Archive for the “Bad Science” Category
I’d have to dig through my Outlook archives to say for sure (and I won’t), but this one may have set the new record for the number of Did you see this?! emails I received.
If you follow the health news (and if you haven’t been on a retreat in the wilderness or otherwise deprived of the internet for the past week), you already know a new study declared that low-fat beats low-carb for weight loss … once and for all, end of story, final word, move along folks, there’s nothing else to see. Let’s look at some media treatments of the news.
From a BBC article titled Low-fat diets ‘better than cutting carbs’ for weight loss:
Cutting fat from your diet leads to more fat loss than reducing carbohydrates, a US health study shows.
Scientists intensely analysed people on controlled diets by inspecting every morsel of food, minute of exercise and breath taken. Both diets, analysed by the National Institutes of Health, led to fat loss when calories were cut, but people lost more when they reduced fat intake.
From a Washington Post article titled Scientists (sort of) settle debate on low-carb vs. low-fat diets:
Seeking to settle the debate, scientists from the National Institutes of Health set up a very detailed and somewhat unusual experiment.
They checked 19 obese adults (who were roughly the same weight and had the same body-mass index) into an inpatient unit at the NIH clinical center, for two-week increments.
For the first five days of each visit, the volunteers were given a baseline diet of 2,740 calories that was 50 percent carbohydrate, 35 percent fat and 15 percent protein. This wasn’t very different from what they were eating before. But for the following six days, they were given either a low-fat diet or a low-carb diet, each having 30 percent fewer calories. Each participant was also asked to exercise one hour a day on the treadmill.
After analyzing everything from how much carbon dioxide and nitrogen they were releasing to their hormone and metabolite levels, the researchers concluded that the calorie-per-calorie, low-fat diets beat out low-carb diets.
My favorite headline was from the Los Angeles Times: For fat loss, low-fat diets beat low-carb diets handily, new research finds.
Low-fat won handily? Must’ve been real butt-whippin’ demonstrated in those results.
It is a central dogma of the low-carb lifestyle: that while avoiding carbohydrates will force the human body into fat-burning mode, any diet that fails to suppress insulin will trap body fat in place and thwart a dieter’s hope of shifting to a leaner, healthier body type.
But researchers from the National Institutes of Health have found that the hallowed creed of Atkins acolytes doesn’t hold up in the metabolic lab, where dieters can’t cheat and respiratory quotients don’t lie.
So it was the Atkins diet that got a butt-whippin’ by low-fat. I repeat: The Atkins Diet. I don’t know about you, but I would take that to mean the diet prescribed by Dr. Atkins.
And how long did the diets last? Let’s check the LA Times again:
As the 19 subjects recruited for the current study dieted their way through four weeks of low-carb and low-fat regimens, Hall and his colleagues conducted brain scans and other tests to glean how diets with differing nutrient compositions affected their mood, motivation and sense of satisfaction.
My goodness … they dieted their way through four weeks of low-carb and low-fat regimens, according to the LA Times. I take it that means the subjects were on diets lasting four weeks. That ought to be long enough for real differences to emerge.
But wait a second … I seem to recall the Washington Post describing the diets a bit differently …
But for the following six days, they were given either a low-fat diet or a low-carb diet, each having 30 percent fewer calories.
Hmmm, we seem to have conflicting stories here. Four weeks vs. six days on each diet. Perhaps we should check the study itself – which I did. After reading it, I suspect we have a case of “let’s design a study to produce the results we want.” In fact, I can’t help but imagine the conversation:
“Okay, Jenkins, grab your laptop and step into my office. We need to design a good, solid, scientific study to settle this low-fat versus low-carb issue once and for all.”
“Excellent, sir. You mean in a metabolic ward and everything?”
“Exactly. Let’s start with the low-fat portion.”
“Well, sir, the usual definition of a low-fat diet is less than 30 percent of total calories, so I suppose we should—”
“Don’t be ridiculous, Jenkins. If we’re going low-fat, let’s really go low-fat!”
“Ahh, I see. Something like the very-low-fat diet Dr. Ornish pushes. Okay, 10 percent of total calories, then.”
“Damnit, Jenkins, you’re not listening! I said really low-fat! Let’s go down to, say, 7.7 percent of total calories from fat.”
“So a diet nobody would ever follow voluntarily in real life for any length of time, then?”
“Correct. Now, for the low-carb side of things …”
“That’s easy, sir. The Atkins books recommend starting at 30 grams of carbohydrate per day, so—”
“Good grief, man, we can’t put human beings on such an extreme diet!”
“So we’ll go with 140 grams per day, including, say, 37 grams of sugar. That should be a fair comparison for our purposes.”
“But that’s twice as many carbohydrates per day as the Atkins diet recommends even in the maintenance stage, must less when starting a—”
“Well, it’s complicated, Jenkins, so let me explain it this way: shut up.”
