January 26, 2018

Philosophiae naturalis

Is red meat killing us?

I wrote this post almost six years ago (March 21, 2012), but it’s the gift that keeps on giving.

by Peter Attia

Read Time 11 minutes

I wrote this post almost six years ago (March 21, 2012), but it’s the gift that keeps on giving.

These days, I feel a lot like Bill Murray in Groundhog Day, where at least a few times a year, my inbox is stuffed with concerned individuals forwarding me a paper (or, much more the case, a story about a paper) implying red meat is going to send me to an early grave. The irony is that being stuck in some sort of sadistic red-meat time loop probably will do the trick. But at least I have meditation to help with that.

To be fair, the red-meat-studies are not the only culprit. As I mentioned in a Nerd Safari on epidemiology, John Ioannidis and Jonathan Schoenfeld picked 50 ingredients at random out of a cookbook and determined if each was associated with cancer. They found that at least one study was identified as showing an association for an increase or decrease in cancer for 40 out of the 50 ingredients. (The 10 that didn’t make the list were more “obscure,” as the authors put it: bay leaf, cloves, thyme, vanilla, hickory, molasses, almonds, baking soda, ginger, and terrapin. Thank heavens I can still have my terrapin.)

It’s probably not unfair to say that I put together this post as a coping mechanism. Fight fire with fire. You want a time loop? You may see the following post make its way to the front of the queue several times year. While it’s of course not the best tack for me to close my eyes and block my ears to the latest article that forces a visceral reaction, it’s important to put things in context first.

This time around, I’m posting not because a new study just came out on red meat and mortality (although I haven’t checked my email in the past five minutes), but because we’re doing a series on this very topic of observational epidemiology.

Studying Studies: Part I – relative risk vs. absolute risk

Studying Studies: Part II – observational epidemiology

Studying Studies: Part III – the motivation for observational studies

I must admit, re-reading this post for the first time, I thought to myself, ‘Wow, Peter. Chill out…you really wrote that?’ Kinda like when I look at a picture of me from the 90’s. Dude, you wore that?

—P.A., January 2018




“For the greatest enemy of truth is very often not the liedeliberate, contrived and dishonestbut the mythpersistent, persuasive, and unrealistic. Too often we hold fast to the clichés of our forebears. We subject all facts to a prefabricated set of interpretations. We enjoy the comfort of opinion without the discomfort of thought.”

– John F. Kennedy, Yale University commencement address (June 11, 1962)

I’m going to devote this post to a discussion on what I like to call the Scientific Weapon of Mass Destruction: observational epidemiology, at least for public health policy

I had always planned to write about this most important topic soon enough, but the recent study out of Harvard’s School of Public Health generated more than enough stories like this one such that I figured it was worth putting some of my other ideas on the back-burner, at least for a week.  If you’ve been reading this blog at all you’ve hopefully figured out that I’m not writing it to get rich. What I’m trying to do is help people understand how to think about what they eat and why.  I have my own ideas, shared by some, of what is “good” and what is “bad,” and you’ve probably noticed that I don’t eat like most people.

However, that’s not the real point I want to make.  I want to help you become thinkers rather than followers, at least on the topic of health sciences.  And that includes not being mindless followers of me or my ideas, of course. Being a critical thinker doesn’t mean you reject everything out there for the sake of being contrarian.  It means you question everything out there.  I failed to do this in medical school and residency.  I mindlessly accepted what I was taught about nutrition without ever looking at the data myself.  

Too often we cling to nice stories because they make us feel good, but we don’t ask the hard questions.  You’ve had great success improving your health on a vegan diet?  No animals have died at your expense. Great! But, why do you think it is you’ve improved your health on this diet?  Is it because you stopped eating animal products?  Perhaps.  What else did you stop eating?  How can we figure this out?  If we don’t ask these questions, we end up making incorrect linkages between cause and effect.  This is the sine qua non of bad science.

Most disciplines of science—such as physics, chemistry, and biology—use something called the Scientific Method to answer questions. A simple figure of this approach is shown below:


Scientific Method

The figure is pretty self-explanatory, so let me get to the part that observational epidemiology inherently omits: “Conduct an experiment.”  There is no shortage of observations, questions, or hypotheses in the world of epidemiology and public health—so we’re doing well on that front.  It’s that pesky experiment part we’re getting hung up on. Without doing controlled experiments it is not possible to distinguish the relationship between cause and effect.   


What is an experiment?

There are several types of experiments and they are not all equally effective at determining the cause and effect relationship.  Climate scientists and social economists (like one of my favorites, Steven Levitt), for example, often carry out natural experiments. Why? Because the “laboratory” they study can’t actually be manipulated in a controlled setting.  For example, when Levitt and his colleagues tried to figure out if swimming pools or guns were more dangerous to children—i.e., Was a child more likely to drown in a house with a swimming pool or be shot by a gun in a home with a gun?—they could only look at historical, or observational, data.  They could not design an experiment to study this question prospectively and in a controlled manner.

How would one design such an experiment?  In a “dream” world you would find, say, 100,000 families and you would split them into two groups—group 1 and group 2.  Group 1 and 2 would be statistically identical in every way once divided.  Because of the size of the population, any differences between them would cancel out (e.g., socioeconomic status, number of kids, parenting styles, geography).  The 50,000 group 1 families would then have a swimming pool installed in their backyard and the 50,000 group 2 families would be given a gun to keep in their house.

For a period of time, say 5 years, the scientists would observe the differences in child death rates from these two causes (accidental drownings and gunshot wounds).  At the conclusion, provided the study was powered appropriately, the scientists would know which was more hazardous to the life of a child, a home swimming pool or a home gun.

Unfortunately, questions like this (and the other questions studied by folks like Levitt) can’t be studied in a controlled way. Such studies are just impractical, if not impossible, to do.

Similarly, to rigorously study the anthropogenic CO2 – climate change hypothesis, for example, we would need another planet earth with the same number of humans, cows, lakes, oceans, and kittens that did NOT burn fossil fuels for 50 years.  But, since these scenarios are never going to happen the folks that carry out natural experiments do the best they can to statistically manipulate data to separate as many confounding factors as possible in every effort to identify the relationship between cause and effect.

Enter the holy grail of experiments: the controlled experiment. In a controlled experiment, as the name suggests, the scientists have control over all variables between the groups (typically what we call a “control” group and a “treatment” group). Furthermore, they study subjects prospectively (rather than backward-looking, or retrospectively) while only changing one variable at a time.  Even a well-designed experiment, if it changes too many variables (for example), prevents the investigator from making the important link: cause and effect.

Imagine a clinical experiment for patients with colon cancer.  One group gets randomized to no treatment (“control group”). The other group gets randomized to a cocktail of 14 different chemotherapy drugs, plus radiation, plus surgery, plus hypnosis treatments, plus daily massages, plus daily ice cream sandwiches, plus daily visits from kittens (“treatment group”).  A year later the treatment group has outlived the control group, and therefore the treatment has worked.  But how do we know EXACTLY what led to the survival benefit?  Was it 3 of the 14 drugs?  The surgery?  The kittens? We cannot know from this experiment.  The only way to know for certain if a treatment works is to isolate it from all other variables and test it in a randomized prospective fashion.

As you can see, even doing a prospective controlled experiment is not enough, like the one above, if you fail to design the trial correctly.  Technically, the fictitious experiment I describe above is not “wrong,” unless someone—for example, the scientist who carried out the trial or the newspapers who report on it—misrepresented it.

If the New York Times and CNN reported the following: New study proves that kittens cure cancer! would it be accurate? Not even close.  Sadly, most folks would never read the actual study to understand why this bumper-sticker conclusion is categorically false. Sure, it is possible, based on this study, that kittens can cure cancer.  But the scientists in this hypothetical study have wasted a lot of time and money if their goal was to determine if kittens could cure cancer.  The best thing this study did was to reiterate a hypothesis. Nothing more.  In other words, this experiment (even assuming it was done perfectly well from a technical standpoint) learned nothing other than the combination of 20 interventions was better than none because of an experimental design problem.


So what does all of this have to do with eating red meat?

In effect, I’ve already told you everything you need to know.  I’m not actually going to spend any time dissecting the actual study published last week [March 12, 2012] that led to the screaming headlines about how red meat eaters are at greater risk of death from all causes (yes, “all causes,” according to this study) because it’s already been done a number of times by others this week alone.  Three critical posts on this specific paper can be found here, here, and here.

I can’t suggest strongly enough that you read them all if you really want to understand the countless limitations of this particular study, and why its conclusion should be completely disregarded.  If you want bonus points, read the paper first, see if you can understand the failures of it, then check your “answer” against these posts.  As silly as this sounds, it’s actually the best way to know if you’ve really internalized what I’m describing.

Now, I know what you might be thinking:  Oh, come on Peter, you’re just upset because this study says something completely opposite to what you want to hear.

Not so.  In fact, I have the same criticism of similarly conducted studies that “find” conclusions I agree with.  For example, on the exact same day the red meat study was published online (March 12, 2012) in the journal Archives of Internal Medicine, the same group of authors from Harvard’s School of Public Health published another paper in the journal Circulation.  This second paper reported on the link between sweetened beverage consumption and heart disease, which “showed” that consumption of sugar-sweetened beverages increased the risk of heart disease in men.

I agree that sugar-sweetened beverages increase the risk of heart disease (not just in men, of course, but in women, too) along with a whole host of other diseases like cancer, diabetes, and Alzheimer’s disease.  But, the point remains that this study does little to nothing to add to the body of evidence implicating sugar because it was not a controlled experiment.  


This problem is actually rampant in nutrition

We’ve got studies “proving” that eating more grains protect men from colon cancer, that light-to-moderate alcohol consumption reduces the risk of stroke in women, and that low levels of polyunsaturated fats, including omega-6 fats, increase the risk of hip fractures in women.  Are we to believe these studies? They sure sound authoritative, and the way the press reports on them it’s hard to argue, right?

How are these studies typically done?

Let’s talk nuts and bolts for a moment.  I know some of you might already be zoning out with the detail, but if you want to understand why and how you’re being misled, you actually need to “double-click” (i.e., get one layer deeper) a bit.  What the researchers do in these studies is follow a cohort of several tens of thousands of people—nurses, health care professionals, AARP members, etcetera—and they ask them what they eat with a food frequency questionnaire (FFQ) that is known to be almost fatally flawed in terms of its ability to accurately acquire data about what people really eat.  Next, the researchers correlate disease states, morbidity, and maybe even mortality with food consumption, or at least reported food consumption (which is NOT the same thing). So, the end products are correlations—eating food X is associated with a gain of Y pounds, for example. Or eating red meat three times a week is associated with a 50% increase in the risk of death from falling pianos or heart attacks or cancer.

