Reading Time: 3 minutes

A common refrain of Health At Any Size people is that, “But only 5% of people achieve sustained weight loss!”

Then follows the suggestion that, therefore, nobody should try to achieve sustained weight loss.

This 5% figure is a fiction, as one can see from scientific reviews of the research literature. Read carefully:

In fact, in the right circumstances, an impressively large % of overweight people can maintain an impressively large amount of weight loss. Read the above. It is simply wrong that long-term weight loss is “impossible”. A large number of people do it, and they do a lot of it.

But for a moment, let’s pretend that the 5% figure was correct: only 5% of people maintain sustained, long-term weight loss, right? Here’s the kicker: for most people we give medical treatments, an even smaller percentage will benefit.

Yep, not only is weight loss possible among a rather large % of people, but even if were only 5%, this would still be better than many of our mainstays of medical treatment.

How can this be? Let us take a look. Statins.

Only about 7% of individuals will benefit from a statin. Now this benefit will be equal to about 99 months of life, but only 7% of people will benefit from a statin.

In many weight loss studies, many more than 7% could sustain long-term weight loss! Does this mean we should throw statins out as a medical treatment, because we’re throwing out weight loss?

Blood pressure medications. Only about 1 in 125 people will avoid death from taking a blood pressure medication. Throw out blood pressure medications?

Mammograms. Only about 1 in 2500 women will avoid death because of mammograms. Throw out mammograms?

Prostate cancer screening. Only about 1 in 50 men will avoid death because of prostate cancer screening. Throw out prostate cancer screening?

Colorectal cancer screening. Only about 1 in 1250 people will avoid death from colorectal cancer screening. Throw out colorectal cancer screening?

Metformin for diabetes. Only about 1 in 14 people will avoid death by being treated by metformin for 10 years. That’s *still* worse than the number who will lose weight in many studies.

Am I cherrypicking? Nope. The case for drugs not causing a benefit in most people was also made on in an article called “Most Patients Get No Benefit from Most Drugs“.

These are easily demonstrable, widely accepted facts. Modern medicine saves lives. It improves the quality of life. But on the whole, it is pretty weak. However, applied many times over and to many people, and we get millions of lives saved. It adds up.

But what about weight loss? How much death would be avoided per person assigned to receive weight loss in a clinical trial setting?

According to this paper, which analyzed a total of 15 weight loss randomized controlled trials involving 17,186 obese participants, about 12 pounds of weight loss in obese subjects over a mean follow-up period of just 27 months resulted in a 15% reduction in death from all-causes. Including only trials with a follow-up period of 4 or more years yielded the same result.

Just 12 pounds? With a mean follow-up of just 27 months? 15% reduction in total deaths.

Still, for comparison’s sake, I calculate the number of people needed to attempt weight loss to avoid one death in the 27-month follow-up period using the findings of the above paper:


Not as good as metformin, roughly comparable to blood pressure medication, vastly superior to mammograms and colorectal cancer screening. So again, throw out blood pressure medications, mammograms, and colorectal cancer screening?

Even though modern medicine saves millions of lives, much of it is still weak compared to long-term weight loss. Yet the HAES people say that because not everyone can lose weight, nobody should try to lose it.

If that’s the argument, then to be logically consistent, the HAES people should reject the screening and treatment of many chronic diseases and much of modern medicine.

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Most popular health experts are unscientific

Many popular health experts claim to be science-based. They will often provide hundreds of references to support their claims. But citing many references does not mean one is scientific. It only means that one has collected many references.

Most self-proclaimed health experts are in fact very unscientific. They over-interpret the scientific literature. They create controversies where there are none. They form strong conclusions from weak data. They cite papers that support their views and ignore ones that don’t. They dedicate their entire body of popular work to buttressing an ideology or set of ideologies.

Their goal is not science per se but rather the promotion of a certain point of view. And, when credible people or organizations express disagreement with their conclusions, like clockwork they deploy conspiracy theories to dismiss that person or organization. They behave like cult leaders more than they behave like scientists.

What is sensational and sciency succeeds in the current media environment, not what is scientific

We want answers regarding how to be healthy. So when someone who is passionate provides us with an extensive, plausible-sounding series of arguments, we want to follow. How else, after all, are we going to become healthy, than by trying SOMETHING? And that something, provided by the extensive scientific-sounding claims from popular health experts, is likely to be better than nothing. So we do it.

But why THIS something? Why this advice?

Because it is sensational. Whatever is sensational generates greater buzz in the popular media. Thus, whatever we are exposed to is likely the result of a selection process, where the sensational survived and the drab perished. Sensational plus sciency equals pop health. (Sciency: appearing to be scientific but not actually being so.)

Whoever can be sensational and sciency at the same time, wins. The work of Gary Taubes and his countless low-carb followers is a perfect example of this. It is very sciency and very sensational. The work of Michael Greger and his followers (as well as his predecessor John McDougall) functions similarly. Sciency and sensational. Overturning the received wisdom. With “science.”

But what we really want are claims that are true. The current media environment that has gotten the claims to our doorstep is not giving us what we really want. We want the best way of achieving health according to a reasonable, scientific understanding of everything published to date. And the media is not giving us this because it rewards sciency and sensational, but it has no mechanism for ensuring that what is sciency is actually scientific.

Popular experts must have a scientific mentality if we want for their advice to be at the cutting edge of science

The true scientific mentality consists of a constant effort to understand the world and then to test–and if necessary–disprove that understanding. This is because the person with the scientific mentality really wants to know what is actually true. The person with the scientific mentality is happy if they discover that their current beliefs are not true, because that brings them one step closer to beliefs that actually ARE true.