Actually, the explanation isn’t particularly complicated. Here’s a quote from the full study:
Given the composition of the baseline diet, it was not possible to design an isocaloric very low-carbohydrate diet without also adding fat or protein. We decided against such an approach due to the difficulty in attributing any observed effects of the diet to the reduction in carbohydrate as opposed to the addition of fat or protein.
In other words, they didn’t want to add or remove protein from either diet, and they didn’t want to add fat to the low-carb diet or carbohydrates to the low-fat diet. They wanted to compare restricting carbs to restricting fat with no other changes, period.
Okay, fine. But in that case, the “low-carb” diet is nothing like the low-carb diet recommended by the Atkins diet books, or by any doctors who promote low-carb diets. So the accurate conclusion and/or headline should be something like Extreme low-fat diet produces more fat loss than a sort-of, kind-of, almost-low-carb diet … at least when the diets last six days.
Yup, six days. It was the Washington Post’s description of the duration that was accurate. The L.A. Times got it wrong. Based on those six days, the researchers then describe in their paper how computer models predict substantially more fat loss for the low-fat group if both diets lasted six months.
Uh-huh. I rank that up there with Al Gore claiming his computer models can accurately predict the climate in 2050 … even though those models didn’t accurately predict the previous 10 years. I’m a programmer, so trust me on this: computer-simulation models tell you what you tell them to tell you. The only way we’ll actually know how these diets perform over six months is to keep people on them for six months.
And we’d also want more than 19 people involved. I just wrote a post last week demonstrating how random chance alone can create “significant” differences in small study groups. Nineteen people, diets that lasted a whopping six days … I wouldn’t bet on those results being reproduced with large groups over a long time.
But about those results … the Los Angeles Times assured us the low-fat diet beat the (ahem) “low-carb” diet handily. So what were the big differences in outcomes?
Well, people on the low-fat diet lost (on average) 1.296 pounds of body fat. People on the (ahem) “low-carb” diet lost (again, on average) 1.166 pounds of body fat. The difference was therefore just a shade over one-tenth of one pound. If you don’t believe random chance can produce that trivial of a difference in a study group of 19 people put on diets lasting six days, I suggest you take a class in statistics.
But wait … did I say 19 people? Well, that’s not quite true. According to the paper, 19 people were enrolled in the study – 10 men and nine women. The study had a crossover design, meaning everyone goes on one diet, then goes back to normal eating for a couple of weeks, then goes on the other diet. They’re randomly assigned to do one diet or the other first.
But the results table shows n=19 for the (ahem) “low-carb” diet and n=17 for the low-fat diet. That means two of the subjects didn’t complete the low-fat diet. So I can’t help but wonder why the researchers didn’t simply toss the results for those two people from the study altogether. Why calculate their results on the (ahem) “low-carb” diet into the average if they didn’t finish the other diet? I thought the goal here was a head-to-head comparison of the same people on different diets.
I also can’t help but wonder why, given the small group, the researchers didn’t just show us the full results for everyone. In studies with hundreds of subjects, sure, you pretty much have to present group-average results to make sense of the numbers. But for the 17 people who completed both diets, heck, just show us everyone’s results and stick the averages at the bottom of the table. If some individuals lost a lot more weight on low-fat vs. low-carb or vice versa, that would be worth knowing. It would also be worth knowing if one or two outliers skewed the averages for the groups.
Well, apparently that did happen. I found this in the paper:
The data were analyzed using a repeated-measures mixed model controlling for sex and order effects and are presented as least-squares mean ± SEM. The p values refer to the diet effects and were not corrected for multiple comparisons. One female subject had changes in DXA % body fat data that were not physiological and were clear outliers, so these data were excluded from the analyses.
Uh … okay. I’d sure like to see those individual results, though.
All those complaints aside, there were some interesting results in the study tables (again, keeping in mind the small groups and short durations). During the six-day diets, triglycerides dropped by 17.5 points in the (ahem) “low-carb” group, and by 4.3 points in the low-fat group. For total cholesterol, the drop was 8.47 points in the (ahem) “low-carb” group and 19.1 points in the low-fat group. HDL dropped by 2.67 points in the (ahem) “low-carb” group and by 7.27 points in the low-fat group.
So if low triglycerides and high HDL are indicators of heart health (and if these results are actually meaningful), I’m sticking with a lower-carb diet … but one with more fat, thank you very much, because I want my HDL to go up, not down.
The results I found most interesting were for glucose and insulin. In the (ahem) “low-carb” group, glucose dropped by an average of 2.69 points … but in the low-fat group, glucose dropped by 7.1 points. So it’s clearly possible to reduce glucose levels with a very low-fat diet, despite the high carb intake, if calories are restricted enough.
