The Drivers of the Herd, Part 5
Catalyst Corrected 5, Dr. Demasi’s Extensive Review
Slide 3 In this video we’re still dealing with Catalyst’s message number 2 about diet-heart. Saturated fat doesn’t raise your cholesterol according to Dr. Demasi. Here’s a reminder of the claim she put forth.
Slide 4 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.”
Slide 5 Here’s that list of studies again. She called them “long-term studies” but many weren’t, and none of them really support her assertion that saturated fat doesn’t raise cholesterol. Let’s look at each one. The first study on her list is The Bogalusa Heart Study.
Slide 6 http://tulane.edu/som/cardiohealth/
I have to say, this was a very strange choice of studies for someone with her point of view. The Bogalusa Heart Study focused on children and how heart disease develops in them as they age.
Slide 7 Frank, G. C., G. S. Berenson, and L. S. Webber. "Dietary studies and the relationship of diet to cardiovascular disease risk factor variables in 10-year-old children--The Bogalusa Heart Study." The American journal of clinical nutrition31.2 (1978): 328-340.
The paper Dr. Demasi likely has in mind is this one, in which it is stated that no correlations were observed between dietary components and serum cholesterol.
Slide 8 But that’s not quite the whole story. The authors reshuffled their data, grouping the kids according to their cholesterol levels.
Slide 9 This analysis revealed that the children with the highest cholesterol had the highest fat intakes. There you can see the researchers said as much in plain English.
Slide 10 And there they say it with numbers. The group with the lowest cholesterol ate much less animal fat. So it’s not quite right to say that this study didn’t show a relationship between fat and cholesterol. Nevertheless, this study didn’t provide especially strong support for the connection between saturated fat and cholesterol. Why not?
Slide 11 Look at this slide again. The average age of the kids was only 10.5. The kids provided the data for the study in the form of a 24-hour diet recall. We’ll see in another video in this playlist that people don’t necessarily report their diets accurately in these situations. There’s no reason to think little children would be especially accurate when remembering what they ate the previous day.
Slide 12 There is evidence of problems with their interviews. According to the reporting of these kids, many of them were consuming less than two-thirds of the calories they should have been eating. It’s terrible to imagine so many kids going hungry back then. But I couldn’t verify that that was the case. It seems more likely to me that some of them just underreported their food intake.
Slide 13 Frank, G. C., et al. "Effect of interviewer recording practices on nutrient intake--Bogalusa Heart Study." Journal of the American Dietetic Association 84.12 (1984): 1432.
A later study backs up my hunch. Children in the same community reported their dietary intakes using the same methods as the other study but this time they were asked to recall the same information to two different interviewers. Some pretty big discrepancies were noticed, including in reported meat consumption, which is usually loaded with saturated fat. The interviewers may have been inconsistent, but it’s more likely the kids just changed their stories.
Slide 14 Frank, G. C., G. S. Berenson, and L. S. Webber. "Dietary studies and the relationship of diet to cardiovascular disease risk factor variables in 10-year-old children--The Bogalusa Heart Study." The American journal of clinical nutrition31.2 (1978): 328-340.
Here’s another issue. The kids who were asked about their diets were only a small fraction of those who had their cholesterol measured. It’s entirely possible that the kids they selected were not quite representative of all the rest.
Slide 15 Another problem here was that the mean intake of hydrogenated fat was 8 grams per day.
Slide 16 p. 58. Institute of Medicine (US). Panel on Macronutrients, and Institute of Medicine (US). Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein, and amino acids. Vol. 1. Natl Academy Pr, 2005.
Just like saturated fats, trans fats will raise your total and LDL cholesterol. I hope you knew that already. This is part of the reason they are so bad for us. As far as I can tell, it looks like this paper we’re discussing from Bogalusa counted those trans fats as unsaturated fats. There is no indication to the contrary. That would have made it harder for the researchers to tell how saturated fats were affecting the cholesterol levels of these kids. Unfortunately, as that number for trans fats would imply, those kids were consuming very bad diets, with more of the carbs in their diets coming from sugar than from starch, more protein coming from animal rather than vegetable sources, and hardly any dietary fiber in the mix at all.
