Tag Archives: nutrition

Revealed Preference, Revealed Belief

Revealed preference is a very important economic concept because quite simply: talk is cheap. You cannot poll people on what they economically most want, because humans are want to lie about ourselves so that we appear more noble, more virtuous, and so on. You cannot poll people, instead you have to look at what people *do*.

To explain revealed preference in simple terms: actions speak louder than words. People like to claim that they eat healthily, that they care about what they’re putting into their bodies. But many of those very same people fill their shopping cart with junk food at the expense of all else. So while they claim to eat healthily, they are revealed to eat junk food. Their revealed preference is that they prefer the taste of junk food over the benefits of healthy food, but you wouldn’t know it by talking to them.

At a societal level, revealed preference also shows up whenever popular causes force people to put their money where their mouth is. Reducing plastic waste polls really well, and large segments of society claim that they would happily pay more for a biodegradable option rather than pay less for a plastic option. But the data from supermarkets doesn’t bear this out, with nearly all consumers continuing to prefer a cheaper plastic option when available compared to a more expensive biodegradable option.

So when economists try to understand what drives people’s economic activity, whether it’s what they buy, where they work, or how they commute, one cannot rely on what people *say* they do, you must instead find out what they *actually* do. Because the gap between words and actions is massive and we all want to appear more noble than we truly are.

With revealed preference comes the tantalizing, but tricky prospect of studying *revealed belief*. Revealed *preference* is just showing what *actions* people take that are contrary to their statements. But revealed *belief* would be about showing *the reasoning behind those actions*.

To give an example, lets dissect the junk food vs healthy food choice. You might find people who adamantly claim that they eat healthy food *not just* for their health. They may claim that healthy food tastes better, is more convenient, and is even cheaper than junk food. But if that same person is revealed to mostly eat junk food, we can surmise that their stated beliefs about healthy food vs junk food (that it tastes better, is more convenient, and even cheaper) are also wrong.

Such a person who claims to eat healthy food but only eats junk food clearly has significant cognitive dissonance, or is just *lying* in order to seem healthier. It isn’t just that their actions belie their beliefs, rather their *revealed beliefs* are contradictory to their *stated beliefs*. They probably don’t actually believe healthy food is tastier and cheaper, they just say that to try to further the lie that they eat only healthy food. Their real belief is that junk food is tastier and cheaper, that’s why they buy it and eat it.

This *revealed beliefs* thing is tricky though because there could be several confounding factors. Say someone *only states* that they believe healthy food is tastier than junk food. If they are then revealed later to be buying junk food, is it because they actually don’t think healthy food is tastier? Or is it because the cheapness of junk food and the expensiveness of healthy food outweighs taste considerations? There can always be some other reason that people take their actions, outside of their stated reasons.

But with recent events, I do think I’ve seen a mass example of revealed beliefs. And it’s with tariffs.

When Trump was coming on the scene, first in 2016 and again in 2024, economists and political commentators from both sides of the Atlantic argued passionately against his tariffs on every conceivable level. Trump’s tariffs weren’t just a good idea taken too far, rather *any tariffs at all* would harm consumers and depress the American economy to unimaginable levels. Even tariffs against geopolitical foes like China should be avoided, as such tariffs harmed America a lot more than they harmed China, and so ultimately would be counterproductive.

Yet today in 2026 I see *many of those exact same people*, primarily from the European and Canadian parts of the Atlantic, argue passionately that the EU and other nations *must respond in kind* to Trump’s tariffs. That Europe and Canada should raise massive counter-tariffs against Trump, equal or greater in value to whatever he is levying against them, and specifically targeted at America’s major industries. When Trump’s team met EU officials and agreed to a “deal” whereby the US would raise tariffs and the EU would not respond in kind, this was seen as a disaster, a surrender, and a damning indictment.

It seems clear that there is a revealed belief going on here. These transatlantic thinkers claim that tariffs hurt America more than they hurt the tariffed countries, but if that were the case, then counter-tariffs would hurt the EU and Canada more than they’d hurt America. The “solution” to Trump’s trade war would then be to do nothing at all. LET Trump tariff every nation to high heaven, he’s primarily hurting America after all, and don’t respond in kind under any circumstances. Don’t tariff American products, don’t go after American businesses, don’t do anything differently than you’d normally do, because any such anti-trade measure would harm your own countries more than it harms America.

