Walter Willett and the Terrible, Horrible, No Good, Very Bad Data

One of the major problems in nutritional epidemiology is that we have a hard time measuring things that we are supposed to be measuring in order to say anything meaningful about relationships between diet and chronic disease. You know, things like how much people are actually eating or how much physical activity they really do get.

Today I had the opportunity to hear Walter Willett, king daddy of the field of nutritional epidemiology, speak on just this dilemma (and yes, he still has that sweet ‘stache).  Introduced as having received “too many awards to mention,” W began his talk–“Energy Balance and Beyond:  The Power and Limits of Dietary Data”–by addressing the recent unpleasantness raised by  researchers who have suggested that the dietary data that we collect simply isn’t worth analyzing (Archer, Pavela, & Lavie 2015; Dhurandhar et al. 2015).

Having been recently immersed in my rhetoric of science readings, I noted that W started right off with some perfunctory boundary work, as way of indicating who was “in” and who was “out” when it came to credibility:  He noted that the investigators questioning the value of dietary self-reports are “funded by Coca-cola,” and even the ones that are “pretty good scientists” are “not epidemiologists” and therefore “a little bit naive.”  So much for evaluating the data and the arguments on their own merits.

Then he trotted out the “slippery slope” argument:  If we throw out self-reported dietary data because it is wildly inaccurate, then not only do we have to “throw out the Dietary Guidelines” (heaven forfend!), but we’d have to throw out occupational safety and drug trial data also–because these are often based on self-reports.  Certainly, there’s very little difference between reporting on events in your workplace or what side effects you might have in response to a pill you’re taking and reporting on what you remember eating over the course of the past year.

Then he got down to the nitty-gritty.  The reason your Average American is fat is, to put it bluntly, because of math:

2500 kcals/day x 1% = 25 kcals/day

25 kcals/day x 365 days/year = 9125 kcals/year

9125 kcals/year  = about 1kg of weight gain/year

Of course, the Average American only gains (on average) about 0.5 kg/year, but  W easily explained the discrepancy:  We gain weight, but then we have to expend more energy dragging our fat asses around–my words, not his–so we don’t gain as much weight as we would, but then the increased energy expenditure makes us hungry, so we eat more, so we gain weight, ad infinitum, only not, because we seem to plateau, but then, well, there’s that.

So here’s the $64,000 (or really a few hundred million in grant money) question:  How good are we at measuring the 1% (or less) difference between “energy in” and “energy out” that we see expressed as weight gain in the population?

The answer, according to the man himself?  Not very.

W then showed a comparison of a set of methods to measure “energy in,” along with their coefficient of variation (you can get the technical explanation here, but it is–simplistically–a measure of the amount of variability in your data; long story short:  larger numbers = more variability, less precision and smaller numbers = less variability, more precision).

It looked something like this:

Method Co-efficient of variation
Food frequency questionaire (FFQ) 15%
Diet record 13%
24-hour diet recall interview 28%
Doubly-labeled water (DLW) 9%
Weight 3%

What W made clear is that, if you want to know whether–or to what extent–Americans are indeed eating more and moving less, you can’t measure “energy in” using FFQs, diet records, and interviews and expect to get anywhere near that “1% of calories” accuracy you’re looking for.  You can’t even rely on doubly-labeled water, typically considered to be a biomarker measurement with a high degree of precision.  In fact, W made the point that DLW samples sent out to different labs would come back with results that differed by up to 50%.

W went on to explain that we have similar difficulties measuring “energy out,” with our very best measurements having a coefficient of variation of nearly 20%.

So in other words, or actually in W’s exact words:

“Weight is the best measure of energy balance.”

Wait? Weight?

As far as I can figure it, using weight as a way of “measuring” (and I use that term loosely) energy balance creates a theoretical–if not a methodological–situation that is, in a word, unfalsifiable. Or–in another word–bogus.

“Weight gain results when the things that we think cause weight gain happen, thus proving that those things have happened.” 

At least one of the reasons for attempting to measure “energy in” and “energy out” is to find out whether or not it makes sense to attribute weight gain (or loss) to the differences between them. Instead, W is saying, we can know all we really need to know about how much people eat or move or both, because, voila, weight.

