Archive for the “Bad Science” Category
Suppose you were an idiot. And suppose you were a nutrition scientist. But I repeat myself.
Sorry, just couldn’t resist borrowing from Mark Twain. Let me try again.
Suppose you’re a nutrition scientist. And suppose you conduct a study, all the while expecting the results to support a hypothesis you already believe. But then — @#$%!! – the results undermine the hypothesis.
Oh, dear, what to do?
We saw one way to handle that sticky situation in our last episode: just don’t publish the results. Ancel Keys conducted a clinical study in which people who consumed vegetable oils instead of arterycloggingsaturatedfats!! had higher mortality rates – including higher mortality from heart disease. Keys didn’t like that result, so the data gathered dust for 40 years. Nice move, Ancel.
Here’s another way to handle results you don’t like: explain them away. I found a couple examples of that method while looking through my database of studies recently.
In one study, researchers looked for a link between consuming dairy fat and heart disease. Here are some quotes from a Brown University press release:
Dairy products can be high in harmful saturated fat but not necessarily in risk to the heart.
Okay, let’s stop right there. Take a moment and wrap your head around that sentence. Saturated fats are harmful. Why? Because according to the Lipid Hypothesis, they cause heart disease. But they don’t necessarily pose a risk to the heart.
A newly published analysis of thousands of adults in Costa Rica found that their levels of dairy consumption had nothing to do statistically with their risk of a heart attack.
To conduct the study, [researchers] Aslibekyan and Baylin analyzed data on 3,630 middle-aged Costa Rican men and women who participated in an epidemiological study between 1994 and 2004 by co-author Hannia Campos of the Harvard School of Public Health.
Ah, so it was an observational study. Perhaps the researchers would be justified in explaining away their own results.
The researchers looked not only at the subjects’ self-reported dairy intake, but also at measurements of dairy fat biomarkers, namely 15:0 and 17:0, in their bodies.
Whoops. Not just an observational study. They actually measured biomarkers that told them how much dairy fat the participants consumed. Let’s look at the results.
What they found is that the dairy intake of people who had heart attacks was not statistically different than the intake of people who did not. After breaking people into quintiles, based on their dairy consumption amount, there was no significant linear relationship between consumption and heart risk, even among the most voracious consumers. The highest consumption quintile consumed an average of 593 grams of dairy foods a day.
Once again, stop and wrap your head around that. We’ve been told for decades to stop consuming cream and butter because the saturated fats cause heart disease. But in this study of more than 3,600 people – a study in which researchers directly measured biomarkers of dairy fat consumption – there was no relationship between consuming those arterycloggingsaturatedfats!! and heart disease.
So how do we explain this result?
Rather than suggesting that the saturated fats in dairy products are harmless, Aslibekyan and co-author Ana Baylin, an adjunct assistant professor of community health at Brown, hypothesize that other nutrients in dairy products are protective against heart disease, for all but perhaps the highest dairy consumption quintile in their study. The potentially beneficial nutrients include calcium, vitamin D, potassium, magnesium and conjugated linoleic acid (CLA).
Well, there you have it: saturated fats cause heart disease, ya see, but people who consume a lot of saturated dairy fats — even the most voracious consumers — don’t have higher rates of heart disease because … uh … because something else in the dairy products is protecting their hearts!
Awesome. Coming soon: nutrition scientists decide there must be heart-protective substances in bacon, eggs and sausage that offset the heart-killing effects of the arterycloggingsaturatedfats!!
Here’s another example of explaining away embarrassing results. In a 2010 study, researchers randomly assigned subjects to one of three groups: no change (the control group), 60 grams of whole grains for 16 weeks, or 60 grams of whole grains for 8 weeks followed by 120 grams of whole grains for 8 weeks.
These are the markers of cardiovascular health the researchers measured, according to the abstract:
BMI, percentage body fat, waist circumference; fasting plasma lipid profile, glucose and insulin; and indicators of inflammatory, coagulation, and endothelial function.
If whole grains are the wunnerful, wunnerful, health-enhancing food we’ve all been told they are, the second group should have shown improvement those health markers, and the third group should be well on its way to immortality. So let’s check the results:
Although reported WG intake was significantly increased among intervention groups, and demonstrated good participant compliance, there were no significant differences in any markers of CVD risk between groups.
No significant difference in any markers. That would mean not one.
Oh dear … and here we have our beloved USDA telling us all we need to eat more whole grains. How do we explain this result? Here’s how:
A period of 4 months may be insufficient to change the lifelong disease trajectory associated with CVD.
Riiiiiiight. Four months of consuming large servings of whole grains doesn’t affect BMI, percentage body fat, waist circumference, fasting plasma lipid profile, glucose, insulin, or indicators of inflammatory, coagulation, or endothelial function. But those whole grains may still have a positive effect on the lifelong disease trajectory associated with CVD.
Yeah, that makes perfect sense.
Well, at least these studies were published. If Ancel Keys had conducted them, the data would still be sitting in a dusty attic somewhere.
43 Comments »
Several people posted comments or sent emails with links to articles about a “rediscovered” study from the 1960s. Let’s look at some quotes from the Washington Post article:
It was one of the largest, most rigorous experiments ever conducted on an important diet question: How do fatty foods affect our health? Yet it took more than 40 years — that is, until today — for a clear picture of the results to reach the public.
The fuller results appeared Tuesday in BMJ, a medical journal, featuring some never-before-published data. Collectively, the fuller results undermine the conventional wisdom regarding dietary fat that has persisted for decades and is still enshrined in influential publications such as the U.S. government’s Dietary Guidelines for Americans. But the long-belated saga of the Minnesota Coronary Experiment may also make a broader point about how science gets done: it suggests just how difficult it can be for new evidence to see the light of day when it contradicts widely held theories.