But the revealed belief here is that Trump’s tariffs *do* harm other countries more than they harm America, because counter-tariffs and other trade barriers are being called upon, on the assumption that they will harm America more than they’ll harm other nations. It seems that many transatlantic thinkers are revealing that all the rhetoric around tariffs was a Noble Lie. All the claims about how tariffs are ineffective and self-destructive were lies meant to dissuade the public from supporting tariffs in the first place. But now that the tariffs are out of the bag, the Noble Lie has no more use, and the Awful Truth about tariffs, that they are harmful to one’s own nation, but are effective at countering trade imbalances, has come to the fore.

Noble Lies such as this beclown the person saying the lie. They reveal the liar to be a hypocrite and untrustworthy. If you found that the person who goes on and on about healthy food was actually eating nothing but junk food, you’d probably never again trust their recommendations to you about healthy eating. And likewise, a lot of poli/econ commentators have lost a lot of credibility in my eyes by going back on their pre-Trump claims about tariffs. By revealing that they never believed those things in the first place, they reveal (to me at least) that I should never trust them again going forward.

So whatever happened with Aduhelm?

Aduhelm and Leqimbi were hot news a few years ago. They are both antibodies that work as anti-Alzheimer’s disease drugs by binding to and hopefully destroying amyloid beta. The hypothesis that amyloid beta is the causative agent of Alzheimer’s, and that reducing amyloid beta will lessen the disease, is known as the Amyloid Hypothesis. And while the Amyloid Hypothesis is still the most widely supported, I wonder if the failures of Aduhelm and Leqimbi to make much of a dent to Alzheimer’s disease has damaged the hypothesis somewhat.

Because think about it, the whole job of an antibody is to help your body clear a foreign object. When antibodies bind to something, they trigger your immune system to destroy it. And this is why you get inflammation whenever you get a cut or scrape, antibodies will bind to whatever microscopic dirt and bacteria that enter your body, and your immune system flooding that area to destroy them is felt by you as inflammation.

And we know that Aduhelm and Leqimbi are working as antibodies against amyloid beta. They bind strongly to amyloid beta, they induce inflammation when given to Alzheimer’s patients (although inflammation in the brain can cause multiple side effects), and tests show that they seem to be reducing the amount of amyloid beta in the patients who take them.

Yet the prognosis for Alzheimer’s is not much better with these drugs than without them. Maybe they just aren’t destroying *enough* amyloid beta, but they are barely reducing the rate at which Alzheimer’s patients decline in mental faculty, and are not at all causing patients to improve and regain their mental state. Maybe the brain just *can’t* be fixed once it’s been damaged by amyloid beta, but you’d hope that there would at least be some improvement for patients if the Amyloid hypothesis is correct.

This has caused the field to seemingly split, with many still supporting the Amyloid hypothesis but saying these drugs don’t target amyloid beta correctly, with others now fractured in trying to study the many, many other possible causes of Alzheimer’s diesease. Tau, ApoE, neurotransmitters, there’s lots of other stuff that might cause this disease, but I want to focus on the final hail mary of the Amyloid hypothesis: that the drugs aren’t targeting amyloid beta correctly.

Because it’s honestly not the stupidest idea. One thing I learned when I researched this topic was the variety of forms and flavors that *any* protein can come in, and amyloid beta is no different.

When it’s normally synthesized, amyloid beta is an unfolded protein, called “intrinsically disordered” because it doesn’t take a defined shape. Through some unknown mechanism, multiple proteins can then cluster together to form aggregates, again of no defined shape. But these aggregates can fold into a very stable structure called a protofilament, and protofilaments can further stabilize into large, long filaments.

Each of these different structures of amyloid beta, from the monomers to the aggregates to the filaments, will have a slightly different overall shape and will bind slightly differently to antibodies. One reason given for why Aduheim causes more brain bleeds than Leqimbi is because Aduheim binds to the large filaments of amyloid beta, which are often found in the blood vessels of the brain. By siccing the body’s immune system on these large filaments, the blood vessels get caught in the crossfire, and bleeding often results.

Meanwhile other antibodies are more prone to target other forms of amyloid beta, such as the protofilaments or the amorphous aggregates.

But what amyloid beta does or what it looks like in its intrinsically disordered state is still unknown, and still very hard to study. All our techniques for studying small proteins like this require them to have a defined shape. Our instruments are like a camera, and amyloid beta is like a hummingbird flapping its wings too fast. We can’t see what those wings look like because they just look like a blur to our cameras.