This is like saying, even though traces of tooth fairy fingerprints, footprints, or fiber samples are extremely difficult to obtain, we can reliably determine the existence of tooth fairies by the presence of quarters under your pillow.

Not only does this completely disregard the ever-growing list of things that may also contribute to weight gain/loss over time,* but it contradicts W’s own assertion just moments later that–even though we can’t do it very accurately–a good reason for attempting to measure total energy intake is that it can act as a “crude measure of physical activity.”

One the one hand, W is saying we can estimate how active you are by finding out how much you eat because people who eat more are also likely to be more active–that’s why they eat more–and people who eat less are typically less active–that’s why they don’t eat as much–with the implication being that “energy in” and “energy out” are positively related; as one changes, the other changes in the same direction.

On the other hand, he’s saying these two variables are completely independent of each other. Eating more doesn’t imply you move more; moving less doesn’t imply you eat less. And the way we know that these two variables are disconnected in any given Average American is, voila again, weight.

At this point, it was hard not to be completely distracted by the cognitive dissonance ringing through the room.

I did hang on long enough to hear W say that we shouldn’t really be worried about energy intake anyway because what really matters is diet quality, which, by the way, we can’t measure accurately either.

With all due respect, all I could think of is that while Emperor W may not be completely without clothes, he was definitely down to boxer shorts today.

emperor needs clothesIn an auditorium full of really smart people, I cannot have been the only person thinking that W and his data looked a little over-exposed. But–as we saw with the circumstances revealed by the Ramsden and Zamora paper last week–it can be hard to contradict a famous colleague, and in nutritional epidemiology, no one is famouser than W. It may be even harder, I suppose, when he is an invited guest and an apparently nice fellow. The Q&A was respectful and polite. Difficult as it is to believe, even I kept my mouth shut.

I know science sometimes advances one funeral at a time, and I truly wish W a long and happy life. But maybe he’ll start to get a little chilly there in his boxers and start thinking about retiring someplace warm. Soon.

************************************************************************

*Genetic factors

Epigenetic factors

Gut microbiome

Environmental toxins

Medications/drug use

Hormonal status

Lifestage

Health status

Infection

Inflammation

Sleep patterns

Stress levels

Non-exercise  activity levels

Smoking status/history

Alcohol consumption

Other unknown factors

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86 thoughts on “Walter Willett and the Terrible, Horrible, No Good, Very Bad Data

  1. Weight measurement is the most accurate way of measuring weight gain? That must have taken a lot of experimentation.

    I suppose this topic is a peculiarly opportune one for a circular definition. 😛

    But the variance coefficient of direct weight measurement is 3%, so by that margin of error, people could be losing weight by 2% and still register as gaining 1%!

    And lastly….. if we shouldn’t be worried about energy intake, favoring diet quality instead, then why by that logic should weight itself be a concern at all?

    1. Avery: I would suggest that it is a concern at the extremes, and among those who experience rapid gain or loss; otherwise, no, it is nothing more than another of those wonderful variations we exhibit because of genetic and environmental differences.

  2. All this talk about W (and WW) made me think of:

    W = Dubya = George W “Mission Accomplished” Bush

    WW = Walter White

    1. Mostly, I got cross-eyed typing his last name (one l and 2 ts? two ls and one two ts? neither? both?). But I’m thoroughly enjoying all of the extrapolations from it.

  3. Some people should be forced to read Gary Taubes’ books again and again until they understand that obesity is not about thermodynamics, but about physiology. Just like every other growth in an animal.

    1. Agreed. When I hang out with the animal science folks, they are stunned by the crapulousity of our methods in human nutrition. Since we can’t cage our subjects & then sacrifice them to see what “really” happened during a feeding trial like they can, it seems we could at least learn a few foundational points from them about physiology.

      1. Adele Sorry, you don’t know more than a doctor, especially one who is an expert in nutrition. You are not in Doctor willet’s area code.You are a pathetic wannabe crybaby, with a little too much penis envy.