For this person, false beliefs are a barrier to truth and must be rooted out. This is what people mean when they talk about falsification. Falsification is central to science because it is central to progress toward a final theory of reality, which is the scientist’s ultimate goal. This sounds very lofty, but it also has important practical applications.

A final theory of reality is extremely serviceable, because if we understand exactly how the world works, we can more readily create useful technologies. Thus, in the field of health sciences, science and benefit to patients go hand in hand.

A scientific mindset is the best way to serve patients: false and harmful/unhelpful theories are discarded while true and beneficial theories remain. It follows that an expert that is truly scientific should be trying to constantly overturn their own beliefs. And that promoting just one set of beliefs without criticizing them is a failsafe sign that one has identified someone who is not scientific.

We therefore reach our simple, singular criterion for identifying which popular health experts are science-based and which are not:

A science-based health expert will consistently and competently criticize the design, methods, and findings of studies that agree with the positions that they have taken previously.

They must demonstrate consistent evidence of a scientific mentality. Such an expert will consistently seek out the limitations to their positions. This is actually easy. Because almost all health science has limitations or flaws, we can constantly be gaining a deeper and deeper understanding of how the new and old science is or might be flawed.

Practical recommendations for nutrition and fitness are almost never 100% certain

Health scientists do not come to conclusions or recommendations based on certainty. In almost no area of health science does certainty exist. This is especially true for nutrition and fitness science. Rather, health scientists come to conclusions and make recommendations DESPITE limitations and flaws. Health scientists must weigh the different bits of evidence, with all of the flaws and limitations that are a part of each, against each other. The scientist will always look at evidence in health science and frown.

The recommendations that the health scientist will make are those that make him frown the least. Recommendations in health science are almost always a matter of nodding solemnly, wishing we had better evidence, and then making the recommendation. It is literally impossible to do that in an unbiased and informed way if one does not systematically understand the flaws and limitations of the different positions. Furthermore, since practical recommendations are always hedges, they should change over time as new evidence comes to light which then tips the scale in one direction or the other.

Therefore, a person who is not actively engaged in trying to understand the problems with the science underlying their own recommendations cannot possibly be coming to conclusions based on a scientific understanding of the evidence, and they cannot be updating their point of view in light of new evidence.

A person not constantly questioning their own beliefs in light of the evidence and growing cannot possibly be at the cutting edge of the science.

What most popular health experts do, versus what they should do

Therefore, ask yourself:

Does your preferred health expert seem to be concerned with findings the flaws and limitations of the evidence supporting his or her recommendations?
Do they go deep in looking at the scientific papers and evaluating the design, methods, or findings?

Because if not, then ask yourself:

What is that popular expert actually doing?

We take it for granted that a popular health expert does not behave in the above way, i.e. in a way that is scientific. We take it for granted that popular health experts constantly hype their beliefs, that they should represent a consistent certain point of view, year after year. And certainly this is a more successful strategy for getting a message out.

But shouldn’t we demand that this be balanced by at least some indication that the health expert is concerned with the objectivity of their position? And shouldn’t we be concerned when we see no indication that they are?

Our current system of health science communication has failed, but the way to change is clear

How has our current system of popular health experts helped us? How has it generated anything but confusion? I suggest that we hold popular health experts up to higher standards, to the standard of actual scientists:

What demarcates whether a person is science-based or not is whether they frequently criticize the evidence supporting their own positions. By this criterion, almost no current public health experts are science-based. And I think almost none in fact actually are, so I think this criterion gets things right. The problem is that we have as consumers incentivized hype.

If we want good health information, we need to start incentivizing earnestness. I believe that evaluating health experts on the basis of the above criterion will help to accomplish that.

In the meantime, we also need to explain to children starting at a young age just what science is. It is NOT the next, best cool thing. It is a laborious and constantly unfolding process, especially in the area of health. And the defining feature of this process is thoughtfulness and self-doubt, and the people who balance thoughtfulness and self-doubt with popular communication are the people we should trust. Not hypesters.

I wrote almost a year ago that I wanted to release a quack list. Well, a quack list could easily be generated based on the above criterion. It would include almost all popular health experts. Almost all claim to be science-based, but almost none actually are science-based.

And I really do think that this criterion is a fair one. It’s just radical. But maybe what we need in this age of insane health claims and gurus is exactly that: a radical point of view.

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Reading Time: 14 minutes

Chris Kresser, a frequent guest on the Joe Rogan Experience, is awful. This post will explain why.

Kresser is not science-based. He spreads misinformation about health and nutrition science. I cannot detail why all of this misinformation is misinformation because it would take many hours, and I have many other things to do.

I can however explain at significant depth why he is wrong about one particular fact. In doing so, I hope that readers will take away how unreliable he has been about this one particular issue. And I hope that this will cause them to be a little more cautious about everything else that they read from him.

Some may argue that everyone is wrong about some things. This might be true, but this argument does not apply to Chris Kresser. Chris Kresser systematically rejects science, opting to instead promote ideas wildly at odds with the evidence and conspiracy theories to explain why he is right and scientists are wrong. He often purports that modern medicine is out of step with the current science and that he is on the cutting edge. (This is false. In fact, Kresser merely riffs off of popular science books that have claimed the same and is himself often not familiar with the actual scientific literature.)

I cannot emphasize how much Chris Kresser is, in a word, systematically wrong. But perhaps the following post can be a lesson. I have titled this “Part 1” in case I need to make more of these posts to convince others and actually have enough energy to keep doing so. Most likely, I will not, but it is always possible.

