Before anyone gets too excited, best to remember that Nina is regarded as something of a joke in nutrition science circles, and tends to take poetic license with the truth.
I cannot comment on Nina specifically, since I’m not familiar with her work. I’d only like to suggest that being “a joke in nutrition science circles” in the recent past is probably something of a compliment. Mainstream nutrition science led to advice such as putting energy-dense grains at the bottom of the food pyramid, and villainizing fat with respect to CVD, leading to “reduced fat” alternatives which instead use sugar (which is highly addictive). Now, debates center around how much added sugar should be the recommended daily amount (hint: it should be 0). Lawmakers are considering funding overpriced Ozempic via Medicare to fight our rampant obesity, while nutrition science has abdicated its role in helping people maintain healthful, satiating diets.
At least in the United States, the nutrition science of the last 100 years has overseen the most incredible deterioration of metabolic health in human history. There are some folks doing good work out there, as there always have been, but listening to mainstream nutrition science as if their word is law is akin to letting the inmates run the asylum.
Adherence to guidelines is laughably low in the developed world.
The recommendations regarding fat hasn't changed in 30 years in most countries. FDA recommended limiting saturated fat already in 1980 (didn't bother looking further) and has recommended not exceeding an energy intake from fat over 30% since at least 1990. 30%e from fat is not a low fat diet.
The guidelines from 1980 explicitly mentions reducing saturated fat and sugar.
I think the problem is that we haven't been listening.
I think outcome is the measure we should look at. With regards to disease and longevity there is nothing saying about 50-65% of energy from carbs has to be bad. What matters is what kind of carbs. Bulgur. Quinoa. Whole Rye. Oats. Beans.
In fact, this kind of diet that is the basis of the modern dietary recommendations because we know it is associated with good outcomes.
Based. I know you might just be taking the agnostic position for the sake of the conversation, but the evidence overwhelmingly suggests 6 servings of carbs would massively improve your ACM risk: https://www.sciencedirect.com/science/article/pii/S000291652...
Oh I know. The Mediterranean diet is universelly associated with good health outcomes. It doesn't seem to matter how many youtubers there are explaining mechanisms why carbs or vegetables are bad for you... It also happens to align with a diet that is much better for the planet than the SAD.
I started following a Mediterranean style diet for my own heath a long time ago, and when I realized the harm of animal agriculture I stopped eating animal products completely. I of course would have preferred to continue eating like before, but evidence told me otherwise.
The worst part of eating almost exclusively plants is all the BS. At first they said I couldn't build muscle, so I started lifting weights. When I could deadlift 3x my weight and do 15 strict pull-ups my diet was not good enough for endurance. So I did a 3.40 marathon after 6 months of preparation. Then I swam 10k in just over 3h.
But every time I get a cold (with 3 kids in kindergarten and school, viruses are obligatory) it is seen as a weakness of my way of life. I even had a congenital condition blamed on my plant-based diet by more than one person, despite me doing a lot better than just about everyone else with that condition (which is probably just luck, my family have done well as well, while eating a standard diet).
Haha. You may be built like Schwarzenegger, but you’ll always be a soyboy (</sarcasm>). I think people find veganism threatening so like to mock those that adhere to those principles instead of performing some soul searching.
> 3 kids in kindergarten and school
I see you have chosen the path of perpetual illness and insomnia.
The food pyramid put whole grains specifically at the base of the food pyramid. Not sure why you consider this objectionable, the body of evidence overwhelmingly points in the direction of benefits for wholegrain consumption.
Reduced fat is an interesting one. If you actually look at what Keys was investigating all the way back in the mid 20th century, the hypothesis was always that saturated fat increased CVD risk. The translation of that into policy and marketing aimed at total fat cannot be placed entirely at the feet of mainstream nutrition science.
As for added sugar - again, you’re labelling policy decisions as nutrition science. The DGs that I’m aware of recommend as little added sugar as possible, but when you’re making policy you have to strike a balance between strict enough to make a difference, but not so restrictive that no one listens. That’s different from what mainstream nutrition science would claim (which is indeed that there are no benefits to added sugar and several risks).
The same point applies to your claim that nutrition science has a role in getting people to adhere to satiating diets. No, nutrition science is to help us understand what those diets might look like. It is not responsible for getting populations to adhere to them.
This is false, in the 90s when I grew up there was no such criterion, and the posters of the pyramid prominently depicted sliced white bread.
The worst part of the food pyramid was the indication to use all fats and oils sparingly. There's never been any point in which the evidence suggested that olive oil or other monounsaturated fats should be avoided
Agree that the wholesale demonisation of fats was a massive failure of policy. Doubly frustrating because this was known - Ancel Keys' hypothesis was always about saturated fat specifically, and the Keys equation he devised showed the beneficial effects of PUFA. So mainstream nutrition science was on the money, but policy makers and companies less so.
Grains are cheap and energy dense, if your goal is to feed a large population it makes a lot of sense to put them at the base of the pyramid, that's what will keep you alive, as in, not starving. Higher up are fruits and vegetables, also cheap, they will provide with nutrients that you need to stay healthy on top of the calories that will keep you alive. Higher up are animal products, expensive but rich in proteins and a few other nutrients that are a bit lacking in the base layers, they help you get stronger and more performant in addition to healthy and alive. On top are pleasure foods, not really necessary for your body, but enjoyable.
I take it like a mirror of the "hierarchy of needs" pyramid rather than nutritional advice for people with effectively unlimited resources.
Yeah I always see it as the minimum thing to get if you have limited money. For poor people, most of your money is better utilized to get grains instead of meat.
When I saw it in my local village's clinic it makes sense because it actually encourages eating some meat and fruit instead of none, which is the norm here because of poverty.
The elephant in the room is that nutrition studies (whose results influence health and economic policy) are frequently funded by dominant players of the food industry, creating a huge conflict of interest. This has to end.
> The food pyramid put whole grains specifically at the base of the food pyramid. Not sure why you consider this objectionable, the body of evidence overwhelmingly points in the direction of benefits for wholegrain consumption.
Citation please or I'm calling extreme bullshit. Everything I've ever read has argued for putting more nutrient dense fruits and vegetables as the basis for a healthy diet.
More importantly, I think the nutrition community was woefully naive to the point of being negligent when they tried to defend the food pyramid. One quote I heard was "When we were recommending lower far intake, we never imagined Snackwells." Well, why TF not??? It should have been blatantly obvious that by demonizing fat and making people feel like carbs were "free" that companies would react appropriately and come up with fat-free, sugar-stuffed replacements that had a huge amount of calories, left you feeling unsatiated, and tasted like sweet cardboard. Probably even worse was frankenfood like Olestra.
I agree with the original point - while I think the field of nutrition science has improved a lot over the past decade, they have a ton to answer for and never did an appropriate "mea culpa" for all the great harm they caused.
Your claims that (1) the food pyramid put whole grains at the base, and (2) that there is any consensus at all that a healthy diet should include more whole grains than fruit and vegetables (which is what "being at the base of the pyramid" means).
Three servings of whole grains per day: 0.79 (21% reduction in ACM)
Three servings of vegetables per day: 0.89 (11% reduction in ACM)
Three servings of fruit per day: 0.90 (10% reduction in ACM)
So the evidence seems to support the suggestion that consumers should focus on whole grain consumption as a base for their diet.
> Citation please or I'm calling extreme bullshit. Everything I've ever read has argued for putting more nutrient dense fruits and vegetables as the basis for a healthy diet.
Wut? Was your comment a joke or satire? This entire thread is about how the food pyramid of that era was an unscientific disaster, so linking to a picture of it is not evidence.
If Americans actually stuck to the food pyramid they would be fine. No one does. It needed refinement to “eat whole grains and pasta, brown rice”, but it was hardly a disaster, the disaster is lack of people (adults) paying attention to it and instead eating crap out of boxes loaded with sugar, hydrogenated fats, and lots of ingredients they couldn’t pronounce let alone know how healthy or unhealthy they are. I saw lots of people paying lip service to it, but few people were sticking to it. Same with the current “my plate” ideas. People won’t tsit for 10 minutes and understand what they mean by protein, veggies, grains, and fruit.
Sorry, I realized now, I quoted that section just to give context. I was really referring to "Not sure why you consider this objectionable, the body of evidence overwhelmingly points in the direction of benefits for wholegrain consumption."
Even with that first sentence though, the base of that shitty food pyramid really just doesn't talk about "whole grains" - it calls it the "bread, cereal, rice and pasta" group, with a graphic that includes spaghetti, crackers, a baguette, a bowl of cereal, etc. And having lived through that time when the food pyramid was taught in school, they certainly weren't delineating between highly refined flours and things like oatmeal, brown rice, quinoa, etc.
> The food pyramid put whole grains specifically at the base of the food pyramid. Not sure why you consider this objectionable, the body of evidence overwhelmingly points in the direction of benefits for wholegrain consumption.
my humble research found that diffs in nutrition between whole grains and refined grains carbs is very small compared to say whole grain to some complex carbs from leaf veggies. The same goes to glycemic index, satiety index, etc.
By definition, the human body cannot convert fiber into carbs the human body can burn (but microbes do turn some of the fiber into short-chain fatty acids, which is fuel for human colon cells). That is how "fiber" is defined.
Yes that is my understanding too. Short chained saturated fat to be exact, so don't tell any of the lipophobics or they will automatically add the prefix "unhealthy" to it as they are accustomed to.
In this thread, I was so eager to make sure you didn't have some wrong belief somehow that I didn't even notice you were agreeing with me (or concisely summarizing). I have a bad habit of focusing too much on any errors the other person might have made.
(Maybe we should think of a word that means "carb that the human body can efficiently convert into glucose or fructose" and try to spread that new word. "Insulinogen"?)
In this comment there’s a link to a meta analysis of food groups and their effect on all cause mortality. A serving of whole grains would appear to be approximately twice as protective as either fruits or vegetables: https://news.ycombinator.com/item?id=41965298
there was no control groups (veggies vs whole grains for example), they selected bunch of studies for metaanalysis with different goals and methodologies, no indications how balanced and what components where in diets in those studies.
Let's get real here: the benefits in the USDA Food Pyramid are benefits for agribusiness and the big subsidized food producers. The benefits that the USDA pushes have nothing to do with good nutrition for the average citizen. This is 100% "regulatory capture" as we call it around here. The Food Pyramid is a scam and a hoax, and the more it can be ignored, the better.
When I joined a Christian Health Sharing ministry, they determined that I needed remedial help, due to hypertension and dyslipidemia. They assigned me to monthly virtual meetings with a dietician. The dietician's advice horrified me, because it would've made me sicker, and exacerbated my conditions. I approached the ministry's administrators, requested a replacement dietician, and they replaced her alright. The new dietician had basically the same credentials and the same letters after her name, but she was way more flexible, listened to my reasoning, and supported my choices with encouragement.
My parents followed every "diet fad" in the 1970s-1980s, from 2% milk, to margarine, to yolk-less-egg-whites, to reducing red meat, to low-sodium everythings, to bottled fluoridated water. It was sheer torture and disgusting. My mother didn't know the first thing about flavor or pleasure in cooking, and never used the spices in her rack. Our food was always bland. For breakfast she'd slap down a jug of milk, a box of Chex, a bowl and a spoon, and abandon me to go do housework. I would sit there and read the mendacious lies known as "Nutrition Panel" on the side, and simply stewed in my resentment for the whole thing. It's a travesty.
Tbh I know it’s not what you’re going for, but your parents’ dietary decisions generally sound based AF (apart from bottled fluoridated water - depending on the fluoride levels in your drinking water that may or may not be beneficial).
Chex, I suppose it depends on whether it was wholegrain or not. Wholegrain cereal is associated with pretty good health benefits, refined not so much.
Yes. Not so much at the time when some margarines had trans fats in, but now? Yes, absolutely. The evidence suggests that doing so significantly reduces one's risk of CVD.
The first study is saying that it's good to replace butter with either PUFA margarine or TFA margarine. Since we already know from other places that TFAs are actually quite harmful, we know to ignore this study.
We should also learn from history that replacing our diets based on "nutritional science" has generally been unlikely to yield good health results, as long as we're not already obese. For example, nutritional science kept recommending replacing SFA with any UFA, and ended up killing many, many people because it didn't know that trans unsaturated fatty acids are actually worse than SFAs for overall health.
We can reasonably expect that similar things will be discovered in the future about other parts of margarine, and that eating traditional foods with a long history of safe human consumption is a much safer path, be they olive oil or butter or lard.
It doesn’t say good, it shows it reduces LDL cholesterol. Since the mechanism by which TFA increases CVD risk is separate to this, this is compatible with TFAs causing harm. So no reason to ignore the study, it’s making no false claims. PUFA reduces LDL-c by a greater degree and there are no known issues like there are with TFA, so substituting SFA for PUFA seems like a no-brainer.
As for nutrition science and its effect on health, just because one intervention had deleterious effects doesn’t mean that you can claim that the net effect of nutrition science on health has been net negative. Again, see no reason to believe that without actual evidence supporting it.
Nutrition science told us that we should start fortifying flour to prevent some horrendous diseases, and the net result of that has been far greater than the problems caused by trans fat consumption, for example.
I see no reason to believe that traditional foods are safer than novel foods. In fact, provided both are equally health promoting during the reproductive window, then it’s more likely that a given novel food is better for longevity than a traditional one.
> Since the mechanism by which TFA increases CVD risk is separate to this, this is compatible with TFAs causing harm.
As far as I know, the main mechanism for that is reduction of HDL-c. However, the study you cite found no reduction of HDL-C from TFA substitution.
> PUFA reduces LDL-c by a greater degree and there are no known issues like there are with TFA, so substituting SFA for PUFA seems like a no-brainer.
Key word being "known issues". One of the major issues with nutrition science is this grouping of vastly different foods based on a single simple category of substance. There are a lot of different PUFAs, and even more different specific oils or fat solids containing PUFAs, and there is no reason to believe that they are completely interchangeable in our nutrition. UFAs were once thought to be the same, before the important distinction between PUFAs and TFAs (and the still unclear position of non-TFA MUFAs) was discovered and recognized.
> As for nutrition science and its effect on health, just because one intervention had deleterious effects doesn’t mean that you can claim that the net effect of nutrition science on health has been net negative. Again, see no reason to believe that without actual evidence supporting it.
Yes, some basic findings in nutrition science did improve things worldwide health. The discovery of vitamins and various other micronutrients was by far the most important. The discovery of dietary fiber and its roles allowed nutrition science to course correct a number of bad recommendations from the earlier era. In very specialized fields, such as high performance athletes, it also show reproducible, predictable results (though not necessarily on long-term health, just measured by competition success).
> I see no reason to believe that traditional foods are safer than novel foods. In fact, provided both are equally health promoting during the reproductive window, then it’s more likely that a given novel food is better for longevity than a traditional one.
Traditional foods have an extremely long history behind them of not being acutely harmful to at least one particular population, with traditionally passed on limits of safe amounts of consumption and safe methods of preparation. They have been consumed by populations that lived with much reduced medical care than today, so they are known to be resilient even in the absence of medical interventions, which often confound nutritional studies, especially in older adults. They are also much more likely to be well adapted to the particular genetics of a certain population, unlike nutritional advice which is almost entirely "universal".
One of the main sources of nutritional discoveries has in fact been the study of traditional diets. From vitamins to fiber to fermented foods' effects on gut microbiota, the discovery has always come from trying to understand why a particular population is thriving nutritionally.
The main drawback of traditional foods is that the mechanism for passing down information on safe preparation and consumption was informal, and can be easily lost. They also tend to be hard to create industrially, so they are likely to be much harder or more expensive to consume compared to modern industrial food products. However, for people who can afford it, they are by far the better option compared to the uncertainty and contradictions of modern nutritional advice.
[Note: this is the same account as tsimiones, I'm not trying to hide behind some new name, it's just related to some software on my work PC]
There have now been several intervention trials investigating whether HDL-raising meds improve health outcomes (there’s no evidence to show they do) and MRs looking at genetically determined HDL-c and various health measures (no evidence of effect either). We don’t actually have any evidence that HDL is anything other than a proxy for other factors, and no evidence that it directly affects anything.
Yes, there are no known issues. You can speculate that there might be, but we could equally speculate that they’re actually superfoods and we don’t know it yet. At the end of the day, speculation is all it is so I believe it’s most sensible to apply the principle of indifference and look only at what we do know. That is, margarine is a sensible replacement for butter on the current evidence.
Because of antagonistic pleiotropy, we can actually make an a priori argument that given two foods that are equally health promoting within the reproductive window (I.e. it’s not killing or neutering people before the age of ~50), then probability holds that the food to which we are least adapted is actually more likely to promote longevity than the ancestral food.
Because adaptations are on net more likely to be antagonistically pleiotropic than not, foods to which we are most adapted are more likely than not making a trade off in favour of reproductive success over longevity. Since we don’t have these adaptations to novel foods, this concern does not apply to them.
Therefore, given butter and margarine are both similar in their effects on reproductive success, with no further information at all we should favour margarine. The fact there are studies confirming this is just icing on the cake.
You're making very strong claims based around broad trends in genetics for a process that isn't entirely genetic. The society that is choosing what to eat and how to prepare it is doing so based on their own set of axioms, not pure genetic biology.
The argument is probabilistic, it’s not required that food seeking behaviours are entirely genetic for it to go through. As long as food seeking behaviours and/or preferences are to some degree genetically determined, then the argument is sound and valid.
If I can safely discount all human behavior through history, then I can also assume that the behavioral changes you are espousing are equally non-relevant. Either human behavior can be a greater driver than genetic probability or it can't.
That first study is -tiny- study which is a good data point but hardly worth changing my diet over. I’ve seen plenty of studies saying that butter in moderate usage is just fine, and the war on saturated fats really should have been limited to hydrogenated oils/margarine
How about a pooled analysis of 350,000 participants suggesting that for every 5% energy in the form of saturated fat that’s replaced with PUFA (like you find in margarine), the risk of coronary mortality drops by 26%.
Surely that’s both a large enough cohort and a large enough effect size to change one’s diet?
This study contradicts another study you were citing in this thread . This one says that replacing SFAs with carbohydrates is a net negative, you have to replace SFAs with PUFAs. The other study was saying that replacing SFAs with either carbohydrates or PUFAs is just as good.
It's almost as if all of these studies are looking at tiny effects that they can't adequately measure, and contradicting each other.
Do you believe there’s a difference in health outcomes between consumption of whole grain carbohydrates and refined carbohydrates?
If yes, do you believe it would be expected to see heterogenous outcomes in studies that don’t disambiguate whole grain and refined carbohydrates when replacing SFA?
If yes, then there’s clearly no contradiction in the above studies. If no for any of the above, I’d love to hear the argument.
I have no idea. I understand there are some a priori reasons to believe whole grains have certain health benefits. From what I quickly found in some basic searches, some studies find an effect, some don't. Those that do are typically population studies, which are often confounded by the correlation-vs-causation issue (are people that eat more whole grain healthier, or are people who live healthier lifestyles in general more likely to also eat whole grain?). Those that don't are typically RCTs, that suffer from the short duration and are unable to capture longer term effects, which are very likely with nutrition.
Also, just as I was mentioning in other comments, I think there is a good chance this reduction of the problem to just whole grain - refined grain is unlikely to tell the full picture. I don't see a priori why eating whole wheat would be exactly as healthy/unhealthy as eating whole rice, or oats, or millet, or barley, or quinoa or any of the many other unrelated plants we call "grains". Maybe we should prefer certain grains and avoid others, regardless of the whole/refined distinction; this difference might also depend on genetic factors, with certain populations perhaps being better suited to certain grains than others. It is very much possible as well that certain grains are better eaten whole, and certain others better eaten refined, say if there are substances in certain husks that are problematic over long time or in certain quantities and so on.
And this is not even going into other factors, like rates of contamination of the grains with pesticides/fertilizers/naturally-occuring substances in certain soils; handling, washing, and preservation; cooking differences; and probably many others that I'm not even thinking of.
And while some of these effects will naturally lead to heterogenous outcomes in studies that don't control for them, this doesn't increase my confidence in those studies. The fact that there are an extreme number of possible confounding variables in everything to do with nutrition is basically why nutrition science is almost hopeless as an entire endeavour: we can only reliably find extremely strong effects ("lack of vitamin C causes scurvy"), and even then we need a bit of luck. The rest is built on a house of cards: every new medical or biological discovery tends to upend nutritional studies and what they control for.
Ok, then if you have no idea then clearly there’s room for heterogeneity in studies that pool those different types. So there’s no contradiction in the studies I posted, which is the original claim you made.
Not a big proponent of saturated fats but dietary LDL has only a modest impact on LDL-c - 5-10%. Other things that have similar or larger impact are exercise, reducing sugar intake, not being overweight, and consuming soluble fibre. Plant sterols/stanols also help
Problem in the 70s was trans fats. Now they're no longer a risk, replacing butter with margarine is a solid evidence-based decision for one's health (though not so much for one's enjoyment!).