This study has been hyped by the anti-Taubes brigades as a refutation of the insulin hypothesis, but the tables show very little difference in insulin levels. The (ahem) “low-carb” group showed a drop in fasting insulin of 2.76 points, while the low-fat group showed a drop of 2.04 points. Nonetheless, here’s how the researchers described the difference:
The experimental reduced-energy diets resulted in substantial differences in insulin secretion despite being isocaloric.
Hmmm … I’m thinking there’s a reason they chose the word “substantial” instead of “significant.” Let’s check the tables again …. Yup, the p value (RC versus RF) for the change in fasting insulin is .48. The threshold for “statistically significant” is .05 or below. So the difference here wasn’t even close to significant — in a study some people are waving around as proof that insulin levels aren’t a factor in the ability to lose body fat … perhaps because they read what the researchers wrote in their conclusions instead of checking the study tables.
And by the way, the p value (RC versus RF) for change in body fat was .78 — so unless I’m misinterpreting the meaning of p value (RC versus RF), we would interpret that as “statistically, the odds of this difference being due entirely to chance are 78 percent.”
Within the obvious limitations, the study does show that restricting calories can produce a drop in insulin even when the overall carb count stays the same. So it’s not as simple as carb intake = fasting insulin level. Total energy intake figures into it as well.
That being said, it would be very, very interesting to see what the differences in insulin levels (among other results) were if 1) the study ran much longer, 2) there were more than 17 people who completed both diets, and 3) the “low-carb” diet was actually low-carb and didn’t include 37 grams per day of sugar.
I believe the less-hype, more-substance reporting on the study was in an article that appeared in Forbes magazine online:
But a well-controlled new study finds that – at least in the lab – low-fat might be slightly better for weight loss over the long term. That does not mean that we should all revert to the low-fat insanity of the ’80s and ’90s. Rather, the more valuable take-home message might be that rejecting carbs may not be so necessary for long-term weight loss as many of us believe, and that a nutrient-balanced diet is probably the smarter strategy in the long term.
And frankly, whatever kind of diet is most doable for an individual is probably the one to be on. If it’s easier to stick to low-carb than low-fat, then by all means do it. But a balanced diet is still king.
Bingo. It’s certainly possible to lose weight on a high-carb, very-low-fat diet. It’s possible to lose weight on any diet if you restrict calories enough. I tried a Pritikin-style diet (10% of calories from fat) twice, and lost a bit of weight both times – and then I had to quit both times because I was miserable, hungry all the time, and eventually felt too lethargic and depressed to continue. Meals were an exercise in monkish discipline, choking down tasteless food and trying to convince myself I was fine with it.
Now I’m not miserable, not hungry all the time, and never depressed … which means when people hype a study like this as “proof” that a low-fat diet is better than an (ahem) “Atkins” diet, I can enjoy a hearty laugh.
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Well, I guess we should have seen this one coming: Big Soda is fighting back, and they’re going to use “science” (ahem, ahem) as a weapon. (They already sell weapons of mass destruction, of course, but those are generally used to commit a drawn-out suicide.)
First, let’s examine why Big Soda is fighting back. Here’s a quote from an article on LewRockwell.com:
Sales of sugar-laden sodas have been declining steadily for years and the beverage giants are scrambling to reinvent their products and dodge the blame for health risks associated with those products. PepsiCo just announced that it is killing off aspartame in its diet sodas, as consumers, better educated by way of online access and social media, are starting to avoid the industrial food machine’s aspartame and high fructose corn syrup.
And another quote from an article in the New York Times:
“Coca-Cola’s sales are slipping, and there’s this huge political and public backlash against soda, with every major city trying to do something to curb consumption,” said Michele Simon, a public health lawyer. “This is a direct response to the ways that the company is losing. They’re desperate to stop the bleeding.”
Soon after Fat Head came out, I engaged in online debates with people who were outraged that I refused to blame McDonald’s for the rise in obesity. The exchanges usually went something like this:
Of course it’s their fault! They draw people in with their advertising and get them hooked on junk food!
I’m sorry their advertising got you hooked on eating at McDonald’s. If only you’d had the willpower to resist the ads.
I’m not talking about me. I never eat at McDonald’s. I’m talking about other people.
The ads didn’t draw you in and get you hooked? So you’re really just concerned for the stupid people who, unlike you, are powerless to resist the advertising?
I didn’t say that!!
Yeah, you pretty much did.
That’s the mindset of people who believe our decisions are controlled by evil corporations: we buy what we buy because it’s what the corporations sell.
That’s not how markets work. We don’t buy what they sell. They sell what we’re willing to buy – and all the fancy advertising in the world won’t convince us to buy products we don’t want. If advertising were that effective, New Coke and the McLean burger would have been smashing successes.