Without further ado, Chris Kresser ladies and gentlemen…

Kresser has an incredibly slick and very aesthetic website. As you can see next to the title, his articles are even “Fact Checked”.

“Fact Checked”! What does that even mean?

From the website:

In other words, people on Kresser’s staff, whose salaries he pays and who are not financially independent of him and his extreme views (as we shall see in a moment), must fact check Kresser.

Anyone got any guesses about just how impartial these “fact checkers” who are fact-checking their boss are likely to be? My guess: anywhere from “not very” to “not at all”.

Kresser opens by citing the World Health Organization and pointing out according to recent studies that cardiovascular disease is largely preventable.

True, but what is the largest risk factor according to this study?

“Raised apoB/apoA1 ratio.” Hmm, what is apoB?

As we see from a seminal 2016 article published by the European Atherosclerosis Society Consensus Panel:

ApoB, short for apolipoprotein B, is the constituent lipoprotein on LDL particles.

What does that mean? This is not a primer on blood lipids, but it basically means this: in order to dissolve in the blood, cholesterol needs a protein carrier. This protein carrier dissolves in the blood. The protein carrier for LDL cholesterol is called apolipoproteinB, or apoB. There is one apoB per LDL molecule.

So, remember, the apoB/apoA1 ratio is the ratio of the protein carrier for LDL to the ratio of… wait, what’s apoA1? Easy peasy. ApoA1 is the lipoprotein carrier for HDL.

Remember that lipid panel you got? LDL and HDL are the major components. Well, this is them.

In other words, the ratio of apoB to apoA1 is roughly equivalent to the ratio of LDL to HDL. So what this paper is saying is that the ratio of LDL to HDL is the most important risk factor for cardiovascular disease.

Let’s jump forward.

Here Kresser claims that he is going to “debunk 3 common myths about heart disease.” One of these myths is that high cholesterol in the blood is the cause of heart disease.

But wait a moment. Isn’t a high ratio of LDL/HDL a risk factor for heart disease?

Let’s keep that question in mind as we move forward.

Here Kresser claims that the medical establishment is still diagnosing and treating heart disease according to science that is 40-50 years old. Interesting, because my cardiologist friends seem to be constantly updating their techniques and approaches to cardiovascular disease. Also: I didn’t know that Chris Kresser is a cardiologist!

Perhaps more interesting is this:

“More recent (and higher quality) evidence doesn’t support it.”

Oh really?

Here’s Kresser’s next paragraph:

Clicking on his reference, we see the following:

In other words, on average eggs do not increase the LDL to HDL ratio, which as we saw above in Kresser’s first reference was one of the best predictors of cardiovascular disease risk.

But then…

We see that in hyperresponders, or 25% of the population, this ratio probably is increased: LDL goes up faster than HDL.

Let’s check out the final two paragraphs of this paper. Read the highlighted portions carefully.

First, here:

In other words, up to one-third of the population (people with type 2 diabetes are about 10% of the population) may be susceptible to atherosclerosis (diabetics, as mentioned earlier in the paper, not shown in this blog post) or to a worsening of the LDL/HDL ratio upon consuming dietary cholesterol.

In other words, things are a lot less clear than Kresser lets on.

This, coming from the very article that he is citing in favor of a dogmatic view that dietary cholesterol is unimportant.

That is not what the article that he is citing says.

To put the icing in the cake, the final sentence comments on current recommendations on dietary cholesterol:

Why? Since a large proportion of the population might respond negatively to intake of dietary cholesterol, the paper suggests that dietary cholesterol might best be minimized.

In other words, the article that Chris Kresser cited to show that dietary cholesterol “does not increase the risk of heart disease”? It recommends to minimize intake of dietary cholesterol.

I do not mention this to argue that dietary cholesterol necessarily should be restricted. I only point this out because it makes clear that Kresser is selectively reading the scientific literature in order to make a biased and partisan case for one point of view, while the very literature he cites makes both a more nuanced case and gives the exact opposite recommendation.

What about saturated fat? Kresser writes:

Let’s take a look at the reference, shall we?

Ah, Mensink and Katan’s classic meta-analysis of 60 trials. “Some studies,” Kresser wrote. “Some?”

Still, it’s an old meta-analysis. A more recent one was published in 2016, with Mensink as the sole author, commission by the World Health Organization:

Clocking in at 72 pages, this report contains everything one would want to know about fatty acid replacement, including 91 studies:

“Some studies.”

Let’s revisit that statement again.

“These studies are almost always short-term, lasting only a few weeks.”


Here is a sampling of one page of the list of 91 studies that Mensink used in his analysis:

84 days, 42 days, 49 days. And that’s just among 10 studies. Some of these studies lasted over 90 days. And many lasted over 50. “Lasting only a few weeks”?

Yeah. OK. Sure.

Here is a characteristic table from the study, showing a powerful relationship between the replacement of saturated fat with other macronutrients on blood cholesterol levels:

In other words, robust changes in blood lipid markers in response to replacement of saturated fat by other macronutrients.

But fine, let’s ignore those studies. What about Chris’s other studies?

Apparently all of those other studies show that cholesterol levels don’t go up with saturated fat?

The reference cited is an article from Stephan Guyenet’s blog.

In it, Stephan makes the case that the observational studies show little relationship between saturated fat and blood cholesterol.

But hey, wait a second…

Observational studies? In other words, nutritional epidemiology? Chris Kresser is now using nutritional epidemiology to demonstrate that there is no relationship between saturated fat intake and blood cholesterol?