The catch, of course, is that correlations hold no causal information.  Just because two events occur in step does not mean you can conclude one causes the other.  Often in these articles you’ll hear people give the obligatory, “correlation doesn’t necessarily imply causality.” But saying that suggests a slight disconnect from the real issue. A more accurate statement is “correlation does not imply causality” or “correlations contain no causal information.”

So what explains the findings of studies like this (and virtually every single one of these studies coming out of massive health databases like Harvard’s)?

For starters, the foods associated with weight gain (or whichever disease they are studying) are also the foods associated with “bad” eating habits in the United States—french fries, sweets, red meat, processed meat, etc.  Foods associated with weight loss are those associated with “good” eating habits—fruit, low-fat products, vegetables, etc.  But, that’s not because these foods cause weight gain or loss, it’s because they are markers for the people who eat a certain way and live a certain way.

Think about who eats a lot of french fries (or a lot of processed meats). They are people who eat at fast food restaurants regularly (or in the case of processed meats, people who are more likely to be economically disadvantaged).  So, eating lots of french fries, hamburgers, or processed meats is generally a marker for people with poor eating habits, which is often the case when people are less economically advantaged and less educated than people who buy their food fresh at the local farmer’s market or at Whole Foods.  Furthermore, people eating more french fries and red meat are less health conscious in general (or they wouldn’t be eating french fries and red meat—remember, those of us who do eat red meat regularly are in the slim minority of health-conscious folks).  These studies are rife with methodological flaws, and I could devote an entire Ph.D. thesis to this topic alone.


What should we do about this?

I’m guessing most of you—and most physicians and policy makers in the United States for that matter—are not actually browsing the American Journal of Epidemiology (where one can find studies like this all day long).  But occasionally, like last week, the New York Times, Wall Street Journal, Washington Post, CBS, ABC, CNN, and everyone else gets wind of a study like the now-famous red meat study and comments in a misleading fashion. Health policy in the United States—and by extension much of the world—is driven by this. It’s not a conspiracy theory, by the way.  It’s incompetence.  Big difference.  Keep Hanlon’s razor in mind—Never attribute to malice that which is adequately explained by stupidity.

This behavior, in my opinion, is unethical and the journalists who report on it (along with the scientists who stand by not correcting them) are doing humanity no favors.

I do not dispute that observational epidemiology has played a role in helping to elucidate “simple” linkages in health sciences (e.g., contaminated water and cholera or the linkage between scrotal cancer and chimney sweeps).  However, multifaceted or highly complex pathways (e.g., cancer, heart disease) rarely pan out, unless the disease is virtually unheard of without the implicated cause.  A great example of this is the elucidation of the linkage between small-cell lung cancer (SCLC) and smoking—we didn’t need a controlled experiment to link smoking to this particular variant of lung cancer because nothing else has ever been shown to even approach the rate of this type of lung cancer the way smoking has (reported relative risk of SCLC in current smokers of more than 1.5 packs of cigarettes a day was 111.3 and 108.6, respectively—over a 10,000% relative risk increase). As a result of this unique fact, Richard Doll and Austin Bradford Hill were able to design a clever observational analysis to correctly identify the cause and effect linkage between tobacco and lung cancer.  But this sort of example is actually the exception and not the rule when it comes to epidemiology.

Whether it’s Ancel Keys’ observations and correlations of saturated fat intake and heart disease in his famous Seven Countries Study, which “proved” saturated fat is harmful or Denis Burkitt’s observation that people in Africa ate more fiber than people in England and had less colon cancer “proving” that eating fiber is the key to preventing colon cancer, virtually all of the nutritional dogma we are exposed to has not actually been scientifically tested.   Perhaps the most influential current example of observational epidemiology [circa 2012] is the work of T. Colin Campbell, lead author of The China Study, which claims, “the science is clear” and “the results are unmistakable.”  Really?  Not if you define science the way scientists do.  This doesn’t mean Colin Campbell is wrong (though I wholeheartedly believe he is wrong on about 75% of what he says based on current data).  It means he has not done sufficient science to advance the discussion and hypotheses he espouses.  If you want to read detailed critiques of this work, please look to Denise Minger and Michael Eades.  I can only imagine the contribution to mankind Dr. Campbell could have given had he spent the same amount of time and money doing actual scientific experiments to elucidate the impact of dietary intake and chronic disease. [For example, Campbell would have designed a prospective study following subjects randomized to one of two different types of diets for 10 years: plant-based and animal-based, but with all other factors controlled for.] This is one irony of enormous observational epidemiology studies.  Not only are they of little value, in a world of finite resources, they detract from real science being done.

Featured Image credit: Design by K. Pauley (CC BY-SA 2.0)

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  • Using climate science as the example of how statistical “science” ought to be done is just about the worst possible example you could have come up with. They make the nutritional science folks look rigorous.

    • Funny…Seriously, though, that’s not what I said. I’m using Levitt’s work and climate change science as contrasts — they have to do statistically analysis. How they do it, I’m not expert enough to comment on. Point is, nutrition science should not be doing this.

    • Elizabeth Miller

      Climate Science is as rigorous as it gets. It’s physics and chemistry. For elucidation check out:http://www.realclimate.org/index.php/archives/2007/05/start-here/ (website by actual climate scientists) and yes, Virginia their predictions are coming true with a bang. To understand the climate denial misinformation I highly recommend:
      http://www.youtube.com/greenman3610 (Climate Denial Crock of the Week)

      Anyway Peter I love your website!

      • Thanks very much, but guys (re: ALL READERS), let us NOT turn this discussion into a debate about climate change. Please? It’s missing the point.

    • Samantha

      Actually, I am a climate scientist (paleoclimatologist) and I will attest that I have days when looking at all the scarce data and *hard* chemistry and physics that I use is just crazy… I completely see the correlation between nutritional chemistry and climate science. For example, I am as anal as they get in the laboratory. I am a chemist. However, I use organisms that lived roughly 250 million years ago. They are mostly recrystallized. I have no idea how badly these shells are affected–we can use the chemistry we know to resolve for some of these chemical problems, but in the end, we have no idea about the biological factors that affected these organisms and there are so many oceanographic factors that we just have no clue about.. so we can make a good educated guess about what happened to change the isotopes or trace metal composition of these organisms, but in the end, we really just do not know the truth and we will never know the truth… whereas, with nutritional chemistry, at least we still have living organisms to study to try to figure out what happens on a cellular level!

  • hi Peter – great blog, but I have to take exception with one of your claims:

    The catch, of course, is that correlations hold no (i.e., ZERO) causal information. Just because two events occur in step does not mean you can conclude one causes the other. Often in these articles you’ll hear people give the obligatory, “correlation doesn’t necessarily imply causality.” But saying that suggests a slight disconnect from the real issue. A more accurate statement is “correlation does not imply causality” or “correlations contain no causal information.”

    This is incorrect. If a correlation exists, then there must be a cause present. A correlation between two variables implies unresolved causation; it may be that one of the variables is causing the other, or that some third variable is causing both, but if there is a non-spurious correlation then there must be a cause. In fact, one CAN infer causal structure from observational data under certain assumptions, using a set of causal inference methods developed in the machine learning literature. For more on these methods, see Pearl’s Causality, Spirtes et al.’s Causation, Prediction, and Search, or the TETRAD toolbox. Unfortunately, these methods seem to be rarely used in the epidemiology literature.

    • Russ, I’m not sure I agree with this, but I appreciate the point. Consider the following (true) example: if you look at the rise (seasonally adjusted) of atmospheric CO2 since about 1960 and compare it to transistor density on microprocessors, they are very strongly correlated rising nearly in lockstep. While there are causes of both, they two events are actually independent, though statistically correlated. The driver of transistor density and atmospheric CO2 are separate. Of course, some correlations ARE related and a cause, either between them or by an external 3rd variable, are at play. But looking at 2 correlated variables does let us draw any causal information.
      I agree that there are several elegant statistical tools to try to sort things out, but to my point in the post, let’s reserve those for the questions that can’t be answered experimentally. To use observational epidemiology to solve nutritional problems is like rubbing two sticks together when you’ve got a Zippo lighter. Why bother?

  • Dave Nelsen

    Nice job. I get tired of telling my co-workers at the lunch table that red meat isn’t bad for you. It’s the myth or record so people think you’re a nut or a caveman and just want to eat a lot of steak if you argue the point. After reading Gary’s books and articles and your blog and others, I’m frightened about the poor quality science that is being dumped on the general public. In my work as an engineer I routinely design experiments and have to prove what I want to do is beneficial or at least does no harm. Luckily I have ways to do this that are rigorous and allow me to make informed decisions. If I let my personal biases get in the way, it could lead to decisions that would kill the product we sell and that wouldn’t be good for me or my company. I have never seen so much cherry picking of data in my whole life as an engineer as I have seen reading various “Studies” which prove Salt is bad, etc. It seems to me the researchers who spend their career saying red meat is bad are so invested in their pre-conceived conclusions that they cannot objectively design their experiments or draw the correct conclusions from their work. Unfortunately, poor health decisions can lead to shortened lives of people who followed the current conventional wisdom.

  • Paul

    A bit off topic, but a study today suggests that aspirin may reduce cancer incidence

    However, no mention of past studies on aspirin-insulin sensitivity linkage:

    Hows that for an epidemiological mash up.

    Any thoughts?

  • Mike

    I remember seeing this article also published by the Harvard School of Public Health shortly after the red meat article.

    Hu EA, et al “White rice consumption and risk of type 2 diabetes: Meta-analysis and systematic review” BMJ 2012; DOI: 10.1136/bmj.e1454.

    It’s also interesting how the results automatically lead the researchers toward whole grains instead of wondering about grains altogether.

    • HSPH is literally a *machine* churning out this sort of “stuff.”

