cholesterol.” Is that not clear? Why would Taubes say such a thing?
Slide 19 Ahrens, Edward, et al. "The influence of dietary fats on serum-lipid levels in man." The Lancet 269.6976 (1957): 943-953.
He says that because as much as Taubes loves to make up his own version of nutrition science, even he won’t try to get away with denying this fact. Back in the 1950s it was clear that saturated fats like butter and coconut oil raise cholesterol.
Slide 20 p.82. Holtzman, Jordan L. Atherosclerosis and Oxidant Stress: A New Perspective. New York, NY: Springer, 2008. Google Books.
Textbooks will tell you this. It’s not a topic for serious debate.
Slide 21 Clarke, Robert, et al. "Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies." Bmj 314.7074 (1997): 112.
Why not? Because many experiments have been conducted under controlled conditions, and their results have been consistent. You’ll see in the next video that Dr. Demasi wishes to dispute whether saturated fat raises cholesterol by citing poorly executed studies of free-living people that weren’t designed to settle this question. Rigorous and controlled studies ended any debate about this many years ago.
Slide 22 Bronte-Stewart, B., et al. "Effects of feeding different fats on serum-cholesterol level." The Lancet 267.6922 (1956): 521-527.
As far back as 1956 researchers were conducting controlled trials to see how fats affected cholesterol. Here you see it was found that animal fats and eggs raise cholesterol levels. Even then it was suspected that saturated fats were to blame.
Slide 23 Phinney, S. D., et al. "The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation." Metabolism32.8 (1983): 757-768.
Here’s an example of a controlled study, conducted by a low-carb-promoting doctor, that exposed elite athletes to a diet that delivered extreme quantities of saturated fat and cholesterol. In only four weeks their blood cholesterol shot up dramatically. There was no genetically preset cholesterol level in these subjects.
Slide 24 Heller, Debra A., et al. "Genetic and environmental influences on serum lipid levels in twins." New England Journal of Medicine 328.16 (1993): 1150-1156.
Genetics do matter, of course, although it’s hard to say how much. This study of twins attempted to help us understand the nature-versus-nurture dynamic for cholesterol. My opinion is that this study couldn’t have answered the question since it was only conducted in Sweden, a relatively high-fat country. Mean cholesterol levels in this cohort were high, just as we’d expect.
Slide 25 Hayes, K. C., et al. "Saturated fatty acids and LDL receptor modulation in humans and monkeys." Prostaglandins, leukotrienes and essential fatty acids57.4 (1997): 411-418.
Studies have been conducted which have given us an idea of how saturated fats affect cholesterol levels, although mechanisms have not been well understood. It was observed that they appear to induce the liver to secrete more apo-B-containing lipoproteins.
Slide 26 Lin, Jiandie, et al. "Hyperlipidemic effects of dietary saturated fats mediated through PGC-1β coactivation of SREBP." Cell 120.2 (2005): 261-273.
They also induce the production of fats and cholesterol by liver cells.
Slide 27 Mustad, V. A., et al. "Reducing saturated fat intake is associated with increased levels of LDL receptors on mononuclear cells in healthy men and women." Journal of lipid research 38.3 (1997): 459-468.
Saturated fats also appear to downregulate the production of LDL receptors relative to other fats.
Slide 28 Mendelson, M., et al. "Impact of Maternal Pre-Pregnancy Dyslipidemia Exposure on Adult Offspring Lipid Levels." Canadian Journal of Cardiology 29.10 (2013): S144-S144.
Dr. Curtis should understand that the effects of saturated fat consumption may not be limited to just the person putting them in her mouth. If she also happens to be pregnant, her child may at a far greater risk of having abnormal cholesterol metabolism, according to the early release of this abstract. It’s possible that children will be harmed by Catalyst’s irresponsible program. You’re looking at a finding from research on the citizens of Framingham, the same ones mentioned by Dr. Demasi in this show.
I’ll next talk about her list of unconvincing studies that she thinks tell us that saturated fats in the diet don’t affect cholesterol. But first, Dr. Curtis expressed another piece of nonsense that I can’t allow to go unanswered.
Slide 29 Curis: “… And veins don't develop atherosclerosis – unless you put them in a situation where they have to function as arteries.”
I’ve talked about his oddball argument in a past video. I realize it doesn’t sound like he’s saying much about cholesterol with that comment.
Slide 30 p.21. Curtis, Ernest. The Cholesterol Delusion. Dog Ear Publishing, 2010. Google Books.
Here he is in his book explaining his belief a bit better. He thinks that since cholesterol is present throughout the circulatory system, if it were so guilty of causing plaques, then plaques would be found equally everywhere. But plaques form at common points of stress. Realize all he’s saying is he doesn’t understand how high cholesterol promotes plaques. He’s not making an actual argument on the subject. He’s just saying, “This is my working model of heart disease that I carry around in my head, and high cholesterol doesn’t fit that model.” But in science, you don’t get to say, “This observation that high cholesterol promotes heart disease does not conform to my model of reality. Therefore, this observation can’t be real.” In science you observe nature and if nature doesn’t conform your model of reality, then it’s your job to learn more so you can update your model.”
Slide 31 The idea that high cholesterol contributes to heart disease and the idea that plaques form at particular areas of shear stress are not mutually exclusive ideas. His observation is an old one and it in no way raises doubts about the lipid hypothesis. Unfortunately, Dr. Curtis thinks that this imaginary contradiction he’s latched onto is a substitute for actually studying the issue, which is technical in nature and about which scientists have conducted research. Here’s a paper that explains how the dual phenomena of shear stress and high cholesterol promote atherosclerosis together. I found this paper quite easily by searching with what I knew to be relevant terms. It was easy. Dr. Curtis didn’t bother to do that, yet he’s put out a book that he thinks is worth your hard-earned money. He doesn’t seem to have studied this much at all.
Slide 32 Reis, Ernane D., et al. "Dramatic remodeling of advanced atherosclerotic plaques of the apolipoprotein E–deficient mouse in a novel transplantation model." Journal of vascular surgery 34.3 (2001): 541-547.
His comment that veins don’t form plaques unless you surgically place them as arteries in places where plaques usually form does remind me of one very interesting study. Follow me here. A mouse was given diseased arteries by feeding it a high-fat, high-cholesterol diet. The researchers took out a section of an artery from that mouse and put it into another mouse that had been eating normal chow, so this mouse had low cholesterol. The cholesterol-filled lesion in the artery went away once it was in the low-fat mouse. In the absence of high blood cholesterol, the artery healed itself. This experiment tells us more about the formation of plaques than Curtis’s point about the stress on arteries, which cannot be avoided as long as you have a strong working heart pumping inside you.
Early in this video you saw Dr. Demasi’s list of studies she thinks tell us something about saturated fat’s effect on cholesterol. We’ll look at that list closely in the next video.