The difficulty lies in the fact that scientists are freakin’ liars.
The story begins in the late 1960s and early ’70s, when researchers in Minnesota engaged thousands of institutionalized mental patients to compare the effects of two diets. One group of patients was fed a diet intended to lower blood cholesterol and reduce heart disease. It contained less saturated fat, less cholesterol and more vegetable oil. The other group was fed a more typical American diet.
Just as researchers expected, the special diet reduced blood cholesterol in patients.
Well then, those patients whose cholesterol dropped must have suffered fewer heart attacks and lived longer.
Today, the principles of that special diet — less saturated fat, more vegetable oils — are recommended by the Dietary Guidelines for Americans, the government’s official diet advice book.
And have been since 1980 – because of all the solid evidence supporting switching from animal fats to vegetables oils, doncha know.
Yet the fuller accounting of the Minnesota data indicates that the advice is, at best, unsupported by the massive trial. In fact, it appears to show just the opposite: Patients who lowered their cholesterol, presumably because of the special diet, actually suffered more heart-related deaths than those who did not.
The higher rate of mortality for patients on the special diet was most apparent among patients older than 64.
In other words, within the group most likely to suffer a heart attack in the first place. Hooray for vegetable oils that lower our cholesterol!
It’s not exactly clear why the full set of data from the Minnesota experiment was never published.
Oh, I think I can guess.
“Had this research been published 40 years ago, it might have changed the trajectory of diet-heart research and recommendations” said Daisy Zamora, a researcher at UNC and a lead author of the study.
And that’s why it wasn’t published.
The results of the study were never touted by the investigators. Partial results were presented at an American Heart Association conference in 1975, and it wasn’t until 1989 that some of the results were published, appearing in a medical journal known as Arteriosclerosis.
Amazing. A big, expensive study is conducted to test the hypothesis that switching from saturated fats to vegetable oils will reduce heart disease by lowering cholesterol. The results show the opposite – at a time when many Americans were being encouraged to follow exactly that advice. What kind of lousy @#$%ing scientist would bury the results instead of publishing them?
The lead investigators of the trial, noted scientists Ancel Keys and Ivan Frantz, are deceased.
You’ve gotta love Ancel Keys. The guy conducts an observational study by giving two dietary questionnaires to a whopping 30 or so people in seven countries. From this itty bitty dataset, he decides he’s proved that saturated fats cause heart disease. Meanwhile, he tries to destroy the careers of other researchers who question his findings.
Then when his own clinical study – involving thousands of patients – shows that switching to vegetable oil increases heart disease and overall mortality, he clams up and doesn’t publish the results. What an awesome scientist he was.
If this story sounds somewhat familiar, perhaps it’s because a similar study was “rediscovered” back in 2013. I wrote a post about that as well and quoted from an article in Forbes:
In an exceedingly strange turn of events, data from a clinical trial dating from the 1960s, long thought to be lost, has now been resurrected and may contribute important new information to the very contemporary controversy over recommendations about dietary fat composition.
“Exceedingly strange” has now happened twice.
One trial that actually tested the hypothesis was the Sydney Diet Heart Study, which ran from 1966 through 1973. In the trial, 458 men with coronary disease were randomized to a diet rich in linoleic acid (the predominant omega 6 PUFA in most diets) or their usual diet. Although total cholesterol was reduced by 13% in the treatment group during the study, all-cause mortality was higher in the linoleic acid group than in the control group. However, in the original publications, and consistent with the practice at the time, deaths from cardiovascular (CVD) and coronary heart disease (CHD) deaths were not published.
Now, in a new paper published in BMJ, Christopher Ramsden and colleagues report that they were able to recover and analyze data from the original magnetic tape of the Sydney Diet Heart Study. The new mortality findings are consistent:
• All cause: 17.6% in the linoleic group versus 11.8% in the control group, HR 1.62, CI 1.00-2.64)
• CV disease: 17.2% versus 11%, HR 1.70, CI 1.03-2.80
• CHD: 16.3% versus 10.1%, HR 1.74, CI 1.04-2.92
People who switched to the vegetable did worse all around: higher all-cause mortality, higher mortality from cardiovascular disease in general, higher mortality from heart disease. But as with the Minnesota study, the results didn’t see the light of day for decades. The explanation offered was that a computer data tape was misplaced and only found 40 years later.
What a strange coincidence. We have two large, well-controlled studies conducted around the same time. Both show that switching from saturated animal fats to vegetable oils actually leads to higher mortality rates (including deaths from heart disease), despite lowering cholesterol significantly. A total poke in the eye for the Lipid Hypothesis. And somehow, the results of both studies were buried for 40 years.
No wonder the researchers who crunched the “lost” Minnesota data wrote this:
Findings from the Minnesota Coronary Experiment add to growing evidence that incomplete publication has contributed to overestimation of the benefits of replacing saturated fat with vegetable oils rich in linoleic acid.
I interpret “incomplete publication” as a polite version of scientists are freakin’ liars.
Naturally, researchers who’ve spent years promoting the switch from saturated fats to vegetable oils immediately called a press conference to offer their apologies and a promise to re-evaluate their positions.
Kidding! Of course that didn’t happen. Here’s what did happen:
“The bottom line is that this report adds no useful new information and is irrelevant to current dietary recommendations that emphasize replacing saturated fat with polyunsaturated fat,” Walter Willett, chair of the nutrition department at Harvard University, said in a blog post from the school. “Many lines of evidence support this conclusion.”
He characterized the new analysis of the old experiment as “an interesting historical footnote.”