        1. Dr. Willet (that’s actually how you write it if you know what you’re doing) isn’t an “expert in nutrition.” He’s an expert in getting grants out of datasets. It’s not the same thing. For one, the datasets can’t sue him for shoddy advice.

    2. I listened to this really fascinating podcast about birds, and something that really struck me is how birds change their bodies for migration.

      http://www.npr.org/2015/10/20/450038490/flights-of-fancy-exploring-the-songs-and-pathways-of-the-living-bird

      Search/scroll down to the part about the bar-tailed godwit (also a great name for a band). Sure they gain fat by eating a massive amount in preparation, but also their organs shrink, and their muscles (including the heart) increase by 50% without “working out” to cause it. That’s pretty incredible.

      1. Very interesting article. Makes me think that we just need to get some anthropologist from Mars to explain, oh I don’t know, let’s say “weight gain without increased food intake at menopause” to folks like Willett. If a bird’s metabolism and eating behaviors can demonstrate a remarkable adaptive mechanism–and ones that seem to defy a strict CICO explanation–why not humans? Also, now I want to learn all the owl calls ..

  4. I’m a longtime fat rights activist. Walt Willett is the opposite of a hero in my community. It’s not because people in fat community are any more likely to be lazy gluttons than any other group of people, say, postal workers or nutrition epidemiologists. It’s because his work has so directly fomented weight bigotry for decades. His legacy, in my view, is simple: he won’t compare all that well to the phrenologists who perpetuated racism and sexism in their day. For people in this field, I hope you will consider examining the intense anti-fat stereotype and prejudice that underpin so much of your research. I suggest looking into the Health At Every Size approach, if you care about how you will be remembered. And hurray for the writer of this post for speaking up here, even if you sat on your hands during the talk. (The W stands for wanker.)

    1. Marilyn, it’s an honor to have you visit & comment. I’m very familiar with your work (I have an “obesity politics” reading list for my upcoming exams).

      W = wanker. Somebody had to say it. Thanks for being that someone.

      I agree that W’s work is at the heart of much of the moralizing around obesity. I was stunned to read in one of his that, if a woman is at a “healthy weight” (which for W is a BMI of no more than 22) during young adulthood, she should gain no more than four pounds over the course of the rest of her life (Willett, Dietz, Colditz, 1999). He has also asserted that, “if your weight corresponds with a BMI below 25, do everything you can to keep it there” (Willett, 2001; emphasis added). Unbelievable.

      I like to think that nutritional epidemiology of chronic disease in general will go the way of phrenology.

      Now, if only I could convince the rest of the alt-nutrition community of the wisdom of the HAES approach–and convince the HAES community that the same crappy data that brought us the idea that only one body size/shape can be “healthy” is the same crappy data that brought us the idea that only one dietary pattern can be “healthy.”

    2. Marlyn, you insane, hypersensitive, crybaby.Your comments are those of someone with much thinner skin than we all know you have.
      Dr. Willett is a medical doctor, researcher, and epidemiologist. he doesn’t care about you, he doesn’t even know you. he could not pick you out of a fat farm.
      His work is based on what are the healthiest ways to eat, for optimal health and minimum disease. He NEVER said anything about fat people having less rights than normal humans. Now go eat yourself to death, and smell bad somewhere else.

      1. “His work is based on what are the healthiest ways to eat, for optimal health and minimum disease.”

        Not working though, is it? (Charles, is that you?)

      1. Back at you. Your post is an excellent illustration of the complexity of the interactions between diet and activity. I highly recommend jumping on over the Aaron’s blog & seeing for yourself.

        1. wow, a “nutritionist”in total agreement with a “fat activist.” That does wonders for your credibility!

          1. I feel so special when I get my own troll. Bragging rights with my kids: See? My blob isn’t just an excuse to never vacuum. Its so edgy and provocative that I even get trolls. Okay, a troll. That still counts.