But wait- I thought- I thought Chris Kresser thinks nutritional epidemiology is worthless.

Here is what Chris Kresser says about nutritional epidemiology:

I quote: “Pseudoscientific”.

And he uses the entire post to take cannon ball shots at nutritional epidemiology from every angle in like fashion, with quotes such as:

And with sections such as this:

In other words, Chris Kresser lambasts nutritional epidemiology. UNLESS… UNLESS… well, unless it shows that there is no relationship between saturated fat intake and blood cholesterol.

Well, why the fuck not! If nutritional epidemiology shows it, it’s probably true! Nutritional epidemiology is proof that there is no relationship between saturated fat intake and blood cholesterol, even when the randomized controlled trial literature shows a strong relationship.

BUT… nutritional epidemiology is wrong about everything else.

Right Chris Kresser?

Still, if I were playing Devil’s advocate, I would say that, well, Chris could shoot back:

“Yeah sure nitpicker Bass. Blood cholesterol responds in the short-term RCTs. Yeah, and maybe I misspelled “months” as “weeks”. But the point is, how do we know over a long period of time that blood cholesterol declines in response to lower saturated fat intakes? It might be a temporary effect rather than a long-term effect. The long-term data we have shows that, on the order of years, there is no effect of saturated fat intake on blood cholesterol. It might be observational, but it is the only data we have. So at minimum, even though I have repeatedly argued that epidemiological data are trash, we have to accept that blood cholesterol might not be reduced by reducing saturated fat.


Maybe Chris is right. Maybe we don’t know if there is any effect of reducing saturated fat on blood cholesterol…

If we were living in the 1960s.

Because two very famous studies that sought to test the diet-heart hypothesis (as he calls it) did, in fact, study this very question: could reduction of saturated fat over the course of years cause reduced blood cholesterol levels?

The first in Circulation, an official journal of the American Heart Association:

And it found:

Oh shi-

Here are the methods. Basically, 40% of calories in fat were replaced in the normal diet by unsaturated fat:

Chris Kresser, ladies and gentleman:

But wait, there’s more!

The Oslo Diet-Heart Study, also published in Circulation, this time in 1970:

What happened to the cholesterol?

Yep, it went down.

Here are the methods (from the 1968 version):

So what is it Chris? Do we believe the randomized controlled trial literature of hundreds of studies, verified by at least two long-term trials?

Or the observational epidemiology?

Another question: why is it that Chris forgot about these incredibly famous studies when reporting the role that unsaturated fat plays on blood cholesterol?

Then Chris Kresser decides that a 6-foot grave isn’t deep enough and wants to go even deeper. So, he talks about low-carbohydrate diets:

What a coincidence! A new, comprehensive, 24-page report on low-carbohydrate diets, including every study and meta-analysis on the various effects discussed was recently published by the National Lipid Association in the Journal of Clinical Lipidology:

To be sure, the National Lipid Association is one of the most respected lipids organizations in the world. And researchers from many of the world’s most prominent universities are on the authors list.

And here is what it found on the effects of low-carbohydrate diets on blood lipids:

“A high saturated fatty acid (SFA) content in low-CHO and very-low-CHO diets is a key factor for an increase in LDL-C.”

In other words, while low-carbohydrate diets higher in mono- and polyunsaturated fats caused lower total and LDL cholesterol, diets higher in saturated fats caused higher total and LDL cholesterol.

And here’s the thing. Kresser could have known that when he wrote this published this article June 11, 2019. There were dozens of papers showing increased LDL cholesterol levels in response to low-carbohydrate diets and a dozens of reviews and meta-analyses that point out that the fatty acid composition is critical in determining the response of LDL cholesterol to these diets.

But did Kresser talk about that at all? Nope.

If he had talked about it, he could have helped people who had high blood cholesterol to keep it lower. Ah, but yes, according to him, blood cholesterol is not important for cardiovascular disease, so he doesn’t need to help his readers prevent increased blood cholesterol levels.

Which brings up an interesting point: why is it important for him to argue that dietary cholesterol and saturated fat don’t increase blood cholesterol if blood cholesterol does not cause heart disease?

My guess: Chris is defending his turf at every point possible as someone who recommends high meat intake and “natural” remedies. It is straight from the denialist’s playbook: make the chain of denial so long, impenetrable, and ridiculous that nobody wants to even bother challenging it.

Oh, but let’s continue:

I can’t even.

He is literally saying that a diet high in saturated fat will cause a decrease in blood cholesterol in half of the people to whom it is fed. This is not supported by a single study out of hundreds, and is totally invented by Chris Kresser.

It’s as if even with his throwaway paragraphs, he wants another opportunity to make things up.

Let us continue.

Ancel Keys claiming that the diet-heart hypothesis is dead? Let’s actually look at the original article.

First let us note that Chris Kresser leaves out the first and last sentences, only quoting the middle to make his point. Let’s take a closer look at these sentences.

The first argues that blood cholesterol is important and that thinking otherwise will cause confusion among the public:

The last sentence points out that fatty acids are important (meaning saturated fats):

In fact, this was a restatement of the positions that he had maintained since the 1950s: Ancel Keys early pointed out that dietary cholesterol had only a modest effect on blood cholesterol levels, while he demonstrated through the Seven Countries Study and subsequent work that saturated fats played a decisive role in cardiovascular disease. Which is exactly what he says again in this letter to the editor.

Yet Chris wants to use this letter to imply that Keys had reversed his position:

It is a total distortion of the facts. Kresser literally took a quotation out of context to make the author look as if he believed the opposite of what he really believed.