So now Big Soda’s sales are tanking — and in case you haven’t noticed, they advertise just as much now as they did 20 years ago. Perhaps more so. But it’s not working. As an article in Slate Magazine explains:
Consumers have gotten a lot more health-conscious, so they’re fleeing both sugar-packed drinks and artificial sweeteners like aspartame. Consumer skepticism has officially replaced New York’s attempted big-drink ban as the biggest threat to the soda industry.
Which is why New York’s attempted big-drink ban was another shining of example of a useless nanny-state regulation dreamed up by The Anointed. Anyway …
So before it’s too late, Coca-Cola is trying to change the narrative. With the best science that money can buy.
How do you get health-conscious consumers to drink Coke? Apparently Coke believes confusing the science will do the trick. From the New York Times article:
Coca-Cola, the world’s largest producer of sugary beverages, is backing a new “science-based” solution to the obesity crisis: To maintain a healthy weight, get more exercise and worry less about cutting calories.
The beverage giant has teamed up with influential scientists who are advancing this message in medical journals, at conferences and through social media. To help the scientists get the word out, Coke has provided financial and logistical support to a new nonprofit organization called the Global Energy Balance Network, which promotes the argument that weight-conscious Americans are overly fixated on how much they eat and drink while not paying enough attention to exercise.
That’s why you’re fat, America! It’s not the sodas; it’s your laziness. Get off the sofa, get active, then go enjoy those sodas jam-packed with all that yummy high-fructose corn syrup.
The PR campaign includes a video that you can watch on this page. Go ahead, I’ll wait.
The bearded dude in the video is one of the scientists now on the Coca-Cola payroll. When I watched the video, I had the same reaction as Karen De Coster, who wrote the article on LewRockwell.com:
The man in the video is Steven Blair, PED, FACSM, a Professor in the Department of Exercise Science in the Arnold School of Public Health at the University of South Carolina. That he’s a mouthpiece for “public health” sends a clear message that he is a paid-for shill for the Industrial Food Machine. And then, am I not supposed to notice, or say, that this Professor of “exercise science” is obese?
Coca-Cola may want to re-think the PR strategy here. They hope to convince us it’s mainly a lack of exercise causing obesity. They’ve got a professor of exercise science saying as much – but he’s clearly a very, uh, large man. So what are we supposed to believe about him? That he knows all about the weight-loss benefits of exercise, but isn’t interested in applying to himself? Shades of Kelly Brownell.
Given that Coke is pumping millions of dollars into this effort, I’m sure it’s tempting to be outraged. Don’t be. The proper response here is a hearty laugh, because Coke may as well pour those millions down the drain. This campaign will be about as effective as the ad campaign for New Coke. I’ll bet you dollars to donuts, and you can keep the donuts.
Some years ago, yeah, maybe the strategy would have worked. That’s because some years ago, information flowed from the top down, through a series of information gatekeepers. Companies like Coca-Cola had the financial muscle, through advertising dollars and otherwise, to give marching orders to many of those gatekeepers.
That’s just not how it works anymore. Not in the days of the internet, social media, and the Wisdom of Crowds. Information flows down, up and sideways. The information gatekeepers are increasingly irrelevant (where they even still exist), and public trust in the “science” presented in Big Media is plummeting. The comments sections of articles promoting grains or low-fat diets are so full of blistering critiques, I’m surprised some news sites even allow comments.
In the final episode of Mad Men, we learned that Don Draper was the advertising genius whose jingle had us all wanting to teach the world to sing and buy the world a Coke. (In the land of TV fiction, that is.) But that was then. Now more and more people don’t even want to buy themselves a Coke – and there’s nothing Don Draper or a bunch of paid shills with PhDs can do about it.
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A production crew from Korea came to the Fat Head farm on Sunday to interview me and to film us collecting eggs and cooking them up with some sausage. The segments will go into a TV special about the controversy over whether saturated fat and cholesterol cause heart disease. I will, of course, be one of those who says nope, they don’t. They’ll interview several other people who share my opinion (Uffe Ravnskov and Chris Masterjohn among them, if I remember correctly) and, of course, the usual suspects who still promote the artergycloggingsaturatedfat! theory.
I wasn’t sure how specific they’d want me to be as far as citing research, so I took some time over the weekend to poke through my database of articles and studies. Turns out their questions were more general (“Do you worry at all about how much saturated fat you eat?”), but what the heck, since I came across a couple of interesting items in what I now think of as the Cold Case Files, I thought I’d share them.
The first is a study published in – wait for it – the Journal of the American Heart Association. The AHA is, of course, one of the organizations most responsible for scaring people away from saturated fat. Saturated fat raises cholesterol, and high cholesterol causes heart attacks, doncha know. At least that’s been their position ever since Ancel Keys joined the AHA board of directors.