  • Elizabeth Miller

    I have taken more courses in statistics than I care to remember and one time in a graduate class we performed a regression analyses on random numbers and got some surprising results.(I’ve done my best to forget the stuff.) What strikes me about the statistics in nutritional studies is how small the correlations are and how little of the variance is accounted for — but you’d never know it from the media hype these studies get.
    In a review of Gary’s GCBC the physicist Robert McCleod makes the following observation:
    “As a physicist, if I get an correlation coefficient, R2 < 0.9997 in an experiment, I would consider that a poor result. A nutritional researcher working with human patients cannot even dream of achieving the degree of control or characterization I can, and their data are overloaded with spurious noise.

    Researchers in the soft sciences typically do not have sufficient math skills to understand the statistical methods that are they are using to evaluate their data. I've lost track of how many times I've seen evaluations of the mean and standard deviation for distributions that are clearly not normal (also known as Gaussian). Don't even get me started on p-values. More importantly, very few medical studies attempt to test a single hypothesis. Far too many studies will compare apples to bananas, rather than apples to no apples, or they'll compare apples, oranges, and bananas to no fruit. Making conclusions from such messily designed experiments is rife with the potential for misinterpretation. Drug studies are often an exception."http://entropyproduction.blogspot.com/2009/02/all-medical-science-is-wrong-within-95.html
    Epidemiology sometimes might be useful in generating hypotheses, but should never be used as a substitute for actual science. And one of the key things that's often missing is the notion of falsifiability — no matter how many time the lipid hypothesis, etc. have been struck down — it's never given the burial it deserves.

    • Thank you, Elizabeth. Very well said. I agree, also, with our point about lack of math skills. In fact, one of the more embarrassing moments for T. Colin Campbell, while defending his assertions from the China Study, stems from his inability to distinguish between univariate and multivariate regression. Imagine the higher order mistakes being made, if something this simple is being fouled up.

    • Bob M

      Drug studies are easier to do because they at least can use placebos. If you look at a proposed diet study to actually (attempt to) answer whether red meat is bad for you, no matter what you do, you’ll change two elements of diet. For instance, if you have a control group and group that eats no red meat (randomized into the two groups, of course), if calories remain the same in the group eating no meat, they have to make up those calories somehow. Are the differences in groups due to eating no red meat or replacing the red meat with something else (whatever that something else is)? But at least you can get closer to an answer than performed by epidemiological studies.

      • We can do MUCH better than this. And we will.

  • Sidamo

    One interesting thing I noticed in the Harvard data, is that there’s a strong inverse correlation between how much red meat was eaten and cholesterol levels, despite a strong negative correlation between how much red meat was eaten and amount of exercise done.

    So people who ate the most red meat, also did the least physical exercise, yet had the lowest incidence of high cholesterol.

    I wonder why I didn’t see “Eating Red Meat Lowers Cholesterol Without Exercise” headlines 🙂

    • Great observation! I can only imagine what we could extract from these data if we had the raw data, instead of just summary data.

  • Brian Salazar

    People, Peter gave us another great post.

    Why is everyone going off on tangents? There are already enough people who will attack us for how we think about nutrition. Why “go after” one of the strongest and clearest voices on the web with tiny little nitpicking based on personal opinions about examples.

    I’ve lost 100lbs in the year since I first read Taubes and started following this lifestyle. Yet my wife still hates how I eat even though I’m eating more green veggies than I ever ate before. She can’t wrap her head around so much meat being healhy because of the all the BS and dogma that the media and government keeps generating.

    Thank you for another great and informative post Peter, now if only I could get my wife to read it.

    • Consider having your wife watch “Fat Heads” on Hulu.com or Netflix.com. Simply enlightening documentary that has intelligent information and is entertaining.

      My parents watched it too, and they were shocked with the information we’ve never been told.

    • Anthony

      I can relate. My wife was wondering why I had turned to eating so much fat compared to what I would normally. In the wash up after she read my copy of Why We Get Fat, I made the point that she forgot about what I said when I first started this dietary change, this was about eliminating carbs, not eating more fat. It is easy to notice the consumption of fat given its current public stigma. It’s all in the evidence, and in your case, its dropped off to the tune of 100 lbs.

    • F. Holland

      I agree. Some of us are looking for real solutions, and if we want to read about the environment, we can go elsewhere. I started losing weight seven years ago, and I’m still 100 pounds down, but i have 60 more to go and it seems almost impossible to reach my ultimate goals. There have been times I have devoted ridiculous amounts of time to exercise and spent tens of thousands of dollars on trainers. So when Peter says exercise doesn’t provide the answers; I can relate. I still wouldn’t trade one hour of exercise for one hour of living with the pain of morbid obesity. I’ve been reading this blog for about 10 days now, and have started trying to follow it. I have a few reservations. While I appreciate the scientific approach, it’s sometimes difficult to follow for a simple mind such as mine. I look for the practical applications, which is why I return to the post about what the good doctor eats. I’m currently devouring as much information as I can find. Today, it just felt really weird when I resorted to eating salami and cheese. I started to re-read because “surely” i’m not understanding something. I am determined. I weighed 345 at my maximum weight, and I can personally attest that living to be healthy is the only way to live.

  • Greg


    Great post. I agree fully with your approach: we should all be critical thinkers and not merely problem solvers, or passive accepters of dogma. Part of the problem is the modern system which has introduced so much complexity that we as a society have come to rely on so-called experts who are under their own social and ideological pressures that influence their work. All segments of academia and other professional schemas suffer from this.

    Right now I am reading with some amazement a couple articles in the NYT related to the new Nestle book. I am trying to accept it with an open mind, but I am finding that premise difficult to swallow. In short, I’m shocked by how strong the “Calories as a thermodynamic calculus on the body” dogma continues to be accepted.

    Keep up the good work on the blog. I look forward to your postings.

    • Thanks for your support. I struggle to read this stuff, too, despite trying to keep an open mind. When you really believe the world is round, it gets tough to listen to the masses drone on about a flat world.

  • Greg

    To really nail it home, observational epidemiology is exactly as it sounds – observational. Going back to your diagram of the scientific process, everything underneath the eyeball is ignored. At best, it’s a tool that helps you sift through obviously worthless observations so that experiments can later be designed and executed on the potentially worthwhile observations. The only notable exceptions are when P values are insane, like P <= 0.00001.

    And a minor nitpick: your chart leaves out the community process of science, such as peer review, duplication by other scientists, and verification via experiments designed to explore any weak spots left from another study. Here's an interesting flowchart from Understanding Science: http://undsci.berkeley.edu/flowchart_noninteractive.php

  • Patrick


    I know nothing about microprocessor manufacture per se, but following up your objection to Russ Poldrack’s comment: are you sure that the manufacture of microprocessors does not produce atmospheric CO2? And while the density of transistors on microprocessors could be independent of the CO2 produced, the increasing density could also contribute to an increase in CO2, for all I know.

    I’m not convinced by your example. But perhaps it’s too pedantic of me. The larger point made by both you and Russ Poldrack, I understand: until we do a proper experiment and get a positive result (or eliminate all negatives), we simply don’t know what causes a correlation (although we know what causes us to see the correlation!).

    One other thing: there’s a post about this study by “Health Correlator” Ned Kock, an academic statistician, that takes a 180-degree different view. He looks at the study’s published data and finds a positive correlation between increased meat consumption and decreased mortality! That tells me that the larger problem has to do with statistical interpretation. It’s worth a read. See: http://healthcorrelator.blogspot.com/

    Statistical interpretation? Forget it! How do we know we’re not fooling ourselves?

    (I like the comment somewhere in one of the critiques you mention: red meat only kills you if it is stronger and faster than you, has an appetite, and eats red meat.)



    • Could be, but pretty unlikely, certainly as the *primary* driver. But you draw the right conclusion — let’s do actual science! I have seen the other review you mention, but have not been able to scrub it yet. My point would still stand, though.

    • Matt Taylor

      Don’t you guys know that it is the shrinking number of pirates that is at the root of global warming? The correlation is clear!

  • Alexandra M

    Very informative post! There’s a lot here that will help me in explaining these concepts to others.

    I thought I was really getting through to one of my scientist friends the other day when he agreed that all these studies go through only 3/5 of the scientific process – but he still fervently believes that saturated fat causes heart disease because that’s the consensus.

    • Just point him in the direction of Ancel Keys and the Seven Country Study (along with a few other nuggets of bad science I hope to write about soon).

  • Cadence Daly

    I recently finished Good Calories Bad Calories and have turned away from the “dark side” forever. I found your blog last month through Gary — love your writing.

    When I saw the news about this study last week I knew all you guys would be turning out great posts to refute it, and I haven’t been disappointed.

    Although this story was covered on a number of media sites, the only one I read which provided a caveat was USA Today. To their credit, their account included this paragraph:

    “This new study provides further compelling evidence that high amounts of red meat may boost the risk of premature death,” said the study’s lead author, An Pan of the Harvard School of Public Health. But, he added, this type of study shows association, which doesn’t necessarily mean causation.”

    Of course, the use of that pesky “necessarily” renders this statement next to useless.

    • Don’t give them TOO much credit. The obligatory caveat is just a convenient way to continue convincing people that it’s a good idea to use sun dials for telling the time when quartz watches have already been invented. Very convenient when you sell sun dials.

  • Dr. Attia,

    Speaking of journalism and science, I came across these guys a couple of days ago:


  • Bob Johnston

    Even though I frequently engage in the futility of trying to change other people’s minds, I think Max Planck had it right:

    “A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it.”

    I think we’re in this fight for the long haul. Nobody likes to believe they were wrong or were fooled, the low fat crowd won’t give up easily. Changing minds occurs one mind at a time.

    • Bob, this is also one of my favorite quotes.

  • Samantha

    I am a climate change scientist–I study climate change from hundreds of millions of years ago to recent time on many different timescales. There are so many similarities between climate science and nutrition science and sometimes it is very frustrating. For example, it seems in general that people with no or limited knowledge of science tend to form the hardest opinions about what is the best science, and that is never based in any type of reality. People like to believe what is easiest to believe. Carbohydrates make for great tasting food and it seems as though it is now a major staple in many cultures. If you tell people that carbohydrates will kill them prematurely, and reduce the quality of the lives they live, they will immediately go on the defense–how will children in India survive without rice and grains? If we eat too much meat, won’t that reduce the availability of grains produced as aid packages? The answer is no, not really. Energy companies rely on the addiction people and societies have developed to carbon based fuels, so if we change our infrastructure to rely upon more solar or hydro based fuels, there may be chaos in the markets. As a scientist, I have no interest in the political side of the argument. I am a human and, as selfish as it may sound, I care most about my own survival, and also as a thinker, about the truth. What does it really take to create a healthy society? Is it *true* that fossil fuels will lead to unstable global heating? Is it true that eating a diet rich in carbohydrates will lead to an unhealthy and *expensive* society with greater medical costs? If today I read something that shows a clear answer to this question and it shows a scientific experiment that the composition of red meat alone (and, was the beef grass fed or grain fed? What was the nutrient composition of the red meat?), reacts with the human body in a way that directly leads to adipose fat storage, inflammation that causes heart disease and cardiac arrest, insulinemia/metabolic syndrome, etc., then I will definitely requestion what I have read about carbohydrates doing all of the above. However, all of the clues that scientists have put together seem to show, at least indirectly, that carbohydrates are the culprit, and every year we have more and more evidence of just that. I just wish the news media that caters to the general/non-scientist public would get with it, but of course it is more sensationalist to publish what caters to the general non-scientist public.