Are we seeing a pattern here? However Chris Kresser can land a shot, he does. He denies that saturated fat raises cholesterol. He denies that cholesterol causes heart disease. He denies that saturated fat causes heart disease. He denies that statins prevent heart disease. He distorts the clinical trial evidence and mischaracterizes it. He cites only epidemiological studies, while in other articles calling epidemiology pseudoscience. He ignores any mention of RCT data that would definitively repudiate his claim. He cherrypicks meta-analyses and declines to provide context. He tries to make it look like Ancel Keys reversed his position.

And no matter what claim he needs to defeat, he can always come up with some way of cherrypicking evidence or quotations or ignoring to make it appear defeated. It is one of the most flagrantly dishonest styles of scientific argumentation that I have read in my life.

We’re not done yet.

In a Research Spotlight, Kresser suddenly reverses his position completely and affirms the pivotal importance of LDL cholesterol for cardiovascular disease:

You couldn’t make this up if you tried. It is one of the most flagrantly ridiculous endings to a ridiculous article that I have read in my life.

Oh it gets worse. You didn’t think it could. But it does.

He continues, describing a recently published study that demonstrated how to reduce blood cholesterol through lifestyle. There were three groups:

And according to Chris, they saw a modest decline in LDL cholesterol:

What did the group interventions consist of? I looked up the methods paper. And I have highlighted the relevant portion:

Yep. That’s right. Saturated fat restriction. In both groups that saw an improvement in LDL cholesterol, there was saturated fat restriction.

Chris concludes, praising the intervention:

And with that, the conclusion:

All of that text. All of that work. Just to show that how dishonestly/incompetently Chris Kresser wrote a single short article. Kresser writes hundreds of articles. A substantial proportion are total BS just like this one, argued using an identical ad hoc, cherrypicking methodology that focuses on proving the point rather than being objective.

But how is it possible to know which ones are good and which are nonsense? Here’s a tip: I recommend not reading anything he writes.

And now I am off to hang myself with my shoelaces.

This world. Too much for me.

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Reading Time: 2 minutes

I recently read this article from Scientific American:

This is a good opportunity to remind the reader–in a very schematic way–why science trumps patient or clinical experience for making recommendations.

Sure, this is obvious to many people. But it is worth repeating, because apparently even the editorial staff at the Scientific American needs reminding.

This post will focus on one statement in the article:

“Because if we dismiss everything that isn’t patented or presciption-only [sic], we dismiss people’s lived experiences.”

It is important to preface: nobody denies that patient experiences are very important, only that they cannot be the direct basis for guidelines or recommendations in the popular press or on social media.

If patient experiences became the direct basis for recommendations, then we would literally have to recommend everything. Placebo, regression to the mean, confounding by other simultaneously applied treatments, and any number of other confounding factors will ensure that virtually every treatment has someone to recommend it.

While treating individual patients, their experiences can be useful or at least they can be navigated when they are not harmful. Patient experiences can also lead to new hypotheses to test using science. If science vets these hypotheses, they can become recommendations.

But to imply that patient experiences should OVERRIDE current scientific findings for making population-based recommendations is deeply offensive to those who think that science is superior to hearsay, folk remedies, etc.

Science does not make medical doctors “gods”. It does however place within our therapeutic arsenal (when we know how to use it appropriately) the most powerful system for generating and testing practical knowledge that humanity has yet devised.

In an age of widespread medical nonsense (spread via social media), this is especially important to emphasize. Science protects people from charlatans, who, exploiting plausible-sounding scientific stories, patient testimonials, and science illiteracy, peddle treatments that are useless, harmful, or divert consumers from getting effective medical treatment–leading to real harm.

Scientific American (@sciam), by publishing such statements, promotes thinking that is diametrically opposed to science. This is disappointing. Because this is Science 101.

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Reading Time: 5 minutes

As a follow-up to the podcast discussion with Dave Feldman, I am musing a bit offline about what exactly his LHMR study would show even if atherosclerosis did not progress in his subjects much.

Because we already know that other factors besides LDL also modify risk.

Here is an interesting calculator that David Nunan (@dnunan79) sent me me:

Now, based on it and using Framingham data, here is what would happen to risk if total cholesterol is 8 mmol/L (310 mg/dl), HDL is high, in a 74-year-old female who is 74 and physically active.

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7% chance of having a cardiovascular event.

Just one-in-thirteen!

Same exact risk factors but 45 years old instead of 74 years old?

Just 2%, or 1-in-50.

Yes, maxed-out total cholesterol but just a 2% chance of having an event at age 45.

Now let’s look at the same exact risk factors but as a 74-year-old male.

Not great, but still only a 15% 10-year risk of heart attack.

What about a 45-year-old male?

Less than 4% chance. With maxed-out cholesterol.

Now here’s what happens if in a 74-year-old male, keeping the same total cholesterol and HDL cholesterol, keep the same age, BUT get a) untreated hypertension, b) diabetes, and c) add a father with heart disease.

Suddenly you go from 7% to 100%!

Now here’s what happens if you keep all those same risk factors and reduce cholesterol from 310 to 77.

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Your risk of heart disease drops from certain to about 56%.

Nothing changes except cholesterol. Big drop in risk, but this drop is clearly not everything, and a lot of residual risk remains.

Now here’s what happens when you go low cholesterol, high physical activity, and take away all those other risk factors as well.

Risk down to less than 3% over ten years! In a 74-year-old.

Basically, non-HDL cholesterol (which roughly approximates LDL cholesterol if I am not mistaken) here accounts for about a doubling of whatever one’s baseline risk is.