Okay, the cereal commercials in the 1980s: they would have some ridiculous cartoon mascot and sing a catchy jingle about their sugary cereal treats, and then at the end, they were legally required to say "Part of this balanced breakfast" while displaying a tray laden with fresh fruit, buttered toast, perhaps a glass of orange juice.
Those commercials played multiple times a day in my childhood, and they never failed to piss me off, because they clearly demonstrated that "milk and a box of Chex" was not by any means a "balanced breakfast".
Not sure why you’re being downvoted, this is one of the best takes here. It sits squarely in the realm of evidence where the majority of these comments are anecdotal and they don’t translate to population level studies.
>The food pyramid put whole grains specifically at the base of the food pyramid. Not sure why you consider this objectionable, the body of evidence overwhelmingly points in the direction of benefits for wholegrain consumption.
Many, many people disagree with that. Most days I eat no grains at all and the rest of the time, I strictly limit my grain intake. For example, I just finished a meal where I used one tablespoonful (uncooked volume) of rice (boiled with some peas). (The meal also included meat and butter, the source of most of my calories.) White rice is the only grain I eat anymore, and I would never eat brown rice, which is loaded with oxalate and other phytotoxins. I added to this just-finished meal B vitamins in the form of pure refined powder (which I liberated from capsules).
It is very obvious from how it makes me feel that brown rice is bad for me.
The cultures that have eaten rice for thousands of years eat almost exclusively white rice. Brown rice was not even possible to make before the spread of tech for precision machining (which reached East Asia in the 1900s). You have to remove the hull from the rice before you can eat it, and before precision machining, removing the hull (traditionally done by pounding the rice with a log) also removed most of the bran and germ. Yes, some bran and some germ remained stuck to the rice -- so it was mostly-white rice, as opposed the polished, completely-white rice we have today with no bran and no germ at all. Still it had only a small fraction of the amount of bran and germ that modern brown rice has.
I don’t find n=1s to be a good form of evidence. Many people may disagree, but that doesn’t mean they’re right.
Look at the dose response curve for wholegrain consumption in this bad boy (and yes, it’s looking at whole cereal grains, not including fruits and vegetables). Greater consumption associated with better outcomes: https://www.sciencedirect.com/science/article/pii/S000291652...
I've read the opposite; that brown rice is just white rice with the bran still attached, and that white rice was only eaten by the elite because of the additional work required to seperate it (like white bread only being for the wealthy during the middle ages), and that beriberi was a noticed more in times specifically because of industrialization increasing the availability of white rice:
https://en.m.wikipedia.org/wiki/Thiamine_deficiency
Apperently a lot of white rice is now enriched with thiamine for this reason
>I've read the opposite; that brown rice is just white rice with the bran still attached, and that white rice was only eaten by the elite because of the additional work required to seperate it (like white bread only being for the wealthy during the middle ages)
I've read that, too, many times, and I stopped believing it after I watched videos (on Youtube) of people preparing rice the traditional way. Particularly, I paid close attention to the color of the rice after the processing steps: it was white with bits of brown stuck to it.
I searched for bookmarks for those videos, but cannot find them.
(I don't know about wheat: I only investigated rice.)
I found the bookmark. Anyone who has ever seen modern brown rice will immediately be able to tell that although there might be bits of bran still stuck to it, this rice has no more than 3 or 4% of the bran of modern brown rice:
I bookmarked another video, but it has been made private since I watched it.
Here is a very illuminating moment: the rice has already been pounded, then winnowed (the separated hulls removed), but there are still many kernels that need to be hulled (roughly one kernel in every 150 or 200 kernels), so the rice
is put back in the mortar for another round of pounding. In other words, although there is more pounding to do to make the rice edible, already most of the bran is off the rice (and thrown away along with the hulls).
(When only a few unhulled kernels remain, she removes them one by one with her fingers.) This supports my assertion that it is impossible with traditional
methods to get the hulls off while leaving on most or even a significant fraction of the bran. Again: I think you need precision machines that only became available in Europe in the 1800s and in East Asia in the 1900s to get the hulls off (which I think you really need to do if you eat rice every day and want to keep your teeth) while leaving most of the bran on the kernel. I.e., people in traditional rice cultures did not have the ability to consume anywhere close to as much rice bran as is possible by eating modern brown rice.
Interesting, though perhaps it is possible the colour change is due to oxidation? It would be interesting either way to see a nutritional comparison of traditionally prepared and modern brown rice, as well as their bran content
> I’d only like to suggest that being “a joke in nutrition science circles” in the recent past is probably something of a compliment.
This is the fallacy that makes pseudoscience thrive right now: The idea that the enemy of my enemy is my friend.
Wannabe influencers position themselves as the anti-establishment position. People who are frustrated with institutions blindly fall in line behind them.
The fallacy doesn’t stand up to even the simplest critical thinking, yet it triggers something subconsciously that leads far too many people to see a contrarian statement and assume it must be true.
Meanwhile, these people are grifting away, selling books and pitching Athletic Greens (or the latest sponsor of the day). This person is no exception.
It’s a shame that our institutions have burned so much good will and credibility that they’ve created an environment for this to thrive.
All metrics I see show faith in these institutions going to zero. Most good science I see is making (and has been making for decades) a really strong case that this loss of faith is deserved.
Credentialism is collapsing under the weight of its own corruption.
The solution is better institutions, not less institutions.
Good institutions have mechanisms in place to correct themselves.
And most of the past failures of our institutions were discovered and corrected by ... the institutions (sometimes the very same institution or other institutions whose role was to counterweight the institution at fault)
Unfortunately the trap we all fell into is that we interpret this success at catching and fixing failures as proof that the institutions have failed and thus that they will never be trustworthy ever again.
We need to train ourselves that the trust we put in the institutions does not mean we trust everything that comes out of them, but we trust that the mistakes will be eventually corrected as they happen.
But that's not what's happening now. The society has equated the point-in-time failure of an institution with the failure of the entire process and also extended that feeling across the board towards areas of our society that haven't failed us much.
Nothing good will come out of that. For one, it will remove any incentive from future institutions to try to be objective and self-correct. If self-correction becomes a "capital sin" for institutions, they will be selected to favour absolute unquestionable truths which cannot possibly ever need a correction.
But also. it completely ignores the fact that most institutions are useful, even while they suffer from failures/corruption and that destroying them altogether is going to throw the baby out with the bathwater.
I haven't seen much self correction out of major institutions, but what I am really looking for is honesty.
I want them to share their uncertainty, nuance, and reasoning. Anything less I view as well intended lies.
Institutions as a concept are critical. Some institutions are net negative. Blindly following and support all institutions because some or even most are useful is a fallacy of its own.
I think the nutritional institution credibility is bankrupt at the moment. given the importance, I am willing to take the risk and put in the work to find my own way in the Forrest.
Furthermore, most institutions can only provide heuristic advice, which even when true, is t always true, or true for everyone. It should never be treated as dogma
Yeah you're right about nuance and the fact that it's hard to have a nuanced conversation nowadays.
For what is worth I'm precisely trying to bring nuance to the discussion about institutions.
Institutions do fail. That's a normal mode of their operation. They fail all the time. When institutions fail, they fail and some other institution (in the broadest case the institution of civil society as a whole) calls them out for the bullshit.
The question is: what to do next.
Should we dismantle that institution and other similar institutions, including the ones that helped provide the data that proved the failed institution wrong just because they are all institutions and guilty of the original sin of being an institution?
I find this approach to be a little bit too extreme.
Yes. many institutions are full of shit. Let's reward people who can reign them back in. But we need professionals. We cannot all be experts in everything. I know it can feel this way because we have an unprecedented source of information at our fingertips but realistically we cannot all just figure out things on our own.
I sure feel I'm super smart and I can figure out everything if I just had a weekend but luckily I grew just wise enough to know foolish and misleading that feeling is.
That's a fair question, I don't know what the mechanism for institutional reform is, or if the public has a role to play in it.
I agree that folks should not condemn the messenger. In this context, that seems to mean science as an institution or individual scientists. The lying institutions should be disregard untill they are shown to actually be reformed.
with regards to who you follow in nutritional circles, just beware that there's a lot of social media content out there by people who are really good at business (seo, social media content gen, etc) but haven't read much nutritional research. Meanwhile the real scientists who know a great deal, have very little social media content, if any at all.
Personally, I follow the advice of Dr Micheal Gregor, one of his most recent books has over 13,000 citations! Their team has read over 20,000 nutritional papers!! And he'll tell you that whole grains and beans are an excellent staple of a healthy diet.
And with regards to Saturated Fat and even dietary cholesterol, he said, to make a really long story short, that they're really bad for you. There's way too many specifics to list but his 500+ page book (How not to age, and How not to Die) goes into great details and backs it up with a ton of research.
Actually, excessive omega-6 arachidonic acid intake is far more problematic than saturated fats. Dr. Gregor knows about the arachidonic acid problem but doesn't seem to understand it. https://nutritionfacts.org/topics/arachidonic-acid/
Compare what Gregor says to this comment by Norwegian animal science researchers. "Chicken meat is commonly regarded as a healthy type of meat; it is popular, and hence the consumption has increased. Chicken meat is lean, protein-rich and rich also in other important nutrients. However, the fatty acid composition is strongly dependent on the diet fed to the birds. A typical modern poultry diet is rich in cereals having a high ratio between omega-6 and omega-3 fatty acids. This diet is very different from the natural diet for the same species containing more green leaves that are rich in the omega-3 fatty acid alpha-linolenic acid (ALA). It has been shown that a diet rich in ALA gives increased concentrations of ALA, eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA) and docosahexaenoic acid (DHA) in broiler muscle and improved, i.e. reduced ratio between total omega-6 and total omega-3 fatty acids. The utilisation of ALA and linoleic acid (LA) for synthesizing EPA and arachidonic acid (AA) depends on feed concentrations of ALA and LA as well as on other factors. Much AA in the diet may contribute to prostaglandin overproduction in disease situations in humans, but some AA is necessary for virtually every body function. Dietary sources of AA are especially meat, eggs and offal, with smaller amounts coming from milk and fish. https://pmc.ncbi.nlm.nih.gov/articles/PMC2875212/
It's likely that the global increase in obesity and diabetes is largely due to increased consumption of grain-fed monogastrics such as poultry and swine. A 2021 paper by Australian zoologist Anthony Hulbert, PhD entitled 'The under-appreciated fats of life' concludes, "As a final comment, I note that we are only beginning to understand the implications of the balance between omega-3 and omega-6 fats in the human diet. Although most animals have a relatively constant diet, we humans are especially diverse (both between individuals and over time) in the types of food we consume. Over the last half-century, the modern human food chain has emphasised omega-6 and diminished omega-3 intake, largely because of: (i) a shift from animal fats to vegetable oils, (ii) an increase in grain-fed meat and dairy, and (iii) a decline in full-fat dairy products from grass-fed livestock (an important source of omega-3). In the opinion of the current author and others, these diet trends are likely to be responsible for the increased incidence of obesity and other modern epidemics of chronic disease, but that is a story for another time." https://journals.biologists.com/jeb/article/224/8/jeb232538/...
This is just mechanistic speculation based on animal studies. There is no good evidence that I’m aware of showing harms from high n6 consumption in humans, outside of their contribution to caloric excess.
The n3:n6 ratio was a hypothesis that never panned out. If you look at the studies that “support” it, the “bad ratio” is brought about by reducing n3 levels below sufficiency, not by keeping n3 levels at the RDA or higher and then boosting n6 further.
So it’s no more evidence that n6 is harmful than taking a cohort of people, reducing half of the group’s iron intake to a minuscule amount and claiming that because that group’s “iron:magnesium” ratio is wrong, then consuming more magnesium is clearly harmful. It just doesn’t add up.
Actually, there is human research. Below is a message Olaf Adam sent to myself and several others on September 5, 2021.
I refer to the very readable review by Philip Calder “A systematic review of the effects of increasing arachidonic acid intake on PUFA status, metabolism and health-related outcomes in humans.” His final statement is that an increase in arachidonic acid intake up to 1.5 grams per day does not significantly change the parameters associated with inflammation, blood clotting or atherogenesis. In this very interesting observation, I was astonished by the fact that the background diet was not taken into account. Although the intake of arachidonic acid with the background diet is reported several times, the resulting metabolic consequences are not discussed.
From the data provided, it can be concluded that the background diet in all studies included in the review was a Western diet, the proportion of arachidonic acid being estimated at 200 to 400 mg per day. Our studies on healthy volunteers were carried out with formula diets and allowed a precisely defined supply of arachidonic acid over a period of 6 weeks. These studies have shown that the exclusion of arachidonic acid from the diet (vegan diet) causes a progressive decrease of this fatty acid from 11 + 3% of the total fatty acids in the cholesterol esters of the plasma to 8 + 2% after 6 weeks. The later studies on patients with rheumatoid arthritis have shown that an intake of arachidonic acid amounting to not more than 80 mg/day does not increase the concentration of arachidonic acid in the phospholipids of the plasma and in the erythrocyte lipids. From these findings I have concluded that the body's own production of arachidonic acid is around 80 mg per day. This means that the Western Diet provides approximately 2.5 to 5 times the estimated need for arachidonic acid.
This intake that is higher than the requirement primarily has no negative consequences. We know from many studies that the "silent inflammation" characteristic for the prevalent diseases of western societies has a latency period of more than 10 years before the consequences such as arteriosclerosis and myocardial infarction become apparent. The body is evidently able to avert the consequences of an unfavorable diet for a long time. To do this, there are numerous regulatory options, such as substrate or product inhibition in the case of enzymes or the inhibition of transport to or incorporation into cells. Arachidonic acid has a very special metabolic pathway that offers possibilities for regulating absorption from the intestine, transport in the chylomicrons, metabolism via the enzymes involved and also for incorporation into the cells. For example, we have found a completely different efficiency for the uptake of arachidonic acid into the cell membrane for platelets compared to erythrocytes or granulocytes. It is therefore very likely that regulation options on the metabolic pathway of arachidonic acid can, to a certain extent, compensate for changes in intake.
Only when too much arachidonic acid is present in the food for a prolonged time do these protective mechanisms apparently fail and inflammation and the manifestation of lifestyle diseases is seen. This explains the long latency period with which the diseases of civilization occur. It is documented in the literature that unhealthy supplementation, such as megadoses of vitamin E, has no deleterious effects on health-related outcomes for humans in the short term. Only long-term observations and meta-analyzes have been able to prove the increased overall mortality. These protective functions with which our body is endowed are very important, because our body is often confronted with megadoses of vitamins or other food stuff or unreasonable diets. Otherwise humans would already be extinct.
In summary, I would like to note that the human metabolism has many opportunities to compensate for unreasonable interventions for a limited time. The studies available so far relate to arachidonic acid intake with the Western Diet. This condition may already have provoked defense mechanisms that delay the occurrence of Western Diet diseases. We all agree that the Western Diet is too meat-based. The studies included in the review gave me the impression that an attempt had been made to further aggravate an already bad situation, present in Western civilizations. The negative result of these studies is reassuring for me, but does not mean that this supplementation has to be harmless and without long-term effects.
From my point of view, it would have been more productive from the experimental approach if vegans had been given the doses of arachidonic acid employed in the studies that are included in the review. This would come closer to the desired goal of the effects of arachidonic acid on PUFA status, metabolism and health-related outcomes in humans. Then one could also come to a result for the desirable intake of arachidonic acid, which I estimate for patients with inflammatory rheumatic diseases at 80 mg per day, corresponding to 560 mg per week. This corresponds to a diet with 5 vegan days and 2 days with consumption of animal products per week.
I don’t mind discussing arachidonic acid after this - I’m less woke on the literature on it and am always up for learning something new. When I was referring to no evidence in humans, I meant with regards to the idea of n3:n6 ratios.
If n3 is at sufficient levels, I see no reason to believe the n3:n6 ratio should be of any concern in terms of health risks. All the evidence I’ve seen cited to support the claim that a given n3:n6 ratio raises risks of negative health outcomes has induced “unhealthy” n3:n6 ratios by dropping n3 levels to insufficiency.
It’s on that point that I believe there is no supporting evidence in humans, and the fears of an issue are rooted in speculation. Happy to be proven wrong, though!
It's an omega-6 toxicity problem. Bruce Hammock writes, "Fatty acid composition in the Western diet has shifted from saturated to polyunsaturated fatty acids (PUFAs), and specifically to linoleic acid (LA, 18:2), which has gradually increased in the diet over the past 50 y to become the most abundant dietary fatty acid in human adipose tissue." https://pmc.ncbi.nlm.nih.gov/articles/PMC9060469/
Vijay p. Singh says, "Separately, on analyzing global COVID-19 mortality data and comparing it with 12 risk factors for mortality, they found unsaturated fat intake to be associated with increased mortality. This was based on the dietary fat patterns of 61 countries in the United Nations' Food and Agricultural Organization database. Surprisingly, they found saturated fats to be protective."https://www.medpagetoday.com/reading-room/aga/lower-gi/86940
It's interesting that fasting and exercise furnish some protection from excessive polyunsaturated fatty acid intake. For example, "The increased proportional intake of dietary fat, decrease in feeding frequency and increased physical activity in free-ranging compared to captive cheetahs are all predicted to result in enhanced mitochondrial FA oxidation through the lowering of circulating glucose concentrations and insulin:glucagon ratios. During fasting/refeeding cycles and increased levels of exercise, tissue PUFA concentrations have been shown to deplete rapidly in both humans and rats. These studies show that most PUFAs, including α-linolenic acid (ALA) and linoleic acid (LA), are preferentially oxidized in periods of exercise or fasting. During refeeding, SFAs and monounsaturated fatty acids (MUFAs), such as palmitic acid and oleic acid, are also more rapidly replaced than any of the PUFAs. Similarly, the concentrations of most plasma PUFAs and MUFAs have been shown to be significantly lower in rats fed a high fat ketogenic diet than in controls. The predicted increase in FA oxidation in free-ranging cheetahs is therefore likely to also skew their serum FA profiles toward lower proportional serum concentrations of PUFAs and MUFAs relative to SFA." https://pmc.ncbi.nlm.nih.gov/articles/PMC5167222/
In the final analysis, dietary saturated fats are benign, if not outright beneficial over a wide range of intakes as long as they are consumed in the context of healthy nutrient configuration as in whole foods. https://pmc.ncbi.nlm.nih.gov/articles/PMC7846167/
I read those papers and I don’t see any compelling evidence anywhere in there that n6s are toxic. The first one is just discussing burn patients and yes, we consume more n6s than we used to. But that’s not evidence of toxicity.
The COVID one is disappointing. I was expecting a longitudinal study where they perhaps hadn’t adjusted for confounding variables like obesity, etc. Unfortunately, the reality is far worse.
The only human outcome data they seem to have is a cross-sectional analysis where (as far as I can tell, correct me if I’m wrong) they just looked at gross consumption at a national level of different FA types, then saw if there was an association with COVID mortality. This is an insane way to test the hypothesis “consumption of n6 increases Covid mortality.” It just isn’t evidence at all.
I would take evidence to be something that is expected on a given hypothesis and not the negation of that hypothesis. For example, “we see the sun rise in the sky” is not evidence supporting the hypothesis “the sun orbits the earth”, because it would also be expected on the negation of that hypothesis, for example under another hypothesis: “the earth orbits the sun”.
In this case, we can think of any number of hypotheses that negate the hypothesis “n6 consumption increases covid mortality”. For example, “n6 consumption proxies for junk food consumption and population obesity, which increases COVID mortality.” The outcomes of the study are equally expected on both hypotheses. The outcomes they’re seeing could be explained by this alternate hypothesis, for all we know.
Fundamentally, though, there’s actually a much bigger issue here - the data are just cross-sectional. We have no idea if the increased COVID mortality is even taking place in the people that consumed more UFA - the data just don’t tell us!
This leads to an awkward bullet-bite one has to make in order to make a causal inference from data like these: you would also have to affirm that smoking increases lifespan. Unadjusted cross-sectional data shows that countries with greater cigarette consumption have longer lifespan (http://web.archive.org/web/20220325085356/http://www.thefunc...). Now, clearly this is not because of the beneficial effects of smoking. Perhaps it’s because more cigarette consumption occurs in those countries that are wealthier. The point is, cross sectional data is unsuitable for making causal inferences like this.
The rest is just mechanistic speculation and animal studies, not something that can be extrapolated to human outcomes (more about why later). So the study doesn’t actually show any negative health outcomes in humans from n6 consumption.
The next study is literally a study of cheetahs. Might be of interest if you’re a cheetah, or deciding on your pet cheetah’s diet. But we’re talking about human health here.
And then the final paper suffers from the issue of earlier one - trying to make a causal inference based on cross-sectional data. We have zero idea if the individuals suffering from SAP are even the ones consuming more n6s. Again, if we are to find this convincing evidence of n6 toxicity then we also have to grant that cigarette consumption increases lifespan.
A commonality in these studies is that they try to back up the cross sectional data with animal modelling and in vitro studies, but we have to bear in mind that the best data we have on translation of animal studies to human outcomes suggests the success rate is atrocious. The confidence interval for toxicity studies in animal studies translating to human outcomes includes .5, so you may well be better off tossing a coin than you are relying on animal studies to make inferences about human health outcomes: https://translational-medicine.biomedcentral.com/articles/10...