But this study is from 1961 – before Keys joined the AHA board. So I find the study’s conclusions rather fascinating. The researchers gathered data on serum cholesterol levels and coronary artery blockage taken from 200 autopsies. Here’s what they found:
The mean atherosclerotic indices, i.e., the amount and severity of atherosclerosis in the aorta and the coronary and cerebral arteries, showed progressive increase with age.
The mean serum total cholesterol concentration rose progressively from the first decade to a maximum level in the fifth decade and subsequently declined.
In other words, cholesterol tends to rise until sometime around age 50, then drop a bit. The buildup of plaque in the coronary arteries, meanwhile, progresses throughout life. The researchers noted those facts because they wanted to avoid a false association:
The mean serum total cholesterol showed a progressive rise from the first to sixth groups of aortic atherosclerosis, but, at the same time, the mean age for each group also increased. Since the amount of atherosclerosis in the aorta increased with age and the serum cholesterol concentration also rose up to the fifth decade, it is important to determine if the significant correlation between the concentration of serum total cholesterol and aortic atherosclerosis is a correlation with severity of atherosclerosis per se or is merely due to the effect of age, or both.
So they compared serum cholesterol and coronary blockage within age groups. The results:
No correlation could be found between the two, indicating that, when the age factor was removed, the positive correlation between aortic atherosclerosis and serum total cholesterol is statistically insignificant.
And later in the same paper:
In the present study, we did not find any significant correlation between the blood serum total cholesterol and atherosclerotic index as a representation of the extent and severity of atherosclerosis for any of the vessels studied. The mean serum total cholesterol concentration in the six groups of aortic atherosclerosis showed a successive rise but, when the age factor was taken into consideration, the correlation between atherosclerosis and serum cholesterol in these same groups was found statistically insignificant.
No significant association once you take age into account. Doesn’t that just make you want to run out and get a prescription for statins?
In my research database, I also found an abstract from a European Journal of Clinical Nutrition study of diets in the U.K. vs. France. It’s a bit of a silly study, based on dietary recall and all that, but I saved it because of this gem:
There were positive and negative trends in food consumption in each country. UK respondents reported eating more beans and pulses, less cheese, red meat, and processed meats than French respondents. However, on the negative side, they ate less fruit and vegetables, fish and poultry, cereals, and more sweets and chocolates and cakes, pastries, biscuits and puddings.
Hey, way to go, UK! Sure, the Brits reported eating more sweets and biscuits. But by gosh, they also reported eating less meat, processed meat and cheese than the French. I’m pretty sure they also eat less butter than the French. And aren’t foods like meat, cheese and butter the causes of heart disease? They raise cholesterol levels, ya know.
The study was published in 2000. I happen to have spreadsheets of World Health Organization data on average cholesterol levels and heart-attack deaths from that period. (Some of it’s from 2000, some from 2002.) I plucked the data for the UK and France. I also added data for the Czech Republic, Germany and Russia. Why? Well, the Russians have low average cholesterol, the Czechs have the same average cholesterol as the French, and the Germans have one of the highest average cholesterol levels in the world.
Here are the average cholesterol levels among men, from lowest to highest:
Czech Republic: 209
According to the Cholesterol Kills! theory, the Russians are in great shape as far as heart disease, while the Germans are probably grabbing their chests and dropping like flies.
Here’s a chart I created in Excel to plot cholesterol levels against rates of heart-attack deaths. The blue line is average cholesterol levels among men; the orange line is annual heart-attack deaths per 100,000 men.
Hmmm, things aren’t looking so good for the Russians after all. And German men have fewer fatal heart-attack deaths as a group than men in the UK, despite an average cholesterol level that’s 23 points higher.
The Russian heart-attack rate is so high, including Russia scrunches the chart. So here it is again with Russia removed.
If high cholesterol causes heart disease, those lines should more or less rise together. But they clearly don’t. If anything, they tend to move in opposite directions.
It was fun digging through the Cold Case Files. But I’ll be happy when the entire Cholesterol Kills! theory is a cold case file.
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Two items have appeared the news lately that ought to change what most people think they know about diets and health – that is, if most people were aware of the news items.
I covered one of them in a recent post about the tipping point: several prominent organizations, including the Academy of Nutrition and Dietetics, have finally admitted that upon further review, cholesterol and saturated fat aren’t health hazards after all. We can’t underestimate that one. Given how entrenched the arterycloggingsaturatedfat! theory was, this is akin to officials in the North Korean government announcing that upon further review, communism doesn’t actually work.
Think about just how profoundly the fear of saturated fat and cholesterol has affected us over the decades. It’s why whole milk was banned from schools and replaced with sugar-laden skim milk. It’s why when you go shopping for yogurt, almost every container is labeled nonfat or low-fat. It’s why doctors and nutritionists wanted to put everyone on a low-fat diet. It’s why Weight Watchers started peddling those ridiculous Smart Ones (one gram of fat) meals. It’s why so many restaurants feature a “heart healthy” section of low-fat foods. It’s why restaurant foods are fried in those lousy vegetable oils. It’s why hospitals feed low-fat carbage to patients, including diabetics.