So Willett, like Ancel Keys, considers his observational studies to be rock-solid evidence, but dismisses clinical trials if the results undermine what he already “knows.”
As Max Planck said, science advances one funeral at a time. Ancel Keys is dead. A few more funerals, and we may finally see the Lipid Hypothesis end up on the Scrap Heap of Wrong Ideas, where it clearly belongs.
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Bacterial pneumonia, once a leading killer of the old and the very young, is caused by (duh) bacteria. If you kill the bacteria, the pneumonia goes away. It doesn’t really matter how you kill the bacteria, either. If a patient is allergic to one drug that kills the bacteria, a doctor can prescribe a different drug that kills the bacteria and – bingo! – the pneumonia goes away. Why?
BECAUSE THE PNEUMONIA IS CAUSED BY THE BACTERIA, FOR PETE’S SAKE!
And how do we know that?
BECAUSE IF WE KILL THE BACTERIA, THE PNEUMONIA GOES AWAY, FOR PETE’S SAKE!
Okay, but let’s suppose we kill the bacteria we believe causes the pneumonia, but the pneumonia remains and the patient dies. And let’s suppose this happens with multiple patients. Then what would we conclude?
IF KILLING THE BACTERIA DOESN’T MAKE THE PNEUMONIA GO AWAY, THEN THE PNEUMONIA ISN’T CAUSED BY THE BACTERIA, FOR PETE’S SAKE! WHAT ARE YOU, AN IDIOT?
No, I’m just pointing out some basic logic here. If we kill the bacteria but the pneumonia remains, we have to conclude that while a bacterial infection may be associated with pneumonia, it isn’t the cause. That’s what we’d expect any honest scientist to say.
But strangely, this basic logic seems to escape researchers when a cholesterol-lowering drug fails to prevent heart attacks. Here are some quotes from a New York Times article:
It is a drug that reduces levels of LDL cholesterol, the dangerous kind, as much as statins do. And it more than doubles levels of HDL cholesterol, the good kind, which is linked to protection from heart disease.
That’s the Lipid Hypothesis in a nutshell: LDL is dangerous. It causes heart disease — just like that nasty bacteria causes bacterial pneumonia. HDL, meanwhile, protects against heart disease.
As a result, heart experts had high hopes for it as an alternative for the many patients who cannot or will not take statins.
Everybody sing: “Oh, we’ve got hiiiigh hopes. Yes, we’ve got hiiiigh hopes …”
But these specialists were stunned by the results of a study of 12,000 patients, announced on Sunday at the American College of Cardiology’s annual meeting: There was no benefit from taking the drug, evacetrapib.
No benefit? But LDL causes heart disease! Did the drug fail to lower the LDL that causes heart disease?
Participants taking the drug saw their LDL levels fall to an average of 55 milligrams per deciliter from 84. Their HDL levels rose to an average of 104 milligram per deciliter from 46.
Well now, that is an amazing improvement in lipids. The American Heart Association would be delighted with those numbers … although strangely, I can’t find recommended LDL levels on the AHA site anymore. Perhaps they hired the former KGB artists who used to make people disappear from official photos once they became an embarrassment to the Kremlin. Anyway …
Yet 256 participants had heart attacks, compared with 255 patients in the group who were taking a placebo.
In other words, no difference. A total fail.
“We had an agent that seemed to do all the right things,” said Dr. Stephen J. Nicholls, the study’s principal investigator and the deputy director of the South Australian Health and Medical Research Institute in Adelaide.
Yup. If high cholesterol – and specifically high LDL – causes heart disease, then you did indeed have an agent that seemed to do all the right things.
“It’s the most mind-boggling question. How can a drug that lowers something that is associated with benefit not show any benefit?” he said, referring to the 37 percent drop in LDL levels with the drug.
Boy, that’s a real head-scratcher. Let me think for a minute … uh … uh … perhaps the fact that two things are associated doesn’t mean one is causing the other? I seem to recall a good scientist or two saying as much.
“All of us would have put money on it,” said Dr. Peter Libby, a Harvard cardiologist. The drug, he said, “was the great hope.”
And how are those Enron shares working for ya?
Researchers have hypotheses, but no one is certain what went wrong. “It may be that the LDL level is less important than how it gets changed,” said Dr. Paul Thompson, a cardiologist at Hartford Hospital.
Ah, yes, that must be it. LDL causes heart disease, ya see, but lowering LDL only works if you do it exactly the right way. And if you have bacterial pneumonia, it’s not wiping out the bacteria that cures you; it’s how you kill them. Kill them the wrong way, and you’ll still have pneumonia … even though bacteria cause the pneumonia.
Here’s an alternate hypothesis about why the latest study was a big, fat fail:
LDL DOESN’T CAUSE HEART DISEASE, FOR PETE’S SAKE!
That would be the most logical conclusion: we beat people’s LDL levels down, but they didn’t have fewer heart attacks. So LDL doesn’t cause heart disease. But beating cholesterol levels down is a $36 billion per year (and climbing) business. So we’re getting the illogical conclusion instead:
Cardiologists still have high hopes for a new class of cholesterol drugs, known as PCSK-9 inhibitors, that cause LDL to plummet to levels never seen in drug treatments.
Try to wrap your head around that one: in a multi-year study of 12,000 people, dramatically lowering LDL levels didn’t prevent heart disease. But cardiologists have high hopes for a new class of drugs that lower LDL levels EVEN MORE!
Everybody sing: “Oh, we’ve got hiiiigh hopes. Yes, we’ve got hiiiigh hopes …”
And here’s the reason for those high hopes:
The PCSK-9 inhibitors can cost more than $14,000 a year …
Fourteen grand per patient, per year, year in and year out. Yeah, that would generate a lot of hope.
