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Borge Fagerli's avatar

The observation that mice fed diets high in polyunsaturated fatty acids (PUFA) versus saturated fats become obese, while humans are often advised to consume PUFA for health, certainly seems paradoxical at first glance. Let's break it down with a skeptical lens.

1. **Species Differences**: *Hmm, mice aren't tiny humans. Their physiology is different.* Mice and humans metabolize fats differently. What causes obesity in mice might not have the same effect in humans. For example, mice have a higher metabolic rate and different lipid processing mechanisms.

2. **Types of PUFA**: Not all PUFA are created equal. Omega-3 and omega-6 fatty acids are both PUFAs, but they have different effects on health. Omega-3s are generally considered anti-inflammatory and beneficial, while excessive omega-6s (which are more common in Western diets) can be pro-inflammatory.

3. **The Role of Diet Composition**: *It's not just about fat types, but the whole diet.* In studies, the context of the entire diet matters. Mice studies often use highly controlled diets, which don’t fully replicate the complexity of human diets. The impact of PUFA might differ in the context of a balanced diet containing fiber, protein, and other nutrients.

4. **Quantity and Quality**: The quantity of PUFA and the overall diet quality in humans matter. Excessive calorie intake, regardless of fat type, can lead to obesity. Also, processed foods high in PUFA may have other unhealthy components.

5. **Long-term vs Short-term Effects**: Mice studies often look at short-term effects, while human dietary guidelines consider long-term health outcomes. Short-term weight gain might not correlate with long-term disease risk.

6. **Generalizing from Animal Studies**: *Mice studies give clues, but they're not conclusive for humans.* Animal studies are a starting point for understanding biological mechanisms, but their findings need to be interpreted cautiously when applied to humans.

7. **Epidemiological Evidence in Humans**: Observational studies in humans have shown that diets high in certain types of PUFA (like omega-3s) are associated with reduced risk of heart diseases and other health benefits.

8. **Clinical Trials**: Controlled trials in humans provide more direct evidence. Many have shown benefits of PUFA-rich diets in reducing risk factors for heart disease.

In summary, while mouse studies are valuable, they can't be directly extrapolated to humans due to physiological differences. The current dietary recommendations for PUFA intake in humans are based on a large body of research, including epidemiological studies and clinical trials, which generally indicate health benefits, especially when replacing saturated fats with PUFA. *It’s a complex picture, and dietary advice must be nuanced.*

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Experimental Fat Loss's avatar

The rodent studies showing that 1% vs 8% LA content makes the difference with total fat content held same are referenced here:

https://tuckergoodrich.substack.com/p/does-linoleic-acid-induce-obesity

> It should be very obvious indeed, if it's true.

> A child should be able to do this experiment:

> Because if it's true, it should be known.

So adorable :)

Did you think this whole time that we were in a "race to find the truth" with Big Science? Of course not. Big Science has no interest in finding out what causes obesity; it'd ruin the whole racket.

It is trivial to test this. It has been tested. A child could do it.

And yet, it's been swept under the rug. When I talk to Actual Serious Scientists about it, they pretend they didn't understand the question or misheard me or radio silence.

I talked to Lamming, the guy who runs the lab with all those isoleucine studies, about this - hey, all your mice are on a high-PUFA diet, even the control mice have 3% LA and seem prediabetic from the glucose tolerance test!

He said he thinks his mice are only 1-2% LA. Turns out he didn't know how much LA is in corn oil, the main fat source in his control chow.

They wear CICO/fat tinted glasses. They cannot see the truth if you hit them over the head with it.

After over a decade on keto, following a bunch of interactions between ketoers and Big Science, I believe very strongly that a lot of mainstream scientists are straight up crooks. They're dishonest, they will lie, they will misrepresent their own findings. Maybe they believe their own lies, though it's hard to see how that could be possible.

Kevin Hall, THE big shot in U.S. nutrition science, likes to post a study of his titled something like "All diets work exactly the same," the title image (!) of which shows that low-carb diets work 30-70% better than low-fat diets.

He also published a study saying "high-fat ketogenic diet is obesogenic." The study: he compared a junk-food "high-fat" (=mixed) diet to a low-fat, practically vegan diet ("Whole Food Plant Based"). The high-fat people ate like 700kcal/day more (IIRC) yet lost the same amount of weight!

Physics defied! First law of Thermodynamics broken! CICO disproven! Right?!

No. Obviously, his finding was "Ketogenic diet is obesogenic by causing increased caloric intake."

He is simply a liar. Maybe he believes his own lies, which would make him a zealot, but there's no functional difference.

You seem to believe in the Efficient Market Hypothesis of Science - if it was easy to demonstrate, it would be common knowledge. I believe the Market for Science is completely rigged, and it is not at all efficient.

There are tons of these experiments. Grant from https://ggenereux.blog/ literally did the experiment you mentioned, just with vitamin A - he bought rodents, put them in cages, and didn't feed them any vitamin A. They never, ever got vitamin A deficiency. It's so trivial a child could do it, yet science "knows" you couldn't possibly survive for more than a few weeks without vitamin A.

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