That’s either massive or modest, depending on your point of view. So, according to Framingham, if you were like Dave’s population of interest and got everything dialed in except LDL cholesterol (in other words, if you were a 45-year-old, male lean mass hyperresponder practicing a healthy lifestyle on a ketogenic diet), what would we expect?

We would expect a very low rate of cardiovascular disease progression.

In other words, the model predicted by Dave Feldman in his LMHR project is the exact same as the one predicted by Framingham.

Only if we saw dramatically high rate of progression of atherosclerosis among LMHRs or a dramatically low rate would we be surprised. And for Dave’s study, we would not expect a sufficiently large sample size or methodologically rigorous design to detect a reduction to an already very low risk.

Despite this, these patients would still be about three times as bad off with respect to heart disease than if they had lower cholesterol.

As a reminder, here is the same risk profile as above except with low instead of high cholesterol:

So having very high cholesterol is roughly three times as bad as having low cholesterol while having a healthy lifestyle. But this three-fold elevation still does not result in an extremely high absolute risk.

As a side note, let’s also take a look at the role of diabetes vs. total cholesterol. Here is perfect everything, age 74, female, physical activity, etc., except for diabetes.

4.4% risk of cardiovascular event in the next 10 years.

Now here is perfect everything, age 74, female, physical activity, etc., except for 310 mg/dl total cholesterol (and no diabetes).

7.1% risk of cardiovascular event in the next 10 years.

So having high cholesterol is clearly worse than having diabetes according to our current knowledge. But they are somewhat comparable.

However, contrary to what Aseem Malhotra says, having high lipids is in fact somewhat worse than having diabetes.

But what if we add high lipids and diabetes together and take away physical activity?

Suddenly risk jumps to 18%.

In other words, all of these risk factors are synergistic. They work together to increase risk of cardiovascular disease.

It’s not one or the other. Insulin resistance or cholesterol or smoking or hypertension or age or sex.

All are important.

Statins are thought to be a great drug not because they are the cure-all of cardiovascular disease (they are not), but because they reduce a major risk factor in a safe way.

The same cannot be said about inflammatory cytokines, which, when blocked in the CANTOS trial, caused an increase in sepsis.

We use statins by reason of historical accident: not because LDL is everything, but because as a species we found a way to reduce a major risk factor and haven’t been able to do the same with the other risk factors to the same degree.

Reducing LDL does not solve the problem of cardiovascular disease. It just causes a substantial reduction in risk. But really reducing risk requires an attack on several fronts. None of these can be neglected if we want to minimize risk of deadly and debilitating heart attacks.

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Find my first podcast interview ever here:

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I have always thought that reasoning from anatomy to the human diet was ridiculous. Humans are unlike any other animal in one very important and relevant respect: we have harnessed fire to make food easier to digest. Cooking is a form of predigestion. Indeed, cooking can be thought of as a form of external digestion. As humans, we have outsourced our digestion: from gastrointestinal tract to fireplace.

This outsourcing provides the human species with a competitive advantage. Because our guts no longer need to do the work of digestion, there is less evolutionary pressure to maintain gut function and length. All of those resources that the body dedicates to maintaining gut length now can be used to maintain other organs, such as the brain. All of that time to chewing food, humans can now use for other activities, like hunting, gathering, and socializing in increasingly complex and sophisticated ways.

Humans, through fire, were liberated, body and mind. Fire was the first revolution of mankind. This is why the Greeks dedicated to this milestone one of the most interesting and terrible of all myths: that of Prometheus.

Fire changed us forever. By giving evolution permission to shrink our guts, fire gave license to the expansion of our brains. By freeing us from the yoke of perpetual chewing, it subjected these enlarged brains to the novel and powerful selective pressures of social life, which further enhanced our cognitive capabilities. And by unlocking the endless bounty of nature–which had hitherto been indigestible–fire made humans resilient to famine and paved the way for our spread across the globe.

That is the story told by Richard Wrangham, anyway, in his influential book Catching Fire. And believing it, I also believed that the relationship between gastrointestinal tract structure and digestive function, as evident in the other animals in the world, was broken in humans. While the herbivores of yore might have very long digestive tracts, humans needn’t. We simply do not follow the same rules as the other animals. So if humans did have gastrointestinal anatomy much like a carnivore, then they might be either a carnivore… or not.

Thus, my judgment was closed: anyone arguing from digestive anatomy to function was, at best, a lost cause. And engaging with such arguments, a waste of time. Besides, every diet tribe claims human gastrointestinal anatomy as their own anyway. Therefore, we simply should not try to derive the optimal human diet from anatomy, but from modern nutritional science. Easy peasy.

That was until Game Changers, anyway. A great monument to pseudoscience, I have been motivated to check everything: every crevice of every fact. Besides, despite all my logical certainty, my curiosity was the greater force. I have always wanted to know: exactly what was human digestive anatomy like?

So when Julianne Taylor tweeted about this–that humans have a digestive tract length similar to that of lions, contradicting the claims from Game Changers–I had to check this out.

And what followed was this:

I really appreciate Julianne. We have followed and interacted with each other for a long time, and I really appreciate the work that she does. So I dove into her references. Because I wanted to really understand.

What follows me is my own fact-checking of Julianne’s fact-checks. I wrote this thread after I discovered that her reference was incorrect: humans do not have the same gut-to-body-length ratio as lions or other carnivores. Without further ado, posted with some minor edits…

I don’t think the reference Julianne uses is credible. The human GI tract is about 8.5 meters. The length from neck to anus is around 0.7-0.8m.