To sum up, this seems to be a collection of data from the lower end of the evidence hierarchy, none of which is even in the category of data suitable to provide information about what is healthful or harmful to humans. I don’t see why we would find this convincing evidence of n6 toxicity on its own, even before we get into all the much higher quality evidence pointing to benefits from n6 consumption.
(1996) "Excessive signaling of arachidonic acid (AA) metabolites has been associated with various chronic degenerative or autoimmune diseases, and intervention with the metabolism of AA is widely employed therapeutically in these afflictions. In essence, AA is the most biologically active unsaturated fatty acid in higher animals. Its concentration in membranes and its magnitude of effects depend on its amount, or that of its precursors and analogues, in the diet. The tendency of the field of nutrition to ignore the role of dietary AA will optimistically be reversed in the future." The article also said, "The underlying rationale for this symposium is that dietary AA is perhaps the single most important nutritional determinant in regulating AA levels in Americans. This may ultimately account in part for the striking differences in chronic diseases between strict vegetarians and the bulk of the omnivorous population." https://pubmed.ncbi.nlm.nih.gov/8642436/
Both animals and humans have endocannabinoid systems that operate identically in terms of physiological outcomes. Consequently, excessive arachidonic acid in cell membranes has pathologically consequences. https://johnditragliamd.substack.com/p/the-other-fat-science
As I said, happy to move onto AA once we’ve closed off the n3:n6 ratio thing. So do you have any evidence that the ratio is an issue in humans, or do you concede there’s no such evidence currently?
I believe the current thinking is to consider the effect on inflammation and bad cholesterol.
If your doctor says your number one priority should be to lower inflammation or lower bad cholesterol, you should consider lowering the amount of red meat.
The issue is that of course we need protein. Older people who tend to lose muscle mass and are at risk of falling should actually increase protein intake and weight resistance exercises. If their stomach tolerates fish legumes nuts, wonderful. If they tolerate red meat better, then they should eat red meat. Like every thing else in life, there are trade offs and nothing is completely healthy or unhealthy.
Personally, I don't think the capitalist-driven agenda anywhere in the world gives a flying fricative about the health of anyone, only the health of the profit motive and it's benefits to shareholders. Food and healthcare is but one more example. Love or hate the JRE, I think this episode [1] provides much food (pun intended) for thought. The common person simply does not matter other than as a(n) (addicted) consumer.
Sure. The government isn't your mommy, and neither are corporations. People have to take responsibility and look out for their own health. Nobody else is going to do it for you.
> they have a unique feedback mechanism that suppresses endogenous cholesterol synthesis that most of us don’t have.
What unique feedback mechanism is this and how can i find out if i have this too ?
circular reasoning "what makes them different is that they are shown to be different"
> they manage to escape heart attacks because their vessels are larger than average. Wow. I don’t know what to make of the Masai, except that they are indeed a unique people.
Maybe they are not "unique people" and there are other non-genetic reasons their blood vessels are larger.
I call BS on this so called review because author didn't bother to explain his points.
If you have a cholesterol synthesis feedback mechanism then as you increased your consumption of foods that are known to increase LDL-c (butter, lard, tallow) then your LDL-c would not rise or would only rise by a smaller amount than would be predicted by the Keys equation.
So you could get your LDL-c checked, up your butter consumption and then get a retest and compare the results to the expected value.
only genetics influence those markers? I thought even stress causes increase in cholestrol levels. How is this person so sure that Masai have some sort of special genetics when there are so many other factors.
It’s literally in the reference given. Just read it yourself and all will be revealed:
Biss, K., Ho, K.-J., Mikkelson, B., Lewis, L. & Taylor, C. B. Some Unique Biologic Characteristics of the Masai of East Africa. N. Engl. J. Med. 284, 694–699 (1971).
"The high ratios of phospholipid to cholesterol and bile acid to cholesterol in their gallbladder bile explain the extreme rarity of cholesterol gallstones. All these characteristics may reflect a long-term biologic adaptation of the tribe."
This is just an hypothesis that says they "may" have adaption? Not sure how that translates to definitive "they have a unique feedback mechanism "
Ok, so you have an issue with the certainty that Yoder used in his discussion of that particular issue. Does expressing certainty when the author of the referenced study uses less certain terms make something a joke?
If so, I have some wonderful things to show you from Teicholz that will have you rolling on the floor with laughter compared to Yoder’s stuff.
In what way was the certainty used to refute the findings? The point Yoder was making was that Teicholz made an inference that was incompatible with the study used to support it.
If you’re discounting a rigorous and well-referenced critique solely because it’s on a “spamtaculous” cite, then my intuition is that either you’re a motivated reasoner and nothing would push you off your position, or your epistemic framework for deciding what is credible and what isn’t is so wild that trying to discuss this issue with you would be like trying to teach French to a dolphin.
Just read the critique, ignore whatever “spamtaculous” things you’re seeing on the site. The content of the review is what we should care about. Happy to discuss that.
It’s large and I’m about to go to sleep and only on my phone, so not easy to go through the whole thing, but in short, yes.
Much like in her book, Nina is grossly misrepresenting the evidence, and I’d say just flat-out lies or at the very least misleads the author. See my comment here for an example: https://news.ycombinator.com/item?id=41958014
Some journals are. Others like to carry these kind of articles because heterodox controversial views like this can generate publicity, traffic and citations. Some journals will just publish any old rot.
The essay you linked to reads an awful lot more like a joke than the article in the OP.
To me it’s no secret that the mainstream nutrition science is a joke. The latest Nordic nutrition guidelines I’ve heard of recommend the same amount of sugar and red meat per week — 350 grams.
If that’s not enough to tell you everything these organisations do is based on false premises, I have a bridge to sell you.
> The latest Nordic nutrition guidelines I’ve heard of recommend the same amount of sugar and red meat per week — 350 grams
Please provide a source. The Danish health authorities absolutely do NOT recommend sugar consumption. Instead, they recommend eating 600g of fruits and vegetables, 100g of legumes, 30g of nuts, and 90g of whole grains DAILY, as well as 350g of fish and no more than 350g of meat WEEKLY. Source: https://foedevarestyrelsen.dk/Media/638651862095615836/AOK-a...
The tone is snarky and condescending, which already means it can't be taken seriously. Your initial comment struggles with the same issue to a lesser extent.
If you dismiss valid points addressing the substance of the claim under discussion because of the tone it’s conveyed in, and that’s the epistemic framework you use to understand whether scientific claims are valid or not, then best of luck to you.
Personally, I think that’s hilarious. Enjoy your bacon and butter.
I shouldn't enter into consideration, but it's a shockingly good heuristic to evaluate the credibility of people.
I repeatedly found that people who are thoughtful and not snarky — and often, nuanced — when discussing a topic I have no deep expertise on were much more correct on topics that I did have expertise on and could properly evaluate.
We're all on a time budget at the end of the day. And I do share the sentiment: the scientific literature in nutrition is known not to be very good. You don't have to be an expert, it suffices to notice that there are a lot of people coming to contradictory conclusions, and that the consensus seems to have changed drastically over the past decades, not being particularly driven by any groundbreaking changes in available scientific methods.
Ok, I don’t share that heuristic personally. That said, if that’s yours, then I encourage you to compare Teicholz’s output with, say, Walter Willett’s (who would take the position that SFA is a risk factor for CVD).
Teicholz is considerably snarkier than Willett so, even by that metric, you should lean in favour of Willett’s position that SFA is unhealthy, I guess?
A heuristic is a heuristic, and we can do some of our own research too. I was just defending the OP.
As for my personal position, I remember looking into things a while back and just coming away with the conclusion that nobody really seemed to know. If there's a truth here, it's either considerably more complex than "SFA good" / "SFA bad" (all these interacting pathways, man), or it just makes little enough difference not to matter at all in a way that we can meaningfully measure above the noise.
It seemed clear SFA are clearly not that deadly. Whether you'd be more healthy or live slightly longer if you chose to consume less of them, I have absolutely no clue.
The evidence overwhelmingly shows that replacing SFA with PUFA leads to a 20-30% reduction in cardiovascular disease incidence. Considering this is one of the top killers in the western world, this is massive.
I’m not sure how you’re determining that it’s otherwise?
I partially agree with you but have some counter thoughts.
Tone is something that can be adopted intentionally or unintentionally. If you hear a pilot on a radio dryly say something in a calm and detached tone, it could be in the context of an emergency. Pilots are enculturated to adopt that tone (for various reasons). Meanwhile particular cultures have different levels of acceptability when it comes to tone: some cultures perceive other cultures as more angry, or detached, because of the norms of communication within those cultures.
In short, I think the tone of “calm, scientific detachment” is often weaponized to lend undeserved credibility to an argument, because people tend to believe people more when they adopt that tone.
Furthermore, tone does have a purpose if used alongside a well done argument. For example, in the article the OP linked to, there is a rather exhaustive refutation of the book in question. The tone of the author previews that their entire opinion on the book is negative, given all the arguments they put forth in their review. If the author of the review had adopted a calm and thoughtful tone, perhaps it would indeed have been more effective because the reader would decide. On the other hand, most people won’t read the entire review, so the tone of the author makes it clear what their opinion is.
That said I am not wholly disagreeing with you: would be interesting to do a study using some varying markers to identify tone, and identify, I don’t know, argumentative complexity, and see if snarkiness is associated with a lack of complexity. Assuming you can find markers with predictive power.
I think what actually convinces me more than tone is nuance. If you can fairly assess arguments on both sides, recognize when either side makes a good point, and mention when you're confused about your conclusion, or when some point of evidence doesn't mesh with the theory. Things that are all one-sided are usually wrong (though I suppose there are cases where the truth is indeed one-sided, it's just pretty rare, and less likely to be things that people that you otherwise consider serious would argue about).
Even that attitude can be weaponized I suppose, if nuance convinced more people, than more people would learn to fake nuance to push their favorite outcome. Though I'd like to think that the process would change them a little bit for the better too.
It distracts from the points, whether they're valid or not. It suggests that the person is driven by something other than getting to the truth. They're more interested in demonstrating superiority and punishing the enemy.
That just seems like an attempt at mind reading to me. Maybe that’s just their writing style? Maybe they’re just fed up with having to deal with the same anti scientific nonsense all the time?
Seems a waste of effort trying to attribute motive to such things. Just read what they have to say, verify what they say against their references and then make an inference based on that. Don’t see why tone has to come into it at all.
I claimed that Teicholz was a joke because she makes misleading and often false claims about nutrition science evidence. The response was that the critique I linked to was more of a joke, not because of its content but because of its tone.
So sure, tone matters in certain contexts. If it matters more to someone than the content of what is being said to someone in the context of assessing scientific research, then I think that person has a wild way of interpreting evidence.
Very true. This fact has been deeply exploited by con men across social media in the past decade. When someone knows they’re coming from an unfounded, misleading, or deliberately wrong position they make up for it by heaping on friendly tone. They present in a warm, welcoming, and empathetic tone that appears inviting and friendly, unlike the cold academic discussions where facts reign supreme and tone is an afterthought.
It’s a real problem right now. There are countless influencers and podcasters pushing bad science who get a free pass because they are all smiles, super nice, and present themselves as helping you (while pitching you products and trying to get you to buy their book)
Although I understand the frustration that comes with feeling like misinformation is being spread, it is also much easier to have a meaningful discussion without such a tone/writing style. Everybody is human, and reading something like that can be quite inflammatory and distract from the conversation. Anyways, that's just my personal opinion, and despite writing this, strong emotions getting involved in public forums with topics like these is kind of inevitable.
There's two kinds of it. One is "This is BS, here's why it's BS, here's more detail on why it's BS, don't fall for this BS." It's heavier on evidence than it is on snark. It uses snark to liven up what could be dull, but all the data is there, and is carefully explained.
The other kind is heavier on snark than it is on evidence. It uses the snark to persuade, rather than the evidence. That's "I can't be bothered to actually make a real case here (whether or not the data is actually on my side), so I'm just going to make the other side look stupid, and hope that you decide to agree with me so that you don't feel stupid too".
The first kind can be persuasive. (In fact, it can be more persuasive than the dry kind of refutation.) The second kind is a huge red flag - if they're right, it's only by accident, because they can't be bothered to really deal with the evidence.
I suspect that, when different people are reacting to snark in such an article, they're reacting to different versions of it.
> Before anyone gets too excited, best to remember that Nina is regarded as something of a joke
Hi KempyKolibri. Was this intervention so important that you needed to signup for HackerNews for the first time to call her a joke ? I think this is quite against this forum guideline but (unsurprisingly) you are being upvoted.
Nutrition science is hard. The effects are long-term and easily confounded by all the other things one eats. Randomized controlled trials are not easy to pull off. It's only loosely regulated and and a big market. And everyone eats, so everyone has an opinion.
Perhaps that's why there is a lot of sketchy results, hyperbole in communication, and a cycle of debunking (of the debunking) around.
I have been deeply involved with monitoring my diet and nutrition for almost 40 years now.
My own metabolism and body is so different than when I started 40 years ago.
Current nutrition "science" is basically studying ensembles of weakly nonstationary processes and arriving at meaningless averages.
The whole method is completely stupid. It is why it feels like we have basically learned nothing in my lifetime in this field because I honestly don't think we have.
Looking at the hype cycle, I am beginning to think that what you eat doesn't really matter, with a few caveats.
And it makes sense. We are omnivores, the entire point of being omnivores is to be able to fuel our body with whatever food is available, and it probably played an important role in the development of the human species. It means our body is very tolerant regarding what we eat, and while some types of food may be healthier than others, the effect will be small compared to other factors like generics, lifestyle, exposure to harm, etc...
What I think is important though is that we should have a diet as varied as possible. It is not necessary, but the less varied your diet is (it includes veganism), the more you need to pay attention. With a varied diet, you are very unlikely to miss something, and if you eat too much of the same thing, you may exceed the ability for your body to deal with a particular substance, making it toxic.
Another problem is the psychological aspect. Essentially, the abundance of food that we have now messes with our brain, causing addictive behavior. And I think this is the focus of most serious nutrition science today, and that's also what Ozempic is all about.
I've also found that particle sizes are also important: keeping things in their natural sizes and chewing them yourself does a couple of important things such as mixing them with enzymes, sending signalling about what's coming into the digestive tract, and making food the right size, instead of ultra fine, which provides a different mix of nutrients to the lower parts of the gi tract (and lowers absorbed calories from nuts).
> Your diet is by far the most important part of your health.
If it was the case, we wouldn't have an article like this. We would have very obvious results, and we don't. Some claim we do, but if you look closer, it is not obvious at all.
Note that by "it doesn't matter", I don't mean that anything goes. Only eating deep fried donuts is not good, for the same reason eating only apples is not good, you won't get everything you need from a single food source. If you do that, you will get what are now very obvious and easily identified diseases, like scurvy, anemia, etc... Also, eating too little or too many calories is also not good, especially too little, but the effect (starving to death) is even more obvious.
What I meant by "it doesn't matter" is that with a varied diet and the right number of calories, the details don't matter. And I am convinced that a base diet of fried donuts to the appropriate amount of calories, with supplementation (vitamins, ...) to compensate for deficiencies is fine, or at least, not terrible.
And I also believe that "the appropriate number of calories" is the tricky part. Hunger mechanisms are supposed to regulate this, but they are not adapted to modern society, where rich food is plentiful. Hence the psychological aspect, which Ozempic targets.
I don't know if variety is actually the most important thing, but it certainly helps. It's probably more like:
1. Eat whole foods—prioritize nutrient-dense vegetables and some fruit in moderation.
2. If you can, vary your whole foods
3. Try not to eat too much sugar, especially with high triglycerides
4. Try not to eat too much salt, especially with high blood pressure
Everything else does seem quite overcomplicated. Nutrition has always been an area rife for capture by grifters, health gurus, and everything in-between.
This is a serious problem. How can we trust institutions that are suppose to provide evidence based advice to the general public? To me this is a crime so large that those involved should be held accountable for a percentage of all heart attacks. Furthermore it erodes trust in government, experts, and science. Right now it seems like the American public is actively feed extremely harmful food and lied to about the health consequences.
Is it possible to create a Reddit style voting system where votes are weighed more depending on a level of trust/expertise to review scientific papers. The voting could be on multiple factors, such as on the different types of validity, the overall impact, how transparent they are with methods and data, how well it fits with other literature, etc. The end result could be a paper titled “A survey of saturated fat’s impact on cardiovascular health” where experts very publicly discuss the papers merits and common people interested in their health can review and understand where the science is. Decentralized informational authority.
> This is a serious problem. How can we trust institutions that are suppose to provide evidence based advice to the general public?
The only serious problem here is that some people immediately trust a random article from someone who denies mainstream science simply because it’s a contrarian take.
I don’t understand the people who will question everything that comes from professionals and institutions, but within minutes of reading an article that is contrarian they think “Yep this all checks out and I have no further questions”. To see it happening in real time in this thread is wild.
Well, we read the article, which cites many studies. Maybe she is doing a super selective review of the field, but she does not merely quote one study, but several, all of which indicate that there is no correlation between saturated fat and cardiovascular problems.
IOW, we did not merely "read and trusted one random article" but assessed the presented evidence. You OTOH, merely provided ad-hominem attack on both the author and anyone who dared believe the presented evidence, which smacks of trying to shame people in not voicing their opinion.
Did you actually follow up and read the studies she cited in detail, though? Much of what she claims is misrepresentation, such as the insinuation that the Cochrane review found no evidence of SFA consumption being associated with risk.
one is based on an entire industry of people working in so many conflicting fields that it would boggle the mind if they could all be bought, and the other is based on one person who built their fame on being contrarian without a lot of evidence.
I think the question still makes sense, why people are willing to ignore a ton of evidence from a lot of different unaffiliated people and focus on one article by one person that really doesn't add up to much of an argument - I think the answer is just that this is what they want to hear, so it must be right.
The claim isn't that everyone in nutrition etc is bought off. You simply don't need to do that.
If you're in the sugar industry, you give funding to people investigating how saturated fat causes heart disease. You support organizations that back up your preferred theory. These orgs run media campaigns, slap a "heart-healthy" label on food products, and sometimes fund research. Forming popular consensus on "fats = bad" leads to additional funding from government or other charitable causes.
Increased funding leads to an increased density of scientists working on the problem, which in turn increases the legitimacy of the field, especially among people just getting into their careers. If it's common wisdom in the cardio field that saturated fats are the worst cause of heart disease, that's where they're going to focus their efforts.
It's one of those things where you simply don't need to buy anyone off. You just put your thumb on the scale early enough, and consistently push popular opinion toward a direction that's beneficial for you.
if somebody can find an even worse cause and they publish it, they stand to found an entirely new field - the incentives are to prove the entire existing field wrong. nobody would hesitate.
Scientific knowledge evolves as new discoveries are made, immutable and unequivocal “truth” is the realm of religion, not science (which makes the former much more appealing to many than the latter).
Trust really should not erode if X acted in good faith based on the consensus knowledge at the time.
If the consensus is evolving, sure. If the consensus is going back and forth for decades, and each time it is presented with the authority of medical or physical science, then it is normal and correct to stop listening at some point.
When scientists have weak theories that they're not sure of, they're not supposed to share those breathlessly with the public, and certainly not try to shape public laws based on the theories they know are weak.
And nutrition science has been guilty of this for over a century. You can find people in the field making confident recommendations and setting dietary standards from the time when they didn't know vitamins were a thing. If you followed the science on nutrition and adjusted your diet accordingly around 150-100 years ago, you could literally get scurvy or other vitamin deficiencies. The field has evolved a little bit, but it's still extremely weak as scientific fields go.
I agree that this reflects poorly on trust. But voting to give more authority to the federal government would make it even worse. Look at how poorly voting works.
It’s nonsense. SFA consumption is a risk factor for cardiovascular disease. Nina is misreading the evidence to come to poor quality conclusions. The most rigorous analysis of RCTs on the subject shows this very clearly:
"We found little or no effect of reducing saturated fat on all‐cause mortality (RR 0.96; 95% CI 0.90 to 1.03; 11 trials, 55,858 participants) or cardiovascular mortality (RR 0.95; 95% CI 0.80 to 1.12, 10 trials, 53,421 participants), both with GRADE moderate‐quality evidence.
There was little or no effect of reducing saturated fats on non‐fatal myocardial infarction (RR 0.97, 95% CI 0.87 to 1.07) or CHD mortality (RR 0.97, 95% CI 0.82 to 1.16, both low‐quality evidence), but effects on total (fatal or non‐fatal) myocardial infarction, stroke and CHD events (fatal or non‐fatal) were all unclear as the evidence was of very low quality. There was little or no effect on cancer mortality, cancer diagnoses, diabetes diagnosis, HDL cholesterol, serum triglycerides or blood pressure, and small reductions in weight, serum total cholesterol, LDL cholesterol and BMI."