Slide 17 Then consider that the diets of these kids didn’t vary all that much. The dietary cholesterol intakes were mostly within a narrow range.
Slide 18 p.60 Bickman, Leonard, and Debra J. Rog. The Sage Handbook of Applied Social Research Methods. Los Angeles: SAGE, 2009. Google Books.
Recall that it is vitally important that contrast be created for effects to be detectable.
Slide 19 http://www.plantpositive.com/24-cholesterol-confusion-7-the/
This observation leads us to the most fundamental problem with this study. They looked at just one population at just one point in time, and that population didn’t have very much variety in their diets. I’ve made a video about why this is not the right approach if you want to understand diet-heart. You’ll see that Dr. Demasi chose other studies that had these deficiencies, too.
Slide 20 Frank, G. C., et al. "Dietary studies of rural school children in a cardiovascular survey." Journal of the American Dietetic Association 71.1 (1977): 31.
In another paper from Bogalusa by some of the same authors, they acknowledged the weaknesses of their methods directly. The people who wrote this paper would never have used this information to argue that saturated fat doesn’t raise your cholesterol the way Maryanne Demasi has. But then they didn’t have the agenda she apparently does.
I don’t think it was especially smart of Dr. Demasi to put Bogalusa first on her list. Other papers have come out of this study that demonstrate the weaknesses of her arguments.
Slide 21 Tracy, Richard E., et al. "Histologic features of atherosclerosis and hypertension from autopsies of young individuals in a defined geographic population: the Bogalusa Heart Study." Atherosclerosis 116.2 (1995): 163-179.
For example, here is a paper from Bogalusa that reported the results of autopsies of young people who were participants in the study. The results were somewhat equivocal, but you can see that serum cholesterol levels were found to correlate to the earliest stages of atherosclerosis.
Slide 22 Tracy, Richard E., et al. "Risk factors and atherosclerosis in youth autopsy findings of the Bogalusa Heart Study." The American journal of the medical sciences 310.6 (1995): S42.
This one was similar. Early heart disease was strongly related to both total and LDL cholesterol concentrations. “Aortic fatty streaks were strongly related to both total and low-density lipoprotein cholesterol.” That’s the reality she doesn’t want you to understand.
Slide 23 Nicklas, T. A, et al. "Dietary factors relate to cardiovascular risk factors in early life. Bogalusa Heart Study." Arteriosclerosis, Thrombosis, and Vascular Biology8.2 (1988): 193-199.
Here’s another paper from Bogalusa that considered diet. The kids who ate more cholesterol had higher serum cholesterol. That’s interesting enough, if not unexpected. Notice also that the kids who ate more animal fat were fatter, too.
Slide 24 Berenson, Gerald S., and Sathanur Srinivasan. "Cholesterol as a risk factor for early atherosclerosis: the Bogalusa Heart Study." Progress in Pediatric cardiology 17.2 (2003): 113-122.
And here is a graph from a study showing the progression of plaques in the aorta in relation to LDL cholesterol, also from the Bogalusa study. So as you can see, the Bogalusa Heart Study supports the lipid hypothesis just fine.
Slide 25 The next study on her list is from Tecumseh, MI.
Slide 26 Nichols, Allen B., et al. "Daily nutritional intake and serum lipid levels. The Tecumseh study." The American journal of clinical nutrition 29.12 (1976): 1384-1392.
I’ve talked about this one already in a past video so I’ll keep this brief. Again, we have a homogeneous population that gave dietary information based on recall, and again we see that cholesterol levels didn’t correspond to that information.
Slide 27 But again we see that the authors understood that their study couldn’t be used to dispute diet-heart. Dr. Demasi says otherwise but these authors probably understood their own study a bit better than she does.
Slide 28 Epstein, Frederick H. "Predicting coronary heart disease." JAMA: The Journal of the American Medical Association 201.11 (1967): 795-800.