… while statins can cost just pennies a day, so determining what portion of patients are truly statin intolerant has become an important question.
Yeah, about that “statin intolerant” problem: funny how research funded by drug companies is starting to demonstrate a real problem with statins isn’t it? In one of his many great posts, Dr. Malcolm Kendrick predicted this would happen:
For years the experts have informed us that this is utter rubbish, statins are wonder-drugs, and adverse effect free. All of a sudden, now that the pharmaceutical industry is about to launch new cholesterol lowering agents, we are suddenly going to find that, why, after all, statins do cause a whole range of nasty adverse effects.
I watch this stuff with a kind of morbid fascination. The marketing game is on, billions are about to be spent pushing PCSK9-inhibitors. The Key Opinion Leaders who tirelessly promoted the wonders of statins, and who told us that they were virtually side-effect free, are now singing a completely different tune.
Sure enough, a big ol’ study just concluded that lots and lots of people have real problems with statins. The study was led by Dr. Steve Nissen, one of the long-time pimps for — er, promoters of statins. Returning to the New York Times article:
A second study presented at the cardiology meeting on Sunday and published online in JAMA, the Journal of the American Medical Association revealed just how vexing the issue is.
The study, directed by Dr. Nissen and paid for by Amgen, a pharmaceutical company, included more than 500 people with extremely high levels of LDL cholesterol who had tried two or more statins and had reported aching or weak muscles so severe that they said they absolutely could not continue taking the drugs.
[The result] indicated that 57 percent of patients actually could tolerate statins. Researchers then randomly assigned the remaining 43 percent to take either Amgen’s PCSK-9 inhibitor, evolocumab, or another cholesterol-lowering drug, ezetimibe, which is often taken by statin intolerant patients but has never been shown to reduce heart disease risk when taken without an accompanying statin. The patients tolerated both drugs.
My, my, my … statins go off patent (thus reducing the cost to just pennies per day), and through sheer coincidence, we get a major new study showing that nearly half of all people can’t tolerate statins – but they can tolerate the new drug that costs $14,000 per year.
And of course, we know this new and very expensive drug will prevent heart attacks because it lowers LDL. High LDL cholesterol causes heart disease, ya see. We’ll just continue believing that even when a drug that dramatically lowers LDL fails to prevent heart attacks.
Perhaps someday, after yet another LDL-lowering drug fails to prevent heart attacks, researchers will respond by going before the cameras and announcing that it’s time to bury the Lipid Hypothesis once and for all.
But I don’t have high hopes.
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How’s this for perfect timing? The day after I wrote a post about weenies, Politico.com posted a news item that demonstrates the weenie mentality in action:
In a sign that the nutrition space is as defensive as ever, Nina Teicholz, an author who has publicly criticized the science behind the government’s low-fat dietary advice, was recently bumped from a nutrition science panel after being confirmed by the National Food Policy Conference. The panel instead will include Maureen Storey, president and CEO of the Alliance for Potato Research and Education. The event is set to take place in Washington next month.
Teicholz, of course, is the author of the terrific book The Big Fat Surprise, which presents a detailed history of how we ended up with our current dietary advice. So why the heck would she be disinvited from a panel on food policy?
Teicholz said she was disinvited after other panelists said they wouldn’t participate with her.
I see. And who are the other panelists?
Margo Wootan, director of nutrition policy at the Center for Science in the Public Interest, will speak on the panel, along with Barbara Millen, the former chairwoman of the 2015 Dietary Guidelines Advisory Committee, and Angie Tagtow, executive director of the USDA’s Center for Nutrition Policy and Promotion. Wootan said that “concerns were raised about Teicholz’s credibility, given the significant inaccuracies in her work.”
Um … as opposed to CSPI’s dead-on-accurate description of trans fats as safe and coconut oil as dangerous back when they were harassing restaurants and movie theaters into switching to trans fats? Or the USDA’s dead-on-accurate description of cholesterol in eggs as a contributor to heart disease? (Maybe my memory is getting faulty in my old age … didn’t both organizations have to reverse those positions?)
If Teicholz doesn’t present credible arguments, then the non-weenie approach would be to welcome her onto the panel and point out where she’s wrong. But of course, this isn’t about credibility. It’s about avoiding a debate against a woman who would kick their asses all over the stage.
But hey, that’s part of the weenie mentality: they hate having to debate people who don’t agree with them. That’s why they demand “safe spaces” where they can’t be challenged. That’s why they accuse people who disagree with them of creating a “hostile environment” as a strategy for stifling dissent. That’s why they’d rather attack the messenger than debate what the messenger has to say.
The Big Question is: if they’re convinced they’re right, why are they so afraid of debate? Why don’t they just stand up and vigorously argue in favor of their positions instead of trying to silence the opposition?
That’s the topic of this post. We’ll be venturing into the political/cultural realm again, so consider this your trigger warning. If you haven’t retreated to your safe space by the beginning of the next paragraph, don’t complain to me if you read something here that annoys you.
Still here? Okay, then.
The brief answer to the “why do weenies hate debates?” question is: their beliefs aren’t based on facts or logic, so they’re scared @#$%less of being challenged by logical people armed with facts … not because we might change their minds (we won’t) but because we might change the minds of other people listening.
Now for the expanded answer.
You may have heard the saying you cannot reason people out of a position they did not reason themselves into. Sooner or later, logical people discover that for themselves – because they end up in debates with illogical people and are stunned to see indisputable facts bounce harmlessly off their brains like little rubber bullets. Apparently it’s always been that way. Even Aristotle explained that some people form their beliefs based on logic and facts, while others form their beliefs based on emotions. Logic and facts have no effect on the emotional thinkers, Aristotle explained.