I don’t believe saturated fat is evil. I believe that consuming more than 10%E from SFA increases risk of CVD, and replacing SFA with PUFA reduces risk of CVD.
And yes, that is my citation in support of that claim. Quote:
“There was a 17% reduction in cardiovascular events in people who had reduced SFA compared with those on higher SFA”
and
“When we subgrouped according to replacement for SFA, the PUFA replacement group suggested a 21% reduction in cardiovascular events”
Yes, and I am talking about subtypes of events in the "summary of findings" table. Those subtypes with "moderate" quality has very insignificant diff in # of events. Those with significant diff in # of events have "very low" quality of evidence.
How would that affect the inference being made here? That is, the claim being made is with regard to combined cardiovascular events. This effect is significant and the GRADE quality is moderate.
One of the main purposes of meta-analyses is to summate multiple studies that may have insufficient statistical power in isolation to find a significant effect, but when summated they do.
I _think_ you're trying to suggest that the insignificant individual event types aren't contributing to the significant findings on the combined event endpoint, so we should ignore the GRADE quality of those (correct me if I'm wrong). But that's not how meta analysis functions - those events are also contributing to the significant finding on that endpoint (which is also why the GRADE quality of the combined endpoint is moderate). They just aren't significant _in isolation_.
> How would that affect the inference being made here?
to me, it looks like several rows clearly don't add up in key findings table(they derive "moderate quality" conclusions from "very low quality" observations), which makes whole publication as data astrology quality.
Well, good luck sustaining the claim that Lee Hooper doesn’t know how to perform a meta analysis and that error got past Cochrane’s notoriously lax peer review process, and you definitely didn’t just make a mistake reading the table.
I salute your self confidence, I must say I’m somewhat envious of it.
If you misread data in the way you appear to, that doesn’t surprise me. I can’t imagine you think many studies’ conclusions appear to follow from their results.
It’s just that you’re blaming the studies, rather than your comprehension.
Honestly, your steadfast insistence that you couldn’t possibly be wrong on this is fascinating to me. I’m happy to admit I made a mistake if I’m misreading the data, so walk me through what you think I’m getting wrong.
Please be specific: name the event subtypes you’re looking at, give specific references to the table numbers etc. If I’m wrong about this, I want to know.
I don’t research the topic for a living, so I don’t know — I’ve read none of the studies.
If the conclusion that comes out of the other end of the pipeline is that we should avoid eating the things we’ve eaten for millions of years, it’s fair to say what went in might have been based on false premises.
Why? Evolution doesn’t select for longevity, it selects for reproductive fitness. We have no reason to believe ancestral foods are more longevity promoting than novel ones, and antagonistic pleiotropy would suggest that all else held equal, ancestral foods are less healthy.
Heck, water treatment plants are novel compared to the pathogen-laced water we’ve been ancestrally consuming, but I doubt you eschew tap water for puddle water.
Anyone else have alternative takes on cholesterol based on personal experience?
Some alternative theories I've come across:
- There's a theory that cholesterol is good for you. It's necessary for brain functioning. Low levels of "bad" cholesterol have been linked to depression.
- There's a theory that the high levels of cholesterol in blood clots found around ripped arteries may be due to the body trying to heal a rupture with cholesterol.
- There's a theory that seed oils and table sugar, which have only been mass consumed for the last 100 years or so, are what cause heart disease.
Personally, I have a very high level of both good and bad cholesterol. They shot up after I started eating a lot of non-veg food. And after they shot up, I stopped having depressive episodes.
> Some alternative theories I've come across:
> - There's a theory that cholesterol is good for you. It's necessary for brain functioning. Low levels of "bad" cholesterol have been linked to depression.
These aren’t alternative theories, they’re just reductive takes that try to ignore the big picture.
Reductive takes are really seductive for people who want to reduce everything into “good” or “bad” categories, but the body doesn’t work like that.
The part that confuses people is that the message has been simplified to “cholesterol bad” for so long that people are confused to discover that cholesterol is actually used by the body. Upon discovering these facts, reductive logic switches from “cholesterol bad” to “cholesterol good”, which is just as reductive.
The truth is that cholesterol is useful within the body, but that doesn’t mean that more of it is better. Despite all of the proponents of alternative theories trying to spin a different story, the bottom line is that cumulative lifetime LDL exposure is still correlated with heart disease.
That is the only thing you need to know about the debate if you want to reduce it to something simple. More LDL over time means more heart disease. A lot of people will try to “well actually…” various things around this, but it’s true.
Even the comments below are trying to tell you your own observation is impossible (that diet can’t affect cholesterol levels) when that’s clearly not true.
Cholesterol has become a hotbed of alternative medicine that doesn’t follow the science but sells well on social media. Don’t put too much confidence behind “alternative theories” when we have decades of evidence that excessively high cholesterol levels over a lifetime are correlated with heart disease.
> excessively high cholesterol levels over a lifetime are correlated with heart disease
You're talking about blood cholesterol levels. Yet we're talking about dietary cholesterol. Totally different things, it's now well known that they're unrelated. The cholesterol in our bodies is produced by the liver by a completely different process. The old science is pretty foolish for assuming dietary -> blood cholesterol, as if we didn't have a digestive system. If your point was "stick to the settled science and don't believe the alternatives" you couldn't have picked a worse example.
To the original topic, dietary saturated fat does appear to increase the risk of heart disease by increasing LDL cholesterol. In other words, blood cholesterol is a problem but it's driven, at least partly, by saturated fat intake. High dietary cholesterol food like eggs do not increase serum levels, unless you deep fry them in butter.
What puts a person at risk for chronic inflammatory diseases is excessive polyunsaturated fatty acid intake; in particular, arachidonic acid. Excerpt: "The Mediterranean diet is low in arachidonic acid and rich in healthy fats such as monounsaturated fats found in extra-virgin olive oil (EVOO), nuts and omega-3 fatty acids from fish, which has been shown to lower the risk of inflammation, heart disease, cancer, diabetes and obesity, and other degenerative diseases." https://advancedmolecularlabs.com/blogs/news/new-red-meat-st...
In the middle decades of the 20th Century the heart attack rate was extremely high. Much of that mortality is likely attributable to the release of heavy metals into the environment. Heavy metals such as lead tend to cause arterial plaques to rupture. Excerpt: It must be theoretically expected that there will be a synergistic (multiplicative) interaction between low Se intake (leading to undersaturation of the blood plasma with selenoprotein P), large exposure to toxic heavy metals (which may be expected to lead to simultaneous inhibition of selenoprotein P and extracellular thioredoxin reductase), a high dietary LA/oleic acid intake ratio and high rates of superoxide anion radical production from endothelial NADPH oxidase as causes of more rapid LDL oxidation - with a high rate of LDL oxidation leading in turn to high rates of atheromatosis development. Against this background it is not unreasonable to speculate that excessive exposure to a number of toxic metals from a wide range of different sources may have been one of the main causes of the post-war epidemic of coronary heart disease both in North America and Western Europe. These include lead from car exhaust and from drinking water (especially in the British Isles), as well as mercury and silver from dental amalgam fillings and cadmium from acid rain, commercial fertilizers and tobacco smoke...This hypothesis would appear to be in reasonably good agreement with what is known about the historical curves both for coronary heart disease mortality and for the use of lead as an additive in gasoline in Western Europe, compared to North America. The use of lead as an additive in gasoline started earlier and ended earlier in the United States than it did in the countries of Western Europe. And the epidemic of coronary heart disease has followed a similar time course with both its start and its culmination occurring earlier in the United States than in Western Europe." https://pmc.ncbi.nlm.nih.gov/articles/PMC3031257/
... in the Standard American Diet. Dr Paul Mason's video "The truth about high cholesterol"[1] at 9:40 he cites a study showing that increasing levels of "light buoyant undamaged LDL" do not correlate with increased heart disease risk over 15 years and 11,000 subjects. Then at 10:20 shows study results that increased levels of oxidised, damaged, small, dense LDL do correlate with increased heart disease. IIRC it's damaged by oxidation, glycation, plant phytosterol cholesterol-mimics (driven by increased seed oil consumption) and involved with disruption to lipid rafts which some medications cause, e.g. statins and anti-psychotics.
Part 2: The shady truth about statins: https://www.youtube.com/watch?v=I7r4j1u42V8& (studies showing they do lower cholesterol, and that doesn't lower the risk of heart disease).
I don't know what it is chemically, but why is that naming confusing? Some tortoises are in the family Giant Tortoise. Within that group some are smaller than others. A "small giant tortoise" is not so confusing? A video card can be mid-range. It can also be upper-mid-range or lower-mid-range. I assume similar of LDL; within the group "LDL" there is some variation in size and density; the smaller denser parts of the range have properties which make them worth talking about as a sub-group.
It's a term people use, e.g.
"Small Dense Low‐Density Lipoprotein Cholesterol Is the Most Atherogenic Lipoprotein Parameter in the Prospective Framingham Offspring Study" -
Hiroaki Ikezaki MD, Elise Lim PhD, L. Adrienne Cupples PhD, Ching‐Ti Liu PhD, Bela F. Asztalos PhD, and Ernst J. Schaefer MD; Journal of the American Heart Association - https://www.ahajournals.org/doi/10.1161/JAHA.120.019140
It’s a fair point, I’ve never even thought about that. I think it’s just something that’s awkwardly come about because there was an early broad categorisation of lipoproteins by density, and then there a subsequent need to divide those species even further by density.
I tried to come up with a corollary but the best I have is “jumbo shrimp”. Sigh.
The problem with the “lbLDL is harmless” argument is that, while it was an interesting theory ten years ago, we have very strong evidence this is not the case now. I could go through exactly why people thought this is the case, and why the hypothesis turned out to be wrong, but this paper does a better job than I could: https://pmc.ncbi.nlm.nih.gov/articles/PMC7369156
Paul Mason is a renowned spreader of misinformation on this topic (and many others). My favourite moment of his is when he tried to teach a clinical research scientist that the lipid hypothesis was false, and in doing so revealed that his entire argument against the lipid hypothesis was based on an undergraduate-level misreading of a study, after which he just ran away from the conversation instead of admitting he was wrong. Absolute chef’s kiss moment, enjoy: https://x.com/avibittmd/status/1335491375073271808?s=46
This just says "it is so" and a page of numbers; X won't let me read the thread because I have no account, so... what is so? What intervention? What outcome is it showing? And how are they doing a six year study measuring people's daily energy intake down to 0.2 of a Calorie?
Because Mason’s making a number of flawed assumptions based on a misunderstanding of what drives atherosclerosis risk. The important factor js number of ApoB tagged lipoproteins (ApoB) and not mass of cholesterol within those lipoproteins. There is significant collinearity between these two things, but in ~30% of individuals there is discordance, which can create this illusion of “lbLDL is harmless”.
This is because a given individual with the same amount of lbLDL-c as someone else’s sdLDL-c (that is, mass of cholesterol in both), the person with the same mass of sdLDL-c will have more ApoB tagged lipoproteins and therefore more risk. But when we stop using LDL-c as the measure, and use ApoB, which is what lipidologists now recommend, then the risk from large and small LDL particles is more or less the same. That is, one particle of sdLDL carries about the same risk as one particle of lbLDL.
It’s not hard to make an X account, but ok. I can link to the individual posts so you can have a laugh: Mason said the entirety of the lipid hypothesis was challenged by the fact that those randomised to reduced fat diets had a higher risk of dying in the 2006 WHI RCT: https://x.com/drpaulmason/status/1335411781557075968?s=46
And then Paul, previously so headstrong and sure he was nailing everyone on this one, just peaces out from the conversation (or runs away, if you were to be less generous). His entire argument against the lipid argument was based on misreading dietary cholesterol as serum cholesterol. So good. No one should take him seriously, he’s either purposefully deceptive or completely incompetent at reading the evidence. Don’t see why anyone interested in reaching the truth should be interested in his arguments in either case.
That is an interesting interview with William Cromwell. When he says insulin resistance goes with lots of small LDL, why does it? I don't know how cells turning down their insulin sensitivity has a connection to fat in the blood, particularly. What's causing what to happen/not happen, there?
That Twitter exchange; separate from the lipid hypothesis bit, are you saying in summary that Avi is not contesting the claim that the reduced fat group had a higher heart attack risk, only contesting which fat was reduced? They intervention group reduced dietary cholesterol by 30% and that didn't change their serum cholesterol at all and they had higher heart attack risk?? How does that track with your comments about you reducing your dietary fat, why are you if doing that doesn't change serum levels or death risk? That seems to track what Dr Davis says about CAC scores and reducing dietary fat not helping them.
From out here in layman's view, what people on many different sides are saying is about insulin resistance and metabolic syndrome being more important (and more modifiable). Say as a layman chain of reasoning: if most cholesterol in the blood is made by the liver rather than by diet, if one use for cholesterol is to shuttle repair materials to damaged sites around the body, if chronic inflammation is a sign of widespread low grade damage which needs lots of repair, if some of that damage is caused by glycation, if insulin resistance means more free blood glucose not being taken into cells so there's more in the blood to cause more damage, if damage is also caused by oxidised and rancid fats, if unsaturated fats oxidise more easily... then reducing (sugars, simple carbs, unsaturated fats) in the diet should result in reduced insulin resistance, in less damage, in lower levels of chronic inflammation, therefore in less cholesterol produced by the liver, in lower blood LDL of any size, in less cholesterol to be damaged and less free glucose to damage it, therefore in less plaque buildup, lower heart disease risk.
(At no point here am I saying "more fat is better" in absolute terms; I don't think that adding butter onto a takeaway makes it healthier).
My understanding is that insulin resistance leads to increase DNL in the liver, so you end up with a greater production rate of LDL particles, but each one contains less cholesterol. I’m not woke on the mechanisms, but there’s a review paper here if you’re interested: https://www.sciencedirect.com/science/article/abs/pii/S10501...
Re: the twitter conversation: the diet heart hypothesis is specifically about replacing saturated fat with polyunsaturated fat. If you just reduce overall fat, you may even be making that P:S ratio worse. In the case of the WHI it means that the study is essentially null by default on that issue.
Dietary cholesterol is an interesting one - basically there is a significant effect of dietary cholesterol on serum cholesterol, but only when you go from very low to low levels. After that, the effect tails off dramatically. So in the general population you might not expect a 30% reduction to make a significant difference.
Additionally, you have to consider the overall picture. Maybe the reduction in dietary cholesterol did have a small beneficial effect, but the fact that the intervention group ended up with lower PUFA consumption than the control group meant this reduction was overshadowed by that effect.
There’s no evidence that oxidised fats in unsaturated fats are a cause for concern for health. Aside from that I don’t think stringing together a bunch of mechanisms and speculating about them is a particularly useful way to carry out science.
What we care about is actual outcomes from actual interventions. So yes, I agree that in those with metabolic disease and insulin resistance, we should address this issue. The evidence seems to suggest this is best done by losing weight. If there’s a certain dietary pattern that helps someone do that, great. If it’s a GLP-1 agonist, go for it. Whatever works.
But we also know that fat quality affects CVD risk too, and by a decent amount. So within whatever dietary pattern one settles on, replacing SFA with PUFA would also be a good idea. We can do both!
> "If you just reduce overall fat, you may even be making that P:S ratio worse."
Ugh.
> "There’s no evidence that oxidised fats in unsaturated fats are a cause for concern for health."
https://openheart.bmj.com/content/5/2/e000898 says: "The low-density lipoprotein (LDL) oxidation hypothesis gained traction during the 1980s because it was noted that in general, native unoxidised LDL does not cause foam cell formation. In other words, LDL had to become oxidised first in order for atherosclerosis to develop [..] what causes LDL to become oxidised in the first place? It was later discovered that the oxidation of LDL was initiated by the oxidation of linoleic acid contained within the LDL particles [..] a more comprehensive theory, the ‘oxidised linoleic acid theory of coronary heart disease’, is as follows: dietary linoleic acid, especially when consumed from refined omega-6 vegetable oils, gets incorporated into all blood lipoproteins (such as LDL, VLDL and HDL) increasing the susceptibility of all lipoproteins to oxidise and hence increases cardiovascular risk [..] cholesterol was protected from oxidation if bound to saturated fat but susceptible to oxidation when bound to linoleic acid"
That is condeming oxidised serum fats, not oxidised dietary fats, but it appears to be condemning "omega-6-rich vegetable oils" in the diet because they are more likely to oxidise in the body(?). I'm guessing if they are already oxidised when eaten that matters, because the only way it couldn't matter is if we deconstructed fats we eat and rebuilt them completely from scratch and if we did that completely then none of any of this would matter. The link's Box 1 has 29 points criticising those fats, Box 2 has 1 point in their favour "reduces total cholesterol and LDL".
> "Aside from that I don’t think stringing together a bunch of mechanisms and speculating about them is a particularly useful way to carry out science."
Well I'm not gonna understand biology, chemistry, lipid science to the level of a PhD researcher, PhD statistician, medical doctor, or an interested smart amateur biologist/chemist, myself. If I also can't have a bro-science chain of layperson reasoning, then your position boils down to "Science is only for experts, and only the experts I choose, not those they believe the wrong things so they're quacks, trust me" which is .. disagreeable.
> "What we care about is actual outcomes from actual interventions."
We can't see those until people don't die of heart disease fourty years later. This is why I'm so on the side of Dr William Davis because the CAC score seems to be the only good non-invasive measure of plaque available, something which can show an almost direct outcome of intervention on plaque. Whereas "serum LDL went down" is easily measurable but doesn't show if plaque formation is slowed, stopped, reversed, or unchanged. I also think that if low-fat did avoid or reverse heart disease, the massive international push over the last 50 years for low-fat foods would have made it absolutely clear, and instead heart disease is up up up. Doubling down on "people simply didn't eat low-fat yoghurt hard enough, do that harder" is just so unconvincing.
> "But we also know that fat quality affects CVD risk too"
When you say fat quality, do you mean PUFA vs SFA? Or do you mean things like presense of Glyphosate, trans-fats, contaminations in the food chain, things ordinary people mean by quality?
> "and by a decent amount. So within whatever dietary pattern one settles on, replacing SFA with PUFA would also be a good idea. We can do both!"
You've made a strong case that reducing serum cholesterol would be a good idea. Not such a strong case that reducing dietary fat would be a good idea. And not much case at all that replacing SFA with PUFA is a good idea. Let's be clear that I'm lost in the details of SFA, PUFA, linoleics, Omegas, LDLs/HDLs, triglycerides, cholesterols, which ones are more important, which ones are a tiny effect but easier to study or more interesting to study. When someone is 150lbs overweight and insulin resistant and never does an exercise it can't possibly come down to wibbling over whether they ate two slices of bacon vs half an avocado, or whether they put butter or margarine on a scone that one time. On the other hand if someone is Mark Sisson[1] a lean former ironman runner and paleo/low-carb enthusiast who got famous for eating a "big-ass salad" everyday, who does intermittent fasting, eats salmon and leaves with avocado oil dressing for lunch, then a ribeye stake with asparagus and avocado for dinner, no snacks, no desert, who cares about health, is he at risk of heart disease because he put heavy cream in his one coffee of the day and has red meat on his plate instead of nutloaf?
I guess you're suggesting to remove a daily Starbucks coffee with whipped dairy cream and sugar, right? No-brainer, I would agree.
But telling Mark Sisson to replace that steak with tofu? He has solved or avoided so many other problems people have with food - no food cravings or hunger, he's not overweight, he's not fatigued or big swings of energy, he's unusually healthy for someone in a Western country at his age (50s IIRC) that he's gotta be doing a lot right, not a lot wrong. He's gotta be somewhere close to a good human diet even if that is too much meat to eat every day for other reasons.
On no, not the DiNicolantonio paper. I really need a copy & paste thing on hand to go over all the wild logical leaps this paper makes but alas, I don't. I'm going to try to keep it brief by just focusing on what's relevant to the discussion.
> That is condeming oxidised serum fats, not oxidised dietary fats, but it appears to be condemning "omega-6-rich vegetable oils" in the diet because they are more likely to oxidise in the body(?)
We can just bypass that entire speculation, because to get there we've already made a logical leap, namely assuming that oxLDL is even something we should care about. All the evidence suggests that the oxidation of LDL almost entirely occurs within the arterial wall (https://pmc.ncbi.nlm.nih.gov/articles/PMC2924812/). When LDL is retained, oxidation is practically inevitable. The important thing is number of ApoB tagged particles.
So what would we expect to see in the real world if this hypothesis (that oxLDL is not an independent risk factor) was the case? Well, presumably if we adjusted oxLDL for ApoB, we would see the risk association disappear, since all oxLDL would be doing is just proxying for "amount of LDL", and the oxidation itself is not driving the risk. What do we actually see when we do this? When we perform a mutual adjustment of oxLDL and ApoB, and the association of risk from oxLDL disappears: https://pubmed.ncbi.nlm.nih.gov/16949489/
So even if the speculation that PUFAs increase oxLDL count were valid (and I'm not granting it is), it would appear to be irrelevant as far as risk of CVD goes.
> your position boils down to "Science is only for experts, and only the experts I choose, not those they believe the wrong things so they're quacks, trust me" which is .. disagreeable.