Take note that the men in Tecumseh who had high cholesterol along with hypertension and poor glucose tolerance were at far greater risk of clinically recognizable heart disease than their peers. High cholesterol was a risk factor in Tecumseh, too.
Slide 29 Next up is Evans County, GA and I’ve discussed this one in an earlier video as well.
Slide 30 Stulb, Sarah C., et al. "The relationship of nutrient intake and exercise to serum cholesterol levels in white males in Evans County, Georgia." The American Journal of Clinical Nutrition 16.2 (1965): 238-242.
This was another look at a population lacking in diversity, and a very small one at that: only 52 men, far too few to be statistically meaningful.
Slide 31 Here again, the authors understood this weakness in their study. Their methods weren’t clear here. For example, there is no way to tell what the ranges of intakes of nutrients were. Was there anyone at all eating a low-fat diet? Probably not.
Slide 32 All we know is that they grouped the men into a half with higher cholesterol and a half with lower cholesterol and then they told us what they ate on average by season. For all appearances, everyone ate pretty much the same amount of animal fat and animal protein. There’s nothing in this paper that indicates otherwise.
Slide 33 Cox, Charlotte, et al. "Individual variation in plasma cholesterol response to dietary saturated fat." BMJ 311.7015 (1995): 1260-1264.
If everyone was eating the same way, then the variation in cholesterol would be explainable by genetics or overall health. You can’t have diet determine the variation because there’s hardly any variation in the diet.
Slide 34 Stulb, Sarah C., et al. "The relationship of nutrient intake and exercise to serum cholesterol levels in white males in Evans County, Georgia." The American Journal of Clinical Nutrition 16.2 (1965): 238-242.
Again, this is all we see. There is no way to know anything beyond this. Let’s just say a low-fat diet was not likely among these white men in the Deep South in the 1960s.
Slide 35 These men were only matched by age and cholesterol. Were some fat and others thin? Did some have cancer or other chronic diseases that might affect their cholesterol? Again, we don’t know. That’s how flimsy their methods were. Dr. Demasi should know that this paper can’t speak to diet-heart the way a controlled experiment in a metabolic ward can.
Slide 36 You see that the next on her list is the Israel Ischemic Heart Study. Again, this doesn’t support her views.
Slide 37 Kahn, H. A., et al. "Serum cholesterol: its distribution and association with dietary and other variables in a survey of 10,000 men." Israel journal of medical sciences 5.6 (1969): 1117.
Here we see that the authors said nothing in the diet was found to relate to cholesterol levels. This time the population was not homogeneous. This was a culturally diverse and large cohort, which makes this one a big improvement over the previous studies on Demasi’s list.
Slide 38 Keys, Ancel. "Diet and blood cholesterol in population surveys--lessons from analysis of the data from a major survey in Israel." The American journal of clinical nutrition 48.5 (1988): 1161-1165.
It is likely this null finding was a consequence of problems with their methods. Ancel Keys found fault with their work, and the authors apparently never responded to his critique. He noted that their cholesterol levels did relate to the characteristic diets of the home countries of the men, if not the information they gave in short interviews. Keys made a good point, but his observation leads us to a more important finding in this group.
Slide 39 Goldbourt, Uri, Shlomit Yaari, and Jack H. Medalie. "Factors predictive of long-term coronary heart disease mortality among 10,059 male Israeli civil servants and municipal employees." Cardiology 82.2-3 (1993): 100-121.
Follow these next few slides closely. Another team of researchers looked at the same population. Look at the middle right. “… A curvilinear increase in fatal CHD risk with increasing total cholesterol was observed.” So here we see that the men in this group with higher cholesterol were more likely to die of heart disease. This is an important finding that undermines Demasi’s claims. Now look at the next sentence I’ve isolated for you. It says that deaths from coronary heart disease associated well with the consumption of saturated fat. This is the lipid hypothesis in a nutshell. The more saturated fat you eat, the higher your cholesterol and the greater your chance of dying from heart disease.