I could go on and on, but I won’t. The point is, fear of arterycloggingsaturatedfat! has underpinned millions of bad decisions over the decades by everyone from food manufacturers to frustrated dieters. Let’s cross our fingers and hope those days are finally coming to end.
Of course, we haven’t just been warned away from fatty foods over the years. Nope, we’ve been warned that all kinds of foods will kills us – red meat, to name an obvious example. And we’ve been assured that some foods will save us – whole grains, to name an obvious example. Most of those warnings and assurances have been based on observational studies. This or that is linked to such-and-such, blah-blah-blah.
I’ve been yammering on about how unreliable those studies are ever since I started blogging six years ago. It’s bad enough that researchers want to draw conclusions from mere correlations. But even the correlations are suspect, because (as I’ve pointed out several times), the data is based on food-recall surveys that simply aren’t reliable. I’ve known that for decades, because when I worked at a magazine, we all had to fill out a food-recall survey for some kind of health evaluation, and it was a joke. We just made stuff up to be done with it.
Now a paper published in the Mayo Clinic Proceedings says the same thing. Here’s part of the abstract:
We assert that uncritical faith in the validity and value of M-BMs [memory-based dietary assessments] has wasted substantial resources and constitutes the greatest impediment to scientific progress in obesity and nutrition research. Herein, we present evidence that M-BMs are fundamentally and fatally flawed owing to well-established scientific facts and analytic truths. First, the assumption that human memory can provide accurate or precise reproductions of past ingestive behavior is indisputably false. Second, M-BMs require participants to submit to protocols that mimic procedures known to induce false recall. Third, the subjective (ie, not publicly accessible) mental phenomena (ie, memories) from which M-BM data are derived cannot be independently observed, quantified, or falsified; as such, these data are pseudoscientific and inadmissible in scientific research.
Pow. Zing. Whamo. The researchers are calling B.S. on M-BMs. But wait, it gets better: they’re also calling B.S. on perhaps the most influential organization to make use of (ahem) “studies” based M-BMs. Here’s how an article in Reason Magazine online describes what the researchers have to say:
A new article by University of Alabama-Birmingham researcher Edward Archer and colleagues Gregory Pavela and Carl Lavie, published this week in the Mayo Clinic Proceedings, argues that the conclusions drawn by the federal government’s controversial Dietary Guidelines Advisory Committee (DGAC) rest on fatally flawed assumptions about unusable data. Consequently, the authors conclude that the DGAC’s work—and the research used to support that work—is so off base as to be scientifically useless.
Pow. Zing. Whamo. Take that, USDA.
The Reason article includes an interview with researcher Edward Archer. Here’s some of what he had to say:
“My coauthors and I wrote this article because for over 50 years, government-funded researchers have been presenting anecdotal evidence as science. Given that these data constitute a majority of the evidence base for the federal nutrition guidelines, we think the greatest problem in nutrition and obesity research is not ignorance; it is the illusion of knowledge created by pseudoscientific methods.”
“My previous work demonstrated that 60-80 percent of the dietary data from the NHANES is physiologically implausible. That is a scientific way of saying that people could not survive on the amount of foods and beverages they report.”
“It defies scientific and common sense to think that anyone can accurately remember and will honestly report the exact amount and specific type of foods and beverages they consumed yesterday, much less last week or last year.”
“The confluence of self-interest, institutional inertia, and scientific incompetence has led us to where we are today. The federal government has massively increased spending on nutrition and obesity research over the past few decades, and now spends over $2 billion of taxpayer’s money per year. Unfortunately, the people that control that funding are the same researchers that use these anecdotal methods, train the next generation of researchers, and control the publication of scientific papers. The same researchers are getting funded to do the same research year after year after year. This inertia and self-interest are exacerbated by the exorbitant amount of grant funding established researchers receive. As with many things in life, follow the money.”
Follow the money … I should use that line someday.
“The government funded researchers control the field by funding only those researchers that use the same flawed methods; they stifle progress by rejecting contradictory evidence, and immediately impugn the integrity and competence of researcher who disagree.”
It doesn’t surprise me in the least that government-funded researchers stifle research and reject contradictory evidence. But let’s set all that aside and focus on the main point: food-recall surveys are a complete joke. I don’t care how much fancy-pants statistical analysis you perform, if the data going in is garbage, then garbage is what comes out the other end.
So once again, think about how many This Food Linked To That Disease articles you’ve seen in the media over the decades. You’ve probably had well-meaning friends and family members shove them in your face while you’re busy trying to dunk a piece of bacon in an egg yolk. I’ve lost count of how many people have told me they don’t eat red meat because they had a near-relative die of colon cancer, and well, you know, red meat is linked to colon cancer. It’s been in the news and everything.
