Nina Tei¢holz, Shai'ster ~ Part II: Applicability of RCTs to the General Population

Part I: Discussed the reporting and makeup of the study diets in Shai  Bottom line, if intake reports are to be believed, the "high fat" group in this study DEcreased absolute fat intake by a few grams to 70% of baseline intake depending on the reporting used.

The study:   Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet

Nina Teicholz on Nightline, link to full story

Will the Real Applicable Clinical Trial Please Stand Up!

In this installment I am going to discuss how Nina Teicholz couches the Shai study and then dismisses another study for reasons that apply equally, if not moreso, to her favored example.  Keep in mind that both in The Big Fat Surprise, and in her media blitz promoting the book, Teicholz makes reference to Keys' bad science contrasted by the definitive, conclusive, rigorously controlled clinical studies from the past decade.

These studieS, boil down mostly to one:  Shai.  In Chapter 7 (of 10, they're mercifully short despite the length of the "book") entitled Selling the Mediterranean Diet:  What is the Science?, after pictures of Keys and other famous luminaries associated with the diet, and after being introduced to Big Olive, in a section entitled A Test of the Real Mediterranean Diet, Teicholz introduces us to Shai:
The first such trial [of the Mediterranean diet], in 2008, was conducted in Israel. It was well designed and rigorous, with an international group of professors on board, including the epidemiologist Meir Stampfer of the Harvard School of Public Health. These researchers selected 322 moderately obese middle-aged people, mostly men, and fed them one of three diets: one low in carbohydrates, one low in fat, and the third, Mediterranean. XXVIII Specially prepared meals were served at a workplace cafeteria, allowing for a high degree of control over what and how much foods were eaten. And the experiment lasted two years, a long time for a trial that involves overseeing the preparation and service of food.   {3652}
** all numbers in {} are the starting Kindle location out of 12033 total, this should give those with hard copies a general idea to where they can find these quotes in a hard copy.
The Roman numerals there are Teicholz's footnotes.  These sometimes link to additional information that would not flow in the text, but tucked at the end of the chapter, they are quite often used to "hide information in plain sight".  By that I mean that many reading a physical book will not leaf to the end of the chapter to see what's up, and by the time they get there forget what the footnote pertained to anyway.   Here, XXVIII informs the reader that the Mediterranean diet is Willett's interpretation.  This is important because she sets this up as a test of the "real" Mediterranean diet and this is a point of contention in nutritional circles.  After the above paragraph, Teicholz goes on to describe the 2013 PREDIMED study.  Teicholz apparently donned her Holmes hat and grabbed her magnifying glass with that study, reading every last word of the appendix (or so the impression is given).   It would appear that she did not do the same diligence with Shai.  But the crux of this section of the book comes in the next paragraph:
If the Israeli trial had never existed, everyone could have assumed that the Mediterranean option in PREDIMED was the best possible regime for health. But that third, low-carb arm in Israel had revealed that an even better option was possible. (Previous shorter trials had found the same thing, as we will see in Chapter 10.)XXXI       {3687}
Now here is a prime example of Teicholz hiding information in plain site.  Read the short paragraph above again, please, and tell me there's any inkling there that another two-year study on the Mediterranean diet even existed.  She only implies that there were shorter trials including low carb as an option.    Here's the footnote:
XXXI . There was one other long-term (two-year) trial comparing a low-fat to a Mediterranean diet, with results in 2004. It showed that the Mediterranean diet performed better. But the study involved men and women with metabolic syndrome, not a normal population, and could not be generalized (Esposito et al. 2004).  {3493}
First, I submit that this is the footnote that should have been placed at the end of the red bolded statement regarding the 2008 Shai study being the *first* long term trial of the Mediterranean diet.   But it's that blue bolded statement that prompted this post.

Devilish Details

As an aside here, the first paragraph is a prime example of how Teicholz weaves her overt bias into much of this book.   Prominent names and prestigious institutions are stressed often -- Harvard appears 52 times -- especially, as in this case, to give the appearance of gravitas or higher standards.  The Shai study was an international effort with a Harvard bigwig on board.  The Esposito study she dismisses?   A bunch of no names I guess.   It's also interesting what she leaves out or saves for (much) later, such as the partial funding of Shai by The Atkins Foundation.

The description of the control in this study will be the subject of my next installment as it contrasts wildly with how she describes the LA Veterans study that she maligns and outright mocks in various interviews.  Suffice it to say, that although the subjects in Shai only had access to their cafeteria at lunch time (during work days I might add), there is not even any indication that they were required to make appropriate selections, how much, etc.  These little "details" in how similar situations are described depending on whether the study supports or refutes Teicholz's views are quite telling throughout the book.

Representative Samples

In her footnote about Esposito, Teicholz inadvertently makes an excellent point.  I say inadvertently because, per what I just discussed, if she applied this standard equally to the Shai study (or for that matter her various fat-eating cultures), there'd be no book.  But it's an excellent point nonetheless, and it's one that should be discussed more when interpreting clinical nutritional research.

All clinical trials are done, necessarily, on samples drawn from the population.  It is important that the sample reflect the population in composition as closely as possible so that the results translate to inferences about that population.  All of these clinical trials do some initial screening so essentially these samples are not representative of the general population.  And that's OK ... it makes no sense to test the effect of an asthma medication on non-asthmatics for example.  But it's not OK to extrapolate the results of such studies to the general population without acknowledging these limitations.