That's not my position at all. Please try to employ the principle of charity when interpreting my position, or this is going to be very slow going, and likely unproductive.
My point is that when you look at mechanisms, you're peering at one tiny part of a process of thousands (or more) moving parts. Just stringing together a bunch of those mechanisms into a narrative doesn't provide any kind of sound basis for making an inference about human health outcomes because it ignores every other mechanism at play. For example: mechanistically, exercise induces oxidative stress. I could do as you did above and string it together into a theory about how exercise is bad for your health, but I hope you'd agree that I'd be making a false inference.
My point is not that we then throw our hands up and say "I guess I'll leave science to the experts". I never said that. I said we have to base our inferences off the summation of all the mechanisms at play.
How do we do that? By looking at human outcome data (prospective cohort studies, mendelian randomisation, RCTs). Why don't we think exercise is unhealthy, despite the oxidative stress mechanism? Because we have human outcome data that shows the benefits of exercise. That is, we look at the exposure we're interested in (exercise) and the outcome we actually care about (say, mortality, or cardiovascular disease). Do people who exercise more have lower mortality rates when potential confounders are accounted for? If so, we have good reason to believe exercise is beneficial. This is how we should look at replacing SFA with PUFA. When we do that, what happens to the things we actually care about (heart disease, mortality etc)? Overwhelmingly, we improve outcomes. Why should we prize mechanisms above human health outcomes? It doesn't make sense to me.
> When you say fat quality, do you mean PUFA vs SFA?
Yes.
> Let's be clear that I'm lost in the details of SFA, PUFA, linoleics
The position I take is:
- There seems to be a point, around 10% total energy from saturated fats, where risk increases significantly. Either side of that, changes to SFA still make a difference, but not to the same degree.
- When it comes to reducing SFA, replacement is important. Replacing SFA with PUFA seems to be the most beneficial approach.
In prospective cohort studies, each 5%E from SFA replaced with PUFA resulted in a 13% lower risk of CVD events, and a 26% reduction in coronary deaths. In RCTs, we see a 21% reduction in CVD events when substituting PUFA in for SFA (https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD...). In general the reduction in risk seems to come out at about 20-30% depending on study characteristics. Considering CVD is one of the top killers in the Western world, I think that's something worth paying attention to.
There’s almost no correlation between cholesterol ingested as food and your own blood serum cholesterol. It’s almost as if we have a digestive system to break down nutrients into their constituents rather than release them unmodified into the bloodstream.
Yup, ingesting cholesterol doesn't lead to higher blood serum cholesterol. Although in this case the article was about ingesting saturated fat leading to higher blood serum cholesterol (in my personal experience this is true, and switching to a low saturated fat diet dropped my LDL cholesterol and triglycerides).
In general it matters what you replace the saturated fat with, though: you should replace it with unsaturated fat. Replacing it with carbs/simple sugars can apparently elevate LDL cholesterol and triglycerides: https://pmc.ncbi.nlm.nih.gov/articles/PMC2943062/
Technically speaking it does, but only if you’re starting from a point of very low dietary cholesterol intake or you’re genetically predisposed to have high sterol absorption.
So if you’re, say, a vegan with very little cholesterol intake then adding some would result in significantly higher serum cholesterol. However, for most people in western populations, they’re already above the point where the effect tails off, which is why dietary guidelines generally don’t focus on dietary cholesterol anymore.
Cholesterol is a necessary part of every cell in our body. It allows flexibility of cell membranes despite variations in temperature, and also converts into steroid hormones.
LDL doesn't mean much, but rather the ratio of HDL:LDL. Low cholesterol is bad for the brain. Of course these are oversimplified statements.
There are known cases of older men with low testosterone level and high LDL, who after testosterone replacement therapy experienced a significant decrease in LDL. It's thought that the liver kept churning cholesterol in attempts to synthetize enough testosterone to no avail.
I believe that depression and cognitive dysfunction is a side-effect of too low cholesterol when people take statins, especially older folks, but excessive LDL also accumulates in arteries and lead to hypertension and/or diminished blood flow to organs, which itself leads to dementia, heart attacks, etc.
Unless research has changed since I las tread, about 75% of your cholesterol is manufactured in the human body and not ingested, so ingested cholesterol is of limited in fluence. I suspect the overall health of the body affects it more than eating saturated fats.
Cholesterol by itself isn't harmful. For most people with typical genetics, cholesterol only becomes a problem when arterial plaques form as a reaction to vascular damage. Limiting cholesterol is one fairly effective approach to preventing those plaques, but a better approach is to avoid the damage in the first place. In other words, it doesn't matter if a little extra cholesterol is floating around in your bloodstream as long as it doesn't stick to the walls.
This is all true. And of course let us remember cholesterol is essential. Many hormones are made from it (cortisol, vitaminD, testosterone, estrogen). Being essential (not intending the meaning of "essential vitamin" which means the body cannot synthsize - as a vitamin it would be non-essential) - but being essential for physiology rather than diet, the body can synthesize cholesterol. So there is this axis of people who have low cholesterol super healthy diets.. and their body just makes lots of cholesterol anyway, so now they have high cholesterol and are taking statin drugs for it, because biology and population variation.
The other thing cholesterol is used to make, also quite nice to have, is bile. Used for fat digestion and such. A lot of bile. From a lot of cholesterol. Seems like a waste though, to excrete all that finely synthesized bodily chemical. BUt aha, the body realizes this and so resorbs it. THus there is a cycle and recycle of cholesterol and bile. Aha! What if we can trick the body to not resorb it and just release it. Such a drug has been developed. Well, hard to call it a drug. There is no fanciness, no elegant molecular binding to an esoteric receptor, no, nothing of the sort. It's called metamucil, and as the name tells us, it mostly works by being a big chonky mucinous blob of very impressively thick goop. The "magic" of how it works is literally the bile gets trapped in the thick goop and excreted. And thus we've bled off some bile from the cholesterol recycling loop, and thus, cholesterol. And that's why this weird blobby old person fiber supplement is cholesterol magic.
Kind of sucks for your guts, though, don't it? Bile is corrosive, that's why reflux is an issue and digestive tablets that contain ox bile shouldn't be taken on an empty stomach. Not fun when it reaches your bowels, either.
Certain famous men in the past smoked pipe all day and lived very long lives. E.g. Winston Churchill and Bertrand Russell. Do you have any theories on why smoking didn't harm them as much. Do you think back then there might not have been some interaction factor that's prevalent today, etc.?
How do you feel about starting with the opening paragraph on Wikipedia?
Cholesterol is the principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. — https://en.m.wikipedia.org/wiki/Cholesterol
If you're going to nail people on specific questions, you need to stick to those specific questions, not read a reaction to your very specific “cholesterol by itself isn’t harmful?” as anything other than an answer to your question.
Do you think the original person making the claim was referring to high serum cholesterol, or shadow boxing against an imaginary interlocutor who claims even a single individual cholesterol molecule is harmful?
I thought it was obvious, hence the original broad quote, but the bizarre Wikipedia response made me think that perhaps I wasn’t clear enough. Hence the clarification with my follow up.
Do you think the original person making the claim was referring to high serum cholesterol, or shadow boxing against an imaginary interlocutor who claims even a single individual cholesterol molecule is harmful?
I thought it was obvious, hence the original broad quote, but the bizarre Wikipedia response made me think that perhaps I wasn’t clear enough. Hence the clarification with my follow up.
> Do you think the original person making the claim was referring to high serum cholesterol
What I think is that your behavior is quite strange, to create a fake profile just to post a link "debunking" the author. Do you have something personal against her?
And then when you got corrected, in place of recognizing you said something wrong, you double-down your irrational behavior: "shadow boxing against an imaginary interlocutor". Yeah because the original interlocutor makes stupid questions.
I have issues with people pushing anti-science that can lead to harms. I have issues with Teicholz for this reason in the same way I have issues with Andrew Wakefield.
By "imaginary interlocutor" I was referring to a misreading of the parent reply, not mine. This was the person who said:
"Anyone else have alternative takes on cholesterol based on personal experience?"
The question is then whether when that person said "alternative takes on cholesterol" they meant "alternative takes on the function of an individual molecule of cholesterol" and not "alternative takes on the significance of high serum cholesterol". Considering their next two bullet points refer to high and low levels of serum cholesterol, I thought it was fairly obvious.
Apparently it wasn't for some people, and those same people are then claiming that making this clear is some sort of dodge/goalpost shift/deceptive behaviour. But it clearly isn't. If you read the above, where someone was obviously referring to high serum cholesterol, and in response someone says "cholesterol by itself isn’t harmful", is it reasonable to quote that claim and ask for evidence, by which you mean "I want evidence that high serum cholesterol isn't harmful"? If it is reasonable, which I believe it is, then no deception, goalpost shifting or correcting has actually taken place here.
That's a broad question. Let's turn that around. What harm do you think serum cholesterol could be causing? Like which specific mechanism of action are you concerned about here?
Sure, that’s fair. I believe that ApoB-tagged lipoproteins are a causal agent in atherosclerosis via the mechanism laid out in the 2019 EAS consensus (that is, the response to retention hypothesis).
Sure, no argument with that but let's go another step back in the casual chain. What's causing the arterial wall injury (or loss of ability to repair damage) in the first place to even allow that mechanism to come into play?
If a patient is already accumulating arterial wall damage then it might be necessary to limit serum cholesterol through dietary changes or statins or something. But I would claim that those interventions usually come too late, and that most of the damage can be prevented through other interventions thus making serum cholesterol levels less relevant.
It's like if you have a truck driving around full of toxic waste. Maybe that's cause for concern, but if you can take other measures to ensure it won't crash and spill the cargo then maybe it's fine.
What’s the evidence that this only takes place in individuals with arterial wall injury or without the ability to repair damage?
These factors may increase the effect of high LDL-c on CVD, but I’m not sure on what basis we should assume that those without them aren’t at risk from high LDL-c.
> "What’s the evidence that this only takes place in individuals with arterial wall injury or without the ability to repair damage?"
Some people live a long time with high(er) fat diets and no heart disease; Cardiologist Dr William Davis[1] selling his heart-scan plan using non-invasive CT scan / calcium measuring as a proxy for atherosclerotic plaque buildup claims that cholesterol is "virtually worthless" for predicting heart disease, and that taking statins or cutting the fat in your diet measurably "does nothing" to affect that measure of plaque buildup. Your suggestion is that cutting fat should do something. He claims his plan of removing wheat, grains, using fish oil, fixing inflammation and insulin resistance, various vitamins and minerals, can measurably stop plaque developing and it can reduce. That seems like it should be a very testable claim.
I haven't read his books, don't know the details of his plan, but if calcium is a solid proxy for plaque buildup, and a CT scan can measure it stay the same in people who switch to low-fat diets, and measure it drop in some people who don't but instead remove grains, that suggests plaque buildup from LDL only takes place in some individuals who eat fat, not all. Arterial wall injury or inability to repair damage are they possible reasons? Or the inflammation and insulin resistance he mentions?
That’s an answer to a different question. I don’t disagree that CVD risk is multi factorial - having T2DM massively increases the risk, for example. But this being the case does not serve as evidence that arterial wall injury or an inability to repair damage is required in order for high serum cholesterol to be a risk.
CAC scores (which it sounds like what you’re referring to) only look at calcified plaque, but not soft plaques. So there’s a whole category of risk that is missed by them. People’s CAC only tends to go up when they’re in a very late stage of atherosclerosis, and calcified plaques also tend to be more stable than soft plaques, so if two individuals had the same mass of plaque, but one’s was soft and the other’s one’s hard (sorry for the “carry on cardiology”) then we’d actually expect the individual with the CAC score of zero to be at greater risk of a CVD event.
It’s my interlocutor’s burden to show that arterial wall damage and/or an individual’s inability to repair damage is required for ASCVD to take hold, and so far they’ve yet to meet it. That’s what I’m looking for, basically.
Sounds like CAC scores are the same thing. I can only link some other doctor's article[1] which says that the CAC does only measures hard plaque, but that a score of 0 has been studied and goes with a very low risk of heart attack (1-2%) over the next ten years. When you say soft plaques are a whole category of risk, that suggests they are not a significant risk factor. So something doesn't add up here.
From what I could gain in the paper you linked in another comment, they write that apoB with less LDL in it goes more easily into the arterial wall, apoB with more LDL in it causes more damage once in the arterial wall, and those two effects cancel out, so overal more LDL is worse.
These things don't add up to a coherent picture. If eating less fat reduced LDL, that should reduces plaque buildup (by your claims and your study's claims) and that should reduces heart disease risk, and that should show up in the CAC scans. And apparently it doesn't. If eating more fat increases LDL and that increases heart disease risk, that should show up in Dr Davis' CAC scans and he should think that worsens heart disease risk, and he doesn't.
> "But this being the case does not serve as evidence that arterial wall injury or an inability to repair damage is required in order for high serum cholesterol to be a risk."
It doesn't, and I don't make that claim. So I have no more comment. Agree that it's multifactorial (or appears that way).
Your Dr Davis just appears to be one person saying something is the case, without providing any evidence for it. I don’t see why we should believe his claims that serum cholesterol is irrelevant over the incredibly robust evidence I’ve brought to the table.
I agree that the two things don’t add up, but why wouldn’t we then just favour the higher quality evidence? Seems like Davis is a quack with historical form for just making things up without any evidence in order to sell a product: https://www.healthyeating.org/blog/detail/rdn-s-book-review-...
> "If there are any other causes of obstructive CAD other than fats getting into the artery walls, those cause would all have to be in that group as well (I don't know of any but I can speculate several)."
Here's one speculation of lay-person reasoning:
- Cosmetics people like Retinol skin creams because it makes skin look better. That's a fact that people recommend it.
- One way it does this by making it plumper, which smooths out wrinkles. I think that's a fact.
- It does this by increasing skin cell "turnover", i.e. what it does at the epithelial layer is trigger stem cells to split, making more skin cells, making thicker skin. That's a claim I've seen and am not sure if it's a fact, but it's a plausible mechanism of action.
- We eat retinol in our food, in the form of Vitamin A, that's a fact.
- Vitamin A gets through the guts into the body, that's a fact - it couldn't be a vitamin if it passed straight through us and out.
- Vitamin A gets into the blood stream; fact, there are lab tests of serum retinol levels.
- Vitamin A in the blood is supposed to be wrapped in Retinol Binding Protein to carry it through the blood, but it isn't always. It's normally captured by the liver, and released from the liver wrapped in RBP, but not all of it is captured by the liver and is free in the blood stream. The more of it in the diet, the more gets past the liver, the more of it is free in the blood stream. I've seen it claimed, have no sources to back it up.
- Blood vessels have an epithelial layer on the inside, an internal skin. Claim.
- Retinol in the diet -> retinol in the blood -> triggers stem cell split in the blood vessel walls -> thickening of the walls ("youthful!") -> narrowed blood vessels. Speculation.
(What do we have in this random link[1] I haven't read? "Until recently, it was thought that the sole important retinoid delivery pathway to tissues involved retinol bound to retinol-binding protein (RBP4). More recent findings, however, indicate that retinoids can be delivered to tissues through multiple overlapping delivery pathways, involving chylomicrons, very low density lipoprotein (VLDL) and low density lipoprotein (LDL)" - retinol is not only able to split stem cells, it's a pretty potent molecule in various forms; "Retinoids and immunotherapy may be used to treat high-risk or recurrent neuroblastoma" says Canadian Cancer Society; there's one bro-science connection for increased total LDL -> increased blood vessel damage which is nothing to do with the LDL per-se, but something it carries along with it. Something we eat a lot of as Vitamin A and carotenoids, something the US and Canada fortify flour and low-fat dairy and margarine with, which is another tie-in to both low-wheat and low-fat diet).
Because if obstructive heart disease can be caused by something other than LDL-plaque (such as thickening of the vessel walls) then your suggestion that soft plaque missed by the CAC score is the cause isn't necessarily true, therefore your suggestion that the CAC isn't good enough isn't necessarily true.
[Edit: it isn't relebant; thickened walls would be non-obstructive CAD].
That is another interesting link; I don't discount that link or try to refute it, although I do note that you present it as "58% had a CAC of zero" which sounds very bad, but they're talking of 23,759 sympotmatic patients, 1278 are under 40, and 39-68 of them (the numbers aren't clear[1]) actually do have CAD, and half of those have zero CAC score. That's 1.5% of people under fourty with symptoms have disease and have zero score. If there are any other causes of obstructive CAD other than fats getting into the artery walls, those cause would all have to be in that group as well (I don't know of any but I can speculate several).
I don't think Dr Davis has said serum cholesterol is irrelevant, the statement I linked is that dietary fat removal doesn't stop CAC score increasing.
Why we should believe him is that he's got a feedback loop with a measuring machine. Science is about settling abstract arguments by testing them against the real world, right? So you can dismiss Paul Mason by saying he's an idiot, he can't read, he's looking at old studies, and he's a sports medicine doctor so he's not treating heart disease anyway, but Dr Davis is actually a cardiologist and he gets a patient with a heart problem, he takes actual measurements (CAC score) then gives advice to change their life, then sees them again for followup over years and years, measures again and sees the results. The measurement is not based on whether he is smart or stupid, it's not affected by which studies he's citing.
He's a quack selling a book? The US Bureau of Labour says Cardiologist is the highest paying job in the USA[2]. He could just as easily be shilling low-fat books instead of low-carb books so that makes no sense that he would be shilling a book which goes against his findings instead of one which goes with his findings. Why does he need to shill any product - his financial incentive is do do more treatments, more stents, more bypass surgery, prescribe more statins for pharma kickbacks.
Could he be totally wrong, and his patients are dying en-masse, and others are leaving him to go to another cardiologist for bypasses, and other patients are eating something different and lying to him - I'd actually believe it, yes, but who knows. If we go with that he appears to have found something which reduces his patients' need for surgical intervention over years and decades, then it seems that the biggest things to affect heart disease risk are metabolic syndrome et al, and they appear to have far more effect on serum fats than dietary fat intake does, and far more effect on fats-causing-plaque-buildup than dietary fat does. Less fat in the blood is better, is something your links claimed, and that can also be something Dr Davis would agree with through insulin resistance improvements; as I asked in my other comment, I have no idea what the link there actually is.
At this point serum LDL seems important, dietary fat intake might be but it seems less important/effective as a way to modulate serum levels than fixing other diesease processes does?
[1] It says: "Results A total of 23 759 symptomatic patients, of whom 12 771 (54%) had a CAC score of 0, were included. Overall, the prevalence of obstructive CAD was relatively low across all age groups, ranging from 3% (39 of 1278 patients) in those who were younger than 40 years [..] In patients with obstructive CAD, 14% (725 of 5043) had a CAC score of 0, and the prevalence varied across age groups from 58% (39 of 68) among those who were younger than 40 years" - how can there be 39 people with CAD under fourty in total and also (__ of 68) under fourty with CAD and zero score? Where did the 68 come from?
I probably should never have entertained the Dr Davis derail. The whole bringing up of this character was your attempt to answer my question "What’s the evidence that [atherosclerosis] only takes place in individuals with arterial wall injury or without the ability to repair damage?"
Your response was "Some people live a long time with high(er) fat diets and no heart disease". But this is not evidence that atherosclerosis only takes place in individuals with arterial wall injury or without the ability to repair damage. That could equally be evidence that some people are genetically less predisposed to arterial retention, regardless of arterial wall injury, for example. There are plenty of hypotheses that negate your proposed one that are equally likely on the evidence you've provided. So this whole thread is just a tangent that doesn't engage with the core question. That said, here goes:
My point on CAC was that your entire argument hinges on being able to look at a CAC score and say "this score is a reliable indicator of whether a person has coronary artery disease". But if you're under 40 and actually have CAD, there's a 58% chance that when you get your test results back, it will show 0 CAC (even though you have CAD!). So demonstrably, CAC is a poor proxy for CAD, and so a lynchpin proposition in your argument is clearly false. Whether the numbers look different when read a different way is irrelevant. The above is true, and demonstrates how CAC is not a reliable metric.
> I don't think Dr Davis has said serum cholesterol is irrelevant, the statement I linked is that dietary fat removal doesn't stop CAC score increasing.
Literally from the article you linked: "Can you look at your cholesterol and say “Oh, my cholesterol is 240. I must have heart disease.”? No, of course not — cholesterol is virtually worthless when it comes to predicting heart disease"
So he says exactly that, unless you're willing to quibble over a semantic difference between "virtually worthless" and "irrelevant".
> Why we should believe him is that he's got a feedback loop with a measuring machine
It's not just "why should we believe him", it's "why should we believe him over meta-analyses of RCTs, and other high quality data?" Look at where "expert opinion" and "case reports" (which is the evidence you're citing, if we're being generous) sits relative to the MAs of RCTs that I'm bringing to the table on the hierarchy of evidence (https://en.wikipedia.org/wiki/Hierarchy_of_evidence). It's not clear to me why you're throwing out robust evidence with comparatively low risk of systematic bias and relying on bottom-tier evidence instead. Can you please explain to me why this is a superior epistemic framework?