Slide 40 Goldbourt, U., S. Yaari, and J. H. Medalie. "Factors predictive of long-term coronary heart disease mortality among 10,059 male Israeli civil servants and municipal employees. A 23-year mortality follow-up in the Israeli Ischemic Heart Disease Study." Cardiology 82.2-3 (1993): 100.
Look here at what other patterns these researchers found in this data. The men who had the most heart attacks were from Central and Eastern Europe. The men who had the fewest signs of heart disease were from the Middle East and North Africa. Got that?
Slide 41 Kahn, H. A., et al. "Serum cholesterol: its distribution and association with dietary and other variables in a survey of 10,000 men." Israel journal of medical sciences 5.6 (1969): 1117.
Now look at the table provided in the other paper. The men in Central and Eastern Europe, the ones with the most heart attacks, ate the most saturated fat. The men from the Middle East and Africa, the two columns to the right, consumed the least. They had the fewest signs of heart disease. You see now that the Israel Ischemic Heart Study actually supports the lipid hypothesis. I doubt Dr. Demasi noticed this.
Slide 42 The fifth one down her list is the Health Professionals Follow-Up Study.
Slide 43 Now remember what her claim is about these studies. She says that these are studies that refute the idea that saturated fat raises cholesterol.
Slide 44 Ascherio, Alberto, et al. "Dietary fat and risk of coronary heart disease in men: cohort follow up study in the United States." BMJ: British Medical Journal313.7049 (1996): 84.
I’m guessing this is the paper she means but it doesn’t help her case. Both saturated fat intake and cholesterol were directly related to the risk of coronary heart disease.
Slide 45 Here you see that saturated fat and dietary cholesterol associated with heart disease, along with trans fats. Those are not helpful findings for Demasi. Now they did say these associations were minimized when they adjusted for fiber. But that’s not the right way to look at the issue. If adjusting for fiber makes trans fats look less bad, and you know trans fats are bad for your heart, then adjusting for fiber might not be the right way to understand what’s happening with trans fats. The same could be said here of saturated fat.
Slide 46 Here they say it again. Before adjusting for fiber, dietary cholesterol and saturated fat were associated with an increased risk of death from heart disease.
Slide 47 p.367. Institute of Medicine (US). Panel on Macronutrients, and Institute of Medicine (US). Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein, and amino acids. Vol. 1. Natl Academy Pr, 2005.
The problem arises from the fact that some types of fiber will lower your cholesterol. Since the main way that saturated fat harms your heart is through its effect on cholesterol, if you were to eat a lot of the right types of fiber you’d reduce the effect that saturated fat has on you. The point is that adding fiber into the analysis actually tells you less about the effects of saturated fat, and we’re discussing the effects of saturated fat in this video.
Slide 48 This paper includes lots of interesting tables. Here’s just a sample of one which addresses what we’re discussing. You can see very clearly that saturated fat consumption and the risk of a heart attack increased together. Once again, this is the reality that Dr. Demasi wants you to doubt.
Slide 49 This study had one other serious defect. They excluded from their analysis the men who they thought had hypercholesterolemia. How high did cholesterol have to be for someone to be excluded? The paper doesn’t say.
Slide 50 Vega, Gloria Lena, and Scott M. Grundy. "Mechanisms of primary hypercholesterolemia in humans." American Heart Journal 113.2 (1987): 493-502.
So I looked up how hypercholesterolemia was defined around that time. Here you see that a year after the Health Professionals Follow-Up Study started, hypercholesterolemia was defined as cholesterol over 250 mg/dL. While I agree that that is very high cholesterol, that wouldn’t have been such an unusual number for American men back then.
Slide 51 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.
For example, do you remember that twins study I mentioned in the previous video? Well the average cholesterol levels in some of their categories were into the hypercholesterolemic range by that standard. Again, we see something in their methodology that will end up giving us less of the information we want, not more. The men with high cholesterol were precisely the men upon whom we should be focused. Were they eating the most saturated fat? We can’t know the answer.
