Posted by mgh2 1 day ago
> the paradoxical epidemiological observation that French people have a relatively low incidence of coronary heart disease (CHD), while having a diet relatively rich in saturated fats,[1] in apparent contradiction to the widely held belief that the high consumption of such fats is a risk factor for CHD.
"Intersalt, a large study published in 1988, compared sodium intake with blood pressure in subjects from 52 international research centers and found no relationship between sodium intake and the prevalence of hypertension. In fact, the population that ate the most salt, about 14 grams a day, had a lower median blood pressure than the population that ate the least, about 7.2 grams a day. In 2004 the Cochrane Collaboration, an international, independent, not-for-profit health care research organization funded in part by the U.S. Department of Health and Human Services, published a review of 11 salt-reduction trials. Over the long-term, low-salt diets, compared to normal diets, decreased systolic blood pressure (the top number in the blood pressure ratio) in healthy people by 1.1 millimeters of mercury (mmHg) and diastolic blood pressure (the bottom number) by 0.6 mmHg. That is like going from 120/80 to 119/79."
[0] https://www.scientificamerican.com/article/its-time-to-end-t...
Saturated fat: the making and unmaking of a scientific consensus - https://news.ycombinator.com/item?id=33942840 - Dec 2022 (6 comments)
By the guidelines nunbers, Low is worse than normal, “normal” is low, a little high is protective when you have other morbidities…
There’s nothing “unmade” in the scientific opinion. It’s her opinion because she insists that saturated fat is good, but provides no scientific evidence. Almost all scientific studies and scientists (including the authors of the few studies she might quote, because she often distorts them including completely presenting the opposite of what they demonstrate) disagree with her saying.
And yeah, she’s not a scientist, does no scientific research herself, and has no particular training in this area.
Summary
The idea that saturated fats cause heart disease, called the diet-heart hypothesis, was introduced in the 1950s, based on weak, associational evidence. Subsequent clinical trials attempting to substantiate this hypothesis could never establish a causal link. However, these clinical-trial data were largely ignored for decades, until journalists brought them to light about a decade ago. Subsequent reexaminations of this evidence by nutrition experts have now been published in >20 review papers, which have largely concluded that saturated fats have no effect on cardiovascular disease, cardiovascular mortality or total mortality. The current challenge is for this new consensus on saturated fats to be recognized by policy makers, who, in the United States, have shown marked resistance to the introduction of the new evidence. In the case of the 2020 Dietary Guidelines, experts have been found even to deny their own evidence. The global re-evaluation of saturated fats that has occurred over the past decade implies that caps on these fats are not warranted and should no longer be part of national dietary guidelines. Conflicts of interest and longstanding biases stand in the way of updating dietary policy to reflect the current evidence.
> [nutrition experts] have largely concluded that saturated fats have no effect on cardiovascular disease, cardiovascular mortality or total mortality
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!).