Saturated fat and cholesterol aren’t health hazards, and pretty much every This Food Linked To That study ever published is a joke.
Those two things ought to change everything.
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Like most people, I’ve long assumed whiskey can have a negative impact on memory. The first time I drank whiskey (as a teenager, I’m sorry to say), my only memory after the fourth or fifth shot was of a glowing star dancing in front of my face. I later realized, while helping my drinking buddy clean the room where we drank the whiskey, that the dancing star was the burning end of a cigarette. Neither of us remembered smoking the cigarettes, but we sure cleaned up quite a few of them.
My belief that whiskey affects memory was strengthened during my college years. My roommate and I mostly drank beer at parties, but occasionally indulged in Jack Daniel’s. The Jack Daniel’s nights sometimes led to a series of next-day phone calls intended to ascertain, say, why my car was parked in the middle of a courtyard, and why some guy I didn’t recognize was snoring in the back seat.
So yeah, I just always figured whiskey is bad for memory, at least in the short term.
Well, I should know better than to form medical opinions based on anecdotal evidence. Turns out whiskey doesn’t affect memory. I know this because I recently conducted a careful study comparing the effects of gin and whiskey on memory, and there was no statistically significant difference. That means we don’t need to be concerned with whiskey’s effect on the brain. I could even write a news article with the headline:
STUDY QUESTIONS WHISKEY, MEMORY LOSS CONNECTION
What, you say that’s a ridiculous conclusion? Well, of course it is. But it’s no more ridiculous than the conclusions from a study that generated this headline:
STUDY QUESTIONS STATIN, MEMORY LOSS CONNECTION
Beginning treatment with a statin was associated with a nearly fourfold increased risk of developing acute memory loss within 30 days in a retrospective cohort study …
Yeah, so that would lead me to conclude statins are bad for memory.
… but a similar increase in risk was seen in patients starting non-statin lipid-lowering drugs.
WTF?!! Does that somehow exonerate statins? Let’s read on.
Compared with non-users, both statin and non-statin lipid-lowering drug (LLD) use was found to be associated with acute memory loss in the weeks following treatment initiation, but there was no difference in memory loss when statins and non-statins were compared with each other, researcher Brian L. Strom, MD, of Rutgers University in Newark, N.J., and colleagues wrote online June 8 in JAMA Internal Medicine.
I see. So Dr. Strom compared the effects of whiskey and gin on memory loss and found them to be the same. No worries about whiskey, then. Next thing you know, Dr. Strom will be suggesting people who drink whiskey and gin just think they’re experiencing more memory loss.
The observation that all LLDs were associated with memory loss suggests that either all drugs used to lower lipid levels cause acute memory loss or that the observed memory loss in the study was due to detection bias, Strom said.
Head. Bang. On. Desk.
In a telephone interview with MedPage Today, Strom said it makes sense that patients on a new drug would be more likely to notice symptoms and attribute them to the drug, and they are also more likely to report such symptoms to their physician.
Riiiiight. Statins (and other lipid-lowering drugs) don’t actually cause memory loss, ya see. It’s just that people on statins who were going to have memory issues anyway are more likely to blame the drug. Kind of like one of those next-day phone conversations in college …
“Hello? Oh, hey, Mark. What? Of course I’m alive! Why wouldn’t I be? Uh-huh … uh-huh … I said WHAT?! YOU’VE GOT TO BE KIDDING ME! Well, hell no, I don’t remember! Look, just do me a favor and tell her it was the Jack Daniel’s talking!”
Several previous studies have shown acute memory loss associated with the use of statins, but others have not shown the association or have even shown improved memory in long-term statin users compared with non-users.
Strom noted that without the non-statin LLD control group in his study, the findings would have shown a strong association between statin initiation and short-term memory loss.
“In the absence of this control group, the finding would have been completely misleading,” he said.
Okay, to illustrate the deep and wide stupidity of that statement, imagine this quote about my whiskey-and-gin comparison study.
Naughton noted that without the gin-only control group in his study, the findings would have shown a strong association between whiskey and short-term memory loss.
“In the absence of this gin-only control group for comparison, the finding would have been completely misleading,” he said.
Strom said the study findings should reassure both patients and physicians who prescribe statins.
Naughton said the study findings should reassure both college students who drink whiskey and the liquor-store owners who sell the whiskey.
“This whole issue of short-term memory loss with statins is really a tempest in a teapot,” he said. “Statins are very effective drugs, and people should not veer away from them for fear of a short-term memory effect, especially given the data suggesting that long-term statin use improves memory.”