    • Brad

      Samantha, I also work in the field of climate change, not as a scientist although I did spend a month or two nearly 30 years ago attempting to reconstruct past climates based on fossil foraminifera when I was at university. My background is environmental science and like Gary Taubes I became a science journalist; I now work mainly in the area of climate change communication.

      To me, the big parallel between climate science and nutritional science is that in both areas I see vigorous challenges to the “consensus” view (I put quotes around consensus because true consensus requires 100% agreement, and that’s very rare in science; there is no consensus on climate change but there is a majority view). These challenges are a vital part of the process of science: we need skeptics to question the accepted wisdom. So far, most of the arguments raised by skeptics on climate change have served ultimately to strengthen confidence in the “consensus” view, because the great bulk of arguments put forward by the skeptics have been shown to be wrong or at least on very weak ground. That doesn’t mean the science is settled: science isn’t done by vote, and one person who’s right is worth 10,000 who are wrong. The history of science is full of good examples of the consensus view being overturned. But with climate change there is so much evidence emerging from so many different quarters (with models playing only a relatively small role) that it seems unlikely the basic hypothesis can be overturned.

      While “consensus” is irrelevant to science, it does matter from a policy perspective, because there is no responsible justification for basing policy on the views of a minority of skeptics. I think this is what we’re seeing in the field of nutrition as well. The “Central Dogma” remains tenacious in guiding public policy and mainstream medical advice, not because nobody is aware of Gary Taubes and the evidence he and others are bringing to light, but because the tide of expert opinion has not yet shifted in that direction.

      Why hasn’t the tide shifted? It could be due to inertia, of the difficulty in shaking deeply held beliefs, the unwillingness to look back at one’s career and accept that you wasted it barking up the wrong tree…there are lots of potential reasons. But I think the caution is appropriate, because in order to effect a shift like this you need extremely convincing evidence. And based on what I’ve been reading, the mainstream experts in the field haven’t been convinced yet.

      I don’t think nutritional advice in America is going to be shifted by gathering thousands of supporters of Gary Taubes and Peter Attia to raise awareness of their findings. It’s going to require publishing convincing evidence, opening it for a thorough probing to explore any weaknesses, and addressing those weaknesses.

      Plate tectonics and other theories and principles that were once minority views and now mainstream demonstrate that central dogmas can be changed. It just takes time to amass enough convincing evidence.

      • Brad, thanks for providing the quote of the day: “That doesn’t mean the science is settled: science isn’t done by vote, and one person who’s right is worth 10,000 who are wrong.”

    • Debbie

      Thanks for this post, Samantha. As one of the lay people with zero understanding of science, I rely on scientists like you, and when I read confirmation of what SEEMS logical to me, it helps.

  • Helga

    “Never attribute to malice that which is adequately explained by stupidity.”

    I would argue that the scientists who do these studies are neither stupid nor malicious. I believe they are motivated more by fear of having their funding pulled. If you spend a bunch of money on a study and don’t find anything useful you’re not going to get more funding. I used to work in science and left because I was so disenchanted by what I saw. Many scientists will publish anything they can that shows a shred of evidence that supports the original hypothesis for which they were funded. This is a sad state of affairs in the scientific community.

    On the other hand, conducting controlled experiments on diet is hard. If you were assigned to the 100 ounces of soda a day group and starting packing on pounds would you really stay in the study? There are ethical implications of asking people to consume things they think might be bad for them. This is other reason we don’t assign people swimming pools and guns to see if it will kill their kids. Who would volunteer for that study?

    The other confounding aspect here is that people want easy answers. When no one understood any of the causes of heart disease, doctors were watching their patients die and didn’t know what to tell them. Doctors want to help their patients! That’s their job. Enter Ancel Keys who tells them, look… it’s the fat and the cholesterol! Then doctors had something they could do, and they felt like they were helping.

    The current system of medicine and science is very broken. Not so much out of malice and stupidity, but out of self preservation and the desire to come up with answers, even if they are not correct.

    • “Never attribute to malice that which is adequately explained by stupidity.” The quote doesn’t say whose stupidity. 🙂

      • I have to leave something to your imagination, don’t I?

  • Dan Hackam

    Great post (as usual)!

    A friend sent me a study suggesting that circulating endotoxin levels spike in diabetics who have eaten a high fat meal (I post this piece of science at the end of this message). I want to suggest that there are other forms of bad science out there, which rely solely on surrogate markers (even high quality randomized trial data, although this was not). A pre-post study design is piss poor epidemiology, even if it is experimental. Where is the high carb control group? And what does an overnight fast plus a single meal composed of *anything* tell us about long-term human health? Absolutely nothing. I’m not even sure what the relevance of endotoxin levels are, although I know that endotoxin has been used as a therapy to cure some chronic infectious diseases for decades, particularly in Europe.

    High Fat Intake Leads to Acute Postprandial Exposure to Circulating Endotoxin in Type 2 Diabetic Subjects
    Alison L. Harte, PHD1, Madhusudhan C. Varma, MRCP1, Gyanendra Tripathi, PHD1, Kirsty C. McGee, PHD1, Nasser M. Al-Daghri, PHD2, Omar S. Al-Attas, PHD2, Shaun Sabico, MD2, Joseph P. O’Hare, MD1, Antonio Ceriello, MD3, Ponnusamy Saravanan, PHD4, Sudhesh Kumar, MD1 and Philip G. McTernan, PHD1?
    + Author Affiliations

    1Division of Metabolic and Vascular Health, University of Warwick, Coventry, U.K.
    2College of Science, Biomarkers Research Programme and Center of Excellence in Biotechnology Research, King Saud University, Riyadh, Saudi Arabia
    3Insititut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain
    4University of Warwick and George Eliot Hospital, Clinical Sciences Research Laboratories, Warwick Medical School (University Hospital Coventry and Warwickshire Campus) Coventry, U.K.
    Corresponding author: Philip McTernan, p.g.mcternan@warwick.ac.uk.

    OBJECTIVE To evaluate the changes in circulating endotoxin after a high–saturated fat meal to determine whether these effects depend on metabolic disease state.

    RESEARCH DESIGN AND METHODS Subjects (n = 54) were given a high-fat meal (75 g fat, 5 g carbohydrate, 6 g protein) after an overnight fast (nonobese control [NOC]: age 39.9 ± 11.8 years [mean ± SD], BMI 24.9 ± 3.2 kg/m2, n = 9; obese: age 43.8 ± 9.5 years, BMI 33.3 ± 2.5 kg/m2, n = 15; impaired glucose tolerance [IGT]: age 41.7 ± 11.3 years, BMI 32.0 ± 4.5 kg/m2, n = 12; type 2 diabetes: age 45.4 ± 10.1 years, BMI 30.3 ± 4.5 kg/m2, n = 18]. Blood was collected before (0 h) and after the meal (1–4 h) for analysis.

    RESULTS Baseline endotoxin was significantly higher in the type 2 diabetic and IGT subjects than in NOC subjects, with baseline circulating endotoxin levels 60.6% higher in type 2 diabetic subjects than in NOC subjects (P < 0.05). Ingestion of a high-fat meal led to a significant rise in endotoxin levels in type 2 diabetic, IGT, and obese subjects over the 4-h time period (P < 0.05). These findings also showed that, at 4 h after a meal, type 2 diabetic subjects had higher circulating endotoxin levels (125.4%?) than NOC subjects (P < 0.05).

    CONCLUSIONS These studies have highlighted that exposure to a high-fat meal elevates circulating endotoxin irrespective of metabolic state, as early as 1 h after a meal. However, this increase is substantial in IGT and type 2 diabetic subjects, suggesting that metabolic endotoxinemia is exacerbated after high-fat intake. In conclusion, our data suggest that, in a compromised metabolic state such as type 2 diabetes, a continual snacking routine will cumulatively promote their condition more rapidly than in other individuals because of the greater exposure to endotoxin.

    Received August 18, 2011.
    Accepted November 4, 2011.
    © 2012 by the American Diabetes Association.

  • David

    Take a look at “Design of Experiments” literature to see that it is actually more mathematically efficient to vary more than one variable at a time. It is unfortunate that most engineering schools don’t teach this subject to their students. I had to learn about this at work from a brilliant statistician.

  • steve

    Excellent post Peter and I am glad you pointed out the smoking example. Sometimes associations do count; afterall, where there is smoke there is fire! Sadly, the nutrition/diet studies never give rise to a statistically significant level of association. As to the unrelated topic of the environment, I can only say that the “talking heads” went to town with the destruction of the ocean,etc, after the BP oil spill, and if they had used there heads-thinking- they would have remembered that the ocean is amazing with its self-cleaning properties which have been demonstrated in past spills.
    Your opening quote of Kennedy said it all. Excellent

  • David

    Here is a link to example 2xw2 Designed Experiment http://web.mst.edu/~psyworld/between_subjects.htm

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  • John

    Great post as always Pete. I can not believe how many posts you respond to – amazing. Keep it up bro!

    • Thanks, John. Glad you enjoyed it. Hope it helps with family questions.

  • David

    This is a terrific post. You take a complicated subject and dissect it in a clear, lucid style that can be easily understood by people who never thought once about the validity of these nutritional studies. Thank you. I’m going to share this article with as many people as I can.

    I read the sugar study as well, and thought, oh, this is coming from the same study on red meat. Well, this is worthless.

    “Whole Paycheck” is what everyone calls it around here.

  • Marilyn

    Peter wrote: “You’ve had great success improving your health on a vegan diet? No animals have died at your expense. Great!”