With the obesity and diabetes epidemics in full bloom, a goodly portion of clinical nutrition trials are aimed at one or both of these populations in terms of potential management, treatment or prevention of the conditions.  But if a diet reduces HbA1c from diabetic levels down into non-diabetic levels and other health markers improve, this does not mean that this diet will have any impact on someone who is not diabetic to begin with.  Further, even if it has a similar effect in the non-diabetic, there is no indication that the result is even clinically meaningful.  I used HbA1c as an example because risk factors really "take off" at around the 8 mark, so that lowering HbA1c even one half of one percent from 8.5 to 8.0 is potentially meaningful.  That same reduction from 7.5 to 7.0 is much less so, and in the normal range from 5.5 to 5.0?  The inferences don't translate.   We so often hear that the dietary rules change for diabetics, which may or may not be as significant as claimed, but we don't often hear the admonition in reverse.  That is to say, what applies to diabetics does not necessarily apply to the majority that are not.

It's important to keep in mind the makeup of study groups when considering the implications of the results.   One knock against Big Pharma is that it used to test drugs predominantly in men -- either young healthy males or middle-aged sick men and seemingly nothing in between.  This is an important point (great strides have been made in this regard), let's apply it evenhandedly.

The Other Two-Year Mediterranean Diet RCT:

So let's take a look at this 2004 Esposito study that Teicholz dismisses because it "could not be generalized":  Effect of a Mediterranean-Style Diet on Endothelial Dysfunction and Markers of Vascular Inflammation in the Metabolic Syndrome. A Randomized Trial.  While this study was smaller over all, it only had two groups so at 90 vs. 104-9 per group in Shai it was roughly similar.   But more importantly, Esposito was conducted in a MORE generalizable (is that a word?!) sample than was Shai -- yet another of Teicholz' mounting "errors" in the book.   Here are the criteria for Esposito and Shai, (apologies, green = inclusions, red = exclusions):

[Esposito] involved men and women with metabolic syndrome, not a normal population, and could not be generalized.        ~Teicholz

In the table below I've provided relevant study subject characteristics.  I've noted the 5 inclusion criteria from Esposito in the Met Syn column, and the * denote disease or medications associated with biomarkers.

This is inexcusable.  Just inexcusable.   Firstly, the gender issue alone should be a red-flag as to the applicability of Shai to the general population.  The Esposito study came far closer to a 1:1 ratio, the Shai study at 82 to 91% male in each group?  Not even in the same ballpark!  This was a study in middle aged men, over a third of whom had CVD or diabetes and whom on average would qualify as having metabolic syndrome.  Further, in the 2009 Adherence report, we learn that women in Shai had a higher drop-out rate than the men, something I hope to address in a future installment.  But Shai specifically included those with active diabetes or heart disease regardless of age or weight status, and those currently taking medications to manage those diseases.  How can one possibly attribute any of the results to diet alone?  Further, Shai included smokers which  I'll address when I take up the LA Veterans study.

The Esposito study, which excluded those with active disease and/or anyone taking any medications that would alter biomarkers being assessed, was truly a test of impact of diet on those headed in the wrong direction from a metabolic health point of view.   Could the results be generalized?  Well, considering that Katie Couric tells us 95% of us will be in this boat or worse in another few decades, and what are the statistics on obesity and metabolic syndrome now?  

Dat Mediterranean Diet:

I've seen Willett's Mediterranean diet described as your standard low fat diet with olive oil poured on top.  The sample menu from Shai at right would make it appear somewhat so.  

How about the diet used in Esposito?
The dietary advice was tailored to each patient on the basis of 3-day food records. The recommended composition of the dietary regimen was as follows: carbohydrates, 50% to 60%; proteins, 15% to 20%; total fat, less than 30%; saturated fat, less than 10%; and cholesterol consumption, less than 300 mg per day. Moreover, patients were advised to consume at least 250 to 300 g of fruits, 125 to 150 g of vegetables, and 25 to 50 g of walnuts per day; in addition, they were also encouraged to consume 400 g of whole grains (legumes, rice, maize, and wheat) daily and to increase their consumption of olive oil.
I note that intake is still self reported, but the dietary recommendations were individualized for caloric intake and the reporting was a 3-day diary instead of a single 24 hour recall or FFQ.  We also get a little more information in the study of what they consumed in terms of foods encouraged by the dietary recommendations.  The few sample menus from Shai raise more questions than they do provide meaningful information.

Oops!  They included legumes with the whole grains in the recs, yet itemize them with fruits, veggies and nuts in the intake table.  We see that in this intervention, the subjects actually made what appear to be meaningful changes in their diet, more than doubling up on the FVN&L and the whole grains, and almost doubling olive oil consumption.   We also get some information on "complex carbs" that is absent from the reporting in Shai.  It is doubtful the Shai Med dieters followed a remotely similar diet to the one here as these Med dieters increased fiber by 18 g/day (vs. an increase of 1 gram per day in Shai).  There is also a fairly significant reduction in saturated fat intake of 5% total energy from 13 to 8%.  In Shai, there was an absolute reduction of 4g of saturated fat resulting in a 0.1% change from 9.7 to 9.6%.   Increases in MUFA are obscured by the change in MUFA:SaFA ratio reported in Shai ... it becomes more apparent with each further look into this study why the reporting is so ... shall we say ... cloudy.

I hope to revisit the Esposito study at some point to give it its full due.

Surprise or Disguise?