9/0.7 = 12
9/0.8 = 11

Human ratio is therefore 11-12x. Game Changers exaggerates but in this case is close-ish.

Let’s look at human GI tract. Here is a paper with 200 subjects: 100 males and 100 females. It shows average is about 8 meters, not including the upper GI tract. Including the upper GI tract takes us to about 8.5 meters.

Now the length from neck to anus in humans is about 0.7-0.8 meters. I’m tall and I measured about 0.8 meters.

Why measure from neck to anus? Because that’s how you would measure a quadruped animal’s body length: neck (or head) to base of tail. That’s how lions are measured. (More on this in a moment.) Measuring to the legs does not work because human legs are elongated compared to what they would be if we were quadrupeds. (Try walking on all fours with legs extended.) Likewise, the human leg joint is pointed downward in the hip, giving additional length. So to make a fair comparison, the legs must be excluded. Otherwise humans for reason of their long legs will have an artificially depressed ratio. In fact, the paper that Julianne cites includes the legs of the humans but excludes the legs of the animals, very erroneously depressing the ratio!

Now, the length of the lion GI tract. This paper gives the lion’s GI tract length at about 8.7 meters.


Yet another gives a very similar value (Panthera leo):


Yet another does the same (Felis leo):


According to the San Diego Zoo, the body length of a lion, measured from head to anus, is about 1.9 meters. Let’s cut down to 1.75 metes to get rid of the head. (We are estimating here, but we want to get things basically right.)

Therefore 8.7 meters / 1.75 meters = 5

Which is strikingly similar to the ratio given in Game Changers.

So according to these calculations, humans have more than double the length of GI tract compared to the African lion.

11-12 vs. 5

This is why is it so important to check and double check references. It is not good enough to just find a paper on the Internet. Many papers are plainly wrong.

For instance, the paper that @juliannejtaylor derived her figures from was entitled “Human adaptations to meat eating”.

The title is a red flag. Maybe not bright red, but definitely red. Why are we talking about human adaptations to meat eating? It sounds like a position paper, i.e. biased. But it gets worse, because the paper is not well-written and the refs are nearly untraceable.

Don’t believe documentaries and don’t believe googled papers on the Internet. Most human beings are not objective or scientific, and the incentive structures that would encourage objective information communication are not in place. Quite the contrary.

And in fact, at face value, I even believed Julianne’s thread without looking deeper.

Until I was alerted by @AdamRMG to look deeper. And the above is what I found. Thanks Adam.

I still think @nutrition_facts sucks for endorsing this terrible film, but the human GI tract ratio:body length is very different from a lion’s, and it is close to the figures provided by Game Changers.

This implies that, at least with respect to total intestinal length, humans are most similar to omnivorous or herbivorous and not carnivorous animals. I won’t claim to understand the subject at greater depth than this. I don’t. But we progress small pieces at a time. Perhaps someday I will be able to discuss this at greater length.

In the meantime, I will communicate what the nutrition science says, and evolutionary arguments will continue to take a back seat.

If you like my stuff, donate below. Any contribution, no matter how small, makes a big difference.

I will also be doing an AMA on December 7-8th.

As mentioned, you will need to be a donor to participate. So do so now if that is something you would like to do.


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Last week, Peter Attia wrote a criticism of Game Changers, where he presented the argument (long repeated him) that nutritional epidemiology is fundamentally flawed. By implication, it cannot be used to make nutrition recommendations. His post can be found here.

I am responding to this post because:

a) Peter’s post made it into my message inbox from friends;
b) it misunderstands the basic purpose of nutritional epidemiology;
c) it is a widespread (if misguided and fallacious) view.

I have many problems with Game Changers, which I have discussed elsewhere and which I hope to review sometime this month in a concise format. I have a video here, but I recommend you wait until I can produce the more concise version.

So this is not a defense of TGC. It is a criticism of a widely held view of nutritional epidemiology.

Now, Peter’s article could have been summed up in the singular phrase: “residual confounding”.

A complete summary might be:

Any diet is better than the standard American diet, plant-based or not. Moreover, plant-based diets are associated not just with lower mortality but also with other healthy behaviors. These other healthy behaviors might cause plant-based diets to appear more healthy than they really are, simply by association. Therefore, the conclusions of nutritional epidemiology are not formally scientifically valid.

And that would be that.

This is the version of the argument that I am responding to. I am summarizing it in this way to avoid having my readers get lost in the weeds, and to focus on the essentials. Now the arguments.

To start with, in nutrition science and much of the biomedical sciences, the hypotheses cannot be directly tested: we cannot lock people in cages for their entire lives and control all variables to directly and precisely test the hypotheses of nutrition science. Even if we could, this confinement would itself confound the results, i.e. we would ask: would free-living humans respond the same way as confined ones? Thus, even confinement might not be a solution, depending on the question, even if it were practical or ethical.

Nutrition science and much of the biomedical sciences must therefore adduce evidence for their hypotheses indirectly. Since many hypotheses are not directly testable, much of nutrition science and the biomedical sciences are not, strictly speaking, falsifiable, and are not, therefore, according to the Popperian definition, sciences.

What is nutrition science, then? To provide a full explanation, let’s progress further through the problem and revisit this question later.

Now, to be sure: Peter is right that restricting meat might not account for the health advantages that we see in the epidemiology of people who eat less meat. Again, his article is just one long way to say “residual confounding.”