  5. If weight is the best we can do, that’s not good. My weight can vary by pounds per day. For instance, on 4/18 at the gym I weighed 207; on 4/20 (a mere two days later), I weighed 200. I was fasting during that time, so I do tend to lose (primarily water) weight (I weigh myself fully clothed in workout clothes at the gym). That’s still 7 pounds in two days. I’ve been taking data since September of last year. In that time, on my home scale (with no clothes on). I started at 205.5, but had a low weight of 196 and a high of 207 to my current weight this morning of 199.5. Also, I had to cease lifting weights in that time, as I reinjured an old shoulder injury, so I’m sure I’ve lost at least a few pounds of muscle mass, as my belts continue to get smaller even with no or little scale loss.

    Here’s a random sampling (at home on left, at gym on right):

    3/2/16 205.0
    3/3/16 201.0
    3/4/16 199.0
    3/6/16 206.0
    3/7/16 209.0
    3/8/16 201.0

    If weight is the best we can do, I say we stop trying to find anything out using data.

    1. 🙂 I think a huge part of the problem is that for W & co. real human beings don’t actually count as data; only datasets count as data.

      Although there may be ecological exposures that might explain why “populations” gain/lose weight (um, the Dietary Guidelines for example–but also changes in the food supply), somehow we still have to be able to explain what is going on through individual physiology. And we can’t/don’t do that.

      There’s an interesting remark in Willett’s book, Nutritional Epidemiology, where he is complaining about the fact that some analyses show that obesity has little relationship to heart disease. He says: “… obesity cannot be stripped of its metabolic consequences by sophisticated statistical methods.” And yet, this is exactly what we do in nutritional epi of chronic disease; we separate the bodies from the numbers, play around with the numbers, then superimpose the numbers (averaged, adjusted, and otherwise messed with) back onto bodies as if we’ve done something meaningful.

      1. I think Gary Taubes had a point similar to this, when he said that (perhaps referring to Willet) they were a new breed of obesity researchers, since they never had to actually get people to lose weight. They just did “research”. So, they’re divorced from reality.

        But if weight is the best we can do, we’re in trouble. It’s a terrible indicator of anything. I can gain or lose pounds for reasons I cannot decipher. And, I’ve lost two inches off my waist (at least by pant sizes) while my weight has barely budged. I personally think recalling what I ate for the last week, month, or even year would be more accurate. 😉 And we know how accurate those are.

        1. And trust me, if you are a woman, undecipherable weight fluctuations are the rule.

          I have more examples than I care to think about of my fellow nutritional epidemiology students saying things about human beings which caused me to wonder, if they’d ever actually met any–much less worked with them on health issues.

    1. No. “Begging the question” currently doesn’t mean anything although people most commonly use it as synonymous with “asking the question.” The original meaning was to use the question in the answer as in criticizing a diet that tries to improve on health guidelines by substituting fat for carbohydrate as being unhealthy because it does not conform to guidelines for low fat. This misuse of language only annoys curmudgeons from my generation.

      1. No, you were right. I was responding to the quotation in my email. “…one of the reasons…is to find out whether or not it makes sense to attribute weight gain (or loss) to the differences between them. Instead, W is saying, we can know all we really need to know about how much people eat or move or both, because, voila, weight.” Yeah. That’s begging the question in the original sense.

  6. As Richard Feinman said “I have always thought that science is continuous with common sense.”

    For comparison with Willett’s tortured logic (did he explain WHY some people eat 25kcal extra every day? And why most stop doing this once they reach their overweight set point then remain exactly as weight stable as Willett himself?) here is John Yudkin’s 1963 explanation of obesity and prediction of its future causes.

    (full text) https://www.dropbox.com/s/0won5trkfrk5a1s/yudkin1963.pdf?dl=0

    (permanent link) http://www.ncbi.nlm.nih.gov/pubmed/14002890

    And here is his explanation of how carbohydrate restriction reverses overweight. No magics involved, and few uncertainties. (Unlike Yudkin I believe in the plausibility of a metabolic advantage at various macronutrient extremes, but I don’t see why it would make you any less hungry than exercise does to waste energy in such a way).

    (full text) https://www.dropbox.com/s/u9crs7fxguej27f/yudkin1960.pdf?dl=0

    (permanent link) http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(60)92019-5/abstract

    This is reason, valid (and beautiful) in and of itself independent of the 1950’s facts being analysed. People still read Montaigne even though he is often discussing the 16th century’s nonsense.
    Willett, meanwhile, seems to be discussing today’s nonsense in a nonsensical way.
    This cannot stand the test of time.
    In fact, Adele, it looks like it didn’t even last long enough for you to get it home in one piece.