    Oh, but animals DID die. That’s the thing that’s so dishonest about the vegans’/vegetarians’ “ethical” stance — and so aggravating when they try to push their agenda on the rest of us. What do they think happens to all the gophers and rabbits and snakes and birds, etc., etc., etc. that are in the fields when the plows and the planters and the combines go through to produce the soy and the grain for their tofu burgers?

    • Birgit

      Good point, especially given that these animals were just chopped up by the machines. For people who are concerned about animal welfare make sure the meat you eat comes from animals that were humanely raised (pasture-fed), transported and slaughtered. That way their meat contains fewer stress hormones and is healthier, too.

    • Spencer

      Most of that corn and soy feed the livestock to support the meat industry. Plus the animals in the meat industry are in prison. They can’t leave and are not free to move to a different field. The animals in the fields have the “FREEDOM” to move to a different field. This simply boils down to intentions: in the meat industry the intentions are to kill. If an animal is sad to say accidentally run over by a plow, then it was an accident. And as I said earlier, most of the corn and soy feed the animals intended to be slaughtered. You can’t win this argument on ethics here. Vegans and Vegetarians give up meat because it actually does save lives of animals. On top of that, most of them try not to hurt flies or spiders in the house. They don’t use mouse traps. They try not to wear leather unless maybe it is from a second hand store. They do a lot for ethics for animals and this is debate will always win because it is so obvious.

  • Birgit

    I love this blog. Perfect science reading for my 14-year-old daughter’s homeschooling for tomorrow. I wish all kids learned this in highschool and we’d have far fewer sick people in this country who believe everything their doctors tell them without asking questions and doing their own research. Keep up the good work. 🙂

  • Sam

    “Reading stupid epidemiology studies INCREASE all causes of MORTALITY”. All the stress and needless excess worrying is killing people that beside all the wrong and contradictory advice they get from them. I just need some funding to show causality. Je,je

    In another matter I wanted to ask you Peter. I have a friend who I recommended a kenotic diet because he needed to lose some weight to lower BP. I talked to him the other day and he told me he was very happy with the results. That also he had been suffering from Fibromyalgia all his life and the kenotic diet had resolved all his symptoms. The pain, mental fog and mood swing etc. I was quite surprise. Do you know of any plausible mechanics on why the kenotic may help with Fibromyalgia?

    • Sam, I have heard this from others also, but have not had the time to really dig into the mechanism of action. Glad to hear he’s having great results.

    • Edmund Brown

      If you google “primal” or “paleo” diet you might find a possible mechanism. I don’t remember the ins and outs precisely, but they propose that many auto-immune disorders are caused by food antigens that screw with the immune response. Something about gluten and other grain based prolamines affecting the trans-glutaminase system which is found in tissues all over the body, and therefore can explain the resolution of neurological/dermatologic/orthopedic/systemic inflammation/etc problems when people go “paleo”.

      It’s an interesting idea, but to my knowledge it has not been rigorously tested yet. The sheer number of people who have resolution of symptoms once they stop eating grains/beans makes me think there is “something” there.

    • Cindy C.

      Hi Sam,

      I started a ketogenic diet 3 years ago, as I heard it can help reduce chronic pain. I was told I had Fibromyalgia. Within a few months, my pain level was reduced. Also my blood pressure was more normal, my low blood sugar was more controlled, and my mood improved. Also my overactive bladder was no longer overactive. My social anxiety was reduced, and I lost the 20 pounds I was overweight. On such a diet, as to pain, well grains and sugar seem to cause inflammation, and we are without those, and the brain runs on ketone bodies, which increases Gaba, and reduces glutamate. This seems to reduce pain levels. Here is one study, but it admits this is a hypothesize. MSG consumption has been suggested as a trigger for Fibro.


      I am just glad I started the diet, but just wish I had known all this years ago. I read Sugar Blues, and 2 more books on sugar in the 1970s, and I cut down a lot, but those books did not mention ketosis(very low carb and high fat), much at that time.

  • Michael Ryan

    At the end of the day, doing a controlled experiment on anything to do with human metabolism is nearly impossible. I am a chemical engineer with a six sigma background and have done my share of experiments following the scientific method. Pick a key input varable, change it and observe the change in output. Simple. With metabolic science, there are too many variables that we can’t control in a sample group greater than n=1. To conduct an even remotely meaningful experiment on red meat consumption, you would have to prescribe (and assume that they are followed) EXACT diets for all participants, with one group getting red meat and the other getting none. Macronutrient composition would have to be identical, calorie intake on some normalized basis would have to be identical, exercise, sleep, sun exposure, climate exposure, and a myriad of other things would all have to be the same for the results to mean anything at all. Not Possible. Then, you can throw in the question of genitics and everything goes right out the window.

    For those of us who have reson to tinker with our diets, the only experiment that matters has n=1. Read everything you like. If you find a hypothesis that you think has merit, do a controlled experiment on yourself. If after changing a variable, you burn excess fat, feel better, have a better lipid profile, can get off your meds or whatever improves your being, then you have proven something that works for you. If you fail to lose fat, feel worse, or whatever, then you go back to the start and try changing something else. Again, simple (if you have the discipline to track inputs and outputs and record results.)

    Seven months ago I started eating a low carb diet. I was 341 lbs with a lean body mass of 210 lbs. Between September and Christmas, I weighed and measured food, wrote down everything I ate, tracked macronutrient consumption and calories, and tracked ketosis. I lost about 40 lbs of fat while keeping lean mass essentially constant. Then the weight loss slowed and stopped. I still felt good but was frustrated and stuck at 300lbs. What changed you ask? I stopped tracing everything because I had been doing it for so long that I just knew what to eat. I recently posted another comment and asked Peter for some suggestion on what to change to restart the fat loss. I knew the answer to the question before I posted it, I had just gotten lazy. Peter suggested changing only one variable at a time and it dawned on me that I was no longer being scientific. I started weighing, writing, and checking again. I was no longer in ketosis despite very low carb intake, but my protein intake had increased. I reduced my protein intake and voila…. ketosis returned and so did fat loss. I am now at 289 and dropping.

    Food is the most powerful drug on the planet. Don’t ever believe otherwise. Unfortunately, unlike other addictive substances, you can’t just stop taking it. The results of that expoeriment would not be good. So, we are stuck trying to manage a necessary addiction while weeding through the advice of the so called “experts” on how best to do so.

    Dr. Attia IS an expert on this stuff and his opinions are very much worthy of your attention. However, he is an expert on what optimizes HIS health and performance, not necessarily yours. He is disciplined enough to do controlled experiments on himself and report the results to the rest of us as a hypothesis that we can attempt to prove in our own n=1 experiments. At the end of the day, n=1 is really all that matters to you.

    Thank you for doing this Peter, it is great and necessary work!


  • Jason Brady

    From the science point of view, what valid cases are there for only doing observational studies?

    You pointed out that in the case of climate science and social economics, it is impossible to do a clinical study. Is this the only valid case? What makes it “impossible” enough to justify only observational studies?

    It sounds to me like there is no valid reason to *not* do clinical studies in nutrition, because “hard” is not “impossible”.

    As a side note, when it is “impossible”, how do you then do science with only observational studies?

    • See post. I address all of these questions.

  • Barbara

    Have you thought of approaching the Gates Foundation to fund research on low carb/high fat diets? While their Global Health Initiative seems to focus mostly on infectious diseases, I think you could make a detailed and strongly supported argument that the “diseases of western civilization” (diabetes, heart disease, etc) also have a strong impact on global health and deserve funding consideration. They see themselves as funding research that is “outside of the box”, which pretty much describes low carb/high fat diets given the current conventional nutrition wisdom. Of course they may open themselves up to ridicule, but they’ve shown with some of their funding decisions that they are willing to weather the controversy…and they have the money and independence to do it.

    • Yes. Lots of ideas like this in store. Of course, not sure if this will interest them, but we’ll ask.

  • Edmund Brown

    I found another good quote,

    “If we are to believe this hypothesis we must forget everything we learned in the last 70 years and start all over again.” Thomas Chamberlain a pre-eminent geologist upon hearing Alfred Wegener talk about “continental drift” and the evidence he’d collected to demonstrate its reality.

    I could so easily imagine somebody saying the exact same thing to Gary Taubes…

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  • Anthony

    Hi Peter,
    Apologies if you have addressed this in another post or question. I haven’t been cheating on you by visiting naughty web sites, but I came across the PCRM site and noted they too are promoting the red meat is killing us so called study. I also noticed the following:
    I wonder if it is the hotdog or the white processed bun with more cancer causing potential? I also noticed than unlike your web site where we are free to comment, free to question, and you are not afraid to answer, there was no way of commenting on their blog pages. What do they have to hide?

  • Peter

    Hi Peter,
    Here’s my n=1 experiment. For years I ate ‘virtuously’: high-complex carbs (300-400 grams per day) from brown rice, legumes, whole-grain flour, fruit and vegs, lean protein, minimal fat (olive/poly veg oil). I exercised 4x per week (4 miles treadmilled @12% incline, weight-lifting). Slim and trim ,I weighted about 127 pounds. Still my TC kept climbing over time.
    Then my lipid panel

    Dec 17, 2010 Pre-statin lipid panel
    Total Cholesterol: 206
    Triglyceride: 61
    HDL: 42
    LDL 152

    alarmed my doc, blamed it on genetic traits and prescribed me statin Simvastatin on 12/24/10. I continued to eat the same high-carb way and maintained the same workout routine. Statin worked its magic on TC as shown in next 2 results:

    Feb 1, 2011 Statin lipid panel
    Total Cholesterol: 121
    Triglyceride: 68
    HDL: 41
    LDL 66

    Aug 3, 2011 Statin lipid panel
    Total Cholesterol: 119
    Triglyceride: 87
    HDL: 35
    LDL 67

    The worsening markers HDL and TG in the statin panels and fingering genetics as root cause bugged me; so I started learning about macronutrients and role of insulin. I shifted paradigm. On 12/20/11 I stopped taking statin and ate LCHF (<50 grams carb per day mostly from green vegs and abstained carb-rich food, about 50 grams protein, lots of mon-unsaturated fat). I did not track caloric intake. I continued the same workout regime.