In a lovely little book titled Explaining Postmodernism, philosophy professor Stephen Hicks wrote about the intellectual heritage of objectivists vs. subjectivists — that is, logical types vs. emotional types.
Objectivism traces its modern roots to the Enlightenment thinkers, most of whom were British: Francis Bacon, Isaac Newton, Rene Descartes (not British), John Locke and Adam Smith. Their works emphasized rationalism, the scientific method and individual freedom. Thomas Jefferson, to name one stellar example, was deeply influenced by Locke. To quote professor Hicks:
Individualism and science are thus consequences of an epistemology of reason. Individualism applied to politics yields liberal democracy … individualism applied to economics yields free markets and capitalism.
Subjectivism, by contrast, began as reaction against the Enlightenment thinkers — ironically, in part to save religious faith from the onslaught of rationality. Its proponents were mostly German: Immanuel Kant, Friedrich Nietzsche, Georg W.F. Hegel, Jean-Jacques Rousseau (not German), Martin Heidegger, and of course Karl Marx. They specifically rejected reason and logic in favor of subjectivism.
Simply put, an objectivist thinks like this: If it’s true, I’ll believe it. A subjectivist, however, thinks like this: If I believe it, it’s true. Or the flipside: If I don’t believe it, it’s not true. If you’ve ever debated a nitwit subjectivist, you may have had the experience of offering some objectively true fact, only to be treated to a reply of “Well, I just don’t believe that.” Oh, okay, that settles it, then.
As Hicks explains, objectivists and subjectivists also have very different ideas when it comes to the function of language. Objectivists view words, ideas, logic, debates, etc., as tools we use to discover the truth. But subjectivists (a.k.a. post-modernists) view language as a weapon to be wielded in the battle for dominance. Therefore, what you say doesn’t have to be true. It merely has to be effective in battle. (There is no “true” after all, except what you believe.) Or as Hicks summarizes the subjectivist strategy when it comes to words, if you can’t debate your opponent on the facts, change the argument by calling him a racist instead.
Hicks explains these differences in the two mindsets to answer a question he poses near the beginning of the book:
A related puzzle is explaining why postmodernists — particularly among those postmodernists most involved with the practical applications of postmodernist ideas, or putting postmodernist ideas into actual practice in their classrooms and in faculty meetings — are the most likely to be hostile to dissent and debate, the most likely to engage in ad hominem argument and name-calling, the most likely to enact politically-correct authoritarian measures, and the most likely to use anger and rage as argumentative tactics.
Whether it is Stanley Fish calling all opponents of affirmative action bigots and lumping them in with the Ku Klux Klan, or whether it is Andrea Dworkin’s male-bashing in the form of calling all heterosexual males rapists, the rhetoric is very often harsh and bitter. So the puzzling question is: Why is it that among the far Left — which has traditionally promoted itself as the only true champion of civility, tolerance, and fair play — that we find those habits least practiced and even denounced?
Hmmm, doesn’t that sound just like college administrators promoting the weenification of students by demanding triggers warnings, safe spaces and speech codes?
Hicks doesn’t claim subjectivists never attempt to cite facts or offer what they consider persuasive arguments. Of course they will. Those are verbal weapons they’re happy to wield in battle. The difference is that they’re just as happy to ignore facts and logic when it suits them. That’s why they cherry-pick their evidence. They’re not interested in weighing the evidence to reach a conclusion; they’re only interested in selecting the weapons that support their cause.
Look at the vegan zealots who show up here now and then. They’ll happily post a link to some weak study showing an association between meat and this-or-that disease. But if I reply with links to studies where the association is exactly the opposite, or point out all the confounding variables, facts and logic become little rubber bullets bouncing off their brains. Then they’ll yell “murderer!” and (if we’re lucky) go away.
Another lovely little book I’d recommend to anyone who wants to understand the weenie mindset is Eric Hoffer’s The True Believer. (Sadly, it’s just as relevant now as when it was written in 1951.) In a nutshell, here’s how Hoffer describes what he calls true believers:
- They often have low self-esteem and are typically frustrated with their own lives or the world in general.
- Fanaticism appeals to them because it provides a sense of idealism, identity and certainty.
- They value the collective more than the individual and believe individuals should be willing to sacrifice themselves for the collective good.
- They believe that by imposing their beliefs, they can bring about a better future.
- They can ignore or rationalize away all contrary evidence, as well as logical inconsistencies in their own beliefs.
- They consider anyone who doesn’t share their beliefs an enemy and want to silence those who disagree.
Here are some direct quotes from Hoffer:
They can feel free only by diminishing the freedom of others, self-confident only by spreading fear and dependence among others, and rich only by making others poor.
It is the true believer’s ability to shut his eyes and stop his ears to facts which in his own mind deserve never to be seen nor heard which is the source of his unequaled fortitude and constancy.
The explosive component in the contemporary scene is not the clamor of the masses but the self-righteous claims of a multitude of graduates from schools and universities. This army of scribes is clamoring for a society in which planning, regulation, and supervision are paramount and the prerogative of the educated.
Sounds just like The Anointed, doesn’t it? It also sounds eerily like the loony-left fringe on college campuses.
So of course the weenies want to stifle debate. In their weenified minds, words are not tools we use to discover the truth. Words are weapons, and if other people are allowed to wield those weapons freely, by gosh, the wrong side might win. People in the audience might be swayed to abandon the “correct” position. They might decide The Anointed got it all wrong about saturated fat and cholesterol and salt and red meat and whole grains. Heck, they might decide The Anointed were wrong about all kinds of things.