    1. As far as I could tell, the reason people eat an extra 1% of calories a day is so that Willett can explain why they gain 1kg (except really only 0.5kg) of weight/year.

      Thanks for the Yudkin articles. He sounds so, well, reasonable.

      No, I could barely get out of the room without wanting to scream.

      1. I totally agree. That is a great article/study. Yudkin also seems very reasonable and notes the problems with his study. I thought it was interesting that the people eating the “high fat” diet actually ate less fat than did the same people when eating their normal diet.

        If Yudkin and not Keys controlled the conversation, think where we might be today. Although I’m hesitant to allow any single person to control the conversation, as this seems to not lead to the scientific method (most people given control push the conversation they way they see fit), Yudkin seems reasonable.

  7. The original paper is too long but I have always thought that science is continuous with common sense. We understand that all measurements have error and it is only a question of what you do with the data. I take Volek’s study of 40 people with MetS as a kind of classic. There are independent checks. You can trust the reports of his people on low-carb diets because they were ketotic and therefore the low-fat people, drawn from the same population, are probably not drastically making stuff up. But it is about the results. Volek’s study had big differences in outcome: half the people in the low-carb group did better than anybody in low-fat and the actual magnitude of the big losers was big. Errors of 20 % in food consumption is not going to change the bottom line. On the other hand, Walter Willett’s parade of epidemiological studies with odds ratios of 1.5 are absurd. And frequently the raw unpolished data are published and actually show the wrong conclusion. My letter to the editor on Pan’s red meat-diabetes study was published and showed that the data had to be massaged because the raw data led to the opposite conclusion. Walter Willett looks like Wyatt Earp but he is not a straight shooter.

    1. Richard, I think if you’d been in the room today, your head might have exploded. You’re right, more uncertainty in data can be tolerated when outcomes are markedly different between groups. This was the part about nutrition epidemiology that I could never grasp when I was in that program: with such problematic data and such low risk ratios, what could we possibly be looking at except the researchers’ own inclinations expressed as statistics?

      1. This kind of data massaging and wishy-washiness would never be accepted in a “hard” science. It’s like a high school kid peppering a paper with absolute nonsense and gobbledygook just to get to the required word count, but not actually caring about what any of it says, and whether or not the data (and argument) make sense.

        1. My biostats buddy who was at the lecture said the same thing. Problem is, nutritional epidemiology thinks it’s (at least) a biological science. I was at a presentation at UNC a few years ago where the speaker kept referring to epidemiology as a “social science”–a murmur/shudder would go through the room each time.

            1. Good question. I’ve been reading a lot of Nancy Krieger’s work lately–she makes the case that in the “web of causation” we pay no attention to the “spider”–and I’m beginning to think maybe we should consider epidemiology a practice, rather than a science. I think epidemiology can be useful–for some things. And even nutritional epidemiology has helped us understand pellagra and other diseases of diseases of deficiency.

              But nutritional epidemiology of chronic disease is a different matter. I’m not yet ready to use the word pseudoscience, but after the lecture yesterday, well, that is what we call science based on theory that can’t be falsified.

            2. I would categorize epidemiology as “pre-science” in the same way that an ethnography or field records kept on animal behavior. It can provide a lot of insight into possible, hypothetical processes and mechanisms that can then be tested scientifically.

            3. Since an untestable theory is not science, how about calling it “wishful thinking,” or “science fiction”?

            4. Yes. In fact much of what is published in the literature and much of the spewings of “experts” is religion masquerading as science.

            5. Epidemiologists of Willett’s stamp are the modern equivalent of those guys in Gibbon who would cut the guts out of a pigeon every time the Roman Emperors wanted to go into battle or start some new venture.
              The method was crap at predicting really though it was state-of-the art for that day, but the soothsayers knew how to massage the data, so if they had a bit of horse sense or inside knowledge they could stay on top.
              But if they’ve lost their touch, and some scientist (or journalist) contradicts them, they’re treated like the explorer in the old adventure stories who accurately predicts the eclipse among the remains of some ancient civiliisation..
              The people are impressed, but the soothsayers start plotting ways to discredit them.