So now I ask you:  Which study was a better test of the Mediterranean diet?  Of the impact of lowering SaFA while raising MUFA?  Of increasing fiber?  Of these "complex" carbohydrates?  Of a high carbohydrate, low fat diet?  

Which study is the *real* test of the diet?

Which study is the more applicable to the general population of males and females for whom we are trying to recommend a healthy diet?

Teicholz, after dismissing Esposito as a study that "could not be generalized" goes on to say this in the final chapter of her book (which is basically propaganda for Atkins funded or affiliated researchers Eric Westman, Jeff Volek and Stephen Phinney and NuSI affiliated Gary Taubes and Ronald Krauss.) 
The one statement that seems safe to make is that the refined carbohydrates and sugars that we were recommended to eat by the AHA as part of a healthy, fat-avoiding diet , are not merely indifferent, “empty calories,” as we’ve long been told, but are actively bad for health in a variety of ways. XXV Moreover, the clinical trials [sic] in recent years imply that any kind of carbohydrate, including those in whole grains, fruits, and starchy vegetables, are also unhealthy in large amounts. Remember that the Shai study in Israel found that the Mediterranean diet group, eating a high proportion of calories as these “complex” carbohydrates, turned out to be less healthy and fatter than the group on the Atkins diet, although they were healthier than the low-fat alternative.    {5356}

Those statements (blue and red), folks, are outright lies.  Although I suppose by the definition of a lie, it might not be as Teicholz summarily dismissed Esposito as being remotely relevant.  So she could, I suppose, claim ignorance ... or scholarly incompetence as her mentor Gary Taubes is wont to do.

This book is such a joke.

More on Nina Teicholz and The Big Fat Surprise:


George said…
So what do you make of this?
charles grashow said…
" Although the author has
been supported by funds from Meat & Livestock Australia, Dairy
Australia, and the Beef Cooperative Research Centre in the past, no meat
or dairy industry body commissioned, funded or had any part in this
review. Any discussion of the role of animal food in human nutrition
these days needs a declaration of biases: the author was raised a strict
whole-food ovo-lacto vegetarian and occasionally relapses to that
state; this review is a response to the author’s question of his own
research, ‘Why are we trying to increase intramuscular fat if animal fat
is so bad for us?’"
George said…
Molecular geneticist with decades of published work on animal fat in situ has been inspired to create a labour of love, one which is full of interesting and useful lore. Addressed to the industry (and not apparently shared with the wider nutritional community at the time of publication by its author, who has no links to the usual suspects) it has ideological purity if that matters - which it shouldn't really.
George said…
So, the increases in total C, LDL on the LC diet were cancelled out by other benefits in the FRS analysis.
What do you prefer? Low TG and high LDL, or low TC and LDL?
For a group with MetSyn, where high TG, low HDL was the sign of that pathology?
charles grashow said…
William Barendse is a
senior principal research scientist at CSIRO Animal, Food and Health
Sciences and an adjunct Professor in the School of Veterinary Science,
the University of Queensland. Bill was born in Cape Town, South Africa,
came to Perth as a teenager, and finished a Bachelor’s Degree in Science
in the Zoology Department of the University of Western Australia. That
led to a PhD in the same department, in Genetics and Systematics of the
species Mygalopsis , with Mike Johnson. A Macquarie University
Fellowship followed, to study the human disorder pre-eclampsia with Des
Cooper, which introduced him to Molecular Genetics and Linkage Analysis.
That led to a position in Rockhampton with CSIRO Tropical Animal
Production to make a linkage map of the cow, in Jay Hetzel’s group. The
cow maps acted as the seed for the genome sequence and genetic history
of the cow, to which he contributed. He and his group have been involved
in the mapping of genes affecting production traits of cattle. These
include the Calpastatin gene for meat tenderness. Since 1994, he
has been studying marbling of beef and fatness of cattle, which has led
almost inexorably to this review.
charles grashow said…
From the article

" Organs and fat were generally preferred to lean meat by these hunter-gatherers who were well aware of the value of eating animal fat: the side effects of eating only lean meat have been replicated in the laboratory and they include diarrhoea and unsatisfied hunger (Stefansson 1912; McClellan and Du Bois 1930; Phinney 2004).During human evolution, how much fat was eaten on a daily or yearly basis is a matter for speculation, and would depend on a host of factors. Given the nausea limit in human responses to large amounts of fat (Man and Gildea 1932), one suspects as much fat as could be stomached. These ancestral patterns of food use do not prescribe any particular modern diet or lifestyle but they do show the likely human nutritional adaptations and responses to food, and point to the nutrients that need to be obtained from food (Cordain et al. 2005; Lindeberg 2009)."

Stefansson, Phinney & Cordain - all I need to know.
MacSmiley said…
Is this Willett's Mediterranean diet? 30% plant oils? Keys described greens with olive oil "sprinkled" on them. Doesn't sound like Willett's if this is what is meant.
Susanne said…
The traditional Greek village diet does contain a ridiculous amount of olive oil, from an American point of view. Although raw salad does get about a tablespoon of oil for 3-4 portions, cooked vegetables and legumes are swimming in it. It was kind of a shock for me and my fellow undergrads on my first archaeological project in the 1980s sitting down to the dinner table set for us by a local lady. One guy compared it to "drinking a bottle of Crisco" with every meal. (Use of olive oil was not yet really common in the states then, at least in our economic/social demographic.)

The calories from the oil (and cheese which is often served with the meal) make up for the fact that traditional meals are often vegetarian or vegan and so quite low-energy.

