Posted by mgh2 10/26/2024
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...
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.
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.
The problem is that we have, unfortunately, been listening.
I am so tired of this crap. Energy intake increased by something like 400kcal/day since 1960. Mostly from processed foods.
At the same time physical activity plummeted.
What do you think is the most probable explanation of obesity: the above or that we halved our SFA intake?
1. Nothing to do with saturated fat.
2. Nothing to do with the dietary guidelines.
In fact, this kind of diet that is the basis of the modern dietary recommendations because we know it is associated with good outcomes.
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.
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).
> 3 kids in kindergarten and school
I see you have chosen the path of perpetual illness and insomnia.
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 to the claims that sugar is addictive, this is unsupported - sugar does not meet the DSM-V criteria for addictive substances based on current evidence (https://link.springer.com/chapter/10.1007/978-1-4899-8077-9_...)
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
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.
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.
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.
As for whole grains vs fruit vs vegetables, here's a SR and MA of studies looking at different food groups and the RR of all cause mortality: https://www.sciencedirect.com/science/article/pii/S000291652...
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.
pic from wikipedia named USDA pyramid 1995-2005: https://en.wikipedia.org/wiki/Food_pyramid_(nutrition)#/medi...
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.
looks like I agree with you on this part: https://news.ycombinator.com/item?id=41964513
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.
(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"?)
yes, because they consists of 90%-95% of water, then if you cook them, water evaporates and you get some amount of carbs.
But leaf veggies is one side of spectrum, with refined carbs on another, there are bunch of stuff in between.
this is not my reading of that study.
This is exact example of junk science.
What differences in goals and methodologies have you identified that you believe renders them so different that they cannot be summated?
Not sure what you mean by “no indications how balanced and what components where in diets”, you’ll have to clarify.
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.
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.
So why wouldn’t replacing butter with margarine be a positive step for one’s cardiovascular risk profile?
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.
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.
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]
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.
Surely that’s both a large enough cohort and a large enough effect size to change one’s diet?
https://www.sciencedirect.com/science/article/pii/S000291652...
It's almost as if all of these studies are looking at tiny effects that they can't adequately measure, and contradicting each other.
The other study I'm mentioning :
https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD...
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.
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.
(And really, margarine can be plenty tasty. As a kid I actually preferred it to butter for some reason.)
https://youtu.be/reLIPoZQZ-8?si=lLXfhsdm89zlOWsI
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".
Policy and advocacy is deceptive, dishonest, and lacks nuance.
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.
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 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.)
https://youtu.be/qGNUPqHvTso?si=WWnY3OLALTBREVMs&t=525
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.
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.
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.
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 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
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.
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.
You see it as similar to something that never happened?
It was generally accepted that the earth was round centuries before there even was a church.
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.
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.
#/media/File:USDA_Food_Pyramid.gif){kind=link}
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.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!
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/
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/
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.
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.
Get a blood lipids panel and see what your ApoB is like!
> Maybe they are not "unique people" and there are other non-genetic reasons their blood vessels are larger.
I don't think this effect has been observed in post mortem of other populations, so that would make them fairly unique, no?
not sure how this tell me if i have 'unique feedback mechanism' . wtf does that phrase even mean.
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.
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).
This is just an hypothesis that says they "may" have adaption? Not sure how that translates to definitive "they have a unique feedback mechanism "
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.
That certainty is what led me to believe i can look up genetic markers in my 23andme.
I did read the book and it seemed well cited.
If there are no more credible reviews do you care to substantiate your specific concerns with her work?
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.
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
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.
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...
Out of curiosity, what fish are popular among Danes?
Also what do they say about milk and cheese? Any particular cheese is healthier?
Why?
Personally, I think that’s hilarious. Enjoy your bacon and butter.
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.
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?
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.
I’m not sure how you’re determining that it’s otherwise?
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.
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.
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'm much more likely to listen to a person who has a calm, neutral or positive tone than someone who is screaming the same words at me.
Words are only a part of human communication, and arguably not the most important part.
"Can I help you?" Has a vastly different meaning depending on the tone and body language of the speaker.
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)
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.
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.
Perhaps that's why there is a lot of sketchy results, hyperbole in communication, and a cycle of debunking (of the debunking) around.
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.
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).
We’re good survivors for sure, but try eating only deep fried donuts for a year and let me know how omnivorous you feel.
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.
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.
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.
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.
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.
Its isn't that someone says "Yep this all checks out and I have no further questions"
It's that this person is at least sharing references and the last person said "shut up and do what I say"
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.
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.
Buying just a couple or maybe even one can be enough, culture can take care of the rest.
Actually, the initial buy isn't even required, culture is often adequate on its own for forming collective incorrect beliefs.
Does trust in X erode when X is wrong? Yes.
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.
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.
Just get rid of the agency altogether.
https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD...
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."
This is your citation for saturated fat is evil?
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”
I explain why the null findings on insensitive endpoints aren’t the gotcha some people think they are here: https://news.ycombinator.com/item?id=41960046
they have table with breakdown of events by type, and in both rows with significant reduction it says that quality of evidence is "very low".
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_.
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.
I salute your self confidence, I must say I’m somewhat envious of it.
It’s just that you’re blaming the studies, rather than your comprehension.
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.
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.
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.
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.
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.
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.
Serum levels of saturated fat are not related to dietary saturated fat intake. https://news.osu.edu/study-doubling-saturated-fat-in-the-die...
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.
That talk is 1 of 3, they are here:
[1] The Truth about high cholesterol: https://www.youtube.com/watch?v=rdgS3PuSuyg "can we tell if we have normal or damaged LDL? Yes"
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).