> He's a quack selling a book?
Yes. I'd take a quack to be anyone wearing the coat of science while violating the standards of modern science. Whether or not he stands to gain (or cares about) the money his book makes isn't relevant to that claim, it's based entirely on the nature of what he has to say/publish.
Indeed, going back to the previous point, dismissing the enormous body of high quality evidence showing LDL cholesterol is a causal agent in atherosclerosis by referring to serum cholesterol measurement as "virtually worthless" merely because of his own personal experience, with the plethora of biases that entails, is textbook quackery. The fact that he's published a pop science book that blames many of the ills of the world on wheat with no evidence to back up such an assertion is just the cherry on top.
So I don't need to speculate why he's a quack, and his salary doesn't alter my point. Maybe he does it because being a number one bestseller satisfies his ego in a way nothing else can. Maybe having that accolade means he can charge more for his cardiology services, so there's an indirect financial benefit. Maybe he genuinely believes wheat is the devil's food? I don't really care, my point is that his output suggests he's not a sound practitioner of the scientific method.
Your entire argument here seems to boil down to "there's this guy who sees patients and he says they're not leaving his practice and they're getting better, how would he have patients if everything he says about heart disease wasn't true?" This is wild, the kind of arguments I see from homeopathy advocates. We should always aim for the evidence base most likely to be free from bias. That is not one clinician's account of how they do things.
> "The above is true, and demonstrates how CAC is not a reliable metric."
From your study link: "Introduction .. Coronary artery calcium (CAC) that is assessed by computed tomography is reliable in evaluating the future risk in both asymptomatic and symptomatic patients with stable coronary artery disease (CAD)".
They call it "unmatched".
OK it isn't perfect, that doesn't make it poor. Still instead of "can it miss something", the other way around - if the CAC score measures something is it always definitely plaque buildup? Because then repeated CAC scores have the potential to be good for telling if plaque buildup is changing over time in response to dietary changes in people with non-zero scores and CAD.
Fine with him saying cholesterol is worthless, yes.
> ""why should we believe him over meta-analyses of RCTs, and other high quality data?""
Because when someone you don't like cites multiple meta-analyses of RCTs you handwave it away with a Twitter thread where he "runs away from an argument chef's kiss". I know of Ben Goldacre's Bad Science, I see plenty of HN links about the reproducibility crises in science about the ways of p-hacking and manipulating data, about the broken incentives to publish and get funding, about the complexities of statistical analysis, things I can't argue through. Medical experts are incentivised to push treatments, academic experts are incentivised to push dodgy results, it's not easy for people who like and care about this stuff to say what's "high quality data" or isn't, let alone me. One can't handwave away measuring the amount of plaque buildup in the heart and say "that's not a measure of the amount of plaque buildup in the heart" as easily. If people change X and their heart health measurably improves, and X isn't reducing dietary fat, that should mean something.
> "Your entire argument here seems to boil down to"
My argument was less about Dr Davis himself and more as a way to bring the CAC score in and to say Dr Davis says the CAC score isn't affected by removing dietary fat. That's a testable claim. That's much nicer than "this expert says that expert is wrong" or "this paper says that paper is wrong". You don't believe Dr Davis, well, presumably somewhere is a researcher or practitioner who has done many CAC measurements and has studied whether cutting dietary fat changes the score or not, at this point I am not going to look for it.
I am interested in the things you've said and linked, and my opinions have changed, but I think I'm well past what I am able to follow or interested to continue.
> I am interested in the things you've said and linked, and my opinions have changed, but I think I'm well past what I am able to follow or interested to continue.
Ok, that's unfortunate but obviously your prerogative! I will try to post some more lay-friendly links in this response that may convey my points more straightforwardly.
> if the CAC score measures something is it always definitely plaque buildup? Because then repeated CAC scores have the potential to be good for telling if plaque buildup is changing over time in response to dietary changes in people with non-zero scores and CAD.
No, it can measure plaque density. Additionally, since calcified plaques are more stable than soft plaques, it can actually go up while risk goes down. We see this occur on some statin regimes, where we have boatloads of data showing statins reduce risk, yet we can see CAC scores go up as soft plaque is stabilised into calcified plaque.
I'm not saying CAC is without its merits, but you are stretching credulity beyond breaking point to suggest that because one cardiologist claims that reducing dietary fats doesn't show a reduction in CAC scores, it therefore disproves the lipid hypothesis. CAC has too many caveats to use it to make such bold inferences, even if we get to the wild epistemic standards required to think one cardiologist's claims are sufficient to overturn decades of well-conducted research. Additionally, as I've stated elsewhere, it still wouldn't be evidence that arterial wall damage or inability to repair damage is required for ASCVD, which, let's remember, is the reason we're even talking about this in the first place.
There's quite an interesting discussion about the pros and cons of the CAC here. Suffice to say, it's not suitable to stand up the kind of arguments you're making: https://www.youtube.com/watch?v=gxIeRUbHauw
> Because when someone you don't like cites multiple meta-analyses of RCTs you handwave it away with a Twitter thread where he "runs away from an argument chef's kiss"
No, that's not why I dismiss Mason's claims. I dismiss Mason's claims because he says "this meta analysis says this" and then when you look at the MA it says nothing of the sort. It's false to claim that I'm handwaving away the evidence itself.
> I know of Ben Goldacre's Bad Science, I see plenty of HN links about the reproducibility crises in science about the ways of p-hacking and manipulating data, about the broken incentives to publish and get funding, about the complexities of statistical analysis, things I can't argue through. Medical experts are incentivised to push treatments, academic experts are incentivised to push dodgy results, it's not easy for people who like and care about this stuff to say what's "high quality data" or isn't, let alone me. One can't handwave away measuring the amount of plaque buildup in the heart and say "that's not a measure of the amount of plaque buildup in the heart" as easily. If people change X and their heart health measurably improves, and X isn't reducing dietary fat, that should mean something.
I think it's really worth taking a second to think about what you're saying here. Some points of order first:
- The reproducibility crisis is about some fields of science re-running individual studies and finding that when they do so, they cannot reproduce the original findings.
- p-hacking is about altering the methodology of a study post-hoc to generate statistically significant findings when such findings were not present under the original methodology.
- the objection of the complexities of statistical analyses, I presume, is an objection based on the fact that when using statistical analyses to try to account for confounders and systematic bias, sometimes these analyses are poorly conducted and thus fail to mitigate these biases.
- "Medical experts are incentivised to push treatments" is presumably an objection that individuals publishing papers may have an implicit or explicit bias that causes them to over or understate the significance of a given finding, or record data incorrectly.
So your argument appears to be:
"Ok, so you've provided evidence that LDL is a risk for CVD based on over 200 prospective cohort studies (that is, the results have been successfully produced literally hundreds of times), mendelian randomisation studies, and randomised controlled trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events. However, I believe it's likely that if we were to re-run those studies again, we would not be able to reproduce those results.
“I'm also concerned that p-hacking and systematic bias is so consistently prevalent within all of these studies that it affects the summated findings so profoundly, and consistently in the same direction, that we cannot trust the findings to be accurate. Additionally, the individuals conducting these studies are all incentivised to push treatments and therefore we should believe it to be more likely than not, without any evidence to actually demonstrate this, that these individuals are biasing the results because of these incentives.
“It's not easy for lay people like me to ascertain whether these data from the top of the evidence hierarchy (that is, the evidence least likely to be affected by bias) are high quality, so we have to find a source of evidence that is less likely to be affected by such bias. To achieve this, I propose that we throw all the above data out, and instead trust the claims of a single cardiologist, who's written a blog post on his website about how serum cholesterol is irrelevant when it comes to cardiovascular disease risk.
“After all, p-hacking can't take place when the evidence is so poor that there are no p-values, calculations of statistical significance, or even recorded data from which one could calculate p-values.
“After all, you can't make errors in your statistical analyses if you don't perform any statistical analyses.
“After all, your attempts to control for bias can't go wrong if you don't attempt to control for bias.
“After all, 'One can't handwave away measuring the amount of plaque buildup in the heart and say "that's not a measure of the amount of plaque buildup in the heart" as easily. If people change X and their heart health measurably improves, and X isn't reducing dietary fat, that should mean something,' despite the fact that there are studies that do measure plaque buildup in the heart and show that it is affected by serum cholesterol. I believe that we can handwave it away when it's published in a peer reviewed journal, but we can't do so when it's a blog post on a cardiologist's website. This is the most reliable way to make sound scientific inferences.”
I don't even understand how one can reach these conclusions. I've tried my absolute best to interpret what you've said generously, but there's only so much I can do given material like this.
This whole line of reasoning is also far closer to what you’re accusing me of - instead of discussing what the data show, we should just “trust the experts”. We can’t analyse Dr Davis’ data because he doesn’t even provide any, but we should just assume he’s telling the truth because he’s a cardiologist and therefore so well paid that he has no motivation to be wrong. We should ignore the evidence I’ve provided because it’s harder for laypeople to understand than this supposed expert just saying “trust me, I ran some CAC tests”.
> presumably somewhere is a researcher or practitioner who has done many CAC measurements and has studied whether cutting dietary fat changes the score or not, at this point I am not going to look for it.
I've already provided you even better evidence than that: a pooled analysis of studies where SFA is replaced with PUFA and cardiovascular events and coronary deaths are reduced. You don't need to go looking, I gave it to you: https://pubmed.ncbi.nlm.nih.gov/19211817/. If you want a more consumable version, here's an excellent podcast on it (all their stuff is good, you should see if there's anything else there of interest to you: https://sigmanutrition.com/episode481/).
It's a shame, but not entirely surprising that you no longer desire to continue the discussion. Fundamentally, I think you will always run into issues until you re-assess your underlying epistemic framework when it comes to assessing evidence. Until you do so, reading studies will be largely pointless as you have no reliable tools to interpret those studies. You're running before you can walk.
If you're interested, the Cut Through Nutrition podcast is quite a nice primer on how to think about nutrition science research, I'd highly recommend working through the episodes. Once you've internalised the concepts, it becomes a lot easier to see how quacks like Mason and Davis are operating, even without a great deal of domain-specific knowledge. Podcast is here: https://podcasts.apple.com/gb/podcast/cut-through-nutrition/...
I do have a fear that staying vegan will have other negative effects, unrelated to cholesterol - esp brain and bone density related. For me that means cutting out cheese, milk, and butter as much as possible. But having fish and lean meats 1-2 times per week.
I tried going vegan for ~10 years after reading the scientific research, then started getting stomach ulcers and constant diarrhea.
Tried with paleo (meat and veggies) as I thought the carbs were the culprit and I decreased the frequence of the accidents.
Finally I went carnivore and within a week I had zero symptoms. I was strict carnivore for 8 weeks (lost 8kgs) then I tried reintroducing other food but without great success.
These days I eat mainly butter, eggs and steak and I've been good for 2.5 years now (I was eating organs too at first but I don't really feel any difference if I don't eat them).
Eating the occasional sweet from a bakery makes me feel a bit bloated. Eating some fruit
For 1.5 years eating vegetables would cause the diarrhea to reappear, after 1.5 years I can eat vegetables occasionally without problems. It's like a "limit" got reset or something.
I was vegan for about ten years but it was socially crippling. These days I am vegan or vegetarian 4 or 5 days a week and have chicken or seafood the other there. A recent angiogram showed my coronary arteries are clear at 62 years old despite higher than acceptable LDL lower than normal triglycerides and an overall cholesterol score of 260
If you're concerned about bone density then why are you cutting out dairy products? Those are one of the best sources for the calcium we need (although it is possible to get enough from other foods or supplements).
Personally (not the parent) I'm vegan for moral reasons, so I'm being vegan despite (not for) it's health effects. As every extreme diet, it requires monitoring nutrition intake and occasional supplementation in order to avoid micro- and macroelement deficiencies and health problems.
> Pregnant women have extremely high cholesterol (ridiculously high).
Cholesterol levels rise during second and third trimesters, but it’s not true at all to say that all pregnant women have “ridiculously high” cholesterol. Around 24% of women who have normal range cholesterol will go over the normal range for a few months, but it’s not accurate at all to say they all have “ridiculously high” cholesterol
Cholesterol metabolism is related to hormones that change during pregnancy, so downstream fluctuations in cholesterol aren’t surprising. Do not mistake this for intentional evolutionary pressure to increase cholesterol.
> if evolution designed pregnant women to have high cholesterol, then cholesterol cannot be the poison it's made out to be.
This is an incredibly pseudoscientific way of thinking. Pregnancy puts many pressures on the body, not all of which are good.
Did you know that blood coagulability also rises during pregnancy, which is clearly linked to cardiac events. There is an increased risk of cardiac events during pregnancy.
Saying “X happens during pregnancy therefore X must be good” is an extremely unscientific and uninformed take. I’m not surprised it’s being leveraged by the cholesterol truthers, but it’s wrong. This is the level of reasoning that seems to appeal to people on TikTok and Twitter who consume feel-good science in 15 second clips, but it makes anyone who has read any actual research on the subject depressed at how susceptible people have become to bad science that is dangerous to their health.
> They shot up after I started eating a lot of non-veg food. And after they shot up, I stopped having depressive episodes.
do you know the parable of the drunk gentleman looking for his keys under a streetlamp at night? a policeman asked him where did he drop his keys, he pointed at a dark alleyway further away, so the policeman asked why he didn't look there instead, he replied "well there's no bloody light over there".
is it possible that you were deficient in some other nutrient, possibly even a trace one like some metal ion or maybe just some amino acid, and that's what caused the improvement in symptoms when you started eating flesh again? is it possible that you simply enjoyed the taste and then felt better about yourself? or any number of other changes in your life at the same time - taking more time cooking your meals, learning new recipes, trying new spices with it, etc?
There’s lot of evidence that excess sugar intake like modern humans do causes issues, especially diabetes, over a long time in a large percentage of people. There’s very little about seed oils though and that’s 90% internet hype
I do not know how much truth exists in the theory that an excess of saturated fats is harmful, but I have acted based on this theory and it was very beneficial for me.
A few years ago, I have been diagnosed with incipient atherosclerosis. This was an unpleasant surprise for me, so I have immediately made serious changes in the food that I eat.
At that time, I was eating very high quantities of dairy, which has a high proportion of saturated fat.
Because I could not see any other factor that could cause the atherosclerosis, I have eliminated dairy from my food and I have changed completely the composition of the fats contained in my food.
I eat only food that I cook myself, so I know exactly which is the composition of the fat contained in it. Nowadays, at least 90% of my daily intake of fat comes from a combination of oils that I use when cooking food (typically 60 mL of extra virgin olive oil + 20 mL of cold-pressed sunflower oil + 10 mL of cod liver oil + 1 drop of an oil containing D3 and K2 vitamins).
Instead of any other kinds of dairy, now I use only a cheese substitute that looks and tastes like melted cheese, but it is made from whey protein concentrate (which has almost no fat) mixed with some vegetable oil and a few other ingredients for better flavor.
After changing completely the fatty acid profile of my fat consumption, after a year the symptoms of atherosclerosis have disappeared and there have been also other very noticeable signs of improved cardiovascular health. For instance, previously, I had cold feet and when sleeping I had to take care to keep them warm. Some months after changing the diet, they had become warm (presumably due to improved blood flow) and I have no longer needed any protection against lower temperatures.
So my diet change has very certainly improved a lot my health in a relatively short time of no more than a year, and that has persisted for the last three years. I cannot know if this is really caused by the change in the fatty acid profile, but I cannot see any other significant difference, except if the abundant dairy that I was eating before contained some other harmful substance or if the significant increase in the amount of eaten EV olive oil and cold-pressed sunflower oil has provided some benefits beyond the better fatty acid profile.
Logically, it is plausible that a reasonable amount of saturated fat, which is correlated with the amount of physical work, should not have any harmful effect.
As long as you burn enough calories daily to use all the fat intake for energy, it should not matter if that fat is saturated fat. However, when the fat is not completely used and some of it is deposited, then it is plausible that it is preferable if oleic acid (mono-unsaturated fatty acid) is the most abundant in food, because in normal conditions this is the most abundant fatty acid in the human reserve fat. When other fatty acids are much more abundant than oleic acid, they must be processed and converted before storage and the capacity for the conversion may be overwhelmed.
The negative connotations for "seed oils" are not applicable to all seed oils, but they refer only to the seed oils where linoleic acid is the most abundant acid.
Linoleic acid is an essential nutrient, but the need for it can be satisfied with 15 to 20 mL per day of a suitable seed oil, like sunflower oil. A greater daily intake than that can cause problems, because the excess linoleic acid must be converted into other fatty acids and also because some of its derivatives have physiological roles for which an excess quantity is not desirable.
Given these, it seems plausible that some fat composition is preferable to others. Like I said, I have acted on this assumption and it has worked very well for me, even if the real mechanism cannot be known, at least not yet.
Glad to hear you’ve improved your condition. The evidence suggests that crossing the 10% total energy as SFA threshold increases CVD incidence. There is no evidence (that I’ve seen) than “using up” this energy changes this risk factor.
Obviously the resulting obesity from consuming excess calories is a risk factor for CVD in itself, but the body of evidence would suggest that someone consuming >10% E from SFA, even if they’re in caloric equilibrium, will be at greater CVD risk than someone consuming less, all else held equal.
The main mechanism by which SFA is thought to increase CVD risk is by downregulation of LDL receptors, which occurs during the digestion/absorption of SFA, and is not a result of excess SFA hanging around in the body in some way. If you consume SFA, this pathway will be in play, regardless of how much is burned vs stored.
There’s no good evidence that seed oils/linoleic acid, refined or not, pose a risk for humans. There’s a lot of talk on the subject about on social media, but it’s almost entirely speculation based on animal studies.
I once bought the anti seed oil line, but on closer investigation of the evidence I changed my view and have replaced most of my SFA intake with MUFA/PUFA, mostly in the form of canola and olive oil.
> "it seems plausible that some fat composition is preferable to others."
However, it seems very implausible (or impossible) that humans evolved to need, or benefit from, industrially processed sunflower seeds and olive oil.
How has the total fat in your diet changed? I find it much more plausible that dramatically reducing cheese, cream, whole milk and full fat yoghurt has helped, than that replacing 20mL of cream with 20mL of sunflower oil has helped. It sounds like you have reduced fat overall - why then attribute the benefit to the vegetable oils / fat profile, specifically?
High cholesterol and heart attacks are common in my family. This year, after my dad had intensive open heart surgery, my doctor recommended trying a strict plant-based diet for 90 days with a blood test before and after. She had been studying medical journals on the topic primarily from Canada (she said it’s easier to find medical research not funded by corporations there).
Before the doing the plant-based diet, I had such high cholesterol that I would have needed to start taking statins before age 35. After the 90 day diet experiment, my cholesterol dropped by 130 mg/dL. I no longer need to be put on medication, and am within a healthy range.
I got a high LDL reading of about 200 (this is like top 3% percentile, if I remember correctly). I panicked and switched to an extremely low fat vegan diet, and I couldn't handle waiting so I paid to have my LDL tested again. My LDL had dropped to 130 after one week on that diet.
For me, at least, saturated fat is the most important nutrient I can monitor and avoid. Low saturated fat, high fiber is the diet for me.
I wasn't able to keep the vegan diet, but it was worth trying for a time because I learned some new recipes and new habits.
This past year I switched to a whole foods diet. I eat eggs, whole milk & cheese, veggies, fruit, white meat, saturated & unsaturated natural oils (nothing manufactured like margarine or anything hydrogenated), root veggies (potatoes, sweet potatoes, turnips), beans/lentils (I'm not afraid of soy based things) grain based breads including whole wheat, whole wheat pasta. I tend to avoid red meat (pork and beef). I quit fast food and anything I suspected of a manufactured element. I was bordering on high cholesterol and pre diabetes. Since then I've dropped 35 lbs and everything is back in the normal range. I don't think you have to go vegan, just get away from all the over salted, over manufactured, sugar "enhanced" garbage. We're omnivores, I think we have the machinery to process normal foods. I admit this worked for me and may not work for everyone. The only "vice" I allow myself is a couple of diet cokes a day, but most days it's just coffee. I only will have a drink or two socially on the weekend and tend to stick to wine or clear spirits and lime/lemon.
For me it was both.. I had pretty bad BP and high enough cholesterol to that my doctor wanted me on a statin. Now my BP is normal, and my cholesterol is in the "low risk" range. My doctor said she'd never seen such an improvement before.
In my case it was not the suggestion of a doctor, but rather dating and now marrying a vegan. I converted to a plant based diet starting with eating plant based just with her, and then I became fully vegan for health reasons.
For what it’s worth, the linked article does not dispute that diet can affect blood cholesterol, but does argue that it doesn’t necessarily equal long term health.
> In other words, although diet could successfully lower blood cholesterol, this reduction did not appear to translate into long-term cardiovascular gains.
That said, as other commenters here have highlighted the author of the study has a spotty track record so, uh, big grain of salt.
> Hen tested (via ultra fast CT scan) the blood flow after the experiment -- there was no change.