Compare for example this Greek recipe for a bean casserole. You can tell it's a Greek-style recipe because it recommends a cup of olive oil for a pound of dry beans, whereas Americanized versions tend to limit the oil to a few tablespoons, as I do when I make it:
Susanne said…
"[Esposito] involved men and women with metabolic syndrome, not a normal population, and could not be generalized."

Grabbing the first three Google results comes up with 31.2% prevalence of the metabolic syndrome in a random sampling of adults at medical centers in Lebanon (based on the International Diabetes Federation classification criteria).

In NHANES, the age-adjusted prevalence of MetS decreased from 25.5% 1999/2000) to 22.9% (2009/2010). The authors suggested this was due to increase in drug treatments, which means that number would be higher without treatment: "Decreases in elevated blood pressure, suboptimal triglycerides, and high-density lipoprotein-cholesterol prevalence have corresponded with increases in anti-hypertensive and lipid-modifying drugs, respectively."

It sounds to me like metabolic syndrome is becoming pretty freaking "normal." Maybe we should find a better word.
charles grashow said…
The calculator will not allow a TC of <130 so it's of no use to me.
charles grashow said…
More contradictions from the godfather Loren Cordain - will these EVER be addressed

"here’s another obscure paper because we’re no longer allowed to perform these experiments in primates in which we feed them atherosclerotic diets and try to induce an MI.

That means a heart attack. A Myocardial Infarction. An MI.

In 10 rhesus monkeys and two other monkeys, they were able to induce myocardial infarctions, and electrocardiographic abnormalities, unexpected and relative sudden death in these non human primates are also consistent with signs that are frequently observed in humans. This is an obscure paper that absolutely needs to be addressed by the unlimited saturated fat type groups."

Cordain also says
"Palmitic acid is atherogenic. And there’s not an experiment in humans or animals or tissue to show that it doesn’t down regulate the LDL receptor. This is a point that is never addressed in Gary Taubes’s book or Eric Westman’s articles, or Ron Krauss. You need to address thedown regulation of the LDL receptor. That controls the flux of oxidized LDL in and out of the intima.So on a molecular basis, you can’t deny this information."

" I think you can tend to eat a high saturated fat diet. A high animal food diet. You’re going to be at risk for osteoporosis, Vitamin A deficiency and some other factors, if you don’t eat some plants in your diet. Now if you eat liver, the Vitamin A is a non-issue. But if you only ate muscle meat and fat, then it’s not going to work.

If you eat organ meats like traditional people consumed then you’re going to be in pretty good shape. The osteoporosis does not clear out, and you can see that in these papers here.

If we believe the results of this pathology, that we have atherosclerosis in people who never consumed carbohydrate, always ate a high fat, high protein diet, this atherosclerosis who always consumed a high fat, high protein diet. Then the question comes up, did they ever suffer a fatal MI. My opinion is that they probably didn’t.

Even though they had hardening of the arteries, plaque, they might not have had the inflammatory conditions that cause heart attacks."

Bingo, there you go!

In that way, you and Steve Phinney might agree.

I’ve always stated that, and I’ve been misquoted so often on this saturated fat issue and atherosclerosis. The devil’s in the detail. So I believe these Inuit women who had never been exposed to Western Food did indeed have atherosclerosis."

SO - this diet will give you atherosclerosis (hardening of the arteries, plaque, etc.)
Nigel Kinbrum said…
VLC'ers will argue that sat fats cause atherosclerosis in studies only because the diets also contain carbohydrates.
Hello_I_Love_You said…
That's actually what Cordain has been saying recently, that the hypocaloric effect of LC/VLCing absolves it from atherogenesis.
Hello_I_Love_You said…
Yes, both Inuits and Masias had atherosclerosis. This was shown. But atherosclerosis is a precondition for MI. And these guys have been saying it's inflammation that instigates MI. But you need atherosclerosis do get to that stage. The Masais had significant atherosclersosis. George Mann found that though the circumferences of their main arteries were significantly higher, presumably as a result of their active lifestyle. So even if you had significant atherosclerosis, the cap event where a plaque would be disloged is less likely to happen. The same with stenosis, which would take significant more plaques to have the same effect in them. But can you say the same for Westerners who're couch potatoes or weekend warrirors on LC diets? How did Seth Roberts die? How did Robert Su and Neil Groves die? They all had significant atherosclerosis and at least 2 of them had a significant risk factor (hypertension) which they did not bother to take medication for. These are supposedly health gurus from whom Paleo and LC were taking their cues form. There should be some serious soul-searching after these deaths instead of more fat fest.
Nigel Kinbrum said…
Fred Hahn is saying that the results in Fig 1 of , also don't count, due to the carb content of the diet. How does one argue against that?
Hello_I_Love_You said…
You know why he staked out these positions before? He was trying hard to differentiate his diet from Atkins. In fact, the original edition of that Paleo Diet is devoted to bashing Atkins big time. He has since evolved but he's trying to preserve his credibility while not completely reversing his prior position. The new knowledge that he's quoting (particle size) is now passe. He knows where the weaknesses of the Paleo diet lie.
Hello_I_Love_You said…
I don't know what Hahn is saying but based on the results, I can understand why it's causing LC bellyaches. Fasting TG doesn't mean much, since it's a confounding and overlapping variable that correlates with HDL, CRP, insulin resistance, etc. However, post-prandial TG in the 2-4 hour window is significant. This TG is associated with coronary events and the strongest correlation is with ischemic stroke. Now, that's understandable because IS results from atherosclerosis-induced stenosis. So that explains the slightly lower correlation with MI, as MI is inflammation-driven for the cap event to happen.