Slide 52 Ascherio, Alberto, et al. "Dietary fat and risk of coronary heart disease in men: cohort follow up study in the United States." BMJ: British Medical Journal313.7049 (1996): 84.
Regardless of all that, the bottom line is that this study showed us that saturated fat and dietary cholesterol were linked to deaths from heart disease. That was not the message of this show by Catalyst.
Slide 53 After the Health Professionals study comes Western Electric.
Slide 54 Shekelle, Richard B., et al. "Diet, serum cholesterol, and death from coronary heart disease: the Western Electric Study." New England Journal of Medicine304.2 (1981): 65-70.
If Dr. Demasi wants to argue that saturated fat doesn’t affect cholesterol levels, she picked the wrong study to bring to our attention. Quoting here: “Further analysis demonstrated that serum cholesterol concentrations varied positively with dietary saturated fatty acids and cholesterol …” What must I say beyond that? She’s just wrong.
Slide 55 Paul, Oglesby, et al. "A longitudinal study of coronary heart disease."Circulation 28.1 (1963): 20-31.
But that isn’t the Western Electric paper she has in mind. The spin doctors for fatty foods like Gary Taubes usually refer to this earlier paper from Western Electric. Please take note, the following is a correction of my previous commentary about this paper. You’ll notice I make note of my errors on my website. Now let’s see what we have here. We are told that the researchers found that more new cases of apparent heart disease occurred in the lower fat group.
Slide 56 Lower fat here refers to the 15% of men consuming the least fat. They are being compared to the 15% of men who ate the most fat. But you see that when they compared them they completely left out their average ages. This omission alone makes this comparison worthless. How do we know the men in the low-fat group weren’t just older? How do we know more of them weren’t smokers? How do we know that more of them didn’t have high blood pressure. We don’t. This is ridiculous! This comparison can’t tell us anything. It’s the same problem we saw in the Evans County study.
Slide 57 Use some common sense here, folks. These were factory workers in Chicago around 1960. You wouldn’t expect that many of them were eating healthy low-fat diets back then. They were probably all eating terribly. On average they all had high cholesterol. Two more died in one group than the other after four years and we aren’t given enough information to know why. This isn’t impressive evidence.
Slide 58 Most studies based off of self-reported food intakes deserve some skepticism but this may have been almost as flawed as the one from Bogalusa with the little kids reporting their diets. Here the study says that many men “conceded that they were embarrassed to list … all that they really had consumed.” So along with the usual issues of dealing with a single population with minimal variation in their diets, now we have to consider whether the participants were too embarrassed to be honest with the researchers? Why would we regard this as good data? Again, this was not a study that was likely to tell us a whole lot.
Slide 59 Black, Alison E., and Timothy J. Cole. "Biased over-or under-reporting is characteristic of individuals whether over time or by different assessment methods." Journal of the American Dietetic Association 101.1 (2001): 70-80.
Here’s a quick reference if you need it that people don’t necessarily give accurate accounts of what they eat in studies like this.
Slide 60 Regardless of all that, this study did find “a definite relationship … between higher blood cholesterol levels … and subsequent incidence of clinical coronary disease.” This is the accurate information that tells us what really was going on there. Their cholesterol data were better than their dietary data because cholesterol levels are not subject to embarrassment. The men couldn’t self-report their cholesterol levels. Again, the lipid hypothesis is affirmed.
Slide 61 Shekelle, Richard B., et al. "Diet, serum cholesterol, and death from coronary heart disease: the Western Electric Study." New England Journal of Medicine304.2 (1981): 65-70.
A longer time interval with the same population found that saturated fat and dietary cholesterol were related to blood cholesterol and those were related to death from coronary disease.
Slide 62 Paul, Oglesby, et al. "A longitudinal study of coronary heart disease."Circulation 28.1 (1963): 20-31.
Please note that the first paper from the Western Electric study also didn’t find a difference in blood sugar levels between those with and without coronary disease. Of course, diabetes is a serious risk factor for heart disease. This was not a perfect study.