> It may sound depressing
I think this is a fundamental misunderstanding of the purpose of enforcing low cholesterol.
The goal would be to prevent further damage and restriction. By all accounts that test is a positive result.
Atherosclerosis is correlated with lifetime exposure to high cholesterol. Once you reach the point of having open heart surgery for severe problems, the goal is to slow further progression as much as possible.
Hoping to reverse a lifetime of accumulated exposure to high cholesterol with 7 years of slightly below average cholesterol just isn’t going to happen. Stopping further progression is great though!
Before, I ate low sugar / carb and high on cheese, meat, whole milk, yogurt, and veggies (close to keto). Now I eat a lot of rice, beans, while grains, and veggies. I’m trying to figure out how to get enough protein though, that’s the trade off.
Not OP, but I recently discovered that I have moderately high lipoprotein-a levels and decided to try to reduce my LDL as a result. I cut most eggs, all butter, all full-fat milk, almost all cheese, and switched from whole to skim yogurt. My LDL dropped about 20% between the beginning of August and the middle of October.
This advice has always come off as paternalistic to me, like the emphasis is on people just not being able to control themselves or something.
The first part is obvious.
The second part smuggles in a fundamentally incorrect take on the "eating too much"/obesity problem, namely that it has something to do with willpower: including "not too much" in the advice implies that we need to be told not to eat too much, but that a diet that naturally induces overeating is otherwise OK.
The third part is arbitrary and unfounded, and if you ignore it you can ignore the second part as well: get some good fatty meat on your plate and you can safely eat to satiety.
Is it, though? It seems like many struggle with the first part.
Does snacking on a vending machine Duchess Honey Bun or a sleeve of Oreos qualify as "eat food?" How about popping open a cup of instant ramen or microwaving some frozen taquitos? I'd call all of that eating junk, but I think that's the root of the issue.
No I guess there must be some people for whom it isn't obvious. I was kind of assuming the intended audience for the advice was people who are interested enough in diet to look at a book on nutrition, for example, not people who just eat junk without thinking about it.
But yes for those people I do think the "eat food" thing should be emphasised and laid out in more detail, maybe. Hard for me to have an opinion there as I just can't put myself in the shoes of someone who eats that kind of stuff.
I don't think of the second part being about self control and obesity, to me it's just a reinforcement of the idea that each person has different caloric requirements and you should respect your own needs. Of course it's vague so open to interpretation.
The third part feels as arbitrary and unfounded as any other dietary advice I read, so I'm inclined to take the simplest advice available.
To be fair, Pollan would specifically not consider a bag of potato chips food. It's not included here but he specifically is talking about "real" food and not ultra processed snacks, etc.
I think it's still an oversimplification - people with large amounts of muscle mass, low body fat, and high levels of daily physical activity just don't get a lot of the same metabolic diseases even if they eat huge amounts of animal protein, outside of really poor genetic luck (or complications related to steroid use, etc.) - but it's a pretty good starting point vs. the modern diet.
If he has his own special meaning of the common word "food", then it's no longer a spiffy quote. And now you need to get into all the nitty gritty of this recommendation to actually take any advice from it.
Even this term "ultra-processed" is highly suspect when you start investigating it more deeply. Plenty of traditional foods are quite processed - bread being one of the oldest. Is it better to eat 200g of bread (artisanal, wood fired, using traditionally-milled non-GMO pesticide free grains), or a steak?
The definition I've heard of his for "food" in this sentence was "things your grandparents would recognise", although by this point it might be "your great-grandparents".
There is no such thing as scientific consensus. In a 2003 lecture at the California Institute of Technology Michael Crichton said, "Let’s be clear: the work of science has nothing whatever to do with consensus. Consensus is the business of politics. Science, on the contrary, requires only one investigator who happens to be right, which means that he or she has results that are verifiable by reference to the real world. In science consensus is irrelevant. What is relevant is reproducible results. The greatest scientists in history are great precisely because they broke with the consensus. There is no such thing as consensus science. If it’s consensus, it isn’t science. If it’s science, it isn’t consensus. Period." https://www.aei.org/carpe-diem/michael-crichton-explains-why...
I hate this Crichton quote so much. It gets thrown around all the time and no one thinks about how demonstrably false it is. Science obviously has plenty to do with consensus.
When an evolutionary scientist publishes a paper, do they have to reference or recapitulate the theory of evolution? No, because that position is scientific consensus. Ditto for the hypothesis that smoking increases cancer risk.
Consensus doesn’t mean “impossible to change”, it just means it is generally agreed upon. If some evidence about smoking and cancer comes out down the line, the consensus can change. It’s still the consensus, though.
You seem to hate lots of things and this subject makes you desperate to call yourself a specialist. There are 3 days you have been desperately trying to shutdown discussions in this thread. What is your problem?
In what way am I shutting down discussion? I’m just participating in it. There’s a great deal of misinformation on this thread that could lead people to make lifestyle decisions that would put them at risk. Don’t see why there’d be an issue in discussing the evidence behind this misinformation so people can come to their own, hopefully informed, decision instead of a misinformed one.
I’m not interested in poor attempts at mind reading (“this subject makes you desperate to call yourself a specialist”) but I’m happy to discuss the evidence on this subject if you’d like.
Although the author of the article appears to be controversial, I am concerned that none of the responses citing her controversial nature are actually rebutting anything in the paper.
I believe most of what was written here appears to be factual. What am I missing?
(Someone attacking the currently held beliefs taught by science is by nature controversial. More important question is whether they are pointing out flaws in those beliefs. )
FWIW I think contrarian scientific viewpoints are important if they're rigorous, and Teicholz makes a reasonable case for the viewpoint that saturated fat reductions are unrelated to mortality.
However, I don't think Teicholz herself is really being entirely "factual", bringing purported conflicts of interest into her discourse when it goes on on both sides. People have pointed out that her organization has its own history with this problem: https://thehill.com/blogs/congress-blog/healthcare/257353-co....
That isn't addressing your question but I guess I disagree that Teicholz is just dispassionately presenting a rigorous argument, even if I find it compelling myself. Some of what she writes is sort of misleading (as that linked piece points out) even if I think her most cogent arguments are reasonable.
A lot of her arguments hinge on how you see things like the Cochrane meta-analysis. Her sensitivity analysis with colleagues is compelling in dismissing the CVE result in that meta-analysis, but at the same time you can whittle away any effect if there's not a big enough N (in a sort of inverse form of p-hacking), so I'm not sure I'm entirely convinced either.
Also as that piece points out, Teicholz seems dismissive of anything that's not mortality as an outcome, which I'm not sure I agree with.
I'm sympathetic to Teicholz's arguments, I guess I just feel like she doesn't make them any more convincingly to me than those she criticizes.
At this point for me personally my reading of the literature is that a lot of things are related to individual physiology, and I'm skeptical of a lot of blanket recommendations regarding nutrition. Reducing saturated fats has been good for me personally so I stick with that.
I think dietary matrix is also important, so dietary patterns can be more useful than focusing on individual nutrients. Hard cheeses seem to be associated with positive health outcomes despite their SFA content, yet for butter the inverse is true.
I think what I find frustrating about Nina is the number of fairly basic misreadings of the evidence she makes, despite having been corrected on it (and admitting the error) multiple times. She also grossly mischaracterises the results of studies repeatedly, so misleads laypeople into thinking the evidence base is more heterogenous than it really is.
Additionally, she frequently makes contradictory statements regarding her own epistemology. For example, she states that observational studies can “only show association” and therefore cannot be used for causal inference, yet her twitter account is full of examples of her using observational data to draw causal inferences.
You mention a sensitivity analysis of Hooper that she conducted. Do you have a link to that?
As for the claims about RCTs, she straight-up lies, quote:
“including by the prestigious Cochrane group, most recently in 2020. Altogether, >20 review papers, including umbrella reviews, have been published, with the vast majority concluding that the data from randomized, controlled trials do not provide consistent or adequate evidence for continued recommendations limiting the intake of saturated fat”
So what did the 2020 Cochrane paper actually say? Let’s look:
“ There was a 17% reduction in cardiovascular events in people who had reduced SFA compared with those on higher SFA”
“When we subgrouped according to replacement for SFA, the PUFA replacement group suggested a 21% reduction in cardiovascular events”
So she invokes the respectability of Cochrane yet claims their findings are incorrect, and tries to pass it off as a Cochrane reviewing showing that saturated fat is unrelated to heart disease? This alone should tell you everything you need to know about Teicholz. She relies on her audience not knowing the papers she references, because she misrepresents them to fit her agenda. She’s completely dishonest.
You picked out the one result in five or six from the summary of result that supports the reducing saturated fats and ignored the rest that said it disnt matter (and of those result all cause and cardiovascular mortality were in there in the saturated fat doesnt affect category). There are straight up lies here but they are in your response.
A null finding in a study does not mean it “doesn’t matter”. Let’s take an extreme example: we want to know if exercise reduces mortality, so we randomise one arm of a cohort of 20 people to an exercise regime, while the other arm does nothing. After four weeks, we compare the death rate in each group. There’s no significant difference.
Does this mean exercise “doesn’t matter” for mortality, or it’s in the “doesn’t affect category”? No, of course not - the finding was null because the timescale was too short and even then, the statistical power from a cohort of 20 is going to be very low.
Likewise, if you look at the study characteristics, most of the studies were too short to find a significant outcome on an insensitive endpoint like CVD mortality or ACM. FWIW, Dayton 1967 had a followup of 8 years and did find significant increases in mortality endpoints in the SFA group, but those results are pulled towards null in the meta summation by the other, shorter studies.
CVD events are more sensitive because they don’t require the participants to die of a heart attack in order to register as a data point.
So no, there’s no lying or cherry picking going on here. In order for that to be the case, you’d have to argue that angina and non-fatal heart attacks are not negative health outcomes. If they are, then it’s demonstrably the case that SFA consumption is associated with negative health outcomes, and Nina is telling porkies.
As for your accusation that I’m lying - what false claim did I make? Be specific.
for cvd risk mortality if you exclude the largest single study that also had a long duration (WHI 2006) it made CVD risk mortality significant, so one of those long duration studies is dragging the results the opposite way.
We need to remember we are talking about relative risk so what does a 17% increase correspond to? 15 more incidents per 1000 participants with a ci of 24 to 2 incidents per 1000 participants among studies that were mostly moderate to high risk individuals. It's a rounding error on a low risk event that is probably an even lower risk event for most of the population. If you look at something that actually exists and is relevant you will see 100% plus changes to relative risk. All cause mortality relative risk is 2.29 in this study on the effect of smoking on women, for example: https://pmc.ncbi.nlm.nih.gov/articles/PMC6219821/
Figure six explores saturated fat cut offs and all but 2 of the events trend down for the last observation which is only at 13% energy from saturated fat, probably need to look at higher saturated fat levels to make sure the chart isn't an upside down U and we aren't stuck in the most deadly part of the curve arguing about whether we should cut more when we could increase consumption more to solve the issue.
> for cvd risk mortality if you exclude the largest single study that also had a long duration (WHI 2006) it made CVD risk mortality significant, so one of those long duration studies is dragging the results the opposite way.
Right, and the proposed pathway by which SFA increases CVD risk is via increases in ApoB/LDL-c. What LDL-c differences did they achieve in WHI 2006?
Additionally, the substitution is important. DGs recommend replacing SFA with PUFA, whereas in WHI the intervention group largely replaced SFA with CHO. Interestingly, the control group had higher levels of PUFA and MUFA, which may also explain the paltry change in serum cholesterol.
If you want to claim that 15 more incidents per 1000 of a disease that is one of the top killers in the western world is a rounding error, then go for it. I don’t think that’s a reasonable position, personally.
As for the speculation about higher levels being healthy - speculate away, but I don’t see why anyone should believe it’s the case when
a) it runs contrary to the body of evidence on the subject
b) there’s no actual evidence backing up that speculation.
But your example is not reflective of the study. Are you saying that the 17% reduction is for some reason significant but the other ones, all of which would inconveniently disagree with the result you want, are not, even though they are in the same study?
IOW, you're saying that among the study results, all that agree with your POV are valid, all that don't are invalid. That's quite some bias there.
The answer to your question is literally answered by my comment that you’re replying to. Frequentist statistics cannot be used to affirm the null. That is, you cannot say “cardiovascular deaths was not significantly associated, therefore SFA does not cause CVD mortality”.
So I’m not disagreeing with or omitting anything in the study. The study said no significant association with CVD mortality. Ok, no problem. That doesn’t mean SFA doesn’t cause CVD mortality.
However, the study does show that SFA is associated with CVD events. So there’s a significant finding. It’s not cherry picking, this is just how frequentist statistics works.
Oh, I see. Unusual use of language, but sure, that’s fairly accurate.
That said, I’m here to discuss the article and any related claims around the healthfulness of saturated fat. It may be that someone has some insight that I’m not aware of and I gain some additional knowledge. So I’m not purely here to point out misinformation (though there’s lots of it here!).
I'm surprised there's no discussion here about the inflammatory role of vegetable oils (aka seed oils). I think it's likely that these oils are actually causing inflammatory diseases generally, through a mechanism that isn't understood.
Anecdotally (fwiw), in my household my daughter had been struggling with severe rashes that appeared to be triggered by food. An elimination diet caused us to conclude that she is highly reactive to vegetable oils (canola (rapeseed) oil, sunflower seed oil and soybean oil have all been introduced as food challenges and all produce a reaction within 3-6 hours)
We currently cook only with tallow and her symptoms have improved considerably (we tried olive oil and avocado oil for awhile but it was unclear on her)
As a challenge to anyone objecting to this comment, I ask you to look up the history of canola oil and say whether such a substance would be accepted into the food supply today.
And my question to everyone is, what is the mechanism by which seed/vegetable oils could lead to rashes? The only theory I've heard has been around omega-3/6 balance, but I am looking for alternative theories. I conjecture it has something to do with heating, as she isn't affected by ice cream containing these oils.
The idea that seed oils cause inflammation is largely based on mechanistic studies that don't seem to bear out when the larger and more complex ecosystem of our biology is introduced.
> And my question to everyone is, what is the mechanism by which seed/vegetable oils could lead to rashes? The only theory I've heard has been around omega-3/6 balance, but I am looking for alternative theories.
Canola oil has high levels of omega-3s. If it was the omega-3/6 balance theory then it would be one of the best options for oil use.
Individuals can have bad reactions for a variety of reasons, of course. And there is a very high correlation between seed oils and food that is just generally shitty for you, so if you cut them out of your diet you are also cutting a lot of garbage out, which will likely have an impact independent of the oils themselves, and this is likely what drives a good portion of anecdotal positive experiences.
There are countless peer reviewed studies and articles on both sides of the argument sure - but the sheer volume of anecdotal evidence and the overwhelming consensus across 100K and even 1M+ subreddits against seed oils is unique. You don’t see this level of unified backlash against most other everyday substances.
Tbh the evidence in the literature on seed oils is actually overwhelmingly in their favour. Studies that find in the opposite direction are few and far between, comparatively.
So then we’re just left with “lots of people on the internet believe a thing to be true, surely there’s something in it.”
Hopefully I don’t need to come up with a counter example here, you can just see how poor an argument this is.
Let’s not forget the entire field of dietary fat and heart disease was dead wrong for decades while the real culprit was sugar. Alzheimer’s research? Decades of faked studies, costing billions. Peer review is hardly the gold standard if universities are dependent on corporate and government money.
The flood of case reports online about seed oils causing issues makes it obvious there's a problem. Ignoring this isn’t just unwise it’s willfully blind.
At best, seed oils might work for some but they’re clearly harmful to a large portion of people.
Not sure what you’re basing that claim on. There are boatloads of data suggesting that replacing SFA with PUFA leads to a 20-30% reduction in CVD events.
Does added sugar seem to be a risk factor too? Sure.
There are floods of case reports online about vaccines causing autism, but I’d hope you wouldn’t think that it’s obvious there’s a problem there too? Such reports should not be the driver of our reasoning when we have high quality studies on the question.
When the public raises concerns or points out issues, it’s important not to take it personally or make it political. These are valuable data points that warrant investigation.
Personally regarding autism, I believe neurotoxins might be contributing to inflammation in the brain, while nutrient deficiencies could be affecting cognitive function, with the root cause of both issues being a fungal infection of the gut, related biofilm formation (blocking nutrient absorption in the small intestine which is where b1 is absorbed) and intestinal permeability. Cross-examine the symptoms of Wernicke encephalopathy (b1 deficiency of the brain) and autism and it is rather surprising how similar these are. Its the rule that the majority of autistic people have small intestinal problems often incorrectly blamed on the brain. The fungal infection is simply an overgrowth due to low number of bacteria. Autistic people have been found to have extremely low numbers and types of bacteria in their microbiome.
Do MMR vaccines have anything to do with this? I would hazard a guess that people with the problem I just mentioned may be at increased risk of adverse events occurring after MMR vaccine intake. Their bodies are already in trouble and MMR vaccines are the straw that breaks the camels back and these case reports online regarding autism and MMR vaccines are entirely valid and useful but the scientific community are unfortunately individually too compartmentalized in their trained medical specializations be it brain, digestive system, infectious diseases and such.
It sounds like you find speculation based on anecdotes more compelling than evidence from higher up the evidence hierarchy. That’s obviously your preference and you’re welcome to it.
When I’m discussing an issue and my interlocutor ends up having to bite a bullet like “I think MMR vaccines might contribute to autism based on speculation and the reports of people on the internet”, then I’m happy to take my hands off the wheel - it’s now clear their standards of evidence are very low.
Since you’ve openly admitting to it then I’ve achieved what I came to do:
1. See if I’m wrong in my view (it doesn’t seem like I am)
2. Ensure that anyone reading can see that in order to believe seed oils are harmful, one has to have a completely wild epistemic framework. You’ve admitted you think MMR vaccines might contribute to the development of autism based on a completely evidence-free view that such vaccines might be “the straw that breaks the camels back.”
I think this conversation has probably run its course - you believe things based on what I would consider anti-scientific reasoning, as you’re welcome to do. I don’t think wild speculation is a useful tool for making inferences about the world. We’re unlikely to bring each other round to our own views on this, I suspect.
There is no evidence that Nina Teicholz should be given the benefit of the doubt when it comes to her arguments and plenty of evidence that she should be treated with skepticism.
> Except the human studies we have suggest that seed oils are probably not inflammatory. A few examples are listed in this video: https://www.youtube.com/watch?v=-xTaAHSFHUU
which part of that do you consider bullying? is it any opinion that goes against the underdog?
I don’t know about rashes and reactions. But in health circles, seed oils are generally considered safe and retain higher nutritional value if cold pressed. This makes them suitable at least for salads, but not frying.
> As a challenge to anyone objecting to this comment,
You are free to comment whatever you want, but I don’t see any evidence to support your hypothesis on a population wide basis.
>I ask you to look up the history of canola oil and say whether such a substance would be accepted into the food supply today.
If you are referring to genetically modified rapeseed plants to be herbicide resistant, then it would most definitely be accepted into the food supply today. Genetically modifying plants still happens all over the world.
It's funny, you're the only person who replied who mentioned my challenge, and it's clear you aren't familiar with the history of canola oil, nor are any of the other people replying. You "don't see any evidence" sounds so authoritative, like you are familar with the topic!
The relevant modification is with respect to erucic acid, which pre-modification, was 50% of the content of rapeseed oil, and which provably causes heart lesions in mammals.
There's no way that someone today could take a plant that naturally produces a useful but toxic industrial lubricant, modify it to be less toxic, and then start feeding it to humans. But in the 1970s you could still get away with stuff like that.
> There's no way that someone today could take a plant that naturally produces a useful but toxic industrial lubricant, modify it to be less toxic, and then start feeding it to humans. But in the 1970s you could still get away with stuff like that.
Why? I am not seeing the causation. Tomatoes came from a family of plants that are not edible, and now they are consumed worldwide.
Could it be some other chemical to blame that you are exposed to day-to-day? With so many additives, preservatives, colorants, detergents, cleaning products, cosmetics, perfumes, paints, disinfectants, plastic packaging, synthetic clothing, herbicides, pesticides, glues in furniture, car exhaust, rubber dust, and other chemicals around us, canola oil would not be my first guess of something causing rashes or allergies.
Although not probable in this case as far as I know: if vegetable oils seem to cause problems for you, you should be aware of sitosterolemia (phytosterolemia), caused by rare mutations in genes ABCG5 and ABCG8. It needs to be homozygous for symptoms.
(I have it, discovered by a full-genome sequencing by myself, accidentally around the age of 50.)
wow, that's extremely useful and interesting! Can you say more about your condition? Did you have any symptoms? Which company did you use for the full-genome sequencing?
It looks like the treatment involves avoiding vegetable oils, but in her case there are no visible xanthomas.
You said that you suspect it is the heating of the oils, but even the oil found in ice creme has been heated somewhere in the process unless it is cold pressed. Can she eat sun flower seeds, olives or avocado without a reaction? Have you tried coconut oil as an alternative?