Part 3: "Hard science on the real cause of heart disease - why you should avoid seed oils" - https://www.youtube.com/watch?v=-xCr3mvFCHM
[2] A comment I've made before about his views on saturated fats generally: https://news.ycombinator.com/item?id=32966148 linking to his talk "Saturated Fat is not dangerous" - https://www.youtube.com/watch?v=NUY_SDhxf4k
"Why your doctor thinks cholesterol is bad" - https://www.youtube.com/watch?v=j-nq60_oEIc
I am so confused. What on earth is a " dense Low-Density-Lipid" ?
Please help me understand whether or not this is an oxymoron?
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
I tried to come up with a corollary but the best I have is “jumbo shrimp”. Sigh.
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
Since I don't have the knowledge to read this, why is this review better than the multiple review papers Dr Mason cites in the videos I linked?
> 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?
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.
If you’d like something more consumable, lipidologist William Cromwell covers the topic very well in this video: https://youtu.be/kplh30RmYo8?si=WvDMwG-Z82voxDMp
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
It was pointed out to him that the lipid hypothesis is about P:S ratio, not total fat reduction: https://x.com/avibittmd/status/1335470882987323392?s=46 Avi explained the criteria a study would need to meet to challenge the LH: https://x.com/avibittmd/status/1335475024854192129?s=46 There’s some back and forth, eventually Mason says the rebuttal that WHI failed to significantly reduce serum cholesterol/was a failed intervention because it targeted total fat doesn’t make sense because the intervention arm of the WHI reduced their serum cholesterol by 30%,so clearly the intervention was significant according to the LH: https://x.com/drpaulmason/status/1335488114534481920?s=46 Avi asks him what he’s talking about, the serum cholesterol between intervention and control was basically the same, showing the table in the study: https://x.com/avibittmd/status/1335488453417562112?s=46
Avi suggests he might have confused serum cholesterol with dietary cholesterol: https://x.com/avibittmd/status/1335489121486299138?s=46 They share the table from the study that confirms this: https://x.com/avibittmd/status/1335491375073271808?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 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).
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!
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.
> 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.
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/
Olive oil is good, candy is bad. (News at 11.)
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.
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.
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.
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.?
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
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.
What’s the evidence for the claim “cholesterol by itself isn’t 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.
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.
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.
So for clarification on your view - do you think that high levels of LDL-C (proxying for ApoB) increase risk of CVD?
The full pathway and supporting evidence can be found here: https://academic.oup.com/eurheartj/article/41/24/2313/573522...
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.
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.
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?
[1] https://drdavisinfinitehealth.com/2019/03/why-you-should-get...
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.
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).
[1] https://myheart.net/articles/ct-coronary-artery-calcium-hear...
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).
[Edit: it isn't relebant; thickened walls would be non-obstructive CAD].
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?
[2] https://cardiovascularbusiness.com/topics/healthcare-managem... (I don't know why they don't say "CEO" but whatever, it's a high paying job, he doesn't need to be shilling anything).
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.
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.
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/...
Have a good week!
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.
Pregnant women have extremely high cholesterol (ridiculously high).
- There's a theory that if evolution designed pregnant women to have high cholesterol, then cholesterol cannot be the poison it's made out to be.
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
Here is a good overview: https://pmc.ncbi.nlm.nih.gov/articles/PMC4989641/
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.
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?
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.
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.
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?
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.
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.
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.
> 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, but it's actually very good for what is normally a progressive disease.
The experimenter is currently now doing another 7 year experiment, eating a somewhat healthier than normal diet + statins.
After getting off the ornish diet, there was hardly any change in total cholesterol.
*The diet was ornish-like because it was hard to get anything to eat when going out. The experimentar ate salmon if there was nothing better.
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!
following the normal course of events leads to subsequent surgical interventions based on the people I've seen...
Truth is, it's complicated and neither your observation, nor mine, is enough to conclude anything.
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.
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.
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.
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.
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?
> Is it better to eat 200g of bread (artisanal, wood fired, using traditionally-milled non-GMO pesticide free grains), or a steak?
I don't think there's a real answer here in a vacuum. It depends on what else you eat, your current health, your level of physical activity, etc.
https://www.nytimes.com/2007/01/28/magazine/28nutritionism.t...
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?
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.
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. )
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 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.
Ref to Cochrane: https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD...
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.
I'm sure there's more but I am out of time.
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.
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.
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.
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!).
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.
Because there's very little scientific evidence to be concerned about seed oils themselves and a lot to show that they're fine to good for you.
If you want to talk specifically about inflammation, there's not really any evidence that inflammatory markers in humans are increased by seed oils themselves, e.g. https://www.ahajournals.org/doi/10.1161/01.ATV.0000163185.28...
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.
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.
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.
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.
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.
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.
https://www.thelancet.com/journals/lancet/article/PIIS0140-6...
The BMJ got in trouble for believing her and had to issue retractions because of it:
https://www.theverge.com/2015/10/26/9616122/bmj-nina-teichol...
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.
which part of that do you consider bullying? is it any opinion that goes against the underdog?
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.
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.
Why? I am not seeing the causation. Tomatoes came from a family of plants that are not edible, and now they are consumed worldwide.
(I have it, discovered by a full-genome sequencing by myself, accidentally around the age of 50.)
It looks like the treatment involves avoiding vegetable oils, but in her case there are no visible xanthomas.
https://raypeat.com/articles/articles/unsaturated-oils.shtml
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?
that's because it's literally a 4chan /pol/ schizo theory
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.)
Here is Paul Saladino explaining it:
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.
We need our carbon chains to be consistenty hydrogenated one way or the other, but not with both types in one molecule.
Have you doing that she has the same issue with coconut oil? Specifically, the saturated ones that come in a jar?