“This whole issue of short-term memory loss with whiskey is really a tempest in a teapot,” Naughton said. “Whiskey is a very effective drink, and people should not veer away from it for fear of a short-term memory effect, especially given the data suggesting that long-term whiskey use improves memory.”
Strom reported receiving research funding from AstraZeneca and Bristol-Myers Squibb and serving as a consultant to Abbott, AstraZeneca, Bayer Healthcare, Bristol-Myers Squibb, Novartis and Pfizer. A co-author reported receiving research funding from AstraZeneca and Bristol-Myers Squibb and serving as a consultant to AstraZeneca, Bayer Healthcare, Bristol-Myers Squibb, and Merck.
Naughton reported receiving research funding from Jack Daniel’s and Old Grand-Dad and serving as consultant to Jim Beam, Johnnie Walker and Jameson’s. A co-author reported receiving research funding from Knob Creek and Barton Reserve and serving as a consulting to Glen Morangie, Glenfiddich, Canadian Club and Bushmill’s.
Here’s the bottom line: beating down your cholesterol is bad for your brain, whether you do it with a statin or another drug. Comparing statins to non-statin LLDs doesn’t change that … any more than drinking gin instead of whiskey will explain why that strange dude is snoring in the back seat of your car.
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I wasn’t planning to write another post this week because I’m busy at work and trying to make headway on the book Chareva and I are producing. But a meat-and-mortality study showed up in my inbox, which prompted me to dig up a few more. In my post dedicated to our vegetarian-zealot friends, I made the point that observational studies (the kind they cherry-pick to “prove” that meat will kill you) are unreliable and inconsistent. Here are some studies that underscore that point.
From Meat consumption in relation to mortality from cardiovascular disease among Japanese men and women:
Moderate meat consumption, up to ~100 g/day, was not associated with increased mortality from ischemic heart disease, stroke or total cardiovascular disease among either gender.
What their data showed is that compared to men with the lowest meat intake, men with the highest meat intake had lower mortality rates from heart disease, a very slightly higher mortality rate from stroke, and the same mortality rate from all cardiovascular diseases combined. Women who ate the most meat had a slightly higher rate of mortality from heart disease, but a lower mortality rate from stroke.
So here’s the story so far: meat reduces heart-disease mortality in men, but raises it in women. But the differences aren’t really significant either way.
From Red meat and poultry intakes and risk of total and cause-specific mortality:
Red meat intake was associated with increased risk of ischemic heart disease mortality and with decreased risk of hemorrhagic stroke mortality. There were suggestive inverse associations of poultry intake with risk of total and all-CVD mortality among men, but not among women.
Okay, then. Red meat causes heart disease – for both men and women – but prevents strokes. Poultry also prevents heart disease for men, but not for women. Got it.
From Meat intake and mortality:
Regarding cause-specific mortality, men and women had elevated risks for cancer mortality for red and processed meat intakes. Furthermore, cardiovascular disease risk was elevated for men and women in the highest quintile of red and processed meat intakes. When comparing the highest with the lowest quintile of white meat intake, there was an inverse association for total mortality and cancer mortality, as well as all other deaths for both men and women.
Stop the presses! Turns out red meat causes cancer and heart disease for both men and women after all. Poultry, on the other hand, prevents cancer and a premature death – for both men and women.
From Red meat and processed meat consumption and all-cause mortality:
In a dose-response meta-analysis, consumption of processed meat and total red meat, but not unprocessed red meat, was statistically significantly positively associated with all-cause mortality in a nonlinear fashion.
Notice what they wrote about unprocessed red meat: it’s not associated with higher all-cause mortality. Now look at the conclusion:
These results indicate that high consumption of red meat, especially processed meat, may increase all-cause mortality.
Somehow red meat is still to blame, but especially processed meat. The accurate statement (based on their data, anyway) would have been that only processed meat is the problem.
So the updated story: red meat and especially processed meat will kill you.
From Meat consumption and diet quality and mortality:
After multivariable adjustment, neither red and processed meat, nor white meat consumption were consistently associated with all-cause or cause-specific mortality. In men, white meat consumption tended to be inversely associated with total mortality, but there was no such association among women.
I see. Red meat, white meat, and processed meat aren’t associated with all-cause mortality, or with mortality from any specific cause. White meat prevents premature death among men, but not women.
So here’s what we know from observational studies: Meat – especially red meat and most especially processed meat – will kill you. However, meat (including red meat) prevents heart disease among men while having no effect on premature death. Unfortunately, the same red meat causes heart disease among women — and among men, except for the men.
White meat prevents heart disease among men, but not women. However, it prevents cancer and premature death for both men and women, but not women.
Oh, and all meats – red, white, processed and unprocessed – also have no effect on specific or all-cause mortality for anybody.
That’s why observational studies are a joke – as are the people who cherry-pick them to (ahem) prove a point about meat and health.
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