That’s why Teicholz was disinvited. It’s also why so many colleges – the supposed centers of free and open inquiry — have become such a joke.
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When readers first linked to the “paleo diet makes you fat!” study in comments, I replied that I generally dismiss mouse and rat studies as irrelevant to humans, except in certain circumstances. I should probably talk about those circumstances.
But first, I’ll explain which studies I dismiss outright: pretty much all diet studies that involve rodents. We’re not rodents. The foods that have negative effects on rodents may have positive effects on humans and vice versa.
The big cholesterol scare started more than 100 years ago when scientists fed cholesterol to rabbits, who rapidly developed heart disease as a result. Oh my gosh, cholesterol must cause heart disease in humans!
Stupid conclusion. Rabbits are herbivores. They don’t eat cholesterol. There’s no reason they should have the biological machinery to deal with cholesterol. So – duh! – it builds up in their systems and causes problems. I’m pretty sure if we fed lions an all-vegetarian rabbit diet, they’d become quite ill. But that doesn’t mean carrots are bad for rabbits or humans. It simply means lions are obligate carnivores.
So even if researchers fed rats and mice a true paleo diet of meats and vegetables, I still wouldn’t give a rat’s ass (pardon the pun) about the results — positive or negative – because there’s simply no reason to assume those results translate to humans. We’re not rats. The diet that’s perfect for them is very unlike the diet that’s perfect for us. The researchers in the dumbass “paleo diet makes you fat!” study mentioned that standard rat chow is 3% fat. Has there ever been a group of paleo humans who lived on a 3% fat diet? I sincerely doubt it. Rats are probably biologically geared to thrive on an extremely low-fat diet. We’re not.
But of course, researchers in these studies rarely feed mice and rats anything like the human diet they’re supposedly testing. The “paleo” diet in the dumbass study consisted largely of isolated casein, sugar and canola oil. It was nothing like a paleo diet. The study has absolutely zero relevance to humans eating an actual paleo diet.
This little sleight-of-hand seems to be a habit among some researchers. More than once, I’ve dug into a mouse or rat study of the “Atkins” (ahem-ahem) diet and found that the primary fats were Crisco or corn oil, and the sole source of protein was casein … you know, just like Dr. Atkins recommended. Then when the rats or mice became fat or sick, dingbats in the media dutifully reported that New Study Show Atkins Diet Causes (insert scary result here)!!
So when should we pay attention to rodent studies? Well, I’ll least give them a look if they test the result of drugs or hormones. In the animal kingdom, hormones are the chemical messengers that trigger the code written into our biological software. Hormones have been around since before humans existed. I think we can safely assume hormones produce similar effects in a man and a mouse.
So if researchers pump male mice full of testosterone and those mice become leaner, stronger, and start throwing punches in bars at the slightest provocation, I’d expect to see similar effects in male humans. If researchers inject rats with high doses of insulin and the rats start eating like crazy and getting fat, I’d expect a similar result in humans. But I’d still take those studies with a grain of salt.
Here’s the type of rodent study I don’t take with a grain of salt: those that disprove a supposed Immutable Law of The Universe. Back in 2011, I wrote about a study in which researchers calculated how much food mice were eating ad libitum. Then they took one group of mice and cut their daily calories by just 5%. Here are some quotes from my post:
Now, according to Jillian Michaels and the other leading experts in thermodynamics, there are only a couple of possible outcomes for these experiments:
- The calorie-restricted mice, who were prevented from making little pig-mice of themselves, ended up weighing less and were leaner.
- If the calorie-restricted mice somehow ended up fatter, it could only be because they were far less active than the mice who ate freely.
Yup … if you get fat, by gosh, it means you’re either eating more or moving less. Now let’s look at the actual results:
At the end of the second experiment (three weeks), the average weight for both groups was virtually identical — it was also virtually identical to their baseline weights. But the calorie-restricted mice had 43.6% more fat mass and 6.4% less lean mass than the free-eating control mice.
Ah, well then, the mice who gained fat mass must’ve been less active, right?
Nope. According to the study data, there was no difference in locomotor activity levels between the two groups.
The calorie-restricted mice ate less, they moved around just as much, but they ended up weighing the same as the mice allowed to eat freely, and also ended up with more fat and less muscle. Oh, dear me … did these mice find a way to violate the laws of thermodynamics?
I paid attention to that study because the calorie freaks insist that according to the laws of physics, if you eat less and move around just as much YOU MUST BURN FAT FOR FUEL AND LOSE WEIGHT. IT’S AN IMMUTABLE LAW OF THE UNIVERSE. But these mice ate less, moved around just as much, and gained fat mass while losing muscle.
Yeah, it’s just a mouse study, but the laws of physics are the laws of physics, period. They don’t apply to humans and then go on vacation when mice saunter into the room. So if the laws of physics say eating less while remaining active must always lead to fat loss, that would apply to both large and small furry creatures.
No, those mice didn’t violate the laws of physics. And no, the experiment didn’t disprove any laws of physics. But it did disprove the calorie-freak argument that cutting calories while remaining just as active MUST ALWAYS LEAD TO BURNING AWAY BODY FAT BECAUSE THE LAWS OF PHYSICS SAY SO.
The laws of physics say no such thing. They merely say that if you lose weight, you burned more calories than you consumed. These mice – despite remaining just as active – slowed down their metabolisms and burned muscle tissue for fuel in order to get fatter. It was probably a programmed reaction to what their little mouse bodies interpreted as a risk of starvation. No laws of physics were harmed in the process.