If the results are to be believed, this is a rich study that destroys many LC myths. First, low fasting TG which many low-carbers are wont to cite as a badge of honor, isn't much of an indicator; you're essentially saying your HDL is high-normal, CRP low and lower on the IR spectrum. But the 2-4h PP TG is an independent risk factor for CVD. What kind of people would have high 2-4H PP TG? Those on a fat, especially SAFA, fest.

This study and the other one ("Postprandial triglyceride-rich lipoproteins promote invasion of human coronary artery smooth muscle cells in a fatty-acid manner through PI3k-Rac1-JNK signaling.") implies that a fatty meal is inordinately atherogenic. It doesn't matter whether your fasting TG is under 50 or even close to zero; the fasting level is dictated by caloric intake and a hypocaloric VLC diet would no doubt sink your TG like a stone. But it's all for naught.

And the TG/HDL ratio is a stupid measure, since TG captures already what HDL and other variables represent. What's unique and meaningful is the 2-4H PP TG; this one stands out like a sore thumb like Lp(a), which trumps all other CVD risk factors and act as a true independent variable. This also demonstrates why TC/HDL is more meaningful than TG/HDL.

Another low-carb myth is the dangerous impression it gives that VLCing will lower either your TC or TG and that's all that counts. We know that's not the case, as 1/4 to 1/3 see their LDL skyrocket over 200 and their TC over 300. LCers then saying not to be alarmed, your TG/HDL will save you. Nope. Then Jimmy Moore comes out of the woodwork and parades his 2 CAC test results (both zero) and say, "See, what did I tell you, hypercholesterolemia doesn't mean shit."

Actually, it does mean shit. Here's why. CAC only measures hardened plaque and the hardening is most pronounced in the over 55-60 age group, not in those who're around 40; the hard plaque detectable via CAC is very sensitive to age. But it will miss subclinical atherosclerosis, which could induce both MI and IS. You're not home-free with a zero CAC score.

Remember Fred Hahn's retort to this doc who urged Jimmy to get a CIMT? "Why doc - what would that reveal?" Fred, ignorance is bliss. In fact, that's probably how Seth Roberts died. His PP NF TG was probably elevated and his atherosclerosis was a lot worse than indicated by his 25-50 CAC score.
charles grashow said…
So the VLC'ers are basically betting their lives on keeping their markers of inflammation low regardless of LDL-C, LDL-P, etc.

Dr Thomas Dayspring
"“Let’s get rid of the nonsense seen all over the internet that atherosclerosis is an inflammatory disease, not a cholesterol disease. That is baloney-with the reality being that it is both. One cannot have atherosclerosis without sterols, predominantly cholesterol being in the artery wall: No cholesterol in arteries – no atherosclerosis. Plenty of folks have no systemic vascular inflammation and have atherosclerotic plaque. However clinicians have no test that measures cholesterol within the plaque – it is measured in the plasma. It is assumed, that if total or LDL-C or non-HDL-C levels are elevated the odds are good that some of that cholesterol will find its way into the arteries, and for sure there, are many studies correlating those measurements with CHD risk. Yet, we have lots of patients with very low TC and LDL-C who get horrific atherosclerosis. We now recognize that the cholesterol usually gains arterial entry as a passenger inside of an apoB-containing lipoprotein (the vast majority of which are LDLs) and the primary factor driving LDL entry into the artery is particle number (LDL-P), not particle cholesterol content (LDL-C). Because the core lipid content of each and every LDL differs (how many cholesterol molecules it traffics) it takes different numbers of LDLs to traffic a given number of cholesterol molecules: the more depleted an LDL is of cholesterol, the more particles (LDL-P) it will take to carry a given cholesterol mass (LDL-C). The usual causes of cholesterol depleted particles are that the particles are small or they are TG-rich and thus have less room to carry cholesterol molecules. Who has small LDLs or TG-rich LDL’s? – insulin resistant patients! After particle number endothelial integrity is certainly related to atherogenic particle entry: inflamed endothelia have inter-cellular gaps and express receptors that facilitate apoB-particle entry. So the worse scenario is to have both high apoB andan inflamed dysfunctional endothelium. Is it better to have no inflammation in the endothelium – of course! But make no mistake the driving force of atherogenesis is entry of apoB particles and that force is driven primarily by particle number not arterial wall inflammation.”
charles grashow said…
"Hello, this is Seth’s mother Justine. I’d like to offer what little information I have to try to answer some of the questions that were posted about Seth’s death. We’re told that we’ll get a full coroner’s report in about 6 months. In the meantime we were given only “Cause A: Occlusive coronary artery disease” and “Other significant conditions: cardiomegaly.”

Most of you won’t be surprised to learn that Seth had not visited his
doctor in Berkeley in many years, and, responding to a recent question,
said that he hadn’t been to a doctor during his stay in Beijing either.
We are left with 3 sets of paper records. The earliest, dated 2009,
reports a Coronary Calcium (Agatston score) screening which he discussed here last October. He obtained a second screening 1-1/2 year later. The first report showed his coronary artery occlusion to be about average for a man his age, with an accompanying risk of heart attack, but no cardiomegaly. The second report, following his conclusion that butter
was beneficial for him, and his heavy ingestion of it, showed an
improvement in his score: “Most people get about 25% worse each year. My second scan showed regression (= improvement). It was 40% better (less) than expected (a 25% increase).” The report showed the calcification to be unevenly distributed, with most found in his left main coronary artery, and none in all but one of the other arteries. Again, no heart enlargement was reported.