    Here’s the first post-statin lipid panel:
    3/17/12 post statin lipid panel
    Total Cholesterol: 241
    Triglyceride: 50
    HDL: 60
    LDL 171
    Low carb gets me low TG. Eating mono-unsaturated fat and fatty meat begets higher HDL. My HDL and TG markers and ratios improved. In hindsight, I should not been alarmed by the results of Dec 17, 2010 Pre-statin lipid panel. All I had to do was to go LCHF. My bad on my ignorance and relying on my doctor’s advice. Books and blogs, such as yours, give me the knowledge and confidence to flip the conventional dogma. Oh, though not my intention, I lost about 4 pounds from 3 months of LCHF.

    • Peter, I’ll be writing a lot about lipids in the future, but based on the standard lipid panels you’re showing, the only thing we can even use remotely as a proxy for your insulin resistance and risk of disease is your ratio of TG to HDL-C, which went from 1.5 to 1.7 to 2.5 to 0.8. Very nice trend. Anything above 3 is pretty bad; below 1.0 is ideal. Of course, these are just indirect proxies for risk (which we can’t be assessed any further from these labs). The only thing that really matters is LDL-P, LDL particle number (vs. LDL-C, or LDL cholesterol, which is what they’re checking).
      It does, however, look like you’ve improved your health a lot.

  • Eating in Orlando


    The NYT has been leading the anti-meat crusade…now they have thrown down the gauntlet with an essay contest.


    I am going to write a response. I’d love to read yours.

    • You just read mine. That’s what this blog post was!

    • Eating in Orlando

      I think they are looking more for a defense of the ethics of eating meat. I’m not sure of I can limit myself to 600 words. My parents are vegetarians, so I am sick of hearing variations of the “save the planet, animals have big brown eyes, kumbaya” hymn over and over again. I’m going to let them have it!

    • Brad

      I’m pretty sure the New York Times contest is set up to demonstrate that in fact there is no ethical argument for eating meat. There are nutritional arguments, of course, and therein may lie the only “ethical” argument because studies have shown that when you supplement the mostly plant-based diets of kids in developing countries with a little bit of meat, they are much healthier. But for Americans with a wealth of food choices available, the crux of the question boils down to “is it ethical to take the life of an animal (one that is clearly capable of feeling pain and fear) for food when alternatives are readily available?” Peter Singer, one of the judges of the essay contest, has spent 30 years studying all the counter-arguments to his position of vegetarianism, and he studies them very deeply; he’s a gifted logician. I’m willing to bet that he will have already heard all of the arguments submitted by participants in the contest, and he will be able to demonstrate that none of them stand up to logical scrutiny.

      I say all of this as an omnivore who ate beef stew last night. I don’t think our model of industrial livestock production treats animals ethically and I try to avoid eating that kind of meat as much as possible. I think the ethical line is less clear when it comes to wild game, or to livestock raised under more humane conditions, but it still boils down to the ethics of killing animals for food when we can meet our nutritional needs through plants and supplements.

      My guess is that the Times contest will either produce no winners, or perhaps a winning essay that comes closest to making a convincing case, but the real purpose of the contest is to demonstrate that it is impossible to make a logical ethical case for eating meat.

    • Debbie

      I scanned the comments section, and was amazed to read – I think – that they’re mostly pro-meat. Very few hard core eating meat is murder comments. Very encouraging, especially considering this is the Times, and it’s cool to be vegan – at least in New York.

      • I think the ethical issue actually detracts from the scientific issue. The two issues are separate. Hope the discussion doesn’t confuse these points.

  • Peter

    The Ornish, Esselyn, Campbell, Willets & cohorts may be idealistic and have good intentions, but their dogma has led to this:
    Today’s NY Times headline blared
    ‘For Diabetes, Surgery a Better Option than Standard Treatment.’
    Oh, maybe it’s about treating gangrene. No, it’s bariatric stomach stapling to cure T2D, costing between $11K to $25K per operation. Has our medical establishment gone insane?

    • I think desperate is the better term than insane. As you say, these are not “bad” people telling us not to eat fat. They are just misled by their failure to understand what constitutes good science, and how to best interpret the bit of data out there.

  • Peter, another brilliant post! Reading this renews my faith in humanity and reason. 🙂

    • Thanks so much, Adam. Always appreciate your support.

  • Peter,

    This is an absolutely fascinating point of view I’ve only recently been aware of.

    Recently, I was introduced to paleo.reddit.com, which today led me to the documentary “Fat Head.” Humorous documentary explaining these things you post about.

    Now I’m obsessed. Researching as much as I can and posting information to social sites, bringing the danger of carbs to light.

    Just wanted to thank you for what you do and I will be reading your posts as much as I can.

  • Dwight Lundell M.D.

    Jimmy Moore and I discussed your site yesterday. I think it is great and so does he, keep up the good work and let us know how to help with the Nutrition Science project

    • Thank you so much. Hope we can meet up at some point.

  • Dave

    The article “Eat More Chocolate, Weigh Less?” on the WebMD site,
    the (OBSERVATIONA) study in “Archives of Internal Medicine” that it’s based on,
    and our tastes suggest the following question:
    Is there a way to eat chocolate in an appealing way without stimulating a spike in insulin levels?

    • Dave, I’m glad you’re getting the hang of spotting an OBSERVATIONAL STUDY from a mile away… A very dark chocolate with little to no sugar would have a minimum insulin response. In fact, I’ve started experimenting with chocolate ice cream (zero sugar, a touch of xylitol).

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  • I. Rubey

    Hi, Peter — I have been following (and loving) a low-carb diet after reading “Good Calories”, your blog, and Richard K. Bernstein’s books. I just saw a study posted on a calorie-restriction mail list I follow that seems to say that animal fats (SFAs) are much worse for you than PUFAs. I’d appreciate your thoughts on this if you get a chance: http://www.ncbi.nlm.nih.gov/pubmed?term=22338035

    • I can’t seem to get this paper for free, which I normally can with this journal. Impossible for me to comment on an abstract. Need all the details.

    • Rubey, I just got a copy of the paper and have skimmed it quickly (mostly because it interests me — please don’t let me set a precedent. I can’t read every paper I get sent). No time for great details, but here it is in short order: 1) All subjects consumed about 35% of their calories from carbohydrates. With carbohydrate content this high (which is obviously lower than “normal,” but not so low to even approach ketosis), the body is not yet efficiently able to prioritize fat oxidation. 2) The test meal (an all-liquid fat ingestion) still consisted of 33% carbohydrate, so whatever impact was observed, was done in the presence of at least moderate, if not high, insulin levels. 3) Virtually all of the differences (to my quick reading, at least; I have not studied this paper in my usual level of detail) seem to vanish after 2-4 hours, so it’s not clear the effect was even observed outside of that window. 4) The PUFA meal was 50% EPA and DHA, which is not even remotely a reflection of how Americans eat PUFA. Americans consume 30-50x more omega-6 than omega-3, not 1:1. I suspect much of the benefit this study saw with the PUFA meal had more to do with this feature. It would have been interesting if the PUFA meal was 95% n-6 and 5% n-6. Wonder if the result would be been the same?

      Interesting study, nevertheless, despite the above limitations.

  • I. Rubey

    Re your comments on the SFA/PUFA study — yes, I thought the ratio of omega 3 vs. 6 for the PUFA feeding was rather odd. I wonder what they could have been thinking that led them to propose that to test.

    Thanks for taking the time to look at the study and analyze.

  • Seeker

    Peter, thank you for your work. To base nutritional decisions and policy recommendations on real science would be an invaluable advance. I understand that you are saying that the entire field lacks rigorous studies. I have recently embarked on a low carb way of eating, and I have been trying to absorb the best of what information is available.

    It seems to me that to be fair-minded in making my own personal dietary decisions, I ought to read the best of the literature that opposes low carb eating. Surely there are some bright, well-informed people who are writing in good faith and have serious criticisms of this style of eating?

    Do you believe this is so, and if so is there anything you would particularly recommend to balance out the perspective of someone who has only been reading low carb advocates? I am not looking for a defense of a low fat diet, as much as critique of low carb. Thanks for your thoughts!

    • Honestly, I have not come across ANY valuable work defending the science of “fat is bad and carbs are good.” It’s all observational work and poorly done statistics. Most of the rejections of “low carb” I have seen are ad hominem attacks (e.g., on Atkins, Gary Taubes). Sad, but true.

    • Dan Hackam MD, PhD

      The only counter-argument I can see is that some individuals may have genetic mutations which result in enhanced cholesterol absorption from the gut. Since this usually can’t be predicted in advance, it may be worthwhile to follow an advanced lipid/lipoprotein panel such as VAP, LDL-P, apoB, etc, on a low carb high fat diet. I do wonder if such individuals should be treated with cholesterol absorption inhibitors (of which there are several molecular species), rather than abandon their diet, which will have other beneficial effects on CRP, blood pressure, HDL/triglyceride axis, insulin sensitivity etc.

    • Nicky Hansard

      I have a hypothesis (is that the right terminology?) that some people might be genetically better able to to handle carbohydrates because of their ancestors diet e.g. maybe their ancestors spent the majority of their evolutionary development in a carbohydrate rich environment. It is a possible reason that some people are able to eat high carb diets and remain healthy (like my girlfriend) and others eating high carb diet develop health issues (like me). I think that could be an argument for a low carb diet not being ideal for everybody but I have not put in any effort to backup these claims and I can’t really find any well structured studies defending high carb.

      • Nicky, that is exactly the right terminology and for what it’s worth, I think it’s a pretty solid one. The thing to keep in mind is that very few of us are genetically “traceable” to one region. So it may not be as simple as “my family is from Norway and I believe the people who descended from Norway 10,000 years ago ate X, therefore I should eat X.” But I think the framework could be helpful.

  • Hi Peter,

    Do you consider any foods to be healthy? If yes, on what basis?


    • I don’t know how to answer this question…sorry.

  • Hi Peter,

    My point is that.for example on what basis do you think fruits and vegetables are good or healthy?

    I haven’t come across any RCT showing Fruits & vegetables lowering mortality or cancer.And we have no question that everyone should eat those.

  • Also from your article” I agree that sugar-sweetened beverages increase the risk of heart disease (not just in men, of course, but in women, too) along with a whole host of other diseases like cancer, diabetes, and Alzheimer’s disease”.

    On what basis do you think sugar-sweetened beverages increase the risk of heart disease”.Do you have any RCT’s showing sugar consumption increase the risk of heart disease or mortality?