So maybe we’ve been looking at the wrong forms of amyloid beta, rather than the filaments and protofilaments which are easy to extract, see, and study, maybe we should have been looking at the intrinsically disordered monomers all along, and we only studied the filaments and protofilaments because we were *able* to study them, not because they were actually important.

There’s a parable I heard in philosophy class about a drunk man looking for his keys. He keeps searching under the bright streetlight but can never seem to find them. But he’s only searching under the streetlight because *that’s where he can see*, he isn’t searching because *that’s where his keys are*.

Endlessly searching the only places you *can* search won’t necessarily bring results, you may instead need to alter your methods to search where you currently can’t. And if the Amyloid hypothesis is to be proven true, that will probably be necessary. Because right now I’ve heard nothing to write home about Aduheim and Leqimbi, many doctors won’t even proscribe them because the risk of brain bleeds is greater than the reward of very marginally slowing a patient’s mental decline, not even reversing the decline.

I no longer directly research Alzheimer’s disease, but the field is in a sad place when just 4 years ago it seemed like it was on the cusp of a breakthrough.

Cope, or good sense?

As I wrote last time, I’ve been following Dr Mike Isratael’s youtube channel in my own quest to lose weight and (maybe) gain muscle. And as I said last time, Dr Mike says all the right words to make me think he knows what he’s talking about, but I’m afraid I only believe him because he knows the shibboleths, not because he’s actually right. What if he’s a charlatan like the rest, but his shibboleths are “basic biochemistry” instead of “pseudo-right wing culture,” and that’s why I believe him? What if what he’s saying isn’t correct, will I have the sense to know?

Well I’ve started… not disbelieving, but rather not following all the advice he gives. On the one hand, this could be proof that I’m a free-thinker, who takes all advice to heart and executes it not based on its source or shibboleths, but on its factual content. On the other hand, maybe that’s all cope and I’m not following it because I don’t want to.

The basic idea comes down to 1 thing: dieting. As I said, my primary goal is to lose weight, but I’m hitting the gym and I’d sure like to gain muscle on the way. Well Dr Mike has a video out about how that entire idea is a myth, and that the most productive way to do things is to eat a calorie surplus to gain weight (and go to the gym to make sure that’s muscle weight), while eating a calorie deficit in order to lose weight (and go to the gym to make sure that’s only fat weight). Trying to gain muscle on a calorie deficit, or lose fat on a surplus, is inefficient and possibly impossible.

Now Mike does caveat this with a few exceptions. If an exceptionally jacked individual was gravely injured and has lost muscle and gained fat while laid up in the hospital, then it’s much easier for them to gain back that fat and lose back that muscle once they get out of the hospital. It’s always easier to get *back* in shape than to get in shape *for the first time*.

Another caveat he talks about is “newbie gains,” where someone who is young and never went to the gym can start gaining muscle/losing fat together. But the caveat to the caveat is that this isn’t sustainable, eventually it will be one or the other.

So I’ve decided to believe that I’m in the “newbie gains” stage, the caveat to my own claim being that I did used to go to the gym a bit and I’m not actually that young. Regardless, I’m choosing to believe that Dr Mike is giving this advice to aspiring bodybuilders, people who are already fairly muscular and with a health amount of bodyfat, and therefore his advice doesn’t apply to me who is very unmuscular and with an unhealthy amount of bodyfat.

To reiterate, my goal is to lose weight and gain muscle. Dr Mike says that’s not usually possible and that I have to pick one and only one goal if I’m going to succeed, and I’ve decided to ignore that advice and believe that his advice is aimed at an audience that I’m not really a part of.

But maybe this is all wrong. Maybe for an obese person to become healthy, they need to lose a lot of weight, and during that time they simply won’t gain much of any muscle no matter how they try. And maybe that obese person is me.

If I were to take Dr Mike’s advice to heart, I would probably restructure my training with the understanding that I need to focus solely on the weight loss, probably by entering a more severe calorie deficit than I’m at now, in order to more quickly lose weight so I can then put on muscle. I’d probably spend a lot less time thinking about my gym technique and a lot more time working on my diet.

Am I ignoring Dr Mike’s advice because I’m a free-thinker making a rational conclusion about whether his advice is right for me? Or am I doing it because this is the first piece of advice I just don’t like?

I don’t know.