The second medical report set, done in December 2011, was from
Beijing and covered an exam that may have been required by his employer, Tsinghua University. This included a physical exam, an x-ray and EKG. All reports were negative, i.e., no abnormal findings and no cardiomegaly.

The third set of reports, from a laboratory in St. Charles, Ill., used data collected in Berkeley. They list toxic and essential elements in his hair. The latest report, dated July 18, 2013, showed one element rated “high.” This was mercury, “found to correlate with a 9% increase in AMI [acute myocardial infarction]” according to the report. His level was assumed to indicate exposure gained from eating fish. Presumably Beijing’s toxic smog contributed directly both to the mercury level of the fish that he ate there, and to the level in his hair.

The only information about his blood pressure was in the Beijing
report where it was recorded at 117/87. I could find no information
about cholesterol levels, though it has not been a familial problem. Of
the remaining Framingham Study risk factors: Seth did not smoke or have
diabetes. He was not overweight and was physically active. Seth’s father
died of a heart attack at 72."

SO - his plaque was INCREASING but at a slower rate than expected - "The report showed the calcification to be unevenly distributed, with most found in his left main coronary artery."

The nickname for the left main coronary artery is the widow maker.
charles grashow said…
Any proof for this cockamamie statement??
Hello_I_Love_You said…
No, I think the study below shows that if you eat high fat it could be atherogenic regardless of whether you're eating above or below your BMI. Post-prandial 2-4H trigs will be highly correlated with fat intake more so than carbs, I think, I'm not 100% sure. That's not the case obviously with fasting TG, which the LC camp has been pinning all its hope on. Looks like low fasting TG tells virtually nothing. And the TG/HDL is bunk.
Lighthouse Keeper said…
Barry Groves was a complete and utter nutter. Cause of shooting sprees in the U.S.? Fluoride in the water or the murderous gunmen were on prozac. Suicide? Too many carbs.
Nigel Kinbrum said…
Hahn still bangs on about how TG's are lower on a LCHF diet, as he either can't or won't grasp the difference between fasting & postprandial TG's. It's like trying to teach a pig to sing :-/
charles grashow said…
The TC/HDL ratio has never been applied in the context of VLC'ers and their diets.

For example, Jimmy Moore's last reported TC was 392 and his HDL was 70 giving a ration of 5.6. I've read that this ratio should be below 5.0, and a value that is less than 3.5 is considered ideal.
Hello_I_Love_You said…
That's the ratio with the highest predictive power based on years of Framingham research. But low-carbers won't embrace it because for 1/3 of them, it will be severely out of whack. That's why they fall back on the TG/HDL ratio, which is bunk, according to the article. But what does TC/HDL really tell?

Another way of measuring it would be just your non-HDL cholesterol, i.e., LDL + VLDL, being less than 71.5% of your TC. LDL is usually the biggest chunk of your TC but if it starts claiming higher and higher proportion of TC, you're in trouble. That usually happens when LDL starts moving above 150, 170, 190, etc. At those levels, I guarantee you, your HDL is not gonna be enough make TC/HDL under 3.5x. You can run marathons but HDL over 100 in men is pretty rare and is not known to be protective. At this level, you gotta control your SAFA, no ifs ands or butts.

The tragedy is this type of hypercholesterolemia is reactive so most low-carbers can control it by limiting SAFA but they won't because they've been told you can't get enough of SAFA.
Hello_I_Love_You said…
Hahn's LDL is ~180. He disclosed this to Jimmy. So his TC is probably around 250-300. His trigs might be low since he VLCs. But when you get to that level, I'm sorry, you need to watch your fat. I wouldn't be so worried if my TC was 200-250. But 250-300 is getting up there since it would be difficult to keep your TC/HDL under 3.5. His ApoB/LDL-P would be in the 25th percentile as well at that level. Given his recent fat fest, his PP NF TG 2-4 would be considerable. He's been brainwashed by Volek and Phinney so he won't listen but he can control this if he wants to by lowering fat and eating some carbs.

It's sad since it's been shown that both Masais and Inuits had considerable atherosclerosis; what saved them was lower inflammation and the absence of contributory risk factors like hypertension, diabetes, etc. That's not the case with most Westerners.
Nigel Kinbrum said…
I'm done with Hahn.
charles grashow said…

Hello, this is Seth’s mother Justine. I’d like to offer what little
information I have to try to answer some of the questions that were
posted about Seth’s death. We’re told that we’ll get a full coroner’s
report in about 6 months. In the meantime we were given only “Cause A:
Occlusive coronary artery disease” and “Other significant conditions:
charles grashow said…

In this large-scale, prospective cohort of initially healthy US women, we observed that higher nonfasting triglyceride levels were strongly
associated with an increased risk of future cardiovascular events,
independent of baseline cardiac risk factors, levels of other lipids,
and markers of insulin resistance. In contrast, fasting triglyceride
levels showed little independent association with cardiovascular events. Associations were particularly strong among individuals who had their blood drawn 2 to 4 hours after a meal, and this relationship weakened as more time elapsed postprandially.