So here’s the one part of the “paleo diet makes you fat!” study I found relevant:
After 3 weeks, mice fed the LCHFD began to diverge from the chow-fed group, and at 5 weeks the difference in body weight was statistically significant. At the end of the study, white adipose tissue mass was also significantly increased. The LCHFD has a higher energy density than the chow diet (24 vs 13.5 MJ kg−1); however, the increased body weight of mice fed the LCHFD was not associated with a higher energy intake.
Yup, the mice fed the full-of-crap “paleo” diet (which tripled their sugar intake) gained more weight and more body fat. We can’t blame it on palatability, because they didn’t say, “Oooh, this is yummy!” and eat more. We can’t blame it on consuming too many calories, because they didn’t consume more calories. So if the researchers kept accurate records on food consumption (and it appears they did), we have a situation where mice eating a crap diet got fatter than their control-group cousins, despite not eating more.
That’s a relevant result, even though it’s a mouse study. It disproves the dearly-held belief among the calorie freaks that getting fatter is always and forever the result of eating too many calories BECAUSE THE LAWS OF PHYSICS SAY SO. And it lends credence to the belief that food quality affects how calories are partitioned, burned and stored. Different foods send different commands to the biological software. That’s the only useful lesson from an otherwise garbage study.
And once again, no laws of physics were harmed in the process.
Of mice and men. Again.
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I saw the scary headlines a couple of days ago. You probably did too. The one that caught my attention was this:
Diabetes expert warns paleo diet is dangerous and increases weight gain
That headline was over an article on the EurekaAlert! website. Here are the opening paragraphs:
A new study has revealed following a low-carbohydrate, high-fat diet for just eight weeks can lead to rapid weight gain and health complications.
The surprise finding, detailed in a paper in Nature journal Nutrition and Diabetes, has prompted University of Melbourne researchers to issue a warning about putting faith in so-called fad diets with little or no scientific evidence.
Goodness, no, we wouldn’t want to make our dietary decisions based on little or no scientific evidence. Luckily for us, someone conducted a rigorous and relevant scientific study before declaring the paleo diet dangerous for humans. That’s why it made such a splash in the news.
Here are some paragraphs from another article that appeared in Medical News Today online:
Scientists have warned against following celebrities into “fad” diets that are not supported by scientific evidence, as findings published in the journal Nutrition and Diabetes reveal that just 8 weeks on the “Paleo” diet can pile on the pounds and raise the risk of health problems.
Adherents of the LCHF diet consume more protein, fiber and fat than the average Western diet and less sugar and starchy carbohydrates.
Suggested “dos” include grass-produced meats, fish or seafood, fresh fruits and vegetables, eggs, nuts and seeds, and healthful oils such as olive, walnut, flaxseed, macadamia, avocado and coconut.
Foods to avoid include cereal grains, legumes – including peanuts – dairy products, refined sugar, potatoes, processed foods, salt and refined vegetable oils.
So apparently, those rigorous and concerned scientists fed people more protein, more fat, and less sugar than a standard diet and were surprised when the paleo dieters experienced rapid weight gain and health complications in just eight weeks.
Damn, that is worrisome. To think I’ve been operating under the assumption that a diet of grass-produced meats, fish or seafood, fresh fruits and vegetables, eggs, nuts and seeds, and healthful oils such as olive, walnut, flaxseed, macadamia, avocado and coconut would be good for me. I was so very, very disappointed to learn than people who spent eight weeks living on grass-produced meats, fish or seafood, fresh fruits and vegetables, eggs, nuts and seeds, and healthful oils such as olive, walnut, flaxseed, macadamia, avocado and coconut got fat and sick.
But since I’m not an idiot, I kept reading. Here are more quotes from the Medical News Today article:
Researchers at the University of Melbourne were concerned about the hazards of a paleo diet, especially for those who are already overweight and living a sedentary lifestyle and for individuals with pre-diabetes or diabetes.
To investigate, they took two groups of overweight mice with symptoms of pre-diabetes.
The mice in one group consumed an LCHF diet for 8 weeks, 60% of which was fat, compared with their usual 3% fat intake. Carbohydrates made up 20%. The mice in the control group ate their usual food.
After 8 weeks, the Paleo diet group had increased in weight, glucose intolerance and insulin. The mice had gained 15% of their body weight, and their fat mass had doubled from 2% to almost 4%.
This “extreme weight gain” is equivalent to a person who weighs 200 pounds gaining 30 pounds in 2 months.
Wowzers. So if you switch to a diet of grass-produced meats, fish or seafood, fresh fruits and vegetables, eggs, nuts and seeds, and healthful oils such as olive, walnut, flaxseed, macadamia, avocado and coconut, you could gain 30 pounds in just two months – if you’re a mouse.
Then again, I’ve seen headlines before about mouse studies that supposedly demonstrated the hazards of a paleo or LCHF diet. The scientists never seem to feed those mice grass-produced meats, fish or seafood, fresh fruits and vegetables, eggs, nuts and seeds, and healthful oils such as olive, walnut, flaxseed, macadamia, avocado and coconut.
So I took a peek at the full study. Let’s see what the researchers themselves have to say:
NZO mice were maintained on either standard rodent chow or an LCHFD from 6 to 15 weeks of age.
What the heck is an NZO mouse? Yeah, I wondered that myself. So I looked it up on the website for a company that supplies them:
NZO mice of both sexes exhibit high birth weights and are significantly heavier at weaning age. Severe obesity (including both visceral and subcuatneous fat depots) develops even when mice are maintained on a standard diet containing 4.5% fat.
I see. So we’re talking about mice bred to become obese, even on a low-fat diet.