But the evidence in favor of eating plants over meat is not just the epidemiology (which I review here; please read if you are not familiar with the epidemiology on meat and animal products versus plants). The evidence in favor of plants can also bee found in the feeding studies in animals, in short-term biomarker studies in humans, and in long-term randomized controlled trials. Peter is aware that protein drives mTOR, IGF-1, etc., and thus potentially cancer. Peter is aware that saturated fat raises LDL in many people and that LDL drives cardiovascular disease. He is aware of the classic long-term studies, which, while incredibly flawed in design, also collectively tend to show superior outcomes when saturated fat is replaced by unsaturated fat:

And he has done much to bring attention to these facts in the growing community of people interested in longevity.

But Peter is making the point that, formally, even though these lines of evidence converge–epidemiology, short-term biomarkers, randomized controlled trials, and animal studies–none of these alone demonstrate the long-term detrimental effect of meat intake in humans.

This is true. As I wrote above, nutrition science–given current methods–cannot formally test the causal linkages between many lifestyle practices and health. And the randomized controlled trials, too, cannot stand on their own, because of their gross design flaws. (Thus a proliferation of contradictory meta-analyses on saturated fat randomized controlled trials.)

As I pointed out, the lack of solid RCT evidence means that formal scientific tests of these linkages are impossible. Short-term biomarkers do not establish the causal linkages, and neither do animal studies, and neither does epidemiology. In his criticism, Peter merely highlights this simple fact, this veritable law of most of nutrition science and much of health science.

Yet in every institution in which the government must make decisions about which foods to serve–schools, prisons, public hospitals, etc.–it must also have some sorts of guidelines governing how those decisions are to be made to maximize the human benefits and minimize human costs. The government must have dietary guidelines, and these guidelines must be based on evidence. This, despite the fact that our evidence is incomplete and weak, and we do not have immediate practical means to decisively test our hypotheses.

This makes criticizing nutrition science markedly different from criticizing more traditional sciences. In medicine, we can conduct a clinical trial and, based on the results of that trial, decide whether or not to use the drug. If the drug does not work, we can in principle decide not to use anything. But this is not the same for nutrition science. For nutrition science, we must eat something; the government must formulate nutrition policy.

It is not just that nutrition science can say little conclusively–but that it must say something, because we must act. This makes nutrition science radically and essentially different from many other sciences.

Let us return to the question: What is nutrition science? The conclusion of the above discussion is that nutrition science is in many cases not a science. It is not a Popperian enterprise relying upon definitive falsification of directly empirically testable (and incorrect) hypotheses but a practice that can, in best case scenario, lean upon falsification but more frequently relies upon accretion of disparate pieces of evidence, many of which are not direct tests of our hypothesis.

In a word, there is no such thing in many areas as nutrition science–though there is sometimes, for some questions. Instead, what researchers are doing is not science but a practice that uses the systematic principles of science, combined with judgment, for practical ends. We are talking therefore not so much about nutrition science but of scientific nutrition.

In this case, a case where we must act with incomplete information, it is not appropriate to apply Popperian scientific criteria to the problem. Rather, as in clinical medicine, we must approach the question using our best judgment to manage the risk. We must do scientific nutrition.

The question then is: what are the likely tradeoffs of reducing meat intake?

The answer: in the average context, it is likely either beneficial or neutral.

It is unlikely, after all, that so much data could point in the direction of meat being harmful relative to plants that the opposite should be true.

To explain: if eating plants instead of meat is harmful, this effect is certainly negligible relative to the many health decisions that are consistently obscuring that fact in the epidemiological literature. After all, the very point to making the “healthy user effect” argument is that the healthy user effect is stronger than diet. In other words, if a meat-heavy diet does happen to be more healthful than a plant-heavy diet, this effect is likely to be very minor compared to other lifestyle practices.

In other words, in the most meat-favorable scenario, eating meat is not likely to be very beneficial to health relative to many other things that one could do.

On the other hand, if the nutritional epidemiology, echoing most other evidence we have from other areas of nutrition research, is onto something with respect to meat, then we only stand to gain by eating more plants and less meat.

In other words, we have very little to lose and something substantial, perhaps, to gain. This is the appropriate framework–a risk management framework–through which to understand the meat versus plants discussion. Not a Popperian one or one that takes as its criteria that from drug trials.

What we have is a situation where someone is saying “meat might or might not be unhealthful; we don’t know.” So why wouldn’t we hedge in the direction of harmful, given that’s all the data we have?

Peter still talks about the dietary guidelines being a disaster. He still believes in low-carbohydrate diets–going so far as to recently have Jason Fung on his podcast, which I believe as a podcaster purporting to promote science was a very serious mistake. But I think that such considerations are what’s driving his views on meat.

As far as no data weighing conclusively against meat, he is scientifically right. But that simply doesn’t matter much: when the data are insufficient, the point in scientific nutrition is not to be scientifically right in pointing out that no point of view is strictly speaking formally scientifically correct, but to help people.

So I think the reason Peter leans away from recommending lower meat intakes is that he still believes in the carbohydrate-insulin model. Otherwise, I don’t understand how someone interested in risk management can ignore the data–as imperfect as it is–on meat. So which way should the recommendations run?

It should run in the direction of best evidence: because that’s all that in many cases, scientific nutrition can achieve. If we are interested in the actual practice of nutrition and the actual helping of patients according to best evidence, “best evidence” and not “scientific definitiveness” is the approach we should all be taking. And even if carbohydrates are as bad as Peter seems to think, there is still the possibility of plant-based low-carbohydrate diets. The question is: in which direction does the net balance of risks weigh? And I think the answer, given current data, is crystal clear.

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It’s kind of a joke but kind of not

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