Slide 63 Paul, Oglesby, et al. "Sucrose intake and coronary heart-disease." The Lancet. 292.7577 (1968): 1049-1051.
By the way, do you remember how that Catalyst show made it seem dietary sugar was the real cause of heart disease? Well, the Western Electric study didn’t show any connection at all between sugar and heart disease. At the bottom you can see they said that they couldn’t back up John Yudkin with their data. Demasi probably didn’t notice that, either.
Slide 64 At last we have reached the Japanese Living in Hawaii. Let’s look at this.
Slide 65 Yano, K., et al. "Dietary intake and the risk of coronary heart disease in Japanese men living in Hawaii." The American journal of clinical nutrition 31.7 (1978): 1270-1279.
No dietary variables were found to relate to the risk of heart disease. That would include saturated fat. However, serum cholesterol was an important risk factor for heart disease in this population anyway. Again, that wasn’t Demasi’s message with this show. If I’m correct that this is the paper she has in mind, I don’t see where this speaks directly to her claim that saturated fat was shown to be unrelated to blood cholesterol. I suppose you could infer that since cholesterol was related to heart disease …
Slide 66 And saturated fat was not. That’s my best guess at what she’s thinking. On the left you see that those without clear heart disease after six years ate a bit more saturated fat than those who did suffer heart disease. That’s unexpected and that’s why this study is often mentioned by the saturated fat apologists.
Slide 67 But you can see that the same could be said of simple carbs, which would include sugars, for two of their categories of heart disease. People who ate less simple carbs were more likely to have heart attacks or die of heart disease, as you can see in the second category from the left. So based on this will you conclude that sugar protects against heart attacks?
Slide 68 Demasi apparently missed the line where they said that among those who either had heart attacks or died of heart disease, there was a greater consumption of saturated fat when considered as a proportion of their diets and not in terms of absolute amounts. This wasn’t a big difference but it does take away the possibility of someone saying that saturated fats appeared protective in this study
Slide 69 In explaining their weak findings they appropriately quoted Ancel Keys, who spoke about the difficulty of finding meaningful correlations within populations, as opposed to between contrasting populations. I’m glad Demasi listed this one last because this study allows me to make that important point.
Slide 70 Curb, David. "PROCOR: 1/10/00: The NI-HON-SAN STUDY & Honolulu Heart Program." Procor Global Dialogue. procor.org/, 10 Jan. 2000. Web. 31 Dec. 2013. <http://www.procor.org/globaldialogue/globaldialogue_show.htm?doc_id=722308>.
The cohort that was observed in that study was in the Honolulu Heart Program, and the Honolulu Heart Program was a part of a larger study called the Ni-Hon-San Study. The idea was that it would be more informative to study populations with similar genetics that lived in different places following different lifestyles. This way the contrasts in diet and other factors would be greater, allowing for more meaningful comparisons. They looked at men of Japanese ancestry living in Japan, Hawaii, and California.
Slide 71 p.33. Carson, Jo A. S, Frances M. Burke, and Lisa Hark. Cardiovascular Nutrition: Disease Management and Prevention. Chicago, Ill: American Dietetic Association, 2004. Google Books.
You’ll see that the Ni-Hon-San study is usually cited as great evidence of the lipid hypothesis. It demonstrated that where people eat more saturated fat their cholesterol is higher and they die younger from heart disease.
Slide 72 Marmot, M. G., et al. "Epidemiologic studies of coronary heart disease and stroke in Japanese men living in Japan, Hawaii and California: prevalence of coronary and hypertensive heart disease and associated risk factors." American Journal of Epidemiology 102.6 (1975): 514-525.
Here is one of the well-known graphs that came out of Ni-Hon-San. You can see for yourself how much of an effect cholesterol had on the risk of heart disease. By looking at contrasting populations the consequences of bad diet become much more apparent. Don’t let the games of Demasi and her collection of quacks cause you to ignore this information.
Slide 73 That should cover all of Catalyst’s messages except for the last one. You know enough by now to doubt this one but there is much more that must be said. See you in the next video.