In this large-scale, prospective cohort of initially healthy US women, we observed that higher nonfasting triglyceride levels were strongly associated with an increased risk of future cardiovascular events, independent of baseline cardiac risk factors, levels of other lipids, and markers of insulin resistance. In contrast, fasting triglyceride levels showed little independent association with cardiovascular events. Associations were particularly strong among individuals who had their blood drawn 2 to 4 hours after a meal, and this relationship weakened as more time elapsed postprandially.
charles grashow said…
StellaBarbone said…
Last Tuesday I worked at the polling place for the primary election. I spent 15 hours listening to one of my fellow workers, a Greek immigrant, talk about planting olives, growing olives, picking olives, crushing olives. It was a stunning display of olive minutiae. He even told me how many liters a small family would use in a year. I forget the number, but it implied an enormous intake. As much as I love olive oil, I hope to never discuss the subject again.
Not to mention, in the case of the Masai, a robustly active life-style resulted in arterial enlargement that compensated for the atherosclerosis.

Also, we have no direct observations of any of them being long-lived because they don't have access to evil big pharma. There's little that can be said about resistance to long-term challenges posed--by other inflammatory processes and general deterioration associated with ageing--to their cardiovascular health.
Don't forget the blood sugar cult's concerns as well. ; )
charles grashow said…

"The Cardiac Wellness Program, created and directed by Robert Ostfeld, MD, MSc and
co-directed by Lauren Graf, MS, RD brings a unique, nutrition-centered approach to the management of cardiovascular disease. The program aims to prevent and reverse heart disease with a whole food/plant-based diet.Dr. Ostfeld and Ms. Graf work with patients to embrace a diet that includes no animal products and consists of vegetables, fruits, whole
grains, beans, legumes such as lentils and chickpeas, a small amount of nuts and avocado, as well as dairy alternatives.

In parts of the world where people eat largely a plant-based diet, such as rural China and Central Africa, heart disease is less common. "If you take someone from that kind of environment and move them to the Western world, research shows that within a generation
or two, they catch up to us" on heart disease, explains Dr. Ostfeld. "Genetics don't change that quickly so this is a result of lifestyle–likely in part becaue of the toxic Western diet."
Susanne said…
I've been there! In the area we worked, if you were ever drawn into a conversational topic you didn't want to be in (e.g. American foreign policy) there were two topics that were guaranteed to distract any Greek male: the World Cup rankings, and whether to invest in an irrigation system for your olive grove. (There was a strong contingent which argued that it "diluted the oil.")

There were endless olive groves stretching for miles around over hills and gullies, with no apparent boundaries in between (although sometimes you could tell by the size of the trees that they were different ages). But they were all divided into plots and trees that belonged to specific families, and over time had become split up and (and then bits recombined) in inheritance and marriage. Every village inhabitant, male or female, could march you into one of these unmarked groves and tell you exactly which individual tree(s) belonged to them.
Lighthouse Keeper said…
When a dietary creed keeps zooming in on the Inuit and Masai but turns a blind eye to Blue Zone evidence you know something is rotten in the state of Denmark.
charles grashow said…
This debate took place February 24, 2000 featuring Dr. Atkins, Barry Sears (The Zone), Morrison Bethea, Denise Bruner, Dr.John McDougall, Dr, Dean Ornish
Rosie May said…
Was he not downing inordinate amounts of omega 3 as well? I read somewhere he was taking 3 tablespoons of flaxseed oil a day plus fish oil and probably eating oily fish on top of that. That would probably ring alarm bells with a cardiologist in the same way as his butter consumption. I tried his Shangri-La diet which basically meant downing calories without being able to taste them. A fascinating theory closely allied to Stephan Guyenet's work and it did virtually shut down my appetite.
charles grashow said…
carbsane said…
He wiped the entire thread now. Such an asshat.
carbsane said…
Silly Kade, the elderly Masai just sit around swatting at flies all day.
But swatting flies is so primal and beastly! It's the hearty fitness activity of the stone age übermensch.
carbsane said…
I'm working on a montage of clips where she trashes LA Veterans study. Thanks ... this provided one more!
carbsane said…
I think he used the word "fad" at least a dozen times related to Atkins!
carbsane said…
Yes he was taking like 60g day at one point I think? In the comments of the post announcing his death, someone asked about that.
carbsane said…
carbsane said…
carbsane said…
Thanks as always for sharing your experiences!
carbsane said…
Should animal fats be back on the table? Is there any real evidence that they were ever taken off??

Hint: Go try and find a McLean Deluxe at McD's :-)
carbsane said…
The wording of this "organs and fat were generally preferred to lean meat" leaves the impression that organs were fatty. I've looked at most organ meats, and as expected, they are quite lean. Values from domesticated animals would probably be higher than for wild. The only organs that are more fatty would be the digestive tract and the brains. I'm still waiting for Paleo Chitterlings cookbook.
charles grashow said…
charles grashow said…

Fredrick Hahn I talk to myself frequently. Since I am always right, there is never an argument
Nigel Kinbrum said…
@24:55 Ketoacidosis in T1DM is caused by increased intake of carbohydrate? That's wrong.
scott said…
uhh....what's wrong with it? Do you prefer "inadequate insulin"?
Nigel Kinbrum said…
As it's inadequate insulin that's failing to inhibit hepatic ketogenesis, yes!
carbsane said…
What Nigel said. Haven't had time to watch the video, but ketoacidosis in T1 is unrelated to dietary intake, though I suppose a very high fat intake could make matters worse.