      1. And here is the thought that always pops into my head when I hear the CICO business: if it’s all so tricky to measure, and a mere half a french fry can cause you to gain weight, how is it that all these normal-weight and not-gaining-weight people manage to do it? How do they always, consistently, every day, every meal, know exactly how much to eat and how much to exercise? Because everything is telling me that weight is controlled through volitional actions regarding one’s food and exercise – so how do these non-fats manage such complex and mysterious calculations? Do they have better slide rules or something? Or is it that… maybe… their deliberate actions AREN’T what’s controlling their weight…? oh no that’s crazy. Just crazy talk.

        1. Gingerzini gem of the day: “non-fats.” I love it. Our language is so morally weighted towards “non-fats” that all the other terms for these folks seem to carry a tacit–or even explicit–stamp of approval: slender, thin, “normal” weight, even skinny is “good” these days (which is different from my childhood, when skinny kids got teased just like chubby kids). Now I have the word I need. Thanks!

          I know that there were some behavioral intervention folks in the room with me yesterday, and they didn’t challenge W on these mysterious calculations or magical slide rule advantages (and shame on them for that). I always wondered why, if W is willing to admit his data pretty much stink, why would it be such a stretch to admit that there are mysteries to weight status that his data can’t explain. But now I understand that he’s trapped in a circular logic in which weight gain explains itself. No wonder he can’t see anything else. (Not that this helps my sense of morale about nutritional epi.)

          1. He is indeed trapped in a box of his own making, and will likely happily remain there, like a cat in the suitcase you’re attempting to pack, until he’s ready for the pine box. Astonishing the drivel educated people will politely subject themselves to.

        2. Your comment gives much food for thought. I was a long-distance runner for about fifteen years, but always had a bit of a belly (15-25 pounds more than now). What changed for me was (two years ago) giving up grains and legumes. The belly fat melted off in about three weeks. I’ve replaced those foods with fat, mainly animal fat. We’re all different, thank goodness, but this was an experiment which went well for me. I never get so hungry that I can’t wait two or three hours to eat, if it takes that long to prepare the food. Tim Noakes wrote some interesting stuff recently about insulin resistance being the progenitor for many of these awful things afflicting us, and about the extensive work of Dr. Reaven of Stanford on this.

          1. Sadly, no dietary modifications have caused me to lose weight. I’ve experimented with low carb, high fat, primal, South Beach, low fat, carb cycling, calorie cycling, low calorie, high calorie, moderate calorie, and every combination of diet and exercise regimens. I spent 13 years of my life as an n=1 science experiment, and have come to the conclusion that I wasted a whole lot of time and energy fiddling with my diet, none of which converted itself to weight loss. These days I devote myself to living in a healthy way (by my definition) without hope or regard for losing weight, and with the goal of maintaining my muscle mass, flexibility, and sanity as I age.

            1. Gingerzingi: That’s exactly my approach. I’ve never been on a weight-loss diet in my life. I think what is most sensible is not to aim for weight loss, but for optimal health, and one’s weight will be in an optimal range. Those with good health come in many different sizes and shapes, and it is only media propaganda which has made people (mainly women) feel like there is something wrong with them if they don’t look like the models in ads. Pure BS, but hellish for those who are affected by it. I remember the comic book ads during the ’50’s which made fun of the 98 lb. weakling. Now the 98 lb. weakling’s physique is held up as the ideal! We spend way too much time and energy paying attention to this stuff, rather than living life. And we get way too many blood tests (I’m not getting any more).

            2. Each time I get a blood test, it comes back positive. Yup, I have blood. I don’t think I need any more tests. Hell, if I can feel a pulse, that’s a pretty good indicator that I’ve still got blood in my circulatory system. 😉

            3. Gingerzini, I love your philosophy! Although I don’t agree with everything that the Health at Every Size community says (many are as wedded to a “one size fits all version of ‘healthy’ diet” as anybody from Willett’s camp), it seems clear that we have a lot less control over weight loss/gain than popular thinking would have us believe. I remember my brother trying to gain weight to join the football team in high school. He had about as much success trying to put on 10 pounds as most of us have trying to take them off. But–he turned 40 and the problem pretty much took care of itself.