    • Look at the work of Rob Lustig, Peter Havel, and others (including the group at UC Davis). A great study to look at is this one: http://jcem.endojournals.org/content/early/2011/08/11/jc.2011-1251.abstract
      If you understand that the changes experienced by these subjects — in just 2 weeks — are the sine qua non of metabolic syndrome, and you understand that metabolic syndrome leads to these diseases, then you start to understand the link between sugar and disease.

  • Hi Peter,

    Thanks for the study link, Peter.

    I am not sure why you think this is great study. The fructose used is 25% of total calories. This study is just completely unrealistic! The average US consumption of fructose is 10%! The average US sugar intake is around 16% percent. A 2 week study is too short to make any conclusions about any disease.

    This study would be a good study for someone who consumes 8-10 coke bottles a day.

    I hope you apply the same skeptical thinking to every study.

    • Anoop, this is a good study for several reasons:

      1. It’s well controlled (this group is currently publishing even better, more controlled studies, but this one is better than most).

      2. 25% fructose is not as unreasonable as you suggest (25% of average caloric intake of 2400 kcal/day = 0.25 x 2400 = 600 kcal = 150 gm/day of fructose = 55 kg/year = 120 lb/year. While this is more that what some people consume, it’s actually not far out. Don’t forget the dose-response. No one is saying eating 10 gm/day of fructose is harmful. The purpose of a study like this is not to look at the 10th percentile of consumption. Do you know how many Americans do drink the equivalent of 8-10 Coke’s per day? Factor in the low-fat this and the low-fat that, and you’ll get there pretty quick.

      3. It’s the fact that it was so short that makes it so impressive! I think you may have missed this point, Anoop. If in just two weeks these patients witnessed such a shift towards metabolic syndrome, what do you think it would like if this study continued for 2 years?

      4. There is no credible dispute between metabolic syndrome and the diseases linked to it. Of course, 2 weeks is too short to show a “hard” outcome like more cancer, diabetes, or heart disease. But showing the link to metabolic syndrome is logical equivalent.

  • David Nelsen

    Here’s a study suggesting that Red Meat does reduce life expectancy that I believe:



  • George Henderson

    I hypothesise that people who die earliest tend to eat more, drink more, smoke more because they have less time left to do it all in than other people.
    See, correlation is causation after all!

  • George Henderson

    “No one is saying eating 10 gm/day of fructose is harmful”
    thanks for that Peter, at one point I thought you were!
    John Yudkin discusses this point, canvases various opinions to say that almost everyone should be OK with 25-35g sugar daily. That’s 12.5-17.5 g fructose.
    RD feinman makes the point that on low-carb, more fructose can be tolerated as it is converted to liver glycogen when glucose is low.
    Early low-carb diets were generous with fruit, and worked well; Yudkin, Mackarness, etc.

    • Sure. All of this is correct. Just keep 3 things in mind:
      1) 25-35 gm/day of sugar is less than 25 pounds per year per person. The last time Americans consumed that amount of sugar annually, George Washington was President. Today we’re about 6x that amount.
      2) These points do not diminish the argument that fructose is a toxin — just as most things are toxic at a high enough dose, though, as you suggest, it’s probably not the fruit that’s killing us.
      3) If one is aspiring to be the absolute leanest they can be, it’s worth at least considering a reduction in fruit (especially if currently eating 3 apples, 2 bananas, 3 oranges, and a watermelon each day…you laugh, but some folks think this is “healthy”).

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  • Taylor George

    The link to the study does not offer much. Do we have to pay money to see the actual article/study?

    • Yes, unfortunately, if you don’t have access to the journal.

  • Richard S.


    My stepdaughter is at HSPH and her study about exercise, TV watching, and sperm quality was just published. As I read the study and her comments, I was proud to see how careful she was to point out that these were merely correlations. She noted that the “right” way to do a sudy would be with a prospective, randomized trial using a cross-over design. Only then would we have a good idea for whether less TV and/or more exercise would really help a men’s sperm quality.

    I’ve only read the abstract from this “red meat” study, but I was blown-away by their “substitution” comment and their “estimates” for how many lives could have been saved if everyone had eaten less red/processed meat. We are used to reporters’ crossing the line from correlation to causality, but here the researchers did that for us. Could they have done any more to imply or state causality, without actually using that word? It seems that they violated one of their own cardinal rules.

  • Belgian Beer

    “This doesn’t mean Colin Campbell is wrong (though I wholeheartedly believe he is wrong on about 75% of what he says based on current data). It means he has not done any real science to advance the discussion and hypotheses he espouses. If you want to read the most remarkable and detailed critiques of this work, please look no further than here (Denise Minger) and here (Michael Eades).”

    Wow, that’s really scientific: we should no further than a documented fraud and plagiarist with no training in the sciences and a demonstrably bitter man with zero scientific publications to his name to critique a project conducted by scientists from Cornell and Oxford. *Great* advice.

    • Ah…the classy tried and true ad hominem approach. Great job! Try coming up with an actual argument. Or some logic. Or even a scientific fact or two. Amazing how many people criticize Denise because of her lack of MD or PhD. No need to respond, of course. This is all rhetorical.

  • Belgian Beer

    No? Too many links? Well, how about one, then:

    1. The Journalist Gary Taubes 1: Controlling History

    Come on, Kojak. You’re not afraid of a real debate, are you?

    • Kojak, huh? Belgian Beer, in my experience the probability of someone being an honest intellectual when they begin their “debate” with personal insults (you’ve managed 3 personal insults in 2 comments) is somewhere between zero and, say, zero percent. So while I love debates, I only engage with, you guessed it, intellectuals. Just as I don’t play chess with kittens or puppies, as much as I love both, I don’t debate with folks who lack the ability and honesty to have them based on data and without resorting to insult. Obviously, I’m trying to politely tell you to troll elsewhere. If you’d actually read this post and thought about it, you might appreciate that epidemiology, while a great tool to establish hypotheses, can’t establish cause, save the 2 or 3 times in history the hazard ratios were over 10. You do know what a Cox Proportional Hazard is, right? And presumably you’re familiar with Bradford Hill’s criteria, which don’t come close to being met with the stuff you reference. If you care enough, why don’t you start your own blog? I’m sure you’ll attract an enlightened readership.

    • Christopher Grove

      Frankly, I’m sure that Peter would be more enamored of your Kojak quip, if you did not hide behind a handle/Pseudonym. I’m imagining a huge beer gut here, actually.

  • Sarah

    Thank all powers that be for Peter Attia and Gary Taubes. Seriously. My heroes!!!

  • Holly Hudson, MS, RD

    I hate to post to an old thread, but I just discovered your site. Which is fascinating, by the way — I lean low carb, myself, based on my own readings through the literature and experience with patients, and I’ve noticed standard of care in my field inching slowly in that direction. I think your TED talk is the first time I’ve heard the problem characterized so directly as insulin resistance leads to obesity, rather than the other way around, which is intriguing to think about.

    My question for you is about a particular mechanism by which red meat could be increasing risk of CVD and cancer, as we see in some large and well-controlled epidemiological studies (cited at the end). I, personally, love red meat, and would love to go back to eating it, so if you find anything wrong with this mechanism, that would make me very happy. I don’t know if you’re familiar with the work on Neu5Gc (N-glycolylneuraminic acid) by Ajit Varki, one of the directors of Glycobiology at UCSD. Neu5Gc is a cell-surface sialic acid produced in mammals via an enzyme that humans have lost. As a result, it is found in all mammals except humans (and one other primate). The kicker is that we still produce the enzymes that process Neu5Gc for display on cells, and our immune system makes antibodies to it and will deposit complement in response to its presence. It is incorporated from the diet, confirmed by a feeding test, and within the body it concentrates in vascular endothelial cells and in cancerous tumors. Seeing micrographs of tissue labeled for Neu5Gc, where the dye basically outlines the vascular structure in the tissues, and contimplating my immune cells attacking the lining of my blood vessels in response, has frankly put me off red meat. The antibodies are not numerous, and the response is mild, but presumably enough to provoke inflamation and damage that could accelerate atherosclerosis. The response is strong enough to cause angiogenesis that feeds tumors that are expressing Neu5Gc, causing tumor growth in a mouse model fed a source of Neu5Gc.

    Like I said, if I’m interpretting the literature incorrectly, please set me straight so that I can go back to enjoying lamb. Meanwhile, here are a few citations:

    The paper with the scary micrographs:
    “Evidence for a novel human-specific xeno-auto-antibody response against vascular endothelium”:

    Feeding study:

    Association with tumor growth:

    And there’s more, but if you pull up any of these, you’ll probably stumble upon the rest on your own. And to back up my statement at the beginning, here are two large epidemiological studies that compare red meat vs poultry vs fish, etc., where they control for other dietary factors. I’m waiting for direct studies on red meat vs poultry consumption while tracking Neu5Gc antibody expression and atherosclerotic progression, but these sorts of studies would be complicated and expensive (in part due to the need to control for saturated fat in the diet, which is the reason most people think red meat is a problem), so I’m not holding my breath.

    Epidemiological studies I mentioned:

    • This is a very interesting topic, Holly, though Varki himself has admitted that what he reports in these papers has not be directly linked to human disease. My gut (sorry for the pun) instinct is the the role of Neu5Gc and/or the myriad of other potentially pro-inflammatory factors is highly path- and context-dependent. So it’s quite likely that under some dietary conditions that are otherwise pro-inflammatory, Neu5Gc could mediate disease, while in an otherwise low-inflammation environment, the effect is dwarfed by other factors. It seems impossible to imagine that red meat is universally harmful (or universally benign, for that matter). Context mattes, and most people seem to miss that. As for the epidemiology, my feelings are actually quite strong. The weakness of it suggests a lot. If red meat were universally harmful (say, like tobacco), we would expect to see hazard ratios 10 times — literally — higher than we do.

    • Steve

      Compared to what?

      What is the order of importance of Neu5Gc in the human diet? Sure, perhaps it is one POTENTIALLY harmful chemical in red meat… but there are potentially harmful chemicals in almost (?) everything humans eat. What evidence exists to assert that Neu5Gc in red meat ought to be more of a concern than the thyroid-suppressing goitrogens in broccoli, soy, peanuts, and cabbage, for instance? Evidence does exist that foods high in goitrogens can indeed harm human health. While absence of evidence is not evidence of absence, why is it rational to focus on Neu5Gc instead of all of the other potentially harmful components of food? I am certain there are potentially-harmful components in whatever you would substitute in your diet for red meat.