I've also seen where ketoacidosis is being described as high ketones + high blood glucose in a way that misleads to imply that hyperglycemia is necessariy for ketoacidosis. This is not true, although the two conditions do occur simultaneously due to lack of insulin.
George said…
I had assumed that McD's changed to seed oils to lower the animal fat SFA content of their food.
In any case, the title obviously refers to dietary guidelines, and the "shoulds" and "shouldn'ts" of popular belief.
More seriously, look to the tables in institutions such as prisons, hospitals, mental hospitals and schools for your evidence. I regularly visit a publicly owned rehab facility where the fridge is only ever stocked with a seed oil spread on the advice of government dieticians.
George said…
Someone smokes, and you want to blame his death on fat?
That sounds like epidemiology to me.
George said…
As far as I know, NO risk factor taken in isolation is predictive.
"True" risk factors are not single counts or ratios, but clusters of such things such as MetSyn, plus clinical findings like BP, with a strong input from family history and personal habits, especially smoking and exercise, and BMI.
To be guessing non-imaginary risk from a lipid panel is like guessing the breed of a dog by looking only at its eyes.
George said…
It was lul-worhty and I was about to send it your way, but got side-tracked. Yeah... trendy stuff, right?
George said…
It seems to be once-over-lightly, plagiarized from Tiecholz without attribution. I mean, the information is in the public domain, but the reason it made the Time cover today is not some coincidence.
George said…
True, I think smoking, family history are likely to be independently predictive. But the only way to control for metabolic risk factors is to select cohorts who only present one, with all the rest defined as "healthy". I'm not sure that's been done, or easy to do.
charles grashow said…
On The Trail Of Heart Attacks In Seven Countries

By Henry Blackburn, MD, University of Minnesota School of Public Health
Lighthouse Keeper said…
My all time favourite LLVLC podcast moment was Seth telling Jimmy that he lost weight by drinking sugar water, if 'gobsmacked' had a sound I think I actually heard it. That's like going on Dracula's podcast and telling him you drink garlic smoothies.
Lighthouse Keeper said…
In the UK we now have many producers of cold pressed virgin rapeseed ( canola ) oil grown and bottled on local family farms with a good omega 3 to 6 ratio and available and selling well in supermarkets for around the same price as a decent extra virgin olive oil. This is not an industrially produced oil , GMO free and some are available as organic if that's a concern. Most of the usual seed oil objections put forward by the paleo movement and Weston A Price Foundation are therefore no longer a concern.
George said…
I buy Heinz Seriously Good Mayonnaise for my kids because it is made with canola oil rather than the soybean oil in all other commercial mayo. This makes sense to me. I wouldn't cook with canola oil or use a canola spread, and I wouldn't use it myself because I eat fish and nuts, enough is enough, but personally I don't consider canola oil of the type you describe to be harmful as a raw dressing.
charles grashow said…

"Virtually all popular “diets” such as Atkins, South Beach and others were designed, engineered and created by fallible humans, and as such are rife with our human biases, misinformation and errors concerning the elements of optimal human nutrition. Although, Boyd Eaton, myself and others have been credited with creating “The Paleo Diet”, this
perception is incorrect. The Paleo Diet is and always has been a biological force that shaped the human genome including our present day nutritional requirements. It was created not by fallible human judgment but rather by the forces of evolution acting through natural selection over millions of years. Together with anthropologists, physicians and scientists worldwide, Dr. Eaton and I simply uncovered that which was pre-existing. The Paleo diet has always been the native diet of our species until the beginnings of the agricultural revolution 10,000 years ago (a mere 333 human generations). Our hunter gatherer ancestors consumed a wide variety of fresh plant and animal food depending upon their geographic locale, time of season and food availability – hence there was no single “Paleo Diet” but rather numerous versions of these same two food elements: wild animal and plant foods. Hunter gatherers ate no dairy foods, and rarely ate grains and except for seasonal honey ate no refined sugars. Clearly they ate no modern processed foods.

Under these nutritional stipulations our ancestral diet was almost always high in protein and low in carbohydrate (3). Hence, modern diets designed by diet doctors and fallible humans that are high in protein and low in carbs have at least got these two basic elements of our ancestral diet correct. Nevertheless, it is almost axiomatic that the remainder of these fallible human dietary recommendations will be inconsistent with our ancestral diet and ultimately will result in nutritional shortcomings and health problems."
carbsane said…
Hellmann's used to have a canola mayo that was indistinguishable from its regular. Then somewhere along the line they made it like half the fat. For as rarely as I eat mayo, I use the real deal.
charles grashow said…

"So, where does that leave smoking as a cause of heart disease? Well there are two sides to the debate — and a lot of money to be made out of staying with the status quo. I am not qualified to suggest that smoking does not cause many of the conditions that it is blamed for, including heart disease. But I do think that it is an argument that needs to be looked at with some caution."
Lighthouse Keeper said…
Yes, he was a contrarian with a particular world view that clearly governed his thinking on health and nutrition - a visit to his blog will quickly verify this .
TV53 said…
Very sorry for your loss. Seth sounds like he was a sincere man looking for what is best in life--like all of us. The one thing that jumps out at me in this information is the statement that he saw "an improvement in his (scan) score" after deciding butter was good for him. I may be reading this wrong, but it looks like his score was still getting worse, just not as bad as expected. This is not the same as improvement, and should not be termed as such. Slowing down a disease a bit, is just that. Reversing a disease is improvement. To date, the only diets that have shown reversal of heart disease in both markers and endpoints are whole foods plat based diets.