              In truth, Gingerzini, I would love to interview you (you’d be anonymous) for my dissertation. My last chapter–in my mind–will be on how individuals have resisted, challenged, or reinterpreted the imperatives for health/weight loss that we are surrounded by. Your perspective–tried-every-diet-once & current approach (health defined your way)–should be part of the larger conversation about food and health.

              Your goals sound remarkably similar to mine. For me, adequate protein & yoga work pretty well for the muscle mass & flexibility issues, respectively. I’m still working on the sanity thing …

        3. And how about animals? They not only maintain a surprisingly constant weight without a dietician following them around (except domestic pets who are fed “scientific” diets of course, and farm animals fed grain specifically to fatten them (there’s a BIG hint right there)), but they “know” when and how to gain weight to fuel migration or hibernation.

          1. @Adele, possibly because I haven’t had coffee yet this morning, I couldn’t figure out how to contact you. I pinged you on LinkedIn, I thought it would give me a chance to add a message (like, “Hi, it’s Gingerzingi) but it didn’t.

    1. Really, we live about 20 miles apart? How come we haven’t gone out for coffee yet?

      I moved from “up North” to a small town in eastern NC when I was young & was quite startled to learn a whole different version of American history–not to mention all those words that Southern women say to keep from saying the words that they would never say!

  8. On a different path here, but somewhat related – have recently been reading “Toms River” by Dan Fagin, about the chemical waste pollution in that area of NJ. Really well told, and to me, a non-scientist, a very illuminating look at epidemiology, its development, and related studies of things like workplace illnesses. A review says: “IT’S HIGH TIME a book did for epidemiology what Jon Krakauer’s best-selling “Into Thin Air” did for mountain climbing: transform a long sequence of painfully plodding steps and missteps into a narrative of such irresistible momentum that the reader not only understands what propels enthusiasts forward, but begins to strain forward as well, racing through the pages to get to the heady views at the end.” (like I said, it’s not exactly related, but this is the right crowd to appreciate a book like this).

    1. So maybe Dan Fagin can do this for *nutritional* epidemiology?

      The fact that people are willing to follow my own painfully plodding steps through this muck never ceases to amaze me. Especially since there’s no “heady views” in sight.

      1. LOL, didn’t mean to imply that! I should have just taken an excerpt from that review.

        But it does take a good writer to pull together a long, complicated, complex series of events and discoveries into an understandable – and in this case entertaining – coherent story. Real life is never that obvious and simple.

        My comment was just to share a book that I’m enjoying, but now that I think about it, it’s probably YOU who should do this for nutritional epidemiology…

  9. Astonishing that he takes himself seriously, which I presume he does. Must be one of those for whom curiosity was entirely drummed out in the primary grades (I must say that my own curiosity was whetted and my BS detectors finely honed by the end of fourth grade). I also presume that most of those smart people in that room do not take his “science” particularly seriously, and were polite partly because he has become irrelevant, partly because we’re trained that way, and partly because of his reputation as a nice guy.

    1. Yes. He does seem to take himself–and his critics–quite seriously. But then, he carries the health of a nation on his shoulders, or at least he seems very convinced that he does.

    1. It was weird. Willett himself seemed to be very clear that the reliability of the sort of data we use in nutritional epidemiology was pretty low. On the other hand, his attitude was “it’s all we’ve got & its better than nothing.”

      He ended by pointing to a bunch of improvements in the health of Americans that he attributes to the influence of dietary guidance based on nutritional epidemiology data. Of course, this same influence is in no possible way responsible for the rise in obesity and diabetes in the first place, right?

        1. Lessee. Cholesterol levels (LDL down, HDL up) and incidence of diabetes, down by about 0.3 million. Of course this is all due to removal of transfats from the food supply and warnings about soda consumption.