Both males and females of the NZO/Hl substrain exhibit impaired glucose tolerance (IGT), but subsequent type 2 maturity onset (NIDDM) diabetes development is limited to males, with a phenotype penetrance of 50% or less. NZO/Hl mice also show anti-insulin receptor antibodies, a defect in leptin transport, and hypertension.
Wow, sounds just like me. In fact – amusing story here – I used to wonder why my parents, who were struggling financially when The Older Brother was born, decided to add the expense of a second child a mere 18 months later. I always assumed it was because they were Catholic and that’s what the rhythm method accomplishes: it makes more Catholics.
Eventually, I dared to asked my mom why they had me so soon after my brother. Her reply was something like, “We were very interested in biology and wanted to produce a son who would become severely obese on a standard diet and show impaired glucose tolerance, anti-insulin receptor antibodies, a defect in leptin transport, and hypertension. That was you.”
So I’m totally on board with the idea of applying the results of an NZO mouse study to me. Still, I can’t help but wonder about that diet. Let’s go back to the study:
Prior to the study, all mice were fed a standard rodent maintenance diet. At 6 weeks of age, mice were either transferred to an LCHFD or maintained on the standard diet (chow) for a further 9 weeks. The LCHFD contained 24 MJ kg−1 digestible energy (3.1 MJ or 13% coming from protein, 1.5 MJ or 6% from carbohydrate and 19.5 MJ or 81% from fat. The chow diet contained 13.5 MJ kg−1 digestible energy, with 2.7 MJ or 20% coming from protein, 9.5 MJ or 70% from carbohydrate and 1.4 MJ or 10% from fat.
I see. The standard-chow mice got a diet of 20% protein, while the “paleo” mice got a diet of 13% protein. Wait a minute … how did the Medical News Today article describe a paleo diet again? Let me go find that quote again … okay, here it is:
Adherents of the LCHF diet consume more protein, fiber and fat than the average Western diet and less sugar and starchy carbohydrates.
So the “paleo” mice consumed 35% less protein than the control group. And according to the study documents, the protein the “paleo” mice consumed consisted entirely of casein. Let’s look up the definition of that word.
A protein precipitated from milk, as by rennet, and forming the basis of cheese and certain plastics.
Yup, this is sounding more and more like a true representation of the paleo diet. That’s what most paleo dieters I know do: they precipitate milk as by rennet to isolate the casein and then eat it.
Well, at least the mouse “paleo” diet was high in fat – perhaps ridiculously high in fat, but high in fat. And I’m sure they were paleo fats. After all, as the Medical News Today article clearly stated, paleo dieters avoid cereal grains, legumes, dairy products, refined sugar, potatoes, processed foods, salt and refined vegetable oils.
So I looked up the contents of the “paleo” diet. As a percent of the total, the “paleo” mice got 54% of calories from cocoa butter, 14% from clarified butter, and 14% from canola oil.
Dangit! That is EXACTLY LIKE MY PALEO DIET! I get up every morning and swallow big globs of cocoa butter, then wash it down with clarified butter and canola oil … because it’s not as if butter (or casein) is a dairy product and canola oil is a refined vegetable oil or anything. I take my paleo seriously.
I kept reading to make sure the relative increase in fat intake for the mice was similar to the relative increase in fat for humans who switch to a LCHF diet. Here’s what the study had to say:
Rodent chow is normally low in fat (3% of energy) and high in carbohydrates (approximately 50% starch). In contrast, the LCHFD used here had a very low carbohydrate (only 6% of energy, 100% sucrose) and high fat content (81% of energy).
Just as I feared: the change is totally relevant to humans going LCHF. Compared to their normal diet, the “paleo” mice increased their fat intake by 2567%. Same here. When I switched from low-fat to paleo, the percent of fat in my diet went from 20% to 513% of total calories. I had no idea that would be bad for me — especially the canola oil.
The carb content of the “paleo” diet was low, of course. And since paleo is what it is, those carbs probably came from vegetables, maybe some tubers …
The carbohydrate content of the LCHFD was exclusively derived from simple sugar.
Wait a minute … the paleo mice got 6% of their calories (100% of the carb calories) from simple sugar? Well, I’m sure that was at least a reduction compared to the standard chow.
Typically, rodent chow carbohydrate is contributed to by 50% starch and approximately 2% simple sugars.
I see. So the non-paleo mice got 2% of their calories from simple sugars, and the “paleo” mice got 6% of their calories from simple sugars. Well, once again, that’s exactly what happens when people go on a paleo diet: they triple their intake of simple sugars. That’s why the Medical News Today article mentioned this:
Foods to avoid include cereal grains, legumes – including peanuts – dairy products, refined sugar, potatoes, processed foods, salt and refined vegetable oils.
So there you have it. Mice and men. People who try paleo diets are almost exactly like NZO mice, and the paleo diets they try are almost exactly like the “paleo” diet in this study. So if you go paleo, you’re probably going to get fat and sick. I know it’s true, because the lead researcher said so:
Lead author, Associate Prof Sof Andrikopoulos says this type of diet, exemplified in many forms of the popular Paleo diet, is not recommended – particularly for people who are already overweight and lead sedentary lifestyles.
“Low-carbohydrate, high-fat diets are becoming more popular, but there is no scientific evidence that these diets work. In fact, if you put an inactive individual on this type of diet, the chances are that person will gain weight,” Andrikopoulos, President of the Australian Diabetes Society, said.
Yup, the lead researcher is President of the Australian Diabetes Society, which (like our own Diabetes Society) has been pushing low-fat diets for years. But I’m sure that didn’t affect how he designed or interpreted the study.
And neither did the fact that (according to his bio) he’s received a lot of research money from drug companies. I mean, It’s not as if the paleo diet would reduce the need for drugs or anything.
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