Paul Saladino advocates a theory that humans cannot handle a lot of linoleic acid in the diet: it decreases the performance of membranes, particularly of mitochondria (which in turn causes insulin resistance, obesity and other problems cause by chronic lack of ATP).
Saladino says that it would have been impossible for an ancestral human (particularly in Northern Eurasia where meat from grass-eating animals constituted the majority of calories) to get more than about 3% of calories as linoleic acid whereas the US average is now about 11%. Sunflower seed oil for example is 67% linoleic. corn oil, 53%, soybean oil, 52%. (Most of the omega-6 fatty acid in the human diet is linoleic acid.)
Paul Saladino isn't a credible source of information or theories. He's a non-practicing psychiatrist and social media influencer who's gotten rich making contrarian videos and selling supplements.
Watching Youtube videos can make us believe we understand a topic better, but that's not necessarily the case. And without a good understanding of that topic to begin with, it's hard to know why we're wrong.
Imagine watching a super compelling Youtube video explaining why dinosaurs never existed, and so you now think that's a credible hypothesis. You would probably know more facts about dinosaurs and paleontology than the average person, but I'd argue that your understanding of dinosaurs has actually gone down.
I see a similar thing happening here. You and Paul are able to cite lots of facts about Linoleic Acid. But there's a whole body of experimental human research showing that, if anything, LA-rich oils probably slightly improve insulin sensitivity, inflammation, lipids etc. But Paul either isn't aware of this or chooses not to show you because it contradicts his claims. So you're left with the wrong impression about LA and seed oils, despite thinking that your understanding has gone up.
To be fair, there's a difference between "people who make YouTube videos for a living" and people who make videos to spout contrarian "theories" so they can sell snake oil.
My understanding is that just vegetable oils are generally bad for cooking because of how they retain heat. Even if they have a high smoke point, it's easier for them to get to it.
Have you doing that she has the same issue with coconut oil? Specifically, the saturated ones that come in a jar?
The link between saturated fat and LDL cholesterol is extremely clear. Far from coming from low-quality studies, the relationship has been observed in RCT metabolic ward studies. The best data you can get on the acute effects of diet and we are talking hundreds of these experiments all observing the same relationship.
Does high LDL cause heart disease? That is probably less clear, I am not a scientist, so I really don't know what the latest is on this. LDL is present in Atherosclerotic plaques so it's not crazy to think it plays a role. If I was to guess, as a complete non-expert, low-fiber intake and inflammation probably play a role in turn LDL into atherosclerosis.
> "In the context of cardiovascular disease, AGEs can induce crosslinking of collagen, which can cause vascular stiffening and entrapment of low-density lipoprotein particles (LDL) in the artery walls. AGEs can also cause glycation of LDL which can promote its oxidation. Oxidized LDL is one of the major factors in the development of atherosclerosis."
> "AGEs have been implicated in Alzheimer's Disease,cardiovascular disease, and stroke. The mechanism by which AGEs induce damage is through a process called cross-linking that causes intracellular damage and apoptosis."
(AGE is a bad search term but the term glycotoxin is used as well.)
For me personally there's a very clear link between saturated fat and blood serum LDL and triglycerides: I had very high levels of both despite exercising regularly, switched to a low saturated fat diet with minimal other changes, and my LDL and triglycerides dropped enormously and are now in the "good" range. I don't know enough to know whether cholesterol actually increases heart disease risk, but for me personally there's a clear diet link between saturated fat and LDL cholesterol + triglycerides. YMMV! I suppose something else in the high saturated fat diet could have been causing the problem, but it certainly seems like a good proxy metric for me at least.
> "switched to a low saturated fat diet with minimal other changes"
Does that mean switched fat to non-fat, or switched saturated fat to other types of fat? It seems that would be an important distinction for threads like this.
It’s probably better off if we don’t give a handful of biased people control over the diets of millions. Maybe it is better to make decisions locally from personal connections. Maybe the transmission of knowledge through local groups had the positive effect of a sort of charcoal filter for knowledge. A bit of humility could be good for us. We spent all this time building and abusing a global authoritarian control network without ever considering the side effects.
> the paradoxical epidemiological observation that French people have a relatively low incidence of coronary heart disease (CHD), while having a diet relatively rich in saturated fats,[1] in apparent contradiction to the widely held belief that the high consumption of such fats is a risk factor for CHD.
"Intersalt, a large study published in 1988, compared sodium intake with blood pressure in subjects from 52 international research centers and found no relationship between sodium intake and the prevalence of hypertension. In fact, the population that ate the most salt, about 14 grams a day, had a lower median blood pressure than the population that ate the least, about 7.2 grams a day. In 2004 the Cochrane Collaboration, an international, independent, not-for-profit health care research organization funded in part by the U.S. Department of Health and Human Services, published a review of 11 salt-reduction trials. Over the long-term, low-salt diets, compared to normal diets, decreased systolic blood pressure (the top number in the blood pressure ratio) in healthy people by 1.1 millimeters of mercury (mmHg) and diastolic blood pressure (the bottom number) by 0.6 mmHg. That is like going from 120/80 to 119/79."
7.2 grams a day is still a lot. Low-sodium diets aim for less than 3 grams a day, and it is not that difficult to go even lower. Whether a near-zero sodium intake is good or not, it's another can of worms, but a study looking at a huge-salt diet vs. a high-salt diet does not look very useful.
“The French paradox” is preposterous. Rather than re-assessing the “low fat” model, the approach was to call French nutrition a “paradox”. Resolving the paradox itself should have been done before presenting the low fat model as a fact.
I think it's a combination of low-stress lifestyle and demographics. Or differences of reporting. I am skeptical that there is a genotypical protection to heart disease unique to the French.
Yet within the French population, higher consumption of SFA is associated with higher CVD. So the French paradox doesn’t really seem to be any such thing.
Because LDL drops when you have cancer, or a heart attack. That is, the U shape is a result of reverse causation. When you look at longitudinal data there’s no U shape - it’s straight as an arrow. Higher LDL-c -> more heart disease.
Yes, when we change the URL I almost always post the original link in the thread - I did that at https://news.ycombinator.com/item?id=41957788 but of course these things can get lost in the shuffle
The idea that saturated fats cause heart disease, called the diet-heart hypothesis, was introduced in the 1950s, based on weak, associational evidence. Subsequent clinical trials attempting to substantiate this hypothesis could never establish a causal link. However, these clinical-trial data were largely ignored for decades, until journalists brought them to light about a decade ago. Subsequent reexaminations of this evidence by nutrition experts have now been published in >20 review papers, which have largely concluded that saturated fats have no effect on cardiovascular disease, cardiovascular mortality or total mortality. The current challenge is for this new consensus on saturated fats to be recognized by policy makers, who, in the United States, have shown marked resistance to the introduction of the new evidence. In the case of the 2020 Dietary Guidelines, experts have been found even to deny their own evidence. The global re-evaluation of saturated fats that has occurred over the past decade implies that caps on these fats are not warranted and should no longer be part of national dietary guidelines. Conflicts of interest and longstanding biases stand in the way of updating dietary policy to reflect the current evidence.
Can't tldr this article without including the author's name and reputation, and that many of the representations made are false. In particular, this statement is false:
> [nutrition experts] have largely concluded that saturated fats have no effect on cardiovascular disease, cardiovascular mortality or total mortality
I’ve read that saturated fats from red meat get processed by our gut creating a metabolite called “trimethlylamine N-Oxide” (TMAOs) and that this is what increases one’s risk for CVD.
The book Outlive has a great discussion about CVD and diet. There is a link, and food types matter, but reducing foods to their saturated fat content is of course ridiculous as we now know.
Sort of meta-question: why do nutrition takes from grifters and quacks like this spread so well particularly among the Hacker News community while I see few articles about normal science-based nutrition?
I'm someone who was once taken in by a lot of this nonsense. They're good at finding a handful of studies they can present in a way that seems convincing, and couple that with the general mistrust people have for the modern diet, and you've set the stage quite well. Further prevent people from realizing that no nutritional scientist anywhere is suggesting that the shit we shovel into our mouths daily is the right course of action. Next, present them with diets that necessarily result in caloric restriction, along with cutting out one or two of the half dozen awful things we eat, and have people see personal success in their weight going down, lipid markers improving, etc., from where they were prior when they were eating the absolute worst sort of diet they could.
Now they seem like people who are renegades fighting against the establishment for the good of personal health.
It all unravels once you start really digging in to things, but if you don't have the time or inclination for it, them appearing as a guest on a podcast and presenting you with this snazzy package specifically designed to lead you astray is really coupled with some testimonials from people touting it's efficacy makes a compelling case.
There’s nothing “unmade” in the scientific opinion. It’s her opinion because she insists that saturated fat is good, but provides no scientific evidence. Almost all scientific studies and scientists (including the authors of the few studies she might quote, because she often distorts them including completely presenting the opposite of what they demonstrate) disagree with her saying.
And yeah, she’s not a scientist, does no scientific research herself, and has no particular training in this area.
I'm not sure how we can prevent organizations from being 'bribed' like this, but something has to be done. Misinformation like this has no doubt contributed to the obesity epidemic
The view of SFA consumption as a risk factor for CVD is not the result of bribes, it’s the result of the body of research on the subject pointing in that direction.
It’s rich of Nina to accuse Keys of cherry picking while claiming that there’s no RCT data supporting the diet-heart hypothesis because of the dodgy Hamley meta analysis, while ignoring Hooper 2020, which was far more rigorous and showed a 21% reduction in CVD events when PUFA was substituted for SFA: https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD...
The reduction in that study is 17%, not 21%. And it is 17% of an 8% risk: so, if the study is correct, your risk of CVDs should go from ~9.6% to ~8%. However, this is not associated with a lower risk of all-cause mortality. So even if the effect is real, it seems to be quite small.
No, it's 17% for reduction in SFA. It's 21% for replacement of SFA with PUFA.
Yes, it's not significantly associated with a lower risk of ACM, but that doesn't mean they don't increase ACM risk. It just means that in these relatively short RCTs, a significant finding on a very insensitive endpoint like ACM was not found. That's not surprising, you wouldn't necessarily expect to see such a finding. For that you'd want longer or larger RCTs (unlikely due to cost) or prospective cohort studies (which do show a significant effect on ACM).
The 17% result is for overall reduction of SFA consumption on CHD, and is statistically significant (per the standards of nutrition science). The 21% difference when replacing SFA with PUFA between subgroups is not statistically significant, and neither is the 16% reduction for reducing SFA with carbs, so they should be ignored. The study only finds this modest 17% risk of CHD events from reduced consumption of SFAs.
As noted elsewhere, this is contradicted by other studies, one of which you cite, which find that SFA reduction is not protective if SFA is substituted with CHO (only if it is substituted with PUFA).
Overall, there is no good concluaion to be made, other than that there is a tiny effect from consuming less SFAs, maybe.
Between subgroups is not significant, but the replacement with PUFA is significant in itself.
As I’ve already pointed out to you, that’s not a contradiction when the studies are looking at CHO as a whole and not disambiguating between whole grain and refined carbohydrates.
If you think a 21% reduction in one of the largest killers in the western world is a tiny effect, then that’s genuinely laugh-out-loud funny.
Mechanistically, replacing saturated fats with PUFA reduces the amount of arachidonic acid in cell membranes which dampens excessive inflammatory cell signalling. Here's how that works. "Because arachidonic acid (AA) competes with EPA and DHA as well as with LA, ALA and oleic acid for incorporation in membrane lipids at the same positions, all these fatty acids are important for controlling the AA concentration in membrane lipids, which in turn determines how much AA can be liberated and become available for prostaglandin biosynthesis following phospholipase activation. Thus, the best strategy for dampening prostanoid overproduction in disease situations would be to reduce the intake of AA, or reduce the intake of AA at the same time as the total intake of competing fatty acids (including oleic acid) is enhanced, rather than enhancing intakes of EPA and DHA only. Enhancement of membrane concentrations of EPA and DHA will not be as efficient as a similar decrease in the AA concentration for avoiding prostanoid overproduction." https://pmc.ncbi.nlm.nih.gov/articles/PMC2875212/
The same authors also noted that "The degree of fatty acid unsaturation of mitochondrial membrane lipids has been found to be one of those biochemical parameters that are most strongly correlated with longevity, when different species of mammals and birds are compared, with a low degree of fatty unsaturation being correlated with less lipid peroxidation and a longer normal life-span."
So, mechanistically speaking, replacing saturated fatty acids with PUFAs will dampen inflammatory cell signalling. However, replacing saturated fats with monounsaturated fatty acids will do the same thing without risk of peroxidative damage to cells. Excerpt: "Fatty acid composition in the Western diet has shifted from saturated to polyunsaturated fatty acids (PUFAs), and specifically to linoleic acid (LA, 18:2), which has gradually increased in the diet over the past 50 y to become the most abundant dietary fatty acid in human adipose tissue. PUFA-derived oxylipins regulate a variety of biological functions. The cytochrome P450 (CYP450)–formed epoxy fatty acid metabolites of LA (EpOMEs) are hydrolyzed by the soluble epoxide hydrolase enzyme (sEH) to dihydroxyoctadecenoic acids (DiHOMEs). DiHOMEs are considered cardioprotective at low concentrations but at higher levels have been implicated as vascular permeability and cytotoxic agents and are associated with acute respiratory distress syndrome in severe COVID-19 patients." https://www.pnas.org/doi/10.1073/pnas.2120691119
More info in COVID-19 risk: "Separately, on analyzing global COVID-19 mortality data and comparing it with 12 risk factors for mortality, they found unsaturated fat intake to be associated with increased mortality. This was based on the dietary fat patterns of 61 countries in the United Nations' Food and Agricultural Organization database. Surprisingly, they found saturated fats to be protective." https://www.medpagetoday.com/reading-room/aga/lower-gi/86940
Why would we care about mechanistic speculation from in vitro models when we have evidence from higher up the evidence hierarchy showing direct benefits on human health outcomes when PUFA is substituted for SFA?
It’s like someone providing evidence that exercises decreases mortality risk in humans and countering with “but exercise induces oxidative stress at a cellular level so we shouldn’t do it.”
It’s just turning the evidence hierarchy on its head. I’m curious why you would interpret evidence in this way - why are mechanistic studies with incredibly low internal validity more convincing than RCTs and prospective cohort studies to you?
> not sure how we can prevent organizations from being 'bribed' like this
Statute that makes it fraud for a doctor (or anyone with medical certification) to make unsubstantiated health claims or strong claims based on weak science.
I find I can eat plants along with my beef, lamb and butter as long as those plants are very low in "carbs": fennel, daikon radish, cauliflower, cabbage.
Although plants make up only a small fraction of my caloric intake, because they are much less dense in calories, they make up a large fraction of the mass (and volume) of the food I eat.
Those veggies are mostly fiber. Fiber is technically carbohydrate (hence my putting "carbs" in quotes earlier), but unlike most of the carbs in the typical person's diet, the fiber in the plants I eat doesn't get converted by my gut or my body into fructose or glucose, so fiber is OK for me to eat.
Most of the plant foods people eat that aren't loaded with the kind of carbs that get converted into fructose or glucose are loaded with oxalate, which I have tentatively concluded is a problem for me. Cabbage, cauliflower and radishes are extremely low in oxalate, for plants. Fennel is not particularly high, but also not particularly low in oxalate, so on days I eat fennel I take measures to encourage prompt elimination of the oxalate (i.e., I eat fennel only during the first meal of the day and I make sure to get plenty of calcium every meal that day).
This article is about fats, so what is the relevance of your comment?
Anyway, did any of these people try reintroducing plants in their diet? If not, at most we can say that a change in diet caused these improvements. We cannot say that plants are somehow a contributor to disease.
In fact, I've heard the same anecdotes as yours, except the diet change was the exact opposit: People who stopped eating meat and saw incredible changes to their health. These anecdotes and yours have one thing in common: Change.
We have good evidence that the gut microbiome can change its composition very quickly, in the manner of days, based on food intake. It's possible that some part of the microbiota were reduced or boosted as a result of the radical shift in the diet, and that you'd see a similar effect if you went meat -> plants.
If you're a science-minded person, you could try introducing specific things you eliminated, one by one. That is the principle behind an elimination diet, after all. For example, add broccoli for a week and see what happens. If you get worse, maybe it is the plants.
If you stop eating plants and plant based food (eg. Cereals, baked stuff) you end up eating mostly animal fats and protein (and a bit of lactose if you do dairy) so the poster is related
We ended up here after years of trying other things, following scientific method. We've tried various plant based diets, and they did not work for us. Going to a non-plant diet was a radical change for us, having literally tried everything else.
In case you're interested, here's something to watch that will tie in what we're doing and the success we're having with the article.
To be clear, it's quite possible for a temporary elimination diet to aleviate unexplained symptoms, for instance from an unknown food allergy or intolerance. But then you need to slowly reintroduce foods to find which specific food causes the problem, otherwise your diet is bound to be nutritionally deficient. Eliminating all plants from your diet permanently is insane.
I get that alot. If you only eat plants, people think its a bit quirky maybe, but fully accepted. But stop eating them and get great results, people can't handle it.
The reasons one diet is typically accepted and the other isn't is because the two diets are materially different. It's possible to have a nutritionally complete diet of only plants where the vast majority of the nutrients are naturally occurring in the food. The same is not true of a diet without plants; it's not possible to have a nutritionally complete diet without plants without a significant portion of nutrients coming only from supplementation.
They do, as well as (somehow) omnivores that do not eat game animals regularly. All livestock are supplemented so they stay somewhat healthy AND share a fraction of that b12 with you through that steak. Not very far from a supplemented tofu steak IMHO.
While I am extremely skeptical of the healthy-ness of a diet entirely made of meat and other animal products, I'm not sure what particular nutrients you are thinking of. The only thing that animal products don't contain that can be found in plants is dietary fiber, and it's somewhat debatable whether to call that a nutrient. But otherwise, meat and other animal products contain all of the necessary proteins, fats, and vitamins. After all, we all live entirely on animal products for ~1 year of our lives, when we exclusively drink milk.
The problem with meat is that it doesn't contain carbohydrates, which are a cheap source of energy, so the body has to work a lot more to get its energy, and with a lot more by-products. Also, the lack of fiber will significantly alter the gut microbiome, and almost always leads to stool issues.
Perhaps you're not aware that Inuit lived without plants for most of the year and did well?
Maybe take a look at this documentary, which touches on the story of a vegetarian who ended up living with the Inuit and his experiences. It's a good place to start to expand your knowledge.
The Inuit. The Kazakh people. The Sami. (In fact most Northern Europeans had nothing to eat but meat and maybe fermented vegetables for two thirds of the year.) The Masai. The Metis.
Conversely, there has never been a vegan society. Even the handful of vegetarian cultures that have evolved such as those found in India rely heavily on dairy. Humans simply aren't adapted to be vegetarian.
This is just wrong as far as I know. How are you defining complete nutrition and where did you get the idea that you can get it from an all-plant diet but not an all-meat one?
It's true. I ran into a friend of my wife's yesterday who is a nurse. The topic of food came up and I mentioned I haven't eaten any plants in over two years. She snidely remarked "How's that constipation going for you?" She's 150 lbs overweight and looks 15 years older than her age. Meanwhile, I lost 20 lbs and cleared up a bunch of medical problems. (Including constipation.) People love to sit on their high horses and make snide remarks while evidence is staring them right in the face. It's wild.
"Insane" and "gets working results quickly" are not mutually exclusive categories. You can cut off the limbs you don't need to live if you wanted to lose weight too but that's a very poor and rash decision that will be reciprocated by your lifespan and overall health and fitness.
It’s not a healthy long-term diet. But as a treatment diet, going all in on fat and protein absolutely works for weight loss. You’re probably in ketosis, for example.
Getting "off plants" necessarily means getting off processed foods, which is where most of the benefits lie. The "guidelines" in many places aren't strict enough. This is a rhetorical sleigh-of-hand because the unhealthy Americanized/Western diet is not high in vegetables and fiber, it's high in refined carbs and starches, added oil, and sugar, all of which is derived from plants.
An anecdote isn't that persuasive, talk is cheap. Systematic reviews of randomized control trials won't show a carnivore advantage over whole foods. There's no compelling evidence, this is just brushed aside with conspiracies.
Notwithstanding that in the first place there's evidence that whole foods (plant-based or not) diets can improve life extension and profile.
I'd prefer a higher quality source than a youtube video, and once again, I don't put much stake in an anecdote. It's possible to have a starch-heavy low quality diet even with lower amounts of processed foods. Carnivore is an elimination diet; it has one food, meat. One could opt to survive on nothing but potatoes but that doesn't make it a balanced diet. Meat by itself provides a broader range of nutrients, so the proper comparison would be with e.g. a composition like the mediterranean diet. To date the benefits of including whole foods are thoroughly documented; extraordinary claims require extraordinary evidence.
"argument from silence" is a funny way to say there's no evidence.
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If you’d like to take a look at a critical review of her other work on this topic, I’d highly recommend this damning analysis of her “Big Fat Surprise” book: https://thescienceofnutrition.wordpress.com/2014/08/10/the-b...