          1. The important part of the cholesterol change, much of which will be inconsequential in terms of CVD risk, will be due to the different smoking rates and reduced air pollution etc, and would not be affected if LDL cholesterol increased again, as long as people don’t start smoking.
            Or getting polluted again – this is quite topical – if lead raises cholesterol, no wonder high cholesterol is bad.
            http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1508848/
            Incidence of diabetes is down? Does this mean diabetes has been reversed in 300,000 Americans?
            This is based on clinic sampling and each year’s samples are spread over different locations from from the last. A variety of diagnostics are used (HbA1c, fasting PG, and OGTT results) and the mix of these will vary from year to year. Intersample comparisons are notoriously unrealiable, but “they’re all we have”.Long term trends are more reliable, not sudden upturns or downswings.
            Warnings about soda, the uptake of low carb diets since 2002 – NHANES carb intakes are down a bit recently – and the switch from high PUFA to high oleic oils are some things that might have taken the edge off the diabesity epidemic but I’m not counting on it yet.

            1. Agreed. There are a lot of factors involved in any changes that we see in population health, so for Willett to “claim victory” (we got transfats out of the food supply!) ignores a lot of other influences–and totally disregards the reasons for transfats entering the food supply (thank you, CSPI).

              Fewer new cases of diabetes recently–but again this could be due to many things and, yes, the flattening of carbohydrate intake was the first that came to my mind. We have a long way to go though, until we are back to 1980 levels.

          2. I assume then that Willett believes in the “cholesterol causes heart disease” theory? Talk about a theory with cognitive dissonance! There was a recent study on a drug called evacetrapib, which lowered LDL by 37% and raised HDL by a whopping 130%, yet had no bearing on heart disease. See:

            https://drmalcolmkendrick.org/2016/04/10/lowering-cholesterol-has-no-effect-on-heart-disease/

            If you lower LDL and raise HDL and it has no bearing on heart disease, then raising LDL and lowering HDL not using a drug would mean….?

            Personally, I don’t believe in any of this. I do believe that LDL and HDL are markers for something else, which I think is insulin resistance and high blood glucose levels. You reduce your insulin resistance, and your HDL goes up and LDL usually goes down (my HDL has gone up and LDL and triglycerides have gone down). But it’s not the change in HDL/LDL that has an effect on health; it’s instead the change in insulin resistance.

            1. Bob, I heard a researcher saying this week on BBC radio that type 1 diabetes had risen six-fold in the UK in the last forty years. That’s at the same time as obesity rose ten-fold and type 2 diabetes nine-fold. Another casualty of our revised dietary guidelines? Type 1 is always referred to as not diet related, but the constant demand for insulin resulting from a high carbohydrate diet is surely a strong suspect?

              Of course, the researcher didn’t want to talk about the trigger for this rise, only a drug to possibly deal with it (metformin). In her excellent Ted talk, Professor Wendy Pogozelski, a biochemist and type 1 diabetic, makes clear that she successfully managed her condition by reducing carbohydrates.

            2. Since type 1 diabetes is an autoimmune condition, it is likely that the increase is causally related to the increase in the vaccine schedule over particularly the last thirty years. We’ve seen a fairly dramatic rise in autoimmune conditions of all sorts over those years, and the chronic microglial activation from the aluminum adjuvants (which most pediatric vaccines have) alters the development of immune function to the point of chronic dysfunction in a susceptible subset of children. But you’re right. The evidence is overwhelming, from historical and anthropological research, from the work of Phinney and Volek, Tim Noakes, and a whole host of others, that reducing carbohydrates in the diet and replacing it with fat would benefit most people, both the otherwise healthy and those suffering from an autoimmune condition (such as Dr. Terry Wahls) or other illness.

          3. It’s The American Paradox!

            Probably as much due to people reading this and other blogs and following Real Science and eating Real Food.

            There’s a Swedish Paradox too, I understand their increase in obesity has levelled off since LCHF became established.

            Then of course there’s the Historical Paradox, some of us can remember back to a time when there WERE no epidemics of obesity and metabolic diseases. Then low fat diets were invented . . .

    1. It is a least some progress that we are seeing pushback about data quality–even if it is from those “fringe” scientists!

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