      And, yet, we need to eat something or we’ll starve to death. It is simply impossible to avoid any potentially harmful component of food while eating a diet of natural, whole foods – and most evidence I’m aware of indicates that purified processed foods are much more unhealthy for humans on a macro scale, even if the exact mechanisms are not clear in every case.

      So in discussing the risk, if any, of Neu5Gc from red meat, another question must be: compared to what?

      • Steve, I think you’re approaching this question exactly through the right lens.

  • Gaston


    Once again – great article – nailed it! For an interesting view on pseudo-science and getting things bass-ackwards on causality check out (Nobel Prize winner) Richard Feynman’s “Cargo Cult Science” – it was a commencement address at Caltech.

    All the best

    • A great lecture by a great man… So, so tragic that he’s not around today.

  • Peter, I read with great interest your blog posts on limiting sugar and carbs. I am a 33yo physician, and I have been self-experimenting (along with my wife) for the last few months but have been disappointed with the lack of evidence to guide my choices. My wife and I are both quite healthy and fit (no chronic medical problems). I have low body fat (<10%) and exercise vigorously 5x/wk (heavy weights and high-level soccer). My BMI is 21 and my waist circumference is 28". I have no family history of CV disease. My resting HR is 55 and my BP is <120 systolic. I have not measured my cholesterol in 7y, but at that time it was wnl. Given these facts, I wonder, just how important are my nutritional choices? As long as I am not eating too many calories or quite unhealthy food (I try to limit sugar, carbs, and processed food in general, but I do enjoy 'cheating' on the wknd), do you think there is much of an effect on my long term health by my nutritional choices? Also, how often do you think it's ok to eat read meat, and meat of any kind? I previously had tried to limit my meat (and esp read meat) intake, but after reading your blog and taking a look at the studies am beginning to wonder if there is some real anti-meat bias out there. I'd appreciate your thoughts, thanks!

    • Abilash, I wrote a post a while back called something like, “Is red meat killing us?” It addresses your concern, I believe.

  • Sheila

    Peter – I wanted to ask if you have read the blog of Stephan Guyenet – http://wholehealthsource.blogspot.com/#uds-search-results

    I have read him for a few years now and before including you, he was were I went for my true scientific “fix” on these topics. So, I thought I would search his blog and sure enough you came up. I’m going to go back and see what he has to say about you. I’m guessing since he knows you, you know of him.

    Just spending some time of late reading through many of your posts, I am interesting in seeing your points of difference or agreement with Stephan.


    • Yes, I know Stephan personally. Agree on some things, disagree on some things, but a very cordial relationship. I like Stephan and consider him very thoughtful.

  • Norm

    Hi Peter,

    Wanted to ask if you have had the chance to discuss with dr Rosedale regarding his stance on sturated fat as he suggests to limit it for weight loss? He actually calls it “a second generation of carbohyderates”, he seems to be kind of ok with it once one is fat adapted.

  • Tim Claason

    I’m not sure if this has been explicitly stated here, but I’m just sort of discovering all of these things, and I am trying to understand about the penetration of the endothelial layers in, and subsequent artheriosclerosis.

    My understanding is that, at the foundation of the low carbohydrate/high fat argument, is the assertion that the lipid hypothesis is incorrect, and something else creates the situation where the endothelial wall is vulnerable to penetration. I’ve heard and read several people make the case that one of the problems is the ratio between omega 3 and omega 6 PUFAs.

    Is there a definitive answer on this?

    • Ian

      I share the same interest. The science and increasing real world evidence backs low carb high fat so the next question has to be about the quality of fats in the diet. The various opinions about mono/poly/saturated/omega/dha whatever – I’d really like to see some authoritative information as it’s driving me nuts!

  • Vladimir

    Hi, I am from Slovakia (in Central Europe) and I am in my last year of studying mathematical statistics and applied economics… I ran into your blog maybe a week ago (already swallowed all the articles) searching for deeper info about nutritional ketosis and what made me to continue reading was the rigorous scientific method you used (besides all of the useful and interesting information). Me and my girlfriend (from Czech republic) got on the path of ketosis mere six weeks ago firstly because of the weight loss, but as I was digging deeper I made a decision that being low-carb is evolutionary “normal” for my body a that it makes me feel much better. I am looking forward to sharing my story of successful life-change in two year’s time, but today is too early.

    What I want to comment on and ultimately to praise you for is your scientific approach to this topic. I conduct research in the field of theoretical and applied economics where variables are (from the logic of things) not fixed and it is even harder or mostly impossible to make an experiment. Although some “natural” experiments occurs (as it is with the special mutations in very small groups of patients which the researchers may utilize), most of the time I rely on advanced mathematical methods to somehow (if possible) filter the white noise of millions of souls doing their everyday decisions. The world would be a much better place (from economical point) if that alone was enough.

    The problem is that huge (sometimes for me even disgusting) number of researchers, professors and teachers…virtually all those who should be conveying thoughts only after the rigorous scrutiny are not doing that, even worse, they are doing the exact opposite. The thing is that you are always able to get a number, whether it is a correlation coefficient, regression coefficient or a deep parameter of some exotic probability distribution, but when you don’t know what this number means you have got nothing to say. You ought to be silent, unless you want to ask a question “What does it mean in the context of what have I been researching?”.

    The scientific method ethics always makes me emotional and upset. I perfectly know and understand the party situations where my girlfriend is kicking me under the table just to stop me making this exact point. The world is full of logical fallacies and you can not confirm any hypothesis, you can just reject it. This why it is always more important to find out where the hypothesis is weak and not to be afraid of saying “This paper doesn’t by any means answer all of the questions.” or humble “I don’t know, but I am studying this issue.” The topic of statistical misinterpretations and logical fallacies is a story for a whole new blog (with a very poor number of readers I suppose though).

    Excuse me for the very long comment, but I am very glad that finally someone is giving people the hard painful and lengthy knowledge about this topic. As it gives me hope that such people will occur more and more in all fields of human gnosis. Just a big thank you Peter for the scientific ethic, your argumentation rigour and the well-explained warnings concerning statistical phenomenon.

    Have a nice day or more 🙂

    • Ollie W

      Hi Vladimir, it’s been Four years now since your original 6 weeks so I’d love to know your reflections on your low carb dieting over the medium term? Many thanks, Oliver Wilkinson

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  • Francis

    So what is your opinion on eating meat? Eat more of it? Eat less of it?

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  • Song

    At the risk of sounding like a looney, I just want to say…you are my hero!
    I love that you encourage every one to use their brains and to actually THINK things through.
    After seeing several of your studies I began dramatically increasing my good fats and now I have “cured” my diabeties and my horrific blood sugar swings that tomented and dominated me most of my adult life. Keep up the fantastic work. You are a gem. Song

  • Norm
    • If you’re a mouse, yes, at least worth considering.

  • Peter Silverman

    After reading Richard Feinman’s book “The world turned upside down” it doesn’t make sense to me to disregard all observational studies without looking at the strength of the evidence. That smoking makes us 30 times more likely to get lung cancer seems worth paying attention to, even if it’s not a double blind gold standard study. Similarly, gold standard studies that show very small differences in results seem pretty open to question.

    • Lung cancer (and scrotal cancer and mesothelioma) are very special examples–I’d call them the exceptions, not the rules–that give us great reason to we have cause within the correlation.

  • Conrad

    Almost two years old, still well-sourced and accurate.

    Some of those claims are exactly the ones you’ve set out to prove (or disprove) with NuSI, and my impression is that for each of them you are either already convinced based on the plenty available evidence or else you could bet that new evidence will confirm them.

    You have scrutinized studies more than most people I know. I wonder in your view which of these you personally have highest confidence (close to 100% sure) and which you’d be more like ‘I would bet so, but studies have not been so strong so far and we do actually need more data’.

    At least one caveat I believe you have is on #3 as you expose in the video mentioned in ‘Random finding (plus pi)’ article: that the safety of consumption of SFA seems not to be universal (that is, that not all people physiologically respond to it equally well).

  • Gavin Curtis

    And how does the immoral nature of slaughter and massive environmental degradation fit into your statistical model?

    • Those are important considerations, Gavin. But it’s important to keep the three macro arguments, the two you raise–ethical and environmental–and the individual health considerations separate. Too often people confuse the arguments. They all matter, but I’m asking–very specifically–about the latter.

    • Tomoff

      And how moral is industrial crop-raising and cramming grain and grain-extracted sugar down our gullets, including, by the way, the gullets of industrially raised animals; how environmentally safe is it from a habitat’s point of view? Morally, we’ve been killing animals for food since time immemorial. Today the main reason to be slaughtering them in such numbers is that they’re raised in such numbers, which in turn is possible, because they – can you guess? – are fed on plentiful, subsidized grain.

  • Frances Katrishen

    What do you think of the World Health Organizations conclusions today that people should eat less red meat because it may cause some forms of cancer? How good was the research in terms of establishing causality? They seem to have established a stronger link between processed meat and cancer. In both cases they don’t know why. It is being widely reported and it is giving the anti-meat people more “evidence” for their claims that we should all eat less meat.

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  • Suzy

    Even God says it is ok to eat meat.
    “Only whenever your soul craves it you may slaughter, and you must eat meat according to the blessing of Jehovah your God that he has given you, inside all your gates. The unclean one and the clean one may eat it, like the gazelle and like the stag.” Deuteronomy 12:15.

    • Jeff

      *Your* god says eat meat, at least a subset of available meaty options. Plenty of other gods would disagree.

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  • Benas

    Hi Peter! Huge fan of your blog! I have recently read studies about iron and its role in insulin sensitivity & aging and believe iron levels is a missing link in nutrition science, probably explaining why eastern cultures were OK despite eating carbs, potential harm in red meat, why women are healthier than men until menopause etc.

    Here’s an interesting quote: “Medical scientist Francesco Facchini has done much work in this area. He found that in patients with insulin resistance – what he calls “carbohydrate intolerance” – therapeutic phlebotomy such that the patients got to “near iron deficiency” caused an approximately 50% improvement in insulin sensitivity.”

    P.D. Mangan summarizes the findings of various studies quite well, his series of articles on iron:

    So red meat contains lots of iron, and a person can reduce iron levels by losing/donating blood. So it seems combining low-carb diet with blood donations could be the answer.

    • I’ve been meandering through this lit for the past year. I think there is something to it, but I don’t think it’s the full story. Too many counterfactual examples. But it could matter in extreme states.


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